Carbon Monoxide Poisoning

CARBON MONOXIDE POISONING

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CARBON MONOXIDE POISONING EDITED BY

DAVID G. PENNEY

Boca Raton London New York

CRC Press is an imprint of the Taylor & Francis Group, an informa business

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Dedication ——————— I wish to dedicate this book first to my mother, Gertrude Ellen (Goodhew) Penney, always a source of support and encouragement, to my grandchildren, and to all of those victims of carbon monoxide poisoning who sought but did not find professional help for their suffering.

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Preface Carbon Monoxide Poisoning is a new title covering further areas of the expansive field of carbon monoxide (CO) toxicology that were not covered in the first two books, Carbon Monoxide and Carbon Monoxide Toxicity, both edited by David G. Penney, PhD. Both were published by CRC Press, the first in 1996 and the second in 2000. This book is designed to be complementary to both earlier books, forging into new areas and following new themes. The scope of this book is even broader than the earlier two. The first book took a very scholarly approach, presenting the latest basic and medical science of CO toxicology in 13 chapters. The contents of that book remain current. The second book was broader in its approach, and while extending presentations of basic and medical science, added discussions of human CO exposure under specialized conditions and in geographic locations other than the United States, in 23 chapters. It also presents a large body of new data on both acute and chronic CO poisoning. This present, third book, Carbon Monoxide Poisoning, further extends these presentations both to new areas such as the law, rehabilitation, personal experience with CO poisoning, education of the public about CO using the World Wide Web, and so forth, and adds further new data on chronic CO poisoning. This book contains some unique features: 1. A critical look at the efficacy of hyperbaric oxygen therapy in decreasing the damage caused by CO poisoning 2. The use of exciting new scanning techniques in revealing damage from CO poisoning 3. The introduction of a handheld pulse-oximeter that reads COHb directly and noninvasively 4. New data showing the persistent health damage that can be caused by chronic CO poisoning 5. The dangers of CO poisoning possible in motor homes, recreational boats, and so on 6. The levels of ignorance regarding CO on the part of the general public Interest in the effects of carbon monoxide on human health has grown rapidly during the past 20+ years. Governmental agencies, private groups, and the public are concerned. While an old and familiar poison, CO remains the number one “poison” in our environment in terms of its “brain-killing” potential, and its potential for overall immediate and long-term health harm. The public and the medical community need to obtain quality information about the risks from CO and need the means to identify and manage victims of CO poisoning successfully. It is hoped that this book, and its two previous companions, will in some way be of value in meeting these challenges.

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Author David G. Penney, PhD, is a retired professor of physiology, who taught and conducted research on carbon monoxide at the School of Medicine, at Wayne State University, Detroit, Michigan. He was at one time adjunct professor of occupational and environmental health in the School of Allied Health Professions at Wayne State University. He is also a retired director of general surgical research at Providence Hospital in Southfield, Michigan, where for 12 years he directed the scholarly activities of surgical residents and attending surgeons. Dr. Penney obtained his BSc degree from Wayne State University in 1963, and his MSc and PhD degrees from the University of California, Los Angeles, in 1966 and 1969, respectively. Before coming to Wayne State University in 1977, he was a faculty member at the University of Illinois, Chicago. With his wife, Linda Mae Penney, the couple have six children. Dr. Penney’s professional interests have been focused on carbon monoxide for over 37 years, in both animal models and in humans. His special interests center around chronic CO poisoning, education of the public about the dangers of CO poisoning, the diagnosis and management of CO poisoning victims, and the medicolegal aspects of CO toxicology. Dr. Penney has assisted many national and international government and nongovernment agencies in matters involving carbon monoxide. He was among the earliest consultants to the US Environmental Protection Agency (EPA) in setting CO standards for outside air. He assisted the World Health Organization (WHO) in the late 1990s in setting similar standards for the world. He has worked with the Australian Medical Association (AMA) and with other concerned groups in Australia to attempt to stem the tide of suicides involving CO. Currently, Dr. Penney assists Underwriters Laboratory (UL) as a medical expert on CO in establishing standards for CO alarms and other gas-monitoring equipment, and major gas distributing companies in educating the public about the dangers of CO poisoning. Dr. Penney’s published works on CO include over 65 peer-reviewed research articles, several dozen other articles and abstracts, a number of review articles, book chapters, and three other books in print. At last count, Dr. Penney had more research articles and books published on the topic of CO toxicology than anyone else in the world. He has also published several other books on medical education and on Royal Oak history, and for some years wrote a column on local history for a hometown newspaper.

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Acknowledgments I wish to thank all the authors, former patients, and all who have contributed to this book. It has been a long road and at times it seemed impossible. Now it is done. Thanks to everyone. I also wish to thank Wayne State University School of Medicine and my Department of Physiology chairman, Dr. Joseph Dunbar, for granting me the time off in 2005 to get the book off the ground. I of course thank CRC – Taylor and Francis Publishers and all their employees who have been wonderful to work with these past 12 years, in developing my three books on carbon monoxide. Finally, I wish to thank my wife Linda for her constant support in developing these books, hearing my complaints, providing inspiration and also some perspiration in getting the work done. I of course thank my mother, Gertrude, for her support, encouragement and even late night help with data entry.

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Contributors Rob Aiers

Kosmas Galatsis, Ph.D.

Envirotec (UK) Ltd. Hampshire, U.K.

Microelectronics Advanced Research Corporation Center on Functional Engineered Nano Architectonics University of California Los Angeles, California

Carol L. Armstrong, Ph.D., A.B.P.N. Division of Oncology The Children’s Hospital of Philadelphia Department of Neurology University of Pennsylvania Medical School Philadelphia, Pennsylvania

Steve N.M. Collard, B.A., M.E.D. Adjunct Professor of Law Nova Southeastern University Valrico, Florida

David C. Cone, M.D. Division of Emergency Medicine Yale New Haven Hospital Yale University School of Medicine New Haven, Connecticut

Joseph A. Cramer Wyoming, Michigan

James F. Georgis, O.D. Optometry Clinic Pueblo, Colorado

James M. Gracey, Ed.D. Colorado Institute for Injury Rehabilitation, Inc. Denver, Colorado

Neil B. Hampson, M.D. Center for Hyperbaric Medicine Section of Pulmonary and Critical Care Medicine Virginia Mason Medical Center Seattle, Washington

Jacqueline L. Cunningham, Ph.D. Department of Psychology The Children’s Hospital of Philadelphia Philadelphia, Pennsylvania

Michael F. Hanzlick

Thomas M. Dydek, Ph.D., D.A.B.T., P.E.

Alastair W.M. Hay, Ph.D.

Dydek Toxicology Consulting Austin, Texas

Gas Dynamics Corporation St. Paul, Minnesota

Molecular Epidemiology Unit LIGHT Laboratories School of Medicine University of Leeds Leeds, U.K.

Peter G. Flachsbart, Ph.D., A.I.C.P.

Dennis A. Helffenstein, Ph.D.

Department of Urban and Regional Planning University of Hawaii at Manoa Honolulu, Hawaii

Colorado Neuropsychological Associates Colorado Springs, Colorado

Robert E. Engberg, B.S., P.E.

Hanzlick & Associates Highland Ranch, Colorado

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Contributors

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Gunnar Heuser, M.D., Ph.D.

Joshua A. Mott, Ph.D.

Neuromed and Neurotox Associates Santa Barbara, California Clinical Assistant Professor University of California, Los Angeles Los Angeles, California

CDC/CCID/NCIRD Air Pollution and Respiratory Health Branch National Center for Environmental Health Atlanta, Georgia

S. Gregory Hipskind, M.D., Ph.D. Department of Anthropology Western Washington University Bellingham, Washington

Ramona O. Hopkins, Ph.D. Psychology Department and Neuroscience Center Brigham Young University Provo, Utah

Gary Hutter, Ph.D. Meridian Engineering & Technology, Inc. Glenview, Illinois

David G. Penney, Ph.D. Wayne State University School of Medicine, and Providence Hospital and Medical Centers (retired) St. Augustine, Florida & Beulah, MI

Linda M. Penney St. Augustine, FL & Beulah, MI

Kevin J. Reilly, Jr.

Richard Karg, B.S., M.S.

Training Operations & Firefighter Diversified Security Solutions, Inc. Saddle Brook, New Jersey

R.J. Karg Associates Topsham, Maine

James W. Rhee, M.D.

Michael E. King, Ph.D. CDC/CCEHIP/NCEH Air Pollution and Respiratory Health Branch National Center for Environmental Health Atlanta, Georgia

Jerrold B. Leikin, M.D. Rush Medical College Chicago, Illinois and Evanston Northwestern Health Care Glenview, Illinois

Section of Emergency Medicine & Medical Toxicology The University of Chicago Chicago, Illinois

Frank Ricci New Haven City Fire Department New Haven, Connecticut

Carlos D. Scheinkestel, M.D. Monash University Melbourne, Australia

Jane Brown McCammon, B.S., M.S.

Robert E. Schreter, B.S., P.E.

Double Angel Foundation Broken Circle M Consulting, LLC Littleton, Colorado

R. Schreter and Associates, Inc. Roswell, Georgia

Peter Tikuisis, Ph.D. Ian L. Millar Monash University Melbourne, Australia

Human Modeling Group Defence Research & Development Canada Toronto, Ontario, Canada

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Contributors

Christian Tomaszewski, M.S., M.D., F.A.C.E.P., F.A.C.M.T. Department of Emergency Medicine University of Pittsburgh Medical Center Hannad Medical Corporation Doha, Qatar

Suzanne R. White, M.D., F.A.C.M.T., F.A.C.E.P. Children’s Hospital of Michigan Regional Poison Control Center Department of Emergency Medicine Wayne State University School of Medicine Detroit, Michigan

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Stephen P. Willison, B.S., J.D. Willison & Hellman, P.C. Grand Rapids, Michigan

Wojtek B. Wlodarski, D.Sc., Ph.D., M.Sc. E.E. School of Electrical and Computer Systems Engineering Royal Melbourne Institute of Technology University Melbourne, Victoria, Australia

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Table of Contents Table of Contents for Carbon Monoxide Toxicity, 2000 . . . . . . . . . . . . . . . . . . . . . . . . .

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Table of Contents for Carbon Monoxide, 1996 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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Chapter 1 Introduction to and Overview of the Field . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . David G. Penney

1

Chapter 2 Exposure to Ambient and Microenvironmental Concentrations of Carbon Monoxide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Peter G. Flachsbart Chapter 3 Carbon Monoxide Build-Up in Houses and Small Volume Enclosures. . . . . . . . . Robert E. Engberg Chapter 4 Formation and Movement of Carbon Monoxide into Mobile Homes, Recreational Vehicles, and Other Enclosures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Robert E. Schreter Chapter 5 Carbon Monoxide Emissions from Gas Ranges and the Development of a Field Protocol for Measuring CO Emissions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Richard Karg Chapter 6 Investigating Carbon Monoxide-Related Accidents Involving Gas-Burning Appliances . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Michael Hanzlick Chapter 7 Carbon Monoxide Dangers in the Marine Environment. . . . . . . . . . . . . . . . . . . . . . . . . Jane McCammon

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5

43

57

99

129

157

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Contents

Chapter 8 Application of Warnings and Labels for Carbon Monoxide Protection . . . . . . . . . Gary Hutter Chapter 9 Public Health Surveillance for Carbon Monoxide in the United States: A Review of National Data. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Michael E. King and Joshua A. Mott Chapter 10 Carbon Monoxide Sensors and Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Kosmas Galatsis and Wojtek Wlodarski Chapter 11 Marketing of Carbon Monoxide Information and Alarms in Europe and Beyond: Use of the World Wide Web in Saving Lives . . . . . . . . . . . . . . . . . . . . . . . . . . Rob Aiers

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Chapter 12 Investigating Carbon Monoxide Poisonings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Thomas M. Dydek

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Chapter 13 Carbon Monoxide Detectors as Preventive Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . James W. Rhee and Jerrold B. Leikin

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Chapter 14 Misconceptions About Carbon Monoxide. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . David G. Penney

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Chapter 15 A Survey Study of Public Perceptions About Carbon Monoxide . . . . . . . . . . . . . . . David G. Penney and Linda M. Penney

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Chapter 16 Treatment of Carbon Monoxide Poisoning. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Suzanne R. White

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Chapter 17 The Case for the Use of Hyperbaric Oxygen Therapy in Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Christian Tomaszewski

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Contents

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Chapter 18 Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning: Useful Therapy or Unfulfilled Promise? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Carlos D. Scheinkestel and Ian L. Millar Chapter 19 A Challenge to the Healthcare Community: The Diagnosis of Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . David G. Penney Chapter 20 Neuroimaging after Carbon Monoxide Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gunnar Heuser

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Chapter 21 Recent Advances in Brain SPECT Imaging after Carbon Monoxide Poisoning 457 S. Gregory Hipskind Chapter 22 Neurocognitive and Affective Sequelae of Carbon Monoxide Poisoning . . . . . . Ramona O. Hopkins Chapter 23 Neurocognitive and Neurobehavioral Sequelae of Chronic Carbon Monoxide Poisoning: A Retrospective Study and Case Presentation . . . . . . . . . . . . . . . . . . . . . . . Dennis A. Helffenstein Chapter 24 Chronic Carbon Monoxide Poisoning: A Case Series . . . . . . . . . . . . . . . . . . . . . . . . . . . David G. Penney Chapter 25 Functional and Developmental Effects of Carbon Monoxide Toxicity in Children . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Carol L. Armstrong and Jacqueline Cunningham Chapter 26 Issues in Rehabilitation and Life Care Planning for Patients with Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . James M. Gracey Chapter 27 Treatment of Carbon Monoxide Poisoning with Yoked Prism Lenses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . James F. Georgis

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495

551

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591

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Contents

Chapter 28 Firefighters and Carbon Monoxide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Kevin J. Reilly, Jr., Frank Ricci, and David Cone Chapter 29 The Purpose and the Process of Litigation in a Carbon Monoxide Poisoning Case . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Stephen P. Willison

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Chapter 30 Offering Expert Opinions in a Carbon Monoxide Case . . . . . . . . . . . . . . . . . . . . . . . . . Stephen P. Willison

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Chapter 31 Injury Caused by Carbon Monoxide Poisoning: Defining Monetary Damages Steve Collard

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Chapter 32 My Carbon Monoxide Poisoning: A Victim’s Story . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Joseph A. Cramer

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Chapter 33 Noninvasive Measurement of Blood Carboxyhemoglobin with Pulse CO-Oximetry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Neil B. Hampson Chapter 34 Chronic Carbon Monoxide Exposure: How Much Do We Know About it?—an Update . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Alastair W.M. Hay

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Chapter 35 Essential Reference Tables, Graphs, and Other Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . David G. Penney

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Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

765

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Table of Contents for Carbon Monoxide Toxicity 2000

Chapter 1 History of Carbon Monoxide Toxicology Dieter Pankow Chapter 2 Carbon Monoxide in Breath, Blood, and Other Tissues Hendrik J. Vreman, Ronald J. Wong, and David K Stevenson Chapter 3 Carbon Monoxide Detectors Richard Kwor Chapter 4 The Setting of Health-Based Standards for Ambient Carbon Monoxide and Their Impact on Atmospheric Levels James A. Raub Chapter 5 Effect of Carbon Monoxide on Work and Exercise Capacity in Humans Milan J. Hazucha Chapter 6 The Interacting Effects of Altitude and Carbon Monoxide James J. McGrath Chapter 7 Interactions Among Carbon Monoxide, Hydrogen Cyanide, Low Oxygen Hypoxia, Carbon Dioxide, and Inhaled Irritant Gases David A. Purser Chapter 8 Carbon Monoxide Poisoning and Its Management in the United States Neil B. Hampson

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Contents

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Chapter 9 Death by Suicide Involving Carbon Monoxide around the World Pierre Baume and Michaela Skopek Chapter 10 Carbon Monoxide as an Unrecognized Cause of Neurasthenia: A History Albert Donnay Chapter 11 Update on the Clinical Treatment of Carbon Monoxide Poisoning Suzanne R. White Chapter 12 Treatment of Carbon Monoxide Poisoning in France Monique Mathieu-Nolf and Daniel Mathieu Chapter 13 Acute Carbon Monoxide Poisonings in Poland - Research and Clinical Experience Jerzy A. Sokal and Janusz Pach Chapter 14 Treatment of Carbon Monoxide Poisoning in the United Kingdom Martin R. Hamilton-Farrell and John Henry Chapter 15 Carbon Monoxide Air Pollution and Its Health Impact on the Major Cities of China Qing Chen and Lihua Wang Chapter 16 Use of Scanning Techniques in the Diagnosis of Damage from Carbon Monoxide I.S. Saing Choi Chapter 17 Low-Level Carbon Monoxide and Human Health Robert D. Morris Chapter 18 Chronic Carbon Monoxide Poisoning David G. Penney Chapter 19 Chronic Carbon Monoxide Exposure: The CO Support Study Alistair WM. Hay, Susan Jaffer, and Debbie Davis

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Contents

Chapter 20 Neuropsychological Evaluation of the Carbon Monoxide-Poisoned Patient Dennis A. Helffenstein Chapter 21 Pediatric Carbon Monoxide Poisoning Suzanne R. White Chapter 22 Carbon Monoxide Production, Transport, and Hazard in Building Fires Frederick W. Mowrer and Vincent Brannigan Chapter 23 Approaches to Dealing with Carbon Monoxide in the Living Environment Thomas H. Greiner and Charles V. Schwab

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Table of Contents for Carbon Monoxide 1996

Chapter 1 Carbon Monoxide Analysis Roger L. Wabeke Chapter 2 Carbon Monoxide Formation Due to Metabolism of Xenobiotics Dieter Pankow Chapter 3 Modeling the Uptake and Elimination of Carbon Monoxide Peter Tikuisis Chapter 4 Cerebrovascular Effects of Carbon Monoxide Mark A. Helfaer and Richard J. Traystman Chapter 5 Pulmonary Changes Induced by the Administration of Carbon Monoxide and Other Compounds in Smoke Daniel L. Traber and Darien W Bradford Chapter 6 Effects of Carbon Monoxide Exposure on Developing Animals and Humans David G. Penney Chapter 7 Carbon Monoxide - From Tool to Neurotransmitter Nanduri R. Prabhakar and Robert S. Fitzgerald Chapter 8 Toxicity of Carbon Monoxide: Hemoglobin vs. Histotoxic Mechanisms Claude A. Piantadosi

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Contents

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Chapter 9 Carbon Monoxide-Induced Impairment of Learning, Memory, and Neuronal Dysfunction Masayuki Hiramatsu, Tsutomu Kameyama, and Toshitaka Nabeshima Chapter 10 Behavioral Effects of Carbon Monoxide Exposure: Results and Mechanisms Vernon A. Benignus Chapter 11 Delayed Sequelae in Carbon Monoxide Poisoning and the Possible Mechanisms Eric Kindwall Chapter 12 Treatment of Carbon Monoxide Poisoning Suzanne R. White Chapter 13 Options for Treatment of Carbon Monoxide Poisoning, Including Hyperbaric Oxygen Therapy Stephen R. Thom

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1

Introduction to and Overview of the Field David G. Penney

CONTENTS References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

4

I have designed this book to complete the series on carbon monoxide (CO) begun with Carbon Monoxide, 19961 and continued with Carbon Monoxide Toxicity, 2000.2 This and the second book are NOT new editions of the first book, as has often been assumed. While CO may seem a very narrow subject area, it finds its way into many diverse disciplines and its literature is vast. This third book, Carbon Monoxide Poisoning, completes the trilogy and should become a standard reference source on CO for years to come. The new book covers areas not previously presented, including rehabilitation, education of the public using the WWW, litigation involving CO poisoning, economic loss assessment, and firefighting. There are areas of update, such as the chapter by Dr. Suzanne White, on diagnosis and management. There are two chapters in which the authors take opposing views, one stating the case for use of hyperbaric oxygen therapy (HBOT) by Dr. Christian Tomaszewski and against the use of HBOT by Dr. Carlos Scheinkestel. One chapter deals with toxicology investigation (i.e., forensic) procedures. A series of chapters detail the risk of CO poisoning from kitchen ranges, recreational trailers and motor homes, and recreational powerboats. Three chapters cover the very important area of neuropsychological evaluation of adults and children following CO poisoning. The chapter by Dr. Dennis Helffenstein presents new data on a case series of patients that had sustained chronic CO poisoning. I have written a companion chapter to his in which a retrospective review of 61 chronically CO-poisoned patients were symptomatically evaluated (Chapter 24). Better Education of Physicians: This is essential if CO-poisoned patients are to be properly diagnosed and treated in the future. Several years ago I overheard a prominent emergency room physician say, “the standard of care for CO poisoning in the U.S. is less than the standard of care.” I estimate that in 80% of CO cases reviewed, one, two, or more mistakes were made in diagnosing and/or treating CO-poisoned patients. This may involve misdiagnosis, dependence on faulty pulse-oximetry data, administering NBO with the wrong 1

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2

Carbon Monoxide Poisoning

equipment (e.g., nasal prongs), failure to order HBOT when it was needed and possible, discharge of patients while still symptomatic, and so forth. Physicians should also be informed of the possible serious permanent health harm that chronic or lower-level acute CO poisoning can cause if not diagnosed immediately and treated fully. From my perspective, the CO cases that result from acute poisoning and those most likely to reach the media are actually the smaller fraction of all CO poisonings, while the chronic (i.e., occult) CO poisonings make up by far the largest fraction, and probably result in the most injuries, but they are the very group that physicians are least trained to properly deal with. Better Education of the Public: The public too needs education about the dangers presented by CO exposure. My chapter presenting the results of surveys of public perceptions of CO in Michigan and Florida shows this. While almost everyone knows that CO is a deadly poison, substantial fractions (sometimes most) of the adult and juvenile population cannot intelligently evaluate the risk of CO from automobiles, propane radiant heaters, generators, and recreational powerboats. In some situations people are overly cautious in a given situation, but in other situations people vastly underestimate the risk of injury and death. Youth, as opposed to adults, are particularly uninformed. New Approaches to Treating Acute, Severe CO Poisoning: There appears to be very little new in treating acute severe CO poisoning. We cannot decide for sure whether HBOT is more effective in reducing neurologic sequelae, even though it has been used for approximately 50 years. The pros and cons chapters on HBOT provide detailed discussions of many aspects of the situation, and a few ideas about possible new approaches. The bright light in this area is almost certainly the new generation of pulse-ox devices that read COHb directly and noninvasively. See Dr. Neil Hampson’s chapter about the testing of this device. Requiring Proper Warnings on Combustion Equipment: The lack of proper and adequate warnings on equipment that do, or under foreseeable conditions might, emit harmful or lethal amounts of CO remains a real problem. People continue to die because warnings on combustion devices are not obvious, explicit and direct, and not on the device itself. Warnings in operating manuals should be continued and improved, but they alone are insufficient because manuals are usually separated from the device. Warnings on the device must tell the user what might occur in using the device a certain way. Statements such as “provide adequate ventilation” are useless. The warning must specify where and when not to use the device, and for how long. Warnings in the United States should be written in both English and Spanish, along with standard prohibition symbols. Some of the devices this applies to include portable generators, cement saws, lawn mowers, pressure washers, scissor-lifts, kerosene heaters, propane-radiant heaters, lamps and cook stoves, powerboats, charcoal grills and hibachis, and so forth. See Dr. Hutter’s excellent chapter on warnings.

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Introduction to and Overview of the Field

Rethinking Work Guidelines for Carbon Monoxide that Reflect the Science: Another area that needs immediate attention is threshold limit standards for inhalation of CO. Environmental Protection Agency (EPA) and World Health Organization (WHO) after extensive study and deliberation some years ago set the 8-h standard at 9 ppm, or 10 mg/m3 for outside air. On the other hand, National Institute for Occupational Safety and Health (NIOSH) and Occupational Safety and Health Administration (OSHA) have set different standards for the work environment. We know that people with coronary artery disease, congestive heart failure, asthma, and a state of fetal development are often members of the workforce, and represent a more sensitive, higher risk subgroup of the general population. It is also well known that people, even those with no obvious risk factors, vary widely in their tolerance of CO. Why then should the standards be so different—9 ppm (EPA, WHO) versus 50 ppm (OSHA) for the same species? This is a 5-1/2 fold difference! I believe it is time we in the toxicology community re-examine ambient air CO concentration work standards, and make decisions for new standards based only on the best science. Realization that Brain Damage Resulting from CO Poisoning Is not Dependent on COHb and/or Severity of Poisoning: New studies make it clear what many of us have believed for some time based on experience, that brain damage from CO poisoning is only very poorly correlated with the severity of the poisoning by whatever criteria, even the COHb saturation. Some people with very severe poisoning and/or high initial COHb values make remarkable recoveries, while some with what appears to be minimal poisoning, and even on occasion, near normal COHb when measured, incur substantial damage. Clearly, loss of consciousness is not required for the development of neurologic sequelae, although I sometimes hear the less well-informed say that it is. I believe everyone agrees that a longer (i.e., soaking) exposure is more detrimental than a short one, but strangely some still insist that chronic, lower-level CO exposure can cause no permanent harm. Other markers for brain damage have been proposed such as acidosis, gait/balance/clumsiness on presentation, and release of cellular enzymes, but it remains unclear how useful they are. Carbon Monoxide Disaster Management: Release of CO during certain kinds of disasters could pose significant problems. Fire almost invariably gives off CO as an incomplete combustion product, and fire is a larger or a smaller component in most disasters, especially those that might be instigated by terrorists. It is unclear to me whether any overall planning has been done by agencies of the government with respect to CO. Firefighters regularly encounter CO in the work they do, and have equipment such as self-contained breathing apparatus to deal with it. See the chapter on firefighting by Mr. Reilly, Mr. Ricci, and Dr. Cone. Other concerns for human health that may not yet be fully addressed include indoor car, monster truck, and motocross events, work in coal mines, warehouses, enclosed construction sites, and so forth where significant CO is generated by combustion devices. Since it is dangerous and

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foolhardy to run a portable generator inside a garage or house, why is it not dangerous to human health to run several monster trucks with huge gasolinefueled engines lacking catalytic converters inside a covered sports stadium? The recent Sago Mine disaster where a dozen men died slowly, mainly from CO poisoning, points out the need for adequate emergency equipment that would allow men to live for extended periods of time in the presence of lethal CO air concentrations. Autostarters—are they safe? How often will car engines be started inadvertently (by children, otherwise by mistake) in a closed garage, leading to injury or death from CO poisoning? The wonder is that CO has been with man since prehistory, probably since we first began using fire. Other scourges such as plague, cholera, typhus, smallpox, and so forth are gone, at least from the developed world, whereas this simple, small molecule, CO, continues to afflict us, and probably will, at least as long as we are wedded to the “carbon energy cycle.” I hope you enjoy this book and will use it with its earlier brothers, Carbon Monoxide (1996)1 and Carbon Monoxide Toxicity (2000).2

References 1. Penney, D.G., ed. Carbon Monoxide, CRC Press, NY, 1996, 296 pp. 2. Penney, D.G., ed. Carbon Monoxide Toxicity, CRC Press, NY, 2000, 560 pp.

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2

Exposure to Ambient and Microenvironmental Concentrations of Carbon Monoxide Peter G. Flachsbart

CONTENTS 2.1 2.2

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Standards and Guidelines for Exposure to Ambient Concentrations of Carbon Monoxide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.3 Trends in Carbon Monoxide Emissions and Ambient Air Quality . . . . . . . 2.4 Human Exposure to Carbon Monoxide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5 Microenvironmental Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.1 Residential Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.1.1 Nonfatal Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.1.2 Fatal Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.2 Occupational Exposures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.3 Shopping Center Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.4 Recreational Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.4.1 Exposures on Recreational Vehicles . . . . . . . . . . . . . . . . . . . . 2.5.4.2 Exposures at Indoor Sporting Events . . . . . . . . . . . . . . . . . . . 2.5.5 Commuter Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.5.1 Defective Exhaust Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.5.2 Parking Garages . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.5.3 Service Stations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.5.4 Drive-Up Facilities. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.5.5 Airbag Deployment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5.5.6 Motor Vehicle Emission Standards. . . . . . . . . . . . . . . . . . . . . . 2.6 Exposure to Methylene Chloride . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.6.1 Nonoccupational Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.6.2 Occupational Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.7 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.8 Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

6 7 8 10 17 17 18 19 20 22 23 23 24 25 26 29 29 29 30 30 31 31 32 32 34 34 5

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2.1 INTRODUCTION Carbon monoxide (CO) is a gas commonly produced by incomplete combustion of fuels containing carbon atoms. Many people use these fuels (i.e., coal, gasoline, kerosene, natural gas, oil, propane, and wood) around the globe. As a result, CO is ubiquitous in the atmosphere. However, without sophisticated instruments, a person is unable to detect CO, because the gas is not irritating and has no color, odor, or taste. Moreover, the gas is a potential health hazard, because exposure to CO can starve critical body organs, especially the brain and heart, of oxygen. Once inside the lungs, CO molecules pass easily into the bloodstream and compete with oxygen for hemoglobin (Hb) in the red blood cells. About 95% of the absorbed CO readily binds with Hb to form carboxyhemoglobin (COHb), because the affinity of Hb for CO is over 200 times stronger than it is for oxygen. Thus, the percentage of total Hb in the blood that is in the form of COHb is a biomarker of CO exposure.1 The health effects of CO, which are a function of its concentration and the duration of exposure, range from subtle to severe. They include neurobehavioral, cardiovascular, and developmental effects, observed at low levels of CO exposure, to unconsciousness and death, which occur after acute exposure to high CO concentrations. Lethal CO exposures are usually linked to CO concentrations greater than 1000 parts per million (ppm) by volume. Coma, convulsions, cardiopulmonary arrest, and death have been observed when COHb levels reach 50%, although death from CO poisoning is frequently reported at far lower COHb saturations. The exact COHb concentrations that trigger acute and chronic health effects in different people differ widely. Sublethal levels of CO may cause neurological-type symptoms, including fatigue, headache, nausea, vomiting, deficit in short-term memory, to name a few. Exposures to these CO concentrations are often misdiagnosed as viral illness, clinical depression, and so forth. Still lower CO exposures (i.e., those producing less than 10% COHb) may not be associated under certain circumstances with overt symptoms.2,3 This broad range of effects makes CO relevant to people concerned with ambient air quality management as well as officials responsible for protecting public health and safety. Ambient air quality standards are the foundation of air quality management programs in many countries worldwide. Such standards typically specify maximum permissible concentrations in ambient air for certain pollutants. To achieve ambient standards in the United States, the U.S. Environmental Protection Agency (EPA) implemented progressively tighter tailpipe emission standards for motor vehicles. As a result, these standards have substantially reduced ambient CO concentrations in most metropolitan areas of the U.S. and have had other collateral benefits. For example, the nation had 11,667 fewer deaths from accidental CO poisoning between 1968 and 1998, according to a study by the Centers for Disease Control and Prevention (CDCP).4 Still, an average of 480 U.S. residents died each year during 2001–2002 from nonfire-related unintentional CO poisoning. In addition, an estimated 15,200 persons, that is, people with confirmed or possible nonfire-related CO exposure or poisoning, were treated annually in U.S. hospital emergency rooms.5 In fact, more than 50% of all fatal poisonings reported in many countries may be attributable to CO, because these cases are under-reported or misdiagnosed by medical professionals.2

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This chapter explores reasons behind the paradox of declining ambient CO concentrations in urban areas of the United States coupled with persistent injuries and fatalities from CO poisoning. The chapter is organized around the superposition principle of CO exposure, which may help to explain this paradox. This principle holds that CO concentrations at any given point in time and space consist of both ambient and microenvironmental components. The next section takes a closer look at ambient CO concentrations in urban areas. The chapter then describes how the development of portable monitors enabled measurements of personal exposure to CO concentrations in places where people perform routine daily activities. Since these activities often occur in specific microenvironments, the chapter then describes typical CO exposures where people live, work, shop, play and commute, and factors that affect these exposures. The last section offers some concluding thoughts.

2.2 STANDARDS AND GUIDELINES FOR EXPOSURE TO AMBIENT CONCENTRATIONS OF CARBON MONOXIDE The Clean Air Act (CAA) of 1963 was amended by the U.S. Congress in 1970, 1977, and 1990. The 1977 and 1990 versions largely reaffirmed the course set by the 1970 amendments.6 Under the 1970 CAA amendments, the U.S. EPA established the National Ambient Air Quality Standards (NAAQS) and set deadlines for their attainment. The current NAAQS reflect EPA’s scientific judgments about maximum allowable ambient concentrations and averaging times for certain “criteria” air pollutants including CO. Criteria air pollutants are those that could reasonably endanger public health or welfare. The 1970 and 1990 CAA amendments also mandated stringent motor vehicle emission standards as a means to achieve the NAAQS for CO and other air pollutants that have been linked to mobile sources. Air pollutant concentrations can be expressed either as ppm or as milligrams per cubic meter (mg/m3 ) of air. Many of the studies reviewed in this chapter refer to the NAAQS for guidance on allowable limits of CO exposure. The EPA promulgated identical primary and secondary NAAQS for CO on April 30, 1971. The primary standards specify a level of air quality sufficient to protect public health and the secondary standards are intended to protect public welfare. The standards include “an adequate margin of safety” to reflect scientific uncertainties related to measurement of the effects of air pollutant exposure in the population. In 1985, EPA rescinded the secondary standard for CO, but retained two primary standards: 9 ppm (10 mg/m3 ) as an 8-h average and 35 ppm (40 mg/m3 ) as a 1-h average. Each standard may be exceeded once per year in an air quality control region (AQCR) without violating the standard.7 The NAAQS for CO are designed to keep COHb levels below 2% in the blood of 99.9% of nonsmoking healthy adults and people who belong to probable high-risk groups. Smokers are excluded because they may exhale more CO into the air than they are inhaling from the ambient environment. The high-risk groups include the elderly; pregnant women; fetuses; young infants; and those suffering from anemia or certain other blood, cardiovascular, or respiratory diseases. People at greatest risk

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from exposures to ambient CO levels are those with coronary artery disease. Some of these people suffer myocardial ischemia as identified by ST-segment depression, during exercise when their COHb levels ≥ 2.4%.7 The symptoms of this disease are spasmodic attacks of chest pain (angina pectoris) caused by insufficient oxygen in the heart muscles. Controlled laboratory studies are needed to observe these health effects, because the COHb levels are at or near the lower margin of detection of current instruments.8 Although annual death rates from heart disease have been declining since 1980, heart disease is still America’s leading cause of death.9 Coronary artery disease reduces a person’s circulatory capacity, which is particularly critical during exercise when muscles need more oxygen. Given the widespread prevalence and lack of awareness of coronary heart disease, Godish3 argues that a significant number of people still may be at risk from CO exposure, even if ambient CO concentrations do not exceed the 8-h NAAQS for CO. The World Health Organization (WHO) guidelines for CO (see below) are also relevant to this discussion. Relative to the NAAQS for CO in the U.S., these guidelines have an identical 8-h concentration but a lower 1-h concentration. Unlike the NAAQS, the guidelines specify maximum concentrations for two shorter time spans (30 min and 15 min).10,11 Maximum Concentrations

Averaging Times

9 ppm (10 mg/m3 ) 25 ppm (30 mg/m3 ) 50 ppm (60 mg/m3 ) 90 ppm (100 mg/m3 )

8h 1h 30 min 15 min

WHO’s guidelines are intended to prevent blood levels of COHb from exceeding 2.5–3% in nonsmoking populations even when a person engages in relatively heavy work. Romieu12 reported that average COHb levels are about 1.2–1.5% in the general population and from 3% to 4% in the blood of cigarette smokers.

2.3 TRENDS IN CARBON MONOXIDE EMISSIONS AND AMBIENT AIR QUALITY The CAA amendments have substantially reduced nationwide CO emissions, even as other socio-economic indicators of growth have increased. For example, between 1970 and 2002, nationwide emissions of CO fell 48%, despite national increases of 38% in population, 155% in vehicle miles of travel (VMT), and 164% in gross domestic product.13 The rapid growth of VMT has been attributed to the decentralization of jobs and housing within urban regions during the post World War II era.14 The CAA amendments have also reduced ambient CO concentrations in urban areas of the United States. The U.S. EPA determines compliance with the NAAQS based on measurements of ambient air quality made by a nationwide network of fixed-site monitoring (FSM) stations. Ambient concentrations of air pollutants are

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typically measured in air “external to buildings, to which the general public has access.”15 In urban areas, most ambient stations that measure CO concentrations are located near roadways.16 These stations use nondispersive infrared reference (NDIR) spectrometry to measure ambient CO concentrations. Monitoring instruments based on the NDIR method are large, complex and expensive, and require a vibration-free, air-conditioned facility for the production of accurate and reliable data. The nationwide network consists of state and local air monitoring stations (SLAMS), which send data to EPA’s Aerometric Information Retrieval System (now Air Quality System) within six months of acquisition.17 Several stations within the SLAMS network belong to a network of national air monitoring stations (NAMS) to enable national assessments of air quality. FSM stations typically reveal two peaks in ambient CO concentrations. These peaks usually coincide with periods of congested rush-hour traffic.7 For that reason, some exposure analysts consider CO to be a signature air pollutant for mobile sources. On a nationwide basis, the EPA’s annual emissions inventory revealed that highway vehicles accounted for 62.8% of the 93.7 million tons of CO emitted from all sources except fires in 2003.13 Regional inventories show that motor vehicles account for even higher percentages of all CO emissions released into the ambient air. For example, CO emissions from motor vehicles ranged from 78% of all CO emissions in Fairbanks, Alaska, to 96% of all CO emissions in Phoenix, Arizona. EPA classified both cities as having “serious” levels of ambient CO concentrations in 1999.18 An ambient station is considered to be in violation (i.e., nonattainment) of the NAAQS for CO, if it records a nonoverlapping average concentration that exceeds either the 1-h or 8-h standard more than once per calendar year. The historical record shows that cities have had more difficulty satisfying the 8-h standard than the 1-h standard. For the 8-h standard, the nonoverlapping average omits other high values that occur within 8 h of the first value. Also, values of 9.5 ppm, or greater, are counted as exceeding the 8-h standard due to the standard’s rounding convention. Maximum 8-h average CO concentrations typically exceeded 30 ppm when continuous monitors were first installed in some U.S. cities in the early 1960s. When EPA promulgated the NAAQS for CO in 1971, 91.4% of 58 ambient monitors recorded violations of the 8-h standard and 12.1% of 58 stations recorded violations of the 1-h standard.16 In 1996, EPA’s Office of Air Quality Planning and Standards (OAQPS) reported that CO levels exceeded the NAAQS in seven counties, which had a combined population of more than 12.7 million people.19 The CAA amendments require states to develop plans to achieve and maintain ambient air quality that satisfies the NAAQS. To prepare these plans, states inventory emissions in each AQCR for a baseline year and determine the necessary emission reductions to achieve the NAAQS. Pursuant to the 1977 CAA amendments, many states established inspection and maintenance (I/M) programs as required by their plans for those regions that were in nonattainment of the NAAQS. An AQCR must satisfy the CO NAAQS for two consecutive years to be considered in attainment by EPA. States must submit plans to EPA showing how the region will maintain that attainment for at least 10 years. As of March, 2006, OAQPS reported that there were 38 CO “maintenance areas” in the United States encompassing 89 counties with a combined population of 46.8 million people.20

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Since 1995, 11 cities have reported violations of the 8-h standard and no monitor has reported a violation of the 1-h standard.16 Violations appear to persist in areas with meteorological and/or topographical handicaps. Meteorological handicaps make it particularly difficult for cities to satisfy the standard, because of the stochastic nature of ambient air pollutant concentrations. For example, violations of the NAAQS for CO in Fairbanks, Alaska, have been attributed to stagnant air masses during winter months. The atmosphere is more stable in Fairbanks during winter, because less sunlight causes ground-level temperature inversions to occur more frequently. Also, less air pollutant dispersion occurs in winter, because winds are milder and mountains surrounding the city hinder horizontal dispersion.16 As of March 2006, the EPA had classified five American cities (El Paso, Texas; Las Vegas and Reno, Nevada; the Los Angeles South Coast Air Basin, California; and Missoula, Montana) as urban areas that were in nonattainment of the NAAQS for CO. They represented eight counties with a total population of about 15.4 million people.21 Compared to 1996, there was one more county in nonattainment of the NAAQS for CO by 2006, and the total population living in such areas had increased by 21.3%.

2.4 HUMAN EXPOSURE TO CARBON MONOXIDE The study of population exposure is multidisciplinary and the definition of personal exposure has evolved over time. A recent definition states that exposure is the contact between an agent and a target at a specified contact boundary, defined as a surface in space containing at least one exposure point, that is, a point at which contact occurs. According to this definition, an inhaled CO molecule (the agent) reaches a human (the target) at the lining of the lung (the contact boundary), where CO exchange takes place between air and blood.22 Actual studies of CO exposure use small-scale portable monitors to measure CO concentrations within a few feet of a person’s nasal and oral cavities. These studies assume that the air surrounding the person is well mixed and that measured CO concentrations in that air represent the person’s actual exposure from CO inhalation. Besides inhalation exposure to CO, metabolic degradation of many drugs, solvents (e.g., methylene chloride), and other compounds of CO can elevate levels of COHb in a person’s blood. Because the endogenous production of CO from drugs and solvents may continue for several hours, it can prolong any cardiovascular stress from COHb. Moreover, the maximum COHb level from endogenous CO production can last up to twice as long as COHb levels caused by comparable exposures to exogenous CO.23,24 Hence, this chapter also discusses the literature on exposure to methylene chloride. Figure 2.1 illustrates an individual’s air pollutant exposure over time. In this figure, the function Ci (t) describes the CO concentration to which an individual i is exposed at any point in time t. Ott defined this event as the instantaneous exposure of an individual.25 The shaded area under the curve represents the accumulation of instantaneous exposures over some period of time (t1 − t0 ). This area also is equal to the integral of the air pollutant concentration function, Ci (t), between t0 and t1 . Ott defined the quantity represented by this area as the integrated exposure. An exposure analyst can derive the average concentration to which a person is exposed

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Concentration

Ci (t )

t0

t1 Time

FIGURE 2.1 Exposure of person i to air pollutant concentration (C) as a function of time t.

by dividing the person’s integrated exposure by the period of integration (t1 − t0 ). This average concentration is sometimes referred to as the average exposure. To compare the average concentration with an established air quality standard, the period of integration should equal the averaging period of the standard. This concept of exposure thus combines two parameters, the air pollutant concentration and the time duration of exposure to the air pollutant. An exposure analyst assumes that these two parameters are directly proportional to the dosage of CO in the body, as represented by the level of COHb in the blood stream, and ultimately to health outcomes. Prior to the use of portable monitoring devices, exposure analysts relied on ambient data from FSM stations in urban areas to estimate population exposure. Such data were used to provide crude estimates of population exposure to CO concentrations that violated the NAAQS. For example, the President’s Council on Environmental Quality (CEQ) did a crude estimate of population exposure to CO in the late 1970s.26 This method is based on data collected for each county in the United States. The estimate is derived as follows: TPE =

n


(pi )(di )

(2.1)

i=1

where TPE = the total population exposure in the United States (person-days) = the resident population of county i (persons) pi di = the number of days in a calendar year that violations of the NAAQS for CO are observed in county i (days) n = the total number of counties in the United States in a given year

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For 1978, the CEQ estimated that the nation’s total population exposure above the 1-h NAAQS for CO of 35 ppm was 2.80 billion person-days. This represented about 3.7% of the total possible exposures of 75.555 billion person-days, which was derived by multiplying an estimated 207 million U.S. residents in 1978 times 365 days in a year.26 CEQ’s method was a crude estimate of total population exposure, because the estimate rested on three major assumptions: 1. The CO concentrations measured by the county’s fixed-site monitors were representative of concentrations to which residents were actually exposed. If a county had more than one fixed-site monitor, then the monitor with the worst CO concentration represented the exposure of all residents in the county. 2. Residents did not leave the county on days that violations of the NAAQS for CO occurred for that county. 3. There were no violations of the NAAQS for CO in counties that were not monitored (e.g., rural counties). Several scientific studies have questioned the validity of the first two assumptions as discussed below. The first assumption implies that ambient CO concentrations are spatially homogeneous throughout a county. A study in the early 1970s questioned the ability of FSM stations to accurately represent human exposure to ambient CO concentrations. Using large Tedlar™ bags filled by a constant flow pump over 5-min periods, Ott collected 1128 CO concentrations at “breathing height” at outdoor locations in San Jose, California, on weekdays between October 1970 and March 1971.27 Of 438 samples collected on 21 dates while walking along sidewalks of congested downtown streets, 60% were above values measured concurrently at the nearest FSM station. The correlation between the “walking samples” and FSM values was positive, but low (r = 0.20). On 2 of 7 days, the sidewalk concentrations (13 and 14.2 ppm) averaged over an 8-h period were well above the corresponding concentrations (4.4 and 6.2 ppm, respectively) reported for the FSM station. Overall, the 8-h average CO concentrations for the 7 days ranged between 1.4 and 3 times the values observed simultaneously at the FSM station. The highest values were in late December when streets were heavily congested with traffic due to Christmas shopping.28 The San Jose study confirmed the hypothesis that FSM stations did not represent the CO exposures of a person walking in outdoor settings of a major city. Since the San Jose study measured the CO exposure of only one person, other studies tested the hypothesis for larger groups of people. Some of these studies focused on commuters, because CO is a signature air pollutant of motor vehicle tailpipe emissions. For example, Cortese and Spengler29 recruited 66 nonsmoking volunteers who lived in different parts of the metropolitan area of Boston, Massachusetts. Each volunteer carried an Ecolyzer monitor attached to a Simpson recorder for 3–5 days between October 1974 and February 1975. The study reported that the mean of all commuter exposures (11.9 ppm) was about twice the concurrent concentration measured at six FSM stations (6 ppm). Automobile commuters had exposures nearly twice that of

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transit users, and about 1.6 times that of people who did “split-mode” commuting, which involved both auto and transit. The first assumption of the CEQ method of exposure estimation also raises the following question: To what extent do ambient CO levels reflect the CO concentrations to which people are exposed indoors? Early studies of human activity patterns in America30 and other industrialized countries31 have consistently shown that people spend most of their time indoors. Several studies published in the early 1970s addressed this question.32−34 Each study examined the relationship between indoor and outdoor CO concentrations. In the absence of indoor sources, these studies found that indoor CO concentrations of office buildings tended to follow outdoor CO levels with some degree of time lag and with a tendency not to reach either the extreme high or low values that were found outdoors. The General Electric study also reported that CO concentrations were larger indoors than outdoors at heights greater than 100 ft above the roadway, due to entrapment of CO within the building.33 To simplify the exposure calculation, the CEQ assumed that each person spent 24 h at home, because the method relied on household data provided by the U.S. Census Bureau. The CEQ method also assumed that people did not travel outside the area represented by the FSM station. People who live in cities spend a significant amount of personal time in pursuits away from the home. In a study of metropolitan Washington, DC, residents in 1968, Chapin found that the hours spent away from home, on the average, ranged from 6.33 h on Sunday to 10.64 h on Friday.30 In other words, people spent between 26.4% and 44.3% of their day away from home. Chapin also reported that people travel an average of 14.2 miles per day, which suggested that people moved between areas represented by different FSM stations over the course of the day. By the early 1980s, additional studies raised further questions as to the ability of FSM stations to represent the CO exposures of the public.35,36 As stated previously, FSM stations use the NDIR method to measure ambient CO concentrations. Because NDIR monitors are not portable, they cannot be used to measure CO exposure as a person performs routine daily activities. The advent of microelectronics during the 1970s enabled considerable progress to be made in the development of reliable, compact, mobile air quality monitoring instruments. The most dramatic of these were the new miniaturized personal exposure monitors (PEMs) as described by Wallace and Ott.37 These instruments could go nearly anywhere, as they were equipped with batteries and shoulder straps. The utility of PEMs for measuring personal CO exposure was demonstrated in several early studies. These included a study of automobile commuters in Los Angeles during the summer of 1973,38 and field surveys of personal exposure in many commercial settings of several California cities between November 1979 and July 1980.39 Continued technical improvements of PEMs stimulated scholarly interest in how to use them in studies of personal and population exposure. Both direct and indirect methods in the use of PEMs have evolved. The direct method distributes PEMs to ordinary people who record their CO exposures and activities directly using either a paper diary or an electronic data logger. For example, Cortese and Spengler used this method in their survey of Boston commuters.29 A second method relies on indirect estimates of population exposure, based on the

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following model advocated by Fugas40 and Duan.41 Ei =

n


ck (tik )

(2.2)

k=1

where Ei = the total integrated exposure of person i over some time period of interest (e.g., 24 h) ck = the air pollutant concentration in microenvironment type k tik = the amount of time spent by person i in microenvironment type k n = the number of microenvironment types encountered by person i over the period of interest. The total exposure of a population can be determined by summation of the integrated exposures of individuals who are members of that population. The indirect method assumes that an individual’s total exposure to air pollution is a function of location and time. It follows that variation in the total exposure of an individual occurs because air pollution concentrations vary from one location to another and because time spent in different locations varies substantially from person to person. The indirect method postulates the existence of “microenvironments” in which a person is exposed to an air pollutant at a given concentration over a fixed period of time. Duan described a microenvironment as a “chunk of air space with homogeneous pollutant concentration.”41 Because of the potentially large number of microenvironments, Duan suggested that similar ones should be grouped, either by location (e.g., indoor or outdoor) or activity performed at a location (e.g., residential or commercial) into “microenvironment types.” Under the CAA, the U.S. EPA has authority to perform periodic reviews of the criteria that support the NAAQS. In the early 1980s, EPA scientists developed a riskanalysis framework to support its reviews of the NAAQS for CO.42,43 This framework required estimates of the percentage of an urban population that was exposed to CO concentrations that exceeded the NAAQS. The need for these estimates was partly related to EPA’s proposal to change the form of the primary standard from deterministic to statistical.44 In response to this need, the EPA supported development of several large-scale population models of CO exposure in the early 1980s. These models included the Simulation of Human Activity and Pollutant Exposure (SHAPE) model and the NAAQS Exposure Model (NEM). Subsequently, the EPA supported development of the probabilistic NEM for CO (pNEM/CO) and the Air Pollutants Exposure Model (APEX). To provide data for these models, the EPA funded both direct and indirect studies of urban population exposure. The indirect studies included measurements of CO in various microenvironments and a nationwide survey of human activity patterns as described later. EPA’s direct studies took measurements of the daily CO exposures of the noninstitutionalized, nonsmoking adult populations (ages 18–70 years) living in two metropolitan areas of the United States. The surveys were performed using portable CO exposure monitors equipped with data loggers to reduce the data-collection

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burden on the population. Field surveys of 454 residents of Denver, Colorado, and 714 residents of Washington, DC, occurred during the fall of 1982 and winter of 1983. Study participants carried PEMs equipped with data loggers. They also kept diaries for 48 h in Denver and for 24 h in Washington. The studies revealed that ambient CO levels at the composite network of fixed-site monitors were able to track variation in personal exposures. However, the network overestimated the 8-h exposures of people with low-level personal exposures and underestimated the 8-h exposures of people with high-level personal exposures. With respect to the underestimates, over 10% of the daily maximum 8-h exposures in Denver exceeded the NAAQS of 9 ppm, and about 4% did so in Washington. The end-expired breath CO levels were in excess of 10 ppm, which was roughly equivalent to about 2% COHb in about 12.5% of the Denver participants and about 10% of the Washington participants. Recall, that the NAAQS for CO are designed to keep COHb levels below 2% in the blood of the general public including probable high-risk groups. During the survey period, the composite CO concentrations at fixed-site monitors exceeded the 8-h NAAQS for CO (9 ppm) only 3% of the time in Denver, and never in Washington, DC. Hence, the results of these two surveys raised further doubts as to the ability of fixed-site monitors to represent the total CO exposure of urban populations.45 The results of the population exposure studies in Denver and Washington did not persuade the U.S. EPA to change the form of the NAAQS for CO from deterministic to statistical. In September, 1985, the EPA announced that it would retain the existing primary NAAQS for CO, but that it would rescind the secondary standard to protect public welfare, because there was no evidence to support it.7 However, one could argue that the results of these two studies provided some justification for the tighter CO emission standards that had taken effect for new cars sold outside of California during the 1980 model year. (Under the CAA, the state of California has authority to set its own tailpipe emission standards.) For example, Table 2.1 shows results for selected microenvironments of the Denver study. The table shows that higher CO concentrations were associated with commuting by motor vehicles (i.e., motorcycle, bus, car, and truck). It also shows that indoor CO concentrations in excess of the NAAQS were observed in public garages and in service stations or vehicle repair facilities. In the Washington study, participants who commuted 6 h or more per week had higher CO exposures than those who commuted fewer hours per week. Likewise, participants who had occupations that involved motor vehicles (e.g., professional drivers of trucks, buses, and taxis; automobile mechanics; garage workers; and policemen) had a mean CO exposure (22.1 ppm) that was over three times higher than the average exposure of those who did not work with motor vehicles (6.3 ppm). The Denver population exposure study provided raw data to test the SHAPE model and the probabilistic version of the NAAQS Exposure Model (pNEM/CO). The evaluation of SHAPE showed close agreement between the observed and predicted arithmetic means of the 1-h and 8-h maximum average CO exposures. However, SHAPE over-predicted low-level exposures and under-predicted high-level exposures.48 Likewise, an evaluation of pNEM/CO showed relatively close agreement between simulated and observed exposures for CO concentrations near the

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TABLE 2.1 Carbon Monoxide Concentrations of Selected Microenvironments in Denver, Colorado, 1982–1983 (Listed in Descending Order of Mean CO Concentration) n

Meana (ppm)

Standard Error (ppm)

22 76 3, 632 405 619 9

9.79 8.52 8.10 7.03 3.88 1.34

1.74 0.81 0.16 0.49 0.27 1.20

29 22 12 61 126 16 74 29 21

8.20 7.53 3.68 3.45 3.17 1.99 1.36 0.97 0.69

0.99 1.90 1.10 0.54 0.49 0.85 0.26 0.52 0.24

Indoor Public garages 116 Service stations or vehicle repair facilities 125 Other locations 427 Other repair shops 55 Shopping malls 58 Residential garages 66 Restaurants 524 Offices 2, 287 Auditoriums, sports arenas, concert halls 100 Stores 734 Health care facilities 351 Other public buildings 115 Manufacturing facilities 42 Homes 21, 543 Schools 426 Churches 179

13.46 9.17 7.40 5.64 4.90 4.35 3.71 3.59 3.37 3.23 2.22 2.15 2.04 2.04 1.64 1.56

1.68 0.83 0.87 1.03 0.85 0.87 0.19 0.002 0.48 0.21 0.23 0.30 0.39 0.02 0.13 0.25

Microenvironment In-Transit Motorcycle Bus Car Truck Walking Bicycling Outdoor Public garages Residential garages or carports Service stations or vehicle repair facilities Parking lots Other locations School grounds Residential grounds Sports arenas, amphitheaters Parks, golf courses

a An observation was recorded whenever a person changed a microenvironment, and on every

clock hour; thus each observation had an averaging time of 60 min or less. Source: Johnson, T. A Study of Personal Exposure to Carbon Monoxide in Denver, Colorado, Report No. EPA-600/4/84-014, Environmental Monitoring Systems Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, 1984 as reported in U.S. EPA. Air Quality Criteria for Carbon Monoxide, Report No. EPA 600/8-90/045F, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, U.S. Environmental Protection Agency, Research Triangle Park, NC, 1991.

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average exposure (i.e., within the range of 6–13 ppm for the 1-h standard and within 5.5–7 ppm for the 8-h standard). Like SHAPE, pNEM/CO also over-predicted lower exposures and under-predicted higher exposures for both standards.49

2.5 MICROENVIRONMENTAL EXPOSURES This section describes studies of CO exposures in microenvironments that people use to live, work, shop, play, and commute. In particular, it identifies factors that may contribute to high-level exposures in these microenvironments. High-level exposures deserve more attention, because population exposure models (i.e., SHAPE and pNEM/CO) appear to underestimate high-level exposures in these microenvironments, as stated earlier. These microenvironments were also chosen, because they were identified by the U.S. EPA’s National Human Activity Pattern Survey (NHAPS) as locations relevant to air pollution exposure. That survey collected 24-h retrospective diary data on activities and their locations from 9196 respondents interviewed in the 48 contiguous states from late September 1992 through September 1994. Table 2.2 summarizes the minutes spent on the diary days in six locations for respondents to the survey.50

2.5.1 RESIDENTIAL EXPOSURES Exposure to CO in the home is an important component of a person’s total daily exposure, because an estimated 68.7% of one’s time on average is spent inside a residence.50 Major sources of CO concentrations inside the home include unvented or poorly vented furnaces, gas appliances, fireplaces, wood stoves, kerosene space heaters, and charcoal grills and hibachis. Other CO sources include motor vehicles inside an attached garage. Studies of exposures to nonfatal concentrations are discussed first, followed by studies of unintentional deaths caused by high indoor CO concentrations.

TABLE 2.2 Time Spent in Different Locations by 9196 Participants of The National Human Activity Pattern Survey (NHAPS), October 1992–September 1994 Location In a residence Office-factory Bar-restaurant Other indoor In an enclosed vehicle Outdoors

Overall Mean (min)

Doer %

Doer n

Doer Mean (min)

990 78 27 158 79 109

99.4 20.0 23.7 59.1 83.2 59.3

9153 1925 2263 5372 7596 5339

996 388 112 267 95 184

Source: Modified from Klepeis et al., J. Expo. Anal. Env. Epid., 11, 231, 2001.

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2.5.1.1 Nonfatal Exposures Many Americans have appliances that emit CO in the home. These homes often use gas (natural gas and liquid propane) for cooking, heating water, and drying clothes. Of all participants of the NHAPS study, 38.3% had a gas range or oven at home, and 23.7% said that it had a burning pilot light. The same study showed that some people still use small appliances to heat a room: fireplace (10%); wood stove (6%); and kerosene space heater (2%). In the presence of indoor sources such as gas appliances, indoor CO concentrations often exceed outdoor levels.47 In a 1985 Texas study, CO concentrations were greater than or equal to the NAAQS for CO of 9 ppm in 12% of surveyed homes. Residential CO concentrations were high in cases where unvented gas space heaters were used as the primary heat source.51 According to the Barbecue Industry Association, 44 million American households owned a charcoal grill in 1989, and an estimated 600 million charcoal-barbecuing events took place annually.52 An earlier study showed that the air stream from charcoal grills contained 20–2000 ppm of CO, with 75% of grills emitting 200 ppm and above.53 Another study reported COHb levels ranging from 6.9% to 17.4% in a family of four people in northern California who had been exposed to smoke from cooking indoors on a barbecue grill, which was found by firefighters in the middle of the living room.54 Based on data for ten counties, a study in Washington state reported features of unintentional CO poisoning cases that occurred between 1982 and 1993.52 Most cases occurred when electrical power was interrupted during fall and winter months, because of either regional storms or unpaid utility bills. Of 509 patients treated with hyperbaric oxygen, 79 (16%) were exposed to CO emissions when charcoal briquets were burned for heating or cooking in 32 separate incidents. Non-English speaking Hispanic whites and Asians were disproportionately represented among the cases. The COHb levels of these 79 people averaged 21.6% and ranged from 3.0% to 45.8%. Two studies assessed CO exposure to emissions from unvented portable kerosene heaters in eight small mobile homes with no gas appliances and low air exchange rates.55,56 Each home was monitored for an average of 6.5 h per day for 3 days per week for 4 weeks. For 2 weeks the heater was on, and, for 2 weeks, it was off. When the heater was turned on, it was in use for an average of 4.5 h. When the heater was in use, study participants (all nonsmokers) spent most of their time in the family room or kitchen. Sampling took place in the living area about 1.5–3 m from the heater. The mean 8-h CO concentrations were 7.4 ppm (1-h peak = 11.5 ppm) when the heater was on and 1.4 ppm (1-h peak = 1.5 ppm) when it was off. Peaks usually were observed at the end of the combustion period. The ambient CO level measured 0.5 h prior to heater use ranged from 0 to 8 ppm. When the heater was on, three of the eight homes had 8-h average CO levels that exceeded the NAAQS, and one home routinely had levels of 30–50 ppm. A California study reported CO exposures for a random sample of homes that used gas appliances during a 48-h period from December 1991 to April 1992.57−59 For periods of 48 h, the median CO concentration was 1.2 ppm (indoors) and 0.8 ppm (outdoors), and the median of the maximum 8-h average CO concentration was 2.0 ppm (indoors) and 1.4 ppm (outdoors). Of surveyed homes, 13 of 286 homes (4.5%)

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had indoor CO concentrations above the NAAQS of 9 ppm for 8 h, and 8 of 282 homes (2.8%) had outdoor CO concentrations above this standard. Although most of the exceedances occurred in the Los Angeles basin, these percentages could be low because the basin was under-represented in the statewide sample. The study did not translate these percentages into statewide estimates. The study suggested that a small percentage of California homes would still have indoor CO problems even if outdoor CO levels at these homes complied with federal ambient standards. For a common sample of 277 homes, 17 homes (6.1%) had 1-h maximum concentrations indoors that were at least 5 ppm higher than outdoor levels, and 10 homes (3.6%) had 8-h maximum CO concentrations indoors that were at least 5 ppm higher than outdoor levels. Using univariate regression analysis, outdoor CO concentrations explained approximately 55% of the indoor CO variation. Higher net indoor CO levels (indoor minus outdoor CO concentrations) were traced definitively to space heating with gas ranges and gas-fired wall furnaces, use of gas ranges with continuous gas pilot lights, small home volumes, and cigarette smoke. However, several other factors also may have contributed to the higher CO levels: malfunctioning gas furnaces, automobile exhausts leaking into homes from attached garages and carports, improper use of gas appliances (e.g., gas fireplaces), and improper installation of gas appliances (e.g., forced air unit ducts).59 2.5.1.2 Fatal Exposures Factors contributing to unintentional deaths from CO poisonings were identified by studies in California and New Mexico. In California, two studies collected data for the 1979–1988 period. In the first study, 59 of 444 deaths (13.3%) were caused by improper use of charcoal grills and hibachis.60 Of the 59 deaths, 54% occurred inside motor vehicles (e.g., vans, campers) and 46% in residential structures (e.g., homes, apartments, shacks, tents). Relative to their share of the state’s population, higher death rates occurred amongAsians, blacks, males, and people aged 20–39. The second study identified specific factors that contributed to unintentional deaths caused by CO from several combustion sources (e.g., charcoal grills and hibachis, other heating and cooking appliances, motor vehicles, small engines, camping equipment).61 In this study, there was a strong association between alcohol use and CO poisoning from motor vehicles. Typically, motorists under the influence of alcohol would pull into their garages, leave the engine running while listening to cassette tapes, and then fall asleep. Faulty heating equipment used during winter months was implicated in about 50% of all unintentional deaths in both the California study61 and the New Mexico study.62 The National Center for Health Statistics (NCHS) and the U.S. Consumer Product Safety Commission (CPSC) estimated that 212 deaths in 1992 could be attributed to fuel-burning appliances used in the home. Of these deaths, 13 involved use of gasoline-powered appliances.63 An estimated 3900 CO injury accidents occurred in 1994, of which about 400 were associated with the use of gasoline-powered engines or tools. In response to the problem, several federal government agencies issued a joint alert concerning exposure to CO emitted by these sources.64 These sources involved use of pressure washers, air compressors, concrete-cutting saws, electric generators,

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floor buffers, power trowels, water pumps, and welding equipment. Unintentional CO poisonings frequently happened indoors even when people took precautions to ventilate buildings. Power outages following hurricanes and tropical storms often create demand for alternate sources of electricity (e.g., portable gasoline generators) to run air conditioners and refrigerators. But these generators can be a significant source of CO exposures if they are placed in garages or outdoors near windows. The majority of exposures occur overnight when generators are used to run air conditioners and other appliances. Hurricanes Katrina and Rita, which struck the U.S. Gulf Coast in the late summer of 2005, caused 10 deaths from CO poisoning in 18 storm-affected counties of Alabama and Texas.65 All of the fatalities were caused by gasoline-powered generators placed either inside the home or in a fully enclosed space outside the home. Very few homes had functioning CO detectors. In four hurricanes that hit Florida in 2004, some victims of CO poisoning placed generators inside their homes or garages to protect the devices from weather damage or to prevent theft.66

2.5.2 OCCUPATIONAL EXPOSURES The NHAPS study reported that 20% of Americans spent nearly 6.5 h per day on average working inside an office or factory.50 The National Institute for Occupational Safety and Health (NIOSH) estimated that 3.5 million workers who work in the private sector potentially are exposed to CO primarily from motor exhaust. The number of persons potentially exposed to CO in the work environment is greater than that for any other physical or chemical agent.67 In 1992, there were 900 work-related CO poisonings resulting in death or illness in private industry according to the U.S. Bureau of Labor Statistics as cited in a NIOSH report.64 Three risk factors affect industrial occupational exposure: (1) the work environment is located in a densely populated area that has high background (i.e., ambient) CO concentrations; (2) the work environment produces CO as a product or by-product of an industrial process, or the work environment tends to accumulate CO concentrations that may result in occupational exposures; and (3) the work environment involves exposure to methylene chloride (i.e., dichloromethane), which is metabolized to CO in the body. Proximity to fuel combustion of all types elevates CO exposure for certain occupations: airport employees; auto mechanics; small gasoline-powered tool operators (e.g., users of chainsaws); charcoal meat grillers; construction workers; crane deck operators; firefighters; forklift operators; parking garage or gasoline station attendants; policemen; taxi, bus and truck drivers; toll booth and roadside workers; and warehouse workers.47 Table 2.3 shows results for several occupational studies (typical CO values and/or ranges), averaging periods, and the measured or estimated percent COHb levels for nonsmokers, if reported. The CO exposure of office building workers has received less attention. Flachsbart and Ott83 developed a “rapid method” for surveying CO concentrations inside several high-rise buildings. In one case, they observed CO concentrations in excess of 9 ppm, which is the 8-h NAAQS for CO, on four visits to a 15-story office building in Palo Alto, California. A survey in April 1980, showed that CO concentrations in the building’s underground garage averaged 40.6 ppm. The CO levels ranged from

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5.0–13.6 (0.25 h) 5–300 (0.1–1.7 h) (INT) 5.8–12.5 TWA (0.5–1 h) NA >200 (<2 min) 16.2–24.3 TWA (8 h) 250–300 (5 h) NA (4.4 h) 370–386 (NA) 25–47 TWA (8–12 h) 3–34 (8 h) 42.6% > 35 (1 h) 2.7 (8 h) 1–4.3 (8 h) 5–42 (ENV)

Airport workers NA NA NA 9.2–75.6 in 5 farmers NA > 4 in 10 NS 5–22 for 4 NS 4.2–28.7 for 7 NS 21.1 ± 0.7 6.3–13.3 for 4 NS > 3.25 in 5% of NS > 5 in 45% of NS NA NA <5

Measured or Estimated Percent COHb Massachusetts, U.S. U.S. France U.S. U.S. Germany North Carolina, U.S. North Carolina, U.S. North Carolina, U.S. Colorado, U.S. California, U.S. Ontario, Canada 4 states, U.S. Denmark Massachusetts, U.S.

State/Country

68 69 70 71 64 72 73 74 75 76 77, 78 79 80 81 82

References

Note: ENV = short-term environmental measurements; INT = interior of vehicle; NA = not available; NS = non-smokers; and TWA = time-weighted average Source: Modified from Apte, M. A population-based exposure assessment methodology for carbon monoxide: development of a carbon monoxide passive sampler and occupational dosimeter, Ph.D. thesis, University of California, Berkeley, 1997 and updated.

Garage mechanics Traffic/roadway workers

Forklift operators and workers in facilities with forklifts

Bus drivers Chainsaw/gas tool operators

CO Concentration (ppm) and Averaging Period

Occupational Category

TABLE 2.3 Studies of Occupational Exposures and Dosages

Exposure to Ambient and Microenvironmental Concentrations 21

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10.2 to 18.5 ppm on the first eleven floors of the building, but were only 2–4 ppm on the top four floors. They attributed these findings to three factors: (1) fans ventilating the garage had been switched off to reduce electricity costs, because utility rates had increased sharply due to an international energy crisis; (2) the door connecting the garage with the main stairwell of the building was kept open; and (3) the first eleven and top four floors of the building were served by separate ventilation systems. Once the first two factors were corrected (i.e., the garage fans were switched on and the connecting door to the garage was closed), Flachsbart and Ott83 reported that average CO levels in the garage dropped from 40.6 ppm (before) to 7.9 ppm (after), while typical CO levels in the building fell from 11 ppm to 12 ppm (before) to 1 ppm to 2 ppm (after).

2.5.3 SHOPPING CENTER EXPOSURES The NHAPS study estimated that 59.1% of Americans spent nearly 4.5 h per day on average at other indoor locations, such as shopping malls, stores, schools, churches, health clubs, laundromats, salons, and parking garages.50 Of these locations, major shopping centers, in particular, attract and generate relatively large volumes of motor vehicle traffic that typically circulates at low speeds with frequent stops and starts. This traffic pattern produces relatively high CO emissions, which can accumulate to unhealthy levels if emissions occur in enclosed or semienclosed spaces. Since shopping centers also attract large numbers of people, the potential for human exposure to high CO levels is great. In the 1980s, the Ala Moana Shopping Center in Honolulu, Hawaii, was an example of this type of indoor CO exposure problem. First, the center had 155 business outlets that attracted 40 million people including many tourists each year. Second, the center had an attached structure with 7800 parking spaces on several decks. CO emission rates were high, because the posted speed limit for motor vehicles in the structure was 15 mph for the safety of pedestrians. CO emission rates increase when vehicle speeds fall below 15 mph. Third, one deck of the parking structure functioned as a lid on the exhaust emissions of cars at the street level of the structure. Fourth, many of the 94 outlets at street level kept their doors open during business hours to attract customers. This allowed CO concentrations from the parking area and internal driveways to diffuse into many retail outlets.84 Flachsbart and Brown visited 25 of the 94 street-level outlets at the shopping center every 5 days between November 1981 and March 1982.85 During one visit 4 days before Christmas Day, they estimated that average 1-h concentrations of CO inside ten stores exceeded the federal ambient standard of 35 ppm, but not the occupational standards which were 200 ppm for a 1-h period and 50 ppm for an 8-h period. The average CO levels during 3-min visits to these ten stores on that date ranged from a low of 36.3 ppm to a high of 86.7 ppm. An earlier study of the shopping center’s ground-level parking area found average CO levels ranging from 12 to 37 ppm.86 Although the two studies surveyed different locations of the shopping center, the lower CO levels observed by the 1981–1982 study of the center could be attributed to implementation of the federal motor vehicle emission control program during the 1970s.

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2.5.4 RECREATIONAL EXPOSURES Recreational exposures occur when people use recreational vehicles and when they watch or participate in certain indoor sporting events that involve motor vehicles.

2.5.4.1 Exposures on Recreational Vehicles Two studies examined personal exposure to CO in the exhaust of recreational vehicles. In the first study, Simeone sampled CO concentrations in the passenger areas of large power boats with side-mounted exhausts during routine cruises offshore of Annapolis, Maryland, and Boston, Massachusetts.87 In Boston harbor, CO concentrations averaged 56 ppm during a 60-min cruise and 28 ppm after a 30-min cruise. For the Chesapeake Bay cruises near Annapolis, average stabilized CO concentrations at the helm ranged from 93 to 170 ppm over 20- to 30-min periods and 272 ppm over 30 min on the rear deck near the transom of the boat. In both studies, exhaust gas was affected significantly by airflow about the boat under certain head winds. At head wind speeds of 10–30 knots, turbulent mixing occurred in closer proximity to the rear of the boats, enabling exhaust gases to migrate freely into each boat. In the second study, Snook studied the CO exposure of a second snowmobiler who tailed a lead snowmobiler on a 2- to 3-miles straight trail over level terrain in Grand Teton National Park, Wyoming.88 The CO exposure of the second snowmobiler was measured under stable atmospheric conditions in Tedlar™ bags. The distance between the two snowmobiles ranged from 25 to 125 ft., and speeds ranged from 10 to 40 mph. The second snowmobiler’s maximum average centerline exposure was 23.1 ppm, which occurred at 10 mph and 25 ft. behind the lead snowmobile. Although Snook reported no averaging times for exposures, one can estimate that these times ranged from 3 to 18 min from the data given on the snowmobiler’s travel distance and vehicle speed. In general, the centerline CO concentrations decreased with increasing distance between snowmobiles and increased with greater speeds, but only for distances greater than 25 ft. between snowmobiles. At 15 ft. off centerline, average concentrations fell sharply to levels of 0–7.5 ppm. When the snowmobiler drove alone (self-exposure), the average concentration minus the background concentration was 1.3–3.0 ppm. Background concentrations ranged from 0.2 to 0.5 ppm. At the time of Snook’s study, snowmobile tourism was a booming business across the nation and in several national parks. During the winter of 1993 and 1994, over 87,000 tourists traveled by snowmobile in Yellowstone National Park.89 Under steady-state conditions, a snowmobile may emit from 10 to 20 g of CO per mi, while a modern U.S. automobile equipped with a catalytic converter emits far less (0.01– 0.04 g of CO per mi) at speeds of 10 to 40 mph. Snook and Davis reported that there were no federal laws regulating the exhaust from snowmobile engines, and states were pre-empted from implementing snowmobile emission standards.90 The typical snowmobile utilized a two-stroke engine, because it is less expensive than a four-stroke engine and provides a high power-to-weight ratio. However, a two-stroke engine produces relatively high emissions of CO.

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2.5.4.2 Exposures at Indoor Sporting Events Significant quantities of CO are emitted by certain types of machines during sporting events that occur in poorly ventilated indoor arenas. The CO is emitted by several sources, including ice-resurfacing machines and ice edgers during skating events; gaspowered radiant heaters used to heat viewing stands; and motor vehicles at motocross, monster-truck, and tractor-pull competitions. These competitions usually involve many motor vehicles with no emission controls. Several studies of CO exposure at indoor sporting events are noteworthy. First, Kwok reported episodes of CO poisoning among skaters inside four arenas in Ontario, Canada.91 Mean CO levels ranged from 4 to 81 ppm for periods of about 80 min. The CO levels in the spectator areas ranged from 90% to 100% of levels on the ice rinks. The ice resurfacing machines lacked catalytic emission controls. Second, both Sorensen92 and Miller et al.93 reported CO concentrations greater than 100 ppm in rinks from the use of gasoline-powered resurfacing machines. High concentrations were attributed to poorly maintained machines and insufficient ventilation in one rink. Third, based on data collected in the Québec city area, Lévesque et al.94 developed a linear relationship between CO exposure and the CO concentration in exhaled breath, but could not eliminate other factors affecting the relationship. In a later study, Lévesque et al.95 measured the alveolar CO of 14 male adult nonsmokers who played ice hockey, but who were not exposed in occupational settings. Rink CO concentrations ranged from 0 to 76.2 ppm. The study again found a linear relationship between exposure and absorbed CO, such that for each 10 ppm of CO in the indoor air, the players absorbed enough CO to raise alveolar CO by 4.1 ppm or about 0.76% COHb. In the United States, surveys of CO exposure were done at ice arenas in Vermont, Massachusetts, Wisconsin, and Washington. For a rink in Massachusetts, Lee et al.96 showed that excessive CO concentrations can occur, even with well-maintained equipment and fewer resurfacing operations, if ventilation is inadequate. Average CO levels were less than 20 ppm over 14 h, with no significant source of outdoor CO. Ventilation systems could not disperse pollutants emitted and trapped by temperature inversions and low air circulation at ice level. In another study, Lee et al.97 reported that CO concentrations measured inside six enclosed rinks of the Boston area during a 2-h hockey game ranged from 4 to 117 ppm, whereas outdoor levels were about 2–3 ppm. The alveolar CO of hockey players increased by an average 0.53 ppm per 1 ppm CO exposure over 2 h. Fifteen years earlier, Spengler et al.98 found similar CO concentrations in the Boston area, with levels ranging from 23 to 100 ppm for eight enclosed rinks. In 1991, Paulozzi et al.99 reported that 25 people exposed to CO during a Vermont high-school ice hockey game had mean COHb levels of 8.9%, but did not report whether any of them were smokers. Although Paulozzi et al. were unable to measure CO concentrations at the game, Smith et al.100 reported CO levels of 150 ppm (no averaging time was given) at an indoor ice-hockey rink in Wisconsin. To document the extent of the problem in Vermont, Paulozzi et al. measured CO concentrations during eight high-school games in the state, and reported that average CO levels for the entire game ranged from <5 ppm to 101 ppm with a mean of 35 ppm.101

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Hampson reported a maximum CO level of 354 ppm inside an ice arena in Seattle, Washington, in March 1996.102 Based on data for 17 persons, whose tobacco use was not reported, the average COHb level was 8.6% (range of 3.3–13.9%). The source of the CO was a malfunction in a 20-year-old ice resurfacing machine. The study also reported that CO may have diffused into an adjacent bingo hall through an open door. In view of these studies, the State of Minnesota declared in Regulation No. 4635 that CO measurements taken 20 min after ice resurfacing must be less than 30 ppm.102 Studies also have been done in sports arenas that allow motor vehicles. Boudreau et al.103 reported CO levels for three indoor sporting events (i.e., monster-truck competitions, tractor pulls) in Cincinnati, Ohio. The CO measurements were taken before and during each event at different elevations in the public seating area of each arena with most readings obtained at the midpoint elevation where most people were seated. Average CO concentrations over 1–2 h ranged from 13 to 23 ppm (before the event) to 79 to 140 ppm (during the event). Measured CO levels were lower at higher seating levels. The ventilation system was operated maximally, and ground-level entrances were completely open. High CO concentrations also have been found at motor vehicle competitions in Canada. Luckurst and Solkoski104 recorded CO concentrations at two tractorpull events in Winnipeg, Manitoba. The mean of instantaneous concentrations at 25 locations in the arena ranged from 68 ppm at the start of the first event to 262 ppm by the end. At the second event, the range was 78–436 ppm. Lévesque et al.105 reported CO levels at an indoor motocross competition held in a skating rink in the Québec City region. The May, 1994 event lasted from roughly 8:00 p.m. to midnight. Average CO concentrations determined at five stations located at different points in the arena ranged from 19.1 to 38.0 ppm, with the higher levels measured during the second half of the show. High CO concentrations forced a health official to interrupt the event seven times to help clear the air. Covariance analysis showed that CO levels were related to the initial CO concentration, the event duration, engine size, and especially the number of motorcycles on the track.

2.5.5 COMMUTER EXPOSURES The NHAPS study estimated that 83.2% of Americans spent 95 min per day on average inside a motor vehicle.50 Time spent inside a vehicle, as a percentage of a 24-h day (6.6%), is relatively small compared to the percentage of time spent at home (69.2%) or at work (26.9%). Still, one might expect commuter CO exposure to be high. Highway vehicles accounted for 62.8% of the total CO emitted from all sources except fires in the U.S. in 2003.13 In urban areas, highway vehicles typically account for even higher percentages of total CO emissions.3 Moreover, highway vehicles potentially are a major contributor to a person’s total CO exposure, especially if a person is routinely near motor vehicle emissions.106 Some evidence of this comes from the Denver population exposure study, which indicated that CO exposure while driving was a major component of a person’s daily CO exposure.45,48

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In some ways, driving on congested roadways is analogous to swimming in a polluted river. However, the analogy isn’t perfect, because most commuters have enclosed vehicles, which may not fully protect their occupants from ambient CO concentrations. In a Los Angeles study, Petersen and Allen107 reported that interior CO concentrations averaged 92% of exterior levels. An earlier study by Petersen and Sabersky found that CO concentrations measured outside vehicles exhibit rapid variations and high peaks, while simultaneously measured concentrations inside a vehicle show more gradual variations.38 Several factors affect variation in the CO exposures of commuters as shown in Table 2.4, which lists several American studies in chronological order that have been performed on this subject over a 28-year period since 1974. Table 2.4 includes three studies of actual commuters29,45,108 and five studies of commuter microenvironments.109−113 A Boston study in 1974 revealed variation in the CO exposure of a bicyclist by street type, as defined by traffic volume and number of lanes.109 A few years later, Holland found that automobile commuter exposures varied among four cities surveyed during the winter of 1981.110 A later study attributed Denver’s higher exposures to its colder winter climate and higher altitude.114 Table 2.4 shows that exposures vary by commuting period (morning versus afternoon);29 trip type (residential versus commuting to an urban area);110 mode of travel (automobile, bus, and rail);111 season of the year (summer versus winter);108 trip location (rural, interstate beltway, and urban);112 and year of study.113 Akland et al.45 reported that actual commuters who spent six or more hours per week in travel had greater exposures than those who spent less than 6 h. Finally, Table 2.4 shows that seven of these studies found that commuter exposures typically exceeded concurrently measured ambient concentrations.29,45,108,110−113 2.5.5.1 Defective Exhaust Systems The need to control CO emissions from motor vehicles can be traced in part to studies that tied high CO exposures during commuting to defective exhaust systems and cars without effective emission controls. For example, Amiro115 found that engine and/or tailpipe emissions of CO leaked into passenger cabins of 9 of 19 vehicles studied. CO concentrations inside contaminated vehicles ranged up to 400 ppm. Clements reported that of 645 school buses tested, 7.2% had average CO readings in excess of 20 ppm, and 5.4% had maximum readings above 50 ppm.116 He estimated that CO concentrations in excess of 20 ppm existed in school buses ridden by up to 2.1 million U.S. school children on a daily basis in the 1970s. In a two-step study, Ziskind et al.117 first identified which sustained-use vehicles (buses, taxicabs, and police cars) had faulty exhaust systems, that is, they leaked CO into passenger cabins. Of 120 rides taken in faulty vehicles during the second step, the researchers found that 58% had CO concentrations that exceeded the U.S. NAAQS of 9 ppm for 8 h. In a later study, Hampson and Norkool reported that 20 of 68 children were treated for accidental CO poisoning after riding in the back of eight pickup trucks in Seattle, Washington, between 1986 and 1991.118 Average COHb levels measured in an emergency room were 18.2% ± 2.4% (mean ± standard error of the mean), and ranged from 1.6% to 37.0%. Seventeen of the twenty children rode under a rigid closed canopy attached to

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Auto Auto

October ’74–February ’75

January–March ’81

January–March ’81

January–March ’83

Commuting period Morning Afternoon

City

Trip type Residential driving Urban commute

Mode of travel Washington, DC

Four citiesc

Stamford, CT Los Angeles, CA Phoenix, AZ Denver, CO

Boston, MA

Auto Bus Rail

Auto Auto

Auto Auto Auto Auto

Bicycle Bicycle Bicycle

Boston, MA

Summer ’74

Type of street Narrow-busy 2-lanes Wide-busy 4-lanes Narrow-light 2-lanes

Travel Mode

Study Period

Factor Urban Area

TABLE 2.4 Factors Affecting Commuter Carbon Monoxide Exposure.

9.1–22.3 3.7–10.2 2.2–5.2

2.9–7.6 6.2–16.1

5.2 8.5 6.7 10.3

12.8 13.9

16.4 (17.3)a 14.4 (10.9)a 10.1 (8.8)a

Mean or Median CO Concentration (ppm)

±2 to ±9 ±1 to ±7 0.5 to ±5

±3.6 to ±5.0 ±4.7 to ±7.7

±4.7 ±5.8 ±4.9 ±7.7

±5 ±6

3.3 (4.6)a 3.5 (1.9)a 0.88 (1.5)a

Range or SD of CO Concentration (ppm)

2.3

±2.4 to ±3.9 ±3.9 to ±5.8

4.2–5.5b 3.9–5.8 2.4–3.9 3.1–5.8

6.0

NA NA NA

Typical Ambient CO Concentration (ppm)

(Continued)

111

110

110

29

109

References

Exposure to Ambient and Microenvironmental Concentrations 27

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9.7e 4.8e 1.5e

4 11 13

6.5 10.1

5.04 7.90

Mean or Median CO Concentration (ppm)

±3.1 ±1.7 ±0.8

NA NA NA

±2.2 ±5.8

NA NA

Range or SD of CO Concentration (ppm)

1.3 1.31 0.61

NA NA 2.8

2.8 4.3

3.2

Typical Ambient CO Concentration (ppm)

Note: a Rush hours: 7–9:30 a.m. and 3–5:30 p.m.; (non-rush hour concentrations) b Ambient concentration was measured outside the automobile. c Four cities were Stamford, CT; Los Angeles, CA; Phoenix, AZ; and Denver, CO. d Surveys occurred in the suburbs of Menlo Park, Palo Alto, and Los Altos. e Median of net CO concentrations for 50 trips, where the net value of each trip = average trip CO concentration − background CO concentration. NA = not available

San Francisco, CAd

Raleigh, NC

Los Angeles, CA

Auto Auto Auto

Auto Auto Auto

August–September ’88

Trip location Rural Interstate beltway Urban

February ’80–February ’81 February ’91–February ’92 February ’01–March ’02

Auto Auto

May ’87–March ’88

Season Summer Winter

Year of study

All All

Washington, DC

November ’82–February ’83

Travel Mode

Weekly travel < 6 h/wk ≥ 6 h/wk

Urban Area

Study Period

Factor

TABLE 2.4 Continued

113

112

108

45

References

28 Carbon Monoxide Poisoning

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the bed of the truck, and the other three children rode beneath a tarpulin. Six pickups had a known leak in their exhaust system: three had a rear-end tailpipe and three had a side-mounted tailpipe. 2.5.5.2 Parking Garages Initial studies of CO concentrations in parking garages focused primarily on the garage itself. Trompeo et al.,119 who surveyed 12 underground garages in Turin, Italy, reported that CO levels averaged 98 ppm and ranged from 10 to 300 ppm for 132 observations. Chovin120 measured CO levels of 80–100 ppm on average in poorly ventilated garages in Paris, France. CO concentrations in parking garages can reach a peak in the late afternoon when many drivers leave work and start their cars at the same time. Goldsmith121 and Flachsbart et al.111 found that mass exits from garages can elevate pollutant levels to very high concentrations. The latter study observed spikes in CO concentrations (mean = 94.0 ppm based on 3-min averages, n = 14 cases) inside a test vehicle as it exited the underground garage of a government office building in Washington, DC, during a winter survey in 1983. The study also attributed these spikes in CO concentrations to the fact that many cars were operating under “cold-start” conditions. Once the test vehicle exited the garage, high CO concentrations inside the vehicle gradually dissipated, but the dissipation rate was slow because the vehicle’s windows were kept closed due to cold weather. 2.5.5.3 Service Stations Many motorists typically pump their own fuel at service stations. For safety reasons, most people shut off the engine of their vehicle after they arrive at the station. However, some people may be exposed to CO emitted by vehicles entering or exiting the station. Amendola and Hanes measured CO concentrations in thirteen service stations and two automobile dealerships in the New England area.122 Results varied by season, with CO concentrations ranging from 2.2 to 21.6 ppm in warm weather and 16.2 to 110.8 ppm during cold weather. They cited reduced ventilation as another cause of higher concentrations during winter. Based on a random sample of 100 self-service stations in four counties of southern California, Wilson et al.123 reported a median CO concentration (4.3 ppm), which was about twice that of the ambient level (2.0 ppm) for 5-min averaging times. 2.5.5.4 Drive-Up Facilities Passengers have been exposed to extremely high CO levels when motor vehicles are idling in a queue. During February and March of 1976, Myronuk124 measured CO concentrations inside an automobile at space-confined, drive-up facilities in Santa Clara Valley, California. The in-vehicle CO concentrations ranged from 15 to 95 ppm for 15-min averages, with short-term peaks of 100–400 ppm. High CO averages could be attributed to older vehicles that lacked catalysts, even though these vehicles probably had other forms of emission controls and appeared to be well maintained

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and tuned. Background CO levels were only 2–5 ppm and monitoring occurred when wind speeds were low. Concentrations varied widely if ventilating fans for heater or air conditioning units were in operation. 2.5.5.5 Airbag Deployment Airbags are currently a required safety feature on new cars sold in the United States. On the basis of deployment of four airbags, Wheatley et al.125 reported that time-weighted-average (TWA) CO concentrations ranged from 174 to 370 ppm. Peak CO concentrations occurred 2 min after deployment. 2.5.5.6 Motor Vehicle Emission Standards One of the most significant factors affecting commuter exposure in the United States has been the federal motor vehicle emission control program.126 The CAA amendments of 1970, 1977, and 1990 established a series of progressively tighter motor vehicle emission standards and other controls on new cars sold in the United States. Tighter controls on the tailpipe emissions of new cars had the effect of offsetting the expansion of motor vehicle travel caused by population growth and urban sprawl since 1970.127 Prior to the 1968 model year, the CO tailpipe emissions of passenger cars in the U.S. were 84.0 g per mi. A series of progressively tighter CO emission standards took effect beginning with the 1968 model year, when a standard of 51.0 g per mi took effect. By the 1975 model year, CO tailpipe emissions fell to 15.0 g per mi as a result of the catalytic converter, which became standard equipment on new cars sold in the U.S. The CO emission standard was then lowered to 3.4 g per mi for the 1981 model year and then to 1.7 g per mi by the 2003 model year.3 This amounted to a reduction of nearly 98% in the CO emission rate of new cars between the 1967 and 2003 model years. Several studies show the effects on CO exposure of this trend. First, Flachsbart did a meta-analysis of 16 commuter exposure studies that occurred in the U.S. between 1965 and 1992.128 These studies reported typical (mean or median) CO concentrations for trips, most of which lasted an hour or less. CO concentrations fell from 37 ppm in 1965, as reported by Haagen-Smit129 for a study in Los Angeles, California, to 3 ppm in 1992 for a study by Lawryk et al.130 in the New Jersey suburbs of New York City. A more recent study of an arterial highway on the San Francisco Peninsula indicated that the median CO exposure of 50 trips taken over a 15-month period between 2001 and 2002 was 1.5 ppm.113 If one assumes that the results of these 17 separate studies between 1965 and 2002 are representative of commuter CO exposures in cities nationwide, then exposures fell 96% over the 37-year period. Notice that this percentage reduction in commuter exposure (96%) is nearly identical to the percentage reduction in the CO emission rate for new cars (98%). Also, the time period represented by the CO exposure reduction (1965–2002) is nearly identical to the period used to estimate the emission rate reduction (1967–2003). Finally, Mott et al.4 found that unintentional motorvehicle-related CO death rates in the United States fell from 4.0 to 0.9 deaths per one million person-years between 1975, when the catalytic converter was introduced, and

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1998. They estimated that if rates of unintentional CO-related deaths had remained at pre-1975 levels, then 11,667 more vehicle-related CO deaths might have occurred by 1998. It’s quite possible that modern motor vehicle emission control programs have substantially reduced the sharp peaks in CO exposures observed in older studies of commuting microenvironments. A longitudinal study of commuting in California noticed a lack of sharp peaks in CO measurements during surveys of an arterial highway in 2001–2002 relative to observations of the same highway during previous surveys in 1980–1981 and 1991–1992. The study attributed this finding to California’s implementation of (1) an I/M program (i.e., Smog Check) in 1984; and (2) tougher “durability standards” on emission controls which were adopted in September 1990 and phased-in on new cars sold in California in 1993 and 1994.113

2.6 EXPOSURE TO METHYLENE CHLORIDE Exposure to halogenated hydrocarbons such as methylene chloride, which can be metabolized to CO in the body, occurs when the chemicals are found in contaminated ambient air and groundwater, and in consumer products that contain the chemical as a solvent, flame-retardant additive, or propellant.

2.6.1 NONOCCUPATIONAL EXPOSURE Exposure to methylene chloride in the home, for example, primarily occurs through use of paint and varnish removers. Exposure may also occur through use of aerosol propellants such as those found in hair sprays, antiperspirants, air fresheners, and spray paints. The Agency for Toxic Substances and Disease Registry reported that some aerosol products may contain up to 50% methylene chloride.24 Ambient exposure may occur near production and use facilities or near hazardous waste sites that store methylene chloride. In a study reported in 1983, ambient concentrations of methylene chloride near organic solvent cleaning and paint and varnish removal operations ranged from 7.1 to 14.3 parts per billion (ppb) averaged over one year.131 Although methylene chloride readily disperses when released into the air, it may remain in groundwater for years, and be ingested in drinking water or inhaled when it volatilizes during showering and laundering.24 Exposure to about 500 ppm methylene chloride for several hours can elevate COHb levels to 15%. Increases in COHb levels can be detected in the blood of nonsmokers about 30 min after exposure to methylene chloride. Stewart et al.132 showed that elevated COHb levels were proportional to a series of controlled exposures to methylene chloride. In another controlled experiment, Stewart and Hake133 observed postexposure levels of COHb ranging from 5% to 10% after 3 h use of a liquid-gel paint remover containing 80% methylene chloride and 20% methanol by weight. Concurrent exposure to methylene chloride and methanol prolongs the period of elevated COHb in the body.23,133,134 Peterson reported COHb levels of up to about 10% saturation after inhalation of methylene chloride concentrations ranging from 50 to 500 ppm over 5 days, for 7.5 h per day.135

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2.6.2 OCCUPATIONAL EXPOSURE Certain occupations expose workers to organic solvents such as methylene chloride. The solvent is widely used as a degreaser, paint remover, aerosol propellant, and blowing agent for polyurethane foams. It is used as an extractant for foods and spices, a grain fumigant, and a low-pressure refrigerant. It also is used in the manufacturing of synthetic fibers, photographic film, polycarbonate plastics, pharmaceuticals, printed circuit boards, and inks. More than one million workers have significant potential for exposure to methylene chloride.24 Moreover, the highest levels of exposure to methylene chloride often occur in the workplace. To protect worker health, the 8-h TWA threshold limit value for methylene chloride was set at 50 ppm by the American Conference of Governmental Industrial Hygienists (ACGIH).136 Exposure at this concentration leads to COHb levels of about 1.9% in experimental subjects. Exposure to 500 ppm for several hours may elevate COHb levels as high as 15%. An 8-h exposure to about 500 mg/m3 (3.5 mg/m3 = 1 ppm) of methylene chloride vapor is equivalent to an 8-h exposure to 35 ppm of CO.137 Methylene chloride stored in tissue may continue to be metabolized to CO after several hours of acute exposure. In such cases, COHb levels will continue to rise and peak as high as 25% about 5–6 h after exposure.24 Shusterman et al.138 reported an apparent linear elevation of COHb as a function of hours worked by a furniture refinisher who used paint stripper containing methylene chloride. Ghittori et al.139 reported a significant linear correlation (r = 0.87) between methylene chloride concentration in air and CO in alveolar air of nonsmoking and sedentary factory workers in Italy. Exposure to 600 mg/m3 of methylene chloride for 7.5 h was associated with a COHb level of 6.8% in eight volunteers. Exposure to methylene chloride also can be fatal. Leikin et al.140 reported fatalities of two people who were exposed to unknown concentrations of methylene chloride while they removed paint in an enclosed space. Death was caused not by CO poisoning, but by solvent-induced narcosis. Before they died, their COHb levels continued to rise following cessation of exposure despite treatment with high levels of oxygen.

2.7 CONCLUSIONS This chapter reviewed several types of CO exposure studies. Some studies measured CO concentrations in places where people live, work, shop, play, and commute. Other studies determined the amount of time people spent doing these activities. Still other studies identified factors that contribute to exposures in excess of federal ambient or occupational standards. A few conclusions from these studies follows. The NHAPS found that Americans continue to spend most of their time indoors. On average over a 24-h period, they spent 86.9% of their time indoors either at home, work, bar–restaurant, or elsewhere. They spent 5.5% of their time inside a motor vehicle and only 7.6% of their time outdoors.50 These percentages applied to the entire national sample of 9196 respondents interviewed in the 1990s, not just to the “doers” of various activities. If most Americans spend only a few hours outdoors each day, then indoor and in-vehicle CO exposures are important components of total human exposure.

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The findings of the NHAPS study underscore the importance of studies that compared indoor and outdoor CO exposures. Some of these studies indicated that indoor and outdoor CO exposures differed from those predicted from observations at fixedsite monitors, which are used by the U.S. EPA to determine compliance with the NAAQS. When ambient CO levels are either high or low on a given day, fixed-site monitors still reflect the corresponding high or low aggregates of personal exposures on those days. Otherwise, the stations do not adequately represent the CO exposures of community residents while they are exposed to motor vehicle exhaust during commuting, and to occupational and residential sources of unvented or poorly vented fuel combustion. The mean COHb level of people exposed to CO from these sources is greater than their mean COHb level predicted solely from exposure to CO of ambient origin. Longitudinal studies show that federal and state motor vehicle emission control programs have substantially reduced the CO exposures of urban commuters in the United States. These studies have two implications. First, similar reductions in exposure may exist for other microenvironments, especially those that may be affected substantially by tailpipe emissions from motor vehicles (e.g., office buildings and shopping centers attached to parking garages, as well as service stations, waiting lines at drive-up facilities, and sidewalks along busy streets). Unfortunately, there appear to be no published trend studies of CO exposure for these other microenvironments. Second, one would expect that results of certain population studies (e.g., the Denver–Washington study of 1982–1983) may no longer represent the CO exposures of current urban populations in the United States. More recent studies have shown that people are still exposed to elevated CO levels in certain indoor microenvironments (e.g., unventilated parking garages, motor vehicles with leaky exhaust systems, small homes with unvented or poorly vented gas stoves and space heaters). Moreover, studies report that high-level CO exposures can occur when people use unregulated gasoline-powered appliances, engines, and tools (e.g., chainsaws), even under ventilated conditions. These locations and activities are not part of the regulated ambient environment. However, these microenvironments typically represent settings of fatal and nonfatal CO poisonings. Studies of California homes indicated that elevated CO concentrations (>9 ppm) were caused by several factors, such as attached garages and carports; ranges with continuous gas pilot lights; and improper use and installation of gas appliances, especially in small homes. Other studies have found elevated CO concentrations (>9 ppm) when people ride certain types of recreational vehicles (e.g., snowmobiles, power boats), gather indoors to barbecue food (sometimes to cope with electrical power outages after severe storms), and watch sporting events held at indoor arenas. High-level exposures (>25 ppm) may occur inside arenas when they are used for ice skating or motocross, monster-truck, and tractor pull competitions. Vehicles in these competitions often lack any type of emission controls. At some events, ventilation did not sufficiently lower CO concentrations to safe levels (<9 ppm) for the general public. Finally, CO exposures are high in certain occupations, such as garage mechanics and chainsaw/gas tool operators, and for people who operate or work around forklifts. More than one million people have high exposure to methylene chloride in the

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workplace, which is a concern because it can metabolize to CO in the body after several hours of exposure.

2.8 ACKNOWLEDGMENTS Portions of this chapter are reprinted with permission from: Chemosphere—Global Change Science, vol. 1, M.A.K. Khalil, J.P. Pinto, and M.J. Shearer, Eds., P.G. Flachsbart, “Human Exposure to Carbon Monoxide from Mobile Sources,” pages 301–329, copyright (1999), published by Elsevier; Urban Traffic Pollution, D. Schwela and O. Zali, Eds., P.G. Flachsbart, “Chapter 4: Exposure to Exhaust and Evaporative Emissions from Motor Vehicles,” pages 89–132, copyright (1999), published by the WHO; Journal of Exposure Analysis and Environmental Epidemiology, 11(3), Neil E. Klepeis et al., “The National Human Activity Pattern Survey (NHAPS): a resource for assessing exposure to environmental pollutants,” pages 231–252, copyright (2001), published by Nature Publishing Group; A Population-Based Exposure Assessment Methodology for Carbon Monoxide: Development of a Carbon Monoxide Passive Sampler and Occupational Dosimeter, copyright (1997) by Michael G. Apte, Ph.D. Thesis, University of California, Berkeley; and Human Exposure Analysis, W. Ott, A. Steinemann, and L. Wallace, Eds., Peter G. Flachsbart, “Exposure to Carbon Monoxide,” pages 113–146, copyright (2007), published by CRC Taylor & Francis.

References 1. Burr, M.L. Combustion products, In Indoor Air Quality Handbook, Spengler, J.D., Samet, J.M., and McCarthy, J.F., eds., McGraw-Hill, New York, 2000, chap. 29. 2. Raub, J.A., Mathieu-Nolf, M., Hampson, N.B., and Thom, S.R. Carbon monoxide poisoning—a public health perspective, Toxicology, 145, 1, 2000. 3. Godish, T. Air Quality, 4th ed., Lewis Publishers, Boca Raton, FL, 2004, 156–159. 4. Mott, J.A., Mitchell, I.W., Alverson, C.J., Macdonald, S.C., Bailey, C.R., Ball, L.B., Moorman, J.E., Somers, J.H., Mannino, D.M., and Redd, S.C. National vehicle emissions policies and practices and declining US carbon monoxide-related mortality, JAMA: J. Am. Med. Assoc., 288, 988, 2002. 5. Vajani, M. Unintentional non-fire-related carbon monoxide exposures - United States, 2001–2003, MMWR: Morb. Mort. Wkly. Rep., 54, 36, January 21, 2005. 6. Fiorino, D. Making Environmental Policy, University of California Press, Berkeley, CA, 1995, 25–28. 7. U.S. EPA. Air Quality Criteria for Carbon Monoxide, Report No. EPA 600/P-99/001F, Office of Research and Development, National Center for Environmental Assessment, U.S. Environmental Protection Agency, Washington, D.C., 2000. 8. Raub, J. Environmental Health Criteria 213: Carbon Monoxide, 2nd ed., World Health Organization, Geneva, Switzerland, 1999. 9. Arias, E., Anderson, R.N., Kung, H.-C., Murphy, S.L., and Kochanek, K.D. Deaths: final data for 2001, National Vital Statistics Reports, 52(3), Center for Health Statistics, Hyattsville, MD, 2003. 10. WHO. Carbon monoxide, In Air Quality Guidelines for Europe, WHO Regional Publications, European Series No. 23, World Health Organization, Regional Office for Europe, Copenhagen, 1987, 210–220.

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11. WHO. Updating and revision of the air quality guidelines for Europe, Meeting of the WHO Working Group “Classical” Air Pollutants, Report No. EUR/ICP/EHAZ 94 05/PB01, World Health Organization, Regional Office for Europe, Copenhagen, 1995. 12. Romieu, I. Epidemiological studies of health effects arising from motor vehicle air pollution, In Urban Traffic Pollution, Schwela, D. and Zali, O., eds., E & FN Spon, London, 1999, chap. 2. 13. U.S. EPA. National Air Quality and Emissions Trends Report, 2003 Special Studies Edition, Report No. EPA 454/R-03-005, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC, 2003. 14. Muller, P.O. Transportation and urban form: stages in the spatial evolution of the American metropolis, In The Geography of Urban Transportation, 3rd ed., Hanson, S. and Giuliano, G., eds., Guilford Press, New York, 2004, chap. 3. 15. U.S. Code of Federal Regulations, 40 CFR 50.1(e). 16. National Research Council. Managing Carbon Monoxide Pollution in Meteorological and Topographical Problem Areas, National Academies Press, Washington, D.C., 2003. 17. Blumenthal, D. The use of real-time air quality data in daily forecasting and decisionmaking, EM: The Magazine for Environmental Managers, September, 2005, 18. 18. U.S. EPA. National Air Quality and Emissions Trends Report, 1999, Report No. EPA/454/R-01-004, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC, 2001. 19. U.S. EPA. National Air Quality and Emissions Trends Report, 1996, Report No. EPA/454/R-97-013, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC, 1998. 20. See: http://www.epa.gov/oar/oaqps/greenbk/cmsum. 21. See: http://www.epa.gov/oar/oaqps/greenbk/cntc. 22. Zartarian, V.G., Ott, W.R., and Duan, N. A quantitative definition of exposure and related concepts, J. Expo. Anal. Environ. Epid., 7, 411, 1997. 23. Wilcosky, T. and Simonsen, N.R. Solvent exposure and cardiovascular disease, Am. J. Ind. Med., 19, 569, 1991. 24. Agency for Toxic Substances and Disease Registry. Methylene chloride toxicity, Am. Fam. Phy., 47, 1159, 1993. 25. Ott, W. Concepts of human exposure to air pollution, Environ. Int., 7, 179, 1982. 26. Council on Environmental Quality. Environmental Quality - 1980: The Eleventh Annual Report of the Council on Environmental Quality, U.S. Government Printing Office, Washington, D.C., 1980, 27–40. 27. Ott, W. An urban survey technique for measuring the spatial variation of carbon monoxide concentrations in cities, Ph.D. thesis, Stanford University, Stanford, CA, 1971. 28. Ott, W. and Eliassen, R. A survey technique for determining the representativeness of urban air monitoring stations with respect to carbon monoxide, J. Air Pollut. Control Assoc., 23, 685, 1973. 29. Cortese, A.D. and Spengler, J.D. Ability of fixed monitoring stations to represent personal carbon monoxide exposure, J. Air Pollut. Control Assoc., 26, 1144, 1976. 30. Chapin, F.S., Jr. Human Activity Patterns in the City, Wiley-Interscience, New York, 1974. 31. Szalai, A., ed. The Use of Time: Daily Activities of Urban and Suburban Populations in Twelve Countries, Mouton and Co., The Hague, The Netherlands, 1972.

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Carbon Monoxide Poisoning 32. Yocom, J.E., Clink, W.L., and Cote, W.A. Indoor/outdoor air quality relationships, J. Air Pollut. Control Assoc., 21, 251, 1971. 33. General Electric Company. Indoor–Outdoor Carbon Monoxide Pollution Study, Report No. NTIS-PB220428, National Technical Information Service, Springfield, VA, 1972. 34. Godin, G., Wright, G., and Shephard, R. Urban exposure to carbon monoxide, Arch. Environ. Health, 25, 305, 1972. 35. Meyer, B. Indoor Air Quality, Addison-Wesley, Reading, MA, 1983, 159–160. 36. Spengler, J. and Soczeck, M. Evidence for improved ambient air quality and the need for personal exposure research, Environ. Sci. Technol., 18, 272A, 1984. 37. Wallace, L.A. and Ott, W.R. Personal monitors: a state-of-the-art survey, J. Air Pollut. Control Assoc., 32, 601, 1982. 38. Petersen, G.A. and Sabersky, R.H. Measurement of pollutants inside an automobile, J. Air Pollut. Control Assoc., 25, 1028, 1975. 39. Ott, W.R. and Flachsbart, P.G. Measurement of carbon monoxide concentrations in indoor and outdoor locations using personal exposure monitors, Environ. Int., 8, 295, 1982. 40. Fugas, M. Assessment of total exposure to an air pollutant, Paper No. 38-5 in Proc. Int. Conf. Environ. Sensing and Assess., Vol. 2, Las Vegas, NV, 1975, 1. 41. Duan, N. Models for human exposure to air pollution, Environ. Int., 8, 305, 1982. 42. Padgett, J. and Richmond, H. The process of establishing and revising national ambient air quality standards, J. Air Pollut. Control Assoc., 33, 13, 1983. 43. Jordan, B.C., Richmond, H.M., and McCurdy, T. The use of scientific information in setting ambient air standards, Environ. Health Perspectives, 52, 233, 1983. 44. Federal Register. Carbon monoxide; proposed revisions to the national ambient air quality standards: proposed rule, 45, 55066, August 18, 1980. 45. Akland, G.G., Hartwell, T.D., Johnson, T.R., and Whitmore, R.W. Monitoring human exposure to carbon monoxide in Washington, D.C., and Denver, Colorado, during the winter of 1982–1983, Environ. Sci. Technol., 19, 911, 1985. 46. Johnson, T. A Study of Personal Exposure to Carbon Monoxide in Denver, Colorado, Report No. EPA-600/4/84-014, Environmental Monitoring Systems Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, 1984. 47. U.S. EPA. Air Quality Criteria for Carbon Monoxide, Report No. EPA 600/8-90/045F, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, U.S. Environmental Protection Agency, Research Triangle Park, NC, 1991. 48. Ott, W.R., Thomas, J., Mage, D.T., and Wallace, L. Validation of the simulation of human activity and pollutant exposure (SHAPE) model using paired days from the Denver, CO, carbon monoxide field study, Atmos. Environ., 22, 2101, 1988. 49. Law, P.L., Lioy, P.J., Zelenka, M.P., Huber, A.H., and McCurdy, T.R. Evaluation of a probabilistic exposure model applied to carbon monoxide (pNEM/CO) using Denver personal exposure monitoring data, J. Air Waste Manage. Assoc., 47, 491, 1997. 50. Klepeis, N.E., Nelson, W.C., Ott, W.R., Robinson, J.P., Tsang, A.M., Switzer, P., Behar, J.V., Hern, S.C., and Engelmann, W.H. The national human activity pattern survey (NHAPS): a resource for assessing exposure to environmental pollutants, J. Expo. Anal. Environ. Epid., 11, 231, 2001. 51. Koontz, M.D. and Nagda, N.L. A Topical Report on a Field Monitoring Study of Homes with Unvented Gas Space Heaters: Volume III, Methodology and Results, Contract No. 5083-251-0941, Gas Research Institute, Chicago, 1988.

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52. Hampson, N.B., Kramer, C.C., Dunford, R.G., and Norkool, D.M. Carbon monoxide poisoning from indoor burning of charcoal briquets, JAMA: J. Am. Med. Assoc., 271, 52, 1994. 53. Yates, M.W. A preliminary study of carbon monoxide gas in the home, J. Environ. Health, 29, 413, 1967. 54. Gasman, J.D., Varon, J., and Gardner, J.P. Revenge of the barbecue grill: carbon monoxide poisoning, West. J. Med., 153, 656, 1990. 55. Mumford, J.L., Williams, R.W., Walsh, D.B., Burton, R.M., Svendsgaard, D.J., Chuang, J.C., Houk, V.S., and Lewtas, J. Indoor air pollutants from unvented kerosene heater emissions in mobile homes: studies on particles, semivolatile organics, carbon monoxide, and mutagenicity, Environ. Sci. Technol., 25, 1732, 1991. 56. Williams, R., Walsh, D., White, J., Jackson, M., and Mumford, J. Effect on carbon monoxide levels in mobile homes using unvented kerosene heaters for residential heating, Indoor Environ., 1, 272, 1992. 57. Wilson, A.L., Colome, S.D., and Tian, Y. California Residential Indoor Air Quality Study, Volume 1 - Methodology and Descriptive Statistics, Integrated Environmental Services, Irvine, CA, 1993. 58. Wilson, A.L., Colome, S.D., and Tian, Y. California Residential Indoor Air Quality Study, Volume 1 - Methodology and Descriptive Statistics, Appendix, Integrated Environmental Services, Irvine, CA, 1993. 59. Colome, S.D., Wilson, A.L., and Tian, Y. California Residential Indoor Air Quality Study, Volume II - Carbon Monoxide and Air Exchange Rate: A Univariate & Multivariate Analysis, Integrated Environmental Services, Irvine, CA, 1994. 60. Liu, K., Girman, J.R., Hayward, S.B., Shusterman, D., and Chang, Y. Unintentional carbon monoxide deaths in California from charcoal grills and hibachis, J. Expo. Anal. Environ. Epid., 3, 143, 1993. 61. Girman, J.R., Chang, Y.-L., Hayward, S.B., and Liu, K.-S. Causes of unintentional deaths from carbon monoxide poisonings in California, West. J. Med., 168, 158, 1998. 62. Yoon, S.S., Macdonald, S.C., and Parrish, R.G. Deaths from unintentional carbon monoxide poisoning and potential for prevention with carbon monoxide detectors, JAMA: J. Am. Med. Assoc., 279, 685, 1998. 63. National Center for Health Statistics and U.S. Consumer Product Safety Commission. Death certificate file, U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, Atlanta, GA, 1992. 64. National Institute for Occupational Safety and Health. Preventing Carbon Monoxide Poisoning from Small Gasoline-Powered Engines and Tools [NIOSH alert], Report No. DHHS (NIOSH) 96–118, Public Health Service, U.S. Department of Health and Human Services, Cincinnati, OH, 1996. 65. Tucker, M., Eichold, B., Lofgren, J.P., Holmes, I., Irvin, D., Villanacci, J., Ryan, J., et al. Carbon monoxide poisonings after two major hurricanes—Alabama and Texas, August – October 2005, MMWR: Morb. Mort. Wkly. Rep., 55, 236, 2006. 66. Sniffen, J.C., Cooper, T.W., Johnson, D., Blackmore, C., Patel, P., Harduar-Morano, L., Sanderson, R., et al. Carbon monoxide poisoning from hurricane-associated use of portable generators - FL, 2004, MMWR: Morb. Mort. Wkly. Rep., 54, 697, 2005. 67. Pedersen, D.H., and Sieber, W.K. National Occupational Exposure Survey, Volume III: Analysis of Management Interview Responses, Report No. PB90-193640, U.S. Department of Health and Human Services, National Institute for Occupational Safety and Health, National Technical Information Service, Springfield, VA, 1988. 68. Bellin, P. and Spengler, J.D. Indoor and outdoor carbon monoxide measurements at an airport, J. Air Pollut. Control Assoc., 30, 392, 1980.

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Carbon Monoxide Poisoning 69. McCammon, C.S., Halperin, W.F., and Lemin, R.A. Carbon monoxide exposure from aircraft fueling vehicles, Arch. Environ. Health, 36, 136, 1981. 70. Limasset, J., Diebold, F., and Hubert, G. Assessment of bus drivers’ exposure to the pollutants of urban traffic, Sci. Total Environ., 134, 39, 1993. 71. Kahler, M., Kuhse, W., and Wintermeyer, L.A. Unintentional carbon monoxide poisoning from indoor use of pressure washers - Iowa, January 1992–January 1993, MMWR: Morb. Mort. Wkly. Rep., 42, 777, 1993. 72. Bünger, J., Bombosch, F., Mesecke, U., and Hallier, E. Monitoring and analysis of occupational exposure to chain saw exhausts, Am. Ind. Hygiene Assoc. J., 58, 747, 1997. 73. Baucom, C.D., Freeman, J.I., and MacCormack, J.M. Carbon monoxide poisoning in a garment-manufacturing plant - North Carolina, MMWR: Morb. Mort. Wkly. Rep., 36, 543, 1987. 74. Fawcett, T.A., Moon, R.E., Francia, P.J., Mebane, G.Y., Theil, D.R., and Piantadosi, C.A. Warehouse workers headache: carbon monoxide poisoning from propane-fueled forklifts, J. Occup. Med., 34, 12, 1992. 75. Ely, E.W., Moorehead, B., and Haponik, E.F. Warehouse workers’ headache: emergency evaluation and management of 30 patients with carbon monoxide poisoning, Am. J. Med., 98, 145, 1995. 76. McCammon, J.B., McKenzie, L.E., Heinzman, M. Carbon monoxide poisoning related to the indoor use of propane-fueled forklifts in Colorado workplaces, Appl. Occup. Environ. Hyg., 11, 192, 1996. 77. Apte, M. A population-based exposure assessment methodology for carbon monoxide: development of a carbon monoxide passive sampler and occupational dosimeter, Ph.D. thesis, University of California, Berkeley, 1997. 78. Apte, M.G., Cox, D.D., Hammond, S.K., and Gundel, L.A. A new carbon monoxide occupational dosimeter: results from a worker exposure assessment survey, J. Expo. Anal. Environ. Epid., 9, 546, 1999. 79. Gourdeau, P., Parent, M., and Soulard, A. Exposition à l’oxyde de carbone dans les garages d’automobiles: évaluation chez les mécaniciens, Canada J. of Public Health, 86, 414, 1995. 80. Boeniger, M.F. Description of Facilities and Employee Exposure to Carbon Monoxide at Four Different Bridge and Tunnel Toll Authorities in the United States, Report No. IWS-45-02, National Institute for Occupational Safety and Health, Division of Surveillance, Field Studies, Hazard Evaluations, Cincinnati, OH, 1995. 81. Raaschou-Nielsen, O., Nielsen, M.L., and Gehl, J. Traffic-related air pollution: exposure and health effects in Copenhagen street cleaners and cemetery workers, Arch. Environ. Health, 50, 207, 1995. 82. Kamei, M. and Yanagisawa, Y. Estimation of CO exposure of road construction workers in tunnel, Ind. Health, 35, 119, 1997. 83. Flachsbart, P.G. and Ott, W.R. A rapid method for surveying CO concentrations in high-rise buildings, Environ. Int., 12, 255, 1986. 84. Flachsbart, P.G. and Brown, D.E. Surveys of Personal Exposure to Vehicle Exhaust in Honolulu Microenvironments., Department of Urban and Regional Planning, University of Hawaii at Manoa, Honolulu, HI, 1985. 85. Flachsbart, P.G. and Brown, D.E. Employee exposure to motor vehicle exhaust at a Honolulu shopping center, J. Archit. Plan. Res., 6, 19, 1989. 86. Bach, W. and Lennon, K. Air pollution and health at Ala Moana Shopping Center in Honolulu, Hawaii Med. J., 31, 104, 1972.

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87. Simeone, L.F. The Intrusion of Engine Exhaust into the Passenger Areas of Recreational Power Boats, Report No. DOT-VNTSC-CG-91-1, John A. Volpe National Transportation Systems Center, Cambridge, MA, 1991. 88. Snook, L.M. An investigation of driver exposure to carbon monoxide while traveling in the wake of a snowmobile, Ph.D. thesis, University of Tennessee, Knoxville, 1996. 89. Wilkinson, T. Snowed under, National Parks, 69, 32, 1995. 90. Snook, L.M. and Davis, W.T. An investigation of driver exposure to carbon monoxide while traveling in the wake of a snowmobile, Paper No. 97-RP143.02 presented at the 90th Annual Meeting of the Air & Waste Management Association, Toronto, Ontario, Canada, 1997. 91. Kwok, P.W. Reduction of carbon monoxide in indoor skating arenas, Environ. Health Rev., 25, 60, 1981. 92. Sorensen, A.J. The importance of monitoring carbon monoxide levels in indoor ice skating rinks, J. Am. Coll. Health, 34, 185, 1986. 93. Miller, R.K., Ryan, M.C., and Bilowus, P. Carbon monoxide poisoning in indoor ice skating arenas, Va. Med., 116, 74, 1989. 94. Lévesque, B., Dewailly, E., Lavoie, R., Prud’Homme, D., and Allaire, S. Carbon monoxide in indoor ice skating rinks: evaluation of absorption by adult hockey players, Am. J. Public Health, 80, 594, 1990. 95. Lévesque, B., Lavoie, R., Dewailly, E., Prud’Homme, D., and Allaire, S. An experiment to evaluate carbon monoxide absorption by hockey players in ice skating rinks, Vet. Hum. Toxicol., 33, 5, 1991. 96. Lee, K., Yanagisawa, Y., and Spengler, J.D. Carbon monoxide and nitrogen dioxide levels in an indoor ice skating rink with mitigation methods, Air Waste, 43, 769, 1993. 97. Lee, K., Yanagisawa, Y., Spengler, J.D., and Nakai, S. Carbon monoxide and nitrogen dioxide exposures in indoor ice skating rinks, J. Sports Sci., 12, 279, 1994. 98. Spengler, J.D., Stone, K.R., and Lilley, F.W. High carbon monoxide levels measured in enclosed skating rinks, J. Air Pollut. Control Assoc., 28, 776, 1978. 99. Paulozzi, L.J., Satink, F., and Spengler, R.F. A carbon monoxide mass poisoning at an ice arena in Vermont, Am. J. Public Health, 81, 222, 1991. 100. Smith, W., Anderson, T., Anderson, H.A., and Remington, P.L. Nitrogen dioxide and carbon monoxide intoxication in an indoor ice arena - Wisconsin, MMWR: Morb. Mort. Wkly. Rep., 41, 383, 1992. 101. Paulozzi, L.J., Spengler, R.F., Vogt, R.L., and Carney, J.K. A survey of carbon monoxide and nitrogen dioxide in indoor ice areas in Vermont, J. Environ. Health, 56, 23, 1993. 102. Hampson, N.B. Carbon monoxide poisoning at an indoor ice arena and bingo hall Seattle, 1996 [reprint of MMWR: Morb. Mort. Wkly. Rep., 45, 265, 1996] JAMA: J. Am. Med. Assoc., 275, 1468, 1996. 103. Boudreau, D.R., Spadafora, M.P., Wolf, L.R., and Siegel, E. Carbon monoxide levels during indoor sporting events - Cincinnati, 1992–1993 [reprint of MMWR: Morb. Mort. Wkly. Rep., 43, 21] J. Am. Med. Assoc., 271, 419, 1994. 104. Luckurst, D.G. and Solkoski, G. Carbon monoxide levels in indoor “tractor-pull events”—Manitoba, Can. Dis. Wkly. Rep., 16, 79, 1990. 105. Lévesque, B., Allaire, S., Prud’Homme, D., Rhainds, M., Lebel, G., Bellemarre, D., and Dupuis, K. Indoor motocross competitions: air quality evaluation, Am. Ind. Hygiene Assoc. J., 58, 286, 1997. 106. Colvile, R.N., Hutchinson, E.J., Mindell, J.S., and Warren, R.F. The transport sector as a source of air pollution, Atmos. Environ., 35, 1537, 2001.

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Carbon Monoxide Poisoning 107. Petersen, W. and Allen, R. Carbon monoxide exposures to Los Angeles area commuters, J. Air Pollut. Control Assoc., 32, 826, 1982. 108. Shikiya, D., Liu, C., Kahn, M., Juarros, J., and Barcikowski, W. In-vehicle Air Toxics Characterization Study in the South Coast Air Basin, South Coast Air Quality Management District, El Monte, CA, 1989. 109. Kleiner, B.C. and Spengler, J.D. Carbon monoxide exposures of Boston bicyclists, J. Air Pollut. Control Assoc., 26, 147, 1976. 110. Holland, D.M. Carbon monoxide levels in microenvironment types of four U.S. cities, Environ. Int., 9, 369, 1983. 111. Flachsbart, P.G., Mack, G.A., Howes, J.E., and Rodes, C.E. Carbon monoxide exposures of Washington commuters, J. Air Pollut. Control Assoc., 37, 135, 1987. 112. Chan, C.-C., Ozkaynak, H., Spengler, J.D., and Sheldon, L. Driver exposure to volatile organic compounds, CO, ozone, and NO2 under different driving conditions, Environ. Sci. Technol., 25, 964, 1991. 113. Flachsbart, P., Ott, W., and Switzer, P. Long-term trends in exposure to carbon monoxide on a California arterial highway, Paper No. 69237 presented at the 96th Annual Meeting of the Air & Waste Management Association, San Diego, CA, 2003. 114. Ott, WR., Mage, D.T., and Thomas, J. Comparison of microenvironmental CO concentrations in two cities for human exposure modeling, J. Expo. Anal. Environ. Epid., 2, 249, 1992. 115. Amiro, A. CO presents public health problems, J. Environ. Health, 32, 83, 1969. 116. Clements, J. School Bus Carbon Monoxide Intrusion, Report No. DOT-HS-803-705, National Highway Traffic Safety Administration, U.S. Department of Transportation, Washington, D.C., 1978. 117. Ziskind, R., Rogozen, M., Carlin, T., and Drago, R. Carbon monoxide intrusion into sustained-use vehicles, Environ. Int., 5, 109, 1981. 118. Hampson, N.B. and Norkool, D.M. Carbon monoxide poisoning in children riding in the back of pickup trucks, JAMA: J. Am. Med. Assoc., 267, 538, 1992. 119. Trompeo, G., Turletti, G., and Giarusso, O. Concentrations of carbon monoxide in underground garages, Rassegna di Medicina Industriale, 33, 392, 1964. 120. Chovin, P. CO, analysis of exhaust gas investigations in Paris, Environ. Res., 1, 198, 1967. 121. Goldsmith, J. Contribution of motor vehicle exhaust, industry, and cigarette smoking to community CO exposures, Ann. NY Acad. Sci., 15, 122, 1970. 122. Amendola, A. and Hanes, N. Characterization of indoor carbon monoxide levels produced by the automobile, In Indoor Air Volume 4, Chemical Characterization and Personal Exposure, NTIS Report No. PB85-104214, Berglund, B. et al., eds., Swedish Council for Building Research, Stockholm, 1984, 97–102. 123. Wilson, A.L., Colome, S.D., and Tian, Y. Air Toxics Microenvironment Exposure and Monitoring Study, South Coast Air Quality Management District, El Monte, CA, 1991. 124. Myronuk, D. Augmented ingestion of carbon monoxide and sulfur oxides by occupants of vehicles while idling in drive-up facility lines, Water Air Soil Pollut., 7, 203, 1977. 125. Wheatley, A.D., Sadhra, S., and Beach, J.R. Exposure to toxic gas and particle phase pollutants evolved during deployment of airbags in vehicles, Indoor Environ., 6, 134, 1997. 126. Flachsbart, P.G. Human exposure to carbon monoxide from mobile sources, In Carbon Monoxide, Khalil, M.A.K., Pinto, J.P., and Shearer, M.J., eds. [special issue of papers

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from an international conference, December, 1997, Portland, OR] Chemosphere: Global Change Science, 1, 301, 1999. Transportation Research Board. Expanding Metropolitan Highways: Implications for Air Quality and Energy Use, National Academy Press, Washington, D.C., 1995. Flachsbart, P.G. Long-term trends in United States highway emissions, ambient concentrations, and in-vehicle exposure to carbon monoxide in traffic, J. Expo. Anal. Environ. Epid., 5, 473, 1995. Haagen-Smit, A.J. Carbon monoxide levels in city driving, Arch. Environ. Health, 12, 548, 1966. Lawryk, N.J., Lioy, P.J., and Weisel, C.P. Exposure to volatile organic compounds in the passenger compartment of automobiles during periods of normal and malfunctioning operation, J. Expo. Anal. Environ. Epid., 5, 511, 1995. Systems Applications, Inc. Human Exposure to Atmospheric Concentrations of Selected Chemicals, Vol. II, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC, 1983. Stewart, R.D., Fisher, T.N., Hosko, M.J., Peterson, J.E., Baretta, E.D., and Dodd, H. C. Experimental human exposure to methylene chloride, Arch. Environ. Health, 25, 342, 1972. Stewart, R.D. and Hake, C.L. Paint-remover hazard, JAMA: J. Am. Med. Assoc., 235, 398, 1976. Buie, S.E., Pratt, D.S., and May, J.J. Diffuse pulmonary injury following paint remover exposure, Am. J. Med., 81, 702, 1986. Peterson, J.E. Modeling the uptake, metabolism and excretion of dichloromethane by man, Am. Ind. Hyg. Assoc. J., 39, 41, 1978. ACGIH. Threshold Limit Values for Chemical Substances and PhysicalAgents: Biological Exposure Indices, American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 1996. U.S. EPA. Health Assessment Document for Dichloromethane Methylene Chloride, Report No. EPA/600/8-82/004F, Office of Health and Environmental Assessment, U.S. Environmental Protection Agency, Research Triangle Park, NC, 1985. Shusterman, D., Quinlan, P., Lowengart, R., and Cone, J. Methylene chloride intoxication in a furniture refinisher: a comparison of exposure estimates utilizing workplace air sampling and blood carboxyhemoglobin measurements, J. Occup. Med., 32, 451, 1990. Ghittori, S., Marraccini, P., Franco, G., and Imbriani, M. Methylene chloride exposure in industrial workers, Am. Ind. Hyg. Assoc. J., 54, 27, 1993. Leikin, J.B., Kaufman, D., Lipscomb, J.W., Burda, A.M., and Hryhorczuk, D.O. Methylene chloride: report of five exposures and two deaths, Am. J. Emerg. Med., 8, 534, 1990.

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3

Carbon Monoxide Build-Up in Houses and Small Volume Enclosures Robert E. Engberg

CONTENTS 3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2 Carbon Monoxide Safety and Monitoring Devices . . . . . . . . . . . . . . . . . . . . . . . 3.3 Metabolic Uptake of Oxygen and Room Air Ventilation for Humans . . . 3.4 The Tracer Gas Model for Predicting CO Accumulation in Structures . . 3.5 Ventilation Requirements for Humans in Small Structures . . . . . . . . . . . . . . . 3.6 Oxygen Depletion Sensor Applications to Small Burners . . . . . . . . . . . . . . . . 3.7 Combustion Equations for Gas Burners . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.8 Carbon Monoxide Accumulation Due to Small Engine Exhaust Gases . . 3.9 OSHA and Industry Standards for CO Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . 3.10 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

43 44 45 47 48 48 50 53 54 54 55

3.1 INTRODUCTION The problem of carbon monoxide (CO) production within habitable enclosures (i.e., breathing spaces) has been a chronic problem since the use of hydrocarbon fuels became widespread. We know that CO generation from these fuel sources is commonly caused by the lack of, or starvation of, adequate oxygen during the combustion process whether in a heating appliance, engine, or lighting fixture. The creation of CO becomes a problem when it enters an occupied space used by living creatures, either by accident or by design. Humans cannot sense such occult emissions until the blood saturation with CO begins to affect coordination and mental state. CO is transparent and colorless to the occupant of the space, as well as being odorless and nonirritative. When CO is discovered in significant concentration in a breathing space, the occupants may suffer sickness and even death. The presence of CO is not usually suspected in an enclosed space until dangerous levels are reached. CO generation from burning hydrocarbon fuels in combustion devices is due most often to improper fuel–air combustion ratios. This can be caused by oxygen starvation 43

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at the burner and by improper setting of the fuel–air ratio at the appliance. Testing of combustion devices installed in small enclosures reveals that 4–5 air changes per hour (ACH) is necessary to allow the device to operate safely and not generate a CO concentration of greater than 100 parts per million (ppm). Experience shows that the fuel–air ratio of the burner can be easily upset by lack of inspection and maintenance of the combustion device. Primary air adjustment shutters are commonly obstructed by the collection of dust and lint, while combustion air passages can become restricted or exhaust ventilation ducts plugged. This causes the production of CO in closed spaces. It was not until the 1980s that the use of burner safety devices were legislated and used within the United States to attack the problem of CO deaths and injuries in closed breathing spaces. During the past 10 years, manufacturers of small portable heating appliances have designed and installed burner safety devices to affect shutdown under ambient conditions that might produce dangerous levels of CO. The most common and simple safety device built into fuel consuming appliances has been the oxygen depletion sensor (ODS). It is incorporated into the flame safety system of most burners. A typical ODS consists of a thermocouple that senses flame outage and acts to shut down the fuel valve and the pilot flame. This combination makes up the typical flame safety and ODS assembly on a fuel-burning device. A second option has been to incorporate a CO sensor into devices such as gas engines. The past decades have brought national and state codes and standards to bear in an effort to eliminate CO hazards in fuel burning devices, and in building construction standards and techniques. The American National Standards Institute (ANSI), the National Fire Protection Association (NFPA), the Consumer Product Safety Commission (CPSC), Underwriters Laboratory (UL), Canadian Gas Association (CGA) and the Occupational Safety and Health Administration (OSHA) are at the forefront as agencies that write and enforce CO safety device requirements in commercial products and building construction. One example of a standard is the requirement for minimum exhaust concentration limits generated within a test enclosure that is heated with a liquefied petroleum (LP) gas fueled, infrared (IR) camp type heaters (ANSI and CGA). Technology has greatly advanced in CO monitoring techniques and the measurement of environmental conditions. We can now estimate the oxygen uptake of a human at a given activity level in a closed space, in the presence of CO being produced by a malfunctioning heater operating under specified air exchange and combustion rates. We will discuss each of these techniques in the following sections.

3.2 CARBON MONOXIDE SAFETY AND MONITORING DEVICES It has become commonplace to install CO sensors in breathing spaces that have the potential of accumulating CO due to fuel combustion by heating appliances and engines. CO alarms are available at most hardware and home supply stores. The law requires CO monitors in most new house and apartment construction. For the UL

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standards governing the set points of common CO alarms see Chapter 28 in this book. The way UL has set up the standards, lower CO concentrations take longer to produce audible alarm while higher CO concentrations trip the alarm in less time. The intent is to roughly model the rate of CO uptake by humans. Other types of CO monitors are designed for marine engine rooms, industrial environments, and so forth. Monitoring and data logging CO sensors are available for personal use, where walk around monitoring of an indoor environment may be needed. These units are available in pocket-sized and handheld models that record data from the environment at preset time intervals and store the data for downloading to computer for later display and interpretation. As stated above, the ODS has become popular for the safe shutdown of burner systems. The device has a calibrated shutdown feature that gauges ambient oxygen concentration by changing flame shape. The predetermined pilot flame will degrade in shape with the reduction of ambient oxygen. When this happens, the flame moves off the thermocouple, causing thermocouple output current to decline, which trips a gas valve, shutting down the burner. This principle was developed in Europe. The ODS has been a common safety device required on gas heating appliances since the 1970s. The pilot flame is a common safety device used with gas fueled appliances. It has been used successfully for many decades in the United States and Europe. It assures the ignition of any gas fumes or vapors around the burner and serves to ignite the burner. Its continued operation is also monitored through the use of a thermocouple that senses pilot flame heat. Pilot flames may be ignited either by a match or the everpopular piezoelectric spark igniter. The latter has become an added safety feature on gas burning appliances, since no open continuously burning flame is present, which might present a fire hazard and also consumes fuel over time. Exhaust stack gas analyzers are another type of CO sensor used to monitor boiler burner combustion efficiency. These handheld analyzers and monitors can be used to data-log exhaust stack conditions in terms of CO, oxygen, and carbon dioxide. They may also monitor other burner characteristics such as temperature, draft, excess air, and unburned hydrocarbons. These units also allow burner overall efficiency to be computed in a continuous fashion. Placing a thermocouple near the burner screen on an LP-fueled camp heaters is another safety device. One characteristic of some infrared heaters is the variation of burner screen temperature with respect to declining oxygen levels in a heated breathing space. The manufacturer may chose to design the screen-thermocouple such that it will shut down the burner with decreasing oxygen levels. This will occur before burner CO production is excessive. The details of this option are discussed later in this chapter.

3.3 METABOLIC UPTAKE OF OXYGEN AND ROOM AIR VENTILATION FOR HUMANS A major concern for humans occupying a small breathing space is the provision for adequate ventilation of that space for creature comfort, health, and safety. One design

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question is just how much oxygen is consumed by the human body and how much ventilation is needed. To do that we must estimate the oxygen uptake of the human body. Coupled with this concern will be determining the oxygen depletion within the space that can be expected or allowed. For a description of the metabolic variables necessary for this calculation see Reference 1. All of these variables and concerns are best addressed by an example of a typical breathing space and occupant model. Such an example might be two hunters sleeping in a camp tent. The parameters that will be assumed for this calculation are as follows: 1. A tent will be of a cabin-type design, with nominal floor dimensions of 7.5 × 9.5 × 6.0 ft. (w × l × h), respectively, or 235 cu. ft., approximately. The tent will have been treated with a water repellent coating. 2. Two men sleeping and each weighing 200 pounds, no outdoor wind, and all tent windows and opening flaps closed. 3. A propane fueled, infrared heater set at a low heat setting of 8000 BTU/h, using commercial propane with a higher heating value (HHV) of 2550 BTU/cu. ft.2 4. Ambient air having 20.9% oxygen, and a design lower limit of 18.5% oxygen, where CO begins to be generated when using a typical camp heater. The mathematical variables used in the following equations and calculations are defined as follows with their associated units denoted in [… ..]: ACH = Vm /Ve , where Vm = minimum rate of fresh airflow per person, [cu. ft./h] and Ve = volume of the enclosure [cu. ft.]. M = metabolic rate (met) for a human is given as, 1 met = 18.4 [BTU/h * sq. ft.]. And M = 567(0.23∗ RQ+0.77)∗ QO2 /Ad, where RQ = 0.83 for light and sedentary activity; QO2 = volumetric rate of oxygen consumption at conditions (STPD) of 32◦ F, 14.7 psi (std. atm.) [cu. ft./h], and for a sleeping man the value to be used is M = 13 BTU/h*sq. ft. Now, solving for the oxygen uptake: QO2 = 13∗ 19.6/567∗ (0.23∗ 0.83 + 0.77) = 0.47 cu. ft./h. So, for two men, the oxygen uptake in the tent will be 0.94 cu. ft./h. Now, from our defined limits of minimum oxygen reduction in this space, we have: QO2 avail = (0.209 − 0.185)∗ V = 0.024∗ 235 = 5.64 cu. ft. of oxygen available. We next consider the oxygen uptake by the LP, infrared camp heater set at the “low” heat position, with a fuel flow as defined above. Using the HHV for propane vapor as 2550 BTU/cu. ft. (Reference 2, p. 24) and the stoichiometric combustion of propane, (volume of oxygen reacting for each volume of LP vapor is 5), we have: VO2 /VLP = 5 Therefore, when operating at the ‘low’ heat setting of 8000 BTU/h, we get: VLP = 8000/2550 = 3.137 cu. ft./h of propane used.

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Next, the volume of oxygen utilized by the heater becomes VO2 = 5∗ 3.137 = 15.69 cu. ft./h. The time (t) needed to bring the oxygen level down to the critical minimum level at the onset of CO production will be: t = QO2 avail /(VO2 +2∗QO2 ) = 5.64/(15.69 + 0.94) = 5.64/16.62 = 0.339 h or 20.4 min. We can expect that after this amount of time spent in the tent, CO will begin to be generated by the heater assuming that no air exchange, or infiltration, has occurred during this period of time. The next job is to estimate the amount of infiltration air (ACH) that will be needed to maintain the oxygen level within the tent above 18.5%, remembering that the heater and the two men are competing for the available oxygen. We first write the equation that: QO2 (consumed) = QO2 (infiltrated) = 15.69 + 0.94) = 16.63 cu. ft./h = (0.209 − 0.185)∗ Vair , so, Vair = 16.63/0.024 = 692.7 cu. ft. of air exchange. Thus, ACH = Vm /Ve = 692.7/235 = 2.95 air changes per hour are needed to maintain an 18.5% level of oxygen in the tent. This value for ACH is in good agreement with experimental values for ACH required for LP heaters to not accumulate CO in closed breathing spaces.3

3.4 THE TRACER GAS MODEL FOR PREDICTING CO ACCUMULATION IN STRUCTURES This approach allows one to predict ACH for any enclosure. It is assumed that the tracer gas is distributed uniformly in the initial charge of fugitive gas used for this measurement. It is also assumed that air infiltration into the structure is uniformly distributed throughout the space. The typical tracer gas used for this measurement is sulfur hexafluoride (SF6 ). Its concentration (C) is described by the equation Ct = Co e−kt and solving for kt, ln (Ct /Co ) = −kt The latter equation indicates that a semilog plot of the quantity ln (Ct /Co ) versus time will be linear with time and that the ACH, (k) will be equal to the slope of this line. Since this line is expected to be linear, linear regression can be used to fit a line to the data and the expression describing how well the line fits the data is R2 , where R is the correlation coefficient. Assume that if testing yields an R2 greater than 0.9, then the test is acceptable. Now, if the ACH (k) is known, then the source strength (S) for CO generation of the heater can be computed from a simple mass balance of CO in the chamber. The equation predicting the CO generation rate is St(i+1) =

V ∗ k[Ct(i+1) − Ct(i) ∗ e−k{ti+1 −ti } ] , [1 − e−k{ti+1 −ti } ]

where V = the tent volume; St(i+1) is the generation rate of CO at time ti+1 , k = ACH, Ct(i+1) is the concentration of CO at time ti+1 and Ct(i) is the concentration of CO at time ti . The above equation was derived based on the assumption that the air in the

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chamber is well mixed and that CO is not absorbed or adsorbed into the tent material or its contents.

3.5 VENTILATION REQUIREMENTS FOR HUMANS IN SMALL STRUCTURES The ventilation rate for a small enclosure is much the same as for larger spaces that are designed for occupation by humans. The American Society of Heating, Refrigeration, and Air Conditioning Engineers (ASHRAE) standard 62 specifies guidelines for the minimum ventilation airflow rate for various habitable structures. A flow rate of 15 scfm per person is a common requirement for residential structures. This flow rate will provide enough air to maintain the normal oxygen level for an average adult and will remove most pollutants as they accumulate in typical spaces. To reiterate, the oxygen depletion due to its uptake by two adults using a small camp heater within a tent space requires a minimum of about 3–6 ACH to supply enough oxygen to allow proper metabolism and to prevent the dangerous accumulation of CO. One must look at the geometry of the tent to predict whether the ACH will be effective for the occupants. Please make reference to the ASHRAE Fundamentals Handbook 1 that describes the dynamics of ventilation in a breathing space. It asks designers to incorporate cross ventilation such that lower air levels are systematically exchanged at the prescribed rate. This prevents vent gases or other pollutants from settling down and accumulating in sleeping areas. The method of cross ventilation that incorporates a low level air entry opening with an upper level exhaust or discharge opening of equal area is the optimum design, as it promotes thermal differences and relative ambient winds to power air exchange within the space. The designer should use, as a rule of thumb, about 1 sq. in. per 1000 BTU/h of burner capacity. The definition of a confined space is considered to be 50 cu. ft. for each 1000 BTU/h of input burner rating. No single vent opening dimension should be less than 3 in. This ventilation flow rate will translate to an ACH in the tent computation to be: ACH = 15 cu. ft./min*60 min/h/235 cu. ft. = 3.83. We may compare this value with the calculated ventilation needed to maintain the minimum oxygen level for combustion in the above example of 2.95 ACH. Clearly, a ventilation rate to avoid CO buildup was about 6.0 ACH as shown in Reference 3. This resulted in less than 100 ppm CO.

3.6 OXYGEN DEPLETION SENSOR APPLICATIONS TO SMALL BURNERS An ODS system is simply a pilot burner whose flame impinges on a thermocouple that in turn powers a gas safety valve electromagnet. What is unique about an ODS is the tripping of the gas safety valve at a specified level of oxygen depletion. The tent enclosure computation above specified the oxygen safety valve trip level was 18.5%, as compared to a normal ambient oxygen concentration of 20.9%. Codes and

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standards recognize that it is not healthy or safe for humans to function in oxygen reduced atmospheres (<18%) for more than 8 h. The theory of ODS operation is based on flame geometry changing during a reduction in ambient oxygen (Figure 3.1). Change in position of the pilot flame with respect to the thermocouple allows the thermocouple tip to cool to a point that will cause the electromagnet to trip the safety valve, shutting off the heater’s burner. Safety shutdown is typically designed to occur at 18.5% ambient oxygen. This oxygen level is above the threshold that will cause excessive CO to be produced within the burner. Typical ODS flame geometry changes are shown in Figure 3.1. The ODS was developed and used extensively in Europe for 30 years prior to it being adopted in the United States in 1980. It was first mandated here on ventless,

Pilot burner Thermo couple

Ignition plug

Gas

Pilot burner Thermo couple

Ignition plug

Pilot burner Thermo couple

Ignition plug

Gas

FIGURE 3.1 Operation of an oxygen depletion sensor. Upper panel: Normal operation— 20.9% oxygen. Pilot flame touches tip of thermocouple, generating the thermoelectricity needed to hold the safety valve open. Middle panel: Oxygen level dropping—19% oxygen. The flame begins to lift off the precision pilot burner. The thermocouple begins to cool. Lower panel: Safety shutdown—18% oxygen. The unstable pilot flame moves away from the thermocouple to stop generating the electricity needed to hold the spring-loaded safety valve open. The heater shuts down. (Source: Adapted from a sales brochure, no copyright, ca. 1996.)

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gas space heaters. In the late 1990s, this safety device was beginning to be applied to gas heaters used by the hunters, campers, and the recreational industry generally for satisfying the demand for safe, small, infrared, and catalytic heaters. Many infrared camp heater designs use LP gas to fuel the main burner at relatively high vapor pressures, that is, typically 7–15 psig. Pressure at the burner orifice or gas tip is controlled by a gas regulator on the heater control panel, that is, the heat setting control knob. This knob usually adjusts the regulator to about 7 psig in the low heat range and to about 15 psig in the heater’s high heat range. These regulator pressures are problematic for the ODS pilot burner, because it usually operates at about 3–5 inches water column (in. w.c.), or approximately 0.11–0.18 psig. One solution for this problem is to add a second stage regulator that reduces the high pressure going to the main burner regulator to a lower pressure. Normally, some pilot flame shielding is required to deflect radiated heat from the main burner and also to shield the small ODS flame from wind and drafts, thus stabilizing the ODS flame’s play on the thermocouple. The approximate heat output of a typical ODS flame at 3.5 in. w.c. pressure, using a 0.00665 in. diameter, 60◦ orifice angle, will be 175 BTU/h. This is the maximum amount of gas that may pass through the pilot burner without having a code required safety valve to shut off the pilot gas flow when flame outage occurs. It may be desirable to relax this orifice diameter in order to fit a commercially available drill bit size, for example, 0.006 in. Using this bit and the 175 BTU/h code limitation, we can use a 5.3 in. w.c. orifice pressure. This will produce a desired maximum gas flow and satisfy the safety code. The burner system designer may now determine the most economical arrangement of gas safety shutdown piping and equipment for his product. Also, the heater designer has the choice of commercially available vertical, angled, and horizontally mounted ODS designs in order to best accommodate his design preferences. Some other ODS variants have been used by Copreci, an Italian manufacturer.

3.7 COMBUSTION EQUATIONS FOR GAS BURNERS The reader is advised to refer to Reference 4 for a complete summary of formulae to determine the products of combustion for gaseous fuels such as propane and butane that are typically used to fuel space and construction heaters for small volume enclosures. This reference also details the combustion analysis that relates the amount of combustion air needed for the stoichiometric combustion of various gaseous fuels. Such an equation for the stoichiometric or theoretical oxidation of propane will be Balanced equation: C3 H8 + 5O2 = 3CO2 + 4H2 O Molecular weights: 44.094 + 5∗ 32 = 3∗ 44.01 + 4∗ 18.016 Relative combining weights: 1 lb + 3.629 lb = 2.995 lb + 1.634 lb Combustion data for typical hydrocarbon fuels are given in Table 3.1.2 Additional combustion data and LP-gas properties are found in reference 4. It should be remembered that commercial propane (i.e., LP-gas) contains a number of other hydrocarbons that are limited by the HD5 or HD-5, P grade specification. That is,

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CH4 C2 H4 C2 H3 C4 H10 C5 H12 C2 H4 C3 H6 C4 H8 9.55 16.70 23.86 31.02 38.19 14.32 21.48 28.58

Air 2.0 3.5 5.0 6.5 8.0 3.0 4.5 6.0

Oxygen 1.0 2.0 3.0 4.0 5.0 2.0 3.0 4.0

Carbon Dioxide 2.0 3.0 4.0 5.0 6.0 2.0 3.0 4.0

Water Vapor 7.55 13.20 18.86 24.52 30.19 11.31 16.98 22.58

Nitrogen

Products of Combustion ln Cu. FL. formed by Burning 1 cu. ft.

17.24 16.13 15.71 15.49 15.35 14.80 14.80 14.80

Air 3.98 3.73 3.63 3.58 3.54 3.42 3.42 3.42

Oxygen

Pounds Required for Combustion 1 lb. of Gas or Vapor

Source: Handbook Propane–Butane Gases, 4th ed., Chilton Company, Los Angeles, CA, PP. 22,23 1962.

Methane Ethane Propane Butane Pentane Ethylene Propylene Butylene

Chemical Formula

Cubic Feel Required per Cu. Ft. of Gas or Vapor for Combustion

TABLE 3.1 Combustion Data for Hydrocarbons

2.74 2.92 2.99 3.03 3.05 3.13 3.13 3.13

Carbon Dioxide

2.24 1.79 1.63 1.55 1.50 1.28 1.28 1.28

Water Vapor

13.26 12.40 12.08 11.91 11.80 11.38 11.38 11.38

Nitrogen

Products of Combustion in Pounds from Burning One Pound Gas or Vapor

11.7 13.1 13.7 14.0 14.2 15.0 15.0 15.0

Ultimate Carbon Dioxide ln Flue Products Percent

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TABLE 3.2 Physical and Chemical Properties of LP-Gasa Propane Formula Boiling point (◦ F) Specific gravity of gas (air = 1.00) Specific gravity of liquid (water = 1.00) lb per gallon of liquid at 60◦ F BTU per gallon of gas at 60◦ F BTU per lb. of gas BTU per cu. ft. of gas at 60◦ F cu. ft. of vapor (at 60◦ F) gallon cu. ft. of vapor (at 60◦ F) lb Latent heat of vaporization at boiling point BTU per gallon Combustion data cu. ft. air required to burn 1 cu. ft. gas Flash point (◦ F) Ignition temperature in air (◦ F) Maximum flame temperature in air (◦ F) Limits of flammability percentage of gas in air mixture At lower limit (%) At upper limit (%) Octane number (ISO-Octane = 100)

Butane

C3 H8 −44 1.50 0.504 4.20 91,502 21,548 2488 36.38 8.66 773

C4 H10 15 2.01 0.582 4.81 102,032 21,221 3280 31.26 6.51 808

23.86 −156 920–1120

31.02 N.A. 900–1000

3,595

3,615

2.15 9.6

1.55 8.6

Over 100

92

a Commercial quality. Figures shown in this chart represent average values.

Source: LP-Gas Serviceman’s Manual Engineered Controls International, Inc. (Reg O), Elon College, NC, pp. 2,3, 1962, Revised March, 2000.

propane must constitute a minimum of 90.0% of the gas, propylene can be at most 5.0%, and the butanes and heavier aliphatics must not exceed 2.5%. For a summary of the properties of commercial propane and butane, the reader is referred to Table 3.2.5 The LP-gas is to have a vapor pressure at 100◦ F of greater than 175, but not exceeding 208 psig (Table 3.3). Other reference sources are 4 and 6. It is sometimes necessary to compute CO in combustion products in a specific manner to comply with industry standards as defined on an free-air basis. Instruments can determine the amount of CO on an air-free basis by first measuring the amount of oxygen and CO present in the sample, then using the following equation to calculate CO on a free-air basis: CO air-free = 20.9∗ CO/(20.9 − O2 %)

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TABLE 3.3 Vapor Pressures of LP-Gasesa Temperature (◦ F) (◦ C) −40 −30 −20 −10 0 10 20 30 40 50 60 70 80 90 100 110

−40 −34 −29 −23 −18 −12 −7 −1 4 10 16 21 27 32 38 43

Approximate Pressure (PSIG) Propane Butane 3.6 8 13.5 23.3 28 37 47 58 72 86 102 127 140 165 196 220

3.0 6.9 12 17 23 29 36 45

a Conversion formula: Degrees C = (◦ F − 32) × 5/9

Degrees F = (9/5 ×◦ C) + 32 Source: LP-Gas Serviceman’s Manual, Engineered Controls International, Inc. (Reg O), Elon College, NC, pp. 2,3, 1962, Revised March, 2000.

This computation compensates for the amount of excess air provided by the burner. Excess air from a burner dilutes the products of combustion and causes a test for CO to be understated. A CO air-free measurement eliminates the excess air dilution.

3.8 CARBON MONOXIDE ACCUMULATION DUE TO SMALL ENGINE EXHAUST GASES Some serious injuries and deaths have occurred because the general public is not fully aware of the latent danger in operating internal combustion engines in confined breathing spaces or in poorly ventilated structures. An analysis of the combustion products or exhaust gases from engines fueled by hydrocarbons shows they generally produce CO in great abundance as compared to burners in various heaters and lighting appliances. As a comparison, a gas burning appliance will be “red tagged” in many municipalities if its flue products contain an excess of 400 ppm of CO. Some states have limited the legal level of CO in the automobile engine exhaust at 1.2%. Precatalytic CO production in typical gasoline engines is 12,000 ppm CO or more. A poorly tuned gasoline engine may produce 30 times the CO that a misadjusted gas

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burning appliance will typically generate. In most cases where gasoline engines are operated, engine exhaust is vented directly into the habitable space as opposed to an exhaust stack as with gas burning appliances. Use of a breathing space shared by a running gasoline engine subjects the people to lethal concentrations of CO very quickly and unexpectedly. The consequences of operating a small gasoline engine in a closed space are seen in Reference 7. For example, a 5 hp, four-cycle, gasoline-fueled engine will generate CO at a rate of 1.72 cfm. A simple calculation reveals that for most small structures, a significantly elevated CO concentration will exist there after just a few moments of engine operation. Thus, gasoline-powered engine operation in small rooms becomes hazardous to the occupants very quickly and requires excessive ventilation, that is, many ACH. In fact, the number of ACH necessary to limit CO buildup in such a space may be in excess of 20 just to limit the CO concentration to 400 ppm. The rule of thumb is that small gasoline-fueled engines should NEVER be operated in closed breathing spaces.

3.9 OSHA AND INDUSTRY STANDARDS FOR CO EXPOSURE In times past, a 100 ppm CO exposure level was acceptable for humans over extended periods of time, that is, the 8-h workday. The history of acceptable CO standards for human exposure has been one of a gradual decline in that number over the past 100 years. National Institute for Occupational Safety and Health (NIOSH) and OSHA now use a level of 35 ppm, time-weighted-average (TWA), over 8 h. The concern has been to keep blood carboxyhemoglobin saturation to less than 5% for both chronic exposure in the workplace and for workers with cardiovascular or pulmonary disease. Other approval and standards organizations such as ASHRAE defer in their Standard 62-89 to the Environmental Protection Agency (EPA) standard for outdoor air quality. EPA sets the ambient limit at 9 ppm, averaged over 8 h. EPA also allows exposure to 35 ppm CO or lower, averaged over 1 h. Finally, the ANSI guide number Z21.1, allows the ambient atmosphere surrounding an unvented space heater to achieve a maximum of 200 ppm CO when measured on an air-free basis. On the same basis, a maximum flue gas concentration of 400 ppm is allowed and an unvented gas oven may produce a maximum of 800 ppm. See Section 3.7 for the equation used to calculate CO on a free-air basis. Many state statutes limit flue gas products of combustion for a heating appliance to no more than 400 ppm at anytime in the equipment setup or operating range. Many state and municipal inspectors will “red tag” any fuel burning appliance that is found to exceed that CO limit.

3.10 CONCLUSION The aspects of CO accumulation in small structures introduced by using consumer products such as LP-gas heaters, lanterns, and small gasoline engines motivates a special series of cautions, warnings, designs, and code compliance considerations.

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These concerns must be addressed by the consumers, designers, and certainly by the engineers creating products and structures for the stream of commerce. The number of mishaps and associated litigation speaks for the issue of properly operating fuelburning products in small structures such as tents, fishing shanties, campers, garages, and so forth to name just a few. The first aspect of operating these appliances in small breathing spaces must be that of safety for the consumer, that is, public. The chemical and physiological effects of CO have made it a serious design factor for engineers, manufacturers, and consumers alike.

References 1. Berglund, L.G. ASHRAE Handbook-Fundamentals, American Society of Heating, Refrigerating and Air Conditioning Engineers, Inc., Atlanta, GA, pp. 8.6, 8.7, Chapter 8, 2001. 2. Denny, L.C., Luxon L.L. and Hall, B.E. Handbook Propane–Butane Gases, 4th ed., Chilton Company, Los Angeles, CA, pp. 22, 23, 1962. 3. Tucholski, D.R. Technical Feasibility of a CO Shutdown System for Tank-Top Heaters, U.S. Consumer Products Safety Commission (CPSC), Washington, D.C., p. 53, 2005. 4. Reed, R.J. North American Combustion Handbook, 3rd ed., Vol. 1, North American Manufacturing Company, Cleveland, OH, p. 49, 1986. 5. LP-Gas Serviceman’s Manual, Engineered Controls International, Inc. (RegO), Elon College, NC, 1962, Revised March, 2000. 6. Segeler, C.G. Editor-in-Chief; Ringler, M.D., Assistant Editor; Kafka, E.M., Technical Assistant, Gas Engineers Handbook, The Industrial Press, New York, NY, pp. 6–33, 1966. 7. Earnest, G.S., Mickelsen, R.L., McCammon, J.B. and O’Brien, D.M. Carbon monoxide poisoning from small, gasoline-powered, internal combustion engines: just what is a well-ventilated area? Am. Ind. Hyg. Assoc. J., 58, 787–791, 1997.

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4

Formation and Movement of Carbon Monoxide into Mobile Homes, Recreational Vehicles, and Other Enclosures Robert E. Schreter

CONTENTS 4.1 4.2 4.3 4.4

4.5

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Accident Statistics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Codes and Standards . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Potential Sources of Carbon Monoxide within Motor Homes and Other Enclosures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.1 Internal Combustion Engines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.1.1 Large Vehicle Propulsion Engines . . . . . . . . . . . . . . . . . . . . . . 4.4.1.2 Auxiliary Power Generators . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.2 Interior Devices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.2.1 Ranges . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.2.2 Ovens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.2.3 Gas Refrigerators (LP Gas) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.2.4 Domestic Water Heaters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.2.5 Gas or Oil-Fired Space Heaters . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.2.6 Clothes Dryers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.2.7 Fireplaces (LP Gas) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.2.8 Other Sources . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Primer on the Mechanism of Formation of Carbon Monoxide from Fuel-Fired Appliances found in Mobile Homes . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.5.1 The Physical and Chemical Properties of Carbon Monoxide . . . . . 4.5.2 The Combustion Process . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

58 59 59 60 61 62 62 64 64 64 65 65 65 65 66 66 67 67 68

57

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4.5.2.1

Basic Requirements to Initiate and Perpetuate the Combustion Process . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.5.3 Thermochemical Equations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.5.4 Excess Air Combustion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.5.5 Excess Fuel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.6 Application of Combustion Theory to Actual Carbon Monoxide Poisoning Situations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.6.1 Introduction to the Flow of Exhaust Gases . . . . . . . . . . . . . . . . . . . . . . . . 4.6.2 Total Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.6.3 Stagnation Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.6.4 Thermal Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.6.5 Air Flow Around and Through Enclosures . . . . . . . . . . . . . . . . . . . . . . . . 4.6.6 Wind Rose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.6.7 Scoops, Deflectors, and Openings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.6.8 Resonance, Cyclical Flow into and out of an Enclosure. . . . . . . . . . 4.6.9 Flow into and out of Living Quarters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.6.10 Flue and Chimney Dynamics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.6.11 Back-drafting of Flue Gases into the Enclosure . . . . . . . . . . . . . . . . . . 4.6.12 Dynamics of Generator Tailpipe Exhaust . . . . . . . . . . . . . . . . . . . . . . . . . 4.6.13 Exhaust Flow Through Bent or Displaced Exhaust Pipes . . . . . . . . 4.6.14 Missing Exhaust Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.7 Accumulation of Carbon Monoxide within an Enclosure. . . . . . . . . . . . . . . . . 4.7.1 Rate of Dissipation of Carbon Monoxide from an Enclosure . . . . 4.8 Test Methods for Determining the Location of Leakage into an Enclosure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.8.1 Smoke Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.8.2 Basic Considerations during Smoke Testing . . . . . . . . . . . . . . . . . . . . . . 4.8.3 Positive Pressure Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.8.4 Negative Pressure Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.8.5 Typical Smoke Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.9 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

68 69 71 72 72 72 73 75 76 77 78 78 81 82 82 83 83 85 86 87 89 90 91 91 92 92 93 96 96

4.1 INTRODUCTION This chapter deals with nonfire related carbon monoxide (CO) poisoning accidents that occur in mobile homes, live-in trailers, portable offices and other mobile living or work enclosures containing devices that can produce CO or other toxic gases. The flow mechanisms and equations presented apply equally to all stationary buildings subject to wind and thermal activity. I will briefly discuss American National Standards Institute (ANSI) and National Fire Protection Association (NFPA) codes that apply to recreational vehicles, motor homes and the like and stress the code requirements involved in sealing the living compartment against toxic gases and vapors produced externally. This chapter addresses the individual sources that generate CO within the living compartment and sources that are part of the mobile home but external to the living compartment, as well as those produced in the vicinity. It discusses each

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of the appliances, the mechanisms by which they produce CO and the expected concentration of CO associated with them. It compares the probability of their entering into life threatening asphyxiations. It also discusses other sources of CO emanating from other vehicles or generators in the vicinity. I will discuss the physical properties and behavior of CO and the mechanism of its formation in various types of appliances and internal combustion engines. It discusses the combustion process, thermochemical equations, and how excess air, excess fuel, mixing of air and fuel and available time for the completion of combustion affect its production. I will introduce the concept of total pressure, including wind and thermal pressure and how these pressures are the driving forces that result in CO penetrating leaks into the living compartment. The chapter covers the application of combustion theory and aerodynamics and how they apply to CO accidents. It discusses how wind and the aerodynamic shapes and openings encountered in mobile homes and other enclosures affect air and gas flow movement into, through, and out of enclosures. There is a general discussion of exhaust systems for internal combustion engines and how they play a role in life threatening CO asphyxiations. It discusses how missing or damaged engine generator tailpipes are major contributors to fatal accidents. This chapter presents methods used to evaluate the rate of accumulation of CO within enclosures. Computational methods used to determine CO concentration at any point in time during the inflow are presented. It also presents computational methods to determine the dissipation of CO during periods where the generating source is shut down or its flow rate curtailed. The methods presented predict the partial pressure within an enclosure and how it may be used in conjunction with the Coburn–Forster– Kane equation to predict carboxyhemoglobin (COHb) in a victim’s blood (see other books in this series). Finally, the chapter discusses methods that may be used to determine the locations of leaks into the living compartment and the magnitude of inflow into the enclosure.

4.2 ACCIDENT STATISTICS Between 1995 and 1999, an estimated 10,200 people reported to hospital emergency rooms each year for nonfire-related CO poisoning injuries associated with consumer products.1 There were more than 500 unintentional nonfire related deaths and injuries resulting from CO-poisoning accidents associated with the use of consumer products. An average of 22 deaths per year was associated with engine-driven generators and engine-driven products, which includes deaths associated with mobile homes. Between 1993 and 1997 deaths from motor vehicle exhausts, averaged 534 annually. Many CO accidents are not recognized, and because of data collection problems, many cases go unreported. Nonfatal injuries mostly go unreported, therefore, there are few accurate statistics.

4.3 CODES AND STANDARDS TheANSI 119.2,2 and NFPA501c3 have written and promulgated standards applicable to CO in mobile homes and recreational vehicles. The standards cover fire and life

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safety criteria for recreational vehicles to provide reasonable protection from loss of life from fire and explosion. In particular, the standard sets down requirements for fuel burning devices used in connection with recreational vehicles. They pay special attention to the location of internal combustion engines and their exhaust ports relative to leakage into the living compartment of the vehicle. In essence, the codes state that exhaust gases shall be directed away from the vehicle and that the exhaust system shall be installed in a manner by which the exhaust pipes are not unduly subject to road damage. They also state that all fuel-burning devices, except ranges and ovens, shall be designed and installed to provide for the complete separation of the combustion system from the interior atmosphere of the recreational vehicle. Throughout this chapter, the interior of the recreational vehicle would be referred to interchangeably as the living compartment or living enclosure. Essentially, this means that the combustion air intake, the burner, the combustion chamber, heat transfer elements, and exhaust piping shall be outside the living compartment. It further states that exhaust or flue outlets shall not terminate under the recreational vehicle. The codes further state that internal combustion engines (motor generators), engine driven pumps or the like shall be mounted in compartments that are vapor tight to the interior of the vehicle (living compartment). The wording is somewhat confusing in that of necessity the engine compartment cannot be sealed because the engine requires combustion and cooling air, therefore, cannot be sealed. However, the meaning of the code is quite clear that the living compartment must be sealed to prevent exhaust gas penetrating the enclosure. In addition, the code states that all penetrations into the living compartment shall be sealed. Furthermore, fuel lines and exhaust systems shall not penetrate the living compartment. All recreational vehicles that are equipped with or are equipped to accommodate a future installation of an internal combustion engine shall be equipped with a listed CO detector or alarm. Readers interested in detail information regarding codes or standards are referred to ANSI 119.2 and NFPA 501 c.2,3

4.4 POTENTIAL SOURCES OF CARBON MONOXIDE WITHIN MOTOR HOMES AND OTHER ENCLOSURES Motor homes contain a variety of appliances utilizing combustion that can generate CO as well as other toxic gases. The probability of creating serious injury or death is a function of the amount of CO produced by the appliance and the concentration ultimately trapped in the enclosure. The likely devices and appliances fall into one of two classes depending on level of CO that can be expected 1. Internal combustion engines produce levels of CO ranging from 10,000 to 70,000 ppm or more; CO concentration drops by 95% or more when the

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exhaust system is equipped with a catalytic converter. Without a catalytic converter, the probability of life threatening accidents occurring is very high if exhaust gases leak into occupied enclosures. 2. Ranges, stoves, ovens, water heaters, and so forth produce much lower levels of CO, generally in the range of a few ppm up to a few hundred ppm. The probability of these devices causing life-threatening accidents is considerably lower than with internal combustion engines. However, these concentrations are capable of causing brain damage and other healthrelated injuries and cannot be dismissed out of hand. In any CO asphyxiation incident, regardless of the CO level, it is a good practice to inspect all devices that could potentially generate CO. Measure their output, and catalog emissions even though they may appear to be unrelated to the accident and the environment in which the accident occurred.

4.4.1 INTERNAL COMBUSTION ENGINES Internal Combustion Engines present the greatest hazard from the standpoint of CO poisonings. As stated above, CO concentrations of 10,000–70,000 ppm are not uncommon. CO at these magnitudes, even when diluted 30 or 40 to 1 can be lethal, can quickly result in death. Internal combustion engines produce high levels of CO because of the brief period available to complete combustion. As an example, a single cylinder engine running at 2400 rpm must fire 20 times per second. It must draw in a charge of air, meter and inject an appropriate quantity of fuel through a crude carburetor, and mix the air and fuel in 0.0236 s. The mixture must then be ignited, the flame propagate throughout the cylinder, and finally complete the power stroke in 0.014 s. In this brief period of time, it is virtually impossible to perfectly mix each fuel molecule with the appropriate amount of air and burn it to completion in about 0.04 s. Consequently, incomplete combustion is the inevitable result. In addition, the boundary of the metal cylinder, the cylinder head, and piston are all relatively cold surfaces, therefore cause quenching and additional incomplete products of combustion. As a result, the small internal combustion engine is naturally inefficient and produces high levels of CO and other products of incomplete combustion. Modern automobile and truck engines, although greatly improved, still produce high levels of CO, but because of catalytic exhaust systems now deliver much lower levels of CO to the atmosphere. Of the fatal CO motor home accidents that I have investigated, the majority can be traced to the motor generator and its exhaust system. The majority occurred after the exhaust system was damaged, displaced, or missing. The damage to or the absence of the tailpipe allowed high levels of CO and other toxic exhaust gases to be directed under the motor home where they accumulated and found their way into the living compartment. It should be noted that despite numerous accidents many generator exhaust systems are still located in unprotected areas where they are subject to damage from direct impact from road hazards.

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H

E F

B

G

D I A

J

K

C

FIGURE 4.1 Air flow over and through an enclosure.

4.4.1.1 Large Vehicle Propulsion Engines Older motor home engines, built before mandated emission standards, commonly produced in excess of 4% (40,000 ppm) CO. Modern engines still produce high levels of CO; however, modern catalytic exhaust systems have reduced CO discharge drastically in order to meet the current CO emission standard. Other than intentional suicide, and operating the motor home engine for heating purposes in quiescent zones, the main propulsion engine is rarely the cause of fatal asphyxiations. The propulsion engine is rarely running long enough, when the vehicle is not in motion, to accumulate a high enough concentration of CO. When in motion, the position of the exhaust pipe encourages rapid dilution and dissipation of CO, discharging it away from the vehicle. There is one exception, and that is in the area directly behind the vehicle. Large moving objects create a suction wake directly behind the vehicle, which encourages exhaust gases to accumulate, much like the vortex G, shown in Figure 4.1. Codes recognize this problem and require special sealing to avoid leaks into the living compartment in those areas. In addition, codes require that openings like windows must be permanently sealed to avoid opening. Main propulsion engine exhaust pipes are generally large and structurally strong, with substantial means of attachment to the vehicle. Although they are frequently in unprotected areas, the pipes and supports are strong and can sustain impacts that would damage smaller lighter generator exhaust pipes. Although this does not preclude an accident, it greatly reduces the probability. A motor home if left with the engine idling, for a prolonged period of time, especially, if parked in a protected zone or in a depression, may permit exhaust gases to accumulate underneath. The accumulation of exhaust gases in the vicinity of the discharge end of the tailpipe thwarts the natural dilution of exhaust gases, thereby exposing leakage areas to highly concentrated exhaust gases. The temperature of undiluted exhaust gas is high thereby creating a thermal head that facilitates infiltration into the living compartment through breaches in the vehicle floor. 4.4.1.2 Auxiliary Power Generators The majority of standby power generators, used in motor homes, are driven by single cylinder, four-stroke engines. Some of the larger generators use larger two-cylinder,

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four-stroke cycle engines. The range of sizes run from 2.5 kW (7 bhp) to 7 kW (14 bhp). They are available for gasoline, liquefied petroleum (LP), liquid or vapor state fuels, and occasionally diesel fuel. Codes require that all motor-driven generators be mounted in compartments that are outside of the living compartment. The generators are generally located in a ventilated compartment along the periphery of the motorhome. The generator compartment cannot be sealed and must be open to the outside air to maintain a constant flow of cooling and combustion air to the engine. The code requires that all generators be mounted in compartments that must be outside of the living enclosure. Typically, the generators are equipped with exhaust systems that consist of a muffler, tailpipe, and tailpipe support brackets. The exhaust pipe, approximately 1 in. in diameter, usually made of 16 gauge stainless steel, is routed under the motorhome and generally protrudes out the side or back of, and beneath the lower skirt of the motorhome. Engines are provided with mufflers to reduce exhaust noise levels, which are typically 67–70 dBA (sound pressure level at 10 ft.). On some “Quiet” models sound levels as low as 60 dBA are available. It should be noted that even at 60 dBA the noise signature is loud enough that a defect in the exhaust system can readily be detected by a person, used to the sound, standing in the vicinity of the generator. This provides a safety feature to persons that check the generator in use. In general, low horsepower engines are inefficient and produce very high levels of CO. Exhaust gas composition may range from 4.0% to 7.0%, (40,000–70,000 ppm) of CO with associated carbon dioxide levels ranging from 6% to 10% (60,000–100,000 ppm). Exhaust gases are discharged at a temperature of 400–800◦ F depending on the generator load. Of all appliances, motor generators present the greatest danger to human life and health. The high CO concentration (40,000–70,000 ppm) in the exhaust gas, even when the engine is in good working order, creates a serious poisoning hazard. By comparison, with a few exceptions, other CO-producing devices commonly found in motor homes, produce CO levels up to 400–500 ppm and only then when they are not working properly. These lower CO levels may still present a health hazard, but of a far lower magnitude than a generator. Because generators present such a high exhaust gas hazard, it is required that a special standard of care be exercised to ensure that the generator engine and all its associated components be maintained in first class condition, and be protected against accidental damage. Generator engines are quite reliable when properly maintained. However, the exhaust gas is highly toxic regardless of the operating condition of the engine. Essentially, nothing can be done to relieve the fundamental CO hazard. With regard to life safety, the exhaust system is the most critical component of the motor generator and should be protected at all cost. In general, the exhaust pipe and muffler are located under the engine with the tailpipe projecting below the skirt of the motor home. In the majority of cases, the discharge of the tailpipe is located perpendicular to the side of the motor home and projects out a minimum distance of 1 in. beyond the side of the motor home. For additional protection, codes require that the exhaust pipe may not be located closer

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than 6 in. from any air intake. This assumes that the pipe discharges into clean air to dilute the exhaust products. The tailpipe, by virtue of its location below the vehicle, is in an unprotected position and is subject to impact from curbs, road hazards, uneven terrain, and flying debris. Most frequently, tailpipe support brackets are weak and will not withstand substantial impact. The pipe is normally a thin wall stainless steel tube that is readily subject to impact damage. My experience shows that the majority of fatal accidents are caused by damaged, out of position, or missing tailpipes.

4.4.2 INTERIOR DEVICES 4.4.2.1 Ranges The majority of cooking stoves used in motor homes or trailers burn LP as a fuel. Propane, butane, or a combination thereof are commonplace. Exhaust gases from the burners are vented directly into the living compartment of the motor home. Gravity vents may be provided or a fume hood may be located above the range. A fume hood collects range exhaust products of combustion along with cooking vapors and discharges the gases through a register located on the outside wall or roof of the motor home. The registers are normally equipped with flap type check valves to prevent back flow into the motor home from wind movement. Some fume hoods used over stoves filter out grease and smoke, but return combustion products to the living compartment. These systems do not remove CO, carbon dioxide, or other toxic gases, but simply circulate them within the enclosure. Exhaust fan capacities are typically in the range of 50–125 acfm. All exhaust systems require similar quantities of make-up air to prevent back drafting. Tests conducted by the author show that CO levels, taken just above the visible flame, range from 15 to 70 ppm; properly adjusted burners have blue flames. Badly adjusted or damaged burners, frequently typified by yellow tipped flames, have CO levels of 100–770 ppm (this figure may vary by location). Burner pilot lights can contribute an additional 28–56 ppm. Ranges used for cooking rarely are hazardous because they are used for a limited time. When used for prolonged cooking they are generally used in conjunction with an exhaust hood. Ranges can pose a hazard if used in a small, tight compartment without sufficient air infiltration or when operated for prolonged periods of time. Ranges should never be used for space heating. 4.4.2.2 Ovens Ovens also discharge products of combustion and cooking vapors directly into the living compartment. Ovens having blue flames can produce 35–768 ppm of CO and their pilots can add up to an additional 960 ppm.4 Some ovens use a gravity flue to discharge oven gases outside the living compartment. When used they should be equipped with backflow protection. Because of the relatively low temperature of exhaust gases and the short stack length, the flue draft developed is limited. Back drafting may present a problem when dryers or

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exhaust fans are used simultaneously within the same enclosure. Under back-drafting conditions, CO can increase to dangerous levels. During back drafting, CO levels far exceed the norm expected of the appliance. Like cooking ranges, ovens are used for relatively short periods of time and are generally vented. However, when used in tightly sealed enclosures without sufficient infiltration air, they can present a hazard. Ovens should never be used for space or supplemental heating. 4.4.2.3 Gas Refrigerators (LP Gas) The majority of motor homes and trailers use gas or combination gas-electric refrigerators. The combustion unit for a gas refrigerator is contained in a separate metal enclosure that is located outside the living quarters. Combustion air is drawn into the combustion tube, mixed with vaporized propane, ignited and burned and flue products passed through a heat exchanger and discharged to the outside atmosphere. Thus, combustion gases are isolated from the living compartment. Of all appliances, gas refrigerators show a low frequency of CO poisonings. Negative living compartment pressure does not pose a problem. 4.4.2.4 Domestic Water Heaters The combustion unit for a gas fired water heater is contained in a separate metal enclosure that is located outside the living quarters. Combustion air is drawn into the combustion tube, mixed with vaporized propane, ignited, burned, and flue products passed through a heat exchanger. They are discharged to atmosphere outside the living compartment. Make-up and hot water connections that penetrate the living compartment must be sealed to prevent external gases from penetrating the living compartment. Negative living compartment pressure does not pose a problem except through leaking seals around pipes or electrical connections entering/leaving the living compartment. The risk of dangerous amounts of CO entering the living compartment, except at seals, is small. 4.4.2.5 Gas or Oil-Fired Space Heaters The combustion unit of the space heater must have an air intake and discharge that are external to the living compartment. Hot combustion gases are contained inside a stainless steel heat exchanger that separates them from the living compartment. Pressurized air flow across the outside of the heat exchanger picks up and carries hot air into the living compartment. The risk of dangerous levels of CO penetrating the living compartment is small. 4.4.2.6 Clothes Dryers Clothes dryers when fuel-fired have the combustion unit outside the living compartment. The combustion unit is much like those used in approved space heaters,

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water heaters, and refrigerators. Clothes dryers present an additional but indirect hazard, because the dryer exhaust can lower living compartment pressure to the point where back drafting by other appliances occurs. Lower living compartment pressure also increases the probability of drawing external exhaust gases into the living compartment. If a clothes dryer is used it is imperative that a sufficient make up air supply be provided to prevent back drafting into the living compartment.

4.4.2.7 Fireplaces (LP Gas) Fireplaces and even wood burning stoves have become available for use in mobile homes. Because their flames are exposed inside the living compartment, anything that could result in back drafting will cause exhaust gases to be discharged directly into the living compartment. Gas fireplaces, even in conventional homes, are notorious for discharging CO into living areas. Fireplaces are subject to back drafting any time that living compartment pressure is reduced below atmospheric pressure (see Figure 4.2).

4.4.2.8 Other Sources The use of portable kerosene, gasoline, and propane or natural gas heaters is not recommended. Regardless of the type, they discharge their products of combustion into the living compartment. Even when operating properly they require an adequate supply of combustion air, which may not be present in a tight enclosure. Heaters of this type are portable and can be easily upset, presenting an additional fire and toxic gas hazard. Many of these devices are position sensitive and cannot function in other than a vertical attitude. Their use is prohibited by ANSI 119.2 in that the products of combustion are discharged into the living compartment. There is a history of numerous asphyxiation accidents related to this type heater.

Fresh air

Leakage air Dryer exhaust Dryer exhaust

Exhaust gas back flow

Clothes dryer

FIGURE 4.2 Back-drafting in a fireplace flue.

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4.5 PRIMER ON THE MECHANISM OF FORMATION OF CARBON MONOXIDE FROM FUEL-FIRED APPLIANCES FOUND IN MOBILE HOMES 4.5.1 THE PHYSICAL AND CHEMICAL PROPERTIES OF CARBON MONOXIDE To understand how CO is generated and transported into a motor home, it is necessary to understand its physical properties, where and how it is formed, and how dangerous concentrations are transported into living compartments. CO is a clear gas that is odorless, tasteless and has a density slightly less than air. It is generally a product of incomplete combustion of carbon or hydrocarbon fuels. Its physical properties are seen in Table 4.1.5 The common understanding is that CO is lighter than air, as it is in the pure state. At standard temperature and pressure, it has a density of 0.0779 lb/cu. ft.; air is 0.0807. The difference in density creates a natural buoyancy. However, under most circumstances where we find it, CO is a product of incomplete combustion. Therefore, it is not a pure gas, but contained in a mixture of exhaust gases containing nitrogen, carbon dioxide, and water vapor in proportions dictated by Equation 4.1. Because of the density of these gases, the combined mixture has an essentially neutral buoyancy. For illustrative purposes, assume that a motor generator is fueled by octane, C8 H18 . Its exhaust products are 6% CO and 8% CO2 . Under these conditions the exhaust gas density is 0.0805 lb/cu. ft. at STP (standard temperature and pressure 60◦ F and 29.92 mm Hg), which has essentially neutral buoyancy when compared to air

TABLE 4.1 Physical Constants for Carbon Monoxide∗ Name

Symbol

Chemical symbol Density, STP Molecular weight Specific gravity (air) Specific gas constant Specific heat p = c Specific heat v = c Specific heat ratio Specific volume Speed of sound Heat of combustion Heat of combustion Flammability in air lower Flammability in air upper Flame temperature in air Auto ignition temperature

CO rho MW SG R Cp Cv k nu C

LFL UFL

Value

Units

0.0779 28.011 0.967 55.19 0.248 0.177 1.4 13.557 1154.8 310 4340 12.5 74 3542 1228

lb/cu.ft.

ft. lbf /lbm R◦ Btu/lb◦ F Btu/lb◦ F — cu. ft./lb ft./s Btu/cu. ft. Btu/lb Vol% of total volume Vol% of total volume ◦F ◦F

∗Also see Chapter 35.

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0.0807,lb/cu. ft. at STP. Therefore, an exhaust gas mixture, with neutral temperature differential, will not have natural buoyancy at STP. Any buoyancy characteristics associated with combustion products will be due solely to a temperature differential between the exhaust gas stream and the surrounding air. For example, a hot jet stream of exhaust at 800◦ F in air will be buoyant and have a resultant direction and magnitude that will be the vector sum of the vertical thermal component and jet vector of the initial gas stream. Ahot gas stream jetted into ambient air naturally entrains large volumes of ambient air, thereby lowering its temperature, thus its buoyancy. As the stream gains volume it slows down. Any computations should take into account the momentum exchange, the increasing volume of the stream and diminishing temperature.

4.5.2 THE COMBUSTION PROCESS Under most circumstances, CO is an undesirable product of combustion. It is formed as a result of incomplete or inefficient burning of carbonaceous substances. By definition, combustion is the rapid oxidation of fuel accompanied by the liberation of heat and light. The combustion process, even in its simplest form, say burning methane in air, is not fully understood. Equation 4.2 shows a methane and excess air mixture burning to completion, forming products of combustion containing water, carbon dioxide, and excess air. Unlike the simplified end-points equation shown, there can be up to 31 intermediate steps in the oxidation of methane. If at any time during the combustion process the reaction is chilled or in any way interrupted, the intermediate reactions will freeze leaving one or more intermediate partial products of combustion. One of the more common partial products is CO. If temperatures remain high and oxygen is present some or all the intermediate products may be oxidized to completion. If the temperature drops below the critical reaction temperature or if oxygen is not present, the intermediate products will become stable and be represented in the exhaust gases. The most common causes for incomplete combustion are quenching, incorrect fuel air ratios and inadequate mixing resulting in stratification, and burning in the fuel rich or reducing fuel air region. The combustion process involves mixing of multiple gas products, mass transport, chemistry, and heat transfer. For the purpose of this discussion, many of the more complex processes will be simplified and we will deal, as much as possible, with the reactants and end products of combustion as defined by the thermo-chemical equations. It should be understood that the equations shown are representative of those containing intermediate reaction, but only at the beginning and the end. 4.5.2.1 Basic Requirements to Initiate and Perpetuate the Combustion Process Fuel must be present in a state that is burnable. Liquid and solid fuels will not burn. Fuel must be in a gaseous state for it to combine with oxygen and burn. Liquid fuels have to be atomized to small particles so that on exposure to high temperatures, the pilot flame, they quickly gasify so they can burn. Similarly, solid

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fuels must be pulverized so that on exposure to high temperature, the pilot flame, they quickly gasify and burn. The fuel must also be present in sufficient quantity to be within the flammable limits (Table 4.1), and the initial flame size must exceed the minimum kernel diameter in order to propagate. An oxidizer, air or oxygen, must be present and intimately mixed with the fuel. The mixture must be within flammable limits, at least in a localized area, where ignition is to occur. There must be a source of ignition, of sufficient energy to raise the temperature of a critical mass of the fuel mixture above the ignition temperature to initiate the reaction. If the reaction is to perpetuate itself, the heat generated must be at least equal to the net heat loss from the flame and the heat required to heat the incoming mixture to ignition temperature. If the heat generated is equal to or greater than those requirements, the reaction will propagate.

4.5.3 THERMOCHEMICAL EQUATIONS Combustion like any other chemical reaction may be represented by thermochemical reaction equations. The equations show the fuel and air input and the products of combustion and heat liberated. The typical equation shows the initial ingredients and the final products of combustion, but does not show the intermediate reactions. For those interested in the detailed combustion process, see various sources.6–8 In general, this presentation will concern itself with the end-products of rich combustion, primarily CO and carbon dioxide. There are times when quenching, chilled flames, and blow off create intermediate toxic products of combustion. Essentially, we will concern ourselves with three thermochemical equations, Equation 4.1 for rich or excess fuel (i.e., deficiency of air), Equation 4.2 is for an excess of air, and Equation 4.3 is for secondary oxidation of CO formed in Equation 4.1. The term “E” represents the equivalence ratio or the ratio of actual to stoichiometric air. Stoichiometric air being that amount of oxygen required for perfect combustion. Thermochemical Equation for Methane Excess Fuel CH4 + 2 E O2 + 7.52 E N2 = (4 E − 3) CO2 + (4 − 4 E) CO + 2H2 O + 7.52 E N2 + Heat (1040 BTU/ft 3 )

(4.1)

Thermochemical Equation for Methane and Excess Air. CH4 + 2 E O2 + 7.52 E N2 = CO2 + 2H2 O + 2(E − 1)O2 + 7.52 E N2 + Heat (E∗ 1040 BTU/ft 3 )

(4.2)

Thermochemical Equation for Carbon Monoxide. CO + O = CO2 + Heat (323.5 BTU/ft 3 )

(4.3)

Equation 4.2 is presented in graphic form (see Figure 4.3). This chart gives a quick visualization of how combustion proceeds to either excess fuel or excess air. An equivalence ratio of 1, the abscissa, occurs at stoichiometric or perfect combustion.

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DEN*100 CO2 CO O2

Exhaust gas percent wet methane CH4

18 16

Percent (Wet)

14 12 10 8 6 4 2 0 0

1

2

3 4 Equivalence ratio

5

6

FIGURE 4.3 Exhaust gases from the combustion of methane.

Some notable observations about Figure 4.3. 1. The CO2 curve peaks at an equivalence ratio of 1, and falls off on the reducing and oxidizing side of stoichiometric. 2. Maximum combustion efficiency is achieved when carbon dioxide is maximized. 3. Therefore, the CO2 curve is a good indicator of the quality of combustion. 4. Since CO2 is readily measured, it can be used, in conjunction with a determination of the presence of oxygen to assess the equivalence ratio. 5. Flame temperature also follows the CO2 curve (flame temperature actually peaks slightly on the reducing side of E = 1 but for general purposes the difference can be disregarded). 6. These observations are helpful in determining if a flame is reducing and generating CO. The chart shown is for methane. There are two charts for each fuel: (1) wet gas analysis, where the water of combustion remains in the exhaust gas, and (2) dry gas analysis, assuming that the water of combustion has condensed. Figure 4.3 represents a wet gas analysis. The use of wet gas analysis is appropriate for combustion systems where the exhaust gas temperature is above the dew point. The majority of charts found in the literature are set-up on a dry basis. This was done when the most common combustion analyzer was the Orsat. It being a wet absorption analyzer caused the gas temperature to drop below the dew point, removing all the water, and thereby yielding the products of combustion on a dry basis. Care must be taken when using a chart to determine if analysis is on a wet or dry basis. Section 4.10 shows a similar graph drawn on a dry basis. This approach may be more recognizable and is used more frequently by those involved in general combustion work.

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The maximum CO2 for each fuel will be different and may be calculated from Equation 4.1. Burners are normally adjusted for near peak CO2 on the slightly oxidizing side to insure complete combustion. The majority of good combustion equipment operates with an equivalence ratio in the range of 1.0–1.4. Electronic instruments can be calibrated to read either wet or dry percent. Therefore, it is important to know how the instrument is calibrated.

4.5.4 EXCESS AIR COMBUSTION Excess air combustion occurs at any time that the quantity of combustion air exceeds the stoichiometric requirements. This can occur on an overall basis, where fuel and air are uniformly mixed throughout the combustion chamber, or on a local basis within the combustion envelope, usually classified as stratified mixing. Stratified mixing can result in rich and lean zones occurring within the same flame envelope. One of the fundamental problems that occurs in most combustion systems is that it is difficult to mate every fuel molecule with the correct number of oxygen molecules. Failure to do so can result in rich excess fuel zones and lean excess air zones within the same combustion envelope. When there is too much air for a given amount of fuel, the flame temperature drops because of heating the additional excess air. If the quantity of excess air is sufficient then the flame temperature can drop below the critical reaction temperature and flameout can occur. However, prior to flameout, flame quenching starts and partial products of combustion such as CO and various aldehydes appear and become stable in the exhaust gases. If the quenching is local, and the partial products are subsequently reheated to a temperature in excess of the critical reaction temperature then the partial products may go to completion in the subsequent burn. Figure 4.4 shows a curve of flame temperature (◦ F) versus excess air (%). As excess air, increases flame Temperature versus excess air 4000 Temperature Temperature (F°)

3500 3000 2500 2000 1500 1000 500 0 0

500

1000

1500

2000

2500

Excess air (% )

FIGURE 4.4 Flame temperature versus excess air (%), natural gas. (R. Schreter and Associates, 1997).

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temperature decreases. As the temperature approaches 1200◦ F, the critical reaction temperature, partial products of combustion and unburned fuel emerge. At very high levels of excess air, CO and formaldehyde can be generated.

4.5.5 EXCESS FUEL Excess fuel combustion occurs at any time that the quantity of fuel exceeds the stoichiometric requirements. As with excess air, this can occur on an overall basis or on a local basis within the combustion envelope. As depicted in Figure 4.3, CO appears at any value of E < 1. Small amounts of CO may occur even at E = 1.05, slightly excess air, because of difficulty mixing all the fuel with all the air. The rise of CO is very rapid on the excess fuel side as can be seen in Figure 4.3. Rich reactions contribute to the formation of CO in appliances when they are deficient in combustion air. The same type of reaction occurs when back drafting occurs. During back drafting, the reversal of flow upsets the mixing process and flame stability, resulting in rich combustion, blow off, quenching and formation of partial products of combustion.

4.6 APPLICATION OF COMBUSTION THEORY TO ACTUAL CARBON MONOXIDE POISONING SITUATIONS Aerodynamics and gas dynamics are the primary factors driving exhaust gas leakage into or out of the living compartment of a motor home, or for that matter any enclosure. The following theory is intended for use with motor homes; however, the same approach may be used in any low-pressure flow situation that might occur in a residential or commercial building.

4.6.1 INTRODUCTION TO THE FLOW OF EXHAUST GASES The flow rate of air, CO or a mixture of exhaust gases through leaks in the enclosure boundary is of critical importance to the concentration of toxic gases within the enclosure. The physical conditions governing low pressure gas flow usually encountered in motor homes greatly simplifies calculations, because the compressibility of the gases may be disregarded. The range of total pressure and differential pressure is low, further simplifying the flow equation. Flow is mainly through orifice type openings and friction can generally be disregarded. A discharge coefficient appropriate for the type of opening is required. Discharge coefficients may be found in most sources on fluid flow. Because differential pressures across orifices or leakage holes are low, a simplified velocity equation may be used as expressed in Equation 4.4. Gas Velocity at Low Pressures.
U=

2∗gc ∗R∗

T0 ∗ (P0 − P1 ) P0

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(4.4)

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The continuity equation may then be used to determine the flow rate (Equation 4.5). Gas Flow Q = Cd∗A∗U

(4.5)

For very low pressures where (P0 − P1 /P1 ) ≤ 0.01, a much simplified flow equation may be used. Low Pressure Gas Flow.
Q1−2 = 1658.5∗Cd∗a∗ (h0 − h1 ) ∗

δg δa

(4.6)

where a is area (sq. inches) A is area (sq. ft.) δa is density of air at STP δg is density of gas at flowing conditions F is frictional loss in units consistent with pressure gc is the constant 32.2 h0 is upstream pressure (inches of water) h1 is downstream pressure (inches of water) Cd is discharge coefficient P0 is upstream pressure (lb/sq. ft. abs) P1 is downstream pressure (lb/sq. ft. abs) Q1−2 is flow rate (cu. ft./h) R is universal gas constant (ft lb/lb R0 ) T0 is upstream absolute temperature (R0 ) U is velocity (ft./s)

4.6.2 TOTAL PRESSURE The pressures, ht and Pt , represent total pressures that are used in connection with moving air streams. Total pressure includes static pressure and a velocity component. Moving gas streams have both potential and kinetic energy components. In lowpressure gas flow, they are generally thought of as total, static, and velocity pressures (Equation 4.7). Total pressure is the sum of the static and velocity pressures and may be represented by any consistent set of units. Total Pressure. ht = hs + hv + f

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(4.7)

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where f is frictional loss [in. water column (w.c.)] hs is static pressure (in. w.c.) ht is total pressure (in. w.c.) hv is velocity pressure (in. w.c.) An example will be helpful to illustrate the concept of total pressure and the interchange of static and velocity pressures. Assume a large tank has been pressurized to a static pressure of hs . Because the tank is large and the outflow is small, there is negligible velocity within the tank. Therefore within the tank hv = 0. From Equation 4.7, ht = hs . As the fluid approaches and enters the pipe, it must accelerate and gain velocity. The static pressure diminishes and the velocity pressure increases (see plane a). Concurrently, because of turbulence there is a permanent frictional head loss that causes the total pressure, ht to decline slightly (see point e). In the straight section of pipe, plane (a to b), fluid reaches maximum velocity, requiring a corresponding loss in static pressure (see plane a). The fluid then enters a divergent nozzle (b to c), where the velocity diminishes, restoring static pressure. Throughout the pressure interchange (a to c), there is a gradual loss of total pressure due to friction and turbulence (e to f). As the fluid emerges from the nozzle, it continues to expand and then it impacts the wall. The remaining velocity is converted back into static pressure with an accompanying friction loss (f to g). The static pressure is now equal to the total pressure since velocity is now zero. The regaining of velocity pressure into static pressure, hs , is referred to as stagnation pressure (see Figure 4.5).

Wall h

Flow

Tank

g f

Total pressure

e

Friction Static pressure

Velocity pressure

D

a

b

c

d

FIGURE 4.5 Total velocity and static pressure versus position.

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After striking the wall at point h, the static pressure being higher than the ambient pressure causes the gas to accelerate in a direction perpendicular to the original jet, again causing another interchange between total, velocity, and static pressure. This concept is extremely important and will be used throughout discussions of moving gas streams.

4.6.3 STAGNATION PRESSURE When a moving gas stream impacts a stationary barrier or wall the stream velocity diminishes or approaches zero. The kinetic energy of the moving stream is transformed into potential energy in the form of pressure. The change into potential energy raises the local static pressure, which is termed stagnation pressure. Stagnation pressure plays an important role in the inflow and outflow of gases in a motor home or like enclosure. The stagnation pressure can be due to a moving body, such as a motor home impacting stationary air, or to a moving air stream or wind impacting a stationary body. The magnitude of the stagnation pressure may be calculated from the velocity component and the angle of incidents to the plane of the impact surface. In low-pressure air flow calculations it is traditional to refer to velocity in ft./min and stagnation pressure in terms of inches of water column (see Equation 4.8). Stagnation Pressure.  h =

Um 1096.5

2 ∗ δ ∗ sin φ

(4.8)

Where δ is density of fluid at flowing temperature and pressure (lb/ft3 ) h is stagnation pressure (in. w.c.) φ is angle of incidence of Vm to plane of stagnation degrees Um is velocity of stream (ft./min) A useful chart, Figure 4.6, shows the magnitude of stagnation pressure for air at various wind speeds impacting a stationary surface. To put this in perspective consider the following example: a 20 mph wind impacts a stationary wall at an angle of 90◦ . From Figure 4.6, the stagnation pressure will be 0.20 in. w.c. Assume that there is a single 2 ft. × 4 ft. closed double hung window in the wall. Assume that the window has a 1/64 inch crack along all moving surfaces. The total leakage area will be A=

1 × 12 × (2 + 2 + 2 + 4 + 4) = 2.625 sq.in 64

Using Equation 4.6 we can calculate that the air flow through the window crack will be 1572 acfh, which is a substantial leakage.

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Stagnation pressure in. water column

Stagnation pressure (in. water column) 1.40 1.20 1.00 0.80 0.60 0.40 0.20 0.00 0

10

20

30

40

50

60

Wind speed MPH

FIGURE 4.6 Stagnation pressure.

4.6.4 THERMAL PRESSURE Any time there is a temperature gradient within or between the inside and outside of an enclosure, thermal pressure will develop at the top of the enclosure. Thermal pressure is a function of temperature difference, density of the fluid or fluids, and vertical height from the inlet to outlet in feet. The usual units for thermal pressure are inches of w.c. Equation 4.9 represents the equation for thermal pressure: Thermal pressure.   p∗MW ∗H 1 1 ht = ∗ − 55.77 T2 T1

(4.9)

Where ht is thermal pressure head (in. w.c.) H is height of the enclosure (ft.) MW is molecular weight of gas p is atmospheric pressure (psia) T2 is absolute atmospheric temperature (Rankine degrees) T1 is absolute enclosure temperature (Rankine degrees) Thermal pressure can be treated as any other pressure to determine flow across an opening (see Equation 4.6). Thermal pressure is important in the flow of exhaust because of the temperature gradient between the hot exhaust gas and that of the surrounding atmosphere. To put it into perspective, a temperature gradient of 100◦ F in a 6-ft. high enclosure will create a thermal pressure of 0.0237 in. w.c. That thermal pressure would create a flow of 204 scfh per square inch of leakage area.

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4.6.5 AIR FLOW AROUND AND THROUGH ENCLOSURES Aside from fans, blowers, exhausters, or similar power gas moving devices, thermal head, and wind are the principal cause of flow of gases into or out of enclosures such as motor homes or buildings. Any time that wind moves across or around any object, pressure gradients form around it. It is these pressure gradients acting on openings in the enclosure that create flow into and out of the enclosure. Figure 4.1 shows an elevation view of a simplified enclosure (B) exposed to wind flow. The wind blowing from left to right. The horizontal lines (A) represent stream tubes of air. As the lower stream tubes approach the vertical wall, their horizontal velocity approaches zero, converting kinetic energy to static pressure (stagnation pressure). This builds a positive pressure region along the upwind face. The static pressure gradient on the upwind face is greatest at the bottom where virtually all kinetic energy or velocity pressure is converted to static pressure (C). At higher levels there is flow moving up the wall, therefore static pressure will be somewhat lower due to transition into velocity. Total pressure remains essentially constant across the face with the exception that there is a frictional loss due to turbulence. Air within the positive pressure region (M) flows into the lower pressure region (D) and accelerates to join the higher velocity stream tubes flowing across the top of the object at (B). As the velocity increases, static pressure diminishes forming a low pressure region (F) along the top of the object. This effect may be likened to the low pressure created as air flows across the top of an airfoil. As the stream tubes flow past, the downstream edge of the object they deflect down due to the low-pressure vortex (G) on the downstream side of the body. Surface drag from the stream tubes acting on the low pressure region (G) cause a clockwise rotation to the low-pressure wake (G). At very low Reynolds numbers vortex (G) will remain stable in the cavity formed by the ground and the downstream wall of the object. At Reynolds numbers above 50, which is most common in air flow, vortex (G) becomes unstable and periodically moves downstream, as represented by vortex (H). Then a new vortex is established and grows in size at (G) until it separates. This process is referred to as vortex shedding. While vortex shedding introduces instability downstream for the object, the pressure in the immediate downstream area while variable in magnitude remains essentially negative. When openings exist in the enclosure, as shown in Figure 4.1, positive pressure on the windward side causes flow into the enclosure through openings (I). As a result of the inflow, internal pressure increases. The internal pressure being higher than that on the downwind side causes a pressure differential that results in flow through any openings (K). The negative pressure (G) further increases the pressure differential resulting in a further increase of flow. If the enclosure is divided into rooms or other subdivisions, flow will work its way through openings in the partitions, traveling from high to low pressure. Flow rate will be governed by pressure differential and area of leakage paths, in accordance with Equation 4.6. If multiple leaks are involved, a series of simultaneous equations may be written to determine the net flow through the enclosure. It is apparent that if CO was discharged on the upstream side, then it would be induced into the interior of the enclosure.

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4.6.6 WIND ROSE When a CO-poisoning incident occurs and external wind conditions appear to be a factor, it is desirable to be able to determine the wind effect over the time span of the accident. The wind may be at a constant velocity and direction during the entire incident or it may vary widely in direction and velocity. The wind intensity and direction are a vector quantity that may constantly change with time. Because of the highly variable nature of the wind, it is helpful to develop a graphic image, as well as a mathematical model of the wind effect relative to time. There are three factors that are pertinent: velocity, direction, and duration which add to the difficulty in graphing the event. National Oceanographic and Atmospheric Administration (NOAA)9 hourly weather reports provide all the data necessary to evaluate the role of weather on an incident. The reports give wind direction, speed, temperature, and a number of other factors, for each hourly segment. The NOAA weather service developed a chart called a wind rose used to assess average wind direction and speed for given airport locations for the purposes of runway direction. Using this basic concept as a starting point, I developed a chart that is useful for forensic investigation of wind-related incidents. Initially, the wind direction, wind speed and the time for each hourly segment is logged into a chart (Table 4.2). The data are then plotted on a 360◦ polar graph in which wind direction, degrees, and intensity (knots) is entered on the polar graph. Entries are shown as 1-h segments for any given direction. The length of each vector represents the wind speed for that particular vector. Where there are multiple vectors or any given heading, each alternating sector is colored for easy differentiation. I normally place time in, {0800}, showing the actual time for each sector so that I do not have to refer to the database for that information. Plotting wind impact surfaces on the chart also aids in visualization. The rose (Figure 4.7) shows that during a 24-h period there were two prominent groupings of wind. The one of interest spans from about 2200 on 2/13 to 0800 on 2/14, having a wind direction of from 70◦ to 180◦ , which is predominantly out of the east. In this case, the front of the building is represented by the line from 30◦ to about 210◦ . The concern was for stagnation pressure on the “East East South” face of the building within the time frame of the accident. Study of the data (Table 4.2) showed that during the critical hours winds out of the east created substantial stagnation pressure, thereby, pressurizing not only the face of the building but all the rooms having openings on that side of the building. In the case represented by this wind rose there were a number of large louvers opening into a boiler room that contained the boiler that generated CO. As a result of the wind, the room was pressurized driving CO into other sections of the building, which contained the living quarters. The wind rose also shows that more intense winds out of the southwest occurred later in the day; however, they occurred outside of the critical time and were of no consequence.

4.6.7 SCOOPS, DEFLECTORS, AND OPENINGS It is commonplace to have ventilators and exhaust fans on or in the roof of motor homes and most portable trailers and offices. These ventilators frequently project into

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TABLE 4.2 Weather Data Giving Wind Direction, Wind Speed, and Temperature Date

Time

Wind Direction (degree)

Wind Speed (knots)

Temperature (◦ F)

2/13/2004 2/13/2004 2/13/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004 2/14/2004

2200 2300 2400 100 200 300 400 500 600 700 800 900 1000 1100 1200 1300 1400 1500 1600 1700 1800

90 90 180 126 290 150 0 180 0 0 140 0 0 0 240 260 240 220 220 230 230

4 8 3 1 3 4 0 3 0 0 4 0 0 0 9 11 9 7 6 14 10

33.8 35.6 32.0 30.2 30.2 30.2 37.4 33.8 33.8 30.2 33.8 37.4 44.6 48.2 53.6 55.4 55.4 57.2 55.4 55.4 53.6

North 360°

Front face of building

Wind speed 3 (knots)/ring

270°

90° (2300) (2200) (0100) (0800) (0300) (0500) (2400) 180°

FIGURE 4.7 Wind rose for 02/13/04 (2200 hrs) to 02/14/04 (1800 hrs).

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B

D

C

E

FIGURE 4.8 Ventilator acting as a deflector.

A

B

G −

H −

+ +

C +

+

−

−

−

+

F D E

FIGURE 4.9 Ventilator acting as a scoop.

the wind stream and induce flow during motion of the vehicle, or in windy conditions with the vehicle being stationary. Figure 4.8 and 4.9 show pressure gradients and direction of flow into or out of an enclosure, depending on the direction of wind flow across the ventilator. Figure 4.8 shows wind flow (A) from left to right, that is deflected upward as it encounters the cover sloping up to the right. The increased velocity at B lowers the static pressure resulting in a low-pressure region at D, downstream of the cover. Assuming neutral pressure within the enclosure (C), flow from inside the enclosure (E) will move from the neutral pressure zone (C) to the negative pressure zone (D), downstream of the deflecting cover. Knowing the relative wind velocity, its angle of incidence the shape and configuration of the ventilator, and the area of the opening the flow rate through the enclosure can be calculated using Equation 4.6. Figure 4.9 shows airflow (A) from left to right that impacts the underside of the cover (B), causing partial stagnation of stream (C), resulting in a positive pressure region (D) on the underside of the cover and at the mouth of the ventilator opening. This assumes that the interior of the enclosure is at neutral pressure (E). The pressure differential plus the remaining velocity pressure will result in air flowing into the enclosure. The flow rate entering the enclosure can be calculated using Equation 4.6. If the pressure within the enclosure is other than neutral, then the differential pressure (h0 −h1 ) must be adjusted accordingly.

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4.6.8 RESONANCE, CYCLICAL FLOW INTO AND OUT OF AN ENCLOSURE Airflow across any opening leading into a closed chamber can result in cyclical pressure pulsations within the enclosure. The cyclical pressure pulsations result in a cyclical inflow and outflow of gas from the enclosure. The pulsations, depending on the shape of the opening can result in a net inflow or outflow from the enclosure. This phenomenon is well known to passengers riding inside an automobile when the rear windows are partially open. The cyclical low frequency pressure surges are commonly referred to as buffeting. The pressure surges can go unnoticed or be significant to the extent of being painful to the ears. A similar effect can be experienced inside a motor home or other enclosure when airflow across an open window or ventilator results in buffeting. The frequency of the oscillation is a function of the volume of the enclosure and the physical characteristics of the opening. The technical term for this type of oscillation is helmholtz resonance. The equation that governs this phenomenon is Helmholtz resonance.
1 fo = ∗ ∗ 2 π

c2∗ S lc∗ V

(4.10)

Where c is speed of sound, at flowing temperature and pressure of the gas (ft./s) fo is resonant Frequency (Hz) lc is effective length of the throat opening S is cross-sectional area of the throat opening (sq. ft.) V is volume of the enclosure (cu. ft.) An example will illustrate the significance of Helmholtz resonance. Assume a trailer 8 × 30 × 7 has a volume of a 1680 cu. ft. Assume it has a single partially open window having an open area of 0.44 sq. ft. and a 0.5

throat, thickness of the pane, at the opening. Also assume that the fluid medium is air at 60◦ F. The frequency of the oscillation will be 7.1 Hz (cps). This frequency is well below the range of human hearing; therefore, the oscillation will go undetected. However, it will still induce large volumes of outside fluid during the negative cycle. It should be noted that low frequency pulsations, if of sufficient amplitude, could be detected by feeling. The inducted fluid will then mix with the contents of the enclosure. On the positive cycle, a similar volume of mixture will be expelled. This of course assumes that the opening is bidirectional in configuration. If the atmosphere outside the window contains a significant percentage of CO, then each half cycle will induce CO into the interior. Over a period of time, the interior concentration of CO will increase and could become significant. See Section 4.7 for a discussion of the rate of accumulation.

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4.6.9 FLOW INTO AND OUT OF LIVING QUARTERS After the foregoing discussion it is apparent that flow into or out of an enclosure occurs only if there is a pressure imbalance and an opening that will allow flow. The pressure imbalance can be due to a mechanical device like a pump or fan; thermal activity creating pressure imbalance due to density variations; or wind pressure acting on the enclosure. The leakage areas may be the obvious ones such as windows, doors, ventilators, or unsealed openings around pipes or electrical penetrations into the living compartment. Leaks can also occur at joints in the walls and floors, through cracks or labyrinth openings that are not apparent to an observer. In CO poisonings, the percent CO concentration in the enclosure is of prime importance. CO may be generated within the enclosure or outside and leak into the enclosure, or a combination of the two. Flow into or out of the enclosure is critical because it can increase the concentration within or it can dilute the concentration by bringing in fresh air and washing out CO during the air exchange process.

4.6.10 FLUE AND CHIMNEY DYNAMICS A flue or chimney is used to remove the products of combustion from inside a building or enclosure. It operates on the same principle as thermal pressure except that the pressure is negative when measured at the base of the flue. In addition, because flow is confined within a solid boundary, the chimney or flue, friction within the duct must be considered. Equation 4.11 may be used to calculate the suction created by a flue or chimney. Careful inspection of the equation shows a similarity with that of Equation 4.9, except that there is an additional back end representing the fluid friction inside the chimney. Flue draft h=

     p∗MW∗H 1 1 .09∗H∗U 2 p∗MW ∗ − − 1+ ∗ 55.77 Tf Ta D∗2∗g 10.729∗Ta

Where D is flue diameter (ft.) g is a constant = 32.2 h is flue suction (in. w.c.) H is height of the flue or chimney (ft.) MW Molecular Weight of the flowing gas p is absolute pressure (psia) Ta is absolute temperature of ambient air (R◦ ) Tf is absolute temperature of flowing gas (R◦ ) U is the velocity of the flue gas (ft/sec)

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(4.11)

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To solve Equation 4.11 it is necessary to assume a flue gas velocity. An acceptable range to start with is 14.0–16.5 ft./s

4.6.11 BACK-dRAFTING OF FLUE GASES INTO THE ENCLOSURE Back drafting is one of the common root causes for CO poisoning. Back drafting is a process whereby the normal direction of exhaust flow is reversed because the suction inside the enclosure is greater than the thermal suction created as a result of the temperature difference across the flue. Back drafting can occur in any closed or semiclosed enclosure. The most common cause is a result of an exhaust fan, or similar air removal device, overpowering the flue suction. The exhaust device may be an exhaust fan, a bathroom or kitchen exhauster, clothes dryer or even another chimney of greater height and temperature difference. Figure 4.2 shows an example of back drafting through a chimney as a result of a clothes dryer operating. The room is relatively tight which limits leakage air into the room. The exhaust fan in the clothes dryer has a capacity, which exceeds the leakage rate of air into the room, thereby lowering the pressure within the room. If the suction pressure within the room is equal to or greater than the flue suction, the flow up the chimney stalls, resulting in a reversal of flow in the chimney. Ambient air is drawn down the chimney, providing combustion air to the flame from above. This changes the normal direction of airflow across the flame holder, disturbing mixing and flame stability. The flame instead of being sucked up the stack, is blown toward the inside of the enclosure. The exhaust gases then change direction and are discharged into the enclosure. Additionally, the flow reversal disturbs the normal combustion process and its flame stability, causing the flame to blow off, increasing the production of partial products of combustion. Figure 4.2 shows a back drafting chimney as a result of a suction created by a clothes dryer. Back drafting has become much more common as homes and buildings becoming tighter (less air leaks) and the prevalence of air exhausting appliances like clothes dryers and exhaust fans, roof exhausters and multiple chimneys becomes more common. The way to avoid the problem is to install appliances that have their own outside air intake, which are frequently power driven. Another method would be to install a general outside air intake. Motor homes, trailers and portable buildings, because of their requirement to seal the living compartment tend to have fewer air leaks, thereby, become prone to back drafting when exhaust devices are used.

4.6.12 DYNAMICS OF GENERATOR TAILPIPE EXHAUST Generator tailpipe exhaust, by code, must always be external to the living compartment. As described earlier, the tailpipe is generally perpendicular to the outside wall of a motor home, is below, and protrudes beyond its periphery. For the purpose of perspective, consider that a 4 kW single cylinder, four-cycle gasoline-fueled engine (Octane, C8 H18 , will be used as the formula for gasoline) generator will be used. At a 3 kW load the exhaust volume will be about 2030 acfh at 800◦ F. At the 1.1 in.

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diameter exhaust pipe, typical for that size generator, exit velocity will be 85 ft./s. When the exhaust jet enters stationary ambient air, the surface drag of the jet stream moves ambient air along with it. Ambient air is entrained into the outer portion of the jet stream causing the outer layer to lose velocity and through drag eventually to slow the core stream. The velocity profile across the jet will be Gaussian as shown in Figure 4.10. As cold air is entrained into the hot jet the average temperature of the jet diminishes. Normally it would be expected that the hot jet would have a tendency to rise, due to its buoyancy. However, in the early stages of the jet, the first 20–30 diameters, the horizontal velocity is high compared to the vertical velocity resulting from thermal buoyancy. Therefore, the vertical movement of the jet will be small. In the example shown in Figure 4.10 the vertical rise at 36 diameters is approximately 1.5 diameters, which is not significant. When the horizontal jet velocity slows, the thermal rise becomes more significant. From Figure 4.11, the entrainment at 36 diameters (3 ft.) will be in the order 17:1 and could be as high as 30:1. The example used a 17:1 entrainment ratio.

Gaussian velocity distribution

Entrainment of ambient gas

Thermal rise l.45 D

0D

4D

8D

Exhaust pipe

12 D 16 D

20 D

24 D

36 D

Jet profile

FIGURE 4.10 Expanding jet.

Velocity fps; entrainment ratio

Entrainment ratio versus distance 100 80 60 40

Velocity

20

Entrainment ratio

0 −20

0

5

10

15

20

Distance in nozzle diameters

FIGURE 4.11 Jet velocity and entrainment versus jet distance in diameters.

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Trapped exhaust gas Direction of flow of exhaust gas Motor home Entrained exhaust Tailpipe

Exhaust discharge

FIGURE 4.12 Entrainment in a confined area.

The initial CO concentration would be diluted by a factor of 17:1. The CO concentration in the vicinity of the jet at 3 ft., for an initial CO concentration of 40,000 ppm, would be approximately 2350 ppm. Further dilution would occur at greater distances downstream. If the exhaust jet is discharged into a region that has limited air circulation or that traps or confines the exhaust, then the jet will be immersed in a cloud of exhaust gases (see Figure 4.12). Initially, the exhaust jet entrains ambient air diluting the exhaust concentration. As the jet strikes the wall, its velocity drops to zero and the exhaust gases stagnate. Because of the confinement, the exhaust gases accumulate between the road, the wall, and the motor home. The entraining action of the jet instead of drawing in fresh air and diluting the CO level in the jet, it entrains and re-circulates exhaust gas, gradually concentrating it, up to the maximum concentration in the exhaust jet. On the basis of this behavior, it is important to insure that the exhaust system is in good condition and discharges outside the motor home and into an area, that is unrestricted where exhaust gases can readily dissipate.

4.6.13 EXHAUST FLOW THROUGH BENT OR DISPLACED EXHAUST PIPES Because exhaust systems are usually located in exposed locations they are prone to impact and may become damaged, bent or rotated out of position. When this happens, they may discharge exhaust gases under the motor home or possibly discharge it against the inside of the skirt or other interior surfaces. If the jet discharges under the vehicle, there is a tendency for the exhaust to become stagnant there. As a result, the exhaust jet entrains the locally stagnant exhaust and the CO does not dissipate. If the jet strikes another object, the jet loses its velocity, therefore its entraining ability. The exhaust becomes stagnant and does not dilute or dissipate. The slow moving or stagnant cloud of highly concentrated CO remains under the motor home and inside the generator compartment.

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Without entrainment the highly concentrated CO cloud remains at high temperature, therefore is highly buoyant, creating thermal pressure on any leaks that may exist into the living compartment. In addition, any suction pressure within the enclosure, resulting from wind or other effects, will add to the entrainment of the offending gases. The concentrated pocket of exhaust under the floor of the motor home is in a location where leaks into the living quarters are more likely. If the exhaust jet impinges on the skirt or other surface at an angle, the jet stream will attach to and flow along the wall, (Coanda effect or wall jet attraction, Henry Coanda, French aviator, ca. 1918). The flattened jet is under negative pressure, causing it to entrain local ambient gases. Since this occurs in a confined area under the motor home, the gas being entrained is primarily exhaust gases, resulting in a high concentration of CO. The concentrated gases are in a location that is prone to have leaks into the living compartment.

4.6.14 MISSING EXHAUST SYSTEMS If the exhaust system, either the tailpipe or the muffler has been broken off, the remaining vertical spud directs the exhaust jet toward the ground. The jet characteristics are similar to those previously described. The hot exhaust gas jet entrains ambient gas and the mixed jet then impacts the ground. The hot jet after striking the ground flows outward from the point of impact and because of its buoyancy then flows upward. Thereafter, a recirculation pattern develops (Figure 4.13). The exhaust cloud remains in position, continually being regenerated. The suction in the exhaust jet entrains local gases, which are primarily exhaust gas and fresh air dilution is minimal. The re-entrained exhaust jet builds up a stationary, highly concentrated CO cloud under the generator and motor home. Winds acting perpendicular to the exhaust stream could move the cloud to a safer location depending on the direction and magnitude of the wind stream and terrain or boundaries in the vicinity of the generator. The stationary cloud has a relatively high temperature and therefore creates thermal pressure on the underside of the motor home and generator compartment where the probability of leaks into the living compartment is most likely. Generator compartment

Muffler spud Generator platform

Hot exhaust gas

Pavement

Recirculation vortex

FIGURE 4.13

Jet entrainment and recirculation under a motor generator without a tail pipe.

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4.7 ACCUMULATION OF CARBON MONOXIDE WITHIN AN ENCLOSURE The extent of disability or death of individuals exposed to CO and other toxic exhaust gas products of combustion is directly related to the partial pressure of the toxic gases within the enclosure, the duration of exposure, as well as the physical condition and rate of exertion of the individual and presence of other gases such as carbon dioxide. This discussion does not consider the medical aspects of such poisoning and refers the reader to other authoritative texts on the subject (other chapters in this book, and10,11 ). Earlier I described the sources of exhaust gases that are produced either within the enclosure or the volume flow rate of exhaust gases leaking into the enclosure from exterior sources. This section describes the procedures for determining the exhaust gas concentration at any specific time in the CO accumulation cycle. This information in conjunction with the Coburn–Forster–Kane equation may be used to evaluate the individual exposure to CO and their resultant COHb. Equation 4.14 evaluates the exponential increase of CO concentration within an enclosure that is initially filled with clean uncontaminated air. The program assumes that perfect mixing will occur within the enclosure. This is a reasonable assumption because the contaminating fluid is either jetted into the enclosure or is drawn in as a result of pressure differential, or is due to a thermal plume or jet with a sizable thermal head, all of which create mixing. In addition, the enclosures are generally small and are not subdivided into tight rooms or enclosures, that might create isolation or stratification of the leakage gases. Equation 4.14 allows for simultaneous introduction of exhaust gas, CO and also leakage of uncontaminated outside air. This same equation may be used to evaluate the concentration of other component gases contained in the exhaust gas by substituting the gas concentration in ppm, that is, QCO2 for QCO in ppm. Volume flow of carbon monoxide in incoming exhaust (CFM). QCO = QX ∗ CO/1000000

(4.12)

Total volume of exhaust plus leakage air into the enclosure (CFM). QMm = QLm + QX Concentration of carbon monoxide at time t.   (QMm )∗ tn 100∗ QCO ∗ V Cn,m = 1−e QMm where CO is CO concentration, ppm, in incoming exhaust Cn,m is CO concentration within the enclosure at time tn and QMm , ppm e is a constant = 2.7183

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(4.13)

(4.14)

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m is step iterator (cfm) n is iterator of time (min.) Qco is volume flow of CO in the incoming exhaust gas (cfm) QL m is leakage of air entering the enclosure. Iterated by m (cfm) QMm is total volume of exhaust plus leakage air entering the enclosure (cfm) QX is volume of exhaust entering the enclosure (cfm) tn is the iterated value of time in min V is net volume of the enclosure (cu. ft.) Example: Assume a motor home having a 1680 cu. ft. volume, initially containing clean air, and with two openings, one at the top and one near the floor. Assume there is a 150 cfm roof exhauster located in the ceiling. Assume another motor home is parked parallel to this one whose motor generator is discharging exhaust gases containing 50,000 ppm CO in the direction of the first motor home, near the lower opening. Because of dilution and the size opening, assume that 100 cfm of diluted exhaust containing 2000 ppm of CO is drawn into the lower opening of the first motor home. Simultaneously, 50 cfm of clean air, (150 fan-100 exhaust), is drawn in through the upper opening. Determine the CO concentration with respect to time. Plot CO concentration when the total volume of exhaust plus leakage, QM m = 100, 125, 150, and 175, 200 cfm. Figure 4.14 shows the CO concentration in ppm within the enclosure with respect to time. Iterative computations were done for Qmx = 100 to 200 cfm. The middle dash line (m = 2) represents a flow of 150 cfm, when m = 150, which is equal to the exhaust fan volume of 150 cfm. The series of curves shows how CO concentration changes with higher and lower leakage flow rates, QL, into the enclosure.

CO concentration (ppm) at time tn 2000

C ppm0,n

CO concentration (ppm)

C ppm1,n 1500

C ppm2,n C ppm3,n

1000

C ppm4,n

500

0

0

20

40

60

80

100

tn Time (min)

FIGURE 4.14 Accumulation of carbon monoxide within an enclosure.

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Based on this information it is possible to predict the CO concentration at any period of time or to integrate the area under the curve, and to divide by time to determine the average concentration for any time span. Some important points may be made regarding this set of curves: 1. The solid curve, representing zero air leakage, shows that the CO concentration in the enclosure reaches a maximum concentration in the incoming exhaust gas after about 80 min. 2. Each successive curve maxes out at a lower concentration, all at about 80 min or less. 3. The CO concentration rises to a level dangerous to humans within 6 or 7 min. The CO concentration, for the example given, rises very rapidly for the first 20 min, reaching about 1100 ppm. Thereafter, the rate of rise diminishes and levels off at a maximum CO concentration of 1300 ppm at about 50 min. Thereafter the concentration stabilizes and remains constant. This information derived from this calculation can then be used in conjunction with the Coburn, Forster, Kane (CFK) equation, to determine blood COHb rise for any given period of time.

4.7.1 RATE OF DISSIPATION OF CARBON MONOXIDE FROM AN ENCLOSURE Earlier I discussed the rate of accumulation of CO within an enclosure. This section directs its attention to the dissipation of the accumulated CO when the rate of influx of CO, QCO , decreases or is zero, while a fan or exhauster continues bringing in fresh air. Dissipation of carbon monoxide within an enclosure.   βn,m = ppmx ∗ e−((QCO + Qx) ∗ tn /V ) (4.15) where βn,m is CO concentration in the enclosure at the end of time tn (ppm). n is time iterator (min) ppmx is CO concentration at the start of the reduction QCO is volume flow rate of CO entering the enclosure, if any (cu. ft./min) Qx is volume flow rate of clean air entering the enclosure (cu. ft./min) t is time (min) V is volume of enclosure (cu. ft.) Reconsider the previous example with the following modifications: Assume that after 20 min of operation the motor generator is turned off, but all other conditions remain the same. Determine the rate of dissipation of CO within the enclosure with

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Dissipation of CO versus time

Co concentration (ppm)

1500

1200

β 2, n

900

600

300

0

0

20

40

60

80

100

tn Time (min)

FIGURE 4.15 Dissipation of carbon monoxide from an enclosure.

respect to time. The exhaust fan, still running, takes up 150 cu. ft./min of fresh air which dilutes the 1100 ppm CO concentration within the enclosure. Equation 4.15 may be used to calculate the CO concentration after any time period. Figure 4.15 shows the dissipation curve starting at 1100 ppm at time t = 0 which correlates with Figure 4.14 at 20 min. Calculation of the type shown in section 4.7 and 4.7.1 can be used to calculate CO concentration where the source of CO cycles on and off, as would occur with a thermostatically controlled furnace. Depending on the on-off cycle time, the resultant graph would appear as a saw tooth curve. Integration of the area under that curve divided by time would yield the average concentration over any selected time span. If this information is to be used in the determination of blood COHb, a similar saw tooth curve would have to be produced accounting for the rise in COHb during periods where the CO partial pressure of the atmosphere exceeds the partial pressure of CO in the lungs. Also half-life calculations would have to be done to account for decreasing COHb where the partial pressure of CO in the enclosure is below that of the lungs during off time.

4.8 TEST METHODS FOR DETERMINING THE LOCATION OF LEAKAGE INTO AN ENCLOSURE In cases where CO intrusion into the living compartment occurs, it becomes important to determine the location and relative size of the opening or breach in the living compartment. NFPA3 and ANSI2 safety codes require that the living compartment of a mobile home or trailer equipped with a motor generator must be sealed against

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intrusion of exhaust gases. Therefore, any opening or potential leakage path into the living compartment that is not sealed is of significance. Since exhaust gases, CO, carbon dioxide and nitrogen, are all colorless, odorless, and tasteless, it is not possible to detect their leakage using normal sensory perceptions. Scientific instruments, that detect the presence of the offending gas, may be used as long as it is possible to replicate original conditions regarding flow and generation of CO. Replication, particularly when wind or atmospheric conditions play an active role is usually very difficult. Additives to the gas stream may be used to enhance sensory perception as long as they do not affect the results. Smoke testing has proven to be simple, inexpensive and accurately shows the magnitude and position of leaks.

4.8.1 SMOKE TESTING Injecting smoke into an area where exhaust gases were known to accumulate is a practical way to make leakage into the living compartment visible, without appreciably changing the physical characteristics of the leakage stream. Visual contrast of smoke is good, as are photographic characteristics. Smoke makes it easy to detect the location of small and large leaks as well as to assess their magnitude. It should be pointed out that this is not an attempt to replicate the original exhaust gas stream. It is intended to show leakage paths and give an order of magnitude to the leakage stream. Commercial smoke-producing devices are readily available, which are inexpensive and safe to operate. These include candles of various sizes as well as other smoke generators. Candles will generate smoke over periods from 30 s to 3 min, in volumes from 4,000 to 40,000 cu. ft. Smoke generators can provide a continuous stream of high quality smoke where required. Colored smoke is available in candle form. Colored smoke gives excellent contrast especially in bland backgrounds, however, colored smoke is apt to cause permanent stains. Most manufacturers state that their smoke is not toxic. My experience has been that breathing smoke, even for a short duration, leaves an aftertaste, and lung congestion that is objectionable, and that persists for many hours. The use of a good high quality respirator seems to alleviate that problem. Smoke particle size in ranges from 2 µm (0.00004 in.) to 60 µm (0.0024 in.) therefore, has little effect on changing the flow characteristics of a gas stream. The smoke is stable and persistent, having a settling time of about 1.5 h, which is more than enough for most tests. The smoke, because of its small size will penetrate very small openings. Smoke can be released in open air or injected into the intake of a portable blower, when a pressurized stream is required. The internet is a good source for smoke candles or generators. Smoke candles, or the fluid used for a smoke generators are not permitted as carry on or shipped baggage on commercial aircraft.

4.8.2 BASIC CONSIDERATIONS DURING SMOKE TESTING In order to have either an inflow or an outflow of gases there must be a pressure differential between the inside and outside of the enclosure. The simplest way to

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accomplish the pressure differential is to increase or decrease the enclosure internal pressure while allowing the ambient or outside pressure to remain at atmospheric conditions. Negative internal pressure replicates the conditions that would normally draw CO into the living compartment, therefore tends to replicates the actual accident conditions, assuming that the leakage areas have not been changed. Under some atmospheric conditions, generally high ambient temperatures, a thermal head may develop as a result of temperature differentials occurring during testing and must be overcome by additional pressure differential. Tests can be done by pressurizing or by creating a negative pressure within the enclosure. The specific type of test will be dictated by the circumstances.

4.8.3 POSITIVE PRESSURE TESTING Positive pressure testing requires a means for increasing internal pressure within the motor home or enclosure. This requires the installation of a turbo blower or other device that is not normally found in this type of enclosure. Additionally it requires that exhaust fans, ventilators, dryers, and similar openings be sealed during the test. Observation of small quantities of leaking smoke may be difficult to see in ambient or bright light conditions. Windy conditions will tend to dilute all but very large leakage streams. The diluted streams are much more difficult to photograph in bright sunlight where it may be impossible to control front lighting. Many of these problems can be eliminated if the testing can be done inside a building where wind and lighting can be controlled.

4.8.4 NEGATIVE PRESSURE TESTING Negative pressure testing is done by lowering the pressure inside the enclosure while providing a reservoir of dense smoke on the outside of the enclosure. It is desirable to locate the source of the smoke in the area where leaks are suspected. The advantage of this type of testing is that most motor homes, trailers or portable buildings already have exhaust ventilators, bathroom exhausters, fume hoods and dryers, that can be used to lower the enclosure pressure. Additionally, it is easier to see the smoke in interior controlled lighting conditions, where front and side lighting is easily achieved. Most tests can be performed without modification to the living enclosure. This is a distinct advantage in production testing but it is especially valuable in forensic cases where approval for modifications would have to be obtained, in advance of testing, from opposing counsel. Most CO intrusion incidents are from auxiliary generator engine exhaust that is normally discharged outside the living enclosure. As a generalization, motor homes develop exterior leaks in the floors and transition area of walls to floors, around wheel wells, and around conduits or pipes that penetrate the living enclosure. Frequently the leakage path is convoluted and difficult to detect using a light source or by trying to push a flexible object through the opening. Smoke testing is an easy and efficient way to detect these types of openings.

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4.8.5 TYPICAL SMOKE TESTING Smoke testing will give a good visual picture of the location and magnitude of leaks into a living compartment. Still and video photographs provide a means of recording real time results of the test. If photographs are judiciously taken they can be used to determine relative location and relative magnitude of leaks. Photos and videos are invaluable in forensic cases since they provide visual proof that leakage paths are present in the living compartment, which is in direct violation of NFPA and ANSI safety codes. Pictures are worth a thousand words, but only if it they are clear and depict the objects of interest accurately without distortion. As an example, the photographs in Figures 4.16 through Figure 4.22 tell a story of how and where CO leaked into the motor home. They show a replication, using smoke as a visible medium, of exhaust gas entering a motor home. The desired effect in this case was to show how large volumes of CO entered the motor home in a very short period of time. The photographs clearly show how the accumulation of smoke (the smoke representing CO) occurred. At the start of the test in the example shown, the interior of the motor home was clear without any obstruction. Figure 4.16 shows a view looking toward the back of the motor home. This shows that the internal atmosphere is clear. An additional photograph taken looking forward through the motor home and out the windshield shows that that section of the motor home is also free of haze (Figure 4.17). Figure 4.18 shows the first wisps of smoke appearing through the upper drawer of the end table. This photograph was taken after 1 min of elapsed time (ET) following initiation of smoke. This leak occurred at the left rear corner of the motor home. This was particularly important because that is where the generator was located. The smoke candle was located directly under the generator. The smoke traveled through a convoluted passage that could not be detected during inspection.

FIGURE 4.16 Looking aft before testing.

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FIGURE 4.17 Looking forward before testing.

FIGURE 4.18 Left rear corner, first smoke 1 min elapsed time.

From preliminary testing it was suspected that a large leak existed in the middlearea of the motor home. Thus attention was focused on that area. Figure 4.19 shows a view looking aft from the middle-point of the motor home. A large discharge of smoke was detected coming from the lower part of a storage cabinet. The interior atmosphere has become partially obscured at 2 min ET. Figure 4.20, 25 s later, shows obscuration has all but eliminated all detail in the previous photograph. Figure 4.21 shows total obscuration of the cabinet shown on the right of the previous photograph. This series of six photographs shows the location of the two leaks, and it shows that the mid point leak is the larger of the two. It shows that the rate of leakage is very

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FIGURE 4.19 Looking aft second leak area, 2 min elapsed time.

FIGURE 4.20 Looking aft second leak 2 min 25 s elapsed time.

high in the interior part of the vehicle. The photographs show that the leaks were very large and smoke permeated the interior of the vehicle in a very short time. Total obscuration took place in three minutes. Timing with a stop watch, backed up by the time record from the digital and video cameras, used in conjunction with the known volume of the vehicle, made it possible to approximate the leakage rate of smoke into the interior of the vehicle. I have found that smoke testing is an efficient means of determining the location of leaks and also their relative magnitude. It has proven to be an invaluable asset in forensic cases.

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FIGURE 4.21 Second leak, totally obscured cabinet, 3 min elapsed time. Exhaust gas percent dry methane CH4 20 18

Percent (dry)

16 14 DEN*100 CO2 CO O2

12 10 8 6 4 2 0 0

1

2

3 4 Equivalence ratio

5

6

FIGURE 4.22 Exhaust gas percent dry methane.

4.9 CONCLUSION Using the techniques presented in this paper, the source and magnitude of CO leaks into mobile homes and other enclosures may be determined. Photographs of the smoke intrusion provide a visual demonstration of the presence of leaks.

References 1. Mah, J.C. Non-Fire Carbon Monoxide Deaths and injuries Associated with the Use of Consumer Products U.S. Consumer Products Safety Commission, October, 2000. 2. American National Standards Institute, Washington, DC.

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3. National Fire Protection Association, Quincy, MA. 4. Environmental Protection Agency. Air Quality Criteria for Carbon Monoxide, EPA 600/P-00/001B, Tables 3–7, 1999, Cincinnati, OH. 5. Boltz R. E. and Tuve G. L. Handbook of Tables for Applied Engineering Science, 2nd edition, CRC Press, Boca Raton, FL, 1987. 6. Williams, G. C. et al., The Combustion of Methane in a Jet Mixed Reactor, Twelfth Symposium on Combustion, Pittsburg, PA. 1968. 7. Jones, J.C. Combustion Sciences: Principles and Practices, Millennium Books, Newton, Australia, 1933. 8. Linan, L. and Williams, F. Fundamental Aspects of Combustion, Oxford University Press, Oxford, UK, 1993. 9. National Oceanographic and Atmospheric Administration, Washington, DC 10. Penney, D.G. Carbon Monoxide, p. 296, CRC Press, NY, 1996. 11. Penney, D.G. Carbon Monoxide Toxicity, p. 560, CRC Press, NY, 2000.

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5

Carbon Monoxide Emissions from Gas Ranges and the Development of a Field Protocol for Measuring CO Emissions Richard Karg

CONTENTS 5.1

5.2

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.1.1 Objectives of Karg Field Protocol Development. . . . . . . . . . . . . . . . . . 5.1.2 ANSI Standard Z21.1-1993, Household Cooking Gas Appliances 5.1.3 As-Measured and Air-Free Carbon Monoxide Measurement . . . . . 5.1.4 Single-Zone Mass Balance Model and Room CO Concentrations 5.1.5 Field Testing, Laboratory Research, and Karg Field Protocol Development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.1.5.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.1.5.2 Range Top Burners, Field Testing . . . . . . . . . . . . . . . . . . . . . . . 5.1.5.3 Range Top Burners, Laboratory Testing . . . . . . . . . . . . . . . . 5.1.5.4 Oven Bake Burners, Field Testing . . . . . . . . . . . . . . . . . . . . . . Karg Field Protocol for Measuring Carbon Monoxide Emissions from Gas Ranges . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.2.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.2.2 Visual Inspection and Customer Education . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.2.2.1 Range Top Inspection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.2.2.2 Oven Inspection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.2.3 Measurement of Emissions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.2.3.1 Safety During Measurement of Emissions. . . . . . . . . . . . . . 5.2.3.2 Preparation for Burner Testing . . . . . . . . . . . . . . . . . . . . . . . . . . 5.2.3.3 Range Top Burner Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

100 102 102 103 106 108 108 109 112 115 122 122 122 122 123 124 124 124 125 99

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5.2.3.4 Oven Bake Burner Testing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.2.3.5 Burner or Range Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.3 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.4 Acknowledgment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

125 126 126 127 127

5.1 INTRODUCTION Indoor air quality studies and carbon monoxide (CO) emissions testing from combustion appliances have pointed to a number of factors affecting indoor CO levels: source and source-use characteristics, building features, ventilation rates, air mixing within and between rooms, the existence and effectiveness of contaminant removal systems, and outdoor concentrations.1 Gas ranges are used by a significant percentage of the population and, as an unvented combustion appliance, can contribute to hazardous concentrations of CO in indoor air when they malfunction or are misused. The U.S. Consumer Products Safety Commission (CPSC) estimates that 130 people died in 2001 from nonfire, nonauto related CO poisonings; 75 of these deaths were attributed to heating systems and 10 to gas ranges/ovens.2 From 1990 to 2001 the CPSC estimated between 6 and 14 people died each year from CO emitted from gas ranges/ovens.2−5 Data for the years 1994–1998 show an additional 600–900 per year suffered nonfatal poisonings.3 It is obvious from these data that gas ranges/ovens can malfunction and emit hazardous levels of CO. To reduce injuries and deaths from CO poisonings, gas range top burners and ovens should be tested regularly and maintained properly. Testing combustion appliances for CO emissions during servicing or home weatherization is not currently a standardized practice in the United States, although the low-cost electronic combustion analyzers available today make it easier to test CO emissions in the field. The lack of standard field testing procedures for measuring CO emissions, the uncertainty of the accuracy of field measurements, and the dearth of technicians trained to consider the complex nature of CO diagnostics have led to widely variable emission measurement protocols or to a total lack of field testing.6−10 Heating systems are more likely than gas cooking appliances to receive regular servicing.5 Most natural gas utilities recommend servicing of gas heating systems every 1–3 years. Gas ranges/ovens are seldom, if ever, serviced by a trained technician. Tilkalky suggested: “. . . routine service adjustments on the 10 range set resulted in statistically significant decreases in CO and NO2 following servicing. This finding implies that some servicing of the gas range may be desirable and have an impact on indoor levels of NO2 and CO, and should be investigated further on a larger data set to determine if this initial indication holds true for a larger population.”6 Furthermore, if a homeowner desires servicing of a cooking appliance, anecdotal reports suggest that they might have difficulty finding a trained and willing technician.11,12 From 1995 to 1998 the administrative office for the Ohio low-income weatherization program, funded by the U.S. Department of Energy (DOE), conducted a survey of the 50 state and District of Columbia low-income weatherization programs to determine the CO emission testing methods used by these programs on all combustion

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appliance types. Many of the questions used on these Ohio surveys were related to gas range tops and ovens. Tables 5.1 and 5.2 include oven and range top data from the 1998 Ohio survey.13 The wide variation and arbitrary nature of these testing methods was alarming. This lack of consistency among testing methods within this DOE program demonstrated the need for a standardized CO emissions testing protocol for technicians in the field. In addition, there were other reasons to develop a field protocol,

TABLE 5.1 Gas Range Top Burner Testing Data from Ohio Survey of carbon monoxide Protocols, 51 State Low-Income Weatherization Programs, 199813 Do you have a CO emissions protocol? n = 51 Pan on burner for test? n = 31 Sampling probe height above burner (inches)? n = 28 Highest acceptable CO reading (ppm)? n = 26

Burner warm up time before test (minutes)? n = 25

Yes = 37

No = 14

Yes = 4 Range = 6–36, Mean = 13.8, SD = 8.2, Median = 12, Favored = 12

No = 27

As-measured, n = 25 Range = 9–300 Mean = 58 SD = 62 Median = 50 Favored = 100

Air-free, n = 1 Value = 100

Range = 0.25–20, Mean = 5.4, SD = 3.5, Median = 5, Favored = 5

TABLE 5.2 Gas Oven Testing Data from Ohio Survey of CO Protocols, 51 State LowIncome Weatherization Programs, 199813 Do you have a CO emissions protocol? n = 51 Oven door open or closed? n = 36 Oven control on broil or bake? n = 42 Highest acceptable CO reading (ppm)? n = 32

Burner warm up time before test? n = 34

Yes = 37 Open = 10 Broil = 19 As-measured, n = 28 Range = 9–400 Mean = 110 SD = 103 Median = 100 Favored = 50 and 100

No = 14 Closed = 26 Bake = 23 Air-free, n = 4 Range = 35–400 Mean = 158 SD = 164 Median = 100 Favored = 100 Range = “at startup” to “steady-state”, Favored = 5 or 10 min

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including (1) the use of gas ovens/ranges was widespread, (2) these appliances were often used as space-heating devices dwellings were becoming tighter, and (3) gas ranges and ovens were not regularly cleaned and tuned.14 The author was asked by the U.S. DOE’s Low-Income Weatherization Programs of the Chicago Region to develop the Field Protocol for Gas Range Carbon Monoxide Emissions Testing in 2001, hereafter referred to as the Karg Field Protocol.15,16

5.1.1 OBJECTIVES OF KARG FIELD PROTOCOL DEVELOPMENT The primary objective of developing the Karg Field Protocol was to identify range top and oven burners that are high emitters of CO. As residences are made tighter to save energy, a given CO emission for a gas range can become more hazardous to the occupants. This is discussed in Section 5.1.4 with the use of the single-zone mass balance model. Of course, the possibility of an increased hazard to occupants is a concern to the management and technicians working with weatherization programs. Secondly, the Karg Field Protocol was developed to bring standardization to range testing among 51 DOE low-income weatherization programs. The Ohio survey of emissions testing methods clearly demonstrated this need and made it obvious that there was no existing consensus. The final objective was to minimize arbitrary or biased evaluation by field technicians.

5.1.2 ANSI STANDARD Z21.1-1993, HOUSEHOLD COOKING GAS APPLIANCES Two important questions had to be answered while developing the Karg Field Protocol: What basis should be used to develop the threshold level of CO emissions at burners to ensure an acceptable ambient level for the occupants of a residence? Second, at what time after burner start-up should readings be recorded and what method of measurement should be used to accurately reflect the long-term CO emissions and thus, the potential hazard of a burner’s emissions to occupants. This second question is discussed in Section 5.1.5.4. Manufacturers of gas ranges must comply with American National Standards Institute document Household Cooking Gas Appliances (ANSI Z21.1, 1993).17 This standard states “An appliance shall not produce a concentration of CO in excess of 0.08% (800 ppm) in an air-free sample of the flue gases when the appliance is tested in a room having approximately a normal oxygen supply.”17 The test procedure required by this standard is lengthy, but simply stated: containers filled with five pounds of water are placed on each of the four range top burners. All the range top burners and the oven burner are started simultaneously. After 5 min of operation, the CO air-free is measured in a collection hood above the range. This air-free concentration must be 800 ppm or less. In 1996, the Gas Research Institute published a topical report entitled Critique of ANSI.Z21.1 Standard for CO Emissions from Gas-Fired Ovens and Ranges.8 This Battelle Laboratory appraisal of the 800 ppm emission level, originally set in 1925, found “The underlying basis for and allowable limit set by the original

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CO standard were valid and conservative in 1925, and remain so today. . .”8 The report continues with “Gas ovens/ranges do not pose a public safety or health threat with regard to CO emissions, a performance characteristic that can be reliably validated either in the lab, factory, or field by using the current Z21.1 measurement protocol, and its specified limit of 800 ppm CO, O2 -free.”8 Although not all researchers agree with this conclusion,10 the gas range Karg Field Protocol used this American National Standards Institute (ANSI) level of 800 ppm CO air-free as the basis for the development of CO emission thresholds. It would have been problematic to select a basis for the Karg Field Protocol other than ANSI Z21.1, since it is the current standard by which manufacturers design and build gas ranges and ovens. A field protocol based on values more or less stringent than ANSI Z21.1 would have limited credibility within the industry and would have compromised field technicians. Therefore the Karg Field Protocol was designed to determine if a gas range complies with ANSI Z21.1.

5.1.3 AS-MEASURED AND AIR-FREE CARBON MONOXIDE MEASUREMENT Gas ranges are probably the most common unvented gas appliances in use in North America. Because they are unvented, they have the potential of contributing to unacceptable ambient indoor levels of CO. Fortunately, in most residential situations, they are not operated long enough to adversely affect occupants. However, there are cases where gas oven/ranges can emit enough CO to cause health hazards or trigger CO alarms.18 Examples include: (1) user operation of a gas oven/range as a spaceheating appliance;14 (2) user alteration of the oven, such as lining the oven bottom with aluminum foil, inadvertently covering the secondary air ports;5,19 (3) malfunctioning equipment, including excessive gas pressure, closed air shutters, damaged orifices, and warped oven flame spreaders;16 and (4) baking a large roast or fowl. As the awareness of CO hazards increases, more technicians are using electronic instruments for measurement of CO emissions. These electronic devices are connected to a flexible plastic tube with a hollow metal probe at the other end. When measuring CO emissions from a vented appliance, the metal probe is inserted into a drilled hole in the metal flue pipe. A vacuum pump in the measurement device pulls a combustion gas sample through the metal probe and plastic tube, into the CO measurement cell, and finally expels the gases through an exhaust port. Measurement of CO emissions from a gas oven is performed with a similar technique, however, rather than inserting the probe into a drilled hole in a vent pipe, the metal probe is inserted into the oven-vent port that is typically located at the rear of the range top. There are two scales with which to measure CO: one is “as-measured” and the other is “air-free.” As-measured CO is determined from a sample of combustion gases with no regard for the amount of excess air (oxygen, O2 ) diluting the CO concentrations. Excess air is the amount of oxygen in the combustion gases in excess of the exact amount needed for perfect combustion. When combustion is perfect, just the right amounts of fuel and oxygen are supplied to the combustion process so that all the oxygen is utilized, a process called stochiometric combustion.

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The basic problem with the as-measured method is this: As the amount of excess air increases, the as-measured CO value falls for a given source strength of CO.20 In other words, the amount of excess air in an emissions sample can, by dilution, significantly decrease the as-measured value. This can cause a technician to mistakenly think that a hazardous burner is working properly. On the other hand, air-free measurement of CO takes account of the amount of excess air in an emissions sample, incorporating an adjustment to the as-measured CO ppm value, thus simulating air-free (oxygen-free) conditions in the sample. To do this, a reading of oxygen percentage is taken from the emissions sample along with the CO as-measured ppm. This can be done with an emissions meter having the capability of measuring CO and oxygen percentage. Most emissions meters that measure oxygen and CO as-measured have an integral electronic chip that calculates the air-free level from as-measured CO ppm and oxygen percentage. CO air-free and the firing rate of the burner can be used to determine the CO emission rate; CO as-measured cannot. The use of the CO air-free measurement is generally supported within the scientific community because it is a normalized value.21 Understanding as-measured and air-free CO measurements can be aided with an analogy. If four drops of blue food color are placed in a small glass of water and another four drops in a full pitcher of water, the water in the glass is darker shade of blue than the water in the pitcher. When a sample from each water vessel is analyzed, the concentration of food color in the pitcher is lower than in the glass; this is analogous to CO as-measured. On the other hand, CO air-free is analogous to calculating the number of drops of food color in each vessel by analyzing the concentration by measuring (similar to CO as-measured) and by performing calculations to determine the amount of food coloring in each vessel. Of course, the resulting calculation would reveal four drops of food color in each vessel, a determination that could not be made if only the concentration were measured. Finally, either of these vessels of water, when dumped into a 5 gallon container of water, will color the 5 gallons of water to nearly the same degree. Either of these equivalent equations can be used for determining air-free CO in an emissions sample with values for CO as-measured and oxygen percentage: 
20.9 COAFppm = · COppm (5.1a) 20.9 − O2 or
COAFppm =

COppm 1 − 4.78 (O2 )

 (5.1b)

where COAFppm = Carbon monoxide, air-free ppm COppm = As-measured combustion gas carbon monoxide, ppm O2 = Oxygen in combustion gas, as a percentage From any combustion emission sample, the highest percentage of oxygen possible is 20.9%—that of the earth’s atmosphere—and the lowest is zero, resulting

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(b)

CO as-measured = 43 ppm O2 = 20% CO air-free = 1000 ppm

Oven A

CO as-measured = 522 ppm O2 = 10% CO air-free = 1000 ppm

Oven B

FIGURE 5.1 (a) Oven A has more dilution air than (b) oven B, so the CO as-measured value is lower, but the CO air-free values are the same for each oven, so each oven will pollute the kitchen air to the same degree.

from stoichiometric or oxygen-starved combustion. Whereas the oxygen content of combustion gases from natural gas or propane furnaces or boilers is usually within a range of 4.0–10.0%, the percentage of oxygen for a natural gas or propane range top burner or oven is much higher, normally within a range of 13.6–20.1% and averaging about 19.8%.16 This higher range of oxygen in the combustion gases leads to more diluted and lower as-measured readings. The two ovens pictured in Figure 5.1 demonstrate the inherent problem with as-measured values. For Oven A, the CO as-measured level is 43 ppm; safe by some standards. For Oven B, the CO as-measured level is 522 ppm; considered unsafe by most standards. However, each oven is emitting the same level of CO air-free—1000 ppm, which is unsafe by all standards. (Refer to Equation 5.1a for these calculations.) In other words, the source strength of CO from each oven as indicated by the CO air-free measurement is the same; each oven will lead to the same ambient level of CO in the kitchen air. A technician might pass Oven A and fail Oven B, not understanding that each is contributing equally to hazardous levels of ambient indoor CO. Measuring CO air-free gives the technician a better idea of the impact the CO emissions has on indoor air concentrations. As indicated above, the higher the percentage of oxygen in the combustion gases, the lower the CO as-measured readings will be. If excess air is zero, as-measured and air-free measurements will be equal. As excess air increases, CO as-measured readings decrease, but CO air-free readings do not change. The high excess air percentages for gas ovens and range top burners increases the importance of taking air-free measurements, because the high excess air can significantly lower as-measured readings, thus masking the true CO source strength. It is common to find an oxygen content of 19.8% in range top burner combustion gases. If this value is plugged into Equation 5.1a, the resulting CO air-free level

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is 20 times the as-measured value. This is a rough general guideline relating CO as-measured to CO air-free values for gas range top burners.

5.1.4 SINGLE-ZONE MASS BALANCE MODEL AND ROOM CO CONCENTRATIONS Vented appliances are only a hazard when they spill or backdraft. On the other hand, gas ranges vent into the living space, so it is important to understand the relationship between the source strength of CO emissions and the resulting concentrations of CO in the ambient indoor air. The single-zone mass balance model equation is helpful for demonstrating this relationship.  COppm =

  COAFppm · Vg · Gr · 1 − (1/2.713ACHt ) ACH · v

(5.2)

where COppm = As-measured indoor ambient carbon monoxide, ppm COAFppm = Air-free carbon monoxide, ppm Vg = ft 3 of flue gas per ft3 of fuel gas (8.5 ft3 for natural gas, 21.8 ft3 for propane) Gr = Gas flow rate, in ft3 /h = input rate (Btu/h) / heat value of fuel (Btu/ft3 ) —an average input rate for an oven is 18,000 Btu/h, for a range-top burner 9,000 Btu/h —an average heat value for natural gas is 1000 Btu/ft3 , for propane 2500 Btu/ft3 2.713 = Napierian logarithmic base ACH = Number of natural air changes per hour of room or house t = Time interval, hours v = Volume of room or house, ft3 For example, if a natural gas range with a total input rate of 54,000 Btu/h is emitting CO air-free at a constant rate of 800 ppm in a house of 8000 ft3 having an air exchange rate per hour (ACH) of 1.5, the ambient indoor CO concentration will be 29 ppm after 2 h (Refer to Equation 5.3). The rate of 54,000 Btu/h is the sum of the input of four range top burners and the oven operating at the same time, a possibility if a user were operating the gas range as a space heater.   800AFppm · 8.5 · 54 · 1 − (1/2.7130.5·2 ) = 1.5 · 8000 

COppm

COppm =29

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(5.3)

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This assumes the ambient CO is evenly dispersed throughout the house. In reality, the concentrations are likely to be higher in the kitchen than in remote sections of the living space. If the structure is tightened, reducing the ACH from 1.5 to 0.5, the ambient indoor CO level will increase. As shown in the Equation 5.4, at the end of the 2-h period the average ambient CO concentration will be 58 ppm, rather than 29 ppm. At the end of 4 h, the room concentration will be 80 ppm.   800AFppm · 8.5 · 54 · 1 − (1/2.7130.5·2 ) = 0.5 · 8000 

COppm

(5.4)

COppm =58 It is clear that tightening the house (lowering the ACH) without also lowering range CO emissions or operating a vented range hood during range operation can create a more hazardous indoor condition. This has important implications for the weatherization of residential buildings. Figure 5.2 shows the above examples along with two other house leakage rates— 0.35 to 2.0 ACH. Notice that as the leakage rate decreases the indoor levels of CO increase and the number of hours before reaching a stabilized level increases. For example, at 2.0 ACH the stabilized level of 23 ppm is reached after 2 h. In contrast, at 0.5 ACH the stabilized level of 91 ppm is reached after 10 h. This situation might occur if occupants were operating all the burners for space heating with the oven door

140.00 0.35 ACH Ambient CO level, ppm

120.00 100.00

0.5 ACH

0.35 ACH 0.5 ACH 1.0 ACH 2.0 ACH

80.00 60.00

1.0 ACH

40.00 2.0 ACH 20.00 0.00 0

1

2

3

4

5

6

7

8

9

10

Hours of CO production, 800 ppm air-free

FIGURE 5.2 Room ambient CO concentrations at various house leakage rates over 10-h period. CO production is at a constant rate of 800 ppm air-free from a total burner input of 54,000 Btu/h in an open-plan house of 8,000 ft3 .

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open, thus the duty cycle of the oven would be 100% because the oven thermostat would never be satisfied. Field measurements of 18 gas ovens under the author’s direction in 2001 resulted in 8 of these tested units emitting in excess of 800 ppm CO air-free after 15 min of operation. Although the average gas oven has a firing rate of approximately 18,000 Btu/h—only one-third the value of 54,000 Btu/h input rate used in the total range input rate above—these failed ovens emitting in excess of the 800 ppm air-free CO emissions could cause hazardous ambient CO levels if one of these ovens were used to bake a large turkey or as a space heater. One notable oven emitted CO at a rate of 2270 ppm air-free. In the same example house as above, with a 0.35 ACH and the oven operating at 18,000 Btu/h, this CO emission level would result in an ambient CO of 62 ppm after 2 h and 93 ppm after 4 h. Other field and laboratory studies have revealed that lining the bottom of an oven with aluminum foil to catch spills can lead to higher CO emissions if the foil obstructs the secondary air openings at the oven bottom, as noted in the U.S. CPSC testing.5 This practice interrupts the oven venting path and becomes even more hazardous if the oven is operated with its door open.5 “The worst case situation of a consumer using a gas oven as a space heater with an aluminum foil, protective liner, produced the highest CO emission rates. These high emission rates can push CO ambient air concentrations to dangerous levels.”5

5.1.5 FIELD TESTING, LABORATORY RESEARCH, AND KARG FIELD PROTOCOL DEVELOPMENT The Karg Field Protocol for Gas Range Carbon Monoxide Emissions Testing was completed by the author in 2001. Funding and support for this protocol research and development was provide primarily by the U.S. DOE and the Chicago Region low-income weatherization programs of Illinois, Indiana, Iowa, Michigan, Minnesota, Missouri, Ohio, and Wisconsin. Funding and support for laboratory work was provided by the Gas Research Institute of Des Plaines, Illinois, through GARD Analytics of Park Ridge, Illinois and WEC Consulting of Potomac, Maryland. A group of technical advisors was assembled for the project that included college faculty, scientists from government organizations, indoor air quality experts, technical consultants, and private laboratories. Tim Lenahan of the Ohio Office of Energy Efficiency was the contract manager for the project. 5.1.5.1 Introduction At the foundation of the development of this Karg Field Protocol was research in the field and laboratory. Eighteen oven bake burners, and 81 range top burners were tested in the mid-coast Maine area, and 19 range top burner tests were done at the Gas Research Institute laboratory facility. Of the 21 oven bake burners tested, 4 were natural gas and 17 were propane (LPG). All 21 of the gas ranges tested in the field were in primary residences or summer homes. Laboratory range top burner testing was done over a 3-day period to determine the best method for measuring range top burner CO emissions. No oven testing was done at the laboratory.

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Field testing required approximately 3 h in each house. During emissions testing, the houses were closed up with all windows and exterior doors shut. Range hood fans and other exhaust fans in the houses were not operated during the testing, unless ambient CO levels reached 35 ppm. All test equipment was calibrated with CO span gas at the beginning and end of each house test regimen. After each burner test the instrument was rinsed for 1–2 min. All oven emissions testing was done with two test instruments inserted into the oven vent at the back of the range top. During each 30-min oven test, these instruments were checked for correspondence. The oldest range tested had been in service 53 years; the newest only 1 year. Ten of the ranges had standing pilots and eleven had spark ignitions. Gas pressure was measured in ten of the ranges. Natural gas measured in three ranges was between 4 and 5 in. of water column and propane gas pressure measured in eight ranges was between 7 and 12 in. of water column. The actual firing rate of each burner was not measured, but label firing rates were recorded for 16 ranges. The mean and median range top burner label firing rate were 8,563 and 9,000 Btu/h and the mean and median oven bake burner label firing rate were 17,677 and 18,000 Btu/h. Ambient CO levels were continuously monitored during the field testing for the safety of house occupants and the field analyst. After range top burner testing, the highest ambient CO level recorded was 7 ppm; all other readings were zero. After oven bake burner testing, the highest level was CO level recorded was 78 ppm and the lowest was zero. The mean, median, and standard deviation were 7.8 ppm, 1.5 ppm, and 19.21 ppm for 16 field tests for which this information was recorded. Although the tested ranges were not adjusted after the initial emissions test and then tested again, other research has found evidence that adjustment of a gas range by a knowledgeable technician can lower CO emissions.6 Ranges should be cleaned, tested for CO emissions, and adjusted, if necessary. Anecdotal evidence suggests that gas ranges are seldom adjusted and rarely tested for CO emissions. 5.1.5.2 Range Top Burners, Field Testing Range top burner emission rates are affected by disruption of the burner flame. Air currents and flame impingement greatly affect CO output. In addition, sampling location also affects measured CO and oxygen concentrations. To reduce variability and increase correspondence between measured CO output and actual CO output, a number of devices and methods have been devised. Range top burner testing in the field was done using five different devices and methods to determine which method was the most uniform, repeatable, and best simulated actual burner use in a home. These devices and methods include (1) the CO Hot Pot™ (Figure 5.3), (2) a device similar to the CO Hot Pot™, but with a stainless steel kettle within the cylinder, (3) a device similar to the CO Hot Pot™, but with no bowl or water kettle within the cylinder, (4) a free-standing aluminum kettle on the burner, and (5) testing the burner CO emissions over an open burner with no special device. The first of three devices were designed and fabricated by the author to introduce standardization and increase the accuracy of field testing. The last two methods were found to be in common use

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(a)

(b)

FIGURE 5.3 CO Hot Pot™ for measuring CO emissions from range top burners. Notice the stainless steel bowl at the bottom of the 8-in. diameter by 12-in. high cylinder. (a) Front view and (b) Top view of the CO Hot Pot™.

for testing range top burners by technicians working in the U.S. DOE low-income weatherization program.13 The CO Hot Pot™ was used on each range top burner for a five-minute test. This simple device (Figure 5.3) is an 8-in. round by 12-in. high galvanized sheet metal cylinder with a 6-in. round stainless steel bowl fastened concentrically at the cylinder’s bottom.22 This bowl is intended to simulate a pot or pan on the range burner. The Y-shaped brace at the top of the cylinder strengthens the top of the cylinder and supports an eye-bolt that holds the tip of the electronic instrument probe in place after it is inserted through a hole drilled in the side of the cylinder. A metal handle fastened to the other side of the cylinder facilitates easy placement of the cylinder on the range top burner grate. The cylinder contains the emissions and protects the combustion from lateral drafts that can significantly increase CO emissions as a result of flame impingement. This device was also used during range top burner testing in the Gas Research Institute laboratory. A second device that was field and laboratory tested was a cylinder similar to the CO Hot Pot™, but with a stainless steel water kettle in the place of the bowl. The spout of this kettle passed through a snug opening in the cylinder so that evaporating water from the kettle could escape without affecting the emissions readings taken inside the cylinder just above the kettle. This device had the same Y-brace and eye-bolt to hold the instrument probe. The kettle was always filled with four pounds of 60◦ F water just before a test. The third device tested was an open cylinder that was also used for range top burner testing, a replica of the CO Hot Pot™, but without the stainless steel bowl at the bottom. In addition to these three devices, the fourth method tested in the field and laboratory was a free-standing aluminum water kettle, without a cylinder around it, that was used on each range top burner. The size of this water kettle was similar to the stainless steel one housed in a cylinder. This aluminum kettle was always filled with four pounds of 60◦ F water before a test. Finally, the fifth method tested was the CO instrument probe held at a precise position over the open flame of the range top burner; no cylindrical device or water kettle.

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Left front range top burner, unit10 600

30

500

25

400

20

300

15

200

10

100

5

0

CO as-measured (ppm)

CO air-free ppm CO as-measured ppm 35

700 CO air-free (ppm)

111

0 0

1

2

3

4

5

Time after startup (minutes)

FIGURE 5.4 A typical emission profile of a 5-min range top burner test with CO Hot Pot™ showing CO as-measured and air-free ppm.

When each of these devices and methods were used on a range top burner, the end of the instrument probe was always positioned exactly ten inches above the top of the burner grate. Each test was conducted for 5 min while emissions at the burner were monitored and recorded. All burner measurements for CO as-measured, CO air-free, oxygen (O2 ) percentage, and temperature were logged every 0.25 min and recorded to a computer spreadsheet for analysis. Range top burner testing was always performed before oven testing to prevent the oven from preheating the range top area. Figure 5.4 shows typical profiles of CO as-measured and air-free ppm using the CO Hot Pot™ for a 5-min test. It was common for the emissions to peak within the first 2 min and then begin to fall as the burner parts warm up and steady state is reached. Range top burner emissions are less problematic to measure than oven emissions because the burner does not turn on and off (duty cycle) in order to hold a constant temperature. Notice that the CO air-free and as-measured emissions track each other in parallel, although air-free is approximately 17–20 times greater than as-measured. This is typical. The parallel characteristic of these two measurements is a result of a fairly consistent percentage of oxygen in the emission gases. Of the 81 range top burners tested during the field research, only 1 failed the Karg Field Protocol threshold of 35 ppm CO as-measured, using the CO Hot Pot™ at 5 min. This failed burner had an emissions rate of 38 ppm CO as-measured and 882 ppm CO air-free (20% oxygen). Oxygen percentages were within a fairly narrow range when using the CO Hot Pot™—between 17.9 and 20.8, with a mean of 19.8. Oxygen percentages this high can significantly affect the relationship between CO as-measured and air-free values. For example, for the failed range top burner mentioned above, the multiplier to get from CO as-measured to CO air-free is 23.2 (see Equations 5.1a and 5.1b). The high oxygen levels typically found in emissions from gas range top and oven burners lead to reduced levels of certainty when taking measurements in the field. Although one study by the Gas Research Institute found “The data sets reveal mean CO emissions on the low setting to be much larger than the values obtained

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when the burners were set on high or medium,”6 the author’s testing in the field and the laboratory was done with the range burner setting on high. The highest setting was selected for the Karg Field Protocol because this setting; (1) most closely matches the Btu/h rating on the range name plate; (2) is the easiest setting for the technician to find; and (3) is the only repeatable setting on most range top burners, allowing the technician to retest at the same setting—Btu/h firing rate—after a burner is adjusted. 5.1.5.3 Range Top Burners, Laboratory Testing Laboratory chamber testing was done over a 3-day period at the Gas Research Institute facility to determine the best method of measuring CO emissions from range top burners. The CO Hot Pot™ and four other methods—all described in the previous section—were tested to determine which of the five methods would best predict the ambient emission CO levels in the test chamber. The CO Hot Pot™ was tested seven different times; the four other methods were each tested three times. The CO Hot Pot™ was tested more often because by the third day of testing, it already showed evidence of being the most promising of the five methods. During the chamber testing of range top burners, readings of CO as-measured, CO air-free, and oxygen were recorded with hand-held equipment at the burner with each of the five methods (devices) while the chamber ambient CO concentrations were recorded with stationary laboratory equipment. Both burner and chamber emissions were recorded every 0.25 min during the test periods. The equipment was set up on a range burner in the chamber, the technician left the chamber, the burner and emissions recording equipment was then activated from outside of the chamber. During most of the tests, a small fan was operating on the floor of the chamber to help mix emissions with the chamber air; care was taken to ensure air did not flow across the range top. The burner was operated for 30 min and then turned off from outside the chamber. The decay of the emissions was measured for another 15 min so that the rate of air changes per hour within the chamber could be calculated after each 30-min emissions test. For most of the tests, the chamber was then purged with an exhaust fan operating for 15 min within the chamber before the next test began. All tests were performed with the burners at the highest setting. (See Figure 5.5) The burner input rate is usually printed on the range nameplate for both natural gas and propane fuels. ANSI Standard Z21.1-1993 for manufacturers states “When operated for 5 min, starting with all parts of the appliance at room temperature, the burner adjustment shall be within + 5% of the capacities specified (on the nameplate).”17 Metering gas consumption during laboratory testing for this study showed that the metered consumption in Btu/h of five range top burners on two ranges varied from rated consumption by +15% to –29%. The metered burner consumption closest to rated consumption was –12%. These variations were significantly greater than the 5% required by the ANSI Standard. More field research is needed to determine the typical variation between nominal nameplate ratings and actual burner Btu/h. Figure 5.6 shows the chamber concentrations of CO during three tests using the CO Hot Pot™ over the 30-min test, the 15-min decay, and the 15-min purge. At the end of the 30-min test, the chamber concentrations were within less than 1 ppm of CO for the three tests on the same burner.

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FIGURE 5.5 Chamber testing with CO Hot Pot™ and Testo instrument sending emissions data directly to a computer outside the chamber. Notice the 12-in. square opening in the wall at the upper right and the floor fan to spread combustion emissions within chamber. Photo was taken through a sealed glass observation port.

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FIGURE 5.6 Test chamber CO concentrations for three range top burner tests using CO Hot Pot™. See Figure 5.7 for corresponding burner CO emission rates.

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Test3, Range C, CO air-free Test10, Range C, CO air-free Test15, Range C, CO air-free

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FIGURE 5.7 Burner CO emission rates for three range top burner tests using CO Hot Pot™. See Figure 5.6 for corresponding test chamber concentration.

Figure 5.7 shows the corresponding CO emissions measured at the burner for these three 30-min tests. At the end of the three tests, the CO as-measured values were 21, 21, and 19 ppm and the CO air-free values were 231, 231, and 199 ppm. At 6 min after burner startup, the test time selected for the Karg Field Protocol, the CO as-measured values for the three tests were 15, 14, and 10 ppm and the CO air-free values were 261, 225, and 161 ppm. The higher chamber CO concentrations and emission rate at the burner for test 3 shown in Figures 5.6 and 5.7 might have resulted from the CO Hot Pot™ being positioned slightly off center over the burner (laboratory notes and a photograph support this misalignment), although further tests were not conducted to determine if an off-center position over the burner would affect emissions. After field and laboratory testing, the CO Hot Pot™ was selected over the other four test methods for a number of reasons. 1. The cylinder of this device protects the CO emissions testing from the unpredictable affect of lateral air movement, making testing in the field more consistent and repeatable. During a test in the laboratory chamber with the free-standing water kettle, the chamber air conditioner inadvertently turned on, blowing air across the range top and causing the ambient CO concentration in the chamber to rise to just under 15 ppm. Similar tests with this free-standing water kettle on the same burner without the affect of the air conditioner fan resulted in a chamber CO just above 3 ppm. This minor laboratory accident demonstrated the importance of preventing air flow across burners during emissions measurement and supports the use of the cylindrical protective housing of the CO

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Hot Pot™. Of course, emissions testing with the instrument probe merely held above an oven flame is subject to the same, if not more, variability from lateral air movement than when using a free-standing water kettle. 2. Burner emissions measurements with the CO Hot Pot™ were found to level off to steady-state conditions 5–6 min after burner startup in almost all tests in the laboratory and field. The other four methods were less consistent in performance. 3. Some of the other measurement methods where either too complicated to be practical in the field, or they demonstrated design flaws. The methods not using a cylindrical housing made the emissions testing subject to more error resulting from lateral drafts, as described above. The cylinder with a water kettle inside and the free-standing water kettle required filling with water and yielded variable results because of the changing water temperature. Finally, the open cylinder with no bowl or water kettle concentrically fastened at the bottom of the cylinder created a strong enough draft during some tests to cause the flames to lift off the burner, resulting in artificially high emissions readings. 4. The oxygen percentages in the emission gases when using the CO Hot Pot™ were usually close to 19.85. The field testing mean was 19.84% and the laboratory testing mean was 19.3. This rather tight range for oxygen percentage allowed the adoption of a relatively simple method for the Karg Field Protocol range top burner testing, using the CO Hot Pot™ for CO asmeasured readings rather than the more complex CO air-free measurement. The Karg Field Protocol calls for CO as-measured emissions measured with the CO Hot Pot™ of 35 ppm or less. For an oxygen percentage of 19.85%, this equates to a CO air-free threshold of just less than 700 ppm, 100 ppm less than the ANSI Standard Z21.1 level of 800 CO air-free ppm to which manufacturers must adhere. The ANSI Standard requires measurement at 5 min, whereas the Karg Field Protocol calls for measurement at 6 min. The author’s field and laboratory testing indicated that range top burner CO emissions measured with the CO Hot Pot™ are more likely to have settled into steady-state conditions at 6 min than at 5 min. The later emission measurement of the Karg Field Protocol is likely to yield results closer to the longer-term emissions of a range top burner than ANSI Standard test a 5 min. 5.1.5.4 Oven Bake Burners, Field Testing Oven testing was performed on bake burners only, even if a separate broil burner was installed and working in a tested oven. Oven testing was done at a setting of 350◦ F with the oven door closed, utensils removed from within and under the oven, and foil lining removed from the oven floor (none of the ovens floors were lined with foil when the field analyst arrived to test). Ovens were not cleaned before testing. Testing was done for thirty minutes while emissions at the oven burner and ambient kitchen air were monitored and recorded. All field measurements for CO

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FIGURE 5.8 Redundant testing of CO emissions during field test. Two instrument probes are inserted into oven vent in a manner ensuring that room air will not dilute the sample.

as-measured, CO air-free, oxygen percentage, and temperature were logged very 0.25 min and recorded to a computer spreadsheet for analysis. The oven burner emissions were measured at the oven vent, which in all cases was at the back of the range top surface. Care was taken to measure emissions without the diluting affect of room air. Oven temperature was measured at the end of the emissions probe and with a separate oven thermometer placed in the oven. All emissions measurements were measured with two electronic instruments that were checked during the 30-min test period for correspondence. (See Figure 5.8) All instruments were calibrated before and after each test series at each site with 250 ppm CO calibration gas. Tikalsky et al. used 400◦ F for their field testing while Tsongas suggested a 350◦ F setting for his oven field protocol.6,23,24 The oven temperature setting used for the project field testing was 350◦ F and burner setting selected for the Karg Field Protocol was also 350◦ F. This temperature was selected because it is a common baking temperature and the oven requires less time to reach steady-state conditions than for a higher setting. The actual measured oven temperature at the end of the 30-min field tests for the 18 ovens ranged from 290◦ F to 375◦ F, with a mean of 347◦ F, a median of 340◦ F and a standard deviation of 20.7 F◦ . Separate broil burners were not included in the final protocol because it was thought that the additional time that would be required would not be worth the reduced risk to the range user. It was assumed that broil burners are not used as often as bake burners and, when they are used, they are not operated as long.25 Of the eighteen valid oven field tests that were conducted in 2001, ten passed the Karg Field Protocol and eight failed. The highest CO air-free ppm measured at the 15-min Karg Field Protocol mark was 1907, the lowest 244, the mean 932, the

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Oven setting at 350°F 600

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median 769, and the standard deviation 588. Oven oxygen percentage ranged from a high of 20.9 to a low of 10.4 with a mean of 18.3. Two profiles for oven test data are shown in Figure 5.9 (oven number 15, which passed) and Figure 5.10 (oven number 11, which failed). Each figure shows CO air-free ppm (left Y-axis), CO as-measured ppm (right Y-axis), oxygen percentage times 20 (right Y-axis), temperature in ◦ F (right Y-axis), and time in minutes (X-axis). Notice in both figures how CO emissions peak just after start-up, then fall, and eventually settle into a steady-state, saw-tooth pattern as a result of the burner duty cycle. For each of these profiled field tests, the steady-state condition was reached approximately 11 min after startup. The longest time required to reach steady-state for the 18 oven field tests was 19.5 min, the shortest was just over 3 min, and the mean and median were 10. As a result of these observations, the timing for the oven bake burner CO emissions test for the Karg Field Protocol was set at 15 min from

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FIGURE 5.9 Oven number 15 passed the developed oven bake burner Karg Field Protocol.

Timeafter startup, (min)

FIGURE 5.10 Oven number 11 failed the developed oven bake burner Karg Field Protocol.

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start-up or later. Only one of the 18 field tested ovens required more than 15 min to reach steady-state. As mentioned in Section 5.1.2, two important questions had to be answered before developing the Karg Field Protocol: First, what basis should be used to develop the threshold level of CO emissions at the burners to ensure an acceptable ambient level for the occupants of a residence? This is discussed in Section 5.1.2. Second, at what time after burner startup should readings be recorded and what method of measurement should be used to accurately reflect the long-term CO emissions and thus, the potential hazard of a burner’s emissions to occupants? The Karg Field Protocol time and method of measurement for ovens CO emissions was designed not only to reflect the ANSI Standard, but also to accurately predict the emission rate after the oven bake burner settled into a steady-state pattern.15 To gauge the level of accuracy, the emissions data for the eighteen ovens were used to compare the Karg Field Protocol method of measuring CO air-free ppm emissions at 15 min with the CO air-free emissions averaged from 15 to 30 min. The field testing process collected data every 0.25 min during a 30-min test of each oven. This analysis found that the oven Karg Field Protocol value had a coefficient of linear correlation to the CO air-free emissions averaged from 15 to 30 min of R = 0.95 and R2 = 0.9. (See Figure 5.11). In addition to the Karg Field Protocol, correlation was also checked with protocols developed by ANSI, Tsongas, and Building Performance Institute (BPI). Of the four, the Karg Field Protocol gave the highest correlation. As a result of designing the Karg Field Protocol to give close correspondence from CO air-free values averaged over 15–30 min, the protocol values averaged 102.4% of the longer term CO air-free emissions, whereas the ANSI protocol was found to be 71.6%. The Tsongas and BPI protocols could not be checked for this correspondence because they use a CO as-measured test method. These data for these four protocol comparisons to the author’s CO air-free values averaged over 15–30 min for 18 oven field tests are shown in Figure 5.12. These oven field data were also analyzed to determine the correlation between the CO air-free ppm emissions at 5 min and the CO air-free emissions averaged

CO air-free averaged from 15–30 min, ppm

Karg field protocol, oven measurement 2000 1500 R = 0.95 R2 = 0.90

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FIGURE 5.11 Relationship in 18 tested ovens between Karg Field Protocol oven CO air-free measurement and CO air-free emissions averaged from 15 to 30 min.

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FIGURE 5.12 Data for comparison of CO air-free emissions averaged from 15 to 30 min from 18 oven field tests by the author to 4 oven test protocols. Columns c, f, i, and k are from the author’s oven field test data measured according to the corresponding protocol. A brief description of each protocol CO measurement method is included in the last row.

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ANSI Z21.1 Protocol 2000 1500 R = 0.51 R2 = 0.26

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FIGURE 5.13 Relationship in 18 tested ovens between ANSI Z21.1 standard measurement of CO emissions at 5 min and CO air-free emissions averaged over 15–30 min.

from 15 to 30 min. This was done because the ANSI Standard Z21.1 with which gas range manufacturers must comply, requires CO emissions be measured at 5 min after startup; these emissions must be 800 ppm air-free or less.17 This analysis found that the 18 tested ovens at the 5-min ANSI Standard measurement requirement had a coefficient of linear correlation to the CO air-free emissions averaged from 15 to 30 min of R = 0.51 and R2 = 0.26. (Refer to Figure 5.13) These field data demonstrate that measuring CO air-free from a bake burner at 5 min after start-up is not a good predictor of longer-term CO air-free emissions and that it may underestimate steady-state, long-term emissions. This significant finding indicates that more research is needed to determine the match between the ANSI Standard method and actual field CO emissions from oven bake burners in the field. The oven field test data were analyzed to determine the comparability with two other published oven CO emission field protocols. The first, published in 1995 by Tsongas calls for the first CO as-measured ppm peak to be recorded after startup.23 If this peak is 100 ppm or greater at an oven temperature setting of 350◦ F, the oven fails the protocol. Of the 18 ovens tested in the field on 2001, only 2 passed this protocol with 70 and 39 CO as-measured ppm, with the average time for the first peak in CO as-measured emissions of 2.25 min. The Tsongas protocol was tested with the field data from the 18 ovens to determine how well it predicted the longer term oven emissions. (Results are illustrated in Figure 5.14) The Tsongas protocol did not correlate well with longer term CO air-free emissions. The Tsongas protocol CO as-measured value of 100 ppm appears to be significantly more stringent than the ANSI Z21.1 Standard. (Referring back to the oven emission profiles in Figures 5.9 and 5.10 will help demonstrate this poor correlation.) Finally, the oven field test data were analyzed to determine how well the BPI oven protocol predicts the longer term oven emissions.26 (Results are illustrated in Figure 5.15) The BPI protocol (being used across the U.S. by BPI certified technicians) calls for oven bake burner CO as-measured ppm testing at 5 min at the maximum oven temperature setting, short of broil. If CO as-measured emissions from ovens are from 100 to 300 ppm, or less, a CO alarm must be installed and a recommendation for oven service must be made to the customer. If CO oven emissions are more than 300 ppm, the unit must be serviced before any weatherization work is performed.

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Tsongas oven measurement protocol 2000 1500 1000

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FIGURE 5.14 Relationship in 18 tested ovens between CO as-measured ppm emissions at the first peak after start-up and CO air-free emissions averaged over 15–30 min.

CO air-free averaged from 15–30 min (ppm)

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FIGURE 5.15 Relationship in 18 tested ovens between CO as-measured ppm emissions at 5 min after start-up and CO air-free emissions averaged over 15–30 min.

Of the 18 ovens tested in the field in 2001, 13 passed this BPI protocol (300 ppm). Eight of these BPI passes also passed the Karg Field Protocol and five failed. Of five ovens that failed the BPI protocol, three failed the Karg Field Protocol and two passed. Although the 18 oven field tests were done at an oven setting of 350◦ F and the BPI protocol calls for the highest setting, the field test data at 5 min is valid. This is because at 5 min the oven set at 350◦ F is still moving toward a steady-state condition, just as it would be at a higher temperature setting. Of the four oven protocols compared with the field data of eighteen oven tests, the Karg Field Protocol appears to most accurately predict the averaged emissions from 15 to 30 min. There is no evidence to suggest that the steady-state, saw-tooth pattern of oven CO emissions over 15–30 min will significantly change after the 30-min mark, but because the author’s testing stopped at 30 min, he cannot demonstrate this. Because CO emissions from a gas range burner are seldom, if ever, hazardous unless the burner operates for a long period, this relationship between protocol readings and longer term emissions is important. Any protocol that does not correlate closely with longer term, steady-state emissions will not adequately reflect a CO hazard to occupants.

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5.2 KARG FIELD PROTOCOL FOR MEASURING CARBON MONOXIDE EMISSIONS FROM GAS RANGES 5.2.1 INTRODUCTION The purpose of this protocol is to guide the field analyst through a systematic procedure of gas range testing to determine whether a gas range burner is emitting unacceptable levels of CO. The burner limits for this protocol are 35 ppm CO as-measured for range top burners and 800 ppm CO air-free for oven bake burners. Oven broil burners are not required to be tested. This method covers residential grade floor-mounted gas ranges, drop-in range top burners, and built-in ovens only. If drop-in range top burners or built-in ovens are encountered, follow the appropriate sections of this protocol for these appliances. This protocol is not intended for use with (1) outdoor gas grills, (2) ovens in catalytic cleaning mode, (3) ovens vented into flues or chimneys, or (4) range/ovens with a downward vented exhaust fan while the fan is operating. This protocol is not intended to determine whether gas ranges operate acceptably during misuse, such as when a range is used for space heating. Accurately measuring CO emissions in the field is difficult due to the complex nature of combustion and dilution airflow patterns. Use of this protocol can increase the accuracy of measurements to, perhaps, +30%.8,10 This means that the protocol will sometimes result in false failures and false passes. Because there is a broad variety of gas ranges in the field, there is the possibility that range characteristics not addressed in this protocol will be encountered. Funding and support for this protocol research and development was provided in 2001 primarily by the U.S. DOE and the Chicago Region low-income weatherization programs of Illinois, Indiana, Iowa, Michigan, Minnesota, Missouri, Ohio, and Wisconsin. Funding and support for laboratory work was provided by the Gas Research Institute of Des Plaines, Illinois, through GARD Analytics of Park Ridge, Illinois and WEC Consulting of Potomac, Maryland. Tim Lenahan of the Ohio Office of Energy Efficiency was the contract manager. This section of this chapter includes an abridged version of the Field Protocol and is not subject to the copyright of the publisher of this book.

5.2.2 VISUAL INSPECTION AND CUSTOMER EDUCATION 5.2.2.1 Range Top Inspection Inspect the range top burner area for cleanliness. If the burners or burner area are dirty enough to adversely affect the combustion process, inform the customer that the range should be cleaned to reduce the possibility of unacceptable emissions. Do not test for CO emissions until the problem is corrected. Inspect the burners for proper alignment and seating.

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All cooking vessel support grates should (1) be in place, (2) fit properly in the burner well, and (3) be in the configuration the manufacturer intended, with no broken parts. If any of the grates are missing or in unsatisfactory condition, the customer should not use the affected range burner until the substandard or missing grate is replaced. If a grate cannot be repaired or replaced, the decision whether to replace the range should be made. If the range top burners are ignited with a standing pilot light, verify that the pilot flame is present, is about 5/16 in length, and is soft blue in color (not yellow). 5.2.2.2 Oven Inspection Inspect the oven for cleanliness. If the burners or oven area are dirty enough to adversely affect the combustion process, inform the customer that the range should be cleaned to reduce the possibility of unacceptable emissions. Do not test for CO emissions until the problem is corrected. Check the oven for obstruction of the oven-floor vents. These vent holes must not be blocked by anything in the oven, such as aluminum foil, or anything stored below the oven. These vent openings must never be obstructed because they are a vital part of the oven combustion and venting systems. Check for air blockage at the bottom of the range and drawer and/or broiler compartment under the oven. Dust, lint, pet hair, rugs, or any other obstruction blocking free airflow to the oven bake burner must be removed. Check the oven bake-burner spreader plate (burner baffle). Most bake burners (the one at the bottom of the oven compartment) have a flame spreader plate just under the oven floor bottom and above the bake burner flame. A warped or detached spreader plate can result in flame impingement and quenching (cooling) of the gas flame, causing increased production of carbon monoxide. Many spreader plates are intentionally bent into curved or angular shapes, or dimpled, to add strength. Inspect carefully with a flashlight and inspection mirror to determine if the spreader plate has distorted from its original shape or has detached from the oven bottom. Ignite the bake burner to inspect the flame. The flame should not extend beyond the edge of the spreader plate. Also, inspect for carbon buildup on the spreader plate and the oven bottom. Any carbon build-up can be an indication of incomplete combustion caused by flame quenching or a fuel-rich gas mixture. If the range also has a broil burner at the top of the oven compartment, check its flame for proper size and color. If the oven bake burner is ignited with a standing pilot light, verify that the pilot flame is present, that it is about 5/16 in length, and is soft blue in color (not yellow). Inspect gas range installation for code compliance by referring to the latest edition of the National Fuel Gas Code (NFPA 54). Verify that the range is set up for the appropriate supply gas, either natural gas or propane (LPG). Although a mismatch between supply gas type and range set up is not a common occurrence, each range should be checked. Natural gas (methane) contains 1000 Btu/ft3 , while propane contains 2500 Btu/ft3 . Gas ranges using natural gas usually operate at a gas pressure of 3.5–5 in. of water, while propane operates

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at 10–11 in. of water. Because of these characteristics, natural gas requires a larger orifice size than propane at each burner, and a lower gas pressure. If a range is set up for natural gas but has propane piped to it, it will be over-firing, probably creating unacceptable levels of CO. A gas range in this condition must not be used until the problem is corrected. Symptoms of this problem include noisy, yellow, and large flames rising above the burner support grates on the range top burners; carbon (smoke) emissions; or unacceptable carbon monoxide emissions. If a range is set up for propane but has natural gas piped to it, it will be under-firing. In this case, the customer might complain of the long period required to boil water or the extended time required for baking. This condition is usually not hazardous, but it should be corrected. If the flexible gas line connector can be inspected without moving the range, make sure the flexible connector is (1) not brass, (2) is not a two-piece connector, and (3) has no pre-1973 rings (in some cases, the date can be found on the flare nuts rather than the date rings). Do not move the range for the sole purpose of inspecting the flexible connector; this movement might crack or otherwise damage it. Check for gas leaks at the range top burner area, oven area, and any accessible gas lines with an appropriate combustible gas detector. Check for propane leaks below connections (propane falls) and for natural gas leaks above connections (natural gas rises). If any gas leaks are found, specify repair. Shut off the gas to the appliance and do not proceed with testing until the leak is repaired. If the gas range fails any of these items above (1) specify repair of the gas range or (2) specify replacement of the gas range, depending on the character of the problem. If the range does not fail, proceed, with the measurement of emissions.

5.2.3 MEASUREMENT OF EMISSIONS 5.2.3.1 Safety During Measurement of Emissions While performing the emissions testing, monitor CO concentrations in the kitchen. If indoor air concentrations rise above 35 ppm, shut down the burner(s), discontinue testing, and open windows and/or doors. Be cautious not to burn hands or other body parts on hot test equipment or the range. Also, be mindful not to damage test equipment by open flames or hot surfaces. Do not damage customer’s counters, floors, carpeting, or furniture with hot equipment or open flames. This protocol calls for range top burners to warm up for at least 6 min before recording emissions. Make sure that the open flame is not left unattended during this warm-up period. If the analyst wishes to attend to other tasks during the burner warm-up period, ask the customer to watch the burners during warm up. 5.2.3.2 Preparation for Burner Testing Always calibrate the emissions measurement instrument according the manufacturer’s recommendations. Before using the instrument, make sure that the most recent calibration is valid (check for the calibration label on the instrument). If the calibration

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period has expired, calibrate the instrument before use. Zero the instrument according to the manufacturer’s recommendations before testing. 5.2.3.3 Range Top Burner Testing Test range top burners before testing the oven. Remove all objects from the range top. The range top burners are to be tested in order of right rear (RR), left rear (LR), right front (RF), and left front (LF). Test each range top burner with the CO Hot Pot™. This protocol with its limit of as-measured CO per burner is based on the use of the CO Hot Pot™, exactly as designed.22 The use of any other device or a variation of the CO Hot Pot™ is likely to yield different results. If room air from a fan or open window or door is blowing across the range top burners, ask the customer to turn off or redirect the fan, or close the window or door. The natural flow of combustion gases upward from the burner must not be disrupted during the emissions testing process. Center the CO Hot Pot™ on the burner grate. Prepare the emission measurement instrument for the test. Ignite the burner and turn to the highest setting. Start timing device. Insert the probe of the emission measurement device into the hole on the side of the CO Hot Pot™ and through to the center of the cylinder. At 6 min after ignition, watch the instrument CO readings for 2 min. Record high and low readings for this period. Average the high and low readings to get the 2-min average CO as-measured. The CO measured at the burner averaged over the 2 min must be 35 ppm or less, as-measured, using the CO Hot Pot™. Determine whether the burner passes or fails the limit. Test each of the top burners in the order specified above. 5.2.3.4 Oven Bake Burner Testing Test the oven bake burner only. If the oven has a separate broil burner, do not test it. Clear the oven of all pots, pans, or other objects. Clear area below oven of all objects. Leave oven shelves in place. If the vent holes on the oven bottom are obstructed with foil, catch pans, or anything else, ask the customer to remove the obstructions. Ignite the burner, with the temperature setting at 350◦ F. The oven burner may not ignite immediately; this is normal for some electronic ignition systems. Bake burners with standing pilots usually ignite faster. Start timing device. Insert the probe of the emission measurement instrument into the oven vent sleeve at the back of the range top. Make sure the open end of the instrument probe is fully inserted into the oven vent opening at its center. Do not allow dilution air to mix with the sampled combustion by-products. Ensure that grease or other build-up does not inadvertently block the instrument probe tip. After beginning the oven test, do not open the oven door. If the oven door is opened after the testing period begins, wait at least 5 min or to the end of the 15-min warm up time, whichever is longer, before taking emissions readings.

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It is not necessary to turn on the emissions measurement instrument at the beginning of the warm-up, but it must be ready to take readings after 15 min of oven warm-up time. After 15 min of burner warm up, watch the emission measurement instrument for the minimum and then maximum CO as-measured values. The corresponding CO air-free must be calculated and averaged for these minimum and maximum CO as-measured readings. The step-by-step details of measurement: After 15 min of warm up, watch for the minimum CO as-measured value (not the minimum CO air-free value). Record this minimum CO as-measured value and the corresponding oxygen percentage (if your instrument automatically calculates CO air-free, record this value at the minimum CO as-measured value). Continue to watch the instrument until you detect the next maximum CO as-measured value. Record this maximum value and the corresponding oxygen percentage (if your instrument automatically calculates CO air-free, record this value at the maximum CO as-measured value). Calculate the CO air-free emission rates for the minimum and maximum CO as-measured readings from Equation 5.1a (for natural gas and propane). Average the CO air-free emission rates for the minimum and maximum CO as-measured readings. Some emissions measurement instruments calculate CO air-free automatically. If this is the case, this equation need not be used. Averaged CO air-free must be 800 ppm or less, averaged from the CO air-free values corresponding to the CO as-measured minimum and maximum occurring after fifteen minutes of warm-up, with oven set to 350◦ F. Determine whether the burner passes or fails the limit. 5.2.3.5 Burner or Range Failure If a failed burner can be adjusted in a way that reduces the CO emissions to below those set by the levels of this protocol, then the range passes the protocol after the field analyst retests the range to ensure that the burner(s) now passes limits of the protocol. If the failed burner(s) cannot be tuned or replaced to pass the protocol levels or the gas range construction does not allow for adjustment or parts replacement, the gas range should be replaced.

5.3 CONCLUSIONS The Ohio surveys of the national weatherization program technicians demonstrated a significant lack of uniformity among gas range field testing protocols.13 This diversity of methods demonstrated disagreement about testing protocol and a dearth of understanding regarding reliable field test data and methods. Using the Karg Field Protocol for Gas Range Carbon Monoxide Emissions Testing developed by the author would increase accuracy and standardization and repeatability to field CO testing.15,16 The Karg Field Protocol demonstrates a fairly close correlation between field measurements of oven CO emissions and longer-term emissions averaged from

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15 to 30 min. The 1996 Battelle study to determine the validity of the assumptions of the ANSI Standard Z21.1-1993, Household Cooking Gas Appliances8 did not examine the correlation of CO burner emissions at the 5-min mark of the ANSI test with the longer term oven emissions. The evidence from the author’s field testing suggests poor correlation between the data for ovens at the ANSI Z21.1 prescribed 5-min mark and the longer term, steady-state emissions averaged from 15 to 30 min. The author’s data suggests the longer term, steady-state emissions averaged from 15 to 30 min gives more representative results. This significant finding indicates that more research is needed to determine a valid oven testing method. The field research for the development of the Karg Field Protocol reveals that oven burners were more hazardous than range top burners. While just over 1% of the range top burners tested in the field failed the Karg Field Protocol, 40% of the over burners failed.15 Furthermore, during normal household use, oven burners are usually operated longer than range top burners, increasing the potential hazard of a high-emission oven burner. This increased oven failure rate in the test sample and longer run time for ovens indicates it is more important to field test oven burners than range top burners.

5.4 ACKNOWLEDGMENT I would like to thank Tom Greiner, Ph.D. for reviewing and editing this chapter.

References 1. Persily, A.K., Carbon Monoxide Dispersion in Residential Buildings: Literature Review and Technical Analysis, NISTIR 5906, National Institute of Standards and Technology, Gaithersburg, MD, October 1996. 2. U.S. Consumer Product Safety Commission, Non-Fire Carbon Monoxide Deaths Associated with the Use of Consumer Products: 2001 Annual Estimates, CPSC, Bethesda, MD, May, 2004. 3. U.S. Consumer Product Safety Commission, Non-Fire Carbon Monoxide Deaths and Injuries Associated with the Use of Consumer Products: Annual Estimates, CPSC, Bethesda, MD, June, 1999. 4. U.S. Consumer Product Safety Commission, Non-Fire Carbon Monoxide Deaths and Injuries Associated with the Use of Consumer Products: Annual Estimates, CPSC, Bethesda, MD, October, 2000. 5. U.S. Consumer Product Safety Commission, Summary of Carbon Monoxide Emissions Test Results of Gas Ranges with Self-Cleaning Ovens, Memorandum to Ronald Jordan from Dwayne Davis and Christopher Brown, February 6, 2001. 6. Tikalky, S. et al., Gas Range/Oven Emissions Impact Analysis, Gas Research Institute, Chicago, IL, December, 1987. 7. Reuther, J.J., Billick, I.H., Wiersma, S., Misconception, reality, and uncertainty regarding co-emissions from unvented gas appliances, paper given to Karg in 2001 by Billick. 8. Reuther, J.J., Critique of ANSI Z21.1 Standard for CO Emissions from Gas-Fired Ovens/Ranges, GRI-96/0270, September, 1996 for Gas Research Institute by Battelle, Columbus, OH, 1996.

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Carbon Monoxide Poisoning 9. Greiner, T.H., The case of the CO leak: solving the mysteries of carbon monoxide exposures, Home Energy, 21–28, November/December 1997. 10. Greiner, T.H., Comments concerning carbon monoxide emissions from gas-fired ovens and ranges: with special reference to Battelle’s 1996 Critique of ANSI Z21.1, prepared for Affordable Comfort Conference, Chicago, IL, available from Iowa State University Extension, Ames, IA, 1998. 11. Andrews, T., Ohio Office of Energy Efficiency, personal communication, June 6, 2006. 12. Lenahan, T., Ohio Office of Energy Efficiency, personal communication, June 6, 2006. 13. Andrews, T., Survey Results of State Weatherization Programs Concerning Carbon Monoxide Standards and Testing for Heating and Cooking Appliances, 1998, Ohio Office of Energy Efficiency, Columbus, OH, 1998. 14. Heckerling, P.S. et al., Predictors of occult carbon monoxide poisoning in patients with headache and dizziness, Annals of Internal Medicine, 107, 174–176, 1987. 15. Karg, R.J., Field Protocol for Gas Range Carbon Monoxide Emissions Testing, Chicago Regional Diagnostics Working Group and U.S. Department of Energy, Washington, D.C., 2001. Unpublished. Available at www.karg.com/papers.htm. 16. Karg. R.J., CO testing for the real world, Home Energy, 30–33, January/February 2002. 17. American National Standards Institute, Household Cooking Gas Appliances, Standard Z21.1, American Gas Association, Cleveland, OH, 1993. 18. Greiner, T.H. and Schwab, C.V., Approaches to dealing with carbon monoxide in the living environment, Carbon Monoxide Toxicity, Penney, D.G., (ed.), CRC Press, New York, 2000, chap. 23. 19. Hedrick, R. and Billick, I., Gas Range/Oven Testing at the GRI Research House, slide presentation to GRI Industry Environmental Council, Rosemont, IL, March 15, 2000. 20. Karg, R.J., Air-free measurement of carbon monoxide emissions from gas ranges: analysis and suggested field procedure in Affordable Comfort ’98 Selected Readings, Madison, WI, May, 1998. 21. Reuther, J.J., Interlaboratory Program to Validate a Protocol for the Measurement of NO2 Emissions from Rangetop Burners, GRI-94/0458, December 1994 for Gas Research Institute by Battelle, Columbus, OH, 1994. 22. Karg, R.J., CO Hot Pot™ Assembly Instructions, www.karg.com/COhotpot.htm. 23. Tsongas, G., Carbon monoxide from ovens: a serious IAQ problem, Home Energy, 18–21, September/October 1995. 24. Tsongas, G., Field monitoring of elevated CO production from residential gas ovens, in Proceedings: Indoor Air Quality ’94, St. Louis, MO, American Society of Heating, Refrigerating, and Air Conditioning Engineers, Inc., Atlanta, GA, 1994. 25. Hedrick, R., personal communication, June 20, 2001. 26. Building Performance Institute (BPI), Technical Standards for Certified Building Analyst1, BPI, Malta, NY, 2005.

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6

Investigating Carbon Monoxide-Related Accidents Involving Gas-Burning Appliances Michael Hanzlick

CONTENTS 6.1 6.2 6.3

6.4 6.5

6.6 6.7 6.8 6.9 6.10 6.11

6.12 6.13

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Basic Gas Appliance Design . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The Venting System and Air for Combustion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.3.1 The Draft Diverter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.3.1.1 Safety Problems Associated with the Draft Diverter . . . Gas Appliance Safety Devices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gas Appliance Types . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.5.1 Household Cooking Gas Appliances . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.5.2 Clothes Dryers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.5.3 Space Heating Appliances . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.5.3.1 Central Furnaces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.5.3.2 Room Heaters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.5.3.3 Wall Furnaces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.5.3.4 Low-Pressure Boilers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.5.3.5 Water Heaters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.5.3.6 Special Design Appliances . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gas Appliance Certification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gas Appliance Installation Requirements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . National Fuel Gas Code . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Manufacturers Installation Instructions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.9.1 Proper Fuel Input Adjustments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Fuel Gases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Basic Principles of Combustion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.11.1 Products of Complete Combustion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.11.2 Products of Incomplete Combustion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CPSC Estimates of Carbon Monoxide Deaths . . . . . . . . . . . . . . . . . . . . . . . . . . . . The Heating/Gas Appliance System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

130 130 131 132 133 134 135 135 135 135 135 136 136 136 137 137 138 139 139 139 140 140 143 143 144 145 145 129

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6.14 Failure Modes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.15 Investigation of Root Cause . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.15.1 Initial Discovery and Investigation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.15.2 Follow-Up Inspections and Investigation . . . . . . . . . . . . . . . . . . . . . . . . . 6.15.3 Determination of Root Cause . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.15.4 Estimation of Ambient Carbon Monoxide Levels in Occupied Areas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.16 Case Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.16.1 Investigation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.16.2 Failure Mode. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.16.3 Case Study Conclusions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

146 148 149 149 151 151 151 152 153 153 155

6.1 INTRODUCTION The gas appliance industry is one of the oldest and most stable industries in the United States, having its origin in the early 1800s.1 The industry has prided itself on its record related to the safe and efficient operation of gas appliances and has consistently worked to improve the safety of gas appliances by incorporating design changes when appropriate. Of major concern in the industry is the production of carbon monoxide (CO) during appliance operation. CO is a colorless, odorless, highly toxic gas. While there are many sources for CO, it can be produced in gas burning appliances by the incomplete combustion (burning) of a carbon-based fuel, such as natural gas or propane. In the gas appliance industry, CO has been called the “silent killer” because its victims are normally unaware of any operational problems with the gas appliance or that they have been poisoned. Modern gas appliances, those manufactured within the last 50 years, are designed and safety certified to perform their intended function without producing dangerous levels of CO when installed, operated, and maintained in accordance with the manufacturer’s instructions. However, there are many key factors that are not controlled by the appliance manufacturer that can cause an otherwise safe appliance to begin to produce CO.

6.2 BASIC GAS APPLIANCE DESIGN The efficient and safe operation of a gas-fired appliance is dependent on a number of factors some of which are controlled by the overall design and construction of the appliance. Some of the most basic of these factors are (see Figure 6.1) • The proper amount of fuel must be mixed with the proper amount of oxygen and its temperature raised to the ignition point so that combustion (burning of the fuel to produce heat) takes place. • The actual mixing of the fuel and air takes place within the gas burner assembly contained within the appliance.

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Products of combustion mixed with dilution air exits to outside atmosphere

Vent system Warm air to heated area Draft diverter

Dilution air Enters at draft diverter relief opening

Hot products of combustion (flue gases)

Gas burner assembly

Cool return air from heated area

Air blower

Combustion air Mixes with fuel and is combusted in the gas burner assembly Fuel Natural gas or propane lgas

Blower compartment

FIGURE 6.1 Typical gas-fixed appliance (furnace).

• The initial ignition of the fuel is often accomplished by the use of an electric ignition device or by a small constant burning flame referred to as a pilot light or pilot burner. • The actual burning of the fuel and production of heat takes place in a confined combustion chamber within the appliance. • As the fuel is combusted or burned, hot products of combustion (flue gases) are formed and travel through the appliance. • Heat energy is removed from the hot products of combustion in the heat exchanger and used to provide useful functions (heat air to heat a home, cook food, dry clothes, or even produce light.) • Finally, the flue gases exit the appliance and are dispersed into the atmosphere through a venting system.

6.3 THE VENTING SYSTEM AND AIR FOR COMBUSTION As the appliance operates, products of combustion (flue gases) must be removed from the appliance and new air for combustion supplied. New air for combustion is mixed with the fuel and combusted at the main burner. This process establishes a “natural”

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draft through the appliance due to the buoyancy of the hot flue gases, and establishes the rate at which heat is extracted from the appliance through its heat exchanger. This effect also acts to establish the overall operating efficiency of the appliance. In order for an appliance to operate at an efficient and safe level on a consistent basis, this natural draft through an appliance must be maintained at as near a constant level as possible. Products of combustion for a properly adjusted gas appliance contain amounts of carbon dioxide, nitrogen, excess oxygen, and water vapor.2 If the appliance is in poor condition, poorly maintained or installed incorrectly, products of combustion can also contain dangerous levels of CO. The products of combustion and flue gases are removed from the appliance and vented to the outside atmosphere through a venting system. The venting system that an appliance is connected to can have a dramatic effect on the draft through an appliance. The draft rate through a vent system can increase or decrease depending on a number of variables some of which include • • • • • •

Height of the vent terminal above the appliance Size of the vent system The difference between inside and outside temperatures (stack effect) Adequate supply of new makeup air for combustion to the appliance Outside wind conditions Obstructions near the vent terminal

The venting system must not be allowed to restrict or block the natural draft of combustion products through an appliance. If the natural draft through an appliance is blocked, incomplete combustion resulting in the production of CO and possible fire hazards are created. A continuous source of new combustion air containing oxygen must be supplied to the appliance to maintain proper combustion and operation of the appliance. If the supply of new combustion air is restricted incomplete combustion resulting in the production of CO can result.

6.3.1 THE DRAFT DIVERTER The draft diverter, or draft hood, is one method utilized to “couple” the gas appliance to the venting system and neutralize the effects that a vent system may have on the operation of the appliance. The draft diverter is a device that is built into an appliance and is designed to • Provide a path for the escape of the flue gases from the appliance in the event of no draft, back draft, or stoppage beyond the draft hood in the vent system. • Prevent a back draft from entering an appliance. • Neutralize the effect of stack action of the gas vent upon the operation of the appliance.

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In its most basic form, a draft diverter is in the shape of a “box.” It has an inlet for the products of combustion to enter, an outlet at the top connecting to the vent system and a “relief” opening on one side that is open to the area around the appliance. A draft diverter may contain one or more baffles to control how the products of combustion flow through the draft diverter. In operation, products of combustion from the appliance enter the draft diverter through the inlet, collect in the diverter box, and exit the draft diverter through the outlet to the venting system. During normal operation “dilution” air, air from the area around the appliance, enters the draft diverter through the relief opening and mixes with the products of combustion. This process of adding dilution air through the relief opening acts to allow the flow rate through the vent system to increase or decrease, depending on vent system design and outside atmospheric conditions, while maintaining a constant natural draft through the appliance. The design of the draft diverter also allows products of combustion to exit the appliance through the relief opening in the event that the vent system should become blocked or if a down draft or reverse draft should develop in the venting system. 6.3.1.1 Safety Problems Associated with the Draft Diverter While a draft diverter provides an important safety function of protecting the appliance from the effects of the venting system, the basic design of the draft diverter presents a serious safety concern in itself. Specifically, a blocked vent or a down draft condition in the vent will cause products of combustion to “spill” out of the draft diverter relief opening into the area around the appliance. This is normally not a problem if the blockage or down draft condition is caused by a temporary condition and the spillage only occurs for short periods of time. However, if the spillage condition is allowed to continue for a prolonged period of time a serious safety condition will develop. Products of combustion will be drawn back into the appliance, replacing the normal supply of combustion air, causing the appliance to have “incomplete” combustion resulting in the production of CO. This cycle, if allowed to continue, can generate sufficient amounts of CO in the area around the appliance to cause a serious threat to human life. Spillage of products of combustion from the draft diverter can be caused by • Blockage or restriction in the vent system • A poorly designed, maintained or installed vent system • Back draft in the vent system An inadequate supply of combustion air can also cause spillage. As oxygen is depleted in the combustion process, in the area around the appliance, new air containing oxygen for combustion will be drawn to the appliance from the path of least resistance. If the appliance is installed in a confined area, the path of least resistance can be through the venting system, which creates a back draft. This back draft causes the products of combustion to exit the appliance through the relief opening of the draft diverter.

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6.4 GAS APPLIANCE SAFETY DEVICES All modern day appliances are equipped with basic, and sometimes very complicated, safety devices in an attempt to ensure the safe operation of the appliance. Some of these safety controls include • Thermocouple used on constant burning pilot systems—A device that utilizes the heat from the constant burning pilot flame to generate an electric current to hold open a gas valve piped in series with the main gas burner. If the constant burning pilot flame is extinguished the gas valve closes and shuts off all gas to the appliance. The appliance user must manually relight the constant burning pilot flame. This type of safety is the most basic and is commonly found on all appliance types. • Electronic ignition systems—Electronic ignitions systems are either spark ignition systems or some form of a hot wire or carbon bar system. These systems eliminate the constant burning pilot flame and either ignites a small pilot flame or the main burner flame directly. The presence of a flame must be “proven” electronically within a very short time frame. If the flame fails to ignite all gas to the appliance is shut off and the appliance will not operate. This type of system can be very complicated and most require a trained service representative to repair. • High limit control—An electrical switch that senses the operating temperature of the appliance. The control is electrically connected to the appliance so that if the switch senses an over temperature condition the switch will act to shut down the operation of the appliance. Normally, the switch will automatically reset itself after the appliance cools down and allows the appliance to operate without any intervention by the user. • Flame rollout switch—A flame rollout switch is an electric temperature sensitive switch that monitors the temperature in the area around the main burner area. If a malfunction occurs that would cause the main burner flame to burn outside of the burner compartment, the rollout switch will act to shut down the operation of the appliance. In some cases this switch must be manually reset after it senses a malfunction. Although the technology for flame rollout switches has existed since at least the early 1950s, appliance manufacturers did not begin to routinely install flame rollout switches on appliances until the mid 1980s. • Vent safety shutoff system—A vent safety shut off system normally consists of an electrical switch that senses the temperature of the air in the draft diverter relief opening area. During normal operation the temperature in this area is at, or near, room temperature. If the vent system malfunctions causing products of combustion to spill out of the relief opening, the temperature at this location will rapidly rise to an elevated temperature because hot flue gases are exiting the appliance through the relief opening. The switch is electrically connected to the appliance so that if the switch senses an over temperature condition the switch will act to shut down the operation of the appliance. Normally, the switch will automatically reset itself after the appliance cools down and allows the appliance to operate

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without any intervention by the user. Although the technology for vent safety shut off systems has existed since at least the early 1950s, appliance manufacturers did not begin to routinely install this safety device on appliances until the mid 1980s.

6.5 GAS APPLIANCE TYPES Although all modern gas appliances share the same basic design concepts, not all appliances are designed to operate alike or provide the same function to the consumer. The most common types of gas appliances are:

6.5.1 HOUSEHOLD COOKING GAS APPLIANCES Commonly referred to as gas stoves or gas ranges. Most household cooking appliances contain small top burners for cooking food in pots or pans, an oven for baking food and a broiler for broiling or grilling food. Household cooking appliances may be free standing, built-in or a combination of the two. Household cooking appliances are normally not equipped with a draft diverter and are not connected to a venting system. Instead, household cooking appliances usually exhaust the products of combustion directly into the area just above the appliance. This is the same area that is normally occupied by the user of the cooking appliance. For this reason, household cooking appliances are of special concern when considering the overall safety of operation of the appliance.

6.5.2 CLOTHES DRYERS Primarily used in the family living environment to dry clothes after washing. The gas fired clothes dryer looks very much like its electric counter part. Clothes dryers are not equipped with a draft diverter. Clothes dryers depend on an internal blower to circulate the hot products of combustion directly around and through the wet clothes to achieve the drying action. This same blower then forces the very wet cooler products of combustion from the clothes dryer through the dryer vent to the outside atmosphere. Clothes dryers consume an enormous amount of air from the living environment during the drying operation. For this reason it is critical that clothes dryers (both electric and gas) not be installed in the same room as other gas fired appliances.

6.5.3 SPACE HEATING APPLIANCES There are four basic types of space eating appliances: 6.5.3.1 Central Furnaces The most typical gas appliance utilized to heat a home. A central furnace is a selfcontained gas-burning appliance for heating air by the transfer of heat through a heat exchanger. The warm air is then circulated to the home through a heat distribution system (heating ducts.) A central furnace is normally equipped with an air blower

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that provides the primary means for circulating the air. There are three variations of the central furnace • Upflow—The blower is located at the bottom of the furnace and air flows up through the appliance. • Downflow—The blower is located on the top of the furnace and air flows down through the appliance. • Horizontal—The furnace appears to be laying on its side; the blower is located at one end of the furnace and air flows horizontally through the appliance. Central furnaces are often equipped with a cooling coil in the warm air outlet of the furnace. During the hot summer months the furnace blower is utilized to circulate cool air to the home. Central furnaces are normally equipped with a draft diverter and are connected to a venting system. 6.5.3.2 Room Heaters Aself-contained, freestanding gas appliance utilized to heat a small area. Like a central furnace, room heaters heat air by the transfer of heat through a heat exchanger. The warm air is then allowed to circulate into the area to be heated. They may be equipped with a small fan or blower to assist the circulation of the warm air through the area being heated. Unlike a central furnace, a room heater is not connected to a heat distribution system. Room heaters are normally equipped with a draft diverter and most room heaters (vented) are connected to venting system. However, some room heaters (unvented) are designed to exhaust their products of combustion directly into the room being heated and are not connected to a venting system. 6.5.3.3 Wall Furnaces A self-contained gas appliance utilized to heat a small area. Wall furnaces are either recessed into a wall of the room being heated or installed flush on the wall. Like a central furnace, wall furnaces heat air by the transfer of heat through a heat exchanger. The warm air is then allowed to circulate into the area to be heated. Wall furnaces may be equipped with a small fan or blower to assist the circulation of the warm air through the area being heated. Unlike a central furnace, a room heater is not connected to a heat distribution system. Some wall furnaces are designed to provide heat to two adjacent rooms. In this case the wall furnace is located on the common wall between the two rooms and a small opening from the back of the wall furnace allows heat to flow into the second area. Wall furnaces are normally equipped with a draft diverter and are connected to a venting system. 6.5.3.4 Low-Pressure Boilers A self-contained gas burning appliance for supplying hot water for space heating. The boiler heats water by the transfer of heat through a heat exchanger. The hot water is

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then circulated to the home through a piping distribution system and utilizes radiators to heat specific areas inside the home. A hot water heating system is normally equipped with one or more circulator pumps that circulate the hot water from the boiler to the areas being heated (zones.) Each area, or zone, may operate independently of the other zones. Low-pressure boilers normally maintain the water contained in the boiler at a constant temperature, usually around 180˚ F. Low-pressure boilers are normally equipped with a draft diverter and are connected to a venting system. 6.5.3.5 Water Heaters A water heater is a closed vessel in which water is heated through a heat exchanger by the hot products of combustion. The most common type of water heater is the automatic storage type that heats and then stores water, within the appliance, for delivery to the user on demand. Typical automatic storage type water heaters have 30 gallon, 40 gallon, or 50 gallon water capacities and deliver water between 100˚ F and 120˚ F. They are normally equipped with a draft diverter and are connected to a venting system. Water heaters are normally installed in the same area of the home as the central heating appliance. When this is the case, the water heater and the central heating appliance will usually share the same venting system. Each appliance is connected to the “common” vent system through its own vent connector. The vent connector consists of a short section of vent pipe that connects the outlet of each appliance to the inlet of the common vent system. In this type of installation, any failure of the common portion of the venting system will affect both appliances connected to it. 6.5.3.6 Special Design Appliances While most gas-fired appliances are equipped with draft diverters and are connected to a venting system, there are two special designs that eliminate the draft diverter and in some cases eliminate the need for a typical venting system. Direct Vent—A system consisting of an appliance, combustion air, and flue gas connections between the appliance and the outside atmosphere. The appliance, flue gas connections, and vent termination cap are supplied by the appliance manufacturer and constructed so that all air for combustion is obtained from the outside atmosphere and all flue gases are discharged to the outside atmosphere. In this type of system there is no draft diverter. The appliance, normally a wall furnace, is installed on an outside wall of the structure, and the combustion and flue gas connections are directly to and from the appliance through the wall to the outside atmosphere. Induced Draft—A system that utilizes a small air blower to induce or force the products of combustion through the venting system to the outside atmosphere. The blower takes the place of the draft diverter and forces the products of combustion through the system. This type of system is more efficient than the type of system that utilizes a draft diverter and is normally utilized on mid and high efficiency central space heating

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systems. Both of these types of special design appliances are safer designs because they eliminate most of the problems associated with the draft diverter and the vent system.

6.6 GAS APPLIANCE CERTIFICATION In the United States, most building codes in effect today require that the building code authority approve any gas appliance before it is installed. Normally any gas appliance that has been tested and certified (listed) by an approved testing agency will be considered “approved” by the building code authority. Most gas appliance manufacturers in the United States voluntarily have their products tested and certified through a certification program provided by the Canadian Standards Association (CSA)3 and the Z21/83 Committee. The CSA and the Z21/83 Committee are jointly accredited by the American National Standards Institute (ANSI) to develop the Z21 series of standards for gas burning appliances and related accessories. These standards cover construction requirements, safe operation, performance aspects, and laboratory test methods. CSA provides the administrative services required to operate the program, and the Z21/83 Committee, along with its Technical Advisory Groups, develop the Z21 series of standards in accordance with ANSI approved procedures. CSA is accredited by ANSI as a Nationally Recognized Testing Laboratory and is considered to be an approved testing agency as required under most building codes. For gas appliances manufactured in the United States, the CSA Star indicates that the appliance has been tested under the applicable Z21 ANSI Standard and is certified to meet the requirements of that standard. (see Figure 6.2) Before the CSA, the American Gas Association (AGA) was recognized as the approved testing agency and used the same star certification seal as an indication that the appliance was certified to meet the requirements of the applicable Z21 standard. This seal, in some form, has been found on certified appliances manufactured since 1925.

D

ESIG N

C

ER

TIFIE

D

®

FIGURE 6.2 CSA Star.

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6.7 GAS APPLIANCE INSTALLATION REQUIREMENTS The installation, adjustment, operation, and repair of gas burning appliances are governed by national building codes adopted by the building authority having jurisdiction in a local community such as a city or county. There are currently four major national building code groups in the United States. • Building Officials and Code Administrators International, Inc. (BOCA) Primarily used in the Northeastern region of the United States. BOCA publishes the National Mechanical Code and the National Plumbing Code. • International Conference of Building Officials (ICBO) Primarily used in the Western half of the United States. ICBO publishes the Uniform Mechanical Code. • Southern Building Code Congress International, Inc. (SBCCI) Primarily used in the Southeastern region of the United States. SBCCI publishes the Standard Mechanical Code and the Standard Plumbing Code. • International Association of Plumbing and Mechanical Officials (IAPMO) Primarily used in the Western half of United States. IAPMO publishes the Uniform Mechanical Code (jointly with ICBO) and the Uniform Plumbing Code. In 1972 the Council of American Building Officials (CABO) was established by BOCA, ICBO, and SBCCI to compile and standardize the code requirements published by BOCA, ICBO, and SBCCI. The International Code Council, Inc. (ICC) was organized on December 9, 1994 as successor to CABO. The ICC publishes the International Fuel Gas Code, the International Mechanical Code, and the International Plumbing Code. While each national building code group has developed its own set of codes that apply to the installation of gas appliances, the codes are very similar to one another with only minor differences between them. In some cases, the local building authority may supplement sections of a national code with more stringent requirements.

6.8 NATIONAL FUEL GAS CODE The National Fire Protection Association (NFPA) was organized in 1896 to improve the methods of fire protection and to obtain and circulate information on these subjects.4 The NFPA in its efforts has developed a set of National Standard Codes that includes the National Fuel Gas Code—NFPA 54. The National Fuel Gas Code— NFPA 54 was developed by gas industry experts, and is considered to be the industry standard for the installation of gas piping and gas appliances.

6.9 MANUFACTURERS INSTALLATION INSTRUCTIONS The appliance manufacturer supplies each gas-burning appliance with detailed installation instructions. All of the national building codes referenced above require

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that the appliance be installed in accordance with the manufacturer’s installation instructions. Most manufacturer’s installation instructions require the installation to comply with the National Fuel Gas Code—NFPA 54 and provide instructions for • • • • •

Proper gas appliance location Adequate gas piping supply Adequate combustion and ventilation air supply Proper venting system Proper fuel input adjustment

All of these topics are covered in detail in the National Fuel Gas Code— NFPA 54.

6.9.1 PROPER FUEL INPUT ADJUSTMENTS Even though all of the items listed in the installation instructions are critical for a safe installation, the most common installation requirement that is often overlooked is the proper fuel input adjustment. The fuel input rating for a gas-burning appliance can be found on the appliance rating plate attached to the appliance. This rating is the amount of fuel, expressed in British Thermal Units (BTUs), which the appliance will consume or burn during each hour of operation at sea level (zero feet in elevation.) Gas-burning appliances are preadjusted to burn this amount of fuel by the manufacturer before shipment to the distributor. The appliance installer will often assume that the fuel input is correct because it was pre-adjusted by the manufacturer. While this practice may be valid at sea level, at higher elevations above sea level it is not valid. A cubic foot of fuel (natural gas or propane gas) requires a specific amount of oxygen (supplied in the air) for proper and safe combustion. As the elevation above sea level increases, the amount of oxygen in the air decreases. Because an appliance is physically designed to burn a specific amount of gas with a specific amount of oxygen supplied in the combustion air, the fuel input rate to the appliance must be adjusted down, or derated, to account for the lower levels of oxygen at increased elevations. As stated in most appliance installation instructions, at elevations above 2000 ft. the fuel input rate must be reduced by 4% for each 1000 ft. above sea level. For example, a central furnace rated at 100,000 BTU/h as listed on its rating plate, would only be rated at 80,000 BTU/h when installed at 5,000 ft. above sea level (Denver, Colorado.) If the installer of this furnace did not check and adjust the fuel input rate for the increased elevation, the appliance would be burning a too rich mixture of fuel and air with the increased probability of producing dangerous amounts of CO.

6.10 FUEL GASES There are four major groups of fuel gases; natural gases, liquefied petroleum (LP) gases including propane and butane, manufactured gases, and mixed gases. The most common type fuels for household use in the United States are natural gas followed by propane and then to a much lesser extent butane. Natural gas, propane gas, and

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butane gas are all classified as hydrocarbon gases. A hydrocarbon gas is a gas that is made up of both hydrogen and carbon atoms, thus the term hydrocarbon. Natural gas is a naturally occurring mixture of hydrocarbon gases as well as small amounts of nonhydrocarbon gases found in porous formations beneath the earth’s surface. The principle component of most natural gases found in the United States is methane. Lesser amounts of ethane, propane, butane, and other gases are also found in natural gas. The major source of propane and butane in the United States is crude petroleum. Another important source of propane and butane is from natural gas through a process known as absorption. These fuels are absorbed from natural gas in oil and then refined into propane, butane, and natural gasoline. The boiling point of natural gas at atmospheric pressure is −260◦ F.5 In order to liquefy natural gas it is necessary to cool it to its boiling point. As the pressure of natural gas is increased the boiling point also increases. The critical temperature of natural gas is about −116◦ F at about 673 pounds per square inch (PSI) of pressure. Simply put, this indicates that natural gas will always be in a vapor state whenever the temperature of the gas is above −116◦ F regardless of the pressure. A natural gas utility company normally provides natural gas to the end user through a distribution system of underground pipes. The boiling point of propane is −44◦ F at atmospheric pressure.6 When propane is enclosed in a container at room temperature it will reach a state in which some of the propane will be in a vapor state and some of the propane will liquefy. The propane vapor causes the pressure inside the container to increase. The pressure inside the container will depend on the temperature (see Table 6.1). This characteristic of propane allows the fuel to be stored very easily in a storage tank as a liquid and then vaporized and used as a fuel in a gas-fired appliance. Propane gas is most often found on portable appliances (outdoor grills), on recreational vehicles, and in rural areas as a heating fuel. The boiling point of butane is 32◦ F at atmospheric pressure. Like propane, when butane is enclosed in a container at room temperature it will reach a state in which some

TABLE 6.1 Vapor Pressures of Propane and Butane Gases Temperature (◦ F) −40 −20 0 20 40 60 70 80 100

Propane Vapor Pressure (psi)

Butane Vapor Pressure (psi)

1.3 10.7 23.5 40.8 63.3 92.5 109.3 128.1 172.3

3.0 11.5 16.5 22 37

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of the butane will be in a vapor state and some of the butane will liquefy. Because the boiling point of butane is 32◦ F it will always remain a liquid at temperatures below 32◦ F. This characteristic makes it very difficult to use butane as a heating fuel in locations where the storage temperature is below 32◦ F. Another important characteristic shared by natural gas, propane gas, and butane gas is how the number of atoms affects the gases. Referring to Figure 6.3, note that methane has fewer carbon and hydrogen atoms than ethane, propane has more atoms than ethane, and butane has more atoms than propane. As the number of atoms increase the actual weight or density of the gas increases. Also as the number of atoms increases the heating value of the gas increases. The weight of a gas is normally expressed as a ratio of the weight of the gas compared to the weight of the same volume of dry air. This ratio is referred to as the specific gravity of the gas. A specific gravity greater than 1 indicates the gas is heavier than air and if the gas is released into the air it will sink to the lowest level. A specific gravity less than 1 indicates the gas is lighter than air and when released into the air it will rise. Referring to Table 6.2, note that natural gas is lighter than air. H H

C

H

H

H Methane CH4

H

H

H

C

C

H

H

H

Ethane C2H6

H

H

H

C

C

C

H

H

H

H

Propane C3H8

H

H

H

H

H

C

C

C

C

H

H

H

H

Butane C4H10

FIGURE 6.3 Carbon atoms and hydrogen atoms linked together; the aliphatic series.

TABLE 6.2 Specific Gravity and Heating Values of Several Hydrocarbon Gases

Specific gravity (Air = 1.00) Heating value BTU/cu. ft.

Natural gas

Propane

Butane

0.58 − 0.79

1.53

2.00

900 − 1200

2516

3280

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Also propane and butane are both heavier than air. This characteristic makes natural gas a safer fuel because if released into the air it will rapidly dissipate into the atmosphere while propane and butane will tend to collect and pool at floor level. The heating value of a gas is normally expressed in British Thermal Units per cubic foot (BTU/cu. ft.) One (1) BTU is the amount of heat required to raise one (1) pound of water one (1) degree Fahrenheit (◦ F.) Referring to Table 6.2, note that butane has a higher heating value than propane and propane has a higher heating value than natural gas. This characteristic makes it critical that the gas-fired appliance be properly adjusted to burn the type of fuel that is supplied. A gas-fired appliance that has been adjusted to burn propane fuel will not operate safely on natural gas just as a gas-fired appliance adjusted to burn natural gas will not operate safely on propane.

6.11 BASIC PRINCIPLES OF COMBUSTION Combustion, or burning, of a fuel is defined as the rapid oxidation of the fuel. It is the process of oxygen acting with the fuel to produce heat and light very rapidly. Some people have defined combustion as the controlled explosion of a mixture of fuel and oxygen to produce controlled amounts of heat or light. For combustion to take place the proper amount of fuel must be mixed with the proper amount of oxygen (air.) Heat must be added to raise the mixture to its ignition point. Once ignition takes place the combustion process will continue as long as the fuel and air supply is maintained. About 10 cu. ft. of air containing normal amounts of oxygen is required to burn 1000 BTU of either natural gas or propane gas at optimal conditions. However, the limits of flammability, or explosive limits, of natural gas is between about 4% and 14% gas in air and for propane between about 2.4% and 9.6% gas in air. If the fuel mixture is below the explosive limit the mixture is too lean to burn; and, if the mixture is above the explosive limit the mixture is too rich to burn. The ignition point of natural gas and propane gas is normally between about 900◦ F and about 1000◦ F.

6.11.1 PRODUCTS OF COMPLETE COMBUSTION When a hydrocarbon fuel gas, like natural gas, is burned in a mixture of air containing a sufficient amount of oxygen (O2 ) the normal products of combustion are carbon dioxide (CO2 ) and water vapor (H2 O.) Included with the combustion products is the nitrogen (N2 ) that was contained in the combustion air. Nitrogen, because it is an inert gas and does not burn, passes through as part of the flue gases. The total volume of the flue gases contains (see Figure 6.4) CO2 and H2 O (products of combustion), N2 (carry through from the combustion air), and excess air. Heat as shown refers to ignition of the gas mixture. Excess air is air that was drawn into the appliance with the combustion air but was not needed for combustion. When burning a fuel such as natural gas or propane in a gas-designed appliance, the volume of gas burned on a per hour basis remains constant. Therefore, the volume of the products of combustion, CO2 and H2 O, will remain constant. However, the total volume of the flue gases will vary depending on the amount of excess air that

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100 cu.ft. carbon dioxide Products of combustion

1000 cu.ft. combustion air (Oxygen + Nitrogen)

200 cu.ft. water vapor

100 cu.ft. natural gas 250 cu.ft. excess air

800 cu.ft. nitrogen

HEAT

250 cu.ft. excess air

1350 cu.ft. (fuel + combustion air + excess air)

1350 cu.ft. flue gases

FIGURE 6.4 Products of complete combustion.

is drawn into the appliance. Appliance manufacturers utilize excess air as a built-in safety factor when designing the combustion system in an appliance to ensure that complete combustion results. CO is not a product of complete combustion.

6.11.2 PRODUCTS OF INCOMPLETE COMBUSTION Sometimes when a hydrocarbon fuel gas is burned incomplete combustion results. When this occurs, CO is one byproduct of the incomplete combustion in addition to the normal byproducts of complete combustion, carbon dioxide (CO2 ) and water vapor (H2 O). The most common cause of incomplete combustion in a gas-fired appliance is an inadequate supply of combustion air. Another less common cause of incomplete combustion is flame cooling, and to a lesser extent, insufficient mixing of the fuel and combustion air. Flame cooling results when the flame impinges on a cool surface, such as a heat exchanger wall. This causes the flame to cool to below the ignition point of the fuel. When this occurs the mixture is not fully combusted and CO, as well as other byproducts, is an unwanted by product. CO is actually a hydrocarbon fuel similar to propane or butane. The heating value of CO is about 322 BTU/cu. ft. and the specific gravity is 0.9672, making it slightly lighter than air. CO has no odor. Although CO has no detectable odor, there is another byproduct of incomplete combustion that does. Just as CO is the byproduct of the carbon component in the fuel, there are also byproducts of the hydrogen component, namely aldehydes, hydrogen, and other hydroxylated compounds. Aldehydes usually have a sharp penetrating odor that acts to sting the nose and eyes. Very small amounts of aldehydes in air are detectable by the normal human nose. The presence of aldehydes indicates the presence of CO. However, the lack of a detectable odor does not necessarily indicate that combustion is complete since CO and hydrogen are both odorless.

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TABLE 6.3 CPSC Estimated Annual Carbon Monoxide Poisoning Deaths 1994–2002 (Nonfire Related)

Unspecified gas heating LP gas heating Natural gas heating Gas water heaters Gas cooking ranges/ ovens All other causes Total

1994–1998

1999

2000

2001

2002

Total

Percent of Total (%)

25 46 35 7

3 22 19 1

7 29 37 3

6 26 28 0

15 50 22 1

56 173 141 12

7.3 22.6 18.4 1.6

7 80 200

6 58 109

11 51 138

10 60 130

3 97 188

37 346 765

4.8 45.2 100.0

6.12 CPSC ESTIMATES OF CARBON MONOXIDE DEATHS The Consumer Product Safety Commission (CPSC) has tracked deaths in the United States due to CO from the late 1970s. In a report7 titled “Non-Fire Carbon Monoxide Deaths Associated With The Use Of Consumer Products 2002 Annual Estimates”, published on July 12, 2005, the Commission has estimated the number of deaths that has occurred each year from 1994 due to gas-fired appliances (see Table 6.3). As demonstrated in Table 6.3, the majority of deaths were caused by natural gas and LP gas (propane and butane) heating systems followed by gas-fired cooking ranges/ovens and to a lesser degree gas-fired water heaters. As noted in the CPSC report, these are estimates of documented deaths and do not include reported and nonreported injuries and illness caused by CO or deaths that were misdiagnosed as non-CO deaths. Table 6.3 also indicates, regardless of any advances in appliance design, the number of deaths each year attributed to gas-fired heating systems has remained fairly constant over the past 10 years. This supports the concept that the manner in which the gas appliance is installed and how the appliance is serviced and maintained has a huge influence on the safe operation of the appliance. Or, simply stated, the operating condition of the heating system as a whole has just as much influence, if not more, on the safe operation of the gas-fired appliance.

6.13 THE HEATING/GAS APPLIANCE SYSTEM When evaluating the operation of a gas-fired appliance, it is critical to consider the operation of the appliance including all of the external factors that impact the safe operation of the appliance. The gas-fired appliance and all of the external components impacting the operation of the appliance make up the heating system or gas appliance

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system. As a minimum, the following external components or factors, along with the gas-fired appliance make up the system • The fuel supply— As discussed earlier, it is critical to adjust the appliance for the type of fuel that is supplied. In addition to the fuel type, the fuel line pressure and quality of the fuel is also important. If the fuel line pressure is too low improper mixing of the fuel and combustion air could result causing incomplete combustion. Conversely, too high of a fuel line pressure could cause the appliance to malfunction resulting in a fire hazard. The quality of the fuel, moisture content, and other contaminants could also cause the appliance to malfunction. • The combustion and ventilation air supply—For an appliance to operate as designed, it is critical that a sufficient amount of air for combustion is supplied to the appliance. A deficient supply of combustion can cause the venting system to malfunction resulting in a down draft through the vent system rendering the vent system inoperative. This causes all of the products of combustion to vent out of the appliance through the draft diverter relief opening. As discussed under the section “Safety Problems Associated With The Draft Diverter,” this condition can, and often does, result in the production of CO. It is just as important to ensure that a sufficient amount of ventilation air is also supplied to the appliance. An adequate amount of ventilation air will ensure that the draft effect in the venting system, and the appliance itself, will be maintained. Ventilation air is used to help cool the area around the appliance and, more importantly, provide air for dilution at the draft diverter as needed. • The venting system—The proper design, installation, and operation of the venting system is the single most important factor in the safe operation of a gas-fired appliance. Normally, if the venting system is functioning as intended, any CO produced by the appliance will be vented to the outside atmosphere. If the vent system fails, it is probable that the appliance will produce CO at some point in its operation. • The service personnel—Even if the gas-fired appliance system is properly installed and adjusted, it is critical that the operation of the system be checked annually and repaired as necessary. Normally it requires a minimum of two failures for CO to find its way into the living occupied area of a home. There must be source of CO (failure 1) and there must be a pathway into the occupied area (failure 2). Proper servicing of the system will help to ensure there are no failures during the useful life of the appliance.

6.14 FAILURE MODES As noted above, it normally requires at least two failures of the system to result in CO reaching the occupied area. For example, the first failure would cause the appliance to produce CO and the second failure would cause the CO to travel to the occupied area rather than being vented to the outside atmosphere.

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The following failure modes can result in incomplete combustion causing the appliance to produce CO: • Appliance burning too much fuel resulting in a rich mixture • Incorrect combustion air adjustment on the burner causing the flame to lift and impinge on a cooler surface • Restricted internal flue passageway resulting in poor draft through the appliance • Insufficient combustion air supply Normally the appliance will appear to operate safely under the above listed failures provided that the venting system is operating to vent the products of combustion to the outside atmosphere. The following failure modes can cause the venting system to malfunction: • Improper design, improper size, or insufficient vent height above the roof line. • Missing or damaged vent terminal cap at the vent terminal. A damaged or missing vent cap will allow wind to enter the vent system causing a back draft or no draft. A damaged or missing vent cap will also allow birds and other animals to enter the vent in an attempt to nest. • Insufficient combustion air supply can cause the vent to downdraft, or reverse flow. The lack of combustion air causes the pressure inside the room containing the appliance to be reduced. A downdraft through the vent system occurs when the pressure inside the room containing the appliance is decreased to a point below the outside atmospheric pressure. Note that an insufficient supply of air can cause two failures in the system, incomplete combustion resulting in the production of CO and the failure of the vent system. Other failure modes that can cause two failures in the system include • Excessive leakage in the return air system of a forced air furnace. Excessive leakage causes air from around the furnace to be pulled into the return air system of the furnace. Depending on the severity of the leakage this effect can cause the vent system to fail. In severe cases it can cause the burner flame to be pulled out of the furnace causing not only a CO hazard but a fire hazard as well. Once the furnace starts producing CO a direct path into the heated area is provided by the furnace heat distribution system pumping the CO into all areas of the heated space. • Cracked heat exchanger. A cracked heat exchanger can interfere with the draft effect through the appliance causing the appliance to produce CO. Depending on the location and size of the crack, products of combustion containing CO can enter the heated air stream rather than exiting the appliance through the venting system. Some appliances, such as a gas-fired cooking appliance (range/oven) and unvented room heaters, are not connected to a vent system. These appliances vent the products of combustion directly into the area above the appliance. For example, when the top

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burners of a gas range are operated the products of combustion are vented directly into the area occupied by the user of the appliance. When the oven is used the products of combustion from the oven are vented from the appliance at a location at the back of the cook top directly into the area occupied by the user. In these types of appliances it is critical that the appliance be installed, operated, and maintained so that CO is not produced. Any failure causing incomplete combustion can result in a hazardous condition.

6.15 INVESTIGATION OF ROOT CAUSE Gas appliances are designed and performance certified using ANSI standards developed by the Z21/83 Committee. For example, gas-fired central furnaces are certified under ANSI Z21.478 to produce CO levels less than 400 parts per million (ppm) in an air free (no excess air) sample of the flue gases when tested in an atmosphere having a normal oxygen supply. While ANSI standards allow some amounts of CO, most gas appliances when installed in accordance with national and local codes and properly maintained will produce only trace amounts of CO (normally less than 10 ppm.) When investigating an incident it may or may not be evident that CO poisoning was the cause of the illness or death. However, even in those cases where it is obvious from the beginning that CO poisoning was the cause, it may not be as obvious as to what the root cause or source of the CO poisoning was. Many times police and fire investigators, and sometimes well trained heating technicians, base a conclusion on an obvious observable factor while missing the root cause of the accident. Most of the time, in CO accidents involving gas appliances, there are a number of factors that contribute to the cause. Many of these factors may have been present for a number of years before an observable incident has occurred. A malfunction in any one of the components of the heating system could cause the appliance to produce CO. When this happens, the appliance may seem to operate in a safe manner because the CO is being vented to the outside atmosphere through the venting system. However, if the venting system should fail for some reason or if a second malfunction should occur (i.e., faulty heat exchanger), dangerous levels of CO could be circulated to the occupied areas of the structure. Besides the obvious causes of failure, other less obvious causes are faulty installations, poorly maintained heating system components, and sometimes poorly designed features within the appliance itself. Many times a deteriorating condition is noticeable before a serious failure occurs. Rusted and discolored vent pipes, odors, unexplained gas pilot outages, water vapors condensing on windows during cold periods, and complaints of poor heating are all indicators of a malfunctioning heating system which, if left uncorrected, could result in a CO poisoning. Many times the people who first respond to an accident disturb key evidence while evaluating the scene and attempting to make the location safe. Typical actions taken by response personnel include moving boxes or furniture that may be blocking combustion air openings and removing panels from gas fired appliances to shut off the gas. In order to minimize any destruction of key evidence it is imperative that a

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qualified expert who specializes in forensic investigations be contacted and allowed to inspect the site as soon as possible. When investigating the CO accident the following factors must be evaluated before a probable root cause can be determined. Extensive photographs and videotaping of the scene should be completed to document the conditions as found. Every effort should be made to preserve key evidence for evaluation. The conditions as found (initial discovery) must not be changed or corrected until the investigation is completed. In most cases the gas appliance and venting system components should be removed after the follow-up inspection and investigation and preserved as evidence. While it is preferred that a forensic expert be involved from the initial discovery through the completion of the investigation, this is normally not the case. What usually occurs is the forensic expert is called in at some point after the initial discovery and investigation is completed. From a forensic viewpoint it is important to involve an expert, at least on a consulting basis, as soon as possible after the incident.

6.15.1 INITIAL DISCOVERY AND INVESTIGATION • First discovery—Who discovered the victim? How did they discover the victim? What happened to cause them to find the victim? • Ambient conditions in the space as found—What were the conditions when the victim was first discovered? Was the room cool, warm or hot? Was there water moisture on the windows? Was there an odor in the room and if so what did it smell like? • First response—Who responded? What did the police and fire departments find? Did the local building code department respond? Did the local gas supplier or gas utility respond? Did they take photographs? What conditions did they find? Did they turn off the appliance? If so, how? Were any tests conducted on the appliances? Did they prepare a report? What conclusions did they reach? • Make safe—Did the local authorities call in someone to inspect the gas appliances to make safe? Was the building evacuated? If so, why? What actions were taken to make the building safe? Was the suspect gas appliance repaired or altered after the incident? If so, how and by whom?

6.15.2 FOLLOW-UP INSPECTIONS AND INVESTIGATION • Weather data—What was the local weather conditions preceding the incident? Outside temperature patterns, wind speed and direction, snow cover, rain, sleet, and so forth all may have a bearing on the operation of the venting system and combustion air and ventilation system. Weather data should be collected from local sources such as the state university and local newspapers. • Building orientation and construction—What direction is the building facing? Make a sketch of the building and rooms showing location of the victims, heating appliances, other gas burning appliances, fireplaces,

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•

•

•

•

•

•

and other air consuming devices such as exhaust fans and exhaust hoods. Record all dimensions, including ceiling height and window and door locations. Note the age of the construction and construction type (frame, brick, etc.) and the tightness of the building (weather stripped, caulked, etc.). Mark locations of gas vents and sources of combustion air including size and type of air grills and air louvers. Overall condition and appearance of the building and gas appliances— Does it appear that the building and appliances are in good condition? Is there an existing hazardous condition? Is there a hazard tag on the gas appliance? If so, when was it placed and by who? What action is recommended to correct the hazard? Maintenance history—Have there been any previous problems reported? What types of repairs have been completed in the past? When were the problems reported and when were the repairs completed? Who discovered the problems and who made the repairs? Evaluate appliance installation—Is the appliance installed in compliance with the manufacturer’s installation instructions? Does the installation comply with national standards (NFPA 54) and local building codes? Record locations of fuel lines, gas pressure regulators including gas pressure regulator vent lines and propane tanks if fired on propane. Sketch the existing appliance installation and venting system. Identify sources of combustion and ventilation air and any other information that may be pertinent to the operation of the appliance. Note the condition of the appliance and venting system. Collect appliance data—Record all nameplate data for all appliances. Include serial numbers and model numbers on all automatic gas control valves. Also note any special devices or controls that may be installed on the appliances. Examples of special devices may include automatic vent dampers, heat reclaimers, and other retrofitted energy conservation devices. Conduct combustion tests—Test the gas appliance(s) to determine what their normal operating characteristics are. Test all gas appliances in the structure. Repeat all tests under different conditions to duplicate conditions that existed at the time of the incident. At a minimum, test for CO at the flue outlet (inlet to draft diverter) and measure stack temperature. Also it is necessary to measure oxygen or carbon dioxide content to be able to calculate CO on an air free basis. Note burner ignition and operating characteristics (yellow tip, blue flame, primary air adjustments, etc.). Ambient CO levels in the appliance area, as well as in the area where the victim was found, should be recorded and monitored. Measure the fuel input rate—Is the appliance properly adjusted for the elevation? The nameplate rating for certified appliances must be derated at the rate of 4% for each 1000 ft. in elevation. The actual heat (fuel) input should be determined and recorded. For propane-fired appliances it is necessary to measure the burner orifice sizes and compute the actual input. For natural gas fired appliances it is necessary to measure the actual

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input by “clocking” the gas meter. It is necessary to contact the local gas utility for actual heating (BTU) and specific gravity values. • Miscellaneous factors—Are there any other factors or conditions that might have a bearing on the cause of this incidence? Such factors may include faulty maintenance by a third party or failure of a third party to provide a warning when they had knowledge of a hazardous condition.

6.15.3 DETERMINATION OF ROOT CAUSE Although the cause of the incident may seem obvious at first, guard against premature conclusions. Only after all of the items and information discussed above have been collected and analyzed is it possible to determine the root cause or causes of the CO poisoning. As stated earlier, with modern gas- fired appliances there are usually two or more failures that finally result in a tragic accident. The key is to collect as much data as soon after the incident as possible and evaluate that data to reach a determination of probable cause.

6.15.4 ESTIMATION OF AMBIENT CARBON MONOXIDE LEVELS IN OCCUPIED AREAS As a last step in evaluating a CO incident in a structure, it may be feasible to estimate the ambient CO levels inside the structure caused by the failures identified in the investigation. The factors that must be identified before an estimate of the ambient CO level can be calculated are • Type of fuel, heating value, and total volume of combustion products produced in cubic feet per 1000 BTU, dry basis (water vapor removed.) • Actual fuel input rate, BTU/h. • Combustion data indicating amount of CO produced by the appliance on an air free basis (excess air removed.) • Type of construction and estimated air exchange rate in the structure, expressed as air changes per hour. • Estimate of the operating cycle based on appliance usage and weather data. • Failure mode indicating how much of the produced CO actually enters the structure. After all of the above listed factors have been identified, an estimation of the ambient CO level within the structure can be calculated. As an illustrated example consider the following case study.

6.16 CASE STUDY During the early morning hours on January 12, two adults, male and female, were transported from their home to a local hospital emergency room suffering from severe headaches, nausea, and confusion. Blood tests indicated carboxyhemoglobin

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(COHb) levels in the adult male of 32% and in the female of 35%. Neither individual smoked. As a result of this incident the couple’s single level home was inspected and an investigation conducted in an effort to locate the cause of the CO exposure.

6.16.1 INVESTIGATION • Incident location 1. Northern New Mexico 2. 5000 ft. elevation • Home description 1. Determined from local records and inspection a. Frame construction completed in 1972 b. Single level built over a crawl space c. 1680 sq. ft. in area d. 9 ft. ceilings e. 15,120 cu. ft. internal volume • Type appliance 1. Determined by inspection a. Forced air furnace, upflow b. Rated fuel input rate i. 125,000 BTU/h nameplate ii. 100,000 BTU/h at local conditions c. Atmospheric venting system with draft diverter d. Furnace installed in confined space utility closet. e. No combustion air supplied to utility room (operation depends on normal infiltration of air from the outside for combustion air.) • Fuel type—Natural gas supplied from the Texas Panhandle area. 1. Published data a. Heating value i. 1013 BTU/cu. ft. at sea level ii. 858 BTU/cu.ft. at local conditions b. Total volume of combustion products—8.545 cu. ft. dry basis • Actual fuel input rate 1. Determined by measurement a. 122.55 cu. ft. per h natural gas b. 105,149 BTU/h (5.1% over fired) • Combustion data at steady state conditions 1. Determined by measurement a. % O2 = 12.6 b. CO, ppm with diluted with excess air = 1650 c. CO, ppm excess air free = 4125

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• Air changes per hour and type construction 1. Determined by measurement and calculation utilizing published American Society of Heating, Refrigerating And Air-Conditioning Engineers (ASHRAE) tables and formula.9 a. Estimated air exchange rate i. 0.75 air changes per hour at design conditions ii. 0.56 air changes at average temperature difference (January) b. Average to tight • Weather conditions for time period 1. Local data sources a. January time period i. Average outdoor temperature 29.9◦ F b. Indoor temperature 72◦ F c. Average temperature difference 42.1◦ F d. Design outdoor temperature −1◦ F • Furnace operating cycle 1. Calculation based on furnace size and average weather data for time period a. Duty cycle 57.7% b. Burner cycles per hour 4

6.16.2 FAILURE MODE • Determined by investigation 1. Production of CO by furnace (source) a. Over fired (contributing cause of CO) b. Insufficient combustion air supply c. 4125 ppm CO air free basis 2. Total vent system failure caused by insufficient combustion air resulting in vent draft reversal 3. 100% spillage of combustion products into area around furnace 4. Excessive leakage of air into return air system of furnace at furnace base and junction of furnace to return air plenum connection (pathway into heated area) 5. 100% of combustion products circulated into occupied area

6.16.3 CASE STUDY CONCLUSIONS Figures 6.5 and 6.6 were generated by applying the collected data to standard formulas to calculate estimated ambient indoor CO levels.10−13 These plots indicate that after about 7 h of total elapsed time from start, the ambient CO level inside the structure has increased from 0 to around 250 ppm. The plots also indicate that the ambient

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Ambient Co level (ppm)

300 250 200 150 100 50 0 Time 0–7 h

FIGURE 6.5 Estimated ambient carbon monoxide levels from starts to 7 h of elapsed time.

265.0

Ambient CO level (ppm)

260.0 255.0 250.0 245.0 240.0 235.0 230.0 Time 7–14 h

FIGURE 6.6 Estimated ambient carbon monoxide levels from 7 to 14 h of elapsed time.

level of CO within the structure stabilized after about 10 h from start and then varied between 245 and 260 ppm as the furnace cycled on and off. The Environmental Protection Agency (EPA)14 has published maximum allowable exposure limits for CO of 9 ppm for an 8-h exposure or 35 ppm for a 1-h exposure. The EPA has established that this exposure limit not be exceeded more than once per year. Exposure above these levels is considered harmful to public health. The estimated ambient CO levels demonstrated in this case study exceed the EPA recommended maximum allowable CO exposure limits for humans and indicate that the occupants were exposed to an extremely hazardous risk of CO poisoning.

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References 1. American Gas Association, Gaseous Fuels, Properties, Behavior, and Utilization, 1954. 2. American Gas Association, Fundamentals of Combustion Revised, Catalogue No. XH9601. 3. Canadian Standards Association, CSA in the USA, http://www.csa-international.org/ testing_certification_us/ 4. National Fire Protection Association, National Fuel Gas Code Handbook, 1999, Lemoff, T.C., ed., Inc., NFPA No.: F9-54HB99. 5. Gas Engineers Handbook, Fuel Gas Engineering Practices, 1977, Industrial Press, Inc., NY, Segeler, C.G., editor First ed.—5th Printing. 6. Engineered Controls International, Inc. LP-Gas Serviceman’s Manual, L-545, 1962. 7. Consumer Product Safety Commission, Non-fire carbon monoxide deaths associated with the use of consumer products 2002 annual estimates, July 12, 2005. 8. American National Standards Institute, Inc., ANSI Z21.47, American National Standard for Gas-Fired Central Furnaces. 23rd ed., 1987. 9. American Society of Heating, Refrigerating and Air-Conditioning Engineers, 2005 ASHRAE Fundamentals Handbook. 10. Calspan, Investigation of Safety Standards for Flame-Fired Furnaces, Hot Water Heaters, Clothes Dryers and Ranges, Report No. YG-5569-D-3, July, 1975, Contract No. CPSC-C-74-131. 11. Calspan, Safety Devices For Gas-Fired Appliances, Report No. 6608-D-1, May, 1980, Contract No. CPSC-C-79-1007. 12. Gas Research Institute, Environmental and Safety Research, September 1996, Topical Report, Critique of ANSI Z21.1 Standard for CO emissions from gas-fired ovens and ranges, Prepared by J.J. Reuther, Battelle. 13. Thomas H. Greiner, Ph.D., P.E., Associate Professor, Iowa State University, Comments concerning carbon monoxide emissions from gas-fired ovens and ranges with special reference to Battelle’s 1996 Critique of ANSI Z21.1 (1) 14. Environmental Protection Agency, National Ambient Air Quality Standards (NAAQS) for pollutants considered harmful to public health and the environment, http://epa.gov/air/criteria.html.

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7

Carbon Monoxide Dangers in the Marine Environment Jane McCammon

CONTENTS 7.1 7.2

7.3

7.4

7.5

7.6

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Identifying Marine CO Poisonings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.2.1 Identification of Marine CO Poisonings at Lake Powell. . . . . . . . . . 7.2.2 Identification of Marine CO Poisonings Nationwide . . . . . . . . . . . . . 7.2.3 Additional Carbon Monoxide Poisoning Case Identification . . . . . Descriptive Characteristics of Known Marine Carbon Monoxide Poisonings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.3.1 Demographics, Distribution, and Outcome of Poisonings . . . . . . . . 7.3.2 Location of the Victim and Source of Carbon Monoxide . . . . . . . . Medical Characteristics of the Cases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.4.1 Carboxyhemoglobin Measurement Limitations . . . . . . . . . . . . . . . . . . . 7.4.2 Boat-Related Carbon Monoxide Poisonings Resulting in Death . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.4.3 Carbon Monoxide Exposure as a Drowning Risk Factor . . . . . . . . . 7.4.4 Non-Fatal Boat-Related Carbon Monoxide Poisonings . . . . . . . . . . Boats and CO Sources Related to Marine Poisonings, with Case Study Presentations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.5.1 Ski Boats . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.5.2 Cabin Cruisers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.5.3 Houseboats . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Airborne Carbon Monoxide Concentrations Measured on and Near Boats. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.6.1 Methods for Measuring, Analyzing, and Evaluating CO in Air . . 7.6.2 Carbon Monoxide Concentrations Associated with Boat-Related CO Poisonings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.6.2.1 Ski Boats . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.6.2.2 Cabin Cruisers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.6.2.3 Houseboats . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.6.2.4 Carbon Monoxide Exposure in Areas of Congested Boat Traffic (Lake Havasu Study). . . . . . . . . . . . . . . . . . . . . . .

158 159 160 160 161 161 161 162 164 164 164 165 166 166 166 170 171 175 175 177 177 177 178 179 157

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7.7

180

Prevention Efforts. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.7.1 U.S. Coast Guard Regulation of Boat Manufacturing/Recall Authority . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.7.2 Environmental Protection Agency Regulation of Marine Engine Emissions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.7.3 State Legislative Action . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.7.4 Effectiveness of Marine Carbon Monoxide Detector/Alarms in Prevention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.7.4.1 Case-Based Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.7.4.2 Marine Carbon Monoxide Detector Evaluation . . . . . . . . 7.7.5 Engineering Control Research and Development . . . . . . . . . . . . . . . . . 7.7.6 Innovations in EMS Medical Management . . . . . . . . . . . . . . . . . . . . . . . 7.8 Summary and Future Directions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.9 Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

180 181 182 183 183 183 184 187 188 190 191

7.1 INTRODUCTION Although carbon monoxide (CO) poisoning has been recognized since the earliest medical writings, CO exposure continues to be a major cause of death and illness. Many fatal and nonfatal exposures go undetected and unreported. The development of effective prevention programs is severely hampered by the absence of a centralized, coordinated surveillance system. CO poisonings in the marine environment began receiving attention as early as 1984, with poisonings occurring inside living quarters (also referred to as the boat cabin) being recognized early on.1 In 1990 and 1991, the United States Coast Guard (USCG), responsible for regulating recreational boat manufacture, investigated issues related to intrusion of engine exhaust into boat cabins.2,3 CO poisoning associated with occupancy of cabins of recreational boats was first described in the scientific literature in 1995.4 Subsequently, the American Boat and Yacht Council (ABYC—a nonprofit membership organization that develops safety standards for boat building and repair) developed standards for CO detection systems for boats manufactured after July 31, 1998.5 However, CO poisonings occurring outside the boat cabin were another matter. Reports of outdoor CO poisonings in any setting are scant.6−9 Published reports of boat-related CO poisoning outside of a boat cabin, in which the boat occupant was swimming behind a motorboat10 and behind a houseboat11 appeared in 1998. The absence of data on outdoor CO poisonings confused National Park Service (NPS) Emergency Medical Services (EMS) providers on Lake Powell (within the Glen Canyon National Recreation Area—GCNRA) who had noticed a number of poisoning incidents involving boat occupants losing consciousness outdoors, beginning in the early 1990s. Through the early years of these poisonings, park officials sought evidence of other outdoor CO poisonings, but failed to find documentation of this problem elsewhere in the United States. When the first verified fatal marine CO poisoning occurred at Lake Powell in 1994, NPS EMS personnel had treated a total of 29 nonfatal CO poisonings associated with boats.

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On an August evening in 1994, NPS officials at the GCNRA dispatch center received an emergency call from boaters requesting assistance regarding the possible drowning of a 12-year old boy. Three boys had been swimming near the rear of a houseboat while family members were inside the air-conditioned living quarters of the boat. One of the boys became ill, and parents took him inside the boat to rest, attributing his illness to the hot weather. The other two boys continued swimming. The victim (the second boy) was on the swim platform at the time and complained to his companion about his legs feeling funny. The third boy climbed onboard and went inside the boat, complaining to his mother that he, too, did not feel well. The victim remained on the swim platform at the rear of the boat while others attended to his companion. Nearly an hour later, the group discovered that the victim was missing and began to search for him, concurrently summoning NPS assistance. NPS divers recovered the boy’s body from 21 ft. of water more than 2 h later. During the course of their investigation of this drowning, NPS discovered that the onboard gasoline-powered generator had been operating when the boys were swimming, and communicated this information to the medical examiner. As a result, a carboxyhemoglobin (COHb) analysis was requested as part of the autopsy. The analysis, repeated due to the high initial concentration, revealed a COHb of 61% documenting that the boy’s drowning was secondary to CO poisoning, the source of which was the generator.12 Although NPS requested assistance from the USCG after this boy’s death, and again in 1998 when two CO-related drownings occurred within 12 days of each other behind houseboats of a similar design, active response was lacking. This changed in August 2000, when two brothers, Dillon and Logan Dixey (aged 8 and 11 years), swimming at the rear of their family houseboat on Lake Powell, died as a result of CO poisoning. Their deaths were quick, occurring within minutes of exposure to generator exhaust under the swim deck, and were strikingly similar to five previously recognized fatalities on this lake behind houseboats of the same design. The brothers’ deaths, combined with the growing body of evidence at Lake Powell, triggered an interagency, multidisciplinary investigation, the goal of which was to identify effective prevention strategies at this lake.13 The interagency investigation rapidly grew to cover similar poisonings nationwide, with a number of local, state, and federal governmental agencies, individual boat and equipment manufacturers, boat rental companies, trade organizations, nonprofit organizations representing consumers, and individual boaters joining the effort to identify poisonings and interventions.

7.2 IDENTIFYING MARINE CO POISONINGS Data discussed in this chapter were derived from a variety of sources, and vary in level of documentation and detail available from the source. The most important thing to remember is that these are not all the poisonings that have occurred, but rather are the poisonings we know about from the sources discussed below. Case data are influenced by reporting bias (such cases were not recognized early on, recognition of cases has improved only slightly, awareness of reporting requirements is scant, and many cases

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were reported because of increased news coverage); and misdiagnosis of disease and death etiology (many deaths were and are classified as drownings that were actually CO poisonings first).

7.2.1 IDENTIFICATION OF MARINE CO POISONINGS AT LAKE POWELL Todate, nearly 1/3 of all recognized cases occurred at Lake Powell, and were identified through extensive case-finding research conducted jointly by the Centers for Disease Control and Prevention’s (CDC), National Institute for Occupational Safety and Health (NIOSH), the Medical Advisor for Prehospital Care at GCNRA, NPS GCNRA staff, and the US Department of the Interior. The isolation of the lake, and related centralization of NPS emergency response and patient transport, resulted in early identification and thorough documentation of fatal and nonfatal marine poisonings by Glen Canyon NPS medical and law enforcement personnel. Computerized and hard copy records were abstracted to identify and describe Lake Powell CO poisonings.14 These included: NPS GCNRA law enforcement dispatch logs; NPS EMS response sheets; Page Hospital Emergency Department treatment records; hospital discharge data; and medical examiner/coroner autopsy reports.

7.2.2 IDENTIFICATION OF MARINE CO POISONINGS NATIONWIDE In the United States, data related to boating accidents are collected through the USCG Boating Accident Report Database (BARD), which provides vital information for USCG regulation of the manufacture and recall of recreational boats and boatingrelated equipment. Data used to compile the BARD statistics come from two sources: (1) Boating Accident Report data forwarded electronically to the USCG by recognized reporting authorities, typically the state boating law administrator in each state; and (2) reports of USCG investigations of fatal boating accidents that occurred on waters under Federal jurisdiction.15 To obtain the most accurate data, BARD relies as much as possible on recreational boating accident investigations conducted by local law enforcement personnel and submitted to the USCG electronically by the recognized reporting authority. In the absence of investigational data, information is collected from accident reports filed by recreational boat operators, who are required to report boating accidents that involve the vessel or its equipment.16 Included in the USCG database are recreational boat-related or equipment-related accidents in which: 1. A person dies; or 2. A person is injured and requires medical treatment beyond first aid, that is, treatment at a medical facility or by a medical professional other than at the accident scene; or

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3. Damage to vessels and other property totals $2000 or more or there is a complete loss of any vessel; or 4. Aperson disappears from the vessel under circumstances that indicate death or injury. CO poisonings were specifically added to the listed USCG reporting guidelines in 2001, in response to confusion expressed among the reporting authorities as to whether recreational marine CO poisonings met the reporting requirements. Thus, a fraction of marine CO poisonings were reported to the Coast Guard prior to 2001.

7.2.3 ADDITIONAL CARBON MONOXIDE POISONING CASE IDENTIFICATION Intense national news coverage of the poisonings at Lake Powell, as well as technical presentations and other information dissemination, resulted in the identification of additional cases by researchers closely identified with this issue. The pattern that emerged from collection of related records from these independently identified cases indicated a broader problem, and pointed to emerging problems nationwide related to the design of houseboats and swim platforms on other types of motorboats. These randomly identified cases were added to those identified in the Lake Powell investigation and those contained in BARD to comprise a document now known as the National Case Listing.17 Data discussed below are derived from the January 2006 listing and analysis of the supporting database.

7.3 DESCRIPTIVE CHARACTERISTICS OF KNOWN MARINE CARBON MONOXIDE POISONINGS 7.3.1 DEMOGRAPHICS, DISTRIBUTION, AND OUTCOME OF POISONINGS The National Case Listing contains detailed information about 607 US boat-related CO poisonings requiring medical treatment or emergency response occurring on water bodies in or adjacent to 32 states. Further information is described in publications by the CDC.13,18,19 One-hundred-twenty-two (20%) of the 607 people died as a result of the poisoning. Ninety-eight percent of the poisonings occurred between 1990 and 2005. Age was known for 432 (71%) of the cases: 42% of the 432 cases were children (aged 18 or younger). Gender was known for 393 (64%) of the cases, which was fairly evenly divided between males (204 or 52%) and females (189 or 48%). Figures 7.1 through 7.3 show the distribution of cases by year, month, and state. The decline in cases in 2005, shown in Figure 7.1, is primarily an effect of the time lapse between the occurrence of the incident and reporting or verification of the case. (As of this writing, we have preliminary information regarding 13 additional cases for 2005.) Monthly distribution of marine CO poisonings is opposite that of

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Number of boat-related CO poisonings by year Total poisonings identified =607

Date of chart: 1/2006

80 70 60 50 40 30 20 10 unk

2005

2004

2003

2002

2001

2000

1999

1998

1997

1996

1995

1994

1993

1992

1991

1990

1989

1988

1987

1986

1985

1984

0

Fatal

Non–fatal

FIGURE 7.1 Distribution of boat-related carbon monoxide poisonings by year. Distribution of boat-related CO poisonings by month

Number of people poisoned

120 100 80 60 40 20

K N U

EC D

O V N

T C O

P SE

G AU

L JU

N JU

AY M

R AP

AR M

B FE

JA N

0

FIGURE 7.2 Distribution of boat-related carbon monoxide poisonings by month.

other poisonings (higher in the summer instead of higher in the winter) and reflects the pattern of boat use.

7.3.2 LOCATION OF THE VICTIM AND SOURCE OF CARBON MONOXIDE Location (on the boat) was known for 546 of the cases. Two of every three victims (353/546) were documented to be inside the boat’s living quarters when poisoned.

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163

1

13 15 7

7

1 30

Lake powell 176 (29%)

19* 1

5

*Excludes lake powell cases

15

1 6 3

5

44

30

10

29

2 22*

2

1

45

3

4

2 4 20

1

12

Location unspecified 39 17

FIGURE 7.3 Distribution of boat-related carbon monoxide poisonings by state.

These poisonings in the boat cabin occurred in 88 incidents primarily involving multiple victims (as many as 17 victims at a time). In contrast, 190 people were poisoned outside the boat cabin, in 149 incidents which were more likely to involve one to three victims. Thus, the higher number of incidents of poisoning occurred outside the boat. The specific location of the victim was documented for 100 of the CO-related deaths, with 56 of the victims exposed to CO outside the boat’s living quarters, 44 exposed inside the living quarters or within a full boat canopy. Location on the boat was characterized for 446 of the 485 survivors of marine CO poisonings: 309 were exposed to CO inside the boat cabin in 69 incidents; 134 were exposed outside a boat cabin in 103 incidents; and 3 people (1 incident) were characterized as having been at various locations inside and outside. Again, although more poisoning survivors were inside boats when poisoned, more incidents occurred outside boat cabins. The specific source of CO exposure was documented for 487 of the 607 poisonings. Exhaust from onboard gasoline-powered marine generators used to produce electricity for onboard appliances (air-conditioners, televisions, refrigerators, etc.) was the most common source, linked to 302 of the 480 poisonings. Gasoline-powered propulsion engine exhaust was linked to 168 poisonings. Twelve people were exposed to exhaust from both types of engines (generators and propulsion engines) when they were poisoned. Source was undifferentiated (e.g., the record said “engine exhaust” or “exhaust fumes” but did not clearly define which engine) or unspecified for 120 cases. At this point, there are no poisonings known to have been associated with marine diesel-powered engines of either type.

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7.4 MEDICAL CHARACTERISTICS OF THE CASES Medical characteristics of marine CO poisonings to be discussed here include COHb as an indicator of exposure, death and loss of consciousness (LOC) as indicators of exposure severity, and Glasgow Coma Scale (GCS—a scale that assesses the degree of brain function) as a measure of victim status when EMS personnel arrived on the scene.

7.4.1 CARBOXYHEMOGLOBIN MEASUREMENT LIMITATIONS Many boat-related CO poisonings occur while the victim is swimming near the boat. In such incidents, the victim loses consciousness, sinks into the water or lays face down in the water, ultimately drowning as a result of the poisoning. As such, COHb concentrations are often lower than those typically associated with CO-related fatalities. As is true with all CO poisonings, there is no consistency regarding timing of the COHb measurement. Reported COHb concentrations must be viewed as indicators of exposure, because of the many factors impacting that measurement (i.e., oxygen therapy duration, number of half-lives that have passed since the CO exposure ended, activity level of the victim between exposure cessation and COHb measurement, etc.). COHb analysis related to fatal boat-related poisoning may be complicated by the fact that victims who are poisoned and subsequently drowned sometimes are submerged for extended periods before their bodies are found. In such cases, body decomposition, and related degradation of blood cells, may impact the ability to accurately measure COHb.

7.4.2 BOAT-RELATED CARBON MONOXIDE POISONINGS RESULTING IN DEATH COHb concentrations were available for 50 of the 122 marine CO-related fatalities. Six of those 50 people received oxygen therapy prior to blood analysis. Reported COHb concentrations for people that were poisoned outside the cabin ranged from 1.9% (after 440 min of oxygen treatment by intubation) to 100%. The related estimated CO exposure duration for these victims was surprisingly short, ranging from 30 s to 30 min. Most (47) of the 56 people who died as a result of poisoning outside the boat’s living quarters were in the water when they were exposed to CO, likely losing consciousness and sinking. Reported duration of submersion for those that drowned as a result of the poisoning ranged from 5 min to 13 days. Six people that died outside the living quarters were on the boat, either sitting in the rear seat or rear section of the boat, or leaning over the transom. Specific location of the victim was unknown for three people. COHb concentrations for deaths that occurred inside the cabin or a full canopy ranged from 27% to 77%. With one exception, the people that died in the cabin of boats had gone there to sleep or watch videos, and were found dead the following morning when someone had noticed them missing, or when someone noticed the boat adrift. The exception to this is an incident in which four children were found

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Swim platform

165

Zippered canopy opening

FIGURE 7.4 Cabin cruiser with full canopy deployed.

unconscious (one of which was dead) in the rear area of a cabin cruiser boat that was covered with a full canopy (see Figure 7.4). The children were using a shower device that drew heated water from the operating propulsion engine’s cooling system. They unzipped a panel in the canopy and stood on the swim platform to use the shower hose. About 45 min after they had gone to the boat to shower, two of the boys were found unconscious on the bed in the boat cabin, and two (one of which died) were found unconscious in the area covered by the canopy. CO from the operating propulsion engine had apparently entered the canopied area and cabin. The COHb of the boy who died was 46.6%.

7.4.3 CARBON MONOXIDE EXPOSURE AS A DROWNING RISK FACTOR To assess the proportion of drownings and boat-related drownings for which CO poisoning was a contributing or primary cause of death, drownings that occurred on Lake Powell from 1994 to 2004 were identified.14 (The starting point was based on the year of the first confirmed CO-related drowning at Lake Powell.) Seventy-two people died of unintentional drowning within GCNRA during that time period. Seventeen percent (12 of the 72 people) of all drownings were CO-related. Twenty-five of the 72 people drowned in BARD-reportable boat-related accidents. This meant that nearly half (12/25) of all the boat-related drownings at Lake Powell were CO-related. These surprising numbers indicate that CO exposure may be a factor in many more drownings on other open water bodies than are currently recognized. This under-recognition is likely to continue unless COHb analyses are routinely included in autopsy protocols and hospital emergency room patient care procedures.

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To assess under-reporting of these cases, researchers examined the Coast Guard surveillance system (BARD) data and found that one of three Lake Powell boatrelated drownings were absent from BARD, and that CO-related and nonCO-related drownings were missing in similar proportions.

7.4.4 NON-FATAL BOAT-RELATED CARBON MONOXIDE POISONINGS As mentioned earlier, 485 people are known to have survived marine CO poisoning that required at least emergency medical treatment. It is important to remember that these patients did not always have easy access to transport (because they are out on a lake, river, or ocean), and that transport to a local hospital where blood is drawn (or equipment for breath analysis is available) often takes a while. These delays impact the COHb result significantly, especially if oxygen is being delivered to the patient during a lengthy transport. COHb concentrations were available for 128 of these poisoning victims, of which nearly half (i.e., 63) were treated with oxygen prior to COHb analysis (ranging from 10 to 645 min in duration). Measured COHb ranged from 1.9% to 47.8%. Information about LOC was available for 250 of the 485 survivors of poisoning, and just over half (i.e., 130) of the 250 were documented to have lost consciousness. GCS ratings were available for 112 of the survivors, with assessment ratings ranging from 3 (unconscious and unresponsive to deep pain) to 15 (indicating normal mental status at the time of EMS response and assessment). It was striking to note that 85 of the 112 GCS-rated patients were assessed as having normal mental status (GCS of 15), despite the fact that nearly 40% (33) of those patients reported profound LOC during their exposure to CO. Half of these patients (17/33) were evaluated by EMS personnel within 10–35 min of experiencing LOC, indicating that CO poisoning etiology can be easily missed if emergency response personnel do not know that CO exposures outside of an enclosure can result in rapid, serious poisoning.

7.5 BOATS AND CO SOURCES RELATED TO MARINE POISONINGS, WITH CASE STUDY PRESENTATIONS Types of boats involved in marine poisonings are categorized as follows: ski boats; cabin cruisers; houseboats; other pleasurecraft (fishing boat, personal water craft, etc.), or unspecified. The distribution of poisonings by boat is shown in Table 7.1, and are discussed below.

7.5.1 SKI BOATS Ski boats are typically a high-performance craft designed for speed and agility. They vary in size, but are typically about 21 ft. long and about 8 ft. wide. Ski boats associated with the outside poisonings (shown in Figures 7.4–7.6) are typically equipped with a high horsepower (310–400 hp) gasoline-fueled inboard direct-drive propulsion

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TABLE 7.1 Distribution of Marine Carbon Monoxide Poisonings by Boat Type Boat Type Ski Cabin cruiser Houseboat Other or unknown Total by outcome

Inside Cabin 0 31 2 11 44

Fatal Outside Cabin 23 3 23 7 56

Unknown Location 0 4 0 18 22

Inside Cabin 0 102 177 30 309

Nonfatal Outside Cabin 45 14 54 21 134

Unknown Location 3 4 1 34 42

Total by Boat Type 71 158 257 121 607

Swim platform

Exhaust

Propeller

FIGURE 7.5 Ski boat transom, platform, exhaust, and propeller configuration.

engine, the propeller of which is under the belly of the boat and thus removed from close proximity to the victim and thought by many to be out of harm’s way. Most of these boats have a water level rear platform (see Figure 7.5) used to facilitate easy access to the water and donning of ski and wakeboard gear. Engine exhaust is dual piped, exiting the boat hull just below the rear platform. All fatal and nonfatal poisonings associated with ski boats occurred outside of any enclosure, and were caused by exposure to propulsion engine exhaust (this class of boat is not typically equipped with a generator). The details of these incidents are strikingly similar: 45 (63%) of 71 people poisoned on this type of boat were sitting on or holding onto the swim platform; 18 of the 45 people died and 27 of them survived poisoning (19 of whom experienced LOC). The ages of victims occupying the swim platform ranged from 2 to 23 years. Five people were poisoned, four of whom lost consciousness, while occupying the padded sunning deck at the rear of ski boats.

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168 (a)

“Teak surfing” or “platform dragging” Surfer Displacement wave

Engine exhaust outlet (x2) Vessel is operated at a speed that will create the largest possible displacement wave, usually 10–12 miles per hour

(b)

Boat transom (rear wall)

FIGURE 7.6 Teak surfing. (a) Side-view showing position of surfer, (b) View toward transom of boat showing same.

Much media, legislative, and educational attention has centered on a thrill seeking activity that has been labeled as “teak surfing” or “dragging” (shown in Figures 7.6 and 7.7), in which the person holds onto the rear swim platform (which is often made of teakwood, thus the term “teak surfing”) until the boat reaches a speed (typically 10–12 mph) and orientation that allows them to briefly release their grasp and be pulled forward by the displacement wave directly behind the boat. Five of the poisonings associated with platform occupancy (three fatal and two nonfatal) occurred during teak surfing. The predominance of incidents associated with platform occupancy actually occurred when the boat was moving at idle speed (5 mph) through the water, while the victim was being pulled from here to there, or was sitting on the platform dangling his/her feet in the water. In addition, one person who died on the platform and eight survivors were sitting there while the ski-boat was not moving at all, but the propulsion engine was idling. One of the later incidents involved the poisoning of a 4-year-old girl exposed to propulsion engine exhaust while she sat on the swim platform, playing with a shower device that is fed hot water by the operating engine. (This is the same device previously mentioned in Section 7.4.2) Case 1. In June 2001, an 18-year-old passenger of a ski-boat drowned in Lake Powell as a result of CO poisoning. Three of the ten boat passengers were being

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Exhaust

Propeller

FIGURE 7.7 Position of teak surfer relative to engine exhaust terminus and propeller.

pulled behind the boat, teak surfing. Approximately 2 min after they began, one of the teenagers was unable to maintain her hold on the platform. She was reported as having “jerky arm movements” and difficulty in communicating. She was pulled into the boat by the passengers. Not recognizing the cause of her symptoms, another teen took her position on the platform, and they began teak surfing again. Approximately 1–2 min later, one of the three teens began to experience a severe headache and weakness. This teen pulled herself up onto the swim platform while the boat continued to move forward. The third surfer, still positioned for teak surfing, suddenly lost consciousness and released his hold on the platform. He sank beneath the surface. His body was retrieved from the water 3 days later. His COHb on autopsy was 57%. Case 2. In July 2000, a 15-year-old girl survived CO poisoning while she was lying on the rear padded sunning deck of a ski-boat on Lake Minnetonka in Minnesota. Boat occupants were waiting for a fireworks display, with the propulsion engine operating to power the onboard music system. Other occupants thought the girl was sleeping until they tried unsuccessfully to awaken her. She had stopped breathing. Her COHb measured upon transport to the local hospital was 30%. Case 3. In July 2005, a 21-year-old woman drowned as a result of CO poisoning. The woman was boating on the Gulf of Mexico with her husband and a group of friends in a 21 ft. ski boat. She and her husband were floating in the water, holding on to the swim platform of the stationary boat. The boat operator started the engine and began moving at about 5 miles per h when the woman slipped from the platform and sank. Her husband was unable to locate her. Several hours later, her body rose to the water’s surface and was discovered. Her COHb upon autopsy was 67%.

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FIGURE 7.8 Cabin cruiser.

7.5.2 CABIN CRUISERS A cabin cruiser is generally a large motorboat that has a cabin, and plumbing and other conveniences necessary for living onboard. The hull of a cabin cruiser (see Figure 7.8) is shaped like a conventional motorboat. Many modern cabin cruisers are equipped with air-conditioning and other electrical appliances that necessitate the use of an onboard generator for power. Most (31) of the 44 deaths inside a boat of any kind occurred in a cabin cruiser. Source of CO was known for 24 of the 31 deaths occurring in cabin cruisers: 18 of these deaths were associated with generator exhaust that infiltrated into the cabin; 5 from propulsion engine exhaust; and 1 from emissions from both types of engine. Four deaths occurred outside cabin cruisers, with the source being generator exhaust in three of the deaths and propulsion engine exhaust in the remaining incident. Case 4. In June 2005, a 36-year-old man and his 35-year-old wife died of CO poisoning while inside a cabin cruiser. The couple’s boat was moored at Lake George Inlet, Florida near two other boats; all three boats’ generators were operating to power the air-conditioners. When the victims’ generator ran out of gas at about 10:00 a.m., friends opened the door and found the occupants’ bodies. When emergency workers entered the cabin, they found high concentrations of CO. It was unclear if the CO was from the boat on which the couple died, or from the combined exhaust of all three generators. Autopsy results revealed that the husband’s COHb was 75.2%; the wife’s COHb was 77.2%.

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Case 5. In September 2001, a 62-year-old man was swimming near his cabin cruiser boat on Shasta Lake, California, talking with his wife who was on the boat. The boat was not moving, but the propulsion engine was operating at the time, charging the boat batteries. The man went to the swim platform at the rear of the boat to rest. While resting for approximately 1–3 min, he started splashing water at his wife. His eyes then became fixed, and he lost consciousness. His wife tried to pull him from the water, but couldn’t. She moved his body to a nearby island. Although the medical examiner initially listed his cause of death as a heart attack, this was changed upon receipt of forensic toxicological test results two months later indicating that his COHb concentration was 89.3%. The test was repeated, this time indicating a COHb concentration of 80.8%. Case 6. In August 2002, two 9-year-old girls were poisoned outside of a moored cabin cruiser on Lake Powell. One girl died and one survived. They were observed playing in shallow water (about 30 in. deep) near the rear of the boat very near the exhaust terminus of the operating generator. One girl was called into the boat by her parents, and when she climbed out of the water onto the swim platform, she stumbled and fell onto the floor. She was thought to be suffering from dehydration. The other girl was discovered to be missing about 15–30 min later. She was found lying on the bottom of the lake. Attempts to resuscitate her were unsuccessful. The survivor’s COHb was 15.1% after more than 70 min of oxygen therapy. The girl who died had a COHb of 39% after more than 40 min of resuscitative efforts, including CPR and intubation.

7.5.3 HOUSEBOATS A houseboat typically looks a bit like a house trailer mounted on a large floating barge (referred to as a monohull) or pontoons. Houseboats vary substantially in size, with some reaching 90 ft. in length and 16 ft. in width, dependent upon the requirements of the purchaser, restrictions of the water body on which the boat will be placed, transport restrictions, and so forth. Many of the fatal poisonings associated with houseboats (and all of the fatal houseboat poisonings on Lake Powell) were related to a specific design, shown in Figures 7.9 through 7.11. This design incorporates a monohull structure with an attached extended swim deck at the rear of the boat. The rear deck structure creates a cavity or air space between the hull and the water level swim platform. Exhaust of both propulsion engines, and sometimes that of the gasoline-powered generator, is directed into this air space, which came to be referred to by many as the “Death Zone” (a designation that will be used throughout this chapter for ease of reference). When the engines or the generator are operating, the build-up of CO in this cavity is so high that it creates an imminent danger of death for anyone who enters the cavity. Exhaust lingers in this cavity for on extended period following deactivation of either type of engine. CO poisonings have also been associated with the very high CO concentrations measured on or near the swim platform of houseboats. The common practice of continuous generator operation to provide power for air-conditioning, entertainment centers, and electronic suites while the houseboat is moored has exacerbated the problem.

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Living quarters/ boat cabin

Swim step

Extended deck

Engine compartment

FIGURE 7.9 Houseboat design associated with fatalities.

Propulsion engine outdrive

Generator exhaust terminus

FIGURE 7.10 Cavity beneath the extended deck (showing one of two propulsion engine outdrives and rear-directed generator exhaust location) - commonly referred to as “the Death Zone”.

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Exhaust from engine and generator

DANGER! Air pocket and water under step Swim platform

Used by permission. Copyrigh  2007 Boat Ed www.boat-ed.com

FIGURE 7.11 Diagramatic depiction of exhaust accumulation within the cavity.

Poisonings outside of houseboats were typically attributed to exposure to generator exhaust (15 fatalities and 44 nonfatal poisonings). In other incidents, the source of CO was a combination of generator and propulsion engine exhaust (two deaths and one nonfatal). Five people were poisoned by propulsion engine exhaust only (two deaths and three nonfatal). All poisonings that occurred inside the living quarters of houseboats (2 fatalities in 1 incident; 177 nonfatal poisonings in 27 incidents) were attributed to generator exhaust infiltrating the cabin. Case 7. In July 2004, a 34-year-old woman drowned and two others lost consciousness as a result of CO poisoning on Perry Lake, Kansas. A group of women were swimming behind several tethered (rafted) houseboats on which one or more generators were operating. There was little wind when the incident occurred. Two of the women were found unconscious. One of the women was not breathing, but was revived, and the second was unconscious and unresponsive. A few minutes later, someone noted that the third woman was missing. Her body was recovered approximately 30 min later. On autopsy, her COHb was 45%. Case 8. In September 2002, a 42-year-old man entered the airspace beneath the extended rear deck of a houseboat on Lake Powell shortly after the propulsion engines were deactivated. Just prior to the incident, the boat occupants were attempting to moor the boat during windy weather. As they maneuvered the boat, the anchor ropes became entangled in one of the engine propellers. Just after the engines were deactivated (estimated to be more than 3, but less than 5 min), the victim entered the air space beneath the stern deck to remove the lines from the propeller. He was wearing

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a personal floatation device (PFD) at the time. After his first entry into the airspace (estimated to have lasted about 2 min), he emerged and removed the PFD because he was unable to access the propeller. After approximately 2 min, he entered the space again, and stayed there about 2 min. He emerged for 2 min, and then re-entered the space a third time. After about 2–3 min elapsed, he no longer responded to questions from the boat occupants and failed to emerge from the space. His overall time of exposure was thought to have been 6 min, with a total of approximately 15 min transpiring before he was no longer heard from. Although divers made many attempts to find him, they were unsuccessful. His body floated to the surface 3 days later. Autopsy results indicated that his COHb was 51%. Case 9. In June 1998, a 4-year-old girl was swimming at Lake of the Ozarks, Missouri with a group of children behind the rear deck of a houseboat. She was wearing a PFD, and was under the direct supervision of adult swimmers. She swam to the swim platform, held on to the ladder while her mother applied sunscreen to her face, and then swam away. Within moments she was observed floating face up on the water, unconscious, and rigid. She was quickly brought into the boat where her mother, a registered nurse, checked her for respirations and pulse. She appeared pale and stiff at that time, was unresponsive with poor respiratory effort. After 2–3 min of aggressive stimulation, the child began responding with grunts but was described as disoriented and sleepy. Paramedics were called and arrived 10–15 min later. They administered oxygen and transported the child to the nearest hospital emergency department within 30–45 min. Her COHb level at the hospital after approximately 1 h of oxygen therapy was 22.2%. Upon examining the houseboat during their next visit to the lake, the child’s parents discovered that the exhaust terminus for the onboard generator that was operating at the time of this poisoning was located at the edge of the swim platform, in the center of the rungs of the ladder that the child was holding onto when the sun screen was applied. Case 10. In June 2000, 15 people, ages ranging from 16 to 47 years, were overcome by CO on two rented houseboats on Lake Cumberland, Kentucky. The boats were tied together and anchored in a cove. Both boats had gasoline-fueled generators; the generator on one of the boats had a side-directed exhaust terminus. The exhaust of one of the generators seeped into the adjacent boat through an open bathroom window. CO was circulated through the full interior of the boat by the central air-conditioning system. A few boat occupants awoke at about 5:00 a.m. with headaches and nausea. Realizing they had a problem, the group radioed the marina and ambulances met the boats at the shore. The water patrol officer that responded to the emergency witnessed that two occupants were unconscious when he arrived, and others were drifting in and out of consciousness. All 15 people were treated at the emergency department of a nearby hospital; 3 were admitted as hospital inpatients for further treatment. There were six CO detector/alarms on this boat, but none were properly connected when the boat was inspected after the poisoning incident.

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7.6 AIRBORNE CARBON MONOXIDE CONCENTRATIONS MEASURED ON AND NEAR BOATS 7.6.1 METHODS FOR MEASURING, ANALYZING, AND EVALUATING CO IN AIR Four methods, each with different upper range of measurement capability, were used for collecting CO air samples in the investigations discussed below. Method 1: Direct-reading infrared instruments, more conventionally used to measure CO directly in engine emissions, were used to analyze air samples of very high CO concentrations (i.e., collected in the “Death Zone” and on swim platforms) from houseboats and ski boats. Emissions analyzers are capable of measuring CO in the ranges of percentages (1% CO equals 10,000 ppm) as high as 100%, and also measure oxygen concentration. Method 2: Direct-reading instruments with electrochemical sensor technology were used to measure CO in concentrations between 0 and 1000 ppm. These sensors can be damaged when exposed to excessive CO concentrations for extended periods. Method 3: Detector tubes (a glass tube filled with media that changes color when CO in air is passed through it) capable of measuring 30,000–70,000 ppm were used primarily to confirm ranges of measurement, and to indicate which technology could be safely used in different locations of measurement. Method 4: A laboratory analytical method was used to confirm very high CO concentrations measured by direct-reading instruments. Grab samples were collected using glass air-evacuated containers, which were then shipped to a laboratory for analysis. The sample inside each vial was then analyzed for a number of components, including CO and oxygen. This method was capable of analyzing 0–100% CO, as well as oxygen concentration. How much CO is too much? The answer to this question involves both duration of exposure (minutes, hours, days, etc.) and air concentration. Units of measure for CO concentration in air are parts of CO per million parts of air (ppm). Exposure to CO concentrations (in ppm) results in a rise in CO in the blood, referred to as COHb—expressed as percent saturation. Various health and safety agencies recommend or require limits for CO in air. Table 7.2 shows the limits for general populations and for workers. These limits are presented as evaluation criteria to help the reader understand the hazard associated with the air sampling data presented below.

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TABLE 7.2 Evaluation Criteria for Carbon Monoxide

Agency

Intent of the Limit

US Environmental Protection Agency

Established to protect the most sensitive members of the general population by maintaining increases in COHb to less than 2.1%77

World Health Organization

Recommendations established to protect the general population by maintaining increases in COHb to less than 2.5% when a normal subject engages in light or moderate exercise78

National Institute for Occupational Safety and Health

The 8-h limit is recommended to protect workers from health effects associated with COHb levels in excess of 5%. The IDLH (Immediately Dangerous to Life and Health) limit is recommended as a concentration at which an immediate or delayed threat to life exists or at which an individual’s ability to escape unaided from a space would be compromised. The ceiling limit is recommended based on acute effects of exposure79

Limit (in parts of CO per million parts of air) 35

1h

9 87

8h 15 min

52 26 9 1200

30 min 1h 8h IDLH value

200

American Conference of Governmental Industrial Hygienists

The 8 h limit is recommended to protect workers from increases in COHb levels in excess of 3.5%. The agency similarly recommends a Biological Exposure Index (BEI) of 3.5% COHb for end of shift exhaled breath analysis in nonsmoking workers80

Occupational Safety and Health Administration

Required limit to protect workers from health effects associated with a COHb of 8–10%81

Time Period

35 125

25 50

Ceiling limit— never to be exceeded 8h Excursion limit (5 times the 8-h standard)

8h 8h

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7.6.2 CARBON MONOXIDE CONCENTRATIONS ASSOCIATED WITH BOAT-RELATED CO POISONINGS 7.6.2.1 Ski Boats In June and July 2001, CO air samples were taken as part of the investigation of the Lake Powell death of an 18-year-old boy that succumbed to exposure to CO while “teak surfing” (see Section 7.5.1, Case 1).20 CO concentrations as high as 23,800 ppm in the unobstructed airspace above the swim platform (where the teak surfer’s face and upper body would be during the activity) were measured. When the airflow above the platform was obstructed by a form simulating the shape of the upper torso of a person with extended arms (like a “teak surfer”), CO concentrations above the platform were consistently between 10,000 and 26,700 ppm, despite the fact that engine maintenance had been conducted. In an August 2001 Connecticut incident, a 15-year-old boy who was teak surfing for an estimated 10–15 min, released the platform, floated briefly, lost consciousness, and sank. His COHb measured during the autopsy was 56%.21 An investigation involving air sampling for CO was later conducted on the boat. (The upper limit for equipment used to measure CO in air for this investigation was 1000 ppm.) CO concentrations exceeded 1000 ppm on the swim platform (and in what would be the breathing zone of simulated swimmers/teak surfers) at varying engine speeds, and whether the platform was obstructed or unobstructed. The operator of the boat was exposed to as high as 410 ppm during idle, depending on the wind direction. Average concentrations consistently exceeded 200 ppm during the entire sampling event when the boat was operating.

7.6.2.2 Cabin Cruisers In response to reported incidents that identified a potential safety problem involving CO for recreational boater occupants inside cabins, the USCG contracted a study to evaluate intrusion of CO into the passenger areas of gasoline-powered recreational cabin cruiser boats.2 Tests results reported in 1991 showed that under certain conditions, CO accumulated in the passenger spaces at a rate of about 1 ppm per minute, posing a health and safety threat to occupants. In areas at the rear of the boat (on the transom, in the rear deck passenger area, etc.) peak CO concentrations as high as 400 ppm, and 30 min average concentrations as high as 272 ppm, were measured. The authors concluded: “It is apparent that the potential exists for a serious health and safety problem for power boaters.” Results of an interagency investigation of a fatal and nonfatal CO poisoning that occurred near a cabin cruiser were reported in 2002.22 (See Section 7.5.2, Case 6 for details of the incident.) CO concentrations as high as 41,600 ppm, and oxygen concentrations as low as 12%, were measured in the open air within inches of the boat’s generator exhaust terminus (approximately where the poisoned children were exposed). In addition, CO concentrations consistently exceeded the upper limit of the air monitors placed on the swim platform and at locations one and five ft. from the exhaust terminus, indicating that the CO concentration at these locations were

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somewhere between 1000 ppm and the maximum value measured at the exhaust terminus (41,600 ppm). Concentrations as high as 570 ppm were measured 10 ft. away from the exhaust terminus. 7.6.2.3 Houseboats Unless otherwise specified, all data discussed below pertain to houseboats designed similarly to those in Figures 7.9 through 7.11. In 1995, a 43-year-old man died in Florida as a result of a 5-min CO exposure within the airspace under the extended rear deck of a houseboat. The boat’s electrical power generator, which released exhaust into the airspace, was activated just before he entered; propulsion engines were not operating. Approximately 5 min after he entered the airspace, he was observed unresponsive floating face down in the shallow water; he subsequently died. His COHb measured in the hospital 2 h after exposure, and after more than an hour of oxygen therapy, was 29.7%. A forensic toxicologist estimated that the man’s COHb was greater than 70% when he collapsed. CO concentrations measured as part of the investigation of this death were reported in legal proceedings.17 Inspection and testing of the houseboat revealed that CO concentrations in that airspace would reach 4,000–10,000 parts per million (ppm) within 2–5 min after the generator was activated. As part of the initial investigation of the death of two young brothers exposed to generator exhaust in the airspace under the rear deck of their family houseboat at Lake Powell in August 2000, the NPS conducted air sampling to define the incident circumstances.23 CO concentrations at water level below the rear deck of three similar houseboats exceeded 2000 ppm (which was the maximum CO concentration the instrument could measure) approximately 10 min after generator activation. CO measurements collected above the swim platforms of the three boats were 800, 100, and 1156 ppm. Two of the people conducting the test began to experience headache, mild nausea, and weakness while conducting this air sampling. As other agencies joined in the investigation of past and ongoing CO poisonings at Lake Powell, air sampling on houseboats continued. In September 2000, air sampling in the airspace beneath the rear deck on similar houseboats documented the following maximum CO concentrations: 13,000 ppm when one propulsion engine operated; 30,000 ppm when the generator operated (with concurrent oxygen deficiency, 13% measured); and 20,000 when both the propulsion engines and generator operated. CO concentrations exceeding 1200 ppm above and around the water level swim platform were also measured. Repeat testing in November, 2000 confirmed these very high concentrations of CO in the “Death Zone” of similar boats, as well as on the upper rear deck and swim platform.24 Further testing was conducted on houseboats at Lake Cumberland in Kentucky, with results reported in December, 2000.25 This study again documented that CO concentrations near and under the rear deck of houseboats were very high (4,078 ppm measured near water level off the back of the swim platform when the gasolinepowered generator operated, and 10,224 ppm measured at the same location when the generator and propulsion engines operated). These measurements confirmed that there was significant potential for poisonings on houseboats on lakes other than Lake

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Powell. This study was the first to characterize emissions of diesel generators—with a maximum CO concentration of 10 ppm measured when the diesel generator operated near the exhaust terminus and at the back of the boat. However, when the gasoline motors were in operation, CO concentrations increased considerably, with 455 ppm measured on the swim platform. In March, 2003, an interagency group collected air sampling data as part of a supplemental investigation of a fatal poisoning at Lake Powell.26 (See Section 7.5.3, Case 8 for a description of the death.) The purpose was to provide further information about clearance of propulsion engine exhaust from the “Death Zone” airspace. (Previously reported data documented that the CO concentration in that airspace decayed to 0 ppm within 8 min following deactivation of the generator and propulsion engines.27 ) In repeated tests conducted on two boats in the 2003 study, rates of decay varied widely—with initial CO concentrations as high as 88,200 ppm decaying to 2 ppm in widely varying time periods (from 10 to 30 min), indicating that CO clearance times in that airspace are unpredictable, and could feasibly be much longer than documented in these tests. 7.6.2.4 Carbon Monoxide Exposure in Areas of Congested Boat Traffic (Lake Havasu Study) During summer holiday weekends, as many as 700 boats collect in the Bridgewater Channel of Lake Havasu at any given time, some moored to the shoreline of the channel and many cruising slowly through it (see Figure 7.12). The City of Lake Havasu estimates that about one-third of the boats in the channel have engines operating, representing exhaust roughly equivalent to that of 40,000 automobiles. As a result of initial reports of poisonings occurring in an area congested with boats at Lake Havasu, Arizona, CO exposures among municipal employees and visitors at the Bridgewater Channel were evaluated through air sampling and expired breath measurements. Air sampling was conducted during summer holidays in 2002 and 2003, when boat traffic within the channel was congested.28 Initial sampling documented that CO concentrations in channel air exceeded all short-term exposure criteria listed in Table 7.2; and 4 of 12 boating patients reporting to a local hospital emergency department for any cause (injury, LOC, etc.) had COHb levels of 9.4–28.3%. In response to these findings, an interagency investigation of CO concentrations in the channel was conducted during Memorial Day weekend (May), and during June–September, 2003. These surveys documented excessive CO exposure and confirmed the health risk among vacationers and employees working in the channel near crowded motorboat gatherings, with a trend of higher exposures later in the day. Sixty-nine percent of monitored workshift exposures of 36 municipal employees involved short-term CO exposures that exceeded the NIOSH ceiling limit of 200 ppm. Overexposures were confirmed by postshift measurements of exhaled breath: 67% of sampled workshifts resulted in estimated COHb levels equal to or greater than the recommended limit of 3.5%,29 with the average COHb among nonsmoking employees increasing from 1% in the morning to 6% in the afternoon (maximum was 13%). Among 46 nonsmoking vacationers that volunteered for exhaled breath

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FIGURE 7.12 Boats in Lake Havasu’s Bridgewater Channel.

measurements, the estimated COHb increased from a mean of 1% in the morning to 11% in the afternoon (maximum was 23%).19

7.7 PREVENTION EFFORTS 7.7.1 U.S. COAST GUARD REGULATION OF BOAT MANUFACTURING/RECALL AUTHORITY The USCG Recreational Boating Product Assurance Division of the Office of Boating Safety is responsible for such things as developing and enforcing federal safety standards and investigating consumer complaints. Specific responsibilities of the division includes inspecting and testing recreational boats for compliance, and issuing recalls of recreational boats and associated equipment. For this reason, boats are excluded from the jurisdiction of the US Consumer Product Safety Commission. After the August 2000 deaths of two brothers at Lake Powell (and related subsequent data collection), the Coast Guard determined that the houseboat design shown in Figures 7.9–7.11 (specifically a houseboat with an extended rear deck, water level swim platform, and rear-directed generator exhaust terminus that empties into the air space beneath the rear deck) was defective and fell within their recall jurisdiction. The agency contacted 71 houseboat builders, informing them about data documenting a deadly combination of generator exhaust and houseboat swim platforms on boats of this design.30 As a result of this and following mailings,

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six manufacturers agreed to a voluntary recall.31 Initially, it was estimated that more than 2000 boats would have to be retrofitted with the new design suggested by manufacturers (rerouting rear-directed generator exhaust terminus from within the cavity to the side of the boat outside of the cavity), but that number was adjusted downward to 1087 boats. Manufacturers self-certified that over 800 boats were retrofitted as a result of the voluntary recalls.32 Side exhaust was seen as an improvement in design, but not a solution, as there had been poisonings associated with water level exhaust outside of any enclosure (such as the one formed by the cavity beneath the deck). In addition, the common practice of “rafting” several houseboats together raised concerns about side exhaust that would now be directed towards the next boat when the generator operated. The Coast Guard also acted to prevent poisonings associated with the use of a shower system at the back of the boat that draws heated water from the operating propulsion engine (thus exposing the user to propulsion engine exhaust). This device was associated with two poisoning incidents (one fatal and four nonfatal poisonings). In December 2005, the Coast Guard notified the manufacturer of the system that there were CO and other safety hazards for recreational boaters who use the shower system directly connected to the operating propulsion engine. The manufacturer responded with assurances that the system installation would be changed to eliminate connection to an operating propulsion engine, and that they would provide additional CO warnings in printed materials.30

7.7.2 ENVIRONMENTAL PROTECTION AGENCY REGULATION OF MARINE ENGINE EMISSIONS The Clean Air Act directs Environmental Protection Agency (EPA) to regulate nonroad engines, a classification that includes marine propulsion engines and marine generators. Initial EPA regulations for gasoline-powered marine engines, published in 1996, pertained to outboard engines and personal watercraft only. These standards, phased in from 1998 to 2006, achieved approximately a 75% reduction in hydrocarbons (HC) and oxides of nitrogen (NOx ) from new engines. Although a cap in CO emissions was proposed in these regulations, none was finalized. However, some of the methods used to reduce outboard engine HC emissions also result in a reduction in CO emissions.33 In 2001, the California Air Resources Board adopted emission standards for new gasoline-powered sterndrive and inboard marine engines that are expected to require use of catalytic converters beginning in 2007.34 There are currently no federal standards for emissions from gasoline-fueled sterndrive and inboard marine propulsion engines. Consequently, while these engines remain uncontrolled, calculations conducted by Sonoma Technology, Inc. indicated that an average marine engine emits the same amount of CO as 188 automobiles35 EPA gave notice of its intent to develop a proposal for these engines in 2002.34 EPA regulates new gasoline-powered marine generators under 2 sets of rules. Rules for small generators (≤ 19 kW) vary depending on size of the engine, include limits for HC, NOx , and CO, and were phased in from 1997 to 2005. Regulations

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relevant to large gasoline-powered marine generators (>19 kW) were effective in 2004, with substantial reductions in HC, NOx , and CO required for 2007 models.34

7.7.3 STATE LEGISLATIVE ACTION The National Association of State Boating Law Administrators (NASBLA) provides model language for individual state legislation related to boating safety. In 2003, NASBLA approved language related to marine CO poisoning, with revisions approved in 2005.36 The model act, referred to as the Safe Practices for Boat-Towed Watersports Act, and aimed at the practice referred to as “teak surfing”, included the following provisions: [Requirements.] a) No person shall operate a motorboat or have the engine of a motorboat run idle while a person is teak surfing, platform dragging, or body surfing behind the motorboat. b) No person shall operate a motorboat or have the engine of a motorboat run idle while a person is occupying or holding onto the swim platform, swim deck, swim step, or swim ladder of the motorboat. [Exemptions.] The provisions of this act do not apply when a person is occupying the swim platform, swim deck, swim step, or swim ladder while assisting with the docking or departure of the motorboat, while exiting or entering the motorboat, or while the motorboat is engaged in law enforcement activity. To date, five states have promulgated legislation or regulations intended to prevent marine CO poisonings, most using the model language proposed by NASBLA. Pennsylvania was the first state to revise boating regulations related to unacceptable boating practices in 2003.37 In 2004, the California State Legislature passed Assembly Bill (AB) 2222, the Anthony Farr and Stacy Beckett Boating Safety Act of 2004.38 This bill added to the NASBLA language by: 1. Requiring that all state-sponsored or approved boating safety courses include information about the dangers of CO poisoning at the stern of a motorized vessel and how to prevent that poisoning; 2. Requiring that any new or used motorized vessel, when sold, bear warning stickers as to the danger of CO poisoning on boats; and 3. Requiring that boat registration materials include similar informational about the dangers of CO poisoning and boats. Nevada followed in 200439 Oregon in 200540 and Washington state41 and Utah42 in 2006, each state adopting and embellishing the NASBLA model language.

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7.7.4 EFFECTIVENESS OF MARINE CARBON MONOXIDE DETECTOR/ALARMS IN PREVENTION 7.7.4.1 Case-Based Data Investigative records related to Lake Powell CO poisonings that occurred in the living quarters of houseboats were evaluated with regard to CO detector/alarm presence and function. From 1990 to 2004, 80 people survived poisonings inside houseboats in 15 incidents.14 Fifty of the eighty people were poisoned in boats that were known to have had CO detectors in the living quarters. However, in only one incident (four people poisoned) did the alarm sound alerting the occupants to the hazard. Twenty people were poisoned in three separate instances involving disarmed or “broken” detectors. Twenty-two people were poisoned in four instances involving functional detectors that failed to sound during the poisoning incident. Ten people were poisoned in a houseboat that was not equipped with CO detectors. Twenty people were poisoned in houseboats in which the record failed to document the absence or presence of detectors. In May 2005, an analysis of boat-related CO poisonings conducted by the National Marine Manufacturers Association (NMMA) pointed out that documentation was available regarding CO detectors in 12% (66) of 506 cases they analyzed, and for half of these cases (33), the exposure occurred with the CO detector disconnected.43 In 11 of the 66 cases (17%), the CO detector malfunctioned, and in only 1 of 66 poisonings did a CO detector sound. The failure of onboard CO detectors in the living quarters of houseboats on Lake Powell, as well as data related to detectors elsewhere, raises concern about the impact of such devices in CO-poisoning prevention. Improving the effectiveness of these devices is complex, as there were four types of problems identified, each indicating a different corrective strategy. (Identified problems included: failure to alarm; alarming when they shouldn’t; disarmed or dysfunctional detector; and absence of detectors.) Failure of functional detectors to warn occupants of high CO concentrations and the sounding of alarms for no discernable cause are related to detector sensor technology. A likely explanation of disabling of detectors by boaters is that the detectors are sounding frequently and the boater either cannot identify a cause for the alarm (also a detector technology issue) or cannot resolve the issue that is causing CO to enter the cabin (an issue related to boat design, technology, and boater education).

7.7.4.2 Marine Carbon Monoxide Detector Evaluation In 2004, the USCG Office of Boating Safety Recreational Boating Product Assurance Division released a contracted study of CO detector performance in the marine environment.44 The purpose of the study was to evaluate the reliability of CO detectors that, in 2002, were advertised as being suitable for marine environments. About 90 detectors (five different products) were evaluated; 54 had metal-oxide sensors, 18 had electrochemical sensors, and 18 had biomimetic sensors. The goal was to determine the impact of one or more factors (humidity, salinity, temperature

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variants, or out-gassing of new boat construction materials) on detector performance, using the Underwriter Laboratories, UL 2034 standard for CO alarms on recreational boats, as evaluation criteria. The study also included data on performance of detectors following nonpowered storage, as is common with boats that have seasonal use. Results and related recommendations included: 1. Future studies should be performed over two season extremes. This was based on results of the study that indicated the detectors may be affected by seasonal changes. 2. The effect of long-term exposure of sensors to volatile compounds resulting from out-gassing of vessel construction materials and related impact on sensor functionality should be investigated. This was based on the data characterizing new and increased existing volatile organic compounds over time when ambient temperatures rise, and when the boat is in a “closed condition” as would be the case during storage in nonuse seasons. 3. The recovery time of the sensors used and the time required for the sensor to reach a stable operating condition should also be investigated. This was based on results of nonpowered detector testing of the metal-oxide sensors, documenting that prolonged storage in a nonpowered condition (as is the case during storage of the boat or periods of nonuse) can affect sensor performance. Instructions from the sensor manufacturer stated that these conditions may require a longer preheating period to stabilize the detector before use, and recommends storing the sensor in a sealed bag containing clean air and nothing else (as in, no silica gel). No other manufacturer provided any information regarding the proper or recommended storage practices when the detector is not in use and not under power. 4. Detectors should be installed on various types of vessels and a portable test chamber testing capability should be developed to allow for testing detectors in a real world setting.

7.7.5 ENGINEERING CONTROL RESEARCH AND DEVELOPMENT By the time data from the investigation of boat-related CO poisonings at Lake Powell were published in December, 2000,13 work was already underway to develop controls to reduce the CO hazard. Initial efforts were directed towards houseboat generators, primarily based on Lake Powell data. (Of the 111 poisonings identified at Lake Powell at that time, 74 were on houseboats, and 64 of these were associated with exposure to generator exhaust. In addition, 7 of 11 deaths there had occurred near houseboats of the design shown in Figures 7.9 through 7.11, and 5 of the deaths were associated with generator exhaust only.) In May 2001, the USCG Office of Boating Safety cosponsored the first of what became a series of workshops to focus on ways to reduce marine CO hazards, bringing together boat manufacturers, control innovators, and government agencies.45 The initial meeting focused primarily on controls for houseboat generators, and spawned a number of research and development projects.

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FIGURE 7.13 Generator exhaust terminus—side exhaust (marked by arrow).

Houseboat generator control alternatives developed and evaluated since then included 1. Rerouting generator exhaust to the side (as shown in Figure 7.13)46,47 2. Rerouting generator exhaust through a hybrid wet/dry vertical stack exhaust system with an exhaust terminus several feet above the upper deck (Figure 7.14)27,47−57 3. Retrofitting generators with an emission control device (Figure 7.15)45,46,49,57 4. An electrical interlock device to deactivate the generator when conditions indicated that boat occupants were swimming (lowered swim ladder, open gates, etc.),48 and finally, 5. New manufacture of emission-controlled generators55,58 Control directly at the source is the preferred and most effective intervention. In February, 2004, Westerbeke was the first manufacturer to introduce a series of reduced-emission gasoline-powered marine generators, reporting a 99% reduction in CO emissions. This reduction was confirmed through Coast Guard-sponsored field testing of two generators (14 and 20 kW) installed and used on houseboats.55 Final results for the second round of tests, designed to assess longevity of effectiveness of the emission controls after 2300 and 1300 h of use (calculated to be equivalent to 92,000 and 52,000 miles of use for an average automobile) indicated little or no deterioration in the effectiveness of the controls.58 In 2005, Kohler

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FIGURE 7.14 Stacks directing generator exhaust upward (marked by arrows).

FIGURE 7.15 Emission control device for retrofit of generators.

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also announced a new line of marine generators reported to reduce CO emissions by 99%.59 By 2002, focus shifted towards control of propulsion engine emissions. The Coast Guard and ABYC began semiannual meetings to discuss the progress of research and development of all marine engineering controls. These are held in conjunction with the International Boatbuilders Exposition meetings, and minutes of the meetings are available through ABYC. These periodic CO workshops have greatly facilitated the exchange of both technical information among manufacturers and the public, and also the sharing of accident information, and a general rising of awareness in the industry, government, and the public. The workshops have also served to accelerate other mitigating technologies, including diesel engines as viable alternatives for recreational boats.60 The result has been to highlight a much broader scope of research by adding express cruisers, towed activities, etc. The workshops have also served as a catalyst for revision of ABYC TH-23 (Design, Construction, and Testing of Boats in Consideration of CO),61 and addition of dry stack exhaust considerations to ABYC P-1.62 Concurrent with the workshops, the Coast Guard sponsored evaluations of CO emissions on recreational boats.63,64 Safe distances from the boat were evaluated to address the issue of potential CO exposures for those being towed on water “toys” behind the boat (tubers, wake surfers, etc.).65,66 Evaluations of the effectiveness of devices designed to reroute the exhaust of ski-boat engines were also conducted.67,68 Prototype catalyzed propulsion engines were introduced at the International Boat Builders Exposition in February 2005, and evaluations of the catalyzed engines continued.69−71 In March 2006, Indmar introduced the first production inboard propulsion engine with controlled emissions to be available on 2007 model year boats.72 Most recently (January 2006), results of a Coast Guard sponsored study of CO emissions and exposures on a class of cabin cruiser boat known as express cruisers were reported.73 The study was performed to better understand how CO poisonings may occur on express cruisers, identify the most hazardous conditions, and begin the process of identifying controls to prevent/reduce CO exposures. Many of the evaluated boats generated hazardous CO concentrations: peak CO concentrations often exceeded 1100 ppm, while average CO concentrations were well over 100 ppm at the stern (rear). Two boats with a combined exhaust system (exhausting at the sides and underwater) had dramatically lower CO concentrations than any of the other evaluated boats (about 40% lower).

7.7.6 INNOVATIONS IN EMS MEDICAL MANAGEMENT With the support of the USCG, in 2003 NPS EMS personnel at Lake Powell began using equipment that allowed noninvasive estimation of COHb concentration from analysis of exhaled breath samples for more effective triaging of patients. The decision logic shown in Figure 7.16 is used to guide medics in acting upon results of the analysis. A decision logic for use of a new noninvasive blood pulseoximeter has also recently been published74 and is discussed in another chapter of this book.

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CARBON MONOXIDE POISONING The micro CO meter is to be used on anyone who has been or you suspect has been exposed to or poisoned by carbon monoxide (CO) Consider scene safety for rescuers and patients. Rapid extrication from hazardous environment PRN.(1)

Address airway issues

NO

YES

Obtain exhaled CO measurement

Micro CO meter immediately available?

Administer high flow oxygen via nonrebreather mask

Administer high flow oxygen via non-rebreather mask

Obtain exhaled CO measurement as soon as Micro CO meter available Patient is pregnant, has abnormal cerebellar testing, COHb level of 25% or greater, exhibits cardiovascular dysfunction, continued abnormal mental status or had any of loss of consciousness or seizure?

YES

PATCH

Consider rapid transport to hyperbaric facility(3)

NO YES

NO Patient exhaled COHb level > 20%

Is patient symtomatic?

YES

NO

Transport to nearest medical facility for continued evaluation, treatment, and monitoring (2)

PATCH

Consider field treatment with no transport. Continue treatment with oxygen until COHb is <5% (or 10% in smoker) (2) (1) (2) (3)

Rescuers will be equipped with SCBA for extricating patients from hazardous environmentt. Continue measuring exhaled CO with Micro CO meter Q 15–30 minute intervals. Initiate preplanning with receiving facility. Refer to transfer guideline: Hyperbaric oxygen therapy for acute carbon monoxide poisoning.

FIGURE 7.16 Glen Canyon NPS decision logic for patient triage.

7.8 SUMMARY AND FUTURE DIRECTIONS On the positive side, in a span of just over 5 years, many agencies, companies, and individuals have joined to improve identification of marine CO poisoning, characterize risks, develop and evaluate control technologies, and launch a plethora of prevention programs. The resulting developments are impressive: (1) two manufacturers successfully developed low-emission marine generators that are on the market; (2) two major manufacturers developed and participated in testing of catalyzed inboard propulsion engines, with one introducing it in production engines; (3) devices for rerouting generator and propulsion engine exhaust were developed and tested; and (4) several states passed safe towing legislation or regulations.

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So what is left to do? We must remember that there are more than 12.8 million boats registered for use on US waters, more than 12 million of which are propelled by outboard, inboard, or sterndrive engines.75 The only engines that have emission controls are newly manufactured outboard engines and one inboard engine model. Thus, a large proportion of the gasoline-powered marine engines in use have no emission controls. Thus, even if EPA increases the scope of emission standards by regulating inboard and sterndrive engines, a lot of boats will continue to emit a lot of CO for a long time. EPA regulation of CO emissions for all marine engines is vital for prevention of marine CO poisonings. A reduction in automobile-related CO poisonings followed the EPA Clean Air Act regulations requiring emission control on automobiles.76 The same would likely follow similar requirements for marine engines. The key to improved prevention of boat-related CO poisonings lies in improved recognition and reporting. Until there is more comprehensive testing for COHb by physicians and those involved in death investigation, CO poisoning cases will continue to be missed. This results in inadequate or incorrect treatment of cases, related increased morbidity, inaccurate assignation of cause of death, and related failures in prevention. Development of standardized autopsy protocols, combined with more extensive training of the responding medical and law enforcement personnel to facilitate collection and transfer of adequate incident detail are needed for improved recognition. Adequately recognized poisonings must then be reported so that the full scope of the problem can be defined for prevention programs. Reporting of marine CO poisonings is low. This can be easily examined by comparing Lake Powell data for fatal and nonfatal boat-related CO poisonings, identified, and documented through extensive searches of EMS records, against Coast Guard data for reported CO poisonings. From 1990 through 2002, there were 13 fatal boat-related CO poisonings and 151 nonfatal boat-related CO poisonings requiring medical attention documented at Lake Powell (thus a total of 164 boat-related CO poisonings at that one lake). In that same period, Coast Guard data documented 170 injuries and 62 deaths related to CO reported from incidents across the entire country. Clearly, marine CO poisonings are not extensively reported to the Coast Guard. State Boating Law Administrators (the recognized reporting authority) should be encouraged to develop liaisons with other state-based surveillance efforts (i.e., state-based child fatality review boards, vital records departments, injury surveillance efforts), as well as Federal surveillance systems, to enhance identification and reporting of boat-related CO poisonings reporting. In addition, more extensive training of municipal law enforcement officers and first responders is needed, so that they can better understand the need to report CO poisonings. While developments in control have been impressive, implementation of new controls and retrofitting existing boats remains problematic, as evidenced by recent poisonings (not included in the 607 cases analyzed here). Recent Coast Guard data identified two new poisonings (one fatal + one nonfatal) related to entry into the “Death Zone”. Newspaper reports and related autopsy results document a June, 2006 death associated with ski-boat platform occupancy (COHb = 51%). The list of marine CO poisonings continues to grow.

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Boat manufactures must assess and address design features that attract occupancy at the back of the boat, redesigning to eliminate hazards. Consumer education, vital to the success of retrofit programs, must continue and increase. If boat owners don’t understand the problem, they won’t be motivated to go to the trouble of complying with recalls and consumer advisories. Failure of onboard CO detector/alarms raises concern about the impact of such devices in CO poisoning prevention. Improving the effectiveness of these devices is complex, as there were four types of problems identified, each indicating a different needed corrective strategy. Failure of functional detectors to warn occupants of high CO concentrations and the sounding of alarms for no discernable cause are related to much needed improvements in detector sensor technology. A likely explanation of disabling of detectors by boaters is that the detectors are sounding frequently and the boater either cannot identify a cause for the alarm (also a detector technology issue) or cannot resolve the issue that is causing CO to enter the cabin (an issue related to boat design, technology, and boater education). As has been documented here, quick death can and does occur from exposure to CO in the marine environment, even in the open air. Acceptance of this possibility remains difficult for technical audiences as well as consumers. Anecdotal accounts of medical examiners and hospital emergency departments failing or refusing to order COHb analyses related to incidents on boats continue. The need for increased awareness of the problem was recently underscored in the following quote by a family dramatically impacted by a teak surfing death: Unfortunately, widespread understanding of the issue among the boating public remains elusive. We still see kids teak surfing between wake boarding runs. Most people we talk to are surprised at the severity of the CO risk behind a boat. In spite of all our efforts, most seem not to realize the potential peril. I recently talked to two families from Canada who said they teak surfed all the time and were amazed when I told them it could be deadly. This risk is just not self-evident and consequently more kids die unnecessarily every year. Our family, the Dixey family, and people like us that have lost loved ones certainly know the costs of not knowing about or under-estimating this hazard. We who have now been warned have the responsibility to sound the dangers for others. By lifting our voice in warning, we can do our part to make sure that great kids don’t continue to die. This quote certainly applies to all types of gasoline-powered marine engines, all boaters, and to all deaths from this preventable cause of CO poisoning.

7.9 ACKNOWLEDGMENTS Much of the work described in this chapter, including initial recognition of the problem and call for engineering changes, would not have happened without my colleague and good friend, Dr. Robert Baron. I am grateful for his guidance, wisdom, and partnership. Thanks to Claire Babik, who has worked so hard for prevention in honor of the brother she lost. In addition, gratitude is owed to Tim Radtke; to National Park

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Service Rangers, Divers, Emergency Medical Technicians (EMTs), and Medics at GCNRA; and to the researchers at the National Institute for Occupational Safety and Health. All of these fine public servants have devoted many hours to the cause of identifying and preventing marine CO poisonings. I pay respect to the families that have lost so much to this unnecessary cause. And to my own family, I want to say thanks for everything.

References 1. USCG, Boating Safety Circular 58, A good way to die, US Department of Transportation, United States Coast Guard, June, 1984. 2. Simeone L.F. The intrusion of engine exhaust into the passenger areas of recreational power boats, United States Coast Guard Office of Navigation Safety and Waterway Services Report DOT-VNTSC-CG-91-1, 1991. 3. Simeone L.F. A simple carburetor model for predicting engine air-fuel ratios and carbon monoxide emissions as a function of inlet conditions, United States Coast Guard Report CG-079, 1990. 4. Silvers S.M. and Hampson N.B. Carbon monoxide poisoning among recreational boaters. JAMA, 274, 1614–1616, 1995. 5. American Boat and Yacht Council, A-24, Carbon monoxide detection systems, American Boat and Yacht Council, Inc., 1997. 6. Struttman T. et al. Unintentional carbon monoxide poisoning from an unlikely source, JABFP, 11, 481–484, 1998. 7. Huff J.S. and Kardon E. Carbon monoxide toxicity in a man working outdoors with a gasoline-powered hydraulic machine, NEJM, 320(23), 1564, 1989. 8. First M.W. and Murphy R.L.H. Carbon monoxide exposures from snow melting machines. Am Ind Hyg Assoc J., 31, 754–757, 1970. 9. Hampson N.B. and Norkool D.M. Carbon monoxide poisoning in children riding in the back of pickup trucks, JAMA, 267, 538–540, 1992. 10. Jumbelic M.I. Open air carbon monoxide poisoning, J Forensic Sci, 43, 228–230, 1998. 11. Easley R.B. Open air carbon monoxide poisoning in a child swimming behind a boat, South Med J, 93, 430–432, 2000. 12. GCNRA NPS, Investigative Report, Case 94-4012, Glen Canyon National Recreation Area National Park Service, 1994. 13. CDC, Houseboat-associated carbon monoxide poisonings on Lake Powell—Arizona and Utah, 2000. Centers for Disease Control and Prevention, Morbidity and Mortality Weekly Report, 49(49), 1105–1108, Dec 15, 2000. 14. NIOSH, Hazard evaluation and technical assistance report: 2000-0400 and 20020325, Glen Canyon National Recreation Area, Arizona and Utah, US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, 2005. Available http://www.cdc.gov/niosh/hhe/reports/pdfs/20000400-2956.pdf 15. US Coast Guard. Boating statistics—2004. US Department of Homeland Security, COMDTPUB P16754.17, 2005. Available http://www.uscgboating.org/statistics/ accident_stats.htm 16. 33 CFR 173.55, Vessel Numbering and Casualty and Accident Reporting, Code of Federal Regulations, Washington, DC, US Government Printing Office, Office of the Federal Register, 2002.

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Carbon Monoxide Poisoning 17. DOI, Boat-related CO poisonings on US waters national case listing, Safety Management Information System (SMIS), US Department of the Interior (DOI), 2006. Available http://safetynet.smis.doi.gov/cohouseboats.htm 18. CDC, Carbon-monoxide poisoning resulting from exposure to ski-boat exhaust, June 2002 - Georgia, Centers for Disease Control and Prevention, Morbidity and Mortality Weekly Report (MMWR) 51(37);829–830, September 20, 2002. Available http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5137a3.htm 19. CDC, Carbon monoxide poisonings resulting from open air exposures to operating motorboats—Lake Havasu City, Arizona, 2003. Centers for Disease Control and Prevention, Morbidity and Mortality Weekly Report, 53(15), 314– 318, April 23, 2004. Available http://www.cdc.gov/mmwr/preview/mmwrhtml/ mm5315a3.htm 20. McCammon, J.B. Letter to Joe Alston, Park Superintendent, Glen Canyon National Recreation Area from J.B. McCammon, NIOSH, CDC, PHS, DHHS, Denver, Colorado, July 31, 2001. Available http://safetynet.smis.doi.gov/teakfinal.pdf 21. Ritter G. Air monitoring for Connecticut Department of Environmental Protection Division of Conservation Law Enforcement boating accident reconstruction, Prepared by TRC Environmental Corporation, September 13, 2001. 22. McCammon J.B. et al. Letter to Joe Alston, Park Superintendant, Glen Canyon National Recreation Area, Page, Arizona, from J. McCammon (National Institute for Occupational Safety and Health, Centers for Disease Control), T Radtke (US Department of Interior), and DP Bleicher (National Park Service), December 3, 2002. Available http://safetynet.smis.doi.gov/searayfinal.pdf 23. GCNRA NPS Investigative Report, Case 2000-4627: Carbon monoxide testing, August 25, 2000, Glen Canyon National Recreation Area National Park Service, 2000. 24. Hall, R.M. and McCammon, J.B. Letter to Joe Alston, Park Superintendent, Glen Canyon National Recreation Area from R.M. Hall and J.B. McCammon, NIOSH, CDC, PHS, DHHS, Cincinnati, Ohio, November 21, 2000. Available http://safetynet.smis.doi.gov/HHE2powell.pdf 25. Hall, R.M. Letter to Dr. Rice Leach, Commissioner, Cabinet for Health Service, Commonwealth of Kentucky from R.M. Hall, NIOSH, CDC, PHS, DHHS, Cincinnati, Ohio, December 18, 2000. National Institute for Occupational Safety and Health Hazard evaluation and technical assistance report: 2001-0026. Available http://www.cdc.gov/niosh/hhe/reports/pdfs/2001-0026-letter.pdf 26. McCammon J.B. et al. Letter to Joe Alston, Park Superintendant, Glen Canyon National Recreation Area, Page, Arizona from J. McCammon (National Institute for Occupational Safety and Health, Centers for Disease Control), T. Radtke (US Department of Interior), and D.P. Bleicher (National Park Service), March 17, 2003. Available http://safetynet.smis.doi.gov/notoriousfinal.pdf 27. Dunn K. et al. An evaluation of an engineering control to prevent carbon monoxide poisonings of individuals on houseboats at Sumerset Custom Houseboats, Somerset KY, National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-26a, May, 2001 Available http://www.cdc.gov/niosh/surveyreports/pdfs/ectb-171-26a.pdf 28. NIOSH, Hazard evaluation and technical assistance report: 2002-0393, Lake Havasu Municipal Employees, Lake Havasu City, Arizona, February 2004, US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, 2004. Available http://www.cdc.gov/niosh/hhe/reports/pdfs/2002-0393-2928.pdf

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29. ACGIH, TLVs® and BEIs®. American Conference of Governmental Industrial Hygienists, 2006. 30. McCormick D. Personal communication, 2006. 31. NBSAC, Minutes of the National Boating Safety Advisory Council 67th meeting, Cleveland OH, 2001. Available http://www.uscgboating.org/nbsac/MtgMin/pdf/ 67thNBSAC_Minutes.pdf 32. USCG, US Coast Guard Recall website, accessed Jan 30, 2006. Searched for “generator exhaust” and “exhaust system”. Available http://www.uscgboating.org/ recalls/recalls_database.htm 33. EPA, Regulatory update: Overview of EPA’s emission standards for marine engines, Publication EPA420-F-04-031, August 2004. Available http://www.epa.gov/otaq/regs/ nonroad/marine/420f04031.pdf 34. EPA, Program Announcement: Marine engine manufacturer develops low emission inboard marine engines. Publication EPA420-F-06-057, July 2006. Available http://www.epa.gov/oms/regs/nonroad/marine/si/420f06057.htm 35. Roberts P. Unpublished data. Sonoma Technology Inc., Petaluma, California. 36. NASBLA, Safe practices for boat-towed watersports act. NationalAssociation of State Boating Law Administrators, 2005. Available http://www.nasbla.org/pdf/Model% 20Acts/new/Boat-Towed%20Watersports%2092105.pdf 37. The Pennsylvania Code, 105.3 Unacceptable boating practices, 2003. Available http://www.pacode.com/secure/data/058/chapter105/s105.3.html 38. California Code, Harbors and Navigation Code, Section 680-685, Anthony Farr and Stacy Beckett Boating Safety Act of 2004, 2004. Available http://www.leginfo.ca.gov/ cgi-bin/displaycode?section=hnc&group=00001-01000&file=680-685 39. Nevada Code, NAC 488.435 Prima facie evidence of reckless or negligent operation, 2004. Available http://www.leg.state.nv.us/NAC/NAC-488.html#NAC488Sec435 40. Oregon Legislative Assembly, Senate bill 56 amending ORS 830.990, 2005. Available http://www.leg.state.or.us/05reg/measpdf/sb0001.dir/sb0056.en.pdf 41. Washington Senate Bill 6364, An act relating to the regulation of recreational vessels; amending 2 RCW 79A.60.610; adding a new section to chapter 79A.60 RCW; adding new sections to chapter 88.02 RCW; creating a new section; prescribing penalties; and providing an effective date, 2005. Available http:// www.leg.wa.gov/pub/billinfo/2005-06/Pdf/Bills/Senate%20Passed%20Legislature/ 6364.PL.pdf 42. Utah Administrative Code R651-224. Towed Devices. Available at http://www.rules. utah.gov/publicat/code/r651/r651-224.htm R651-224-2. Unlawful Methods of Towing. 43. Taylor R.K. et al. National Marine Manufacturers Association carbon monoxide label study. Design Research Engineering, Novi, Michigan, 2005. 44. US Coast Guard Contract Number DTCG39-00-D-R0009, Task Order 01-F-00016, September 2002. 45. US Coast Guard, Houseboat industry workshop on carbon monoxide, Summary record, Lexington, Kentucky, May 3, 2001. USCoast Guard Office of Boating Safety, Recreational Boating Product Assurance Division, Report prepared by Potomac Management Group. 46. Earnest G.S., Beamer B., and Dunn K.H. Evaluation of side exhaust and prototype and production emission control devices to prevent carbon monoxide poisonings on houseboats. National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-29a, May 2002. Available http://www.cdc.gov/niosh/surveyreports/pdfs/ectb-171-29a.pdf

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Carbon Monoxide Poisoning 47. Dunn K.H. et al. Comparison of a dry stack with existing generator exhaust systems for prevention of carbon monoxide poisonings on houseboats. National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-28a, August 2001. Available http://www.cdc.gov/ niosh/surveyreports/pdfs/ectb-171-28a.pdf 48. Earnest G.S. et al. An evaluation of an engineering control to prevent carbon monoxide poisonings of individuals on houseboats. National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-25a, March 2001. Available http://www.cdc.gov/niosh/surveyreports/pdfs/ectb171-25a.pdf 49. Earnest G.S. et al. An evaluation of an emission control device, exhaust stack, and interlock to prevent carbon monoxide poisoning of individuals on houseboats. National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-27a, August 2001. Available http://www.cdc.gov/niosh/surveyreports/pdfs/ectb-171-27a.pdf 50. NIOSH, Evaluation of two exhaust stack configurations on two houseboats at Table Rock Lake, Missouri. HETA Report Number 2003-0318-2936. Cincinnati, OH: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, June 2004. Available http://www.cdc.gov/niosh/hhe/reports/pdfs/2003-0318-2936.pdf 51. Earnest G.S. et al. An evaluation of vertical exhaust stacks and aged production emission control devices to prevent carbon monoxide poisonings from houseboat generator exhaust. National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-32a, October 2003. Available http://www.cdc.gov/niosh/surveyreports/pdfs/ectb-171-32a.pdf 52. Hammond D.R. and Marlow D.A. Followup evaluation of design changes to a houseboat generator exhaust stack system. National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-34a2, July 2004. Available http://www.cdc.gov/niosh/surveyreports/pdfs/ectb-171-34a2.pdf 53. Hammond D.R., Earnest G.S., and Hall R.M. An evaluation of factors that might influence exhaust stack performance to prevent carbon monoxide poisonings from houseboat generator exhaust. National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-34a1, January 2004. Available http://www.cdc.gov/niosh/surveyreports/pdfs/ectb-171-34a1.pdf 54. Hammond D.R. et al. An evaluation of conditions that may affect the performance of houseboat exhaust stacks in prevention of carbon monoxide poisonings from generators, JOEH, 3, 308–316, June, 2006. 55. ZimmerA.T., Earnest G.S., and Kurimo R.An evaluation of catalytic emission controls and vertical exhaust stacks to prevent carbon monoxide poisonings from houseboat generator exhaust. National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-36a, September 2005. Available http://www.cdc.gov/niosh/surveyreports/pdfs/ectb-171-36a.pdf 56. Dunn K.H. et al. Carbon monoxide and houseboats, Prof Safety, 48, 47–57, Nov., 2003. 57. Earnest G.S. et al. An evaluation of an engineering control to prevent carbon monoxide poisonings of individuals on and around houseboats, AIHAJ, 63, 361–369, May/Jun, 2002. 58. Earnest G.S. et al. An evaluation of catalytic emission controls to prevent carbon monoxide poisonings from houseboat generator exhaust. National Institute for Occupational Safety and Health/Division of Applied Research and

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Technology/EPHB Report 17/-38a, October 2006. Available http://www.cdc.gov/ niosh/surveyreports/pdfs/ectb-171-38a.pdf Kohler, Press Release: New generation gasoline generators from Kohler reduce carbon monoxide emissions by 99 Percent. Kohler Power Systems, Kohler WI. August, 2005. Available http://www.kohlerpowersystems.com/pr/GasolineEmission_2005.html Carlan K, Mastry Engine Center Presentation at the 2004 USCoast Guard / ABYC Carbon Monoxide Workshop, IBEX 2004, Miami Beach, FL, October 27, 2004. Minutes of the meeting available at http://safetynet.smis.doi.gov/miami10-04_cominutes.pdf; presentation slides available at http://safetynet.smis.doi.gov/miami10-04_slides.pdf ABYC, TH-23: Design, Construction, and Testing of Boats in Consideration of Carbon Monoxide, American Boat and Yacht Council, Edgewater, Maryland, 2004. ABYC, P-1: Installation of Exhaust Systems for Propulsion and Auxiliary Engines, American Boat and Yacht Council, Edgewater, Maryland, 2002. Earnest, G.S. et al. Carbon monoxide emissions and exposures on recreational boats under various operating conditions. Lake Mead, Nevada and Lake Powell, Arizona. National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-05ee2, February 2003. Available http://www.cdc.gov/niosh/surveyreports/pdfs/ectb-171-05ee2.pdf Echt, A. et al. Carbon monoxide emissions and exposures on recreational boats under various operating conditions, Lake Norman, N.C. National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-31a, April 2003. Available http://www.cdc.gov/niosh/surveyreports/pdfs/ectb171-31a.pdf USCG and ABYC, Carbon monoxide safe distance study. US Coast Guard, American Boat and Yacht Council, September 2003. Mann, L.W. Carbon monoxide exposure while operating an inboard boat and related water sports activities. [Online] Available at http://www.FreshAirExhaust.com (Accessed July 2004). Marlow D.A. et al. Evaluation of the “Fresh Air ExhaustTM ” system to reduce carbon monoxide exposure during motor boating and wake surfing. National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-35a, August 2004. Available http://www.cdc.gov/niosh/surveyreports/pdfs/ectb-171-35a.pdf Marlow D.A., Hammond D., and Earnest G.S. Evaluation of the SideswipeTM exhaust system to reduce carbon monoxide poisoning during motor boating and wake surfing. National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 171-37a, December 2005. Available http://www.cdc.gov/niosh/surveyreports/pdfs/ectb-171-37a.pdf Hall R.M. et al. Case study: Evaluation of carbon monoxide emissions from engines on recreational boats equipped with prototype catalysts, JOEH 3(2), D4-D7, Feb., 2006. White J.J. Cleaner pleasurecraft: Lower-emission boats may be coming soon to a lake near you, Southwest Research Institute, 2004. Available http://www.swri.org/3pubs/ttoday/summer04/craft.htm Carroll J.N. Catalyzed marine engine saltwater durability, Presentation by Southwest Research Institute at the USCG Carbon Monoxide Seminar, Miami, Florida, October 2005, Minutes and presentation available from American Boat and Yacht Council, 3069 Solomon’s Island Road, Edgewater, Maryland, 21037. Indmar, Press release: Indmar introduces first production catalyst for inboard engines. Indmar Products Co., Millington TN. March 7, 2006. Available http://www.indmar.com/news/newsroom_article.cfm?id=31

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Carbon Monoxide Poisoning 73. Garcia A., Beamer B., and Earnest G.S. In-depth survey report of carbon monoxide emissions and exposures on express cruisers under various operating conditions, National Institute for Occupational Safety and Health/Division of Applied Research and Technology/EPHB Report 289-11a, January 2006. Available http://www.cdc.gov/niosh/surveyreports/pdfs/ECTB-289-11a.pdf 74. Hampson N.B. and Weaver L.K. Noninvasive CO measurement by first responders: A suggested management algorithm, Elsevier Public Safety, Lethal Exposure, Supplement to J. Emerg. Med. Services, 10–12, Spring, 2006. 75. NMMA, 2005 recreational boating abstract. National Marine Manufacturers Association, 2005. Available http://www.nmma.org/facts/boatingstats/2005/files/ populationstats3.asp 76. Mott J.A. et al. National vehicle emission policies and practices and declining US carbon monoxide-related mortality. JAMA, 288, 988–995, 2002. 77. EPA, Air quality criteria for carbon monoxide, Publication No. EPA-600/8-90/045F, US Environmental Protection Agency, Washington, D.C., 1991. 78. WHO, Environmental health criteria 213 - carbon monoxide (Second Edition), World Health Organization, Geneva, ISBN 92 4 157213 2 (NLM classification: QV 662) ISSN 0250-863X, 1999. 79. NIOSH, Recommendations for occupational safety and health: Compendium of policy documents and statements, US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, DHHS (NIOSH) Publication No. 92–100, 1992. 80. ACGIH, 2005 TLVs® and BEIs®: threshold limit values for chemical substances and physical agents. American Conference of Governmental Industrial Hygienists, 2005. 81. CFR 29 CFR 1910.1000, Code of Federal Regulations, Washington, D.C., US Government Printing Office, Office of the Federal Register, 1997.

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8

Application of Warnings and Labels for Carbon Monoxide Protection Gary Hutter

CONTENTS 8.1 8.2

8.3

8.4 8.5

8.6

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Characteristics of Carbon Monoxide Formation and Movement as Related to Warnings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.2.1 Physical Characteristics of Carbon Monoxide . . . . . . . . . . . . . . . . . . . . 8.2.2 Combustion and Formation of Carbon Monoxide . . . . . . . . . . . . . . . . 8.2.3 Buoyancy, Migration, and Dilution of Carbon Monoxide . . . . . . . . 8.2.4 Exit Velocity Considerations for Different Carbon Monoxide Producing Equipment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.2.5 Absorption and Dissipation of Carbon Monoxide . . . . . . . . . . . . . . . . Common Sources of Carbon Monoxide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.3.1 Consumer Products . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.3.2 Industrial Products and Processes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . What are Warnings, Labels, Instructions, and Other Forms of Communications? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The Content, Configuration, and Design of Labels, Warnings, and Instructional Materials . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.5.1 Design of Labeling and Warnings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.5.2 Written Instructional Information on Safety Materials . . . . . . . . . . . 8.5.4 Workplace Area Warnings and Labeling . . . . . . . . . . . . . . . . . . . . . . . . . . 8.5.4.1 Examples of General OSHA Warning Signage . . . . . . . . . 8.5.4.2 Examples of Specific OSHA Exposure Warning Signage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.5.4.3 Other OSHA and Industry Warning Criteria . . . . . . . . . . . . The Reasons, Rationale, and Scientific Bases for Providing Safety Information for Carbon Monoxide with Selected Examples . . . . . . . . . . . . . 8.6.1 Ethical and Philosophical Reasons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.6.2 Research Basis: the Need for Safety Information . . . . . . . . . . . . . . . . . 8.6.3 Voluntary Standards for CO Warnings (Examples in Chronological Order) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.6.4 Mandatory Safety Information Regulations . . . . . . . . . . . . . . . . . . . . . . .

198 198 198 199 200 202 204 204 204 205 206 206 207 209 211 211 212 213 214 214 216 219 219 197

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8.6.4.1 State-Based Examples . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.6.4.2 Federal Government Examples. . . . . . . . . . . . . . . . . . . . . . . . . . 8.6.5 The Custom and Practice of Carbon Monoxide Safety Information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.6.6 Litigation-Driven Safety Information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

223 223 224 227 230

8.1 INTRODUCTION Other chapters in this book discuss about the chemical, physical, toxicological, and health concerns of exposure to carbon monoxide (CO). This chapter addresses warnings, labeling, instructions, and other communication modes (i.e., safety information) about the hazards of exposure to CO. This chapter addresses (1) the conditions that may lead to the static and variable formation of CO, (2) characteristics that may impact the need to provide user-safety information, (3) common sources of CO, and (4) the characteristic movement of CO through the air that may prompt a need for user-safety information. The mid-portion of the chapter discusses the functions, criteria, research, and basis for CO safety information. Finally, details about the current practices in communicating this information to those who are potentially exposed to CO is provided. Examples of codes, standards, and recommended practices are offered, and real-life examples of warnings, labeling, and instructions are provided from products currently in the stream of commerce. Under some subject headings, the impact of the subject on the need for warnings are provided.

8.2 CHARACTERISTICS OF CARBON MONOXIDE FORMATION AND MOVEMENT AS RELATED TO WARNINGS To understand better why CO exposure necessitates warning for the at-risk population, it is helpful to know the characteristics of CO that influence its hazardous nature.

8.2.1 PHYSICAL CHARACTERISTICS OF CARBON MONOXIDE CO is extremely toxic. It is often called a poison. It causes a broad array of symptoms that precede possible death. Kandarjian1 list 22 different symptoms that arise from CO exposure. (There are actually many more symptoms, signs, and conditions that can result from CO exposure.) CO is an invisible, odorless, nonirritating, and tasteless gas that in and of itself has no (or extremely poor) sensory warning characteristics for those exposed. This fact contributes to the insidious nature of CO exposure. However, some combustion processes that release CO also produce aldehydes and/or particles that have distinct odors, which may alert someone to the possible presence of CO. This is more likely

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to occur from the combustion of solid (wood, charcoal) or liquid fuels (fuel oil), and is much less likely to occur from the refined gaseous fuels (e.g., methane, propane, butane). Natural gas and propane often have odorants added to the fuel mixture for leak detection purposes. Unfortunately, they are typically consumed in the combustion process, which eliminates the benefit of possible olfactory warnings. Under unusually poor combustion processes containing these odorants, some of the odor may be detectable in the exhaust stream. (It has been suggested that a substance be used that only gives odor when there is incomplete combustion, but none with complete combustion.) Labeling Implications: Carbon monoxide has poor sensory warning characteristics.

8.2.2 COMBUSTION AND FORMATION OF CARBON MONOXIDE Carbon-containing fuels that generate CO may originate as solids (e.g., charcoal, wood), liquids (e.g., kerosene, gasoline), or gases (e.g., methane, propane, butane). The combustion process actually takes place with the hydrocarbon components in the gaseous phase even though they may originate from a solid or a liquid. Therefore, the following discussion is written in terms of the gas phase of the fuel component. Given the correct initial conditions, carbon (typically from a hydrocarbon molecule) and oxygen will react to initially form CO as an intermediate compound, with carbon dioxide as the final product of combustion. CO generation as the final product of combustion is most often the result of interruption of the combustion process at the intermediate step (quenching) and incomplete combustion of carbon-containing materials. Stoichiometry is the evaluation of the fuel and air ratios associated with combustion efficiency of the gas phase. In theory, at an ideal stoichiometric mixture of carbon-based fuels, there would be sufficient amounts of oxygen, on a mass basis, to react with all of the carbon. This would allow the oxidation reaction to go to completion. In this case, there would be no CO remaining. An obvious corollary is that under insufficient oxygen conditions, CO is produced because there are not enough oxygen molecules to react completely with the carbon molecules. This incomplete combustion can be done intentionally, as is the case with iron ore refining blast furnaces or coke ovens. Both these processes intentionally operate under nonideal (oxygendeficient) stoichiometric conditions to refine (chemically reduce) the iron oxide to iron, and to thermally distill coal into coke. In both these processes, large amounts of CO are intentionally produced (
1%), are an unavoidable part of the process, and are recovered as a fuel for other operations. Oxygen-deficient combustion that leads to the formation of CO can also be unintentional. This occurs because of restricted air supplies, inadequate exhaust gas management, or an overabundance of fuel. Examples of these scenarios include (1) comfort heating furnaces that are installed in closet-like locations with insufficient fresh (combustion) air supply vents, (2) chimneys that have developed internal blockages, and (3) burners that incorporate jets and/or orifices for the passage of

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gaseous carbon fuels of different molecular weights (such as natural gas furnaces fueled with propane). All of these conditions can result in combustion problems and the subsequent generation and release of CO into people’s houses or other living spaces. A less obvious condition that leads to the formation of CO occurs when stoichiometrically correct ratios of carbon and oxygen do not have sufficient time, molecular intimacy, or energy (in the form of heat) in a combustion process to completely react, resulting in an interrupted or incomplete reaction. To avoid these conditions, gaseous fuels are often premixed with the combustion air in a turbulent fashion to provide the time and contact for a complete reaction. For example, in gas burners there are various fuel jets and mixing chambers that swirl the air and fuel together. This facilitates the dispersion of oxygen within the combustible fuel, and thus enhances combustion. Combustion temperatures influence the creation of CO, and reflect the heat available for a carbon–oxygen reaction to go to completion. These temperatures are typically controlled so that there is sufficient energy available for completing the reactions. Quenching the temperatures can shift the reaction kinetics and allow some of the carbon to react only to the CO state, resulting in the presence of CO in the exhaust. In low-temperature combustion processes, a catalyst can be used to lower the threshold combustion temperatures. This method better assures complete combustion and is used in catalytic heaters and reactors. Combustion processes depending on catalytic reactions are prone to the elevated formation of CO if the catalyst becomes damaged or poisoned. Finally, even well-managed combustion mixtures of carbon-based fuels and air can produce some finite quantity of CO simply because the processes are not ideal. Incomplete combustion occurs, and if not vented properly can result in the formation of even greater amounts of CO. For example, natural gas in a stove-top burner or oven may produce several parts per million (ppm) of CO,2 especially when at low settings. The CO is then diluted in the relatively large space of a typical home kitchen. The same stove-top burner or oven, operating under the same conditions in a small camper or motor home, results in higher concentrations of CO because of reduced dilution and the decline of oxygen content in the surrounding feed-air supply. These various combustion scenarios all produce CO concentrations, mass amounts, and temporal exposure variations that may repeatedly alternate from harmless, to chronic exposure levels, to acute exposure levels. Because of this, exposures may go unnoticed until a dangerous or even deadly situation occurs. Labeling Implications: The combustion processes most often associated with the production of CO can and do vary significantly due to small changes in ambient or process conditions resulting in situations where little CO is produced to situations where significant amounts of CO are produced.

8.2.3 BUOYANCY, MIGRATION, AND DILUTION OF CARBON MONOXIDE CO has a molecular weight close to that of air (CO = 28, Air = 28.9) and following the ideal gas laws would have approximately the same density as air across

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the normal ambient temperature range. This would tend to make the gas neutrally buoyant; neither wanting to migrate upward or downward due to density differences when released into the environment. Therefore, if room temperature gas with CO escaped from a calibration tank, it would not pool on the floor or raise to the ceiling. Rather, its movement would be affected by the forces of the pressure drop at the leak, concentration-driven diffusion, Brownian movement, and local air disturbances.3 [Of course once mixing of the CO and air (oxygen, nitrogen, etc.) molecules occurs, separation of the molecules cannot take place once again without the addition of large amounts of energy, lest it violate the Second Law of Thermodynamics.] CO does not have any unusual adiabatic heat loss or gain characteristics. Therefore, it does not have a vertical lapse rate that is different from air, and there are no additional internal physical driving forces on it. Under local atmospheric “inversion” conditions, ambient temperature CO would move similar to other neutrally buoyant gases. On the other hand, certain conditions can cause CO to move upward. CO recently produced by a combustion process (e.g., in a residential furnace or boiler) is apt to be warmer than the surrounding ambient air, and therefore will be thermally buoyant and migrate upward, at least initially. For example, a few inches from the combustion zone of propane heaters, gases are typically several hundred degrees Fahrenheit above ambient temperatures. The extent of this temperature-driven density difference and accompanying upward migration is controlled by the ability of the exhausting plume to maintain the boundary of its thermal envelope. Further, mechanisms like cross air movement and heat sinks cause a loss of heat and buoyancy. These air movements and heat sinks can quickly inhibit further vertical movement. Certain conditions can also cause CO to migrate large distances. For example, the continual release of hot exhaust gases that contain CO (e.g., a leak in a basement furnace) produce their own convection currents that can effectively fumigate distant areas. A furnace located in a cooler portion of a building can release products of combustion—including CO—that move along the colder building cavities and migrate several floors above the original leak. This phenomenon is enabled by nonthermal volumetric expansions of simple gaseous carbon fuels due to changes in pressure (e.g., from a pressurized cylinder), and by the increased number of moles of gas in the by-products. The basic combustion equations for methane, ethane, propane, and butane are given in Table 8.1. Comparing the volume (or moles of gas) in the products of combustion (VP) to the volume of the reactants (VR), reveals a positive volumetric change for all but methane during the combustion process. Dilution of airborne gaseous contaminants typically follows an exponential decay profile. Ten thousand (10,000) cu. ft. of gas containing 500 ppm would require another 10,000 cu. ft. of clean dilution air to reduce the concentration to 250 ppm. It would take another 20,000 cu. ft. of dilution air (10, 000 + 20, 000 = 30, 000 cu. ft.) to reduce the concentration to 125 ppm; and a total dilution of 90,000 cu. ft. of dilution air (100,000 − initial 10,000 cu. ft. = 90,000 cu. ft.) would be required to reduce the level to the Occupational Health and Safety Administration (OSHA) 50 ppm PEL. Hence, a short-term release of 10,000 cu. ft. of exhaust from a furnace containing 500 ppm CO would need to be diluted into 90,000 cu. ft. along its path before it is

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TABLE 8.1 Volumetric Expansion Due to Reaction and Released Heat from Reaction Gas Methane Ethane Propane Butane

Ideal combustion equation

VP/VR

CH2 + 2O2 = CO2 + 2H2 O CH2 H6 + 3.5O2 = 2CO2 + 3H2 O C3 H8 + 5O2 = 3CO2 + 4H2 O C4 H10 + 6.5O2 = 4CO2 + 5H2 O

3/3 5/4.5 7/6 9/7.5

Heat released (BTU/ft3 average) 1100 2500 3200

500

CO (ppm)

400 300 200 100

20,000 40,000

60,000 80,000

100,000

Total Volume of Air to Dilute Concentration

FIGURE 8.1 Effect of dilution on concentration.

reduced to 50 ppm. This exponential dilution decay mechanism allows for significant migration before the gas is rendered harmless (Figure 8.1). Labeling Implications: On the basis of molecular weight, CO is neutrally buoyant. It is thus more likely to move from its originating combustion process based on its thermal buoyancy. This buoyancy is more profound under conditions of greater temperature differential and with prolonged and continued releases compared to smaller “puff” releases. There are additional forces driving volumetric changes resulting from the combustion process. Owing to these characteristics, the contaminant moves in significantly variable ways depending on seasonal and ambient conditions.

8.2.4 EXIT VELOCITY CONSIDERATIONS FOR DIFFERENT CARBON MONOXIDE PRODUCING EQUIPMENT Some mechanisms that release CO have attached exhaust systems, so the exiting gases may have considerable range in their volumetric flow rates and initial exit velocities.

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The role that this range in exit velocity plays in the dispersion and distribution of the exhaust gas can be deceptive. For example, consider an engine’s exhaust system (seen in cars, construction vehicles, small gasoline-powered engines). These exhaust systems often accommodate at least an order of magnitude change in volumetric exhaust flow across their normal operation range. Under low speed operation, the volume of gases, and their ability to be propelled to a great distance from their exit point, may be extremely low. At high speeds, the velocity at the point of exit may be significantly greater. The general rule of thumb is that at approximately 20 diameters away from the exit point, the horizontal velocity has dropped to 10% of its initial value.4 Hence, it is a myth that the exhaust plume from most conventional engines can be propelled great distances backwards from their initial release point. In many combustion processes that have dedicated exhaust systems, there are relatively small changes in volumetric exhaust flow during normal operation. Furnaces, hot water heaters, and boilers are examples of this category of equipment, and they are typically operated at a constant firing rate, with burners either on or off. Thermal efficiency may be a consideration in the purchase of these devices, and therefore they are designed to achieve low exhaust gas temperatures, and incorporate large diameter exhaust systems to lower the resistance to exhaust flow, and sometimes utilize flue dampers5 to conserve heat during the “off” portion of the operation. Owing to the relatively small, thermally induced pressure differential in these systems, it is common to see some back flow and/or spillage of combustion products into the area where this equipment is located, at least under initial start-up conditions.6 The duration, cause, and consistency of this is highly dependent on the maintenance of the system, ambient conditions, and weather conditions. The footprint of this gas “spillage” is a sooty residue on air supply vents in residential furnaces and hot water heaters. While a small amount of “spillage” may be acceptable, consistent spillages can result in chronic exposure conditions. Some combustion sources do not have exhaust systems with well-defined exit velocities (e.g., stoves, welding torches, portable heaters). These devices exhaust directly into the area they operate in. They depend on their small size, clean exhaust, or area ventilation for the removal and dilution of the CO that they may produce. This is problematic when combustion is high in CO content, or when proper ventilation is not present. There have been numerous situations in which industrial welders or torch operators have been overexposed because they were working in a location with a poor ventilation system. Further, campers have been injured or killed because they used a portable heater or other combustion process in a tent that they thought was naturally ventilated. Labeling Implications: Automobile or other engine-powered equipment do not project their exhausts a significant distance horizontally due to high exit velocities; thermal effects are probably a greater driving force for movement of the CO. Installations with low forced exit velocities and low thermal content depend on their mechanical state of repair and ambient conditions for removal of the products of combustion. For CO removal, systems without dedicated exhaust systems rely heavily on the user, and on factors associated with their location.

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8.2.5 ABSORPTION AND DISSIPATION OF CARBON MONOXIDE CO is preferentially absorbed in comparison to oxygen. CO absorption and purging times (body dissipation time) from the blood system are a function of rate of respiration, and the oxygen content in the subsequent breathing air. The respiratory system is the only significant pathway for excretion of CO. The removal of the CO-exposed person and the introduction of oxygen-enriched breathing air are the most common means of removing CO from the body. The intravenous addition of blood can dilute the total amount of CO held within the body, but there are limits to the quantity of blood that can be added. Absorbed mass or body burden is a function of the rate of uptake and the size of the person. This means that large people generally take up a larger amount of CO than people with smaller body mass. Individuals who have a higher respiratory (i.e., ventilatory) rate will also take up CO faster. People with compromised respiratory systems, decreased levels of hemoglobin, or circulatory system problems are more at risk. Accelerated rate of absorption due to higher CO concentrations during exposure may compress the normal display of symptoms, whereas slower or chronic exposure may produce progressive steps in the symptomology. Symptoms may include flulike conditions, nausea, headache, sleepiness, and so forth followed by confusion, decreased cognitive capability, and unconsciousness. Variants in the symptoms of CO and variations among individuals can result in (1) CO exposures that go undiagnosed, (2) chronic exposures that cause long-term health problems, or (3) loss of consciousness and death. Safety and accident history information indicate that a significant percentage of total CO nonworkplace deaths occur through the use of camping and heating equipment that is used under poorly vented conditions, and from malfunctioning furnaces and water heaters. Both groups could benefit from warnings.

8.3 COMMON SOURCES OF CARBON MONOXIDE CO is associated with the following sources and locations:

8.3.1 CONSUMER PRODUCTS • Automobile and truck internal combustion engines (typically gasolinefueled types) • Cigarettes and side stream smoke • Combustion of charcoal/gas grills (typically propane) • Camp lanterns/stoves/gas or liquid fuel • Fire places, chimneys, flues, flue damper • Gasoline-powered engine implements: Lawn mowers Snow blowers High-pressure washers

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• • • • • •

205

Power generators Air compressors Chain saws Hot water heaters (gas or oil) Kitchen stove burners and ovens (gas and propane fired) Motor boats, house boats Portable and stationary gas, liquid, and solid-fueled comfort and camp heaters Residential furnaces (gas or oil) Wood burning furnaces and heaters

8.3.2 INDUSTRIAL PRODUCTS AND PROCESSES • • • • • • • • • • • • • • • • • • • •

Blast furnaces Boiler operations (typically gas or oil) Calibration gases Cement kilns Chemical manufacturing (e.g., methanol, formaldehyde, ethylene) Coke ovens Construction site combustion space heaters Fuel gas generators (e.g., water gas, coal gas, producer gas) Gasoline engine powered tools and equipment Heat treating ovens (typically gas or oil) Industrial furnaces and space heating furnaces (gas, liquid, solid fuel) Industrial trucks and vehicles (typically gasoline or propane) Inert atmosphere generators Inhaling methylene chloride vapors (metabolizes to CO) Material handling/receiving docks (industrial trucks) Meat packaging additive Metallic ore refining Sewers and other underground structures Welding and torching operations Production of reducing oxides

This list demonstrates the ubiquitous consumer and industrial sources of CO. History has documented the numerous deaths and injuries associated with unexpected exposures. This situation has prompted the codification of methods to provide warnings and to investigate such hazards. Subsequent sections detail warning information; and an example of this investigation codification in contained in ASTM E2292-03 Standard Practice for Investigating Carbon Monoxide Poisoning Incidents. The scope of that standard states 1. Scope 1.1. This practice covers guidelines for collecting and preserving information and physical evidence related to incidents involving the poisoning of individuals by carbon monoxide.

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8.4 WHAT ARE WARNINGS, LABELS, INSTRUCTIONS, AND OTHER FORMS OF COMMUNICATIONS? In the context of this chapter, the phrase “warnings, labeling, instructions, and other forms of communications” (e.g., safety information) refers to those textual messages, words, pictures, alarms, and figures that are intended to eliminate or mitigate possible exposure to CO by alerting the person at risk, informing the person at risk, or reminding the person at risk of possible dangers. This last function of warnings to remind is especially important in situations where use of the equipment is highly intermittent, as may occur with seasonal camping equipment; or under circumstances where the manifestation of the hazard of CO may be transient. These warning items may appear as a label or tag directly on the product. They may be a part of the products’ packaging that includes depictions of the use of the product, or part of an instructional insert in the packaging. They may be a workplace sign or alarm that indicates when elevated levels of CO are detected. Warnings can be found in manuals that accompany products, or in locations where the products are used. There are also brochures compiled by CO hazard awareness advocate organizations. Many of these warning materials are now also available on the Internet or as inserts in promotional literature. This safety information is based on philosophical issues, safety research, voluntary, or regulatory requirements, the custom and practice of a given industry, or is litigation driven. Regardless of the forces at play, safety efforts have manifested themselves in a broad variety of warning schemes and warning materials.

8.5 THE CONTENT, CONFIGURATION, AND DESIGN OF LABELS, WARNINGS, AND INSTRUCTIONAL MATERIALS The term “label” is generally associated with writing or graphics that are attached to a product. Warnings may be a part of that “attached” label. They can also be included in other locations such as on the product packaging or on inserts provided within the packaging. The word warning itself is used as a specific “signal word” within a properly designed warning scheme. Warnings or safety information may also be found in certain locations rather than “on” a product. It is normal to see various warnings in the instructions, on packaging, and on doors and in areas of industrial facilities. Complicated safety instructions may be difficult to apply to an individual machine or use in an industrial setting, whereas some consumer products will have fairly detailed safety-related instructions. Instructions may also be a stand-alone item that contains both operational instructions and safety information. Usually when there are warnings that are difficult to actually apply to the product (e.g., or will not survive the life or usage of the product), there will be an instruction on the product to consult or “read the instructions” before operating or performing certain functions. On some products, there may even be a pouch or a compartment so that one can store the safety instructions along with the product.

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Arecent development on some chemical containers for lawn, garden, and pesticide products is a “fold out” label that provides additional space for written information.

8.5.1 DESIGN OF LABELING AND WARNINGS Although there is some latitude about the configuration and content of labeling, certain designs have become generic. Typically, the signal words of “Notice,” “Caution,” “Warning,” and “Danger” and the associated colors of blue, yellow, orange, and red are progressive with increasing degrees of danger (Figure 8.2). Often a triangular shape with an exclamation point or lightening bolt in its center is used to denote that the sign is related to safety concerns (Figure 8.3). These are called alert symbols. Typically, product warnings have well-defined borders or textual boxes containing the different elements of the warning. Figure 8.4 identifies 8 of the common elements of warnings based on a review of 11 publications addressing the design and configuration of warnings as tabulated in Table 8.2. Several American National Standards Institute (ANSI) standards provide guidelines on the minimum size of font height for warning signs, with 0.08 in. height being the minimum at a viewing distance of 1 ft. or less, 0.16 in. at 5 ft., and 0.22 in. at 8 ft. Konz,4 Woodson,7 McCormick and Sanders,8 and other authors on human factors provide considerations on the display of information with respect to letter size and readability, reading speeds, configurations, and conditions that may lead to errors in reading content. Table 8.2 compares the contents of 11 publications9−19 on 12 items related to the contents of warnings and shows a consistency across these items.

Pictorial

Your information here

Pictorial

Your information here

Pictorial

Your information here

Pictorial

Your information here

FIGURE 8.2 ANSI 535.2 type labels.

FIGURE 8.3 Typical alert symbols ANSI, ASAE, and SAE.

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Signal word Alert symbol Symbols & pictograph

DANGER Standard border

Hazard identification Result of ignoring warning

How to avoid hazard

Additional information

FIGURE 8.4 General vertical layout for warming label.

TABLE 8.2 Documents (A–K) Addressing Labeling/Warning Content Items (1–12) Content items 1. Hazard alert/symbols 2. Signal word 3. Color(s) 4. Symbols and pictures 5. Hazard identification 6. Result of ignoring hazard 7. How to avoid hazard 8. Location of label 9. Font size 10. Contents disposal 11. Material/durability 12. Fire/handling/Ref.

A9

B10

C11

D12

E13

F14

G15

H16

I17

x x x x x x x x x x

x x x x x x x

x

x

x

x x x x x x x

x

x x x x x x x x x x

x

x

x x x x x x x x x

x x

x

x

x

x

x

x x x

x

J18 x x x x x x x x x

K19 x x x x

x x

x

One other labeling approach included in the ANSI standards is ANSI A13.120 for piping systems. It includes a color scheme, arrows to indicate the direction of flow, a signal word to identify the chemical content, and font size requirements. In a section entitled “Legal/Litigation Driven” there is an additional discussion of the contents of warnings/labels based on court decisions and legal interpretation. There are other places and products where specific warning designs are required by regulation and may not follow the criteria referred to above. The most ubiquitous of these is one of the warnings on cigarette packages (Figure 8.5). This particular warning is required by specific legislation,21 and does not conform to the criteria often found in the standards and guidelines for CO warnings.

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“SURGEONS GENERAL’S WARNING: Cigarette Smoke Contains Carbon Monoxide”

FIGURE 8.5 U.S. Government required CO warning on cigarette packages.

8.5.2 WRITTEN INSTRUCTIONAL INFORMATION ON SAFETY MATERIALS Safety instructions may require more space than is available on a label. In these cases instructions are described in a separate document. It is common to see warnings within manuals and other instructional materials that have the general appearance of an “on-product” warning, but are instead found in the accompanying materials. An example of a CO warning that is found with a product manual is shown in Figure 8.6. These messages are either bundled together into one section of the product literature or distributed in various sections of the literature. The Handbook of Technical Writing22 contains guidelines for the writing style that may be used in composing instructional materials. Writing and Designing Operator Manuals15 provides strategies for the composition and detail of safety manuals. The content found in these publications is the basis for instructional warnings about CO. Various gasoline engine-powered equipment have warnings in their instructional manuals about CO. Exemplar of this is the American Honda Motor Company Owner’s Manual23 for a line of small displacement engines that are used on lawn mowers, small portable generators, power washers, air compressors, and snow throwers. Their manual starts out with a brief discussion of what “Safety Messages” mean and how to identify them by a safety symbol, a signal word, and the box-like border around them. The manual uses the word “Warning” and the alert symbol and addresses the carbon monoxide hazard by stating Carbon monoxide gas is toxic. Breathing it can cause unconsciousness and even kill you. Avoid any areas or actions that expose you to Carbon monoxide.

This manual also contains a text under the title “Safety Information” that states Your engine’s exhaust contains poisonous carbon monoxide. Do not run the engine without adequate ventilation, and never run the engine indoors.

Under “Maintenance Safety,” there are additional “Safety Precautions” that state Carbon monoxide poisoning from engine exhaust. Be sure there is adequate ventilation whenever you operate the engine

(It should be noted that the exhaust emissions are met in part by the use of a catalytic converter system.)

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_____________________________________________________________________________________________ Instruction Manual: COSTAR® P-1, 9V Personal CO Detector QGI P/N 099-0062-01 REV 07/25/01 Page 1 of 4

Personal Carbon Monoxide Detector Model P-1 OWNER’S MANUAL PLEASE READ AND SAVE! Personal & Automobile Use Dear New COSTAR® Model P-1 Owner, Congratulations as you have taken steps to help insure the health and life safety of you and your family. We are proud to offer you our unique, patented CO Sensor technology that detects CO in a manner similar to the human body's response. The COSTAR® P-1 is an ideal and low-cost way of warning you of both the acute and chronic effects of CO poisoning. Please read this owner's manual carefully so you will have a better understanding of the effects of CO poisoning and the COSTAR® P-1 Detector, as we work together pursuing a safer, healthier air quality for us all. To your good health and safety, Mark Goldstein, Ph.D. President Quantum Group Inc. 1.0 WHAT YOU SHOULD KNOW ABOUT CO Carbon monoxide (CO) is an insidious poison. It is a colorless, odorless and tasteless gas. It is a cumulative poison. Even low levels of CO have been shown to cause brain and other vital organ damage in unborn infants with no effect on the mother. The following symptoms are related to CARBON MONOXIDE POISONING and should be discussed with all members of the household: • MILD EXPOSURE: Slight headache, nausea, vomiting, fatigue (often described as “flu-like” symptoms), giddiness • MEDIUM EXPOSURE: Severe throbbing headache, drowsiness, confusion, fast heart rate • EXTREME EXPOSURE: Unconsciousness, convulsions, cardio-respiratory failure, death Many reported cases of CARBON MONOXIDE POISONING indicate that while victims are aware they are not well, they become so disoriented they are unable to save themselves by either exiting the building/automobile or calling for assistance. Also, young children and household pets may be the first affected. Your CO detector is designed to detect the toxic CO fumes that result from incomplete combustion, such as those emitted from appliances, furnaces, fireplaces and auto exhaust. (DO NOT put your detector next to the vehicle’s tailpipe. It may damage the detector permanently.) A CO detector is NOT A SUBSTITUTE for fire alarms, smoke alarms, or other combustible gas alarms. This carbon monoxide detector is designed to detect carbon monoxide gas from ANY source of combustion. CAUTION: This detector will only indicate the presence of carbon monoxide gas at the sensor. Carbon monoxide gas may be present in other areas at a higher concentration than at the detector’s location; therefore, immediately get fresh air. WARNING: This product is not designed to comply with the Occupational Safety and Health Administration (OSHA) commercial or industrial standards. Individuals with medical problems may consider using detection devices that provide audible and visual signals for CO concentrations under 30 PPM. 2.0 WHAT YOU SHOULD DO IF THE ALARM SOUNDS

WARNING: Actuation of this device indicates the presence of carbon monoxide (CO) which can KILL YOU.

_____________________________________________________________________ FIGURE 8.6 COSTAR® P-1, 9 V, personal CO detector.

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All of these statements are part of an effort to alert users of the potential release of CO, its poisonous nature, the need to vacate exposed areas, and means of mitigating exposure. More common are CO warnings found on internal combustion engine-powered cars and trucks. In the Hyundai 2003 Santa Fe Model Owner’s Manual,24 there is an entire page dedicated to engine exhaust emissions, predominantly associated with CO. That warning uses the alert symbol, the signal word “Warning,” and black lettering on a yellow background to garner attention and states that Exhaust fumes contain carbon monoxide, a colorless gas that can cause unconsciousness and death by asphyxiation.

Additional information is provided about how to avoid this hazard, what to look for in detecting this hazard, and other precautions.

8.5.4 WORKPLACE AREA WARNINGS AND LABELING Several ANSI and American Society for Testing and Materials (ASTM) standards provide warning and labeling criteria for workplaces or work-related areas. They include Environmental and Facility Safety Signs, ANSI Z 535.2, 1991; Accident Prevention Signs, ANSI Z 535.5, 1998; Criteria for Safety Signs, ANSI Z 535.3, 1991. Standard Practice for Labeling Art Materials for Chronic Health Hazards, ASTM D 4236

On November 18, 1990 the Labeling of Hazardous Art Materials Act (Public Law 100-695) went into effect which embraces ASTM D 4236 (above) and requires labeling in that industry. OSHA has both general and activity-specific information about warning signs. Below are several examples. 8.5.4.1 Examples of General OSHA Warning Signage • For construction, 29CFR 1915.16(b) Posting of large work areas. A warning sign or label required by paragraph (a) of this section need not be posted at an individual tank, compartment or work space within a work area if the entire work area has been tested and certified: not safe for workers, not safe for hot work, and if the sign or label to this effect is posted conspicuously at each means of access to the work area. • For maritime, 1926.200(a) General. Signs and symbols required by this subpart shall be visible at all times when work is being performed, and shall be removed or covered promptly when the hazards no longer exist.

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• For general industry, 1910.145(a) Scope. 1910.145(a)(1) These specifications apply to the design, application, and use of signs or symbols (as included in paragraphs (c) through (e) of this section) intended to indicate and, insofar as possible, to define specific hazards of a nature such that failure to designate them may lead to accidental injury to workers or the public, or both, or to property damage. These specifications are intended to cover all safety signs except those designed for streets, highways, railroads, and marine regulations. These specifications do not apply to plant bulletin boards or to safety posters.

8.5.4.2 Examples of Specific OSHA Exposure Warning Signage • For asbestos activities, 1910.1001(j)(3) Warning signs. 1910.1001(j)(3)(i) Posting. Warning signs shall be provided and displayed at each regulated area. In addition, warning signs shall be posted at all approaches to regulated areas so that an employee may read the signs and take necessary protective steps before entering the area. 1910.1001(j)(3)(ii) Sign specifications. 1910.1001(j)(3)(ii)(A) The warning signs required by paragraph (j)(3) of this section shall bear the following information: DANGER ASBESTOS CANCER AND LUNG DISEASE HAZARD AUTHORIZED PERSONNEL ONLY • For cadmium and cadmium containing compounds, in all forms, 1910.1027(m)(2) “Warning signs.” 1910.1027(m)(2)(i) Warning signs shall be provided and displayed in regulated areas. In addition, warning signs shall be posted at all approaches to regulated areas so that an employee may read the signs and take necessary protective steps before entering the area. 1910.1027(m)(2)(ii) Warning signs required by paragraph (m)(2)(i) of this section shall bear the following information: DANGER CADMIUM CANCER HAZARD CAN CAUSE LUNG AND KIDNEY DISEASE AUTHORIZED PERSONNEL ONLY RESPIRATORS REQUIRED IN THIS AREA

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1910.1027(m)(2)(iii) The employer shall assure that signs required by this paragraph are illuminated, cleaned, and maintained as necessary so that the legend is readily visible. 1910.1027(m)(3) “Warning labels.” 1910.1027(m)(3)(i) Shipping and storage containers containing cadmium, cadmium compounds, or cadmium contaminated clothing, equipment, waste, scrap, or debris shall bear appropriate warning labels, as specified in paragraph (m)(3)(ii) of this section. 1910.1027(m)(3)(ii) The warning labels shall include at least the following information: DANGER CONTAINS CADMIUM CANCER HAZARD AVOID CREATING DUST CAN CAUSE LUNG AND KIDNEY DISEASE 1910.1027(m)(3)(iii) Where feasible, installed cadmium products shall have a visible label or other indication that cadmium is present. 8.5.4.3 Other OSHA and Industry Warning Criteria There is no OSHA standard specific to CO signage. However, by following the criteria for general signage, hazard mitigation, and OSHA’s criteria for other chemicals, OSHA can utilize the “General Duty Clause” (a.k.a. “5a Clause”) to issue citations about inadequate CO warning signs. Other locations and industries have their own guidelines. Within the iron producing and steel manufacturing industry, CO is knowingly produced in blast furnace operations and in coke ovens. It is common in these industries to see warnings about the possibility of a CO outbreak (from a blast furnace) and the location of safe areas and evacuation routes. Since CO is produced in large quantities and at such elevated concentrations, blast furnace work areas are often equipped with monitors that continuously check CO concentrations. Safe rooms, rescue respirators, and signs about CO hazards are typical in these facilities. The Department of Defense Hazardous Chemical Warning Labeling System25 provides detailed labeling requirements including a mechanism for “rating” chemicals. The format for these Department of Defense (DOD) labels is unique, in part because of their use in wartime or under the stress of military conditions. They do not use the alert symbol, but do use the same hierarchy of signal words. They use a small selection of pictograms, including a skull and cross bones, which under their criteria is appropriate for CO. The DOD Hazardous Chemical Warning Label follows criteria set out in the 29 CFR 1910.1200 Hazard Communication Standard. It is often 8.5 by 11 in. in size, and contains information about specific categories of health, contact, fire, and reactivity. Following this format, a label for CO is rated as moderately toxic, severely flammable, and slightly reactive.

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8.6 THE REASONS, RATIONALE, AND SCIENTIFIC BASES FOR PROVIDING SAFETY INFORMATION FOR CARBON MONOXIDE WITH SELECTED EXAMPLES Many books and treatises have been written about the issues surrounding informing consumers of risk through warnings and informational means. A brief discussion of some of the bases for warnings, labeling, instructions, and safety communications is given below.

8.6.1 ETHICAL AND PHILOSOPHICAL REASONS The concept of “do no harm”26 is widely accepted as a moral and ethical obligation and may be an underling element (although not a part of) the Hippocratic Oath. All products, processes, and workplaces are capable of harm, and at a minimum people should be informed of hidden or unexpected risks that cannot be eliminated. Much of “being informed” comes from education, life experiences, and simple observation. With the added complications of modern technology, keeping oneself informed of product and workplace risks is difficult and in some cases impossible. From an ethical perspective, when hazards cannot be eliminated or reasonably safe guarded, it is necessary to provide information in the form of warnings, labeling, instructions, or other communications, so as to “do no harm.” One of the basic safety philosophies originating in part from the engineering and safety professional codes of ethics includes the notion that designers of equipment, products, and process have the three basic goals of (1) making a product/process that is functional, (2) making a product/process that helps human welfare by being available (and therefore is cost efficient), and (3) making a product/process that is reasonably safe. In other words, products have to work, be inexpensive enough for availability to the general public, and be reasonably safe.27 User information (warnings, labeling, and instructional information) affects all three of the items above. For most products and processes to function, there is a need for some directions and information. For most combustion processes, instructions about how the equipment is to function includes information that reduces the formation, accumulation, and concentration of CO. Instructional manuals, labels, and warnings all increase the cost of products. They can also delay the introduction of products into the market place. However, they can significantly increase consumer awareness about safety concerns. On complicated pieces of equipment and processes, informational materials often require testing and evaluations via “task analysis” to determine the effectiveness of the material before a new product enters the market place. Gordon and Hall28 and others suggest that a task analysis of a product and its accompanying documents should be a part of the normal product development sequence. In essence, warnings, labeling, instructional materials, and other forms of safety information should not be thought of as pieces of paper or decals, but as part of a vital scheme to do no harm.

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Within the safety community there is a general consensus that has developed over the years concerning steps that should be taken to ensure safe products and safe workplaces.29 The order to these incremental steps are 1. 2. 3. 4.

Eliminate the hazard Apply safeguarding technologies to control the hazard Warn potential users about the hazard and its features Provide training and/or personal protective equipment to mitigate exposure to the hazard

With CO, there is no real opportunity to “eliminate” the hazard as long as carbonbased fuels are in use. In some circumstances it is possible to provide safeguarding technologies. These include CO alarms, oxygen deficiency sensors (ODS),30 CO protective respirators, self-checking flue dampers, temperature sensors positioned to detect hot gas leaks (indicative of a leak of combustion gases), timers on space heaters, and the use of catalysts to enhance certain types of combustion processes. Providing information manifests itself in items (3) and (4). Unfortunately, this approach does not take into account the importance of safe product design in ensuring user safety. This factor is especially important in our technological world. Figures 8.7 through 8.12 show several excerpts of CO warning criteria that are not based on general codes or standards (though they may follow code criteria for their specific content and form), but are based on a range of ethical and philosophical safety criteria. Some of these warnings originate from an association or industry collective, while others are for products that do not produce CO, but are associated with other equipment that may produce CO. A diverse product mix is provided for instructional purposes.

“Carbon Monoxide Hazards from Small Gasoline Powered Engines Fact Sheet HS05-023B (8-05) “Tool Rental Agencies Should: …• Put warning labels on gasoline-powered tools. For example: WARNING - CARBON MONOXIDE PRODUCED DURING USE CAN KILL - DO NOT USE INDOORS OR IN OTHER SHELTERED AREAS.” FIGURE 8.7 Warning information from Texas Department of Insurance Division of Workers’ Compensation (TDI/DWC), E-mail: [email protected]

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Carbon Monoxide Poisoning “Important Alert for Gasfitters The Office of Gas Safety (OGS) alerts gasfitters that all open-flued instantaneous gas water heaters (IGWH) in toilets and bathrooms should be replaced as a matter of urgency…. Open-flued IGWH’s, in a confined living space, can expose gas users to the risk of carbon monoxide poisoning…. • Provided the Important Safety Warning including the dangers and symptoms of carbon monoxide poisoning .”

FIGURE 8.8 Warning information from Office of Gas Safety Level 1, Wool House, 369 Royal Parade, Parkville, Victoria 3052.

Informational Brochure On CO Poisoning From Boating “Apply the enclosed carbon monoxide warning decals at the helm and by the swim deck as a reminder. Additional carbon monoxide warning decals may be obtained from any boating enforcement officer.”

FIGURE 8.9 Warning from National Marine Manufacturers Association, 200 East Randolph Drive, Suite 5100 Chicago, IL 60601-6528, Available at: www.nmma.org.

8.6.2 RESEARCH BASIS: THE NEED FOR SAFETY INFORMATION Much research into the efficacy of safety information has been conducted over the years. The findings are curiously polarized: safety information either helps or is not universal in effectiveness. However, there is not any substantial body of research finding that safety information hurts or causes a new harm. The literature repeatedly comes down to a discussion of to what extent safety measures help. Somewhere on this continuum, between safety measures being marginal to them being extremely useful, there is a middle ground wherein safety efforts help sufficiently and are reasonable in their design and application. A brief review of the safety literature over the past 25 years indicates that safety efforts are directed at the performance and efficacy of warnings, and that whether or not warnings should or should not be used is a less debated consideration. For example, in the publication entitled “Human Factors Perspectives on Warnings, 1980 to 1993,”31 the terms “effectiveness” or “effect(s)” appears in the title of listed papers and abstracts at least 27% of the time. These researchers are attempting to establish the threshold of effectiveness in warnings. In volume 2 of the same publication,32 covering the period 1994–2000, the research continues in that vein, with the added inquiries as to what aspects of a warning improves the effectiveness of the warning. Research into the colors by Braun et al.,33,34 symbols by Caird et al.,35 risk perception and warning dilution from multiple warnings by Chen et al.,36 legibility by Ringseis and Caird,37 and effects of age by Hancock et al.38 on word content are all examples of the direction the most recent

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1.1.SAFETY ALERT SYMBOLS AND SIGNAL WORDS 1.2.14.1. Generator If your trailer is equipped with a gasoline or diesel generator, you must have and follow the generator manufacturer's instructions. You must also have one or more carbon monoxide detectors in the trailer's accommodation spaces. Carbon Monoxide is an odorless gas that can cause death. Be certain exhaust from a running generator does not accumulate in or around your trailer, by situations such as :

Being drawn in by fans or ventilators operated in a trailer ; Prevailing wind; Being trapped between your trailer and other trailers, vehicles or buildings; or Being trapped between your trailer and, or in a snow bank, or other nearby objects.

Operating gasoline and diesel generators can lead to death or serious injury by:

Carbon Monoxide Fire and Explosion Electrocution Have a working carbon monoxide detector in th e accommodation spaces before operating a generator. Do not refuel a running generator or refuel near ignition sources. 1.2.14.3. LP Gas Fuel System

You can die or be brain damaged by Carbon Monoxide. Make certain the exhaust from LP appliances is directed to the outdoors. Have a working carbon monoxide detector in th e accommodation spaces of your trailer before operating any LP gas appliance. Do not operate portable grills or stoves inside th e trailer.

FIGURE 8.10 Brockmann Trailers (a trailer manufacturer) (http://www.bockmann.co.uk/ supporta.asp), Lastrup, Northern Germany. Available at: http://www.bockmann.co.uk/ abouta.asp.

research has taken. None of these authors reports findings that product or process warnings are useless. Other research includes the role of “on-product” warnings, the interplay between warnings and training, and the relative effectiveness of verbal and nonverbal warnings. Examples of nonverbal warnings are included in Analysis of Workplace Factors on Auditory Warning Alarm Location by Nanthavanij.39 CO alarms and oxygen

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!WARNING Failure to properly vent the water heater to the outdoors as outlined above and in the following section can result in unsafe operation of the water heater causing bodily injury, explosion, fire, or death. To avoid the risk of fire, explosion, or asphyxiation from carbon monoxide, NEVER operate this water heater unless it is properly vented and has an adequate air supply for proper operation.

FIGURE 8.11 Rheem, water heater manufacturer power vent residential gas water heater, use and care, AP10960-11 (04/02) manual (www.rheem.com/documents/resourcelibrary/use/ and care/rheempowervent/ap10960-11.pdf).

“Carbon Monoxide is a product of the reaction of H2 and CO2. Carbon monoxide (CO) is a colorless, odourless, tasteless and flammable gas which is acutely toxic. CO is introduced into the blood stream through the lungs and binds with the hemoglobin preventing it from carrying oxygen around the body. This can result in rapid damage to body tissues due to oxygen starvation. Since CO is an accumulating toxin it can be dangerous even when present in quite low concentrations over long periods of time.” ( note: triangular alert symbol is used)

FIGURE 8.12 Carbolite “coal ash fusion furnace,” installation, operation, maintenance instructions (industrial furnace), (industrial furnace) Hope Valley, S33 6RB, England CAF 16/38, MF45-1.0, Copyright 2002, 11/14/02.

depletion systems are prime examples of nonverbal warnings/alerting systems for exposure to CO. Some of the older research concerning the warning requirements for CO are contained in the Encyclopedia of Chemical Labeling.14 This book classifies CO as a chemical requiring identification as “extremely hazardous,” ”vapor extremely hazardous,” “poisonous if inhaled,” and a “poison.” The National Institute for Occupational Safety and Health (NIOSH) suggested in 1972 that CO cylinders and other containers be labeled “fatal if inhaled” and “do not breath gas.”40 For areas where CO gas may be present, they recommended signage stating that “high concentrations may be fatal.” In 1974, the American Insurance Association referenced the research work of the Consumer Product Safety Commission (CPSC) and concluded that, The Consumer Product Safety Commission (CPSC) has repeatedly warned manufacturers of equipment which may produce carbon monoxide to label the equipment so as to inform the general public of the toxic hazards if improperly vented or used.41

Further, in 1971 through 1985, the Environmental Protection Agency (EPA) had a variety of research-based rules42 concerning ambient air quality. These included rules concerning CO content and how to alert or warn the public if they are at risk

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of overexposure. The 1986 40 CFR Ch. 1, Par. 51.16 “Prevention of air pollution emergency episodes” required “Communication procedures for transmitting status reports [on carbon monoxide] for contact with the public officials, major emissions sources, public health, safety, and emergency agencies and news media”43

to warn the public of air pollution episodes.

8.6.3 VOLUNTARY STANDARDS FOR CO WARNINGS (EXAMPLES IN CHRONOLOGICAL ORDER) Numerous nongovernmental codes, standards, and guidelines recognize the need to inform workers and consumers of the hazards of CO. Figures 8.13 through 8.20 show some examples for different time periods, locations, and products.

8.6.4 MANDATORY SAFETY INFORMATION REGULATIONS Regulations regarding product warnings and labeling are based in part on our social value system. Our society has allowed for the formation of various regulatory bodies, and it is generally through these regulatory agencies that mandatory requirements “Carbon Monoxide DANGER! EXTREMELY FLAMMABLE GAS UNDER PRESSURE MAY BE FATAL IF INHALED Avoid breathing gas. Keep container closed. Use with adequate ventilation. Keep away from heat, sparks and open flames. Never drop cylinder. Keep cylinder out of sun and away from heat.”

FIGURE 8.13 Manufacturing Chemist Association (MCA) “Guideline for Chemical Labeling.” “NOTE: The 0.01% level of CO in indicated to protect the test personnel…”

FIGURE 8.14 Society of Automotive Engineers (SAE) “Test Procedure for Measuring Carbon Monoxide Concentrations in Vehicle Passenger Compartments,” SAE J989, Approved 1968, 1971 Handbook. “Para:8.4.(b) WARNING: during an extended hot idle period of up to 60 minutes, idle exhaust CO from the test or traffic simulation vehicle will probably remain constant.”

FIGURE 8.15 Society of Automotive Engineers (SAE) “Test Procedure for Measuring Carbon Monoxide Concentrations in Vehicle Passenger Compartments,” SAE J989a, Revised 1978, 1985 Handbook.

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“1.34.7 INSTALLATION MARKINGS… (c)… This appliance must be properly connected to a venting system. This appliance is equipped with a vest safety shutoff system. WARNING: Operation of this wall furnace when connected to a properly installed and maintained venting system or tampering with the vent safety shutoff system can resultin carbon monoxide (CO) poisoning and possible death.”

FIGURE 8.16 ANSI Z 21.49—1989 “Gas Fired Gravity and Fan Type Vented Wall Furnaces.”

“ Operation and Installation Instructions: 21.1J The word “WARNING”, and the following or equivalent text: “TO REDUCE THE RISK OF CARBON MONOXIDE POISONING, TEST DETECTOR OPERATION IF NOT IN USE FOR 10 DAYS OR MORE. (K) The word “WARNING”, and the following equivalent text: “This device may not alarm at low carbon monoxide levels. The Occupational Safety and Health Administration (OSHA) has established that continuous exposure to levels of 35 ppm should not be exceeded in an eight hour period”

FIGURE 8.17 Use,” 1989.

UL 1524 “Standard for Safety—Carbon Monoxide Gas Detectors for Marine

WARNING! Do not use equipment and tools powered by gasoline engines inside buildings or other partially enclosed spaces unless the gasoline engine can be placed outdoors and away from air intakes

Tool rental Agencies Should: • Place warning labels on gasoline-engine-powered tools. For example: WARNING – CARBON MONOXIDE PRODUCED DURING USE CAN KILL – DO NOT USE INDOORS OR IN OTHER SHELTERED AREAS.

FIGURE 8.18 National Institute for Occupational Safety and Health, NIOSH ALERT:1996, Pub. No. 96-118 “Preventing Carbon Monoxide Poisoning from Small Gasoline-Powered Engines and Tools.”

for product safety information are created. These efforts are a compromise between no regulation at all, or banning products that cannot be made safe without such information.44 Government regulatory agencies have to balance public demand, business interests, and political intrigue, with a well-established scientific basis for implementing safety standards.

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All unvented Servel Refrigerators shall have a warning label, protected from the environment, that is either affixed to the outside of the front door or inside the Un-Vented Servel Refrigerator in a location that is readily visible. The warning label shall have the following wording: Warning This refrigerator is prone to the production of Carbon Monoxide in levels that may be lethal. This refrigerator may only be operated in an area that is isolated from the living space such as: a remote shed, garage or open porch. The refrigerator shall be located a minimum distance of 12 inches from any opening to the living space

FIGURE 8.19 Technical Standards and Safety Authority, 14th Floor, Certre Tower, Toronto, Ontario, CAN, Ref. No FS-076-06, March, 2006, Director’s Order, Fuels Safety Program, Roland Hadaller, Director.

Using a generator indoors WILL KILL LYOU IN MINUTES. Exhaust contains carbon monoxide, a poison gas you cannot see or smell.

NEVER use in the home or in partly enclosed areas such as garages.

ONLY use outdoors and far from open windows, doors, and vents.

FIGURE 8.20 UL offered CO warning label (www.ul.com/media/newsrel/generatorCOMarking.pdf).

Scientific research into chemical hazards often has implications for the development of mandatory safety regulations. For example, Viscusi44 reports that “the Food and Drug Administration’s (FDA’s) predominant risk standard for carcinogens is a lifetime risk of 1/1,000,000. This is ten times as conservative as the 1/100,000 lifetime risk embodied in California’s Proposition 65 (which mandated hazard warnings for risks of cancer and reproductive toxicity from products, jobs, and the environment).” Determining the accuracy of this risk assessment is difficult since there are no public death registries for CO, whereas there are well-established registries and protocols for cancer deaths (e.g., Centers for Disease Control, National Program for Cancer Registries). Typically, manufacturers have an idea concerning the number of deaths from CO related to their products. However, this information is generally kept at high levels of confidentiality. Burd (2002)45 reports in his research of a single county (Bexar County, Texas, population 1.4 million, 2000 census) over a six decade time period (1935–1995) that for the past 5 years (1991–1995) the death rate from CO was 40 deaths per 1,000,000

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residents. Although a direct comparison to the FDA or the California numerical risk criteria noted above is not perfectly correct, there is a close correspondence. The CPSC has also investigated deaths from CO. In Non-fire Carbon Monoxide Deaths Associated with the use of Consumer Products 2001 Annual Estimates (www.cpsc.gov/LIBRARY/coed04.pdf) the CPSC reports that: In 2001 there were an estimated 130 unintentional non-fire CO poisoning deaths associated with consumer products under the jurisdiction of the U. S. Consumer Product Safety Commission. Fifty-eight percent of the estimated deaths in 2001 were associated with the use of heating systems. Natural gas heating accounted for 37 percent and liquefied petroleum (LP) gas heating accounted for 35% of the estimated heating deaths. An estimated 18% of the 2001 annual CO poisoning deaths were associated with enginepowered tools, nine percent were associated with charcoal grills, eight percent were associated with gas ranges and ovens, one percent were associated with camp stoves and lanterns, and seven percent were associated with other or multiple appliances.46

Meanwhile, in the CPSC’S “Incidents, Deaths, and in-Depth Investigations Associated with Carbon Monoxide from Engine-Driven Generators and Other Engine-Driven Tools, 1990–2004” (December 1, 2005, Natalie E. Marcy, www.cpsc.gov/LIBRARY/coed05.pdf) there are reportedly 317 incidents of poisoning and 318 deaths from exposure. Both these reports indicate a significant death rate from CO, and are the basis for some of the mandatory regulations concerning warnings and labeling. In 1993, the OSHA published their “Final Rule” on confined spaces: Entry Permits: The entry permit.. shall identify: (7) The hazards of the permit space to be entered.

Applying this criteria to a space that may contain CO requires postings about the hazards of carbon monoxide. In 1994, OSHA implemented mandatory rules about chemical hazards, primarily directed at workers but that have labeling implications for both worker and consumer populations. The “Hazard Communication” provision of 29 CFR 1910.1200 requires specific information be provided on “all chemicals produced or imported” into the country. This section specifically states that: label means any written, printed, or graphic material displayed on or affixed to containers of hazardous chemicals.

Section (f) contains detailed labeling requirements addressing the use of: appropriate hazard warnings, or alternatives, words, pictures, symbols, or combination thereof …regarding the hazards of the chemical …

Applying this criteria to containers of CO, there would be information about the highly toxic nature of exposure, the need to take appropriate protection measures, and the necessity of ceasing contact with the gas. Figures 8.21 through 8.26 show examples of the current federal, state, and local regulations concerning safety information for the hazard of CO.

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Tennessee OSHA has instituted a Special Emphasis Program for Carbon Monoxide (CO). This is established to focus state-wide attention on carbon monoxide and to reduce employee exposure to, and eliminate deaths from, carbon monoxide.

Carbon Monoxide Warning Sign

WARNING CARBON MONOXIDE A colorless, odorless, toxic gas is produced from incomplete combustion of gas, oil, kerosene, and wood. May cause dizziness, nausea, or headache Excessive exposure may cause unconsciousness and death May aggravate heart and artery diseases

FIGURE 8.21 State of Tennessee OSHA F:\TN Department of Labor and Workforce Development.htm “Special Emphasis Program—Carbon Monoxide, The Hidden Killer.”

Mandatory Carbon monoxide Warning Decals Now Available Contact: June lljana (916) 263-0788 e-mail: pubinfo.dbw.ca.gov April 29, 2005 Sacramento – As of May 1, California boaters will be required to place stickers on their newly purchased boats warning against the threat of carbon monoxide poisoning The Farr and Stacet Beckett Boating safety Act of 2004 requires that a set of carbon monoxide warning stickers be placed on the transom and helm of all new and used motorized boats sold in California. The bill, AB 2222 (Koretz), was signed by Governor Schwarzenegger in September.

FIGURE 8.22 State of California, Department of Boating and Waterways, F:\Mandatory Carbon Monoxide Warning Decals Now Available.htm.

8.6.4.1 State-Based Examples Figures 8.21 through 8.23 show state-based examples. 8.6.4.2 Federal Government Examples Figures 8.24 through 8.26 show Federal Government examples.

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NECESSITY, FUNCTION, AND CONFORMITY: KRS 217.690 authorizes the Cabinet for Human Resources to adopt administrative regulations to regulate the control of hazardous substances in Kentucky. The purpose of this administrative regulation is to provide uniform standards relating to the "conspicuousness" of labeling requirements; to specify requirements to identify hazardous substances that present special hazards and require specialized labeling to protect the public health; and to prevent the deceptive use of disclaimers on labelsof hazardous substances.Section 1. Conspicuousness of Labeling Requirements. (1) The signal word, the statement of the principal hazard or hazards, and instructions to read carefully any cautionary information that may be placed elsewhere on the label shall appear together on the main panel of the label. The information shall be placed together and distinctively apart from other wording or designs. The necessary prominence shall be achieved by placement within the borders of a square or rectangle with or without a borderline, and by use of suitable contrasts with the background achieved by distinctive typography or color, and by both color and typography if needed. Section 2. Special Labeling Requirements. In addition to the requirements of KRS 217.670 the following hazardous substances are deemed to be misbranded unless the label includes the requirements stated below: (1) Charcoal briquettes and other forms of charcoal for cooking or heating. Because inhalation of the carbon monoxide produced by burning charcoal indoors or in confined areas may cause serious injury or death, containers of the products shall bear the following borderlined statements: "WARNING; Do Not Use for Indoor Heating or Cooking Unless Ventilation is Provided for Exhausting Fumes to Outside. Toxic Fumes May Accumulate and Cause Death".

FIGURE 8.23 Labeling and identification standards. Relates to: KRS 217.650-217.710. Statutory authority: KRS 194.050, 211.090, 211.180, 217.690, 902 KAR 47:020.

“(2) It shall be unlawful for any manufacturer or importer of cigarettes to advertise or cause to be advertised (other than through the use of outdoor billboards) within the United States any cigarette unless the advertising bears, in accordance with the requirements of this section, one of the following labels:… SURGEON GENERAL'S WARNING: Cigarette Smoke Contains Carbon Monoxide.”

FIGURE 8.24 Title 15—Commerce and Trade Chapter 36—Cigarette Labeling and Advertising §1331. Congressional declaration of policy and purpose.

8.6.5 THE CUSTOM AND PRACTICE OF CARBON MONOXIDE SAFETY INFORMATION “Custom and Practice” in the safety and engineering profession is a term referring to common customs and practices in the design of equipment, products, and processes. “Custom” having the meaning “a usual practice or habitual way of behaving; habit,” and “practice” having the meaning “to do or be engaged in frequently or usually.”47 Custom and practice is all around us. It is what we are accustomed to and what multiple designers have coalesced to in their designs. For example, the ubiquitous use of right-handed threads on nuts and bolts is the custom and practice for most threaded fastening applications. The introduction of metric threads was a change to a preexisting custom and practice in the United States. For some things the custom and practice is regional. In certain dryer portions of the southwest, residential air cooling is performed by evaporative coolers, while in more humid areas, compression cycle cooling units are used.

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To direct the Consumer Product Safety Commission to issue regulations concerning the safety and labeling of portable generators. (1) WARNING: portable generator sold to the public for purposes other than resale shall have a large, prominently displayed warning label on the exterior packaging, if any, of the portable generator and permanently affixed on the portable generator regarding the carbon monoxide hazard posed by incorrect use of the portable generator.

The warning label shall include the word “DANGER” printed in a large font, and shall include the following information, at a minimum, presented in a clear manner: (A) Indoor use of a portable generator can kill quickly. (B) Portable generators should be used outdoors only and away from garages and open windows. C) Portable generators produce carbon monoxide, a poisonous gas that people cannot see or smell. (2) PICTOGRAM.--Each portable generator sold to the public for purposes other than resale shall have a large pictogram, affixed to the portable generator, which clearly states “POISONOUS GAS” and visually depicts the harmful effects of breathing carbon monoxide.”

FIGURE 8.25 109th U.S. Congress (2005–2006) S. 2084: Portable Generator Safety Act, Introduced December 13, 2005.

Requirements for Labeling of Retail Containers of Charcoal; proposed Amendments AGENCY: Consumer Product Safety Commission. ACTION: Proposed rule.\1\ SUMMARY: Under the Federal Hazardous Substances Act, the Commission is proposing a rule to change the required labeling for retail containers of charcoal intended for cooking or heating. The labeling addresses the carbon monoxide hazard associated with burning charcoal in confined spaces. The proposed amendments, which include a pictogram, are intended tomake the label more noticeable and more easily read and understood and to increase the label's ability to motivate consumers to avoid burning charcoal in homes, tents, or vehicles. DATES: Comments on the proposal should be submitted no later than October 24, 1995.”

FIGURE 8.26 Consumer Product Safety Commission, 6 CFR Part 1500. Available at: http://www.cpsc.gov/businfo/frnotices/fr95/95-40785.html.

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CAUTION CARBON MONOXIDE MAY BE PRESENT

FIGURE 8.27 Seton Style No. M9699.

In some cases, the custom and practice is dictated by codes, standards, or guidelines. OSHA’s Standard Interpretations: Fluor Constructors, Inc. v. OSHRC, No. 87- 4029 1/22/1988 states that, a Commission judge agreed with the Secretary that both OSHA’s standards and industry custom and practice plainly distinguish between lifelines and lanyards.

This concept, or pattern of practice, is generally accepted as a means to establish what safety measures are reasonable. Where codes do not require user-safety information, custom and practice can be the basis for requiring notice of a hazard. In the United States Occupational Safety and Health Review Commission’s decision in “SECRETARY OF LABOR, Complainant, v. CITY OIL WELL SERVICE CO., Respondent”48 the Commission stated that, The evidence indicates that the custom and practice of the industry is for the well servicer to rely on the well operator or owner to advise it if H2 S hazards are present.

The phrase “of the industry” in the decision above associates custom and practice with the multiple providers of goods or services that comprise an industry. When there are few providers of these items, or if there is a single provider, it is difficult to say this “practice” is the “usual” in that it may be the “only” practice. In this context, one provider’s design does not establish enough of a pattern for there to be a custom and practice to evaluate safe design. In some cases, custom and practice criteria has been “institutionalized” into standalone business enterprises. Several firms sell standard and customized warning signs and labels, including ones directed at CO exposure (Emedco, Seton, VMC, Inc., Safetysign Inc.) (Figure 8.27). There does appear to be a general custom and practice with respect to safety warnings within the United States both with regard to their content and to a lesser extent concerning on what products or places warnings should be applied. The content aspect is well documented. The content of warnings and other safety information generally include (1) a signal word, (2) a pictorial, (3) a signal symbol, (4) a description of the hazard, (5) a statement of the consequences, and (6) a statement of how to avoid the hazard.9,10,14,28 With regards to which products and places require safety information, there is some variation among different products, product groups, and processes. With respect to CO, there are several established customs and practices for different products and places. In Carbon Monoxide: Its Hazards and the Mechanisms

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INSTRUCTIONS “! WARNING! … Actuation of your CO alarm indicates the presence of carbon monoxide (CO) which can KILL YOU. … CAUTION: This alarm will only indicate the presence of carbon monoxide (CO) gas at the sensor. CO gas may be present in other areas of the RV.”

FIGURE 8.28 Model 3400 Carbon Monoxide Gas Alarm 5052 (CO Alarm for RVs) CCI Controls Co., Cecelia Street, South Gate, CA 90280. Phone: (323) 560-6060; Fax: (323) 560-1136; available at: www.ccicontrols.com.

Assembly Instructions “WARNING CARBON MONOXIDE HAZARD Burning charcoal inside can kill you. It gives off carbon monoxide, which has no odor. NEVER burn charcoal inside homes, vehicles or tents….”

FIGURE 8.29 Tabletop Grill™ (Drum-type Barbeque Grill), New Braunfels, Model 03407610.

of Its Actions (1944), published by the United States Public Health Service,49 there is reference to the early warning needs of CO exposure: In spite of these efforts, a large number of accidents from CO poisoning occur which are due to acts of carelessness of uninformed persons, as pointed out by Brumbaugh (1926) and it seems to be imperative that the public be informed about the proper handling of such appliances (bolding added for emphasis) [gas appliances and space heaters]… it appears that the public is not aware of the dangers resulting from the improper handling of gas appliances capable of forming CO due to incomplete combustion.

To the present time, the custom and practice is to continually inform the public of the hazards of CO exposure. Automobile manuals, for example, consistently and for many years have warned the public about the possibility of CO overexposure from operation of a vehicle’s engine in an enclosed space. Figures 8.28 through 8.31 show examples of warnings, labels, or instructions about CO that are the result of an existing or emerging custom and practice, and are not the result of voluntary standards or mandatory regulations.

8.6.6 LITIGATION-DRIVEN SAFETY INFORMATION It is not unusual for an injured party to complain about insufficient warnings or instructions in product defect or workplace injury cases. Since warnings and instructions can influence the safe use of a product, it is reasonable to consider them in

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OPERATING INSTRUCTIONS AND OWNER’S MANUAL “WARNING: Early signs of carbon monoxide poisoning resemble the flu, with headache, dizziness and/or nausea. If you have these signs, heater may not be working properly. Get fresh air at once! Have heater serviced. … WARNING: Combustion by-products producedwhen using this product contain carbon monoxide, a chemical known to the State of California to cause cancer and birth defects (or other reproductive harm).”

FIGURE 8.30 Mr. Heater (Portable Propane Space Heater). Model # MH18B Enerco Group, Inc., 4560 W. 160th Street, Cleveland, OH 44135 · 216-881-5500 05/04 Revision L1 # 78435.

Operating and Maintenance Instructions“ WARNING_Engine exhaust contains carbon monoxide, an odorless, colorless, poison gas. …Breathing carbon monoxide can cause nausea, fainting and death.”

FIGURE 8.31 Briggs & Stratton, Power Products Group, Model AA0101 (four-stroke outboard engine), Milwaukee, WI, Form number MS-5682-9/03.

evaluating their effects on the safe use of the product or workplace. Safety criteria can be based on the precedence of prior cases or regional law. Individual states and the federal bench have their own juristically developed labeling, warning, and instructional criteria for product safety. Below is just one example of these criteria: Adequate warning: 1) it must be of such form that it could reasonably be expected to catch the attention of the reasonably prudent man in the circumstances of its use; and 2) the content of the warning must be of such a nature as to be comprehendible to the average user and to convey a fair indication of the nature and extent of the danger to the mind of a reasonably prudent person … the question of whether or not a given warning is legally sufficient depends upon the language used and the impression that such language is calculated to make upon the mind of the average user of the product. Implicit in the duty to warn with the degree of intensity that would cause a reasonable man to exercise.… the caution commensurate with the potential danger… A clear cautionary statement setting forth the exact nature of dangers involved would be necessary to fully protect the seller… .50

Weinstein and Twerski51 in 1978 reports (p. 41)

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The court in Muncy vs Magnolia Chemical Company set forth its requisite for adequate warnings: ‘1) it must be of such form that it could reasonably be expected to catch the attention of the reasonably prudent man in the circumstances of use; and 2) content of the warning must be of such a nature as to be comprehensible to the average user… Implicit in the duty to warn is the duty to warn with a degree of intensity that would cause a reasonable man to exercise… the caution commensurate with the potential danger….’

In The Restatement of Torts: Products Liability,51 the American Bar Institute addresses the relationship between dangerous product design and product warnings and instructions. Section 402A states that, One who sells any product in a defective condition unreasonably dangerous to the user or to his property is subject to liability for physical harm thereby caused to the ultimate user or consumer.

In The Restatement of Torts: Products Liability—the tension between product design and product warning, the author explains that, courts have interpreted [section] 402A to mean that a product may be unreasonably dangerous because of a defect in manufacturing, design, or warnings and instructions.

Silvergate expands this by including the third restatements of torts language in conjunction with proper design: [A Product] is defective because of inadequate instructions or warnings when the foreseeable risks of harm posed by the product could have been reduced or avoided by the provision of reasonable instructions or warnings by the seller or other distributor, or a predecessor in the commercial chain of distribution and the omission of the instructions or warnings renders the product not reasonably safe.

But that, In general, when a safer design can reasonably be implemented and risks can reasonably be designed out of a product, adoption of the safer design is required over a warning…

Hence, warnings and instructions have a second place behind proper design in the eyes of the judicial system, but they are a vital element in deciding if a product (or place or process) is reasonably safe. Many of these and other legal admonitions are passed on to the engineering community. In a how-to book for engineers called What every Engineer Should Know About Products Liability,52 the authors detail the four components of a warning communication (p. 58): 1. Intelligibility 2. Adequacy

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3. Completeness 4. Placement and add that: If a product has obvious dangers, there is no duty to warn, since the danger is a matter of common knowledge. For example, the fact that a sharp knife is capable of cutting a careless user is a matter of common knowledge and is obvious. Similar remarks can be made for guns, blowtorches, and so forth. The hazards that must be warned against are the less obvious ones - inherent, latent, or concealed dangers the manufacturer has knowledge of but the user cannot foresee.

In the publication, Injury and Litigation Prevention, by Freeman, 1991,53 the author presents eight considerations that may be used in a judicial evaluation of warnings. Many of these are consistent with those detailed in previous sections, but also included is the concept of “motivate[ing] behavioral change.” Warnings should not just provide weak warnings, but the “consequences of continuing the forbidden activity must be clear, not remote or hidden.” Finally, while the courts and legal systems around the world have very different traditions and bases for their laws and judicial processes, Huber54 discusses the positions of several judicial systems around the world in regards to safety, liability, and warnings. Comparisons are made among English, Japanese, German, French, and Canadian case law, and reports that product warnings may be a basis for concluding a product is defective.

References 1. Kandarjian, L. Federal Policy Options for Indoor Air Pollution from Combustion Appliances, Transactions of Combustion Processes and the Quality of the Indoor Environment, Harper, J., ed., International Specialty Conference, Air and Waste Management Association, September 1988. 2. Flickinger, J. Characterization of Emissions and Indoor Air Quality Impacts Resulting from Vented and Unvented Gas Appliances in Ten Homes, Dames & Moore, Transactions of Combustion Processes and the Quality of the Indoor Environment, Harper, J., ed., International Specialty Conference, Air and Waste Management Association, September 1988. 3. Carbon monoxide. Material Safety Data Sheet, Genium Publishing Company, Schenectady, NY, January 1986, MSDS # 35. 4. Konz, S. Work Design, Industrial Ergonomics, 4th ed., Publishing Horizons, Inc., Scottsdale, AZ, p. 388, 1995. 5. Heating System Check Recommended for Carbon Monoxide—CPSC Release 88–92, November 1989. 6. Fugler, D. Indoor Pollution Measured in Combustion Spillage Testing, Research Division, Canada Mortgage and Housing Corp., Ottawa, ON, Transactions of Combustion Processes and the Quality of the Indoor Environment, Harper, J., ed., International Specialty Conference, Air and Waste Management Association, September 1988. 7. Woodson, W.E. Human Factors Design Handbook, 2nd ed., McGraw Hill, NY, 1992.

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8. McCormick, E.J. and Sanders, M.S. Human Factors in Engineering and Design, 5th ed., McGraw Hill, New York, NY, 1982. 9. Product Safety Label Handbook, Westinghouse Electric Company, Traftord, PA, 1981. 10. Product Safety Sign and Label System, FMC Corporation, Santa Clara, CA, Copyright 1990. 11. Holkham, T. Label Writing and Planning, Blackie Academic, London; Melbourne, 1995. 12. Holmes, N. Wordless Diagrams, Bloomsbury, USA, 2005. 13. Recchia, N. Warnings, Mark Batty, West New York, NJ, 2005. 14. Mellan, I. Encyclopedia of Chemical Labeling, Chem. Publishing Co., Newyork, NY, 1961. 15. Schoff, G. Writing & Designing Operator Manuals, Lifelong Learning Publications, Division of Wadsworth, Inc., Belmont, CA, 1984. 16. Product Safety Signs and Labeling, ANSI Z 535.4, 1998; “Safety Color Code”, ANSI Z 535.1, 1991; Environmental and Facility Safety Signs, ABSI Z 535.2, 1991; Accident Prevention Signs, ANSI Z 535.5, 1998; Criteria for Safety Signs, ANSI Z 535.3, 1991. 17. For Hazardous Industrial Chemicals—Precautionary Labeling, ANSI Z 129.1, 1994. 18. Ryan, J. Design of Warning Labels and Instructions, Van Nostrand Reinhold, 1991. 19. Specifications for Accident Prevention Signs, USA Standard, USAS Z38.1, 1959. 20. Scheme for the Identification of Piping Systems, ANSI A13.1, 1981. 21. Title 15—Commerce and Trade, Chapt. 36—Cigarette Labeling and Advertising. 1999. 22. Brusaw, C. Handbook of Technical Writing, 5th ed., St. Martins Press, NY, 1997. 23. Honda Owner’s Manual, GC160–GC190, American Honda Motor Co., 31Zl8A08 00X31-ZL8-A080, 2003–2005 copyright. 24. 2003 Owner’s Manual—Santa Fe, Hyundai Motor Co., A030A020-AAT. 25. Department of Defense Hazardous Chemical Warning Labeling System, Office of the Assistant Secretary of Defense, 93-17976, DOD 6950.5 H, June 1989. 26. Hippocrates, The Epidemics, Bk. I, Sect. XI. 27. Professional Engineering Codes of Ethics, 1999. 28. Gordon, S. and Hall, P. Systematic Training Program Design, University of Idaho, Englewood, Cliffs, NJ, p. 70, 1994. 29. Barnett, R.L. and Brickman, D. Safety Hierarchy, Triodyne Inc., Safety Brief, Vol. 3, No. 2 Revised, Niles, IL, June 1985. 30. A.G.A. Requirements for Carbon monoxide Safety Shutoff Systems and Carbon Monoxide Warning Devices, Supplement to American National Standard for Automatic Gas Ignition Systems and Components, ANSI Z 21.20, as contained in report No. 2-86, Nov 10, 1986. 31. Human Factors Perspectives on Warnings, 1980–1993, Human Factors and Ergonomics Society, 1994. 32. Human Factors Perspectives on Warnings, Vol. 2, 1994–2000, Human Factors and Ergonomics Society, 2001. 33. Braun, C.C., Greeno, B., and Silver, N.C. Differences in Behavior Compliance as a Function of Warning Color, Proceedings of the HFES 38th Annual Meeting, USA pp. 379–383, 1998. 34. Braun, C.C., Holt, R.S., and Silver, N.C. Signal Word and Color Specifications for Product Warnings, Proceedings of the HFES 38th Annual Meeting, USA, pp. 1104–1108, 1994.

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Carbon Monoxide Poisoning 35. Caird, J.K., Wheat, B., and McIntosh, K.R. The Comprehensibility of Airline Safety Card Pictorials, Proceedings of the HFEWS 41st Annual Meeting, USA, pp. 801–805, 1996. 36. Chen, J.C., Gilson, W.D., and Mouloua, M. The Comprehensibility of Airline Safety Card Pictorials, Proceedings of the HFES 41st Annual Meeting, USA, pp. 801–805, 1997. 37. Ringseis, E.L. and Caird, J.K. The Comprehensibility and Legibility of Twenty Pharmaceutical Warning Pictorials, Proceedings of the HFES 39th Annual Meeting, USA, pp. 974–978, 1995. 38. Hancock, H.E., Rogers, W.A., and Fisk, A.D. Understanding Age-related Differences in the Perception and Comprehension of Symbolic Warning Information, Proceedings of the HFES 43rd Annual Meeting, USA, pp. 617–621, 1999. 39. Nanthavanji, S. Analysis of Workplace Factors on Auditory Warning Alarm Location, In Advances in Industrial Ergonomics and Safety VII, Taylor & Francis, Bristol, PA, 1995. 40. Criteria for a recommended standard …Occupational Exposure to Carbon monoxide, U.S. Department of Health, Education and Welfare, National Institute for Occupational Safety and Health (NIOSH), 1972. 41. Chemical Hazards Bulletin, Engineering and Safety Services, American Insurance Association, 85 John Street, NY 10038, August, 1974. 42. In 1971 Primary and Secondary National Ambient Air Quality Standards (36 FR 8186), in 1985 Review of the National Ambient Air Quality Standards for Carbon Monoxide, 40 CFR Part 50, FR Vol. 50, No. 176, September 13, 1985. 43. 40 CFR Ch. 1, 7-1-86 Edition, Para 51.16(e) (3). 44. Viscusi, W.K. Product-Risk Labeling—A Federal Responsibility, Am. Enterprise Institute, p. 1, Washington, DC, 1993. 45. Burd, L.T. CO Morbidity and Mortality Six Decades of Carbon Monoxide Poisoning, Master of Public Health Thesis, University of Texas, Health Science Center at Houston, School of Public Health, August, 2002. 46. Non-fire Carbon Monoxide Deaths Associated with the use of Consumer Products 2001 Annual Estimates, CPSC, Susan Carlson, Directorate of Epidemiology, May 13, 2004. 47. Webster’s New World Dictionary of the American Language, 2nd College ed., World Publishing Co., 1970. 48. Decision in Secretary of Labor, Complainant, vs. CITY OIL WELL SERVICE CO., Respondent. OSHRC Docket number 81-1797, Buckley, Chairman; Cleary, Commissioner, September 30, 1986. 49. von Oettingen, W.F. et al. Carbon Monoxide: Its Hazards and the Mechanisms of Its Actions, Federal Security Agency, United States Public Health Service, Public Health Bulletin No. 290, 1944. 50. Weinstein, A.S. and Twerski, A.D. Products Liability and the Reasonably Safe Product, Wiley, p. 41, 1978. 51. Silvergate, S.H. The Restatement (Third) of Torts: Products Liability—The Tension Between Product Design and Product Warnings, Florida Bar J., Vol. 75, pp. 10–17, December 1, 2001. 52. Thorp, J.F. and Middendorf, W. What Every Engineer Should Know About Products Liability, Marcel Dekker, Basel and NY, 1978. 53. Freeman, S.H. Injury and Litigation Prevention, Van Nostrand Reinhold, NY, 1991. 54. Huber, P.W. The Liability Maze, The Brookings Institute, Washington, DC, 1991.

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9

Public Health Surveillance for Carbon Monoxide in the United States: A Review of National Data Michael E. King and Joshua A. Mott

CONTENTS 9.1 9.2

Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9.2.1 Public Health Surveillance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9.2.2 Carbon Monoxide-Caused Mortality . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9.2.2.1 Recent Studies of National CO Mortality. . . . . . . . . . . . . . . 9.2.3 Carbon Monoxide-Caused Morbidity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9.2.3.1 Recent National Studies of Nonfatal Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9.3 Toward a National Surveillance System for Carbon Monoxide . . . . . . . . . . 9.3.1 Case Definitions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9.3.2 Mortality Limitations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9.3.3 Morbidity Limitations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9.4 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

233 234 234 236 237 241 242 243 243 244 245 246 248

9.1 OVERVIEW This chapter provides a review of epidemiologic studies describing national surveillance related to carbon monoxide (CO) poisoning in the United States. We discuss sources of surveillance data and recent studies of CO-caused mortality and morbidity. We conclude with a summary of national estimates and provide recommendations for improving public health surveillance efforts and establishing a national system specifically designed to track CO poisoning. 233

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9.2 INTRODUCTION CO poisoning is an important public health problem in the United States, resulting in over 400 fatal unintentional poisonings annually.1 The burden of CO poisoning has been shown to vary from state to state,2 and risk factors for poisoning may vary across regions and populations, particularly in the wake of natural disasters.3,4 Ironically, CO poisoning in indoor environments “is almost entirely preventable by the correct installation, maintenance, and operation of devices that may emit CO indoors, combined with the appropriate use of CO detectors” (i.e., alarms).5 Surveillance activities are a critical component of any prevention effort and public health professionals rely on timely accurate surveillance to describe the magnitude and etiology of poisonings to better target interventions. Yet, despite increasing awareness of the dangers of CO poisoning, a timely national surveillance system is not in place to monitor CO poisonings or deaths in the USA. The purpose of this chapter is twofold: (1) to provide a review of epidemiologic studies describing national surveillance for CO poisoning in the United States, and (2) to discuss issues relevant to the development of an ongoing, national surveillance system for CO.

9.2.1 PUBLIC HEALTH SURVEILLANCE Environmental public health surveillance is broadly defined as: “the ongoing systematic collection, analysis, and interpretation of data, closely integrated with the timely dissemination of these data to those responsible for preventing and controlling disease and injury.”6 This definition emphasizes the importance of surveillance for CO poisoning, since information about the epidemiological aspects of CO poisoning is essential for targeting, monitoring, and evaluating risk factors and public health interventions. Surveillance activities are conducted routinely for diseases or conditions that are highly prevalent, result in excess emergency department (ED) or hospital use, and for which primary or secondary prevention is possible. However, with the exception of isolated reports from states responding to public health emergencies7,8 surveillance has not neen conducted for CO poisoning in the United States. The absence of a national system has resulted in “basic gaps in our knowledge of the epidemiology and outcomes of CO poisoning, including the long -erm sequelae, prevention, and risk behaviors.”5 The primary challenge for environmental surveillance is relating health outcomes, such as CO intoxication, to specific environmental exposures, and hazards.9 To facilitate this linkage, surveillance systems must collect, characterize, and disseminate data on health hazards, exposures, and interventions, in addition to health outcomes.9 Environmental health hazards are defined as chemical, physical, and biologic agents or biomechanical stressors in the air, food, and water.6 Exposure surveillance involves monitoring individuals for “the presence of an environmental agent, its metabolites, or its clinically inapparent (e.g., subclinical or preclinical) effects”.6 Tracking interventions includes monitoring programs and policies intended to prevent agents from becoming hazards or minimize exposures and health outcomes. Given the variety of data necessary to achieve these diverse surveillance objectives, no single dataset currently available is sufficient to serve as the sole source of surveillance data. Currently,

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TABLE 9.1 Components of an Environmental Public Health Surveillance System and Potential CO Poisoning Data Sources, United States Surveillance Components Hazard surveillance Examples: • CO emissions data • Gas leak public call-data Exposure surveillance Example: • Carboxyhemoglobin level data Health outcomes Examples: • Nonfatal poisoning occurrences • Occupational poisoning data • Outpatient visits • Emergency department visits • Hospitalization data • Mortality data Interventions Examples: • Data on the presence of working catalytic converters in automobiles • CO-detector ownership data • Gasoline-powered generator safety knowledge/attitude data • Emission and CO-detector legislation data

Data Sources • US Environmental Protection Agency National Emission Inventory database • Utility companies/fire departments • Electronic lab reporting databases (e.g., the National Electronic Disease Surveillance System) • American Association of Poison Control Centers Toxic Exposure Surveillance System (TESS) • Consumer Product Safety Commission CO Poisonings database • National Electronic Injury Surveillance System (NEISS) • National Ambulatory Medical Care Survey • National Hospital Discharge Survey • National Vital Statistics System • Environmental Protection Agency • Behavioral Risk Factor Surveillance System • Private national surveys (e.g., Porter-Novelli annual Healthstyles survey) • National Conference of State Legislatures electronic legislation databases

Source: Adapted from Thacker et al. Am. J. Publ. Health, 86, 633–638, 1996. The National Workgroup on Carbon Monoxide Surveillance Carbon monoxide: A model environmental public health indicator. ONLINE. 2006. Available: http://www.maine.gov/dhhs/eohp/epht/documents/CO_White.pdf. (Oct. 1, 2006).

“there are 31 federally funded national data systems that collect data on injury mortality, morbidity, and risk factors.”10 However, a limited number of them are potentially useful for tracking CO poisoning. Table 9.1 provides examples of different types of data and data sources for surveillance of environmental hazards, exposures, health outcomes, and interventions related to CO in the United States. To date, the majority of national surveillance studies for CO have focused on health outcomes, and, in particular, estimates of mortality. This focus is perhaps due to the absence of a single system that captures national CO-related morbidity reliably. Likewise, CO is often only recognized as the cause-of-death upon postmortem examination, because the symptoms of CO poisoning are nonspecific and are frequently attributed to other causes or overlooked altogether by clinicians and the public.11

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Most of the studies reviewed in this chapter concern poisonings resulting from unintentional and nonfire-related (NFR) events because both intentional and fire-related CO poisonings have distinctly different public health prevention strategies and are outside of the scope of this discussion.

9.2.2 CARBON MONOXIDE-CAUSED MORTALITY All US death certificates are compiled by the National Center for Health Statistics into the Multiple Cause-of-Death Mortality Database as part of the National Vital Statistics System (NVSS).12 To date, this system has served as the primary source of data for estimating national rates of poisoning death related to CO in the United States. This database provides mortality data by multiple-cause of death for all fatalities occurring in the United States. Each record is on the basis of information abstracted from death certificates filed in vital statistics offices of each state and the district of Columbia. Death certificates contain demographic and geographic information of the decedent, as well as up to 20 conditions that contributed to the death, coded according to the World Health Organization format International Classification of Diseases (ICD).13,14 The causes of death codes are compiled in two forms: the entity axis, which contains conditions as stated on the death certificate, and the record axis, which is edited by a computer algorithm to remove duplicate records and revise ICD codes to best describe the overall medical certification portion of the death certificate.15 It is important for researchers using Multiple-Cause data to be aware of the format and structure of the data file prior to use; documentation accompanying public use mortality data files specifies that the “record axis is designed for the generation of person-based multiple-cause statistics” and “by definition, the entity data cannot meet this requirement.”16 In other words, codes on the record axis may be used for CO surveillance to count people with conditions, whereas the entity axis data may only be useful for counting the number of times a particular condition was coded. The 8th Revision of ICD coding (ICD-8) was used for 11 years, from 1968 to 1978, the 9th Revision (ICD-9) from 1979 to 1998, and the 10th Revision (ICD-10) from 1999 to the present year. At the time of this writing, the most recent year of mortality data available was 2003 as there is a delay of 2–3 years before national mortality data are released to the public. As a reference, the ICD codes that have been used for the national surveillance of CO are provided in Table 9.2. One alternative source of national mortality data for the surveillance of CO is the Centers for Disease Control and Prevention (CDC), Wide-ranging Online Data for Epidemiologic Research (WONDER) data system. This system provides access to an array of health-related datasets, including the NVSS underlying cause-ofdeath files from National Center for Health Statistics (NCHS) and injury mortality reports generated by the Web-based Injury Statistics Query and Reporting System (WISQARS) maintained by the National Center for Injury Prevention and Control (NCIPC). Although WONDER may be used to estimate national CO mortality, it is important to note that the system can only identify cases of CO poisoning using a single cause-of-death. Hence these data are likely to underestimate the burden of unintentional poisoning because of the inability to select cases using codes in multiple-cause-of-death codes fields.

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TABLE 9.2 International Classification of Diseases Codes Specific to Carbon Monoxide Poisoning and Additional Codes Useful for Case Identification Underlying or contributing cause of death Toxic effect of carbon monoxide ICD-10: T58 ICD-8 and ICD-9: N986 Intent of death Unintentional injury ICD-10: X47 ICD-8 and ICD-9: E800-E949 Intent undetermined ICD-10: Y17 ICD-8 and ICD-9: E980-E989 Mechanism of death Fire-related (exclude from analyses) ICD-10: X00-X09 ICD-8 and ICD-9: E837, E890-E899, E923, or N940-N949 Motor vehicle-related ICD-10: No X-code specific to CO ICD-9: E800-E807, E810-E825, E830-E836, E838, E840, E841, E843-E847, E868.2, E929.0, E929.1, E952.0, E958.5, E958.6, E982.0, E988.5, and E988.6 ICD-8: E800-E807, E810-E825, E830-E836, E838, E840, E841, E843-E845, E873, E927, E940-E941, and E952.0 Nonmotor vehicle-related ICD-10: No X-code specific to CO ICD-9: E867, E868.0, E868.1, E868.3, E919, E920, E951, E981 ICD-8: E870-E872, E874, E920, E927, E928, E951, E981 Source: Adapted from Mott et al., JAMA, 288, 988–995, 2006.

9.2.2.1 Recent Studies of National CO Mortality The most recent analysis of unintentional, nonfire-related (UNFR), CO-related mortality data in the United States was produced by the National Center for Environmental Health’s Air Pollution and Respiratory Health Branch at the CDC.17 This study estimated national and state-specific CO mortality rates and described the demographic, seasonal, and geographic patterns in CO-related deaths for 1999–2002.17 Death certificate data were obtained from the NVSS using the underlying cause-of-death field and record axis fields from the multiple-cause-of-death files. A case of unintentional CO-related death was defined as a US resident death coded using the ICD-10 code T58 (toxic effect of CO) as the underlying cause-of-death and for which poisoning by accidental exposure (code X47) or exposure of undetermined intent (code Y17) to gases or vapors was listed as a contributing cause in one of the 20 record axis fields. All records of deaths caused by intentional or fire-related exposure to CO, coded as X00–X09, were excluded from the analysis. This study found that during

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1999–2002, there were 11,132 CO-related deaths among U.S. residents, of which 1982 (18%) were classified as both unintentional and NFR. From 1999 to 2002, the total average age-adjusted annual death rate for UNFR CO was 1.8 deaths per million persons in the United States. Death rates were highest for adults (2.2 per million for adults aged >18 years, versus 0.4 per million for children aged 17 years or younger) and men (2.8 per million men versus 0.9 per million women). The average daily number of CO-related deaths was greatest during the months of January and December (277 per month) and lowest during the months of July and August (91 per month). For the period from 1999 to 2002, only 32 states had a sufficiently large number of UNFR CO-related deaths to calculate stable mortality rates (Figure 9.1). Although numerous states had rates above the national four-year average annual rate, the state with the highest statistically reliable UNFR CO mortality rate was Nebraska (5.6 deaths per million person-years) and the state with the lowest reliable rate was California (0.6 average deaths per million) (Figure 9.1). Reporting of acute CO poisoning by healthcare providers was mandated for 13 states, although there was no clear pattern of differences in CO-related mortality between states with mandated reporting and those without.17 In 2005, the National Center for Injury Prevention, in conjunction with the National Center for Environmental Health, used multiple-cause-of-death mortality data to estimate the annual incidence of fatal and nonfatal unintentional, NFR CO poisoning.18 This study provided national crude annual UNFR CO death rates by demographic characteristics and season for 2 years: 2001 and 2002. In addition, case-fatality rates were estimated by dividing the number of deaths by the sum

UR

UR (NH) UR (VT)

UR

UR

UR UR

MR MR

UR MR

UR

UR (ME) UR/MR (MA)

MR

MR

UR (RI) UR (CT) MR (NJ) UR/MR (DE) UR (DC)

MR UR MR

UR UR(HI)

CO Death Rate* > U.S. Average = U.S. Average

*Rate per 1,000,000 population per year, age-adjusted to 2000 US Census population . UR = Rate unreliable MR = CO death is a mandated reportable condition

< U.S. Average

FIGURE 9.1 Average rates of unintentional, nonfire, carbon monoxide-related death, by state, United States, 1999–2002.

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of UNFR CO deaths and nonfatal exposures multiplied by 100. Fatal UNFR CO poisoning deaths were identified as those with ICD-10 code T58 as a leading or contributing cause of death and an underlying cause of death code indicating either accidental poisoning (X47) or poisoning of undetermined intent (Y17). This study found that the crude annual UNFR CO death rate for the United States was 0.17 per 100,000 with an average of 480 deaths per year. The annualized incidence of fatal UNFR CO exposures was greatest during the fall and winter months, with more cases occurring during December (56 deaths) and January (69 deaths). The crude death rate from CO was highest for adults over 65 years (0.32 per 100,000), males (0.24 per 100,000), and nonHispanic whites and blacks (0.17 per 100,000). The case-fatality rate increased with age, ranging from 0.6% for children under 4 years to 5.5% for adults aged 55–64 years. Overall, males had a 2.3 times higher casefatality rate than women and 23.5% of deaths occurred among adults aged 65 years or more.18 In 2002, Mott et al.19 conducted an ecological analysis of national CO death data from the NVSS and annual CO emissions estimates for light-duty vehicles obtained from the US Environmental Protection Agency. This study estimated the percent change in CO emissions and CO mortality rates by intent and mechanism for the years 1968–1998. The main outcome from this study was US resident deaths from 1968 to 1998 coded with ICD-8 or ICD-9 code N986 (toxic effect of CO) as a contributing cause -of -death or those records with an ICD external cause of injury code exclusive to CO poisoning (Table 9.2). From 1968 through 1998, this study identified 116,703 NFR deaths due to CO in the United States. During this same time period, crude mortality rates associated with NFR CO declined from 20.2 deaths to 8.8 deaths per million person-years in the United States. There were 2.2 intentional deaths for every one unintentional NFR CO-related death. Between 1968–1998, motor vehicles were identified as the mechanism for 70.6% of deaths and, following the introduction of the catalytic converter in 1975, annual estimates of NFR CO emissions decreased by 76.3%. In addition, unintentional motor vehicle-related NFR CO death rates declined by 81.3% and rates of motor vehicle-related NFR CO suicides declined by 43.3%.19 In 1996, the CDC published a summary of findings from an investigation of deaths associated with multiple motor-vehicle related CO poisonings in Colorado and New Mexico, together with national estimates of CO deaths from 1979–1992.20 This report presented the geographic pattern of national unintentional CO mortality associated specifically with stationary motor vehicles (UMVR). Deaths were identified using ICD-9 code E868.2, a code specific to deaths due to accidental poisoning by CO or another utility gas from the following sources: farm tractor not in transit, gas engine, motor vehicle not in transit, or any type of combustion engine not in a watercraft. This analysis found that crude death rates for UMVR CO were highest in states in the northern regions of the United States from 1979 to 1992, although no specific national or state rates were provided.20 In the early 1990s, Cobb and Etzel2 published a descriptive analysis of unintentional NFR CO-related deaths (UNFR) in the United States. This study calculated crude and age-adjusted death rates by demographic characteristic, season, and state for the years 1979–1988. All US resident deaths coded using ICD-9 code N986 were

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identified between 1979–1988, excluding those coded as intentional (codes E950– E959 and E960–E969), intent undetermined (E980–E989), and those owing to fire (E837, N940–N949, E923). The 10-year average crude UNFR CO death rate for males (0.78 per 100,000 persons) was found to be 3 times higher than that for females (0.26 per 100,000 persons). Overall, 83% of UNFR CO-related deaths occurred among whites, yet “race-specific death rates were more than 20% higher for blacks (0.63 per 100,000) than for whites (0.51 per 100,000).”2 Annual incidence of unintentional CO-related death was found to be highest in the month of January, with an average of 181 deaths, and lowest in the month of July, with an average of 44 deaths. The state with the highest age-adjusted UNFR CO death rate for the 10-year period was Alaska (2.72 per 100,000) and the lowest rate was found in Hawaii (0.05 per 100,000).2 In addition to the above-mentioned surveillance reports produced by the CDC, national estimates of CO-related mortality produced by the Consumer Products Safety Commission (CPSC) may provide useful national surveillance for CO-related mortality. These reports combine data from multiple sources, such as the NVSS and National Electronic Injury Surveillance System (NEISS), with proprietary CPSC datasets21 on the basis of death certificate data purchased directly from states and in-depth follow-up investigations of select deaths. These data are used to produce annual national estimates of unintentional NFR CO exposures and fatalities by product, victim age, and incident location. However, the reports currently available are limited to estimates associated specifically with the use of consumer products under the jurisdiction of the CPSC (e.g., engine-powered tools, charcoal grills, gas ovens, and other appliances). CPSC reports do not capture fatalities associated with motor vehicles, despite the fact that CO in motor-vehicle exhaust has been found to account for the majority of poisoning deaths in the United States.22 The most recent year for which a complete CPSC report of CO-related mortality is available is 2002.23 In 2002, CPSC identified 188 unintentional, nonfire CO-related deaths and the average annual estimate from 1999 to 2002 was 141 deaths. Heating systems were associated with 55% of deaths and engine-powered tools were associated with 28% of deaths in 2002. An estimated 71% of CO deaths occurred in the home. Overall, 81% of fatal CO incidents involved a single death, with adults over 45 years of age accounting for 55% of all unintentional, nonfire CO deaths in 2002.23 Although CPSC memoranda have been published covering both non-fatal CO exposure incidents and fatalities for the periods 1990–2004 and 2002–2005, respectively, CPSC notes that the counts for recent years contained in these reports may not be complete.24 Briefly, from 1990 to 2004, there were 318 nonfire CO-related deaths identified by CPSC, 274 of which were associated with the use of generators. Most of these deaths (39%) occurred during winter and 77% took place in the home. From 1990 to 2004, an estimated 33% of deaths occurred among adults aged 45–64 years and 75% of all “engine-driven tool” CO-related deaths were males.24 From 2002 to 2005, preliminary counts from CPSC indicate that 253 nonfire CO-related deaths were associated with engine-driven tools in the United States. An estimated 218 (86%) of CO deaths were associated with gasoline-powered generators.20

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9.2.3 CARBON MONOXIDE-CAUSED MORBIDITY National surveillance for nonfatal CO exposures is challenging, given the limited number of data sources currently available (Table 9.1). One potential source for national nonfatal CO poisoning data is the NEISS, operated by the CPSC since 1971.25 The NEISS has been used to monitor consumer product-related injuries resulting from consumer products under the regulatory jurisdiction of the CPSC. In 2000, the surveillance system was expanded to collect data about all types and causes of injuries and poisonings treated in hospital EDs, whether or not they were associated with consumer products. This expanded system is called the NEISS All Injury Program (NEISS-AIP). NEISS data are currently collected from a nationally representative sample of 100 EDs, selected from a stratified probability sample of all US hospitals that have at least 6 beds and provide 24-h emergency services, while NEISS-AIP data are collected from a 66 hospital subsample. Data from approximately 500,000 injuryrelated ED cases are collected annually by NEISS and coded for cause and intent of injury using guidelines consistent with coding guidelines in the ICD-9-CM.25 Use of these data for CO surveillance is limited, however, they exclude incidents owing to occupational exposure, those associated with motor vehicles, and cannot provide state or local estimates.25 Another source of national nonfatal CO poisoning surveillance data is the National Hospital Ambulatory Medical Care Survey (NHAMCS) conducted by the National Center for Health Statistics of the CDC. The NHAMCS collects data on the utilization and provision of ambulatory care services in hospital emergency and outpatient departments. Findings are on the basis of a national sample of visits to the emergency and outpatient departments of noninstitutional general and short-stay hospitals, exclusive of federal, military, and veterans administration hospitals, located in the 50 States and the District of Columbia. Annual data collection began in 1992. Similarly, the national Toxic Exposure Surveillance System (TESS) operated by the American Association of Poison Control Centers has demonstrated capability to serve as a source of CO data for both state-based26 and national studies.27 Implemented in 1983, TESS is a comprehensive database that contains detailed toxicological information about over 24 million poisoning incidents reported to 61 poison control centers in the United States.28 The calculation of rates of calls to TESS for a given exposure is facilitated because participating poison control centers also report the size of the population they serve. However, the use of TESS data for CO surveillance may be limited by the fact that most reports pertain to the treatment of nonfatal poisonings. Therefore, TESS data may underestimate the incidence of fatal CO exposures. As of October, 2006, annual reports summarizing TESS data are available online for the years 1983–2004 (http://www.aapcc.org/annual.htm). Finally, recent studies have suggested that data obtained from hyperbaric oxygen (HBO) therapy centers may serve as an indicator of CO burden.27,30 HBO is typically used to treat those patients with the most severe CO poisoning,27 comprising approximately 6% of all patients seen for CO in EDs.30 According to Hampson, “as long as the spectrum of severity of the condition and treatment practices has not been recognized to have changed significantly during the period surveyed, the national rate of HBO therapy should serve as a qualitative marker of total disease incidence”.27

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Using data from HBO therapy facilities for national CO surveillance is limited by the lack of general availability and the fact that these data do not include less severe cases, those not referred for HBO, or those treated at EDs using HBO. Likewise, a patient’s state of residence may differ from that in which they received the HBO therapy, complicating the calculation of valid state rates. 9.2.3.1 Recent National Studies of Nonfatal Carbon Monoxide Poisoning A 2005 study by Hampson27 used TESS data and information from a recent survey of HBOT facilities29 to compare trends in the annual incidence of nonfatal CO poisoning in the United States. Hampson27 searched TESS records from 1985 to 2002 for all calls received by poison control centers regarding cases of CO exposure, and calculated annual call rates per million person-years. This study found that annual call rates for CO poisoning increased from 31.1 per million in 1985 to 95.4 per million in 1996. Although the rate decreased to 54.5 per million persons from 1996 to 2002, there was a significant increase in calls for the entire 18 year period (p = .0022).27 Rates of HBOT for CO poisoning and rates of calls to poison control centers were also found to correlate strongly (r = 0.82, p = .0002).27 Also in 2005, the CDC published national estimates of unintentional, NFR CO exposures for 2001–2003 using NEISS-AIP data.18 Nonfatal cases of CO poisoning were considered to be those coded as “CO exposure” or “CO poisoning” in NEISS-AIP hospital data. Additional criteria used to identify nonfatal CO poisonings included: (1) intent of injury unintentional or undetermined, (2) principle diagnosis of “poisoning” or “anoxia”, and (3) additional narrative information indicative of CO. This study estimated that 15,200 patients were treated in EDs annually for nonfatal, unintentional, NFR CO poisoning during 2001–2003. Overall, the rate of nonfatal exposure was similar for males and females, although the rate was highest for children under 4 years of age (8.2 per 100,000 person). While most nonfatal CO exposures (64.3%) occurred in the home, only 9.3% of patients reported owning a CO detector.18 This study also provided national estimates of CO-related mortality discussed earlier in this chapter. Although not pertaining to CO specifically, a CDC report published in 1999 used data from the NHAMCS to describe poisoning-related ED visits from 1993 to 1996 in the United States.31 This study used a variety of ICD-9-CM codes to identify all injury-related ED visits, but did not provide sufficient detail to describe the etiology, intent, or mechanism of CO exposures. From 1993 to 1996, toxic effect of CO (ICD-9-CM code N986) was the sixth leading principle diagnosis identified among poisoning-related ED visits in the United States An annual average of 34,000 ED visits were attributed to CO during the 4 year study period.31 In an earlier study, Hampson30 reported a synthetic national estimate of nonfatal CO poisoning on the basis of a survey of EDs located in Washington, Idaho, and Montana. This survey collected data about the total number of patients seen for acute CO poisoning in 1994, although details regarding the etiology, source, or intent of the poisoning were not collected. This analysis extrapolated data from the three states to the United States as a whole and used state-specific age-adjusted CO death rates

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to adjust for the fact that CO poisoning is more common in the Pacific Northwest region. The study estimated 42,890 ED visits for CO poisoning occurred in 1994 in the United States, resulting in a national ED visit rate of 16.5 per 100,000 persons for CO poisoning.30 The public health literature describing surveillance of CO poisoning included in this chapter is characterized by its variability. Although most studies focus on fire-related CO poisoning, different data sources and definitions of poisoning are used for case ascertainment, thus limiting the comparability of national estimates. In addition, other national estimates of nonfatal CO poisoning are available in the literature, although many of these focus only on poisonings resulting from a specific mechanism (i.e., consumer products) or are very old. For example, recent reports from the CPSC have used data from the NEISS to estimate that approximately 5000 nonfatal CO poisonings associated with motor-driven appliances occur annually in the United States.32 Likewise, a 1974 study estimated that 10,000 nonfatal CO poisonings occurred annually in the United States.33 The variability among national studies and estimates of CO poisoning underscores the need for a national surveillance system for CO.

9.3 TOWARD A NATIONAL SURVEILLANCE SYSTEM FOR CARBON MONOXIDE The lack of information linking environmental hazards to health outcomes has contributed to what has been labeled the “environmental health gap” by The Pew Environmental Health Commission.34 To address this gap and coordinate the development of CO surveillance in the United States., the CDC established The National Workgroup on Carbon Monoxide Surveillance, a partnership of public health professionals and agencies spanning private and federal jurisdictions from environmental health and injury prevention to emergency response.5 This workgroup has noted that the need for nationwide CO surveillance “is recognized in the Healthy People 2010 goal for the United States of ‘increasing the number of Territories, Tribes, and States, and the District of Columbia that monitor carbon monoxide poisoning from 7 to 51.’”5 One indicator of progress toward the Healthy People 2010 goal for CO is the number of states that mandate reporting of CO poisoning as part of the National Notifiable Disease Surveillance System. The National Council of State and Territorial Epidemiologist (CSTE) serves as a partner in the National Workgroup for CO Surveillance and monitors patterns of nonnotifiable diseases and conditions; currently, 15 states mandate reporting of CO poisoning (http://www.cste.org/NNDSSSurvey/ 2004NNDSS/NNDSSstatechrreporcondnona2005.asp). Similarly, although a number of states have mandated the installation of CO detectors, surveillance data are needed to evaluate the effectiveness of ongoing legislative interventions for CO.

9.3.1 CASE DEFINITIONS Although there is a growing recognition of the need to develop a national surveillance system for CO, methods of case identification and ascertainment remain a

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serious challenge for injury and death due to CO. The ability to accurately describe CO-related morbidity and mortality depends heavily on the methods used to identify and classify cases, the rules for coding data, and the type of data available. Effective public health surveillance relies on the establishment of a widely adopted, clear, and reliable case definition that includes criteria describing person, place, and time.35 To date, no such consensus has been reached in the case of CO poisoning. According to the National Workgroup on Carbon Monoxide Surveillance, 2 national public health organizations have published their own version of a case definition for public health surveillance of CO poisoning; The CSTE and the State and Territorial Injury Prevention Directors Association (STIPDA). The STIPDA definition is more conservative than the CSTE definition, that is, if both definitions are applied to the same dataset, the STIPDA definition will identify fewer records as having CO poisoning than the CSTE definition. The CSTE definition has been modified by at least one state to make it a more conservative definition.36 The case definitions suggested by CSTE and STIPDA are listed in Table 9.3. A formal evaluation of these case definitions is the focus of a current study by the National Workgroup for CO Surveillance.36

9.3.2 MORTALITY LIMITATIONS In addition to achieving a uniform case definition for tracking CO poisoning, understanding the limitations of available data is vital to improve national CO surveillance efforts. For mortality specifically, the use of death certificate data for national CO

TABLE 9.3 Two Case Definitions for the National Surveillance of Carbon Monoxide in the United States Carbon Monoxide Case Definitions CSTE Confirmed case: ICD-9 Coded Data: (1) a record in which the Nature of Injury code N-986 “Toxic effect of CO” is listed or (2) a record in which an External Cause of Injury (E-Code) indicating exposure to carbon monoxide (exclusively) is listed such as E868.3, E868.8, E868.9, E952.1, or E982.1. Probable case: ICD-9 Coded Data: A record in which an E-code indicating acute carbon monoxide poisoning inferred from motor-vehicle exhaust gas exposure is listed, ie. E868.2, E952.0, or E982.0. STIPDA Records must have the N-code for CO poisoning (986) in the principal diagnosis field. Because this case definition relies only upon the presence or absence of the N-code, it does not define classification of cases, such as confirmed and probable. Source: National Workgroup on Carbon Monoxide Surveillance. Project to evaluate carbon monoxide surveillance CSTE and STIPDA case definitions with hospital data. 2006 Unpublished report. Obtained October, 2006 from the Air Pollution and Respiratory Health Branch, U.S. Centers for Disease Control and Prevention.

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surveillance is limited by recent changes in the way deaths are coded and classified. As noted earlier, the Tenth Revision of the ICD (ICD-10) was implemented in 1999 and is currently used to categorize causes of death in the NVSS. Earlier versions of ICD coding provided external cause of injury codes exclusive to CO poisoning (ICD 8 = E874, E875, and E952.1; ICD 9 = E868.3, E868.8, E868.9, E952.1, and E982.1) or poisoning from motor vehicle exhaust (ICD8 = E873 or E952.0; ICD9 = E868.2, E952.0, and E982.). Since CO is the only acutely poisonous gas in motor vehicle exhaust, in the past these latter codes could also be used to indicate CO poisoning. Although numerous ICD-10 codes mention CO, the Tenth Revision of ICD has only one code specific to CO:T58. While the latest revision contains codes that indicate the manner or intent of injury or can identify fire-related exposures, much detail has been lost in the ability to describe certain etiologic mechanisms (such as motor vehicle-related injuries) that could be described previously using E-codes related to CO. Hence, estimates of CO deaths classified using ICD-9 are not directly comparable to estimates derived from ICD-10 coded data. In addition to limitations regarding case ascertainment, data from NVSS do not become available to the public in a timely manner and lack other etiologic detail necessary for CO surveillance. For example, NVSS data do not contain sufficient detail to identify multiple victims of the same incident of CO poisoning. Estimating CO-related death from the NVSS requires a thorough understanding of the ICD coding rules and the limitations for case identification imposed by selection criteria for specific years of data. To summarize, the most important implication of the implementation of ICD-10 is that the already limited etiologic detail in the NVSS has been further reduced, thereby substantially decreasing its usefulness as national CO surveillance system. The use of the NVSS for national mortality surveillance indicates that there are roughly 500 unintentional, NFR CO deaths per year in the United States. Follow-up epidemiologic investigations of these deaths, however are needed to provide us with enough etiologic information to suggest meaningful public health interventions. Such investigations remain a high priority until alternate sources of surveillance data can be made available.

9.3.3 MORBIDITY LIMITATIONS Data currently available for the surveillance of nonfatal CO poisoning are limited by difficulties with case ascertainment. CO poisoning is characterized by nonspecific signs and symptoms that are often ignored or attributed to another condition by the public and medical professionals alike.11 In addition, those who experience nonfatal CO poisoning but do not present for medical treatment are not counted in morbidity estimates from medical records. Hence, all estimates of nonfatal poisoning are likely to underestimate the actual incidence of CO poisoning. The variation of populations and methods evident among datasets currently available suggest that no single source can serve as a comprehensive surveillance source for CO poisoning morbidity in the United States at this time. Despite these limitations, the continuing morbidity and mortality associated with acute CO poisoning in the United States necessitates the establishment of a national surveillance system. The goals of a national surveillance system

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for CO range from planning for rapid public health responses following disasters and tracking the burden of CO poisoning over time, to improving our understanding of exposure sources, related hazards, and facilitating research.5,36 To promote and facilitate surveillance at the local, state, and federal levels, the National Workgroup for CO Surveillance has produced a summary report describing the attributes of CO as a model environmental public health indicator (http://www.maine.gov/dhhs/eohp/epht/documents/CO_White.pdf).5

9.4 CONCLUSIONS Although the overall national rate of death from NFR CO declined steadily from 1968 to 1998 in the United States,19 the average annual rate of unintentional nonfire-related (UNFR) CO-related death has remained relatively stable over the past 4 decades.17–19 From 1968 to 1998, the crude death rate for UNFR CO was 7.06 deaths per 1 million person-years.19 The most recent analysis of mortality data from 2002 reported a crude UNFR CO death rate of 1.8 deaths per 1 million person in the U.S.17 There are an average of 494 accidental, NFR deaths and approximately 1,747 intentional deaths due to CO-poisoning each year in the United States.19 Evidence from a recent ecological study suggests the decrease in all CO-related deaths in the United States was driven primarily by a reduction in deaths from exposure to motor-vehicle exhaust.9 This reduction has been attributed to the national implementation of the 1970 Clean Air Act. In contrast to trends in national CO mortality, the incidence of nonfatal CO poisonings rose, while rates of death fell from 1985 to 1996 in the United States27 The annual number of nonfatal poisonings then decreased from 1996 to 2002.27 Published estimates of ED visits due to UNFR CO poisoning suggest there are approximately 15,200 ED visits per year, with 1,676 resulting in subsequent hospitalization.18 Similarly, unpublished estimates from the 2002 National Hospital Discharge Survey using the CSTE-proposed case definition identified 1496 hospitalizations due to UNFR CO poisoning in the U.S.37 Across studies, men and older adults (ranging from over 45 to over 65 years) are most at risk for unintentional death or injury from CO.17–19 Despite the lack of uniform national surveillance data, the burden of CO poisoning in the United States may be summarized using estimates from a variety of related data sources (Figure 9.2). The substantial health burden of unintentional CO poisoning illustrated in Figure 9.3 suggests the need to put CO morbidity and mortality under ongoing public health surveillance. The de facto national surveillance system for CO poisoning in the United States has been the NVSS. However, this system has several limitations for the surveillance of CO poisoning. Although the data have taken two years to process following collection, the recent implimentation of ICD-10 codes has further limited the utility of the NVSS for CO surveillance due to the removal of several important ICD codes that denote etiologic mechanism of poisoning. Public health professionals must consider these recent changes in the ICD coding system when assessing CO-related mortality derived from the NVSS. When estimating nonfatal CO poisoning, data from multiple sources should be used to cross-validate estimates of morbidity, to reduce the likelihood of under-estimation from any single source of data. To obtain a complete picture of

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120

10

100

8

80

6

60

4

40

1975– catalytic converters required on all new passenger cars

2

20

0

CO Emissions control timeline Grams of CO emited per VMT

CDR per1,000,000 personyears

Suicides 12

1975: Catalytic converter introduced on new passenger cars to meet new CO emissions standard of 15 g/mile. 1978:1975 and newer model year cars make up 34% of the U.S.passenger vehicle fleet.

0

5

120

4

100 80

3 60 2 40

98 19

94

96 19

92

19

90

19

88

CDR: Nonmotor vehicle

19

86

19

84

19

82

19

80

19

78

CDR: Motor vehicle

19

76

19

74

19

19

19

19

19

72

0 70

20

0 68

1

COEmissions (g/mile)

Gramsof CO emited per VMT

Unintentional deaths CDR per1,000,000 personyears

1970:Congress enacts Clean Air Act. CO emissions standard at 34.0 g/mile.

1980: All new passenger cars required to meet new CO emissions standard of 7.0 g/mile. 1975 and newer model year cars make up 50% of US.passenger vehicle fleet. 1981:All newcars required to meet new CO emissions standard of 3.4 g/mile. 1990:1975 and newer model year cars make up 91% of the U.S.passenger vehicle fleet. 1992: Standards setting emission limits for carbon monoxide at temperatures <20°F are established. Oxygenated gasoline is introducedin cities with high CO levels. Source: EPA CO emissions inventory data,and Fact Sheet OMS-12.

FIGURE 9.2 Annual crude death rates (CDR) from carbon monoxide poisoning, and annual estimated grams of CO emitted per vehicle mile traveled (VMT), United States, 1968–1998 (From Mott et al., JAMA, 288, 988–995, 2006.)

494 deaths17

1,496 hospitalizations37

13,201 emergency department visits18

15,633 calls to poison control centers27

FIGURE 9.3 The nonfire-related, carbon monoxide poisoning pyramid, 2002, U.S.

CO poisoning, surveillance systems must be established in a variety of settings and must be comprehensive, capturing the incidence, causes, and circumstances of both nonfatal and fatal poisonings in a timely manner. Likewise, innovative approaches may be necessary to gather surveillance data on nonresident populations, such as

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undocumented immigrants who may be at increased risk for CO poisoning, but for whom the calculation of valid rates is challenging. Ultimately, the standardization of an ICD-coded case definition for CO-related morbidity and mortality is a necessary 1st step to describe the national burden of CO poisoning, to better target interventions, and to evaluate the impact of public health prevention efforts.5 Until additional resources can be identified and allocated to surveillance at the federal, state, and local levels, epidemiologic investigations of recent CO-related deaths will need to remain the foundation for obtaining the etiologic information necessary to mount effective public health campaigns.

References 1. U.S. Centers for Disease Control and Prevention. Poisonings fact sheet. ONLINE. 2006. National Center for Injury Prevention and Control. Available: http://www.cdc.gov/ncipc/factsheets/poisoning.htm. (Oct. 1, 2006). 2. Cobb, N. and R. A. Etzel. Unintentional carbon monoxide-related deaths in the United States, 1979–1988. JAMA 266: 659–663, 1991. 3. U.S. Centers for Disease Control and Prevention. Carbon monoxide poisoning after Hurricane Katrina—Alabama, Louisiana, and Mississippi, August–September, 2005. MMWR, 54: 996–998, 2005. 4. Daley, W. R., A. Smith, E. Paz-Argandona, J. Malilay, and M. McGeehin. An outbreak of carbon monoxide poisoning after a major ice storm in Maine. J. Emerg. Med. 18: 87–93, 2000. 5. National Workgroup on Carbon Monoxide Surveillance. Carbon monoxide: A model environmental public health indicator. ONLINE. 2006. Available: http:// mainegov-images.informe.org/dhhs/eohp/epht/CO_WHITE.pdf. (Oct. 1, 2006). 6. Nsubuga, P., M. White, and S. Thacker et al. Public health surveillance: A tool for targeting and monitoring interventions. In Disease Control Priorities in Developing Countries, 2006, D. Jamison, J. Breman, A. Measham, G. Alleyne, M. Claeson, D. Evans, P. Jha, A. Mils, and P. Musgrove, eds., pp. 997–1015, New York, NY: Oxford University Press. 7. U.S. Centers for Disease Control and Prevention. Unintentional carbon monoxide poisonings in residential settings—Connecticut, November 1993–March 1994. MMWR 44: 765–767, 1995. 8. Girman, J., Y. Chang, S. Hayward, and K. Liu. Causes of unintentional deaths from carbon monoxide poisonings in California. W. J. Med. 168: 158–165, 1998. 9. Thacker, S. B., D. Stroup, R. Parrish, and H. Anderson. Surveillance in environmental public health: Issues, systems, and sources. Am. J. Publ. Health 86: 633–638, 1996. 10. Institute of Medicine, Surveillance and data. In: Reducing the Burden of Injury: Advancing Prevention and Treatment, Bonnie, R., C. Fulco, and C. Liverman, eds., 1999, 60–81. National Academy Press, Washington, DC. 11. Raub, J., M. Mathieu, N. Hampson, and S. Thom. Carbon monoxide poisoning—A public health perspective. Toxicology 145: 1–14, 2000. 12. U.S. Centers for Disease Control and Prevention. U.S. census populations with bridged-race categories. ONLINE. 2004. National Center for Health Statistics. Available: http://www.cdc.gov/nchs/about/major/dvs/popbridge/popbridge.htm. (Oct. 1, 2006).

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13. World Health Organization. Manual of the International Statistical Classification of Diseases, Injuries, and Causes of Death, 1967: 8th revision. Geneva. 14. World Health Organization. Manual of the International Statistical Classification of Diseases, Injuries, and Causes of Death, 1977: 9th revision. Geneva. 15. U.S. Centers for Disease Control and Prevention. Public use data file documentation: multiple cause of death for ICD-9, 1994. 1996, Hyattsville, MD: National Center for Health Statistics. 16. U.S. Centers for Disease Control and Prevention. Public use data file documentation: mortality for ICD-10, 1999. 2002, Hyattsville, MD: National Center for Health Statistics. Available: http://0-www.cdc.gov.mill1.sjlibrary.org/nchs/data/dvs/ Mort99doc.pdf. (Oct. 1, 2006). 17. U.S. Centers for Disease Control and Prevention. Update of unintentional, non-fire, carbon monoxide-related death rates, United States, 1999–2002. 2006, Unpublished data, Air Pollution and Respiratory Health Branch. 18. U.S. Centers for Disease Control and Prevention. Unintentional non-fire-related carbon monoxide exposures in the United States, 2001–2003. MMWR 54: 36-39, 2005. 19. Mott, J., M. Wolfe, C. Alverson et al. 2002. National vehicle emissions policies and practices and declining U.S. carbon monoxide-related mortality. JAMA 288: 988–995, 2006. 20. U.S. Centers for Disease Control and Prevention. Deaths from motor-vehicle related unintentional carbon monoxide poisoning, Colorado, 1996, New Mexico, 1980, 1995, and United States, 1979–1992. MMWR 45: 1029–1032, 2006. 21. Consumer Product Safety Commission. Non-fire carbon monoxide fatalities associated with engine driven generators and other engine driven tools in 2002 through 2005. ONLINE. 2006, August. Available: http://www.cpsc.gov/library. (Oct. 1, 2006). 22. Baker S., B. O’Neill, M. Ginsburg, and G. Li. The Injury Fact Book, 1992, 2nd ed., New York: Oxford University Press. 23. Consumer Product Safety Commission. Non-fire carbon monoxide deaths associated with the use of consumer products: 2002 annual estimates. ONLINE. 2006, Available: http://www.cpsc.gov/library. 24. Consumer Product Safety Commission. Incidents, deaths, and in-depth investigations associated with carbon monoxide from engine-driven generators and other engine-driven tools, 1990–2004. ONLINE. 2005, December. Available: http://www.cpsc.gov/library. 25. Kessler, E. and T. Schroeder. The NEISS sample: Design and implementation. 2000. Washington, DC: U.S. Consumer Product Safety Commission. 26. U.S. Centers for Disease Control and Prevention. Monitoring poison control center data to detect health hazards during hurricane season—Florida, 2003–2005. MMWR 55: 426–428, 2006. 27. Hampson, N. Trends in the incidence of carbon monoxide poisoning in the United States. Am. J. Emerg. Med. 23: 838–841, 2005. 28. Watson, W., T. Litovitz, C. Rubin et al. Toxic Exposure Surveillance System [abstract]. In: Syndromic Surveillance: Reports from a National Conference, 2003. MMWR 53: 262, 2004. 29. Hampson, N. and C. Little. Hyperbaric treatment of patients with carbon monoxide poisoning in the United States. Undersea Hyperb. Med. 32: 21–26, 2005. 30. Hampson, N. Emergency department visits for carbon monoxide poisoning in the pacific northwest. The J. Emerg. Med. 16: 695–698, 1998.

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Carbon Monoxide Poisoning 31. McCaig, L. and C. Burt. Poisoning-related visits to emergency departments in the United States, 1993–1996. J. Toxicol. 37: 817–826, 1999. 32. Mah, J. C. Non-fire carbon-monoxide deaths and injuries associated with the use of consumer products: annual estimates - October 2000. ONLINE. 2001, August. U.S. Consumer Product Safety Commission. Available: http://www.cpsc.gov/ library/co00.pdf. 33. Schaplowsky, A., F. Oglesbay, and J. Morrison et al. Carbon monoxide contamination of the living environment: A national survey of home air and children’s blood. J. Environ. Health 36: 569–573, 1974. 34. Pew Environmental Health Commission. America’s Environmental Health Gap: Why the Country Needs a Nationwide Health Tracking Network, 2000. Technical Report. Baltimore, MD: Pew Environmental Health Commission. 35. Teutsch, S. Considerations in planning a surveillance system. In Principles and Practice of Public Health Surveillance, 2000, S. Teutsch and R. Churchill, eds., pp. 17–29. New York: Oxford University Press. 36. National Workgroup on Carbon Monoxide Surveillance. Project to evaluate carbon monoxide surveillance CSTE and STIPDA case definitions with hospital data. 2006 Unpublished report. Obtained October, 2006 from the Air Pollution and Respiratory Health Branch, U.S. Centers for Disease Control and Prevention. 37. U.S. Centers for Disease Control and Prevention. Estimates of unintentional, non-fire, carbon monoxide-related hospital discharges, National Hospital Discharge Survey, United States, 2002. 2006 Unpublished data, Air Pollution and Respiratory Health Branch.

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10

Carbon Monoxide Sensors and Systems Kosmas Galatsis and Wojtek Wlodarski

CONTENTS 10.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10.2 Sensor Technologies for Carbon Monoxide Gas Detection . . . . . . . . . . . . . . . 10.2.1 Semiconducting Metal Oxide (SMO) Gas Sensors . . . . . . . . . . . . . . . 10.2.2 Optical Gas Sensors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10.2.3 Electrochemical Gas Sensors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10.3 Sensor Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10.4 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10.5 Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10.6 Appendix 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

251 253 254 256 261 263 265 265 265 267

10.1 INTRODUCTION Carbon Monoxide (CO) is one of the most important gases in the field of sensor technology. This is because its toxicity combined with its properties of being odorless, colorless, tasteless, and nonirritating to the respiratory tract. Attempts at detection of CO date back to the famous French physiologist, Claude Bernard, circa 1846,1 who performed experiments with CO poisoning dogs. Small birds and mammals were used for decades in mines as living CO detectors. CO has been called the “silent killer,” the “stealthy-poison,” and even the “smart poison” because it enters the body without notice and leaves so quickly with little trace. See an earlier discussion of CO detectors by Kwor in Carbon Monoxide Toxicity, 2000. Today’s CO detectors/alarms are small electronic devices. Such devices are installed in homes near heating devices or in garages where sources of CO such as combustion burners and/or motor vehicles may potentially pollute the breathing space. If a sufficient level of CO is detected, the device audibly alarms, giving occupants a chance to ventilate the area or safely vacate. Unlike smoke, CO is undetectable by the unaided human senses, and hence, people often find themselves in environments polluted with CO without knowing it.

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During the mid 1990s, the installation of residential, wall-mounted CO alarms grew rapidly in the United States. This was a result of the availability of low cost CO alarms, marketing campaigns, education campaigns by the American Lung Association and advocacy by the US Consumer Products Safety Commission (CPSC). In 1995, Chicago was the first municipality in the United States to mandate CO alarms in all single and multiple family housing, and in some special use buildings such as schools, churches, theaters, museums. By 1998, approximately 20 million units had been shipped and an estimated 8–15% of homes had at least one CO alarm installed.2 CO alarms today retail for $20–$60 (U.S.), are widely available, and can either be battery-operated or AC (mains) powered. Other locales such as Massachusetts have followed Chicago in acknowledging CO poisoning as a priority and have enacted state legislation which requires CO detectors in homes. Such domestic detectors are required to meet performance standards such as BS EN 50291 (UK and Europe), UL 2034 (USA), and CSA 6-19-01 (Canada). The Canadian standard has been argued to be superior as it requires “time of manufacture” and test for “lifetime reliability.” As an example, the British–European standard requires domestic CO alarms to behave in the following way: • • • •

No alarm within 60 min at 45 ppm CO Alarm within 30 min, but not less than 10 min, at 150 ppm CO Alarm within 6 min at 350 ppm CO Recovery from the alarm state within 6 min in clean air

Although these design standards help set a benchmark for performance, they do not specify the degree to which alarms must maintain their performance, and hence has contributed to CO detectors known to becoming notoriously unreliable with age. Poor sensitivity at low humidity was a major problem in one field experiment, showing as much as 79% of alarms failed when tested at 5% RH and that 3 of the 10 brands tested worked well.3 Other than the domestic need for CO alarms, another important CO sensing application that has recently gained considerable interest is vehicle cabins. Exhaust pollutants find their way into the cabin through the ventilation system, also known as the heating, ventilation, and air conditioning (HVAC) system. Independent studies4−7 have shown that vehicle cabins commonly show concentrations of toxic gases such as CO, hydrocarbons (HC), volatile organic compounds (VOC), and oxides of nitrogen (NOx ) higher than safety limits set by Occupational Safety and Health Administration (OSHA) and World Health Organization (WHO). Among the array of toxins found in vehicle exhaust gases, CO is the most deadly poison. It is a major subject of overlooked issues concerning motor-vehicle cabin air quality and suicides involving CO.8,9 Of the 2320 suicides registered for the year 2002 in Australia, 416 persons (18%) died from use of motor-vehicle exhaust gases.10 By understanding the problem of CO pollution within vehicle cabins, CO sensor technology can be employed to circumvent the danger. See Chapter 9 of Carbon Monoxide Toxicity, 2000, and Appendix 1 for additional discussion of this issue.

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10.2 SENSOR TECHNOLOGIES FOR CARBON MONOXIDE GAS DETECTION At the heart of any gas alarm and detecting system are the sensors. The sensor detects target gases, and then converts the information into an electrical signal for processing. There are numerous ways to sense gas. However, as cost, size, and simplicity are critical sensor attributes, three main sensing technologies have dominated domestic CO alarms. These are 1. Semiconducting metal oxide (SMO) technology 2. Electrochemical (EC) technology 3. Infra-red/optical technology (IR) SMO gas sensors are currently the smallest CO sensors available. These sensors have a small heated element, causing reducing/oxidizing gases to react with the surface of a metal oxide film, changing the semiconductor’s conductivity proportionally to the gas concentration. Electrochemical gas sensors have electrodes placed in contact with a liquid electrolyte to form an Electrochemical sensor. As the gas diffuses, it reacts with the working electrode, changing its electrical potential proportional to the gas concentration. And third are IR sensors, where the optical sensing element undergoes light transmission changes when exposed to the target gas. Table 10.1 compares the technologies against seven key sensor device criteria. Domestic CO alarms predominantly employ either the semiconductor or Electrochemical sensor. Semiconductor based CO sensors have penetrated the market with companies such as Figaro (Japan), Microchemical (MiCS) (Switzerland), and FiS (Japan). Some Electrochemical sensor manufactures include City Technology (U.K.), Monox (UK), and Kidde (USA). Optical CO sensors have been pioneered by Quantum (USA). For vehicle cabin air quality monitoring installed within the HVAC systems of vehicles, metal oxide sensors have dominated as they are small, have a long lifetime and the technology allows for the sensor element to be conveniently

TABLE 10.1 Comparison of Three Gas-Sensing Technologies with Respect to Desirable Carbon Monoxide Domestic and Vehicle Air Quality Monitoring Criteria Criteria Cost Life time Sensitivity Selectivity Response time Size Ease of use

Infra Red—Optical

Electrochemical

Metal Oxide

6 years Very good Excellent Seconds Medium Good


6years Very good Poor Seconds Small Excellent

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optimized for various toxic gases. However, for aftermarket vehicle CO detectors, optical sensors from Quantum have dominated.

10.2.1 SEMICONDUCTING METAL OXIDE (SMO) GAS SENSORS SMO gas sensors are relatively small, reliable, durable, and have low cost. Traditionally, the major disadvantages of SMO as gas sensitive devices has been their poor gas selectivity, and the influences of humidity and temperature.11,12 The introduction of noble metal catalysts (such as platinum and palladium), filters (activated carbon), and modification to the SMO microstructure and nanostructure has enabled SMO sensor manufacturers to improve selectivity and stability performance.13 For reducing gases such as CO, molecules react with adsorbed oxygen ions (from ambient air) on the surface of the oxide. The adsorbed oxygen loses its electron by reacting with the reducing gas molecule, thereby increasing the films conductivity. A simple model consisting of three possible reactions is shown below14,15 : 2CO + O2− ←→ 2CO2 + e− CO + O− ←→ CO2 + e− CO + O2 ←→ CO2 + 2e− From this reaction it is obvious that a change in ambient oxygen concentration will also change the rate of this redox process and influence the output signal of the sensor. The relationship between film conductivity (σ ) and gas concentration (c) follows a power law that can be described by16 : σ = kcn where k is a measured proportionality constant unique to the film/sensor and the exponent n can range from 0.3 to 0.8. Owing to this intrinsic nonlinear semiconducting nature, linearization circuitry within hardware/software is usually required. In addition, for the SMO material to react with a gas, the material is elevated to temperatures between 90◦ C and 250◦ C enabling the reduction/oxidization process to occur. Elevating the sensor to high temperature requires an integrated heater circuit to be fabricated below or adjacent to the sensing element. Owing to this high temperature requirement, SMO gas sensors require relatively high power consumption. Traditional SMO sensors fabricated on alumina substrates typically consume above 350 mW. One way of reducing power consumption is by fabricating gas sensors using a thin Si membrane as done by MiCS in Switzerland. Power consumption of the MiCS sensor is about 30–50 mW. Typically for detecting CO gas, the sensitive film material used in SMO sensors is tin oxide (SnO2 ). Other transitional metal oxides such as tungsten oxide (WO3 ), indium oxide (In2 O3 ), chromium titanium oxide (Cr2 TiO3 ) fabricated at a thickness between 200 nm and 10 µm have also been shown to be effective CO sensing materials.17−24 For automobile air quality monitor (AQM) applications, MiCS manufactures dual element sensors for detecting both reducing gases such as CO and HC’s and oxidizing

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gases such as NO2 and O3 . This allows for detection of gasoline pollution from cars and motorbikes, and diesel pollution from diesel-powered cars as well as trucks and buses. The Si based sensor chips (Figure 10.1a) are bonded to either transistor outline (TO) packages or SMD (surface mount device) packages. Figure 10.1b shows two sensor chips on the same housing developed for the automobile industry, capable of detecting both CO and NOx . Typically, the sensor is integrated on a printed circuit board with peripheral electronics and packaged as a CO alarm for domestic or automobile use.

(a)

(b)

(c)

(d)

FIGURE 10.1 Photographs of commercial CO gas sensors. (a) The MiCS Micro-ElectroMechanical Systems (MEMS) chip 2.1 × 2.3 mm. This chip is made up of a thin Si membrane, which is a micromachined silicon platform that includes an integrated heater and interdigital electrodes. The sensitive layer is a thin (about 200 nm in. thickness) metal oxide polycrystalline film; (b) Dual MiCS MEMS chips mounted and bonded onto a TO5 package. These sensors are used in automobile applications to control the HVAC system, (c) The FIS SB series sensing element made up of a platinum coil heater (as shown in the inset) with a sensing platinum electrode in the middle of the coil. The structure is coated and covered with sensitive semiconducting metal oxide, tin dioxide (SnO2 ). The SnO2 material is made up of many small particles in the size range of submicron to several tens of microns, (d) The FIS SB series sensor package for integration within CO detectors. These sensor structures are encapsulated in nickel plated brass (as shown in the inset) with an attached active charcoal filter and then enclosed in an outer plastic housing. These sensors are typically employed within domestic CO detectors. (Courtesy of MicroChemical of Switzerland and FIS of Japan).

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Figure 10.1c and d shows the sensor design of the FiS (Japan) sensor employed in domestic CO detectors. Compared to MiCS, the FiS design is based on a tin dioxide coated over a platinum coil and a sensing electrode. The coil heats the structure at an elevated temperature while the working electrode senses the conductance changes. Figure 10.2a shows the FiS sensor responding to CO gas. Some important characteristics to note are: (1) The sensor signal returns to its original baseline. This characteristic ensures that the sensor remains calibrated, free of drift that will result in signal errors. (2) The response time and decay time of the sensor is a few minutes which is adequate for either domestic or automobile applications. (3) The magnitude of sensor signal changes as a function of concentration (i.e., exponent n, based on Equation 10.1). This permits a greater signal to noise ratio and signal dynamic range. Figure 10.2b is a typical selectivity test performed to determine cross-sensitivity to other gases. As shown, the SMO sensor does not offer absolute CO selectivity. Improving selectivity requires optimizing calatyst concentration (such as platinum), optimizing material annealing temperature and optimizing crystal and grain properties. Figure 10.2c shows a stability test of the FiS CO sensor. The slight change in baseline is a result of the complicated nature of the crystallization process due to operation at elevated temperatures. The sensor is extremely stable over 1000 days—even after 1000 days a baseline change of only 10% occurs, which is usually mitigated by intelligent microprocessor algorithm programming. Improving this characteristic of SMO sensors is a great challenge that drives the active research disciplines of semiconductor metal oxide gas sensors.

10.2.2 OPTICAL GAS SENSORS IR-based sensors are relatively physically small, consume low power, are selective, and are rapidly decreasing in cost. These sensors are considered as solid state and have a lifetime of over 6 years (depends on IR source degradation/failure) with good resolution, relatively high selectivity, and broad dynamic range. These sensors identify gases by taking advantage of a gas’s unique IR absorption spectra. Most gases (more than one type of atom) can be detected by measuring their absorption at a particular IR wavelength, which corresponds to the resonance of the molecular bonding between dissimilar atoms. Figure 10.3a shows an IR absorption spectrum of some common gases. For example, to detect CO, the wavelength at which one carbon atom and one oxygen atom resonate in a carbon monoxide molecule is 4.7 µm. Therefore, the IR system will be filtered to detect radiation at a bandwidth centered at 4.7 µm. There are certain basic components common to all IR gas sensors: an IR source (e.g., incandescent lamp), an IR detector (e.g., thermopiles, pyroelectric detectors, photodiode), a means to select appropriate wavelengths (e.g., band pass interference filter) and a sample cell. The simple sensing setup is shown in Figure 10.3b. The IR source is at one end and the IR sensor at the other. The band pass optical filter must correspond with the absorption wavelength of the gas being measured. As the concentration of the gas being measured increases, the output signal from the sensor reduces as the IR is absorbed by the target gas molecules. The relationship between

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257

5.0 CO 100 ppm clean air

CO 300 ppm clean air

CO 100 ppm clean air

VRL (V )

4.0 3.0 2.0 1.0 0

(b)

0

5

10

15 Time (min)

20

25

30

100000

Rs (Kohm)

10000

1000

100

CO 400 ppm

CO 60 ppm CO 100 ppm CO 200 ppm

Air

CO 30 ppm

Isopropyl alcohol 200 Carbon dioxide 5000p

Butane 300 ppm 2hr

Heptane 500 ppm 2hr Ethyl acetate 200 ppm

Methane 500 ppm 2hr

CO 400 ppm

1

Air CO 30 ppm CO 60 ppm CO 100 ppm CO 200 ppm

10

FIGURE 10.2 FIS SB series CO sensor data showing, (a) exposure to 100, 300, and 100 ppm CO with clean air cycles. The x-axis represents time (minutes) and the y-axis represents the proportional voltage response from the sensing element. The sensor is stable when responding to CO gas, returning to baseline within a few minutes. In addition, the repeatable response characteristic at 100 ppm also is another desirable sensing attribute, (b) selectivity to other gases following the UL2034 specification. The largest cross-sensitivity is with heptane (error bars overlap with an equivalent CO error signal of about 30 ppm), (c) long-term stability. The sensor’s stability over 1000 days shows extremely stable characteristics, even after 1000 days a baseline change of only 10% occurs, which is usually mitigated by intelligent microprocessor algorithm programming. (Courtesy of FIS, Japan).

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R /R0(CO100)

R /Ro

R /R0(CO300)

1

0.1 0

100

200

300

400

500

600

700

800

900

1000 1100

Time (days)

FIGURE 10.2 Continued.

IR transmission, I, and gas concentration, c, can be explained by Beers Law of Absorption: I = Io e(−kc l) where I is the intensity of IR radiation at the IR detector, Io is the IR radiation emitted from the IR source, k is the absorption coefficient, and l is the optical path length. To improve the signal to noise ratio, an improved IR detection setup as shown in Figure 10.3c was developed. The difference is that a reference detector was added to compensate for humidity, vibration, source intensity deterioration, detector contamination, vibration, and aging. As a result, a dual beam topology is typically employed with most IR gas sensors. A reference detector senses IR at a neutral wavelength where almost no absorption takes place (i.e., 4 µm). By taking the ratio of both detector voltage U1 and reference signal U2 , the common Io coefficient is cancelled, and the target gas signal component remains which corresponds to the target gas concentration. The Quantum Group (US) is the leading manufacturer of optical gas sensors for domestic CO alarms. They have developed a unique type of solid state IR gas sensor based on the “biomimetic” phenomena. The company has been successful in developing a broad range of domestic CO alarms and it is the first company to offer an aftermarket CO detector for vehicle safety applications. The IR-based “biomimetic” sensors are designed to replicate the CO uptake by hemoglobin in the blood, hence the name “biomimetic.” In doing so, the sensing element can be set to alarm based on the replicated blood level of carboxyhemoglobin (COHb). Figure 10.4a shows the elements of the biomimetic CO sensor. The patented sensing elements are made from a porous transparent disk coated with a monolayer

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(a)

Absorption (arbitrary value)

1014

NO (5.3)

101

H2O (1.4)

SO2 (4)

CO (4.7)

HC (3.4) CO2 (4.3)

H2O (1.9)

0 1

2

3 4 Wavelength (µm)

(b)

5

6

IR bandpass filter

IR detector IR source

(c)

U1∝I0 exp (kcl) U2∝I0

Gas filter Reference filter IR light

FIGURE 10.3 IR sensor design that is based on, (a) the absorption bands of various gases in the IR region, (b) A simplified diagram of a single beam IR absorption gas detector and, (c) an improved version of the dual beam arrangement makes the gas detector insensitive to source performance deterioration. (Courtesy of PerkinElmer Optoelectronics, Germany).

of supramolecular organometallic complex. This complex is formed through a selfassembly process to generate the sensing elements that mimic hemoglobin. Upon exposure to CO, one or both of the sensing elements changes its spectral character and absorbs photons of light at a rate dependent on the concentration of CO in the surrounding environment. The sensing elements reverse their spectral shift by a selfgeneration process whose rate depends upon the decrease of CO in the environment.

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Retainer clip

Filter element

Red sensing element Sensor housing

Window

Yellow sensing element

Photodiode

IR lED

Sensor holder

(b)

FIGURE 10.4 A commercialized optical CO gas sensor, (a) components and structure of Quantum’s biomimetic CO gas sensor, and (b) a photograph of the CO sensor cell incorporated within Quantum’s line of domestic and automobile CO detectors. (Courtesy of the Quantum Group, USA).

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Carbon Monoxide Sensors and Systems CO Exposure

Recovery period

120 110 100 90 80 70 60 50 40 30 20 10 0

Temperature = 0°C/15% RH Temperature = 25°C/30% RH

600

540

480

420

360

300

240

180

120

60

Temperature = 50°C/30% RH

0

I%

Preconditioning

261

RH = Relative humidity

Time (min)

FIGURE 10.5 Response curves of a Quantum biomimetic sensor towards 100 ppm CO for 90 min with varying ambient temperatures from 0◦ C to 50◦ C and relative humidity from 15% to 30% RH. It can be seen that varying these parameters influences the response time and baseline of the optical sensor. (Courtesy of the Quantum Group, USA).

This mechanism acts as a variable IR bandpass filter. By monitoring the rate of change in the amount of light transmitted through the sensing elements, the concentration of the CO in the surrounding environment can be determined accurately. The sensing elements are held in optical alignment by the sensor-housing placed between an IR light emitting diode (LED) and a photodiode. Pulses of light emitted by the LED pass through the first sensor-housing window and are attenuated by the sensing elements. The attenuated light exits through the second sensor-housing window and is then detected by the photodiode. The light transmittance follows Beer’s Law (Equation 10.2). Figure 10.5 shows the response of the Quantum Group’s biomimetic sensor over 90 min to a 100 ppm concentration of CO at varying temperatures and relative humidity. After the 90 min, the CO is removed and the sensor begins regenerating. When exposed to CO, the sensor rapidly absorbs photons at 940 nm. In a fixed alarm point detector, a value of 30% is typically set as the alarm point. Thus in such a detector, the alarm would be triggered within 40 min of exposure, which is well within the UL safety guidelines. When the sensor is again exposed to clean air (marked as recovery time), the biomimetic component begins a self-regenerating process. As the sensor reverses its spectral shift, the signal increases and within hours the sensor has fully recovered. Although the response time is slower than the SMO sensor, incorporating sensing algorithms based on the rate of change of signal, improves response time.

10.2.3 ELECTROCHEMICAL GAS SENSORS Electrochemical gas sensors are also small electronic devices. A City Technology CO sensor commonly found in CO domestic alarms is shown in the inset of Figure 10.6. In their simplest form they are comprised of two electrodes: sensing and counter,

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Capillary diffusion barrier

Sensing electrode Separator Counter electrode Current collectors

Electrolyte Sensor pins

FIGURE 10.6 A simplified schematic of a two electrode electrochemical cell manufactured by City Technology. The inset show photographs of the complete sensor package. These sensors are employed within domestic CO detectors. (Courtesy of City Technology, U.K.).

separated by a thin layer of electrolyte. The structure is enclosed in a plastic housing that has a small capillary tube to allow gas entry to the sensing electrode and includes pins which are electrically attached to both electrodes and allow easy external interface. These pins may be connected to a simple resistor circuit that allows the voltage drop resulting from any current flow to be measured. Gas diffusing into the sensor is either oxidized or reduced at the sensing electrode and, coupled with a corresponding (but converse) counter reaction at the other electrode, a current is generated through the external circuit. Since the rate of gas entry into the sensor is controlled by the capillary diffusion barrier, the current generated is proportional to the concentration of gas present outside the sensor. Of great importance to any electrochemical gas sensor is the design of the diffusion barrier, which limits the flow of gas to the sensing electrode. The electrode is therefore able to react with all target gas as it reaches its surface, and still has electrochemical activity in reserve. The reactions that take place at the electrodes in a CO sensor are: Sensing: CO + H2 O− CO2 + 2H+ 2e− Counter: 12 O2 + 2H+ + 2e− > H2 O And the overall reaction is: CO + 12 O− 2 > CO2 Similar reactions take place for all other toxic gases that are capable of being electrochemically oxidized or reduced. From the reaction at the counter electrode, it is evident that oxygen is required for the current generation process to take place. This is usually provided in the sample stream by air diffusing to the front of the sensor, or by diffusion through the sides of the sensor (a few thousand ppm is normally sufficient).

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However, continuous exposure to an anaerobic sample of gas may result in signal drift, despite the oxygen access paths which may cause the sensor to be poisoned. Similar to SMO gas sensors, electrochemical gas sensors are also affected by temperature variations. The baseline signal of most electrochemical sensors tends to increase exponentially with temperature, approximately doubling for every 10◦ C rise in temperature which proves problematic for domestic applications as the baseline shift with temperature could seriously affect the ability to measure these gases accurately and result in false alarming. Nevertheless, by compensating for this drift either in the hardware or software, such temperature influences can be reduced.

10.3 SENSOR SYSTEMS The CO sensor is the main component within all domestic CO detectors. Support electronics are also required to provide the sensor with intelligence so that it will actuate alarms according to compliant standards. Most detectors incorporate at least one microprocessor that allows them to be quickly reprogrammed and the behavior of the alarm to be altered to suit various applications or standards. For domestic applications, CO alarm design and alarm requirements are well defined by associated performance specifications. However, in emerging CO and air quality monitoring applications such as monitoring vehicle cabin air quality, specifications, and standards have yet to evolve. Vehicle cabin air quality concerns are usually generated by the following four scenarios: (1) Pollutant gases entering the vehicle through the ventilation system, (2) A lack of fresh airflow resulting in low oxygen and high carbon dioxide concentrations due to occupant respiration, (3) Pollutant gases entering from the external environment through window openings, imperfect seals, and other holes, and (4) Toxic gases entering the vehicle cabin by redirected exhaust fumes for self-harm (i.e., suicide) purposes. Currently, no system or aftermarket product addresses all four vehicle AQM concerns. Only two commercial AQM solutions currently exist for vehicles: (1) The most common are AQM systems controlling HVAC ventilation flaps, and (2) Less common are aftermarket toxic gas alarms for vehicle cabin applications, such as that commercialized by the Quantum Group (U.S.). Currently, the demand for AQM systems is driven by the increasing concern for passenger safety, health, comfort, and by automakers aiming for features and attributes that differentiate their vehicles. In turn, this growth has increased demand for reliable automotive air quality sensors. Figure 10.7 shows a simplified view of an AQM system controlling the HVAC ventilation flap. External gases enter the vehicle cabins through the ventilation system. Mounted in the air intake of the HVAC system, the AQM sensor sends a signal to the fresh air inlet flap to close when pollutant gases are detected and automatically reopen when the external air quality returns to an acceptable level. Although a driver could close the air inlet manually, forgetting to reopen it could cause the oxygen concentration in the cabin to decrease and carbon dioxide levels to increase. Therefore, a compromise must be reached. One way of tackling the problem to implement with the system an air quality factor. For instance, the absolute concentration of particular gas (Cx ) in the vehicle cabin is dependent on the exhaust flow rate (F), time (T ), cabin

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CO2

O2 OPEN

3. Ventilation system/flap 2. Electronics/algorithms

CLOSED

1. Sensor response

CO NOx HC Particulates

FIGURE 10.7 An overview of a typical automobile air quality monitor (AQM) employed within a heating, ventilation and air conditioning (HVAC) system. When the ventilation flap is open, dangerous pollutants such as CO and NOx may enter the cabin. To mitigate this, electronics automatically close the ventilation flap. High carbon dioxide and low oxygen concentrations may result through occupant respiration. High carbon dioxide and low oxygen concentrations are dangerous because they induce fatigue and drowsiness, reducing driver attention and response times.

volume (V ), and cabin seal (S). Therefore, Cx = f (F, T , V , S) Concentrations of carbon monoxide (CCO ), and oxygen (CO2 ) have been identified as important gas species contributing to poor cabin air quality. The summation of each absolute gas species concentration gives rise to an air quality factor (AQcabin ) such as: AQcabin = αCO + δ(CO2 )−1 Where α, and δ are proportionality coefficients. It should be noted that other gas species such as hydrocarbons and nitrogen oxides have been ignored. Absolute threshold limits could then be set for scenarios such as suicide (AQsuicide ) and driver fatigue (AQfatigue ). For increased reliability and effective suicide attempt identification, the change of air quality with time (dAQcabin /dt) should also be incorporated into the driver fatigue and suicide detecting algorithms: ∂CCO ∂(CO2 )−1 dAQcabin =α +δ dt ∂t ∂t An alarm threshold, dAQsuicide /dt, could also be incorporated as done so by Quantum Group. Therefore, the cabin gas-sensing system should include both absolute and changing air quality factors, to determine if alarms need to be activated. Software solutions to improve CO detectors are commonplace. In addition, rate of change, humidity compensation (through humidity sensors) and temperature

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compensation (through temperature sensors) are also common within sensor systems. However, compensation for environmental variables increases the cost of the CO detector. Data referenced above showing that 79% of alarms failed when tested at 5% RH3 is compelling evidence of performance standards not meeting real-life long-term requirements for adequate domestic CO monitoring.

10.4 CONCLUSIONS Detection of CO has gone far beyond the primitive approach of Claude Bernard and others. CO sensors and detectors employ advanced materials, electronics, and software to ensure reliable and selective performance while maintaining economic sensitivity and feasible for the domestic market. This chapter has discussed the three major sensing techniques employed in mainstream CO detector/alarms. SMO sensors depend on chemi-absorption between the oxide and CO molecules for CO detection. Various methods are employed by industry to increase selectivity through the introduction of catalysts such as Pt and Pd, and filters using activated carbon. Optical sensors depend on CO energy absorption by incident photons. Humidity, temperature, and pressure are environmental factors that may affect sensor components. Electrochemical sensors are also vulnerable to cross sensitivity, temperature, and humidity variations. The intrinsic deficiencies of materials and electronic components that make up commercial CO sensors and systems have been documented and are well known. These issues have plagued manufacturers and the research community for many years and continue to be areas of active scientific interest. Nevertheless, economic forces, government legislation, competition, and customer demand drive CO detector products to be sold at the lowest possible prices, while high customer standards, product superiority, competitive advantage and market reputation drive product quality and innovation. Hence, these forces lead to the classic economic balance between price and performance.

10.5 ACKNOWLEDGMENTS The authors kindly thank all contributors including Dr Mark Goldstein from Quantum Group, Inc. (USA), Dr Herve Borrel from MiCS (Switzerland), Dr Nobuaki Murakami from FiS (Japan), Dr Jürgen Schilz from PerkinElmer Optoelectronics (Germany), and City Technology Sensors (UK).

10.6 APPENDIX 1 (D.G. PENNEY) Suicide in Australia, especially that of young men, had attained an alarming rate in recent years, higher than that in the USA and most other countries. The use of motorvehicle exhaust gas for this purpose was the most popular method. For this reason, in 1998 the Australian Medical Association in cooperation with other governmental and industrial groups as well as various individuals in Australia, invited me to provide conceptual solutions for reducing this tragic loss of young life.

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Almost immediately, it was felt that by limiting the availability of the lethal component of motor-vehicle exhaust gas, carbon monoxide (CO), the use of this method of commiting suicide would decline, possibly saving several hundred lives per year. The use of CO was often chosen because of its availability, ease of use, and supposed painless induction of unconsciousness. Making CO unavailable would defeat this approach. Several solutions were considered: (1) Accelerate the rate of installation of effective catalytic converters on Australian motor vehicles, possibly by instigating a retro-fit program. (2) Require the sale or retroinstallation of CO detectors on all motor vehicles in Australia that would warn drivers/occupants of the danger, and/or, immediately shut-down the engine and prevent restarting. (3) Place a distinctive odorant in petrol/gasoline that would give motor-vehicle exhaust an unpleasant odor and thus discourage/warn potential suicide attempters. (4) Design ignition systems that would prevent motor vehicles from remaining in an “idle” mode for more than a short time. Catalytic converters are expensive, eventually wear-out, are slow to come on-line in Australia owing to a long mean vehicle life, and retro-fitting would be difficult and place financial burdens on people least able to pay. Also, current catalytic converters still permit exhaust gases to contain lethal CO concentrations. Finally, the fact that catalytic converters only become effective in reducing CO at elevated temperatures means that exhaust gases would continue to contain supra-lethal concentrations of CO during the “warm-up” period. CO detectors that produce engine “shut-down” would have to be carefully designed so as not to exacerbate traffic problems due to elevated ambient CO concentration. This approach appeared to be the best overall solution, and could have provided some additional health benefits separate from the suicide issue. Solutions involving odorants in motor-vehicle fuel might cause public discomfort and complaints and undesirable environmental pollution. Most motor vehicles need the capability to idle, for example, waiting for traffic or stop lights, taxis, and vehicles being repaired. Australia represented just 1% of the world motor-vehicle market. The average age of Australian motor vehicles (8 × 106 ) in 1997 was 12–14 years. It was my charge in visiting Australia in early April, 1998, to recommend to the Australian Medical Association (AMA) and the Working Group on Motor Vehicle Exhaust Suicide, a CO concentration that might be set as the threshold at which engine shut-down would occur. Mathematical modeling of motor vehicle exhaust gas revealed a “unique signature” that might be used to quickly and unequivocally identify a suicide attempt, distinct from simple leakage of outside gases into the vehicle. Motor vehicles would be equipped with a sensor array in the passenger compartment that was sensitive to: carbon monoxide, carbon dioxide, and oxygen. Sensor output would be directed to a microchip with an embedded program such that: (1) measured CO concentration was integrated over time in a manner modeling human CO uptake, and thus provides a Low warning alarm at 35 ppm (7% COHb), and a High warning alarm at 100 ppm (14% COHb), and (2) A CO concentration at 100 ppm and above, as well as rapidly rising CO2 concentration and rapidly falling O2 concentration would immediately trigger engine shut-down.

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There were several advantages to this scheme: Low and high alarms give warning of CO presence at levels shown to impair psychometric performance (“drowse alarm”) and known to produce health damage in at-risk groups (congestive heart failure (CHF), coronary artery disease (CAD), fetus). These would give warning of elevated ambient CO and/or abnormal exhaust gas leaks into the motor-vehicle driver/passenger compartment. With concentration × time computer integration, neither heavy cigarette smoking, auto tunnels, nor congested roads would be likely to trigger even the low CO alarm. Use of CO2 concentration and O2 concentration changes along with CO concentration would prevent “false positives,” that is, inappropriate engine shut-down. Changes in the concentrations of these three gases would provide a unique “signature” of the suicide attempt. A second sensor array might be placed outside the motor-vehicle, preferrably near the rear tailpipe. This would cause engine shut-down in those instances where people attempt to commit suicide outside of the car, behind the tailpipe (in a garage, outside, etc.). If the cost of the three-sensor array proved too great, only one sensor responding to CO might instead be used. In this event, threshold CO concentration might be set somewhat higher in order to avoid inappropriate engine shut-downs. CO detectors are standard equipment in households in the USA, warning of furnace malfunction, etc. They are also required in motor homes, recreational powerboats, and other devices where people are fully or partially enclosed and in proximity to an internal combustion engine. Why shouldn’t such devices now become standard equipment in motor vehicles, considering that cars are such prodigious generators of CO and in such close proximity to the driver and passengers, and the fact that cars already incorporate minimally several microcomputers in their normal operation. For further details of the proposed scheme, see www.coheadquarters.com/CO1.htm.

References 1. C. Bernard, Introduction a l’etude de la medecine experimentale. Paris: J.B. Bailliere et Fils, 1865, pp. 85–92, 101–104, 107–112, 265–301. 2. Revised Standards to Improve Carbon Monoxide Alarm Performance, Gas Research Institute Digest (GRID), Chicago, vol. 21, pp. 24–25, 1998. 3. P. K. Clifford, Evaluating the Performance of Residential CO Alarms, Mosaic Industries, Inc., Newark GRI–02/0112, 2002. 4. K. Galatsis, W. Wlodarski, Y. X. Li, and K. Kalantar-zadeh, Vehicle cabin air quality monitor using gas sensors for improved safety, presented at COMMAD 2000 Proceedings. Conference on Optoelectronic and Microelectronic Materials and Devices (Cat. No. 00EX466). IEEE. 2000, pp. 65–68. Piscataway, NJ. 5. K. Galatsis, W. Wlodarski, L. Yongxiang, and K. Kalantar-zadeh, Ventilation control for improved cabin air quality and vehicle safety, presented at IEEE VTS 53rd Vehicular Technology Conference, Spring 2001. Proceedings (Cat. No. 01CH37202). IEEE. Part vol. 4, 2001, pp. 3018–3021, Piscataway, NJ. 6. K. Galatsis, B. Wells, and S. McDonald, Vehicle cabin air quality monitor for fatigue and suicide prevention, SAE Transactions, vol. 2000-01-0084, 2000. 7. S. Sato, R & D Review of Toyota CRDL 39, vol. 1, 36, 2004.

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Carbon Monoxide Poisoning 8. V. H. Routley and J. Ozanne-Smith, The impact of catalytic converters on motor vehicle exhaust gas suicides, Med. J. Australia, vol. 168, pp. 65–67, 1998. 9. M. A. Skopek and R. Perkins, Deliberate exposure to motor vehicle exhaust gas: the psychosocial profile of attempted suicide. Australian and New Zealand J. Psychiatry, vol. 32, pp. 830–838, 1998. 10. Motor Vehicle Census, Australian Bureau of Statistics, Canberra Cat. 0309.0, 2001. 11. W. Gopel, New materials and transducers for chemical sensors, presented at Sensors and Actuators B (Chemical), vol. B18, no. 1–3, March, 1994, pp. 1–21. Switzerland. 12. N. Yamazoe, New approaches for improving semiconductor gas sensors, presented at Sensors and Actuators B (Chemical), vol. B5, no. 1–4, Aug.–Dec., 1991, pp. 7–19. Switzerland. 13. G. Sberveglieri, Recent developments in semiconducting thin-film gas sensors, presented at Sensors and Actuators B (Chemical), vol. B23, no. 2–3, Feb. 1995, pp. 103–109. Switzerland. 14. M. J. Madou and S. R. Morrison, Chemical Sensing with Solid State Devices: Academic Press, San Diego, 1989. 15. S. R. Morrison, In Semiconductor Sensors, S. M. Sze, ed., New York: J. Wiley, 1994. 16. H. Meixner, J. Gerblinger, and M. Fleischer, Sensors for monitoring environmental pollution, presented at Sensors and Actuators B (Chemical), vol. B15, no. 1–3, Aug., 1993, pp. 45–54. Switzerland. 17. G. Kiriakidis, N. Katsarakis, M. Katharakis, M. Suchea, K. Galatsis, W. Wlodarski, and D. Kotzias, Ultra sensitive low temperature metal oxide gas sensors, presented at 2004 International Semiconductor Conference. CAS 2004 Proceedings (IEEE Cat. No. 04TH8748). IEEE. Part vol. 2, 2004, pp. 325–331, vol. 2. Piscataway, NJ, USA. 18. K. Galatsis, Y. Li, W. Wlodarski, C. Cantalini, M. Passacantando, and S. Santucci, MoO3 , WO3 single and binary oxide prepared by sol-gel method for gas sensing applications, J. Sol-Gel Sci. Tech., vol. 26, pp. 1097–1101, 2003. 19. S. Kaciulis, L. Pandolfi, S. Viticoli, G. Sberveglieri, E. Zampiceni, W. Wlodarski, K. Galatsis, and Y.X. Li, Investigation of thin films of mixed oxides for gas-sensing applications, Surface and Interface Analysis, vol. 34, pp. 672–676, 2002. 20. L. M. Cukrov, P. G. McCormick, K. Galatsis, and W. Wlodarski, Microcharacterisation and gas sensing properties of mechanochemically processed nanosized iron-doped SnO2 , presented at Proceedings of IEEE Sensors 2002. First IEEE International Conference on Sensors (Cat. No. 02CH37394). IEEE. Part vol. 1, 2002, pp. 443–447, vol. 1, Piscataway, NJ. 21. Y. X. Li, D. Wang, Q. R. Yin, K. Galatsis, and W. Wlodarski, Microstructural characterization of sol-gel derived Ga2 O3 -TiO2 thin films for gas sensing,” presented at COMMAD 2000 Proceedings. Conference on Optoelectronic and Microelectronic Materials and Devices (Cat. No. 00EX466). IEEE. 2000, pp. 363–366. Piscataway, NJ. 22. Y. X. Li, K. Galatsis, W. Wlodarski, J. Cole, S. Russo, J. Gorman, N. Rockelmann, and C. Cantalini, Polycrystalline and amorphous sol-gel derived WO3 thin films and their gas sensing properties, presented at COMMAD 2000 Proceedings. Conference on Optoelectronic and Microelectronic Materials and Devices (Cat. No.00EX466). IEEE. 2000, pp. 206–209. Piscataway, NJ. 23. L. Yongxiang, W. Wlodarski, K. Galatsis, S. H. Moshli, J. Cole, S. Russo, and N. Rockelmann, Gas sensing properties of p-type semiconducting Cr-doped TiO2 thin films, presented at Transducers ’01. Eurosensors XV. 11th International Conference on Solid-State Sensors and Actuators. Digest of Technical Papers. Springer-Verlag. Part vol. 1, 2001, pp. 840–843, vol. 1. Berlin, Germany.

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24. K. Galatsis, L. Yongxiang, W. Wlodarski, E. Comini, G. Sberveglieri, C. Cantalini, S. Santucci, and M. Passacantando, Comparison of single and binary oxide MoO3 , TiO2 and WO3 sol-gel gas sensors, presented at Transducers ’01. Eurosensors XV. 11th International Conference on Solid State Sensors and Actuators. Digest of Technical Papers. Springer-Verlag. Part vol. 1, 2001, pp. 836–839, vol. 1, Berlin, Germany. 25. For availability: www.coheadquarters.com/CO1.htm

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Marketing of Carbon Monoxide Information and Alarms in Europe and Beyond: Use of the World Wide Web in Saving Lives Rob Aiers

CONTENTS 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8

My Introduction to CO Alarms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Use of the Internet . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Department of Health . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The Department of the Environment, Transport, and the Regions . . . . . . . The Department of Trade and Industry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The Health and Safety Executive . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Appendix 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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11.1 MY INTRODUCTION TO CO ALARMS I have been involved with carbon monoxide (CO)-related issues for 8 years. My work and indeed my passion for getting the message out has resulted in our website becoming the number one CO-related issues website based on Google searches. From time to time we swap places with David Penney’s website. My background is in marketing, although I am an aircraft engineer by trade, serving 13 years in the Royal Air Force (RAF) and culminating in the first Gulf War. On leaving the RAF, I completed a diploma in sales and marketing management. I have worked for a number of large organizations and have been consulting in my own marketing business for 5 years. 271

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My entre’ to the problem of CO exposure came when working for the world’s largest water utility company, as a consultant, with a remit for new and innovative products. My goal was to find a product that could be known outside the water company’s geographical area (water utilities in the United Kingdom cover a geographic area for their core business, but can own a number of such businesses in various areas) and thus make nonregulated profits (core business profits are regulated in the United Kingdom). The first product that I was asked to market was a product called Water Fuse. It was a water-related product that the water company took on before I joined. Although Water Fuse was a good product, it had a number of problems. It measured water usage and if a leak was detected, would shut off the water. We did a number of commercial trials for the product and found it to be very reliable, however that was not the whole story. We found that the cost of the product combined with the installation costs made it prohibitively expensive, around $550. Most people in the market for this type of product (i.e., the domestic user) were happy if they had a problem their insurance would cover. Indeed most people’s insurance premiums were less than the cost of Water Fuse and covered all elements of liability including fire, theft, and so forth. I set out to find a replacement for Water Fuse that would be cheaper and easier to install. It was at this time that we came across many wacky products. One that springs to mind is Eco-Balls. This was a product that one used in place of detergent. Its marketing blurb read, “unleash the ionic power of your washing machine.” The premise of this product was that when you put the balls in with your washer, the power of ions would clean your clothes. When tested in the lab, it was found to be only marginally more effective than water alone. On my travels I met with a company that had done a trial of a product that was similar to Water Fuse, but was much less expensive and easier to install. This product could also be expanded to cover small leaks in all parts of a property by utilizing the electrical ring main of the house to send a signal back to the master unit, turning off the water. At the end of the meeting I asked what other products they were working on. “We have a product that we think could be a major lifesaver, but it does not fit the water company profile.” The product it turns out was a CO detector. We spent more time talking about this product than about the Water Fuse replacement. I was amazed how little I knew about CO. I spent the next few weeks researching the topic and discovered I was by no means alone in my ignorance. I was further astounded at the conflict in the numbers of deaths and injuries from CO exposures/poisonings. The figures ranged from an official government statistic of around 50 deaths a year to as many as 1500 deaths per year from nonofficial sources. I was appalled that there wasn’t more information available and that the government did not and still doesn’t, recognize or promote CO safety. Every now and then, late at night on TV, there is a puny campaign about CO exposure consisting of a public relations commercial. I am quite cynical about why the government does not publicize the CO problem. I believe that if they made people more aware of CO, the government would be compelled to follow up with a plan to resolve the problem. The government in the

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UK owns about 2.5 million homes, mostly “social housing.” If it publicized the problem, it would have to protect the residents from danger—the costs would be great. A CO alarm costs around $20.00. Multiply that by 2.5 million homes and the total is roughly $50 million. I saw the CO alarm to be a perfect public relations vehicle for a water company. It could be a true win-win situation. The water company had around 11 million customers and had access to the rest of the 60 million UK population through other water utilities. They could publicize the dangers of CO and also sell a product that could protect its users from future exposure. This might drastically reduce deaths. The company who first had the CO alarm was small, but it was innovative. It also had all the problems inherent to small companies, namely cash on hand. The product had been prototyped, with a short manufacturing run in Taiwan. However, the company had no money to move into full production. We concluded a deal where we had exclusive access to the product. The CO alarm was inserted directly into the wall electrical power receptacle. It incorporated some clever technology that allowed it to predict carboxyhemoglobin (COHb) levels, that is, blood CO content. We agreed to pay for an increase in product run once we had seen the product being built in a factory in Taiwan and were convinced that all was okay. Some colleagues and myself flew out to Taipei, Taiwan to verify the situation. This took a total of 5 days, either on the road or at manufacturing facilities. At every location we were dressed in full medical whites (“clean garb”), as the facilities also produced computer and automotive industry components. My view at that time was that Taiwan was just a producer of cheap toys for Christmas, crackers, and so forth. Nothing was further from the truth. All the facilities we saw were high-tech—at the top end of the computer industry. The costs of the CO alarms were a problem. If the selling price was too high, we’d be unable to sell many units. Not only would we not make projected profits, but more importantly, people would not be able to protect themselves from CO poisoning. Clearly the profit element was important and getting unit costs down was vitally important. We had to have the best product at the best price, so that when we advertised, we had an affordable solution for all. Ideally I would have liked to get the product down to a price of around £10 ($17). That is about the same price as a smoke alarm. We soon realized that the CO alarm was a much more complicated product and it may never be possible to make it as cheap as a smoke alarm. The smoke alarm industry had become a mature market, unlike that for CO alarms. It is worth drawing some parallels with what had allowed the smoke alarm industry to gain so much ground. In the 1980s, UK market penetration for smoke alarms was around 9% of households. At that time the government mounted a big campaign through the fire service and TV advertising. The “Smoke kills” campaign was responsible within a 9-year period of raising market penetration to around 65%. Recently, government legislation has caused that penetration to be near 100%. By law now, all new houses must have a smoke detector hard-wired into the construction, and it is now considered the norm to have such a device in place. The smoke kill’s campaign still goes on, but the focus is now more on maintaining existing devices. I think that the world would be a safer place if the same regulations existed for CO alarms.

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We had to look for manufacturing facilities that would get CO alarms to market at a price that would ensure that most people would buy them. Many of the Taiwanese factories also had Chinese manufacturing facilities. These involve much reduced cost, since labor costs in the Republic of China are less than that of Taiwan. This would have been the next move had not something happened. It became clear that the price that I was trying to achieve was not realistic and that CO alarms would never be as cheap as smoke alarms. As stated above, this is because smoke alarms detect danger as the danger is occurring (by either optical sensors or ion detection), but do not require the complex circuitry required in a CO alarm. It is possible to have a large release of CO that causes an immediate audible alarm, or to have much lower levels of CO released over prolonged periods of time. The best type of CO alarm is one that can make the correct calculations regarding human CO uptake. As stated above, I also wanted to sell the best alarm, so it had to be a unit that measured CO concentration over time. Inexpensive card-type detectors are available that change color in the presence of CO, but these can be contaminated by chemicals, don’t give satisfactory low-level indications, and have no audible alarm. I am not totally opposed to this type of CO detector, as they play a role in raising CO awareness. Nonetheless, they are not sufficiently reliable for constant usage. We had by this stage fully evaluated the CO alarm market and were excited to get on with marketing the product and making the public aware that there was a problem. We hit on a major problem at this time—the water company was likely to be sold. This was happening at a high level in the company so none of us was aware of the impending sale. Orders came down from on high that we were to stop all unnecessary marketing and to get back to the core business. My vice-president at that time was a very talented woman who was not held in high regard by the company board. There followed a free for all with junior managers stepping on each others heads to try to gain political high ground. In particular, while I was on leave, an alliance was formed between two managers who were determined to steal our thunder, or better still, to totally kill our work. In the end they won and all of the people who had been working for me were let go or moved to other departments. With that, all of our efforts were dashed. I then left the company to move on to other things, but the company had no idea what contracts had been signed. Consequently a legal dispute ensued, because contracts had been signed for the water company (by me) that tied them to marketing and supply agreements. The company with whom we had been dealing needed the agreements in order to move forward, but foolishly had signed an agreement with a third party to sell the product before the legal wrangle was resolved and they ultimately lost everything.

11.2 USE OF THE INTERNET I resumed my marketing business at this time, after working initially on a consulting basis for the water utility. I worked for a number of large clients, but also felt the government could and should publicize the CO issue. It was around this time that I spawned the idea of a CO information website, that is, www.carbonmonoxidekills.com. I immediately began getting it set up.

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Unfortunately I knew nothing about the internet, so I needed to team up with someone who was familiar with its complexity. It was at this time I met Frank Tiarks, a Danish chap who had been educated in the UK. Frank had a very good understanding of what was required to make website content user friendly, and of the content necessary to cause the major web search engines to list it first. I soon learned that it is no use just having a website—it has to be seen. I would liken it to having a shop that sells great products that people really need, but the shop is located down a dead-end road or in the depths of the countryside where no one will find it. One of the most important factors for success here is having a “Frank” who knows how to do it. There are many reasons why the world wide web (WWW) is an excellent way of getting your message out. First, the WWW is democratic. You have the same chance of getting your message across to the public if you are a small corner toy shop, as Toys-R-Us does. From that perspective it didn’t matter where you were geographically located as long as you could speak English. Anyone who has visited our website and has acted on the information there owes a debt to Frank Tiarks who has worked tirelessly to get CO-related information to the public. We needed to have a website with immediate impact, so we came up with the name, www.carbonmonoxidekills.com. As a capitalist, I had to generate a profit from the website simply to be able to continue running it. Over the past 5–6 years, some $80,000 has been spent on it, of which only a small percentage has been recouped. I am proud of the fact that we have become one of the most highly utilized, web-based CO information sites in the world. Approximately 5500 people per day look at the information on www.carbonmonoxidekills.com (see Figure 11.1). If we have saved one life or helped one sufferer improve his life, it has been money well spent. Some of the respondents have been referred to Dr. Penney for evaluation. More recently we have added some law firms as consultants, so some of our viewers have been helped with their legal problems. As you might guess, the website is quite comprehensive. Where questions are not answered, we pass the visitor on to an expert to answer the question (see Figure 11.2). It should also be noted that what you can see here is only the front page of the website. There are many additional layers, so almost any subject relating to CO poisoning can be found. It took some time to get us where we are now in terms of a web presence. We constantly re-examine the content of the website to insure that it has the best information for our visitors. We now get around 2 million visitors a year, many of whom e-mail us to thank us for the website. It is a sad indictment of those official government sources that should be doing this job and not be relying on individuals like me to do the job for them. Unfortunately we only get visitors who already are aware that there is a problem involving CO. In the words of Donald Rumsfeld, “we don’t know what we don’t know.” A clumsy way of saying that is, if you have never heard of CO, why would you look for information about it. That is the main issue here. If governments would just get the word out, people would be better able to decide for themselves whether there is a problem. The United States is much better at this than the United Kingdom. It may have to do with the fact that America is a more litigious society. We do not have a punitive damages system in the United Kingdom, so where someone may get an award of

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FIGURE 11.1 The front page of www.carbonmonoxidekills.com

several hundred-thousand dollars in the United States, in the United Kingdom the award is more likely to be £10,000 at best. The questions we are asked through the website are diverse to say the least. In some cases they are downright stupid. In one case an American youth asked me if it was dangerous to travel in the trunk of his friend’s car. The great bulk of the questions from an uninformed public are completely justified (see Figure 11.3). About 75% of the website’s visitors are American—15% are from the United Kingdom (we have a lot of UK links from other websites, especially government sites), with the remaining visitors coming from the rest of the world. The reasons for this are several-fold. First, the United States has a larger population than the United Kingdom. Second, America is more web-savvy than most of the world. However the most important reason is that Americans are more aware of the dangers of CO, and are thus better able to seek out information. It should be noted that our website is in English alone, so other language speakers may not be able to use it. While there are charities and experts who work hard to get the message out, the same cannot be said of everyone. People with vested interests in CO issues have not,

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FIGURE 11.2 The law connection to the Web.

in my view, been ready to sing from the same song sheet. There are three or four government departments in the United Kingdom who have some responsibility with regard to CO. From a public health perspective there is the Department of Health, from an environmental point of view (i.e., housing, etc) there is the Department of the Environment, and from a business perspective there is the Department of Trade and Industry. There is also the Health and Safety Executive who looks at the industrial side of safety.

11.3 DEPARTMENT OF HEALTH This department’s charge is the state of the nation’s health, with its remit covering doctors, nurses, and the general health infrastructure. Health concerns cover every part of people’s lives and some areas are covered better than others. Let me draw a parallel if I may. Meningitis affects about the same number of people in the United Kingdom as those who are affected by CO, based on government statistics. It is a

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FIGURE 11.3 The forum associated with www.carbonmonoxidekills.com.

very serious disease that can kill or maim. Unchecked, CO poisoning can also kill, or damage people’s lives either through an acute poisoning episode or through chronic exposure. You would be hard pressed to find a parent in the United Kingdom who was not aware of the symptoms of meningitis and what to do if he/she suspected his/her child was suffering from it. This is just as it should be and is so because the government and the media have spent a good deal of time and effort publicizing its dangers. There was scarcely a time 3 years ago when you turned on the TV that this issue was not being aired. Please excuse me if I shout, “CO EXPOSURE IS AS DANGEROUS AS THE MANY STRAINS OF BACTERIA AND VIRUS THAT CAUSE MENINGITIS.” It is about time that politicians and health experts in the United Kingdom took a lead from some of the US states and began taking the CO exposure/poisoning issue more seriously. It is my opinion that most medical practitioners here and in the United States are only slightly better than useless when it comes to diagnosing and treating their

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patients exposed to CO. If you visit your physician with flu-related symptoms, CO poisoning is usually the last cause he/she will include in the differential diagnosis, if it is included at all. Physicians are poorly trained about the dangers of CO poisoning— after all, the concern is primarily toxicological, not internal medicine. Physicians generally don’t know the correct questions to ask. For example, they usually fail to ask how your house is heated? Whether several people and even animals are sick at the residence? I very much doubt it. However, this is not an excuse for complacency. We must train our medical personnel better to recognize the symptoms of CO exposure. There are few ways for a physician to investigate the living circumstances of the person who has presented for treatment. That patient could be residing in a property where someone previously suffered similar symptoms. It is possible that over an extended period of time many people suffered CO poisoning in that building because no medical professional was alert. This scenario could go on for years. Early in 2006 I had a meeting at the Department of Health with a number of people. This included a lawyer who had represented victim’s interests in CO cases that had gone to court in the United Kingdom. There were a couple of representatives from a CO charity and the head of the Health Protection Agency, whose responsibility it is to deal with preventive health measures. I found the way the meeting was conducted to be astounding. We were informed that a leaflet had been sent to all UK physicians regarding CO. The leaflet was fairly brief. We asked if the department had followed up the leaflet to make sure that physicians had received it, and whether they had read and understood the information. The answer was no. We were also told that if there was a high demand for the leaflet there would be a reprinting, and that it was also available on the Department of Health’s website. If the physicians had not read the information in the first place how was there going to be a high demand? I told department personnel that I would help them in whatever way I could to get the message out, but that they needed to help me. One of the ways that this could be done quite simply and at very little cost, was for them to call TV stations to alert them to the problem. In the United Kingdom we have a morning program called GMTV. They spearheaded a brilliant campaign for meningitis and could do the same for CO. I have been unsuccessful in getting through to them. However one call from the chief medical officer would spur them into action at the cost of a phone call. At the meeting, a vice-president of CO Awareness said that she had tested the department’s system by calling “NHS Direct” (a phone hot line that gives health advice). She was told that the best people to speak with about CO was CO Awareness, her own charity. When questioned about the computer menu on their help line which advises what should be done when certain syptoms are mentioned, the official said that unexplained headaches and drowsiness would NOT be related to CO exposure by the operator. Of course this is incorrect. The problem goes much deeper. I asked the chief medical officer what would be the recommendation from physicians should they suspect CO poisoning? He replied that “the patient should be tested.” Do they have the appropriate equipment I asked? “I’ll have to get back to you,” he said. “So let’s accept the fact that they have the relevant testing equipment,” I said. “When do you recommend that the patient be tested?” “Well, during their consultation” was his reply. I had to point out that if the

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FIGURE 11.4 www.codetection.com, which is lined to form carbonmonoxidekills.com

patient had been away from the source of the CO poisoning for more than a few hours, then they would likely give a negative test. In this event, someone who was suffering an episode of CO poisoning, but who happened to get an appointment at the end of the day might have CO dismissed as a potential cause of his/her illness, and then might go on being exposing needlessly to a life threatening situation. In some ways this is much worse than not being diagnosed at all. This problem was dismissed almost out of hand, likely because I was not a medical professional. The Department of Health should in my view be recommending that all homes be fitted with CO alarms (see Figure 11.4). There are a number of different views about CO alarms and their efficacy, but I think they are a good weapon in the arsenal for combating CO poisoning. They should also be recommending that all combustion appliances be checked annually. Only landlords have to perform an annual safety check. I am sorry to be bashing the Department of Health, because on the whole they do a great job. They are often hog-tied by a lack of government funding.

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11.4 THE DEPARTMENT OF THE ENVIRONMENT, TRANSPORT, AND THE REGIONS This department is responsible for a numbers of areas. It is concerned with amongst other things, the air we breathe. Many people think that CO is only caused by vehicular emissions. There are major crossovers with other departments and I am loathe to list the full responsibility of this department, since by the time this book goes to print, it may have changed or there may be a new administration. This Department is responsible for dangers that lurk in our homes. It is responsible for planning regulations and for new building laws, for example, requiring newly built homes to have hard-wired smoke detectors. In my view, it is remiss in this respect in not also requiring CO detectors. The Department of the Environment requires landlords to have a safety check each year of accommodations where fossil or wood burning appliances are used. Because many people in the United Kingdom own there own homes, it means that a large fraction of residences are not covered by any regulation. It is unfortunately the way of the world that we buy “stuff” for which we can see a direct benefit. A CO detector costs about the same as a take-away meal, and at the end of that meal we are happy to part with our cash. Because it costs a bit more to get our furnace/boiler serviced (i.e., $100/200), many of us might shy away from the cost. It usually doesn’t make us feel good—in fact quite the reverse. We will only pay this charge if compelled to do so. We do not like paying our house or car insurance, but do it because we are compelled to. New York has the right idea in that landlords must by law install a CO alarm, and in turn can collect $25 from each tenant to help pay for it. Do yourself a favor. Purchase a recommended CO alarm to protect yourself and your family. Better yet, buy two CO alarms. By its nature CO is colorless, odorless, and has no taste. It does not occur to us that there will ever be a problem. You would not leave small children near a staircase lacking a gate to prevent them from falling.

11.5 THE DEPARTMENT OF TRADE AND INDUSTRY This department deals with the interests of trade, but also regulates some of the peripheral issues related to CO. One of the main areas of authority regarding CO are the gas supply companies, which until recently was reduced to just one supplier, “British Gas.” British Gas lost its monopoly and now there are many suppliers in the market place. These companies came into being as a result of denationalization, a trend in the United Kingdom. The majority of gas users still use British Gas. Some credit has to be given to British Gas for recent initiatives, but they are not on the whole completely altruistic in their nature. I will paraphrase a conversation that I had with one senior British Gas executive. He said that “if we publicize the fact that gas could be dangerous and that in certain circumstances gas appliances will give off CO, then we denigrate our product.” This is a bit like saying that we should not install seat belts in automobiles because it makes them appear unsafe. From a trade point of view they are missing the point. Their product is not the problem, it is what is done with that product when it leaves the pipeline that is key.

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British Gas now sells CO detectors. In fact, they are the biggest UK distributor for the SF-350 CO detector, the best selling unit in Europe. Most of these have been given away with service, which is sold on a commercial basis. British Gas has a large service division that must make a profit. In my opinion, if they played the white knight and told people that there was a major problem, they would be seen as a responsible company with their customer’s interest at heart. They would benefit from their customers coming to them and asking for service. Also, people would in turn buy the CO detectors, and not expect them to be free. The company would not be held up as irresponsible as they are now by some groups for not publicizing the CO danger. In this way, they could benefit financially from making CO a safety and health issue.

11.6 THE HEALTH AND SAFETY EXECUTIVE This department, HSE, is responsible primarily for safety. I recently attended a meeting of their Gas Safety Committee. I had been invited by the head of a leading charity to present my views to the committee. A number of things came up in that meeting that I found astounding and frustrating. The Department had a £100,000 surplus at the end of the financial year which they had to spend quickly, otherwise it would disappear from the following year’s budget. They didn’t ask the charities who endeavor to get the message about the best course of action. They didn’t call on our firm for suggestions. Instead they called CORGI. CORGI is the regulatory body for heating engineers. You cannot work on gas appliances in the United Kingdom unless you are qualified and a member of CORGI. CORGI’s suggestion was to give it to them and they would do a survey; so they did. The HSE could not provide us with a qualitative or quantitative evaluation of what they were going to get for their money. I guess they will get a survey back which will form part of the departments future strategy that says, “CORGI are really good guys and are in the opinion of the people who where surveyed, a top organization?” The HSE Department has tried to develop a cohesive plan to alert people to CO dangers. They have not called on me. I have on occasion called them, but they seem to have no clue as to what is going on in the world outside government. An independent enquiry stated in 2000 that it would be desirable to impose a fuel levy on gas, oil, and coal of about 0.25%, which would be used to fund CO awareness publicity. The HSE has now said that they will not implement the tax after being lobbied hard by the gas companies. They can see this going the way of all taxes, that is, once introduced, the taxes will only go up. Consequently, they don’t want even a small tax that they could absorb. Instead they have said to the HSE, “We have spent £2 million this year on CO awareness.” In actual fact, they had a campaign about service that was high profile, with many UK celebrities in ads. Unfortunately the ads never mentioned CO. The ads were mainly about getting the British public to buy their service—service which I might add, will go on making millions for years because it is annual service. The net effect of this is that less people will be harmed by CO, but don’t for a minute think that they have done it for purely altruistic reasons, they want your buck.

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All of these government departments have budgets which in and of themselves are not really that much, maybe a couple hundred thousand pounds each. If however, they combined their resources, they could do some real good. Also, if they had one team looking at this rather than many disparate groups, they would not be duplicating effort and could reduce spending. The effort could also be better coordinated so that we have something tangible to show for it. People would readily be able to see the dangers immediately, not months or years later. People would also be more aware about protecting themselves in the first place. In the last few months I have been to meetings at the House of Lords and subsequently with Lord McKenzie who is tasked with getting all the information on CO together in one place with one agency responsible. It seemed at last that there was some momentum, however that was some months ago and I have heard nothing since. We have created a website brand www.carbonmonoxidekills.com which is well recognized throughout the English-speaking world. Since I am a capitalist, our website is linked to a number of others. I submit that most problems in the world could be resolved by entrepreneur’s looking at them as opportunities to earn revenue. The more money that we make in this venture, the more we are able to plow it into CO awareness. It’s a win-win situation. Also, the more we get out there, the more information that we acquire, the more we can educate people about the issue. Dr. Penney asked me to write this chapter partly because we have a relationship going back a few years. He had kindly agreed to be our online “doctor” some years ago. As such, he responds to enquiries regarding CO from the public. We feel that he is an integral part of our online organization. We also have relationships with law firms who are able to answer legal questions. Therefore, we are able to get the best representation for people who have suffered CO poisoning episodes. As mentioned above, we sell CO detectors through another link on our website, that is, www.carbonmonoxidekills.com. This has been hard work and it has taken a great deal of effort to get where we are. People often contact me, asking how they can set up there own website. They are more than welcome to try, but we are the experts and that is why over the years we have arrived at the position that we hold. To achieve this, you have to get as much information about your subject on the website. That information needs to be updated regularly so that the search engine spiders can recognize new information. This keeps the rankings up. A spider is a computer routine that runs on search engines like Google, Yahoo, and so forth. Working for a high ranking is a bit of a catch 22 situation. Unless you have a good ranking, you can’t get one. Another factor in terms of search engine rankings, is how many other websites link to yours and the type of organizations they are. The best types of organizations are government departments, the next are educational establishments such as universities, and so forth. Media institutions are also good in that they attract lots of visitors on a given subject such as CO that appears in the news. Thus, you will get renewed interest at the time of newsworthy items. One has to be very careful when approaching these kinds of websites. They will not link to you if your information is commercial or inflammatory. Many charities suffer for the latter reason, because they will often hold someone accountable for an incident making them on occasion being seen as biased and having a narrow manifesto. No government department will link to them. It is also sometimes difficult to get

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a government body—and most educational institutions are government influenced— to link to you unless another government institution has linked first. No one wants to be first to link because they are scared that it will impact their impartiality and position. The first one to come on board is the hardest to get. If I call an institution now and ask them to link to us, they are only too willing because we have 100s of other links. There is now a comfort factor for them. There has not been a willingness in the United Kingdom to grasp the nettle and do something about the issue of CO. Proper unbiased research need to be done, and we need to have a better understanding of the issue. Statistics on CO need to be consistent. Some of the country’s top toxicologists state numbers that differ greatly from the government’s official figures. I mentioned above that most physicians are ill-prepared to diagnose and treat CO poisoning. Moreover, if a physician has not identified the connection to CO, then people may never know that they had CO-exposure. They may have relocated from their house, their job, left home, etc. They may exhibit effects of CO in later life that will never be attributed to CO. Death certificates may not tell the whole story either for very similar reasons. The physician may list just one of the symptoms as the cause of death. The coroner’s office in the United Kingdom is not attached to the Department of Health—it is part of the Home Office. I was amazed to learn that until recently, the job of coroner was a part time job. I am glad to say that we are now going to get a full-time chief coroner. This may clarify the position and he/she will liaise closer with the Health Department. In short, we need to know who and how many people are affected. Only then can the problem be properly addressed. In Paris, France all cadavers are tested for poisoning of all types. As a result, more people are recorded to have died from CO than in all of the United Kingdom. This is probably not because Paris has a worse problem, but just that better monitoring is in place. Take for example the murderer Harold Shipman, who was a UK general practitioner. No one is quite sure how many people he killed. His story has been recognized as one shortcoming of the coroner’s office. As a result, certain remedial measures were suggested. The one I am most interested to see implemented is the checking of all bodies for poisons, including CO, as a matter of course. This could prove a real breakthrough and give us proper statistics so that the problem will be highlighted and solutions found.

11.7 CONCLUSIONS There is much work to be done. Combining the budgets of disparate government departments, along with some coordinated thinking would result in a better understanding. I have offered government departments use of our website facility. If they wish, we are able to run studies and research at little cost through our valued visitor stream. We are very well-placed to be able to assist. While recognized for the efforts that we have made, we are never seen as part of the solution. My ambition is that www.carbonmonoxidekills.com will be the world-wide marketing tool for all CO-related issues. I want to make myself redundant, in as much as

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we have done the job so well, there is no more need for publicity because the whole world has got the message and deaths and injury from CO are a thing of the past. I would like people to know as much about CO as about meningitis. If the government picked up the ball and ran with it, the issue of CO may actually pay for itself. Get the message out and people will be empowered to protect themselves. People would not be taking up the valuable time of physicians with mysterious illnesses or have to be hospitalized. I make no apologies for the fact that this chapter lacks high academic content. Instead, I hope you will appreciate the journey that we at www.carbonmonoxidekills.com have made over the last few years. We have tried to be the most open information platform possible, and not an exclusive high brow intellectual website that turns visitors off, indeed those that need us most. It has sometimes been tough, and I have thought about giving it up at times. It takes a lot of my time. Then I get an e-mail from a distraught mother, father or other relative or friend, that thanks us for our help and it all seems worthwhile. It is sad to say that unless governments do more, we are the only outlet for some people. I only wish that we could get through to more people, but language barriers make that difficult. It would be difficult for us to translate our website into other languages, such as Chinese. The paradox is that as the markets in the developing world get bigger, it is they who will need it most.

11.8 APPENDIX 2 Carbon Monoxide Headquarters known as COHQ, or “coheadquarters.com,” is one of the oldest carbon monoxide (CO) information sites on the web. It was started in 1996, so is now more than 11 years old. That is very old in terms of the history of the web! Initially COHQ ran on an old Macintosh computer in my research laboratory at the Medical School at Wayne State University in Detroit, MI. It had a long URL because it did not have its own registered domain name. In the late 1990s the website received its own domain name and I migrated it over to a commercial server in Texas. The new URL and the one used today is “coheadquarters.com/CO1.htm.” From a collection of a few dozen linked pages in the early days, COHQ has grown to a site containing hundreds of pages dealing with many subtopics in the field of CO toxicology: chronic CO poisoning, dangers to high risk groups, neuropsychological effects, FAQs, CO alarms/detectors, and so forth. COHQ was begun as a way to provide the public with straightforward, unbiased, information about CO and its effects on humans. It has been my operation from the beginning. With the exception of a few dozen pages written at first by my student Amy Derusha, all of the content, architectural design, art (whether good or bad), and maintenance was been done by me. The website was produced by writing HTML in “text” by hand—it never involved using a web-editor. As crude and lacking in flash as COHQ is, it still comes up in the top 15 sites in doing a Google search using the terms “carbon monoxide poisoning.” The goals of COHQ were: (1) To act as a platform for public information about CO, (2) To act as an educational resource for all viewers, including medical professionals,

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(3) To act as a data resource—“look-up” and retrieval of information, and (4) To present new ideas and information at the forefront of research in the field. Like other good expert sites, it (1) Provides reliable, in-depth information in a narrow, defined span of knowledge, (2) Is accessible, understandable, and useful to the lay public as well as professionals in field, (3) Remains current as the field progresses and as viewers needs change, and (4) Is unbiased; that is not supported or influenced by a commercial interest in the field. The web was a very different place a decade ago. The number of websites was miniscule as compared to today. Google was not yet operating. “My Space” was years away. There were search engines running there, but they didn’t have the power and speed of today’s. It is hard to believe that in the middle 1990s it was difficult for us to even find sources of instruction for the HTML language. Much of the early writing was hit or miss—whatever worked was used. The objective of COHQ was never to sell new furnaces, to provide furnace maintenance, and so forth as so many thousands or tens of thousands of websites found by a “carbon monoxide” search pulls up today. I have been accused of using the site as an advertising vehicle. Any good information source, whether a book, storefront, or website inadvertently advertises the author/owner when people go there. Nonetheless, unlike most CO sites, COHQ has no axe to grind. It provides both simple and technical information free about CO to whoever wishes to look at it. The constant theme is public health, for groups and for individuals—educating and protecting people from this age-old poison [see other chapters in this book on misconceptions about CO (Chapter14) and on public perceptions of CO (Chapter15)]. The moto on the home page reads, “CARBON MONOXIDE HEADQUARTERS, (to) provide information, public service, help people, maintain health, save lives.” I was pleased when “carbonmonoxidekills.com” came along in the late 1990s as another major CO information source, in this instance, emanating from the United Kingdom. As you have now read, its major objective is to safe-guard everyone by everyone having CO alarms. Carbonmonoxidekills.com is currently number 1 when the same search noted above for COHQ is run on Google. So I was thrilled some years ago, when Rob Aiers, the owner, asked me to answer questions on CO from his website. I have continued in that role to this day. Thus, it was natural when this book was being planned that I would ask Mr. Aiers to tell us about his experience in developing a very successful website similar to COHQ.

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Investigating Carbon Monoxide Poisonings Thomas M. Dydek

CONTENTS 12.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12.2 Signs and Symptoms of Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . 12.3 Assessments of Carbon Monoxide Exposure Level and Duration. . . . . . . . 12.3.1 Carboxyhemoglobin Levels as a Measure of Carbon Monoxide Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12.3.2 Occupational Exposure Standards for Carbon Monoxide . . . . . . . . 12.3.3 Community Exposure Standards and Guidelines for Carbon Monoxide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12.3.4 Carbon Monoxide Exposure Duration Assessments . . . . . . . . . . . . . . 12.4 Treatments for Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12.5 Other Factors to Consider in Investigations of Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12.6 Case Study of Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12.7 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

287 288 289 290 291 291 292 295 296 297 299 300

12.1 INTRODUCTION Carbon monoxide (CO) is a colorless, odorless, tasteless, and potentially toxic gas. These properties have earned it the title of “the silent killer”.1 CO poisoning is responsible for more than one half of the poisoning fatalities reported in this country every year. It is the leading cause of death in industrial accidents as well. Fatalities and CO-related injuries are also common throughout the world. Another factor that makes CO an especially dangerous toxin is that the early symptoms of poisoning are easily confused (and often misdiagnosed) as the onset of a cold or the flu, stomach virus, or other common diseases.2 CO is produced by natural sources and by man-made sources. Natural sources include forest fires, oxidation of nonmethane hydrocarbons, and oxidation of methane. Plants can also emit CO as a metabolic by-product.3 Anthropogenic sources of CO are mostly associated with incomplete combustion of organic materials such as

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gasoline, fuel oil, natural gas, wood, or plastics. Common man-made sources of CO include improperly vented cooking or heating devices, tobacco smoke, agricultural burning, and internal combustion engines. Exposure to CO is one of the chief dangers associated with the fighting of fires in buildings and forest fires. Workers in occupations in which routine exposures to CO occur include truck and bus drivers, mechanics, highway toll takers, garage attendants, and police officers. Everyone who drives a car or truck, especially in areas of congested traffic, has some exposure to CO.4 This chapter covers topics related to the investigation of CO-poisoning events. These investigations can occur in a number of different situations. Oftentimes these investigations are undertaken as part of legal proceedings. Many people have commented that we in the United States today are the most litigious society in the history of the world. While this may be a somewhat dramatic statement, there is a large element of truth in it. Many people in this country feel that pursuing legal remedies for perceived injuries which they believe they have suffered should be a first, rather than a last, resort. Expert witnesses in engineering, industrial hygiene, and toxicology are often called to investigate CO-poisoning incidents and to render opinions about whether or not the CO exposure reported was of at a sufficient level or duration to have caused the health harm alleged. The topics covered in this chapter include signs and symptoms of CO poisoning, exposure level and duration assessments, treatments for CO poisoning, differences in susceptibility between people, how the above factors affect the acute effects of exposure, and the long-term prognosis for CO victims, and other toxic exposures or conditions that mimic CO toxicity (differential analysis). All of these factors are important in the investigation of CO poisonings.

12.2 SIGNS AND SYMPTOMS OF CARBON MONOXIDE POISONING CO poisoning results in a decreased level of oxygen in the body. The brain and other parts of the central nervous system are the areas of the body which are among the most sensitive to oxygen lack.5 When oxygen levels in tissues fall, aerobic metabolism decreases and lactic acid accumulates. Neurons begin to break down, leading to cell death and brain damage.6 The longer the brain is deprived of adequate oxygen, the more widespread the damage will be. Similar effects occur in muscle tissues deprived of oxygen. This is of special concern when the muscle involved is in the heart. For many years most toxicologists believed that COs toxicity was fully explained by this hypoxic effect. More recent research has shown, however, that CO exerts direct toxic effects by inhibiting the activity of cytochrome a3 oxidase and by causing lipid peroxidation. These latter findings help to explain the clinical experience that carboxyhemoglobin (COHb) levels (an indicator of the risk of tissue hypoxia) are a very poor predictor of a patient’s medical condition and his or her prognosis.2,5,7

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The acute symptoms seen with CO-poisoning depend on the concentration of CO and the duration of the exposure. At low levels of exposure there may be subtle changes in time discrimination, visual vigilance, and choice response. Exposure to higher levels will aggravate preexisting angina pectoris. Symptoms seen in people with higher level CO exposure include severe headache, dizziness, nausea, vomiting, mental confusion, visual disturbances, reddening of the skin (not always), compartment syndrome, loss of muscle tissue, fatigue, hypotension, and coma. Severe exposure can of course be fatal.8 The COHb levels measured in the CO-poisoned patient are sometimes used to classify CO exposures in terms of mild, moderate, or severe poisonings. In this system, COHb levels of less than 30% are termed “mild” poisonings. “Moderate” poisonings are those in which the victim has a COHb level of from 30% to 40% and “severe” poisonings occur when COHb levels are greater than 40% . This construct, while sometimes useful at a simplistic level,7 should be used with great caution since other signs and symptoms are known to be far more important in determining how and when to treat a patient poisoned by CO. Depending on the level and duration of CO exposure, delayed or prolonged symptoms can also occur in CO-exposed individuals. Some of these effects can be severe and can last for years. These symptoms can include sleep disturbances, vision problems, hearing loss, tinnitus, peripheral neuropath, mental deficits, memory problems, and difficulty concentrating, to name but a few. While there is often some recovery of mental function in CO poisoned individuals over time, many brain tissues damaged by CO show little, if any capability for regeneration. Similarly, the neurological or other damage done in cases of compartment syndrome is not generally reversible. Therefore, many of the chronic medical conditions brought on by severe CO poisonings are likely to be permanent.5,9,10

12.3 ASSESSMENTS OF CARBON MONOXIDE EXPOSURE LEVEL AND DURATION In any poisoning case the investigator must try to determine the amount of exposure an individual has had. The cornerstone of toxicology is the “dose makes the poison.” Knowledge of the “dose” as reflected by the exposure a person has experienced helps to assess the potential for adverse health effects the person may exhibit, guides treatment that the individual will require, assists in assessing the patient’s follow-up care needs, and determines his/her prognosis. In the legal arena, a large part of job of the expert witness as a poisoning incident investigator is to determine what the exposure level was. Exposure assessments are also required in the workplace to ascertain whether or not occupational exposure standards were exceeded. Community exposure standards and guidelines have also been established by federal and state environmental agencies and by private organizations. Monitoring ambient air levels of CO and keeping outdoor CO levels below applicable standards and guidelines is one of the jobs of federal and state air pollution control agencies.

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12.3.1 CARBOXYHEMOGLOBIN LEVELS AS A MEASURE OF CARBON MONOXIDE EXPOSURE When measurements of the CO level in the air have not been made or if made are not representative of the actual CO exposure levels a poisoning victim has experienced, other methods have been used to estimate CO exposure levels. One such method is to rely on COHb levels in the victim’s blood. When CO is inhaled, it is readily absorbed into the blood. Once there, the vast majority of the CO binds to hemoglobin in the erythrocytes to form COHb. CO binds to hemoglobin with an affinity more than 200 times that of oxygen. Thus CO displaces the oxygen from the hemoglobin, impairing oxygen delivery to critical body tissues such as the central nervous system, heart, and other organs.5 COHb levels in people exposed to CO reach a peak or plateau if the exposure lasts for 5–10 h. Further exposure to CO will not increase the COHb saturation of the hemoglobin if the air CO concentration remains constant. This is referred to as the “equilibrium” (or steady-state) COHb level. Estimates have been made as to what COHb level will be reached on the basis of concentration of CO in the air to which a person is exposed. For example, a person exposed to 30 ppm CO for an extended period of time will eventually have about 5% of their hemoglobin as COHb. An exposure to 100 ppm CO will yield an equilibrium COHb level of 20%. Exposures to 600 ppm gives a COHb level of more than 50%.11 In the latter case 50% of the hemoglobin is in the “carboxy” form. Whether more subtle toxic effects occur after this “plateau” COHb level is attained is the object of ongoing research. Various investigators have attempted to correlate health effects with COHb level. Such data nearly always show a huge variability, presumably because it is not just the effect of CO on hemoglobin that is important, but also the effects of CO on tissue and cells (e.g., on the cytochromes) and the effects of lipid peroxidation. Some studies have shown decreased vigilance in subjects with only 2–3% COHb.12,13 Others have shown no effects on vigilance or other health endpoints at COHb levels up to 12.6%.14−27 Conversely, there are studies that showed effects in addition to decreased vigilance at relatively low (less than 13%) COHb levels. These effects included small changes in the electrocardiogram, increased minute volume, reduction in exercise stamina, driving skill deficit, increased heart rate, visual sensitivity decrement, fatigue, and increased reaction time.28−41 Mild headaches are reported in people with COHb levels of 13–20%,16 but other effects have not generally been reported until COHb levels exceed about 30%.31,42−49 Symptoms seen at COHb levels of from 30% to 40% have been associated with severe headache, dizziness, difficulty concentrating, nausea, vomiting, polycythemia, and loss of consciousness.50,51 Subjects with COHb levels from 40% to 45% were unable to perform any tasks requiring even minimal physical exertion.52 Coma and convulsions usually occur at COHb levels of 50–60%, or below.51 Acute COHb levels near 70% are almost always lethal. Note that the median COHb saturation of people dead from CO-poisoning is near 53%. While such crude relationships between COHb levels and health effects may serve as a general guide, the toxicologist must be cognizant of the fact that different individuals are affected differently by CO. This issue is discussed more fully below.

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12.3.2 OCCUPATIONAL EXPOSURE STANDARDS FOR CARBON MONOXIDE Many CO exposures (and poisonings) occur in occupational settings. There are two main types of occupational exposures to CO: accidental exposures and routine exposures. In the case of accidental poisonings, the challenge for the investigator (who is usually not present at the accident itself) is to determine what the exposure levels might have been. It is rare for there to be air quality measurements in such situations and the actions of emergency response personnel may complicate the exposure level assessment. Obviously, the first duty of safety personnel is to assist the CO-poisoning victim. In this effort, first responders may open doors or windows or turn on fans or institute other ventilation efforts before they take measurements of ambient CO levels. Measurements made after ventilation has taken place will be lower that those responsible for the poisoning. CO levels during routine industrial operations are easier to obtain and interpret. Airborne CO levels are routinely monitored in some industrial settings, but in some cases where CO intoxication is suspected, monitoring may not be available. A typical function of the occupational safety investigator is to go to the place of business in question and to obtain CO levels in the air under normal plant operating conditions. These measured CO levels can then be compared to the existing occupation exposure standards. Occupational exposure standards have been set to protect worker’s health. There are three major types of occupational exposure standards and guidelines for CO in this country. The current Occupational Safety and Health Administration (OSHA) standard (which carries the force of law) is an 8-h average of 50 ppm. The National Institute of Occupational Safety and Health (NIOSH) recommended standard is an 8-h average of 35 ppm.53 The American Conference of Governmental and Industrial Hygienists threshold limit value (TLV) over 8 h is 25 ppm.54 OSHA originally proposed lowering their standard to that recommended by NIOSH, but this rule was remanded by the U.S. Circuit Court of Appeals.55 These occupational standards and guideline limits were supposedly set to protect against adverse cardiovascular, respiratory, and neurobehavioral effects. These limits were set to also be protective of pregnant workers and their unborn children, and other workers at high risk, although whether this is actually true is open to question. NIOSH has also established a “ceiling” exposure limit for CO of 200 ppm. This level is not to be exceeded at any time during a working day. The “Immediately Dangerous to Life and Health” (IDLH) for CO is 1200 ppm. Exposure to levels of CO greater than the IDLH “is likely to cause death or immediate or delayed permanent adverse health effects or prevent escape from such an environment.”53

12.3.3 COMMUNITY EXPOSURE STANDARDS AND GUIDELINES FOR CARBON MONOXIDE Air pollution investigators are often called upon to access the levels of CO in community air. CO levels are typically highest near highways or major industrial facilities having combustion sources. As in the case of the industrial environment,

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there are methods available to measure the levels of CO in community air. These measured levels can then be compared to air quality standards or guidelines set by federal or state agencies or by other organizations. A variety of community exposure guidelines have been set up to protect public health from air pollutants, including CO. Table 12.1 summarizes the current community exposure standards and guidelines for this chemical. The agencies and organizations that have set community exposure limits for CO include the American Industrial Hygiene Association (AIHA),56 the U.S. Environmental Protection Agency (EPA),57 and the California Air Resources Board (CARB).58,59 Like the occupational exposure standards mentioned in the previous section, these limits have been set to protect members of the general population from the adverse effects of CO exposure.60 Since these standards and guidelines are subject to change, the reader is urged to consult with the agency or organization involved to get the most current exposure levels of interest.

12.3.4 CARBON MONOXIDE EXPOSURE DURATION ASSESSMENTS As mentioned briefly above, the CO exposure duration as well as the exposure level has to be considered in investigations of CO poisonings. In occupational and in some nonoccupational settings, the frequency of exposure is also important. One general rule in toxicology that reflects the importance of both exposure level and duration is referred to as Haber’s Law or Haber’s Rule. This rule can be stated as follows: C×t =k where C is the toxicant concentration or exposure level, t is the time of exposure, and k is a constant reflecting the severity of the toxic effect. For example, if a toxic substance obeys Haber’s Law, a 30 min exposure to 100 ppm of the chemical should give a similar level of toxic effect that a 60 min exposure to 50 ppm would (30 min × 100 ppm = 3000 ppm-min = 60 min × 50 ppm).61 The formation of COHb in CO-poisoned people does not seem to follow Haber’s Law. Data from research studies and from clinical experience is summarized in Table 12.2.62 Three different ranges of COHb levels are shown below: 2.0–2.7%, 7.0–8.5%, and 11.0–12.6%. These data show that the product of CO exposure level and exposure duration is in no way indicative of COHb levels. This may be partially explained by the fact that COHb levels reach an equilibrium concentration at some point in time and do not increase even when exposure duration does. If C remains constant and t is increasing, k, the COHb level in this case will not increase. The deviation from Haber’s Law may also explained by the fact that responses to CO exposures are highly variable from one individual to another. In any case, the duration of exposure is important to the CO investigator. Unless CO levels are very high, an exposure of a few minutes will rarely if ever cause adverse effects. On the other hand, long-term exposures to quite low levels of CO for extended periods of time (months to years) can lead to serious health consequences.

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TABLE 12.1 Summary of Existing Community Air Quality Standards and Guidelines Agency or Organization AIHA AIHA AIHA AIHA AIHA AIHA AIHA EPA EPA CARB CARB CARB

Type of Standard TEEL-0 TEEL-1 TEEL-2 TEEL-3 ERPG-1 ERPG-2 ERPG-3 NAAQS-1 NAAQS-2 AQS-1 AQS-2 REL

Carbon Monoxide Level (ppm) 50 83 83 330 200 350 500 35 9 0.25 0.04 20

Averaging Time 15 min 15 min 15 min 15 min 1h 1h 1h 1h 8h 1h 24 h 1h

The AIHA is the American Industrial Hygiene Association. The EPA is the U.S. Environmental Protection Agency. The CARB is the California Air Resources Board. TEEL-0, the threshold concentration below which most people will experience no appreciable risk of health effects. TEEL-1, the maximum concentration in air below which it is believed nearly all individuals could be exposed without experiencing other than mild transient adverse health effects or perceiving a clearly defined objectionable odor. TEEL-2, the maximum concentration in air below which it is believed nearly all individuals could be exposed without experiencing or developing irreversible or other serious health effects or symptoms that could impair their abilities to take protective action. TEEL-3, the maximum concentration in air below which it is believed nearly all individuals could be exposed without experiencing or developing life-threatening health effects. ERPG-1, the maximum concentration in air below which it is believed nearly all individuals could be exposed for up to 1 h without experiencing other than mild transient adverse health effects or perceiving a clearly defined objectionable odor. ERPG-2, the maximum concentration in air below which it is believed nearly all individuals could be exposed for up to 1 h without experiencing or developing irreversible or other serious health effects or symptoms that could impair their abilities to take protective action. ERPG-3, the maximum concentration in air below which it is believed nearly all individuals could be exposed for up to 1 h without experiencing or developing life-threatening health effects. NAAQS-1, the 1-h average National Ambient Air Quality Standard as established by the US EPA. NAAQS-2, the 8-h average National Ambient Air Quality Standard as established by the US EPA. AQS-1, the 1-h average air quality standard as established by the CARB. AQS-2, the 8-h average air quality standard as established by the CARB. REL, the Reference Exposure Level as established by the CARB. RELs are levels at or below which even the most sensitive members of the community would not suffer any adverse health effects.

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TABLE 12.2 Carboxyhemoglobin Levels for Different Carbon Monoxide Exposure Levels and Durations CO Exposure Level (C in ppm) 50 12 50 100 50 650 75 100 200

Exposure Duration (t in h) 1.33 192 0.42 2.5 192 0.75 168 8.0 2.67

COHb Level (%)

C × t (ppm-h)

2.0 2.4 2.7 7.0 7.1 8.5 11.0 12.0 12.6

67 2304 21 250 9600 488 12600 800 534

Another factor that comes into play in evaluating a person’s risk of CO exposure is the frequency of exposure as compared to the half-life of CO excretion in the body. For example, in the occupational world, workers normally work 8 h shifts. Unless a worker has significant CO exposures outside of the work place (a possibility, especially if the worker has a long daily commute through heavy traffic) he or she will have 16 h away from work to recover from CO exposure on the job. If a person takes in CO more quickly than it can be eliminated from the body, elevated COHb will tend to persist during off-work times. The half-life (expressed in units of time) of an exogenous chemical in an organism is the time it takes for a given level of that chemical to be reduced by one-half. In two half-lives, the chemical level would be 25% of the original level, after three half-lives, it would be 12.5%, and so on. In CO poisonings, it is sometimes useful to know what initial COHb level in a particular individual. This can be done if the COHb level is measured a short time after the CO-poisoning, and then back-calculating to get the initial level known at to , based on how many COHb half-lives have transpired. The half-life for COHb of a person breathing ambient or room air is roughly 4–5 h.63 Next consider the previously mentioned example of a worker exposed for 8 h on the job and then having little or no CO exposure for the following 16 h. Sixteen hours is approximately four half-lives for COHb for people breathing ambient air. After four half-lives have passed, COHb levels should be reduced by 94%. While this is a large reduction, it should be pointed out that the COHb levels would not return to the baseline levels before the worker went back to work the next day, again to be exposed to CO. On the second day of exposure the COHb level would start at a higher baseline and would then reach a higher level than reached on the first day. The intervening 16 h “rest” periods would decrease the COHb levels by 94% each day, but there would be some accumulation over the work week. Fortunately, the 63 h between 5:00 p.m. Friday afternoon and 8:00 a.m. Monday morning affords almost 16 half-lives, during which the COHb level would be reduced to less than 0.002% of the level on Friday afternoon.

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12.4 TREATMENTS FOR CARBON MONOXIDE POISONING Medical treatments administered to CO-poisoned patients are designed to reverse the effects that CO has on the body; namely, the effects on the blood oxygen carrying capacity, the binding to myoglobin in muscle, the interference CO exerts on the cytochrome oxidase system, effects on lipid peroxidation in the brain and other tissues, and so forth. The type of treatment provided can influence the investigator’s conclusions concerning the nature and extent of the damage caused by CO poisoning. Emergency medical technicians (EMTs) and other “first responders” are trained to administer 100% oxygen to people they suspect have been poisoned by CO. This treatment has the effect of reducing the COHb levels in the patient’s blood at a faster rate than would be expected without such treatment. As mentioned earlier, the halflife of COHb without supplemental oxygen is 4–5 h. The half-life of COHb in patients breathing 100% oxygen centers around 60–80 min.63,64 Oxygen treatment functions to promote the dissociation of COHb65 and to reduce tissue hypoxia. A more controversial treatment regime for the CO-poisoning victim is hyperbaric oxygen treatment (HBOT). See in-depth discussions of this treatment modality elsewhere in this book. HBOT is accomplished by placing the patient in a large sealed chamber, giving the patient 100% oxygen, and gradually increasing the pressure inside to levels several times greater than of atmospheric. It is clear is that HBOT can greatly decrease the half-life of COHb—to roughly 20–30 min.63,65,66 HBOT has also been shown to promote CO dissociation from cytochrome a3 oxidase in animal studies and to reduce brain lipid peroxidation.65 The efficacy of HBOT in humans has not been conclusive. Some studies have shown marked reductions in the number and severity of both acute symptoms and the incidence of delayed neuropsychological sequelae.67,68 Other investigators have reported either no advantage to HBOT69 or have even found that HBOT worsened the patient’s condition.70 One explanation for these conflicting findings, besides the variability in susceptibility expected in those CO-poisoned, is that the groups of patients studied came from a wide variety of CO poisoning situations. Some HBOT was done at less than the optimal pressures of from 2.5 to 3.0 atm., while in other studies there had been a delay in initiating the HBOT. Some groups of CO-poisoned individuals studied, included individuals who had lost consciousness, while others did not and some studies had flaws in design and execution.5,65,71 The current consensus seems to be that HBOT should be applied selectively. There are risks of side-effects to this treatment and the transport of critically injured patients to the nearest HBOT center also poses risks. HBOT may not be the best approach for all patients. HBOT is more likely to have benefits outweighing its risks for patients having one or more of the following characteristics: 1. Severe intoxication as evidenced by coma, seizures, focal neurological deficits or cardiac effects65 2. Those who can be given HBOT within 6 h of the poisoning event67

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3. Those presenting with COHb levels in excess of 25%.5,71 4. Some studies suggest that patients with less severe CO poisoning may do just as well after normobaric treatment (i.e., sea level) with 100% oxygen.66

12.5 OTHER FACTORS TO CONSIDER IN INVESTIGATIONS OF CARBON MONOXIDE POISONING The investigator of CO-poisoning events needs to be aware of other causes of the symptoms that are associated with overexposure to CO. The process by which other causes are dealt with is called the “differential diagnosis.” Other conditions that can have symptoms in common with CO poisoning include viral infections, food poisoning, depression, anxiety, transient ischemic attacks, coronary artery disease, cardiac arrythmias, Parkinson’s disease, meningitis or encephalitis, epilepsy, migraine, drug overdose, ethanol intoxication, pneumonia, and sinusitis.10,65 Clues exist by which to discern whether the case being investigated is actually a CO-poisoning case. For example, if all of the occupants of a residence or business establishment are affected, many of the above alternate explanations can be eliminated. If symptoms improve when the victims depart the site, this usually points the finger at suspected site as the likely culprit. Indications of incomplete combustion, such as yellow flames on gas appliances or heaters provide an indication that CO exposure is possible/likely.70 In the occupational environment, CO exposures can occur wherever there is a source of combustion. Some examples include propane or gasoline powered forklifts (i.e., hi-lows, lift trucks), generators, bobcats, scissor lifts, cherry pickers, concrete saws and chain saws, floor strippers and polishers, and so forth. The toxicity of CO is enhanced at high altitudes, at elevated temperatures, and in people having increased ventilation or metabolic rates. The human fetus is at particularly high risk from CO poisoning because of its normal development in a somewhat oxygen-deprived environment. Children are at higher risk of CO poisoning because they generally have higher metabolic rates than adults. People with preexisting diseases such as anemia, cardiovascular, or cerebral vascular disease, hypovolemia, or those with increased endogenous CO production are also at higher risk of adverse effects from CO exposure.10 Exposures to some other chemicals either in the home or in the workplace can mimic CO exposures and are easy to confuse with those exposures. For example, exposure to methylene chloride (i.e., dichloromethane) can cause the same types of effects as exposure to CO. This is because methylene chloride is metabolized to CO and carbon dioxide in the body. An 8-h exposure to 150 ppm of methylene chloride produces the same elevated carboxyhemoglobin level that a 35 ppm exposure to CO would produce over the same time period. While causing less of an effect per ppm of exposure, it has been found that the half-life of methylene chloride-induced COHb is greater than that of CO-induced COHb, so effects may last for longer periods of time.7 Exposure to cyanide can mimic CO intoxication, mainly because cyanide also disrupts the functioning of cytochrome a3 oxidase.

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12.6 CASE STUDY OF CARBON MONOXIDE POISONING The following is an account of an actual case in which three individuals were severely poisoned by CO. This particular situation involved a faulty swimming pool heater at a hotel. Malfunctions of heaters are a common cause of CO-related poisonings and fatalities. The names of the victims, the other individuals involved in this incident, and the name of the hotel have been omitted to maintain privacy. The three individuals involved were staying at a hotel near Denver, Colorado. Victim #1 went jogging the evening of October 31 and returned to his room at about 7:00 p.m. He soon felt ill and probably passed out around 8:00 p.m. that evening. Housekeeping staff entered his room the next morning at 8:20 a.m., but seeing him on the bed, assumed he was just sleeping soundly and left the room. A colleague of Victim #1 who was staying at another hotel called Victim #1’s hotel at 9:45 a.m. on November 1 and asked the desk clerk on duty to check on his friend. The clerk went to Victim #1’s room, knocked on the door, but did not enter. He stated that it was against hotel policy to enter a room unless the guest gave them authorization to do so. Later that morning after repeated calls from the colleague, the hotel staff did enter Victim #1’s room. Hotel records show that Victim #1’s door was opened at 11:04 a.m. and 11:15 a.m. by the desk clerk trying unsuccessfully to rouse him. The colleague finally came to the hotel to check on Victim #1 at about 11:30 a.m. and went to his room. Finding him unconscious, the colleague asked the desk clerk to call 911 and to summon emergency medical personnel. Victim #1 was finally removed from the room at about 11:55 a.m. Victim #1 therefore had an approximately 17-h exposure to CO. In this case the duration of exposure could be obtained from what is known as an “audit trail.” At some hotels each time the card key is used to open the door, the time and whose card was used (guest, housekeeping, desk clerks, etc.) is recorded on the hotel computer. This victim suffered severe brain damage. Victim #2 has stated that she got into her room at the hotel at about 5:00 p.m. on October 31. After 15–20 min she felt confused and nauseated. Maids working at the hotel entered her room at about 8:30 a.m. the next day and found her passed out on the floor and thought that she had had too much to drink (example of a “misdiagnosis”). Upon reporting this to the hotel management, the maids apparently were told to leave Victim #2 alone. Nothing was done to aid her until the emergency personnel (who had been summoned to assist Victim #1) arrived and removed her from her room just before noon. She was therefore exposed to the CO for a total of about 19 h. This victim incurred cognitive deficits and had to have a leg amputated because of compartment syndrome she suffered caused by the CO exposure. Victim #3 entered her room at about 5:00 p.m. on October 31. She believed she passed out by about 6:00 p.m. Victim #3 awoke at about 6:30 a.m. the next morning, showered, got dressed, and passed out again. She called some friends to come and get her at about 8:00 a.m. Sometime shortly thereafter, she also called the front desk to let them know she had vomited and that the carpet needed to be cleaned. Her friends arrived at about 9:00 a.m. and seeing her condition took her to the hospital. Therefore, she was in her room and exposed to the CO for about 15.5 h. Her outcome involved limited neuropsychological deficits.

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Blood tests done after these three victims reached the hospital showed that each had elevated COHb levels. This confirmed that they had been exposed to CO. All three people were diagnosed by physicians at the hospitals as having CO-poisoning. Their symptoms at the emergency room (ER) included severe headache, dizziness, nausea, vomiting, reddening of the skin, compartment syndrome, loss of muscle tissue, fatigue, hypotension, and coma. These are consistent with what would be expected from CO exposures. In addition, all three victims suffered ongoing health damage involving sleep disturbance, vision problems, hearing loss, tinnitus, peripheral neuropathy, mental deficits, memory problems, and difficulty concentrating. During their investigations of this incident, local fire department personnel measured CO concentrations in the rooms occupied by the three individuals. They were all in excess of 200 ppm. These readings were taken after the doors to the rooms had been opened and some ventilation of these rooms had occurred. Because of this, the CO levels to which the victims were exposed would certainly have been higher than that recorded by the fire department. The source of the CO was traced to the swimming pool heater in the hotel. CO levels in this mechanical room were found to be “extremely high” according to fire department personnel. Police investigating this incident looked for, but did not find any evidence of the presence of drugs, drug paraphernalia, or alcohol in the Plaintiffs’ hotel rooms. Furthermore, there was no evidence of any violence or trauma to the victims. Victim #1 suffered occasional headaches and visual problems prior to the incident, but these became much worse afterwards. Otherwise, the Plaintiffs’individual medical histories prior to this incident were unremarkable. Thus, it was possible to rule out other possible causes for the victims’ adverse health effects. The conclusion reached in this CO-poisoning investigation was that the adverse health effects suffered by the victims were caused by their exposures to CO at the hotel. The bases for this conclusion are as follows: 1. Elevated levels of CO in excess of 200 ppm were found in the hotel rooms occupied by the individuals even after some ventilation of these rooms had occurred 2. The victims were exposed to high levels of CO for periods of time ranging from 15.5 to 19 h 3. The presence of elevated levels of COHb in the blood of these three individuals confirms that they did sustain an exposure to CO 4. Both the acute and the long-term symptoms exhibited by the three victims were entirely consistent with those associated with an overexposure to CO 5. Finally, the three victims in this case had no significant medical or psychiatric conditions or problems prior to the incident, and no other likely explanations could be found for the health harm suffered by the individuals. Another conclusion was that the victims’ injuries would have been less severe if they had been removed from their hotel rooms earlier. The housekeeping staff went into each of the three victims’ rooms at about 8:30 a.m. on November 1. Although the first two victims were found unconscious at that time, they were not taken out of their rooms until about noon. This resulted in each of them sustaining an extra three and

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one-half hours of CO exposure. The odds of more serious injuries go up with each additional hour of exposure. Victim #3 was fortunate to have been able to summon aid on her own. Notably, she suffered fewer and less severe effects than the other two individuals who had 2–3 h more exposure to CO at the hotel. The basis for this finding is that neurological damage from CO poisoning is progressive. It becomes more severe the longer tissues are without adequate oxygen as explained above. If Victim #1 had been taken out of his room earlier and had received medical treatment sooner, he would have probably suffered less severe brain damage. If Victim #2 had been rescued earlier, she may not have suffered such a severe injury to her leg. Victim #3’s continuing injuries (problems with memory loss and other mental deficits), while not as great as those suffered by the other two victims, would most likely not have been as severe or taken as long to overcome had she been able to get to the hospital sooner.

12.7 SUMMARY CO poisoning is a leading cause of accidental injuries and fatalities in this country and throughout the world. Exposures to CO are possible wherever there is a source of combustion; for example, heating systems, fires, petroleum product fueled vehicles, and industrial equipment, to name a few. This chapter has been an overview of how investigations of CO-poisoning incidents are carried out and the types of information required in such investigations. Investigations include evaluations of the signs and symptoms of the intoxication, assessments of exposure level and duration, reviewing the medical treatments that may have been administered, and the ruling out of other factors that may have caused the poisoning. The investigator first of all should be familiar with the signs and symptoms of CO poisoning. Many of the symptoms are common to other conditions such as viral infections, alcohol intoxication, coronary disease, and other disease states. This can complicate a positive determination of CO’s involvement. Other chemicals can cause similar symptoms and should be also investigated as possible causes. It is crucial in an investigation of CO poisonings to determine how great a “dose” of CO the victim received. This may be done using CO measurement instruments, or by determining COHb levels subsequent to the poisoning incident. Measured airborne CO levels can be compared to occupational and community exposure standards and guidelines, to assess health risk in more routine human exposure scenarios. The medical treatment that an individual received can influence the investigation of CO poisonings. Whether a victim received no supplemental oxygen, was given 100% oxygen to breathe, or had HBOT, will influence the immediate health condition and the long-term prognosis for that individual. CO poisonings have occurred for tens of thousands of years, and probably even before humans inhabited the earth (from volcanic activity, forest fires, etc.). The advent of man’s use of controlled fires for warmth and cooking no doubt signaled a sharp rise in the risk and incidence of CO poisonings. Even with all of the technological advances that have been made over the millennia, CO poisoning is still common

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and continues to be a major threat to public health. One objective of this chapter is to assist those who are involved in investigations of CO poisoning. This chapter and the others in this book also serve to raise awareness of this threat and to hopefully reduce the number of CO poisonings.

References 1. Shephard, R.J. Carbon Monoxide, The Silent Killer, Charles C. Thomas Publisher, Springfield, Illinois, 1983. 2. Kindwall, E.P. Carbon monoxide, In: Occupational Medicine, 3rd ed., Zenz, C., Dickerson, O.B., and Horvath, E.P., eds., Mosby, St. Louis, 1994, Chapter 29. 3. U.S. Environmental Protection Agency, Air Quality Criteria for Carbon Monoxide, USEPA Publication No. EPA 600/P-99/001F, U.S. Government Printing Office, Washington, DC., 2000. 4. Lipsett, M.J., Shusterman, D.J., and Beard, R.R. Inorganic compounds of carbon, nitrogen, and oxygen, In: Patty’s Industrial Hygiene and Toxicology, 4th ed., Vol. II, Part F, Clayton, G.D., and Clayton, F.E., eds., John Wiley & Sons, Inc., New York, 1994, pp. 4523–4552. 5. Tomaszewski, C. Carbon monoxide, In: Goldfrank’s Toxicological Emergencies, 6th ed., Goldfrank, L.R., et al., eds., Appleton & Lange, Stamford, Connecticut, 1998, pp. 1551–1563. 6. Victor, M., and Adams, R.D. Metabolic Diseases of the Nervous System, In: Harrison’s Principles of Internal Medicine, 9th ed., McGraw-Hill Book Company, New York, 1980, pp. 1978–1979. 7. Hathaway, G.J., Proctor, N.H., and Hughes, J.P. Carbon monoxide, In: Proctor and Hughes’ Chemical Hazards of the Workplace, 4th ed., Van Nostrand Reinhold, New York, 1996, pp. 113–116. 8. Smith, R.P. Toxic responses of the blood, In: Casarett and Doull’s Toxicology, The Basic Science of Poisons, 5th ed., Klaassen, C.D., Amdur, M.O., and Doull, J., eds., McGraw-Hill, New York, 1996, Chapter 11, pp. 343–344. 9. Smith, J.S., and Brandon, S. Morbidity from acute carbon monoxide poisoning at three-year follow-up, Br. Med. J. 1, 318, 1973. 10. Respiratory Toxicology, In: Ellenhorn’s Medical Toxicology, 2nd ed., Ellenhorn, M.J., et al., eds., Williams & Wilkins, Baltimore, pp. 1465–1476, 1997. 11. Seinfeld, J.H. Air Pollution, Physical and Chemical Fundamentals, McGraw Hill Book Company, New York, 1975, pp. 22. 12. Fodor, C.G., and Winneke, C. Effect of Low CO concentrations on resistance to monotony and on psychomotor capacity, Staub-Reinhalt Luft, 32, 46, 1972. 13. Beard, R.R., and Grandstaff, N.W. Carbon monoxide and human functions, In: Environmental Science Research, Vol. 5, Behavioral Toxicology, B. Weiss and V.G. Laties, eds. New York, Plenum Press, 1975,pp. 1–27. 14. Sievers, R.F., Edwards, T.I., and Murray, A.L. A Medical Study of Men Exposed to Measured Amounts of Carbon monoxide in the Holland Tunnel for 13 Years, Public Health Bulletin No. 278, U.S. Government Printing Office, Washington, DC., 1942. 15. Mikulka, P.R., et al. The effect of carbon monoxide on human performance, Ann. N.Y. Acad. Sci. 174, 409, 1970. 16. Stewart, R.D., et al. Experimental human exposure to carbon monoxide, Arch. Environ. Health 21, 154, 1970.

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17. Horvath, S.M., Dahms, T.E., and O’Hanlon, J.F. Carbon monoxide and human vigilance, a deleterious effect of present urban concentrations, Arch. Environ. Health 23, 343, 1971. 18. O’Donnell, R.D., et al. Low level carbon monoxide exposure and human psychomotor performance, Toxicol. Appl. Pharmacol. 18, 583, 1971. 19. Raven, P.B., et al. Effect of carbon monoxide and peroxyacetyl nitrate on man’s maximal aerobic capacity, J. Appl. Physiol. 36, 288, 1974. 20. Ettema, J.H., et al. Effects of alcohol, carbon monoxide and trichloroethylene exposure on mental capacity, Int. Arch. Occup. Environ. Health 35, 117, 1975. 21. O’Hanlon, J.F. Preliminary studies of the effects of carbon monoxide on vigilance in man, In: Behavioral Toxicology, Weiss, B., and Laties, G., eds., Plenum Press, New York, 1975, pp. 61–75. 22. Benignus, V.A., et al. Lack of effects of carbon monoxide on human vigilance, Perception and Motor Skills. 45(3, Pt 1), pp. 1007–1014, 1977. 23. Luria, S.M., and McKay, C.L. Effects of low levels of carbon monoxide on vision of smokers and nonsmokers, Arch. Environ. Health 34, 38, 1979. 24. Davies, D.M., et al. The effects of continuous exposure to carbon monoxide on auditory vigilance in man, Int. Arch. Occup. Environ. Health 48, 25, 1981. 25. DeLucia, A.J., Whitaker, J.H., and Bryant, L.R. Effects of combined exposure to ozone and carbon monoxide (CO) in humans, In: Advances in Modern Environmental Toxicology, Vol. 5, Lee, S.D., Mustafa, C.G., and Mehlman, M.A., eds., Princeton Scientific Publishers, Princeton, N.J., 1983, pp. 145–159. 26. Mihevic, P.M., Gliner, J.A., and Horvath, S.M. Carbon monoxide exposure and information processing during perceptual-motor performance, Int. Arch. Occup. Environ. Health 51, 355, 1983. 27. Benignus, V.A., et al. Effect of low level carbon monoxide on compensatory tracking and event monitoring, Neurotoxicol. Teratol. 9, 227, 1987. 28. McFarland, R.A., et al. The effects of carbon monoxide and altitude on visual thresholds, J. Aviat. Med. 15, 381, 1944. 29. Ray, A.M., and Rockwell, T.H. An exploratory study of automobile driving performance under the influence of low levels of carboxyhemoglobin, Ann. N.Y. Acad. Sci. 174, 396, 1970. 30. Bender, W., Goethert, M., and Malorny, G. Effect of low carbon monoxide concentrations on psychological functions, Staub-Reinhalt Luft, 32, 54, 1972. 31. Ekblom, B. and Huot, R. Response to submaximal and maximal exercise at different levels of carboxyhemoglobin, Acta. Physiol. Scand. 86, 474, 1972. 32. McFarland, R. Low-level exposure to carbon monoxide and driving performance, Arch. Env. Health 27, 355, 1973. 33. Ramsey, J.M. Effects of single exposures of carbon monoxide on sensory and psychomotor response, Am. Ind. Hyg. Assoc. J. 34, 212, 1973. 34. Wright, G., Randell, P., and Shephard, R.J. Carbon monoxide and driving skills, Arch. Env. Health 27, 349, 1973. 35. Drinkwater, B.L., et al. Air pollution, exercise, and heat stress, Arch. Env. Health. 28, 177, 1974. 36. Gliner, J.A., et al. Man’s physiologic response to long-term work during thermal and pollutant stress, J. Appl. Physiol. 39, 628, 1975. 37. Horvath, S.M., et al. Maximal aerobic capacity at different levels of carboxyhemoglobin, J. Appl. Physiol. 38, 300, 1975.

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Carbon Monoxide Poisoning 38. Putz, V.R., Johnson, B.L., and Setzer, J.V. Effects of CO on Vigilance Performance. Effects of Low-Level Carbon monoxide on Divided Attention, Pitch Discrimination, and the Auditory Evoked Potential, Publication Number DHEW (NIOSH) 77–124, U.S. Department of Health, Education, and Welfare, National Institute of Occupational Safety and Health, Cincinnati, Ohio, 1976. 39. Putz, V.R., Johnson, B.L., and Setzer, J.V. A comparative study of the effects of carbon monoxide and methylene chloride on human performance, J. Env. Pathol. Toxicol. 2, 97, 1979. 40. Davies, D.M. and Smith, D.J. Electrocardiographic changes in healthy men during continuous low-level carbon monoxide exposure, Env. Res. 21, 197, 1980. 41. Bunnell, D.E. and Horvath, S.M. Interactive effects of heat, physical work and CO exposure on metabolism and cognitive task performance, Aviat. Space Env. Med. 60, 428, 1989. 42. Chevalier, R.B., Krumholz, R.A., and Ross, J.C. Reaction of non-smokers to carbon monoxide inhalation, cardiopulmonary responses at rest and during exercise, JAMA. 198, 1061, 1966. 43. Pirnay, F., et al. Muscular exercise during intoxication by carbon monoxide, J. Appl. Physiol. 31, 573, 1971. 44. Vogel, J.A. and Gleser, M.A. Effect of carbon monoxide on oxygen transport during exercise, J. Appl. Physiol. 32, 234, 1972. 45. Vogel, J.A., et al. Carbon monoxide and physical work capacity. Arch. Environ. Health 24, 198, 1972. 46. Parving, H.H. The effect of hypoxia and carbon monoxide exposure on plasma volume and capillary permeability to albumin, Scand. J. Clin. Lab. Invest. 30, 49, 1972. 47. Stewart, R.D., et al. Effect of carbon monoxide on time perception, Arch. Environ. Health 27, 155, 1973. 48. Hudnell, H.K. and Benignus, V.A. Carbon monoxide exposure and human visual detection thresholds, Neurotoxicol. Teratol. 11, 363, 1989. 49. Schulte, J.H. Effects of mild carbon monoxide intoxication, Arch. Environ. Health 7, 524, 1963. 50. DiMarco, A. Carbon monoxide poisoning presenting as polycythemia, N. Engl. J. Med. 319, 874, 1988. 51. Chiodi, H., et al. Respiratory and circulatory responses to acute carbon monoxide poisoning, Am. J. Physiol. 134, 683, 1941. 52. Stewart, R.D. The effect of carbon monoxide on humans, Ann. Rev. Pharmacol. 15, 409, 1975. 53. NIOSH Pocket Guide to Chemical Hazards, Department of Health and Human Services, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, DHHS (NIOSH) Publication Number 97–140, U.S. Government Printing Office, Washington, DC, 2003. 54. 2005 TLVs and BEIs, American Conference of Governmental Industrial Hygienists, ACGIH Signature Publications, Cincinnati, Ohio, 2005. 55. Department of Labor, Occupational Safety and Health Administration, 29 CFR Part 1910, Air Contaminants, Federal Register, 54, 2651, 1989. 56. Current values for the American Industrial Hygiene Association can be found at the Internet Web Site http://www.eh.doe.gov/chem_safety/teel.html. 57. Current National Ambient Air Quality Standards can be found at the USEPA Internet Web Site http://www.epa.gov/air/criteria.html. 58. Current values for California Air Quality Standards can be found at the CARB Internet Web Site http://www.baaqmd.gov//pln/air_quality/ambient_air_quality.htm.

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59. Current values for the California Reference Exposure Limits can be found at the CARB Internet Web Site http://www.oehha.ca.gov/air/pdf/acuterel.pdf. 60. Craig, D.K. Derivation of temporary emergency exposure limits (TEELs), J. Appl. Toxicol. 20, 11, 2000. 61. Pastenbach, D.J. The History and Biological Basis of Occupational Exposure Limits for Chemical Agents, In: Patty’s Industrial Hygiene and Toxicology, 5th ed., Volume 3, VI, Harris, R.L., ed., John Wiley & Sons, Inc., New York, 2000, pp. 1953–1954. 62. National Research Council, Carbon monoxide, In: Review of Submarine Escape Action Levels for Selected Chemicals, National Academy Press, Washington, DC, 2002, pp. 69–96. 63. Varon, J. and Marik, P.E. Carbon monoxide poisoning, J. Emerg. Int. Care Med. 1, 1, 1997. 64. Weaver, L.K., et al. Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure, Chest. 117, 801, 2000. 65. Gill, A.L. and Bell, C.N.A. Hyperbaric oxygen: Its uses, mechanisms of action, and outcomes, Q. J. Med. 97, 385, 2004. 66. Leach, R.M., Rees, P.J., and Wilshurst, P. ABC of oxygen: hyperbaric oxygen therapy, Brit. Med. J. 317, 1140, 1998. 67. Thom, S.R., et al. Delayed neuropsychological sequelae after carbon monoxide poisoning: Prevention by treatment with hyperbaric oxygen, Ann. Emerg. Med. 25, 474, 1995. 68. Ducasse, J.L., Celis, P., and Marc-Vergnes, J.P. Non-comatose patients with acute carbon monoxide poisoning: Hyperbaric or normobaric oxygenation?, Undersea Hyperb. Med. 22, 9, 1995. 69. Weaver, L.K., Hopkins, R.O., and Larson-Lohr, V. Neuropsychological and functional recovery from severe carbon monoxide poisoning without hyperbaric oxygen therapy, Ann. Emerg. Med. 27, 736, 1996. 70. Scheinkestel, C.D., et al. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: A randomized controlled clinical trial, Med. J. Aust. 170, 203, 1999. 71. Harper, A. and Croft-Baker, J. Carbon monoxide poisoning: undetected by both patients and their doctors, Age Ageing 33, 105, 2004.

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Carbon Monoxide Detectors as Preventive Medicine James W. Rhee and Jerrold B. Leikin

CONTENTS 13.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13.2 Carbon Monoxide Detector Technology: A Brief Review . . . . . . . . . . . . . . . . 13.3 Setting an Initial Standard . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13.4 The Chicago Experience. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13.5 Clinical Implications. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13.6 Some Data Regarding Effectiveness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13.7 Current and Future Directions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

305 306 306 307 308 308 309 310

13.1 INTRODUCTION Carbon monoxide (CO) is odorless, colorless, tasteless, and nonirritating. As such, CO has no warning properties that can alert unwary individuals to its presence. When people become ill owing to CO toxicity, the symptom complex can be nonspecific and variable making the diagnosis of CO poisoning difficult. Given its lack of warning signs and lack of distinct clinical features, CO has been labeled by some as a “silent killer.” Data analyzed by Cobb and Etzel from the National Center for Health Statistics, attributed 53,133 deaths to CO from 1979 to 1988—making it the most common cause of acute poisoning deaths.1 When Shepherd and Klein-Schwartz examined the mortality data from 1979 to 1994 for persons aged 10–19 years, they found 3034 out of 7936 poisoning deaths were attributable to carbon monoxide.2 As these numbers were derived from databases, they are likely to be significant under representation of the true number of deaths caused by CO. They also do not take into account the significant morbidity that may occur from severe CO exposures. Given the “silent” nature of CO and its significant impact on public health, a need for residential-based CO detectors was identified. In 1989, the Consumer Product Safety Commission (CPSC) urged Underwriters Laboratories (UL) (Northbrook, Illinois) to develop a standard that would serve as a guideline for residential 305

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CO detectors. This standard (UL 2034) applying to single and multiple station CO detectors was published in April, 19923 —subsequently, the first two CO detectors were listed later that year.4

13.2 CARBON MONOXIDE DETECTOR TECHNOLOGY: A BRIEF REVIEW Most of the residential CO detectors utilize one of the two methods of sensing the presence of CO—either a biomimetic sensor or a metal oxide sensor. The types of technology usually involved in residential sensors include the “Gel cell” metal oxide and electrochemical sensor. The nondispersive infrared technology (NDIR) is usually utilized for industrial purposes. The “Gel cell” based sensor sends a light beam through a biomimetic sensor to a photosensitive component which alarms at appropriate set points. This colorimetric sensor essentially mimicked the hemoglobin uptake of CO, thus changing the spectral response. These types of sensors exhibit proper sensitivity to CO and can achieve a unique accumulation of CO. There is some interference with other gases and vapors along with humidity, and these types of sensors take a longer time to recover in the setting of CO removal (slower response reversibility). The “Gel cell” detectors are rarely equipped with digital displays. The metal-oxide (usually tin-oxide) sensor detects CO by measuring the resistivity of the metal component through oxidation of CO to carbon dioxide, which reduces the resistance of the sensor. These sensors usually require main (i.e., AC) power and cannot use batteries as a primary power source. Upon exposure to CO, the electrochemical sensors will generate electricity through an acid electrolyte (usually sulfuric acid or phosphoric acid). This technology has been utilized as portable or fixed gas monitors in industry owing to its resolution (down to 1 ppm) and stability, and is probably the primary type of sensor used in residential detectors. These sensors can also be affected by cross-contamination of gases. The NDIR can measure CO concentrations with an accuracy of ±2 ppm, but are expensive and therefore usually not utilized in residential detectors. Metallocorroles utilizing cobalt (111) can selectively absorb CO gas on a molecular complex and may provide a future matrix in sensor development.5

13.3 SETTING AN INITIAL STANDARD UL is a well-known organization located in Northbrook, Illinois that develops standards and test procedures for materials, components, assemblies, tools, equipment, and procedures, chiefly dealing with product safety and utility. The CPSC worked closely with UL to develop standards for CO detectors. Part of setting this standard required UL to create thresholds at which the detectors would alarm. The threshold at which the residential CO detectors would alarm presented a unique challenge. Initially, set points were generated on the basis of extrapolating what levels of CO over what period of time would generate a carboxyhemoglobin (COHb) concentration of 10% in a nonsmoking individual. These values were based

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TABLE 13.1 UL 2034 (1992–1996). Carbon Monoxide Concentration Versus Time for Alarm Test Points Air Concentration (ppm)

Maximum Response Time (min)

100 200 400

90 35 15

on the Coburn–Forster–Kane equation. (In addition, the CO detector should alarm at an exposure of 6000 ppm within 3 min.)6 This initial standard (UL 2034) was set in place in 1992.3 Soon afterwards CO detectors were sold across the United States. Table 13.1 illustrates the original set points for activating the audible alarm in the CO detectors. Other standards, such as loudness of the alarm and the response to other gases needed to be clarified as well. Similar to smoke detectors, the CO detector was set to emit an 85-dB alarm (at 10 ft.), which is loud enough to wake most people when sounding outside a bedroom through a closed door. However, unlike smoke detectors, CO detectors have computer processor-based software which allow it to alarm at certain set points. Sensors were set to not alarm when exposed for 2 h to methane (at 500 ppm), butane (at 300 ppm), heptane (at 500 ppm), ethyl acetate (at 200 ppm), isopropyl alcohol (at 200 ppm), carbon dioxide (at 5000 ppm), toluene (at 200 ppm), and acetone (at 200 ppm).7 Other major features include a red lightemitting diode (LED) as a trouble signal, a green LED indicating normal operation and a reset mechanism for testing and resetting purposes. Some detectors utilize a digital display (over 30 ppm).

13.4 THE CHICAGO EXPERIENCE The state of Illinois, in the past had one of the highest fatality rates from CO— accounting for 8.7% of all unintentional CO deaths nation-wide, with a rate of about 0.9 deaths per 1000 people between 1979 and 1988.1 In light of this statistic, Chicago, Illinois, passed a mandatory CO detector ordinance in March, 1994 requiring CO detectors to be present in all homes, apartments, class “B” and “C” buildings with heat sources that generate CO.8 During the first 3 months of the ordinance implementation, 68 individuals were transported with suspected CO poisoning attributed to CO detector alarms.9 However, during this time period (October 1–December 31, 1994), the Chicago Fire Department received over 12,000 calls of CO detector alarming. In about 85% of these cases, less than 9 ppm of CO was reportedly measured by the Chicago Fire Department.9–12 This was climaxed on December 21–22, 1994, when the Chicago Fire Department was involved in 3464 CO investigations.11 It was subsequently determined that a thermal air inversion (upper atmosphere warmer than lower atmosphere) had caused a fivefold

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elevation of ambient CO concentration, of 13–20 ppm, thus setting off multiple CO alarms. CO detector sensitivity or resistance specifications were 15 ppm over an 8-h period at that time.9,10 In response to the inordinate number of “nuisance alarms,” UL increased the 15 ppm resistance specification from 8 h to 30 days in the 1996 revised standard.7 The UL standard 2034 is under a continuous maintenance process and was last revised in 2006.

13.5 CLINICAL IMPLICATIONS Given the variable presentation of CO toxicity—it is apparent that healthcare providers could use assistance in diagnosing occult CO poisoning. Patients with CO poisoning are often misdiagnosed as having a viral syndrome or food poisoning.13 Earlier studies have shown that among adult patients presenting to an emergency department during the winter months with complaints of headache or dizziness, 3–5% have COHb levels greater than 10%.14 Because CO is a colorless, odorless, tasteless, and nonirritating gas, the physician and the patient have few clues as to the contribution of CO to the illness (see other chapters in this book). The CO detector can act as a useful screening tool to identify CO exposure. The CO detector should allow the clinician to obtain a history of exposure and prompt the clinician to begin investigating the potential for CO poisoning.

13.6 SOME DATA REGARDING EFFECTIVENESS CO detectors/alarms have made death from CO poisoning completely preventable. CO detectors can save lives. Despite the high number of false alarms in Chicago after the initial mandatory CO detector ordinance was established in 1994, only one CO-related death was reported in the Chicago media between September 1994 through February 1998. Compared to other cities during this same time period, Chicago (the only city to have a CO detector ordinance during the study period) had the lowest case fatality rate.15 And despite the loudly voiced criticisms and objections to the ordinance from various sources, a Chicago Sun-Times poll (though hardly scientific) reported that 77% of respondents supported such a mandatory ordinance. Krenzelok et al.16 found that in an investigation of emergency responses to possible CO poisoning, residences with CO alarms had lower CO concentrations (18.6 ppm with CO detectors versus 96.6 ppm without CO detectors) and fewer symptomatic patients (11.7% with CO detectors vs 63.4% without CO detectors).16 They concluded that audible CO detectors were effective in alerting people to the presence of abnormal levels of CO, thus resulting in less exposure to CO. This subsequently lead to a lower incidence of CO-related symptoms.16 A study conducted by Bizovi et al.10 found similar results where only about 5% of individuals at a site where a CO detector had activated displayed signs of CO poisoning, suggesting that the CO detector may have prevented more serious exposure.10

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Yoon et al.17 estimate that 78 out of 136 unintentional deaths due to CO poisoning that occurred during a 15-year period in New Mexico, may have been prevented if audible CO detectors were in use.17 In North Carolina, a couple of studies evaluated the impact of a local CO detector ordinance (which exempted all-electric heated homes) was conducted.18,19 While, the ordinance did not seem to decrease the amount of CO exposures, the relative incidence of severe poisoning requiring hyperbaric oxygen treatment was diminished.18 Another study evaluating a CO poisoning outbreak during a winter storm in 2002 demonstrated that the North Carolina county CO detector ordinance did not eliminate a CO poisoning outbreak, but it did mitigate its effects.19 Of note, the study found that none of the patients who developed symptoms of severe CO poisoning had a functioning CO detector.19 Despite the apparent effectiveness of CO detectors at saving lives, only 29% of respondents to a survey conducted by Runyan et al.20 reported the presence of CO detectors in their homes.20 The lack of widespread use of these detectors intuitively limits the effectiveness of these devices to have a profound impact on mortality and morbidity due to CO poisoning.

13.7 CURRENT AND FUTURE DIRECTIONS Newer aspects of CO detector specifications include an alarm reset within 6 min if the CO concentration exceeds 70 ppm, secondary power supply considerations, and alarm tests point revision (revised November, 2001—see Table 13.2). Usage in recreational vehicles/marine units and unconditioned areas was added in 1997.7 The revised UL 2034 standard is similar to that of the International Approved Services (IAS) and the British Standards Institute (BSI). While these new standards and new sepcifications for CO detectors facilitate the design and development of newer and better CO detectors, the potential impact these CO detectors can have on public health is limited by the prevalence of their use.

TABLE 13.2 UL 2034, revised November, 2001. Carbon Monoxide Concentration Versus Time for Alarm Test Points Based on 10% Carboxyhemoglobin (COHb) A. Carbon Monoxide Concentration (ppm) and Response Time Concentration, ppm Response time, min 70 ± 5 60–10 150 ± 5 10–50 400 ± 10 4–15 B. False Alarm-Carbon Monoxide Concentration Resistance Specifications Concentration, ppm Exposure time, (no alarm) 30 ± 3 30 days 70 ± 5 60 min

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This problem can potentially be remedied by CO detector ordinances set at the state and local levels, since the ordinances already in place have had a demonstrable impact on public health.

References 1. Cobb, N. and Etzel, R. A. Unintentional carbon monoxide-related deaths in the United States, 1979 through 1988, JAMA, 266, 659, 1991. 2. Shepherd, G. and Klein-Schwartz, W. Accidental and suicidal adolescent poisoning deaths in the United States, 1979–1994, Arch. Pediatr. Adolesc. Med., 152, 1181, 1998. 3. Standard for Safety UL 2034 Single and Multiple Station Carbon Monoxide Detectors, Underwriters Laboratories, Northbrook, IL, 1st ed., 1992. 4. Hrones, T. L. and Patty, P. E. Carbon monoxide detectors: protection against the silent killer, In Poisoning and Toxicology Compendium, Leikin, J. B., and Paloucek, F. B., eds., Lexicomp, Hudson, Ohio, 1998, 630. 5. Barbe, J. M., Canard, G., Brandes, S., Jerome, F., Dubois, G., and Guilard, R. Metallocorroles as sensing components for gas sensors: remarkable affinity and selectivity of cobalt(III) corroles for CO vs. O2 and N2 , Dalton Trans., 1208, 2004. 6. Coburn, R. F., Forster, R. E., and Kane, P. B. Considerations of the physiological variables that determine the blood carboxyhemoglobin concentration in man, J. Clin. Invest., vol. 44(11), 1899–1910, 1965. 7. Standard for Safety UL 2034 Single and Multiple Station Carbon Monoxide Detectors, Underwriters Laboratories, Northbrook, IL, 2nd ed., 1996. 8. City Council of the City of Chicago: Amendment of Title 13, Chapter 64 of the Municipal Code of Chicago by addition of new sections 190 through 300 requiring CO detectors in various buildings. Meeting of March 2, 1994. 9. Leikin, J. B. Carbon monoxide detectors and emergency physicians, Am. J. Emerg. Med., 14, 90, 1996. 10. Bizovi, K. E., Leikin, J. B., Hryhorczuk, D. O., and Frateschi, L. J. Night of the sirens: analysis of carbon monoxide-detector experience in suburban Chicago, Ann. Emerg. Med., 31, 737, 1998. 11. Eversole, J. M. Carbon Monoxide Detector Ordinance: Review of the Chicago Fire Department experience, In Poisoning and Toxicology Compendium, Leikin, J. B., and Paloucek, F. B., eds., Lexicomp, Hudson, Ohio, 1998, 633. 12. Leikin, J. B., Krenzelok, E. P., and Greiner, T. H. Remarks to the Illinois House of Representatives Executive Committee hearing regarding state carbon monoxide detector act (HB 603), J. Toxicol. Clin. Toxicol., 37, 885, 1999. 13. Barret, L., Danel, V., and Faure, J. Carbon monoxide poisoning, a diagnosis frequently overlooked, J. Toxicol. Clin. Toxicol., 23, 309, 1985. 14. Heckerling, P. S., Leikin, J. B., and Maturen, A. Occult carbon monoxide poisoning: validation of a prediction model, Am. J. Med., 84, 251, 1988. 15. Clifton, J. C. N., Leikin, J. B., Hryhorczuk, D. O., and Krenzelok, E. P. Surveillance for carbon monoxide poisoning using a national media clipping service, Am. J. Emerg. Med., 19, 106, 2001. 16. Krenzelok, E. P., Roth, R., and Full, R. Carbon monoxide: the silent killer with an audible solution, Am. J. Emerg. Med., 14, 484, 1996. 17. Yoon, S. S., Macdonald, S. C., and Parrish, R. G. Deaths from unintentional carbon monoxide poisoning and potential for prevention with carbon monoxide detectors, JAMA, 279, 685, 1998.

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18. Tomaszewski, C., Lavonas, E., Kerns, R., and Rouse, A. Effect of a carbon monoxide alarm regulation on CO poisoning, J. Toxicol. Clin. Toxicol.,41(5), 167–168, 2003. 19. Lavonas, E., Tomaszewski, C., Kerns, W., and Blackwell, T. Epidemic carbon monoxide poisoning despite a CO alarm law, J. Toxicol. Clin. Toxicol.,41(5), 711–712, 2003. 20. Runyan, C. W., Johnson, R. M., Yang, J., Waller, A. E., Perkis, D., Marshall, S. W., Coyne-Beasley, T., and McGee, K. S. Risk and protective factors for fires, burns, and carbon monoxide poisoning in U.S. households, Am. J. Prev. Med., 28, 102, 2005.

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Misconceptions About Carbon Monoxide David G. Penney

CONTENTS 14.1 Properties, Presence, and Detection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14.2 Physiology of Carbon Monoxide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14.4 Treatment and Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14.5 Miscellaneous . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

313 316 318 320 322 323

14.1 PROPERTIES, PRESENCE, AND DETECTION There are many many misunderstanding about carbon monoxide (CO), even today, by the general public, healthcare professionals, and others who ought to be better informed. The first grouping of these misconceptions are shown in Table 14.1. CO is known as the “Silent Killer” or the “Stealthy Poison” because it is impossible to detect by humans—we cannot smell, taste, or see CO gas, no matter what the concentration. For this reason gas supply companies often put smelly tracers in fuel gases to assist us in detecting their presence. With school groups and nonscientists I often refer to CO as a “smart poison,” as opposed to “dumber poisons” like hydrogen sulfide and others that we have warning of by our chemoreceptors (i.e., taste, smell). CO is also smart in that it enters our bodies simply by our breathing, and does not have to be “picked up” by ingestion through the mouth as lead largely is. Another element of “smartness” is that it leaves the body quickly, although damage may already have been done, while dumb poisons remain (lead, mercury, etc.) to be detected days, weeks, even years later. CO is of course slightly lighter than air, being made up of one carbon atom and one oxygen atom. It has about the dimensions of an oxygen molecule (i.e., diatomic oxygen), contributing to several others of its properties (i.e., ability to diffuse easily, attach to hemoglobin where oxygen sits). The molecular weight of CO is roughly 28 (see Reference Data, Chapter 35). Calculating the molecular weight of air, a mixture of nitrogen (28), oxygen (32), argon (40), carbon dioxide (44), and water vapor (18), gives a weighted average of approximately 29. Thus, CO is about 4% lighter than

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TABLE 14.1 Misconceptions: Properties, Presence, and Detection • • • • • • • • • • • • • •

CO is easy to detect. CO is lighter than air and therefore rises (to the ceiling) and stays there. CO is not combustible. CO adsorbs and absorbs to fabric, crockery, walls and thus remains long after it has left the air. CO and natural gas are the same thing. Natural gas contains considerable amounts of CO. You can always tell if CO is present because of a peculiar odor that is present. A brand new, well designed, perfectly “tuned” heating/cooking device cannot produce toxic/lethal amounts of CO. Diesel engine exhaust never contains enough CO to cause harm. Heating, ventilation, and air conditioning (HVAC) and gas company service personnel always check for CO when performing maintenance/service on home heating systems. CO will be detected immediately by service personnel if it is present in a home heating system. When your home CO detector shows low levels of CO, it is probably just an instrument malfunction. Cracks in heat exchangers are responsible for the production of CO. Home CO detectors/sensors are the best devices to ferret out CO because they react to very low levels of the gas.

air. However, the assertion that CO rises to the ceiling when released into the air of a structure is incorrect. The CO is always mixed with vast quantities of excess air, mixes thoroughly and completely, and cannot unmix lest it violate the Second Law of Thermodynamics. The key to observations of higher CO concentration near ceilings stems from the fact that hot air rises, and exhaust containing CO is often warmer than the surrounding air. CO is of course combustible and has been used as a fuel gas. It will burn to carbon dioxide, which it does with the release of additional heat. CO was used as a fuel source in past years, for both lighting and heating. This property should be kept in mind when working around high concentrations of CO, where ignition may occur. We may forget about this property because usually the toxic effects are of greatest significance at far lower concentrations. CO does NOT attach in any way to fabric, glass, crockery, and so forth. I heard that a physician when seeing a patient who had sustained acute CO poisoning, told his patient’s mother to clean everything in the apartment after the incident because CO “sticks.” She did this as well as giving away all the furniture and clothing that had been in the apartment. This was of course entirely needless; the result of inadequate education in toxicology. Natural gas as it is used in the United States, contains little CO. Its main component is methane, CH4 . I understand there are also small amounts of other gases too, of the aliphatic series (e.g., ethane). CO may only be present around a combustion device using natural gas after the gas is combusted, and when that combustion process is incomplete, that is, not all of the gas is burned to form carbon dioxide and water vapor. Other possible incomplete combustion products include soot (i.e., elemental carbon).

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All common combustion devices involve some amount of incompelete combustion, although under certain circumstances this may be very small. So, all such devices produce some CO. Usually the concentration of CO generated is below levels set as safe by regulatory standards. But even these devices may under certain conditions produce extraordinarily high, even lethal concentrations of CO if something else in the heating system is inadequate or fails (compromised combustion air source, broken exhaust system), or if slow or catastrophic failure of the heating device itself takes place through corrosion, lack of cleaning, physical impact by outside forces, and so forth. Diesel engines generally produce lower CO concentrations in exhaust gases than gasoline-fueled engines. On the other hand, the Environmental Protection Agency (EPA) over the past several decades has required gasoline-fueled vehicles in the United States to have catalytic converters that work on the exhaust gases. This device converts the CO to carbon dioxide using various catalysts. They only work effectively when they are hot, that is, they are not effective at cold start. The key point here is that diesel engine equipped vehicles lack catalytic converters, so ALL the CO generated by the engine goes out the tailpipe. Thus, the CO emissions from many diesel powered vehicles are above those from gasoline-fueled vehicles. Heating and cooling technicians and gas company personnel should always monitor for CO when checking a combustion device. Unfortunately, this is not always done. “Sniffing” for natural gas or propane (LPG) is more common, to detect leaks that could lead to fire or explosion. Checking for CO that can lead to injury and/or death is sadly often not done. Unfortunately, even when CO is checked, a problem may be missed. A high CO reading is proof-positive of a problem with a combustion device or the system it is operating in. Failure to find CO on one attempt does not entirely rule out the possibility of a problem during that time frame and under slightly different environmental conditions. Of course measurements must be made when the combustion device is operating, and for sufficient time to catch possible delayed build-up. Often measurements will have to be made several times, and under slightly different conditions, for example, when other combustion devices are also operating, when exhaust fans are being run, when outside wind conditions change, and so forth. One of the most common, possibly lethal mistakes made by people is to assume that a residential CO alarm (i.e., detector) showing low, or even high levels of CO, is malfunctioning. “It never did before,” “it must be the battery,” “The smoke alarm is not sounding,” “take the battery out and go back to bed.” I recommend that people have a minimum of two CO alarms in their residence, one located very near where they sleep, and another near where they are when awake, reading, watching TV, and so forth. Two alarms sounding simultaneously make it much less likely that a person will come to the conclusion that the warning is due to malfunction. If there are two or more floors to the residence, an additional alarm should be installed for each additional floor. Home CO alarms are not the best devices to discover where CO is coming from in a breathing space. After all, they are built as “alarms,” not as instantaneous sensing devices. They have mathematical algorithms built in to simulate human CO uptake, and thus to provide warning before we have taken very much of the CO up into our blood and tissues. Also, their cost is minimal, making them affordable to the general

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public, but by no means professional grade in accuracy. The best devices to ferret out CO sources and monitor it accurately are what we call “monitors.” They measure CO almost instantaneously and produce a reading in parts per million (ppm). They are usually portable and the readings are highly reproducible. As one might imagine, these kind of devices are more costly than home CO detectors.

14.2 PHYSIOLOGY OF CARBON MONOXIDE CO binds to hemoglobin reversibly (Table 14.2). While this binding is avid, as we know it is some 230 times that of oxygen, it is nonetheless a competitive process with oxygen. As the oxygen partial pressure rises, the CO is forced off the site on the hemoglobin molecule and oxygen takes its place. This mechanism is one of the major reasons for using hyperbaric (high pressure) oxygen in treating CO poisoning. CO-induced hypoxia is far more serious than hypoxic hypoxia. The presence of CO in the blood occupying the oxygen sites on the hemoglobin decreases the oxygen transport capability of the cardiovascular system, not unlike increasing high altitude does by desaturating arterial blood as lung partial pressure of oxygen falls. In addition to this, however, CO causes the remaining oxyhemoglobin to hold its oxygen more strongly, thus shifting the oxygen dissociation curve (ODC) to the left and making it harder to unload what oxygen remains in the blood to the tissues. People tend to forget this second action of CO on the ODC. Hypoxic hypoxia does just the opposite, shifting the ODC to the right and enhancing the unloading of oxygen to the tissues. Thus, CO inflicts a “double-whammy” on the body in terms of oxygen delivery capability that is much more serious than is that of hypoxic hypoxia. CO poisoning is also far more serious than a comparable simple anemia, where it may appear that there is the same amount of total hemoglobin able to carry oxygen. Like hypoxic hypoxia, anemia causes a right-shift in the ODC, which enhances oxygen

TABLE 14.2 Misconceptions: Physiology • • • • • • • • •

CO binding to hemoglobin is irreversible. CO (caused) hypoxia is no more serious than any other type of hypoxia. CO poisoning is no more serious than an anemia in which there is a comparable amount of hemoglobin able to carry oxygen. Small animals (birds, mice, etc.) die more quickly because their hemoglobin binds CO more avidly than that of humans, thus they were used as alarms for CO in mines. The fetus is protected from CO by the maternal body. Good COHb measurements can be obtained 1 day to a week after a person leaves the site of the CO poisoning. Breathing “clean” air for 2–3 h will eliminate all CO from the body. Breathing 100% oxygen for 20–30 min will eliminate all CO from the body. Breathing (filter) masks protect the wearer from the inhalation of CO.

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unloading to the tissues, whereas CO does the opposite. A condition where the body has only one-half of its normal hemoglobin concentration (i.e., anemia) is welltolerated, whereas a condition where half of the hemoglobin has CO attached [i.e., 50% carboxyhemoglobin (COHb) saturation] is usually quickly lethal. Small birds and mammals were at one time used as CO alarms in mines and other closed places where CO occurred. Canaries and other like small birds were especially popular in this capacity because they would fall off their perches when incapacitated, making it obvious to the observer there was a problem. The reason for their usefulness was not that the small birds or mammals were necessarily more sensitive to CO, but because their warm-bloodedness and high surface to volume ratio caused their metabolic rate to be necessarily much higher than that of humans, making their ventilation rate greater than that of humans. Hence they take up the CO much faster. This provided a living “early warning” system for CO. The fetus residing inside the maternal body is subject to the CO breathed by the mother. Being a nonirritating gas, unlike chlorine or nitrogen dioxide, it is taken up silently and without notice through the maternal lungs. The CO reaches the placenta through the circulating maternal blood, and again, it passes silently and readily across the membranes into the fetal circulation where it attaches to the fetus’ hemoglobin. While CO compromises oxygen delivery to tissues in the maternal circulation by the mechanisms described above, the situation is much more serious for the fetus, which normally is operating in an oxygen-depleted environment. The presence of CO makes the situation worse by further degrading the oxygen carrying capacity of the fetus. The right time to draw blood for accurate measurement of COHb is one of the biggest misunderstandings by lay people, and even members of the medical community. The half-life of COHb in humans breathing sea level ambient air centers around 4–5 h. That is, one-half of the COHb will be gone in 4–5 h, and half of what remains will be gone in another 4–5 h (i.e., two half-lives). Within one day, COHb level in the blood will be at or near background (0.4–1.4%) no matter how high it was to start with. For accurate measurement, blood sampling should be done within 2–4 h of leaving the site of the CO poisoning. Physicians must not say when contacted by a patient on Friday or on the weekend, “just come to the office on Monday and we’ll do the COHb test.” It will be too late and the results will be useless. On the basis of what we know of COHb half-life, it is clear that breathing “clean” air for 2–3 h. will not eliminate all the CO from the body—approximately 24 h is required. In the same way, breathing 100% oxygen for 20–30 min at sea-level pressure, known as normobaric oxygen therapy, will not eliminate all the CO from the body, since the half-life of COHb when breathing 100% oxygen under normal conditions centers around 50–70 min. A number of hours will be required to do this. Another misconception involves the use of masks in polluted environments. Dust masks or more complicated filtering respirators will remove particulates of various sizes. Virtually none of these devices will remove CO. Donning a mask that does not remove CO when the wearer believes it will, can be a very dangerous, even deadly mistake. In order to safely enter an atmosphere containing CO, self-contained breathing apparatus (SCBA) is required, such as that used by firefighters and hazmat personnel.

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14.3 SYMPTOMS While CO poisoning is classically described as causing the skin, nail beds, and exposed mucous membranes to turn pink or bright red, this is rarely seen in actual fact. Often dead CO victims appear gray or yellow. The COHb saturation must be high enough for the COHb to show; people dying in the water from acute CO poisoning usually reach only 40–45% COHb, the level at which incapacitation occurs. Breathing then ceases below the water’s surface. The pink color is of course difficult to see in darkly pigmented people (i.e., negroids), those with severe sunburn, and so forth. (see Table 14.3) Fever is rarely associated with CO poisoning, especially chronic CO poisoning. Nonetheless, thermoregulatory dysfunction is a common outcome of CO poisoning, and is thought to be due to brain damage caused by the poison. Victims with this condition usually feel cold in thermally neutral surroundings, and occasionally report being hot, however, in the latter instance actual body temperature is rarely above normal. Fever is reported following severe acute CO poisoning, probably associated with cerebral tissue damage and edema, gastrointestinal damage, and so forth. The lungs along with the nasal passages, throat, and trachea are generally unaffected by CO. Most of the CO uptake by the body occurs through the former route, and the CO goes directly into the blood. While congestion, cough, and hoarseness are not caused by CO inhalation, other substances that often accompany CO, particulates, nitrogen oxides, sulfur oxides, aldehydes, and so forth will do this. A recent book on CO (Dwyer et al., 2003, p. 5)1 lists “wheezing” or bronchial constriction” and “persistent cough” as “signs and symptoms of CO poisoning.” In my experience this is incorrect. Such symptoms may be due to other components of

TABLE 14.3 Misconceptions: Symptoms • • • • • • • • • • • • • • •

The skin, nail beds, and so forth of people with CO poisoning are invariably red or pink in color. Fever is a common symptom of CO poisoning. Nasal congestion, cough, and hoarseness are symptoms of CO poisoning. The lungs are inflammed by low to moderate levels of CO and appear abnormal by x-ray. Hyperventilation is a response to low and moderate CO poisoning Symptom clusters involving prolonged headache, dizziness, nausea, and fatigue of the whole family should be blamed on viruses, bad food, or group craziness. Everyone responds to CO in the same way, that is, all people show the same symptoms. Depression is not a residual effect of CO poisoning. Loss of short-term memory capability is not a residual effect of CO poisoning. Muscle and/or joint pain is not a residual effect of CO poisoning. Difficulty with attention and concentration is not a residual effect of CO poisoning. Blurry vision is not a residual effect of CO poisoning. Personality change is not a residual effect of CO poisoning. More people experience acute CO poisoning than the chronic type There is a good dose–response relationship between CO in the air and COHb and immediate symptoms or long-term health damage.

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exhaust gases (e.g., Particulates, aldehydes, sulfur, and/or nitrogen oxides), but not to the CO specifically. As noted above, the lungs are virtually transparent to CO. In life-threatening CO poisonings, the lungs become edematous and begin to fill with fluid. This congestion is coughed up as a light to more darkly tan fluid, often mistaken for vomitus. It is usually observed at scenes of lethal CO poisonings, combined or not combined with vomitus. Tachypnea is not a symptom of low to moderately severe CO poisoning, since the carotid chemoreceptors are insensitive to percent saturation of the arterial blood, responding only to changes in arterial PO2 and pH, which generally change little until the CO poisoning becomes very severe. That is why hyperventilation with simple CO poisoning is so rare, and its presence suggests a more complicated poisoning. As discussed at length earlier, CO poisoning usually presents with a number of nonspecific symptoms; few if any of the symptoms are specific (i.e., pathognomonic) to CO poisoning. We often speak of symptom clusters, since CO usually induces symptoms involving so many organ systems. “Flu-like” is the way the symptoms are often described. Yet the “flu” may continue for weeks or months, affect everyone in the same breathing space (i.e., house, apartment) at the same time, subside when an individual leaves the space, etc. characteristics which are very “un-flu-like.” Historically, chief among misdiagnoses, has been viral or bacterial flu, food poisoning, psychosomatic behavior, and so forth. Sometimes medical providers will continue to insist on traditional causes for weeks and months, when they are clearly impossible, and fail to recognize the ear-marks of a site-specific poisoning. See my chapter on misdiagnosis of CO poisoning (Chapter 19). Although there is a commonality of responses to CO, not all people respond exactly the same, or have the same overall sensitivity to CO. This is the basis for the problems with tables of symptoms seen in articles and books on CO, as they occur at increasing concentrations of CO or COHb. I’ve often said that “people are not lab rats.” We vary in age, gender, race, height, body weight, and so forth and in ways that are difficult to describe or at present unknown, that influence our sensitivity (or tolerance) to CO. In any group of people exposed to what appears the same CO concentration for the same period of time, a diversity of responses develop. Some individuals suffer few immediate or even long-term health effects, while others can be severely affected, or even die during the initial CO exposure. Then there is a third group who respond in an intermediate manner, with mild initial symptoms and mild long-term effects. Thus, we usually see a “normal distribution” of responses, approximating a bell-shaped curve. This pattern appears to occur whether the CO poisoning is extremely mild, or extremely severe. Clinical depression is seen with a high frequency in people who have suffered long-term health damage from CO exposure. This is documented by the Utah group, principally Dr Ramona Hopkins (see chapter 22 in this book). The depression appears to have at least two components, that caused by the realization of the loss of functionality by the CO-injured individual, and by direct CO-induced damage to the brain. The latter pathway is often overlooked by those health professionals unfamiliar with CO poisoning. The depression is usually treatable with standard antidepressant medications.

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Along with chronic fatigue, decrement in short-term memory capability is probably the most common long-term damage caused by CO poisoning. It is described by victims as involving problems in remembering appointments and what was already said in a conversation, losing keys, wallet/purse, finding the right word, and so forth. It is embarrassing, affects a person’s confidence and self-esteem, and often forces that person to become less social, and even a recluse. Damage to longterm or remote memory, is far less common. In fact, it is rarely seen by this author, although it is reported in the literature. In the CO Support Study (see Hay et al., Carbon Monoxide Toxicity, 2000),2 muscle and joint pain were the most common long-term outcome of CO poisoning. My studies of chronic CO poisoning in particular, verify the frequency of these symptoms. Because clinical testing of the complaining muscles and joints rarely show evidence of local damage, it is my working hypothesis that the damage is wholey in the brain, and that the pain is referred, ie. sited in the brain. I don’t suggest that it is imagined or fabricated, that it is in fact real, but is simply another product of the CO-induced brain damage, not unlike that that causes the well-recognized cognitive and memory deficits. Like short-term memory damage, problems with attention–concentration are extremely common after CO poisoning. People become more distractible, with even minor auditory or visual distractions. Combined with this, and closely related to attention–concentration, is usually a vastly reduced ability to do more than one task at a time (i.e., multitasking). Having to have the TV off when talking on the phone, the radio off when entering a freeway, and having to study in a totally quiet environment, is often reported. While blurry vision is a common complaint during CO poisoning, it can continue for some time after poisoning has ended. It is one of several dozen visual complaints that may be persistent and residual. See Dr Helffenstein’s chapter in this book (Chapter 23). One of the most common statements by family and friends of a CO victim is that he/she is no longer the same—there has been “a personality change.” This usually occurs in the direction of increased irritability, anxiety, depression, apathy, and so forth. CO poisoning does not cause personalities to improve! I have written elsewhere (Chapter 1) that the most frequent kind of CO poisoning is the chronic type, that it is the least likely to be diagnosed, and probably results in the largest amount of total injuries. New studies make it clear that brain damage from CO poisoning is only very poorly correlated with severity of poisoning, whether that be gauged by air CO concentration, COHb saturation, loss of consciousness, and so forth.

14.4 TREATMENT AND OUTCOME I often see cases where nasal prongs were used following CO poisoning. Just because the oxygen in the tank is 100%, that doesn’t mean the oxygen coming through the nose to the lungs will be 100%. It could be just a bit over 21%, that is, room air, owing to dilution with copious amounts of fresh air (see Table 14.4).

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TABLE 14.4 Misconceptions: Treatment and Outcome • • • • • • • • •

Inhalation of 100% oxygen from a rebreathing mask or from nasal prongs are the best immediate means of removing CO from the body. Victims of CO poisoning should be released from medical care immediately following 1–2 h of oxygen treatment, whether or not their symptoms have disappeared. There is no need for repeat COHb measurements, psychometric tests, or other clinical tests following medical treatment for CO poisoning. People who recover from CO poisoning are always completely normal. Use of 100% oxygen therapy at normal atmospheric pressure (NBO) is a proven approach to eliminate the residual effects of CO poisoning. Use of 100% oxygen at increased atmospheric pressure (HBO) is a proven approach to eliminate the residual effects of CO poisoning. CO exposure never produces brain damage unless there is a period of unconsciousness. Low/moderate CO exposure cannot produce brain damage or significant changes in functional performance. Venous blood measurement of COHb is not as accurate as arterial.

CO poisoning victims should be kept in-hospital for observation, usually for a minimum of one night. All too often patients are seen for 2–3 h, given oxygen, then released and continue to be symptomatic—headache, nausea, dizziness, and so forth. Patients should never be discharged until they are completely symptom-free. An extra night in the hospital gives staff a chance to observe them. Delayed sequelae are such well-known complications of CO poisoning, even in patients who appear to be doing very well patient. Discharge documents should clearly warn of possible delayed effects, that is, sequela and how to recognize them. CO washout rates vary tremendously among people, even when body mass, gender, age, and so forth are taken into consideration. Second COHb measurements should be done to confirm that normal or near-normal COHb levels exist after treatment. This is an area that needs great improvement. COHb should be measured increasingly by the newer methods (breathlyzer, multiwavelength pulse-oximeters). Their advantage is that they can be done as often as necessary until COHb is sufficiently reduced. Psychometric testing should also be done on a more frequent basis in the emergency room (ER), especially in those patients who presented with symptoms of altered consciousness or gait/balance problems. It is recognized that a fraction of people who recover from CO poisoning are left with decrements in function. Mainline medicine has been slow to recognize the physical symptoms that often persist, and also the sensory, motor, cognitive, and psychological deficits that many patients are left with, instead only chosing to focus on the gross neurologic problems. The use of 100% normobaric oxygen (NBO) has been used for many years to treat CO poisoning. On a mechanistic basis, it should be efficacious simply because it more quickly removes CO from the body than breathing room air. In recent studies, it was the therapy to which hyperbaric oxygen (HBO) treatment was compared. The use of

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NBO is proven only in the sense that aside from HBO, it appears to be the best approach available. See the chapters by Drs Tomaszewski (Chapter 17) and Scheinkestel and Millar (Chapter 18) on the use of NBO and HBO therapies. Studies during the past 20 years make it abundantly clear that loss of consciousness is not required for development of neurologic sequelae. Even more recent studies demonstrate the lack of correlation between brain damge and air CO concentration, COHb saturation, and many other traditional markers of poisoning severity. For the measurement of blood CO alone, a venous sample is just as good as an arterial sample. The use of noninvasive methods (breathylizer, new generation pulse-oximeters) for this purpose is encouraged.

14.5 MISCELLANEOUS Medical students and residents receive virtually no training in the diagnosis and treatment of CO poisoning, and usually have little or no contact with CO-poisoned patients in their practice (see Table 14.5). This is a large part of the reason for the high misdiagnosis rate of CO poisoning by physicians. As a result few physicians have an adequate index of suspicion for CO poisoning when presented with appropriate symptoms and when they take a situational history. The gold standard for the cognitive-memory problems that occur with such a frequency following CO poisoning is neuropsychological testing. This should be done by a neuropsychologist who understands the pathology of CO poisoning and who has evaluated many patients with this condition. Psychiatry is well-suited to assist medically in the treatment of emotional and personality problems that often arise after CO poisoning. Neurology can be brought to bear for patients with gross neurologic problems (i.e., aphasia, gait disturbance) caused by CO poisoning. It must

TABLE 14.5 Misconceptions: Miscellaneous • • • • • • • • •

Physicians receive adequate training in the diagnosis and treatment of CO poisoning in medical school and residency/fellowship. Physicians get adequate experience with CO poisoning in treating their patients. Physicians generally have a high enough index of suspicion relative to CO poisoning in order to diagnose it reliably. Psychiatrists and neurologists are the medical professionals of choice to determine the extent of central nervous system (CNS) damage caused by CO. High-tech imaging devices (CT, MR, SPECT) always show areas of brain damage from CO poisoning, if they exist. Two wavelength pulse oximeters are excellent devices for determining oxygen saturation and also whether a person is suffering from CO poisoning. In environments containing CO, the levels of CO2 , oxygen and other gases are unimportant in the degree of poisoning. The presence of green plants in a closed space will remove CO from the atmosphere. Toxicology is central to medicine.

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be kept in mind however, that professionals in neither of these disciplines of medicine have training in toxicology. Computed tomography [CT, Computerized Axial Tomography (CAT)] is a form of computer-enhanced x-ray scanning. Magnetic resonance imaging (MRI) shows internal anatomy without the use of ionizing radiation. Both of these techniques allow us to look at structure only, not function. Single photon emission computed tomography (SPECT) permits the imaging of function in living tissue (see Chapters by Drs. Heuser [20] and Hipskind [21]). Pulse oximeters currently in use are “blind” to COHb, thus giving incorrect values for oxygen saturation in the presence of COHb. These pulse oximeter devices should never be used when there is suspicion of CO poisoning. In that case arterial blood should immediately be drawn for measurement of total blood gases, which includes COHb and oxygen saturation. See the chapter by Dr. Hampson [33] and mine [19], regarding the new generation of pulse CO-oximeters marketed by Masimo. Elevated carbon dioxide concentrations causes hyperventilation and an increased rate of CO uptake. Depressed oxygen (i.e., depletion) does the same, and also increases the final COHb saturation by shifting the Haldane equation. A recent article on residential CO poisoning published in the January, 2007 issue of “Woman’s Day” magazine, states that the presence of green plants will remove CO from the atmosphere. This was reportedly told to a patient by a treating physician. There is in fact no basis for this statement. Maybe he was confused by the fact that plants take up carbon dioxide (not carbon monoxide), converting it to oxygen through the process of photosynthesis. Toxicology might be likened to a poor relation to medicine. For most physicians the normal circles of training and practice experience in internal medicine rarely intersect with the toxicology circle. Thus, the constant complaints I receive from CO-victims, saying that few if any physicians they see are helpful in the diagnosis, evaluation, or treatment of their conditions.

References 1. Dwyer, Leatherman, Manclark, Kimball, Rasmussen. Carbon Monoxide: A Clear and Present Danger, ESCO Press, USA, 3rd ed., 2003 (www.escoinst.com). 2. Hay, A.W.H., Jaffer, S., Davis, D. Chronic carbon monoxide exposure: The CO Support study. In: Carbon Monoxide Toxicity, D.G. Penney, ed., CRC Press, NY, 2000, pp. 419–438.

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15

A Survey Study of Public Perceptions About Carbon Monoxide David G. Penney and Linda M. Penney

CONTENTS 15.1 Background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.2 Electric Generator Use . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.3 Propane Radiant Heater Use . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.4 Recreational Powerboat Safety . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.5 Conditions Affecting Exhaust Gas Danger . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.6 Safe Use Indoors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.7 The Greatest Risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.8 The Worst Poison . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.9 The Best Advice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.10 Duration of Time in the Body . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.11 Properties of CO . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.12 Experience with CO Poisoning? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.13 Use of CO Emitting Devices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

325 327 329 331 332 333 334 335 336 338 338 338 339 339 339

15.1 BACKGROUND On the basis of the large numbers of accidents involving carbon monoxide (CO), recent studies have asked questions about the public’s knowledge of the dangers of this gas.1 Our survey was conducted in the latter half of 2006 by sampling the opinions of people in Michigan (MI) and Florida (FL). The data derived from this survey are shown in Tables 15.1–15.13. Adult respondents belonged to civic and athletic social clubs. These data were analyzed by age groupings and by gender. Youth data were obtained by surveying students in both junior high and senior high school classes. The Michigan school was a large public school in Benzie County (first set of four rows). In Florida, one school was a large public high school in St. John’s County (first set of four rows), while data from two smaller parochial schools in the county were combined (second set of four rows). The youth data were also analyzed 325

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TABLE 15.1 Assume the Electric Power is Off, but Can be Restored by the Use of a Gasoline-fueled, Portable Generator. If Started in a Room, How Much Ventilation is Adequate for the Generator to be Run Safely? Percent of Total Male Michigan

Female

Mean Age

A

B

C

D

E

38 — 14–15 — 49 14–15 29 — 16–18 — 48 16–19 20 8 30–59 31 14 60–69 34 7 70–81 85 — 31–81 — 29 30–79 Florida (rows 1–4 public; 5–8 private)

14.4 14.4 16.7 16.8 48.5 64.9 74.2 64.9 62.3

13.2 28.6 0 12.5 7.1 11.6 13.2 12.1 7.7

10.5 18.4 37.9 22.9 14.3 14.0 10.5 10.8 19.2

26.3 24.5 17.2 27.1 3.6 7.0 5.3 6.0 3.9

26.3 18.4 24.1 31.3 21.4 18.6 36.8 26.5 23.1

23.7 10.2 20.7 6.3 53.6 48.8 34.2 44.6 46.2

38 — 15 — 9 — 44 — 56 16 72 — *20

15.6 15.5 17.1 17.2 13.9 13.5 16.5 16.6 44.8 71.1 50.8 46.9 57.5

15.8 21.4 8.3 7.1 22.2 7.7 4.7 2.6 1.4 5.6 2.9 0 4.4

13.2 19.1 0 28.6 22.2 15.4 4.7 15.4 2.8 11.1 5.7 0 8.7

23.7 14.3 0 21.4 0 30.8 9.3 20.5 4.2 16.7 7.1 5.3 8.7

23.7 28.6 41.7 35.8 33.3 15.4 46.5 33.3 15.7 22.2 14.3 31.6 21.7

23.7 16.7 50.0 7.1 22.2 30.8 34.9 28.2 75.0 44.4 70.0 63.2 56.5

— 43 — 14 — 14 — 40 18 2 — 20 *5

Range

14–16 15–16 17–18 17–18 13–15 11–15 16–18 16–18 18–59 60–83 19–83 26–69 26–80

A = One window open; B = Two windows open; C = Three or more windows open; D = All windows and the door open; E = None of the above. ∗ “medical”—all adults, MI and FL, with self-reported medical, biological occupations.

by age group and gender. The questions put to respondents in the survey are printed above each table, and the “correct” answer is indicated in bold. The survey asked only for age, gender, and occupation to be written in. Before the survey was administered, respondents were instructed to answer quickly, not to agonize over their responses, and told the survey was not an intelligence test. When we could not be present for administration of the survey, the survey takers (teachers) were provided instructions to be read to the class prior to starting. There was an initial un-numbered fill-in question that asked yes or no, whether respondents (or if students, their parents) had rented or owned various small combustion devices (Table 15.12). A final question on the survey asked respondents about their experience with CO poisoning incidents. This

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TABLE 15.2 Portable Propane Radiant Heaters are Available to Provide Heat, for example, when Camping. Which One of the Situations Below is Safe? Percent of Total Male Michigan

Female

Mean Age

A

B

C

D

E

38 — 14–15 — 49 14–15 29 — 16–18 — 48 16–19 20 8 30–59 31 14 60–69 34 7 70–81 85 — 31–81 — 29 30–79 Florida (rows 1–4 public; 5–8 private)

14.4 14.4 16.7 16.8 48.5 64.9 74.2 64.9 62.3

0 2.0 0 2.1 0 2.3 2.7 2.5 0

7.9 14.3 3.5 4.2 3.6 2.3 10.8 6.2 3.7

34.2 49.0 41.4 66.7 10.7 11.6 13.5 12.4 11.1

18.4 4.1 13.8 8.3 17.9 11.6 24.3 21.0 7.4

39.5 30.6 41.4 18.8 67.9 72.1 48.7 58.0 77.8

38 — 15 — 9 — 44 — 56 16 72 — *20

15.6 15.5 17.1 17.2 13.9 13.5 16.5 16.6 44.8 71.1 50.8 46.9 57.5

5.3 0 7.7 0 0 0 2.3 0 1.3 0 1.4 0 0

21.1 18.6 0 15.4 0 7.1 9.1 15.0 0 0 0 0 4.2

44.7 44.2 30.8 53.9 55.6 64.3 36.4 37.5 22.7 55.6 25.0 45.0 16.7

5.3 28.6 15.4 7.7 11.1 0 4.6 5.0 5.3 0 4.2 5.0 8.3

21.7 16.7 46.2 23.1 33.3 28.6 47.7 42.5 70.7 44.4 69.4 50.0 70.8

— 43 — 14 — 14 — 40 18 2 — 20 *5

Range

14–16 15–16 17–18 17–18 13–15 11–15 16–18 16–18 18–59 60–83 19–83 26–69 26–80

A = Use in a closed tent while sleeping; B = Use in a tent with the door flap loose/open; C = Use for a short time before going to sleep in order to warm up the closed tent; D = Use in a tent with two windows open; E = None of the above. ∗ “medical”—all adults, MI and FL, with self-reported medical, biological occupations.

question had no “correct” answer. Sources of CO involved in CO poisonings were written in on the survey by respondents, and are compiled in Table 15.13.

15.2 ELECTRIC GENERATOR USE (QUEST. 1) In most cases a majority of respondents believed that a gasoline-fueled electric generator could be operated inside a closed space (i.e., room) if some ventilation were provided. This is of course false—no amount of ventilation will make this scenario safe. The generator MUST be operated outside, preferably 20–25 ft. from the nearest structure. In general, adults responded with the highest percent of correct answers,

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TABLE 15.3 When Using a Recreational Powerboat, What is Safe (one only)? Percent of Total Male Michigan

Female

Mean Age

A

B

C

D

E

38 — 14–15 — 49 14–15 29 — 16–18 — 48 16–19 20 8 30–59 31 14 60–69 34 7 70–81 85 — 31–81 — 29 30–79 Florida (rows 1–4 public; 5–8 private)

14.4 14.4 16.7 16.8 48.5 64.9 74.2 64.9 62.3

7.9 6.3 6.9 4.4 3.7 0 2.8 1.3 3.9

5.3 2.1 3.5 4.4 0 0 0 0 0

5.3 8.3 0 4.4 0 0 0 0 0

79.0 66.7 89.7 82.6 81.5 97.6 91.7 91.1 92.3

2.6 16.7 0 4.4 14.8 2.4 5.6 7.6 3.9

38 — 15 — 9 — 44 — 56 16 72 — *20

15.6 15.5 17.1 17.2 13.9 13.5 16.5 16.6 44.8 71.1 50.8 46.9 57.5

13.2 7.1 6.7 14.3 33.3 28.6 13.6 7.7 2.8 0 1.5 5.3 0

2.6 0 6.7 0 0 0 0 7.7 0 0 0 0 0

7.9 9.5 0 0 0 0 2.3 0 0 0 0 0 0

68.4 73.8 73.3 71.4 55.6 71.4 68.2 82.1 93.1 93.8 94.1 89.5 96.2

7.9 9.5 13.3 14.3 11.1 0 15.9 2.6 4.2 6.3 4.4 5.3 3.9

— 43 — 14 — 14 — 40 18 2 — 20 *5

Range

14–16 15–16 17–18 17–18 13–15 11–15 16–18 16–18 18–59 60–83 19–83 26–69 26–80

A = Sitting on the transom with the boat engine idling; B = Teak surfing (hanging on to the swim platform behind the boat); C = Wake surfing (body surfing in the wake immediately behind the boat); D = Water skiing 100 ft. behind the boat; E = Sitting on the boat moored near other boats whose engines are idling. ∗ “medical”—all adults, MI and FL, with self-reported medical, biological occupations.

youths the least. People in healthcare-science fields answered correctly no more frequently that other adults generally. On the basis of the responses of many people, and especially so youths, who thought that opening one window will be enough, many of them would not have survived that scenario if it had really happened. In fact, for many of the cohorts of teenagers, the vast majority of the individuals would be at risk for death or injury from CO poisoning from a generator based on their faulty knowledge and perceptions of this gas. People die on a regular basis from CO poisoning because of improper use of generators, and especially after severe storms and hurricanes when main electrical power is not available. The study by Hampson and Zmaeff1 cited a number of incidents of injury and death from improper use of generators following storms and hurricanes. This included

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TABLE 15.4 What Weather Condition Might Greatly Affect the Levels of Exhaust Fumes on Board a Boat? Percent of Total Male Michigan

Female

Mean Age

A

B

C

D

E

38 — 14–15 — 49 14–15 29 — 16–18 — 48 16–19 20 8 30–59 31 14 60–69 34 7 70–81 85 — 31–81 — 29 30–79 Florida (rows 1–4 public; 5–8 private)

14.4 14.4 16.7 16.8 48.5 64.9 74.2 64.9 62.3

13.9 4.2 0 2.0 8.0 2.6 0 2.8 3.7

16.7 10.4 17.2 10.2 8.0 0 2.9 2.8 3.7

8.3 10.4 3.5 6.1 0 7.7 0 2.8 3.7

22.2 31.3 20.7 14.3 28.0 33.3 25.7 27.8 33.3

38.9 43.8 58.6 67.4 56.0 56.4 71.4 63.9 55.6

38 — 15 — 9 — 44 — 56 16 72 — *20

15.6 15.5 17.1 17.2 13.9 13.5 16.5 16.6 44.8 71.1 50.8 46.9 57.5

16.2 7.3 7.1 0 22.2 14.3 6.8 7.5 2.9 13.3 4.6 5.6 0

8.1 9.8 14.3 21.4 0 14.3 18.2 12.5 7.1 6.7 9.1 0 0

5.4 9.8 7.1 0 0 21.4 2.3 5.0 4.3 0 3.0 5.6 4.2

37.8 26.8 35.7 50.0 33.3 28.6 29.6 25.0 34.3 26.7 31.8 33.3 25.0

32.4 46.3 35.7 28.6 44.4 21.4 43.2 50.0 51.4 53.3 51.5 55.6 70.8

— 43 — 14 — 14 — 40 18 2 — 20 *5

Range

14–16 15–16 17–18 17–18 13–15 11–15 16–18 16–18 18–59 60–83 19–83 26–69 26–80

A = Sun out/overcast; B = Air temperature; C = Rain; D = Humidity; E = Wind direction. ∗ “medical”—all adults, MI and FL, with self-reported medical, biological occupations.

26 people in January, 1993 (Washington), 74 in January, 1998 (Maine), 71 in December, 2002 (North Carolina), and 2 in September, 2003 (Hurricane Isabel). Lovanas, at the Centers for Disease Control and Prevention (CDC), found that about one-third of generator incidents involved non-English speaking patients.2

15.3 PROPANE RADIANT HEATER USE (QUEST. 2) A small percentage of respondents believed that it is safe to sleep in a tent with an operating propane radiant heater. While these heaters produce little CO when burning in the open air, they can produce prodigious amounts of CO if oxygen in the ambient air becomes depleted and limiting to complete combustion. A somewhat larger percentage, but usually still far less than a majority, realized that when using these much smaller (i.e., than generators) sources of CO, the secure opening of two windows

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TABLE 15.5 Which One of the Following May Safely be Used Indoors? Percent of Total Male Michigan

Female

Mean Age

A

B

C

D

E

38 — 14–15 — 49 14–15 29 — 16–18 — 48 16–19 20 8 30–59 31 14 60–69 34 7 70–81 85 — 31–81 — 29 30–79 Florida (rows 1–4 public; 5–8 private)

14.4 14.4 16.7 16.8 48.5 64.9 74.2 64.9 62.3

5.3 2.1 17.2 6.3 0 2.3 0 0 3.6

76.3 60.4 72.4 68.8 76.9 84.1 84.6 82.7 82.1

2.6 4.2 0 0 0 0 2.6 0 3.6

2.6 0 3.5 2.1 0 4.6 0 2.5 0

13.2 33.3 6.9 22.9 23.1 9.1 12.8 14.8 10.7

38 — 15 — 9 — 44 — 56 16 72 — *20

15.6 15.5 17.1 17.2 13.9 13.5 16.5 16.6 44.8 71.1 50.8 46.9 57.5

5.3 9.3 0 0 11.1 0 9.1 10.0 4.1 6.7 2.9 10.0 8.0

73.7 58.1 73.3 78.6 55.6 50.0 79.6 60.0 82.4 66.7 79.4 80.0 72.0

2.6 2.3 6.7 0 0 7.1 4.6 2.5 0 0 0 0 4.0

0 2.3 6.7 0 0 0 0 0 0 0 0 0 0

18.4 27.9 13.3 21.4 33.3 42.9 6.8 27.5 13.5 26.7 17.7 10.0 16.0

— 43 — 14 — 14 — 40 18 2 — 20 *5

Range

14–16 15–16 17–18 17–18 13–15 11–15 16–18 16–18 18–59 60–83 19–83 26–69 26–80

A = Hibachi grill; B = A dozen candles; C = Gasoline-powered generator; D = Gasoline-powered pressure washer; E = I don’t know. *“medical”—all adults, MI and FL, with self-reported medical, biological occupations.

of a tent, guarantees safe operation. This requirement is specified by manufacturers. Many people believed that warming up the tent prior to going to bed was safe. This, in fact, may be one of the most unsafe practices that has resulted in may deaths: (1) CO can accumulate in the closed tent during warm-up, which then poisons the person after he/she comes inside to sleep, or (2) the heater is operated while people are inside the tent in order to heat up, the people then fall asleep, CO accumulates, and death occurs silently. The warmed inside environment, combined with fatigue, CO uptake, and possible alcohol use readily induces sleep. An opened door flap is not safe, because unless it is secured it could inadvertently be brushed closed or be closed by wind. In either case, the end result is predictable. One manufacturer’s propane radiant heaters are known to have killed over 75 people during the past 16 years.

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TABLE 15.6 Which One of Those Below is Known on Average to Represent the Greater Risk of Immediate Injury or Death from Carbon Monoxide Poisoning? Percent of Total Male Michigan

Female

Mean Age

A

B

C

D

E

38 — 14–15 — 49 14–15 29 — 16–18 — 48 16–19 20 8 30–59 31 14 60–69 34 7 70–81 85 — 31–81 — 29 30–79 Florida (rows 1–4 public; 5–8 private)

14.4 14.4 16.7 16.8 48.5 64.9 74.2 64.9 62.3

50.0 38.6 79.3 76.6 76.0 88.6 91.9 88.8 80.8

15.8 6.8 0 8.5 8.0 0 0 2.5 0

7.9 20.5 3.5 4.3 16.0 9.1 8.1 8.8 15.4

2.6 6.8 0 2.1 0 0 0 0 0

23.7 27.3 17.2 8.5 0 2.3 0 0 3.9

38 — 15 — 9 — 44 — 56 16 72 — *20

15.6 15.5 17.1 17.2 13.9 13.5 16.5 16.6 44.8 71.1 50.8 46.9 57.5

68.4 73.2 53.9 64.3 55.6 64.3 65.1 59.0 77.5 62.5 75.0 72.2 96.0

5.3 4.9 15.4 14.3 0 0 7.0 2.6 2.8 12.5 2.9 11.1 0

15.8 9.8 15.4 7.1 22.2 28.6 11.6 15.4 14.1 18.8 14.7 16.7 4.0

2.6 0 7.7 0 11.1 0 9.3 10.3 0 6.3 1.5 0 0

7.9 12.2 7.7 14.3 11.1 7.1 7.0 12.8 5.6 0 5.9 0 0

— 43 — 14 — 14 — 40 18 2 — 20 *5

Range

14–16 15–16 17–18 17–18 13–15 11–15 16–18 16–18 18–59 60–83 19–83 26–69 26–80

A = An automobile; B = A gasoline-powered lawn mower; C = A ski-boat with inboard gasoline engines; D = A snow thrower; E = An electric water heater *“medical”—all adults, MI and FL, with self-reported medical, biological occupations.

15.4 RECREATIONAL POWERBOAT SAFETY (QUEST. 3) While the vast majority of respondents believed that the safe activity was water skiing 100 ft. behind the powerboat, some respondents believed that sitting on the boat transom (the side to side structure at the back of a ship or boat) with the engine idling, teak surfing (holding onto the swim platform and being dragged through the water), wake surfing (being pulled behind the boat on a board via a very short rope), and sitting on a boat near other boats whose engines are idling was also safe. All four of the latter behaviors of course expose individuals to the potential for injurious or lethal CO poisoning. In general, younger people were more likely to endorse these

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TABLE 15.7 Which Poison Debilitates or Accidentally Kills the Most People Each Year in the USA? Percent of Total Male Michigan

Female

Mean Age

A

B

C

D

E

38 — 14–15 — 49 14–15 29 — 16–18 — 48 16–19 20 8 30–59 31 14 60–69 34 7 70–81 85 — 31–81 — 29 30–79 Florida (rows 1–4 public; 5–8 private)

14.4 14.4 16.7 16.8 48.5 64.9 74.2 64.9 62.3

0 6.3 0 2.1 0 2.3 0 1.2 0

0 2.1 0 0 0 0 0 0 0

97.4 83.3 92.9 79.2 100 97.7 97.4 97.5 100

2.6 2.1 3.6 8.3 0 0 0 0 0

0 6.3 3.6 10.4 0 0 2.6 1.2 0

38 — 15 — 9 — 44 — 56 16 72 — *20

15.6 15.5 17.1 17.2 13.9 13.5 16.5 16.6 44.8 71.1 50.8 46.9 57.5

2.6 4.9 7.1 0 0 0 4.6 2.5 1.4 6.7 3.0 0 0

5.3 4.9 0 7.1 0 0 4.6 5.0 0 0 0 0 0

68.4 78.1 85.7 85.7 100 78.6 81.8 87.5 90.0 93.3 91.0 88.2 96.0

5.3 7.3 0 0 0 0 4.6 5.0 0 0 0 0 0

18.4 4.9 7.1 7.1 0 21.4 4.6 0 8.6 0 6.0 11.8 4.0

— 43 — 14 — 14 — 40 18 2 — 20 *5

Range

14–16 15–16 17–18 17–18 13–15 11–15 16–18 16–18 18–59 60–83 19–83 26–69 26–80

A = Chlorine; B = Hydrogen sulfide; C = Carbon monoxide; D = Cyanide; E = Carbon dioxide *“medical”—all adults, MI and FL, with self-reported medical, biological occupations.

risky behaviors, especially, sitting on the transom with the engine running by the Florida youth.

15.5 CONDITIONS AFFECTING EXHAUST GAS DANGER (QUEST. 4) There was considerable confusion among respondents about what conditions will affect exhaust fume distribution on a boat. Greater fractions of adult respondents thought wind direction would be the major factor, while fewer young people made this choice. Approximately one-third of respondents thought humidity would be most important. Some even thought sunshine versus overcast, air temperature, or rain might be major influences. Studies show that wind velocity and wind direction, combined

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TABLE 15.8 If Carbon Monoxide Exposure is Suspected, What is the Best Advice? Percent of Total Male Michigan

Female

Mean Age

A

B

C

D

E

38 — 14–15 — 49 14–15 29 — 16–18 — 48 16–19 20 8 30–59 31 14 60–69 34 7 70–81 85 — 31–81 — 29 30–79 Florida (rows 1–4 public; 5–8 private)

14.4 14.4 16.7 16.8 48.5 64.9 74.2 64.9 62.3

36.8 30.4 37.9 16.7 44.4 34.1 51.3 48.8 25.0

7.9 4.4 3.5 0 0 0 0 0 0

52.6 63.0 51.7 75.0 55.6 65.9 48.7 51.2 75.0

2.6 2.2 6.9 6.3 0 0 0 0 0

0 0 0 2.1 0 0 0 0 0

38 — 15 — 9 — 44 — 56 16 72 — *20

15.6 15.5 17.1 17.2 13.9 13.5 16.5 16.6 44.8 71.1 50.8 46.9 57.5

31.6 23.8 21.4 38.5 33.3 21.4 25.0 32.5 35.7 31.3 34.3 38.9 44.0

7.9 2.4 0 7.7 11.1 0 9.1 0 1.4 0 1.5 0 0

52.6 69.1 78.6 46.2 55.6 78.6 59.1 65.0 62.9 68.8 64.2 61.1 56.0

5.3 2.4 0 7.7 0 0 2.3 2.5 0 0 0 0 0

2.6 2.4 0 0 0 0 4.6 0 0 0 0 0 0

— 43 — 14 — 14 — 40 18 2 — 20 *5

Range

14–16 15–16 17–18 17–18 13–15 11–15 16–18 16–18 18–59 60–83 19–83 26–69 26–80

A = Go outside and breathe some fresh air; B = Ignore it and it will go away; C = Go immediately to an emergency center and be evaluated by a physician; D = Call your doctor for an appointment in a few days; E = Take an aspirin or Motrin for headache. *“medical”—all adults, MI and FL, with self-reported medical, biological occupations.

with boat speed and direction, greatly influence the concentrations of CO found on boat decks, in cabins and immediately behind the boat.

15.6 SAFE USE INDOORS (QUEST. 5) A high percentage of respondents recognized the burning of a dozen candles as being the safe choice indoors. Candles are small combustion sources and produce very little CO. Nevertheless, a significant number of people didn’t know the answer (in one instance >40%), and some even endorsed the use of a hibachi or an internal combustion engine indoors. Younger respondents appeared to be the less knowledgeable, and in some cases significant percentages of the youth (>10%) thought very risky, even lethal behaviors were okay (e.g., use of a hibachi indoors).

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TABLE 15.9 How Long Does Carbon Monoxide Stay in the Human Body? Percent of Total Male Michigan

Female

Mean Age

A

B

C

D

E

38 — 14–15 — 49 14–15 29 — 16–18 — 48 16–19 20 8 30–59 31 14 60–69 34 7 70–81 85 — 31–81 — 29 30–79 Florida (rows 1–4 public; 5–8 private)

14.4 14.4 16.7 16.8 48.5 64.9 74.2 64.9 62.3

10.5 6.4 10.3 4.2 0 4.6 5.1 3.6 3.7

5.3 2.1 17.2 18.8 3.7 11.4 0 4.8 7.4

10.5 8.5 10.3 4.2 11.1 9.1 5.1 8.4 7.4

15.8 2.1 17.2 6.3 7.4 6.8 10.3 7.2 11.1

57.9 80.9 44.8 66.7 77.8 68.2 79.5 75.9 70.4

38 — 15 — 9 — 44 — 56 16 72 — *20

15.6 15.5 17.1 17.2 13.9 13.5 16.5 16.6 44.8 71.1 50.8 46.9 57.5

7.9 11.9 20.0 0 0 7.1 11.4 10.0 5.6 6.7 6.1 5.3 0

15.8 4.8 13.3 7.1 0 0 11.4 10.0 8.5 6.7 10.6 0 12.5

13.2 9.5 6.7 7.1 0 7.1 13.6 5.0 12.7 6.7 12.1 10.5 16.7

10.5 2.4 6.7 7.1 0 0 11.4 7.5 15.5 6.7 16.7 5.3 20.8

52.6 71.4 53.3 78.6 100 85.7 52.3 67.5 57.8 73.3 54.6 79.0 50.0

— 43 — 14 — 14 — 40 18 2 — 20 *5

Range

14–16 15–16 17–18 17–18 13–15 11–15 16–18 16–18 18–59 60–83 19–83 26–69 26–80

A = Once breathed, it stays always; B = For 65 days; C = For 1 week; D = For 1 day; E = I don’t know. * “medical”—all adults, MI and FL, with self-reported medical, biological occupations.

15.7 THE GREATEST RISK (QUEST. 6) The vast majority of respondents viewed the automobile as the greater risk from CO poisoning. This of course is out of line with the fact that automobiles produce only extremely low levels of CO today when properly used and maintained, thanks to the US Environmental Protection Agency (US EPA) and the catalytic converters required at manufacture. Internal combustion engine-driven devices without catalytic converters represent far greater hazards today for the individual user. The greatest of these are those with the largest engines, therefore the greatest CO generating capacity. That would be gasoline-powered powerboats—ski-boats, cabin cruisers, fishing boats, and so forth, especially those with inboard engines. Generally, the bigger the boat and engines, the more dangerous. Only 10–20% of respondents were aware of this fact. A few thought that lawn mowers or snow throwers were most

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TABLE 15.10 Which One of the Following is a Property of Carbon Monoxide? Percent of Total Male Michigan

Female

Mean Age

A

B

C

D

E

38 — 14–15 — 49 14–15 29 — 16–18 — 48 16–19 20 8 30–59 31 14 60–69 34 7 70–81 85 — 31–81 — 29 30–79 Florida (rows 1–4 public; 5–8 private)

14.4 14.4 16.7 16.8 48.5 64.9 74.2 64.9 62.3

23.7 6.4 13.8 18.8 7.1 20.5 7.7 12.1 14.3

5.3 21.3 27.6 25.0 42.9 18.2 38.5 38.6 10.7

34.2 4.3 6.9 2.1 0 2.3 0 1.2 0

21.1 21.3 27.6 20.8 28.6 29.6 25.6 31.3 17.9

15.8 46.8 24.1 33.3 21.4 29.6 28.2 16.1 57.1

38 — 15 — 9 — 44 — 56 16 72 — *20

15.6 15.5 17.1 17.2 13.9 13.5 16.5 16.6 44.8 71.1 50.8 46.9 57.5

7.9 9.8 20.0 21.4 22.2 21.4 13.6 15.0 22.2 12.5 18.8 27.8 32.0

23.7 17.1 33.3 14.3 11.1 0 20.5 15.0 25.0 37.5 30.4 16.7 12.0

21.1 19.5 6.7 7.1 0 7.1 9.1 10.0 1.4 0 1.4 0 0

15.8 12.2 20.0 21.4 11.1 7.1 34.1 22.5 27.8 6.3 2.7 33.3 28.0

31.6 41.5 20.0 37.7 55.6 64.3 22.7 37.5 23.6 43.8 27.5 22.2 28.0

— 43 — 14 — 14 — 40 18 2 — 20 *5

Range

14–16 15–16 17–18 17–18 13–15 11–15 16–18 16–18 18–59 60–83 19–83 26–69 26–80

A = It is much lighter than air; B = It is much heavier than air; C = It has a strong odor of burning materials; D = It is about the same density as air; E = I don’t know. * “medical”—all adults, MI and FL, with self-reported medical, biological occupations.

dangerous in terms of CO. Certainly they too can be dangerous because even though they have much smaller engines, they also lack catalytic converters. The basis for CO risk posed by electric water heaters, which as many as 27% of one student group chose, is unclear. It may represent a total misunderstanding of how CO is generated. School teaching programs should take note of this abberation.

15.8 THE WORST POISON (QUEST. 7) This question makes it clear that while people of all ages may have confusion on other issues relating to CO, high percentages know that CO debilitates and kills people. Instances of this are frequently reported in the newspapers and on TV. Some groups, especially young people chose carbon dioxide. Confusion between these two carbon oxides could be serious. The one we breathe out is not toxic until very high

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TABLE 15.11 Have YOU Experienced the Toxic Effects of Carbon Monoxide Poisoning? Percent of Total Male Michigan

Female

Mean Age

A

B

C

D

E

38 — 14–15 — 49 14–15 29 — 16–18 — 48 16–19 20 8 30–59 31 14 60–69 34 7 70–81 85 — 31–81 — 29 30–79 Florida (rows 1–4 public; 5–8 private)

14.4 14.4 16.7 16.8 48.5 64.9 74.2 64.9 62.3

5.3 4.3 13.8 4.2 10.7 11.1 0 6.0 10.3

5.3 4.3 0 2.1 3.6 4.4 5.1 4.8 3.5

60.5 59.6 55.2 75.0 64.3 55.6 79.5 63.9 72.4

5.3 14.9 69.9 8.3 7.1 11.1 5.1 8.4 6.9

23.7 17.0 24.1 10.4 14.3 17.8 10.3 16.9 6.9

38 — 15 — 9 — 44 — 56 16 72 — *20

15.6 15.5 17.1 17.2 13.9 13.5 16.5 16.6 44.8 71.1 50.8 46.9 57.5

7.9 0 0 0 11.1 7.1 4.6 7.5 4.1 6.3 5.8 0 8.0

2.6 0 0 0 0 0 0 0 6.9 0 5.8 5.3 4.0

76.3 71.4 66.7 100 55.6 64.3 77.3 52.5 67.1 75.0 65.2 79.0 64.0

0 4.8 0 0 11.1 0 9.1 7.5 5.5 6.3 7.3 0 16.0

13.2 23.8 33.3 0 22.2 28.6 9.1 32.5 16.4 12.5 15.9 15.8 8.0

— 43 — 14 — 14 — 40 18 2 — 20 *5

Range

14–16 15–16 17–18 17–18 13–15 11–15 16–18 16–18 18–59 60–83 19–83 26–69 26–80

A = Yes, once; B = Yes, more than once; C = No; D = No, but I know of someone who has; E = I don’t know. * “medical”—all adults, MI and FL, with self-reported medical, biological occupations.

levels are reached, while its sibling with one less oxygen atom is deadly at very low concentrations. Science classes in school could do better in teaching these important distinctions.

15.9 THE BEST ADVICE (QUEST. 8) The majority of respondents recognized that the best action to take when CO exposure is suspected, is prompt presentation at an emergency center for evaluation and treatment by a health professional. A small but substantial percentage of respondents believed that simply going outside and breathing fresh air was adequate to conteract the effects of CO. This is the general wisdom of many older individuals in the medical community, even though it is wrong. CO poisoning is not to be trifled with.

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TABLE 15.12 Sources of Carbon Monoxide for Survey Respondents Michigan Automobile—7 In trunk—1 In garage with door shut—1 Exhaust—2 Suicide attempt—2 In house—1 Furnace—4 Heater—2 Pilot light failure—1 Kerosene heater—2 Water heater (electric)—1 Fire (electrical)—1 Plugged chimney—1 Lawn mower—1 Pool heater/AC—1 Gas refrigerator—1 Golf cart—1 Boat—1 Exhaust gases—1 Race car with bad ventilation system—1 U.S. Army tank + 2-1/2 tn truck—1

Florida Automobile—3 Repair facility—1 In garage—1 Exhaust—1 Tractor—1 Gas oven—1 Gas heater—1 Coal heater—1 Heating system—1 Camp fires—1 Fire—1 Fireplace leakage—2 Lawn mower—1 In garage—1 Boat (anchored)—2 Inside cabin—1 Generator—1 Generator during hurricane—1 Commercial diving—1 Drag race—1 In chemistry class—1

TABLE 15.13 Rental and Ownership of Selected Combustion Devices by Survey Respondents in Michigan and Florida, Adults and Juveniles∗ Rental

Ownership

Chain Press, Kerosene Chain Press, Kerosene Saw Washer Heater Generator Saw Washer Heater Generator Michigan Men (85) Women (29) Boys (67) Girls (97) Florida Men (72) Women (20) Boys (106) Girls (111)

4.7 0 16.4 9.3

16.5 6.9 11.9 11.3

1.2 0 7.5 8.3

5.9 0 16.4 8.3

65.9 48.3 68.7 54.6

27.1 20.7 35.8 21.7

17.7 20.7 28.4 18.6

21.2 20.7 37.3 22.7

25.0 0 22.6 12.6

34.7 25.0 34.9 36.0

6.9 0 7.6 1.8

13.9 5.0 21.7 17.1

44.4 25.0 50.0 45.1

31.9 20.0 45.3 33.3

6.9 0 15.1 8.1

27.8 25.0 40.6 36.0

∗ It is assumed that this reflects rental and ownership by the juvenile’s families.

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A substantial fraction of those poisoned develop long-term health damage. It must be treated immediately and correctly! Likewise, ignoring it as a few respondents thought, will not guarantee that it will go away. Finally, action must be prompt— calling a physician for an appointment days to weeks hence is of no value relative to maintenance of health after CO poisoning, and is equivalent to doing nothing.

15.10 DURATION OF TIME IN THE BODY (QUEST. 9) Probably the greatest confusion related to the length of time CO remains in the body. Being a very smart poison, as it has been characterized, it “washes out” quickly when one breathes clean air. The half-life of carboxyhemoglobin (COHb) is approximately 4–5 h, so within 24 h (5–6 half-lives) body CO concentration (i.e., COHb) is back at or very near background level (0.4–1.4% for nonsmokers). The healthcare-scientific subgroup did only slightly better on this question than lay people in any age group. Fifty percent of the people in that group didn’t know the answer. This is consistent with my experience with physicians, nurses, and so forth. Physicians will often ask patients to come to their office or a hospital on Monday to have blood drawn for COHb measurement, when the fact of CO exposure was discovered the previous Friday. Consequently, measurements made in this way are useless, and when used as a forensic tool may be directly injurious to the CO victim, since the finding of a normal COHb value may cause the patient to be sent back to the same site for continued CO exposure, injury, and even death.

15.11 PROPERTIES OF CO (QUEST. 10) This question gave respondents almost as much trouble as number 9. Only 15–30% knew that CO has about the same density as air (actually 4% lighter). An approximately equal or even larger percentage indicated they didn’t know CO’s properties. Of the healthcare-scientific subgroup, 28% got the question correct and 28% said they didn’t know the answer. Significant fractions of people thought CO was either much lighter or much heavier than air. An elementary knowledge of chemistry (molecular weights of the gases) allows one to easily compute density without recourse to pencil and paper, providing the information necessary to answer this question. Again, the educational establishment must take note. Of the select group of healthcare-scientific respondents, 32% believed CO was much lighter than air. CO mixed with air only rises when the air is warmer than surrounding air—that is, hot air rises! As stated elsewhere, CO cannot separate from air and rise as cream may separate from milk. That would violate the Second Law of Thermodynamics. Gases containing CO may have a strong or a weak odor, but CO plays no part in that. It is odorless and tasteless.

15.12 EXPERIENCE WITH CO POISONING? (QUEST. 11) As many as 10–15% of respondents believed they had experienced CO poisoning once or more than once. Up to another 15% knew of someone who had. That means

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that as many as one-fifth of respondents had some direct or indirect experience with CO poisoning. Another significant fraction of respondents didn’t know whether they had or not. Table 15.12 lists the sources of CO poisoning that were written in by respondents. Vehicles and heaters were prominent sources, both in Michigan and in Florida. Other sources included water heaters, fires, lawn mowers, boats, generators, and so forth. The percentages of respondents indicating poisoning at least once was not different between Michigan and Florida, and almost equal numbers of sources were given in both areas of the country. This tends to repudiate assertions that CO poisoning is much more prevalent in the cold north as opposed to the warm south.

15.13 USE OF CO EMITTING DEVICES Table 15.13 provides data about rental and ownership of CO emitting devices by respondents in Michigan and in Florida. Chain saws were owned by the largest percentages of respondents, both adults and juveniles or their parents, whether in Michigan or in Florida. Ownership was higher in the north than in the south. In all cases, a higher percentage of males owned chain saws than females. Ownership of generators was higher in Florida than in Michigan. A male–female difference was not clear-cut. Ownership of pressure washers was somewhat higher in the south than the north, but for ownership of kerosene heaters this difference was reversed. Chain saw, pressure washer, and generator rental tended to be higher in the south than in the north. Clearly, whether in the north or in the south, a significant percentage of people own or rent one or more small CO emitting devices that potentially expose them to CO. Improper use of these devices because of misperceptions and/or lack of education could result in injury or death.

ACKNOWLEDGMENTS In Benzie County Michigan, we wish to thank the Rotary club of Frankfort, the Benzie Sunrise Rotary Club, and the Benzie Bicycle Club. Our many thanks go to Mr. Gary Waterson, science teacher at Benzie County Central High School in Benzonia. In St. Johns County Florida, we wish to thank the St. Augustine Rotary Club, the St. Augustine Sunrise Rotary, and the Ancient City Road Runners. Many thanks also to St. Augustine science teachers Karen Ford, Ph.D. at Pedro Menendez High School (Public), Becky Melton, M.D. at St. John’s Academy (Christian School), and Mr. Peter Bugnet at St. Joseph Academy (Catholic High School).

References 1. Hampson, N.B., Zmaeff, J.L. Carbon monoxide poisoning from portable electric generators. Am. J. Prev. Med., 28, 123–125, 2005. 2. Centers for Disease Control and Prevention. Use of carbon monoxide alarms to prevent poisonings during a power outage—North Carolina, December, 2002. Morb. Mortal. Wkly. Rept., 53, 189–192, 2004.

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16

Treatment of Carbon Monoxide Poisoning Suzanne R. White

CONTENTS 16.1 16.2 16.3 16.4

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Historical Perspective . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mechanisms of Carbon Monoxide Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Currently Available Neuroprotective Treatments . . . . . . . . . . . . . . . . . . . . . . . . . 16.4.1 Normobaric Oxygen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16.4.2 Hyperbaric Oxygen Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16.4.3 Allopurinol and N-acetylcysteine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16.4.4 Insulin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16.4.5 NMDA Receptor Antagonists . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16.4.6 Brain-Derived Neuropeptides . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16.4.7 Hypothermia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16.5 Approach to the Patient with Carbon Monoxide Poisoning . . . . . . . . . . . . . . 16.5.1 General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16.5.1 Neuroimaging. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16.5.2 Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16.5.3 Children . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16.6 Management of the Sequelae of Carbon Monoxide Poisoning . . . . . . . . . . . 16.7 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

341 342 344 348 348 348 351 352 354 355 355 355 355 358 360 360 361 362 362

16.1 INTRODUCTION Carbon monoxide (CO) poisoning is the leading cause of toxicologic death in the United States of America, with 5600 fatalities reported annually.1 Worldwide CO remains the most lethal toxin in every community in which it has been studied.2 While mortality rates associated with acute exposure to CO may have declined over the past two decades, the total public health burden has not decreased.3 Most notably, delayed neuropsychiatric sequelae in a significant percentage of CO-poisoning survivors continues to pose an enormous challenge.4−9 The following chapter will focus primarily on the various treatment aspects of acute CO poisoning. It should be kept in mind that our present knowledge regarding 341

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therapy for CO poisoning is limited for several reasons. First, effective medical treatment is ideally guided by diagnosis of either positive or negative outcomes following exposure to toxic substances. For example, blood or urine levels of toxins, combined with characteristic signs or symptoms of toxicity often aid in the institution of appropriate therapy. Unfortunately, symptoms relating to CO exposure are notoriously vague, and some studies estimate that the diagnosis is missed in 30% of cases presenting to the emergency department.10 For instance, when all neurologic admissions over a 5-month period were screened, it was determined that three out of 29 patients admitted with impaired consciousness and no lateralizing neurological signs had serious CO intoxication.11 A further toxicological challenge is that carboxyhemoglobin (COHb) levels neither correlate with toxicity nor predict the risk for development of long-term effects.12,13 Although other predictors of long-term neuropsychiatric sequelae have been proposed (i.e., loss of consciousness,14 cerebral edema on brain computed tomography,15 elevated blood glucose16 or a history of a “soaking” type exposure,17 )their sensitivity and specificity are largely unproven. As a result, how best to treat patients with these clinical warning signs and symptoms remains controversial. Second, appropriate therapy for poisoned patients is ideally guided by an understanding of the toxic mechanisms of that poison. Unfortunately, even though CO has most likely been present since the beginning of time, and has been studied clinically for over 100 years, an adequate understanding of its toxic mechanisms continues to elude us. Lastly, treatment guidelines should ideally be on the basis of prospective, well-controlled, peer-reviewed studies. There is a dearth of such studies relating to CO-poisoning treatment in the literature. Despite these limitations, a general approach to treatment will be described. As an overview, treatment is on the basis of cessation of tissue hypoxia, the removal of CO from the body, the consideration of potential neuroprotective interventions, and management of the long-term sequelae of CO poisoning. First, a review of historical, often failed treatments for CO poisoning will be presented, followed by a discussion of promising neuroprotective agents. Finally, a clinical approach to the CO-poisoned patient will be outlined.

16.2 HISTORICAL PERSPECTIVE Oxygen therapy has been the mainstay of treatment for CO poisoning since it was first used therapeutically by Linas and Limousin in 1868.18 Haldane subsequently was able to experimentally demonstrate that mice exposed to “carbonic oxide” were unaffected if oxygen was provided during the exposure. In this seminal work, Haldane concluded that “the higher the oxygen tension the less dependent an animal is on its red corpuscles as oxygen carriers, since the oxygen simply dissolved in the blood becomes considerable when the oxygen tension is high.”19 Indeed, sea level oxygen decreases the half-life of CO from 320 to 80 min. Unfortunately, sea level oxygen alone has not been entirely effective in the treatment of CO poisoning, particularly with regard to the prevention of delayed neuropsychiatric sequelae. This realization has prompted researchers and physicians to search for yet other treatment modalities.

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The use of resuscitative gasses other than oxygen has been proposed. Studies by Killick demonstrated more rapid clearance of COHb with 5% carbogen (5% carbon dioxide, plus 95% oxygen), which was thought to be related to increased ventilatory drive.20−21 Schwerma et al.,22 exposed dogs to 0.3% CO until near-respiratory arrest occurred. Upon removal from exposure, 36% survived with fresh air alone. The survival rate increased to 50% when mechanical ventilation was used, 69% when ventilation with 100% oxygen was applied, and 66% when mechanical ventilation was combined with 7% carbogen. There was no clinical advantage to the use of carbogen in terms of improved survival, normalization of pH or lactate, or decreased incidence of neurologic sequelae in animals relative to breathing 100% oxygen alone.2 Thus, this method of treatment has subsequently fallen out of favor. Several other fascinating drug therapies for CO poisoning have not proven to be effective, and are mentioned here only for historical interest. Methylene blue, succinic acid, persantine, iron and cobalt preparations, and ascorbic acid have all been tried, without benefit.23 In animals, cytochrome c, theorized to activate cytochrome oxidase upon supplementation, has not been associated with clinical improvement.24 Hydrogen peroxide infusions do reduce COHb content in experimental animals, but the absence of human experience with this chemical and the danger of air embolism preclude its clinical use.25 While ultraviolet radiation was proposed to facilitate the dissociation of COHb from red blood cells during transit through skin capillaries and to decrease mortality in animals,26 these results were not able to be duplicated in a subsequent animal trial.27 Intravenous procaine hydrochloride does not improve the anoxia of CO poisoning in humans.28 Intravenous lidocaine was advocated, on the basis of its facilitation of neuronal recovery after cerebral ischemia in experimental animals, but has not yet been employed in CO-poisoned humans.29 Dipyridamole pretreatment in rats with inhalational CO toxicity inhibited ultrastructural changes in capillary endothelial cells, myocardial mitochondria, and myocardial myofilament arrangement,30 but follow-up studies were never peformed. Exchange transfusion has been reported to improve survival following CO poisoning in an animal model.31 Despite the fact that this method has been utilized in only a single patient,32 it is still promoted by some clinicians as an alternative to hyperbaric oxygen therapy (HBOT).33 While exchange transfusion does in fact lower COHb levels, given the complex mechanisms for CO toxicity that extend well beyond the toxicity of COHb, this technique is not likely to be effective as a sole therapy. Furthermore, given the potential for exchange transfusions to deplete valuable blood product resources and place the patient at risk for blood-borne pathogen infections, this treatment modality can no longer be recommended. Perfluorochemical infusions have been used in animal models as treatment for CO toxicity.34,35 Recently, pyridoxalated hemoglobin-polyoxyethylene conjugates (PHPs) have been developed. These agents act as blood substitutes capable of transporting oxygen through chemical modification of hemoglobin derived from human blood erythrocytes whose shelf-life has expired. Affinity of PHP for oxygen is almost identical to that of whole blood. PHP use in rabbits poisoned by CO was associated with prolonged survival time, temporary recovery of PO2 and PCO2 , and elevations in pH and blood pressure in comparison with animals treated with saline.36 Beyond the fact that human use of this product has not yet been reported, its efficacy as

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a sole therapy is unlikely, for the same reasons as discussed above with exchange transfusion. HBOT was first suggested as treatment for CO poisoning in 1901 by Mosso.37 The first clinical use of HBOT in the treatment of human CO poisoning, occurred in 1960.38,39 This modality has subsequently become the mainstay of therapy for severe CO poisoning in an average of nearly 1500 patients treated annually.40

16.3 MECHANISMS OF CARBON MONOXIDE TOXICITY To gain an understanding of the available methods of treatment for CO poisoning, a review of what is known about mechanisms for CO toxicity, albeit an incomplete comprehension of the problem, is presented here. Hypoxic ischemia plays a significant role in the neurotoxicity of CO, which binds slowly to hemoglobin, but with extremely high affinity (240 times that of oxygen). Oxygen binding sites are occupied by CO at very low partial pressures of the gas, decreasing the oxygen carrying capacity of the blood and subsequently decreasing the usual facilitation phenomenon for further unloading of oxygen at the tissue level. The net result is an abnormally hyperbolic oxygen dissociation curve that is shifted to the left. Those tissues most susceptible to the hypoxic effects of CO are those that are the most metabolically active. Oxygen delivery may further be impaired through the alteration of erythrocyte diphosphoglycerate concentration.41 In adults, COHb half-life is dependent upon the concentration of inspired oxygen, and is most commonly reported to be approximately 4.5 h on room air, 90 min on normobaric 100% oxygen, and 20 min with oxygen applied at hyperbaric concentrations. It should be noted that reported half-lives are extremely varied in the literature. In children, the half-life of COHb has not been well-studied, but is reported by one author42 to be 44 min on 100% oxygen at normobaric pressure, on the basis of measurements performed on 26 school-aged children. The half-life of COHb in the fetus is approximately 7 h.43 Over and above hypoxia, CO induces ischemia secondary to hypotension. Hypotension may be mediated through CO binding and activation of guanylyl cyclase which increases cGMP and triggers cerebral and peripheral vasculature smooth muscle dilatation or myocardial suppression. It may further be compounded by CO triggered release of nitric oxide from platelets with subsequent central and peripheral vasodilation. The degree of central nervous system (CNS) damage observed following poisoning correlates well with the degree of hypotension noted.44 Additional mechanisms of toxicity have been proposed given observations that (1) COHb levels did not correlate with toxicity, (2) COHb formed by noninhalational routes did not produce the same lethal consequences as inhalational exposure to CO, and (3) that delayed neuropsychiatric sequelae were common after apparent complete recovery from the initial CO insult. Early researchers such as Haldane,45 Brabkin,46 and Goldbaum47−49 suggested intracellular uptake of the gas as a possible mechanism for toxicity. In competition with oxygen, CO will bind iron or copper scontaining proteins such as myoglobin, mixed-function oxidases, and cytochrome c oxidase in vitro. The binding to cytochrome c oxidase (a, a3 ) has been proposed as the mechanism

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for intracellular CO toxicity and has been demonstrated in animals.50 It has also been demonstrated that during recovery, the ultimate restoration of mitochondrial function lags behind clearance of COHb.51 However, the Warburg constant for cytochrome oxidase is unfavorable for CO binding relative to the other hemeproteins.52 Furthermore, only reduced cytochrome a, a3 binds CO. It is likely, then, that other hemeproteins act as “CO buffers,” thus preventing significant binding to cytochrome c oxidase at COHb levels of less than 50%. At high levels of COHb, depletion of high energy stores and intracellular neuronal acidosis occurs, which may favor CO-cytochrome binding. On the other hand, in vivo data from Rivers53 supports hemoglobin binding with impaired oxygen delivery, rather than mitochondrial poisoning as the etiology of the metabolic acidosis in CO poisoning. In this model, even at extremely high COHb levels, dogs were able to fully extract and utilize oxygen, indicating a lack of mitochondrial effect. In addition work by Ward54 demonstrated that expression of the heat shock proteins 72 and 32 (sensitive markers of acute neuronal stress) did not occur following CO poisoning in rats who were maintained normotensive throughout the exposure. This caused the authors to question the role of CO as a direct neurotoxin, and to suggest that neuronal injury results from hypotension-induced ischemia. The role of iron as a promoter or attenuator of CO toxicity is not clear. Iron deficiency, results in lowered hemoglobin, cytochrome and myoglobin levels in the animal model.55 These combined effects could potentially predispose to CO toxicity. Conversely, neuronal tissues high in iron content, such as the basal ganglia seem particularly vulnerable to the effects of CO. In fact, limiting iron availability confers neuroprotection from CO in the developing auditory system.56 Myoglobin binding may play a role in CO-mediated toxic effects. Myoglobin is a hemeprotein with similar three-dimensional configuration to hemoglobin that can bind CO reversibly. Myoglobin binds CO more slowly and with greater affinity than does hemoglobin in vivo. Normally, myoglobin is an O2 carrier protein that facilitates oxygen diffusion into skeletal or cardiac muscle cells and serves to place oxygen stores in close proximity to mitochondria. Cardiac and skeletal muscle injury could theoretically result from impaired myoglobin function. While the clinical significance of COHb formation is not yet clear, there is increasing emphasis on cardiac injury related to CO poisoning in the literature. Cardiac injury has historically been observed at COHb levels of 20–40%.57 Recently, Aslan reported on 83 young, healthy patients with severe CO poisoning. These victims had loss of consciousness in 63% and an average COHb level 34.4%. They were evaluated with echocardiogram (ECHO) and myocardial perfusion single-photon emission computed tomography (SPECT) scanning. Findings included diagnostic ischemic electrocardiogram (EKG) changes in 14.4% and abnormal SPECT results in 11%. Six of the latter group had confirmatory and corresponding ECHO abnormalities.58 Henry and colleagues noted ischemic EKG changes in 30% of 230 patients with moderate to severe CO poisoning. Cardiac biomarkers were elevated in 35% of these patients and in-hospital mortality was 5%.59 In a subsequent outcome study, these investigators noted an association between moderate to severe CO exposure and myocardial injury, finding this injury to be a strong predictor of mortality. It was further suggested that patient subsets include those with a “stunned myocardium” and others with “unmasking” of underlying coronary artery disease.60 Longer durations of CO exposure predisposed people to myocardial

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injury, but not mortality in this study. Defining the earliest and most sensitive cardiac markers of injury is clearly an important area of future investigation.61,62 The mechanisms underlying the delayed effects of CO poisoning have been longstanding toxicological conundrums. An increasingly complex body of literature suggests that brain ischemia/reperfusion injury, lipid peroxidation, vascular oxidative stress, neuronal excitotoxicity, apoptosis, and immunotoxicity all play significant roles. After removal from the CO environment, animal models demonstrate marked changes in neutrophil structure and function. Abnormal adherence to brain endothelial cell receptors quickly occurs, possibly as a result of endothelial damage. Up-regulation of endothelial intercellular adhesion molecules (ICAMs) is demonstrated on endothelial cell surfaces as a result of activation by inflammatory mediators. ICAMs bind beta 2 integrins located on PMN surfaces, resulting in aggregation of polymorphonuclear cells (PMNs) onto endothelial cells in the neuromicrovasculature. Subsequent degranulation of PMNs results in release of destructive proteases, which cause oxidative injury and trigger further inflammatory responses. Thom’s work63−65 has been instrumental in elucidating the CO-induced perivascular oxidative changes that occur during recovery from CO poisoning and ultimately lead to superoxide formation, prolonged lipid peroxidation reactions, reactive oxygen species (ROS) generation, vascular injury, and neuronal death. Even lower level CO exposure can produce vascular oxidative stress as evidenced by platelet-mediated nitric oxide release and deposition of peroxynitrate, a highly oxidative substance.66 Peroxynitrite, which forms from NO released from platelets and endothelial cells, can further inactivate mitochondrial enzymes and damage vascular endothelium of the brain.67,68 ROS generation can be attributed to several other sources including mitochondria and cycloxygenase. ROS production increases notably during CO hypoxia, with the highest oxidative stress occurring in the most vulnerable brain regions.69 This stress may result from lower antioxidant capacity or higher tissue concentrations of iron. In fact, limiting iron availability confers neuroprotection from CO.56 In mitochondria, decreased ratios of reduced oxidized glutathione are seen following CO poisoning, and may reflect decreased ability to detoxify ROS.70 As in animal models, acute CO poisoning in humans has resulted in intravascular platelet-neutrophil interactions and neutrophil activation. Thom71 demonstrated these phenomena in 50 patients by measuring actual aggregates and myleoperoxidase (MPO) concentrations. It was noted that patients with exposures of greater than 3 h duration had increased neutrophil expression of CD18 surface receptors and MPO. In animal models, MPO was deposited along the brain vascular lining and colocalized with nitrotyrosine. Changes did not occur in thrombocytopenic models or those using platelet–neutrophil interaction inhibitors such as tirofiban. Lastly, theses changes were not noted when l-nitroargninine methyl ester, a nitric oxide synthesis inhibitor, was given or in knock-out mice lacking MPO.71 Reactive products of lipid peroxidation like malonylaldehyde can cause adduct formation with neuronal myelin basic protein (MBP). The altered cationic state MBP triggers an adaptive immunological cascade that includes antibody-mediated degradation of MPB over the course of days. This triggers a secondary influx of macrophages and CD-4 lymphocytes that exhibit an autoreactive, proliferative

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response to the altered MPB. Brain microglial activation ultimately occurs. These neuropathological changes are associated with decrements in learning that are not seen in rats immunologically tolerant to MBP.72 CO-mediated oxidative stress leads to the release of excitatory amino acids (EAA).73 Subsequent neuronal excitation leading to cell death may also play a role in the development of delayed toxicity following CO poisoning. These effects have been extensively reviewed by Piantadosi,74 and are paraphrased here. Excitatory amino acids such as glutamate, accumulate in synaptic clefts during neuronal depolarization owing to both excessive presynaptic release and failure in ATP-dependent reuptake mechanisms.75 Interstitial glutamate concentration increases in the hippocampus during and after CO exposure. Postsynaptic binding to at least three glutamate receptors including N-methyl-d-aspartate (NMDA), Kainic acid (KA), and α-amino3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) occurs with a secondarily increased influx of calcium into postsynaptic neurons. This hypercalcemia is associated with neuronal death. ROS production follows increased excitatory amino acid (EAA) release as well. NMDA receptor antagonism attenuates delayed neuronal degeneration in the hippocampus after CO poisoning, and is discussed further below. Physiological amounts of CO generated by heme breakdown seem to act to impact neurologic processes such as long-term potentiation of memory and neurotransmitter release. Conversely, in toxic doses, CO alters the modulating influence of local NO on soluble guanylate cyclase, an effect that is most evident at 7 days after exposure.76 Despite its role in vasodilation and peroxynitrite formation, NO has therefore been proposed to also mediate the toxic effects of CO.77 Given these disparate data, the exact role of NO as an attenuator or mediator of CO toxicity is still under investigation.78 Catecholamine excess may also be detrimental following CO exposure. EAA release causes excessive surges of norepinephrine and dopamine release and synaptic accumulation of these neurotransmitters. This effect appears to somehow be linked to NO production, as both events can be prevented by nitric oxide synthase (NOS) inhibition. CO induces both heme oxygenase and NOS in cortical pyramidal neurons. While it is unclear whether the resulting altered cerebral blood flow is a pathological or protective response, worsened outcome in sheep treated with hemoxygenase (HO) and NOS blockers suggests the latter.79 Therefore, EAA release, catecholamine release, and NO production are under tight regulation in vivo and can be influenced by COinduced oxidative stress. Furthermore, auto-oxidation or oxidative deamination of catecholamines occurs during ischemia and reperfusion by type B monoamine oxidase and contribute to further ROS formation.80 ROS production after CO exposure can be inhibited by partially blocking type B monoamine oxidase, located predominantly in glia.81 Gliosis, a known neuronal response to injury, and a condition found in Alzheimer’s disease, develops and may play a role in the delayed toxicity seen after CO hypoxia. ROS are capable of triggering programmed cell death or apoptosis. Apoptotic cell death requires activation and/or expression of specific cellular processes, some of which may act through oxidant pathways. In animals, CO-induced neuronal loss was slight at Day 3, increased at Day 7 and persistent at Day 21 following exposure. Neuronal apoptosis was observed to be present upon histopathological examination

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of the animals in this model.82 Others have not demonstrated apoptosis in rats, despite moderately severe poisoning,83 but have observed gliosis. Caspase-1 and NOS inhibitors both block CO induced apoptosis.84 As eloquently summarized by Piantadosi,74 “impaired mitochondrial energy provision in CO hypoxia/ischemia leads to neuronal depolarization, EAA and catecholamine release, and failure of re-uptake until energy metabolism is restored during reoxygenation. These processes, normally modulated by NO production, could contribute to degeneration of neurons in vulnerable regions, possibly by enhancing mitochondrial ROS generation which can initiate apoptosis.”

16.4 CURRENTLY AVAILABLE NEUROPROTECTIVE TREATMENTS 16.4.1 NORMOBARIC OXYGEN There are limited data to suggest that normal neuropsychiatric outcome is possible after treatment with normobaric oxygen (NBO). In one study, 33 patients with acute CO poisoning (mean COHb 29.4%, 10 patients above 40%, 7 comatose on arrival) were treated with 100% NBO. Recovery was reportedly rapid, with no neurological deficits at discharge. Formal neuropsychiatric testing and follow-up were not performed, however.85 Similarly, four patients presenting comatose from CO poisoning who did not receive HBOT were identified retrospectively, but then evaluated with formal neuropsychological testing at 6 and 12 months after exposure. All had normal neuropsychiatric examinations.86 Meert looked retrospectively at the outcome of children treated with NBO, and concluded that acute neurologic manifestations resolve rapidly without HBOT.87 However, neurologic outcome was assessed from nursing and physician records, physical and occupational therapy evaluations, and unspecified neuropsychological examinations in an unspecified number of patients. Therefore, the major limitation of this study is the lack of detailed neurologic assessment both at presentation and at follow-up that would allow detection of those specific neuropsychiatric changes known to result from CO poisoning. Nonetheless, the authors noted “gross” neurologic abnormalities in nine (8.5%) survivors, with seven of those persistent at various stages of follow-up (2 months to 3.3 years). Three patients developed delayed neurologic syndromes including tremors, hallucinations, seizures, occipital lobe infarctions, defects in cognitive, and interpersonal skills. The presence of serious comorbidities, such as smoke inhalation, burns, need for mechanical ventilation, and need for surgical procedures certainly confounds the outcomes reported by these investigators, which are not reflective of pure CO exposure. Overall, given the small size of these trials and their significant methodological limitations, they do not significantly add to our understanding of predictors for good outcome after treatment with NBO therapy.

16.4.2 HYPERBARIC OXYGEN THERAPY In addition to the aforementioned effects of increasing both the amount of dissolved oxygen in the blood and the rate of displacement of CO from hemoglobin, HBO may

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have other beneficial effects. In animal models, HBO at 3 atmospheres absolute (ATA) also prevents functional neurological impairment88 and HBO at 2.5–3.0 ATA reversibly inhibits PMN CD18 beta 2 integrin activation therefore decreasing adherence of PMNs to endothelial cells.89,90 This effect has also recently been noted in patients with acute severe CO poisoning, in whom HBO modulated neutrophil generation of ROS and surface expression of CD18 receptors.91 Moreover, HBO is known to regenerate inactivated cytochrome oxidase, and may thereby restore mitochondrial function.92 An astroglial structural protein S100B that is a proposed marker for neuronal injury is elevated in CO-poisoned rats treated with ambient air or NBO, but not in those treated with HBO.93 Other proposed beneficial effects of HBOT include decreased production of ROS,94 protection against cerebral edema and increased cerebrospinal fluid (CSF) pressure,95,96 induction of production of protective stress proteins (SP72), and antagonism of NMDA excitotoxic neuronal injury. Conversely, HBO has not been effective in animal models as a treatment for nonCO mediated acute cerebral ischemia with reperfusion.97 Anecdotal human case reports suggest significant clinical improvement from CO poisoning during HBOT.98−105 In addition, numerous other case series report on the beneficial effects of HBOT, but these are limited by either their retrospective nature, or prospective design without the use of randomization, double-blinding, or controlled methodology.106−112 Three pioneering research efforts attempted to discern potential benefit from HBOT, through randomization of CO-poisoned patients into HBO and NBO treatment groups. Raphael113 studied 343 mildly poisoned CO-patients (those who had not lost consciousness) and found no difference at 1 month follow-up in neurologic outcome between HBO and NBO-treated groups, and no benefit to multiple HBO treatments in a more severely poisoned group (those who had lost consciousness), randomized to either one or two HBO treatments. Criticisms of this study regarding the method of neurologic evaluation used, the application of inadequate doses of oxygen therapy, and potential delays in HBO treatment have been raised.114 Ducasse115 randomized noncomatose patients to HBO and NBO groups and found significantly improved differences in quantitative electroencephalogram (EEG) and cerebral vascular responsiveness to acetazolamide in the HBO group during the first 24 h. Differences at 3 week follow-up are not reported consistently. Early improvements in clinical signs and symptoms, such as headache, reflex impairment, and asthenia were significant in the HBO group. Thom116 randomized patients with mild to moderate CO poisoning into NBO versus HBO groups. The incidence of delayed neuropsychiatric sequelae (DNS) was 23% after treatment with oxygen at ambient pressures and 0% in the HBO group. DNS persisted for an average of 41 days following exposure. The author concluded that HBOT decreased the incidence of DNS. Limitations of this study117 are the lack of double-blinding, inconsistent NP testing methods used, and exclusion of severely poisoned patients. Recently, several additional more rigorously designed trials have been carried out. All are prospective, randomized, double-blinded, controlled clinical trials assessing the benefit of HBO versus NBO in the treatment of CO poisoned patients. Two have been completed and one has resulted in publication of the interim data analysis. These are reviewed below.

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Scheinkestel et al. peformed the first large prospective, randomized, double blinded, controlled clinical trial investigating the neurologic sequelae in 191 patients with all grades of CO poisoning after treatment with HBO and NBO.118 Sham HBO treatments were given to those randomized to the NBO group. Pregnant women, children, and burn victims were excluded. Higher doses of oxygen were utilized than reported in most previous studies, averaging approximately 37 COHb-dissociation half-lives in the HBO group and 28.5 in the NBO group (up to three daily treatments in those not improving). Neuropsychiatric evaluations were performed at completion of treatment and at discharge. No benefit and possible adverse effects of HBO were found. Overall mortality was 3%, with persistent neurologic deficits in 71% at hospital discharge and 62% at one-month follow-up. All five patients with delayed onset of neurologic deficit occurred in the HBO group. Limitations of the study are that 44% of victims had ingested other drugs, there was a mean treatment delay of 7.1 h, 56% of patients were lost to 1-month follow-up, and 76% were suicidal, which could impact neuropsychological testing. These results led the investigators to conclude that HBOT should no longer be recommended for CO poisoning treatment. A similarly designed longitudinal follow-up study employing sham treatments, found approximately 30% of patients with acute CO poisoning have neurocognitive problems 1 year after poisoning. Of these patients, approximately one-third have the delayed neuropsychiatric syndrome and two-thirds have persistent neurocognitive problems, mainly difficulties with memory and executive function. 119 Patients in the treatment arm received three HBO sessions. This randomized control trial demonstrated a 46% reduction in cognitive sequelae in HBO-treated patients at 6 weeks following poisoning, which was maintained at 1 year after poisoning.120 It should be noted that nonspecific symptoms were the primary determinant of a statistical difference between treatment groups. A third randomized controlled trial (RCT) performed on noncomatose CO-poisoned patients showed no benefit between HBO and NBO at 1 month, 6 months, or 1 year postexposure. Since the study is published only in abstract form, details are minimal.121 Interim results from a 4th RCT trial employing one HBOT session in patients with moderate to severe CO poisoning showed no difference in outcome.122 Assessments were made by questionnaire and a blinded neurology examination. A high rate of symptoms in both groups was noted (39–42%) at 1 month after poisoning. The use of repetitive HBOT is controversial but common with 23% of US HBOT facilities automatically giving more than one HBO treatment per CO-poisoned patient.40 Some investigators perform additional treatments if lack of improvement is noted after the 1st HBO treatment.104,123−125 Others report no benefit to multiple HBO treatments.113 Turner et al.124 recently proposed the use of the initial hydrogen ion concentration (degree of metabolic acidosis) as a marker for repetitive HBO treatment requirement, on the basis of a retrospective analysis of 48 patients. McNulty et al.126 found impairment of short-term memory for verbal material to be predictive of the number of HBO treatments needed. Finally, the use of peak alpha frequency on EEG as an indicator of need and efficacy of repetitive HBO treatments has been proposed.127 While generally safe, unusual risks of HBOT include complications arising from transport to an HBOT facility, barotrauma, oxygen toxicity with resultant seizures in 1–3% of CO-poisoned patients128 and fire or explosion hazard. Historically, the lack of definitive results from RCTs have rendered the indications for HBOT in CO poisoning

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arbitrary and tremendously varied. Recommendations have primarily been derived from patient history, presenting neurologic and cardiovascular signs and symptoms, and laboratory data such as glucose, lactate, arterial blood gases, electrocardiography, and COHb levels. Unfortunately, none of these clinical or laboratory findings at presentation are entirely predictive of long-term outcome following CO exposure. Those that show future promise, such as SB100 and neutrophil response, are not yet clinically available. Of note, recent preliminary work suggests that HBOT benefit may be limited to reducing the incidence of persistent neuropsychiatric sequelae (PNS) but not DNS, perhaps through modulating early but not later mechanisms for brain injury.129 Overall, the evidence favoring HBOT as protective against DNS and PNS remains under fire as experts continue to debate the results and limitations of each of the randomized controlled trial performed to date.130−138 These uncertainties definitely suggest that greater future research emphasis be placed on non-HBOT methods of therapy.

16.4.3 ALLOPURINOL AND N-ACETYLCYSTEINE As described above, there is considerable evidence that reactive oxygen metabolites mediate neurologic injury in models of CO poisoning. Lipid peroxidation is documented in rats after CO exposure at concentrations sufficient to cause unconsciousness. Products of lipid peroxidation are increased by 75% over the baseline values 90 min after CO exposure. Unconsciousness is associated with a brief period of hypotension, so brief that in itself it causes no apparent insult. Lipid peroxidation occurs only after the animals are returned to CO-free air; and there is no direct correlation between the degree of lipid peroxidation and COHb level.63 This suggests that ischemia and reperfusion may play a role in the ultimate neurologic injury. Xanthine oxidase also has a central role in this toxicity. During the COinduced PMN degranulation described above, released proteases convert xanthine dehydrogenase to xanthine oxidase. Xanthine oxidase generates superoxide free radicals and lipid peroxidation occurs.65 The xanthine oxidase enzyme is an NADdependent dehydrogenase that under ischemic conditions converts to an oxidase, utilizing molecular oxygen rather than nicotinamide adenine dinucleotide (NAD) as an energy source and generates the superoxide radical and hydrogen peroxide. These products in turn cause tissue injury, the brain being particularly susceptible with its low content of catalase and glutathione peroxidase.139 The restoration of xanthine dehydrogenase functional activity is accomplished through the use of xanthine oxidase inhibitors (allopurinol)140 and sulfhydryl donors [N-acetylcysteine (NAC)]141 in nonCO-mediated neuronal injury. Fechter et al.142 noted that acute CO poisoning produces preferential high-frequency hearing impairment, noted to be a consequence of other types of anoxic exposure. These investigators also discovered that either allopurinol or phenyl-n-tert-butyl-nitrone (PBN), a free radical scavenger blocked the formation of characteristic compound action potential threshold elevation and cochlear microphonic amplitude. Therefore, both agents were effective in blocking loss of CO-mediated auditory threshold if given prophylactically in the guinea pig model. Allopurinol and N-acetylcysteine have been used in the treatment of CO-induced neuronal injury. Thom63 demonstrated decreased conversion of xanthine dehydrogenase to xanthine oxidase with decreased lipid peroxidation in rats pretreated with

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allopurinol. Only one human case report demonstrated effectiveness of such combined therapy for the treatment of CO poisoning. A 26-year-old male with a COHb level of 25%, 40 h postexposure, who was comatose for 4 days with cerebral edema on computed tomography (CT) was treated with both a xanthine oxidase inhibitor (allopurinol) and a sulfhydryl donor, NAC. NAC was given intravenously over a 20-h period and allupurinol was given orally for 2 weeks. Eight hours after the completion of this regimen, the patient became responsive and gradually improved over the next three weeks. “Neurological and mental examination at six weeks followup were normal.”143 Although no formal neuropsychiatric testing was reported, this type of therapy may perhaps provide a basis for further study. Since allopurinol theoretically prevents the formation of free radicals, it remains to be seen whether any benefit exists for postexposure administration. Other antioxidants such as dimethyl sulfoxide and disulfiram have been shown to prevent learning and memory deficits in CO-poisoned mice in preliminary reports.144 Such agents may someday serve as useful adjuncts in limiting free radical mediated injury.

16.4.4 INSULIN In humans and animals numerous studies have shown that elevated blood glucose is associated with worsened neurologic outcome after brain ischemia caused by stroke or cardiac arrest. Acute severe CO poisoning is characterized by hyperglycemia and this elevation has been linked to increased severity of brain dysfunction in the rat.145 Indeed, animal studies show that CO exposure raises blood glucose in a dosedependent manner, and is an independent predictor of neurologic outcome. A few similar observations have been made in CO-poisoned patients. Penney146 observed that elevated admission blood glucose was associated with worse neurologic outcome after CO poisoning in patients. Leikin found elevated blood glucose in most patients presenting with COHb saturation above 25%.147 Furthermore, anecdotal evidence in the human literature suggests that the neurologic outcome in diabetics poisoned with CO is generally worse than in nondiabetics.148 Considerable basic research has been directed at identifying molecular mechanisms of tissue injury and potential interventions to allow the preservation or rescue of neurons after stroke and cardiac arrest. On the basis of the aforementioned association between elevated blood glucose and poor outcome, insulin has recently been investigated as a potential therapeutic agent in various models of brain and spinal cord ischemia, and indeed appears to substantially ameliorate neuronal death induced by ischemia in these studies. Surprisingly, this neuron-sparing effect is known to be independent of insulin-induced reductions in blood glucose, and is hypothesized to be mediated through cell signal transduction mechanisms, in common with other growth factors. The question of whether insulin ameliorates neuronal injury secondary to CO toxicity was investigated in rats who were exposed to a CO LD50 of 2400 ppm for 90 min. Survivors were treated for 4 h with (1) normal saline infusion (2) continuous infusion of glucose to clamp blood glucose levels at 250–300 milligrams per deciliter (mg/dL) and (3) continuous infusion of glucose to maintain blood glucose levels at 250–300 mg/dL with intraperitoneal (IP) injections of 4 units/kg of regular insulin.

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Neurologic scoring was performed at time 0, 5.5, 24, 48, 72, and 96 h. It was noted that significant neurologic deficit occurred in all groups after the CO exposure and treatment period. Induced hyperglycemia after CO exposure was associated with significantly worsened neurologic scores as compared to saline-treated controls. Insulin therapy simultaneous with induced hyperglycemia significantly improved neurologic scores at all times despite maintenance of comparable hyperglycemia with respect to the group treated only with glucose. No significant difference in mortality was found between treatment groups.149 Several theories have evolved regarding the postreceptor binding protective effect of insulin on the neuron. Insulin has been shown to provide neuromodulatory inhibition of synaptic transmission in vivo and in vitro. As an inhibitor of glial uptake of gamma amino butyric acid (GABA), insulin may increase the availability of this inhibitory neurotransmitter and may decrease neuronal firing, beneficially reducing cell metabolism.150 The additional effect of sodium extrusion from the cell which affords subsequent protection against water accumulation may prevent neuronal swelling.151 Furthermore, it has been suggested that an insulin-induced elevation of brain catecholamines through both inhibition of catecholamine uptake and stimulation of release might be a contributory neuroprotective mechanism, since catecholamines have been found to attenuate ischemic brain damage. Of these theories regarding insulin’s neuroprotective activity, however, the most recent highlights its role in stimulating second messengers, and emphasizes its potential genomic effects, that is, the regulation of protein synthesis, enzymatic activity, and the signaling of cell proliferation. It is well established that the neonatal brain is rich in insulin-like growth factor receptors. Indeed, insulin is similar in structure to other growth factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin-like growth factor-1 (IGF-1). Such peptides are involved in basic neuron development and differentiation. Once bound to its receptor, like other growth factors, insulin triggers signal transduction by internal autophosphorylation of tyrosine on the insulin receptor, which subsequently enhances further phosphorylation reactions of other tyrosine containing substrates by tyrosine kinase, located on the insulin receptor. This type of tyrosine phosphorylation is important in signaling pathways for such growth factors and products of proto-oncogenes. Insulin is a progression growth factor in replication G0G1 phase and works synergistically with other growth factors to generate both competence and progression of cells. Through tyrosine phosphorylation of phosphokinase C, other second messengers such as diacyglycerol are formed, which increase intracellular calcium, activate the sodium–hydrogen pump, and increase intracellular pH. This pH change in turn activates the sodium potassium ATPase pump, which signals cell proliferation.152 Insulin also regulates specific mRNA levels through diacylglycerol153 and may increase mRNA efflux from the nucleus through nuclear triphosphatase activation.154,155 More importantly, insulin stimulates lipid neogenesis. It appears therefore, that the effects of insulin are fundamental with regard to cell signaling, proliferation, replication, and repair following injury. These processes are crucial to cells such as neurons which normally are terminally differentiated and contain little if any capacity to replicate or to synthesize repair lipids.

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Certainly, anatomic correlates to the above proposed mechanisms are in place. For example, it has been demonstrated that the location of insulin and IGF-1 receptors correlates with phosphotyrosine products in the brain.156 Moreover, the basal ganglia, areas typically found to be damaged by CO, possess low levels of insulin receptors. Although the initial results of animal studies such as those above may provide building blocks for clinical work, any recommendations regarding the use of insulin in humans as treatment for CO poisoning will of course await further studies.

16.4.5 NMDA RECEPTOR ANTAGONISTS Recent evidence implicates the endogenous excitatory amino acids such as NMDA in ischemic neurodegeneration.157−159 Moreover, the NMDA receptor antagonist, MK801, prevents nonCO induced ischemic neurodegeneration in animal models.160 Successive CO exposures induce a consistent pattern of degeneration of hippocampal CA1 pyramidal neurons, a selective neuronal death that resembles that seen with other models of cerebral ischemia. This observation has prompted the study of NMDA receptor antagonists in CO poisoning in mice. Ishimaru pretreated animals with a competitive NMDA antagonist, CPP; a noncompetitive NMDA antagonist, dizocilpin (MK-801); a glycine binding site antagonist, 7-CK; a polyamine binding site antagonist, ifenprodil; glycine; and saline. Seven days postexposure the number of hippocampal CA1 pyramidal cells was quantified using an image analyzer. A decrement of 20% in the number of hippocampal CA1 pyramidal cells was noted relative to the control group. Those animals receiving high doses of MK-801, 7-CK, and CPP had significant reductions in neuronal damage. No clear protective effect was obtained with ifenprodil. Interestingly, glycine, a facilitory neurotransmitter at the NMDA receptor complex did not exaggerate the CO-induced neuronal damage as might be expected.161 Although no neurologic outcome correlates or survival data are reported, this work may provide valuable mechanistic and possibly future therapeutic insights. Similar work by Lui162 suggested beneficial effects of MK 801 when administered either systemically or directly to the cochlea in protecting against CO-induced ototoxicity. Glutamate is another excitatory neurotransmitter acting at the NMDA receptor complex. Postexposure treatment of mice with glutamate antagonists prevents CO-induced learning and memory deificits.163 Finally, NOS inhibitors prevent NMDA receptor activation and were protective of learning deficits in CO poisoned mice.73 Ketamine is a widely used dissociative anesthetic agent, which is known to have NMDA receptor-blocking properties.164 It has been shown to be neuroprotective in various animal models of ischemic and anoxic neuronal injury. It has also been observed to blunt hypotension, a condition known to worsen CO-mediated neuropathologic changes. Promising work by Penney165 demonstrated significantly reduced cerebral edema, more rapid recovery from hypotension, and suppressed lactate formation following CO-poisoning when 40 mg/kg ketamine was administered to rats before and during CO exposure.165 This same study did not yield positive results with the use of verapamil, which could theoretically block NMDA-mediated postsynaptic calcium uptake in neurons.

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16.4.6 BRAIN-DERIVED NEUROPEPTIDES Cerebrolysin, a drug,produced by enzymatic breakdown of lipid free proteins of porcine brain is a putative neuroprotective agent of unknown mechanism. Proposed neurotrophic effects are supported by reports that cerbrolysin-treated rats had increased brain protein synthesis,166 prevention of neuronal degeneration,167 and enhanced neuronal growth in tissue culture.168 Effects on the blood brain barrier have also been noted. Interestingly, cerebrolysin increases expression of the blood brain barrier glucose transported gene in brain endothelial cell cultures. It is hypothesized that cerebrolysin may accelerate repair of the blood brain barrier in regions compromised by hypoxia.169 Recently, a model of acute CO poisoning combined with spreading depression-induced metabolic stress was used to examine the protective effects of cerebrolysin on the development of electrophysiological, behavioral, and morphological signs of hypoxic damage in rats. Spreading depression waves reflect the recovery of cerebral cortex in the peri-ischemic areas, or penumbra zone. After a 90 min exposure to 0.8–5% CO, microinjections of 5% KCl into the cortical and hippocampal areas were performed and the duration of spreading depression was noted. At 9 and 18 day follow-up, repeat spreading depression measurements were taken, and a decrease in amplitude was used as an index of brain damage. Postexposure cerebrolysin-treated animals had significantly improved hippocampal recovery. Better performance was also noted on behavioral testing, and no apparent histological damage was apparent in the hippocampus as compared to controls.170 This very promising neuroprotective agent, which appears to be effective even if given postexposure, certainly deserves further study to elucidate any possible beneficial role in humans.

16.4.7 HYPOTHERMIA Hypothermia was found to be beneficial in the management of CO poisoning by Sluijter,171 an effect that was thought to be secondary to increased dissolved oxygen in the blood at lower temperatures. Peirce et al.,172 howeve, was unable to demonstrate any synergistic effect when hypothermia was used in conjunction with HBO in a dog model.172 An interesting report of the use of mechanical ventilation and hypothermia in patients with abnormal motor activity or coma to treat CO toxicity, noted complete reversal of these manifestations in three patients when therapy was initiated within the first 24 h. No beneficial effects were noted in a fourth patient who did not receive hypothermic treatment until 5 days after exposure. HBO was not available to these patients.173

16.5 APPROACH TO THE PATIENT WITH CARBON MONOXIDE POISONING 16.5.1 GENERAL The most critical step in managing the patient poisoned with CO is the cessation of tissue hypoxia. This involves supplementation with 100% oxygen, delivered

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by either a tight-fitting continuous positive airway pressure (CPAP) mask or by endotracheal intubation. Intubation may be necessary in the patient with chronic obstructive pulmonary disease (COPD), to avoid carbon dioxide retention secondary to high concentrations of oxygen. NBO should be initiated as soon as the diagnosis is entertained, and should not be delayed for confirmatory COHb levels. As discussed above, the use of 5% carbon dioxide mixed with 95% oxygen (carbogen) has been proposed by some to facilitate the release of CO from hemoglobin by increasing ventilatory response. This therapy is of questionable value, and has fallen out of favor. Even though not demonstrated in animals,174 the potentially life-threatening possibility of carbogen-induced carbon dioxide retention and subsequent worsening of an already existing acidosis would contraindicate it use in the patient with COPD, concurrent poisoning with respiratory depressants, or altered mental status. The duration of oxygen therapy is guided by a knowledge of the COHb half-life and allows for a margin of safety. Generally this would involve at least 6 h of therapy on 100% oxygen, longer if the patient is gravid or an infant. An early chest x-ray is mandatory to assess for evidence of pulmonary edema resulting from CO or other inhaled toxins. Once airway control and oxygenation are assured, attention should be directed toward the cardiovascular system. Continuous cardiac monitoring is advisable and a 12 lead EKG should be obtained to assess for subclinical cardiac ischemia. Myocardial enzymatic changes with or without EKG changes, are increasingly described in adults with CO poisoning as outlined above. It is prudent therefore to perform a cardiac evaluation on patients with CO poisoning. It is not clear, however, whether CO-induced myocardial injury, particularly the “stunned myocardium” is a predictor of poor clinical outcome or mortality. Should arrhythmias, ischemia, or hemodynamic instability occur despite therapy with 100% oxygen, the patient could be considered a candidate for HBOT. Myocardial depression and arrhythmias may occur secondary to extremely low arterial pH, such as has been noted in patients with severe lactic acidosis. Severe acidosis should therefore be treated aggressively. However, correction of mild acidosis with sodium bicarbonate is not advisable as this could result in a further shift of the oxyhemoglobin dissociation curve to the left, and impair the unloading of oxygen to hypoxic tissues. A novel calcium sensitizer, levosimendan, improves myocardial contractility and increases coronary artery flow. Its use in a single patient with cardiogenic shock from CO-induced myocardial stunning was associated with improved hemodynamics relative to dobutamine. Improvement was assessed by cardiac magnetic resonance imaging.175 In those patients with altered mental status, causes of rapidly reversible causes of coma should be considered and treated by the bedside assessment of a fingerstick glucose and the administration of thiamine and naloxone, a narcotic antagonist. Supplemental glucose may be needed to correct hypoglycemia, but every attempt should be made to maintain euglycemia, and avoid iatrogenic hyperglycemia. A thorough physical assessment for burns, odors, toxidromes, skin findings, and signs of smoke inhalation, trauma, or abuse is indicated. Acareful history regarding the circumstances surrounding the exposure must be obtained once the patient is stabilized. Considerations should be made to gastric or skin decontamination and activated charcoal

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administration in the setting of suspected intentional drug abuse, suicide attempt, or dermal chemical exposure (methylene chloride). Removal of CO from the body is best accomplished through displacement by oxygen, either normobaric or hyperbaric. Other less conventional therapies have been used anecdotally with favorable outcomes, and include both exchange transfusion and extracorporeal oxygenation.176 These invasive approaches however, would be recommended only in unusual circumstances, for example if HBOT was not available in a deteriorating or moribound patient. Should the patient be CO-poisoned from smoke inhalation, numerous other products of combustion may be contributing to the metabolic and pulmonary derangements seen. Of particular concern is cyanide, a lethal combustion product, that is commonly elaborated when plastics or synthetic materials burn. The patient with CO poisoning and evidence of smoke inhalation who remains significantly acidotic despite treatment with oxygen should be suspected to have concomitant cyanide toxicity. Specifically, cyanide poisoning is associated with enclosed space fires, the presence of soot in mouth or sputum, altered consciousness, hypotension, and an elevated lactate >8–10 mmol/L without significant burns.177 Some authors advocate empiric treatment of fire victims with suspected cyanide poisoning with the sodium thiosulfate component of the cyanide antidote kit. The other components, methemoglobin-forming agents such as amyl nitrite and sodium nitrite, have been traditionally withheld if CO poisoning is suspected in order to avoid further hemoglobinopathy and worsened hypoxia. Moore et al.178 demonstrated a 25% increase in mortality in sodium nitrite-treated animals with CO-poisoning compared to the untreated controls. Despite this, a human study demonstrated that five of seven patients with CO poisoning were safely treated with the antidote kit in its entirety.179 These patients however, had only moderate COHb levels, with a mean level of 26%. Coupled with the fact that only a small number of patients were studied, this form of empiric treatment for cyanide poisoning in victims of smoke inhalation cannot yet be widely recommended. Another cyanide antidote, hydroxycobalamin is under Food and Drug Administration (FDA) consideration for approval. While not yet readily available in the United States, this new antidote will not harbor the risk of methemoglobinemia found with nitrites and will ultimately offer a safer option for victims of smoke inhalation. For now, given the relative safety of the sodium thiosulfate component of the cyanide antidote kit, its sole use may be advisable for the treatment of the patient dually poisoned with CO and cyanide. Once the patient has been stabilized, consideration of the use of possible neuroprotective agents including HBO should be made. If the patient is awake, a mental status examination should be performed. Abbreviated neuropsychologic tests (CONSB) have been developed specifically for the CO poisoned patient, but often are not practical for use in the emergency department or in those with moderate or severe acute intoxication. Examples of tasks performed by the patient during administration of the CONSB include placing pegs in a board, complete rapid finger tapping, memorization, construction, number processing, and subjective stress response.180 Memory impairments are the most frequent cognitive impairment noted following CO poisoning, some improving over time.181 Other common deficits include visual tracking,

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visuomotor skills, visuospatial planning, and abstract thinking. Impaired executive function, information processing speed, attention and concentration are also common.

16.5.1 NEUROIMAGING Neuroimaging studies can be valuable adjuncts to the neuropsychiatric assessment. They should be considered in CO-poisoned patients with altered mental status, abnormal, or lateralizing neurologic examinations, or a history of head trauma. Increasingly, correlates are described between cognitive impairment and neuroimaging findings (see other chapters in book), particularly relative to basal ganglia atrophy, fornix atrophy, and white matter hyperintensities.182 Moreover in adults, CT abnormalities have been prognostic with regard to neurologic outcome in several studies.183−185 Pathologic lesions seen on CT owing to CO intoxication are variable, including cerebral edema, symmetrical low density areas in the basal ganglia, symmetrical and diffuse white matter low density areas, and, as late changes, ventricular dilation, and sulcal widening. The classic finding of bilateral symmetrical hypodensities in the basal ganglia, especially the globus pallidus, most typically becomes evident within 24–48 h of exposure. However, such abnormalities have been reported to appear anywhere from the first day to 5 years following CO exposure. Remarkably, such basal ganglia lesions have been reported to occur in 32% to 86% of CO-poisoned patients.186 These lesions are not pathognomic for CO poisoning, however, and when encountered, the differential diagnosis includes methanol, cyanide, or hydrogen sulfide toxicity; hypoxia; hypoglycemia; the hemolytic uremic syndrome; osmotic myelinolysis; encephalitis; inborn errors of metabolism; and Huntington’s disease.187 Likewise, white matter lesions are frequent and include hyperintesities in the periventricular and centrum semiovale or deep regions, generalized white matter degeneration, and generalized atrophy. Several studies suggest that white matter lesions occur even more commonly than do basal ganglia lesions.188 Magnetic Resonance Imaging (MRI) may be superior to CT in detecting white matter, cerebral, cerebellar, substantia nigral, and basal ganglia lesions following CO poisoning.189−195 Quantitative MRI may be more sensitive in evaluating the hippocampal regions in patients with DNS following CO poisoning. Some authors report a good correspondence between MRI and memory deficits on neuropsychological evaluation in adults.196−198 Conversely, Prockop199 noted a significant percentage of patients with normal MRI examinations had intellectual impairment on neuropsychological testing. Functional imaging such as SPECT scanning provides an indicator of the severity of cerebral damage and correlates with outcome.200 The combination of EEG with SPECT scanning may provide greater sensitivity for detecting anomalies than EEG alone.201 In a cohort of adult patients with acute severe CO poisoning, treated with HBO, positron emission tomography (PET) scan findings of globally increased oxygen extraction ratios and decreased blood flow in the frontal and temporal cortex were most severe in those patients with DNS or PNS. These changes are temporary in patients who appear normal following CO exposure and in those with temporary neurological and psychiatric deficits. This suggests that ischemia is ongoing after

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CO intoxication, even after apparent normalization of the clinical status.202 Others have noted prolonged perfusion and metabolic abnormalities in patients with neurologic deficits following exposure.203 In a small case series, PET abnormalities in the basal ganglia of CO victims were undetected by CT or MRI, suggesting possible greater sensitivity with PET.204 Newer techniques in SPECT scanning may allow for even earlier detection of regional CO-induced anomalies.205 Specifically, decreased perfusion in the basal ganglia and cortex correlated with parkinsosian symptoms and cognitive deficits, respectively. More recently, magnetic resonance spectroscopy (MRS) detected decreased n-acetyl aspartase in the basal ganglia bilaterally in one-third of CO-poisoned patients studied.199 Should the patient perform abnormally on the CO neuropsychiatric screening battery (CONSB), have a history of a soaking-type exposure or loss of consciousness, have abnormal neurologic findings (particularly cerebellar findings,119 exhibit cerebral edema on CT scan, or have evidence of cardiac ischemia, HBOT should be recommended. Despite this general practice, clinical predictors of DNS or PNS remain elusive and controversial. Even syncope unreliably predicts the need for HBOT.119 Similarly, laboratory markers such as COHb level, lactate level, or base deficit are unreliable factors in predicting DNS or PNS. Preliminary animal evidence points us toward the potential future use of laboratory markers such as peripheral lymphocyte cytochrome c oxidase, cyclic GMP, cholinergic muscarinic receptors and S100 B protein for determining patient prognosis.206,207 As suggested above, the use of COHb levels to guide therapy is controversial. A survey of medical directors of US and Canadian facilities indicated that 62% use a specific COHb level as the sole criterion for asymptomatic patients. The same survey found that when a specific COHb level was used as the indication for HBOT, 25% was the most common level chosen.208 See Table 16.1. Others suggest that HBOT is prescribed on the basis of COHb level in 40% of patients and in 60% on the basis of central nervous system or cardiac dysfunction.209 The patient’s clinical findings and history are of equal importance relative to COHb in determining the need for HBOT. Patients who could be considered candidates for HBOT include the pregnant patient with a COHb level greater than 10–15%, the patient with a history of coronary artery disease and a COHb level greater than 20%, the asymptomatic patient with a level

TABLE 16.1 Proposed Indications for Hyperbaric Oxygen Therapy in Pregnancy 1. 2. 3. 4. 5. 6. 7.

Abnormal CONSB (CO neuropsychiatric screening battery) Neurologic abnormalities (particularly cerebellar findings) Loss of consciousness (syncope) COHb > 25–40% Ongoing myocardial ischemia Worsened, recurrent,or refractory symptoms on NBO Relative considerations: soaking exposure, cerebral edema on CT scan

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greater than 25% to 40% COHb, or the patient with recurrent or persistent symptoms despite 6 hours of therapy with NBO. If HBOT is indicated, treatment within 6 h is desirable.210 Patients should undergo a full neuropsychiatric evaluation prior to discharge. Close follow-up is necessary with repeat neuropsychiatric examinations at 6 weeks, 6 months, and 12 months.

16.5.2 PREGNANCY The effects of CO on the fetus has been extensively reviewed by Penney.211 The fetus is particularly vulnerable to the effects of CO, which readily crosses the placenta, and, in animal models, is even more tightly bound to fetal hemoglobin than adult hemoglobin. The fetus also reaches higher peak COHb levels than does the mother. Fetuses that survive a significant CO poisoning may be left with limb malformation, hypotonia, areflexia, persistent seizures, mental and motor disability, and microcephaly.212,213 The only prospective, multicenter study of acute CO poisoning in pregnancy recently reported adverse outcomes in 60% of children whose mothers suffered severe CO toxicity. Of those babies born to mothers with mild to moderate CO exposure, normal physical exams and neurobehavioral development were reported.214 Since CO elimination from the fetus is prolonged (7–10 h), it is generally accepted that HBOT is indicated at lower maternal COHb levels than would be acted upon in the nongravid patient. In addition, surface oxygen therapy should be extended to four to five times the normal duration. Although controversial, HBO has been reported to be safe in the pregnancy,215 despite theoretical dangers of fetal hyperoxia in animal models.216−218 (Such animal models exceeded the time and pressure routinely used in clinical therapy). A recent report of 44 women undergoing HBOT during pregnancy for CO exposure suggests that it is safe and should be considered, although miscarriages did occur, and six patients were lost to follow-up.219 It should be noted that HBO was implicated in the induction of labor in one pregnant patient, the pregnancy however, was near term when the CO exposure occurred.220 Proposed indications for HBOT in the pregnant patient are listed in Table 16.2, although these are not well-studied.

16.5.3 CHILDREN Pediatric CO poisoning has been reviewed by White.221 Younger children have traditionally been viewed to be more susceptible to CO poisoning on the basis of more

TABLE 16.2 Proposed Indications for Hyperbaric Oxygen Therapy in Pregnancy 1. 2. 3. 4.

Maternal COHb level > 10–15% at any time during the exposure Any neurological signs or symptoms other than headache Evidence of fetal distress (fetal tachycardia, decreased beat-to-beat variability, late decelerations) If maternal neurologic symptoms or fetal distress persist 12 h after initial therapy, additional HBO treatments may be necessary

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rapid metabolic rate and higher oxygen demands. They may also have more atypical presentations relative to adults. Both persistent and delayed sequelae are described in the children, however, formal neuropsychiatric testing is generally difficult and not well-documented in such case series.222 The use of HBOT in the treatment of pediatric CO poisoning is controversial, and recommendations vary, even among pediatric toxicology experts. Until further knowledge and experience is gained in this area, children are likely be treated as aggressively as adults who are CO-poisoned.

16.6 MANAGEMENT OF THE SEQUELAE OF CARBON MONOXIDE POISONING Delayed sequelae from CO poisoning is devastating and occurs in 10–43% of persons recovering from the acute exposure. Parkinsonism, the most dramatic long-term neurologic complication has a grim prognosis. Fortunately, most cases of DNS associated with mild CO poisoning resolve within two months.119 Unfortunately, only one-third of severely CO-poisoned patients surviving to HBOT have resolution of DNS. Conventional therapy of DNS-related parkinsonism with l-dopa has been disappointing. Use of another centrally acting dopaminergic agonist, bromocriptine has been reported. Nine patients (mean age 61 years) suffering from CO-induced parkinsonism who were given bromocriptine (5–30 mg/day), displayed improvement in Webster’s scores while under treatment.223 Clearly no definitive conclusions regarding bromocriptine therapy can be made on the basis of small study, but perhaps it will provide a basis for future investigations. Treatment with ziprasidone, a newer atypical antipsychotic agent resulted in improved neuropsychiatric symptoms and cognitive function in a patients with CO-induced severe DNS refractory to HBOT, bromocriptine, conventional antipsychotics, and other atypical antipsychotics, risperidone and quetiapine.224 Similar success was noted using aripiprazole in managing CO-induced psychotic symptoms and parkinsonism.225 One report involving hyperpyrexia and muscle rigidity as sequelae of CO poisoning was treated successfully with a prolonged course of dantrolene sodium, a peripheral skeletal muscle relaxant.226 Given that the patient manifested signs characteristic of severe hypoxic/ischemic encephalopathy, this therapy was symptomatic for that condition, and not specific to CO poisoning. Dantrolene would not likely provide any benefit beyond other safer sedatives, such as benzodiazepines, in treating such complications. Another common sequelae from CO poisoning is memory impairment. Recent work by Hiramatsu et al.227 focused on treating delayed amnesia in mice. The investigators treated mice with documented amnesia 5 days postexposure with dynorphin A (1–13). They found this treatment regimen to be effective in reversing CO-induced memory impairment. Nor-binaltrophimine (kappa opioid receptor antagonist) blocked the effect of dynorphin A (1–13), suggesting that kappa receptors mediated the reversal of impairment in memory seen from CO poisoning in this animal model.227 The authors reported similar findings with a second kappa receptor agonist, U-50488H, which appeared to additionally activate the cholinergic neuronal system, known also to play an important role in cognitive deficits associated with

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other conditions such as aging and neurodegenerative diseases.228 These agents may hold promise for the future in treating the persistent or delayed detrimental effects of CO on acquisition and consolidation of memory. Delayed, sometimes repetitive, HBOT has been advocated by some to improve the long-term neurologic deficits from CO toxicity, even if instituted weeks after the initial CO exposure.229−235 Such practice which is advocated by several treatment centers in the United States lacks validation by well-controlled, blinded clinical studies that utilize neuropsychiatric testing data. Interestingly, behavioral treatment has been successful when guided by formal neuropsychiatric testing. In certain patients, indirect measures of learning are better predictors of treatment efficacy.236 Patients who present to health care facilities late or have suffered recurrent or chronic lower level CO exposures pose particular treatment challenges to the clinician. Any proposed therapeutic approach to such patients should be considered carefully given the fact that no definitive clinical or animal studies in this area exist.

16.7 CONCLUSION Much remains to be learned about CO, including the mechanisms of toxicity, predictors of outcome after poisoning, and best treatments. Further research is needed to formulate clear-cut clinical indications for the use of potentially neuroprotective agents (i.e., insulin, sulfhydryl donors, allopurinol, ketamine, brain-derived peptides, kappa receptor agonists). Given that multiple pathways are involved in the ultimate neuronal injury, how to best use these agents, perhaps synergistically as a “cocktail” approach, remains to be seen. Other areas that deserve further study are the clarification of risk factors for adverse fetal outcome following CO exposure during pregnancy, the delineation of the true incidence of PNS and DNS in children, and the best test for indicators of risk for these sequelae. The future for HBOT in CO poisoning remains to be seen. Given the disparate results from randomized clinical trials using HBOT, we are compelled to continue to carefully select patients for this therapy, and to promote further study to delineate subpopulations such as children and pregnant women who may potentially benefit.

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computed tomography in carbon monoxide poisoning, Ann. Emerg. Med., 24, 947, 1994. DeReurck, J., Decoo, D., Lemahieu, I., et al. A positron emission tomography study of patients with acute carbon monoxide poisoning treated by hyperbaric oxygen, J. Neurol., 240, 430–434, 1993. Shimosegawa, E., Hatazawa, J., Nagata, I., and Okudera, T. Cerebral blood flow and glucose metabolism measurements in a patient surviving one year after carbon monoxide intoxication, J. Nucl. Med., 33, 1696, 1992. Hon, K.E., Yeung, W., Assunta, C., Leung, W.A., Li, A.M., Chu ,W.C., and Chan, Y. Neurologic and radiologic manifestations of three girls surviving acute carbon monoxide poisoning, J. Child Neurol., 21: 737, 2006. Kao, C.H., Hung, D.Z., ChangLai, S.P., Liao, K.K., and Chieng, P.U. HMPAO brain SPECT in acute carbon monoxide poisoning, J. Nucl. Med., 39, 769–772, 1998. Castoldi, A.F., Coccini, T., Randine, G., Hernandez-Viadel, M., Felipo, V., and Manzo, L. Lymphocyte cytochrome c oxidase, cyclic GMP and cholinergic muscarinic receptors as peripheral indicators of carbon monoxide neurotoxicity after acute and repeated exposure in the rat, Life Sci., 78, 1915, 2006. Brvar, M., Mozina, M., Osredkar, J., Suput, D., and Bunc, M. Prognostic value of S100B protein in carbon monoxide-poisned rats, Crit. Care Med., 32, 2128, 2004. Hampson, N.B., Dunfored, R.G., Kramer, C.C., et al. Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning, J. Emerg. Med., 13, 227, 1995. Sloan, E.P., Murphy, D.G., Hart, G., Cooper, M.A., Turnbull, T., Berreca, R.S., and Ellerson, B. Complications and protocol considerations in carbon monoxide-poisoned patients who require hyperbaric oxygen therapy: report from a ten-year experience, Ann. Emerg. Med., 18, 629, 1989. Goulon, M., Barois, A., Rapin, M., et al. Carbon monoxide poisoning and acute anoxia due to breathing coal gas and hydrocarbons, J Hyperbaric Med., 1, 23, 1986. Penney, D.G. Effects of carbon monoxide exposure on developing animals and humans, In Carbon Monoxide, Penny, D.G., ed., Boca Raton, FL, CRC Press, Inc, 1996, Chap 6, pp. 109–144. Ginsberg, M.D., and Myers, R.E. Fetal brain injury after maternal carbon monoxide intoxication, Neurology, 26, 15–23, 1976. Ginsberg, M.D., and Myers, R.E. Fetal brain damage following maternal carbon monoxide intoxication, Acta. Obstet. Gynecol., 53, 309–317, 1974. Koren, G., Sharav, T., Pastuszak A., Garrettson, L.K., Hill, K. Samson, I., Rorem, M., King A., and Dolgin J.E. A multi-center, prospective study of fetal outcome following accidental carbon monoxide poisoning in pregnancy, Reprod. Toxiol., 5, 397–403, 1991. Brown, D.B., Mueller, G.L., and Golich, F.C. Hyperbaric oxygen treatment for carbon monoxide poisoning in pregnancy: a case report, Aviat. Space Envir. Md., 63, 1011–1014, 1992. Ferm, V.H. Teratogenic effects of hyperbaric oxygen, P. Soc. Exp. Biol. Med., 116, 975–976, 1964. Fujikura, T. Retrolental fibroplasia and prematurity in newborn rabbits induced by maternal hyperoxia, Am. J. Obstet. Gynecol., 90, 854–858, 1964. Miller, P.D., Telfored, I.D., and Haas, G.R. Effects of hyperbaric oxygen on cardiogenesis in the rat, Biol. Neonatorum, 17, 44–52, 1971.

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219. Elkaharrat, D., Raphael, J.D., Korach, J.M., Jars-Guincestre, M.C., Chastang, C., Harborn, C., and Gajdos, P. Acute carbon monoxide intoxication and hyperbaric oxygen in pregnancy, Intens. Care Med., 17, 289–92, 1991. 220. Farrow, J.R., Davis, G.J., Roy, T.M., et al. Acute carbon monoxide intoxication and hyperbaric oxygen in pregnancy, Intens. Care Med., 17, 289–292, 1991. 221. White, S.R. Pediatric Carbon Monoxide Poisoning. In: Carbon Monoxide Toxicity, Penney, D.G., ed., CRC Press LLC, Boca Raton 2000, Chapt. 21. 222. Seger, D., and Welch, L. Carbon monoxide controversies: neuropsychologic testing, mechanism of toxicity, and hyperbaric oxygen, Ann. Emerg. Med., 24, 242, 1994. 223. De Pooter, M.C., Leys, D., Godefroy, O., DeReuck, J., and Peter, H. Parkinsonian syndrome caused by carbon monoxide poisoning. Preliminary results of the treatment with bromocriptine, Rev. Neurol., 147, 399–403, 1991. 224. Hu, M.C., Shiah, I.S., Yeh, C.B., Chen, H.K., and Chen, C.K. Ziprasidone in the treatment of delayed carbon monoxide encephalopathy, Prog. Neuro-psychoph. , 30, 755, 2006. 225. Pae, C.U., Kim, T.S., Lee, C., and Paik, I.H. Effect of aripiprazole for a patient with psychotic symptoms and parkinsonism associated with delayed sequelae of carbon monoxide intoxication, J. Neuropsych. Clin. Neurosci., 18, 130, 2006. 226. Ten Holter, J.B.M, and Schellens, R.L.L.A.M., Dantrolene sodium for treatment of carbon monoxide poisoning, Brit. Med. J., 296, 1772, 1988. 227. Hiramatsu, M., Sasaki, M., Nabeshima, T., and Kaemyama, T. Effects of dynorphin A(1–13) on carbon monoxide-induced delayed amnesia in mice. Pharmacol. Biochem., 56, 73, 1997. 228. Hiramatsu, M., Hyodo, T., and Kameyama T. U-50488H a selective k-opioid receptor agonist, improves carbon monoxide-induced delayed amnesia in mice, Eur. J. Pharmacol., 315, 119, 1996. 229. Myers, R.A., Snyder, S.K., and Emhoff, T.A. Subacute sequelae of carbon monoxide poisoning, Ann. Emerg. Med., 14, 1163–1167, 1985. 230. Smith, J.S., and Brandon, S. Morbidity from acute carbon monoxide poisoning at three-year follow up, Brit. Med. J., 1, 318–321, 1973. 231. Myers, R.A., Mitchell, J.T., and Cowley, R.A. Psychometric testing and carbon monoxide poisoning, Disaster Med., 1, 279–281, 1983. 232. Myers, R.A., Snyder, S.K., Linberg, S., et al. Value of hyperbaric oxygen in suspected carbon monoxide poisoning, JAMA, 246, 248, 1981. 233. Coric, V., Oren, D.A., Wolkenberg, A., and Kravitz, R.E. Carbon monoxide poisoning and treatment with hyperbaric oxygen in the subacute phase, J. Neurol. Neurosur. Ps., 65, 245, 1998. 234. Maeda, Y., Kawasaki, Y., Jibiki, I., Yamaguchi, N., Matsuda, H., and Hisada, K. Effect of therapy with oxygen under high pressure on regional cerebral blood flow in the interval form of carbon monoxide poisoning: observation from subtraction of Technetium-99m HMPAO SPECT brain imaging, Eur. Neurol., 31, 380, 1991. 235. Samuels, A.H., Vamos, M.J., and Taikato, M.R. Carbon monoxide, amnesia and hyperbaric oxygen therapy, Aust. NZ. J. Psychiat., 26, 316, 1992. 236. Heinrichs, R.W. Relationship between neuropsychological data and response to behavioral treatment in a case of carbon monoxide toxicity and dementia, Brain Cognition, 14, 213–219, 1990.

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17

The Case for the Use of Hyperbaric Oxygen Therapy in Carbon Monoxide Poisoning Christian Tomaszewski

CONTENTS 17.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17.2 Carbon Monoxide Effects at the Cellular Level . . . . . . . . . . . . . . . . . . . . . . . . . . . 17.2.1 HBOT Reverses the Cellular Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17.3 Clinical Efficacy of HBOT in Carbon Monoxide Poisoning . . . . . . . . . . . . . 17.3.1 Negative Trials . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17.3.2 Positive Trials . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17.4 Indications for HBO Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17.5 Delayed Administration of HBOT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17.6 Repeated Treatment with HBOT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17.7 Future Directions in Better Targeting HBO . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17.8 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

375 376 377 378 378 379 382 383 384 384 385 385

17.1 INTRODUCTION Carbon monoxide (CO) is a serious but complex poison. If one is lucky enough to survive the acute hypoxic event from avid binding of hemoglobin, the patient still has to contend with a potential of up to 40% chance of delayed and/or persistent neurological deficits.1–6 These effects can be debilitating including dementia, amnestic syndromes, parkinsonism, movement disorders, and cortical blindness.7–9 The problem is that patients may appear initially well, and following several days to weeks, develop delayed neurological sequelae (DNS).9 These problems can last for a year or longer.10 The main issues in treating CO poisoning is identifying those that are at risk for neurological sequelae and referring these patients to a treatment modality that will prevent such sequelae. These issues are important once the patient has reached the 375

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hospital, having been resuscitated and stabilized. Traditionally 100% oxygen was advocated as initial first aid to enhance removal of CO from hemoglobin and reverse any concomitant hypoxia. But starting in the 1960s, especially in the United States, hyperbaric oxygen therapy (HBOT) had started to be advocated for treating all such poisonings.11 Anywhere between 450 and 2500 HBO treatments are done for CO poisoning each year in the US alone.12,13 According to recent review articles, the weight of evidence does not appear to support the use of HBO for CO poisoning.14–17 But most of these critical review articles give equal weighting to all controlled studies. Almost all the studies failing to show benefit from HBO in CO poisoning have critical flaws in treatment regimen or follow-up. They also contradict consistent studies showing benefit in animal models, in which the pathophysiology for improvement is now being elucidated. All these studies, along with some recent randomized trails, suggest that a safe modality like HBO has the potential to offer hope in a poisoning with often unforeseen devastating neurological consequences.

17.2 CARBON MONOXIDE EFFECTS AT THE CELLULAR LEVEL The simplest explanation for the utility of HBO is that it accelerates the removal of CO from hemoglobin. Normally, the half-life of carboxyhemoglobin (COHb) with 100% oxygen averages 74–92 min, on the basis of three studies.6,18,19 With HBO, COHb half-lives are reduced to as low as 20 min.20,21 Should someone be hypoxic, HBO also increases dissolved oxygen by about ten times, sufficient to supply metabolic needs.22 But on entry into the HBO chamber, in Weaver’s trial of ill CO-poisoned patients, the mean COHb was less than 5%.6 So in most cases of CO poisoning, COHb clearance is not an issue because of aggressive treatment with normal pressure oxygen prior to ability to arrange HBO treatment. The consensus is that there must be an alternative mechanism for HBOT efficacy in CO poisoning. This is why the percentage of COHb does not always correlate with degree of acute toxicity and with eventual neurological outcome.2,10,23,24 Once a patient is stabilized, the real target organ of interest is the brain. CO is delivered intracellularly, where it can bind to heme proteins other than hemoglobin. At high levels, CO interferes with cellular respiration by binding to and inhibiting mitochondrial cytochrome oxidase.25 This is particularly exaggerated during episodes of hypoxia and hypotension. The inhibition of cellular respiration may contribute to the ischemic reperfusion that occurs in rat brains during CO poisoning ultimately leading to lipid peroxidation.26 These free radicals cause endothelial damage, which allows lymphocytes to attach and release proteases that promote more production of oxygen free radicals.27 The end result of this process is delayed central nervous system (CNS) damage that is accompanied by learning decrements. Part of the neuronal damage may also be mediated by excitatory amino acids.28,29 Glutamate binds to N-methyl-d-aspartate (NMDA) receptors causing intracellular calcium release, thus causing delayed neuronal cell loss. Accompanying this may

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be apoptosis.30,31 Some of the most sensitive areas for neuronal cell loss from these processes are the basal ganglia and hippocampus, resulting in impaired learning and memory.32 All these rodent studies demonstrate that CO is not a simple chemical asphyxiant. The CO molecule sets in a motion a cascade of cytochemical events that days later result in CNS cell loss. So in spite of COHb clearance from the bloodstream early on with normal pressure, or normobaric oxygen (NBO), HBO may still have an essential role in most cases of CO poisoning in preventing these delayed neurological events.

17.2.1 HBOT REVERSES THE CELLULAR EFFECTS HBO has been shown to reverse many of the biochemical effects of CO in the same rodent models that elucidated CO’s neurochemical and immune effects. First, HBO accelerates regeneration of inactivated cytochrome oxidase.25 This reduction in potential for oxidative stress is accompanied by prevention of lipid peroxidation. Rat models show a dose response effect from HBO, maximal at 3 atm. absolute (ATA), in decreasing the lipid peroxidation products in the brains of rats exposed to CO.26 The critical event that precedes lipid peroxidation is the vascular abnormalities that CO induces in cerebral endothelium. Adherence of neutrophils amplifies CO-mediated oxidative stress.27,33 The end result of this is necrosis and apoptosis of critical areas of the brain for learning and memory, particularly the hippocampus.28,30,34 HBOT is able to prevent neutrophil adherence to the brain microvascular endothelium, an essential step for amplification of CNS damage from CO.35 This blockage of lipid peroxidation prevents the precipitation of abnormalities in myelin basic proteins. Therefore, the CO-mediated oxidative stress that causes alteration in myelin basic protein and leads to immunologic effects is blocked by HBO.36 The final outcome is that HBO reduces mortality in rodent models of serious CO poisoning. This appears to be due to protection against cerebral edema. All control rats died in one study from cerebellar herniation as opposed to 100% survival in those that received HBO.38 The end result is that cognitive decrements from CO are prevented by HBO, as demonstrated in radial maze performance.36 The histological manifestation of this protection is lack of lesions in the globus pallidus and hippocampus in rats, which are seen after CO poisoning.32 One recent study does not support this, but there were issues with excessive toxicity from concomitant hypoxic stress.39 In conclusion, animal models show that the mechanism for CO toxicity is more than hypoxia. The poisoning initiates an immune cascade in the brain that includes changes in vascular endothelium, adherence of leukocytes, and lipid peroxidation. The end result of these events is neurological deficits in learning and memory. HBO, but not NBO, prevents all of these events, usually in a dose-related fashion. None of these mechanisms are related to the continued presence or clearance of COHb. This lends support to the use of HBO in symptomatic CO-poisoned patients once they have been stabilized regardless of the lack of remaining COHb. These patients are still at risk for delayed or persistent neuropsychological sequelae and therefore could benefit from HBO.

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17.3 CLINICAL EFFICACY OF HBOT IN CARBON MONOXIDE POISONING HBOT has been advocated as the treatment of choice for patients with significant CO exposures.11,40 However, clinical studies have not consistently demonstrated efficacy for HBO in preventing neurological damage from CO, as basic science studies discussed above suggest. Initially, interest in HBO for CO poisoning was fueled by uncontrolled human clinical series. In such studies, the incidence of persistent neuropsychiatric symptoms, including memory impairment, ranged from 12% to 43% in patients treated with 100% oxygen, and was as low as 0–4% in patients treated with HBO.4,5,40–42 Such early studies were obviously biased. So although HBO was advocated widely for CO poisoning, no randomized controlled trials (RCTs) existed to support such a stance.

17.3.1 NEGATIVE TRIALS The first truly randomized study in acutely poisoned CO patients did not come until 1989.2 The study failed to show the beneficial effect of HBO in over 300 patients. Patients who presented without loss of consciousness (LOC), n = 343, were randomized to one HBO session or 100% oxygen at room pressure by mask. Outcome criteria were not strict and were mainly based on questionnaire responses regarding symptoms. At 1 month, there was no difference in both groups with respect to self-reported neurological symptoms: 32% in the HBO group, 34% in the room pressure oxygen group. Another outcome, return to prior occupation, was 97% in both groups. Major flaws in this study, besides the lack of blinding and poor endpoints, were suboptimal HBO pressure used, 2.0 ATA, and almost half of the patients receiving HBO over 6 h from end of CO poisoning, which was a major delay.43 After the Raphael trial described above2 , a larger, double-blinded trial was hailed by many as conclusive proof that HBO was not useful in CO poisoning.44 This trial involved 191 patients who up to 24 h after poisoning were randomized to HBO (2.8 ATA maximum) versus sham HBO treatments. Patients were treated aggressively at a maximal pressure of 2.8 ATA. They received daily treatments for 3 days, and up to 6 additional daily sessions if they did not recover. HBO provided no benefit in this trial with the majority of each group having adverse neurological outcomes at 1 month: 74% in HBO-treated patients, and 68% in controls (reported odds ratio (OR) = 1.7; 95% confidence interval (CI) = 0.8–4.0; P = 0.19, not significant (NS)). The major flaw in this study was a mean delay of over 6 h to treatment with HBO. In addition 54% of the original subjects were lost to follow-up. Disproportionate numbers of suicide cases (about two-thirds) and drug toxicity (44%), with accompanying excessive neuropsychological defects, could have confounded any beneficial effect from HBOT. Other work shows that depression can contribute to poor neuropsychological testing.45 Because of these multiple flaws, it is not surprising that HBO failed to show any benefit in what was initially a well designed study. The most recent study showing no beneficial effect from HBO in CO poisoning is only available in abstract form.3 One hundred and seventy-nine patients that had transient LOC, but who were not comatose, were randomized to one session of HBO

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at 2 ATA versus 6 h of normal pressure oxygen. Outcome was self-assessed symptoms and blinded neurological examination at 1 month. Recovery was the same in both groups: HBO 46/79 (58%) versus control 45/74 (61%). As in Raphael’s previous study2 , lack of sufficient pressure, at 2.0 ATA, may have undermined the efficacy of HBO. There are consistent themes in the negative studies failing to show beneficial effects of HBO in CO. The first is delay in treatment. Animal studies show that the biochemical effects begin within hours after exposure to CO.36 The issue is whether delayed treatment can reverse this once it has started.43 The other problem is that treatment may have not been optimal. Three ATA is the pressure at which animal studies show the most benefits on tissue effects and neurological outcomes after CO poisonings.25,46,47 In fact, to prevent human neutrophil adherence, only marginal inhibition occurs at 2.0 ATA; 2.8 ATA gives almost complete inhibition.46 Other issues with these studies include poor outcome data due to both quality and quantity of follow-up.

17.3.2 POSITIVE TRIALS As the critics of HBO mounted, studies began to show the beneficial effects of HBO with CO poisoning. The first randomized positive study used mildly poisoned patients.1 Sixty-five patients without LOC were randomized to one session of HBO or 100% oxygen by face mask at room pressure. A decrease in any one of six neuropsychological tests immediately after poisoning versus at 4 weeks defined outcome. No patient [95% C.I. 0–12%] in the HBO group versus 23 [95% C.I. 10–42%] in the control group showed deterioration. Critics point out that the neurological deterioration was seen in only one test, Trail-Making; but neurological sequelae persisted for a mean of 41 days, and 10% of the controls had difficulties with daily activities. The success of this trial can be partially attributed to the adequate pressure used, maximum 2.8 ATA, and that all patients were treated within 6 h of discovery. A subsequent study by Mathieu et al.48 examined the efficacy of HBO at 2.5 ATA for 90 min versus NBO for 12 h. All patients had to be within 12 h of poisoning termination and noncomatose on presentation. At one and three months there was a lower incidence of persistent neurologic manifestations in the HBO group. This was significant at 3 months: HBO 9.5% versus NBO 15%, p < .02. This difference resolved over the following year. This study suffers from lack of detail and the fact that it is an interim analysis with no final analysis published. Regardless, early aggressive treatment, using pressures above 2.0 ATA, confirm the efficacy of HBO in CO poisoning. The landmark randomized control trial showing efficacy of HBO in CO poisoning differs from the other positive trials, in that all patients, including intubated cases (13%), were enrolled. Patients, n = 152, who presented with symptoms from acute CO poisoning were randomized to three sessions of HBO, with the first hour at 3.0 ATA, versus 100% oxygen at room pressure.6 Rather than looking at the absolute difference between the two groups on neurological testing, neurological sequelae were defined a priori. Aggregate performance on six neuropsychological tests at least one standard deviation below published norms, or an aggregate score greater than

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or equal to two standard deviations below expected, was defined as neurological sequelae. At 6 weeks, HBO caused an absolute reduction of 21% [95% C.I. 6–34%] in the proportion of neurological sequelae: 24% in the HBO group; 46% in control, which equates to a number needed to treat 5. At 1 year, there was still some benefit, albeit less, with an absolute reduction of 15% [95% C.I. 1–28%]. As stated earlier, the patients were seriously ill on presentation, with a mean initial COHb level of 25% and half having suffered LOC. Although patients could be entered up to 24 h post CO-poisoning, the mean time to treatment was less than 2 h. The combination of high pressure and early treatment probably contributed to the success of this trial. The main criticisms with Weaver’s study6 lie in the statistical definition of neurological sequelae.14 Although there were individual differences in the neuropsychological test of Trail-Making, there was no difference at 6 weeks in the parametric comparison of mean neuropsychological score. In addition, there was no difference in activities of daily living at 6 weeks and 12 months. In defense of the study and HBO, patients had decreased self-reported memory problems at 6 weeks (28% versus 51%), and the beneficial effect on cognitive sequelae lasted up to one year. Another criticism leveled on the Weaver study was that patients in the control group were more ill, with a higher incidence of cerebellar dysfunction on presentation, which ended up being a predictor for cognitive sequelae.17 But, when doing a logistic regression to adjust for this incidental finding, HBO was still protective (OR=0.45, 95% C.I. 0.22–0.92).6 In conclusion, Weaver’s study appears methodologically sound, especially when considering that outcome measures were determined a priori and the fact that the trial was double-blinded including sham HBO treatments in the control group. The Cochrane Review recently examined all six controlled studies published as of 2006 that examined the effect of HBO versus NBO in CO poisoning.15 (Table 17.1). The common outcome was the presence of neurological symptoms or signs at time of primary analysis 4–6 weeks postpoisoning. With a collective 1335 participants, the incidence of persistent signs and symptoms was 29% (202/691) in the HBOT group versus 34% (219/444) in the normobaric group. The overall odds ratio favored HBO at 0.78 [95% C.I. 0.54–1.12]. Because of the lack of statistical significance their conclusion was that existing trials do not support use of HBO in CO-poisoned patients in order to reduce neurological sequelae. Similarly, the American College of Emergency Physicians, on the basis of the same data, formulated a similar conclusion in their 2007 Clinical Policy for the management of acute CO poisoning.49 They concluded that although HBO should not be mandated for CO poisoning, it “remains a therapeutic option to potentially reduce the incidence of neurological sequelae.” The consensus among all these expert reviews is that further RCTs are needed, particularly with regard to identifying which CO-poisoned patients are most likely to benefit from HBO. Using the same studies, the Underwater and Hyperbaric Medical Society recommends HBO treatment for any CO-poisoned patients with signs of serious intoxication.11 With little risk,50 almost 1500 patients are treated with HBO for CO poisoning in the United States each year.51 The main risk with HBO is related to barotraumas such as tympanic perforation.6 Less likely, and not usually associated with

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HBO 2 h vs. 100% NBO until asymptomatic HBO 1 h (min × 3) vs. NBO 100 min HBO 2 h (×3) vs. NBO 2 h (×1)

Thom 19951

2.0 ATA

3.0 ATA

2.8 ATA

2.8 ATA

2.0 ATA

2.5 ATA

Maximum HBO Pressure

∗ Odds ratio less than 1.00 favors treatment with HBO.

Raphael 20043

Weaver 20026

HBO at 2.0 ATA 60 min vs. 6 h NBO

HBO 2.0 h vs. 6 h NBO

Raphael 19892

Scheinkestel 199944

HBO 90 min vs. 12 h NBO

Design

Mathieu 199648

Study

< 12 h

Mean 5.6 h

Mean 7.1 h

Mean 2.0 h

Mean 7.1 h

<12 h

Time To RX

33/79 (42%)

19/76 (25%)

30/48 (63%)

0/30 (0%)

51/159 (32%)

69/299 (23%)

Treatment

29/74 (39%)

35/76 (46%)

25/40 (63%)

7/30 (23%)

50/148 (34%)

73/276 (26%)

Control

TABLE 17.1 Patients with Signs or Symptoms at 4–6 Weeks Post Carbon Monoxide Poisoning

1.11(0.58– 2.12)

0.39(0.20– 0.78)

1.00(0.42– 2.38)

0.05(0.00– 0.95)

0.93(0.57– 1.49)

0.83(0.57– 1.22)

Odds Ratio∗

No difference in overall neuropsychological scores or daily activities Abstract. Subgroup data on transient loss of consciousness group

69% attempted suicide, 56% lost to follow up

Abstract. Excluded coma. 3 months outcome favorable for treatment: 9.5 vs. 15% (P = 0.016) Subjective outcome. Subgroup data on transient loss of consciousness group. No patient with LOC entered

Comment

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any demonstrable neuronal damage, are oxygen induced seizures.40,52 On the basis that at least three randomized trials that used early and adequate pressure demonstrated a benefit for HBO, and the fact that it is a relatively safe modality, it is surprising that the consensus of opinion is not stronger in support of HBO for serious CO poisoning.

17.4 INDICATIONS FOR HBO THERAPY The Cochrane review pointed out that studies are needed with regard to the particular role of HBO in CO poisoning.15 Although specific indications for HBO after acute CO poisoning are widely published (Table 17.2), none have been prospectively evaluated.11,53 The patients with the most to gain from this procedure are those with the greatest potential for persistent or DNS. Traditionally COHb levels have been advocated, with specific cut offs, for deciding if HBO is needed.53 However, COHb levels do not correlate with clinical findings acutely nor with final outcome.10,40,54–56 The target organ, once a patient has been resuscitated and stabilized, at the time at which one would consider HBO, is no longer the blood but the CNS. A single COHb level does not describe the actual area under the dosage curve, which more likely represents the true degree of poisoning. Before all the intricacies in the cellular action of CO were known, many authors advocated treating all patients with COHb levels of 40% or greater with HBOT. Many HBO centers arbitrarily use a more conservative level of 25% as an indication for HBO. In Weaver’s recent trial, post hoc analysis predicted that patients with COHb levels greater than 25% were one of the subgroups to benefit most from HBO.57,58 However, other studies suggest that no absolute COHb level on presentation has been found to be necessarily predictive of outcome, and therefore, the need for HBO.2,10,24 Another traditional marker for serious CO poisoning, and therefore the need for HBO, has been syncope, or LOC.59 This may represent the episode of hypotension that is necessary for causing neuronal damage from CO-induced ischemic-reperfusion

TABLE 17.2 Suggested Indications for Hyperbaric Oxygen Therapy After Carbon Monoxide Poisoning • Syncope (loss of consciousness) • Coma • Seizure • Persistent altered mental status (GCS < 15) or confusion • Abnormal cerebellar examination • Carboxyhemoglobin level > 25% (Adapted from Tomaszewski, C., Goldfrank’s Toxicologic Emergencies, Goldfrank, L.R., Flomenbaum, N.E., Hoffman, R.S., Howland, M.A., Lewin. N,A., Nelson, L.S (Eds), McGraw-Hill, New York, 2006.)

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injury in animal models.60,61 However, syncope is not entirely predictive for cognitive sequelae.6 Patients with long exposures, or “soaking” periods, are also at greater risk for neurological sequelae.62,63 Animal models and human cases suggest that “soaking,” that is, prolonged exposure to high levels of CO, is a factor that actually predicts final neurological outcome, rather than any particular COHb level.64,65 The presence of a significant metabolic acidosis may be a surrogate marker for this. A base excess lower that −2 mmol/L was an independent predictor for cognitive sequelae and the potential for benefit from HBO in Weaver’s study.6,58 Other studies confirm the utility of metabolic acidosis as a predictor of HBO requirement.10,66,67 It is still unclear if mild neurological symptoms (e.g., confusion, headache, dizziness, visual blurring) or abnormal mental status testing on initial presentation after CO poisoning is prognostic for cognitive sequelae. These symptoms simply represent CO poisoning, which, at COHb levels approaching 10% in volunteers, can cause temporary impairment of learning and memory.68 To date, neuropsychological screening tests have not been found to be reliable indicators of the need for HBO because they do not consistently predict neurological sequelae.1 In a recent prospective clinical trail of CO poisoning, the incidence of cerebellar dysfunction portended a higher incidence of cognitive sequelae (odds ratio 5.7 [95% C.I. 1.7–19.3]).6 Therefore, difficulty with finger-to-nose, heel-to-shin, rapid alternating hand movements, or even ataxia, should all be considered indications for HBO. Some authors recommend selective use of HBO because of cost and difficulties in transport if the primary facility lacks a chamber.69 However, complications that may make such transfers and treatment unsafe are rare.50 Although HBO cannot be recommended for every patient with CO poisoning, it is a relatively safe treatment that should be considered in all serious exposures. Post hoc analysis of Weaver’s data showed that the patients most likely to benefit were those who presented with a base deficit greater than 2 mmol/L, unconsciousness, age ≥50 years, and COHb level greater than 25%.6,70 Therefore, most clinicians refer any CO-poisoned patient with any of these criteria for HBO (Table 17.2). One group of patients who could probably be excluded from HBOT are those who have had a cardiac arrest from CO; these cases have been universally fatal.71

17.5 DELAYED ADMINISTRATION OF HBOT The optimal timing of HBO treatment for CO poisoning is unclear. Patients treated later than 6 h after exposure tend to have worse outcomes in terms of delayed sequelae (30% versus 19%) and mortality (30% versus 14%).72 Randomized trials with longer times to treatment have generally failed to show benefit from HBO.73 In the recent randomized trial showing beneficial effects from HBO, with a number needed to treat of 5 in order to prevent one case of neurological sequelae, patients were entered into treatment up to 24 h post-poisoning.6 In fact 38% of the patients were treated later than 6 h. Studies purporting beneficial effects much later are anecdotal and lack controls.4 Therefore, at this time it seems reasonable to attempt treatment up to 24 h post-exposure.

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17.6 REPEATED TREATMENT WITH HBOT Repeated HBO treatments have been advocated for patients that do not initially improve from CO poisoning, particularly those in coma.74 In the recent randomized study showing beneficial effects from HBO, all patients received three HBO treatments within 24 h of presentation.6 A retrospective review of records on patients who received two versus one treatment showed a reduction in DNS from 555 to 18%.75 Prospective studies comparing single versus multiple courses of HBOT have failed to confirm any benefit from repeated HBO treatment.2,3 Therefore, multiple HBO treatments cannot be recommended at this time. The most recent clinical guidelines from the Underwater and Hyperbaric Society state that the optimal number of HBO treatments for CO poisoning is unknown, reserving multiple treatments for patients who fail to recover after the initial treatment.11

17.7 FUTURE DIRECTIONS IN BETTER TARGETING HBO A search has been made for plasma markers for CO exposure that predict degree of toxicity and therefore, perhaps, the potential for neurological sequelae and the need for HBO. Many plasma markers of oxidative stress, such as glutathione release from erythrocytes, increase within hours of CO poisoning.76 Multiple peripheral vascular cells have been implicated in CO poisoning: erythrocytes, platelets, leukocytes, and endothelial cells.27,46,77 They actually appear to mirror what is going on in the target organ of concern, the CNS.78,79 One recent study showed that CO exposure in rats resulted in a 50% decrease in cyclic guanosine monophosphate (GMP) activity, as measured in leukocytes, that started at 24 h post-exposure.80 No human series of plasma markers are available to show if they are predictive of final outcome and therefore a potential need for HBOT. Plasma markers are still only surrogates for the real target organ of CO poisoning, the brain. S100B is a neurobiochemical marker of brain damage. It is found in astroglial cells and is released into the blood with brain injury. Rat studies show that it is elevated after severe CO poisoning and is a better predictor of death than level of consciousness.81 In patients presenting with Glasgow Coma Scores (GCS) of less than eight after CO poisoning, but who did not experience LOC, immediate blood samples show elevated peripheral blood levels of SB100B.82 HBO prevents this rise in SB100B when given immediately after CO poisoning in rats.83 A recent clinical study, however, showed no increase in S100B levels after CO poisoning.84 Therefore, it is unclear if SB100B can be used as a consistent marker of CO poisoning and the need for HBO. As an alternative to serum markers, various types of neurological imaging are available that show early changes from CO poisoning. Except for xenon enhancement, computed tomography does not show early changes from CO.85 More sensitive is Magnetic Resonance Imaging (MRI), which can show changes within the first day post-exposure.86 Diffusion-weighted is even more sensitive, detecting changes in subcortical white matter within hours of CO poisoning.87 However, MRI changes have not been shown to correlate with eventual outcome.57,87

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A more sensitive radio imaging modality is single-photon emission computed tomography (SPECT), which gauges regional blood flow noninvasively. It shows perfusion changes within watershed regions that are associated with delayed neuropsychological impairment months after CO poisoning.88,89 With HBO, an improvement in oxygen extraction of the frontal and temporal cortices was demonstrated on positron emission tomography (PET) scan.90 Because of practicality considerations, along with lack of prospective data, no neurological imaging technique can be advocated at this time to predict who needs HBO treatment.

17.8 SUMMARY HBOT may originally have been a “therapy in search of a disease” with respect to CO poisoning. But now several controlled studies show early benefits in preventing cognitive sequelae from CO poisoning. Although these studies are not perfect, the alternative negative clinical controlled studies suffer from serious flaws. In addition, the positive clinical results corroborate the findings of animal studies that show that HBO can prevent the cascade of neurochemical events that occur during recovery from acute poisoning. The biggest challenge though will be to decide who can really benefit from this therapy. To date, there is no consistent marker to predict who will suffer DNS and therefore, who has the most to gain. Until more studies are available confirming HBO’s utility, and owing to the inherent delay with such, we probably should not be subjecting patients to extraordinary transports to receive such therapy. But based on the safety of the procedure, and relative low resource utilization, there is no reason not to at least attempt one HBO treatment in any seriously ill CO-poisoned patients.

References 1. Thom, S.R., and Taber, R.L., Mendiguren II et al. Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Ann. Emerg. Med. 25, 474–480, 1995. 2. Raphael, J.C., Elkharrat, D., Jars-Guincestre, M-C et al. Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet 2, 414–419, 1989. 3. Raphael, J.C., Chevret, S., Driheme, A., and Annane, D. Managing carbon monoxide poisoning with hyperbaric oxygen. J. Toxicol. Clin. Toxicol. 42, 455–456. 2004. (Abstract) 4. Myers, R.A.M., Snyder, S.K., and Emhoff, T.A. Subacute sequelae of carbon monoxide poisoning. Ann. Emerg. Med. 14, 1167, 1985. 5. Mathieu, D., Nolf, M., and Durocher, A. Acute carbon monoxide poisoning: risk of late sequelae and treatment by hyperbaric oxygen. J. Toxicol. Clin. Toxicol. 23, 315–324, 1985. 6. Weaver, L.K., Hopkins, R.O., Chan, K.J et al. Hyperbaric oxygen for acute carbon monoxide poisoning. NEJM 347, 1057–1067, 2002. 7. Lee, M.S., and Marsden, C.D. Neurological sequelae following carbon monoxide poisoning: clinical course and outcome according to the clinical types and brain computed tomography scan findings. Movement Disorders 9, 550–558, 1996.

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Carbon Monoxide Poisoning 8. Ginsberg, M.D. Carbon monoxide intoxication: clinical features, neuropathology, and mechanisms of injury. J. Toxicol. - Clin. Toxicol. 23, 281–288, 1985. 9. Choi, I.S. Delayed Neurological Sequelae in Carbon Monoxide Intoxication. Arch. Neurol. 40, 433–435, 1983. 10. Sokal, J.A., and Kraldowska, E. The relationship between exposure duration, carboxyhemoglobin, blood glucose, pyruvate and lactate and the severity of intoxication in 39 cases of acute carbon monoxide poisoning in man. Arch. Toxicol. 57, 196–199, 1985. 11. Thom, S.R., and Weaver, L.K. Carbon monoxide poisoning, Hyperbaric Oxygen 2003 Indications and Results: The Hyperbaric Oxygen Therapy Committee Report, Feldmeier, J.J., Ed, Chap 2. Dunkirk, M.D., Undersea Hyperb. Med. Soc., 2003, pp. 11–17. 12. Hampson, N., Dunford, R.G, Kramer, C.C et al. Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. J. Emerg. Med. 13, 227–231, 1995. 13. Watson, W.A., Litovitz, T.L., Rodgers, G.C et al. 2004 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am. J. Emerg. Med. 23, 589–666, 2005. 14. Buckley, N.A., Isbister, G.K., Stokes, B et al. Hyperbaric oxygen for carbon monoxide poisoning: a systematic review and critical analysis of the evidence. Toxicol. Rev. 24, 75–92, 2005. 15. Juurlink, D.N., Buckley, N.A., Stanbrook, M.B., Isbister, G.K., Bennett, M., and McGuigan, M.A. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database of Systemic Reviews 4(2), CD002041, 2006. (Abstract) 16. Silver, S., Smith, C., and Worster, A. Should hyperbaric oxygen be used for carbon monoxide poisoning? Can. J. Emerg. Med. 8, 43–46, 2006. 17. Judge, B.S., and Brown, M.D. To dive or not to dive? Use of hyperbaric oxygen therapy to prevent neurological sequelae in patients acutely poisoned with carbon monoxide. Ann. Emerg. Med. 46, 462–464, 2005. 18. Levasseur, L., Galliot-Guilley, M., Richter, F et al. Effects of mode of inhalation of carbon monoxide and of normobaric oxygen administration on carbon monoxide elimination from the blood. Hum. Exp. Toxicol. 15, 898–903, 1996. 19. Weaver, L.K., Howe, S., Hopkins, R et al. Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure. Chest 117, 801–808, 2000. 20. Myers, R.A., Jones, D.W., and Britten, J.S. Carbon monoxide half-life study, In: Proceedings of the 9th International Congress on Hyperbaric Medicine, Kindwall, E.P., Ed, Flagstaff, AZ, Best Publishing, 1987, pp. 263–266. 21. Sasaki, T. On half-clearance of carbon monoxide hemoglobin in blood during hyperbaric oxygen therapy. Bull. Tokyo Med. Dent. Univ. 22, 63–77, 1975. 22. Boerema, I., Meyne, I., Brummelkamp, W.H et al. Life without blood. Arch. Chir. Neer. 11, 70–83, 1959. 23. Seger, D., and Welch, L. Carbon monoxide controversies: neuropsychologic testing, mechanism of toxicity, and hyperbaric oxygen. Ann. Emerg. Med. 24, 242–248, 1994. 24. Myers, R.A.M., and Britten, J.S. Are arterial blood gases of value in treatment decisions for carbon monoxide poisoning? Crit. Care. Med. 17, 139–142, 1989. 25. Brown, S.D., and Piantodosi, C.A. Recovery of energy metabolism in rat brain after carbon monoxide hypoxia. J. Clin. Invest. 89, 666–672, 1991. 26. Thom, S.R. Antagonism of carbon monoxide-mediated brain lipid peroxidation by hyperbaric oxygen. Toxicol. Appl. Pharmacol. 105, 340–344, 1990.

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27. Thom, S.R. Leukocytes in carbon monoxide-mediated brain oxidative injury. Toxicol. Appl. Pharmacol. 123, 234–247, 1993. 28. Ishimaru, H., Katoh, A., Suzuki, H et al. Effects of N-methyl-D-aspartate receptor antagonists on carbon monoxide-induced brain damage in mice. J. Pharmacol. Exp. Ther. 261, 349–352, 1992. 29. Thom, S.R., Fisher, D., Zhang, J et al. Neuronal nitric oxide synthase and N-methyl-Daspartate neurons in experimental carbon monoxide poisoning. Tox. Appl. Pharmacol. 194, 280–295, 2004. 30. Piantadosi, C.A, Zhang, J., Levin, E.D et al. Apoptosis and delayed neuronal damage after carbon monoxide poisoning in the rat. Exper. Neurology 147, 103–114, 1997. 31. Thom, S.R., Fisher, D., Xu, Y.A et al. Adaptive responses and apoptosis in endothelial cells exposed to carbon monoxide. Proc. Natl. Acad. Sci., USA 97, 1305–1310, 2000. 32. Thom, S.R. Learning dysfunction and metabolic defects in globus pallidus and hippocampus after CO poisoning in a rat model. Undersea Hyperb. Med. 23 (Suppl.), 20. 1997. (Abstract) 33. Ischiropoulos, H., Beers, M.F., Ohnishi, S.T et al. Nitric oxide and perivascular tyrosine nitration following carbon monoxide poisoning in the rat. J. Clin. Invest. 97, 2260–2267, 1997. 34. Nabeshima, T., Katoh, A., Ishimaru, H et al. Carbon monoxide-induces delayed amnesia, delayed neuronal Death and change in acetylcholine concentrations in mice. J. Pharmacol. Exp. Ther. 256, 378–384, 1991. 35. Thom, S.R. Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. Toxicol. Appl. Pharmacol. 123, 248–256, 1993. 36. Thom, S.R., Bhopale, V.M., and Fisher, D. Hyperbaric oxygen reduces delayed immune-mediated neuropathology in experimental carbon monoxide toxicity. Tox. Appl. Pharmacol. 213, 152–159, 2006. 37. Jiang, J., and Tyssebotn, I. Normobaric and hyperbaric treatment of acute carbon monoxide poisoning in rats. Undersea Hyperb. Med. 24, 107–116, 1997. 38. Jiang, J., and Tyssebotn, I. Cerebrospinal fluid pressure changes after acute carbon monoxide poisoning and therapeutic effects of normobaric and hyperbaric oxygen in conscious rats. Undersea Hyperb. Med. 24, 245–254, 1997. 39. Gilmer, B., Kilkenny, J., Tomaszewski, C et al. Hyperbaric oxygen does not prevent neurologic sequelae after carbon monoxide poisoning. Acad. Emerg. Med. 9, 1–8, 2002. 40. Norkool, D.M., and Kirkpatrick, J.N. Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: a review of 115 cases. Ann. Emerg. Med. 14, 1168–1171, 1985. 41. Goulon, M., Barios, A., Raphin, M et al. Carbon monoxide poisoning and acute anoxia due to breathing coal gas and hydrocarbons. Ann. Med. Intern. 120, 335–349, 1969. 42. Smith, G.I., and Sharp, G.R. Treatment of carbon monoxide poisoning with oxygen under pressure. Lancet 2, 905–906, 1960. 43. Brown, S.D., and Piantadosi, C.A. Hyperbaric oxygen for carbon monoxide poisoning. Lancet 2, 1032, 1989. 44. Scheinkestel, C.D., Bailey, M., Myles, P.S et al. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. Med. J. Aust. 170, 203–210, 1999.

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Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning: Useful Therapy or Unfulfilled Promise? Carlos D. Scheinkestel and Ian L. Millar

CONTENTS 18.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18.2 Hyperbaric Oxygen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18.2.1 Hyperbaric Oxygen Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18.2.2 Basic Science Overview in Use of Hyperbaric Oxygen . . . . . . . . . . 18.2.3 HBO for Carbon Monoxide Poisoning: Human Evidence. . . . . . . . 18.2.3.1 “Trial of Normobaric and Hyperbaric Oxygen for Acute Carbon Monoxide Intoxication” by Raphael . . . . 18.2.3.2 “Non-Comatose Patients with Acute Carbon Monoxide Poisoning: Hyperbaric or Normobaric Oxygenation?” By Ducasse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18.2.3.3 “Delayed Neuropsychologic Sequelae after Carbon Monoxide Poisoning: Prevention by Treatment With Hyperbaric Oxygen” by Thom . . . . . . . . . . . . . . . . . . . . . . . . . . 18.2.3.4 “Randomized Prospective Study Comparing the Effect of HBO Versus 12 h NBO in Noncomatose CO Poisoned Patients: Results of the Interim Analysis” by Mathieu . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18.2.3.5 “Managing Carbon Monoxide Poisoning with Hyperbaric Oxygen” by Raphael . . . . . . . . . . . . . . . . . . . . . . . . 18.2.3.6 “Hyperbaric or Normobaric Oxygen for Acute Carbon Monoxide Poisoning: a Randomised Controlled Clinical Trial” by Scheinkestel . . . . . . . . . . . . . . . . . . . . . . . . . . 18.2.3.7 “Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning” by Weaver . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18.3 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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18.4 Where to Now? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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18.1 INTRODUCTION Superficial consideration suggests that hyperbaric oxygen (HBO) should be the optimal antidote for acute carbon monoxide (CO) poisoning. It is a well-established form of therapy, albeit with a limited distribution of facilities, and the side-effect and complication profile is well established, manageable and rarely associated with longterm sequelae. By generating the highest tolerable intravascular partial pressure of oxygen, HBO provides the most rapid means available of simultaneously reversing cellular hypoxia and accelerating the elimination of CO, not only from its binding with hemoglobin, but also from intracellular binding sites. Human clinical use of HBO for this purpose appears to have first occurred in 19421 and was proposed again by Pace in the publication “Acceleration of CO elimination in man by high pressure oxygen” in 1950. This US Navy study measured acceleration of elimination of CO in volunteers treated with 2.5 atmospheres absolute (ATA) pressure oxygen after a brief loading exposure with CO, producing carboxyhemoglobin (COHb) in the range of 20–30% 2 . CO poisoning subsequently became established as one of the principal indications for HBO therapy (HBOT) as clinical use of HBO grew in the 1960s. Acute CO poisoning has subsequently been listed as an indication for HBO in the guidelines produced by multiple international hyperbaric medicine societies. Despite this, HBO has failed to become the standard of care for CO poisoning. For instance, in the US northwest, it was estimated in 1994 that only 6.9% of CO poisoning patients presenting to emergency departments received HBO.3 The historical reasons for this were probably related to the limited availability of hyperbaric chambers, limited awareness of this form of therapy, a reluctance to expose patients to the hazards of transfer for treatment, as well as a degree of general scepticism regarding the therapy. In recent times, clinical trial results and debate surrounding these have questioned the effectiveness of HBO in producing significant improvements in outcome. In the US, the number of CO-poisoned patients treated with HBO has remained relatively constant since 1992 at about 1500 per annum4 despite a more than doubling of hyperbaric facilities in that time. The lack of increase in patients treated in this environment may be a result of increasing doubt as to the effectiveness of HBOT, although any change in usage must be interpreted in the light of changes to the rates of poisoning. In the US, survey results and toxicology service data indicate that while the CO related death rate has fallen, nonfatal CO emergency calls have remained relatively stable. This correlates with the situation regarding HBO use.4 In Australia, by contrast, the number of CO poisoning patients treated by hyperbaric units fell from 240 per annum to 60 over the last 10 years. In Australia the most common cause of CO poisoning has been automobile exhaust suicide attempt. The incidence of this has fallen in association with depression recognition, suicide prevention campaigns and the reduction in CO production mandated for newer model vehicles.5,6 At the same

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time, it is likely that public health measures have reduced occupational and domestic exposures. The decline in CO poisoning numbers treated with HBO may thus be as much a result of reduced incidence of poisoning as it is of reduced provision of treatment arising from implementation of evidence from clinical trials. Meanwhile, our understanding of the biology, pharmacology, and toxicology of both CO and HBO has become much more complex, and it is clear that both these low molecular weight gases (i.e., CO and oxygen) are two edged swords—essential elements of normal physiology but toxic at higher doses, and thus potentially useful therapeutically yet capable of harm at doses which overlap with those required for therapeutic effect.7−13 Alongside the sometime impassioned debate about interpretation of clinical trials, there is thus a fascinating and rapidly evolving stream of basic science research which will hopefully soon deliver us a better basis for designing future clinical trials aimed at answering the question of whether HBO has a place in the routine treatment of CO poisoning, and if so, in what clinical settings, and at what dose.

18.2 HYPERBARIC OXYGEN HBO provides a means of elevating oxygen concentration in the body to the maximum tolerable, in order to seek therapeutic effects not achievable with administration of oxygen in the normal ward environment, with its 1 ATA pressure at sea level, or less at altitude. Hyperbaric chambers are used to expose patients to pressures that are normally 2–3 times atmospheric, that is, 2–3 ATA. Combined with 100% inspired oxygen breathing, this can deliver arterial partial pressures as high as 15–20 times normal. As a result, not only is the volume of oxygen delivered to tissues increased but more importantly, intracellular partial pressures of oxygen increase well beyond normal, providing potentially useful effects both directly and by inducing a response to the oxidant stress generated. The technology for providing HBOT is well established. Pressure vessels for human occupancy have been built for clinical use for over 150 years, although the early proponents of HBOT mostly believed that it was pressure that was therapeutic and increased levels of oxygen were not used, limiting the therapeutic effects possible. During the 1930s, Cunningham used an air pressurized hyperbaric chamber for patients with severe acute respiratory disease, probably maintaining life through a crisis period by effectively increasing the partial pressure of oxygen available to patients, albeit in a much more complicated fashion than achievable now via administration of facemask (normobaric) oxygen (NBO) therapy. The clinical combination of increased oxygen with increased pressure was first promoted in the 1950s as a means of increasing the time window for cardiovascular surgery requiring circulatory arrest and in the 1960s a significant number of large hyperbaric chambers were constructed in hospitals around the world. Many of these are still in use today although surgery is now rarely performed under pressure. These operating theater chambers and smaller chambers evolved from commercial diving industry recompression chambers. They have been the basis for the development of the modern “multiplace” chamber. Over a similar period, single person, oxygen filled

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“monoplace” chambers have evolved as an alternative, originally used to enable coadministration of HBO and radiotherapy, but now widely used for both hospitalized and ambulatory patients. Ideally, hyperbaric facilities should be located inside the building structure of a hospital, close to relevant patient care areas to minimize transport difficulties, and they should have good critical care support. The most versatile multiplace chambers have multiple compartments, are quiet and well lit, have doors that will readily admit a trolley or even better a full sized patient bed and have a floor level matching that of the surrounding building. In recent years, a number of manufacturers have provided rectangular chambers that have further advanced the aim of making hyperbaric chambers as close to a normal clinical room as possible. Multiplace chambers are pressurized with air to minimize fire risk and cost. Oxygen must be administered to patients via a mask or hood, or in the case of intubated patients, via a suitable ventilator. In most cases a hyperbaric nurse, doctor or paramedic attends patients undergoing treatment which typically lasts from 1.5 to 2 h overall. Although there are safety and functional limitations on what equipment can be used inside a chamber, most major hospital facilities can provide intensive care including positive pressure ventilation, arterial pressure monitoring, and inotrope infusion. There are many variations in chamber size and configuration but the predominant alternative type of chamber in use is the single person, horizontal acrylic cylinder style monoplace chamber. These are much smaller, cheaper, and easier to install than properly designed clinical multiplace chambers and are thus in widespread use in many parts of the world, especially in facilities that concentrate on using HBO for problem wound cases and the late side effects of radiotherapy. While most hyperbaric centers with a routinely used critical care capability have multiplace chambers, monoplace chambers can be used for critical care patients by experienced teams.14

18.2.1 HYPERBARIC OXYGEN EFFECTS HBO provides it’s effects via multiple mechanisms. These can be grouped into those related to gas dynamics, to restoration of function by normalization of oxygenation and those that are a therapeutic result of the oxidative challenge achieved by very high pO2 . Some, such as elimination of gas bubbles and those underlying HBO’s anti-infective and wound healing promotion effects, are probably not directly relevant to CO poisoning. It is interesting to note, however, that in many cases, effects previously thought to be brought about merely by reversing hypoxia are now understood to result from HBO triggering intracellular signaling via various oxidative and nitric oxide related biochemistry.15−18 Other mechanisms of HBO that would seem to have particular potential in CO poisoning include accelerating elimination of CO,2,19 reversing cellular hypoxia,19,20 reducing edema,21−25 up-regulating antioxidant systems,26,27 inhibiting reperfusion injury18,28 and possibly modulating other elements of the secondary injury cascade.29,30 Some models show reduced cellular necrosis and apoptosis,31−37 although the mechanisms for these effects are still emerging.

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A key element of HBO therapeutics is that hyperbaric sessions are of limited duration—usually a maximum of around 2 h. The limited duration and intermittent nature of HBO is an essential factor in the safety profile of this therapy. Pulmonary, optic, and central nervous system (CNS) toxicity are well recognized complications of excess exposure to oxygen at pressure and the threshold of toxicity overlaps with the therapeutic dose range.38,39 Of particular interest is acute CNS oxygen toxicity, manifested most frequently by short duration loss of consciousness (LOC) and tonicclonic seizure activity which self-terminates as toxic levels of oxygen fall in the temporary absence of respiration. The incidence of acute CNS oxygen toxicity can be very low in comparatively well, ambulatory patients, with Yildiz40 reporting only two cases in 80,000 treatments,40 although most recent author’s estimates are in the order of 3/10,000.39,41 The incidence rises significantly with higher pressure treatments and results of this are seen in the treatment of acute patients such as those suffering decompression illness.42 In CO poisoning patients suffering neurological injury, the rate of acute CNS toxicity can be significant,43 with Sloan38 reporting a 5% incidence in 297 patients seen over 10 years.38 As applies to CO poisoning, the rapidly evolving field of free-radical and oxidant/antioxidant research has major implications for our understanding of the therapeutic and toxic effects of HBO. Some years ago, there were significant concerns that short-term benefits seen with HBO might be associated with at least some burden of oxidative stress related problems such as acceleration of cardiovascular disease or even premature aging. Reassuringly, the balance of findings to date suggests that although HBO is an oxidative stressor, it up-regulates antioxidant systems sufficiently to avoid significant net damage or even, in some cases, to provide a paradoxical and beneficial net antioxidant effect. An important caution must remain, however, that the net result of HBO probably depends upon the physiology of the host receiving HBO. Without adequate nutritional substrates for antioxidant production, when faced with excessive total oxidative stress or when specific processes are in train such as lipid peroxidation, HBO might well exacerbate the problem rather than ameliorate it, at least in some doses or at some time points.

18.2.2 BASIC SCIENCE OVERVIEW IN USE OF HYPERBARIC OXYGEN The history of using HBO for CO poisoning is sometimes claimed to date back to Haldane’s classic 1895 paper: “The relation of the action of carbonic oxide to oxygen tension”.44 This paper in fact demonstrates that, in a mouse model, the high levels of oxygen achievable in the hyperbaric environment can make normally lethal levels of CO exposure tolerable without mortality. Confusing this demonstration of the competitive inhibition of CO uptake with the therapeutic use of HBO after CO poisoning underscores one of the major challenges to date in trying to draw clinically useful conclusions from animal studies. Most human CO poisoning patients experience a delay of many hours between the termination of CO poisoning and the start of HBO, while most animal researchers have initiated HBO soon after termination of CO exposure, and often immediately. The effectiveness of HBO and indeed the entire basis for interaction between HBO and CO poisoning pathology are likely to

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be very different at different time points after exposure: from the acute rescue and resuscitation phase, through the period when it may be possible to prevent secondary injury, to modulating established secondary injury processes, attempting to prevent delayed neurological sequelae (DNS) and even using HBO to accelerate recovery or for delayed treatment for established residuae. Although there is some debate regarding the degree to which the acute manifestations of CO poisoning are mediated by a shortfall in intracellular oxygen availability, there is no doubt that hypoxia is a significant factor, at least in severe cases.45,46 . It may be that the level of hypoxia that is critical for any particular individual’s physiology is a key determinant of susceptibility to toxicity at any given level of CO exposure. The elderly, collapsed patients and those affected by certain drugs and co-toxins will have limited capacity for compensatory cardiac output and cerebral blood flow increase as the oxygen carrying-capacity of blood falls. This may underlie the susceptibility of these populations to CO poisoning. High altitude (hypoxic/hypoxia) exposure increases the toxicity of CO.47−52 HBO dissolves sufficient oxygen in plasma to meet physiological demands, meaning that oxygen can be immediately delivered to cells despite the presence of high COHb levels. Clinically this can be demonstrated by resolution of abnormal electrocardiogram (ECG) activity and rapid recovery of consciousness, which are sometimes but not always seen when HBO is used for CO poisoning. HBO also reduces COHb levels much more rapidly than can be achieved by NBO. Although there are interindividual and inter-study differences in actual numbers reported, the human half-life reduction is in the order of 4.5 h on air, to 90 min on 100% oxygen, to 20 min with HBO at 2.5–3 ATA.53 In the patient with significant cellular hypoxia resulting from CO poisoning, HBO can therefore expedite resolution of this problem and this would be expected to not only provide immediate benefit but to reduce the risk of ongoing hypoxia compounding existing injury. Because the uptake of CO within cells is slower than the association of CO with hemoglobin, it could be hoped that early HBO might prevent the onset of cellular toxicity.46 HBO will also speed the dissociation of CO from intracellular sites, although the proportional acceleration is different for different biochemical processes and varies with species studied. All of this would seem to provide a case for the immediate use of HBO for CO poisoning where this is can be made available. Some high risk industrial site and paramedic rescue systems have been established using portable hyperbaric chambers for this purpose.54,55 Whether very early HBO actually produces more survivors and better outcomes than NBO has not been definitively established, given that all major clinical trials to date have had insufficient numbers of patients treated within, say, the first hour after CO poisoning. Of the randomized human studies, only that of Ducasse56 came near to this with all patients treated within 2 h of CO exposure. However, this study was small and used outcome measures that are difficult to interpret as will be discussed. Most animal studies to date do seem relevant to the question of early therapy benefit, however with therapy usually provided to exposed animals commencing either immediately after cessation of poisoning or after a relatively short delay—most usually between 15 and 60 min.

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In many animal models of CO poisoning, HBO has shown benefit on a range of measures including survival, recovery of consciousness, recovery of brain function and reduction in postmortem neuropathology, including reductions in cellular necrosis and apoptosis. Despite early initiation of treatment, it is noteworthy that not all animal studies show benefit of HBO over NBO, however, or even of any kind of oxygen therapy over air breathing. Amongst recent studies looking at mechanisms underlying longterm sequelae, Brvar et al.57 did demonstrate that in rats poisoned without loss of consciousness (LOC), 30 min of 3 ATA HBO, but not 30 min of NBO, significantly reduced an immediate post-CO rise in blood levels of S100B, an astroglial structural protein that shows promise as a marker of CO poisoning severity.57 The CO exposure was 3000 ppm for 60 min. The same group has also reported however, in the same model, that both NBO and HBO resulted in a dramatic but effectively equal reduction in pyknotic cells in the hippocampus when the rats were sacrificed two weeks later.58 By contrast, in a mouse model of more severe poisoning with LOC, Gilmer et al.59 found that neither NBO nor HBO commenced 15 min after poisoning provided any significant protection against learning dysfunction or hippocampal pyknosis.59 LOC was induced in this model with a 4–9 min exposure to 50,000 ppm of CO after 40 min at 1000 ppm. It could be argued that this produces a sufficiently severe injury to be irreversible. This experimental poisoning regimen can be compared with Thom’s well established rat model which uses 3000 ppm for up to 20 min in order to induce LOC after 40 min of exposure to 1000 ppm.60 Treatment commences after a more clinically relevant interval of 45 min and the HBO regimen used is 45 min at 2.8ATA. This model was used to demonstrate that another structural protein, myelin basic protein (MBP) is released after CO poisoning and triggers delayed neuropathology via a cell mediated immune response.61 Most recently, Thom62 has shown that intervention with HBO, but not NBO, reduces learning dysfunction and the sensitization of lymphocytes to MBP, but this effect is only partial.62 This study adds to work showing that early HBO can block leukocyte adherence to endothelium and reduces leukocyte mediated oxidative damage that compounds CO-related injury upon reoxygenation.63 Interpreted together, the mechanisms of action of HBO and the studies referred to above suggest there is potential for benefit from early HBO. It is not clear, however, to what extent reversal of acute toxicity is responsible for outcome benefit as opposed to secondary injury reduction via mechanisms such as modulation of delayed immune-response and up-regulation of antioxidant systems. It is also not clear whether these effects are useful if HBO is applied much later after termination of CO exposure. Oxygen dosing is another major variable, with various pressures between 1.5 and 3.0 ATA used in therapeutic research, for durations between 45 min and 2 h. Single dose therapy and multiple dose therapy at varying intervals, have been used. In clinical practice, therapeutic oxygen is used in variable amounts and durations before and during hospital admission and therapeutic and toxic effect in animals should ideally be studied with varying doses of HBO and both with and without NBO in the periods before and after HBO, if findings are to be translated into human clinical practice or research design. It is also important to remember that developing a satisfactory animal model is critical to laboratory research. An experimental poisoning regimen must be found that produces sufficient toxicity to be associated with measurable pathology but the

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animals must survive and the damage should not be so severe as to be irreversible. Such controlled exposures are not the reality for humans and even in the animal models, demonstrated benefit may only apply in certain degrees of injury severity and both the optimal HBO dose and level of poisoning amenable to therapy seem likely to be species specific. The issue of animal model generalizability to humans is particularly important in CO poisoning. Most CO poisoning studies are done in rodents, which have the advantages of being relatively cheap, easy to handle and importantly, they are now available in a wide range of genetically altered strains which can be used to test biochemical mechanism hypotheses. Although rodents are mammals, they have critical differences from larger species. Their small body mass and high metabolic rate result in much more rapid uptake and distribution of gases than is the case for humans.52,64 More importantly, rodents are relatively hypoxia and carbon dioxide resistant, presumably evolved traits associated with survival in the rodent environment but ones which may have critical impacts on the interpretability of findings regarding CO poisoning, given the importance of hypoxia in the pathology of CO poisoning. This is not to argue against rodent research; it has generated and will continue to generate significant advances in our knowledge regarding the mechanisms of both CO and HBO. Generating clinical outcome predictions, case selection criteria or dosing requirements from rodent work has significant potential for error however. Gorman argues this in reporting results from his instrumented sheep model of CO poisoning. In this model, animals lose consciousness with an exposure to 1% CO for 120 min and seem to tolerate LOC-inducing levels of CO poisoning without the same neuropathology described in other models, although some peri-ventricular white matter infarcts and gliosis do occur. In addition to species differences, tolerance almost certainly depends upon cardiovascular and cerebrovascular reflex responses being intact and sufficient to maintain ongoing cerebral oxygenation. This has required chronic instrumentation of the animals, as if CO poisoning is provided too early after cannulation of the carotid vessels, more severe neuropathology was seen, localized to the side of instrumentation possibly related to impairment in the normal compensatory increase in cerebral blood flow.45,65−68 In summary, most animal studies suggest benefit should arise from using HBO as a therapy for CO poisoning, but much caution is needed in translating findings from pure and highly controlled CO exposure in healthy animals, treated rapidly with HBO, to the messy and complicated realities of human CO poisoning.

18.2.3 HBO FOR CARBON MONOXIDE POISONING: HUMAN EVIDENCE In October 2006, the American College of Emergency Medicine released its draft “Clinical Policy: Critical Issues in the Management of Adult Patients Presenting to the Emergency Department with Acute Symptomatic CO Poisoning”.69 This document uses an evidence-based approach. In response to the question “Should HBOT be used for the treatment of patients with CO poisoning; and can clinical or laboratory criteria identify CO-poisoned patients who are most likely to benefit from this therapy?”—the best it could do was “Level C” recommendations, that is, recommendations based

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on preliminary, inconclusive or conflicting evidence. The Level C recommendations were: 1. HBOT should not be mandated for the treatment of CO poisoning. 2. HBOT remains a therapeutic option to potentially reduce the incidence of neurological sequelae. 3. Do not use COHb levels alone to choose therapy in CO poisoning. 4. The available evidence does not identify either a subgroup of patients for whom HBOT is clearly indicated, or a subgroup of patients who clearly have no potential to benefit from HBO. Prior to this, Phin,70 in reviewing the evidence for therapy of CO poisoning, concluded that there was no evidence to support HBOT being of clear effectiveness. Evidence—based on call: Acute Medicine in 200171 recommended avoiding HBO in CO therapy, classifying this as an A class recommendation. In November 2000, The Medicare Services Advisory Committee of the Department of Health and Aged Care of the Australian Government,72 released its Report on HBOT. It concluded that there should be no support for “public funding for HBOT in either a multi-place or mono-place chamber for CO poisoning.” On February 9, 2001, the Minister for Health and Aged Care accepted this recommendation and such funding was withdrawn. This recommendation was based on a systematic review by Juurlink et al.73 in 2000 on behalf of the Cochrane Database of Systematic Reviews. “The review collected six reports of randomized controlled trials involving nonpregnant adults acutely poisoned with CO. Only three studies scored ≥ 3/5 on the Jadad quality scale (assessment based on randomization, double blinding and withdrawals and dropouts),74 and these three by Raphael,75 Thom,76 and Scheinkestel77 were analyzed. Juurlink et al.73 found that the severity of CO poisoning varied between trials and each trial employed different doses of HBO. The results for a total of 455 patients were available for analysis. Nonspecific neurological symptoms were present in 81/237 patients (34.1%) in the HBO group compared to 81/218 (37.2%) in the NBO group [odds ratio (OR) = 0.82; 95% Confidence Interval (CI) = 0.4, 1.66]. This systematic review failed to demonstrate a significant reduction in neurologic sequelae following HBOT for CO poisoning.” The German government has similarly recommended discontinuation of HBOT for CO poisoning78 stating “no studies could be identified, which could justify a continuation of HBOT for CO poisoning.” The review by Juurlink et al.73 underwent a substantive amendment in November, 2004 and was subsequently published in the Cochrane Library 2006.73 In this review, six trials were evaluated, the previous three plus a further one from Raphael,79 one from Mathieu,80 and one from Weaver.81 Of these, the latest one from Raphael is in abstract form only and that from Mathieu is an interim analysis. Using the Jadad scale again,74 Mathieu’s trial scored 2/5, the two from Raphael and the one by Thom scored 3/5 with those by Weaver and Scheinkestel scoring 5/5. Juurlink et al.73 state: “Of the six trials included, four found no benefit of HBO for the reduction of neurologic sequelae, while two did. While pooled analysis does

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not suggest a benefit for HBOT, (OR for neurological deficits = 0.78; 95% CI = 0.54, 1.12, p = 0.18), significant methodological and statistical heterogeneity means that this result must be interpreted with caution. Design and analysis flaws were evident in all the trials and importantly, the conclusion of one positive trial may have been influenced by failure to adjust for multiple hypothesis testing while the other positive trial is hampered by apparent changes in the primary outcome during the course of the trial.” Juurlink et al.73 again concluded that: “there was no evidence to support the use of HBO for treatment of patients with CO poisoning.” It is worth carefully reviewing all these studies, and also including for review that by Ducasse,82 which is also a prospective, randomized trial, but not usually included because of the use of surrogate outcome measures. Most of the discussion will concentrate on the two main studies: Weaver’s and Scheinkestel’s. Case series, retrospective reviews, nonrandomized studies, animal work and manuscripts based on theory have not been included in this review. They are discussed in chronological order below. 18.2.3.1 “Trial of Normobaric and Hyperbaric Oxygen for Acute Carbon Monoxide Intoxication” by Raphael Raphael’s study published in 1989,75 enrolled only patients poisoned in the 12 h prior to hospital admission. Three hundred and forty-three (343) patients with mild CO poisoning (no impairment of consciousness) were randomized to receive either NBO or HBO. Two hundred and eighty six (286) severely poisoned patients (with impairment of consciousness) were randomized to either one or two sessions of HBO, 12 h apart. Critically ill patients were excluded. Patients refusing the allocated treatment after randomization (n = 19), were still retained in the study and analyzed according to treatment intended. NBO therapy consisted of 6 h of 100% inspired oxygen by facemask or endotracheal tube. HBOT was 2 h of HBO in a mono-place chamber (0.5 h for compression, 1 h at 2.0 ATA and 0.5 h for decompression), plus 4 h of NBO. Eleven percent (11%) of patients were lost to follow-up. Thirty-nine patients (39) were intolerant of HBO and five had confirmed barotrauma. Raphael reported persistent neurological sequelae (PNS) in 32–34% of the patients with no LOC, and in 46–48% of those with LOC. The diagnosis of PNS was based on gross signs and symptoms, as neuropsychological testing was not performed. Patient assessment at 1 month consisted of a self-assessment questionnaire and a physical examination performed by the patients’ own doctor. If there was no response to the questionnaire, patients were telephoned. Raphael concluded that in patients without LOC, HBO had no advantage over NBO. At the 1-month review, recovery occurred, respectively, in 66% of 170 NBO patients and 68% of 173 HBO patients. Ninety-seven percent of patients resumed their usual occupation and social activities irrespective of treatment. In patients with transient LOC, he found no difference in outcome at 1 month between those patients having one or two HBO treatments (54% versus 52% recovery, p = 0.42).

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The problems identified with this study include: • Individuals were excluded on the basis of COHb measurement alone. • Those patients who refused randomization were retained in the study and included in the final analysis as members of intended treatment group.83 • NBO was given by facemask only, making the exact percentage of inspired oxygen unclear. • Lack of true controls. Only less severely CO poisoned patients were randomized to HBO versus NBO groups.78 All severely poisoned patients received HBO. • The HBO regimes used are considered by some to be ineffective (2.0 ATA instead of 2.8 ATA).84 • The times from poisoning to treatment entry criteria (up to 12 h) were too long.85,86 Oxygen treatment did not begin until after more than 6 h after poisoning in approximately half the cases.75 • Patients were not stratified according to interval between exposure and therapy.83 • Neither the investigators nor the patients were blind to treatment group. • The use of insensitive outcome measures (self-assessment questionnaire by telephone or mail one month after poisoning, discussion with the patients’ personal physicians),87 with recovery being determined by a lack of symptoms and/or resumption of former activities and delayed neurologic sequelae (DNS) being diagnosed when patients reported any of a variety of complaints.88 • Not using neuropsychometric tests to assess outcome resulted in an absence of objective or quantitative evaluation of cortical function. • The physical examination was performed by the patients’ own physician, rather than a physician experienced in CO-poisoning. Inexperienced physicians, not used to assessing these patients, may miss the more subtle signs and symptoms. • The use of multiple physicians precluded consistency. • 70 of 629 (11.1%) patients were lost to follow-up at 1 month. 18.2.3.2 “Non-Comatose Patients with Acute Carbon Monoxide Poisoning: Hyperbaric or Normobaric Oxygenation?” by Ducasse Ducasse’s56 series comprised 26 noncomatose patients with a glasgow coma score (GCS) of 15 on admission; 13 patients were randomized to HBO and 13 patients were randomized to NBO. They started treatment at a mean time after CO exposure of 53 min. The HBO group received HBOT for 120 min at 2.5 ATA pressure, followed by 100% NBO for 4 h and a further 6 h of 50% NBO. The NBO group received oxygen through a face-mask at 100% for 6 h, then at 50% for 6 h. Patients were assessed on clinical signs and symptoms, electroencephalogram (EEG) and cerebral blood flow response to acetazolamide. No neuropsychological assessments were performed. The reported incidence of both persistent neurologic sequelae (PNS) and DNS was zero.

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Clinical assessment at 2 and 12 h favored the HBO group. Two patients in the NBO group were changed to HBO at 12 h and were asymptomatic at completion of treatment. All 26 patients were discharged home well, an average of 28 h after presentation. There was no difference in the EEG at 24 h between HBO and NBO groups. Eight of twenty-six patients (31%) were lost to follow-up (three in the NBO group and five in the HBO group). Follow-up EEG in the remainder was worse in the NBO group (p ≤ 0.02), but all patients were clinically normal. Cerebral blood flow was assessed in 20 patients (four HBO, six NBO, and ten controls). There were no differences between HBO, NBO and controls with regard to perfusion of the basal ganglia or in cerebral blood flow values. Reactivity to acetazolamide was similar in the controls and the HBO group, and were said to be statistically significantly different from the NBO group (p ≤ 0.04). Adverse events due to HBO are not mentioned. Ducasse concluded that HBO reduced the time to initial recovery and the number of delayed functional abnormalities in noncomatose patients with acute CO poisoning. He attributed some of his success to the rapidity of treatment. The problems identified with this study include: • • • • • • • • • • • •

Small study with few patients.26 Only patients with mild CO poisoning were enrolled. The study was nonblinded. The use of surrogate outcome measures which are of questionable significance.85,87,89 The significance of an abnormal EEG in clinically normal patients is unclear. No statistical significance values were reported for the EEG results. Thirty-one percent (31%) of subjects we lost to follow-up. While controls were part of the 3-week evaluation, the authors did not define this subgroup’s characteristics. There were no measures of cognitive function, as standardized neuropsychiatric testing was not performed. The test data appear to conflict with one of the author’s conclusions: that HBO treated patients showed a better cerebral blood flow response and greater improvement in the 3 week EEG studies.83 Inadequate allocation concealment.89 Statistical significance of reactivity to acetazolamide is questionable, given the small numbers and large range of results.

18.2.3.3 “Delayed Neuropsychologic Sequelae after Carbon Monoxide Poisoning: Prevention by Treatment With Hyperbaric Oxygen” by Thom Thom’s study76 also included only mild poisonings. Patients with a history of LOC were excluded. Patients presented within 6 h of exposure and usually commenced

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treatment in about 1 h. Thirty-two patients were allocated to NBO and thirty-three to HBO. HBO patients were treated once for 30 min at 2.8 ATA, followed by 90 min at 2.0 ATA. NBO patients received 100% oxygen through a nonrebreather face-mask until all symptoms resolved (4.2 ± 3 h). The presence or absence of five signs and symptoms together with a COHb level were used to assume the two groups were of similar severity of poisoning. Thom used a CO neuropsychological screening battery (CONSB) designed by Myers after completion of treatment. Formal neuropsychological testing was performed at 1 month. The 3-month review consisted of a telephone interview only. Twelve of sixty-five patients (18%) were lost to follow-up. Thom reported no DNS in the HBO group, while 7 of 30 in the NBO group developed problems (p < 0.05). No specific treatment was given to those who developed DNS. Three of these patients refused follow-up. In the remaining four, neuropsychometric testing was repeated at intervals of 2–3 weeks until scores returned to baseline. It would appear that all DNS resolved. No adverse events resulted from HBO treatment. Thom concluded that HBOT decreased the incidence of DNS after CO poisoning. Problems reported with this study include: • • • • • • • •

•

Neither the patients nor the investigators were blinded to treatment. The randomization process is unclear. The consent procedures are unclear. Only patients with mild poisoning were included, sick patients were excluded.90 While a COHb level was one of the measures used to assume that the two groups were of similar severity of poisoning, the delay taken in measurement of COHb is not mentioned. Baseline neuropsychometric testing was not performed to ensure that the two groups were similar. There was greater comorbidity in the NBO group at randomization.85,87 . NBO patients were slightly older and had a higher incidence of cardiovascular and respiratory disease. Neuropsychological tests were repeated at intervals of 2–3 weeks until scores returned to baseline. The effect of repetition and learning of tests on outcome was controlled by comparing to the effects achieved by practice on learning in a control group of eight patients. This is an insufficient number of control subjects to assist with the interpretation of neuropsychological tests86,91 and no details of the characteristics of the control group were provided, in particular how they matched with the HBO and NBO groups.90,91 The location and conditions for neuropsychometric testing were inconsistent. Some were performed immediately on completion of treatment, but if patients were “fatigued”, the tests were performed in the patients’ homes within the next 12 h. No details are provided as to how the neuropsychometric testing was performed on the controls.

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• The paper does not state the number of clinicians involved in performing the neuropsychometric testing, nor their experience. • The neuropsychological tests used (CONSB) are said not to adequately measure memory. • The definition of DNS was a deterioration in one or more subtest scores on the neuropsychological test battery, but this “deterioration” is not defined in the paper.91 • The incidence of delayed sequelae may have been significantly altered in the normobaric group if normal psychometric testing had been a prerequisite for discharge.88 • At the 4 week follow-up, the NBO group had a worse score in one subtest only, Trail-Making, which Thom states may reflect the presence of a subtle impairment of learning ability when these patients first took the psychometric test and hence a lack of familiarity on retesting.76 • The 3-month review consisted of a telephone interview only. • 18% of patients were lost to follow-up.86 • All patients reported complete resolution of symptoms. Hampson89 states that this study was stopped early due to a treatment advantage in the HBO group, but the actual paper makes no mention of this. In fact, Juurlink73 points out that in an interim analysis describing the outcome of 58 patients, published in 1992, there was no difference in symptoms between patients in the NBO versus HBO groups (4 of 29 patients versus 0 of 29 patients, respectively). Juurlink notes that seven additional patients were recruited after this interim analysis, three to the NBO arm (all of these patients experienced neurological sequelae), and four to the HBO arm (none of these experienced neurological sequelae). He states that although the recruitment of seven additional patients with this distribution of allocation and outcomes could be due to chance (p = 0.014 by Fisher’s exact test), it may reflect premature termination of the trial after recruitment of only seven more patients, greatly exaggerating the treatment effect. A statistical penalty to adjust for inflation of the type I error rate was not introduced, and would have rendered the final result statistically insignificant.73 Had adjustment for multiple comparisons been performed, no significant difference between treatments would have been identified.92 18.2.3.4 “Randomized Prospective Study Comparing the Effect of HBO Versus 12 h NBO in Noncomatose CO Poisoned Patients: Results of the Interim Analysis” by Mathieu Mathieu80 reported on an interim analysis after 3 years of a 5-year multicenter study. Only patients noncomatose on hospital admission, and poisoned in the preceding 12 h were enrolled. Delay to treatment is not specified. Treatment was either one HBO session of 90 min at 2.5 ATA (299 patients), or 12 h of 100% NBO (276 patients). Patients were neurologically normal at the time of hospital discharge, but at 1 month approximately one quarter had sequelae with no difference between HBO and NBO (23% versus 26%). At three months, the incidence

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fell and there was a statistically significant difference between HBO and NBO (9.5% versus 15%; p = 0.016), but this was no longer evident at 6 months (6.4% versus 9.5%; p = 0.09) or 12 months (4.3% versus 5%). The limitations of this report are: • • • • • • • • • •

It is only available in abstract form. There was no blinding. The definitions of the primary outcome are missing.92 There was a long entry time of 12 h from poisoning to treatment.85 No details of the neurological assessment are provided. Neurological manifestations are referred to as PNS, but given that the patients were neurologically normal at the time of hospital discharge, it is not clear why they are PNS and not DNS. Neuropsychological assessments were not performed either pre- or posttreatment. Mathieu provides no details of attrition rates for follow-up.92 Recovery was considered complete if the patient had no complaints.88 Had the investigators adjusted their analysis for multiple comparisons, no significant difference between treatments would have been identified at any interval.92

18.2.3.5 “Managing Carbon Monoxide Poisoning with Hyperbaric Oxygen” by Raphael Raphael79 in 2004, published in abstract form the results of a second randomized controlled trial. Patient recruitment took place between 1996 and 2000 and involved 385 victims of accidental, domestic CO poisonings presenting within 12 h of CO exposure. One hundred and seventy nine (179) patients had transient LOC and were randomized to receive either 6 h of NBO (A0 group, 86 patients) or one treatment with HBO (at a plateau of 2 ATA for 60 min), plus 4 h of NBO (A1 group, 93 patients). Two hundred and six (206) comatose patients were randomized to receive either one (B1 group-101 patients) or two (B2 group-105 patients) HBO treatments (at a plateau of 2 ATA for 60 min) plus 4 h of NBO. The primary end-point was the proportion of patients who recovered at 1 month, with recovery being defined by a normal self-assessment questionnaire and normal blinded neurological examination. The trial was stopped prematurely because the interim analysis showed that giving two HBO sessions rather than one, was associated with a poorer outcome in comatose patients. Furthermore, in patients with transient LOC, the recovery rate was not modified by addition of HBO to NBO. The percentage who had recovered at 1 month were as follows: A0 61% 45/74 A1 58% 46/79 (OR = 0.90, 95% CI = 0.47–1.71, p = 0.87) B1 68% 54/80 B2 47% 42/90 (OR = 0.42, 95% CI = 0.23–0.79, p = 0.007)

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There were four deaths and four survivors with severe neurological sequelae in the B2 arm, (two HBO treatments). All but one of the deaths and severe neurological sequelae were in the B group, that with comatose patients receiving HBO treatment. Severe neurological sequelae occurred only in those with coma at presentation. Seventeen (17%) percent of patients were lost to follow-up. The authors concluded “There is no evidence supporting the routine use of HBO in patients with acute CO poisoning” The limitations of this report are: • All the ones of his previous study, as the trials are essentially the same: • Lack of true controls. Only less severely poisoned patients were randomized to HBO versus NBO.73 All severely poisoned patients received HBO. • The HBO regimes used are considered by some to be ineffective (2.0 ATA instead of 2.8 ATA).84 • The times from poisoning to treatment entry criteria (up to 12 h) were too long.85,86 • Patients were not stratified according to interval between exposure and therapy.83 • Neither the investigators nor the patients were blind to treatment group. • The use of insensitive outcome measures (self-assessment questionnaire by telephone or mail 1 month after poisoning, discussion with the patients’ personal physicians),87 with recovery being determined by a lack of symptoms and/or resumption of former activities and DNS being diagnosed when patients reported any of a variety of complaints.88 • Not using neuropsychometric tests to assess outcome resulted in an absence of objective or quantitative evaluation of cortical function. • The physical examination was performed by the patients’ own physician, rather than a physician experienced in CO-poisoning and inexperienced physicians, not used to assessing these patients may miss the more subtle signs and symptoms. • The use of multiple physicians precluded consistency. In addition, • The study is only available in abstract form. • 17% of patients were lost to follow-up. 18.2.3.6 “Hyperbaric or Normobaric Oxygen for Acute Carbon Monoxide Poisoning: A Randomised Controlled Clinical Trial” by Scheinkestel We98 commenced a trial in 1993 in which we aimed to overcome the shortcomings of the previous trials. We randomized patients with all grades of CO poisoning, including severely poisoned patients, within 24 h of poisoning, used sham treatments in the multiplace chamber for the NBO group with both patients and the outcome assessor

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blinded to treatment group. Our primary end-point was outcome at completion of treatment. Our secondary end-point was outcome at 1 month. In the absence of universally accepted recommendations for depth or duration of pressurization for HBO treatments, we used what was at the time, the best available data to determine the HBO treatment protocol, which consisted of three treatments of 100 min with 60 min at 2.8 ATA over 3 days, based on the conclusions of Gorman and Runciman93 that such protocols were associated with the lowest mortality and neurological deficits and would provide the maximum potential advantage for HBOT. In between treatments, patients received high-flow oxygen by nonocclusive facemask. In order for the treatment and control groups to be identical in every way except for the hyperbaric component, the NBO group had exactly the same treatment as the HBO group but had NBO in the chamber. Patient assessment at entry included the clinical effects of poisoning and a minimental examination. After the third treatment, patients were reassessed medically and underwent full neuropsychological testing. Patients with a poor outcome had a further three treatments (NBO or HBO as previously allocated) and continued with high flow oxygen between treatments. We used a pretreatment, baseline minimental examination, an extended series of neuropsychological tests to assess both persistent and delayed neuropsychological deficits, a clinical psychologist trained in neuropsychological assessment of brain injured patients to perform all the tests (at completion of treatment and at follow-up), and computerized testing to standardize administration and increase objectivity of these tests. Following consent, patients were stratified into four groups: suicide versus accidental, then mechanically ventilated versus non-ventilated prior to randomization to HBO (104 patients) or NBO (87 patients). In our prospective randomized controlled trial of 191 patients, in which both groups received high doses of oxygen, the HBO regimen used, did not benefit and may have worsened outcome. More patients in the HBO group required additional treatments (28% versus 15%, p = 0.01 for all patients; 35% versus 13%, p = 0.001 for severely poisoned patients). HBO patients had a worse outcome in the learning test at completion of treatment (p = 0.01 for all patients; p = 0.005 for severely poisoned patients) and a greater number of abnormal test results at completion of treatment (3.4 versus 2.7, p = 0.02 for all patients; 3.7 versus 2.6, p = 0.008 for severely poisoned patients). A greater percentage of severely poisoned patients in the HBO group had a poor outcome at the completion of treatment (85% versus 65%, p = 0.03). DNS were restricted to the HBO patients (p = 0.03). No outcome measure was worse in the NBO group. The comprehensive assessment of all patients at completion of treatment showed no benefit for HBO. Our study has attracted a number of criticisms: •

Cluster randomization

In the accompanying editorial, Moon and DeLong,99 while acknowledging that “the study design is amongst the most rigorous yet published”, expressed concern about

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cluster randomization. Kao87 and Weaver100 expressed similar concerns. To minimize the impact of the trial on daily practice, cluster randomization was used for simultaneously presenting patients from the same exposure: the treatment group assigned to the first patient was allocated to the other simultaneously presenting patient(s). Randomization took place only after the group was assembled. Cluster randomization accounted for the difference in numbers between the HBO and NBO groups. We used cluster randomization, allocating more than one person simultaneously to the same treatment on 22 occasions, (2 patients on 12 occasions, 3 patients on 5 occasions and 4 patients on 5 occasions). Overall 14 clusters (40 patients) were allocated to HBO and 8 clusters (19 patients) to NBO. As patients presenting simultaneously could be uniquely identified by having identical measurements for three continuous baseline severity measurements (exposure time, time to COHb measurement and time to treatment), any effects due to cluster randomisation could be controlled and adjusted for by including these variables in the generalized linear model. Continuous outcome variables were also analyzed by the mixed procedures in statistical analysis software (SAS)94 which allows a repeated measures analysis of variance, with the variable cluster being treated as a random repeated measurement, thus “adjusting for” within cluster variation. We also repeated the analysis excluding all patients who were allocated as part of a cluster. It has been shown95,96 that the effect of cluster randomization is to increase the size of standard errors and p-values. By including these three variables we found that the standard errors and the p-values were increased in comparison to models excluding these variables. To further validate results, sensitivity analysis was performed for the binomial outcome variables by comparing results with those obtained by excluding all participants who were randomized into a cluster.

Variable

Original OR (95% CI)

Results Excluding All Clusters

Required > 3 treatments 2.8 (1.3–6.2) 3.3 (1.3–8.2) Required > 3 treatments (severe) 5.4 (2.0–14.8) 5.3 (1.7–16.0) Poor outcome 1.7 (0.8–4.0) 2.2 (0.8–5.9) Poor outcome (severe) 3.6 (1.1–11.9) 3.2 (0.9–11.9) This analysis produced consistent results for all variables which suggests that our results have not been biased by cluster randomisation.97,98 • Allocation Concealment The Cochrane review73 scores our study a “B” for allocation concealment because of concern of failure of concealment related to fixed block sizes if the treating team were aware of previous assignment. We specifically addressed this by having blocks of various sizes so that you could not predict the next treatment. Randomization (HBO or NBO) was performed by a hyperbaric technician who opened progressively numbered, sealed, opaque envelopes (from random blocks of 4, 6, 8 and 10 envelopes, each block containing equal numbers of HBO and NBO selections).

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Delay to Treatment

Both Moon99 and Weaver100 also express concern about our delay to treatment (geometric mean of 7.1 h (95% CI = 1.9–26.5 h). Firstly this is not dissimilar from some of the other studies. Raphael’s inclusion criteria was up to 12 h in both his studies74,79 with a mean time to treatment of 6.4 h74 . Mathieu’s80 entry criteria was also within 12 h of exposure. Weaver’s study81 included patients within 24 h of exposure and the mean times in his study were only marginally different from ours: for HBO 5.8 ± 2.9 versus 7.5 (6.6–8.6), NBO 5.7 ± 2.9 versus 6.6 (5.7–7.5), respectively, for Weaver’s and Scheinkestel’s patients. As Tighe points out,101 “these time delays are representative of most clinical practice because of late presentation and the need for stabilization and transport to a remote hyperbaric facility.” Although the geometric mean treatment delay was 7.1 h, we performed subgroup analysis of patients treated within 4 h (all patients and just severely poisoned patients). There were 44 patients treated within 4 h (22 HBO and 22 NBO), 33 of which were severely poisoned (15 HBO and 18 NBO) with no outcome measure favoring the use of HBO. We further analyzed time to treatment in quartiles (<3, 3–6, 6–12, >12 h) and found no difference in outcome between HBO and NBO. Further multivariable analysis did not identify delay in treatment as a predictor of poor outcome. Thus there was no evidence that delay in treatment could have explained the lack of benefit of HBO.97 •

Concomitant depression, suicide attempt and use of psycho-active drugs

Weaver,100 Shank,85 and Moon99 express concern that we included patients whose exposure was due to suicidal intent, had consumed cointoxicants and had a history of depression. They question whether this might have influenced the outcome of the neuropsychological tests and therefore the results of the study. While it is true that depression and the use of medication may have resulted in a higher incidence of poor outcome overall, this would not in any way have biased the comparison between normobaric and hyperbaric groups as patients were specifically stratified for suicide attempt prior to randomization to therapy. As we also stated, analysis of accidental poisonings (excluding suicide attempts) also showed no differences between HBO and NBO groups.77 Furthermore the incidence of self-administration of drugs and alcohol was identical in both groups (44%).77 In a subsequent letter to the British Medical Journal (BMJ)102 Weaver states “I agree that attempted suicide probably did not bias the outcome between the two arms”. • Lack of pretreatment neuropsychological assessment Our lack of pretreatment neuropsychological assessment has been considered a problem by Moon,99 Schiltz103 and Denson and Hay.104 In order to address our specific research question, whether HBOT is superior to NBO therapy in preventing residual cognitive impairment following CO poisoning,

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two alternative research designs were considered: a cross sectional design wherein subjects are randomly assigned to two groups (HBO versus NBO), and a longitudinal design where within group comparisons are made (pre-treatment verses post-treatment). When employing neuropsychological tests to evaluate patient outcome within a longitudinal design, both practice effects and spontaneous recovery may over-estimate treatment benefits. As Dr. Schiltz points out,103 it would be pertinent within a longitudinal design to take into account premorbid intelligence and psychiatric status. In selecting a randomized cross-sectional design (where both assessor and data analyzer were blind to treatment membership) however, statistical comparisons are not confounded by practice effects nor spontaneous recovery. Additionally, while we acknowledge that we could not clearly establish that our two groups (NBO and HBO) were equal with respect to premorbid intellectual activity and level of depression, there was no difference in initial mini-mental score between groups (27.0 (26.1–27.9) versus 26.4 (25.4–27.4), p = 0.27). There was similar improvement in mini-mental score in both groups, for all patients (p = 0.53), and for severely poisoned patients (p = 0.71). The score improved further to normal levels in both NBO and HBO groups in those attending follow-up for all patients as well as severely poisoned ones. Clinical considerations were equally important in selecting the most appropriate research design and methodology. Firstly, there is the issue of obtaining meaningful data. In an acutely ill, disoriented, agitated and distressed patient, prolonged psychometric testing is not practical or meaningful. In more cases than not, the patient would not be able to sustain concentration for a 1.5-h assessment. Further, availability of a trained psychologist 24 h a day, 7 days a week to perform pretreatment full neuropsychological assessments and delaying treatment by a further 90 min was not practical. We therefore performed the mini-mental test on admission, which is quick and easy to administer, rather than comprehensive neuropsychological assessment which was performed at completion of treatment once patient’s mental status had stabilized. • Type of tests There has been criticism that the neuropsychological tests we used were not standard ones.87 Neuropsychological assessment of the CO population is challenging in light of the confounding psychiatric variables. A further challenge to researchers is the collection of data in a clinical setting that needs to be sensitive to patient motivation, level of cooperation and imminent discharge. For these reasons, highly sensitive cognitive tests were selected that sampled the pertinent neuropsychological realms (attention, new learning, visuo-construction and executive functioning) in 90 min in order to maximize cooperation and minimize fatigue. The choice reaction time (RT) measure we used, required participants to respond to stimuli that appeared at various positions around the periphery of the screen and as such required rapid visual scanning. RT is considered sensitive to cerebral lesions of any localization. Should specific visuo-spatial deficits occur in the CO-poisoned population, it is likely that they would be reflected in the RT. In addition to being sensitive to diffuse cerebral lesions, the choice RT task can be argued to be sensitive specifically to visuospatial deficits.

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Multitude of tests

Moon99 and Denson and Hay104 raise the matter that we performed a multitude of tests and that only one showed a statistically significant result (in favor of NBO). Although we performed a multitude of tests, not one showed a benefit in favor of HBO. We were not trying to prove a statistically significant advantage for NBO, rather we could not demonstrate a benefit in favor of HBO. As multiple tests were considered, there is an increased likelihood of a type I error. But, given that an outcome measure based on combining all tests was used, in conjunction with death and > 3 treatments, the chance of a spurious result was minimized. We agree that there were two major limitations to our study: •

Low follow-up rate

While our study was inclusive with 83% of potential patients being entered (4% were excluded and 13% refused consent), only 46% of patients entered attended the followup at 1 month. Thus, longterm follow-up was only available in 38% of all potential patients. This unfortunate result occurred despite significant effort. Patients were requested to attend for review at 1 month. The review appointment was confirmed by mail and if required, patients were actively pursued by telephone. Despite repeated efforts, only 46% of patients attended follow-up. This low rate of attendance at follow-up is indeed a major problem in interpreting our patients’ outcomes. Our different patient population, with characteristics associated with suicide attempts and depression, many referrals from distant locations and lack of incentive, probably contributed to the low follow-up rate, which was however, equal in both groups, and evenly distributed across subgroups. For those attending follow-up, our assessment was rigorous (as opposed to a telephone survey) and failed to show any benefit for HBO. The previously published randomized studies have experienced lower but significant nonattendance rates at delayed review of 11.1%,75 31%,82 18%,76 17%,79 with Mathieu’s study not quoting the attrition rate. • The treatment regimens We have been criticized for using nonstandard HBO and NBO therapy46,87,99 because this is not representative of usual practice. The treatment regimens in our study were not conventional. It should be noted however, that established practice continues to vary very widely.4 In the absence of universally accepted recommendations for depth or duration of pressurization for HBO treatments, our protocol for the management of CO poisoning consisted of three treatments of 100 min with 60 min at 2.8 ATA over 3 days, based on the conclusion of Gorman and Runciman93 that this achieved the lowest mortality and neurological deficits and would provide the maximum potential advantage for HBOT. Our hyperbaric treatment regimen for CO poisoning included interval NBO. To retain blinding, we also provided the control group with NBO for 3 days. As a result, our normobaric group received more NBO than used in previous studies and this may have been a factor in the lack of outcome difference between the treatment groups.105

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As Tighe comments,101 “previous studies have been flawed by a failure to optimize treatment in the normobaric group, and Scheinkestel et al’s study clearly shows that such cheap, available, safe treatment is also effective.” Moon99 raised the concept that repetitive treatments at 2.8 ATA could have been neurotoxic and offset any potential benefit from HBO. This proposal of oxygen neurotoxicity is a valid one, but it is important to note that repeated daily treatments at 2.8 ATA is standard therapy for CO poisoning in many centers and also for cerebrally-impaired patients with decompression illness. We set out to demonstrate an advantage for HBO and selected the optimum treatment regime to achieve this. We have now demonstrated that there is no advantage in outcome for HBO over 3 days of high flow oxygen therapy. What we cannot now answer is whether the same outcomes can be achieved with less days of high flow oxygen therapy. Piantadosi46 states that the difference in O2 doses between the groups was negligible. We calculated that the HBO group received oxygen therapy equating to approximately 35.7 COHb dissociation half-lives, while the NBO group received the equivalent of 28.5 COHb dissociation half-lives, a difference of 7.2 COHb dissociation half-lives. Most other studies have used total oxygen doses of less than 7.0 COHb dissociation half-lives.74,75,80,82 The difference in our two groups is greater than the difference in doses used in these other studies. We just used a higher baseline oxygen dose. 18.2.3.7 “Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning” by Weaver Weaver81 in 2002 reported on the outcome of 152 patients enrolled within 24 h of exposure to CO in his double-blind randomized trial. Seventy-six patients were assigned to have three hyperbaric sessions within a 24-h period and 76 had one NBO treatment and two sessions of exposure to normobaric room air. Patients were stratified according to whether or not they had lost consciousness, the interval between end of exposure and entry into the chamber (<6 h or >6 h) and age (<40 years or >40 years). Treatments took place in a Sechrist monoplace chamber. The first HBO session was with 100% O2 for 2.5 h with 55 min at 3.0 ATA, the second and third were with 100% O2 for 2 h with 90 min at 2.0 ATA. It is not clear from the paper as to the exact NBO treatment given. In one section it states: “patients in the NBO group were exposed to air at one ATA for all three chamber sessions.” In another section it states: “100% oxygen was delivered to those in the NBO group during chamber session 1. During NBO sessions 2 and 3, patients were exposed to 1 ATA and breathed air” unless the patients were intubated and ventilated or had arterial oxygen saturations <90%, in which case they received 100% oxygen. Neuropsychological assessments were administered after chamber sessions 1 and 3, at 2 weeks, 6 weeks, 6 months, and 12 months. The primary outcome was cognitive sequelae at 6 weeks. The trial was stopped after the third of four scheduled interim analyses. Cognitive sequelae at 6 weeks were less frequent in the hyperbaric group (25%) than in the normobaric group (46%), p = 0.007, even after adjusting for cerebellar

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dysfunction and for stratification variables (adjusted OR = 0.45, 95% CI = 0.22 − 0.92, p = 0.03. The presence of cerebellar dysfunction before treatment was associated with the occurrence of cognitive sequelae (odds ratio:5.71 (95%, CI 1.69–19.31), p = 0.005, and was more frequent in the normobaric group (15% versus 4%, p = 0.03). Cognitive sequelae were less frequent in the hyperbaric group at 12 months, according to intention to treat analysis (p = 0.04). The authors concluded that three HBO treatments within a 24-h period appeared to reduce the risk of cognitive sequelae at 6 weeks and 12 months after acute CO poisoning. An abstract by Weaver117 further analyzed the data and concluded that HBO improved outcome if any of the following were present: LOC, COHb > 25%, age > 50 and metabolic acidosis. In patients with none of these four criteria, HBO did not improve outcome. While proponents of HBO for CO-poisoning consider this to be a landmark paper, and Dr Weaver believes his paper to be the only one worth considering and the definitive paper on HBO in CO-poisoning,78 we believe there are some fundamental problems with the Weaver study: •

Primary Outcome analysis

Dr. Juurlink summarizes this eloquently.78 “In 1995, Weaver and colleagues published the first interim analysis of their study.106 In that report, the only test of statistical significance was applied to DNS, and the investigators indicated that enrollment would continue because the p value had not achieved the threshold required for premature termination of the trial. That same year,107 Weaver presented a description of his ongoing trial and gave an explicit definition of its primary outcome: “Our major question is, does HBO2 reduce the incidence of DNS?” He also wrote: “During the course of the trial, it became evident that operational definitions of DNS and PNS were needed . . . Our definition for DNS is: development of a new neurologic abnormality not present at day 1, and/or decrement of neuropsychologic subtest score of more than two SDs below the mean or two subtest scores more than one SD below the mean compared to standardized norms (prior normal neuropsychologic test). If the prior neuropsychologic test is abnormal, then we use a decrement of an abnormal subtest of more than one SD compared to the prior score or more than 0.5 SDs below each of at least two abnormal subtests.” In his letter to the editor,107 written with the study underway and 47 patients enrolled, neither the definition of DNS nor that of PNS includes patient symptoms. They are both clearly defined and these definitions are solely based on the outcome of neuropsychological tests.” DNS appears to be the original intended outcome of the trial. This outcome has never been subsequently reported in any forum. “In 2001, a discussion of his soon-to-be published study89 contained no mention of DNS. Indeed, a very different outcome (“cognitive sequelae”) had been defined: “Cognitive sequelae were considered present if any 6-week neuropsychological subtest score was >2 standard deviations below the mean (or if at least two

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subtest scores were each more than one SD below the mean) of demographically corrected standardized scores. Cognitive sequelae were present if a neuropsychological subtest score was >1 SD below the mean or if two subtest scores each were >0.5 SD below the mean and the patient complained of memory, attention, and/or concentration difficulties.” In the final publication,81 the cut-off values used to define abnormal results changed yet again. It is not clear why the statistical analysis on the T-scores for the neuropsychological subtests is performed on the aggregate of the three scores obtained after chamber session 3, at 2 weeks and at 6 weeks, given that “the primary outcome was cognitive sequelae at 6 weeks”. The other two scores (after chamber session 3 and at 2 weeks) are not relevant to this end-point.” In summary, the original intended outcome of this trial was DNS defined by rigorous clinical criteria. In contrast, the final publication reports “cognitive sequelae,” a distinctly different outcome. PNS and DNS have been bundled together. The definition of a poor outcome was changed to include a subjective component of patient symptoms and the results of neuropsychological tests after treatment, at 2 weeks and at 6 weeks have also been bundled together. Juurlink states: “Dr. Weaver and his coinvestigators have obviously collected the data necessary to examine DNS as an outcome, and we urge them to present this analysis.73 Juurlink states, “doing so would help settle the present debate. While HBO enthusiasts may argue that ‘cognitive sequelae’ is a meaningful outcome, skeptics may legitimately wonder if the revised outcome was simply that which cast the most favorable light on HBO once all the data were collected.” Buckley108 asserts that a significant difference between HBO and NBO would almost certainly not have been demonstrated if the originally intended outcome had been analyzed. Other problems identified with Weaver’s study include: •

Early termination of the study

In 1999, Weaver wrote109 “Blinded interim analysis showed no difference in outcome between the two groups after 50 and 100 patients. Yet after 52 additional patients, the results were so clear-cut, that the trial was terminated early, “after the third of four scheduled interim analyses”. We interpret this to mean that there was one more interim analysis scheduled and presumably 100 more patients still to enroll. When Weaver adjusted for differences in baseline severity (cerebellar dysfunction—see section on failure of randomization), the difference between groups only just makes statistical significance at p = 0.05, well below the predetermined “stopping rules.” •

Enrollment and follow-up

Only 33% of potential patients were entered: 28% were excluded and 39% refused consent, thus introducing the possibility of significant selection bias. The 95% followup rate of these highly selected patients resulted in only 31% of all potential patients being assessed. Weaver argues110 that he has followed up 91 of the 180 who declined to be in the trial. They had a lower suicide rate (16% versus 30%) and a lower COHb (20% versus 25%). Weaver concludes that they were similar to those enrolled in the

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study. Further he states that the incidence of 6 week cognitive sequelae of 43% was similar to that of the NBO group in the trial (46.1%), but it is clear from his reasons for “declined enrollment in the trial” group,81 that at least some of these declined because the referring physician insisted on HBO. •

Failure of randomization

This is the only study to have a large difference in baseline severity. Despite randomization, Weaver et al.’s normobaric group appeared to have suffered more severe CO poisoning. The normobaric group had a CO exposure of 22 ± 64 h, almost double that of the hyperbaric group (13 ± 41 h), and the COHb saturation at first entry to the chamber was significantly higher (p = 0.02). Furthermore, the incidence of pretreatment cerebellar dysfunction was 15% in the normobaric group and only 4% in the hyperbaric group, an almost fourfold difference that was also statistically different (p = 0.03). The presence of cerebellar dysfunction before treatment was associated with cognitive sequelae (p = 0.005). Shorter exposure to CO, a lower level of COHb, and a lower incidence of cerebellar dysfunction would be expected to favor a better outcome in the hyperbaric group. It is also worth noting that the COHb was actually only available in 83 patients (in 36 HBO, less than half of the 76 HBO patients enrolled, and in 47 NBO). In the other 69, missing values were imputed on the basis of the data in the other 83 patients. The duration of exposure to CO has been presented as a mean with a standard deviation. From these results (13 ± 41 versus 22 ± 64) it is clear that the distribution of duration is skewed. Variables measuring duration are often well characterized by a log-normal distribution and would have been more appropriately presented as geometric means with 95% confidence intervals, or if the distribution was unknown (nonparametric), as medians with interquartile ranges. It is likely that there are significant outliers included and this may have had a detrimental effect on the significance of baseline differences and therefore on the multivariate analysis as a whole. Weaver argues that the CO exposure was not statistically significant and produces the requested statistics:110 • Median exposures: 4.2 (range 0.2–308 h) for HBO versus 5.0 (0.3–397 h) for NBO • Geometric means: 4.0 h (95% CI = 2.9–5.4) for HBO versus 5.4 (95% CI = 3.8–7.6) for NBO, p = 0.2 • Interquartile range 7.3 h (1.6–8.9) for HBO versus 9.5 (2.0–13.5) h for NBO, p = 0.2 These all confirm a trend, albeit non-significant, towards increased exposure in the NBO group, which is confirmed by the statistically, significantly higher COHb in the NBO group and is in keeping with the increased cerebellar signs in the NBO group. Weaver argues however that the difference in COHb is of no consequence as there is no relationship between COHb and outcome.110 This still leaves the fourfold increase in prechamber cerebellar signs in the NBO group compared to the HBO group. If these patients are not excluded, his intention to treat analysis finds a highly significant difference in six weeks outcome (25.0% versus 46.1%, p = 0.007) in favor of HBO.

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If only patients with normal cerebellar function are analyzed, the benefit for HBO only just reaches statistical significance (23.2% versus 39.0%, p = 0.05) and the trial would not we assume have been terminated early. • Inadequate oxygen dose to normobaric group The amount of oxygen therapy given to the normobaric group may have been suboptimal. In all studies, patients received variable amounts of NBO therapy prior to hospital arrival. Current recommendations for in-hospital NBO administration most commonly involve occlusive face-mask and reservoir bag for 6–12 h or until symptoms resolve. In this study, unless the patient’s oxygen saturation was less than 90%, or they were intubated, the normobaric group only received 135 min of oxygen therapy with a reservoir and a nonocclusive face-mask while in the chamber. Thus in-hospital oxygen treatment was, by conventional criteria, short. The four other randomized studies that have been published all utilized longer duration of oxygen therapy in the normobaric group: 6–12 h80 6 h75 12 h,82 and an average of 4.2 h.76 Weaver argues110 that the sum of oxygen therapy for the NBO group was 6.9 h, 135 min in the chamber and 4.5 ± 2.2 h before chamber session 1. The range was 3.9–18.8 h. However, he is including the prehospital time, whereas all other studies provide at least 6 h once at the hospital. The median duration of oxygen therapy in Weaver’s NBO group was 6.2 h. By definition 50% of patients had less than 6.2 h of oxygen therapy. Further, Weaver states109 that referring physicians gave NBO therapy to CO patients, but there is no statement to guarantee that these patients were given high flow oxygen from a reservoir through a non-rebreathing face mask prior to arrival at LDS Hospital. Conventional teaching is that hyperoxia is required in CO poisoning to help “offload” CO. Not providing oxygen therapy to patients whose oxygen saturations were >90% would be considered inappropriate by most centers. Weaver argues110 that they treated all CO-poisoned patients with NBO until the COHb was less than 5%. This is not stated in the paper. In fact, the paper is quite clear in several sections, that supplemental oxygen was only provided if the oxygen saturation was <90%. Nor is there a statement that COHb was remeasured at intervals to establish there was no rebound rise in COHb postcessation of treatment, as is common. Further, he does not state how oxygen saturation was monitored to ensure it was >90%. If this was done using pulse oximetry, as is the norm, then there is considerable literature as to the inadequacy of pulse oximetry to monitor oxygen saturation as this cannot differentiate between COHb and oxyhemoglobin, and therefore over-estimates oxyhaemoglobin.111 •

Non-conventional HBO regime

Kao raised concerns that Weaver used a nonstandard HBO protocol.87 The first HBO session was with 100% O2 for 2.5 h with 55 min at 3.0 ATA, the second and third were with 100% O2 for 2 h with 90 min at 2.0 ATA. These are not the normally used treatments and are not in keeping with The HBOT Committee Report 2003,112 which states as follows: “the optimal number of hyperbaric treatments, the time following poisoning after which therapy is no longer effective and the optimal treatment pressure

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will require additional study . . . all patients at high risk deserve a single treatment . . . subsequent treatments may be performed within 6–8 h and continued once or twice daily until there is no further improvement . . . the optimal dose cannot be clearly stated . . . between 2.5 and 3.0 ATM seems appropriate.” Weaver’s HBO regime was less conventional than Scheinkestel’s. Weaver only gave three treatments, 18% of the HBO group did not complete the three treatments and the treatments were at lower ATA than recommended in the HBO Committee Report. This compares with Scheinkestel’s treatment regime that gave a further three treatments (total of six) if abnormalities persisted and all were at the recommended ATA. •

Unjustified assumptions made in interpreting six week data

The intention to treat analyzes used by Weaver as “patients with missing data for neuropsychological tests at six weeks were assumed to have cognitive sequelae.” This is contrary to the standard intention to treat (ITT) approach of carrying the last observation forward. Further, only one patient was lost to follow-up in the HBO group whereas four were lost in the NBO group, thus this assumption favored the HBO group.92 The impact of such arbitrary definitions on outcomes can be seen in Weaver’s 2002 abstract113 where he took the opposite approach and if data were missing, the outcome was deemed to be “favorable.” Data from the 6 and 12 month follow-up are apparently combined. Weaver states “a favorable outcome was found in 62/76 (82%) of HBO patients compared with 50/76 (66% treated with NBO (p = 0.027). If data from patients with unknown 6 and 12 month outcome data were excluded, a favorable outcome was present in 49/58 (84%) treated with HBO compared to 42/60 (70%) treated with NBO (p = 0.061).” •

Unjustified assumptions made in interpreting 6 and 12 month data

In the final publication,81 the definitions change again. With respect to the outcomes at 6 and 12 months, these were performed on the basis that ‘if patients had cognitive sequelae at 6 weeks, and missing data at 6 or 12 months, they were assumed to have cognitive sequelae at those times. This is invalid, as it does not allow for the improvement with time, which was demonstrated in patients with complete data. Such a definition couples the first outcome to later events and creates a spurious outcome dependent on the first. The statistical differences reported at 6 and 12 months merely reflect the results at 6 weeks, not necessarily the true longterm outcome. If the analysis is restricted to those patients with complete data, the statistically significant difference in late outcome is lost. Dr Weaver disputes110 that statistical significance is lost at 12 months but a p = 0.08 is not statistically significant. •

Soft outcome measures

The entire positive outcome of this study is based on reported symptoms. These were the primary determinant of a statistical difference between treatments. In the final publication,81 neuropsychological testing identified no difference between HBO and NBO; indeed, the mean neuropsychological testing scores for patients treated with NBO were within the normal range.78,92

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HBOT patients reported fewer difficulties with memory (p = 0.004) and this was the only significant symptom difference between the two groups. However, there were no statistically significant differences between groups on any of the memory-related neuropsychology test scores. •

Interpretation of neuropsychological tests

Disproportionate numbers of patients with cerebellar problems entered one arm of the Weaver study. Neurological sequelae occurred more commonly if there were cerebellar signs at the time of enrollment into the study. This was particularly so because two of the six neuropsychiatric tests involved “Trail-Making,” and this would be affected by even minor degrees of cerebellar dysfunction.78 This imbalance alone could have accounted for half the actual observed difference between groups because the absolute difference between arms was 16 individuals, yet there were 8 more individuals with cerebellar dysfunction and neurological sequelae in the NBO group.92 Olsen is more critical114 and states: “The neuropsychological data presented by Weaver are clinically underwhelming. The raw scores show a statistically significant difference between treatment groups in only one of six subtests (Trail-Making, Part 1), and even in this subtest, the normobaric group was at the mean demographically corrected score for a normal population at 6-week follow-up.” Buckley also comments that the mean performance of patients in the NBO group was normal for five of the six neuropsychiatric tests and above normal in the sixth.92,115 He questions how a meaningful outcome could label 46% of patients in the control group as having “cognitive sequelae,” when in fact, five of six of the mean test scores in that group were actually normal or above average. Weaver 110 responds that the neuropsychological test scores of patients with dysfunction are obscured by those without sequelae and that therefore the group mean scores do not detect a difference between groups, but no data are provided to support this. It is also of interest to note that the frequency of cognitive sequelae amongst patients who completed three HBO sessions was not different from those who did not complete the three sessions, and 18.4% of the hyperbaric group did not complete the required number of chamber sessions. Weaver et al.’s outcome measures were performed by any of ten different psychologists. Weaver states that the examiners were all psychology Ph.D. candidates with proper training, with inter-rater reliability being well established for these tests at 0.9 or higher. He also states that as the trial took 6 years, this necessitated multiple examiners. • Interpretation of 6 and 12 month data Weaver claims115 that “Cognitive sequelae at six months and 12 months were less frequent in the HBO group than in the NBO group, both according to the intentionto-treat analysis (p = 0.02 at 6 months, p = 0.04 at 12 months) and according to the efficacy analysis, (p = 0.03 at 6 months, p = 0.08 at 12 months).” Interestingly, in his presentation at the Undersea and Hyperbaric Medicine Society Annual Scientific Meeting July, 2002, and presented in abstract form, Weaver states “if data from patients with unknown 6 and 12 month data were excluded, a “favorable

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outcome” was present in 49/59 (84%) treated with HBO compared to 42/60 (70%) treated with NBO (p = 0.061).” • Lack of pretreatment neuropsychological assessment Weaver’s study performed no baseline neuropsychological assessment. As Raphael states, baseline information on abnormal cognitive tests is not provided. Given the heterogeneity of the population and the rather small sample size, one cannot rule out an imbalance between the treatment groups with respect to abnormal results of cognitive tests just as there was an imbalance with respect to cerebellar signs.116 •

Outcomes of other tests

There were no statistically significant differences between groups on the Geriatric Depression Scale, the Katz index of activities of daily living, nor in scores on the subscales of the SF 36 (social function, physical role, mental health, and energy). Weaver argues110 that these tests do not test cognition and confirm that the cognitive impairment is not due to depression. He also states that the “activities of daily Living” measures gross abilities to perform daily activities not cognition. He also states “the SF36 measures health related quality of life. It does not measure cognition but rather the patients’ perception as to whether the CO poisoning resulted in decreased quality of life for physical and psychological functioning.” However, in regard to the latter, his paper states: “We found no treatment-related differences in scores on the subscales (social function, physical role, mental health and energy) of the SF36. Clearly then, the conclusion is that the patients did not have the perception that the CO-poisoning results in decreased quality of life for physical and psychological functioning. • Adverse events Weaver reports a significant difference in the incidence of nystagmus post-treatment, with hyperbaric patients having a 12% incidence compared to 2.7% for the normobaric group (p = 0.05). The reason for this adverse effect in the hyperbaric group is not clear. It is also worth noting that 18.4% of the hyperbaric group did not complete the required number of chamber sessions for reasons including anxiety and middle ear problems. In an abstract presented to the ASM of UHMS117 in 2001, Weaver states that the NBO group tolerated chamber therapy better (96% versus 82%, p = 0.002). While these adverse events are not major, they must be taken in the context of the degree of benefit obtained from the treatment. •

Cost analysis

In his 1995 letter to the editor of the Annals of Emergency Medicine,107 Weaver states that other questions his trial may answer include differences between the two therapies (HBO and NBO) related to cost (including transport). This analysis is yet to be seen. Other criticisms include the following: • Small number of intubated patients (12) prevents interpretation of what HBO may or may not have to offer seriously injured patients.

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• Having stratified for time to treatment less than or greater than 6 h, Weaver does not report if there was a difference between these two groups, yet he is so critical of those studies where there was a delay of >6 h. • Weaver’s subsequent analysis concluded that: “HBO improved outcome if any of the following: LOC, COHb >25%, age > 50 and metabolic acidosis were present. In patients with none of these four criteria, HBO did not improve outcome. This conclusion uses an absolute value of COHb at the time this was first sampled and the recommended selection criteria could therefore exclude patients with significant exposure but delay in COHb measurement. It is worth noting that the actual COHb levels were only available in 55% of his patients. This statement is in contradiction with the literature and Weaver’s previous and subsequent declaration that “the difference in COHb between the groups is of no consequence as there is no relationship between COHb and outcome.110 Further it is difficult to understand the choice of age > 50, when his study stratified for age > 40 years and did not present the data for age greater than or less than 40. • The outcome should not be derived, as Weaver’s was, from complex interpretations of pooled differences in test scores, especially when those tests are not routinely conducted in clinical practice.115 Buckley92 concludes overall that the unbalanced recruitment, changed primary outcome, and the intention to treat (ITT) assumption when considered with the very small number of patients (16) resulting in the finding in favor of HBO, could easily mean that the trial outcome would have changed from significant to nonsignificant had these factors been otherwise. Given all the above, Weaver et al.’s conclusion of benefit arising of HBOT is not convincing. The benefit of HBOT demonstrated in this study, if there is one, may not be clinically significant.

18.3 CONCLUSIONS There are significant difficulties with comparing the outcomes of these investigations. Variations in study design, HBO and NBO protocols used, outcomes measured and patient populations included, make it difficult to draw firm conclusions.87 In addition, many of the studies show bias towards use of HBO in the more severely affected patients, follow-up is incomplete and overall, the numbers of patients studied is low. No reliable method to identify patients at high risk for neurologic sequelae has been identified. The efficacy of one HBO protocol over another has not been determined. Timing of evaluation (discharge, 1 month, 6 weeks, 1 year) has also not been determined. The ongoing debate about the efficacy of HBO is driven largely by these discrepant results.

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The best, most sophisticated, unbiased and comprehensive analysis of published human trial work to date, without conflicts of interest, and no pre-existing financial or reputational bias either pro or against HBO, was performed by Buckley92 who concluded that “The role of HBO remains unclear and the weight of the available evidence neither confirms nor refutes a clinically meaningful net benefit.” Buckley assessed the effectiveness of HBO compared with NBO for the prevention of neurological sequelae in patients with CO poisoning. Eight randomized controlled trials were identified. Two had no evaluable data and were excluded. A pooled OR for the presence of neurological symptoms at 1-month follow-up was calculated. At 1 month follow-up after treatment, sequelae possibly related to CO poisoning were present in 242 of 761 patients (36.1%) treated with NBO compared with 259 of 718 patients (31.8%) treated with HBO. The OR for neuropsychiatric symptoms with HBO was 0.77 (95% CI = 0.51, 1.14). A further analysis was performed by removing the results of trials with a Jadad score of less than 3/5 (the two trials published in abstract form only), leaving a total of 146 of 383 patients (38%) randomized to HBO with neurological sequelae at one month compared with 152 of 368 patients (41%) randomized to NBO [OR for neurological sequelae 0.70 (95% CI = 0.34, 1.47)]. When restricting the analysis to the two studies that enrolled more severely poisoned patients (the only two with a Jadad score of 5/5) the results remained inconclusive [OR for neurological sequelae 0.73 (95% CI = 0.22, 2.48)]. Buckley states that there were methodological shortcomings in all trials and empiric evidence of bias in some, particularly those suggesting benefit from HBO. The trials enrolled patients with CO poisoning of varying severity, employed different regimens of HBO and NBO. Only two were conducted with double-blinding through sham treatment. Pooled analysis of such inconsistent studies should be interpreted with caution. In the following issue of Toxicological Reviews, four knowledgeable clinical toxicologists from different parts of the world were asked to provide editorials on the subject. Brent, the editor, comments: “Given six relevant randomized clinical trials involving 1479 patients, if the effect of HBO were real and large, it is difficult to imagine that the trials would not be more definitive.118 Even the positive ones can be interpreted as having only marginal benefit.” “There are clearly insufficient data to consider HBO as a standard of care and it should be considered to be a therapy of as yet unproven benefit. Further, any benefit deriving from HBO is likely to be small. Thus, no physician or poison center should be held liable for withholding HBO given the uncertainty and even possibility of harm associated with this treatment.” Henry119 states: “Most of us would probably choose HBO because we know there is no real evidence of harm and “because it might do some good.” However, the benefit is not likely to be great.” Olsen114 concludes: “There is no recognized standard of care mandating the use of HBO.” Bentur120 was the most positive in favor of HBO, stating “it is impossible to state that HBOT should not be offered.” He goes on to provide an algorithm for treatment of CO poisoning based on the results of Weaver’s and Scheinkestel’s studies.

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Seger121 states: “believers believe that the studies that support HBO have fewer limitations than the studies that do not support HBO (the believers are very fervent, and tend to lump the atheists and agnostics together and suggest both be put to the sword). The more sceptical nonbelievers feel that the studies demonstrating no benefit have fewer limitations. The camps are divided,” with many in each camp seeming to have an investment in maintaining their belief system, regardless of the data. Lastly, there is in fact a downside to HBO. There is a cost both for providing the service and transport to the facility. This has not to-date been quantified. Transports of critically ill patients are associated with risk and while this has not specifically been quantified for CO-poisoning, there is considerable evidence for this in critically-ill patients. Further, there is documented morbidity to patients due to the treatment in a hyperbaric chamber. A report by the Department of Health and Human Services, Office of Inspector General, June Gibbs Brown, in October 2000 on HBOT: Its Use and Appropriateness,122 states: “According to our review, 18% of beneficiaries exhibit side effects (significantly greater than the literature suggests). The most common side effect is ear-related trauma, representing 63% of all observed side effects. While side effects are generally not severe, two individuals within our sample showed signs of oxygen toxicity. This relates to 1.3% of the population which also is significantly greater than the expected value cited in the literature. These statistics were based on our analysis of the 1998 National Claims History file maintained by Health Care Financing Administration (HCFA).”

18.4 WHERE TO NOW? While independent reviewers have, predictably, called for large, multi-center randomized, controlled and blinded, clinical trials, many in the hyperbaric community appear to believe this is either unnecessary, unethical or impractical, if not all three. Plans are therefore emerging for further randomized studies comparing different doses of HBO, selected from existing regimens and a pilot has been conducted.123 The optimal dose of HBO is certainly an important question for all indications for HBO, but it could be argued that at the present time we know too little about HBO for CO to select either the optimal doses or the optimal patient eligibility criteria for an optimal study. It will be apparent from the preceding that we agree that it would be absolutely necessary for further randomized trials to provide proof of benefit before HBO could be generally and unconditionally recommended for CO poisoning. We also believe that it would not in any way be unethical to randomize patients, given the lack of clear-cut evidence for the superiority of any one form of treatment over any other. It is not clear to us, however, that another randomized controlled trial is the appropriate next step. Large multicenter studies carry a large financial cost however and sometimes there can be a significant opportunity cost as well. If one study consumes the limited numbers of eligible patients, capable centers and research funding available for several years, this can be to the detriment of potentially better studies conceived after

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new basic science or epidemiologically generated information becomes available. It is therefore most important that any future studies have an optimal design and conduct, and are designed to answer a reasonable hypothesis. Herein arises a significant issue. Simple and broad hypotheses applied to heterogeneous populations with many confounding variables require very large studies to ensure matching of active and control groups, to ensure that relatively small but significant outcome improvements are detected and to allow for the subgroup analyses necessary to identify response in important subpopulations. Another factor that mandates large sample sizes is low incidence of the outcome measure of importance and this applies to the CO poisoning outcomes of death after rescue and development of delayed onset neurological sequelae (DNS). As an example, a highly important 50% reduction in mortality or DNS rate from, say, 10% to 5% would require a two armed randomized study sample size of nearly 1000 subjects to provide 80% likelihood of detection at p = 0.05 (2-tailed T test). The alternative trial design strategy is to utilize tight enrollment criteria to identify a specific subgroup for a test of therapy thought to provide significant benefit, based upon pilot data or coherent and generalizable large animal research. This could allow for smaller study sizes if the therapeutic effect is powerful and the outcome measure is relatively close to evenly distributed in the control group. Caution is subsequently needed in generalizing the results of any such study to different populations, doses or treatment timings. Patient selection for any therapy is clearly important and this could be a critical issue in the case of CO poisoning. To date, recommendations regarding the optimal population for treatment with HBO have generally used combinations of age, COHb level, history of LOC and presenting signs and symptoms. Consideration of age and indicators of cardiovascular or cerebral disease do seem very logical given the way that cerebral or cardiac hypoxia can exacerbate the severity of clinical poisoning that results from any given COHb level. It is not clear from the studies published to date whether such criteria are valid. While outcome for patients who have suffered CO-poisoning-related cardiac arrest is universally bad,124 there may or may not be a definable larger group of patients so severely brain injured as to have no reasonable prospect of recovery. It is clear that long-term harm can occur with and without LOC and recovery can follow severe as well as mild poisoning. It is not yet clear, however, whether there is a minimum threshold for injury and most significantly, whether there is better response to HBO amongst any particular CO poisoning population. In attempting to generate potential clinical study designs, a number of relevant hypotheses can usefully be generated from the existing human and animal data and from basic principles: • The value of HBO may vary significantly with the stage of injury. • The optimal dose of HBO may vary with stage of injury. • Optimal dose, especially in very early stage treatment, may be variable with degree of poisoning and this would indicate the need for therapy tailored to some measurable variable. • HBO and even NBO might be harmful at certain stages of the secondary injury process, perhaps only in susceptible individuals, by increasing

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•

• • • • • • •

lipid peroxidation or other manifestations of oxidative injury rather than reducing them. Unconsciousness or gross neurological deficit on admission is correlated with poorer outcomes and this is usually taken to be an indicator of severity of brain injury but this may not mean that this is the most treatment-responsive group. If one could measure and allow for the effects of residual intracellular CO and/or cellular hypoxia this seems likely to correlate with injury severity, but again might not select for the most treatment responsive group. LOC may be possible without harm, provided that cerebral oxygen delivery is maintained by greatly increased cerebral blood flow, and this might be a group of patients who can recover without any active therapy. Overall outcomes and response to therapy may be different depending upon the presence or absence of cotoxins such as volatile hydrocarbons, cyanides and other products of combustion. There may be significant inter-individual variability in susceptibility to CO mediated secondary cerebral injury and in the degree of recovery possible. There may be a significant inter-individual variability in response to HBO. Such variabilities may have both genetically determined and acquired elements. If HBO does accelerate recovery and reduce hospital stay, this may be sufficiently valuable to be worthwhile even if there is no net change in longterm outcome. If so, therapy could be most valuable to populations selected for characteristics other than susceptibility, for instance working age patients, parents, and carers or the psychiatrically disturbed.

The size and complexity of the studies likely to be needed and the extent of the above and, no doubt, other unknowns would suggest that the time is not yet right for large and costly human randomized controlled trials. Given that the provision of HBO for CO poisoning is established practice in some centers, it is not unreasonable for these centers to undertake studies comparing different but commonly used doses of HBO provided adequately powered, well governed, collaborative studies can be achieved at moderate cost, with study designs that address the limitations of previous work. Meanwhile, a huge natural experiment is continuing, unfortunately with little analyzable data being collected; CO poisoning is common and patients currently receives a wide range of different oxygen doses in both the normobaric and hyperbaric treatment environment. A well-designed clinical registry has the potential to generate specific hypotheses for testing with clinical trials and even to answer many questions outright. Meaningful data must be collected, however, and this will require agreement on markers of poisoning severity and outcome measures. It would also be much more valuable if any registry drew data from centers that do not use HBO as well as from the hyperbaric community’s patients. In addition to enabling comparison of outcomes between patients receiving NBO and HBO, the optimal initial duration of NBO for different poisoning severity is unknown, as is the place of increased inspired oxygen fraction during the postpoisoning, secondary brain injury phase.

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Animal and cell based research will continue to produce information that should be taken into consideration and of particular note here is the field of CO therapeutics. In recent years, identification of the role of CO as an intracellular signalling molecule and element of the hemoxygenase stress response system has led to two important conclusions: some elements of the pathology of CO poisoning may be related to disturbances of the physiological role of CO45,125,126 and exogenous CO might be a useful therapeutic substance.9,127−139 . Both of these ideas have implications for CO poisoning therapeutics. Exogenous CO can inhibit ischemia-reperfusion injury and appears to have neuro-protective, cardio-protective and lung protective properties in some animal models and this has already led to some human clinical trials. The doses used in these trials have been as high as 500 ppm,140 an order of magnitude above current occupational health limits and a level that has been associated with pathological outcomes, a fact which has been pointed out in critical commentaries.11,12 Nevertheless, the potential for exogenous CO to modulate immune and oxidative stress-related processes raises the question as to whether residual CO may have some protective effects after the bulk of excessive CO is eliminated following CO poisoning. It is clear that both CO and HBO biochemistry are in a state of evolution that should be closely monitored by toxicologists and clinical researchers. Work in other types of neurological injury is also likely to yield important information, both with regard to the potential for HBO use in the later and delayed onset stages of CO-related injury and with respect to alternative therapies to minimize CO related brain injury. Strategies which show promise for diffuse and hypoxic brain injury, such as moderate hypothermia and various anti-oxidant drugs,141,142 could well provide benefit for CO poisoning patients. If alternative neuroprotective strategies show significant benefit for CO, it would be appropriate to compare these with HBO and to test combined therapy. CO-related cardiac injury is also be a field needing further investigation. Recent work indicates that measurable injury is far more common than previously considered143 and HBO may moderate this, although this needs investigation. Cardiac injury might also prove a useful and more easily measured outcome than neurotoxicity for research aiming to select optimal dosing of oxygen and might even prove to be a usable surrogate enabling early assessment of overall severity of injury. Given the lack of predictive power of clinical signs and current biochemical markers, new markers of neurological injury severity would be useful if they were shown to correlate with either outcome or response to therapy. Cleaved tau, nonspecific enolase, MBP and S100B57,144−146 are amongst markers being considered. Serum could be readily collected from CO poisoning patients to produce a database which could yield useful information, provided good follow up and outcome measures are available to enable correlations to be sought. Medical imaging is advancing rapidly and various markers of severity have been proposed based upon Computed Tomography (CT), Magnetic Resonance Imaging (MRI) and Tc-Hexamethylpropyleneamine Oxime (HMPAO) Single Photon Emission Computed Tomography scanning (SPECT).147−157 To date none have become established as reliable determinants of response to treatment and any such markers would need to be readily available with rapid turn-around if they are to be

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useful in deciding therapeutic directions. Quantitative EEG monitoring has also been tested as a marker of response, no doubt, will other measures.158 A final critical factor is that it seems likely that there are variations in innate susceptibility or resistance to injury and responsiveness or resistance to therapy for CO poisoning, as is increasingly seen as important in many other areas. Gender is almost certainly significant, as is the case in trauma and stroke.159−161 As this may be based upon antioxidant protective mechanisms of female hormones, it is conceivable that response to exogenous oxygen therapy could be different and any future research should look for potential gender differences. Recently, Hopkins162 has reported in abstract that ApoE typing is a significant predictor of outcome in patients followed-up at his institution. The ApoE e4 allele, associated with poor outcomes in many other forms of degenerative and acute brain conditions, was associated with higher incidence of cognitive sequelae after CO poisoning and benefit from HBO appeared to be confined to patients with ApoE4—in those without the e4 allele there was no difference in outcome between HBO and non HBO treated groups. At present this measure is not available as a point of care test but this and other markers, including those drawn from the fields of genomics and proteomics may hold the future of case selection and progress monitoring for specific treatments such as HBO. Despite over four decades of hope and persistence, HBO has, as yet, failed to live up to it’s promises as a valuable therapy for CO poisoning. While there are sufficient indications of potential benefit to support ongoing research, there is insufficient evidence to support promotion of HBO use outside of clinical trials or for the development of new HBO facilities specifically for CO poisoning treatment. Given an ongoing problem with CO poisoning and an increasing availability of high standard hyperbaric facilities incorporated into major hospitals, the infrastructure for next generation clinical trials exists. Hopefully lessons will be taken from trials to date in developing future trials but it should not be assumed that existing protocols are optimal and an open mind should be kept to alternatives. Meanwhile, those facilities treating CO poisoning regularly will hopefully contribute data to registries which will also gather data on patients treated with NBO, which continues to be the standard of care, albeit without any good data regarding the optimal duration of therapy.

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140. Mayr FB, Spiel A, Leitner J, et al. Effects of carbon monoxide inhalation during experimental endotoxemia in humans. Am. J. Resp. and Crit. Care Med. 2005; 171(4): 354–360. 141. Giffard RG, Jaffe RA. Advances in understanding protection from cerebral ischemia. Curr. Opin. Anaesthesiol. 2002; 15(5): 495–500. 142. Wang KK, Larner SF, Robinson G, Hayes RL. Neuroprotection targets after traumatic brain injury. Curr. Opin. Neurol. 2006; 19(6): 514–519. 143. Henry CR, Satran D, Lindgren B, Adkinson C, Nicholson CI, Henry TD. Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. JAMA 2006; 295(4): 398–402. 144. Rasmussen LS, Poulsen MG, Christiansen M, Jansen EC. Biochemical markers for brain damage after carbon monoxide poisoning. Acta Anaesthesiologica Scand 2004; 48(4): 469–73. 145. Berger RP, Adelson PD, Richichi R, Kochanek PM. Serum biomarkers after traumatic and hypoxemic brain injuries: insight into the biochemical response of the pediatric brain to inflicted brain injury. Develop. Neurosci. 2006; 28(4–5): 327–335. 146. Brvar M, Mozina H, Osredkar J, et al. S100B protein in carbon monoxide poisoning: a pilot study. Resuscitation 2004; 61(3): 357–360. 147. Gale SD, Hopkins RO. Effects of hypoxia on the brain: neuroimaging and neuropsychological findings following carbon monoxide poisoning and obstructive sleep apnea. J. Int. Neuropsychol. Soc. 2004; 10(1): 60–71. 148. Wu CI, Changlai SP, Huang WS, Tsai CH, Lee CC, Kao CH. Usefulness of 99mTc ethyl cysteinate dimer brain SPECT to detect abnormal regional cerebral blood flow in patients with acute carbon monoxide poisoning. Nucl. Med. Comm. 2003; 24(11): 1185–1188. 149. Sener RN. Acute carbon monoxide poisoning: diffusion MR imaging findings. AJNR 2003; 24(7): 1475–7. 150. Teksam M, Casey SO, Michel E, Liu H, Truwit CL. Diffusion-weighted MR imaging findings in carbon monoxide poisoning. Neuroradiology 2002; 44(2): 109–113. 151. Kesler SR, Hopkins RO, Blatter DD, Edge-Booth H, Bigler ED. Verbal memory deficits associated with fornix atrophy in carbon monoxide poisoning. J Int Neuropsychol. Soc 2001; 7(5): 640–646. 152. Hurley RA, Hopkins RO, Bigler ED, Taber KH. Applications of functional imaging to carbon monoxide poisoning. J. Neuropsychiatry and Clin. Neurosci. 2001; 13(2): 157–160. 153. Gale SD, Hopkins RO, Weaver LK, Bigler ED, Booth EJ, Blatter DD. MRI, quantitative MRI, SPECT, and neuropsychological findings following carbon monoxide poisoning. Brain Inj. 1999; 13(4): 229–243. 154. Silver DA, Cross M, Fox B, Paxton RM. Computed tomography of the brain in acute carbon monoxide poisoning. Clin. Radiology 1996; 51(7): 480–483. 155. Pracyk JB, Stolp BW, Fife CE, Gray L, Piantadosi CA. Brain computerized tomography after hyperbaric oxygen therapy for carbon monoxide poisoning. Undersea Hyperb. Med. 1995; 22(1): 1–7. 156. Murata T, Itoh S, Koshino Y, et al. Serial cerebral MRI with FLAIR sequences in acute carbon monoxide poisoning. J. Computer-Assisted Tomogr. 1995; 19(4): 631–634. 157. Gotoh M, Kuyama H, Asari S, Ohmoto T, Akioka T, Lai MY. Sequential changes in MR images of the brain in acute carbon monoxide poisoning. Comput. Med. Imaging Graph. 1993; 17(1): 55–59.

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158. Murata M, Suzuki M, Hasegawa Y, Nohara S, Kurachi M. Improvement of occipital alpha activity by repetitive hyperbaric oxygen therapy in patients with carbon monoxide poisoning: a possible indicator for treatment efficacy. J. neurol. Sci. 2005; 235(1–2): 69–74. 159. Vink R, Nimmo AJ, Cernak I. An overview of new and novel pharmacotherapies for use in traumatic brain injury. Clin. Exper. Pharm. Physiol. 2001; 28(11): 919–921. 160. Roof RL, Hall ED. Gender differences in acute CNS trauma and stroke: neuroprotective effects of estrogen and progesterone. J. Neurotrauma 2000; 17(5): 367–388. 161. Choudhry MA, Bland KI, Chaudry IH. Gender and susceptibility to sepsis following trauma. Endocrine, Metab. Immune Disorders Drug Targets 2006; 6(2): 127–135. 162. Hopkins RO. Effects of the ApoE4 allele on cognitive outcome in acute CO poisoning. Undersea Hyperb. Med. 2006; 33(5): 337–338.

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19

A Challenge to the Healthcare Community: The Diagnosis of Carbon Monoxide Poisoning David G. Penney

CONTENTS 19.1 19.2 19.3 19.4

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Problems in the Diagnosis of CO Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Chronic Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Addendum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19.4.1 The RAD-57 cm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

437 439 443 446 446 448

19.1 INTRODUCTION Overview Statement: If you were able to chose the kind of brain injury you were to incur, it would be better in terms of the potential for recovery to have a stroke, a concussion in a motor vehicle accident, etc. than carbon monoxide poisoning.

There are many problems with CO poisoning generally (Table 19.1). Although CO is a very simple molecule, its mechanisms of action are complex and multiple. There is more to its pathophysiology than simply the tying up of hemoglobin such that oxygen cannot be transported. It traverses the blood-barrier and dissolves in the protoplasm of cells, attaching there to a variety of molecules. As stated elsewhere in this book, CO is a very “smart poison.” It is colorless, tasteless, odorless, and is completely nonirritating to respiratory and mucous membranes. Thus it is undetectable by humans with unaided senses. Unlike other “dumb” poisons, it leaves the body quickly when the victim again breathes unpolluted air, leaving behind just the damage it has done. CO doesn’t hang around to be detected and identified weeks, months, or years later, like lead and mercury. 437

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TABLE 19.1 Some of the Major Problems in Dealing with Carbon Monoxide Poisoning1 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Mechanisms of toxicity involve more than CO attaching to hemoglobin. Lack of public awareness of the dangers of accidental CO poisoning. Insufficient professional awareness in the diagnosis of CO poisoning. Extent of suicidal use of motor exhaust and other fumes. Assessment of the severity of the poisoning. Criteria to be used in the treatment of poisoned patients. Pathogenesis and prediction of the development of delayed sequelae. Effectiveness of hyperbaric oxygen therapy is largely unproven. Are there any effective alternative treatments to HBO? Unknown morbidity and mortality of undiagnosed cases.

The public and indeed most members of the healthcare community are ignorant of many of the risks involved in working and playing around equipment that emits CO (see Chapter 15). While automobiles have enjoyed the reputation of being extremely dangerous in terms of CO emissions, this is no longer the case when they are in good repair and are used properly. Because of catalytic converters, virtually all of the CO produced by the automobile engine is now converted to harmless carbon dioxide and water vapor. Other vehicles such as high-powered, watercraft fueled by gasoline and using engines similar to those used in cars, now pose the greatest risk of deadly CO poisoning to individuals. Some of these boats, such as a single inboard, twin-engine ski boat may emit as much CO as 250–300 automobiles. CO concentrations immediately behind such boats may range to over 20,000 ppm depending on boat movement, wind direction, and speed, CO concentrations at least 40 times the lethal dose for humans. People have difficulty recognizing and appreciating the danger posed by these boats, since it usually occurs in the open air, not inside a structure. Medical personnel have traditionally underappreciated the frequency of CO poisonings, both the acute and the chronic types, but especially the latter, and have been notorious in misdiagnosing CO poisoning. Because the symptoms produced are mostly general and nonspecific, they are usually associated with other diseases that lie more central to internal medicine, conditions that result from bacteria, viruses, hormonal changes, physical trauma, and so forth. In fact, the very nature of the multiplicity of symptoms that CO poisoning produces, tends to confuse physicians and nurses. If the flu, hypothyroidism, stroke, and so forth are not suggested, then psychosomatic or psychiatric conditions often are. Since few symptoms or signs are produced that occur only with CO-poisoning (i.e., pathognomonic), it is often difficult to immediately identify a cause. Identification of CO poisoning as the cause is made easier by the taking of a full situational history. When possible, this consists of determining where the patient was during the past few hours. Who was with him and were the others also sick? Was it a house, apartment, recreational vehicle, and so forth? Were pets also sick or died? How was the space heated? Did the patient notice

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a pattern in that he/she was less sick when he/she left the site, and became sicker again upon return? Had there been reports of heating devices malfunctioning, or the use of internal combustion engines near or within the structure? Assessment of the severity of CO poisoning has been a thorny problem. Far too much reliance has been placed on carboxyhemoglobin (COHb) measured at the emergency center, and too little on evaluation of the conscious state and behavior of the victim. Recent studies suggest that gait and balance may be among the most important prognostic signs, and should be used far more often in deciding the course of treatment. Long or “soaking” exposures to CO invite more rapid and aggressive therapy than shorter CO exposures. The early use of the new generation of pulse CO-oximeters (see addendum and Chapter 33), possibly even at the site of discovery, will aid in assessing poisoning severity and treatment regimen. As long as the use of hyperbaric oxygen therapy (HBOT) has been available to treat CO-poisoned patients, it remains unclear whether it is really effective in reduced long-term health damage. Two other chapters in this book discuss in detail the pros and cons of the half a dozen or so clinical studies that have tested the HBO hypothesis. Little progress appears to have been made in the past decade in developing new approaches to treating CO poisoning, or in understanding HBOT.

19.2 PROBLEMS IN THE DIAGNOSIS OF CO POISONING CO poisoning is difficult to diagnose for a number of reasons, and the rate of misdiagnosis has been in some cases, shockingly high. Part of the problem has to do with its special properties, and some has to do with healthcare workers ignorance of the symptoms by which it presents (Table 19.2). There has been overreliance on COHb level, and also the fact that COHb is not routinely measured in patients

TABLE 19.2 Major Reasons for Failure to Diagnose Carbon Monoxide Poisoning in the Emergency Room 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

Usually a low (or zero) index of suspicion for CO poisoning by physicians. Lack of training in toxicology and myopic thinking by physicians. Too many disparate, seemingly unrelated, multisystems symptoms involved. Nonspecific symptoms confused physicians. Incorrect clue given by patient or companion. Failure to obtain complete situational histories. Presentation in ER that appears not to require emergency measures. Mistaken belief that COHb must always be greatly elevated. Distraction by other traumatic or metabolic condition/disease. Dependence on old style, two wavelength pulse-oximeter for measurement of O2 saturation. Use of less than the best, even irrelevant clinical tests for CO, unless goal is R/O (i.e., rule out). COHb is NOT routinely measured in the ER.

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TABLE 19.3 Carbon Monoxide Exposure Types •

Acute, brief exposure

•

Acute, “soaking”

•

Chronic (>24 h)

Immediate presentation Delayed presentation + 100% oxygen Immediate presentation Delayed presentation +100% oxygen Immediate presentation Delayed presentation +100% oxygen

high COHb COHb may be low COHb may be low - high COHb COHb may be low COHb may be low COHb high to low COHb may be low COHb may be low

TABLE 19.4 A Situational History • • • • • • • • • •

Living abode - house, apartment, etc. Heating systems Other people sick there Pets sick/dead Feel better when away, worse when return Periodicity with work, weekends, vacations/season Car driven - year, engine Use of small gasoline engine/attached garage Prolonged illness/seen other docs previously/recently New vs. old building

entering a physician’s office or an emergency room (ER). Recent studies show that there is virtually no relationship between reported COHb saturation and long-term outcome. In some cases COHb was barely elevated or even normal, yet the patient sustained brain damage. The grid of the various types of CO poisonings shown in Table 19.3 indicates why COHb may be normal or well below levels considered toxic in individuals who sustained serious CO poisonings. We see oxygen saturation obtained by two-wavelength pulse oximeters continuing to be printed on the charts of CO-poisoned patients although it has no reality in such cases. The falsely high number could even lead to tragic action by a healthcare worker who does not understand that the number is not accurate. There are numerous examples of healthcare workers failing to avail themselves of all of the clues available to them when a patient presents with symptoms consistent with CO poisoning. Many of these cases end tragically. A high index of suspicion must be maintained about possible CO poisoning when seeing patients (Table 19.4). One very important tool in diagnosing CO poisoning, and indeed other poisons, is the “situational history”. Table 19.5 shows some of the components, that is, questions asked when and if possible, when building a situational history.

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TABLE 19.5 Index of Suspicion (for CO Poisoning) Should be Raised by: • • • • • • • • • • •

Presentation during winter Several/many people presenting “ill” from same household Elevated plasma glucose c/o Memory problems c/o Furnace/heat problem at home Presentation after electrical power outage c/o Pets sick/dead c/o Headache, Nz, Dz, fatigue/weakness c/o “Illness” when going to/staying at, one place, not at others Flushed pink/cherry red skin Unexplained LOC/syncope

Very recently in Florida, a man and his adult son were staying at a motel resort. Overnight both were poisoned by CO. The son died, while the father survived. It was later learned that other motel patrons had been sick the week before, had gone to the hospital, where they were eventually diagnosed with CO poisoning. With an appropriate index of suspicion of CO, the use of proper diagnostic techniques by emergency personnel, and effective communication, tragedies like this can be averted. Clearly, getting the right diagnosis can be critical with possible CO poisoning. Table 19.6 lists possible misdiagnoses of CO poisoning, and Table 19.7 lists the frequency of reported incidences of major misdiagnoses of CO poisoning. In another instance several years ago, a prominent urologist was attending a meeting in the west with his wife, a surgical nurse. After the first night in a posh new ski hotel, both became violently sick. They went to the local ER. Upon entering the facility the urologist said he believed they had eaten some “bad” chicken sandwiches on the plane coming from the east. The ER personnel, hearing this from a fellow physician, accepted his diagnosis and treated him and his wife with antiemetics, and so forth. The doctor and his wife then went back to the hotel to continue the urology meeting, skiing, and dining. The next morning the urologist was dead, and his wife was in a coma that lasted several days. She suffered permanent, irreversible brain damage, involving changes in cognitive ability, personality, physical pain, and so forth. If only COHb had been measured at the ER. Later it was learned through testimony and examination of internal memos that employees and management of the hotel had been aware of a “CO problem” there for over 6 months before the doctor died. In another case in a large eastern US city, an elderly woman was taken to a very prominent local hospital known for its expertise and training programs in emergency and trauma medicine. ER personnel there failed to diagnose the patient with CO poisoning, apparently because the emergency medical technicians who went to her house and transported the woman saw a bottle near the chair she was found in. She was treated as an alcohol overdose case. Shortly afterward, it was discovered that there

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TABLE 19.6 Some Possible Mistaken Diagnoses in Patients with Carbon Monoxide Poisoning1 Misdiagnosis

Cause

Neurological Cerebrovascular accident Migraine, tension headache Epilepsy Meningitis, encephalitis Parkinsonism

Cerebral ischemic accident due to CO poisoning Headache Anoxic convulsions Vomiting, headache, bizarre neurological symptoms Late-onset parkinsonian symptoms

Psychiatric Depression Anxiety state Hyperventilation syndrome Acute confusional state

Lethargy, somatic symptoms Hyperventilation, headache, malaise Hyperventilation Confusion, hallucinations

Cardiac Myocardial infarction Cardiac arrhythmias

A critical coronary artery lesion decompensated through hypoxia Conduction system hypoxia

Pharmacological and toxicological Drug overdose Ethylene glycol poisoning Ethanol intoxication Drug abuse

Hypoxic coma, nontraumatic rhabdomyolysis Coma and renal failure Vomiting, ataxia, slurred speech, coma Agitation, confusion, hallucinations

Infections Influenza and other viral infections Post viral syndrome Gastroenteritis and food poisoning Pneumonia Sinusitis

Muscle aches, tachypnea, headache, exhaustion Lethargy, myalgia Nausea, vomiting Dyspnea, delirium Headache, malaise

Others Cholecystitis and other acute abdominal conditions

Abdominal pain, nausea, vomiting

was no liquor of any kind in the house. The woman had been sitting, then slumping, in the same chair for as long as 3 days. At the hospital the usual “tox screen” found no alcohol or other drugs in her body. Shortly after that, substantial concentrations of CO were discovered in her house by the woman’s daughter. The woman remained comatose for many days in hospital, had a long drawn out period of recovery, and sustained severe brain damage. This is the second example of comments by less qualified personnel being allowed to influence the decision about the proper medical work-up to achieve an accurate diagnosis. In this case the patient failed to receive the proper treatment, which in this case would almost certainly have been HBOT.

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TABLE 19.7 Common Misdiagnosis for Carbon Monoxide Poisoning by Reported Frequency2 Food poisoning Psychiatric disease, hysteria, confusion, depression Heart disease presenting as angina or syncope Alcohol intoxication or delirium tremens Acute solvent intoxication Migraine headache Ischemic cerebral disease Cerebral hemorrhage Cerebral tumor (convulsions)

38% 18% 13% 7% 7% 6% 4% 4% 3%

TABLE 19.8 Characteristics of Chronic Carbon Monoxide Poisoning6 1 2 3 4 5 6 7 8 9

Lasts more than 24 h Often goes long undetected Masquerades as the flu, fatigue, and so forth. Often many people “sick” simultaneously The “sickness” may show a periodicity synchronous with season May go away upon leaving poisoning site (to work, on vacation, etc.) Nearly always misdiagnosed by physicians May involve pets “sick,” dead at same time Rarely involves sinus congestion, cough [when present, it may be due to other compounds (e.g., NOx , SO2 ) in exhaust gases]

19.3 CHRONIC CARBON MONOXIDE POISONING Working Assumption: For every single case of chronic carbon monoxide poisoning reported / successfully diagnosed, there are 10 cases that go unreported/undiscovered/undiagnosed.

Chronic CO poisoning as I define it is an exposure to CO of more than 24 h, whether continuous or discontinuous.3 Beyond this, the characteristics of such CO poisonings (Table 19.8) often go long undetected, sometimes for years. It may masquerade as the flu, chronic fatigue, fibromyalgia, chemical hypersensitivity (MCS), and so forth. Often several or many people are “sick” simultaneously, and for extended periods uncharacteristic of viral or bacterial infections. The condition often subsides or disappears when the victim leaves the poisoning site, but reappears when the victim returns. It may show a seasonal periodicity if it is the primary space heating appliance that is malfunctioning. This type of CO poisoning has the highest misdiagnosis

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CO ignored

CO regarded as rare

Patient ill and stays at home

Chronic exposure to CO

Misdiagnosis

Effects not understood

FIGURE 19.1 Cycle of misunderstanding and misdiagnosis.

rate by healthcare professionals. In the CO Support Study in the UK it was the heating professionals who were most likely to diagnose the problem.4 This type of CO poisoning may result in pets sick with symptoms not unlike those of the humans. It rarely involves sinus congestion, cough or sneezing, although leaking exhaust gases containing irritants could do this—CO alone will not.5 Figure 19.1 illustrates the cycle of misdiagnosis often encountered with chronic CO poisoning. The presence of CO in a breathing space usually goes long undetected, and even when it is detected may be denied by those in authority. The presence of the CO and its possible health damaging effects are often misunderstood by those being poisoned, and worse, by the medical personnel consulted. Finally, people feeling ill from what eventually turns out to be CO, almost invariably spend increased time in the contaminated breathing space attempting to recover, but only become worse or possibly even die with severe poisoning. Some of the comments that I hear from the public regarding such poisonings are found in Table 19.9. I have condensed these comments into what I call “commonalities.” The symptoms consist of headache, fatigue, nausea, dizziness, and so forth.3 Nearly everyone who contacts me is certain he/she was exposed to CO in one way or another. There has to be a source, since CO doesn’t come out of thin air. A dominant theme I’ve heard hundreds of times is that “my doctor won’t take my complaints seriously,” that “CO comes, goes (once you are in fresh air), and then you are ok,” and finally, “there are no medical people in my area who understand CO’s effects!”. The public wants to know how it is diagnosed, when he/she will get better, and what the treatments are. Diagnosis of CO poisoning is a problem as discussed above, particularly if the victim has left the site of exposure for some days or weeks, since CO quickly leaves the body. Making pronouncements about when people will

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TABLE 19.9 Inquiries About Carbon Monoxide Poisoning—Commonalities in my Experience6 • • • • • •

Complaints of continuous headache, fatigue, nausea, dizziness, and so forth. Certainty by complainant that CO exposure occurred. “My doctor won’t take my complaints seriously!”—“CO comes, goes, and . . . (he/she says) you are ok!” “There are no medical people are in my area who understand CO’s effects!” How is it diagnosed? When will I get better? What are the treatments? What long-term damage might the CO have caused to my child/children?

TABLE 19.10 Clues to the Discovery of Chronic Carbon Monoxide Poisoning6 • • • • • • • • •

Lethargy, headache, and so forth of long duration Long-standing “illness” intractable to medical solutions Multiple cases of similar illness at one location “Illness” that may suddenly improve when leaving site “Illness” that improves when combustion device(s) is turned off or taken away Morbidity/mortality of pets CO alarm sounding, once or repeatedly Presence of malfunctioning furnace, water heater, and so forth. Measurement of CO by fireman, service personnel, and so forth at the presumed site of poisoning.

be well again is very risky even under circumstances of thorough knowledge of a case, and telling people it is unlikely they will get well or that their health damage is permanent is very hard to do. I do make recommendations about treatment, but as we all know, brain damage currently remains irreversible. Finally, many people ask what long-term damage might the CO have caused their children, born and unborn. Many effects of CO on both children and fetuses have been described by Penney,7 but identifying damage caused by CO in any one case is difficult. There are many clues to discovery of chronic CO poisoning (Table 19.10). Headache and lethargy of long duration should raise the suspicion of CO exposure. Similar to the comments above, a long-standing “illness” intractable to medical solutions should have CO poisoning placed high on the differential diagnosis list. Likewise, the incidence of multiple cases of similar “illness” at one location is an important clue, and an “illness” that suddenly improves when the victim leaves the site, or when a key combustion device is rendered nonfunctional or is removed, should cause the investigator to suspect a site-specific poisoning. As above, morbidity or even mortality of pets is important. “CO is an equal opportunity poison,” not discriminating on the basis of skin color, gender, religion, or even species. If the organism is warm-blooded and uses hemoglobin as its circulating oxygen carrier, it is subject to injury or death from CO poisoning. The degradation of a heating appliance

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TABLE 19.11 Common Misdiagnoses for Chronic Carbon Monoxide Poisoning6 • • • • • • • • • • • • • • •

The “flu” Other viral or bacterial pulmonary or gastrointestinal infections Bad/tainted/poisoned food Psychosomatic problem, malingering General “run-down” condition A “female” problem Allergy/asthma Psychiatric condition, for example, depression Chronic fatigue syndrome Chemical hypersensitivity (i.e., MCS) Fibromyalgia Multiple sclerosis (MS) Lymes disease Endocrine problem (e.g., hyper- or hypo-thyroid condition) Immune deficiency

such as furnace through corrosion of one or another part, often produces chronic CO poisoning, while discovery of the problem usually occurs when the CO problem is particularly severe. A CO detector/alarm that sounds intermittently over a period of days or weeks is probably identifying a site of chronic CO poisoning. Table 19.11 lists common misdiagnoses made in cases of chronic CO poisoning. The “flu” is probably the most common misdiagnosis. Lack of a fever does not guarantee that the condition is not being caused by a “bug.” “Bad or tainted” food may be pronounced the cause, but this curse is more commonly encountered as the misdiagnosis in cases of acute CO poisoning, as revealed in the tragic story above. A third large area of false cause identification centers around accusations of mental illness, depression, psychosomatic condition, malingering/faking it, and exaggerating minor irritations. This usually stems from the confusion that CO poisoning causes in medical personnel owing to the large number of symptoms generated. Other classic misdiagnoses for chronic CO poisoning include multiple sclerosis, lyme’s disease, fibromyalgia, chronic fatigue syndrome, hypothyroidism, chemical hypersensitivity, allergic reaction, immune deficiency, a “female” problem, general run-down condition, and endocrine problem. Many of these can be easily ruled out by doing the appropriate clinical test.

19.4 ADDENDUM 19.4.1 THE RAD-57 CM Masimo is the innovator of Signal Extraction Technology (SET)® pulse oximetry and the inventor of pulse CO-oximetry. This technology is capable of continuously and noninvasively measuring COHb and methemoglobin (MetHb) in the blood.

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FIGURE 19.2 Masimo Rad-57, hand-held pulse CO-oximeter. It allows clinicians and others to continuously and noninvasively measure carbon monoxide levels in the blood, reducing the need for invasive and expensive arterial blood gas analysis. (From Masimo Corporation website. Rad-57 Pulse CO-oximeter. Available at: http://www.masimo.comlrad-57/index.htm. Accessed September 26, 2005.)

Masimo Rainbow SET™ was developed out of Masimo SET® . It informs the operator about the vascular oxygen status of patients, while continuously and noninvasively monitoring other species of hemoglobin, such as COHb (SpCO%) and MetHb (SpMet%). Rainbow extends Masimo SET® through the addition of signal analysis algorhithms that run in parallel with it, to reveal the presence and levels of these hemoglobin species (see Figure 19.2) Because the Masimo parallel engines and adaptive filters receive more than seven discrete wavelengths of light (note incoming signal λ1 . . . λn ), multiple constituents of hemoglobin are detectable and can be quantitated, as compared to conventional pulse-oximeters that employ only two wavelengths. The wavelengths used span those necessary to recognize oxygenated hemoglobin as well as COHb and MetHb. For example, when CO is bound to hemoglobin, a conventional red/infrared oximeter misreads COHb essentially as oxygenated hemoglobin, producing a falsely high SpO2 value that may have disastrous immediate, delayed, or even chronic effects on brain and cardiac function. Pulse CO-oximetry relies on the same principles of spectrophotometry used to determine blood oxygen saturation in the laboratory. The underlying physical principle in pulse oximetry is the absorption of specific light wavelengths while passing

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through tissues. In pulse CO-oximetry the percent of total hemoglobin found as either COHb (SpCO%) and/or MetHb (SpMet%) is measured. The Masimo Rainbow sensor emits multiple wavelengths of light. Output of the adjoining photo detector is sent to the instrument, where Rainbow SET™ technology employs parallel algorhithms and adaptive digital filters to process the data. The Rainbow device displays as percentages: oxyhemoglobin (SpO2 %), COHb (SpCO%), and MetHb (SpMet%), plus the core parameters derived from the Masimo SET technology platform, pulse rate (PR), perfusion index (PI), and signal IQ® (SIQ). A number of single-use, latex-free, adhesive sensors are available for patients . . . from adults to neonates. Reusable adult and slender finger clip sensors are also available for short-term monitoring and spot checks. Note that a Rainbow-empowered device provides a choice of two wavelength sensors for SpO2 , pulse rate, and perfusion index measurements, or Rainbow SET® multiple-wavelength sensors to add COHb (SpCO%), MetHb (SpMet%), or both to the pulse-oximeter. Editors note: This section has been included in this book for informational purposes only. The editor is not an employee of Masimo Corporation and has taken no money, gifts, whatever, and will not do so in the future, for providing this inclusion.

References 1. Lowe-Ponsford, F.L., Henry, J.A. Clinical aspects of carbon monoxide poisoning. Adverse Drug Reactions and Acute Poisoning Reviews, 8, 217–240, 1989. 2. Bartlett, R. Carbon monoxide poisoning. In: Clinical Management of Poisoning and Drug Overdose, 3rd ed., Haddad, L.M., Shannon, M.W., Winchester, J.F., ed., W.B. Saunders Co., Philadelphia, Chapt.70, pp. 885–898. 1998. 3. Penney, D.G. Chronic carbon monoxide poisoning. In: Carbon Monoxide Toxicity, D.G. Penney, Ed., CRC Press, NY, 2000, Chapt. 18, pp. 393–418. 4. Hay, A.W.H., Jaffer, S., Davis, D. Chronic carbon monoxide exposure: The CO Support study. In: Carbon Monoxide Toxicity, D.G. Penney, ed., CRC Press, NY, 2000, Chapt. 19, pp. 419–438. 5. Dwyer, B., Leatherman, Manclark, Kimball, K., Rasmussen, R. Carbon Monoxide: A Clear and Present Danger, ESCO Press, USA, 3rd ed., 2003 (www.escoinst.com). 6. Available at: www.coheadquarters.com/CO1.htm 7. Penney, D.G. Effects of carbon monoxide exposure on developing animals and humans. In: Carbon Monoxide, D.G. Penney, Ed., CRC Press, NY, 1996, pp. 109–144.

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Neuroimaging after Carbon Monoxide Exposure Gunnar Heuser

CONTENTS 20.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20.2 Sequential Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20.3 Location and Symmetry of Lesions, and Hypofrontality and Disinhibition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20.4 Review of the Recent Literature . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20.5 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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20.1 INTRODUCTION Neuroimaging was previously reviewed by I.S.S. Choi in the book Carbon Monoxide Toxicity, by Penney, published in 2000.1 His review included representative Computed Tomography (CT), Magnetic Resonance Imaging (MRI), Single Photon Emission Computed Tomography (SPECT), and Magnetic Resonance Spectroscopy (MRS) scans. My review is meant to update and complement that of Choi’s. Neuroimaging helps to understand the clinical picture and to correlate findings with other evaluations. The field has advanced in recent years in that the techniques are in some respects vastly improved. The reader is invited to compare the SPECT scans presented in Choi’s chapter with the ones presented here. Present-day imaging of anatomical (MRI, CT) and functional [(SPECT, Positron Emission Tomography (PET)] impairment provides a significant visual aid to the assessment of brain anatomy and function, especially when presented in color. Brain scans now also lend themselves to statistical analysis, comparing a given scan to a control population or analyzing regions of interest (ROI) with other regions in the same brain scan.2

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20.2 SEQUENTIAL STUDIES CO exposure, acute and chronic, can result in long lasting (i.e., years) impairment of neurological and other functions. The need for sequential follow-up exams is obvious in view of the potential long-term effects of CO poisoning. Follow-up neuroimaging and other testing is often mandatory for assessment of a given patient as the clinical picture evolves. It is also important if one wants to assess the efficacy of the course of treatment. Sequential neuropsychological testing is a very useful assessment tool. However, it is expensive. Also, some tests administered suffer from potential learning effects, thus giving the false impression of improvement at the time of follow-up, because the patient has learned to perform better in the follow-up test since he or she is repeating the test. Examinations by a neurologist are not always comparable, especially if the patient is not followed by the same physician. In view of the above limitation, sequential neuroimaging studies appears to be the procedure of choice in assessing a patient over time, provided the patient returns to the same imaging facility which uses the same imaging protocol.

20.3 LOCATION AND SYMMETRY OF LESIONS, AND HYPOFRONTALITY AND DISINHIBITION From a diagnostic point of view, abnormalities after CO exposure would be expected to be present in similar locations and to be symmetrical. This is not the case. One would also expect clinical observations and neuroimaging abnormalities to show a correlation. Often, this is actually not the case. Finally, one would naively assume that damage in different brain regions should be viewed as a focal abnormality which is not functionally connected to other areas of the brain. This is also not true since frontal hypofunction (hypofrontality) may result in hyperfunction in the posterior areas of the brain and also in subcortical areas. Since the frontal brain exerts an inhibitory function, frontal lobe damage may result in disinhibition.3,4 While neurotoxic exposure (e.g., solvents, pesticides, mold toxins) in general may not be obvious on the MRI at all, or result in nonspecific small high intensity (demyelinating/vascular) lesions (foci), MRI studies in CO-exposed patients very frequently show abnormal MRIs with multiple and significant abnormalities, especially in the white matter and the globus pallidus. This is in contrast to other neurotoxic insults and therefore, allows for a tentative diagnosis of CO poisoning on the basis of an anatomical MRI study. Functional SPECT, PET, and MRS studies are frequently abnormal, but not diagnostic of CO poisoning. In other words, the abnormalities seen are compatible with but not diagnostic of CO-induced impairment. Heuser and Mena in 19982 studied more than 70 patients after neurotoxic (pesticides, fumes, perfumes, etc.) exposure and found hypoperfusion in frontal, temporal, and parietal lobes using SPECT. The abnormalities were often asymmetrical, but showed no specific signature after exposure to a given neurotoxin. In other words,

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Baseline data versus adult normals I Right lateral view

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FIGURE 20.1 (See Color insert following page 422) A SPECT scan of cortical function after carbon monoxide poisoning. The color scale (left side) displays normal perfusion in gray, subnormal perfusion in green and blue, and hyperperfusion in red. In other cases hypoperfusion is found in the frontal areas. Thus, the abnormalities found vary from one patient to another. (Credit to J. Michael Uszler)

unrelated neurotoxins resulted in similar, if not identical abnormalities on SPECT. This is why we cannot show a typical, that is, diagnostic SPECT or PET brain scan after CO exposure. Figure 20.1 shows a SPECT brain scan of a patient who was chronically exposed to CO and became symptomatic on a long-term basis. This figure is meant to illustrate the advance in technology which now allows us to display SPECT brain scans in an understandable and almost three-dimensional fashion. The technology and display of SPECT was developed by Ismael Mena at UCLA (now in Santiago, Chile).

20.4 REVIEW OF THE RECENT LITERATURE More than 100 publications on neuroimaging after CO exposure were reviewed for this chapter and the results of significant contributions are summarized below.

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Hopkins and Woon provide an excellent review in 20065 of structural and functional neuroimaging and neuropsychological evaluation after CO poisoning. They also discuss in some detail the mechanism of CO-induced injury. Globus pallidus lesions are described more frequently than all others.6−22 White matter lesions are described by many authors.9,13,15,18,21−26 Lesions can occur in many other locations such as centrum semiovale, hippocampus, fornix, frontal, temporal, parietal, occipital lobes, cerebellum, and of course, the basal ganglia. These locations are discussed in some detail by Hopkins and Woon.5 While lesions can occur in any part of the brain, they are predominant in the globus pallidus and also in the white matter. Wu et al.27 studied ten patients within 2–5 h after CO exposure and found SPECT to be more sensitive than CT scanning. SPECT scans showed hypoperfusion in seven patients. Denays et al.28 studied 12 patients on admission day and found abnormal SPECT scans in the temporo-parietal-occipital areas in eight patients. Abnormalities were unilateral in some patients, bilateral in others. These findings confirm my earlier comment that lesions after neurotoxic exposure are not always symmetrical. Parkinson et al.29 studied 73 patients during the acute exposure phase and then followed these patients and retested them 6 months later. White matter lesions could not be correlated to the clinical severity. Centrum semiovale lesions were correlated with cognitive impairment—periventricular lesions were not. Devine et al. in 200230 compared MRI and neuropsychological evaluations in one patient who had multiple bilateral lesions in the basal ganglia 15 months after exposure. Porter et al.31 studied MRIs and neuropsychological evaluations on the day of exposure and 6 months thereafter in 62 patients. They found corpus callosum atrophy and described correlation in detail. The neuropsychological test results did not correlate with the level of corpus callosum atrophy. Kim et al.32 studied the diffusivity of white matter lesions in five patients, describing periventricular and centrum semiovale demyelinating hyperintense bilateral lesions. Ku et al. in 20064 describes a case of mania and discusses the possible disinhibition of the frontal lobes as a possible mechanism after CO poisoning (this case had frontal white matter lesions on MRI). This discussion supports my earlier comments on disinhibition from frontal lobe lesions. MRI and/or CT scans were done in conjunction with neuropsychological evaluation by many authors: n = 16,7 n = 5,13 n = 156,14 n = 9,16 n = 21,33 n = 69.34 Sequential studies were performed and discussed: n = 5,13 n = 69,34 n = 2135 and others. Reports from various studies show patients being followed for 80 days,7 3 months,37 6 months,38 3 years,36 4 years,22 6 years,39 9 years,24 10 years,40 and 33 years.23 In one study, MRI and CT scans were performed in 107 patients.18 Parkinsonism was described, but does not necessarily correlate with the location of the anatomical or functional lesions.14,16,21,41 Cerebellar lesions were also described.7,15,23,24,30 Gale et al.33 used MRI, quantitative MRI (QMRI), SPECT, and neuropsychological evaluation in 21 patients and found SPECT and QMRI to be the most sensitive neuroimaging tools for the evaluation of CO poisoning.

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Durak et al. in 20057 describe cortical atrophy, cerebellar atrophy, vermian atrophy, corpus callosum atrophy, having examined eight patients. Neuroimaging changes may be present even if patients are asymptomatic. Kesler et al.34 showed that cognitive impairment can occur in the absence of abnormal imaging studies. However, they specifically describe fornix atrophy associated with verbal memory deficits. Uchino et al.22 examined thirteen patients, 25 years after a coal mine explosion. Globus pallidus and white matter lesions were found and the parieto-occipital region was the most affected cortical area. Seven patients had definite asymmetrical cortical and subcortical lesions. Dunham, et al.42 showed that almost identical exposure in some of their patients, did not lead to the same neuropsychological impairment. Silver et al.18 studied 107 patients. Eight had CT scans. Seven of those had typical globus pallidus and white matter lesions. Bianco and Floris in 19966 described hemorrhagic infarction of the globus pallidus in two patients after CO exposure. Silverman et al.19 also described hemorrhage in the globus pallidus in a patient three years after exposure. Pinkston et al. in a remarkable study in 2000,38 describe abnormal test studies in two adults 3 years after chronic CO exposure and correlate these abnormalities with the neuropsychological evaluation of these same two adults. Neuroimaging studies showed decreased functionality in the pre-frontal cortex and the temporal lobe. Tom et al.20 studied eighteen patients and found globus pallidus lesions in seven patients and white matter lesions in five of those patients. Pach et al.43 studied SPECT, MRS and neuropsychological test results in 10 patients. They found only partial correlation in acute and 6 months postexposure studies. Hurley et al.44 showed an increase in choline and a decrease in N-acetyl-aspartate using MRS in one of their patients. Prockop in a 2005 study16 described abnormal MRS studies in nine patients, some of whom showed decreased N-acetyl-aspartate, especially in the basal ganglia. In some patients the changes were asymmetrical, if not unilateral. MRI and neuropsychological studies were also performed in these patients. Sohn et al.45 studied a husband and wife pair like Pinkston et al.,38 with apparently identical exposure to CO, but different clinical outcomes—only the husband developed parkinsonism. Scanning revealed more severe white matter damage in the husband. Only the wife had bilateral pallidal necrosis. This study illustrates the fact that the same exposure can have different results in different people. No review of this type would be complete without mentioning the important contributions of Lapresle and Fardeau,46 who published anatomical–pathological studies of 22 cases after severe CO poisoning.

20.5 CONCLUSIONS A review of the literature and my own experience show that no single neuroimaging or other test can be used as the one and only diagnostic or prognostic indicator. In other words, a good clinical or otherwise pertinent history, a review of medical records, a physical examination, neuropsychological testing, and neuroimaging

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studies (structural and functional) are essential for a correct diagnosis, appropriate treatment, and for thorough follow-up evaluation.

ACKNOWLEDGMENTS Dr Luke Curtis and Sylvia Heuser contributed valuable ideas to the subject discussed in this manuscript. Virginia Salisbury accomplished the difficult and meticulous task of typing the manuscript. Dr. J.M. Uszler of Santa Monica Imaging contributed the SPECT scan in Figure 20.1.

References 1. Choi, I.S.S., Use of scanning techniques in the diagnosis of damage from carbon monoxide, In: Carbon Monoxide Toxicity, David G. Penney, Ed., CRC Press, 2000, pp. 363–380. 2. Heuser, G., and Mena, I. Neurospect in neurotoxic chemical exposure. Demonstration of long-term functional abnormalities, Toxicol. Industr. Health, 14, 813–827, 1998. 3. Heuser, G., and Wu, J.C. Deep subcortical (including limbic) hypermetabolism in patients with chemical intolerance: Human PET studies, In: The role of neural plasticity in chemical intolerance, B.A. Song and I.R. Bell, Ed., Ann. NY Acad. Sci., 933, 319–323, 2001. 4. Ku, B.D., Shin, H.Y., Kim, E.J., Park, K.C., Seo, S.W., and Na, D.L. Secondary mania in a patient with delayed anoxic encephalopathy after carbon monoxide intoxication, J. Clin. Neuroscience, 13, 860–862, 2006 (Epub, 2006, Aug. 28). 5. Hopkins, R.O., and Woon, F.L.M. Neuroimaging, cognitive, and neurobehavioral outcomes following carbon monoxide poisoning, Behav. Cogn. Neurosci. Rev., 5, 141–155, 2006. 6. Bianco, F., and Floris, R. MRI appearances consistent with hemorrhagic infarction as an early manifestation of carbon monoxide poisoning, Neuroradiology, 38 (Suppl. 1), 870–872, 1996. 7. Durak, A.C., Coskun, A., Yikilmaz, A., Erdogan, F., Mavili, E., and Guven, M. Magnetic resonance imaging findings in chronic carbon monoxide intoxication, Acta Radiol. 46, 322–327, 2005. 8. Fine, R.D., and Parker, G.D. Disturbance of central vision after carbon monoxide poisoning, Aust. NZ. J. Ophthalmol., 24, 137–141, 1996. 9. Gotoh, M., Kuyama, H., Asari, S., Ohmoto, T., Akioka, T., and Lai, M.Y. Sequential changes in MR images of the brain in acute carbon monoxide poisoning, Comput. Med. Imaging Graph, 17, 55–59, 1993. 10. Horowitz, A.L., Kaplan, R., and Sarpel, G. Carbon monoxide toxicity: MR imaging in the brain, Radiology, 162, 787–788, 1987. 11. Kanaya, N., Imaizumi, H., Nakayama, M., Nagai, H., Yamaya, K., and Namiki, A. The utility of MRI in acute stage of carbon monoxide poisoning, Intensive Care Med., 18, 371–372, 1992. 12. Kleinert, A., Sinczuk-Walczak, H., and Goraj, B. Acute poisoning by carbon monoxide affecting the extrapyramidal system, Med. Pr., 49, 573–577, 1998. 13. Klostermann, W., Vieregge, P., and Bruckmann, H. Carbon monoxide poisoning; the importance of computed and magnetic resonance tomographic cranial findings for the clinical picture and follow-up, ROFO, 159, 361–367, 1993.

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14. Mimura, K., Harada, M., Sumiyoshi, S., Tohya, G., Takagi, M., Fujita, E., Takata, A., and Tatetsu, S. Longterm follow-up study on sequelae of carbon monoxide poisoning, Seishin Shinkeigaku Zasshi, 101, 592–618, 1999. 15. O’Donnell, P., Buxton, P.J., Pitkin, A., and Jarvis, L.J. The magnetic resonance imaging appearances of the brain in acute carbon monoxide poisoning, Clin. Radiol., 55, 273–280, 2000. 16. Prockop, L.D. Carbon monoxide brain toxicity: clinical, magnetic resonance imaging, magnetic resonance spectroscopy, and neuropsychological effects in 9 people, J. Neuroimaging, 15, 144–149, 2005. 17. Sawa, G.M., Watson, C.P., Terbrugge, K., and Chiu, M. Delayed encephalopathy following carbon monoxide intoxication, Can. J. Neurol. Sci., 8, 77–79, 1981. 18. Silver, D.A., Cross, M., Fox, B., and Paxton, R.M. Computed tomography of the brain in acute carbon monoxide poisoning, Clin. Radiol., 51, 480–483, 1996. 19. Silverman, C.S., Brenner, J., and Murtagh, F.R. Hemorrhagic necrosis and vascular injury in carbon monoxide poisoning; MRI demonstration, Przegl. Lek., 52, 267–270, 1995. 20. Tom, T., Abedon, S., Clark, R.I., and Wong, W. Neuroimaging characteristics in carbon monoxide toxicity, J. Neuroimaging, 6, 161–166, 1996. 21. Tvedt, B., Krogstad, J.M., and Berstad, J. Hypoxic brain damage after carbon monoxide poisoning, Tidsskr Nore Laegeforen, 116, 3005–3008, 1996. 22. Uchino, A., Hasuo, K., Shida, K., Matsumoto, S., Yasumori, K., and Masuda, K. MRI of the brain in chronic carbon monoxide poisoning, Neuroradiology, 36, 399–401, 1994. 23. Coskun, A., Yikilmaz, A., Guven, M., and Erdogan, F. Cranial MR imaging findings of carbon monoxide poisoning in asymptomatic patients, the chronic stage, Tani Girisim Radvol 9, 146–151, 2003. 24. Mascalchi, M., Petruzzi, P., and Zampa, V. MRI of cerebellar white matter damage due to carbon monoxide poisoning: case report, Neuroradiology, 38 (Suppl. 1), 873–874, 1996. 25. Murata, T., Itoh, S., Koshino, Y., Sakamoto, K., Nishio, M., Maeda, M., Yamada, H., Ishil, Y., and Isaki, F. Serial cerebral MRI with FLAIR sequences in acute carbon monoxide poisoning, Comput. Assist. Tomogr., 19, 631–634, 1995. 26. Prockop, L.D., and Naidu, K.A., Brain CT and MRI findings after carbon monoxide toxicity, J. Neuroimaging, 9, 175–181, 1999. 27. Wu, C.I., Changlai, S.P., Huang, W.S., Tsai, C., Lee, C.C., and Kao, C.H., Usefulness of 99mTc ethyl cysteinate dimer brain SPECT to detect abnormal regional cerebral blood flow in patients with acute carbon monoxide poisoning, Nuclear Med. Comm., 24, 1185–1188, 2003. 28. Denays, R., Makhoul, E., Dachy, B., Tondeur, M., Noel, P., Ham, H.R., and Mois, P. Electroencephalographic mapping and 99mTc HMPAO single photon emission computed tomography in carbon monoxide poisoning, Ann. Emerg. Med., 24, 947–952, 1994. 29. Parkinson, R.B., Hopkins, R.O., Cleavinger, H.B., Weaver, L.K., Victoroff, J., Foley, J.F., and Bigler, E.D. White matter hyperintensities and neuropsychological outcome following carbon monoxide poisoning, Neurology, 58, 1525–1532, 2002. 30. Devine, S.A., Kirkley, S.M., Palumbo, C.L., and White, R.F. MRI and neuropsychological correlates of carbon monoxide exposure: A case report, Environ. Health Persp., 110, 1051–1055, 2002.

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Carbon Monoxide Poisoning 31. Porter, S.S., Hopkins, R.O., Weaver, L.K., Bigler, E.D., and Blatter, D.O. Corpus callosum atrophy and neuropsychological outcome following carbon monoxide poisoning, Arch. Clin. Neuropsychology, 17, 195–204, 2002. 32. Kim, J. Chang, K., Song, I.C., Kim, K.H., Kwon, J., Kim, H.C., Kim, J.H., and Han, M.H. Delayed encephalopathy of acute carbon monoxide intoxication: diffusivity of cerebral white matter lesions, Am. J. Neuroradiol., 24, 1592–1597, 2003. 33. Gale, S.D., Hopkins, R.O., Weaver, L.K., Bigler, E.D., Booth, E.J., and Blatter, D.D. MRI, quantitative MRI, SPECT, and neuropsychological findings following carbon monoxide poisoning, Brain Inj. 13, 229–243, 1999. 34. Kesler, S.R., Hopkins, R.O., Blatter, D.D., Edge-Booth, H., and Bigler, E.D. Verbal memory deficits associated with fornix atrophy in carbon monoxide poisoning, J. Int. Neuropsychol. Soc., 7, 640–646, 2001. 35. Hayashi, R., Hayashi, K., Inouse, K., and Yanagisawa, N. A serial computerized tomographic study of the interval form of CO poisoning, Eur. Neurol., 33, 27–29, 1993. 36. Quattrocolo, G., Leotta, D., Appendino, L., Tarenzi, L., and Duca, S. A case of cortical blindness due to carbon monoxide poisoning, Ital. J. Neurol. Sci., 8, 57–58, 1987. 37. Sawada, Y., Takahashi, M., Ohashi, N., Fusamoto, H, Maemura, K., Kobayashi, H., and Yoshioka, T. Computerised tomography as an indication of long-term outcome after acute carbon monoxide poisoning, Lancet, 1, 783–784, 1980. 38. Pinkston, J.B., Wu, J.C., Gouvier, W.D., and Varney, N.R. Quantitative PET scan findings in carbon monoxide poisoning: deficits seen in a matched pair, Arch. Clin. Neuropsychol., 15, 545–553, 2000. 39. Bruno, A., Wagner, W., and Orrison, W.W. Clinical outcome and brain MRI four years after carbon monoxide intoxication, Acta. Neurol. Scand., 87, 205–209, 1993. 40. Pasquier, F., DePoorter, M.D., Jacquemotte, N. Adnet-Bonte, C. and Petit, H. Cerebellar syndrome after carbon monoxide poisoning, Magnetic Resonance imaging single photon emission tomography, Rev. Neurol. (Paris), 149, 805–806, 1993. 41. Ikeda, K., Sasaki, S., Ichijo, S., Matsuoka, Y., and Irimajiri, S. Atlas of cranial and spinal MRI--magnetic resonance imaging in carbon monoxide poisoning and Parkinsonian syndrome, No To Shinkei, 50, 86–87, 1998. 42. Dunham, M.D., and Johnstone, B. Variability of neuropsychological deficits associated with carbon monoxide poisoning, four case reports, Brain Inj., 13, 917–925, 1999. 43. Pach, D., Urbanik, A., Szczepanska, L., Hubalewska, A., Huszno, B., Groszek, B., and Jenner, B. (99m)Tc-HmPAO single photon emission tomography, magnetic resonance proton spectroscopy and neuropsychological testing in evaluation of carbon monoxide neurotoxicity, Przegl. Lek., 62, 441–445, 2005. 44. Hurley, R.A., Hayman, L.A., and Taber, K.H. Applications of functional imaging to carbon monoxide poisoning, J. Neuropsychiatry Clin. Neurosci., 13, 157–160, 2001. 45. Sohn, Y.H., Jeong, Y., Kim, H.S., Im, J.H., and Kim, J.S. The brain lesion responsible for parkinsonism after carbon monoxide poisoning, Arch. Neurol., 57, 1214–1218, 2000. 46. Lapresle, J., and Fardeau, M. The central nervous system and carbon monoxide poisoning. II. Anatomical study lesions following intoxication with carbon monoxide (22 cases), Prog. Brain Res., 24, 31–74, 1967.

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Recent Advances in Brain SPECT Imaging after Carbon Monoxide Poisoning S. Gregory Hipskind

CONTENTS 21.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21.2 Neuroimaging Modalities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21.3 Anatomical Imaging Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21.3.1 Computerized Tomography (CT) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21.3.2 Magnetic Resonance Imaging (MRI) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21.4 Functional Imaging Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21.4.1 Positron Emission Tomography (PET) . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21.4.2 Functional Magnetic Resonance Imaging (FMRI) . . . . . . . . . . . . . . . . 21.4.3 Magnetic Resonance Spectroscopy (MRS) . . . . . . . . . . . . . . . . . . . . . . . 21.4.4 SPECT Findings in Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . 21.5 Neuroimaging Findings in Chronic, Lower-Level CO Poisoning . . . . . . . . 21.6 High Resolution SPECT Findings in Ten Cases of Delayed Carbon Monoxide-Induced Encephalopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21.7 Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21.8 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

457 458 458 458 459 460 460 461 461 462 464 464 471 473 474

21.1 INTRODUCTION It has been established in this book and earlier books in this series, that carbon monoxide (CO) poisoning is an insidious cause of death and disability in the United States and throughout the world.1 Tissue anoxia is most commonly implicated as the underlying pathophysiologic mechanism of toxic CO exposure as a result of its displacement of oxygen from hemoglobin forming carboxyhemoglobin (COHb). In addition, CO has been shown to have a direct effect on several key biochemical

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processes by binding directly to hydroxyperoxidase, cytochrome oxidase, and cytochrome p 450 and other key enzymes in the oxidative metabolic process.2,3 Furthermore, it has been shown that CO binds directly to the heme iron in the globus pallidus in substantia nigra.4 Among the various types of neurotoxins, CO produces a unique clinical syndrome in which, after survival of an acute intoxication, a lucid period of variable duration can ensue followed by the onset of delayed neurological symptoms (DNS) in sequelae or a fraction of patients.4 The mechanism for the delayed a fraction effects of CO poisoning is not well understood, but involves elements of reperfusion injury, vascular oxidative stress by generation of reactive oxygen species, lipid peroxidation,5 neuronal exitotoxicity, and apoptosis.6,7 When these molecular changes affect large enough areas of neural tissue, they may be visualized by various neuroimaging techniques. We will see later how the pattern, distribution, and nature of these induced neuropathalogic changes may provide characteristic neuroimaging clues associated with CO poisoning. The role of specific neuroimaging modalities during the various stages of CO poisoning will be reviewed.

21.2 NEUROIMAGING MODALITIES Various neuroimaging modalities have been employed over the years to evaluate the neuropathological changes associated with both acute and chronic CO poisoning. Also see Chapter 20 in this book. Typically, these modalities are divided into two general categories—anatomical or structural studies and functional modalities. Each modality, anatomic and functional, has made its own unique contribution to our understanding of the neuropathological changes associated with CO poisoning. For purposes of this discussion, functional brain imaging will refer to those imaging modalities that assess the level of regional differences in the metabolic activity of brain tissue. Current prominent examples of functional brain imaging include Single Photon Emission Computed Tomography (SPECT), Positron Emission Tomography (PET), Functional Magnetic Resonance Imaging (fMRI), and Magnetic Resonance (MR) Spectroscopy. The primary anatomical modalities include Computerized Tomography (CT) and Magnetic Resonance Imaging (MRI) with its various perturbations—Diffusion Weighted Imaging (DWI) and Fluid Attenuation Inversion Recovery (FLAIR). A summary of the recent functional and anatomical imaging findings in CO poisoning will be presented.

21.3 ANATOMICAL IMAGING FINDINGS 21.3.1 COMPUTERIZED TOMOGRAPHY (CT) The most common finding in acute CO poisoning on CT imaging is symmetrical, diffuse frontal lobe white matter damage (low density findings). In two relatively large series, one by Muira (n = 60) and one by Choi (n = 129), the sensitivity of CT imaging in acute CO poisoning in detecting these changes was shown to be 38.5% and 48.0%, respectively.8,9 The second most common finding was that of low density areas seen in the globus pallidus, occurring in 30% of patients in

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the Muira study8 and in 25.6% of the patients in the Choi study.9 It was suggested that the low density lesions in the cerebral white matter and globus pallidus were related to necrosis. Although patients with white matter lesions seemed to have a worse prognosis than those with lesions in the globus pallidus, no consistent or reliable prediction of outcome could be established with this imaging modality because of its relatively low sensitivity, particularly for cortical lesions. These suggested neuropathological changes are similar in location and pathology to those found in the pathology studies of Lapresle and Fardeau who performed autopsies on 22 patients who died of acute CO poisoning.10 Decreased CT sensitivity was confirmed in a 2003 study by Wu et al.,11 using 99 m Tc -ECD SPECT in ten patients with acute CO poisoning. All ten patients had negative CT scans. However, brain SPECT imaging showed areas of abnormal hypoperfusion in the basal ganglia of five patients and in the cortical areas of seven patients. The ongoing role and utility of the use of standard CT imaging in the evaluation of CO poisoning continues to be an issue.

21.3.2 MAGNETIC RESONANCE IMAGING (MRI) Although anatomical MRI findings have a slightly superior sensitivity relative to CT, the findings are essentially the same as CT with the exception that, in the 1992 study by Chang,7 additional abnormalities were seen in the subcortical gray matter of the thalamus, putamen, and caudate nucleus. In addition, 9 of 15 patients demonstrated abnormal findings in the globus pallidus bilaterally. Abnormal cortical findings were minimal. Subsequent studies by Gale and Bigler, et al. in 1999,12 using a 1.5 Tesla magnet found cerebral abnormalities in only 38% of 21 patients by MRI who had sustained moderate to severe acute CO poisoning. The majority of the abnormalities detected were subcortical. By contrast, they identified significant abnormalities in 67% of these same patients by using either SPECT or Quantitative Magnetic Resonance Imaging (QMRI). The low sensitivity of MRI for the detection of cortical lesions in CO poisoning somewhat limits it’s utility as either a diagnostic aide or in guiding interventional strategies. However, in a study by Murata et al. in 199513 using serial MRI with FLAIR pulse imaging to follow a single patient with acute CO poisoning, abnormal findings in cerebral white matter were noted which suggested progressive demyelination in spite of normal SPECT and neuropsychological testing. This anecdotal observation seemed to suggest a possible prognostic role for MRI with FLAIR for detecting early neuropathological changes which might require more aggressive interventional strategies. However, in 2005 Durak et al.14 studied 16 patients between 1 and 10 years after their acute episode of CO poisoning using MRI with FLAIR enhancement. All patients initially presented in an unconscious state in the acute setting. At the time of follow-up, eight patients were asymptomatic and eight continued to experience chronic neuropsychiatric sequelae from their acute episode. MRI with FLAIR detected white matter abnormalities in all 16 patients, with lesions noted predominantly in the centrum semiovale area. It thus appears that early evaluation of acute CO poisoning using MRI with FLAIR enhancement carries little prognostic value.

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21.4 FUNCTIONAL IMAGING FINDINGS 21.4.1 POSITRON EMISSION TOMOGRAPHY (PET)

993TC

derived rCBF (ml/min/100g)

PET gets its name from positron emitting metabolic substrate analogs, typically [18 F]—Fluorodeoxyglucose (FDG) or [15 O]H2 O. These isotopes are typically shortacting and are generated in cyclotrons. With their capability to directly measure either glucose metabolism or oxygen consumption, regional differences in cerebral metabolic activity can be expressed quantitatively in units of mL/min/100 g brain tissue. Traditionally, PET imaging has been considered superior to SPECT in that it has been shown to achieve intrinsic spatial resolutions of 4–5 mm versus 6–10 mm for SPECT. In addition, PET’s ability to quantify regional differences in cerebral metabolism directly has been considered a more accurate measurement of cerebral function in comparison to SPECT’s relative measurements of regional cerebral blood flow (rCBF). However, because of PET’s increased cost, decreased availability, and the need for cyclotron-generated pharmaceuticals, it is a less practical neuroimaging modality. In addition, with the advent of cheaper, more readily accessible SPECT cameras which can now achieve intrinsic spatial resolutions of 2.3 mm and less (NeuroQuad, NC Systems), PET’s advantage of superior spatial resolution no longer exists. Furthermore, it has been shown that a very close relationship exists between oxygen consumption, glucose metabolism, and CBF. As seen in Figure 21.1, a very tight correlation between CBF and metabolism is seen when inhaled Xenon 133, which measures CBF quantitatively, is compared with 99mTc-HMPAO, the most common radiopharmaceutical used in SPECT studies. Therefore, the differences between these modalities now become somewhat academic. In a 1993 PET study, DeReuck et al.15 demonstrated a global decrease in cerebral metabolic activity, localized primarily in the frontal and temporal cortices. A PET study by Yoshii et al.16 of a patient two months following acute CO poisoning demonstrated findings primarily in the basal ganglia, but with some involvement of the caudate and amputamen. Pinkston et al.17 studied two patients, man and wife, 3 years following their acute exposure. Using statistical parametric mapping to a

120

120

ECD

100

100

80

80

60

60

40

m = 0.85 b=6 r = 0.86

20 0

0

20

40

133Xe

60

80

100 120

rCBF (ml/min/100g)

HMPAO

40

m = 0.83 b = 11 r = 0.93

20 0

0

20

40 133Xe

60

80

100 120

rCBF (ml/min/100g)

FIGURE 21.1 Comparison of the “derived” regional cerebral blood flow (rCBF) for 99m TcECD (left) or 99m Tc HMPAO (right) scanning techniques relative to rCBF (With permission of Ismael Mena).

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control group they demonstrated decreased metabolic activity in the bilateral orbit frontal, dorsolateral prefrontal, and temporal cortices. Subsequently, Tengvar et al.18 evaluated a patient five months following acute CO poisoning with PET and noted decreased metabolic activity in the frontal lobes, anterior singular gyri, and sub-cortical white matter. In a study of three patients with acute CO poisoning, Ellis-Hon et al.19 noted significant decreases in basal ganglia metabolism in two of three patients using PET imaging. As discussed earlier, it is apparent from the review of the four prior articles which evaluated a total of seven patients only, that PET is not that widely used as a neuroimaging modality for the evaluation of CO poisoning. It remains to be determined whether or not this modality will continue to be utilized in the ongoing neuroimaging evaluations of CO poisoning patients.

21.4.2 FUNCTIONAL MAGNETIC RESONANCE IMAGING (FMRI) FMRI, when employed with blood oxygen level determination (BOLD) enhancement, is able to quantitatively assess regional differences in cerebral metabolic activity. Essentially, by measuring the oxygen extraction between the arterial and venous circulation in various brain regions, with the increased deoxyhemoglobin levels in the venous circulation being detected on T2 images, quantitative measurements of oxygen consumption can be expressed in terms of mL/min/100 g brain tissue. A study by Kondo in 200620 on one patient poisoned with CO, revealed abnormal findings in the deep cortex, hippocampus, and globus pallidus. Hantson21 found symmetrical distribution of deep gray and basal ganglia abnormalities in a study of five patients with delayed effects of CO poisoning. Again, the limited availability of this technology, along with the lack of studies with adequate sample size limit fMRI’s ability to appropriately study the neuropathological changes that occur following recovery from acute CO poisoning.

21.4.3 MAGNETIC RESONANCE SPECTROSCOPY (MRS) This relatively new functional neuroimaging modality uses the response of metabolic protons to an electromagnetic field to evaluate areas of abnormal cerebral activity. It has been shown that the metabolic byproducts of such neuropathological processes as demyelination, neuronal degeneration or ongoing anaerobic glycolysis can result in regional differences in NAA (N-acetyl-aspartate). MRS detected decreases in NAA are associated with neuronal loss or degeneration. Increased choline concentration has been associated with active demyelination. In 1995, Murata et al.13 performed serial MRS, MRI, and SPECT on a patient after the onset of symptoms associated with a delayed CO encephalopathic process. Initially, increased choline was detected which suggested axonal demyelination. The patient was followed with serial MR spectroscopy scans which later revealed increased levels of lactate and NAA which suggested neuronal death. These findings were detected before changes were noted on either MRI or SPECT. In 1998, Sakamoto et al.22 studied three patients with the chronic encephalopathic form of CO poisoning using MRI, electroencephalogram (EEG),

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N-isopropyl-p-[1231]iodoarmphetamine (IMP) SPECT, and HMRS. A white matter lesion detected by MRI persisted long after the improvement of the patient’s clinical symptoms. SPECT findings did not always correlate with clinical symptomatology. MRS studies in the frontal lobe area revealed increases in choline-containing compounds and reductions of NAA in all cases. There was close correlation between clinical symptomatology and levels of lactate suggesting a possible role for MRS as a predictor of clinical outcome in patients with the “interval form” of CO poisoning. In 2005, Pach et al.23 studied ten patients following recovery from acute CO poisoning. Neuropsychological testing and 99m Tc –HMPAO-SPECT was performed at 6 months following the acute injury and MRS was performed at 8 months following the acute episode. SPECT revealed significant abnormalities in the frontal cortex, basal ganglia and parietal cortex. All ten patients evaluated by MRS at 8 months post acute CO exposure exhibited elevations in either mobile lipid and/or lactate concentration in the frontal lobes and basal ganglia.

21.4.4 SPECT FINDINGS IN CARBON MONOXIDE POISONING A growing body of scientific information has evolved in the area of the SPECT evaluation of acute CO poisoning. In a study of 12 patients with acute CO poisoning in 1994, Denays et al.24 demonstrated abnormal CBF in the temporal, partial, and occipital lobes in eight of them. In a study of ten acutely poisoned CO patients in 1998, Kao and colleagues25 identified abnormal cortical findings in seven out of ten patients and abnormal basal ganglia findings in six out of ten patients. In 2003, Wu11 found abnormalities in the cortex of seven acutely poisoned patients and abnormalities in the basal ganglia of five out of ten patients. See the chapter on scanning techniques by Choi in Penney, 2000.26 In a 2004 study of 20 acutely poisoned CO patients by Pach et al.,27 brain SPECT imaging with 99 mTc-HMPAO revealed abnormalities in 17 of the 20 patients (85%). Predominant findings in this study included decreases in perfusion in the frontal and parietal cortices and basal ganglia. Their conclusion was that the use of 99 mTcHMPAO brain imaging seemed to be useful in the demonstration of early central nervous system (CNS) dysfunction. A follow-up study by the same investigators of ten patients revealed the same findings. Another study in 2004 of five patients with the chronic effects of CO poisoning by Kon Chu et al.28 showed decreased bilateral white matter, globus pallidus, and frontal cortex. A summary of the SPECT findings noted above is given in Table 21.1. In 1995, Choi29 studied 13 patients with delayed neurological sequelae of CO poisoning and found a diffuse, patchy, decreased pattern which was more prominent in the frontal lobes. Seven of these patients were seen in follow-up six months later at which time their SPECT scans showed increased frontal blood flow in six out of seven patients which was also associated with improved neuropsychological performance. In 1999, Gale and Bigler et al.12 evaluated 21 patients with delayed sequelae of CO poisoning with the multiple modalities of MRI, QMRI, SPECT, and comprehensive neuropsychological testing. In their study, 14/21 patients were noted to have abnormalities on both SPECT and QMRI imaging, but only 38% of patients were noted to have abnormal findings on routine MRI imaging. In the patients with

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TABLE 21.1 SPECT Areas of Decreased Perfusion Seen in Studies of Carbon Monoxide Poisoning Year

Author

1994

Denays24

1995

Choi26

1998

Kao25

1999

Gale12

2002

Watanabe30

2003

Wu11

2004

Pach23

2004

Chu28

Brain Area Temporal lobe Parietal lobe Occipital lobe Diffuse patchy cortical Bilateral frontal Cortex Basal ganglia Frontal lobes Parietal lobes Bilateral frontal lobes Bilateral insula Right temporal lobe Cortex Basal ganglia Parietal cortex Frontal lobes Basal ganglia Frontal cortex Globus pallidus

Perfusion Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased

abnormal SPECT findings, the perfusion abnormalities were noted in the frontal lobes (71%), parietal lobes (57%), and temporal lobes (36%). The QMRI findings demonstrated decreased hippocampal size, increased ventricle to brain ratio (VBR) and evidence of cortical atrophy. In 2002, Watanabe et al.30 studied eight patients with delayed neurosequelae of acute CO poisoning and ten patients with no neuropsychiatric sequelae. Using statistical parametric mapping and comparing them to a control group of 44 normal patients, patients with delayed neuropsychiatric sequelae had significantly reduced perfusion in the bilateral frontal lobes, bilateral insula, and right temporal lobe. Interestingly, patients with no neuropsychiatric sequelae had significantly reduced bilateral frontal perfusion as well, worse on the left, compared to controls. This study suggests that relative preservation of left frontal lobe function following acute CO poisoning may have some prognostic value and that right frontal lobe dysfunction may result in more significant neurosequelae. This observation deserves further investigation. In the 2004 study by Chu et al.,28 five patients who manifested delayed hypoxic encephalopathy following acute CO poisoning showed the typical T2 -weighted MRI findings of abnormalities in bilateral periventricular white matter and white matter in the frontal and parieto-occipital areas. In addition, symmetrical abnormalities were found in the globus pallidus. Simultaneous brain SPECT imaging using 99 mTcHMPAO revealed decreased profusion in the bilateral frontal cortex, globus pallidus, and bilateral white matter.

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21.5 NEUROIMAGING FINDINGS IN CHRONIC, LOWER-LEVEL CO POISONING Beck’s 1936 axiom is that “No noxious gas so potent when inhaled in atmospheric dilutions of 1% or even less as to cause almost instantaneous death, can be incapable of producing symptoms if inhaled at a lesser concentration for a longer period of time”.31 Population studies have shown that even small increases in the ambient CO concentration can lead to significant increases in mortality,32 low birth weight,33 and psychiatric hospitalizations.34 In a 1998 study by Bayer,35 it was reported that chronic COHb levels between 0.4% and 5.8% were associated with persistent neurological symptoms (PNS). Furthermore, in a 2006 study of chronic CO exposure Tellez and colleagues36 described lack of memory, attention-concentration, and Parkinson type movements as the main neuropsychological and neurological symptoms occurring most frequently. If one assumes that the basic neuropathologic damage of PNS is the same in chronic, lower-level, “occult” CO poisoning as it is in the “interval form” of CO poisoning, it might be anticipated that the neuroimaging findings in these two entities would also be similar. A review of the literature reveals very few neuroimaging studies performed for this entity. A single case of chronic CO exposure in a 2 12 month old infant in 1990 revealed bilateral basal ganglia hypodensities on MRI.37

21.6 HIGH RESOLUTION SPECT FINDINGS IN TEN CASES OF DELAYED CARBON MONOXIDE-INDUCED ENCEPHALOPATHY As much as it is useful to describe the imaging findings of the neuropathological changes which occur in the acute CO poisoning setting from a public health standpoint, the ability to identify those cases of chronic lower-level CO exposure would seem relevant. As has been shown, chronic lower-level CO poisoning often presents clinically as a confusing constellation of seemingly unrelated symptoms which have been variously described as neurasthenia, chronic fatigue syndrome, fibromyalgia, hypochondriasis, and other psychiatric conditions. As such, it often goes undiagnosed and therefore is improperly treated. To the extent that brain function imaging might reveal a characteristic perfusion pattern, it might prove a useful diagnostic tool when the clinical presentation is unclear. This author has had the opportunity to perform high resolution brain SPECT imaging on a series of ten patients over the last 18 months, who were experiencing the long-term effects of acute CO poisoning. A brain dedicated four headed gamma camera (NeuroQuad SPECT, NC Systems Inc.) with an intrinsic spatial resolution of two mm was used. In addition, Mirage software from Segami Corporation which used a normative database allowed comparisons of individual patients on a Brodman area by Brodman area basis for the cortical structures and the subcortical structures of the thalamus, lentiform nucleus, and caudate. A representation of the type of data obtained are seen in Table 21.2.

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TABLE 21.2 Baseline Data versus Adult Normals

ROI # 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 22

ROI Label

# ELTS

Volume (ml)

Area 1,2,3-Both Area 1,2,3-Left Area 1,2,3-Right Area 4-Both Area 4-Left Area 4-Right Area 5-Both Area 5-Left Area 5-Right Area 6-Both Area 6-Left Area 6-Right Area 7-Both Area 7-Left Area 7-Right Area 8-Both Area 8-Left Area 8-Right Area 9-Both Area 9-Left Area 9-Right Area 10-Both Area 10-Left Area 10-Right

5756 2878 2878 9944 4972 4972 2610 1305 1305 15932 7966 7966 15052 7526 7526 9226 4613 4613 8432 4216 4216 11378 5689 5689

21 10 10 37 18 18 9 4 4 59 29 29 56 28 28 34 17 17 31 15 15 42 21 21

Maximum (sd)

Minimum (sd)

Mean (sd)

Standard deviation (sd)

1.3 1.3 1.3 3.0 3.0 3.0 0.3 0.3 0.5 1.8 1.8 1.4 1.9 1.9 1.7 2.3 2.2 2.3 3.6 3.6 3.3 5.0 5.0 5.0

−5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0 −5.0

−2.6 −3.1 −2.1 −2.6 −2.7 −2.5 −2.7 −2.6 −2.8 −2.4 −2.7 −2.2 −1.3 −1.3 −1.1 −2.2 −2.3 −2.1 −2.4 −2.4 −2.3 −1.7 −1.7 −1.7

1.9 1.8 1.8 1.7 1.7 1.7 1.5 1.8 1.1 1.6 1.6 1.6 1.7 1.7 1.6 2.1 2.1 2.1 2.3 2.2 2.3 2.4 2.3 2.5

Four adults and six children underwent high-resolution brain SPECT imaging with 99mTc-HMPAO. The average age of the adults was 34.8 years (range 31.3–44.6 years) and the average age of the children was 10.3 years (range 7.4–12.8 years). In nine of the patients the average time from acute exposure to imaging was 2.7 years. These nine individuals, six children and three adults, were all apparently exposed to the same level of CO and all were found in an unconscious state. One adult was seen 4.1 years following acute exposure in which unconsciousness was also a factor in the acute setting. All patients were experiencing various delayed neuropsychological sequelae from their acute poisoning and most had been found to have significant abnormalities on neuropsychological testing which primarily involved problems with executive function and memory, as well as such affective disturbances as depression and anxiety. Tables 21.3 and 21.4 represent a summary of their SPECT findings. The following data (Table 21.5) are a summary of the number of statistically abnormal findings in the Brodman areas of the nine patients experiencing the same level of acute CO poisoning.

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Bilateral frontal Bilateral temporal Bilateral parietal Patchy cortical

1, L—2.5 2, L—2.5 3, L—2.5 4, L—2.6, R—2.6 5, L—2.0, R—2.3 6, L—2.2 11, L—4.6, R—4.5 25, L—2.1 28, L—2.14, R—2.1 31, R—1.9

D

E

Bilateral frontal Bilateral occipital Patchy cortical

Bilateral frontal Bilateral temporal L > R Left medial temporal Patchy cortical

21, L—1.7 23, L—1.9, R—2.1 24, L—2.6, R—3.0 28, L—2.3, R—2.3 32, L—2.5, R—2.3

C

21, L—2.2, R—2.4 24, L—3.5, R—3.2 25, L—4.5, R—4.1 28, L—2.7, R—2.4 32, R—2.1 38, L—2.5, R—2.6 47, L—2.9, R—3.1

Bilateral medial temporal Patchy cortical

Bilateral frontal L > R Bilateral temporal L > R Bilateral occipital L > R Patchy cortical

24, L—1.8, R—2.6 32, R—2.3

(Area), (Left value), (Right value) 17, L—1.9, R—2.0 18, L—1.9

A

Cortical Findings

B

Broadman Areas (S.D.)

Patient

TABLE 21.3 Summary of SPECT Findings in 10 individuals designated as A–J

Left globus pallidus Right posterior thalamus Left caudate

Bilateral lentiform Right posterior thalamic Bilateral caudate

Left caudate body

R Globus pallidus Bilateral posterior thalamic R > L

R Globus pallidus

Sub-Cortical Findings

466 Carbon Monoxide Poisoning

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32, L—2.8 36, L—2.7, R—2.9 38, L—2.4, R—2.9 47, R—2.1

20, L—2.3 21, L—2.4 24, L—3.8, R—3.2 25, L—2.6, R—2.6 28, L—3.4, R—2.4 32, L—3.2, R—2.7 20, L—2.1 R—2.0 21, L—2.1 R—0

G

H

Right cerebellar Patchy cortical Bilateral frontal Left medial temporal Right occipital Patchy cortical Bilateral frontal Bilateral cerebellar Bilateral posterior temporal Bilateral occipital

17, L—1.9 24, R—1.9

5, L—2.1 17, L—2.6, R—2.5 28, L—2.0 31, L—2.0, R—2.0

J

Left occipital

Bilateral temporal

Patchy cortical Bilateral frontal

Bilateral Frontal Bilateral Temporal L>R Bilateral Parietal Left Occipital Patchy Cortical

Bilateral orbital frontal Bilateral temporal Bilateral occipital L > R

I

25, L—3.1 R—3.5 28, L—3.6 R—3.7 31, L—2.0

24, L—3.9 R—2.4

36, L—2.6 38, R—2.3 44, L—2.9 R—2.3 45, L—2.1 R—2.5

17, L—2.2, R—1.9 21, L—1.9 24, R—2.0 25, R—2.1 28, L—2.4, R—2.1 38, L—2.5, R—2.0

F

Bilateral globus pallidus Right putamen Left posterior thalamus Left caudate

Bilateral putamen Right thalamus Bilateral globus pallidus

—

Bilateral globus pallidus Bilateral posterior thalamus Left caudate

Bilateral lentiform Left globus pallidus

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TABLE 21.4 Summary of Regional Abnormal Areas in Nine Patients Using High Resolution SPECT Cortical Diffuse, decreased patchiness 8/9

Cerebellar 2/9

Frontal 8/9

Temporal 8/9

Parietal 1/9

Occipital 5/9

Subcortical Globus pallidus 7/9

Caudate 4

Putamen 4/9

Thalamus 5/9

TABLE 21.5 Abnormal Cortical Findings by Age after Carbon Monoxide Exposure Patient

Gender

Age (years)

Number of Abnormal Brodman Areas

C H D Adult average A B E F I J Child average

Male Female Male

31 31 33 31.7 12 11 12 11 7 9 10.3

11 17 15 14.3 3 1 4 9 2 6 4.2

Male Male Male Male Male Male

As can be seen, given the same level of acute CO poisoning, the general cortical and subcortical pattern of involvement was similar in both children and adults, while the number of statistically abnormal Brodman areas in the children were less than those seen in the adults. This finding suggests that children sustain milder neuropathological effects from the same level of acute CO poisoning. Various explanations have been offered for this previously observed phenomenon which are consistent with the findings of other observers that children are more resistant to the acute effects of CO poisoning.38 In addition, the sole adult female in the group experienced a smaller number of statistically abnormal areas than the two adult males. This, too, is consistent with the epidemiological evidence suggesting that women are more resistant than men to the effects of acute CO poisoning.39,40 (see Figures 21.2–21.6).

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Finding No. 1(cont.): Toxic injury from carbon monoxide poisoning

"CO poisoned"

Normal

FIGURE 21.2 (See color insert following page 422). Example of diffuse neuronal injury two years after acute carbon monoxide poisoning.

Mild

Medium

Severe

FIGURE 21.3 (See color insert following page 422). SPECT scans of three patients with mild, medium and severe cognitive defects two years after acute carbon monoxide poisoning.

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Adult male

Adult female

FIGURE 21.4 (See color insert following page 422). SPECT scans of male and female patients two years following acute carbon monoxide poisoning with identical carboxyhemoglobin levels (34.5% vs. 34.9%)

LC

RL

IG

TM

BAW

SP

BRW

FIGURE 21.5 (See color insert following page 422). Superior, transverse views of SPECT perfusion findings in isolated lentiform nuclei of seven patients, two years following acute carbon monoxide poisoning. Yellow areas in the color plates are areas of abnormally decreased perfusion.

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ROI label

# Elts

Volume

Maximum

Minimum

471 Standard deviation

Mean

Caudate nucleus—Left

975

0.3 %

71.1 %

26.9 %

42.6 %

9.3 %

Caudate nucleus—Right

975

0.3 %

74.1 %

37.9 %

52.9 %

7.7 %

Right lateral view

Anterior view

Superior view

Left lateral view

Posterior view

Interactive view

FIGURE 21.6 (See color insert following page 422). Six SPECT isolation views of caudate nuclei of a patient two years following acute carbon monoxide poisoning. All areas other than red in the color plates represent areas of abnormally decreased perfusion.

21.7 DISCUSSION CO poisoning, for the purposes of discussion, can be divided into three distinct categories: 1. Acute CO poisoning. This may involve immediate deficits, that is, PNS. 2. Acute CO poisoning which displays delayed effects, that is, DNS (the so-called “interval form” of CO poisoning). 3. Chronic, lower-level or “occult” CO poisoning, which can also result in long-term health effects. In acute exposures, multiple organ systems can be affected with life-threatening results. Suicide by voluntary CO inhalation remains the number one cause of toxic death in the United States.1 Severe acute exposures can result in the development of cardiac arrhythmias, pulmonary edema, renal failure, and metabolic acidosis which must be managed aggressively. High concentrations of CO can cause neuropathologic changes that may manifest themselves immediately or at some interval following the acute, possibly life-threatening episode. Unfortunately, it has been shown that the degree of neuropathologic damage caused by CO does not always correlate with longterm prognosis.41 Although other organ systems can be permanently affected, it is the neurological, neuropsychological, and neuropsychiatric sequelae of CO poisoning that accounts for the bulk of the chronic morbidity often seen in this disorder.42 To the extent that the neuropathological changes that occur in the acute setting are significant and sufficiently widespread, they create “pathological

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footprints” that can be identified by various neuroimaging techniques. In the acute setting, from a neuroimaging standpoint, it is important to establish, if possible, the location and extent of the brain injury. This not only aids in the prediction of clinical outcomes, but can assist in the determination of the need for ongoing interventional measures. Perhaps the greatest potential contribution that neuroimaging might make is the ability to aid in the identification of cases of lower-level, chronic CO poisoning. As has been pointed out, chronic CO poisoning has been associated with various vague neuropsychiatric conditions such as neurasthenia, chronic fatigue syndrome, fibromyalgia, and other nonspecific, yet debilitating illnesses which often go undiagnosed and improperly treated.43,44 To the extent that neuroimaging might be capable of identifying certain characteristic perfusion patterns associated with the chronic effects of CO poisoning, improved diagnosis, and better treatment might be possible for these vague syndromes with their protean manifestations. The focus of this chapter, therefore, is the review of current neuroimaging findings in acute CO poisoning, delayed neurosequelae of acute CO poisoning and chronic CO poisoning. In addition, an attempt has been made to assess its current role in the evaluation of the various forms of this insidious illness. As we have seen, CO poisoning, either acute and life threatening, with delayed neuropsychological sequelae or of the lower-level, insidious chronic type, can cause serious neurological damage to various areas of the brain. The damage, from frank necrosis of gray matter to demyelination of white matter, to impaired mitochondrial, and aerobic metabolic processes, results in impaired neuronal activity. This often results in significant neuropsychological disability and morbidity and represents a significant disease burden for our society. Evidence from the anatomic neuroimaging studies, CT and MRI, suggest a regional predilection for CO to damage frontal lobe white matter including corpus callosum and the centrum semiovale as well as subcortical gray areas, particularly the globus pallidus. These changes are often seen earlier in the course of CO poisoning relative to the changes seen with PET or SPECT. CO’s affinity for the high iron content contained within the globus pallidus and substantia nigra is the proposed mechanism whereby the globus pallidus and the substantia nigra are selectively damaged. Subcortical damage has also been seen in the caudate, putamen and thalamus. Regarding CO’s affect on cortical brain matter, numerous studies have shown PET and SPECT’s superiority to CT and MRI. Since PET and SPECT primarily measure rCBF in the more metabolically active gray matter, white matter abnormalities are only occasionally detected. The preponderance of the functional neuroimaging data suggest a predilection of CO to damage the frontal and temporal lobes, often the more medial aspects of the temporal lobes. However, almost every other cortical lobe has been implicated as well including the parietal, occipital, and cerebellar lobes of the brain. MR Spectroscopy may serve as an alarm modality because of its apparent ability to detect active pathologic changes sooner after the onset of the delayed sequelae of CO poisoning as compared to MRI, PET, or SPECT. Further studies are needed to confirm this initial impression. The apparent earlier ability of MRS to detect the onset of neuropsychological symptoms related to CO poisoning may allow for earlier intervention with modalities such as hyperbaric oxygen (HBO). HBO therapy has

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been shown to be effective in treating many aspects of brain injury, including CO poisoning (see chapter 17 in this book). The data from the various anatomic and functional neuroimaging modalities suggest that a prototypical pattern of CO’s affects on the brain is evolving. This picture appears to be one which demonstrates abnormalities of function in the globus pallidus, bilateral frontal, and bilateral temporal cortices with a tendency toward medial versus lateral temporal involvement. In addition, a patchy cortical pattern of decreased activity as seen in various toxic-anoxic insults to the brain is also observed often but is fairly nonspecific. The proper neuroimaging evaluation of these findings would suggest that a combination of CT and MRI with SPECT or PET is required on the basis of the relative sensitivities and intrinsic spatial resolution anatomical studies for the globus pallidus and the superior sensitivity of functional studies for cortical structures. However, newer generation, high resolution SPECT cameras with intrinsic spatial resolutions of 2.0 mm (NeuroQuad SPECT, NC Systems) may prove useful as a single imaging modality. When one considers this from a radiation exposure standpoint, the ability to do a functional neuroimaging scan with 0.26 rems of radiation exposure versus a CT involving 6.0 rems of radiation exposure, the choice seems obvious. Although there is zero radiation exposure associated with MRI, the ability to avoid two separate procedures and the associated increased cost would also seem preferable. The series of nine patients imaged with the brain-dedicated NeuroQuad SPECT system at Brain Matters, Inc. in Denver, CO confirms its ability to not only assess cortical neuroactivity, but also functional activity in smaller subcortical structures, particularly the globus pallidus. From a public health perspective, the ability of neuroimaging studies to detect CO poisoning of the lower-level chronic type would seem very important. As has been discussed, this insidious malady with its many manifestations often goes undiagnosed and inappropriately treated. Increased awareness and education, particularly in the primary care setting will be important in assisting clinicians in detecting this occult illness in many of their patients who may present with a myriad of seemingly unrelated symptoms. In this setting, clinicians should consider a neuroimaging evaluation to include either a combination of CT or MRI with standard resolution SPECT, or where available, newer generations of high resolution, brain-dedicated SPECT cameras. With the improved diagnostic capabilities of the newer neuroimaging modalities and increased knowledge of CO’s evolving “fingerprint,” earlier intervention and better outcomes after CO poisoning can be achieved.

21.8 CONCLUSIONS 1. Anatomical neuroimaging studies such as CT and MRI are capable of detecting pathological changes in frontal lobe white matter and subcortical gray matter, particularly the globus pallidus, following the development of the neuropsychological sequelae of CO poisoning. 2. Functional neuroanatomical studies such as PET and SPECT appear more sensitive to changes in the regional metabolic activity and rCBF in cortical grey matter, particularly in the frontal and temporal lobes.

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3. A prototypical, but not necessarily pathognomonic neuroimaging profile for CO poisoning is evolving which suggests preferential involvement of the globus pallidus subcortically and the frontal and temporal lobes cortically. 4. MR Spectroscopy may serve as an early indicator for evaluating neuropathological changes which develop following the onset of the neuropsychological sequelae of CO poisoning. 5. Neuroimaging studies, either CT or MRI coupled with SPECT or PET, or alternatively high resolution SPECT should be considered as part of the evaluation process for patients presenting subacutely in the primary care setting with various vague, ill-defined symptoms which are often confused with chronic fatigue syndrome, fibromyalgia, flu, Lyme’s disease, multiple sclerosis, psychiatric condition, and so forth.

References 1. Cobb, N., and Etzel, RA. Unintentional carbon monoxide-related deaths in the United States, 1979 through 1988, J. Am. Med. Assoc., 266, 659, 1995. 2. Brown, S., and Piantadosi, C. In vivo binding of CO to cytochrome oxidase in rat brain, J. Appl. Physiol., 68, 604,1990. 3. Goldbaum, L.R., et al. Mechanism of the toxic action of carbon monoxide, Ann. Clin. Lab. Sci. 1976; 6: 372–376. 4. Auer, R.N., Benveniste H. Hypoxia and related conditions. In: Graham DI, Langtos PL (eds): Greenfield’s Neuropathology, London, Arnold, 1997, pp. 275–276. 5. Thom, S.R. Dehydrogenase conversion to oxidase and lipid peroxidation in brain after carbon monoxide poisoning. J. Appl. Physiol., 73: 1584–1589, 1992. 6. Thom, S.R. Carbon monoxide-mediated brain lipid peroxidation in the rat. J. Appl. Physiol., 68, 997, 1990. 7. Chang, K.H. Delayed encephalopathy after acute carbon monoxide intoxication: MR imaging features and distribution of cerebral white matter lesions, Radiology. 1992; 184: 117–122. 8. Miura, T., Mitomo, M., Kawai, R., and Harada, K. CT of the brain in acute carbon monoxide intoxication: characteristic features and prognosis, AJNR, 6, 739, 1985. 9. Choi, I.S., Kim, S.K., Choi, Y.D., Lee, S.S., and Lee, M.S. Evaluation of outcome after acute carbon monoxide poisoning by brain CT, J. Kor. Neurol. Assoc., 8, 78, 1993. 10. Lapresle, J., and Fardeau, M. The central nervous system and carbon monoxide poisoning. II. Anatomical study of brain lesions following intoxication with carbon monixide (22 cases), Prog. Brain Res. 1967; 24: 31–74. 11. Wu, C.I., et al. Usefulness of 99mTc ethyl cysteinate dimer brain SPECT to detect abnormal regional cerebral blood flow in patients with acute carbon monoxide poisoning. Nucl. Med. Commun. 2003; 24: 1185–1188. 12. Gale, S.D., Bigler, E.D., et al. MRI, quantitative MRI, SPECT, and neuropsychological findings following carbon monoxide poisoning, Brain Inj. 1999; 13: 229–243. 13. Murata, T., et al. Serial proton magnetic resonance spectroscopy in a patient with the interval form of carbon monoxide poisoning, J. Neurol. Neurosurg. Psychiatry. 1995; 58: 100–103.

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14. Durak, A.C., et al. Magnetic resonance imaging findings in chronic carbon monoxide intoxication, Acta. Radiol. 2005; 46: 322–327. 15. De Reuck, J., Decoo, D., Lemanhieu, I., Stijckmans, K., Boon, P., Man Maele, G., Buylaert, W., Leys, D., and Petit. H. A positron emission tomography study of patients with acute carbon monoxide poisoning treated by hyperbaric oxygen, J. Neurol., 240, 430, 1993. 16. Yoshii, R., Kozuma, R., Takahashi, W., Haida, M., Takagi, S., and Shinohara, Y. Magnetic resonance imagin and 11c-n-methylspiperone/positron emission tomography studies in a patient with the interval form of carbon monoxide poisoning. Neurol. Sci. 160, 1, 1998. 17. Pinkston, J.B., Wu J.C., and Gouvier W.D. Varney NR. Quantitative PET scan findings in carbon monoxide poisoning: deficits seen in a matched pair. Arch. Clin. Neuropsychol. 2000; 15: 545–553. 18. Tengvar, C., Johansson, B., and Sorensen, J. Frontal lobe and cingulate cortical metabolic dysfunction in acquired akinetic mutism: a PET study of the interval form of carbon monoxide poisoning. Brain Inj. 2004; 18: 615–625. 19. Ellis-Hon, K.L., Yeung W.L., Ho C.H., Leung W.K., Li AM., Chiu-Wing Chu W., and Chan Y.L. Neurologic and radiologic manifestations of three girls surviving acute carbon monoxide poisoning. J Child Neurol. 2006; 21: 737–741. 20. Kondo, A., Saito, Y., Seki, A., Sugiura, C., Maegaki, Y., Nakyama, Y., Yagi, K., and Ohno, K. Delayed neuropsychiatric syndrome in a child following carbon monoxide poisoning. Brain Dev. 2007; 29(3): 174–177. 21. Hanston, P., and Duprez, T. The value of morphological neuroimaging after acute exposure to toxic substances. Toxicol. Rev. 25, 2, 1993. 22. Sakamoto, K., et al. Clinical studies on three cases of the interval form of carbon monoxide poisoning: serial proton magnetic resonance spectroscopy as a prognostic predictor, Psychiatry Res. 1998; 83: 179–192. 23. Pach, D., et al. Evaluation of regional cerebral perfusion using 99mTc-HmPAO single photon emission computed tomography (SPECT) in carbon monoxide acutely poisoned patients, Przegl Lek. 62, 6, 2005. 24. Denays, R., et al. Electroencephalographic mapping and 99mTc HMPAO singlephoton emission computed tomography in carbon monoxide poisoning, Ann. Emerg. Med. 1994; 24: 947–952. 25. Kao, C.H., et al. HMPAO brain SPECT in acute carbon monoxide poisoning, J. Nucl. Med. 1998; 39: 769–772. 26. Choi, I.S.S. Use of scanning techniques in the diagnosis of damage from carbon monoxide. In: Carbon Monoxide Toxicity, D.G. Penney, Ed., CRC Press, 2000, Chapt. 16, pp. 363–380. 27. Pach, D., et al. Evaluation of regional cerebral perfusion using 99mTc-HmPAO single photon emission computed tomography (SPECT) in carbon monoxide acutely poisoned patients, Przegl Lek. 61, 4, 2004. 28. Chu, K., et al. Diffusion-weighted MRI and 99mTc-HMPAO SPECT in delayed relapsing type of carbon monoxide poisoning: evidence of delayed cytotoxic edema, Eur. Neurol. 2004; 51: 98–103. Epub Jan. 28, 2004. 29. Choi, IS., et al. Evaluation of outcome of delayed neurologic sequelae after carbon monoxide poisoning by technetium-99m hexamethylpropylene amine oxime brain single photon emission computed tomography, Eur. Neurol. 1995; 35: 137–142. 30. Watanabe, N., et al. Statistical parametric mapping in brain single photon computed emission tomography after carbon monoxide intoxication, Nucl. Med. Commun. 2002; 23: 355–366.

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Carbon Monoxide Poisoning 31. Beck, H.G. Carbon monoxide asphyxiation: a neglected clinical problem, J. Am. Med. Assoc., 107, 1025–1029, 1936. 32. Hexter, A.D., and Goldsmith, J.R. Carbon monoxide: association of community air pollution with mortality, Science, 172, 265–276, 1971. 33. Ritz, B., and Yu, F. The effect of ambient carbon monoxide on low birth weight among children born in southern California between 1989 and 1993, Environ. Health Perspect., 107, 17–25, 1999. 34. Strathilevitz, M., Strahilevitz, A., and Miller, J.E. Air pollutants and the admission rate of psychiatric patients, Am. J. Psychiatr., 136, 205–207, 1979. 35. Bayer, M.J., Orlando, J., McCormick, M.A., Weiner, A., and Deckel, A.W. Persistent neurological sequelae following chronic exposure to carbon monoxide, in Carbon Monoxide: The Unnoticed Poison of the 21st Century, Satellite Meeting, IUTOX VIIIth International Congress of Toxicology, Dijon, France, July 3–4, 1998. 36. Tellez, J., Rodriguez, A., and Fajardo A. Carbon monoxide contamination; an environmental health problem, Rev. Salud Publica, 8, 1, 108–117, 2006. 37. Piatt, J.P., Kaplan, A.M. Bond, G.R., and Berg, R.A. Occult carbon monoxide poisoning in an infant, Pediatr. Emerg. Care, 6, 21, 1990. 38. White, S. Pediatric carbon monoxide poisoning. In: Carbon Monoxide Toxicity, Penney, D.G., Ed., 2000, Chapt. 21, 463–491. 39. Howe, S., Hopkins, R.O., and Weaver, L.K. A retrospective demographic analysis of carbon monoxide poisoned patients [abstract]. Undersea Hyperb. Med., 23 (Suppl.), 84, 1996. 40. Dodson, W.W., Santamaria, J.P., Etzel, R.A., Desautels, D.A., and Bushnell, J.D. Epidemiologic study of carbon monoxide poisoning cases receiving hyperbaric oxygen treatment [abstract], Undersea Hyperb. Med., 24 (Suppl.), 38, 1997. 41. Vieregga, P., Klostermann, W., Blumm, R.G., and Borgis, K.J. Carbon monoxide poisoning: clinical, neurophysiological, and brain imaging observations in acute disease and follow up, J. Neurol. , 236, 478, 1989. 42. Choi, I.S. Peripheral neuropathy following acute carbon monoxide poisoning. Muscle Nerve, 9, 965, 1986. 43. Roy, B. Crawford, R. Pitfalls in diagnosis and management of carbon monoxide poisoning, J. Accid. Emerg. Med. 1996; 13: 62–63. 44. Grace, T.W., and Platt, F.W. Subacute carbon monoxide poisoning; another great imitator, J. Am. Med. Assoc., 246, 1698–1700, 1981.

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22

Neurocognitive and Affective Sequelae of Carbon Monoxide Poisoning Ramona O. Hopkins

CONTENTS 22.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22.2 Mechanisms of Brain Injury. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22.3 Cognitive Sequelae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22.3.1 Persistent and Delayed Neuropsychological Sequelae. . . . . . . . . . . . 22.3.2 Cognitive Impairments in Lower Level Carbon Monoxide Poisoning. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22.3.3 Markers of Carbon Monoxide Poisoning Severity and Outcome 22.3.4 Effect of HBO on Cognitive Impairments. . . . . . . . . . . . . . . . . . . . . . . . . 22.3.5 Relationship between Cognitive Sequelae and Neuroimaging Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22.3.6 Functional Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22.4 Affective Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22.4.1 Depression and Anxiety . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22.4.2 Obsessive Compulsive Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22.4.3 Kluver–Bucy Syndrome. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22.5 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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22.1 INTRODUCTION Carbon monoxide (CO) is a colorless, odorless, tasteless, and nonirritating gas produced as a by-product of combustion of carbon-containing compounds. CO is the leading cause of poisoning injury and death worldwide,1 and the most common cause of accidental and intentional poisoning in the United States. CO results in approximately 40,000 emergency department visits2 and 470 unintentional deaths per year in the United States.3 The brain and heart are particularly vulnerable 477

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to the pathological effects of CO.1 Neurologic morbidity following CO poisoning includes neurologic sequelae,4 abnormalities on brain imaging,4 affective changes,5 and cognitive impairments.4

22.2 MECHANISMS OF BRAIN INJURY Exposure to CO may damage multiple organ systems with high oxygen utilization, especially the cardiovascular and central nervous systems. For more detail on this topic, see the Raub et al. review published in 2000.1 The mechanisms of CO-induced neural damage are complex and multifactorial. Although the neuropathological injury associated with CO poisoning are related to CO-induced hypoxia (CO binds to hemoglobin),6 other biochemical mechanisms appear to be involved. Mechanisms of brain injury following CO poisoning include: binding to intracellular proteins cytochrome c-oxidase, myoglobin, or cytochrome c (P-450) reductase, leading to mitochondrial dysfunction and disruption of cellular metabolism.7 Other mechanisms include hypoxia,8 release of excitatory amino acids (e.g., glutamate) resulting in calcium influx and cell damage or death,9 interference with intracellular enzyme function,10 lipid peroxidation leading to oxidative injury,11 deposition of peroxynitrate and subsequent blood vessel endothelium damage,12 oxidative stress from intracellular iron deposition,13 and apoptosis.14 CO-mediated oxidative stress alters myelin basic protein, resulting in an immune response and inflammation in the central nervous system.15 Consistent with the multifactorial neuropathologic mechanisms, the resultant neuropathology, cognitive, affective, and neurobehavioral sequelae are heterogeneous.

22.3 COGNITIVE SEQUELAE Cognitive impairments frequently occur following CO poisoning in healthy individuals.16 It is estimated that between 15% and 49% of individuals with diagnosed CO poisoning will develop cognitive sequelae.17 Some CO-poisoned people will develop persistent neuropsychological sequelae (i.e., initial impairments that persist over time);16 however, others who have intact initial cognitive performance may present with delayed neurologic or cognitive sequelae (i.e., normal initial cognitive scores with impairment developing from 2 to 40 days post-CO poisoning; see discussion below). CO-related cognitive sequelae are heterogeneous regarding onset, severity, and cognitive domain affected.4 A list of some CO-related cognitive impairments are shown in Table 22.1. Common CO-related cognitive sequelae include impaired memory,18 executive function,19 slow mental-processing speed, decreased intellectual function,4 apraxia, aphasia, and agnosia.20 Cognitive sequelae lasting 1 month21,22 or more16,23 occurs in 25–50% of participants with loss of consciousness (LOC) or carboxyhemoglobin (COHb) levels greater than 25%.22,24 Even people with less severe CO poisoning may develop cognitive impairments.25 Recent studies utilizing comprehensive standardized neuropsychological tests find significant cognitive impairments both immediately and several years after recovery from the

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TABLE 22.1 Carbon Monoxide-Related Cognitive Impairments Shown by Cognitive Domain Cognitive Domain Arithmetic Attention

Executive function

Intelligence Memory

Motor

Processing speed Spatial

Verbal

Visual

Impairments Acalculia Distractibility Divided attention Preservative errors Sustained attention Decision making Disorganization Impulsivity Planning Working memory Verbal intelligence Performance intelligence Anterograde memory Delayed memory Recall Recognition memory Retrograde memory Short term or working memory Apraxia Athetosis Ballism Bradykenesia Chorea Dyskenesia Dystonia Incoordination Myoclonus Parkinsonism Rigidity Tremor Mental-processing speed Visuoconstruction Visuoperception Visuospatial Aphasia Dysarthria Hypophonia Mutism Achromotopsia Apperceptive agnosia Cortical blindness Homonymous hemianopsia Prosopagnosia Scotomas Visual form agnosia

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initial CO-poisoning symptoms.4,26 The cognitive impairments range in severity from mild, to moderate, and severe. While impairments in memory, attention, and executive function occur most frequently, a consistent pattern of neuropsychological deficits, or a CO “syndrome,” has not been observed. A recent review of the literature from 1995 to 2005 assessed cognitive impairments following CO poisoning identified by standardized neuropsychological tests.27 Hopkins and Woon27 identified 18 group studies that included 979 CO-poisoned patients and 16 case studies that included 35 CO-poisoned patients, for a total of 1014 patients. The mean age of the patients was 38.1 years and 40.2 years for the group and case studies, respectively. While some studies included elderly individuals (age >65 years), the majority of studies contained predominately young to middle age adults. CO-poisoning severity was moderate to severe, with a mean COHb level of 23% (normal ≤2.0%) for both the group and case studies. LOC occurred in 30.1% (295/979) of patients in the group studies and 42.8% (15/35) of patients in the case studies, with a range of 10.8–100% for the group studies. All of the studies reviewed demonstrated the adverse effect of CO poisoning on cognition. The cognitive impairments occurred in multiple cognitive domains and were heterogeneous regarding onset, severity, and cognitive domain affected. Of the group studies, impaired memory was the most frequently reported impairment, followed by impaired attention, motor impairments, executive dysfunction, slow mental-processing speed, and impaired visual spatial abilities. Similarly, in the case studies, memory impairments occurred most frequently, followed by executive dysfunction, impaired attention, motor impairments, visual spatial deficits, and slow mental-processing speed (Figure 22.1). These data indicate that memory is the most common cognitive domain affected by CO poisoning.27 Memory impairments following CO poisoning can be mild, moderate, or severe. For example, a 48-year-old male with LOC and a COHb of 9.1%

Case studies

Processing speed

Cognitive impairments

Group studies Visual spatial Executive function Motor Attention Memory 0

20

40 60 Percent of studies reporting

80

100

FIGURE 22.1 Percent of group and case studies reporting cognitive impairments following carbon monoxide poisoning.

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had severe memory impairments associated with hippocampal atrophy (structure in the temporal lobe associated with the formation and recall of memories) 6 months postCO poisoning.28 Memory impairments following CO poisoning include impaired short-term memory, anterograde memory, retrograde memory, recall, and recognition memory.28−31 While memory impairments usually include the inability to learn or remember new information, global amnesia (both anterograde and retrograde memory impairments) are reported.31 There was the case of a patient with CO-induced amnesia and bilateral hippocampal atrophy who recovered recognition memory, but remained impaired for verbal and spatial memory over time.32 This suggests that some types of memory may improve, whereas other memory impairments may not improve over time. Other CO-induced cognitive impairments included impaired attention, executive function, motor, visual spatial, and slowed mental-processing speed. Significant deficits in visual tracking, visuomotor skills, visuospatial planning, and abstract thinking occur following CO poisoning.25 Impaired executive function, attention and concentration, visual–perceptual abilities, and information processing speed are also reported.33 Although the common wisdom has been that most people who survive initial CO poisoning will recover, recent studies suggest that the cognitive impairments they incur may last years and sometimes become permanent. The identification of CO-related neurocognitive deficits may be instrumental for future studies in determining if they are lessened through therapy, such as cognitive rehabilitation or medications. In addition to the more common cognitive impairments such as impaired memory and executive function, CO poisoning can produce other impairments such as visual agnosia.34 As an example, a 34-year-old female (patient DF) who sustained severe CO poisoning developed visual form agnosia (e.g., inability to visually recognize objects), owing to bilateral diffuse damage to the ventral portion of the lateral occipital regions, including the ventral visual pathway.34 DF was unable to recognize objects, especially line drawings of common objects. She could not discriminate between vertical and horizontal line gratings or between simple geometric shapes.35 Her color vision was intact and she was able to draw objects from memory, but could not recognize the objects she drew. Despite the problem with object recognition, she had no problem adjusting her finger-thumb grip to the width of objects.36 She was adept at interacting manually with objects and she used the structural features of objects to control visually guided grasping movements, showing the capacity to act upon visual information that she was unable to report at a conscious level.36 Further, she was able to negotiate obstacles when walking though a room.35 The ability to interact with objects or avoid obstacles when walking was due to preservation of the dorsal visual pathway. Thus, she had impaired ability to visually recognize objects but, preserved visual processing for object orientation and location of objects in a room, even though she denied “seeing” the objects.

22.3.1 PERSISTENT AND DELAYED NEUROPSYCHOLOGICAL SEQUELAE Neurological or cognitive sequelae can occur immediately and persist over time (“persistent neurocognitive sequelae,” PNS), or the onset can be delayed in its

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onset (“delayed neurocognitive sequelae” or the so-called interval form, DNS).16,22,23 Delayed neurologic or neurocognitive sequelae presentation includes a lucid period of between 2 and 40 days after CO poisoning onset.37 A number of studies have assessed CO-associated DNS,17,22,23,38 however few studies recognize or assess PNS.16 PNS and DNS are common following acute CO poisoning. Delayed neuropsychological sequelae occur in 0.06–40% of CO poisonings.17,38 Symptoms of DNS include mental deterioration, urinary and/or fecal incontinence, gait disturbance and other neurologic problems such as cognitive impairments.39 There was the case of a 50-year-old male, who sustained LOC owing to CO poisoning and developed DNS 1 month later with behavioral changes, disorientation, impaired memory, masked face, hypophonia, muscle rigidity, and bradykinesia manifested by slow movements and gait disturbance.40 At 4 months all symptoms had resolved. Other studies show that DNS persists over time.23 There are a paucity of data regarding risk factors for DNS, however, COHb levels are not associated with the severity of the symptoms.41 The etiology(s) of PNS and DNS are unknown, although it has been hypothesized that DNS is due to extensive myelin and neuronal loss.42 Other theories include immuopathological damage due to activation of polymorphonuclear leukocytes leading to demyelination and dopaminergic and serotonergic disturbances.43 One method that appears to be sensitive to the underlying pathophysiology of DNS is magnetic resonance spectroscopy (MRS). In proton MRS of the brain, signals are present from N-acetylaspartate (located primarily in neurons, a marker for neurons and axons), choline (principally phosphotidyl choline, a membrane constituent), and creatine (used as an internal standard because its level is usually stable). For comparison purposes, N-acetylaspartate and choline are expressed relative to creatine. MRS appears to be sensitive to CO-poisoning related changes in white matter.44 Data show that N-acetylaspartate/creatine were below normal and choline/creatine were elevated at the time of DNS symptom onset, yet both structural magnetic resonance (MR) and cerebral blood flow measures were normal.45 Increased severity of the spectral changes at the onset of DNS was related to more profound clinical symptoms. Clinical recovery correlated with normalization of the spectral changes.44 Thus, proton MRS may provide a much-needed marker of the development of DNS following CO poisoning. Weaver and colleagues46 assessed both PNS and DNS in a prospective outcome study. Participants (N = 238) with acute CO poisoning were followed prospectively. Persistent neuropsychological sequelae were defined as cognitive dysfunction initially, which persisted at 2 weeks and 6 weeks after CO poisoning. Delayed neuropsychological sequelae are defined as a decline of at least one standard deviation on a neuropsychological subtest score from a prior score, and meeting the definition for cognitive sequelae at 6 weeks.46 Thirty-seven percent of participants had cognitive sequelae at 6 weeks, of which 59% had PNS and 28% had DNS, a ratio of 2:1. Hyperbaric oxygen (HBO) reduced the incidence of PNS but not DNS.46 One possible explanation for the effect of HBO on PNS, but not on DNS is that HBO favorably modulates mechanisms of early brain injury but does not influence mechanisms that may be involved in the development of DNS.15

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22.3.2 COGNITIVE IMPAIRMENTS IN LOWER LEVEL CARBON MONOXIDE POISONING Many clinicians believe that only patients who experience LOC37 or have moderate to severe CO poisoning (COHb > 25%)47 will develop sequelae. A survey of hyperbaric medical centers in North America indicated that nearly all treating facilities would use HBO for a CO-poisoned patient with a COHb level of 40% and a COHb level of 25% was identified most often as an indication for HBO therapy.48 While most studies of cognitive impairments following CO poisoning include patients with moderate to severe poisoning, information is accumulating regarding cognitive impairments in patients with lower-level or less severe CO poisoning. Less severe CO poisoning has been defined using a variety of criteria. It has been defined as COHb level of ≤10%,49 a COHb level of 10%,50 a COHb of 5–15%,47 or COHb of 0.01–11%.25 Most studies agree that less severe CO poisoning occurs at COHb levels of <15% with no LOC. The effects of less severe CO poisoning can be difficult to detect as the symptoms are often mild, therefore such individuals may not seek medical care. Symptoms of less severe CO poisoning are similar to acute poisoning and include headache, fatigue, and dizziness. Syncope can occur with COHb levels as low as 0.1–0.3%.25 Less severe CO poisoning can impair visual thresholds, driving skills, and auditory discrimination at COHb levels of 0.2–0.5%.25 Impaired vigilance to incoming sensory stimuli51 and decreased auditory-evoked potentials, impaired memory, and altered mood17 have been reported following less severe CO poisoning. People with COHb levels as low as 4.4% have reduced work capacity.52 Cave painters who were exposed to lower-level CO developed hallucinations.53 Studies that assess the cognitive effects of less severe CO poisoning are limited. Current data suggest that impaired memory and slow mental-processing speed occurs in individuals with less severe CO poisoning.17 Amitai and colleagues25 investigated the cognitive effects of acute lower-level CO poisoning in healthy students who were majoring in science, law, psychology, medicine, international relations, and social work. The healthy students were exposed to CO from kerosene stoves used to heat the space and compared to matched controls. The students exposed to the CO showed significantly worse performance on measures of memory, learning, visuomotor skills, abstract thinking, and visuospatial planning compare to the students not exposed to CO.25 Thus, even less severe CO poisoning is associated with development of cognitive impairments. Prospective studies of the cognitive outcomes of less severe CO poisoning are lacking. Chambers et al.54 compared the cognitive outcomes of CO poisoned patients with less severe poisoning to patients with more severe CO poisoning at 6 weeks, and 6 and 12 months following their poisoning. Less severe CO-poisoning was defined as no LOC and a COHb level ≤15%, while more severe CO-poisoning was defined as LOC or a COHb level >15%. About 55 patients had less severe and 201 had more severe CO poisoning. Cognitive sequelae occurred in 35% versus 39% for patients with less severe versus more severe CO poisoning, respectively. There was no difference in the prevalence of cognitive sequelae (P = 0.91) in patients

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with less severe compared to the more severe CO-poisoning at 6 weeks, 6 and 12 months. Regardless of less severe or more severe CO poisoning, CO-poisoned patients had significant cognitive sequelae.54 These data suggest that CO-related cognitive outcomes may be independent of poisoning severity.

22.3.3 MARKERS OF CARBON MONOXIDE POISONING SEVERITY AND OUTCOME One common belief is that markers of CO-poisoning severity, such as LOC and COHb levels are good predictors of patient outcome. One study found the length of LOC was related to outcome55 and development of DNS.37 Alternatively, COHb level is not a reliable predictor of CO-poisoning severity, symptoms, or neurologic outcome.55−57 Similarly, COHb levels do not correlate with severity of poisoning or cognitive outcomes.58−60 For example, the rate of cognitive sequelae in patients with severe CO poisoning with mean COHb levels of 25.2 ± 9.2% did not differ from that of patients with less severe CO poisoning with mean COHb levels of 6.8 ± 4.7%.54 Other studies have shown that COHb levels are not associated with cognitive deficits.61 Alternatively markers of poisoning severity such as LOC, duration of coma, elevated COHb, or duration of exposure do not predict cognitive sequelae.23 Several studies have assessed the relationship between markers of CO poisoning severity (LOC and COHb levels) with brain imaging findings and cognitive impairments. Hopkins et al.62 found that LOC was not required for the development of cognitive sequelae following CO poisoning. Another study found no association between corpus callosum atrophy and COHb and or LOC. Even with significantly elevated COHb levels and LOC in approximately 50% of the patients, these markers (e.g., COHb level and LOC) did not correlate with the presence of corpus callosum atrophy or development of cognitive impairments.62 Similarly, neither fornix atrophy nor verbal memory impairments correlate with COHb or LOC following CO poisoning.61 Findings in primates indicate that neither severity nor duration of CO-exposure is related to the severity of white matter damage.63 In summary, neither symptoms of poisoning, cognitive impairment4,23 white matter hyperintensities,64 fornix atrophy,61 or corpus callosum atrophy65 are related to COHb levels or LOC. The lack of association between COHb levels and cognitive and neuropathological outcomes raises the question as to why this may be the case. One possible explanation is that the lack of association between COHb and outcome measures is due part in to the variability in measured COHb levels in CO-poisoned individuals. The variability in measured COHb levels is directly related to the delay in removal from the CO environment to medical treatment and the amount and duration of supplemental oxygen given prior to COHb measurement.66,67 Thus, the time to COHb measurement and supplemental oxygen impacts the result in decreased COHb levels.

22.3.4 EFFECT OF HBO ON COGNITIVE IMPAIRMENTS The usual treatment for acute CO poisoning is 100% normobaric oxygen, commonly delivered by a reservoir nonrebreathing face-mask, or by HBO.41,68 HBO

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therapy is recommended for patients with acute CO poisoning, especially if they have experienced LOC, or have severe poisoning.2,41,69,70 Comparisons of the several randomized clinical trials in the treatment of acute CO poisoning is difficult owing to methodological differences.22,23,71,72 A recent prospective double-blind, randomized treatment trial found that HBO therapy reduced cognitive sequelae by 46% at 6 weeks compared to normobaric oxygen.16 Both groups of participants improved over time, but the difference in cognitive sequelae was maintained at 12 months. Those patients with cognitive sequelae had moderate to severe cognitive impairments, falling below the 16th percentile of the normal distribution.29 They communicate and perform activities of daily living normally, but find activities that require executive function, memory, and attention/concentration skills as challenging or impossible.16 Similar findings of benefit for HBO have been reported.23 Alternatively, Scheinkestel et al.71 reported that HBO might worsen outcome in CO-poisoned patients. The study by Weaver et al.16 differed substantially from that of Scheinkestel et al. regarding the number of intubated patients, CO exposure duration, time from the end of the CO exposure to HBO therapy, randomization methods (equal proportions versus cluster), follow-up rate (97% versus 46%), suicide rate (31% versus 69%), statistical analyses, and oxygen treatment protocols.71

22.3.5 RELATIONSHIP BETWEEN COGNITIVE SEQUELAE AND NEUROIMAGING FINDINGS CO poisoning may result in focal and generalized neuroanatomical abnormalities observed on MR and Computed Tomography (CT) imaging. Brain lesions following CO poisoning occur in cortex,73 cerebellum,74 thalamus,75 and substantia nigra.76 Subcortical lesions are found in the white matter77 and basal ganglia including the globus pallidus,78 caudate and putamen.79,80 White matter hyperintensities are common in the periventricular and centrum semiovale or deep white matter regions.64 Generalized atrophy of white matter structures like the corpus callosum65 and white matter degeneration in the temporal, parietal and occipital regions are reported post-CO poisoning.73 A prospective study in consecutive CO-poisoned participants demonstrated that white matter lesions occur more frequently than basal ganglia lesions.64 While some studies indicate that white matter lesions are the most common lesion following CO poisoning,77,81 others indicate basal ganglia lesions are the most common.82,83 Alternative evidence supporting basal ganglia lesions as the most frequent CO-related lesion comes from a recent review that found globus pallidus lesions occurred in 32–86% of patients.84 Early (within 24 h post-CO poisoning) brain imaging can be normal with basal ganglia lesions observed on subsequent scans.64 Alternatively, basal ganglia lesions can occur within the first day following CO poisoning.85 Basal ganglia lesions have been reported at 1 month,86 6 months,31 1-year,87 2 years,86 4 years,74 and 5 years88 post-CO poisoning. It appears that COHb levels are not associated with the development of basal ganglia lesions, as the lesions occurred with COHb levels as low of 9.1%28 and as high as 54%.89

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In addition to neural lesions, CO poisoning may cause neuronal cell loss and concomitant structural atrophy. Atrophy has been reported in the fornix,61 hippocampus,4 and corpus callosum.65 Generalized atrophy can occur with brain volume reduction manifested by reduced gyral volume, increased sulcal space, and passive ventricular enlargement.4 A recent study found CO-poisoned patients had atrophy in the putamen, caudate, and globus pallidus in the absence of basal ganglia lesions.90 The relationship between neuropathologic findings and cognitive impairments has only recently been assessed. Slow mental-processing speed and impaired memory were associated with smaller putamen and globus pallidus volumes in CO-poisoned patients. Impaired verbal memory was associated with fornix atrophy,61 while slow mental-processing speed was associated with white matter hyperintensities64 following CO poisoning. Thus, basal ganglia atrophy, fornix atrophy, and white matter hyperintensities likely all contribute to the observed cognitive impairments in CO victims. There are significant correlations between neuropsychological impairments and abnormalities in cerebral perfusion, clinical MR, and/or brain volumetric measures in CO poisoned patients.4 A study of consecutively CO-poisoned patients using quantitative MR (brain volumetric measures) compared neural volumes from the initial MR scan (e.g., day of CO poisoning) with MR 6 months post CO exposure. The patients had atrophic changes of the fornix, corpus callosum, and basal ganglia 6 months postexposure compared to their initial MR scans that correlated with cognitive impairments.61,65 Alternatively, MR and CT structural imaging carried out at the onset of the symptoms of DNS found no association between the symptoms and the imaging abnormalities. Pavese et al.91 found 50% of patients (11/22) had abnormalities on MR imaging, whereas 27% of the patients had adverse symptoms 1 month after the CO poisoning. Other authors report many patients with delayed symptoms (30–42%) have normal neuroimaging examinations.92,93

22.3.6 FUNCTIONAL IMAGING Measures of cerebral blood flow may be more sensitive to CO poisoning-related neural changes than standard structural imaging. Decreased glucose metabolism on positron emission tomography (PET),94 hypoperfusion on single photon emission computed tomography (SPECT),4,95 and abnormal electroencephalography (EEG)20,21 parallel the focal and diffuse changes observed with structural imaging following CO poisoning. Regional cerebral blood flow (using PET) abnormalities may also be present in the absence of abnormalities on CT or MR.96 Neuropsychological impairments are associated with abnormalities in cerebral perfusion, clinical MR, and/or brain volumetric measures.4 A SPECT study found patchy hypoperfusion in patients that developed delayed neurological sequelae.95 Parkinsonian symptoms are associated with decreased perfusion of the basal ganglia and cognitive deficits are associated with decreased cerebral blood flow in cortical areas.96 CO poisoningrelated cerebral blood flow abnormalities predict poor outcome (death, remote memory impairment).97 In contrast, cerebral blood flow abnormalities did not predict outcome 3–5 days after CO poisoning.98

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TABLE 22.2 Carbon Monoxide-Related Affective and Neurobehavioral Changes Affective Sequelae Depression Anxiety Apathy Irritability Mood swing Elated mood Neurobehavioral Changes Obsessive and compulsive behaviors Delusions Hallucinations Violent outbursts Fear Disinhibition Anger

22.4 AFFECTIVE DISORDERS 22.4.1 DEPRESSION AND ANXIETY Some affective and behavioral changes associated with CO poisoning are shown in Table 22.2. Affective and personality changes following CO poisoning appear to be heterogeneous regarding time of onset, severity, and duration.26,89,99,100 While depression is frequently reported following CO poisoning, fewer studies have assessed anxiety.4,26,92,101 Other psychological and personality changes following CO poisoning include obsessive and compulsive behavior,26,92,102,103 delusions and hallucinations,20,21,92 violent outbursts,20 fear,26 and elated mood.21 Jasper and colleagues found depression and anxiety in 45% of CO-poisoned patients at 6 weeks, 44% at 6 months, and 43% at 12 months following CO poisoning.5 The prevalence of depression and anxiety following CO poisoning varied by study from a low of 33% to a high of 100%.4,99,104 Differences in patient populations, patient selection, affective measures, and length of follow-up may account for the between study differences. The consistent between study findings include the high rate of depression and anxiety in CO-poisoned people. Similar prevalence rates of depression and anxiety occur in other pulmonary disorders with depression reported in 25–28% of patients with cardiac and pulmonary disorders105,106 and anxiety in 10–40% of patients with pulmonary disorders.107,108 Accidentally CO-poisoned patients are as likely as those with intentional CO poisoning to have depression and anxiety at 6 and 12 months.5 Other studies have reported significant depression and anxiety in participants who attempt suicide with CO.99,104 Hay et al.99 found that depression in CO-poisoned participants was

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similar to control patients who had a psychiatric disorder. Smith and Brandon109 found a higher prevalence of depression and personality changes in patients with intentional CO poisoning (35%) compared with accidentally poisoned patients (21%) and psychiatric controls (9%). Thus both intentional and accidentally CO-poisoned patients are at risk to develop depression and anxiety. CO-poisoned patients with cognitive impairments may develop CO morbid depression and anxiety.4,74 Alternatively, depression following CO poisoning can occur in the absence of cognitive impairments.78,109 Mori et al.78 described a patient with no prior history of psychiatric disorders who developed dramatic personality changes in the absence of cognitive deficits following accidental CO poisoning. Smith and Brandon109 found that 33% of CO-poisoned patients developed personality and affective morbidity, but only 11% developed cognitive impairments. CO poisoning appears to result in a high rate of depression and anxiety.

22.4.2 OBSESSIVE COMPULSIVE DISORDER Symptoms of obsessive-compulsive disorder include behavior mannerisms associated with Tourettes syndrome and obsessive thoughts. Compulsive stereotypic routines may develop in patients with basal ganglia lesions.102 A case of obsessive-compulsive disorder secondary to CO poisoning was reported in the 34-year-old male.102 Shortly after hospital discharge, the patient reported an irresistible urge to spit and pull the hair on his legs. He developed obsessive thoughts of harming his friends and family, fear of germ contamination, and sexual fantasies. His compulsive behaviors included repetitive hand-washing, checking behaviors, and counting rituals. Neuroimaging showed bilateral globus pallidus lesions. Thus, CO poisoning can lead to acquired obsessive-compulsive disorder with concomitant bilateral globus pallidus lesions.102

22.4.3 KLUVER–BUCY SYNDROME Muller110 reported the case of an 18-year-old female with LOC due to CO poisoning. Her COHb was 14%. During rehabilitation she had oral tendencies (i.e., put everything into her mouth), decreased social distance, and object agnosia. She had flattened affect and appeared placid and indifferent toward people and events. She was diagnosed with a Kluver–Bucy-like syndrome. Neuropsychological testing showed cognitive deficits similar to dementia. Lesions on brain imagining were located in the lateral temporal lobes sparing the hippocampus. The Kluver-Bucy like symptoms resolved 6 months later, but the cognitive deficits including impaired attention, distractibility, and amnesia persisted.110

22.5 CONCLUSION CO poisoning is common, often goes unrecognized and may result in significant morbidity. Morbidity following CO poisoning includes neurologic sequelae, neuropathologic abnormalities on brain imaging, affective sequelae, and cognitive impairments. Morbidity appears to be independent of poisoning severity as measured

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by COHb level and LOC. Most CO poisoning is preventable, therefore the associated morbidity is also preventable. Given the high rate of brain related morbidity and the fact that the majority of CO poisoning is avoidable, awareness and prevention of CO exposure is warranted. With increased awareness of the dangers and causes of CO exposure, and with the availability of CO alarms, CO poisoning and its adverse effects may be significantly reduced.

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87. Shimosegawa, E. et al. Cerebral blood flow and glucose metabolism measurements in a patient surviving one year after carbon monoxide intoxication, J. Nucl. Med., 33, 1696, 1992. 88. Vion-Dury, J. et al. Sequelae of carbon monoxide poisoning: An MRI study of two cases, J. Neuroradiol., 14, 60, 1987. 89. Jaeckle, R.S. and Nasrallah, H.A. Major depression and carbon monoxide-induced parkinsonism: Diagnosis, computerized axial tomography, and response to L-dopa, J. Nerv. Ment. Dis., 173, 503, 1985. 90. Pulsipher, D.T., Hopkins, R.O. and Weaver, L.K. Basal ganglia volumes following carbon monoxide poisoning: A prospective longitudinal study, Undersea Hyperb. Med., 33, 245, 2006. 91. Pavese, N. et al. Clinical outcome and magnetic resonance imaging of carbon monoxide intoxication. A long-term follow-up study, Ital. J. Neurol. Sci., 20, 171, 1999. 92. Lee, M.S. and Marsden, C.D. Neurological sequelae following carbon monoxide poisoning clinical course and outcome according to the clinical types and brain computed tomography scan findings, Mov. Disord., 9, 550, 1994. 93. Choi, I.S. and Cheon, H.Y. Delayed movement disorders after carbon monoxide poisoning, Eur. Neurol., 42, 141, 1999. 94. de Reuck, J. et al. A positron emission tomography study of patients with acute carbon monoxide poisoning treated by hyperbaric oxygen, J. Neurol., 240, 430, 1993. 95. Choi, I.S. et al. Evaluation of outcome of delayed neurologic sequelae after carbon monoxide poisoning by technetium-99m hexamethylprophylene amine oxime brain single photon emission computed tomography, Eur. Neurol., 35, 137, 1995. 96. Kao, C.H. et al. HMPAO brain SPECT in acute carbon monoxide poisoning, J. Nucl. Med., 39, 769, 1998. 97. Turner, M. and Kemp, P.M. Isotope brain scanning with Tc-HMPAO: A predictor of outcome in carbon monoxide poisoning?, J. Accid. Emerg. Med., 14, 139, 1997. 98. Sesay, M. et al. Regional cerebral blood flow measurements with Xenon-CT in the prediction of delayed encephalopathy after carbon monoxide intoxication, Acta Neurol. Scand. Suppl., 166, 22, 1996. 99. Hay, P.J. et al. The neuropsychiatry of carbon monoxide poisoning in attempted suicide: A prospective controlled study, J. Psychosom. Res., 53, 699, 2002. 100. Vieregge, P. et al. Carbon monoxide poisoning: Clinical, neurophysiological, and brain imaging observations in acute disease and follow-up, J. Neurol., 236, 478, 1989. 101. Jefferson, J. Subtle neuropsychiatric sequelae of carbon monoxide intoxication: Two case reports, Am. J. Psychiatry, 133, 961, 1976. 102. Escalona, P.R. et al. Obsessive-compulsive disorder following bilateral globus pallidus infarction, Biol. Psychiatry, 42, 410, 1997. 103. Lugaresi, A. et al. "Psychic akinesia" following carbon monoxide poisoning, Eur. Neurol., 30, 167, 1990. 104. Skopek, M.A. and Perkins, R. Deliberate exposure to motor vehicle exhaust gas: The psychosocial profile of attempted suicide, Aust. N. Z. J. Psychiatry, 32, 830, 1998. 105. Silverstone, P.H. Prevalence of psychiatric disorders in medical inpatients, J. Nerv. Ment. Dis., 184, 43, 1996. 106. Silverstone, P.H. et al. The prevalence of major depressive disorder and low selfesteem in medical inpatients, Can. J. Psychiatry., 41, 67, 1996. 107. Karajgi, B. et al., The prevalence of anxiety disorders in patients with chronic obstructive pulmonary disease, Am. J. Psychiatry, 147, 200, 1990.

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108. Pollack, M.H. et al., Prevalence of panic in patients referred for pulmonary function testing at a major medical center, Am. J. Psychiatry, 153, 110, 1996. 109. Smith, J.S. and Brandon, S. Morbidity from acute carbon monoxide poisoning at three-year follow-up, Br. Med. J., 1, 318, 1973. 110. Muller, N.G. and Gruber, O. High-resolution magnetic resonance imaging reveals symmetric bitemporal cortical necrosis after carbon monoxide intoxication, J. Neuroimaging, 11, 322, 2001.

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23

Neurocognitive and Neurobehavioral Sequelae of Chronic Carbon Monoxide Poisoning: A Retrospective Study and Case Presentation Dennis A. Helffenstein

CONTENTS 23.1 Background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.1.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.1.2 Incidence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.1.3 Physical, Cognitive and Emotional/Affective Sequelae of Chronic Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.1.4 Published Chronic Carbon Monoxide Studies Utilizing Neuropsychological Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2 Helffenstein Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.1 Sample and Exposure Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.1.1 Admission Criteria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.1.2 Sample Demographics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.1.3 Source and Location of Exposure . . . . . . . . . . . . . . . . . . . . . . . 23.2.1.4 Level of Carbon Monoxide Exposure . . . . . . . . . . . . . . . . . . . 23.2.1.5 Duration and Frequency of Exposure . . . . . . . . . . . . . . . . . . . 23.2.1.6 Time Since Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.2 Battery Administered . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.3 Norms Utilized . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.4 Symptoms Experienced by Participants During Carbon Monoxide Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.5 Persisting Symptoms Reported by Participants . . . . . . . . . . . . . . . . . . .

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23.2.5.1 Physical Symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.5.2 Visual Symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.5.3 Cognitive Symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.5.4 Psychological / Behavioral Symptoms . . . . . . . . . . . . . . . . 23.2.6 Neuropsychological Testing Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.6.1 Index Scores . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.6.2 IQ Tests . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.6.3 Halstead–Reitan Tests . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.6.4 Memory Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.6.5 Academic Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.6.6 Visual–Visual Perceptual Testing . . . . . . . . . . . . . . . . . . . . . . 23.2.6.7 Speed of Information Processing . . . . . . . . . . . . . . . . . . . . . . 23.2.6.8 Other Motor Skills . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.6.9 Miscellaneous Tests of Executive Function . . . . . . . . . . . 23.2.6.10 Language Comprehension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.7 Minnesota Multiphasic Personality Inventory-2 . . . . . . . . . . . . . . . . . . 23.2.8 Vocational Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.2.9 Summary of Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.3 Case Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.3.1 Patient Demographics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.3.2 Exposure Information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.3.3 Educational History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.3.4 Persisting Symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.3.5 Results from Initial Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.3.6 Neuropsychological Re-evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.3.6.1 Circumstances of Re-evaulation . . . . . . . . . . . . . . . . . . . . . . . 23.3.6.2 Self-reported Symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.3.6.3 Comparison of Test Scores . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.3.6.4 Results from Re-evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.3.7 Summary of Case Study. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.3.8 Takeaway Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23.4 Addendum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

513 513 515 515 516 516 518 522 522 523 525 527 528 529 530 531 536 538 540 540 540 540 541 541 542 542 542 543 543 545 545 546 547 548

23.1 BACKGROUND 23.1.1 Introduction Carbon monoxide (CO) is the most common cause of poisoning in the United States and may result in neuropathologic changes which in turn result in a wide range of cognitive, visual, affective, and neurologic sequelae. The effects of moderate to severe acute CO poisoning have been well documented in the literature. For example, Gale et al.1 utilized neuropsychological testing in addition to brain imaging techniques [i.e., Single Photon Emission Computed Tomography (SPECT),

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Magnetic Resonance Imaging (MRI), and quantitative Magnetic Resonance Imaging (qMRI)] to identify the patient’s residual neuropsychological and neuropathological impairments. Ninety-three percent of the sample group showed cognitive impairments on neuropsychological testing, including difficulties with attention, memory, executive function, and mental processing speed. Ninety-five percent of the patients were experiencing ongoing problems with depression and anxiety. The results of the imaging studies revealed that 38% of the patients had abnormal MRI scans, 67% had abnormal SPECT scans, and 67% had abnormal qMRI findings. The qMRI technique identified hippocampal atrophy and/or diffuse cortical atrophy. The SPECT identified cerebral profusion deficits, most notably in the frontal and temporal lobes. Significant correlation was identified between the neuroimaging techniques and deficits noted on neuropsychological testing. The effects of chronic CO poisoning are less well researched and documented. Most CO poisoning studies to date have focused on short-term effects of a one time, lower-level exposure to CO in experimental settings or on the long-term effects of accidental acute CO poisoning. As with any toxin, there are three components in determining the severity of exposure. These include the level or amount of toxin the individual is exposed to, the frequency of exposure, and the duration of each exposure. One difficulty faced in evaluating the effects of chronic CO poisoning is that it is often difficult to calculate the above variables with any degree of certainty. However, the health risks of exposure to lower levels of CO repeatedly or for an extended duration should not be minimized. Wright2 states, “There is a strong possibility that low level exposure to CO is responsible for widespread and significant morbidity. However, the clinical syndrome produced is often overlooked because of a range of presentation, obscure symptoms, and a lack of awareness of the problem” (p. 387). There is now a growing body of evidence, which clearly shows that chronic exposure to CO can, and often does, result in permanent neurological, cognitive, and visual dysfunction. Regarding this issue, Penney3 states, “Clearly, prolonged exposure to this poison even at what were previously thought to be ultra-low levels is capable of producing many and varied residual health effects. Furthermore, the incidence of such unpleasant and often debilitating effects is far higher than was previously believed by the medical and public health community and can continue for a very long period of time” (pp. 414–415). Indeed, there is some evidence to suggest that because of the repeated exposures, which typically occur in cases of chronic CO poisoning, the pathophysiological changes and damage to the brain may actually be more significant than in cases of acute poisoning.4

23.1.2 INCIDENCE CO exposure is the most common cause of death by poisoning in the US and results in an estimated 40,000 emergency room (ER) visits per year.5 Typically, these are acute poisoning incidents which have resulted in severe medical problems requiring emergency intervention. Townsend and Maynard6 note, “The Institute for Environment and Health commented in their 1998 publication on CO that, ‘It is likely that many more sub-acute CO intoxications occur than are brought to the attention of medical practitioners.’ Because of the difficulty in recognizing the effects of exposure

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to low concentrations of CO, there is currently limited knowledge on the size of the problem” (p. 708). These authors go on to note that there are two key questions, which must be addressed. One, the number of people potentially affected by low levels of CO in their homes, workplaces or other settings, and, two, the likelihood of long-term negative health effects. With regard to the second question, there is some evidence to suggest that a significant proportion (43%) of individuals who experience a chronic exposure to CO have permanent neurological sequelae at 3-year follow-up.7 The number of individuals potentially affected by low levels of CO is more difficult to estimate, but is certainly more common than acute poisoning events. Hampson8 points out that the signs and symptoms of CO poisoning are nonspecific and that under-diagnosis in ERs is well described in the literature. He goes on to point out that not all patients chronically exposed to CO are treated in ERs and are often seen in medical offices or clinics and, therefore, their statistics would not appear in the national database. It is also noted that these patients will often attribute their nonspecific symptoms to alternate causes (e.g., viral illness) and not seek medical attention. This latter event is typically referred to as “occult CO poisoning.”2 The problem with accurately diagnosing chronic CO poisoning has been well documented by other authors. Regarding this issue, Penney3 states, “For every single case of chronic CO poisoning reported/successfully diagnosed, there are ten cases that go unreported/undiscovered/undiagnosed” (pp. 396–397). The answer to the question regarding the frequency of chronic CO poisoning remains elusive. Heckerling et al.9 estimated that 3–5% of individuals who present to urban ERs for headaches and dizziness might well be victims of chronic CO poisoning. Whatever the number of chronic occult CO poisonings, it is clearly a significant health risk in the United States. Regarding this issue, Halpern10 states, “Chronic occult CO poisoning is a diagnosis that is not frequently recognized in patients seen initially in an ER or by a primary care provider. It is not readily recognized because of a limited history, vague and variable clinical presentation and a failure of emergency care providers to suspect the cause of symptoms. It is a serious and potentially lethal condition and should be suspected whenever a person is seen at a health care facility for multiple ‘flu-like’ complaints, especially during the winter months when homes are heated, or in the late fall when furnaces are started” (p. 107).

23.1.3 PHYSICAL, COGNITIVE AND EMOTIONAL/AFFECTIVE SEQUELAE OF CHRONIC CARBON MONOXIDE POISONING To date, there has been several retrospective survey studies conducted concerning the residual or persisting symptoms associated with chronic CO poisoning. These include two studies conducted by Penney3 and a comprehensive questionnaire study of individuals chronically exposed to CO in the United Kingdom conducted by CO Support in 1996, a registered charity, headed by Ms. Debbie Davis. The CO Support Study was originally published as a technical paper in October 1997,11 and a detailed summary of that study was later published by Hay et al.12 Penney3 conducted two retrospective studies of chronic CO poisoning. Study A included data from 66 individuals who had sustained chronic CO poisoning, defined as CO exposure lasting more than 24 h. Data were obtained through the Internet.

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Duration of exposure, as reported by 29 participants ranged from 0.18 to 120 months. The mean duration of exposure was 30.7 months plus or minus 6.0 months (SEM). Air CO concentrations reported in 15 instances were 427.8 ppm, plus or minus 115.2 ppm. Carboxyhemoglobin (COHb) level, as reported in 11 instances was 9.65%, plus or minus 2.46%. Study A assessed symptoms that respondents indicated they experienced during their chronic CO exposure, as well as their residual or persisting symptoms. Respondents reported 103 different symptoms in total during their exposure. The typical respondent reported multiple symptoms in multiple systems. A partial list of these symptoms appears in Table 23.1. Penney notes that the misdiagnosis rate in cases of chronic CO poisoning is very high. He believes chronic CO poisoning is not better recognized because “It almost invariably presents with too many disparate, seemingly unrelated and for the most part, nonspecific symptoms. This tends to confuse physicians who act mainly on pattern recognition of one or a few symptoms to come up with a probable diagnosis, or at least a ‘short list.’ The result of being presented with 5, 10, or 15 or more symptoms is likely to yield a diagnosis of hypochondriasis (faking), psychiatric condition, or both” (p. 395). When an ER or family physician is presented with a history of multiple symptoms in multiple systems, it is easy to understand how they may misdiagnose chronic CO poisoning. Halpern10 emphasizes that, “A high index of suspicion is necessary to recognize this condition.” In addition, accurate and detailed history taking is important in identifying chronic CO poisoning.

TABLE 23.1 Symptoms Reported During Chronic Carbon Monoxide Poisoning Exposure—Penney Study A, 20003 Physical

Cognitive

Emotional/affective

Headaches Nausea Vomiting Fatigue/lethargy Dizziness/vertigo Shortness of breath Muscle/joint aches Balance problems Hearing problems Tremors Short-term memory Mental confusion Attention/concentration Word finding Depression Anxiety Irritability

Weakness Tinnitus Syncope, partial/total Sleep disturbance Vision problems Heart palpitations Paresthesias Muscle cramps Chest pain/tightness Spelling Speech Disorientation Personality changes Mood swings Apathy

a Summarized and reprinted with permission of author.

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TABLE 23.2 Persisting Symptoms Following Chronic Carbon Monoxide Exposure— Penney Study A, 20003 Physical

Cognitive

Emotional/affective

Ataxia Balance Muscle/joint pain Temperature deregulation Chest pain/tightness Choking Motor incoordination Muscle cramps Dizziness Dysarthria Fatigue Shortness of breath Tinnitus G. I. problems Attention/concentration Short-term memory Mental confusion Disorientation Executive dysfunction Slow speed of information processing Math Paraphasias (literal and verbal) Verbal fluency (word finding) Depression Anxiety Panic attacks Irritability Personality change

Headaches Hearing problems Multiple chemical sensitivity Nausea Paresthesias Peripheral neuropathy Heart palpitation Motor tremors Photophobia Phonophobia Sleep disturbance Vision problems

Reading Speech Spelling Writing Vocabulary (reduced)

Aggression Libido (reduced) Motivation (reduced)

a Summarized and re-printed with permission of author.

Study A also assessed residual or persisting symptoms experienced by the 66 respondents. Ninety-five different persisting symptoms were identified. A select sample of those symptoms is presented in Table 23.2. Penney’s Study B3 involved the analysis of questionnaires completed by 82 individuals who claimed to have suffered chronic CO poisoning. The mean duration of exposure was 28.4 months, plus or minus 4.4 months, with a range of 3 weeks to 120 months. The mean period after termination of the CO exposure, to the time their responses were given was 21.4 months, plus or minus 2.2 months, or nearly 2 years after the exposure stopped. This study reviewed only residual or permanent symptoms that the respondents were experiencing at the time they completed their questionnaires. Regarding physical symptoms, 100% reported persisting problems with fatigue. Greater than 80% reported residual problems with headaches, muscle

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and joint pain, dizziness/balance problems, and sleep disturbance. Greater than 50% reported ongoing difficulties with chest pain, tingling and numbness, and vision problems. More than 45% reported ongoing change in their perception of or sensitivity to smell or taste. From a cognitive standpoint, greater than 70% reported ongoing problems with decision-making, following directions, short-term memory, and attention and concentration. More than 40% reported ongoing difficulties with spatial disorientation and organization. With regard to emotional and affective symptoms, more than 80% of the sample reported ongoing problems with mood change/swings, temper problems/irritability, and personality changes. More than 40% reported ongoing social and family problems. Thirty percent reported school problems. Regarding these results, Penney3 states, “This study suggests that a multitude of physical, cognitive, and emotional symptoms persist for very long periods of time following chronic exposure to CO. The CO exposure need not produce altered consciousness at any time for this to occur. In fact, the CO concentrations and COHb saturations are quite low and in the range previously thought incapable of producing lasting health harm in humans” (p. 413). The CO Support study11 involved the analysis of questionnaires completed by 65 individuals who were chronically exposed to CO. None of those individuals lost consciousness (LOC) as part of their exposure. The results of 12 questionnaires completed by individuals who did experience LOC were also reviewed. Ten of those individuals were involved in chronic CO poisonings and two experienced acute poisonings. This study is unique in that it used controls matched for gender, age, and income. For the chronically exposed patients, data regarding symptoms experienced during exposure were summarized as well as persisting symptoms. A detailed summary of this study will not be presented as part of this chapter. For a detailed review of the results of this study, the reader is referred to Hay et al.12 It is important to note, however, that as in the Penney studies; respondents experienced multiple symptoms in multiple systems during their exposure. It is important to note that results of this study also suggest that, while some symptoms do abate to some degree once the exposure stops, in every case the symptoms may persist long-term. The CO Support study also gathered data regarding employment outcome. Although this was not discussed in detail in the Hay et al.12 summaries, a review of the original technical paper provide more detail regarding employment outcome. Those results are presented in Table 23.3. Of note, 32% of the patients chronically exposed to CO were unable to return to work following the exposure. When LOC occurred because of the CO poisoning, 75% were unable to return to competitive employment. This would suggest that when LOC occurs in conjunction with CO poisoning, the possibility of total and permanent vocational disability increases dramatically. Both of these figures stand in contrast to the control group where none of those individuals was disabled from employment. Hay and his colleagues12 conclude their summary of this study by stating, “The results of this survey indicate that there is a continuing and unrecognized problem associated with chronic exposure to CO. Most physicians do not recognize the symptoms of CO poisoning, and, therefore, do not diagnose it. Many individuals

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TABLE 23.3 Employment Outcome—CO Support Study, 199711

Able to work full time Able to work part time Unable to work Not applicable Working full time Working part time Unable to work Not applicable

Chronic CO Poisoning (N = 65)

CO Poisoning with LOC* (N = 12)

35% 8% 32% 22%

17% 8% 75% 0%

Matched Nondisabled Control Group (N = 65)

44.6% 24.6% 0% 30.8%

∗ This group included ten individuals chronically exposed to CO and two individuals who experienced acute exposures.

suffer for many years because of their exposure to this gas, and as the survey indicates, many people continue to suffer symptoms years after the exposure has stopped. Respondents of the questionnaire indicate that they have experienced a wide range of symptoms up to 2 years after the exposure ended” (p. 434).

23.1.4 PUBLISHED CHRONIC CARBON MONOXIDE STUDIES UTILIZING NEUROPSYCHOLOGICAL ASSESSMENT In 1990, Ryan13 presented the case study of a 48-year-old, right-handed, married woman who reported a 3-year history of constant headaches, lethargy and memory problems. She indicated that she did not have any difficulty recalling events from the distant past but had difficulty recalling information that is more recent. She was reporting ongoing episodes of mental confusion, periods of depression, and anxiety. She reported that on one occasion she nearly LOC in her basement and, therefore, had the gas company check her furnace. The furnace was found to be releasing 180 ppm CO. The patient was running a typing service out of her basement and the possibility existed that the exposure may have persisted for up to 3 years. No COHb level was obtained and it is noted that the patient never LOC. While the woman’s headaches stopped once her furnace was replaced, her memory problems persisted. Her history was negative for alcohol or drug abuse, head trauma, and psychiatric problems. She had never previously been exposed to any other toxic substances. The results of her neuropsychological testing revealed deficits in the area of incidental memory, as measured by the Digit Symbol Incidental Memory Test, as well as clear deficits in her ability to both learn and recall verbal and visual information. Dr. Ryan summarizes the results by stating, “There is no doubt that this patient has developed a clinically significant memory disorder. Prior to her exposure, she worked in positions that placed demands on concentration and memory skills; following

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this exposure, she was unable to keep track of verbal information that was presented seconds earlier, and had difficulty accurately retrieving both verbal and visual information that she had learned within the past 30 min” (p. 64). Based on his overall assessment of the case, Dr. Ryan attributed her neuropsychological disturbance, affective disorder, and somatic complaints to her 3-year history of low level CO exposure. Dr. Ryan further notes that memory disturbances are one of the most frequently reported cognitive problems following CO poisoning. He also notes that this case supports the conclusion that a LOC is not necessary for the development of neuropsychiatric symptoms following a period of CO exposure. Roy Myers et al.14 state that “Chronic exposure to CO produces a clinical syndrome that is often overlooked because of obscure symptomatology, a range of presentations, and a lack of awareness of the problems” (p. 555). They go on to note that neurological exams will often not identify subtle changes in functioning and that neuropsychological testing is often more sensitive to the neurotoxic effects of chronic CO poisoning. Seven patients were included in this study. Each individual had been exposed to CO intermittently or constantly over periods ranging from 3 weeks to 3 years. Once the exposure was identified, each was sent for hyperbaric oxygen (HBO) treatment. Each of the individuals was exposed to a minimum of 200 ppm CO. Each individual was administered the CO Neuropsychometric Screening Battery, as well as other specific neuropsychological tests including the WAIS-R, Trails A and B, Finger Tapping Test, Logical Reasoning and Visual Reproduction from the Wechsler Memory Scale, and Minnesota Multiphasic Personality Inventory (MMPI) or MMPI2. Six of the seven individuals received HBO therapy, ranging from 5 to 59 treatments. The individual who received only five treatments was intolerant to the chamber and that individual’s treatment was considered incomplete. One individual was included in the study who did not receive any HBO treatment. Individuals who received HBO treatment were tested every 2 weeks “until the psychometric tests reached a plateau or returned to normal” (p. 557). The individual who did not receive HBO treatment was tested at two months after the exposure stopped, and then after 10 months of rehabilitation, was tested again at 1 year after the exposure stopped. In addition to neuropsychological testing, a questionnaire was also completed by each participant regarding his or her symptoms. The most common symptoms experienced during the exposure (acknowledged by 50% or more of the group) included problems with headaches, dizziness, motor tremors, difficulties with shortterm memory, sleep disturbance, cognitive set loss, anxiety, reading comprehension, vision, gait/balance, muscle tremors, paresthesias, altered sense of smell, body aches, tinnitus, and spatial disorientation. One participant who received ten HBO treatment sessions reported significant resolution of their symptoms following treatment. One individual who received 50 HBO treatments reported moderate resolution of their symptoms. Three of the participants who received 19, 59, and 29 HBO treatments, respectively, reported minimal or no functional improvement of their symptoms. The individual who received five incomplete treatments reported only minimal improvements in his symptoms. The individual, who received no HBO treatment, but ten months of rehabilitation, reported that his condition improved significantly, but that patient continued to report ongoing and multiple symptoms. In summary, five of the seven (71% of the sample) reported minimal or no resolution of their symptoms

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after a period of recovery from the exposure, HBO treatment, and/or rehabilitation services. With regard to the neuropsychological testing, the authors found that the CO Neuropsycho-metric Screening Battery was of little value in identifying residual cognitive deficits and recommended neuropsychological evaluation that is more detailed. By the completion of testing, four of the seven participants continued to demonstrate a significant split in their Verbal and Performance IQs (PIQs). Three of those individuals had Verbal IQs (VIQs) significantly greater than PIQs. One had PIQ significantly greater than VIQ. Three of the seven continued to demonstrate impairments on the Trails B Test, a test of alternating attention and logical sequencing. Three of the seven also demonstrated residual deficits in fine motor speed. One weakness of this study is that there is no discussion of the impact of practice effects. It appears that most individuals in this study were tested every 2 weeks and repeated exposure to these tests can result in significant gains due to practice. The authors note that ongoing problems with emotional lability, irritability, depression, and anxiety are common sequelae of chronic CO poisoning. Pinkston et al.15 conducted Positron Emission Tomography (PET) scans and neuropsychological testing of two adult patients 3 years following a chronic CO poisoning. The patients were both right-handed, middle-aged individuals who had been married for many years. Both worked in professional occupations and they had no history of prior psychiatric or neurologic conditions. They suffered exposure to CO for a 3-year period due to faulty furnace exhaust/ducting. Neuropsychological testing was conducted on both subjects four times over a 3-year period. The results of the testing indicated a significant anterior frontal lobe syndrome. In addition, both individuals demonstrated frontal symptoms in their activities of daily living, such as indecisiveness, mental passivity, and disorganization. Both individuals experienced a significant vocational disability because of their persistent and ongoing symptoms. Indeed, both individuals were rendered vocationally disabled because of their residual deficits. In addition, both experienced losses in their level of independence and both experienced difficulties with various activities of daily living. Both subjects demonstrated a similar pattern of hypometabolism on PET imaging. Substantially reduced metabolism was evident in the orbital frontal and dorsal lateral prefrontal cortex, as well as areas of the temporal lobe for both individuals. It was determined that the individual scans were consistent with the patients’ presenting symptoms and reduced level of functioning. While hypometabolism was evident in various regions of the temporal lobe, both individuals were performing within normal limits on memory tests by the time of their final evaluation. However, both individuals were reporting and experiencing significant memory dysfunction in their day-to-day activities and activities of daily living. It is noted that one of the subjects received a more significant exposure, being in the home for significant more prolonged periods of time. That subject demonstrated more problems on neuropsychological testing and his PET scan demonstrated more areas of significant hypometabolism. That individual also demonstrated more severe behavioral/affective problems. Both patients ultimately developed epilepsy and were begun on Depakote. The authors note that the development of a seizure disorder was

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not surprising given the temporal and hippocampal dysfunction noted on the PET imaging. Hartman,16 presents a case study of a 65-year-old woman chronically exposed to CO over a six-to-seven-year period. The exposure occurred because of improper installation of a water heater. The woman had 2 years of college and a professional degree. Her symptoms began within a year of the new water heater being installed. As is typical for cases of chronic CO poisoning, her symptoms gradually emerged and worsened over time. Physical symptoms that she developed during the exposure were fatigue, muscle spasms, loss of muscle tone in her face, paresthesias, muscle fatigue, migrating neuritis (sharp pains), problems with balance, her fingernails, and toenails turned black, sleep disturbance, and one near-blackout episode. Other symptoms that she experienced included depression, panic attacks, sleep disturbance, problems with short-term memory, spatial disorientation, and difficulties with vision. By the end of the exposure, she had severe body pain, even at rest. Also during the exposure period, she experienced frequent urinary tract infections, other chronic infections, and developed severe allergies, suggesting a possible compromise of her immune system. It was also noted during the exposure that house plants died and silverware turned black quickly. It was noted that her symptoms did abate to some degree when she would leave the house for several days at a time, but worsened upon returning home. Once the exposure stopped, some symptoms resolved but some persisted, most notably difficulty with her vision, short-term memory, allergies, and sleep disturbance. It was also noted that she had become sensitive to a variety of chemicals and substances (e.g., perfume). The patient underwent serial neuropsychological testing. By the time she was evaluated several years after the exposure stopped, she was functionally reporting ongoing problems with language comprehension, verbal short-term memory, and occasional episodes of spatial disorientation, mild emotional lability, and intermittent sleep disturbance. She was continuing to note ongoing sensitivity to various chemicals and substances (e.g., pesticides). The patient had also developed Crohn’s disease. On neuropsychological testing, she was demonstrating persistent sensory/motor and spatial integration deficits. There was a bilateral loss of her ability to discriminate one versus two-point touch on her fingertips and some errors in fingertip localization. Fine motor coordination on the Grooved Pegboard Test was severely impaired. The patient’s ultimate DSM-III-R diagnosis was 294.80 Organic Mental Disorder, not otherwise specified/probable CO exposure etiology. Divine et al.17 present a case study of a 45-year-old woman chronically exposed to CO for approximately 1 year. The exposure occurred because of a faulty furnace at her place of employment where she worked as a cook. For approximately 1 year, she experienced the following symptoms: “severe flu,” inability to walk in a straight line, bumping into things, problems with balance, severe headache, fatigue, verbal fluency, hearing problems, paresthesias, irritability, and facial pain. Her condition was misdiagnosed as a sinus infection. She had been off work for a period of 5 days and upon returning to work immediately became ill and contacted the gas company. “Extremely high” levels of CO were identified in her work area, at which point she left the premises. The exact CO concentration in her work space was not given.

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Seventeen months following cessation of the exposure, many of her symptoms had resolved. However, she was reporting ongoing problems with reading, writing, speaking, verbal fluency, and dysarticulation. An MRI performed at 15-months after the exposure ended was read as abnormal. The scan revealed multiple small lesions bilaterally in the basal ganglia. The lesions were more severe in the globitus palidus than in the putamen. The radiologist concluded that the lesions were consistent with chronic CO poisoning. The patient had a Bachelor’s degree and no prior neuropsychological history. Neuropsychological testing conducted at 17-months after the end of exposure revealed deficits in attention and concentration, learning and memory retrieval. Testing also suggested problems with depression at that time. Behaviorally, during the course of the evaluation, lapses in attention, perseverations, sequencing problems, slight concreteness, and verbal fluency difficulties were noted. The authors concluded that the testing was consistent with subtle frontal lobe dysfunction. Retesting was performed 12-months later and similar deficits were found, suggesting persistent frontal lobe dysfunction.

23.2 HELFFENSTEIN STUDY 23.2.1 SAMPLE AND EXPOSURE DATA 23.2.1.1 Admission Criteria Participants in this study were 21 consecutively evaluated patients who had been chronically exposed to CO. There were a number of criteria established for admission to the study: 1. The full WAIS-III was administered as part of the evaluation 2. No prior psychological or psychiatric history requiring treatment 3. No prior neuropsychological history (e.g., no prior head injuries, toxic exposures, or neurological illness) 4. No history of substance abuse As all participants were involved in some type of active litigation, no patient was admitted to the study if there was any indication of symptom magnification or exaggeration. All 21 participants of this study performed satisfactorily on three symptom validity tests. Eighty-one percent of the participants were administered and passed the Tombaugh Test of Memory Malingering, Hiscock Digit Recognition Test, and Rey II 15 Item Memory Malingering Test. The remaining 19% of the cohort were administered and passed the Computerized Assessment of Response Bias, Word Memory Test, and Tombaugh Test of Memory Malingering. In addition, the MMPI-2 profiles of all 21 participants were devoid of any indications of symptom magnification or exaggeration. In addition, all 21 participants demonstrated behavioral indicators of good effort during the neuropsychological testing process. Participants were admitted to the study only if there was some documented evidence of dangerous levels of CO in their living or work environments. In 14 cases, measurements of CO in ppm had been made in the living or work space. For two of the

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participants, COHb levels were obtained shortly after the exposures were identified. For five of the participants high levels of CO were identified as being emitted from a furnace or other appliance and there was a reasonable mechanism by which CO entered the living or workspace of the individual. 23.2.1.2 Sample Demographics The mean age of participants in this study was 39.6 years (range 16–78). The mean level of education was 13.8 years (range 9–20 years of formal education). All participants in this study were Caucasian. Eighteen were female and three were male. All participants were right-handed. Nineteen of the participants were working full time at the time of the exposure and two were full-time students. 23.2.1.3 Source and Location of Exposure Fifteen of the 21 participants experienced chronic CO poisoning in their homes. Six of the participants experienced CO exposure at work. Eleven of the participants experienced CO exposure because of a faulty furnace or boiler. Five were exposed as a result of a faulty furnace and water heater combination. One experienced CO exposure because of a faulty gas range and water heater combination. Two participants experienced CO exposure as a result of faulty gas fireplace installation. One participant experienced CO exposure because of a faulty water heater installation. One participant experienced CO exposure because of auto exhaust fumes from a parking garage entering his apartment. 23.2.1.4 Level of Carbon Monoxide Exposure As noted above, in 14 of the cases included in this study, actual measurements of CO in parts per million were made in the living or work space of the individual. The average concentration of CO was 123 ppm, with a range of 13–467 ppm. It is important to note that 100-ppm CO exposure over many hours will result in a COHb saturation of 14%. Two of the participants had their COHb levels measured shortly after the presence of CO was discovered. Regression (i.e., back) calculations were performed to determine the COHb levels at the time the participant left the toxic environment. On average, these two individuals had COHb saturations of 14.5% at that time. For four of the participants in the study, a furnace and water heater at their place of employment were housed in a confined space, which limited combustion air. This created a situation where both the furnace and water heater had a tendency to back draft. The furnace was producing 200+ ppm CO and the water heater was producing 2000+ ppm CO. These readings were taken at the exhaust vents. When back drafting occurred, CO was entering the work space of these individuals. 23.2.1.5 Duration and Frequency of Exposure For each of the 21 participants, it was possible to estimate with some certainty the duration of exposure. The mean duration was 28.9 months (2.4 years) with a range of

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0.5–120 months. It was also possible to estimate with some certainty the frequency of exposure. The average frequency of exposure was 6.3 days per week with a range of 3–7 days per week. 23.2.1.6 Time Since Exposure Each of the 21 participants was evaluated because they were experiencing persisting symptoms, which were great enough to negatively impact their day-to-day, academic, and/or work activities. Clearly, this sample represents the sub-set of chronically exposed CO patients who do not make a full and complete recovery. Testing was conducted an average of 46.8 months (3.9 years) postexposure. The range was 16–111 months postexposure (1.3–9.25 years).

23.2.2 BATTERY ADMINISTERED Each participant was administered a comprehensive battery of neuropsychological tests. Each individual received the Expanded Halstead–Reitan Neuropsychological Test Battery, as well as most of the tests renormed for age, gender and education by Heaton, Grant and Matthews.19 Each individual was administered the complete WAIS-III, as well as the Peabody Individual Achievement Test (PIAT). In addition to the above, the following tests were administered: 1. Complex ideation subtest of the Boston Diagnostic Aphasia Examination 2. Nonverbal agility and verbal agility subtest of the Boston Diagnostic Aphasia Examination 3. Ruff Figural Fluency Test (Ruff FFT) 4. Hooper visual organization test 5. Padula visual midline screening test20 6. Line bisection test 7. Behavioral dyscontrol scale 8. Buschke verbal selective reminding test 9. Rey-Osterreith complex figure test 10. Paced Auditory Serial Addition Test (PASAT) (Levin version) In addition to the above, each of the participants completed a MMPI-2 or Minnesota Multiphasic Personality Inventory-Adolescent (MMPI-A). For each of the participants, the following index scores were generated: 1. 2. 3. 4.

Halstead Impairment Index (HII) Average Impairment Rating (AIR) Global Deficit Score (GDS) General Neuropsychological Deficit Scale (GNDS)

For an earlier discussion of neuropsychological testing in a case study of CO-poisoning by this author, see Helffenstein, 2000.18

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23.2.3 NORMS UTILIZED For the purpose of this study, the Heaton et al.19 demographic norms were used. These norms are demographically corrected for age, gender, and education. In addition, for the purpose of this study, the performance levels proposed by Heaton et al. were utilized. Table 23.4 shows the ranges of performance proposed by Heaton et al. as well as the accompanying T-scores and percentile scores. Where nondemographically corrected scores (i.e., non-Heaton norms) are utilized, those norms will be individually identified by level of performance and will be discussed using the Heaton guidelines.

23.2.4 SYMPTOMS EXPERIENCED BY PARTICIPANTS DURING CARBON MONOXIDE EXPOSURE Table 23.5 is a summary of the most common symptoms reported by the participants of this study during chronic CO poisoning. Consistent with prior studies of chronic CO poisoning, people experienced multiple symptoms in multiple systems. Table 23.5 clearly shows that the symptoms involve a wide variety of physical, sensorymotor, visual, cognitive, and affective/mood conditions. Penney3 discussed in some detail misdiagnosis of chronic CO poisoning, and notes that common misdiagnoses include chronic fatigue syndrome, viral/bacterial/pulmonary or gastrointestinal infection, “rundown condition,” endocrine problem, immune deficiency disorders, psychiatric/psychosomatic problems, allergies, and food poisoning. As noted earlier in this chapter, prior studies have found that during chronic CO poisoning, individuals typically experience multiple symptoms in multiple organ systems. On average, the participants in the current study experienced 25 symptoms during the chronic CO poisoning event, and, as noted by Dr. Penney, most of these individuals received a variety of misdiagnoses during their exposure. Often, when

TABLE 23.4 Heaton Range of Performance on Neuropsychological Testing (Heaton, et al.19 ) Level of Performance Above average Average Below average* Mild impairment Mild/Moderate impairment Moderate impairment Moderate/severe impairment Severe impairment

T-Scores

Percentile Scores

55+ 45–54 40–44 35–39 30–34 25–29 20–24 1–19

68+ 30–67 12–29 6–13 3–5 1–2 <1 <1

∗ Some authors (e.g., Jarvis and Barth21 ) also refer to this range of scores as the

“Borderline” range.

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TABLE 23.5 Symptoms Reported During Chronic Carbon Monoxide Exposure, Helffenstein Study (N = 21) Symptom Headaches Fatigue Dizziness Mental confusion Attention and concentration Sleepiness Irritability Nausea Muscle/joint aches Short-Term memory Shortness of breath Sleep disturbance Chest pain (tightness) Word finding Slow mental processing Heart palpitations Motor incoordination Paresthesias Cough Balance problems Anxiety Light sensitivity Depression Motor weakness Muscle spasms/tremors Noise sensitivity Diarrhea Tinnitus Vomiting Sensitivity to chemicals Blurry vision Emotional lability

% of Participants Reporting 100 90 90 90 90 86 86 81 81 81 76 76 71 71 71 67 67 67 57 57 57 57 52 52 52 48 48 43 38 38 38 33

they did not respond to various treatments, their medical providers concluded that they were likely suffering from a psychological or psychiatric disorder. Dr. Penney notes that, because of a lack of training with regard to chronic CO poisoning, and human CO poisoning generally, most health care providers have a low index of suspicion for this condition, which results in “shockingly high rates of misdiagnosis.” In addition, to the symptoms listed in Table 23.5, some percentage of the cohort also experienced the following symptoms: constipation, blackouts, double vision, decreased fine motor skills, spatial disorientation, problems with multitasking,

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paraphasic errors in their speech, cognitive set loss, difficulties with planning and organization, metallic taste in their mouth, hair loss, decreased hearing, bruising easily, change in skin color, decreased night vision, abdominal pain, incontinence of feces, incontinence of urine, hypersensitive sense of smell, and visual inattention resulting in them bumping into things frequently.

23.2.5 PERSISTING SYMPTOMS REPORTED BY PARTICIPANTS Each of the 21 participants in the study underwent a comprehensive clinical interview with this author concerning their residual or persisting symptoms. Again, consistent with prior studies, these individuals typically experience a wide range of persisting symptoms. For the purposes of this study, the symptoms were clustered into persisting physical symptoms (Table 23.6), persisting visual symptoms (Table 23.7), persisting cognitive symptoms (Table 23.8), and persisting psychological/behavioral symptoms (Table 23.9). Again, the norm was for each participant in the study to experience multiple symptoms in all four areas of functioning. As noted above, each of the participants of this study underwent a comprehensive structured clinical interview. A list of possible symptoms was generated based on a

TABLE 23.6 Persisting Physical Symptoms, Helffenstein Study (N = 21) Symptom Chemical sensitivity Fatigue Physical pain (e.g., joints, muscles) Headaches Muscle cramps/spasms Motor incoordination Phonophobia (noise sensitivity) Impaired auditory gating (filtering background noise) Temperature deregulation Tinnitus Shortness of breath Paresthesias Gait/balance problems Dizziness Motor Tremors Altered sense of smell Nausea/vomiting Altered sense of taste High blood pressure Metallic taste Compromised immune system Vertigo

% of Participants Reporting 100 100 95 95 81 81 81 81 81 76 67 67 67 62 62 52 43 43 29 29 29 19

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TABLE 23.7 Persisting Visual Symptoms, Helffenstein Study (N = 21) Symptom Photophobia Visual scanning deficit Accommodation Depth perception Bumps into things Perception of movement in peripheral vision Eye fatigue Veers off center Blurry vision Oscillopsia Double vision Decreased visual acuity at night

% of Participants Reporting 90 90 86 86 86 86 76 76 71 24 14 5

Note: Bumping into things more frequently and veering off center when walking or driving in a straight line are common manifestations of hemispatial inattention.

TABLE 23.8 Persisting Cognitive Symptoms, Helffenstein Study (N = 21) Symptom Attention and concentration Cognitive set loss Short-term memory Verbal fluency (word finding) Slow speed of processing Multitasking Problem solving/decision making Paraphasic errors in speech Reading comprehension Planning and organization Math Language comprehension Spelling Transposition errors Spatial disorientation Accessing remote memories Writing skills Memory confabulation Memory contamination Initiation

% of Participants Reporting 100 100 100 100 100 90 90 86 86 86 81 76 71 71 71 57 48 29 19 14

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TABLE 23.9 Persisting Psychological/Behavioral Symptoms, Helffenstein Study (N = 21) Symptom Irritability Depression Sleep disturbance Decreased libido Emotional lability PTSD/specific phobia Appetite (inconsistent or decreased) Generalized anxiety Social isolation Anhedonia Decreased motivation

% of Participants Reporting 90 81 76 63 52 48 48 24 33 19 14

review of prior chronic CO poisoning outcome studies. Given the multiple possible symptoms in multiple organ systems, this type of interview was highly preferable to a more “open-ended” style interview. 23.2.5.1 Physical Symptoms A review of the symptoms in Table 23.6 reveals that patients chronically exposed to CO often have residual physical symptoms in a wide variety of organ systems including auditory, gustatory, motor, sensory, vestibular, pulmonary, gastrointestinal, and auto-immune. As discussed above, such a wide variety of symptoms can create a significant diagnostic challenge for primary healthcare providers, especially if the chronic CO poisoning has gone unidentified. It is important to note that 100% of the sample reported persistent problems with fatigue. In most instances participants in the study found that they became more tired more quickly whether performing physical or cognitive activities. All were reporting reduced stamina and endurance to varying degrees. In some instances participants in the study were already utilizing a psychostimulant medication (e.g., Concerta, Adderall, Provigil, or Ritalin) at the time of their evaluation. In some instances a prescription for a psychostimulant was recommended as part of the individual’s treatment plan. It was this author’s impression that the fatigue experienced by the majority of the sample was organically based and did not relate to the patient’s psychological status. 23.2.5.2 Visual Symptoms A variety of visual problems have been well documented following moderate to severe acute CO poisoning. The Penney studies A and B,3 as well as the CO Support study,11 document that “vision problems” in general are common following chronic CO

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poisoning. However, neither study describes in detail what types of vision problems are likely to occur. The current study helps to define in some detail the constellation of visual problems, which are common following chronic CO poisoning. We now understand that acquired brain injuries of all types can result in a wide variety of vision problems, which as a group has come to be referred to as a PostTraumatic Vision Syndrome (PTVS). Indeed, PTVS is extremely common following any neurotrauma, including toxic encephalopathy. Many of the functional vision problems identified in Table 23.7 relate to organically based problems, such as: Esotropia—one eye turns inward Exotropia—one eye turns outward Convergence insufficiency—ability to aim the eyes accurately at a target and then track the target as it moves closer or further away Accommodation—ability to accurately focus on a target, sustain focus, and change focus when focal length changes Binocular vision—eyes working/tracking together as a team so that accommodation, convergence, and eye alignment are all integrated Hemispatial inattention—inconsistent ability of the brain to attend to one visual field Nystagmus—shaking of the eyes, which the individual cannot control For a more detailed understanding of these types of visual deficits, the reader is referred to Politzer.21 A brief description of some of the vision problems listed in Table 23.7 follows: Photophobia: Sensitivity to bright sunlight and at times flourescent lighting. Visual scanning deficit: Patients will often report that their eyes do not track effectively. They will, for example, lose their place when they are reading or miss things they are looking for. Accommodation: Patients will often report that their eyes are slow to refocus when shifting their gaze from near to far, or vice versa. Depth perception: Patients will often report that they have difficulty accurately judging distance. This problem often presents itself in driving situations. Hemispatial inattention: Reduced attention to one visual field. Two of the more frequently reported functional problems related to hemispatial inattention is bumping into things more frequently and veering off center when walking or driving in a straight line. Unilateral saccades: Refers to a unilateral eye-tracking motion. One eye will scan to the side independently, at which time the individual will often perceive motion in their peripheral vision when there is nothing there. Oscillopsia: Refers to the perception that stationary objects are moving.

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When a patient who has been chronically exposed to CO reports a constellation of visual problems consistent with a PTVS, referral for further evaluation and treatment is indicated. Referral to a neuro-optometrist or neuro-ophthalmologist familiar with these types of brain-related vision problems can often be beneficial. In this author’s experience, neuro-optometric rehabilitation (i.e., vision therapy) and/or use of yoked prisms can both be helpful in ameliorating many of the above vision problems. 23.2.5.3 Cognitive Symptoms Table 23.8 presents a list of the persisting cognitive problems most commonly reported by the participants of this study. As a group, the participants in this study felt that their residual cognitive deficits constituted some of the most disabling and debilitating aspects of their injury. For the most part, these symptoms can be placed into four general categories: executive functions, memory skills, academic abilities, and language skills. The ultimate findings of this study suggest that executive and memory functions are cognitive abilities most impacted by chronic CO poisoning. In addition, the findings of this study suggest that left hemisphere functions are typically more susceptible than right to the effects of chronic CO poisoning. Thus, there is a high degree of consistency between the participants’ self-reported persisting cognitive symptoms and the ultimate findings of this study. 23.2.5.4 Psychological / Behavioral Symptoms Table 23.9 presents a summary of the most common persisting psychological and behavioral symptoms reported by the participants in this study. Organically based mood disorders and personality change are extremely common following moderate to severe acute CO poisoning. The CO Support study11 found that 38.5% of their sample reported persisting problems with depression, 49.3% reported persisting problems with personality/emotional problems, 29.2% reported persisting problems with panic attacks, and 47.7% reported ongoing problems with sleep disturbance. The Penney A and B studies also found that a significant percentage of the sample reported persisting problems with depression and mood disturbance. Again, the current study has elaborated on these findings. Ninety percent of the sample reported ongoing problems with irritability. Specifically, the participants often reported that they would become easily upset and angry over small things that would not have bothered them previously. As a group, they tended to report reduced coping and stress management abilities. In many instances, this problem was so significant that it would negatively impact personal, family, and work relationships. Persisting problems with depression was reported by 81% of the sample. By far, this was the most common affective or mood problem reported by the participants in this study. Commonly reported clinical symptoms of depression included feelings of sadness, reduced energy, emotional lability, decreased motivation, anhedonia, social isolation, reduced appetite, and decreased libido. However, it is important for clinicians to understand and take into account that many of these classic indicators of depression may occur independently of depression because of organic brain injury.

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As a group, the participants in this study responded well to use of an antidepressant medication in the Select Serotonin Re-uptake Inhibitor (SSRI) class. In some instances, the participants were already utilizing an SSRI-type antidepressant at the time of their evaluation or began use of such an antidepressant following the evaluation. In each case, the participants reported that use of an SSRI medication typically resulted in improvements in their mood, a reduction in their irritability, improvement in their stress tolerance, improved stamina, and endurance, and reduced emotional lability. Sleep disturbance was also a commonly reported persisting symptom by the participants in this study. Seventy-six percent were experiencing some disruption of their sleep pattern. Most of the sample had difficulty getting to sleep and an even greater percentage had difficulty staying asleep. Many of the participants in the study reported they would frequently wake up during the night and had difficulty getting back to sleep. Many also reported a sense that their sleep was now “restless.” In most cases, it was evident that the sleep disturbance was compounding the individual’s organically based fatigue. For most of the participants in the study, they were either already utilizing a sleep aid at the time of their evaluation or one was recommended following their assessment. Anxiety was another commonly reported symptom by the participants in this study. Forty-eight percent of the participants were diagnosed with post-traumatic stress disorder (PTSD) or a specific phobia directly related to the CO poisoning event. Another 24% were experiencing more generalized anxiety. In many cases, this related to performance anxiety. The individuals were well aware that they were not functioning as well as they had prior to the exposure and were thus experiencing some anxiety associated with their reduced performance.

23.2.6 NEUROPSYCHOLOGICAL TESTING OUTCOME 23.2.6.1 Index Scores As noted above, four index scores were generated as part of each participant’s test battery.22 These included the HII, AIR, GDS, which is generated from the Heaton battery of tests19 and the GNDS. A summary of performance on three of these index scores is presented in Table 23.10. The HII, which incorporates seven of the individual test scores, was found to be the least sensitive of the index scores when demographically corrected norms were utilized. Sixty percent of the participants scored within normal limits on this index. Fifteen percent of the sample had a HII score in the below average/borderline range. Only 25% had HII scores in the impaired range. The HII score ranges from 0.0 to 1.0, with a higher score reflecting more significant impairment. Dr. Ralph Reitan, who originally developed the HII, has historically reported that a score of 0.5 or greater on this index is reflective of an acquired brain injury. In this study the mean HII score was 0.395 (range 0.1–0.9). The modal HII score was 0.3. Only 25% of the sample had HII scores of 0.5 or greater. Therefore, whether using the demographically corrected norms or the traditional cut-off score of 0.5, only one-fourth of the participants had impaired scores on this index.

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TABLE 23.10 Index Score Performance: Percentage of Participants Scoring in Each Range of Performance Above Average H.I.I. (7 Scores) A.I.R. (12 Scores) G.D.S (20 Scores)

Average

15

45

23.8

33.3

5.5

11

BA/ Bdl. 15 9.5 28

Mild Impairment

Mild/ Moderate Impairment

Moderate Impairment

Moderate/ Severe Impairment

10

10

5

0

14.3

14.3

4.8

0

44.5

11

0

0

Note: Demographically corrected norms have never been generated for the GNDS. B.A = Below Average; Bdl. = Borderline

The AIR, which takes into account 12 of the individual test scores, was somewhat more sensitive to the effects of chronic CO poisoning. Scores on this index range from 0.0 to 5.0 with higher scores suggesting more impairment. Thirty-three point four percent of the sample performed in the impaired range, 9.5% performed in the below average/borderline range, and 57.1% performed within normal limits when demographically corrected norms were utilized. The mean AIR score was 1.14 with a range of 0.5–3.0. The GDS, which in this study took into account 20 of the demographically corrected scores, was even more sensitive to the effects of chronic CO poisoning. The Boston Naming Test was not administered as part of the test battery and, therefore, only 20 of the 21 tests that comprise the GDS were utilized. In this sample, 55.5% of the participants had GDS scores in the impaired range, 28% had scores in the borderline/below average range, and only 16.5% had scores that were within normal limits. The mean GDS score was 0.634 with a range of 0.0–1.40. The GNDS takes into account 42 of the individual test scores. The GNDS produces a score ranging from 0 to 116 with higher scores representing more significant cerebral dysfunction. When Drs. Reitan and Wolfson23 first developed this index, they found that a cut-off score of 26 best differentiated a group of known moderately to severely brain-injured individuals from a group of nonbrain injured individuals. In this study, the mean GNDS score was 26.67 with a range of 16–47. Eleven (or 52%) of the participants had GNDS scores of 26 or greater. Therefore, 48% of the sample had GNDS scores that were below the recommended cut-off score of 26. In summary, it appears that the GDS is the index score most sensitive to the effects of chronic CO poisoning. It is important to note, however, that three of the participants had scores within normal limits on all of the index scores. Two of the participants had scores within normal limits on three of the indexes, and only one below average/ borderline score. Therefore, as is true for other neurological conditions, these index scores appear to be sensitive to generalized moderate to severe cerebral dysfunction,

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but may be insensitive to more subtle or localized cerebral dysfunction. For example, when the GNDS was originally developed, a cut-off score of 26 was found to be the most effective in differentiating a group of nonbrain-injured individuals from a group of moderate to severely impaired brain-injured individuals. Indeed, when a cut-off score of 26 was utilized, this cut-off score only misidentified 8% of moderate to severely brain-injured individuals as nonbrain-injured (sensitivity 92%) and only misidentified 10% of nonbrain-injured individuals as brain injured (specificity 90%). In the current study, 52% (11/21) of the participants had GNDS scores of 26 or greater. Forty-eight percent (10/21) of the participants had scores of 25 or less. As with other neurological populations (e.g., mild traumatic brain injury) where the individual’s cognitive deficits may be more subtle or localized, the traditional GNDS score of 26 is not recommended for patients who have been chronically exposed to CO. As a result, it would be more important to consider the individual’s GNDS score in comparison to the nonbrain-injured control group and the results of the current study. It is also important to note that the Global Deficit Scale is the only index score that incorporates performance on tests of short-term memory. The GDS takes into account performance on tests of both verbal and visual short-term memory. As memory deficits are by far the most common following chronic CO poisoning, this index score would be especially important to consider. 23.2.6.2 IQ Tests WAIS-III Full-Scale, VIQ and PIQ results are presented in Table 23.11. Also presented are the Verbal Comprehension Index (VCI), Perceptual Organization Index (POI), Working Memory Index (WMI), and Processing Speed Index (PSI) score results. In summary, 19.1% of the sample had impaired Full Scale IQs; 14.3% had Full Scale IQs in the below average/borderline range; and 66.6% had Full Scale IQs within normal limits. Therefore, approximately one-third of the sample obtained Full Scale IQs, which were below expectation or clearly impaired.

TABLE 23.11 WAIS-III I Q Testing: Percentage of Participants Scoring in Each Range of Performance

FSIQ VIQ PIQ VCI POI WMI PSI

Above Average

Average

2.4 23.8 38.1 38.1 42.9 4.8 38.1

42.8 23.8 33.3 28.6 47.6 19 23.8

BA/Bdl.

Mild Impairment

Mild/ Moderate Impairment

Moderate Impairment

14.3 28.6 19 9.5 0 33.3 9.5

9.5 14.0 0 19 0 14.3 9.5

4.8 9.5 0 0 4.8 19 4.8

4.8 0 9.5 4.8 4.8 4.8 4.8

Moderate/ Severe Impairment 0 0 0 0 0 0 9.5

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With regard to VIQ, 23.5% of the sample had impaired VIQs; 28.6% had VIQs in the below average/borderline range; and 47.6% had VIQs within normal limits. VIQ subtest score performance is presented in Table 23.12. With regard to PIQ, 9.5% of the sample had PIQs in the impaired range; 19% had PIQs in the below average/borderline range; and 71.4% had PIQs that were within normal limits. PIQ subtest score performance is presented in Table 23.13. Contrary to studies with other neurologically impaired populations, VIQ appeared to be more significantly impacted by chronic CO poisoning than PIQ. It is important to note that one-third or more of the participants obtained borderline or impaired scores on five of the seven verbal

TABLE 23.12 WAIS-III Verbal Subtest Scores: Percentage of Participants Scoring in Each Range of Performance

Vocabulary Letter-Number Sequencing Arithmetic Digit Span Information Similarities Comprehension

Mild/ Moderate Impairment

Moderate Impairment

Moderate/ Severe Impairment

Above Average

Average

BA/ Bdl.

Mild Impairment

33.3 4.8

42.9 28.6

14.3 19

4.8 19

4.8 23.8

0 0

0 0

19 0 19 23.8 19

38.1 33.3 2.9 47.6 47.6

9.5 33.3 9.5 14.3 19

19 14.3 19 14.3 14.3

4.8 14.3 4.8 0 0

0 4.8 0 0 0

0 0 0 0 0

TABLE 23.13 WAIS-III Nonverbal Subtest Scores: Percentage of Participants Scoring in Each Range of Performance

Digit Symbol Symbol Search Picture Arrangement Picture Completion Block Design Matrix Reasoning

Mild/ Moderate Impairment

Moderate Impairment

Moderate/ Severe Impairment

Above Average

Average

BA/ Bdl.

Mild Impairment

23.8 52.4 28.6

33.3 14.3 33.3

9.5 9.5 19

19 9.5 9.5

9.5 9.5 4.8

0 0 4.8

4.8 4.8 0

33.3

33.3

19

4.8

4.8

0

0

47.6 47.6

42.9 38.1

4.8 4.0

0 0

4.8 0

0 0

0 9.5

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Carbon Monoxide Poisoning

subtests. These included the Comprehension, Information, Digit Span, Arithmetic, and Letter-Number Sequencing subtests. Difficulties with the Digit Span and Letter-Number Sequencing subtests most likely relate to problems with sustained auditory attention and concentration. Problems with the Arithmetic subtest most likely relate to a working memory deficit. Difficulties with the Information subtest most likely relate to a reduced ability to access previously learned information (i.e., memory retrieval) and difficulties with the Comprehension subtest most likely relate to problems with verbal reasoning and problem solving. To some degree, each of these problems can be related to frontal lobe dysfunction, which is found to be common in cases of chronic CO poisoning in other studies. Within the PIQ subtests there were three subtests where one-third or more of the sample performed in the below average to impaired ranges. This included the Picture Completion subtest, Digit Symbol Coding, and Picture Arrangement. Picture Completion assesses attention to salient visual detail. Digit Symbol Coding assesses sustained visual attention and concentration as well as eye-hand coordination. Picture Arrangement assesses logical planning and organization. More than one-third of the sample performed in the below average to impaired range on the Symbol Search subtest as well. This test evaluates sustained visual attention and accurate visual discrimination. Difficulties with planning and organization on the Picture Arrangement subtest may relate to aspects of sequencing and organization as mediated by the frontal lobes. Exposure to CO is known to negatively impact a variety of visual and visual perceptual functions that may account for the sensitivity of the Picture Completion and Symbol Search subtests to this mechanism of injury. Difficulties with the Digit Symbol-Coding task most likely relate to difficulties with sustained visual attention and concentration, which again may be frontally mediated. Table 23.14 lists in descending order the percent of the sample who scored in the below average to impaired range on each of the WAIS-III subtests. It is important to note that three of the four subtests that appear to be most sensitive to the effects of chronic CO poisoning are verbal subtests. This may account for why VIQ appears to be more significantly affected by chronic CO poisoning than PIQ. It is also important to note that all 13 of the WAIS-III subtests, which were administered as part of this study can be negatively affected by chronic CO poisoning. As part of the current investigation, VIQ/PIQ difference or “split” was also studied. For the purposes of this study, a significant VIQ/PIQ split was considered to be 15 points or one standard deviation. Such a difference occurs in the nonbrain injured population less than 10% of the time. In the current study 9 of the 21 participants or 42.9% had VIQ/PIQ splits of 15 points or greater (range 15–22 points). For three of the participants (14.3% of the sample) their VIQ was greater than the PIQ. For six of the participants (28.6% of the sample) their PIQ was greater than their VIQ. Thus, twice as many participants had a PIQ that was significantly greater than their VIQ. This is yet another indication to suggest that VIQ appears to be more susceptible to the effects of chronic CO poisoning. There is some evidence to suggest that blood flow is slightly greater in the left cerebral hemisphere for individuals who are right-hand dominant. This may be due to greater oxygen requirements of the dominant hemisphere. Therefore, the hypoxia

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TABLE 23.14 WAIS-III Subtests: Percentage of Participants who Scored in the Below Average to Impaired Range Digit Span Letter-Number Sequencing Digit Symbol-Coding Arithmetic Picture Arrangement Information Picture Completion Symbol Search Comprehension Similarities Vocabulary Matrix Reasoning Block Design

66.7 66.6 42.8 42.8 38.1 38.1 33.4 33.3 33.3 28.6 23.8 14.3 9.6

created by chronic CO poisoning may have a greater impact on the left hemisphere, as its oxygen requirements are greater. In addition, since blood flow is greater in the left hemisphere, more CO is likely to be “downloaded” into this hemisphere of the brain resulting in greater injury. Both of these theories could explain why VIQ was more impacted than PIQ in this study. As a group, the sample demonstrates greater subtest variability than would typically be seen in nonbrain-injured individuals. Utilizing the Heaton et al.18 demographically corrected norms, the average subtest variability was 2.79 standard deviations with a range of 1.6–3.9 SDs. The average Scaled Score variability was 7.2 with a range of 5–10. In addition, scores from the WAIS-III that were analyzed included the Digit Symbol-Coding, incidental learning, free recall, and pairing tasks. Thirty-six percent of this sample had below average to impaired scores on the free recall task; 25.5% had borderline to impaired scores on the pairing task. Table 23.15 presents the percentage of participants who scored in the Below Average to Impaired Range on each of the summary IQ Scores and summary Index Scores. The results of this study support the notion that WMI Score and the VIQ score are most susceptible to the effects of chronic CO poisoning. More than half of the sample scored in the below average to impaired range on these two summary scores. It is important to note that the WMI score is based on scores from the subtests that measure working memory with verbal material. This is yet another finding to suggest that left hemisphere function is especially vulnerable to the effect of chronic CO poisoning.

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TABLE 23.15 WAIS-III Summary Scores: Percentage of Participants who Scored in the Below Average to Impaired Range Working Memory Index (WMI) Verbal IQ (VIQ) Processing Speed Index (PSI) Full Scale IQ (FSIQ) Verbal Comprehension Index(VCI) Performance IQ (PIQ) Perceptual Organization Index (POI)

71.4 52.1 38.1 33.4 33.3 28.5 9.6

23.2.6.3 Halstead–Reitan Tests Table 23.16 presents the percentage of the cohort who scored within each level of performance on the scores that can be generated from the standard Halstead–Reitan Neuropsychological Test Battery. Table 23.17 identifies the percentage of the sample who scored in the below average to impaired range on each of the standard Halstead– Reitan tests. Of these tests it appears that the Category Test, Tactual Performance Test (TPT) Memory, Rhythm Test, TPT-Localization, Trails B, and Speech-Sounds Perception Test are the most sensitive to the effects of chronic CO poisoning. The Category Test is a measure of the patient’s ability to generate solutions to a new and ambiguous problem. The TPT Memory and Localization tests are both measures of incidental memory. The Rhythm Test and Speech-Sounds Perception Test are both sensitive to sustained auditory attention. The Trails B test measures alternating attention and logical sequencing abilities. Consistent with prior studies, it appears that frontal functions such as sustained attention and concentration and problem solving abilities as well as memory (as measured by the TPT Memory and Localization tasks) are most sensitive to the effects of chronic CO poisoning. 23.2.6.4 Memory Testing Each participant was administered two tests of verbal learning and retention and two tests of nonverbal (visual) learning and retention. Tests used were the Story Memory Test and Figure Memory Test as renormed and administered via the Heaton et al.18 guidelines. In addition, the Buschke Verbal Selective Learning Test utilizing the Larabee norms and the Rey–Osterreith Complex Figure Test utilizing the Meyers and Meyer’s norms were used. Table 23.18 summarizes the percentage of the sample that scored in each level of performance for each of the above memory tests. Table 23.19 summarizes the percentage of the sample scoring in the below average to impaired range for each of the above memory tests. It appears well established in the literature that CO poisoning typically has a profound effect on short-term memory abilities. The literature is also clear that the temporal lobes and hippocampus are brain structures that are highly vulnerable to the effects of CO poisoning. These are brain structures

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TABLE 23.16 Halstead–Reitan Tests: Percentage of Participants who Scored in each Range of Performance Mild/ Mod./ Above BA/ Mild Moderate Moderate Severe Average Average Bdl. Impairment Impairment Impairment Impairment Category Test TPT-Dominant TPTNondominant TPT-Both TPT-Memory TPT-Location Rhythm Test Speech-Sounds Perception TappingDominant TappingNondominant Trails A Trails B Grooved Pegboard Dominant Nondominant

30 50 35

10 30 5

25 10 10

20 5 0

10 5 0

5 0 0

0 0 0

35 5 15 9.5 4.3

30 35 30 3.3 38.1

20 20 20 23.8 28.6

10 25 20 19 9.5

0 10 15 14.3 9.5

0 0 0 0 0

5 5 0 0 0

28.6

47.6

9.5

0

4.8

4.8

4.8

45

49

5

10

5

0

0

28.6 23.8

38.1 28.6

9.5 28.6

19 4.8

0 9.5

0 0

4.8 4.8

33.3 25

38.1 55

4.8 10

9.5 10

9.5 0

0 0

4.8 0

that play a major role in short-term memory. The results of this study are consistent with prior studies, suggesting that memory skills are highly vulnerable to the effects of chronic CO poisoning. The results of this study clearly indicate that verbal and nonverbal learning and retention are all extremely vulnerable.

23.2.6.5 Academic Testing Each participant of this study was administered the original PIAT of reading recognition, reading comprehension, and spelling subtests, as this was the version of the PIAT which Dr. Heaton used in his norming process. The math section from the PIAT-R utilizing those published norms was also administered. Table 23.20 presents the percent of the sample that scored within each level of performance. Table 23.21 summarizes the percentage of the sample scoring in the below average to impaired range. Results suggest that reading, math, and spelling skills are all vulnerable to the effects of chronic CO poisoning, with spelling being the most sensitive.

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TABLE 23.17 Halstead–Reitan Tests:Percentage of Participants who Scored in the Below Average to Impaired Range Category Test TPT-Memory Rhythm Test TPT-Localization Trails B Speech-Sounds Perception TPT-Nondominant TPT-Both Trails A Pegs-Dominant Tapping-Dominant Tapping-Nondominant Peg-Nondominant TPT-Dominant

60 60 57.1 55 47.7 47.6 35 35 33.3 28.6 23.9 20 20 20

TABLE 23.18 Memory Testing: Percentage of Participants that Scored in Each Range of Performance Mild/ Moderate Mild/ Moderate Moderate/ Severe Severe Above BA/ Impair- ImpairImpairImpair- ImpairAverage Average Bdl. ment ment ment ment ment Story memory Learning Retention Figure Memory Learning Retention Buschke VSR Learning (CLTR) 30-min. Recall Rey-osterreith Complex Figure Initial recall 30-min. Recall

14.3 14.3

19 14.3

4.8 0

9.5 4.8

33.3 33.3

9.5 9.5

0 9.5

9.5 14.3

19 14.3

14.3 23.8

23.8 28.6

23.8 0

14.3 9.5

4.8 19

0 4.8

0 0

5 10

15 20

25 10

25 10

0 15

30 0

0 35

0 0

10

10 25

20 5

10 15

10 29

15 9

15 25

20 9

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TABLE 23.19 Memory Tests: Percentage of Participants Scoring in the Below Average to Impaired Range Buschke (CLTR) learning Story Memory 4-h delay recall Buschke 30-min delay recall Rey-Osterreith IR (Learning) Figure Memory-learning Story Memory-learning Rey-Osterreith-30-min delay recall Figure Memory-4-h delay recall

95 71.4 70 70 66.7 66.6 65 61.9

TABLE 23.20 Academic Testing: Percentage of Participants that Scored in Each Range of Performance Mild/ Moderate/ Above BA/ Mild Moderate Moderate Severe Average Average Bdl. Impairment Impairment Impairment Impairment Math Reading Recognition Reading Comprehension Spelling

15 40

45 35

15 20

15 5

10 0

0 0

0 0

30

25

5

15

15

5

5

15

25

20

30

5

0

5

TABLE 23.21 Academic Testing: Percentage of Participants Scoring in the Below Average to Impaired Range Spelling Reading Comprehension Math Reading Recognition

60 45 40 30

23.2.6.6 Visual–Visual Perceptual Testing The literature clearly shows that a wide variety of visual and visual perceptual functions are vulnerable to the effects of CO poisoning. As part of the battery administered to each of the participants, a number of tests were administered to evaluate

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constructional praxis, including copy of a key figure, the Spatial Relations score from the Heaton battery, and an analysis of the patient’s copy of the Rey-Osterreith Complex Figure. For the key drawing which was administered as part of the Reitan-Indiana Aphasia Screening Test, scoring guidelines outlined in Reitan and Wolfson24 were utilized. About 27.6% of the sample had key constructions that were considered to be within normal limits. About 28.6% produced keys that were considered to be borderline and for 23.3% of the cohort, their key drawings were considered to be clearly impaired. For the Rey–Osterreith Complex Figure test scoring guidelines presented in the manual25 were utilized. Sixty percent of the sample had Rey drawings that were clearly impaired. Ten percent produced Rey drawings that were in the below average to borderline range. Thirty percent of the sample-produced drawings were considered to be within normal limits. It is important to note that 45% of the sample produced Rey copies were poorly planned and organized, suggesting a frontal quality to the construction. Fifty-seven percent of the sample had Spatial Relations scores that were in the below average to impaired range. Forty-two point eight percent had Spatial Relations scores that were considered to be within normal limits. In summary, constructional praxis appears to be a cognitive ability, which is vulnerable to the effects of chronic CO poisoning, and this problem can be observed in a number of visual-constructional tasks. As part of the test battery, each participant was administered the Line Bisection Test,26 a measure of hemispatial inattention. There was a suggestion of a possible subtle hemispatial inattention evident in 15% of the participants. The results were suggestive of possible left hemispatial inattention for two of the participants and a right hemispatial inattention for one participant. Amuch more pronounced hemispatial inattention was evident in the results of two of the participants, one suggesting a clear right hemispatial inattention, and one suggesting a clear left hemispatial inattention. The Padula Visual Midline Screening Test20 was also sensitive to identifying hemispatial inattention. This task found that 14% of the sample was experiencing a left visual inattention, 19% were experiencing a right visual inattention, and that one participant tended to miss visual stimuli in both visual fields (i.e., bifixation). When bifixation occurs, the individual will tend to miss important stimuli in one visual field if there is competing stimuli in the opposite visual field. Reitan and Wolfson24 present a case of a woman who suffered severe CO poisoning and loss of consciousness for 5 h following an attempted suicide by running her car engine in a closed garage. The individual demonstrated a right homonymous hemianopsia, suggesting that CO poisoning can result in lateralized visual defects. The results of this study suggest that chronic carbon CO has the potential to cause less severe visual field problems in the form of hemispatial inattention. All participants were administered the Digit Vigilance Test, a test of visual scanning speed and accuracy. Thirty percent of the participants obtained scores in the below average to impaired range on the speed component of the Digit Vigilance Test, whereas 70% had scores that were within normal limits. Half of the sample had visual scanning accuracy scores in the below average to impaired range. Fifty percent had scores that were within normal limits. These results suggest that both visual scanning speed and accuracy are vulnerable to the effects of chronic CO poisoning.

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TABLE 23.22 Visual/Visual Perceptual Tests: Percentage of Participants Scoring in Each Range of Performance

Digit Vigilance Test Speed Accuracy Spatial Relations Hooper VOT

Above Average 20 30 38.1 15

Average

BA/ Bdl.

Mild Impairment

Mild/ Moderate Impairment

Moderate Impairment

50 20 4.8 60

15 20 23.8 20

5 25 9.5 5

5 0 14.3 0

5 5 9.5 0

TABLE 23.23 Visual/Visual Perceptual Tests: Percentage of Participants who Scored in the Below Average to Impaired Range Spatial Relations Score Digit Vigilance Test Accuracy score Speed score Hooper Visual Organization Test

57 50 30 25

The Hooper Visual Organization Test27 was also administered to 20 of the 21 participants. One participant performed in the mildly impaired range and four performed in the below average to borderline range on this test of complex visual organization. Seventy-five percent of the sample tested performed within normal limits. Table 23.22 summarizes the percentage of participants who scored in each range of performance for the Digit Vigilance Test, Hooper Visual Organization Test, and Spatial Relations Score. Table 23.23 summarizes the percentage of participants who scored in the below average to impaired range on these measures. 23.2.6.7 Speed of Information Processing Twenty of the 21 participants were administered the PASAT, a test of complex attention and speed of auditory information processing. Table 23.24 summarizes the percentage of the sample score at each level of performance. In summary, 10% of the participants were not able to proceed past the practice trial of this task. For 30% of the sample, the task was discontinued after Trial 2 as a result of poor performance and high levels of frustration. Twenty percent went on to obtain below average or impaired scores on trial three. Forty percent of the sample (8 out of 20 participants) were able to perform within normal limits on all four trials of this task. Sixty percent had some

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TABLE 23.24 Paced Auditory Serial Addition Test: Percentage of Participants Scoring in Each Range of Performance

PASAT T1 (N = 18) T2 (N = 18) T3 (N = 12) T4 (N = 12)

Average

BA/ Bdl.

Mild Impairment

Mild/ Moderate. Impairment

Moderate Impairment

Moderate/ Severe Impairment

5.5

38.9

5.5

5.5

16.7

16.7

11.1

11.1

38.9

5.5

11.1

11.1

5.5

16.7

8.3

58.3

8.3

16.6

0

8.3

0

0

66.7

8.3

0

0

Above Average

25

0

Note: The PASAT was not attempted with one subject. Two subjects were unable to proceed past the practice trials. The test was stopped after Trial 2 for six subjects as a result of high levels of frustration and poor performance.

level of difficulty. This would suggest that speed of auditory information processing is a cognitive ability commonly affected by chronic CO poisoning. The best measure of visual information processing speed contained in the battery was the PSI score from the WAIS-III. Thirty-eight percent of the sample performed in the below average to impaired range. Sixty-two percent performed within normal limits. In summary, 60% of the cohort had some level of difficulty with auditory information processing speed, whereas only 38% demonstrated problems with visual information processing speed. This would be another indicator that left hemisphere functions are more susceptible to the effects of chronic CO poisoning.

23.2.6.8 Other Motor Skills Fine motor speed and dexterity, as measured by the Finger Tapping Test and Grooved Pegboard, were discussed under the heading of Halstead-Reitan Tests. Several additional tests of motor skills were also administered as part of the battery. Grip strength was measured by use of the Hand Dynamometer. Grip strength with the dominant hand was in the borderline to impaired range for 33.4% of the sample. Sixty-six point six percent had scores that were within normal limits. Grip strength with the nondominant hand was in the borderline to impaired range for 15% of the sample. Eight-five percent had grip strength within normal limits for the non-dominant hand. Executive motor skills were evaluated by the Behavioral Dyscontrol Scale. This is a set of tasks designed to measure motor programming and sequencing abilities. Forty percent of the sample performed within normal limits on this task. Twenty-five

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percent of the sample obtained scores that were below average/borderline, 20% demonstrated mild impairment, 10% demonstrated mild/moderate impairment; 5% demonstrated moderate impairment. Of those who demonstrated scores in the below average/borderline and impaired ranges, 60% demonstrated motor perseveration type errors. Fifty-five percent demonstrated motor disinhibition type errors. Sixty-five percent demonstrated right-left confusion errors. Fifty-five percent demonstrated echopraxic errors and 85% demonstrated motor sequencing errors. In summary, executive motor dysfunction, as measured by motor programming and sequencing abilities, appears to be quite common following chronic CO poisoning. Executive motor functioning was also evaluated by the nonverbal agility and verbal agility subtest of the Boston Diagnostic Aphasia Examination. Ten percent of the sample demonstrated impairment on the Verbal Agility subtest. A striking 90% demonstrated impairment on the nonverbal agility subtest, indicating that oral-motor dyspraxia is a common sequelae of chronic CO poisoning. Table 23.25 summarizes the percentage of participants who scored in the below average to impaired range on the supplemental motor tasks.

23.2.6.9 Miscellaneous Tests of Executive Function As part of the battery, we attempted to administer the Wisconsin Card Sorting Test to each participant. Four of the subjects (19% of the sample) were unable to complete the task. Of the 17 subjects who were able to complete the Wisconsin Card Sorting Test, 23.6% had scores in the below average to impaired ranges. Therefore, 38% of the total sample had some degree of difficulty with the Wisconsin Card Sorting Test, a test of mental flexibility and problem solving. Twenty-one percent of the sample demonstrated from one to three losses of cognitive set on the Wisconsin Card Sorting Test. Verbal fluency was measured by the Thurstone Word Fluency Test. Thirty percent of the sample performed in the below average to impaired range. Seventy percent performed within normal limits.

TABLE 23.25 Other Motor Functions: Percentage of Participants who Scored in the Below Average to Impaired Range Hand Dynamometer Dominant hand Nondominant hand Behavioral Dyscontrol Scale Boston Diagnostic Aphasia Exam Verbal Agility subtest Nonverbal Agility subtest

33.4 15 60 10 90

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TABLE 23.26 Miscellaneous Tests of Executive Function: Percentage of Participants Scoring in each Range of Performance Mild/ Moderate/ Above BA/ Mild Moderate Moderate Severe Average Average Bdl. Impairment Impairment Impairment Impairment WCST

65 11.8 11.8 0 11.8 0 (Note: Four [4] participants were unable to successfully complete this task.) Thurstone VFT 40 30 10 5 5 0 Ruff FFT • Unique design Score 40 30 20 5 5 0 Error Ratio Score 35 35 15 15 0 0 • Perseverations 25 60 0 10 5 0 Stroop Interference Score 25 50 20 0 5 0 Behavioral Dyscontrol Scale 0 40 25 20 10 5

0 10

0 0 0

0

0

Figural fluency was measured by the Ruff FFT. Thirty percent of the sample had below average to impaired scores on the Unique Design score, a measure of figural fluency. Thirty percent had below average to impaired Error Ratio scores, a measure of planning efficiency. Fifteen percent demonstrated a significant number of perseverations on this task. Response inhibition was measured by the interference score of the Stroop. Twentyfive percent of the sample scored in the below average to impaired range on this task. For each of these miscellaneous tests of executive function, the percentage of participants scoring in each range of performance is presented in Table 23.26. Table 23.27 presents the percentage of participants who scored in the below average to impaired range on each of the measures of executive function. Clearly the PASAT (speed of auditory information processing and complex attention) and the BDS (motor programming and sequencing) were the most sensitive to the effects of chronic CO poisoning. 23.2.6.10 Language Comprehension Language comprehension was evaluated utilizing the Complex Ideation subtest of the Boston DiagnosticAphasia Examination. Forty-three percent of the sample performed in the below average to impaired range. Fifty-seven percent performed within normal limits. The percentage of participants scoring in each range of performance is presented in Table 23.28.

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TABLE 23.27 Executive Function Tests: Percentage of Participants who Scored in the Below Average to Impaired Range PASAT Behavioral Dyscontrol Scale Ruff FFT Unique Design score Ruff FFT Error Ratio score Stroop Interference WCST Thurstone Word Fluency Test

62 60 30 30 25 23.6 20

TABLE 23.28 Language Comprehension: Percentage of Participants Scoring in Each Range of Performance

Complex Ideation subtest of BDAI

Above Average 33.3

Average

BA/ Bdl.

Mild Impairment

Mild/ Moderate Impairment

Moderate Impairment

23.8

14.3

14.3

9.5

0

Moderate/ Severe Impairment 4.8

Note: 43 percent of the sample scored in the Below Average to the Impaired Range.

23.2.7 MINNESOTA MULTIPHASIC PERSONALITY INVENTORY-2 The MMPI-2 was completed by 19 of the subjects in this study. The other two participants were adolescents and completed the MMPI-A. The MMPI-2 and MMPI-A are the most commonly used of all paper-and-pencil personality tests and are widely utilized by neuropsychologists as part of a comprehensive neuropsychological test battery. As part of the MMPI-2, the patient reports current or longstanding symptoms or personality traits by responding true or false to 567 statements. The inventory produces 14 Clinical Scales, 9 Restructured Clinical Scales, 15 Content Scales, and a variety of alternate subscales are also available. Four validity scales provide information about the patient’s approach to this inventory, as well as the validity of the profile. The validity scales of the MMPI-2 also provide information about symptom magnification/exaggeration, as well as symptom denial. The profile produced by the ten Clinical Scales is compared to those of normal control subjects as well as psychiatric patients with a wide variety of diagnoses. In addition to providing information

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about the patient’s personality traits and characteristics, the MMPI-2 also provides information about the patient’s current emotional and psychological status. The MMPI-2 is an objective test of personality and emotional status and should be viewed as a self-report symptom checklist. The MMPI-2 is a “here and now” questionnaire and the patient is asked to report their current symptoms or problems. As a result, the effects of actual impairment may be manifested in the patient’s response to items associated with physical, cognitive, emotional, or behavioral changes, which may relate directly to their injuries and resulting impairment. Indeed, 111 of the MMPI-2 items relate directly to symptoms commonly associated with a wide range of neurological disorders. With regard to this issue, Lezak et al.28 state, “Since so many MMPI items describe symptoms common to a variety of neurological disorders, selfaware and honest patients with these symptoms may produce MMPI profiles which could be misinterpreted as evidence of psychiatric disturbance even when they do not have a psychiatric or behavioral disorder” (p. 749). Lezak notes that the most commonly elevated MMPI-2 scales for individuals who have sustained some type of neurological injury are Scale 1, Hypochondriasis; Scale 2, Depression; Scale 3, Hysteria; Scale 7, Psychesthenia; and Scale 8, Schizophrenia. Cripe29 also notes that neurologic patients as a group tend to elevate on Scales 1, 2, 3, 7 and 8. With regard to this issue, Dr. Cripe states, “The basic reason neurologic patients elevate on Scales 1, 2, 3, 7, and 8 is that the inventory is loaded with many items that can be endorsed by a neurologic patient because of their neurologic disorders and the resulting real world problems rather than necessarily due to psychiatric disorders, emotional factors and maladjustment” (p. 296). Dr. Cripe goes on to note, “The safest and most logical assumption to make if a medical or neurologic patient elevates on Scales 1, 2, 3, 7, or 8 is that the patient has some awareness of his/her problems and is reporting the problems within the limitations and constrictions of the MMPI item pool. The patients simply see themselves as having difficulties related to their medical problems and are trying to communicate this awareness. The fact that they are aware of the problems does not necessarily indicate that they are distraught about the problems or emotionally maladjusted” (p. 300). A similar pattern of elevations has been identified in patient populations exposed to a variety of neurotoxins. Morrow et al.30 identified elevations on Scales 1, 2, 3, and 8 in workers seen in an occupational health clinic with complaints of cognitive problems following exposure to a variety of neurotoxins. Bowler et al.31 identified a 1, 2, 3, 8, 7 MMPI profile among women workers exposed to organic solvents. As noted above, 19 of the 21 participants in the current study were administered the MMPI-2. The mean T-scores for all of the validity and clinical scales, as well as the T-score range of these 19 profiles, are presented in Table 23.29. Consistent with prior studies, as a group patient’s chronically exposed to CO demonstrated elevations on Scales 3, 1, 2, 7, and 8 in order of descending T-score elevation. In each case the elevation was above the clinical cut-off level of T = 65. A group MMPI-2 profile of these 19 individuals is presented in Figure 23.1. The elevations on Scales 1 and 3 reflect the group’s on-going report of physical concerns and symptoms. Their elevation on Scale 2 likely reflects feelings or other symptoms of depression. However, this scale also contains a number of items related to cognitive dysfunction, which may well relate to the chronic CO poisoning. The elevation on Scale 7 most

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TABLE 23.29 MMPI-2 Validity and Clinical Scales Summary (N = 19) Scale

T-Score Mean

T-Score Range

VRIN TRIN F F(b) F(p) L K S 1. HS 2. D 3. Hy 4. Pd 5. Mf 6. Pa 7. Pt 8. Sc 9. Ma 10. Si

47.26 57.63 60.37 61.52 46.37 53.79 52.16 52.21 79.11 76.05 87.63 59.47 48.32 62.53 74.68 72.06 54.31 52.53

38–66 50–73 41–96 42–108 41–73 38–76 35–65 33–65 49–101 46–105 49–120 37–76 30–74 45–85 51–103 44–114 37–72 34–80

100

87.63 79.11 74.68 72.06

76.05 65T 60

62.53

60.37 59.47 53.79

54.31

52.16

52.23

Ma

Sc

Pt

Pa

Mf

Pd

Hy

D

Hs

K

F

40

L

48.32

Si

T-scores

80

FIGURE 23.1 Group MMPI-2 validity and clinical scales profile of 19 patients chronically exposed to carbon monoxide—Helffenstein Study.

likely reflects ongoing feelings of anxiety. Scale 8 contains many items associated with organic brain injury. Table 23.30 presents the mean T-scores and T-score ranges for the Content Scales. As a group, the patients chronically exposed to CO were elevated on the Anxiety

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TABLE 23.30 MMPI-2 Content Scales Summary (N = 19) Scale

T-Score Mean

T-Score Range

ANX FRS OBS DEP HEA BIZ AMG CUM ASP TPA LSE SOD FAM WRK TRT

66.58 49.79 58.37 58.31 73.32 52.42 51.31 44.21 42.05 50.10 57.79 54.42 47.73 62.37 56.63

43–89 35–72 41–75 39–83 49–96 39–70 31–72 38–64 33–56 36–64 44–92 32–82 36–65 50–82 39–95

TABLE 23.31 MMPI-2 Health Concerns Subscales Summary (N = 19) Subscale Gastrointestinal symptoms Neurological symptoms General health concerns

T-Score Mean

T-Score Range

61.3 75.5 72.1

43–86 45–114 48–89

and the Health Concerns Content Scales. This would be consistent with the clinical interviews conducted with each of these patients in which they discussed their anxiety and concern regarding their current and future health status. Table 23.31 contains the mean T-scores and T-score ranges for the three Health Concerns subscales. As a group, the patients chronically exposed to CO demonstrate an elevation on the General Health Concerns subscale and the Neurological Symptoms subscale. Thus, as a group, these individuals appear to be anxious and concerned about their health status, particularly their neurological symptoms. Table 23.32 presents the mean T-scores and T-score ranges for the MMPI-2 Restructured Clinical Scales. Figure 23.2 presents a group MMPI-2 Restructured Clinical Scales profile for the 16 participants in this study for which the Restructured Clinical Scales were calculated. As a group, they were elevated on RC1, RC2, and RCd, in descending order of profile elevation. The elevation on RCd (Demoralization) is interpreted as an indication of overall emotional discomfort that the individual

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TABLE 23.32 MMPI-2 Restructured Clinical Scales Summary (N = 16) Scale

T-Score Mean

T-Score Range

RCd RC 1 RC 2 RC 3 RC 4 RC 6 RC 7 RC 8 RC 9

65.06 75.0 67.31 42.0 47.5 47.5 53.38 56.44 44.75

50–55 55–99 42–100 33–66 37–60 41–70 32–84 39–82 34–61

100

80 T-scores

75 67.31

65.06 60

56.44 53.38

47.5 47.5

dem = Demoralization som = Somatic Complaints lpe = Low Positive Emotion

cyn = Cynicism asb = Antisocial Behavior per = Ideas of Persecution

RC9 hpm

RC8 abx

RC7 dne

RC6 per

44.75 RC4 asb

RC3 cyn

RC2 lpe

RC1 som

40

RCd dem

42

dne = Dysfunctional Negative Emotion abx = Aberrant Experiences hpm = Hypomanic Activation

FIGURE 23.2 Group MMPI-2 Restructured Clinical (RC) scales profile of 16 patients chronically exposed to CO-Helffenstein Study

is experiencing.32 Individuals with similar elevations often describe themselves as discouraged, generally demoralized, insecure, and pessimistic. In addition, they will also frequently report poor self-esteem. As a group, this population also appears to elevate most notably on RC1 (Somatic Complaints). Individuals with elevations on RC1 are typically experiencing a variety of physical and other health problems. An elevation on RC1 does not necessarily indicate that the individual is excessively preoccupied with bodily concerns but may simply be accurately reporting their ongoing physical symptoms associated with an actual injury. This scale contains many

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TABLE 23.33 DSM-IV GAF Scores, Helffenstein Study (N = 21) Level of Functioning Mild symptoms (GAF 61 → 70) Moderate symptoms (GAF 51 → 60) Serious symptoms (GAF 41 → 50)

% of Sample 19 76 5

items related to fatigue, motor weakness, and chronic pain, all of which are common sequelae of chronic CO poisoning. Also as a group, this sample elevated on RC2 (Low Positive Emotions). Individuals who elevate on this scale typically are reporting a lack of positive emotions in their lives and may also relate to feelings of depression, unhappiness, and a sense of failure or helplessness. Table 23.33 presents a summary of the DSM-IV GlobalAssessment of Functioning (GAF) scores for the participants in this study. Clearly, the majority met the criteria for “Moderate Symptoms” or moderate difficulty in social, occupational, and school functioning.

23.2.8 VOCATIONAL OUTCOME Nineteen of the 21 participants of this study were working full time at the time that they were exposed to CO. Two of the participants were students. The results of the study clearly documents the residual cognitive deficits, inconsistencies, or relative weaknesses associated with chronic CO poisoning. The study also documents that fatigue is a sequelae of CO poisoning that was experienced by all of the subjects. To some degree, all reported that their stamina and endurance for physical and cognitive activities had been compromised. To some degree, all subjects reported that they became more tired more quickly whether performing physical or cognitive activities. For the majority of the subjects of this study, it appeared that to a large degree the fatigue that they were experiencing was organically based. In some cases, sleep disturbance, chronic pain, and depression were serving to exacerbate further their fatigue. Table 23.34 presents vocational outcomes for the 19 participants of the study who were working at the time of exposure. Only one of the participants was able to return to his prior job on a full-time basis. However, this individual owned and personally managed two film processing plants on opposite sides of the city where he lived. Following the exposure, he found he was unable to manage successfully both plants. To some degree, this related to a cognitive inability to manage effectively all aspects of both plants. To some degree, it also related to the residual fatigue that he experienced postexposure. As a result, he was forced to close one of his plants, which led to a significant reduction in his earning potential. At the time of follow-up, it was learned that this patient had made the decision to sell his remaining plant and to seek alternate employment. The patient made this decision because he had lost so

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TABLE 23.34 Vocational Outcome (N = 19 Working At Time of Exposure) Return to prior job full time Return to prior job part time Return to lower level job full time Return to lower level job part time Opted to retire Total and permanent vocational disability

5% (1/19)* 0% (0/19) 21% (4/19) 37% (7/19) 11% (2/19)** 26% (5/19)

∗ This individual owned his own business but in order to

effectively manage his business postexposure, he had to close one of his two plants which significantly reduced his earning potential. ∗∗ These two individuals were close to retirement but would have worked longer had it not been for their CO positioning

many commercial contracts postexposure that the business was no longer financially viable. Loss of the contracts was attributed by this author directly to the sequelae of his CO poisoning. None of the participants who were working at the time of the exposure returned to their prior employment on a part-time basis. However, this author suspects this is a fairly common vocational outcome for this population. If an individual is working in a job that is over-learned, they may well be able to continue performing that job from a cognitive standpoint postexposure. If that individual experiences ongoing problems with fatigue, then return to his prior job on a part-time basis would certainly be a viable possibility. Four of the 19 participants who were working fulltime at the time of the exposure were able to return to work in a cognitively less challenging (i.e., lower level) job on a full-time basis. For these individuals, while they were experiencing some ongoing problems with fatigue, they were able to continue to work full-time, but from a cognitive standpoint were unable to perform successfully the job that they were doing prior to the exposure. One of the more striking findings of the study is that 7 of the 19 individuals who were working full-time at the time of the exposure (37%) were able to return to work, only in less cognitively complex jobs on a part-time basis. For this subset of the study, the individual’s residual cognitive deficits and fatigue combined to impact negatively their vocational functioning in two separate ways. Two of the participants of the study who were working full-time at the time of their exposure made the choice to retire postexposure. Each of these individuals was close to retirement but would have worked longer had it not been for the CO poisoning. In each case, they made the decision to retire because of the combined effect that their cognitive deficits and fatigue was having on their vocational functioning. Another striking finding of the study is that five of the 19 individuals who were working full-time at the time of the exposure (26%) were totally and permanently

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vocationally disabled because of the exposure. In each case, the individual’s residual cognitive dysfunction, fatigue and other deficits combined to render them totally and permanently disabled from a vocational standpoint. None of these individuals was able to maintain successfully substantial gainful work activity postexposure. This figure is consistent with the results of the CO Support Study11 in which 32% of their cohort were totally and permanently disabled. In summary, all 19 of the individuals who were working full-time at the time of their chronic CO poisoning experienced some degree of vocational disability postexposure.

23.2.9 SUMMARY OF FINDINGS Table 23.35 summarizes the 32 measures from the neuropsychological test battery that were most sensitive to the effects of chronic CO poisoning. That is, at least 38% (or slightly more than one-third) of the participants obtained scores in the below average to the impaired range on these measures. A review of these measures finds that they tend to cluster in a meaningful fashion. Twelve of the 32 measures (37.5%) relate to executive functions. These functions include sustained attention and concentration, speed of information processing, alternating attention, and logical sequencing, generating solutions to new and ambiguous problems, planning and organization, and executive motor skills, such as motor programming and sequencing, and oral motor dyspraxia. Eleven of the 32 measures (34.4%) relate to some aspect of short-term memory functioning. This includes various measures of verbal and non-verbal (visual) learning and retention, as well as incidental memory and working memory. Analyzing the data in this manner clearly suggests that executive functions and memory functions are most susceptible to the effects of chronic CO poisoning. It is also important to note that 7 of the 32 measures (21.9%) relate to some aspect of language or academic skills. Two of the measures (6.3%) relate to some aspect of vision or visual perceptual functions. As noted in the introduction to this chapter, Gale et al.1 identified hypoperfusion in the frontal and temporal lobes on SPECT studies of patients that had experienced acute CO poisoning. This frontal-bilateral temporal pattern appears to be fairly well established in the literature associated with acute CO poisoning. Results of the current study would suggest that these same regions of the brain are most vulnerable to the effects of chronic CO poisoning. Pinkston et al.15 identified hypometabolism in the frontal regions of the brain in two individuals chronically exposed to CO. Their neuropsychological testing identified a variety of deficits in executive functioning. Executive dysfunction is frequently associated with frontal lobe involvement. In that same study, the participants were reporting significant ongoing problems with shortterm memory. That study also identified hypometabolism in the temporal regions of the brain, which would be consistent with the types of memory problems the patients were reporting. This finding is consistent with several known aspects of brain physiology. The blood brain barrier is more permeable in the frontal and temporal regions, which would result in more uptake of CO into these regions. In addition, the frontal and temporal regions of the brain are less able to compensate for a hypoxic event. Thus, we would expect that these regions would be more vulnerable to the effects of chronic CO poisoning, which is supported by the current study.

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TABLE 23.35 Combined Battery: Percentage of Participants Scoring in the Below Average to Impaired Range Buschke (CLTR) learning Oral Motor Dyspraxia Story Memory 4-h delay recall Working Memory Index (WAIS-III) Buschke 30-min delay recall Rey-Osterreith IR (Learning) Digit Span (WAIS-III) Figure Memory—learning Story Memory—learning Letter-Number Sequencing (WAIS-III) Rey-Osterreith 30-min delay recall PASAT Figure Memory—4-h delay recall Category test TPT—Memory Spelling (PIAT) Behavioral Dyscontrol Scale Rhythm Test Spatial Relations score TPT—Localization Verbal IQ DVT—Accuracy Trails B test Speech Sounds Perception test Reading Comprehension (PIAT) Language Comprehension Digit Symbol—Coding (WAIS-III) Arithmetic (WAIS-III) Math (PIAT) Processing Speed Index (WAIS-III) Picture Arrangement (WAIS-III) Information (WAIS-III)

95 90 71.4 71.4 70 70 66.7 66.7 66.6 66.6 65 62 61.9 60 60 60 60 57.1 57 55 52.1 50 47.7 47.6 45 43 42.8 42.8 40 38.1 38.1 38.1

A review of Table 23.35 also suggests that left hemisphere functions are more susceptible to the effects of chronic CO poisoning. As noted earlier in the chapter, there is literature to suggest that, for right-hand dominant individuals, blood flow is slightly greater in the left hemisphere. As noted earlier in this chapter, all 21 participants of this study were right-hand dominant. Again, the theory is that because of greater blood flow in the left hemisphere this resulted in greater uptake of CO into that hemisphere which resulted in greater injury to left hemisphere functions. In addition, the left hemisphere would be expected to be more susceptible to the effects of a hypoxic event given its greater demand for oxygen. Heuser and Mena33 conducted SPECT studies

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on 72 right-handed adults who had been exposed to a wide variety of neurotoxic chemicals including solvents, pesticides, CO, chlorine gas, polychlorinated biphenyls (PCBs), formaldehyde, herbicides, and heavy metals. Each participant of the study was experiencing persisting cognitive dysfunction including problems with shortterm memory. The SPECT studies were abnormal for all participants when their scans were compared to normal controls. Heuser and Mena33 state, “Bilateral, often asymmetrical, impairment of perfusion was found, mostly in the frontal, temporal and parietal lobes. This hypoperfusion was predominantly left-sided in young patients and predominantly right-sided in the elderly” (p. 813). The findings of this study suggest that the left cerebral hemisphere is more vulnerable to the effects of a wide range of neurotoxins in right-hand dominant, nonelderly adults. Clearly, this represents a subset of the population totally consistent with the population of the current chronic CO poisoning study.

23.3 CASE STUDY 23.3.1 PATIENT DEMOGRAPHICS The patient (H.H.) was one of the two adolescents included in the above study sample. At the time of her initial neuropsychological evaluation, she was 16 years old. She is Caucasian and is right-handed. At the time of her original evaluation, she was in the tenth grade in high school.

23.3.2 EXPOSURE INFORMATION H.H. was chronically exposed to CO in her home. A new furnace had been installed in the family home and fitted with a natural gas orifice. The home had liquid propane (LP) gas, which required a different orifice. This error led to over-firing of the burner and incomplete combustion of the gas, producing large amounts of CO (1500 ppm CO found in the furnace exhaust). Inspection of the furnace revealed pinhole cracks in the heat exchanger, which allowed CO to enter the living space around the furnace. In addition, it was determined that there was passive infiltration of CO into the home because of CO filtering back through the water heater exhaust vent. On testing, 30 ppm CO was found in the furnace room and 33 ppm CO was found being emitted from the registers in the home. It is likely that the CO exposure occurred over a 7-year period and began when H.H. was 7 months old, continuing until she was approximately 7 years old.

23.3.3 EDUCATIONAL HISTORY H.H. and her mother reported that she had not had any major difficulty learning and had been an A/B student all of her school career. However, they are aware that each year school was becoming more difficult and that she was having to study harder to maintain good grades. She had never had any behavioral or social problems. At the time of her initial evaluation, H.H. reported that her goal was to complete a college degree and then pursue some type of higher education in the healthcare field. H.H. had

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never been diagnosed with any type of learning disability nor had she ever received special education or remedial services.

23.3.4 PERSISTING SYMPTOMS During the course of her clinical interview, H.H. reported a variety of persisting physical symptoms and problems. This included occasional right leg spasms, daily headaches, tinnitus, photophobia, difficulty filtering out background noise, temperature deregulation, shortness of breath, cognitive and physical fatigue, and chemical sensitivity. Cognitively, she was aware of ongoing problems with attention and concentration, cognitive set loss, short-term memory, verbal fluency, reduced speed of processing, difficulties with problem solving, spatial disorientation, and occasional problems with initiation. Visually, she was aware of difficulties with visual scanning, depth perception and photophobia with headaches. At the time of her evaluation, she was utilizing Celexa, 20 mg per day, as an antidepressant medication. She denied any feelings of depression at the time of testing. She was acknowledging some inconsistent motivation and appetite.

23.3.5 RESULTS FROM INITIAL TESTING On her original neuropsychological evaluation, H.H. demonstrated a pattern of deficits suggestive of executive dysfunction. On the testing, she demonstrated inconsistent sustained attention and concentration abilities, which ranged from the 8th to the 95th percentiles. Figural fluency was mildly to moderately impaired at the 3rd percentile. Verbal fluency was in the borderline range at the 21st percentile. Speed of auditory information processing was inconsistent, ranging from the 12th to the 48th percentile. Cognitive flexibility was in the borderline range at the 18th percentile. She demonstrated a severe oral motor dyspraxia, as well as other problems with motor programming and sequencing. Left temporal/hippocampal involvement was suggested by verbal learning, ranging from the 2nd to the 21st percentile. Some right temporal/hippocampal involvement was suggested by a mild impairment of her ability to learn new complex visual information at the 12th percentile. Therefore, her initial test results did suggest a frontal/bilateral temporal pattern of dysfunction. In addition, on her original testing, she demonstrated a mild constructional dyspraxia on two separate tasks and she also showed deficits in the areas of math and incidental memory. With regard to the pattern of deficits identified on testing, the following observation was made in her narrative neuropsychological report, “Her pattern of weaknesses and deficits is subtle but nevertheless consistent with chronic CO poisoning. From her report and a review of school records, it appears that she is compensating well, but she reports it is becoming more difficult each year to maintain the same grades. The areas particularly affected by CO are the frontal and bilateral temporal lobes of the brain, which are areas affected in H.H. Further, these areas of the brain do not fully develop until a person is at least 21 years of age. Therefore, the full extent of H.H.’s difficulties may not be currently evident. In addition, it is common that, when someone is in school and they can devote extensive amounts of time to homework, they can compensate for

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their residual cognitive deficits. Unfortunately, when cognitive demands increase at the college level and in the work world and it is no longer possible to spend extended periods of time to compensate for residual cognitive deficits, her subtle problems on testing may become more evident at a later date.” Although her cognitive deficits, inconsistencies, and relative weaknesses were rather subtle at age 16, our concern was that over time executive and memory function deficits would become more notable when compared to her demographically similar peer group. Because of injury to the frontal and temporal regions of the brain, our concern was that these functions would not develop normally. As a result, a neuropsychological re-evaluation was recommended at a later date.

23.3.6 NEUROPSYCHOLOGICAL RE-EVALUATION 23.3.6.1 Circumstances of Re-evaulation H.H. underwent a neuropsychological re-evaluation when she was 19 years old. She had graduated from high school with a cumulative grade point average of 3.7 (A-minus average). At the time of her re-evaluation, she had successfully completed 1 year of college (32 semester hours) and her grade point average was 2.8 on a 4.0 scale. Her major was elementary education. H.H. was clear in reporting that, since the time of her last evaluation, she has experienced greater and greater difficulty cognitively and academically. At the time of her re-evaluation, she was extremely concerned about her ability to successfully complete her college degree and function successfully in the world of work. 23.3.6.2 Self-reported Symptoms H.H. was continuing to experience a wide variety of persistent physical symptoms, including ongoing problems with headaches, restless leg syndrome, tinnitus, problems with auditory gating, increasing problems with fatigue (most likely due to the increased cognitive demands of college), shortness of breath on minor exertion, and left-sided weakness. She continued to be sensitive to a wide variety of chemicals and substances. Visually, she was noting ongoing problems with double vision, blurry vision, visual scanning, depth perception, accommodation, photophobia, and eye fatigue. From a cognitive standpoint, she was reporting increasing problems with attention and concentration, cognitive set loss, multitasking, short-term memory, new learning, and cumulative memory. She was continuing to note a variety of languagebased problems, including difficulties with verbal fluency, reading comprehension, paraphasic errors in her speech, and language comprehension. As her math courses became more difficult, she has noted increasing problems with math. In addition, as speed demands and time pressures increased in college, she was becoming more aware of slowed speed of information processing. At the time of her re-evaluation, she was acknowledging minimal feelings of depression, most significantly related to the cognitive problems she encountered in college and concern about her long-term academic and vocational future. Since the time of her last evaluation, she developed panic attacks and was experiencing increased problems with emotional lability. Since

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the time of her last evaluation, she began participating in individual psychotherapy and was being followed by a psychiatrist. She was utilizing Celexa as an antidepressant medication and Clonazepam on an as-needed basis for anxiety. Her psychiatrist attributed her affective and mood disturbance directly to the CO exposure. 23.3.6.3 Comparison of Test Scores A detailed comparison of H.H.’s re-evaluation test scores was made to her test scores obtained as part of her original evaluation. A clinically significant change was considered to be any increase or decrease of 0.7–0.9 standard deviations. A statistically significant change was considered to be any increase or decrease of 1.0 or more standard deviations. Her performance remained essentially the same on 41 of the individual neuropsychological test scores. She demonstrated three clinically significant gains and ten statistically significant improvements on testing. She demonstrated 11 clinically significant declines and 18 statistically significant declines when her reevaluation test scores were compared to her prior test scores. Thus, she demonstrated 13 gains versus 29 significant declines. As part of her re-evaluation, it was noted that, while specific scores did not fall into the impaired range or even the borderline range on the re-evaluation, the fact that she demonstrated a significant decline in cognitive functioning over time was clinically significant. It was felt that this finding suggested that these were cognitive abilities whose development had not “kept pace” with her demographically similar peers. The relative declines, which she demonstrated from her prior testing, clustered almost exclusively into three areas: (1) Executive/frontal functions; (2) Memory functions; and (3) Academic/Language functions. There were also several declines in motor/sensory functions and visual/visual-perceptual functions. Therefore, the areas of cognitive functioning where H.H. demonstrated her most significant relative decline were areas of functioning found to be most vulnerable to the effects of chronic CO poisoning in the current study. It is also important to note that H.H. demonstrated a notable decline in all seven of the summary scores generated as part of the WAIS-III testing when compared to her demographically similar peers. 23.3.6.4 Results from Re-evaluation As noted in the body of this chapter, the index scores generated as part of the test battery are not always sensitive to the more subtle or localized effects of chronic CO poisoning. Indeed, H.H.’s scores on all four of the indexes used as a measure of generalized cognitive functioning were within normal limits. However, her performance on the WAIS-III was suggestive of some residual and more subtle cognitive dysfunction. Her VIQ was in the borderline range at the 27th percentile. Her VCI score was also in the borderline range at the 27th percentile. Her WMI score was at the low end of the average range at the 31st percentile. When utilizing demographically corrected scores, subtest variability ranged from the 14th to the 92nd percentile. This represented a 2.5 standard deviation variability. H.H. demonstrated a clear pattern of executive dysfunction on the re-evaluation. Sustained attention and concentration abilities were inconsistent, ranging from the

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16th to the 82nd percentile. Abstract verbal concept formation, as measured by the Similarities subtest of the WAIS-III, was in the borderline range at the 18th percentile. Reasoning and judgment abilities, as measured by the comprehension subtest of the WAIS-III, were in the borderline range at the 24th percentile. Planning, organizing and logical sequencing abilities, as measured by the Picture Arrangement subtest of the WAIS-III, was in the borderline range at the 24th percentile. Verbal fluency was mildly to moderately impaired at the 4th percentile. Speed of auditory information processing, as measured by the PASAT, was inconsistent and far below expectation, ranging from the 3rd to the 28th percentile. Visual information processing speed was well within normal limits at the 62nd percentile. Severe oral motor dyspraxia remained evident on the non-verbal agility subtest of the Boston Diagnostic Aphasia Examination. Left temporal/hippocampal dysfunction was suggested by a mild impairment of her ability to learn new narrative verbal information presented in paragraph form (Story Memory Test-Learning Component, 11th percentile). Retention of this information following a 4-h-delay period was in the borderline range at the 21st percentile. H.H. was unable to recall 14.3% of the information that she had previously learned. Cueing was of some help to her memory. Learning of new rote verbal information, as measured by the Buschke Verbal Selective Reminding Test (CLTR score), was severely impaired at <1st percentile. Retention of this information following a 30min-delay period was mildly to moderately impaired at the 4th percentile. Language comprehension was in the borderline range at the 21st percentile. Right temporal/hippocampal dysfunction was suggested by a mild impairment of her ability to recall newly learned complex visual information following a 30-min delay period (Modified Taylor Complex Figure Test, 30-min delay, 10th percentile). H.H. was unable to recall 17% of the information that she had previously learned following a 30-min delay. H.H. also demonstrated a variety of academic problems on her re-evaluation. Reading Recognition was in the borderline range at the 16th percentile (10.3 grade level). Reading Comprehension was mildly impaired at the 10th percentile (10.7 grade level). These were essentially the same scores that she obtained when she was 16 years old. Therefore, her re-evaluation suggested that she had made no appreciable improvement in her reading skills or abilities since that time. Indeed, she was reporting increased reading problems over time. Although there had not been a decline in her actual reading skills and abilities, there was obviously an increase in the reading demands, which would have appeared to H.H. as a decline in her reading skills and abilities. It was felt that this represented an excellent example of how H.H.’s cognitive abilities had not developed at a pace commensurate with her demographic peer group. Over time, the lack of development had led to an increased functional cognitive problem. The same type of relative decline, when compared to her demographic peer group, was evident in her vocabulary and arithmetic skills. Her general fund of information, as measured by the Information subtest of the WAIS-III, was in the mildly impaired range at the 14th percentile on retesting. It was concluded that her general fund of information of the type generally acquired in school and through various life experiences had not kept pace with her demographic peer group.

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On her re-evaluation, H.H. demonstrated a moderate to severe right visual inattention on the Padula Visual Midline Screening Test. She also continued to demonstrate deficits or relative weaknesses in the area of incidental memory. There are multiple indicators in H.H.’s re-evaluation to suggest that left hemisphere functions had been more significantly affected than right. Indicators of more lateralized cerebral dysfunction included the following: (1) PIQ, well within normal limits and VIQ being in the borderline/low average range; (2) POI being 14 points greater than VCI; (3) Verbal short-term memory being notably more impaired than visual short-term memory; (4) Moderate to severe right visual inattention; (5) Tactile sensitivity on the right being in the borderline range, whereas tactile sensitivity on the left was well within normal limits; (6) Visual processing speed being in the high average range versus verbal processing speed being in the borderline to mildly to moderately impaired range; and (7) Verbal fluency being mildly to moderately impaired at the 4th percentile, whereas figural fluency was within normal limits.

23.3.7 SUMMARY OF CASE STUDY This case study was chosen because it demonstrates several key points and because it correlates well with the overall results of the study. This study demonstrates that the effects of chronic CO poisoning on neuropsychological testing may at times be quite subtle, as evidenced by H.H.’s original neuropsychological evaluation. The results of her re-evaluation also emphasize that the index scores are not always sensitive to the effects of chronic CO poisoning and in many instances it is more important to look at the overall pattern of individual deficits, relative weaknesses, and inconsistencies. This case study emphasizes the importance of conducting re-evaluations in late adolescence or early adulthood in cases of chronic CO poisoning. Clearly, if one is evaluating a child or adolescent following chronic CO poisoning, the full extent of their long-term cognitive deficits may not be evident until their early 20s. The pattern of dysfunction identified in H.H.’s initial neuropsychological evaluation was consistent with the pattern identified in the study. It was also confirming of the overall results of the study that on re-evaluation H.H. demonstrated her most notable declines in the areas of executive/frontal functions, memory functions, and academic/language functions. Those are areas of cognitive functioning found to be most sensitive to the effects of chronic CO poisoning. It was also confirming that on re-evaluation she was demonstrating more significant left hemisphere dysfunction, which was again consistent with the findings of this study.

23.3.8 TAKEAWAY MESSAGES 1. Chronic CO poisoning can and often will result in permanent neurocognitive and neurobehavioral dysfunction. 2. Loss of consciousness during exposure is not required for the exposure to result in permanent impairment. 3. During the exposure, expect that the individual will have experienced multiple symptoms in multiple systems. 4. Expect to see frequent misdiagnoses during the period of exposure.

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5. If the patient does not make a full and complete recovery, again expect to see multiple residual deficits and problems in multiple systems. Expect to find persisting physical, fatigue, visual, cognitive, affective, mood, and behavioral changes. 6. This study clearly documents that a wide range of cognitive functions can be affected by chronic CO poisoning. However, this study also suggests that executive/frontal, memory, and language/academic functions appear to be highly susceptible to the effects of chronic CO poisoning. 7. This study also clearly suggests that left hemisphere functions tend to be more susceptible to the effects of chronic CO poisoning than right hemisphere functions. However, as expected, right hemisphere functions are not immune to the effects of chronic CO poisoning. 8. When evaluating a child or adolescent following chronic CO poisoning, it is important to realize that, because the human brain does not fully develop until the early 20s, neuropsychological re-evaluation is recommended. Over time, the individual may well experience increasing cognitive problems and deficits when compared to their demographically similar peers. Essentially, brain development does not keep pace with their demographically similar peers and, therefore, over time they will functionally experience greater and greater cognitive difficulty. In addition, mood and affective problems can develop long after the CO poisoning stops. 9. When individuals experience permanent residual neurocognitive and neurobehavioral deficits associated with chronic CO poisoning, this will almost always have a negative impact on their vocational functioning. Indeed, total and permanent vocational disability is quite common following chronic CO poisoning.

23.4 ADDENDUM Just prior to the publication of this chapter, Pearson Assessments, who have the scoring rights to the MMPI-2, made the decision to provide the Lees-Haley Fake Bad Scale34 score as part of their Extended Score Protocol. It is important for clinicians to understand that the construct validity of the Lees-Haley Fake Bad Scale (FBS) has been criticized in the literature (e.g., Butcher, et al.35 and Arbisi and Butcher36 ). The primary concern regarding the construct validity of this scale is that it contains many symptoms common to a wide variety of medical and neurological disorders. Twenty-four of the 43 items contained in this scale relate to possible neurological symptoms including problems with attention and concentration, physical pain, headaches, fatigue, reduced stress tolerance, tinnitus, vision problems, sleep disturbance, temperature deregulation, alteration in sense of taste, dizziness, and decreased libido. Therefore, if a neurologically impaired individual is honestly reporting their symptoms on the MMPI-2 profile, then they are likely to demonstrate artificially elevated scores on the FBS. Regarding this issue, Butcher35 states, “The results indicate that the FBS is more likely to measure general maladjustment and somatic complaints rather than malingering. The rate of false-positives produced by this scale is unacceptably

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high, especially in psychiatric settings. This scale is likely to classify an unacceptably large number of individuals who are experiencing genuine psychological distress as malingerers. It is recommended that the FBS not be used in clinical settings nor should it be used during disability evaluations to determine malingering” (pp. 473–474). The potential for a false-positive error is recognized by Pearson Assessments and their website contains a cautionary statement regarding use of the FBS. The PearsonAssessment website states, “Scores on the FBS should be considered in the context of scores on the other validity scales, the circumstances of the assessment and any conditions such as a significant physical injury or disease that could artificially elevate scores on the FBS.” As has been noted earlier, the current study clearly supports that individuals who have sustained chronic exposure to CO will often experience multiple persisting symptoms in multiple systems. As a result, this population would be at risk for obtaining elevated FBS scores simply because they are honestly reporting their persisting symptoms on the MMPI-2. Therefore, prior to publication of this chapter, the FBS score was calculated for each of the 19 adults who completed the MMPI-2 as part of this study. The Pearson Assessment website suggests that raw scores above 23 on the FBS should “raise concerns” about the validity of self-reported symptoms and that raw scores above 28 should raise “very significant concerns” about the validity of self-reported symptoms. Of the 19 participants in this study, only seven had FBS scores of 23 or less. Three had FBS scores ranging from 23 to 27 and 9 had FBS scores of 28 or greater. The average FBS score was 26.2 (range 17–38). As noted earlier in the chapter, no individual was admitted to this study if there was any indication of symptom magnification, exaggeration, or malingering. None of the 19 adults in this study demonstrated any behaviors suggestive of symptom magnification. They all passed three formal symptom validity tests and the standard and well accepted validity indicators of the MMPI-2 did not suggest any symptom over reporting. A critical item analysis of each participant’s FBS score was conducted. It was determined that 50% or more of the subjects acknowledged persisting problems with attention and concentration, physical pain, headaches, fatigue, reduced coping and stress management, vision problems, sleep disturbance, gastro intestinal (GI) distress, temperature deregulation, and dizziness on the FBS items. The current study supports that these are common residual symptoms experienced by many individuals who have been chronically exposed to CO. It was this author’s opinion that the fact that they honestly reported these symptoms on the MMPI-2 artificially elevated their FBS score. It is also this author’s opinion that the FBS should not be used, or at least be used with extreme caution, as a validity indicator or an indication of symptom over reporting for individuals who have been chronically exposed to CO.

ACKNOWLEDGEMENT I would like to thank our psychometricians, Doug Wise, B.A., Amber Wolffrum, B.A., and Vickie Novak, M.A. who administered the test batteries and also assisted with organizing the volumes of data generated by this study. My wife, Diana, was, as always, a wonderful support to me throughout this project. Technical support was

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provided by C.N.A.’s Director of Operations, Brian Reusink, M.Ed. My thanks to Robert Sokol, PhD who “helped to polish” the final product.

References 1. Gale, S.D., Hopkins, R.O., Weaver, L.K., Bigler, E.D., Booth, E.J., and Blatter, D.D. MRI, Quantitative MRI, SPECT and neuropsychological findings following carbon monoxide Poisoning, Brain Inj., 13, 22–243, 1999. 2. Wright, J. Chronic and occult carbon monoxide poisoning: we don’t know what we’re missing, Emerg. Med. J.; 19: 386–390, 2002. 3. Penney, D.G. Chronic carbon monoxide poisoning, In: Carbon Monoxide Toxicity, Penney, D.G., Ed., CRC Press, Boca Raton, FL, 2000. 4. Hopkins, R.O. Neuropsychological and neuroimaging effects of carbon monoxide, National Academy of Neuropsychology, 22nd Annual Conference, Miami Beach, FL, October 11, 2002. 5. Weaver, L.K. Carbon monoxide poisoning, Critical Care Clinics, 15, 297–317, 1999. 6. Townsend, C.L., and Maynard, R.L. Effects on health of prolonged exposure to low concentrations of carbon monoxide, Occup. Environ. Med.; 59: 708–711, 2002. 7. Broome, J.R., Pearson, R.R., and Skrine, H. Carbon Monoxide Poisoning: forgotten not gone!, Br. J. Hosp. Med., 39, 298–305, 1988. 8. Hampson, N.B. Carbon Monoxide Poisoning and Its Management in the United States, In: Carbon Monoxide Toxicity, Penney, D.G., Ed., CRC Press, Boca Raton, FL, 2000. 9. Heckerling, P.L., Leikin, J.M., Maturen, A., and Perkins, J. Predictors of occult carbon monoxide poisoning in patients with headache and dizziness, Ann. Intern. Med., 107, 174–176, 1987. 10. Halpern, J.S. Clinical Notebook: Chronic occult carbon monoxide poisoning, J. Emerg. Nursing, 15, (Part 1), 1989. 11. Carbon Monoxide Support The Effects of Chronic Exposure to CO: A Research Study Conducted by CO Support, Technical Paper, 1–47 pp., appendices, October, 1997. 12. Hay, A.W.M., Jaffer, S., and Davis, D. Chronic Carbon Monoxide Exposure: The CO Support Study. In: Carbon Monoxide Toxicity, Penney, D.G., Ed., CRC Press, Boca Raton, FL, 2000. 13. Ryan, C.M. Memory Disturbance Following Chronic, Low-Level Carbon Monoxide Exposure, Arch. Clin. Neuropsychology; 5, 59–67, 1990. 14. Myers, R.A.M., DeFazio, A., and Kelly, M.P. Chronic carbon monoxide exposure: A clinical syndrome detected by neuropsychological tests, J. Clin. Psychology, 54, 555–567, 1998. 15. Pinkston, J.B., Wu, J.C., Gouvier, W.D., and Varney, N.R. Quantitative PET scan findings in carbon monoxide poisoning: Deficits seen in a matched pair, Arch. Clin. Neuropsychology, 15, 545–553, 2000. 16. Hartman, D.E. Neuropsychological Toxicology Identification and Assessment of Human Neurotoxic Syndromes (2nd ed.), Plenum Press, New York and London, 1995. 17. Devine, S.A., Kirkley, S.M., Palombo, C.L., and White, R.F. MRI and neuropsychological correlates of carbon monoxide exposure: A case report, Environ. Health Perspect., 101, October, 2002. 18. Helffenstein, D.A. Neuropsychological evaluation of the carbon monoxide-poisoned patient. In: Penney, D.G., Ed., Carbon Monoxide Toxicity, CRC Press, Boca Raton, FL, 2000, Chapt. 20, pp. 439–461.

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19. Heaton, R.K., Grant, I., and Matthews, C.G. Comprehensive Norms for an Expanded Halstead-Reitan Battery, Psychological Assessment Resources, Odessa, FL, 1991. 20. Padula, W.V., and Argyris, S. Post-trauma vision syndrome and visual mid-line shift syndrome, Neuro Rehab., 6, 165–171, 1996. 21. Politzer, T. Vision function, examination and rehabilitation in patients suffering from traumatic brain injury. In: Minor Traumatic Brain Injury Handbook: Diagnosis and Treatment, Jay, G.W., Ed., CRC Press, 2000. 22. Jarvis, P.E., and Barth, J.T. The Halstead-Reitan Neuropsychological Test Battery: A Guide to Interpretation and Clinical Application, Psychological Assessment Resources, Odessa, FL, 1994. 23. Reitan, R.M., and Wolfson, D. Traumatic Brain Injury, Vol. II, Recovery and Rehabilitation, Neuropsychology Press, Tucson, AZ, 1988. 24. Reitan, R.M., and Wolfson, D. The Halstead-Reitan Neuropsychological Test Battery: Theory and Clinical Interpretation, 2nd ed, Neuropsychology Press, Tucson, AZ, 1993. 25. Meyers, J.E., and Meyers, K.R. Complex Figure Test and Recognition Trial: Professional Manual, Psychological Assessment Resources, Inc., Odessa, FL, 1995. 26. Schenkenberg, T., Bradford, D.C., andAjax, E.T. Line Bisection and unilateral neglect in patients with neurologic impairment, Neurology, 30, 509–517, 1980. 27. Hooper, H.E. Hooper Visual Organization Test. LA: Western Psychological Service, 1983. 28. Lezak, M.D., Howieson, D.B., and Loring, D.W. Neuropsychological Assessment, 4th ed, Oxford University Press, NY, 2004. 29. Cripe, L.I. Use of the MMPI with mild closed head injury. In: The Evaluation and Treatment of Mild Traumatic Brain Injury, Varney, N.R. and Roberts, R.J., Eds., Lawrence Erlbaum Associates, Mahwah, NJ, 1999. 30. Morrow, L.A., Ryan, C.M., Hodgson, M.J., and Robin, N. Alterations in cognitive and psychological functioning after organic solvent exposure, J. Occup. Med., 32, 444–449, 1990. 31. Bowler, R.M., Mergler, D., Rauch, S.S., et al. Affective and personality disturbances among female former microelectronics workers, J. Clin. Psychol., 47, 41–52, 1991. 32. Tellegen, A., Ben-Porath, Y.S., McNulty, J.L., Arbisi, P.A., Grahm, J.R., and Kaemmer, B. The MMPI-2 Restructured Clinical (RC) Scales - Development, Validation, and Interpretation, University of Minnesota Press, Minneapolis, MN, 2003. 33. Heuser, G., and Mena, I. NeuroSPECT in neurotoxic chemical exposure demonstration of long-term functional abnormalities, Toxicol. Industr. Health, 14, 813–827, 1998. 34. Lees-Haley, P.R., English, L.T., and Glenn, W.J. A Fake Bad Scale on the MMPI-2 for Personal Injury Claimants, Psychol. Rep., 68, 203–210, 1991. 35. Butcher, J.N., and Arbisi, J.L. The Construct Validity of the Lees-Haley Fake Bad Scale – Does this scale measure somatic malingering and feigned emotional distress? Arch. Clin. Neuropsychol., 18, 473–485, 2003. 36. Arbisi, P.A., and Butcher, J.N. Failure of the FBS to predict malingering of somatic symptoms: response to critiques by Greve and Bianchini and Lees-Haley and Fox, Arch. Clin. Neuropsychol., 19, 341–345, 2004.

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24

Chronic Carbon Monoxide Poisoning: A Case Series David G. Penney

CONTENTS 24.1 Study Background and Demographics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24.2 Symptomatic Evaluation Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24.3 Use of Self-Report Questionnaires . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24.4 Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24.5 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

551 553 558 564 565 565

24.1 STUDY BACKGROUND AND DEMOGRAPHICS This is a retrospective chart-review study. Patients data files were enrolled on two bases, (1) they were exposed to carbon monoxide (CO) for more than 24 h (i.e., chronic), and (2) they were adult, that is, 18 years of age and above. The cohort was subdivided into those patients who were active smokers (18) and those who were not smokers (43). Diagnostic questionnaires on file had been completed by the patients, some completing two or even three questionnaires over the course of their evaluation. In all instances, the most recently completed questionnaire (i.e., longest time period since CO exposure) was chosen for use. The questionnaires used were dated from 2001 to 2006. Patients resided throughout the United States. The most highly represented states were Michigan, Texas, and Washington, four each; Nevada, New York, West Virginia, California, Florida, Kansas, and Missouri, three each; New Mexico, Pennsylvania, Utah, Virginia, Georgia, Idaho, Indiana, and Maine, two each, and the rest with one each—Alaska, Alabama, Connecticut, Iowa, Illinois, Montana, North Carolina, Nebraska, Rhode Island, South Carolina, and Vermont. Table 24.1 lists the sources of CO identified by each of the patients, as they knew it. Notice that “furnace” contributed 38.8% to the total of sources. Related to that was “heater” at 8.9%, fireplace at 14.9%, “boiler” at 4.5%, and “heating system” at 1.5%. Therefore, space heating equipment contributed over two-thirds of the sources of CO identified. Water heaters made up 10.4%. Motor vehicles in total contributed 551

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TABLE 24.1 Sources of Carbon Monoxide in Study C Nonsmoker

%

Smoker

%

Total

%

Furnace Fireplace Heater Water heater Automobile Boiler Stove Truck Heating system Oven Race car Track hoe Lift truck Diesel engine Rocket fuel

17 10 4 4 3 2 1 1 1 1 1 1 1 0 0

36.1 21.3 8.5 8.5 6.4 4.3 2.1 2.1 2.1 2.1 2.1 2.1 2.1 0 0

9 0 2 3 1 1 1 1 0 0 0 0 0 1 1

45.0 0 10.0 15.0 5.0 5.0 5.0 5.0 0 0 0 0 0 5.0 5.0

26 10 6 7 4 3 2 2 1 1 1 1 1 1 1

38.8 14.9 8.9 10.4 6.0 4.5 3.0 3.0 1.5 1.5 1.5 1.5 1.5 1.5 1.5

Total

47

20

67

TABLE 24.2 Demographics of Patients Enrolled in Study C Male/ Female

Age (years)

CO (ppm)

COHb (%)

Exposure Duration (months)

Time After CO poisoning (months)

Nonsmokers n=

12/31

41.9 ± 2.2 43

150.5 ± 24.2 20

8.1 ± 1.5 7

24.9 ± 4.1 30

23.4 ± 3.2 39

Smokers n=

8/10

48.9 ± 3.3 18

143.3 ± 32.0 3

10.5 ± 1.7 5

33.9 ± 8.9 18

22.3 ± 3.7 17

Combined n=

20/41

43.9 ± 2.3 61

149.6 ± 23.4 23

9.2 ± 1.3 12

27.8 ± 4.7 56

23.0 ± 3.0 56

less than 10% as the source of chronic CO poisoning. It is not clear why none of the smokers identified “fireplace” as the CO source. It may be related to the fact that this group was quite small compared to the nonsmoker group. The demographics of the two subgroups and of the total enrollees in the study are shown in Table 24.2. The nonsmoker group of 43 individuals contained 12 men and 31 women, with an average age of 41.9 ± 2.2 years (mean, standard error of the mean). The smoker group of 18 individuals contained 8 men and 10 women, with an average age of 48.9 ± 3.3 years. This difference verges on significance at the p > .05 level. Mean Air CO concentration on the nonsmoker group was 150.5 ± 24.2 ppm,

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and 143.3 ± 32.0 ppm in the smoker group. Combined mean CO concentration was 149.6 ± 23.4 ppm. All values of CO are those at the time of measurement, and may or may not be representative of CO concentration at other times during exposure. Carboxyhemoglobin (COHb) was measured in only twelve of the enrollees, seven nonsmokers, and five smokers. The latter had COHb of 8.1% and the former, 10.5%. Overall, cohort COHb was 9.2 ± 1.3%. No “back-calculation” to time zero (i.e., time of leaving site of CO poisoning) was attempted. Mean overall exposure duration was 27.8 months, with the smokers being nonsignificantly longer by 9 months. The time after the CO poisoning at which the diagnostic questionnaire was completed was about 23 months in both groups, that is, approximately 2 years.

24.2 SYMPTOMATIC EVALUATION DATA The initial/immediate symptoms experienced by the enrollees are shown in Table 24.3. The symptoms are listed in decreasing order of frequency of complaint, down to a total of two. As in my earlier studies of chronic CO poisoning,1 a wide variety of symptoms were involved. The data show that headache was the most frequently reported symptom in both the nonsmoker and smoker groups. This was followed by nausea, dizziness, fatigue, confusion, forgetfulness, and so forth. The immediate symptoms reported only once are as follows: allergies; anger; apathy; appetite poor; arm pain; back pain; back spasm; backache; blacking out; body pain; brain buzzing, burning, sizzling; bruising, bleeding; congestion; coordination, loss; couldn’t get out of bed; couldn’t identify people; couldn’t move; cramps; déjà vu; digestive problems; dreams, horrible; dropping things; dry skin; ear aches; ear pain; eyes burning; eyes, spots; face numb; fainting; fever; frustration; hair falling out; head rushes; hearing loss; heart painful when active; heart squeezed; heartbeat irregular; hoarseness; ill; incontinence; intestinal problems; irritable bowel; itchy; light-headedness; lost in familiar place; miscarriage; motivation lacking; palpitations; paralysis; poor coordination; pressure in head; projects, trouble completing; respiratory problems; restless leg syndrome; runny nose; skin red hot; sore throat; standing up, fell down; stomach, with gas in it; “strobing,” stumbling; throat burning; transient ischemic attack (TIA); trembling; urine output reduced; vertigo; walking all night; and wheezing. Table 24.4 lists the symptoms or conditions that existed when the questionnaire was completed many months after termination of the CO exposure. Of the persistent physical symptoms (Table 24.4A), “fatigue” was said to be present by 93.4% of enrollees. Next in line at decreasing frequency were “sleep problems,” “headache,” “muscle pain,” “weakness,” and so forth. Note that headache, reported as the most frequent immediate symptom is less frequently reported as a longterm, persistent symptom. The most frequently reported sensory-motor symptom is “eye/vision problems,” and the most frequently reported gross neurologic condition is reduced “physical strength.” Of the persistent cognitive-memory symptoms (Table 24.4B), “memory” problems were said to be present by 98.4% of enrollees. Next in line at decreasing frequency were “attention-concentration,” “more distractible,” “multitasking,” and so forth. The affective-emotional symptoms seen with

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TABLE 24.3 Immediate Symptoms during the Carbon Monoxide Exposure in Study C Symptom/Condition Headache Nausea Dizziness Fatigue Confusion Forgetfulness Sleepy Disorientation Dyspnea/S.O.B. Flu-like symptoms Vomiting Weakness Numbness Sleep problems Irritability Tiredness Chest pain Muscle pain Blurred vision Memory problems Depression Pain Vision problems Diarrhea Tingling Loss of balance Tinnitus Attention-concentration Decreased mental capacity Cough Leg pain Sweating Cold in day Joint pain Sleeping longer Thinking difficulty Tachycardia Stomach problems Double vision Panic attacks Nervousness Moodiness Anxiety Photosensitivity Abdominal pain Hallucinations Felt like rubbed raw inside with sandpaper Sleepiness Neck pain Consciousness altered Crying Blood pressure increased

Nonsmokers

Smokers

Combined

32 24 21 13 9 8 6 6 6 3 4 3 4 5 7 7 3 5 4 6 6 3 2 3 3 3 4 5 3 4 1 2 2 3 3 3 1 1 1 1 1 2 2 2 2 2 2 2 2 2 2 2

13 7 6 9 8 3 4 3 2 4 3 4 3 2 0 0 3 1 2 0 0 2 3 2 2 2 1 0 1 0 2 1 1 0 0 0 2 1 1 1 1 0 0 0 0 0 0 0 0 0 0 0

45 31 27 22 17 11 10 9 8 7 7 7 7 7 7 7 6 6 6 6 6 5 5 5 5 5 5 5 4 4 3 3 3 3 3 3 3 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

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TABLE 24.4A Incidence of Persistent Symptoms (Physical, Sensory-Motor and Gross Neurologic) after Carbon Monoxide Exposure in Study C Symptom/Condition Fatigue Sleep problems Headache Muscle pain Weakness Balance Physical strength Joint pain Numbness Eye vision problems Tingling Fine motor problems Walking problems Dizziness Taste/smell changes Shortness of breath Hearing problems Handwriting changed Thermoregulatory dysfunction Chest pain Tremor Other gross motor problems Nausea Vertigo Urinary incontinence Diarrhea Paresthesia Vomiting

Nonsmokers 41/43 38/43 37/43 35/43 36/43 32/40 34/41 32/43 35/43 31/43 34/43 30/40 29/42 28/43 27/43 33/43 28/43 26/42 25/41 24/43 21/43 26/41 21/43 20/39 17/43 16/43 5/14 8/43

Smokers 16/18 17/18 16/18 17/18 15/17 15/16 15/18 17/18 13/17 16/17 13/18 11/16 13/18 14/18 14/18 7/17 11/18 12/18 12/18 9/18 12/18 7/17 7/18 4/17 7/17 7/18 2/4 4/18

Combined 57/61 55/61 53/61 52/61 51/60 47/56 49/59 49/61 48/60 47/60 47/61 41/56 42/60 42/61 41/61 40/60 39/61 38/60 37/59 33/61 33/61 33/58 28/61 24/56 24/60 23/61 7/18 12/61

Combined Percent 93.4 90.2 86.9 85.3 85.0 83.9 83.1 80.3 80.0 78.3 77.0 73.2 70.0 68.9 67.2 66.7 63.9 63.3 62.7 54.1 54.1 56.9 45.9 42.9 40.0 37.7 38.9 19.7

greatest frequency was “more anxiety/fear” at 98.2%. This was followed by “irritability,” “mood changes,” “anger/temper,” “depression,” “more apathetic,” and so forth. The belief that others perceived them as “different than before” the CO poisoning was endorsed by 94.6% of enrollees. One-fifth of enrollees indicated they had had thoughts related to suicide after the CO poisoning. Table 24.5 presents the severity of each of the persistent physical symptoms as reported by the enrollees, for the nonsmoker, smoker, and combined group. Overall, “fatigue” was reported to have the greatest severity, 3.5 ± 0.2 (mean, ± standard error of the mean). The intensity scale ranged from 0 to 5. The absence of a symptom is equivalent to a zero. Above zero, 1 = slight, 2 = mild, 3 = moderate, 4 = severe, and 5 = extremely severe. Thus, 3.5 is midway between moderate and severe. Because the value for fatigue is a mean carrying with it some variance [as expressed by standard

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TABLE 24.4B Incidence of Persistent Symptoms (Cognitive-Memory, Affective-Emotional) after Carbon Monoxide Exposure in Study C Symptom/Condition Memory Attention-concentration More anxiety/fear Irritability More distractible Mood changes Anger/temper Depression More apathetic Loss of interest in life Seen as different than before Loss of motivation Multitasking Word-finding Panic attacks Lose track in actions Mental confusion Stays in room/home Weep/cry Slow mental processing Makes more mistakes Lower self-esteem Understanding others Avoids social situation Afraid of CO poisoning again Decision difficulty Initiation of actions Following directions Less pleasure taken Diminished libido Sorting/organizing Speaking problems Mental/written math Reading problems More suspicious Disorientation Finding familiar places Can’t balance checkbook More compulsive Suicide thoughts

Nonsmokers

Smokers

Combined

Combined Percent

42/43 42/43 39/40 40/41 26/27 42/43 35/37 33/34 37/36 23/25 38/40 22/24 40/43 40/43 28/31 38/41 39/43 38/42 16/18 27/31 25/29 24/27 26/29 37/42 36/41 36/43 26/32 32/39 27/32 31/39 36/43 36/43 24/30 22/29 20/26 29/42 26/41 27/39 18/25 3/25

18/18 18/18 16/16 16/16 12/12 17/18 15/15 16/17 12/13 14/14 15/16 13/13 16/17 16/17 13/13 16/18 16/18 15/17 9/10 13/14 14/15 12/14 13/15 14/17 15/18 16/18 14/15 15/18 10/13 14/16 13/17 11/17 11/15 10/14 9/14 11/16 14/18 12/17 5/13 4/9

60/61 60/61 55/56 56/57 38/39 59/61 50/52 49/51 47/49 37/39 53/56 35/37 56/60 56/60 41/44 54/59 55/61 53/59 25/28 40/45 39/44 36/41 39/44 51/59 51/59 52/61 40/47 47/57 37/45 45/55 49/60 47/60 35/45 32/43 29/40 40/58 40/59 39/56 23/38 7/34

98.4 98.4 98.2 98.2 97.4 96.7 96.2 96.1 95.9 94.9 94.6 94.6 93.3 93.3 93.2 91.5 90.2 89.8 89.3 88.9 88.6 87.8 86.6 86.4 86.4 85.3 85.1 82.5 82.2 81.8 81.7 78.3 77.8 74.4 72.5 69.0 67.8 69.6 60.5 20.6

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H.A. = Headache, SOB = Shortness of breath (dyspnea), Dz = Dizziness, Nz = Nausea.

3.3 ± 0.2 58 1.7 ± 0.2 54 2.0 ± 0.2 59 2.3 ± 0.2 57 0.4 ± 0.1 61 1.1 ± 0.2 53

1.2 ± 0.2 57

1.8 ± 0.2 60

2.8 ± 0.2 59

3.5 ± 0.2 60

1.2 ± 0.2 60

0.8 ± 0.2 60

1.9 ± 0.2 59

2.4 ± 0.2 60

2.7 ± 0.2 59

2.8 ± 0.2 60

Combined n=

3.0 ± 0.3 17 1.8 ± 0.4 16 1.8 ± 0.4 17 1.9 ± 0.4 16

0.4 ± 0.2 18 1.2 ± 0.3 17

0.9 ± 0.3 17

2.1 ± 0.3 17

2.9 ± 0.4 16

3.3 ± 0.3 17

0.8 ± 0.3 17

0.6 ± 0.2 17

1.1 ± 0.4 17

2.5 ± 0.3 17

2.9 ± 0.2 17

2.7 ± 0.3 17

Smokers n=

3.4 ± 0.2 41 1.6 ± 0.3 38 2.1 ± 0.2 42 2.4 ± 0.3 41

0.4 ± 0.1 43

1.1 ± 0.2 36

1.3 ± 0.3 40

1.7 ± 0.2 43

2.8 ± 0.3 43

3.6 ± 0.2 43

1.4 ± 0.2 43

0.9 ± 0.2 43

2.3 ± 0.3 42

2.4 ± 0.3 43

2.7 ± 0.3 42

2.9 ± 0.2 43

Nonsmokers n=

Sleep Problems

Therm Reg. Dys Tingling

Numbness

Vomiting

Vertigo

Nz.

Dz.

Weakness

Fatigue

Chest Pain

Diarrhea

S.O.B

Joint Pain

Muscular Pain

H.A.

TABLE 24.5 Physical Symptoms in Study C

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error of the mean (SEM)], some enrollees reported less fatigue and some reported more than the mean. Recall that nearly all enrollees reported fatigue of some degree (i.e., 93.4%). A symptom of slightly lesser severity was “sleep problems,” at 3.3. This was followed by “headache” and “weakness” at 2.8, and then “muscle pain” (2.7), “joint pain” (2.4), “numbness” (2.3) and “tingling” (2.0). There appeared to be no significant differences between smokers and nonsmokers. The symptoms reported at the lowest level of severity were “diarrhea” (0.8) and “vomiting” (0.4). Table 24.6 presents the severity of each of the persistent sensory-motor and gross neurologic symptoms as reported by the enrollees, for the nonsmoker, smoker, and combined group. Overall, problems with “physical strength” were rated most highly, at 2.5. Following this was “eye/vision” problems (2.2), “balance” problems (2.1), and “hearing” problems, “fine motor” problems, and “walking” problems, all reported at the same mean level of severity (1.8). There appeared to be no significant differences between smokers and nonsmokers. The symptoms reported at the lowest level of severity were “paraesthesia” and “urinary incontinence” (1.0). Owing to the amount of data on cognitive and memory symptoms, Table 24.7 was divided into A and B sections. Each section contains ten aspects each of cognitive-memory data, as reported by the enrollees for the nonsmoker, smoker and combined group. Overall, problems involving “memory” (Table 24.7A) and “attention-concentration” (Table 24.7B) were reported to persist with the highest level of intensity after CO poisoning, 3.5 ± 0.2 for both. Following these were “multi-tasking” (3.3), “more distractible” (3.1), “word-finding” problems (3.0), and “decisions difficult” and “makes more mistakes”, both at 2.9. There appeared to be no significant differences between smokers and nonsmokers. The symptoms reported at the lowest levels of severity were “finding familiar places” (1.9) and “disorientation” (1.5). Owing to the amount of data on affective-emotional symptoms, Table 24.8 was divided into A and B sections. Each section contains ten aspects each of the affectiveemotional data, as reported by the enrollees for the nonsmoker, smoker, and combined group. Overall, problems involving “mood changes” (3.6) and “increased anxiety”, “depression” and “irritability” (all 3.5) (Table 24.8A) were reported to persist with the highest level of intensity after CO poisoning. Other affective-emotional aspects were reported to persist at somewhat lower levels of intensity: “afraid of CO poisoning again” and “anger/temper” at 3.2, “different per others” at 3.1, and “loss of motivation” at 3.0. There appeared to be no significant differences between smokers and nonsmokers. The symptoms reported at the lowest level of severity was “suicide thoughts” (0.3).

24.3 USE OF SELF-REPORT QUESTIONNAIRES The use of questionnaires is basic to clinical psychology, the health sciences, and other fields in attempting to understand a person’s background, thoughts, beliefs, health status, and so forth. For this reason a number of special purpose questionnaires were devised to obtain such data relative to the study of chronic CO poisoning. As such, the questionnaires used are information gathering tools, not testing tools.

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0.8 ± 0.3 17 1.0 ± 0.2 60

2.4 ± 0.4 18 2.5 ± 0.2 59

1.7 ± 0.4 18 1.8 ± 0.2 58

1.1 ± 0.6 9 1.2 ± 0.3 35

1.6 ± 0.4 16 1.8 ± 0.2 53

0.9 ± 0.3 16 1.6 ± 0.2 54

1.2 ± 0.4 17 1.3 ± 0.2 59

2.2 ± 0.3 15 2.1 ± 0.2 55

1.0 ± 1.0 3 1.0 ± 0.4 17

1.4 ± 0.3 16 1.7 ± 0.2 58

1.8 ± 0.4 17 1.8 ± 0.2 56

2.5 ± 0.4 15

2.2 ± 0.2 53

Smokers n=

Combined n=

∗ Eye-vision, hearing, and so forth abnormalities.

1.1 ± 0.2 43

2.6 ± 0.3 41 1.9 ± 0.3 40 1.2 ± 0.4 26

1.9 ± 0.3 37

1.9 ± 0.3 38

1.3 ± 0.3 42

2.0 ± 0.2 40

1.0 ± 0.4 14

1.8 ± 0.3 42

1.9 ± 0.3 39

2.1 ± 0.3 38

Nonsmokers n=

Urinary Incontinence Physical Strength Walking Problem

Hand Writing

Tremor

Balance

Paresthesia

Hearing

Vision

Fine Motor Problems

Other Gross Motor Problems

TasteSmell

∗ Eye-

TABLE 24.6 Sensory–Motor and Gross Neurologic Symptoms in Study C

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Memory Problems 3.5 ± 0.2 42 3.5 ± 0.3 17 3.5 ± 0.2 59

Word-Finding Problems 3.1 ± 0.2 42 2.9 ± 0.3 17 3.0 ± 0.2 59

Speaking Problems

2.4 ± 0.2 39

1.9 ± 0.4 17

2.3 ± 0.2 56

Nonsmokers n=

Smokers n=

Combined n=

TABLE 24.7A Cognitive–Memory Symptoms in Study C

2.9 ± 0.2 61

2.9 ± 0.4 18

2.9 ± 0.3 43

Decisions Difficult Reading 2.3 ± 0.3 29 2.4 ± 0.3 14 2.3 ± 0.3 43

Understanding Others 2.5 ± 0.2 29 2.5 ± 0.3 15 2.5 ± 0.2 44

2.6 ± 0.2 57

2.4 ± 0.3 18

2.6 ± 0.3 39

Following Directions

Disorientation 1.5 ± 0.2 42 1.6 ± 0.3 16 1.5 ± 0.2 58

Confusion 2.7 ± 0.2 41 2.7 ± 0.3 17 2.7 ± 0.2 58

Finding Familiar Places 1.8 ± 0.3 41 2.3 ± 0.4 18 1.9 ± 0.2 59

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More Distractible 3.1 ± 0.2 27 3.1 ± 0.4 11 3.1 ± 0.2 38

Starting Projects 2.9 ± 0.3 32 2.4 ± 0.3 15 2.7 ± 0.2 47

Attention Concentration Problems

3.6 ± 0.2 43

3.4 ± 0.3 18

3.5 ± 0.2 61

Nonsmokers n=

Smokers n=

Combined n=

TABLE 24.7B Cognitive–Memory Symptoms in Study C (cont.)

2.8 ± 0.2 45

3.3 ± 0.3 14

2.6 ± 0.3 31

Slower Mental Processing

2.9 ± 0.2 44

3.1 ± 0.4 15

2.8 ± 0.3 29

Make More Mistakes

2.9 ± 0.2 59

2.8 ± 0.4 18

2.9 ± 0.2 41

Lose Track of Self

2.7 ± 0.2 60

2.5 ± 0.4 17

2.8 ± 0.3 43

Sorting/ Organizing

Balance Check Book 2.5 ± 0.3 39 2.2 ± 0.5 16 2.4 ± 0.3 55

Multitasking 3.4 ± 0.2 41 3.2 ± 0.3 17 3.3 ± 0.2 58

2.4 ± 0.3 41

2.4 ± 0.5 14

2.4 ± 0.3 27

Mental/ Written Math

Chronic Carbon Monoxide Poisoning: A Case Series 561

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More Compulsive 2.6 ± 0.4 23 1.5 ± 0.6 13 2.2 ± 0.3 36

More Suspicious 2.7 ± 0.4 24 1.9 ± 0.5 13 2.4 ± 0.3 37

Afraid of CO Again

3.3 ± 0.3 39

3.1 ± 0.4 17

3.2 ± 0.2 56

Nonsmokers n=

Smokers n=

Combined n=

TABLE 24.8A Affective–Emotional Symptoms in Study C

2.8 ± 0.2 38

2.9 ± 0.5 13

2.7 ± 0.3 25

Decreased Self-Esteem

3.6 ± 0.2 52

3.3 ± 0.4 14

3.7 ± 0.2 38

Mood Changes

Depression 3.5 ± 0.2 34 3.3 ± 0.4 17 3.5 ± 0.2 51

More Apathy 3.1 ± 0.2 36 2.4 ± 0.5 13 2.9 ± 0.2 49

Panic Attacks 2.8 ± 0.3 31 3.2 ± 0.3 13 2.9 ± 0.2 44

Increased Anxiety 3.4 ± 0.2 40 3.7 ± 0.3 16 3.5 ± 0.2 56

3.5 ± 0.2 57

3.3 ± 0.3 16

3.6 ± 0.2 41

Irritability

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Nonsmokers n= Smokers n= Combined n=

Suicide Thoughts 0.1 ± 0.1 25 0.8 ± 0.4 9 0.3 ± 0.1 34

Loss of Motivation 2.7 ± 0.3 24 3.4 ± 0.4 13 3.0 ± 0.2 37

Loss of Interest in Life 2.7 ± 0.3 25 3.4 ± 0.4 14 2.9 ± 0.2 39

Anger Temper 3.4 ± 0.3 37 2.9 ± 0.3 15 3.2 ± 0.2 52

Weeping/ Crying

2.4 ± 0.3 18 2.9 ± 0.5 10 2.6 ± 0.3 28

TABLE 24.8B Affective–Emotional Symptoms in Study C (cont.)

2.6 ± 0.3 31 2.9 ± 0.5 14 2.7 ± 0.3 45

Depressed Libido 2.8 ± 0.3 36 2.9 ± 0.5 16 2.9 ± 0.2 52

Avoid Social Situations

Different Per Others 3.1 ± 0.4 17 3.0 ± 0.8 5 3.1 ± 0.3 22

Gets Less Pleasure 2.8 ± 0.34 31 2.8 ± 0.5 13 2.8 ± 0.3 44

Stay in Room 3.3 ± 0.3 37 3.4 ± 0.4 17 3.3 ± 0.2 54

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A history questionnaire (not used here) was designed to gather historical information regarding medical, social, and psychological events, as well as basic demographic data about the patient. It is six pages in length and requires 30–60 min to complete. The diagnostic questionnaire used here asks respondents about their health, broadly defined, at the time of the toxic event, as well as at the present time, termed “now.” The responses elicited are both qualitative and quantitative—does the symptom or condition apply to the respondent and what is the intensity of the symptom or condition as they sense it. The intensity scale runs from 0 to 5, that is, 0, 1, 2, 3, 4, and 5. An answer of “no” is equivalent to a zero. Zero indicates the symptom or condition is not present, 1 = slight, 2 = mild, 3 = moderate, 4 = severe, and 5 = extremely severe. The collateral A questionnaire (not used here) is designed for a third party who knows the patient extremely well (i.e., intimately) to answer. This person is usually a “significant other.” This questionnaire is also both qualitative and quantitative like the diagnostic questionnaire. Respondents are asked to complete the form from his/her own knowledge of the subject, not by quering the subject. Routinely, during analysis of questionnaire data, the threshold of significance is set at “mild” (= or >2). That means that responses that fail to reach a level of 2.0 are considered not to be significant. The collateral B questionnaire is another kind of third party questionniare. It is designed for a person to answer who knows the subject well, but may not know him or her intimately. It is qualitative only—did the symptom or sign preexist the CO poisoning incident, or did it occur immediately afterward. The credibility and validity of a patient’s responses can be evaluated in a number of ways. Patients can be asked to complete questionnaires several times over, separated by several month intervals. When this is done, patients are asked to attest to the fact that they have not retained photocopies of previously completed questionnaires. Responses on these questionnaires are examined for consistency over time. A second approach to the problem of credibility and validity of responses has been to embed questions in the questionnaire whose function is to reveal those who would blindly indicate that they have every symptom/sign presented (i.e., “control items”). A third approach is to perform cluster analysis of symptoms. This looks at multiple questions concerned with a related symptom or condition. Again, information about a patient’s consistency can be determined in this way. Finally, the use of questionnaires completed by third parties (i.e., collaterals), indicate whether significant others, close friends, family, and so forth see the same symptoms as the patient reports, the same intensity of those symptoms, and whether the symptoms are new after the toxic insult or predated the insult. Some patients unconsciously under-report their symptoms, while others over-report. Information regarding such tendencies can also be gained though use of collateral questionnaires.

24.4 DISCUSSION This study describes extensive and severe symptoms residual after lower-level chronic CO poisoning where the mean reported COHb was 9.2%. COHb in Study A was 9.65% and 9.0% in Study B, corrected in the later instance to 14.0% after allowance

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for CO washout prior to the drawing of blood. Similar extensive and severe health damages are shown in the study of chronic CO poisoning by Dr. Helffenstein in this book2 (Chapter 23), which parallels and also greatly extends this one to areas of neuropsychological damage. Dr. Hopkins (Chapter 22) discusses how less-severe CO poisoning has been defined in terms of COHb by various investigators as ≤10%, 5–15%, and 0.01–11%.3 She described the study by Chambers et al.4 who compared the cognitive outcomes of CO victims with less-severe acute poisoning to those with more severe CO poisoning at 6 weeks, and 6 and 12 months after their poisoning. Less-severe CO poisoning was defined as no loss of consciousness (LOC) and COHb saturation ≤15%. More severe CO-poisoning was defined as involving LOC or a COHb saturation of >15%. Two-hundred and one patients were included in the more severe CO-poisoning group and 55 in the less severe CO poisoning group. Cognitive sequelae occurred in 39% of the first group and in 35% of the second group. The difference was not statistically significant at any time. Thus, both the more and the less severe groups had significant cognitive sequelae. Therefore, CO-induced cognitive outcomes appear to be unrelated to measures of apparent CO poisoning severity. One could ask why it has taken so long for the effects of less severe, acute, and chronic CO poisoning to be recognized. With respect to chronic CO poisoning, this has come about primarily through the work of neuropsychologists such as Bronstein et al., Ryan, Hartman, Pinkston, Devine, Helffenstein, Hopkins, and others,2,3,5−9 toxicologists such as Hay and Penney1,10,11 and epidemiologists such as Ritz, Morris, and others,12,13 not largely through the work of physicians. This is probably owing to the fact that most of the symptoms produced by chronic CO poisoning are not considered seriously by those in mainline medicine and the practice of neuropsychological evaluation is a discipline that has grown up outside of internal medicine. In my case as a specialized toxicologist, I may have recognized them because they were thrust into my face by victims of chronic CO poisoning, and moreover since I entered the field from pure science and had no preconceived ideas about what to expect.

24.5 CONCLUSION This study of a series of 61 patients demonstrates that chronic CO poisoning is not without long-term health consequences. The study results show not only the frequency of the reporting of symptoms known to be part of the Carbon Monoxide Poisoning Syndrome1 but now also the intensity with which each of these symptoms is reported. Again, we see a multiplicity of symptoms and signs in the five arenas, many more than most of the other usual or more common diseases seen by health care professionals. And again, these symptoms and signs appear to involve a number of organ systems, but all with the common connection of the central nervous system and the well recognized damage that CO can do to this organ system.

References 1. Penney, D.G. Chronic carbon monoxide poisoning. In: Carbon Monoxide Toxicity, D.G. Penney, Ed.,CRC Press, NY, 2000, Chapt. 18, pp. 393–418.

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Carbon Monoxide Poisoning 2. Helffenstein, D.A. Cognitive and behavioral sequelae of chronic CO poisoning: Data on large case series. In: Carbon Monoxide Poisoning, D.G. Penney, Ed., CRC-Taylor and Francis Press, NY, 2007, Chapt. 23. 3. Hopkins, R.O. Neurocognitive and affective sequelae of carbon monoxide poisoning In: Carbon Monoxide Poisoning, D.G. Penney, Ed., CRC-Taylor and Francis Press, NY, 2007, Chapt. 23. 4. Chambers, C., Hopkins, R.O., and Weaver, L.K. Cognitive and affective outcomes compared dichotomously in patients with acute carbon monoxide poisoning. Undersea Hyperbar. Med., 48, 2006. 5. Bronstein, A.C., Kadushin, F.S., and Teitelbaum, D.T. Neurobehavioral findings in two cases of chronic low level carbon monoxide poisoning Veter. Human Toxicol., 29, 479, 1987 (abstract only). 6. Ryan, C.M. Memory disturbances following chronic, low-level carbon monoxide exposure. Arch. Clin. Neuropsychol., 5, 59–67, 1990. 7. Hartman, D.E. Neuropsychological Toxicology Identification and Assessment of Human Neurotoxic Syndromes (2nd ed.), Plenum Press, New York and London, 1995. 8. Pinkston, J.B., Wu, J.C., Gouvier, W.D., and Varney, N.R. Quantitative PET scan findings in carbon monoxide poisoning: Deficits seen in a matched pair. Arch. Clin. Neuropsychol., 15, 545–553, 2000. 9. Devine, S.A., Kirkley, S.M., Palumbo, C.L., and White, R.F. MRI and neuropsychological correlates of carbon monoxide exposure: A case report, Environ. Health Perspect., 2002; 110: 1051–1055. 10. Hay, A.W.H., Jaffer, S., and Davis, D. Carbon Monoxide Support. Effects of chronic exposure to CO:Aresearch study conducted by CO Support. Technical Paper. October, 1997. 47 pp, appendices. 11. Hay, A.W.H., Jaffer, S., and Davis, D. Chronic carbon monoxide exposure: The CO Support study. In: Carbon Monoxide Toxicity, D.G. Penney, Ed., CRC Press, NY, 2000, Chapt. 19, pp. 419–437. 12. Ritz, B., and Yu, F. The effect of ambient carbon monoxide on low birth weight among children born in Southern California between 1989 and 1993. Environ. Health Perspect., 107, 17–25, 1999. 13. Morris, R.D. Low-level carbon monoxide and human health. In: Carbon Monoxide Toxicity, D.G. Penney, Ed., CRC Press, NY, 2000, Chapt. 17, pp. 381–391.

Editor’s note: On March 7, 2007 I presented a 50 minute talk in a room at the House of Lords, London, UK, along with others. Several lords and members of parliament were in attendance at various times. The meeting was organized by “CO Awareness”, an English “charity”, whose mission is the reduction of injuries and deaths from unintentional CO poisoning in that country. I spoke about the dangers of CO poisoning, its proper diagnosis, this book, and particularly about the patient (case) series described in this chapter. The impression I gained at the meeting and in talking to a number of participants, live and via E-mail, was that some British are suspicious of statistics released by the government on the numbers of deaths from CO poisoning. Many believe the numbers are far higher than official values. They are also frustrated by what they perceive as inaction on the part of governmental agencies that could address the problems of CO exposure. For more on this, see the comments by Rob Aiers

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in Chapter 11, who manages the number one website for CO poisoning matters, “carbonmonoxidekills.com”. Another impression I gained at the House of Lords meeting is that in Britain there are inadequate numbers of people with special training and experience in CO poisoning. Victims see, for the most part, only physicians, who are principally general practitioners, and who are unschooled and inexperienced in toxicology and in the outcomes of CO poisoning. The same can be said for the neurologists, internists, cardiologists, etc. that they see. As discussed elsewhere (Chapters 14 and 19) these are not generally the health professionals who can be most helpful in the diagnosis, testing and management of people with CO poisoning. In some respects this is similar to the situation in the USA. Finally, it was my impression that high quality neuropsychological evaluation for CO victims such as we have in the USA (see Chapters 22, 23 and 25) may not be encouraged by the medical establishment and/or is unavailable to most victims of CO poisoning in Britain, even though it is often needed. Since the majority of the lasting health effects of CO poisoning generally occur in the cognitive-memory and affective-emotional arenas, and neuropsychological evaluation is considered the gold-standard for assessing CO-induced brain damage, this problem is extremely serious with regard to the proper testing and long-term management of CO poisoned patients.

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25

Functional and Developmental Effects of Carbon Monoxide Toxicity in Children Carol L. Armstrong and Jacqueline Cunningham

CONTENTS 25.1 25.2 25.3 25.4 25.5 25.6

Prevalence and Symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mechanisms of Toxicity Effects on the Brain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Evidence of Structural Brain Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Neurobehavioral Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Carbon Monoxide Toxicity as a Model of White Matter Injury . . . . . . . . . . Developmental Effects of Carbon Monoxide Toxicity . . . . . . . . . . . . . . . . . . . . 25.6.1 Pediatric Vulnerability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25.6.2 Age as a Critical Variable . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25.6.3 Developmental Neuropsychological Approach to Assessing Toxicity Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25.7 Case Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25.7.1 Observations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25.7.2 Case Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25.8 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

569 570 571 571 572 573 573 574 575 577 577 585 586 587

25.1 PREVALENCE AND SYMPTOMS Carbon monoxide (CO) poisoning is a relatively common environmental toxic exposure risk that can masquerade as other illnesses. Attribution to CO toxicity can be made based on clinical findings and knowledge of a malfunctioning heater, without evidence of elevated carboxyhemoglobin (COHb) levels or acute mental status changes. In the United States, CO toxicity is implicated in more than 40,000 emergency department visits made annually.1,2 CO is found wherever there is incomplete combustion of carbonaceous material, and, after carbon dioxide, it is the most

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abundant air pollutant.3 Common sources of CO are fires, faulty combustion heating systems, exhaust from internal combustion engines, and heating gases other than natural gas. Auto exhaust and exhaust gases from oil heat were most commonly associated with elevation of COHb in a study of serially admitted children to an urban emergency department who had elevated COHb levels.2 Normal COHb saturation is 0.4–0.7% at rest, while the ambient level is 0.5–1.5% in the general population due to added environmental exposure. Tobacco smokers have COHb levels ranging from 4% to 20%; the mean for one-pack/day smokers is 5–6%. COHb levels may be higher during pregnancy. Infants of mothers who smoke may have COHb elevations up to 4.3%. The presenting symptoms of a chronic CO exposure are occult, different and less specific than those that are more readily (though not easily) diagnosed in an acute/peak exposure. These differences in presenting symptoms, neuroimaging, COHb measurements, and other clinical characteristics often lead to misdiagnosis.4 Symptoms of chronic exposure may be mistaken as flu-like symptoms or other etiology, especially if there was no loss of consciousness (LOC). Early symptoms of an acute or a peak CO exposure are more obvious. These may include headache (experienced at COHb levels of ≥ 10%), fatigue and lethargy, dizziness, paresthesias, chest pain, palpitations, and nausea. Severe exposures result in obtunded consciousness, reducing the victim’s ability to recognize danger. Peak exposure may be followed by an acute encephalopathy, abnormal hyperintensity signal changes in the brain on magnetic resonance imaging (MRI), and long-lasting neurobehavioral and cognitive changes. Delayed sequelae, or encephalopathy, follows a period of apparent recovery after acute encephalopathy. Problems in functioning can have a delayed onset, and appear suddenly after days or weeks of apparent normal functioning. Symptoms may progress to severe neurocognitive impairments and neuropsychiatric (personality) changes, indicating evidence of hypoxic/anoxic brain damage.

25.2 MECHANISMS OF TOXICITY EFFECTS ON THE BRAIN The harm created by CO exposure is mainly due to reduction in oxygen transport rather than to any significant poisoning effect on respiratory enzymes.5 The major determining factors of toxicity are CO concentration, duration of exposure, and alveolar ventilation. The disruption to cerebral blood flow created by reduction in oxygen transport produces brain injury through hypoxia. The basic mechanisms of behavioral changes are hypoxic brain damage resulting from: (1) the displacement of O2 when CO binds with hemoglobin and interferes with O2 delivery to tissues, (2) the inhibition of mitochondrial oxidative respiration and cardiomyopathy due to displacement of O2 from myoglobin by CO, with associated hypotension and systemic acidosis, and (3) the increased permeability of the vascular endothelium caused by CO. Neural inflammatory processes may also be involved in delayed neurobehavioral problems because of brain iron extravasion into neural tissues and release of myelin basic protein following CO poisoning.6

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Minimal effects on cognitive performance are reliably observed at 7% COHb level, and a 5% COHb level causes decrements in vigilance tests and in difficult dual task tests. A 2–4% COHb level has been associated with reduced video game performance.7−10

25.3 EVIDENCE OF STRUCTURAL BRAIN INJURY Although initial COHb levels do not predict later impairment well, radiographic neural changes are predictive of functional impairments. Peak exposures are more likely to produce obvious structural changes on clinical MRI scans of the brain when caused by hypoxia and by cardioembolic or hypotensive strokes related to myocardial ischemia. The most common MRI finding on T2-weighted images and Fluid Attenuation Inversion Recovery (FLAIR) is often, but not always, bilateral symmetric hyperintensity of the white matter, greater in the centrum semiovale, with relatively less involvement of the temporal lobes and anterior frontal lobes.11,12 The incidence of white matter hyperintensities varies in natural history group studies. In one large prospective controlled group study (N = 73), the incidence was 12%, significantly more in the periventricular area than in the centrum semiovale.13 Cognitive impairment was greater in those patients with hyperintensities in the centrum semiovale, and signal changes persisted over the 6-month study period. Atrophy is common in chronic CO exposure. Most reports of structural abnormalities are based on case reports, but one group report cited cerebral cortical atrophy in 60% of adults, mild atrophy of cerebellar hemispheres in 50%; vermian atrophy in almost 70%, with less common atrophy found in the globus pallidus and corpus callosum.6,12 Atrophy of the hippocampus,11 basal ganglia,14 thalamus and medial temporal lobe15 can also occur. Structures with high-energy demands, including the hippocampus and the cerebellum, are particularly vulnerable to hypoxia,11 as are those high in iron content, including the basal ganglia.16 Initial Computed Tomography (CT) or MRI often fails to detect low-density lesions in the globus pallidus, a frequent site of injury, and has poor clinical correlation as abnormalities seen on the scan may be found in both wellrecovering and comatose patients. At follow-up, lesions may disappear, diminish, or remain unchanged, and resolution of white matter lesions, ventricular enlargement, and cortical atrophy later on may be represented by an improved clinical picture with persistent neurocognitive and neuropsychiatric impairment at a less severe level.6,17,18 However, neurocognitive impairments are likely even when neurological symptoms resolve. Visual evoked potentials are often done, but may miss effects, if white matter lesions result in demyelination in other parts of the brain.19 The most robust findings may be found at long-term follow-up.

25.4 NEUROBEHAVIORAL FINDINGS Neurobehavioral symptoms vary and correspond with damage to cortex, subcortical nuclei, and white matter. The following symptoms and signs have been reported: amnesia,11,20 apraxia,21 visual object agnosia,22 akinetic mutism,23,24 parkinsonism,25 choreoathetosis,26 peripheral neuropathy,27,28 cortical blindness,29,30 depression and

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anxiety,31 and impaired attention and executive functioning.32 Varied memory processes have been implicated in CO toxicity, including incidental memory, recognition, paired associate learning, delayed recall, and visual short- and long-term memory, without effects on intelligence, visuospatial functions, speed, dexterity, nor letter fluency.33

25.5 CARBON MONOXIDE TOXICITY AS A MODEL OF WHITE MATTER INJURY Chang et al.34 identified three types of white matter injury that occur following CO poisoning: (1) multiple small necrotic foci in the centrum semiovale and interhemispheric commissures; (2) areas of necrosis in the deep periventricular white matter that is associated with axonal destruction and lipid-laden macrophages; and (3) demyelination in the deep white matter.13,32,35,36 The multifocal and diffuse injuries associated with CO toxicity link it with traumatic brain injury (TBI) in terms of its commonality with the latter as a white matter disease.37 Whereas the acute clinical course of CO toxicity is differentiated from that of deceleration or rotational brain injury, the chronic state of either condition is associated with events, including the production of free radicals and excitatory amino acids and the disruption of normal calcium homeostasis, which act in concert to exacerbate the hypoxic-ischemic insult that can occur in association with diffuse axonal injury (DAI).38 Given the commonality of neurochemical mechanisms underlying axonal injuries, TBI may be a relevant comparison when examining the neurobehavioral effects of CO toxicity, as well as in speculating on the responsiveness of either condition to similar approaches to rehabilitation.39 In the cognitive domain, a pattern of relative strengths and weaknesses has long been known to characterize DAI: the relative preservation of “crystallized” and prior-learned knowledge, and the severe effects on “fluid” processing,40 which is resource-limited. Resource-limited processes require higher levels of processing resources for optimal performance and are affected by inter-and intra-task competition.41 Fluid intelligence is largely nonverbal and a culture-reduced form of mental efficiency that is used when a task requires adaptation to a new situation. Crystallized intelligence is content-related, and represents the corpus of what has been learned. Whereas no narrowly defined cognitive pattern has been identified as characterizing CO toxicity,33 a frequent cognitive profile obtained in the neuropsychological evaluation of the CO-poisoned patient is one that mirrors that found in TBI in that the profiles demonstrate relative sparing of crystallized abilities, but serious involvement of fluid processes.42 Most common deficits in the CO-poisoned patient are observed in executive functioning (i.e., planning, monitoring, resisting distraction, and maintaining flexibility in thinking), attention and concentration, memory, visual perceptual abilities, and speed of information-processing.42 In both adults and children, deficits in these areas are also expected to occur, singly or in combination, as sequelae to closed head injury.43

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25.6 DEVELOPMENTAL EFFECTS OF CARBON MONOXIDE TOXICITY 25.6.1 PEDIATRIC VULNERABILITY It is important to differentiate the typical CO exposures in adults as compared to children. Adults often are exposed to more lethal doses, but children have heightened vulnerability to CO toxicity based on constitutional factors.44 Low birth weight is a well-known sequelae of CO exposure.45,46 Across all pediatric age groups, roughly 50% of fatalities are unintentional and of those, 50% are related to motor vehicle exhaust inhalation.47 Parameters that are relevant to neural development are the duration of exposure (chronic or peak exposure); acute, subacute or delayed symptoms, timing of exposure (prenatal vs postnatal), and dose (moderate levels analogous to cigarette smoking or higher levels). Symptoms in children appear to manifest more variably than in adults, with even poorer clinical correlation with a wider range of COHb levels,16 and with variable outcomes occurring even in related individuals with similar exposure levels.48 This variability can lead to the conclusion that no clear relationship can be predicted between severity of CO poisoning (COHb levels at admission) and residual neuropsychological deficits.13,48 Even in cases of known elevated COHb levels, some individuals demonstrate little chronic cognitive impairment, although a degree of impairment remains likely. There are very few reported case outcomes for CO-exposed children. Severe memory impairment was reported in four pediatric cases with chronic exposure over several years; in three of the four children, exposure was lower-level and without LOC.33 Physiological factors putting children at greater risk than adults include children’s rapid uptake of CO into the bloodstream, high metabolic needs coupled with small blood volume, reduced pulmonary transport of CO while sleeping (occurring for longer periods in children), and reduced pulmonary transport of CO due to young age.16 There is also heightened risk for children, as compared with adults, from exposure to CO in utero. CO is a known potent fetotoxin and teratogen with prenatal toxicity retarding growth and development.49 Direct effects on cognition are shown by translational studies. Long-lasting learning and memory deficits have been seen to result from gestational exposure of rats to levels of COHb in the maternal blood supply equivalent to cigarette smoking in humans. Postnatal exposure to this dose of CO from 1 to 10 days postbirth has resulted in no memory or learning deficits at 3 and 18 months of age in rats.50 However, exposure to the same level of CO from day 0 to day 20 of gestation in rats has led to impairments in habituation, working memory, and the ability to explore novel objects, but no alteration in spontaneous motor activity.51 The behavioral effect of prenatal exposure may be caused in part by changes in mesolimbic dopaminergic transmission52 and in cholinergic and catecholaminergic pathways.53 In one study, guinea pigs were exposed to CO for 10 h a day from Day 23 to 25 of gestation until term at 68 days. The fetus brains were examined 5–7 days prior to birth. Prenatal exposure to CO affected cholinergic and catecholaminergic pathways in the medulla, particularly in cardio-respiratory centers, a finding which may be related to smoking and increased rate of sudden infant death

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syndrome.53 Prenatal exposure can also cause developmental alterations in the areas of the brainstem responsible for respiratory control, causing increased sensitivity to CO after birth.54 Other factors mediate the impact of CO as a toxicant on child development, some potentiating and some moderating. The level of CO poisoning, age at the time of exposure, and the intellectual level of the child mediate long-term functional capacity.55

25.6.2 AGE AS A CRITICAL VARIABLE Because the growth of children is incomplete at any one point in time, the developmental stage reached at the time of a brain insult holds particular importance in assessing the injury’s significance. The primary challenge to successful coping imposed by pediatric brain injury, is that an acquired brain injury generates “rippling effects” that have long-term consequences over the whole course of a child’s future development.56 The most enduring effects are thus expected to occur at the youngest ages when the child has not yet had the opportunity to master fundamental developmental tasks. In the period from birth to 2 years of age, the child is expected to achieve an understanding of cause-and-effect relationships. By understanding that certain events are routinely paired together, he/she becomes capable of basic self-regulation, an essential achievement that paves the way for the ability to integrate thinking, emotion, and behavior—the task of the developmental period from 3 to 5 years. In the middle-childhood years, the achievement of classroom self-organizational skills forms the precursor for the development of the planning and goal-direction capacities necessary for movement and problem-solving through the middle school years. Failure to develop age-appropriate skills at any stage in the developmental trajectory thwarts the development of the judgment skills eventually necessary for successful progress toward adolescent autonomy.56 The commonly reported finding that permanent deficits in mood regulation and executive functioning, in areas including decision-making and attention-monitoring57 frequently follow CO poisoning, warrants looking at developmental factors which are influential in the expression of impairment. Disruptions in achieving major milestones in the first year of life create lock-step constitutional changes that affect overarching consequences as the child matures. For example, the infant who fails to understand that certain events are routinely paired together becomes despondent when the mother does not immediately attend to his/her cry, resulting in the infant’s difficulty in regulating the sleep-wake cycle.58 Taking a developmental perspective on pediatric CO toxicity extends the focus from the physiological mechanisms causing dysfunction to psychosocial considerations. In the absence of such a perspective, valuable information may be lost because subtle signs, such as irritability, are not detected as markers of organicity. The paradoxical results obtained in a study59 that rated infants with relatively high levels of COHb as asymptomatic have in hindsight been attributed to failure to consider the significance of feeding difficulty and irritability in interpreting the findings.16

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Empirical findings of CO toxicity in children, both in utero and in early childhood, have shown wide-ranging degrees of neurobehavioral injury. Faulty heater installation resulted in a family being exposed to high levels of accumulated CO in an apartment in which they had lived for 1 year. A 4-year-old boy and a 5-year-old girl were hospitalized with COHb levels of 20% and 13% respectively, and were treated with oxygen through masks. Over the course of a year following exposure, behavioral symptoms were recurrent: headaches, lethargy, sleepiness, hyperactivity, violent tantrums, and extreme mood swings in the boy, and irritability, intermittent fatigue, and falling asleep in school in the girl. However, testing of cognitive ability (receptive language, vocabulary, adaptive behavior) was normal in both children 5 months after admission for treatment. The mechanism of the effect was thought to be hypoxemia (rather than hypoxia) partly because psychometric tests were normal.60 In another study, a 22-year-old pregnant woman exposed to elevated CO levels, who developed neurologic symptoms as well as tachycardia, tachypnea, signs of preterm labor, and a mildly elevated COHb level, delivered her baby at full term, without sequelae for the infant, following treatment with hyperbaric O2 .61

25.6.3 DEVELOPMENTAL NEUROPSYCHOLOGICAL APPROACH TO ASSESSING TOXICITY EFFECTS The particular imprint CO toxicity bears on a child’s functioning may represent the toxicant’s direct impact on specific cell groups or brain structures. Impact on neural structures which are vulnerable to CO toxicity and which are essential to the expression of certain functions will be represented as focal effects of injury. As examples, injury to the globus pallidus and the basal ganglia will affect the development of motor repertoires, and injury to structures critically involved in memory, such as the hippocampus, will disrupt this domain of cognitive functioning.11 In contrast to the specific brain-behavior relationships which can, at least to a significant degree, be ascribed to injury in the well-differentiated adult brain, the assessment of injury in the less-differentiated brain must consider the injury’s potential for interfering with complex processes that interact with one another and that represent consequences of both biological and psychosocial developmental forces. A multiplicity of neural and nonneural factors interact to determine a toxin’s impact in children’s functioning.62 In the child, whose behavioral repertoire is in the process of developing, toxins do not simply hit given neural structures—the “where”; they hit a “what” at both a “where” and a “when”.63 Because knowledge of a toxin’s particular signature in behavior demands a consideration of how injury to specific structures (the “where”) disrupts a developing system over time (the “what” and the “when”), the evaluation of the functional effects of toxicity in a child suspected of CO poisoning is necessarily multifaceted. A developmental neuropsychological approach to assessing effects of toxicity proposed by Bernstein64 stipulates that two levels of data-gathering are needed to account for the interactions possible between exposure to a toxicant and the developmental events occurring at the time of exposure. At a first level of assessment, data are obtained in broad domains of functioning to determine whether or not

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deficits actually exist. Domains of interest include behavioral regulation, attentional capacities, learning skills, memory capacities, problem-solving skills, motor skills (gross, fine, graphomotor), sensory capacities, general cognitive ability, communicative competence/language abilities, visuospatial processing, social cognition, socio-emotional status/adjustment, and academic achievement. These domains are tapped by the direct physical and neurological examination of the child, administration of standardized tests, and observation of the child’s behavior in both naturalistic and structured situations. Naturalistic observations complemented by information from behavioral questionnaires and history-taking interviews, contributed by caretakers including parents, teachers, and health-care professionals, form relevant components of assessment. Their importance resides in the fact that the well-structured condition of formal testing may not detect the derailing of self-regulatory functions in the child’s familiar and habituated settings. Often, the injured child’s behavior is much worse at home than in school in part because behavioral disruption may actually be leading to a child’s inability to organize moment-to-moment behavior when the situation is not strongly structuring environmental stimuli. That such derailing is possible as a result of toxicity requires documenting the child’s ability to adapt to the demands of ordinary situations as an important aspect of evaluation, one usually based on family report. As proposed by Bernstein,64 the second level of a developmental neuropsychological assessment moves from identifying deficits to determining their linkages to a particular neurotoxicant. Knowledge of the toxicant’s mode of action and predilection for specific brain systems and/or processes, as well as of the developmental significance of the timing, amount, and duration of exposure, determines the ability to address the questions of specificity, sensitivity, and causation posed at this level. Information on the where, when, and what of CO toxicity comes from animal studies on early brain injury. However, the “where” of CO toxicity (decreased oxygenation of blood) and the “when” (last trimester) in the association between developmental age and CO’s power to produce injury, leave open the knowledge of “what” is disrupted as a result of damage. In work with pre- and postgestational rats and kittens, different functional outcomes have been robustly associated with the precise age at injury.65 The most optimal outcomes have been associated with embryonic stages characterized by maximal astrocyte generation and synapse development, when the developing brain carries the potential for recovery due to the redundancy in neural generation occurring at that point. Conversely, the developing brain is at its worst time for compensation when it is in a stage of neural migration and of the initiation of synaptic formation. In rats, this is the first week of life, a period that is likened to the third trimester in the human fetus.65 During a period when the fetus is most vulnerable to CO poisoning owing to pulmonary development, it is also at a stage when genetically-programmed developmental processes work against its ability to withstand the effects of neural toxicity. Thus, the timing of a CO insult can cause cumulative biological risks66 to a developing system, which can be diverse and lifelong in their aversive impacts).67 Four case studies are next presented to describe the wide-ranging variability in outcomes possible in cases of pediatric CO toxicity.

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25.7 CASE STUDIES The following case studies are shown to illustrate the complexity of consequences possible in young children following CO exposures. The first three cases, CB, LB and DB, are siblings with chronic lower-level exposures lasting from 4.5 years in two children (ages 18 months and 3 years at the beginning of exposure), to lower level in utero exposure plus 2.5 postnatal years in the youngest. A fourth case is presented, HK, who had chronic exposure in utero and postnatally, with a probable peak exposure at almost two years of age. Table 25.1 summarizes psychometric test data as well as information obtained clinically. The children’s neuropsychological findings demonstrate a range of outcome morbidity. Test batteries for the children vary largely because of the applicability of measures at different age groups. For example, there was no neuropsychological battery for the 4-year-old at the time of the assessment, and the Wechsler Intelligence Battery for Children68 was a primary instrument, whereas by age six, a theoretically based neuropsychological battery 69 could be used. However, the constructs that the different tests measured are given, and all tests are converted to a single standard (i.e., percentile), in order to facilitate comparisons.

25.7.1 OBSERVATIONS The two cases exposed in utero (DB and HK) showed respiratory symptoms (postnatal plethora, chronic respiratory infections, asthma, premature lung development). Respiratory problems were not observed in the other two children whose exposure onset was at 4.5 and 2.5 years of age. Skin conditions were observed in three of the four children, all from the same household and thus the same exposure conditions. Systemic problems that were observed in all cases were nervous habits, difficulty concentrating, emotional lability and irritability, and attention deficit disorders. Partial autistic behaviors were observed in the child with the most severe exposure (HK), which included regression in speech at age two years, poor eye contact, difficulty playing rule-guided games, lack of imaginative play, and little social cognition. Furthermore, the longitudinal observations in this child with the most severe exposure indicated that he changed from a pleasant-appearing but poorly concentrating child at age four years, to a rigid, fearful, and easily frustrated child at age six and a half. Motor development was delayed in two of the four children (LB and HK). Some dyspraxia was measured in all four children. In the child with longitudinal data, his ability to copy figures (constructional or graphomotor praxis) declined significantly in relation to developmental expectations. By 6.5 years of age, he was significantly impaired in all motor skills tested. Tactile discrimination (identifying two fingers touched simultaneously) was impaired in the two oldest children in whom this could be tested. Developmental language impairment was often observed by the parents as poor comprehension or impaired articulation, and slow or regressed speech development in two children (LB and HK). The child with the most severe exposure as well as a history of familial reading disability (HK) had receptive and expressive language

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8417: “8417_c025” — 2007/9/11 — 12:14 — page 578 — #10 Faulty furnace emissions and ventilation into house 4 years, 4.0 months

Faulty furnace emissions and ventilation into house 7 years, 0 months

Faulty furnace emissions and ventilation into house 8 years, 7.5 months

Age at test

Chronic

Chronic

Chronic

Peak or chronic CO exposure Source of CO exposure

2.5 years + in utero

4.5 years

4.5 years

From conception

DB

Years of CO exposure

LB 1.5 years

CB

Cases

Clinical characteristics Age at initial CO 3 years exposure

Case Initials

TABLE 25.1 Summary of Psychometric Test and Clinical Data for Four Case Studies

4 years, 1.5 months

Faulty furnace

Chronic low-level in utero, and peak exposure age 1 year, 11 months Possible chronic exposure in utero, one documented peak exposure with unresponsiveness, vomiting, diarrhea, pallor, dilated, equal, slowed pupil responses; other less severe peak exposures possible. Total exposure 2 years + in utero Chronic + peak

HK Time 1

6 years, 6.0 months

Faulty furnace

HK Time 2

578 Carbon Monoxide Poisoning

4 years college 2 years college None, though doesn’t enjoy school

Right None known

Hand dominance Other risk factors including family history

Parental educational level Mother Father Depression

Chronic cough, fatigue, skin bumps, itching, restlessness, difficulty concentrating, difficulty learning, sleep disturbance, chronic diarrhea, frequent muscle cramps, nausea/vomiting, irritable, hyperactive, episode of lethargy and hallucination, nervous habits, messy habits/smearing of feces, temper tantrums

Symptoms observed by family without other known cause

4 years college 2 years college None, happy, even-tempered

Right None known

Skin bumps, flushing of cheeks, speech problems, loss of appetite, nausea, irritability, severe constipation, incident of acute flu-like symptoms and cyanotic hands, fine motor incoordination and dressing difficulty at age of 6 years, problems of speech articulation

4 years college 2 years college None, happy, outgoing, verbally quiet

Right None known

Red skin at birth that normalized, became plethoric 2 days after birth and required suctioning, chronic cough and respiratory problems that onset postnatally, often tired, low energy, frequent knee pain, impaired articulation and reduced intelligibility of speech, dysphagia, asthma, borderline anemia

12th grade 10th grade None reported, pleasant presentation

Right Paternal reading disability (mild); mother smoked 15 cigarettes/day during pregnancy

Asthma onset postnatally, premature lung development, failed to crawl, hyperactive, falls often, impaired concentration, emotional lability, bites fingernails, temper tantrums, fatigued

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(Continued)

None, fearful, easily frustrated, rigid

Same

Symptoms persist with exception of hyperactivity but Attention Deficit Disorder persists, poor attention/concentration, poor comprehension, overly dependent on parents, partial autistic-like behaviors (regression in speech at age 2 years following peak exposure) with recovery of speech, lacks imaginary play, poor eye contact, difficulty playing rule-guided games, little interest in others No change Same

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Slow, first noticed after 2 years of exposure

Timing of onset of symptoms

Neuropsychological findings Sensory and motor function Copying hand 9th percentile movements Copying figures 25th percentile (NEPSY) Grooved Pegboard test 63rd percentile on right 25th percentile on left

Normal

CB

Early motor and speech development

Case Initials

TABLE 25.1 (Continued)

25th percentile 63rd percentile (NEPSY)

9th percentile (NEPSY) 32nd percentile on right 19th percentile on left

Lethargy and viral-like symptoms postnatally

Normal

DB

9th percentile

Slow

Motor development normal prior to CO exposure; speech development slowed following 6 months of CO exposure

LB

Cases

66th percentile (Beery)

Developmental and neurological evaluations at age 2 years 7–8 months revealed clumsiness, impaired balance, lack of speech or language progression after 3 months of therapy; delay in behaviors: cognitive 8 months, gross motor 10 months, fine motor 7 months, personal/social 9 months Respiratory symptoms postnatally; speech/motor symptoms after peak exposure

HK Time 1

5th percentile (NEPSY)

5th percentile

Globally impaired, with greater expressive speech impairment—first sentence structure at age 5.5 years, communicates primarily by gesture; genetic syndrome and autism ruled out

HK Time 2

580 Carbon Monoxide Poisoning

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Impaired: age seven equivalent

Body part naming Attention and information processing speed Symbol digit 47th percentile modalities test—oral version (coding) Coding (digit symbol subtest—written version) Trail making test—A 31st percentile (tracking of numbers) Trail making test—B 19th percentile (tracking of letters and numbers) Visual cancellation 63rd percentile tests Language Word fluency 99th percentile (phonemic) Semantic fluency 84th percentile Token test (linguistic 81st percentile comprehension) Comprehension of instructions Peabody picture 77th percentile vocabulary test-III

Visuomotor precision Oral praxis Finger localization test

77th percentile

>80th percentile 19th percentile

5th percentile

63rd percentile

1st percentile

1st percentile

n/a

Impaired: age six equivalent

73rd percentile

84th percentile

75th percentile

75th percentile

84th percentile

50th percentile

75th percentile 1st percentile

<1st percentile

1st percentile

1st percentile

1st percentile

1st percentile

(Continued)

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Verbal memory Paragraph story recall Face-name associative memory Word list learning, 5 trials Learning rate over 5 trials

Vocabulary knowledge Boston naming test Picture naming Speeded naming Spelling— phonological decoding Reading (word and sentence) Sentence repetition Written expression

Case Initials

TABLE 25.1 (Continued)

1st percentile

23rd percentile

92nd percentile

2nd percentile Severely impaired graphia, unable to sequence alphanumeric symbols, impaired orthographic quality to letters of his name

1st percentile

75th percentile

63rd percentile

16th percentile

High rate of letter and numeral reversals (58% numeral reversals)

Impaired graphia, numeral reversals, poor allographic alpha quality, impaired number sequencing, symbol matching

HK Time 2

75th percentile

77th percentile

8th percentile

99th percentile

HK Time 1 5th percentile

37th percentile 75th percentile

25th percentile 42nd percentile

37th percentile 13th percentile

DB

84th percentile 84th percentile

39th percentile

LB

77th percentile

CB

Cases

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Recall after distractor 28th percentile list Recall after 30 min 77th percentile Visuospatial perception and memory Benton facial 59th percentile recognition Road map test 85th percentile Visuospatial performance subtests from IQ battery Complex figure copy 57th percentile Immediate recall of 51st percentile complex figure Delayed recall of 39th percentile complex figure Memory for faces 50th percentile Delayed recall of faces 37th percentile Executive functions Wisconsin card sorting 68th percentile test—Categories achieved Wisconsin card sorting 33rd percentile test—Perseverative errors Average

6th percentile (mean)

1st percentile

3rd percentile

22nd percentile

84th percentile

25th percentile 37th percentile

6th percentile

31st percentile 11th percentile

20th percentile

50th percentile

1st percentile

15th percentile

(Continued)

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Porteus maze test Tower test Knock-tap test (Go, no-go task) Similarities test Comprehension test Wide range achievement test-III: Arithmetic

Case Initials

TABLE 25.1 (Continued)

19th percentile

32nd percentile

19th percentile

LB

27th percentile

CB DB

Cases

1st percentile 2nd percentile

HK Time 1

1st percentile

25th percentile 26th percentile

HK Time 2

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impairment in areas including vocabulary knowledge, sentence repetition, and written expression at age 6 years. Another child also demonstrated reading impairment in both word recognition and phonological decoding (spelling). In this child (CB), her toxic exposure from age 3 to 7 occurred during the period of development of prereading and productive reading skills—beginning age 5—which is a possible basis for impairment in her reading ability. Both this child and her sister (who was exposed from age 1.5 to 5 years of age and who had no impairment in reading) demonstrated a high rate of letter and number reversals in writing. Such reversals are thought to represent impairment in tactile or somatosensory mapping,70 and both children had impairments in tactile mapping. The most severely affected child developed the most severe graphic impairment. Therefore, development of written expression appears to be very sensitive to CO toxicity. Memory impairment was not common among the children with lower-level exposure only, but in the child with a known peak exposure (HK), despite treatment with oxygen during hospital transfer, memory impairment was severe. The likelihood of hippocampal involvement in ischemic effects of peak exposure may be greater in this case. In a second child (LB), with lower-level CO exposure from age 1.5 to 5 years of age, the only memory deficit was delayed recall (two of three measures were impaired showing an abnormal decline in recall over time), suggesting hippocampal injury.11 Executive functions require a high level of cognitive control of resource-driven processing, and are dissociated from crystallized knowledge. However, only the most severely CO-exposed child demonstrated defective reasoning; the two other children of sufficient age for such testing, had scores in the low average, but not statistically impaired range.

25.7.2 CASE DISCUSSION Bernstein’s recommendations for assessment of toxicity effects on children begin with the examination of functional domains sensitive to disruption and which include behavioral regulation, social cognition, emotional adjustment, adaptability, attentional capacities, memory, and specific cognitive abilities. Radiographic demonstration of common foci of neural injuries (globus pallidus, basal ganglia, hippocampus, and centrum semiovale) predict residual motor and memory dysfunction. Such injuries carry the potential to interfere with complex processes, resulting from rippling effects on development. Predictions of functional effects of CO toxicity in these various domains appear to be accurate on the basis of assessment findings in the cases presented. Furthermore, the prediction of aversive consequences of injury during neural migration and initiation of synaptic formation in the human third trimester, is consistent with the finding that the child or children with significant CO toxicity during fetal development demonstrated the strongest effects. The children with the most severe exposure or with the longest lower-level exposure had the most severe cognitive disorders. The children with the lower-level, chronic CO exposures had impairments mainly limited to motor development and praxis, tactile mapping, and written language development, with some memory impairment (in delayed recall). The conditions of their exposure put them at risk for milder neurodevelopmental effects. Chronic CO

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concentrations that are from small, localized sources, in their case faulty furnaces and ventilation systems, can raise the ambient level and thereby increase the destructive effects of that local source.71 CO also has a greater effect during cold temperatures because its effects are amplified by decreased indoor air exchange, increased use of furnaces, and other indoor sources of combustion,71 all of which also raise the ambient level that can be augmented to a very dangerous level by a small local source, such as a faulty furnace. All the children met these risk criteria, especially the three siblings who resided in the north at approximately 43◦ latitude. CO levels also have significant adverse cardiological effects, putting at risk those with underlying disease. The children demonstrated many of the residual symptoms associated with chronic CO exposure: tiredness/fatigue, sleep problems, gastrointestinal problems, breathing difficulties, difficulty concentrating, and emotional lability. Moreover, they demonstrated developmental problems which ran the gamut from mild to severe, and which disrupted maturation of important adaptive skills, such as dressing, social engagement, involvement in physical play, learning, and complex skill development. Thus, their presentations differed from those expected in adults whose neurobehavioral impairments following CO toxicity are primarily in memory, concentration, and personality change. In these children, their impairments disrupted future development.

25.8 CONCLUSIONS This chapter provides an overview of the functional effects of CO poisoning. It discusses the differences in outcomes predicted for adults versus those for children. Case studies serve to illustrate the difference between the disruption of a whole system of development as opposed to changes from an a priori functional status, as expected for adults. If symptoms in the latter case can be said to represent delta— change, in children they can be said to represent omega—the future endpoint of a system. A developmental approach to neuropsychological assessment was found to be a useful approach to understand the complex factors governing outcomes, including age at the time of CO exposure, severity and length of exposure, fetal exposure, source of CO, and risk from raised ambient levels. Mitigating influences, such as the child’s preinjury intellectual level as demonstrated by parental achievement, were also relevant to these cases. As a conclusion to the discussion, it is proposed that a developmental approach to rehabilitation be also considered important with regard to knowing how to alleviate consequences of injury. Well-publicized work in the TBI literature has advocated for such a developmental approach and can provide a guide to approaches to moderating the far-reaching consequences of a brain insult sustained in development. Brain injury can be considered a rippling event in a child’s life.56 Rippling biological events are greater in children than in adults because of the incompletely developed status of the child’s brain, which needs time and experience to mature. Because new abilities build on established skills over time, a point of departure driving rehabilitation goals is the identification of the critical developmental task missed as a result of injury and

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the provision of a program systematically designed to teach mastery of the task. The critical task for developmental ages, birth-to-two years, is achieving understanding of cause-effect relationships; at ages, 3–5 years, the integration of thinking, emotions, and behaviors; at ages, 6–11, school skills; at ages 12–15, planning and organization; and at 16–19, judgment and autonomy. A developmental rehabilitative model has clear relevance to the treatment of the child following a toxic insult. Moreover, given the often insidious character of CO toxicity, a caretaker’s knowledge of developmental expectations and aberrations may be essential for generating the rehabilitative decisions and actions that could reduce or halt a chronic and undetected course of injury created by poisoning.

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38. Novack, T.A., Dillon, M.C. and Jackson, W.T. Neurochemical mechanisms in brain injury and treatment: A review. J. Clin. Exp. Neuropsyc., 18, 685, 1996. 39. Bigler, E.D. Brain imaging and behavioral outcome in traumatic brain injury. In Childhood traumatic brain injury: Diagnosis, assessment, and intervention, Bigler, E.D., Clark, E. and Farmer, J. E., Eds., PRO-ED: Austin, TX, 1997; p. 7. 40. Horn, J.L. and Cattell, R.B. Age differences in fluid and crystallized intelligence. Acta. Psychol., 26, 107, 1967. 41. Norman, D.A. and Bobrow, D.G. On data-limited and resource-limited processes. Cognitive Psychol., 7, 44, 1975. 42. Helffenstein, D.A. Neuropsychological evaluation of the carbon monoxide-poisoned patient. In Carbon Monoxide Toxicity., Penney, D.G., Ed., CRC Press: Boca Raton, FL, 2000; p. 439. 43. Yeates, K.O. Closed-head injury. In Pediatric neuropsychology: Research, theory, and practice, Yeates, K.O., Ris, M. D. and Taylor, H. G., Eds., The Guilford Press: New York, 2000; p. 92. 44. Gemelli, F. and Cattani, R. Carbon monoxide poisoning in childhood. Br. Med. J. Clin. Res. Ed., 291, 1197, 1985. 45. Secker-Walker, R.H., et al. Smoking in pregnancy, exhaled carbon monoxide, and birth weight. Obstet. Gynecol., 89, 648, 1998. 46. Ritz, B. and Yu, F. The effect of ambient carbon monoxide on low birth weight among children born in southern California between 1989 and 1993. Environ. Health Persp., 107, 17, 1999. 47. Cobb, N. and Etzel, R.A. Unintentional carbon monoxide-related deaths in the United States 1979 through 1988. J. Amer. Med. Assoc., 266, 659, 1995. 48. Dunham, M.D. and Johnstone, B. Variability of neuropsychological deficits associated with carbon monoxide poisoning: Four case reports. Brain Inj., 13, 917, 1999. 49. Penney, D.G. Effects of carbon monoxide on developing animals and humans. In Carbon Monoxide, Penney, D.G., Ed., CRC Press: Boca Raton, FL, 1996; p. 109. 50. Tattoli, M., et al. Effects of early postnatal exposure to low concentrations of carbon monoxide on cognitive functions in rats. Pharmacol. Res., 40, 271, 1999. 51. Giustino, A., et al. Prenatal exposure to low concentrations of carbon monoxide alters habituation and non-spatial working memory in rat offspring. Brain Res., 844, 201, 1999. 52. Cagiano, R., et al. Effects of prenatal exposure to low concentrations of carbon monoxide on sexual behaviour and mesolimbic dopaminergic function in rat offspring. Brit. J. Pharmacol., 125, 909, 1998. 53. Tolcos, M., et al. Chronic prenatal exposure to carbon monoxide results in a reduction in tyrosine hydroxylase-immunoreactivity and an increase in choline acetyltransferase-immunoreactivity in the fetal medulla: Implications for sudden infant death syndrome. J. Neuropath. Exp. Neur., 59, 2000. 54. McGregor, H.P., Westcott, K. and Walker, D.W. The effect of prenatal exposure to carbon monoxide on breathing and growth of the newborn guinea pig. Pediatr. Res., 43, 126, 1998. 55. Klees, M., Heremans, M. and Dougan, S. Psychological sequelae to carbon monoxide intoxication in the child. Sci. Total Environ., 44, 165, 1985. 56. Dise-Lewis, J.E., Calvery, M.L. and Lewis, H.C. Brain Stars Manual. Brain Stars Program: Denver, CO, 2002. 57. World Health Organization (WHO), Environmental Health Criteria 213. Carbon Monoxide, 2nd edition, Geneva, Switzerland, 1999.

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Carbon Monoxide Poisoning 58. Hofer, M.A. The organization of sleep and wakefulness after maternal separation in young rats. Dev. Psychobiol., 9, 189, 1976. 59. Lattere, M., Raspino, M. and Vietti, R.M. Acute carbon monoxide poisoning in children. Pediatria Medica e Chirurgica, 16, 565, 1994. 60. Khan, K. and Sharief, N. Chronic carbon monoxide poisoning in children. Acta Paediatr., 84, 742, 1995. 61. Silverman, R.K. and Montano, J. Hyperbaric oxygen treatment during pregnancy in acute carbon monoxide poisoning: A case report. J. Reprod. Med., 42, 309, 1997. 62. Greenough, W.T., Black, J.E. and Wallace, C.S. Experience and brain development. Child Dev., 58, 539, 1987. 63. Nowakowski, R.S. Basic concepts of CNS development. Child Dev., 58, 568, 1987. 64. Bernstein, J.H. Assessment of developmental toxicity: Neuropsychological batteries. Environ. Health Persp., 102 (Suppl. 2), 141, 1994. 65. Kolb, B. and Gibb, R. Early brain injury, plasticity, and behavior. In Developmental cognitive neuroscience, Nelson, C.A., Luciana, M., Eds., MIT Press: Cambridge, MA, 2001; p. 175. 66. Dennis, M. Childhood medical disorders and cognitive impairment: Biological risk, time, development, and reserve. In Pediatric neuropsychology: Research, theory, and practice., Yeates, K.O., Ris, M. D. and Taylor, H.G., Eds., The Guildford Press: New York, 2000; p. 3. 67. Koger, S.M., Schettler, T. and Weiss, B. Environmental toxicants and developmental disabilities: A challenge for psychologists. Am. Psychol., 60, 243, 2005. 68. Wechsler, D. Wechsler Intelligence Battery for Children-III. The Psychological Corporation: San Antonio, TX, 1991. 69. Korkman, M., Kirk, U. and Kemp, S., NEPSY: A developmental Neuropsychological Assessment. The Psychological Corporation: San Antonio, TX, 1998. 70. Zeiner, H.K. and Prigatano, G.P. Information processing deficits in hydrocephalic and letter reversal children. Neuropsychol, 20, 483, 1982. 71. Morris, R.D. Low-level carbon monoxide and human health. In Carbon Monoxide Toxicity, Penney, D.G., Ed., CRC Press: New York, 2000; p. 381.

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Issues in Rehabilitation and Life Care Planning for Patients with Carbon Monoxide Poisoning James M. Gracey

CONTENTS 26.1 Impact of Carbon Monoxide Poisoning on Cognitive, Physical and Emotional/Behavioral Functioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.1.1 Rehabilitation Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.1.2 Cognitive Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.1.3 Physical Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.1.4 Emotional and Behavioral Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.2 Rehabilitation Counseling as a Valued Service for Community Reintegration of Patients with Carbon Monoxide Poisoning . . . . . . . . . . . . . 26.2.1 Rehabilitation Counseling Defined . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.2.2 Rehabilitation Counseling as Part of the Multidisciplinary Team 26.2.3 Rehabilitation Counseling Tools for Community Reintegration . 26.2.4 Functional Capacity Evaluation (FCE) . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.2.5 Work Hardening . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.2.6 Supported Employment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.2.7 Selective Job Development and Prevocational Planning . . . . . . . . . 26.3 Research Relating to Long-Term Community Adjustment of Patients with Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.4 Life Care Planning for Patients with Carbon Monoxide Poisoning . . . . . . 26.4.1 General Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.4.2 Developing the Life Care Plan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5 Case Study of a Patient with Carbon Monoxide Poisoning . . . . . . . . . . . . . . . 26.5.1 General Information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5.2 Activities of Daily Living (ADL) Issues. . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5.3 Transferable Skills Analysis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5.4 Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5.5 Life Care Plan Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5.5.1 Medical Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

592 592 593 595 596 598 598 599 600 600 601 601 602 603 605 605 606 606 606 607 607 608 609 609 591

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26.5.5.2 Therapeutic Modalities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5.5.3 Medication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5.5.4 Laboratory . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5.5.5 Diagnostic Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5.5.6 Recreation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5.5.7 Care Providers/Residential Care . . . . . . . . . . . . . . . . . . . . . . . . 26.5.5.8 Transportation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5.5.9 Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Appendix 1 - Sample Life Care Plan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

609 610 610 610 610 610 610 611 611 611 612

26.1 IMPACT OF CARBON MONOXIDE POISONING ON COGNITIVE, PHYSICAL AND EMOTIONAL/BEHAVIORAL FUNCTIONING 26.1.1 REHABILITATION EVALUATION The challenge for patients with carbon monoxide (CO) poisoning is similar to patients with other serious medical problems, to successfully reintegrate at home and work. The process to achieve that goal begins with a rehabilitation evaluation of the impact of CO poisoning on the patient’s cognitive, emotional, and physical functioning in the community. The rehabilitation evaluation is a systematic, comprehensive assessment process, often using a team approach, which is highly individualized. The goal is to assess residual work potential and skills by means of a variety of tools, including possible testing (or reviewing neuropsychological test data) or other means which are individualized for the patient. The rehabilitation evaluation of a CO-poisoned patient requires specialized knowledge of neuropsychological assessment tools, and in virtually all cases the rehabilitation counselor should consult directly with the neuropsychologist and physician early in the process and prior to initiating any return-to-work plan. The reality of rehabilitation counseling practice today is that counselors have probably had little exposure to assisting CO patients with returnto-work issues and may not be familiar with the myriad of symptoms which are being experienced. Thus, it is critical that counselors begin to share information and knowledge on the subject. Regardless of counselor sophistication on CO, the better rehabilitation plans are ones that represent a consensus of opinion among key professionals and the patient/family members. By working toward a consensus, the rehabilitation counselor improves the probability that the individualized return-towork plan is the right one for the CO poisoned patient. The four steps in the evaluation process include information gathering, analysis, synthesis, and interpretation.1,2 Of critical importance is a comprehensive review of available medical records regarding the CO poisoning and subsequent treatment. The variables to be considered by the rehabilitation counselor in that assessment are extensive, but most are known or can be determined with quality interview and assessment tools. There is no cadre of experienced rehabilitation counselors throughout the United States who specialize in rehabilitative evaluation and treatment for persons with CO poisoning. Virtually all

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states have rehabilitation counselors who specialize in working with persons with brain injuries, but the constellation of chronic symptoms which often accompanies CO poisoning presents unique challenges for community reintegration.

26.1.2 COGNITIVE ISSUES Rehabilitation counselors who are evaluating patients with CO poisoning sequelae must rely on neuropsychologists, neurologists, physiatrists, and psychiatrists for a clear understanding of what the cognitive deficits are. Often it is the neuropsychologist, who after completing a comprehensive assessment will refer the CO patient to a rehabilitation counselor for evaluation and treatment. It would be difficult, if not impossible, to complete a rehabilitation evaluation without a comprehensive neuropsychological assessment because the tests are essential to objectively defining the cognitive, and emotional and behavioral deficits which have resulted from the CO exposure.3 The responsibility of the rehabilitation counselor is to understand the deficits as reported in the neuropsychological evaluation and then determine the functional impact of those deficits on all aspects of the patient’s activities of daily living (ADLs), including work. In addition to reviewing available medical/neuropsychological records, rehabilitation counselors should independently document ongoing cognitive symptoms (through interview) which the patient is reporting, including problems with memory, concentration, verbal and nonverbal learning, reading, speed of information processing, vision, hearing, chemical sensitivity, executive functioning, decision-making, motor speed and coordination and fatigue. Any or all of these symptoms/deficits may be occurring at the time of referral, and the presence of the deficits will negatively impact work and daily living. The rehabilitation counselor’s evaluation focuses on individualized manifestations of the cognitive symptoms. It must be noted that patient response to CO poisoning differs by the extent of brain damage, and the range of neuropsychological dysfunction varies greatly. Helffenstein4 summarized the likely areas of cognitive dysfunction, which are typically impacted following CO poisoning in Tables 26.1 through 26.4. Regarding memory, CO-poisoned patients often have multiple areas of concern as noted in Table 26.2. Regarding sensory-motor functioning, Table 26.3 illustrates common areas of concern which must be considered by the rehabilitation counselor in any rehabilitation planning. Table 26.4 illustrates common vision and information processing deficits of CO-poisoned patients. Common manifestations of the symptoms, which are noted in Tables 26.1 through 26.4 are summarized in Table 26.5. This short list and other manifestations are reviewed by Penney.5 Such manifestations of CO-related cognitive dysfunction will have a negative impact on the patient’s return-to-work capacity and depending on the degree of deficit, often prevent a successful reintegration at work. Several studies5 suggest that these cognitive problems will continue for years, making it likely that the rehabilitation counselor will need to leave cases open or on hold for much longer periods of time than other catastrophic injuries. It is important to corroborate the symptoms/problems which are reported to the rehabilitation counselor with medical records or in conversation with key people who know the patient, especially within a medical-legal practice. Rehabilitation counselors

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TABLE 26.1 Likely Areas of Executive Dysfunction • Generating solutions to problems • Planning organizing sequencing • Initiation • Persistence/follow through • Self-regulation/maintenance of focus • Self-monitoring for errors • Mental flexibility • Working memory • Multitasking Source: Adapted from Helffenstein, located at www. coheadquarters.com/CO1.htm, Penney, D.G., 2007

TABLE 26.2 Likely Areas Dysfunction

of

Short-Term

Memory

• Verbal • Visual (nonverbal) memory • Learning • Retention • Incidental memory • Contamination/confabulation • Cumulative memory • Lateralized dysfunction is possible Source: Adapted from Helffenstein, located at www. coheadquarters.com/CO1.htm, Penney, D.G., 2007

TABLE 26.3 Likely Areas of Sensory-Motor Dysfunction • Tactile sensitivity • Stereognosis • Fine motor speed • Grip strength • Motor programming and sequencing (Executive motor-skills) • Verbal and nonverbal agility (Oral motor function) • Psychomotor problem solving Source: Adapted from Helffenstein, located at www. coheadquarters.com/CO1.htm, Penney, D.G., 2007

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TABLE 26.4 Likely Areas of Vision and Information Processing Dysfunction • Visual scanning speed and accuracy • Attention to visual detail • Visual analysis, synthesis and organization (problem solving) • Constructional praxis • Speed of auditory processing • Speed of visual processing Source: Adapted from Helffenstein, located at www. coheadquarters.com/CO1.htm, Penney, D.G., 2007

TABLE 26.5 Common Functional Cognitive Issues • Impaired ability to remember instructions or take medications properly • Fatigue and loss of energy (with or without daily napping) • Increased need for structuring the daily routine with cuing • Reduced capacity for initiating task or problem solving completion • Varying degrees of social disinhibition • Impaired multi-tasking capacity • Poor insight regarding deficits • Compromised safety in the kitchen and around machinery • Tendency toward concrete thinking and planning with a related reduction in generalization capacity • Poor money management skills • Directionality/driving problems (even to familiar places) Source: Adapted from Helffenstein, located at www.coheadquarters.com/CO1.htm, Penney, D.G., 2007

often corroborate symptoms with others who know and observe the patient, including family members, employers, friends, and other care providers (physicians, psychologists, cognitive therapists, physical and occupational therapists, etc.). When discussing the cognitive symptoms with the patient (or family members), it is important to cite examples of how that symptom is affecting their life on a daily basis. By the conclusion of the evaluation process, the rehabilitation counselor should have a solid and down-to-earth understanding of how the cognitive symptoms are affecting the daily functioning of the patient with CO poisoning.

26.1.3 PHYSICAL ISSUES Patients with CO poisoning often experience a variety of physical symptoms which must be factored into the rehabilitation evaluation. Physical factors alone can be a major determinant of how well the patient successfully accommodates at work and

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home, although the cognitive problems are often the major barriers to successful community reintegration. CO-related physical deficits include paresthesias, changes in muscle tone, muscle spasms/tremors, loss of coordination, muscular weakness, headaches, sleep disturbance, changes in vision or hearing, light or noise sensitivity and pain.3,5 As with the cognitive deficits, the rehabilitation counselor reviews each physical symptom in terms of how it is impacting the patient’s daily functioning. Many of the physical problems have probably been reviewed with a physician or other caregiver, but the rehabilitation counselor will focus on the practical implications (functional assessment) of the symptoms for daily living and work. This is an important issue as the counselor determines the impact of specific physical deficits on a patient’s ability to function at home and work. Without this comprehensive review of symptoms, the rehabilitation counselor is not aware of important physical problems which can have a negative impact on the outcome of a rehabilitation plan. Physicians or other caregivers are often not aware of every physical symptom of the CO-poisoned patient which are reviewed during the rehabilitation evaluation process.5 For example, vision and hearing deficits may not be known by the physician of a CO-poisoned high school student who is experiencing significant cognitive, physical, and emotional symptoms. For that student, his primary life role is to study and learn in class and through reading assignments. Vision symptoms in an academic setting are problematic if the student did not previously discuss the problems and how they were affecting reading comprehension, or how a hearing loss is impacting the ability to hear the teacher and other students. For this reason, the rehabilitation counselor should always check with the patient and teacher regarding whether such physical problems are involved. In an active clinical practice, rehabilitation counselors often discuss such symptoms with the patient for the first time since the exposure. In the community-based model of rehabilitation within which most rehabilitation counselors operate, patients do not always bring up important symptoms unless they are asked. In addition, physicians may not be knowledgeable regarding the multiple physical symptoms which are caused by CO poisoning. The rehabilitation counselor should review any new symptom with the physician who can order appropriate assessments in order to make the diagnosis. This level of multidisciplinary give and take is essential to proper case management since caregivers are not always aware of the myriad of physical problems facing the patient who is struggling to reintegrate post-CO exposure at home, work, or school.

26.1.4 EMOTIONAL AND BEHAVIORAL ISSUES Multiple researchers3,5–9 report that emotional and behavioral sequelae post-CO exposure are common and often require treatment intervention. Common symptoms include a sense of personality change, depression, increased irritability and reduced frustration tolerance, generalized anxiety, emotional lability (including frequent episodes of tearfulness), intense fearfulness regarding the future, apathy, impulsivity, and social disinhibition. Post-traumatic stress (PTSD) symptoms should also be assessed by the patient’s neuropsychologist. Other emotional and behavioral sequelae include problems with poor sleep, anger management, and CO-induced psychotic symptoms.

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TABLE 26.6 Likely Areas of Emotional and Behavioral Executive Dysfunction • • • • • • • • •

Reduced self-control/inappropriate behavior Impulsivity Emotional lability Irritability Emotional flattening Excitability Erratic carelessness Rigidity Reduced motivation

Source: Adapted from Helffenstein, located at www. coheadquarters.com/CO1.htm, Penney, D.G., 2007

Helffenstein4 described several emotional/behavioral sequelae as directly related to executive dysfunction as illustrated in Table 26.6. Table 26.6 is instructive for the rehabilitation counselor because the sequelae commonly occur and should be noted during the evaluation process. The rehabilitation counselor can usually review the symptoms in advance by looking at the neuropsychological or neurological reports, and some rehabilitation clinics conduct preintake screenings of the complex symptoms by phone with the patient and significant family members. Preintake screenings are helpful in reducing the amount of time which the patient and family members will have to be present physically in the office. Considering that many patients are significantly sleep-deprived and that they already have multiple outpatient appointments, such techniques are helpful in accurately gathering data, establishing rapport, and reducing in-office patient time. The goal of the rehabilitation counselor is to first identify significant emotional and behavioral symptoms that are interfering with daily functioning. The counselor then documents how each symptom is impacting their life and work. Regarding the emotional and behavioral sequelae of CO patients, the rehabilitation counselor should work cooperatively with the treating neuropsychologist and psychiatrist, including a possible meeting between the rehabilitation counselor, psychologist, psychiatrist, and patient in order to review treatment goals and establish how the rehabilitation counselor will complement the treatment process.10 Neuropsychologists and psychiatrists often welcome such interdisciplinary planning with the goal of all parties ultimately agreeing to a particular return-to-work strategy.10,11 Most rehabilitation counselors are used to working in a community-based model of treatment intervention and can be the ones to initiate these rehabilitation planning sessions. It is not difficult to imagine how such pervasive emotional and behavioral symptoms can interfere at home and work. Patients often report that they no longer recognize who they are and are concerned that they are “losing their minds.” For this reason, psychological and psychiatric follow-up is usually critical as the patient

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struggles with issues related to community reintegration. Patients often feel a sense of having lost control of their lives and do not know how to regain lost self-confidence. Most patients can accurately recall how their lives were before the CO exposure and just “want their lives back.” Such emotional turmoil is inevitable after injury, and the rehabilitation counselor can offer concrete reassurance that the rehabilitation process will be a positive and necessary link between their past and future. Experienced clinicians report that virtually all patients express fearfulness that their capacity to return-to-work is impaired. They are usually looking for a methodology from the rehabilitation counselor to constructively explore the return-to-work process, and that is probably the most important service provision of the rehabilitation counselor during this treatment phase.

26.2 REHABILITATION COUNSELING AS A VALUED SERVICE FOR COMMUNITY REINTEGRATION OF PATIENTS WITH CARBON MONOXIDE POISONING 26.2.1 REHABILITATION COUNSELING DEFINED Community-based rehabilitation counseling services are readily utilized in postacute settings by physicians, psychologists, neuropsychologists, and other disciplines for the purpose of assisting persons with a disability to return (reintegrate) to work and resume as normal a lifestyle as possible.12–14 Patients who have been exposed to CO poisoning are included in that referral network. The actual role and function of the rehabilitation counselor has been actively evolving over the past 40 years, partially through a series of major legislative achievements in the United States. The 1973 Rehabilitation Act for the first time reflected a congressional commitment to serving persons with severe physical, intellectual, and emotional problems/deficits, and that commitment was reiterated in a series of amendments to the Act (1974, 1976, 1978, 1986, and 1992).12 Rehabilitation counseling as a profession has been energized by such legislation changes, which include the removal of architectural and transportation barriers, development of social security disability, individualized educational programs (for school age children), supported employment and developmental disability services expansion and other changes. The Americans with Disabilities Act (ADA)15,16 through its five titles, prohibits discrimination on the basis of disability in employment, public accommodations, public services, and telecommunications. The importance of these legislative accomplishments has been to make it possible for persons who are experiencing significant disability to achieve better functional outcomes at work and throughout their lives. Rehabilitation counselors in the United States work with diverse caseloads including persons with injuries/functional deficits to multiple areas of the body. The issue for rehabilitation counselors throughout the world is how to successfully reintegrate patients who are experiencing significant medical problems back to the workplace and to a normalized home environment.14 The aforementioned legislative changes have been foundational to the development of a community-based model

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for vocational rehabilitation services. In essence, the changes have been helpful in leveling the playing field between able-bodied Americans and persons with all types of disability. In addition to understanding these changes in law and practice, rehabilitation counselors know that there are three fundamental steps to the rehabilitation process. The most important of the three is a thorough rehabilitation evaluation. The second step involves developing an appropriate plan of action which takes into account the client’s strengths, deficits, goals, and values. The third step after plan development is plan initiation. Realistically, proper implementation of this process probably varies greatly by rehabilitation counselor, community, and availability of knowledgeable professionals regarding CO and its long-term consequences. Community-based treatment of CO poisoning requires a blend of interdisciplinary treatment professionals, and the rehabilitation counselor is an important member of that team.

26.2.2 REHABILITATION COUNSELING AS PART OF THE MULTIDISCIPLINARY TEAM Postacute multidisciplinary treatment planning for CO patients is essential in an effort to maximize community reintegration success.3,9 Rehabilitation counselors can play an important role in that treatment process because their goal involves the practical implementation of the patient’s desire to return to normal functioning at home and work. Rehabilitation counselors recognize the importance of defining transient and permanent work limitations that the CO poisoning has caused, but also seek to quantify residual strengths and find ways around the multiple deficits. The CO poisoning and residual symptoms have interrupted normal planning for the high school student, college student, or seasoned worker and without assistance and restructuring their life plans and experiences will be significantly delayed or lost forever. Career planning post-CO poisoning is usually difficult because of the combination of symptoms, hospitalization interruptions, need for multiple outpatient interventions, and low energy for rehabilitation. A common issue for treaters is when to refer for vocational rehabilitation services and whether early referral is beneficial.17,18 Although the research on this variable is not definitive, it is clear that successful longterm community integration is dependent on many factors and not just the timing of the referral.18 More important variables include counselor skill and resourcefulness and whether the right physical, psychological, and cognitive interventions are being implemented at the right time. Even though much is not known about the long-term sequelae of CO poisoning, planning for return to home and work should begin soon after stabilization. The rehabilitation counselor, in concert with other team members, should identify which resources will be utilized, and the choices depend on identification and prioritization of deficits in daily functioning. For example, assisting a student to return successfully to school or a worker to their preinjury employer after stabilization from CO poisoning is a crucial beginning aspect of community reintegration.19 Before deciding upon any particular strategy, the rehabilitation counselor will want to summarize the key postinjury deficits which can be expected to interfere with the return-to-work effort. The counselor will know those deficits from

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the initial evaluation process (including interviews with the patient, physician, neuropsychologist, and other caregivers plus review of medical records). Deficits and expected problems should be prioritized and matched with the patient’s preinjury work history and present goals. To that end the Vocational Diagnosis and Assessment of Residual Employability (VDARE) process1 can be quite useful because it translates data into objective terms, identifies transferable skills, helps to determine a vocational objective, and recommends additional services that are necessary to raise the patient’s level of functioning sufficiently so that he/she can successfully return to school or work. This methodology is helpful to the distraught CO poisoning patient who is having significant doubts that anything can be done for him or her. Decisions can then be made regarding whether the patient is ready to seek competitive employment, return to school, return to a preinjury employer in the same or modified position, do a structured volunteer program or request supported employment assistance. Successful community reintegration starts with helping the patient identify options for services. The rehabilitation counselor should review options with other professionals, especially the neuropsychologist and cognitive therapist. The goal of such interdisciplinary planning is to increase the probability that the final rehabilitation plan for the CO patient is the right one. Considering the complexity of cognitive, physical, and emotional and behavioral sequelae, which typically occur after CO poisoning, the rehabilitation counselor would be well advised to review any return to work or school plans with such treaters.

26.2.3 REHABILITATION COUNSELING TOOLS FOR COMMUNITY REINTEGRATION The rehabilitation counselor has several important rehabilitation tools available which can be helpful in implementing a successful return-to-work/school plan. They include functional capacity evaluation (FCE), work hardening, and supported employment. All three are useful for chronic CO patients who are struggling to reintegrate as productive workers. The following sections will discuss the importance of patients reconnecting with employers, post-CO stabilization, and will review the benefits of utilizing prevocational plans for CO patients who are not yet ready for a competitive work environment.

26.2.4 FUNCTIONAL CAPACITY EVALUATION (FCE) Patients with CO poisoning are often experiencing so many symptoms that an FCE becomes essential in documenting how the deficits are impacting the capacity to sustain work activities over any part of a workday.20 In practice, physicians often prefer such testing techniques because the physical and mental capacity can be stated in occupational terms, such as strength, posture, and mobility tolerances. FCEs offer baseline information which can be compared to job task requirements (determinations of whether the patient can perform the essential functions of a job). FCEs typically include recommendations for task avoidance, temporal pacing, and exertional levels and observational data during testing which is invaluable in planning return-to-work/school strategies. Clinical observation during FCEs is very helpful

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in further documenting how the CO poisoning has impacted the patient’s cognitive, physical, and emotional and behavioral functioning and whether he/she is ready to return to school or work.

26.2.5 WORK HARDENING The concept of work hardening has been variously described as work conditioning, work readiness, or work capability training.21 Work hardening programs can be a useful tool for CO patients because they emphasize real or simulated work activities, and staff observe and assess patients in conjunction with physical/mental conditioning tasks which are designed to improve their biomechanical, neuromuscular, cardiovascular, and behavioral functioning.22 Such programs are readily available and can be an important step for the CO patient because they are very goal directed, professionally staffed, and the focus is on helping the patient explore their capacity over an extended period of time (up to several months). The functional deficits can be readily observed over time, and remediation plans can be developed with the patient, physician, neuropsychologist, rehabilitation counselor, and other providers. The rehabilitation counselor is often the logical team member who will interface with the work hardening staff. CO patients can sometimes move directly to a return-to-work/school plan after completion of a work hardening program.

26.2.6 SUPPORTED EMPLOYMENT The concept of supported employment involves selective placement of persons with severe disability in a quasi-competitive work environment as opposed to a sheltered workshop. As the number of sheltered workshops has declined in the United States, the need for more intensive and long-term follow along services has not. Most CO patients would not be comfortable or appropriate in a closed workshop setting, but many are not ready for competitive interviewing and placement because of the unresolved symptoms. This community-based model of rehabilitation intervention has been available for several decades and offers the multidisciplinary team another alternative if the patient is not ready for competitive employment. The basic theory of such services has been in vogue for the past 35 years. Service provision involves locating a suitable employer and then identifying important job and social skills which can be taught to a client, training clients to utilize such skills (through a job coach, if necessary), and placing them and providing long-term follow-up support. Beginning in the 1970s this author and other providers termed such supported employment services “work stations in industry.” A criticism of such supported work service is around the use of a job coach.23 The job coach is the trainer and follow-up troubleshooter for clients at the job site, and a concern has been noted that the cost of such personnel is prohibitive in many clinical settings. An additional concern is that the role of a job coach is intensive and can stigmatize the client as different at a work site. The reality for clinicians is that such resources are valuable and allow the rehabilitation counselor options for selective placement, namely to re-engage in real work settings.

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26.2.7 SELECTIVE JOB DEVELOPMENT AND PREVOCATIONAL PLANNING The reality for persons with significant disability, including CO poisoning, is that their labor force participation rates and wages are lower than that of able-bodied Americans, and the differences are measurable and significant.24 The vast majority of all persons with disabling conditions want to work competitively,2 and CO-poisoned patients are no exception. CO patients are facing financial stress and typically feel that they must return to work despite their limitations. Several researchers have stressed the difficulties which persons with serious cognitive, physical, and emotional problems face in finding and keeping jobs.25 Because of this problem, rehabilitation counselors should promote return-to-work as soon as possible after stabilization. Most people will want to return to their pre-CO exposure job or career, if possible, and to a different job (career) if not. The rehabilitation counselor will have to determine a reasonable approach, considering the CO patient’s situation. Once an option is determined and agreed upon, a gradual return-to-work process is usually essential, and the rehabilitation counselor will probably want to have access to the employer for feedback on work performance. Depending on symptom severity, a job tryout can last for several months and should include structured follow-up sessions with the counselor for troubleshooting issues. The length of follow-up will vary by severity of problems and employer compatibility, but a range of 3 to 6 months is not unusual. It is not uncommon to find benevolent employers (family members, close friends, etc.) who will do virtually anything to help the person return to work. During the job tryout, it is important to emphasize to both parties that the tryout is to be a learning experience (an evaluation) so that he/she can test out their residual strengths in a supportive work environment where the employer is also a participant in the evaluation and return-to-work process. Over time, problems can be identified and worked through with practical solutions by the rehabilitation counselor or supporting cognitive therapist. Although rehabilitation counselors are uniquely trained to assist patients with developing such return-to-work plans, this does not mean that other disciplines (especially occupational therapists or cognitive therapists) cannot enhance the effort. The dramatic increase in cognitive rehabilitation programs has created various subspecialty professionals such as life skills trainers, behavior specialists, case managers, job coaches, and others. These individuals are often skilled in community reintegration techniques including setting up job tryouts with preinjury or new employers and volunteer placements and then troubleshooting with an employer or volunteer agency and patient during the follow-up phase. In a similar manner, prevocational plans can be developed with a benevolent employer or volunteer placement if the CO patient’s symptoms are stable but still too severe for competitive employment. The important goal here is to assist the patient to be productive again, even in a volunteer setting. Prevocational plans should precede a formal return-to-work plan and should not become permanent unless the CO patient’s symptoms are so severe that he/she is no longer employable.

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26.3 RESEARCH RELATING TO LONG-TERM COMMUNITY ADJUSTMENT OF PATIENTS WITH CARBON MONOXIDE POISONING Prediction of success or failure in the community for persons with significant physical, psychiatric, and cognitive disability is complex, multifaceted, and has been researched extensively for several decades.26–31 A consideration for rehabilitation counselors who work with CO patients is that studies which emphasize long-term community adjustment themes important to them are few and far between. Weaver et al.32 evaluated whether four patients with severe CO poisoning had better functional outcomes with or without hyperbaric oxygen treatment. The study mentions employment status of the four patients several months posthospital discharge and concludes that three of the four had a favorable outcome and had successfully returned to work. The study offers no insight regarding the researchers’ definition of “successful” return-to-work. Likewise, Weaver33 summarized numerous studies regarding the long-term consequences of CO poisoning. The report documents multiple affective, cognitive, and neurologic sequelae including malaise, apathy, memory disturbances, depression, anxiety, focal neurologic abnormalities, parkinson-like symptoms, and other problems. Job-related problems are likely with such severe symptoms, but the study did not document employment outcomes. Likewise, other researchers have noted that CO patients experience a variety of emotional problems with depression, anxiety, and increased lability in 1-year follow-up studies,7 but the articles do not offer much detail as to whether CO patients are working successfully. Most clinicians and researchers regard return to productivity as a reasonable goal of treatment,29 and experienced clinicians realize that the combination of physical, cognitive, and emotional symptoms which result from CO exposure complicate that return-to-work effort. Regarding long-term employability of CO patients, the brain injury literature is instructive since the cognitive and emotional and behavioral components are similar between the two diagnostic categories. Crisp30 reviewed 19 studies that emphasized outcomes for persons with brain injury and identified key factors that were consistently related to vocational outcome. For traumatic brain injury (TBI) patients, employment status was related to post-traumatic amnesia (PTA) and length of coma, and the cognitive deficits which most strongly predicted return to productivity involved verbal and/or visual memory and attention. Employment status was also negatively impacted by major depressive symptoms. An earlier study by Crisp28 reviewed 29 studies (from the 1970s and 1980s) which had identified critical factors of persons with brain injury which were associated with vocational outcomes. In that review of the literature, cognitive and personality deficits (problems with memory, concentration, and personality) were key variables in whether TBI patients successfully returned to work. The next most commonly cited variable in successful return-to-work was whether patients were experiencing postinjury psychosocial adaptive difficulties (social isolation, reduced capacity for engaging in appropriate social interaction and poor family adjustment). Of the 29 studies which Crisp surveyed, only 7 reported re-employment statistics of 68% or better for their respective samples, and 20 studies ranged between 12% and 64% employed. Two studies did not provide employment data. The mean

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TABLE 26.7 Return-to-Work Analysis for 208 TBI Patients at 3.5 Years Postinjury Follow-up Pre-TBI Post-TBI

Employed at date of injury N = 170 Unemployed at date of injury N = 38 Postinjury Variable Working at follow-up Returned to work but no longer working No attempt at return to work Total not working who were employed prior to TBI

N 79 23 68 91

Percentage 46.5% 13.5% 40% 53.5%

Source: Adapted from Fleming et al. Brain Injury, 13, 417–431, 1999.

number of employed persons in those 20 studies was only 38%, and the mean number of years since injury was almost four. Fleming et al.29 studied 208 patients who were admitted to a head injury program between 1991 and 1995. The mean time from initial injury to follow-up was approximately 3.5 years. Table 26.7 presents a postinjury analysis of how many TBI patients had returned to work after an average of 3.5 years from the date of injury. Of the 208 subjects, 170 were working before the TBI, and 38 were not. Of that working group (N = 170), only 46.5% (N = 79) had successfully returned to work after the injury with most of the working group going back to the same or similar jobs. Thirteen and a half percent of the working group (N = 23) had been employed since injury but were not employed at follow-up, and 40% (N = 68) of the preinjury working group had not returned to work at all. Thus, a total of almost 53.5% (N = 91) were not working in any capacity at follow-up even though this same group was employed before the TBI. The authors discussed factors which may contribute to successful community (home and job) reintegration. The results were consistent with previous studies in that the variables of PTA, older age at injury, shorter mean duration of acute hospitalization, premorbid occupational status and cognitive variables were predictive of community integration success or failure. The Fleming et al.29 results are echoed in the CO Support Group research34 regarding return-to-work rate and outcomes of CO-exposed patients. Of the chronic (N = 65) and unconscious groups (N = 12), 32% and 75%, respectively, did not return to any employment. The incapacity of CO-exposed patients was further documented in pre- and postexposure patients by income. The postinjury income drop for the unconscious group was around 50% after exposure, and the two groups overall had a significant and continuing reduction in household earnings. Such results are not surprising, considering the myriad physical, cognitive, and emotional symptoms which interfere with all aspects of personal and vocational functioning after exposure. It is understandable that patients with pain/cramps, pins-and-needles sensation/stiffness, headaches, fatigue/weakness, poor concentration, memory loss, dizziness, gastrointestinal problems, cardiac issues, vision problems, depression, and other sequelae are not easily able to resume a career and re-establish earning capacity.

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Of particular concern for community re-entry programs such as vocational rehabilitation, CO patients in both groups and in large numbers reported that the symptoms were persisting. Although there were postexposure drops in the prevalence of some symptoms, the study noted that significant numbers of people continued to suffer ill health effects long after exposure. For example, 60% of the chronic group continued to suffer from tiredness, pain, headaches, and problems with concentration and memory. Such pervasive and unresolved medical problems will significantly and negatively affect long-term employability and necessitate early vocational rehabilitation intervention. Helffenstein35 has published vocational outcome data on 19 CO poisoned patients who were all employed at the time of exposure, and the results underscore the CO Support Group research and the TBI results. Only one of the 19 returned to his preinjury job, but that individual was self-employed and could only complete the work transition by closing one of his two plants, thus significantly reducing earnings. Fifty-eight percent returned to lower skill part-time or full-time jobs and 26% were determined to be permanently and totally disabled. Dunham and Johnstone31 further document the impact of CO poisoning on cognitive, emotional/behavioral, and vocational functioning. Their study recommends careful vocational planning to include postexposure routinized job duties, frequent monitoring, more time to learn new tasks and alternative methods of instruction than just verbal. Much more research is needed as there are insufficient studies which assess how the unresolved symptoms are impacting work on a long-term basis. As noted above, the traumatic brain injury literature on employability is instructive regarding CO patients. It is likely that the CO exposure will have a major impact on work and earning capacity. As a whole, this problem merits more study, rehabilitation interventions, and awareness training for rehabilitation professionals. The vast majority of patients are working or in school at the time of exposure, and most will want to resume their work or schooling after returning home. This review of literature asserts what experienced clinicians are seeing on a daily basis, namely, that chronic CO exposure has a permanent and negative impact on earning capacity, long-term employability, and ability to readapt to preinjury career plans and goals. The problem is particularly troublesome since few rehabilitation counselors are even aware of these issues.

26.4 LIFE CARE PLANNING FOR PATIENTS WITH CARBON MONOXIDE POISONING 26.4.1 GENERAL INTRODUCTION The International Academy of Life Care Planners defines a Life Care Plan (LCP) as a “dynamic document based upon published standards of practice, comprehensive assessment, data analysis and research, which provides an organized, concise plan for current and future needs with associated costs for individuals who have experienced catastrophic injury or have chronic health care needs.”36,37 The history of life care planning has been carefully reviewed in The Guide to Rehabilitation38 and The Life Care Planning and Case Management Handbook39 and will not be discussed here

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in any detail. In summary, the development of LCPs began in the mid-1980s and has continued to accelerate to the present. The life care planning process has been described as transdisciplinary and is usually undertaken by nationally certified and licensed professionals within a health care or rehabilitation discipline.40 There are specific training programs for life care planners which lead to certification (CLCP). Most CLCPs are nurses or rehabilitation counselors, although other health care professionals who have become certified have degrees in medicine, chiropractic, psychiatry, psychology, speech therapy, and others.41 Developing an LCP for patients who have experienced CO poisoning is challenging since many CLCPs have little background with CO-exposed persons. However, this will be an area of increasing need as more patients and family members are asking what medical and rehabilitation products and services will be required throughout their lifetime because of a CO exposure.

26.4.2 DEVELOPING THE LIFE CARE PLAN The LCP is intended to be a realistic assessment of current and future medical/rehabilitative care needs for a catastrophically injured person or someone with a chronic health condition. The scope of the LCP should include a careful documentation of needs regarding medical care, evaluations, medications, durable medical equipment, supplies, therapeutic modalities, laboratory testing, diagnostics, surgery, transportation, adaptive aids, hospitalizations, home modifications, residential/home care, recreational adaptations, orthotics/prosthetics, and other areas. The life care planning process usually includes a comprehensive review of medical records, patient and family interviews, and consultations with caregivers (physicians, neuropsychologists, therapists, and other relevant health care specialists). The CLCP, in conjunction with other treatment professionals determines each item or service, the duration of need (e.g., lifetime, 1 year, 5 years, etc.), frequency of usage (e.g., 1x/day, 1x/week, etc.), purpose, cost (e.g., per month, year, etc.) and supplier/vendor (if known). Only items/services that are determined to be probable from a medical and rehabilitation point of view (more likely than not) are included in the LCP. Items or services that may become necessary for someone in the future are not included as line items in the LCP except as complications. Life care plans for CO-poisoned patients are being developed in increasing numbers and often in a legal context. However, a well-prepared and documented LCP becomes an excellent plan of treatment for patients and families because it is such a comprehensive assessment of long-term care needs. While this can be said of any good LCP, it is particularly important for recovering CO-poisoned patients because of the complexity and diversity of their ongoing symptoms and care needs.

26.5 CASE STUDY OF A PATIENT WITH CARBON MONOXIDE POISONING 26.5.1 GENERAL INFORMATION Ms. G.B. was 39 years old at referral and was referred for a vocational rehabilitation and LCP evaluation after experiencing a 48-h exposure to CO (caused by a faulty

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heater) in which a roommate died. The exposure was significant and resulted in a 60-day period of initial hospitalization, with 20 hyperbaric dives in the first 20 consecutive days. The diagnoses included: (1) CO poisoning with hypoxic encephalopathy, (2) Aspiration pneumonia, (3) Status postrhabdomyolysis with renal insufficiency, (4) Deep vein thrombosis in the left calf, (5) Bilateral mild hearing loss. She had significant impairments of mobility, cognition, ADLs, speech, and swallowing. Her carboxyhemoglobin (COHb) saturation at admission was 34%. By the end of the initial hospitalization, she was described as having made significant gains in mobility and ADL functioning, but with slower improvements in cognition and communication. She was transferred to an inpatient rehabilitation facility where she had extensive medical and neuropsychological work-ups and was followed closely by a neurologist, neuropsychologist, cognitive therapist, physical therapist, and occupational therapist. At the time of transfer, she was experiencing moderately severe to severe impairments of auditory comprehension, expressive communication, initiation, memory, attention, distractibility, and auditory processing. She had significant visual scanning impairments, was perseverative on two-step commands, and had an apraxic gait. She transitioned to outpatient status after about 45 days but required verbal or visual cuing to remain on task. Ongoing problems with executive functioning and reasoning deficits limited her ability to work. Because of the deficits, she lived with family members and was legally assigned a guardian. She continued to experience mild dexterity problems, tremors, difficulties with going down stairs as well as multitasking, organizing information and problem solving, cognitive flexibility, feeling insecure, being alone, managing finances, and social judgment. She was referred for a vocational rehabilitation and LCP evaluation at about 16 months postinjury. At the time of referral, she had not been able to return successfully to work. Her preinjury vocational background included a postgraduate degree and successful career as a financial planner.

26.5.2 ACTIVITIES OF DAILY LIVING (ADL) ISSUES At the intake interview (16 months postinjury), she was experiencing multiple physical, cognitive and emotional and behavioral symptoms (noted above) which were interfering with all aspects of daily functioning. She was having cognitive problems with fatigue, attention, concentration, short-term memory, reading comprehension, slowed speed of information processing, executive dysfunction, and lack of insight. She was also experiencing physical and emotional problems with balance, headaches, tremors, behavioral dysregulation, low frustration tolerance, and impatience. After the CO exposure, family members noted problems with decision-making and problem solving, although Ms. G.B. insisted that she was doing better than the caregivers and family members believed.

26.5.3 TRANSFERABLE SKILLS ANALYSIS In the case of Ms. G.B., a cognitive therapist was providing routine follow-along sessions with her at the time of referral for a rehabilitation evaluation. The rehabilitation counselor and cognitive therapist agreed that they would closely monitor progress

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once a prevocational plan was developed. A vocational plan should only be initiated after a consensus of opinion has been determined among caregivers (including the rehabilitation counselor), patient and family members that the CO-poisoned patient is more likely than not going to be successful in a return-to-work plan. Although failure cannot be prevented, a systematic rehabilitation evaluation (as described above) will reduce the probability of failure substantially because a thorough evaluation will match the patient’s residual skills with known training or job requirements through a transferable skills analysis (TSA). The TSA is “the foundation of any attempt to identify similar or related jobs that are consistent with or equal to the functional skill levels of the worker.”2 Considering the complex combination of physical, cognitive, and emotional deficits that the CO patient is facing, a careful analysis of residual skills (TSA) is crucial prior to implementing any return to productivity plan. In the case of Ms. G.B., her work skills were significantly diminished from before the CO exposure. As a financial planner before the injury, she was responsible for reviewing assets, liabilities, and earning power of clients and helped them develop plans to increase assets and maximize income. Required skills include an ability to work well with people, perform work with accuracy and analysis, make judgments and decisions, express personal thoughts, make recommendations, and communicate clearly.42 The job also required frequent travel to clients’ homes and long irregular hours. Once her residual skills were matched to the list of essential job duties of a financial planner (through the TSA), it was clear that she could not resume this career in the future. That decision was strongly supported by family members as they were convinced that the deficits were of such severity that she would fail any return-to-work plan as a financial planner. After further discussion and review with her doctors it was further determined that Ms. G.B. was probably not competitively employable. She was experiencing pervasive problem solving inefficiencies, impaired executive functioning, plus moderate problems with attention, speed of information processing, forgetfulness, and disorganization, and she had little to no insight regarding any of these problems.

26.5.4 OUTCOME After referral to the rehabilitation counselor (16 months postinjury), a consensus among caregivers formed that Ms. G.B. could not return to her career as a financial planner. The rehabilitation counselor met or spoke by phone with family members, physicians, neuropsychologist, physical therapist, cognitive therapist, and with her supervisor at the financial firm. The counselor carefully documented her pre- and postexposure home and work functioning. The counselor noted that after the CO exposure family members assumed a primary caretaker role with frequent input from the neuropsychologist. All parties agreed that Ms. G.B. was not employable and that she would require extensive medical and rehabilitation follow-up care throughout her lifetime. The referral of Ms. G.B. to the rehabilitation counselor had the effect of solidifying opinions that she could not sustain competitive employment in the future. However, despite the severity of her problems/deficits, Ms. G.B. wanted to work in some capacity. The rehabilitation counselor, in concert with other treatment

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team members recommended a series of college courses in areas of personal interest, and this was followed by referral to a volunteer organization, which was also of interest to the patient. The patient began a set schedule of volunteer hours with a local nonprofit agency, plus occasional college courses through various schools. The rehabilitation counselor followed up for about a year until satisfied that Ms. G.B. was stabilized at her volunteer placement and at home.

26.5.5 LIFE CARE PLAN ISSUES The LCP for Ms. G.B. was determined through face-to-face and phone consultations with her physicians, neuropsychologist, cognitive therapist, and physical therapist. All caregivers were cooperative in providing recommendations for the LCP, and the attached plan was considered to be an accurate assessment of her current and future medical and rehabilitative care needs. Once the plan was completed in the attached chart format, it was submitted to the caregivers for a final review of its completeness and accuracy. The caregivers were asked to approve or change the recommendations in writing. 26.5.5.1 Medical Care Her doctors recommended that she would require lifetime follow-up by a physiatrist, otolaryngologist (ENT), and psychiatrist. The physiatrist was to provide medical supervision of the CO-related problems with paresthesia, tremors, loss of coordination, headaches, muscle weakness and discomfort, as well as monitor the multiple cognitive and emotional deficits. The ENT was to monitor and treat the mild bilateral hearing loss, and the psychiatrist was to provide psychotropic medication management with particular focus on regulation of depression and behavioral dyscontrol issues. 26.5.5.2 Therapeutic Modalities Her doctors recommended that she would require long-term and community-based cognitive therapy at a rate of between two and four times per month for as long as she continued to live in her own apartment. Her doctors stated that she would probably not remain in her own apartment beyond a period of 15 to 20 years after which time she would need to live in a brain injury assisted living program for the duration of her lifetime. The physicians stated that she would probably experience early onset dementia after that time, although proof for this assertion in the literature is lacking. The community-based cognitive therapy was designed to monitor compensatory strategies and improve/maintain her independent living skills. The neuropsychologist recommended individual therapy at the rate of one to two times per month for life. The psychotherapy focused on crisis intervention, loss of social relationships, behavior management, and depression. Her physicians and physical therapist recommended a few sessions of physical therapy per year for life in order to treat neck and back pain and spasms.

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26.5.5.3 Medication Her physicians recommended medications for depression and pain control. In addition, movement disorder medications were recommended to treat the tremors. It was determined that she would require these or similar classes of medication throughout her lifetime. 26.5.5.4 Laboratory Because of the lifetime need for the aforementioned medications, she also needed periodic comprehensive metabolic panels in order to assess the physiological effects of the drugs. 26.5.5.5 Diagnostic Studies The physicians recommended one Magnetic Resonance Imaging (MRI) during the next 20 years to evaluate the expected neurologic deterioration and early onset dementia, although as stated above, the underlying reason for this remains unclear. 26.5.5.6 Recreation Adult recreational camps for persons with brain injury were recommended to provide an opportunity for supervised recreation and socialization. Ms. G.B. had difficulty sustaining relationships after the CO exposure and was not able to resume normal preinjury recreational outings without significant family support. 26.5.5.7 Care Providers/Residential Care Her caregivers recommended that she would need home care assistance (a companion) as long as she remained at home. She was relatively independent in personal care but required significant daily support with home safety, routine problem solving, shopping, meal preparation, and daily planning. The companion will implement treatment goals in consultation with the cognitive therapist, neuropsychologist, and case manager. The physicians opined that she would probably experience early onset dementia within the next 15–20 years at which point she will have to transition into a brain-injury-assisted living program for life. The assisted living program will provide long-term treatment support in the least restrictive environment. Ms. G.B. also required routine follow-along support with a case manager who continually assessed quality of care issues and level of independence in ADLs. The case manager was available by phone and in person to troubleshoot and problem solve with Ms. G.B. and her family members. 26.5.5.8 Transportation The cost of mileage reimbursement for travel to medical and rehabilitative appointments is included in the LCP.

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26.5.5.9 Complications Ms. G.B. is at risk for a variety of medical complications, which, if they occur, will increase the cost of her future medical and rehabilitative care. These complications include seizure disorder, visual problems, motoric deterioration, and worsening depression. This listing is intended to educate the reader in understanding that there are multiple factors which could influence Ms. G.B.’s future medical needs, but which cannot now be included in this LCP. This LCP includes all of the products and services that can now be anticipated and are considered reasonable and necessary. The future cost of these products and services may vary according to Ms. G.B.’s actual health requirements. Because she is at risk for the complications which are listed in the LCP, the actual costs may be higher if her condition changes from what can now be anticipated. Any evaluation of her future care plan requirements should consider this list of potential complications and expected costs.

ACKNOWLEDGMENTS Thanks to my wife, Anthea Blanas Gracey, for her assistance in editing and finalizing the manuscript; to Ruth Zebarth, nurse and Life Care Planner for her assistance in finalizing the LCP; and to Lynn Dalton and MarLene Nelson for their technical assistance.

References 1. Havranek, J., Grimes, J., Field, T., and Sink, J. Vocational Assessment: Evaluating Employment Potential, Elliott and Fitzpatrick, Athens, 1994, Chapt. 5. 2. Weed, R. and Field, T. Rehabilitation Consultant’s Handbook, Elliott and Fitzpatrick, Athens, 2001, Chapt. 6. 3. Helffenstein, D. Neuropsychological evaluation of the carbon monoxide-poisoned patient, In Carbon Monoxide Toxicity, Penney, D.G., ed., CRC Press, Boca Raton, 2000, Chapt. 20. 4. Penney, D.G. www.coheadquarters.com/CO1.htm, 2006. 5. Penney, D.G. Chronic carbon monoxide poisoning, In Carbon Monoxide Toxicity, Penney, D.G., ed., CRC Press, Boca Raton, 2000, Chapt. 18. 6. Balzan, M., Agius, G., and Debono, A. Carbon monoxide poisoning: Easy to treat but difficult to recognise, J. Postgrad. Med., 72, 470–473, 1996. 7. Hay, P. and Denson, L. The neuropsychiatric effects of carbon monoxide poisoning: Preliminary findings from a prospective study, J. Undersea Hyperbar. Med., 25, 47, 1998. 8. Hopkins, R. and Weaver, L. Longterm outcome in subjects with carbon monoxide poisoning, J. Undersea Hyperbar. Med., 21, 17, 1994. 9. Wilson, F., Harpur, J., Watson, T., and Morrow, J. Adult survivors of severe cerebral hypoxia — Case series survey and comparative analysis, J. Neurol.Rehabil., 18, 291–298, 2003. 10. Barisa, M.T. and Barisa, M.W. Neuropsychological evaluation applied to vocational rehabilitation, J. Neurol. Rehabil., 16, 289–293, 2001.

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Carbon Monoxide Poisoning 11. Ultmann, M., Geller, T., Chilakamairi, J., and Kaplan, S. Multidisciplinary rehabilitation management of depression in the carbon monoxide injured patient, Pediatric Rehab., 2, 101–106, 1998. 12. Rubin, S. and Roessler, R. Foundations of the Vocational Rehabilitation Process, PRO-ed., Austin, 1995, Chapt. 2. 13. Garner, W.E. “An Identification of Competencies Critical to Practicing Rehabilitation Counselors: Implications of Validating the Rehabilitation Counselor Certification Examination.” PhD diss., Southern Illinois University, Carbondale, IL, 1985. 14. Rubin, S., Matkin, R., Ashley, J., Beardsley, M., May, V., Onstott, K., and Puckett, F. Roles and functions of certified rehabilitation counselors (special issue), Rehab. Couns. Bull., 27, 199–224, 238–245, 1984. 15. The Americans with Disabilities Act of 1990, 101, 42, U.S.C., 12112. 16. Berkowitz, E. Disabled policy: A personal postscript, J. Disability Policy Studies, 3, 2–16, 1992. 17. Marnetoft, S. and Selander, J. Long-term effects of early versus delayed vocational rehabilitation — A four year follow-up, Disabil. Rehabil., 24, 741–745, 2002. 18. Marnetoft, S., Selander, J., Bergroth, A., and Ekholm, J. Vocational rehabilitation — early versus delayed. The effect of early vocational rehabilitation compared to delayed vocational rehabilitation among employed and unemployed, long-term sick-listed people, Int.. J. Rehabil. Res., 22, 161–170, 1999. 19. VanLierop, B. and Nijhuis, F. Assessment, education and placement: An integrated approach to vocational rehabilitation, Int.. J. Rehabil. Res., 23, 261–269, 2000. 20. Wickstrom, J. Functional capacity testing, In Multidisciplinary Perspectives in Vocational Assessment of Impaired Workers, Scheer, S., ed., Aspen Press, Rockville, 1990, 73–88. 21. Lett, C., McCabe, N., Tramposh, A., and Tate-Henderson, S. Work hardening, In Work Injury: Management and Prevention, Isernhagen, S., ed., Aspen Press, Rockville, 1988, 195–229. 22. Commission on Accreditation of Rehabilitation Facilities. 1994 Standards Manual and Interpretive Guidelines for Organizations Serving Persons with Disabilities, Tucson, 1994. 23. Rusch, F., Conley, R., and McCaughrin, W. Benefit-cost analysis of supported employment in IL., J. Rehabil., 59, 31–36, 1993. 24. U.S. Census Bureau. Disability – Work Experience and Mean Earnings – Work Disability Status of Civilians 16 – 74 Year Old, by Educational Attainment and Sex, Washington, DC, 2005. 25. McMahan, B. and Shaw, L. Work Worth Doing: Advances in Brain Injury Rehabilitation, PMD Press, Orlando, 1991, Chap. 7. 26. Cattelani, R., Tanzi, F., Lombardi, F., and Mazzucchi, A. Competitive re-employment after severe traumatic brain injury: Clinical, cognitive and behavioral predictive variables, Brain Injury, 16, 51–64, 2002. 27. Cifu, D., Keyser-Marcus, L., Lopez, E., Wehman, P., Kreutzer, J., Englander, J., and High, W. Acute predictors of successful return to work 1 year after traumatic brain injury: A multicenter analysis, Arch. Phys. Med. Rehab., 78, 125–131, 1997. 28. Crisp, R. Return to work after traumatic brain injury, J. Rehabil., 58, 27–33, 1992. 29. Fleming, J., Tooth, L., Hassell, M., and Chan, W. Prediction of community integration and vocational outcome 2–5 years after traumatic brain injury rehabilitation in Australia, Brain Injury, 13, 417–431, 1999. 30. Crisp, R. Key factors related to vocational outcome: Trends for six disability groups, J. Rehabil., 71, 30–37, 2005.

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31. Dunham, M. and Johnstone, B. Variability of neuropsychological deficits associated with carbon monoxide poisoning: Four case reports, Brain Injury, 13, 917–925, 1999. 32. Weaver, L., Hopkins, R., and Larson-Lohr, V. Neuropsychologic and functional recovery from severe carbon monoxide poisoning without hyperbaric oxygen therapy, Ann. Emerg. Med., 27, 736–740, 1996. 33. Weaver, L. Carbon monoxide poisoning, Environ. Emerg., 15, 297–317, 1999. 34. Carbon Monoxide Support group. Effects of chronic exposure to CO: A research study, Technical paper, U.K., 1997. 35. Helffenstein, D. Neurocognitive and neurobehavioral sequelae of chronic carbon monoxide poisoning: A retrospective study and case presentation, In Carbon Monoxide Poisoning, Penney D., ed., Chapt. 23, 2007. 36. International Academy of Life Care Planners (IALCP), Standards of Practice for Life Care Planners, Ankeny, 2000, 1. 37. McCallum, P. Field review: Revised standards of practice for life care planners, J. Life Care Planning, 4, 67–74, 2005. 38. Deutsch, P. and Sawyer, H. A Guide to Rehabilitation, Ahab Press, White Plains, 2005, Chapt. 5. 39. Weed, R., ed. Life Care Planning and Case Management Handbook, CRC Press, Boca Raton, 1999/2004, Chapt. 1. 40. Reavis, S. Standards of practice, J. Life Care Planning, 1, 49–57, 2002. 41. May, R. Certification in life care planning is alive and well, J. Life Care Planning, 1, 59–61, 2002. 42. Eureka. Colorado Career Information System, (ECOCIS) [computer software], Eureka, 2005.

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8417: “8417_c026” — 2007/9/11 — 12:14 — page 614 — #24 Lifetime

Lifetime Lifetime

Duration 15–20 years

Lifetime

Lifetime

Physical medicine and rehabilitation specialist

Otolaryngologist

Psychiatrist

Item or Service

Cognitive therapy∗

Psychotherapy

Physical therapy 4–6 sessions/year

12–24 sessions/year

24–48 sessions/year

Frequency

4x/year

1x/year

5–6x/year for 2 years; then 4x/year for 3 years; then 1x/year

Frequency

Provide cognitive assistance; monitor compensatory strategies to improve executive functioning/frustration tolerance; productivity, socialization and recreational goals Psychological support for crisis intervention, loss of social relationships; behavior management and depression Treat neck and back pain and spasms

Purpose

Psychotropic medication management Life Care Plan Therapeutic Modalities

Evaluate function, cognition, mobility and neurologic status and treat problems related to CO exposure Monitor and treat hearing loss

Purpose

$120–164/session $480–984/year

$150–225/session $1,800–5,400/year

$185–215/h $4,440–10,320/year

Estimated Cost

$200/visit $200/year $86–120/visit $344–480/year

$130/visit $650–780/year for 2 years; then $520/year for 3 years; then $130/year

Estimated Cost

R. Omega, R.P.T.

A. Beta, Psy.D.

Western Rehabilitation Hospital

Supplier/Vendor

A. Smith, M.D.

B. Alpha, M.D.

Western Medical Associates

Supplier/Vendor

∗ Community-based cognitive therapy will no longer be required once she transitions to a brain-injury-assisted living program in 15–20 years owing to early onset dementia.

Duration

Item or Service

Life Care Plan Medical Care

APPENDIX 1 Sample Life Care Plan of a Patient with Carbon Monoxide Poisoning

614 Carbon Monoxide Poisoning

1x/day

Treat neuromotor movement disorder

Analgesic for headaches

Antidepressant

Purpose $2.73/day $996/year $25.99–38.99/30 days $0.87–1.30/day $318–475/year $1.27–5.42/day $464–1,978/year

Estimated Cost

Bigstore Pharmacy

Bigstore Pharmacy Bigstore Pharmacy

Supplier/Vendor

Duration Lifetime

Duration Lifetime

Item or Service

Comprehensive metabolic panel

Item or Service

Brain MRI 1x/next 20 years

Frequency

2x/year

Frequency

Evaluate neurologic deterioration, early onset dementia

Purpose

$1,425–2,755/facility fee $285–551/professional fee $1,710–3,306/Total

Estimated Cost

$99–133/lab $198–266/year

Evaluate physiological effects of medication Life Care Plan Diagnostic Studies

Estimated Cost

Purpose

Life Care Plan Laboratory

Health Partners MRI

Supplier/Vendor

Health Partners Lab

Supplier/Vendor

∗ Ms. G.B. will be on these or similar classes of medications throughout her lifetime. ∗∗ Alternative anti-Parkinson medications were recommended for treatment of the movement disorder. These medications include Mirapex 3 mg per day; Sinemet 25/100 once per day and Requip 5–10 mg per day. The estimated cost for these medications ranges from $1.27 to $5.42 per day. The estimated annual cost is $464–$1978 per year.

Lifetime

1–2 tabs/day

Lifetime

Movement disorder medication∗∗

1x/day

Lifetime

Zoloft 50 mg (Generic) Ultram 50 mg

Frequency

Duration

Item or Service

Life Care Plan Medications∗

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Lifetime

Duration 15–20 years

Begin in 15–20 years for life Lifetime 15–20 years

Duration

Adult recreational camps

Item or Service

Companion

Brain injury assisted living program Case manager

Heavy housecleaning

Item or Service Frequency

2x/month

Purpose

Life Care Plan Transportation

Client advocate; assess quality of care/activities; coordinate care Provide housecleaning and laundry assistance

1–2 h/month

Daily

Provide structure and support; evaluate environment for safety; assist with problem solving needs and shopping; meal preparation and so forth Long-term rehabilitative care and supported living

Purpose

Life Care Plan Care Providers/Residential Care∗

Provide supervised recreation and socialization

Purpose

8–12 h/day

Frequency

1-2x/year

Frequency

Estimated Cost

$18–20/h $144–240/day $52,560–87,600/year $275/day $100,375/year $80–100/h $960–2,400/year $75–100/week $1,800–$2,400/year

Estimated Cost

$200–400/year

Estimated Cost

Supplier/Vendor

Once Over Cleaning

Continuous Services

Rehab Assisted Living

ABC Home Services

Supplier/Vendor

Various

Supplier/Vendor

15–20 years Monthly Mileage $0.445/mile Various Travel to medical/rehabilitative appointments reimbursement $900–1,200/year ∗ Her caregivers have recommended that she will need home care assistance (companion) as long as she remains at home. She is relatively independent in personal care but will require significant daily support with home safety, routine problem solving, shopping, meal preparation, daily planning and heavy housecleaning. The companion will implement treatment goals in consultation with the cognitive therapist, neuropsychologist and case manager. The physicians have stated that she will experience early onset dementia within the next 15–20 years at which point she will probably have to transition into a brain injury assisted living program for life. The assisted living program will provide long-term treatment support in the least restrictive environment.

Duration

Item or Service

Life Care Plan Recreation

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Secondary To Carbon monoxide poisoning Carbon monoxide poisoning Carbon monoxide poisoning Cognitive impairments and limitations

Complication

Seizure disorder Visual problems

Motoric deterioration

Severe depression Lifetime

Lifetime

Lifetime Lifetime

Length of Risk

No

No

No No

Surgery

Life Care Plan Complications

Possible

Possible

Possible Possible

Hospitalization

Additional brain injury, increased care needs Balance disturbance, altered mobility, falls, need for yoked prism lenses and vision therapy Altered mobility and independence, falls, increased care and equipment needs Withdrawal, anger, paranoia, confusion, anxiety, sadness, hostility, reduced self-esteem and self-confidence

Possible Outcome

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27

Treatment of Carbon Monoxide Poisoning with Yoked Prism Lenses James F. Georgis

CONTENTS 27.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27.2 A Review of Visual System Functioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27.3 Visual Midline Shift Syndrome (VMSS) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27.3.1 Symptoms of VMSS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27.3.2 Clinical Testing for VMSS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27.4 Treatment of VMSS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27.5 Rehabilitative and Supplementary Considerations . . . . . . . . . . . . . . . . . . . . . . . . 27.6 Case Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27.7 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

619 620 622 622 624 625 626 634 640 640

27.1 INTRODUCTION Carbon monoxide (CO) poisoning has many clinical manifestations. Malfunctions of the cardiovascular and nervous systems caused by CO are numerous and varied. This chapter discusses damage to brain structures that control spatial awareness, balance, and movement. Treatment of these neurological symptoms requires a multidisciplinary approach. The multidisciplinary team often includes the neurologist, primary care physician, toxicologist, neuropsychologist, psychiatrist, physiatrist, optometrist, and neuro-otologist. A variety of allied health care professionals are also necessary in the rehabilitation of the CO-poisoned patient. These include occupational therapists, vocational rehabilitation specialists, cognitive specialists, and physical therapists. Seventy percent of all the sensory nerves in the body come from the eyes or the visual system. This discussion focuses on the role of the visual system in the rehabilitation of the CO-injured patient. It has been estimated that 30 areas of the brain are intricately involved in the processing of visual information and integrating it with other sensory modalities to bring about appropriate actions. The visual process will be reviewed and specific areas of the brain will be discussed that affect balance and movement. According to the World Health Organization1 virtually all the cortical 619

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structures and many of the subcortical structures of the brain can be affected by CO poisoning. It identified common cognitive and motor deficits following CO poisoning. These included deficits in higher cortical functioning sensory-motor deficits and visual problems. Visual midline shift syndrome (VMSS) is a result of neurological injury to subcortical structures. There is strong neuron cross-talk between subcortical and cortical structures. Yoked prism therapy is the treatment for VMSS. The yoked prism modulates the neural signals from the subcortical system to improve movement, balance, and the perception of space.

27.2 A REVIEW OF VISUAL SYSTEM FUNCTIONING The visual system involves an extreme degree of neural activity. CO poisoning can destroy this activity in a short period of time. The brain uses 20% of the oxygen we take up, an extraordinary amount considering that the brain accounts for only 2% of body mass. A continuous supply of oxygen is essential for brain function. Loss of oxygen delivery for a period as brief as 10 min can result in neural death.2 Visual information is contained in the light reflected from an object we view. In order to understand what we see, we need sensory receptors that respond to reflected light. This light passes through the crystalline lens of the eye, where upon the image is inverted and focused on the back surface of the eye, the retina. The retina is composed of millions of photoreceptors. The photoreceptors change the light stimulus to internal neural signals within the many layers of the retina. These neural signals are processed and form a bundle, the optic nerve. The optic nerve transmits this visual information to the central nervous system. The optic nerve divides once it gets into the brain. Ninety percent of the fibers go to the lateral geniculate nuclei (LGN) of the thalamus and project directly to the cortex; the remaining 10% of the fibers go to subcortical structures like the superior colliculus of the midbrain. However, the fact that these other receiving nuclei are innervated by only 10% of the fibers does not mean these pathways are unimportant. The human optic nerve is so large that 10% of the optic nerve constitutes more fibers than are found in the entire auditory pathway. The superior colliculus plays a big role in visual attention.2 The final projection to the visual cortex is through the geniculo-cortical pathway terminating in the primary visual area of the occipital lobe. The retino-geniculo-cortical pathway contains two different retinal ganglion cells, consisting of the smaller parvocellular cells (P cells) and larger magnocellular cells (M cells). The P and M cells continue their separate paths to the occipital cortex where much of the sensory visual information is processed. The output from the occipital lobe is contained in two major nerve fiber bundles. One bundle contains P cells, which leaves the occipital cortex, which goes inferiorly or ventrally into the inferior temporal cortex. Another nerve bundle which contains M cells leaves the occipital cortex and goes superiorly or a more dorsal path to the posterior parietal cortex. The ventral or occipito-temporal pathway is specialized for object recognition, for determining what it is we are looking at. The dorsal or occipito-parietal pathway is specialized for spatial perception, for determining where an object is. There are two main questions that must be answered in visual perception. We must understand “what” we are seeing and “where” we are seeing. The response

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of neurons in the temporal lobe is activated by fibers from the central vision areas of the retina or fovea. The response of neurons in the parietal lobe is activated by fibers from peripheral vision areas of the retina. The fovea has many more retinal cells and gives us greater visual acuity. We usually look directly at things we wish to identify, thereby taking advantage of the greater visual acuity of foveal vision. The dorsal–parietal and ventral–temporal pathways are not isolated from one another but communicate extensively. We know that the retino-geniculate cortical tract contains 90% of the fibers in the optic tract. Approximately 10% of the remaining nerve fibers terminate in the superior colliculus in the midbrain. This is a subcortical visual pathway that is referred to as the retino-collicular pathway. The superior colliculus is an important neural stimulation for spatial awareness and movement. Gerald Schneider in 1969 at the Massachusetts Institute of Technology found evidence of the importance of the colliculus in studies of hamsters.3 Those animals with cortical lesions could not identify visual subjects. This involved damage to the occipitotemporal pathway, which was affecting the “what” pathway. Hamsters with collicular lesions exhibited reduced ability to orient toward the stimulus and their motor system was impaired. They could not move and acted like they were blind. This superior collicular injury affected the subcortical feedback to the occipito-parietal system and was affecting the “where” pathway. As I mentioned earlier, there is strong cross-talk between subcortical and cortical structures. The superior and inferior colliculi receive input from the visual and auditory pathways and use it to develop a representation of where objects are in space and to generate eye movements to attend to these objects. The neurons in the retino-collicular pathway are almost fully myelinated by 3 months after birth.4 The superior colliculus has a virtually normal adult pattern of neuronal lamination even before birth, in preparation for receiving retinal axons. The retino-collicular pathway is almost fully operational at birth. This pathway allows the infant to have visually directed actions in the first few months of life. This pathway is sometimes referred to as the “ambient system.” Ambient means surrounding on all sides. This retino-collicular system gets its feed from the retinal cells in the peripheral retina. Posner states that this pathway is called ambient because the visuomotor behaviors it produces are directed to the global properties, as converse to their fine details.4 The newborn infant looks at the outline of mother’s face rather than the finite details of her face like her nose and mouth. This allows the infant to receive visual stimulation from its peripheral visual field and to turn its head or eyes to the object of interest. The M cell pathway is sometimes referred to as the ambient system. The P cell pathway is concerned with fine details and the M cell pathway is concerned with global orientation. The neural development of the retino-geniculo cortical pathway, particularly of the P cell subsystem is slower in development. This system is often referred to as the “focal system.” The fovea in the retina is slow to mature and the optic nerve fibers innervating the dorsal lateral geniculate body (dLGN) are not fully myelinated. The dLGN is not fully formed and the visual cortex is not completely developed. These visual systems do not reach full operation until about 2 years of age.4 Thus, the infant is unable to attend to fine details early in life and the retino-collicular pathway is the dominant visual pathway until the child is about 2 years old.

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Massive innervations remain between cortical and midbrain structures. These two structures are constantly communicating in order to plan coordinated actions. Most of our experiences in the real world involve information from many different modalities. We plan our actions by receiving information from the visual, vestibular, auditory, and somatosensory modalities. In order for the visual process to function effectively, it must have normal ocular structure and the more than 30 brain regions that process the visual information must be fully operational. Any neurological injury such as traumatic brain injury, stroke, or CO poisoning would adversely affect the entire visual system. The visual system would then be unable to integrate visual information with other modalities like hearing, tactual information, and motor movement.

27.3 VISUAL MIDLINE SHIFT SYNDROME (VMSS) 27.3.1 SYMPTOMS OF VMSS This syndrome is caused by neurological trauma or CO poisoning to the retinocollicular pathway in the midbrain. This ambient system gets its feed from the peripheral retinal neurons. This system organizes spatial information from the visual, kinesthetic, proprioceptive, and vestibular systems. When there is a mismatch of sensory information coming to the midbrain from the proprioceptive, vestibular, and tactile systems, it affects a person’s perception of space. When this mismatch occurs, the ambient visual system steps in and makes adjustments to alter space perception so that the body can maintain its balance. The reason that this midbrain is so important is that it gathers information from our sensorimotor system to organize balance, posture, and movement. Essentially, the midbrain is responsible for keeping our posture and letting us know our internal concepts of space. This midbrain functions as a platform by which higher perceptual processing in the parietal lobe begins to organize. We know there is direct communication between this spatial collicular subsystem and the parietal lobe spatial system. Once the midbrain spatial system communicates with the parietal lobe spatial system, it in turn organizes sensory information going to the temporal lobe. In other words, the ambient system in the midbrain organizes spatial information so the focal system can function efficiently. The “where” visual system must be intact before the “what” visual system can function. We must know where we are before we know what we are looking at. In the case of CO poisoning, stroke or traumatic brain injury (diffuse axonal injuries), the sensorimotor information coming from the right side of the body may be different from that coming from the left side of the body. This is mismatched information and the injured patient may feel like the midline of his body is off to one side. This person is off balance and may place more weight on one side of his body to maintain balance. The ambient spatial visual system can change its understanding of space and equalizes the sensorimotor information coming in from the muscles, joints, and inner ear. Thus, the ambient system recreates space so the patient’s balance is restored. The symptoms of CO poisoning are varied and numerous. Penney in 2000 presented a study of CO-symptoms in the book Carbon Monoxide Toxicity (pp. 408–413).5 In it, data were obtained by e-mail over a period from late 1997 through early 1999.

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Sixty-six correspondents indicated they had sustained chronic CO exposure, that is, CO exposure lasting 24 h or more. The symptoms are seen in Table 27.1. The total number of symptoms is 93. Of those symptoms, 31 are common to VMSS. The bolded symptoms in Table 27.1 are directly connected to VMSS.

TABLE 27.1 Symptoms Noted During Exposure to Carbon Monoxide Symptoms

Symptoms

Symptoms

Agitation Anxiety Apathy Appetite loss Ataxia Attention, loss Back pains Balance problems Body ache Bronchitis Chest tightness/pain Choking Chronic fatigue Concentration problems Confusion Constipation Coolness Coordination Problems Cough, spells Cramps Depression Diaphragm pain Diarrhea Disorientation Dizziness Drop things Dysarthria Ear problems Emotional problems Energy level Extremities cold Eye pain/ache Fatigue Fibromyalgia

Flu-like symptom Flushed Forgetful Gastrointestinal problems Hair loss Hallucinations Handwriting problems Headache Hearing problems Hypertension Hypoglycemia Ill, violently In fog Incontinence Insomnia Iron level low Irritability Learning problems Lethargy Libido loss Lightheadedness Lips red Liver pain Memory loss Mood changes Moodiness Muscle ache/pain Nausea Neck pain Nerve deafness Numbness Palpitations Panic attack Paralysis Parathesias

Personality change Pressure in head Shortness of breath Seasickness/Motion sickness Seizure Shoulder pain Sick feeling Sinusitis Skin, cherry red Skin, dryness Sleep problems Sleepiness Smile, convulsive Speaking problems Spelling problems Suicidal Sweats Syncope, partial/complete Tachycardia Throat, burning sore Tingling legs/arms Tingling lips Tinnitus Tiredness Tongue, thickened Tremor Twitching fingers Vertigo Vision problems Vomiting Walk, inability to Weakness Weight loss Word-finding problems

Source: From Study A, Penney, D.G., Carbon Monoxide Toxicity, D.G. Penney, ed., CRC Press, 2000.

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TABLE 27.2 Post-traumatic Midline Shift Syndrome 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25.

Balance problems Bumps into doors, walls, and furniture Walks into other family members while walking with them Trips on stairs and must hold on to the handrail Busy patterns in the carpet, tile, or wallpaper are uncomfortable to look at Very nervous when around crowds because of excessive crowd movement and noise Trouble finding objects on shelves of supermarket or department stores; gets lost in the stores Misplaces objects like keys, glasses, wallet that are located right in front of them Drops things and tends to knock things over when using either hand. Hits their teeth when drinking out of a glass. Hits lip with eating utensils Handwriting has become illegible Must look at their hands to type on the computer keyboard Trouble driving. Must use excessive concentration in order to stay within the lines of the road Must turn their entire body to see cars coming from their peripheral field. Peripheral moving cars startle them Trouble judging speed and position of other cars. Trouble changing lanes Must take two or three tries to park the car within the parking space. Hits curbs when making a turn More trouble driving at night. Bright car headlights confuse them. Tendency to get lost while driving and often misses turns Photophobia (light sensitive) to outdoor and fluorescent lighting. Bright lights stimulate headaches. Banks of fluorescent lights in large stores and supermarkets are very bothersome Neck, shoulder, back, hip, and foot pain. Chiropractic, massage therapy, physical therapy only relieves symptoms for one day or less Loses place while reading. Words overlap and move on the page. Must reread a lot and often uses finger or a straight edge to follow the line of print Peripheral hallucinations like shadows out to the side of vision and when they look to the side nothing is there Ringing in ears, ears feel blocked, and trouble hearing. Background noise like the sound of the television makes it difficult to talk on the telephone Not able to listen to radio or hold a conversation while driving. Trouble with multitasks of any kind Dizziness when they stand up quickly or sit up from a lying down position Trouble sleeping Memory problems

This author has diagnosed and treated approximately 1500 patients with this VMSS. Table 27.2 lists the most common symptoms of VMSS.

27.3.2 CLINICAL TESTING FOR VMSS The patient is tested in the sitting and standing position. He is instructed to position his head and eyes in a straight-ahead position. A pen is held vertically 18 in. in front of him in front of his right shoulder. The pen is moved in front of his facial plane in

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a parallel pattern from the right shoulder toward the left. The patient is asked to state when the pen appears to be directly in front of his nose as he follows the pen with only eye movements. The test is then repeated by moving the pen from the left shoulder toward the right. The examiner should be seated or standing at random off to the left or right side at approximately a 30◦ angle to the patient in order to lesson the influence of the subject’s response relative to the examiner’s position. Motor evaluation of VMSS is very important in assessing the patient’s posture and movement. The patient is instructed to walk down a normal hallway and ask which foot he is placing more pressure on the floor. While the patient is walking, note if his shoulders are level or if one shoulder is tilted downward. The next motor evaluation should be directed to the position of the patient’s feet. Visual midline shift will usually show patients walking on the temporal or outside edges of one or both feet. Direction of walking is the next motor evaluation. The patient is instructed to walk down the hallway without trying to stay in the center of the hallway. Use the following command, “Do not try to stay in the middle of the hallway. Just float down the hallway, be aware of the walls and tell me if you are going to the right or left side of the hallway.” VMSS patients have an unequal gait and place more pressure on one foot. Often these patients have a moderate to severe shoulder tilt. The foot posture is almost always abnormal and the direction of walk is rarely straight.

27.4 TREATMENT OF VMSS Patients with symptoms of VMSS often report them to eye care professionals, that is, optometrists and ophthalmologists. Eye care professionals often tell them their problems are not in their eyes and that their eyes appear to be healthy. Patients with stroke, traumatic brain injury and CO poisoning often experience anxiety. In many instances these patients are referred to psychologists or psychiatrists in an attempt to treat their anxiety. The referral for mental treatment is sometimes based on a diagnosis of visual hysteria. The psychiatrist or psychologist may not recognize that many of these patients are suffering from syndromes affecting the visual process in the brain. In the early acute medical setting of CO injury the eye care is typically ophthalmological. In the patients who have survived brain injury, the emphasis is on the immediate effects of the trauma with an evaluation of the patient’s ocular health. Neuro-ophthalmologists address the neurological integrity of the visual system and will order tests to localize injury. Dr. Gianutsos, a research professor of Psychiatry at New York University Medical Center, states that in the United States ophthalmologists are rarely trained, experienced, or interested in visual system rehabilitation or function.6 She indicates that an increasing number of optometrists have experience and interest in rehabilitation which represents a natural extension of the emphasis within optometry on visual function and training.7 It is this author’s experience that optometrists are the logical eye professionals to treat VMSS. Optometrists with an interest in brain injury rehabilitation often use standard vision therapy techniques to treat brain-injured patients. While these

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techniques are often helpful, the treatment is mostly concerned with eye movement and eye focusing procedures. VMSS is a brain problem that relates to body movement and body positioning. Visual therapy techniques do not address the spatial and balance symptoms of the syndrome. The treatment of VMSS with yoked prism was developed by William Padula in 1988. Dr. Padula explains the syndrome and treatment very well in his many publications.8−11 He discovered the syndrome by studying the research of Trevarthen,12 who studied primates at Oxford University, England. He developed a concept that the ambient visual system organizes space and sends information to cells in the higher brain. Dr. Padula found the use of yoked prisms could rebalance the ambient visual process. The prism changes the organization of space. The yoked prism is a wedge of glass or plastic that shifts the image of an object. The patient with VMSS has a distortion of space and the yoked prism will rebalance the ambient visual process. The prism shifts the midline in the direction where it belongs. The prism will change the patient’s posture and weight bearing to equalize his gait. The prism redirects the concept of midline to enable the injured patient to have better posture and movement. The prism is introduced to the patient in small increments and the midline test is readministered. The prism is added in the opposite direction to the midline shift until the prism neutralizes the shift. Motor evaluation with the yoked prism in place is a very important step in refining the power of the yoked prism. When the correct prism power is used, the patients’ gait will be equal, the foot and shoulder posture will be normal and the walk will be straight. Treatment with yoked prisms should be undertaken as soon as possible after the neurological injury. The other disciplines that are necessary to rehabilitate the injured patients rely on the patient’s midline treatment. For instance, cognitive therapy is not as effective if the patients reading ability is compromised by the VMSS. Neuropsychological treatment is not effective if the patients’ visual, auditory, and spatial abilities are not functioning properly. Physiatry pain management is not as effective in treating joint and muscle pain when the posture is not stabilized by the yoked prism. Neuro-otological treatment is also hampered by VMSS when there is a mismatch between the visual and auditory systems. Psychiatry treatment is also affected when the patient is hampered by spatial and peripheral hallucination symptoms. Vocation rehabilitation specialists are more successful in their recommendations when the injured patient has good reading and movement skills.

27.5 REHABILITATIVE AND SUPPLEMENTARY CONSIDERATIONS A variety of allied health care professionals are necessary in the rehabilitation of the CO-poisoned patient. Other disciplines find that yoked prism treatment is extremely beneficial to the patient with midbrain injury. They usually recommend to the patient that they see a neuro-optometrist who is qualified in the diagnosis of CO poisoning and treatment with yoked prism lenses. They generally prefer that the patient be treated with the lenses before thy start their rehabilitative specialty.

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In the next few pages I have included comment from other treating specialists. These include James M. Gracey, rehabilitative consultant and therapist; Timothy O. Hall, physiatrist; Susan Gawey-Apgar, speech and language pathologist; Steven Stockdale, clinical psychologist; Pat McKenna, occupational therapist; and Dennis A. Helffenstein, a neuropsychologist. James M. Gracey: A large percentage of my active caseload of more than 250 patients involves brain injury from trauma or CO exposure. We have been providing rehabilitation and life care planning services for 40 years (see another chapter in this book). One of the most common and pervasive symptoms, which we observe, involves visual dysfunction. Table 27.3 shows the problems patients regularly report. See Chapter 26. The above problems tend to persist if left untreated, often leading to a further reduction of home, work, and community functioning. Such patients are referred to a qualified neuro-optometrist for evaluation and treatment. The combination of special glasses (yoked prism lenses) and monitoring often results in resolution (or near resolution) of the problems, thus freeing the patient to focus on the return to work or school. Such treatment is vital in assisting patients to reengage in their activities of daily living and work. James M. Gracey, EdD, CRC, CLCP Rehabilitation Consultant and Therapist Certified Life Care Planner 1660 S. Albion Street #1010 Denver, Colorado 80223 Timothy O. Hall: While combining the fields of neurology, orthopedics, and occupational medicine, physiatry provides a unique perspective in medicine. This is of great importance in the management of brain injury. The multidisciplinary approach necessary to care for these patients is often managed by physical medicine and rehabilitation. By incorporating various disciplines, a full range of symptoms can be addressed and treated.

TABLE 27.3 Visual System Dysfunction Related Problems • • • • • • • • •

Dexterity, poor handwriting Balance, dizziness, tripping Reading, poor reading comprehension, moving lines/letters on page Photophobia to all kinds of lighting Tracking, blurriness, depth perception Driving/veering to the left or right/night driving Eye discomfort, fatigue, related headaches Nervousness in crowds Losing/misplacing common items

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In the clinical management of head injury patients over the past 17 years, I have learned the critical role played by appropriate treatment of midline shift syndrome and other visual sequelae of brain injury. Many patients present with a complex constellation of symptoms that can be overwhelming in the context of diagnoses and treatment. Often these symptoms can be better understood and more appropriately treated by understanding the visual consequences of brain injury. This includes a connection between postural distortions and chronic myofacial pain, as well as musculoskeletal headache. It is critical for successful outcomes of these complex presentations to manage the visual situation in order to increase the likelihood of success in other areas. Usually one of my first interventions in patient evaluation involves visual testing. Treatment of visual distortions is an integral part of the team put together to manage closed head injury. Although controversial, it has been my experience that the management of midline shift and other visual disturbances in this population is critical for success. In my practice, treatment failures that come my way, often years after injury, are most likely to improve by not only instituting a multidisciplinary approach to their treatment but by including management of undiagnosed visual dysfunction. Timothy O. Hall, MD 559 E. Pikes Peak Avenue, Suite 100 Colorado Springs, Colorado 80903 Susan Gawey-Apgar: Over the past 15 years my practice has consisted of mild traumatic brain injured (MTBI) and CO-poisoned patients who have been referred by a variety of sources. It has been my experience with this population that patients with MTBI and CO trauma suffer from a variety of physical, cognitive, and emotional difficulties that affect their day-to-day activities. Typically, when a patient is referred to my clinic for treatment, a one page document is generated identifying them and providing minimal medical information. It is my job within the first hour with a patient to ask a variety of questions that will help with the initial phase of treatment. The initial phase of treatment is essential for MTBI and CO patients because it is the most critical to the patients overall care. By the time the patient is referred for cognitive rehabilitation, they feel hopeless and depressed because their previous care has only focused on the physical aspects of their injury. The first phase of treatment (there are typically three phases to a patients’program) consists of analyzing the symptom checklist (Table 27.4). It is of interest that the checklist for cognitive symptomatology is closely related to the symptoms of posttrauma midline shift patients. Post-trauma midline shift syndrome patients and cognitive disorder patients, have difficulties processing visual data, have poor reading scanning skills, and show a slow speed of processing, handwriting problems, attentional difficulties, and multitasking problems. The patient, therefore, benefits from seeing a neuro-optometrist during phase one of outpatient rehabilitation. Having both specialties working together maximizes the effects of cognitive intervention and support the patient with state of the art medical care.

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TABLE 27.4 Symptom Checklist Cognitive problems • Attention and concentration problems • Short-term memory loss • Trouble remembering old things • Word finding • Understanding what is said • Understanding what is read • Making decisions or solving problems • Slower speed of thinking • Getting lost or disoriented • Trouble juggling several things at once • Disorganized or confused thinking • Stuttering or slurring Physical symptoms • • • • •

Dizziness Coordination of hands, feet, or legs Ringing in the ears Fatigue Jaw pain

Emotional symptoms • • • • • • • •

Feelings of sadness or depression Crying spells Suicidal feelings Increased or decreased emotion Low motivation Change in sex drive Irritable and easily frustrated Feelings of anxiety or fear

Post traumatic stress syndrome (PTSD) • • • • • • •

Recurrent and intrusive thoughts about the accident Nightmares Flashbacks Anxiety or panic while driving Hypervigilance Fear Does this affect social activities or relationships

CO-poisoned patients like those with MTBI, clearly demonstrate the same profile on both the cognitive symptom checklist and the VMSS check list (see Table 27.2). Key to rehabilitation is approaching the patient holistically in order to promote the maximum rate of medical recovery.

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Susan Gawey-Apgar, MS, CCC-SLP Speech and Language Pathologist Neuro-Cognitive Therapist 208 North Corona Street Colorado Springs, Colorado 80903 Steven Stockdale: Electroencephalogram (EEG) neurofeedback has been used in the treatment of traumatic brain injury, utilizing operant conditioning to normalize brain wave patterns. Many of the symptoms of MTBI, which include physical symptoms, cognitive symptoms, and psychological-emotional symptoms, correlate with the symptoms of post-trauma midline shift syndrome. Physical symptoms of MTBI include sensitivity to noise, tinnitus, dizziness, fatigue, blurred vision, and headaches. This symptom group overlaps with symptoms from post-trauma midline shift syndrome. Many patients that come in for evaluation of MTBI have significant visual problems that were not there previous to their brain injury. In those cases, they are referred for evaluation for post-trauma midline shift syndrome. This syndrome can be corrected by yoked prism lenses. Although pre- and postsymptom changes in vision have been noted through neurofeedback alone, correcting the midline shift problems greatly enhances the outcome of the neurofeedback treatment. Steven Stockdale, PhD Licensed Clinical Psychologist EEG Neurofeedback Specialist 2132 North Nevada Avenue Colorado Springs, Colorado 80907 Pat McKenna: When evaluating a person as an occupational therapist (OT), we need to look at the entire person with regard to what may be affecting them and their ability to perform tasks. Thus, we need to look at the physical, cognitive, sensory perceptual, emotional, and psychological factors that might contribute to the person’s difficulties. When a person has sustained a traumatic injury which may affect the head or neck, this can have caused damage to not only the joints and muscles, but, also to the sensory pathways that can include, not only those that contribute to the sensation of pain, but also those of the sensory perceptual system. This is a less well-known system, but it is at the core of our abilities to function. This includes the proprioceptive and kinesthetic systems as well as the vestibular, touch, olfactory, auditory, and visual systems. It is these systems which work together or individually to provide us with information regarding what is going on around us and happening to us that we need to know, so we can respond appropriately and effectively. It is our safety net. It is what allows us to move through the world without falling down, to reach, to get, or replace objects that we need and even feeding ourselves. It is the system that lets us know we have touched something hot and that we need to move our hand away fast. It lets us know, as we walk down stairs, where to place our feet, or walk in the mountains without falling over on all the rocks and uneven ground. It allows us to learn to drive down

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a highway and stay in the correct lane and to be able to stay out of the way of traffic or other things that are coming at us. Or, if playing ball, to reach appropriately in order to catch a ball. It is our silent sentry and helper that allows us to do virtually everything we do. This is not to downplay the importance of the joints and muscles and the nerves that cause them to move. These are things we are all more familiar with and which are visually very obvious if they are injured. A broken leg would not hold you up. A torn muscle would not let the body parts move correctly, if at all. These, we have all seen and understand. The sensory perceptual system, however, is essential for all of these things to work. If anyone has gone to an amusement park fun house, it is these senses that they are “playing with,” You look at a wavy mirror and it distorts your perception of yourself and your surroundings. You walk on the moving floor that goes up and down and very soon, you want “out of there,” sometimes becoming nauseous, but typically were tense and nervous because you could not trust your senses and were afraid you’d fall. The ability to be able to automatically trust these senses has been built from babyhood. At first the baby is just waving its hands around. Then, as this continues, pathways develop that direct the muscles to respond appropriately to the need, the feel, the desire of a certain response to occur. The baby can now consistently get food from the plate to the mouth. They start to try to walk and keep falling. But soon, they are stable and off they go running. It is this pattern of development that has gone on in everything we do. To go up and down stairs without watching where our feet go; to take a hike in the mountains and not pay attention to the minor unevenness of the surfaces we are walking over. When a person has a traumatic whiplash or brain injury, these pathways can be damaged. Our visual system is one of our major sensory systems that these pathways have learned and depend upon, and it is one vulnerable to injury when the head is struck or shaken or suffers a lack of oxygen. Now, all of a sudden the information that the body has trusted to help to determine “where it is in space,” where and how it needs to move to keep it safe and to perform a task safely, cannot be trusted. The person tries to walk down a flight of stairs, but finds herself losing her balance and falling. Where she automatically thought the foot should go, was not correct. They reach for a glass and knocked it over. They find themselves getting a traffic ticket for driving with their tires to the left of the centerline. They find themselves getting a headache or becoming nauseated when they try to read a newspaper—and even worse, when trying to look at the computer monitor. Often these problems have been subtle enough that the person is not fully aware of what is wrong. They often just feel something is weird, and they’re more tired and have more headaches. They think they must just be getting awkward. Very often they do not even mention such things to their doctors. They are embarrassed and they do not realize it could have had anything to do with their head injury. The role of the OT is to look for any problems that might be present that are affecting function. Since the OT is typically having the person do these more functional tasks in a more real life type of setting, they have the opportunity to observe these things happening and to make an association to their head injury. Once these

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types of problems have been observed and a “red flag” is raised, the OT can do some simple, more specific testing—basic optometric tests to be more clear that, “Yes, indeed, this person needs to be seen by an optometrist knowledgeable about the types of problems that can occur following head injury.” Then, on the basis of the results of the optometrist’s evaluation and the effects of the treatment, and if needed in some cases, can assist the optometrist with visual training exercises. It is usually a good collaboration, as both health care professionals are strongly focused on functional outcomes. From the perspective of an OT, this is the type of evaluation that needs to be done very early after an injury. Often, headaches and neck pain are present from the accident. If the person is tense from his inability to trust that he would not fall, and so forth, any therapy to try to heal or reduce muscle tension in the neck will not be successful. And, with constant pain, headache, nausea and a feeling of being unsafe moving about … depression is hard to avoid. Unfortunately, these are not problems that are typically looked for early on. If not addressed early, the person will not heal well and the injuries become more entrenched and harder to deal with effectively as time passes. Since the visual system is at the heart of so much of what we depend upon to make our way through life, when it is not functioning appropriately, it affects the person’s ability to do many of his basic activities of daily living and work. Driving, shopping, taking the laundry downstairs, and so forth, all become tasks with which the person now feels tense and uneasy … sometimes fearful. Thus, they begin to avoid doing them. Since much of a person’s world of work also depends upon one’s vision, this becomes difficult, if not impossible for the person to do accurately and productively. As an OT, these things are issues that we need to help the person deal with. Thus, recognizing the potential problem and getting them to an optometrist who can appropriately diagnose and treat it is essential, if we are to help that person return successfully to their previous life, or, at the very least, to their highest level of function that is possible. One of the treatments that can often be seen to provide dramatic results is use of yoked prism lenses. When patients are properly diagnosed and appropriately fitted with these lenses, we typically see a dramatic response. Patients comment to us that they “couldn’t believe the difference in how they felt virtually the minute they put them on.” They could actually “see” the steps and feel like, “Wow! I can relax now … I don’t feel like I might fall all the time.” And they are not knocking things over when they reach for them. They’re finding that they can read longer. Granted, not all things are immediately perfect, but the change is so substantial that now, as a therapist, I can begin to work better with them on trying to remediate the problems that are interfering with their ability to do the things they used to do without so much frustration. Pat McKenna, Occupational Therapist, Registered Starting Point 8745 West Fourteenth Avenue, Suite 112 Lakewood, Colorado 80215 Dennis A. Helffenstein: As a neuropsychologist who specializes in evaluating and treating individuals with acquired brain injuries, I am familiar with the wide-range

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of vision problems they can and often do experience (see another chapter in this book). Indeed, a number of the tests, which I routinely administer as part of the test battery, identify and quantify those deficits. In many cases, the visual deficits lead to a significant functional impairment in a wide variety of day-to-day, leisure, academic, and work-related activities. However, as a rehabilitation neuropsychologist, I felt I had little to offer these patients. I would on some regular basis refer them for vision therapy, but even when treatment was successful, many of these people were left with profound visual deficits, which continued to limit their functioning. See Chapter 23. In the mid-1990s, I received neuro-optometric reports from James Georgis, OD. It was then that I was introduced to the term, “yoked prisms.” My patients had been referred to Dr. Georgis for evaluation and treatment at or around the same time that I was evaluating them. Without exception, each of the patients who Dr. Georgis treated with yoked prisms returned to me reporting tremendous improvement in their visual function. More importantly, they were experiencing improved functioning in their driving, reading, work and leisure activities, and so many other aspects of their day-to-day lives. Frequently, I have had the opportunity to retest individuals after they began wearing yoked prisms. On retesting, I routinely administer a number of the vision tests with their yoked prisms on and then with the yoked prisms off. I was surprised to find that in almost all cases the deficit identified by the test with their prisms off is not apparent in test performance when the patient is wearing prism glasses. The most notable improvements were seen on tests of visual scanning and visual inattention. I would also note that in addition to improved visual function, my patients often report a reduction in the frequency and severity of headaches, improved balance and gait, and a reduction in cervical and spinal pain (usually because their chiropractic adjustments are now “holding” better) once they began wearing yoked prisms. In my experience, it is extremely rare to find a treatment modality that has such an immediate positive impact on so many aspects of a patient’s functioning. I now routinely screen for post-traumatic vision syndrome and also administer the Padula visual midline screening test as part of my test battery. When I identify a visual midline shift or the patient is reporting visual symptoms suggestive of a hemispatial inattention or visual midline shift, I consider the use of yoked prisms as a treatment possibility. I would like to extend to Dr. Georgis my thanks for his compassionate and successful treatment of so many of my patients. Dennis A. Helffenstein, PhD, CRC. Licensed Clinical Psychologist Colorado License #1484 Certified Rehabilitation Counselor #00001338 Diplomate, American Board of Vocational Experts #64073 Certified, Health Service Provider in Psychology National Register #41454 3545 American Drive Colorado Springs, Colorado 80917

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27.6 CASE STUDY Ms. SL was a 50-year-old woman referred for VMSS evaluation by her Coloradobased neuropsychologist. She reported that she experienced a chronic (long-term, lower-level) exposure to CO between August 1988 and early November 2000. The exposure was caused by defects in the construction of her furnace ventilation system. The vent for her furnace was too small. She also noted that her house was “extremely tight,” that is, it took 8 h for the air to completely change in her home. This was a problem because the furnace was a “natural draft” furnace, taking oxygen from inside the room as opposed to air from an outdoor air source. This tended to create a negative pressure inside the home, which resulted in downdrafting. That is, the home was taking air in through the furnace vent. This caused exhaust from the furnace to migrate into the living area. This also resulted in incomplete combustion of the fuel gas, which produced CO as well as soot (elemental carbon). Ms. SL noted that from the time she moved into the home in August 1988 she had a problem with black soot build-up around the home. For example, she noted that she had a white carpet in the home which she could “never keep clean.” Negative pressure was present in the home, particularly when there were fans running inside the home (e.g., bathroom fan, range hood exhaust fan, or when the clothes dryer was operating). It was noted that in the winter, downdrafting was more pronounced. There was also a concern that her water heater may have been vented improperly and may have also been downdrafting. A reconstruction of how the exposure occurred was preformed by a local expert who specializes in CO-induced injuries. It was found that the furnace was producing high levels of CO in the range of 1200–1300 ppm, especially during start-up. A significant amount of corrosion was noted on the furnace suggesting the presence of CO. Ms. SL’s exposure occurred on a daily basis during the winter months when the furnace was operating. She experienced a variety of symptoms consistent with CO poisoning. These symptoms gradually became worse overtime. She also noted that during the past summer that she had spent out of her home, she did notice an improvement in her symptoms. Once the problem was identified, she had both her furnace and water heater replaced. This occurred in early November of 2000. Ms. SL noted that her symptoms did begin to abate to some degree when the exposure ceased. Ms. SL experienced multiple symptoms during the exposure consistent with CO poisoning. She reported the following symptoms to her neuropsychologist in December 2000. These involved multiple “flu-like” symptoms, including nausea, headache, fatigue/lethargy, and diarrhea. Other physical symptoms included chest pain/tightness, cough, dizziness, lightheadedness, a metallic taste in her mouth, occasional episodes of vertigo, sleepiness, intermittent tinnitus, restless sleep, and multiple chemical sensitivity. Motorically, she noted motor weakness, motor incoordination, muscle spasms and tremors, tingling and numbness in her hands, phonophobia (noise sensitivity), and balance problems. Visually, she noted difficulties with blurry vision, photophobia (light sensitivity), double vision, and fluctuation in her visual acuity, perceiving flashing lights or black dots, and difficulties with depth perception. Cognitively, she noticed difficulties with attention and concentration, short-term memory, mental confusion, slowed speed of mental processing, multitasking, and

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more frequent blatant errors in her work. From an emotional and psychological standpoint, she noted depression, anxiety, and irritability. Ms. SL noted that when she would spend an extended period of time in the home (e.g., over a weekend without leaving), her symptoms would gradually increase. She noted that she would frequently “call in sick” on Mondays. Educational History: Ms. SL graduated from high school, college, and graduate school with an approximated grade average of 3.75. She was currently taking another course in a related field. She noted the new course work was quite difficult for her and she had to work much harder to obtain good grades. She was currently working as a college professor at a community college. She served as department chair for approximately 5 years. She was carrying a full teaching course load, was writing extensively, and developing extensive instructional materials. When she moved into her home in 1998 she began to notice a “gradual change for the worse.” She began to realize, however, that she was working longer and harder hours in order to accomplish the same amount of work. By 1996 she had to give up some of her outside consulting contracts, as she was unable to manage both the consulting and teaching. By 1998, she resigned her position as department chair. Her student ratings (i.e., the ratings that the students give her upon completion of a course) had deteriorated notably. She noted that it was in approximately 1996 that she began to note a significant deterioration of her physical abilities. Whenever she would leave her home for a significant period of time she would begin to feel better physically. She felt that she was using virtually 100% of her available energy for her work and thus had no social or recreational life. Neuropsychological evaluation stated Ms. SL had developed a variety of vision problems. She noted problems with double vision, particularly when she was fatigued. Her eyes were slow to focus, suggesting problems with accommodation. She had problems with depth perception such as judging distance. She noted that she tended to bump into things more frequently and veered off center when walking. She reported ongoing problems with photophobia (light sensitivity) for both sunlight and fluorescent light. She was aware of ongoing eye fatigue. Occasionally she would perceive motion in her peripheral visual field when there was nothing there. She complained of visual distortion in the left lower quadrant of her visual field. She noted that what she saw was rotated and appeared to pulsate. Neurological evaluation was conducted in July 1999. The neurologist identified the following symptoms which included: paresthesias, deficits in short-term memory, diminished mental sharpness, hand tremors, visual distortions, problems with distractibility, irritability, sleep disturbance, bladder incontinence, fatigue, balance problems, motor weakness in her arms and hands, decreased fine motor dexterity, blurred vision, headaches, and problems with verbal fluency. A Magnetic Resonance Imaging (MRI) and EEG were performed in September 1999. Both scans were determined to be within normal limits. Ms. SL underwent a comprehensive evaluation program at a nationally known medical clinic in March 2000. The fact of her CO poisoning had not yet been discovered when she was evaluated at the medical clinic. The physician and psychologists at the clinic identified a wide variety of symptoms consistent with CO poisoning as they conducted their individual evaluations. None of the clinic evaluators

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suspected CO poisoning and they were at a loss in explaining her numerous and wide variety of symptoms. On the basis of the fact that they could not identify a condition to account for her symptoms, the ultimate conclusion was that the majority of her problems related to emotional and psychological issues. In December 2000, a neuropsychological evaluation in Colorado correctly diagnosed her with chronic CO poisoning. The neuropsychologist recommended that a cognitive therapist work with Ms. SL using a restorative and compensatory strategy. He felt it would be helpful for the therapist to work with Ms. SL in developing strategies to compensate for her residual cognitive deficits. The neuropsychologist felt Ms. SL was experiencing emotional and psychological distress associated with the exposure. He felt she could benefit from individual psychotherapy for her feelings of depression, anxiety, and irritability. The neuropsychologist also felt Ms. SL would benefit from the use of an antidepressant medication in the select serotonin re-uptake inhibitor class (e.g., Celexa). He stated that the medications in this class were extremely helpful for individuals who have sustained organic injuries. The medications were recommended to help stabilize her moods, maximize her energy level, and frustration tolerance. The neuropsychological evaluation found vision problems consistent with VMSS owing to CO exposure. The neuropsychologist recommended further evaluation and treatment by a neuro-optometrist. In the course of the clinical interview with the neuropsychologist, Ms. SL reported ongoing problems with phonophobia (noise sensitivity). He recommended the use of noise attenuation earplugs. The neuropsychologist also recommended she consult with her primary care physician to assist her sleep patterns. He mentioned several options in this area like homeopathic sleep aids, antidepressant medications such as Trazadone or Ambien to help regulate her sleep. The neuropsychologist discussed Ms. SL’s long duration of exposure to CO. He suggested she consult with her physician regarding the beneficial effects of hyperbaric oxygen (HBO) treatment or normobaric oxygen therapy. The final recommendation of the neuropsychologist was to reduce Ms. SL’s workload in order to attend to the needed therapies. Neuropsychological re-evaluation (1 year) was conducted in December 2001. She continued to experience ongoing problems with dizziness. Her dizziness and ongoing visual disturbance continued to negatively affect her balance. She felt that her fine motor speed and dexterity remained less efficient and she did not note any functional improvements in these areas. She reported that her tactile sensitivity bilaterally was somewhat better. She noted ongoing problems with noise sensitivity and was unchanged from the time of the last neuropsychological examination. She continued to have difficulties filtering out background noises, suggesting ongoing problems with her auditory gating mechanism. She had seen some improvement in her stamina, but she still was bothered by fatigue. At the time of the original testing, Ms. SL reported multiple vision problems consistent with VMSS. At the 1 year re-evaluation she reported no improvement in these problems from the time of the original testing. She was evaluated by several ophthalmologists and one neuro-ophthalmologist at a large Midwestern university teaching eye center. Neither the general ophthalomogist nor the neuro-ophthalmologist found any problem nor could they offer any advice or recommendations. The neuroophthalmologist stated, “I can discover no organic explanation for the patient’s

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symptoms. I doubt that they are due to CO exposure.” As part of her visit to Colorado for her 1 year neuropsychological evaluation she was scheduled and referred by the neuropsychologist to undergo a thorough evaluation with a local neuro-optometrist, Dr. Georgis. With regards to her cognitive functioning, Ms. SL reported to Dr. Georgis some improvement in her concentration abilities, but noted these remained highly inconsistent. She lost and misplaced things more frequently and the new learning process was more difficult for her. She noted that she avoided reading whenever possible because it was difficult for her. At the time of neuropsychological retesting, Ms. SL noted ongoing problems with spatial disorientation and carried a compass in her car to help with spatial orientation. She acknowledged more feelings of anxiety and frustration regarding her ongoing physical and cognitive defects, and the limitations that those imposed. She was worried about her job status and future vocational potential. She still had some difficulty sleeping. She felt the Celexa had helped her get to sleep; however, she still had difficulty staying asleep. The Celexa had resolved her mood swings and her frustration, and stress tolerance had improved notably. Since the time of the original neuropsychological evaluation, Ms. SL had undergone six HBO treatments. She felt the treatment helped her think more clearly and the tactile sensitivity in her hands had improved. She felt her moods were more settled and she was less labile. Ms. SL had met her treatment goals and had been discharged by her psychotherapist. Ms. SL had reduced her teaching load since her prior neuropsychological evaluation. She noted she had to use 100% of her available energy to function in her reduced academic and teaching load. As part of the 1-year ongoing assessment of Ms. SL, the neuropsychologist gave a questionnaire to Ms. SL’s mother and two sisters. They reported Ms. SL had difficulty in balance, veering off center, judging distances, motor incoordination, penmanship less legible since the exposure, dropping the chalk while writing on the chalkboard, grabbing objects in her path while walking and shutting her eyes owing to dizziness. They noted Ms. SL complains of double vision and she hugged the curb while driving. They noted she squinted outside owing to photophobia and she had very low energy. After 1 year between neuropsychological tests, Ms. SL’s performance remained essentially the same on 24 of the neuropsychological test measures. She made notable gains on 17 of the neuropsychological test measures when compared to her prior testing according to the neuropsychologist. However, to some degree, some of the gains could be attributed to practice effect. When this variable was taken into account, Ms. SL’s current testing suggested that she was experiencing ongoing inefficiencies and inconsistencies in her sustained attention and concentration abilities. Dr. Georgis first saw Ms. SL in December 2001. She reported about her neuroophthalmology examination at the midwest university eye clinic. She said the neuroophthalmologist examined her for 5 min and diagnosed ovarian cancer. She noticed balance problems beginning about 1992. She was running into the walls in her hallway and would hit her drawers with her hip. Ms. SL had trouble with depth perception and she was unable to hit or catch a ball. She noticed she would stumble while walking and these symptoms increased slowly from 1988. Ms. SL was not comfortable around crowds of people. She would stand off to the side when attending a family

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gathering. The crowd noise was especially bothersome. She complained of having to use excessive concentration to drive a car. Her brother and sisters reported she tended to hug the yellow line. Her siblings could not carry on a conversation with her because she needed her entire concentration to drive a car. Ms. SL also reported four near car accidents because she was unable to recognize cars moving in her peripheral visual field. She also noticed seeing flashes and shadows in her peripheral field and when she looked to the side nothing was really there. Ms. SL noticed a smoky area in her visual field and the area would pulsate with her heartbeat. She complained of missing turns while driving and she misplaced her keys and they were visually in plain sight. Ms. SL reported tinnitus, noise sensitivity and that her ears felt blocked. She felt like she had trouble hearing and she had to turn the radio and TV up loud. Some vertigo was noted while in the prone position and she became very dizzy when she moved quickly. She also noted some carsickness when riding as a passenger in a moving car. Ms. SL reported her typing speed and accuracy had deteriorated and she tended to look at her hands while typing. Other hand–eye coordination problems were apparent such as dropping things and knocking over objects while cooking. She complained of severe photophobia especially while diving at night. Fluorescent lights bothered her at work and she tended to keep her home dark. The computer screen glare was also bothersome. Ms. SL noted reading was very difficult since her exposure. She used to enjoy reading, but reading was simply a struggle. She had to reread and tended to use her finger to follow the line of print. Ms. SL reported hip pain and her right heel had been very painful. A visual spatial evaluation found a moderate visual midline shift towards Ms. SL’s right side. Some body sway was noticed during her motor evaluation. Her gait was uneven with more pressure placed on her right foot. She walked on the temporal edge of both feet and walked toward her left side. Ms. SL was put on midline with a moderate degree of yoked prism. The prism equalized her gait, improved her foot posture, straightened her walk and eliminated her body sway. The prism improved Ms. SL’s ability to judge speed, movement, and position of cars moving within six lanes of moving traffic. Reading evaluation found the prism eliminated the word movement and word overlap. It also improved her ability to follow the line of print without using her finger. Photophobia evaluation found a glare control tint that reduced the glare from the computer screen. Yoked prisms were prescribed for distance and near use with a photochromic bifocal. A near glare control tint was prescribed for near and computer work in the classroom. A phone consultation was completed in March 2002, 2 12 months after receiving the yoked prism. Ms. SL stated, “Wow and thank you! Dr. Georgis has helped me the most, in the shortest period of time, than any other doctor.” She said she was able to walk 2 miles without her foot hurting. She no longer hit walls, dresser drawers, and did not stumble at all while walking. Ms. SL reported being more comfortable around crowds and her peripheral hallucinations had completely resolved. Ms. SL noted her driving had improved significantly. She was able to stay within the lines of the road without difficulty and she was able to see other cars within her peripheral field without difficulty. She was able to talk to her sister while driving the car and had not had any near accidents since receiving her prism. She reported her vestibular symptoms had improved a lot. Her noise sensitivity, ear blocking,

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lightheaded feeling in the prone position, dizziness, and motion sickness had completely resolved. Ms. SL noted her typing speed had increased and she no longer needed to look at her hands while typing. Her ability to grade papers on the computer was comfortable for up to 6 h and the glare from the computer screen was nonexistent. She reported her hand–eye coordination had improved and she did not spill as much while cooking. Ms. SL noted a big improvement in her photophobia especially while driving at night. She reported her reading had become pleasurable again. She no longer had to use her finger while reading. However, her reading volume had continued to be much less since her exposure. Ms. SL noticed her hip pain had completely resolved and she periodically had some discomfort in her right heel. Ms. SL was seen in Dr. Georgis’ office in June 2002, 6 months after receiving the yoked prism. She was wearing her yoked prism all of her waking hours and reported, “Fantastic Improvement” from her December 2001 evaluation. However, she had noticed some pain in her right foot in the last month. Her balance was good and she reported no trouble with crowd noise. She noted her tinnitus, dizziness, and lightheaded feeling in the prone position had completely resolved. Her hand–eye coordination was no longer a problem and the photophobia was totally controlled by the glare control prism. She noticed some problem with peripheral vision in the last month. Ms. SL said her reading was better but she was only reading when it was necessary. Another visual spatial evaluation found Ms. SL’s visual midline shift had completely resolved. Her gait was even and her walk was straight. Her balance was very good and there was no evidence of body sway. Her foot posture was normal. The yoked prism treatment was discontinued and Ms. SL was instructed to return if any of the prior symptoms reoccurred. About 8 months later in February 2003, Ms. SL contacted Dr. Georgis by telephone. She complained of falling three times when walking on uneven surfaces. She noticed crowd movement was bothersome and her peripheral hallucinations had returned. She noticed some difficulty judging position and speed of other cars while driving. She also reported some spatial confusion while driving and was missing turns. Ms. SL lost her glare control lenses and her photophobia had returned. She noticed her hand–eye coordination had regressed somewhat. She reported some dizziness, ear blocking, and trouble hearing around background noise. She was instructed to see Dr. Georgis as soon as possible and to see a neuro-otologist in Colorado. Ms. SL was seen by Dr. Georgis 5 months later in July 2003. She complained of the same symptoms that were reported in the February 2003 telephone consultation. She was unable to afford the consultation with the Colorado based neuro-otologist. Visual spatial evaluation found a moderate visual midline shift towards Ms. SL’s right side. The midline shift was a 20% increase over her February 2001 evaluation. The midline shift was corrected with yoked prism and Ms. SL was instructed to be re-evaluated in 6 months. Ms. SL was last seen in January 2004. She was wearing her yoked prism all of her waking hours. She reported good balance, good hand–eye coordination and no dizziness. She noted her photophobia was totally controlled by the glare control prism. Visual spatial evaluation found a 70% improvement in her visual midline shift.

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Her balance with the decreased prism was very good. Her foot posture was normal and her walk was straight. Dr. Georgis reduced her yoked prism by 70%. Ms. SL was seen in January 2004 by her Colorado-based neuropsychologist for a re-evaluation. She was currently using an antidepressant medication and it was working well to control her depression. She planned to wean herself off the antidepressant in the near future. Ms. SL continued to experience a variety of cognitive problems, which negatively impacted her day-to-day and work functioning. She had implemented multiple strategies to compensate for her residual deficits. She had been unable to identify a cognitive therapist in her area to provide direct cognitive rehabilitation. Ms. SL reported she continued to work a full load at the community college. The work required 100% of her available energy. Ms. SL was instructed to return to Dr. Georgis care on an as needed basis and she was last seen in November 2004.

27.7 CONCLUSION CO poisoning is a common health problem worldwide. Neurological damage to brain structures is a common occurrence. Approximately 30% of the neurological symptoms of CO poisoning are directly related to spatial awareness, balance, and movement. VMSS is a result of CO-induced injury to subcortical structures in the midbrain. These structures affect the injured person’s spatial awareness, balance, and movement. Yoked prism lenses modulate these subcortical structures through the highly sensory visual systems. The yoked prism treatment is effective immediately. The balance, movement, and spatial symptoms are eliminated. The prescription or power of the yoked prism lenses can generally be reduced gradually, dependent on the adaptability of the patient’s brain and the severity of the exposure.

References 1. World Health Organization. Carbon Monoxide Environmental Health Criteria 13. Published under the joint sponsorship of the United Nations Environment Program and WHO, Geneva, 1979. 2. Gazzaniga, M.S., Ivry, R.B., Mangun, G.R. Cognitive Neuroscience: The Biology of The Mind. WW Norton and Company, NY. 2nd ed., 2002. 3. Schneider, G.E. Two visual systems. Science, 1969, 163, 895–902. 4. Posner, M.I., Raichle, M.E. Images of the Mind. Sci. Am. Library, NY, 1994. 5. Penney, D.G. Chronic carbon monoxide poisoning. In Carbon Monoxide Toxicity, D.G. Penney, ed., CRC Press, 2000, pp. 393–418. 6. Gianutsos, R. Visual rehabilitation following acquired brain injury. In: Functional Visual Behavior: A Therapist’s Guide to Evaluation and Treatment Options, Michele Gentile, Editor, The American Occupational Therapy Association, Inc., Bethesda, MD, Chapt. 8, pg. 267, 1997. 7. Cohen, A.H., Rein, L.D. The effect of head trauma on the visual system: The doctor of optometry as a member of the rehabilitation team. J. Am. Optom. Assoc., 1992, 63, 530–536.

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8. Padula, W.V., Shapiro, J.B., Jasin, P. Head injury causing post trauma vision syndrome. N. Engl. J. Optometry, Dec/Winter, 1998, 16–21. 9. Padula, W.V., Argyris, S. Post-trauma vision syndrome and visual midline shift syndrome. J. Neurol.Rehabil. , 6, 1996, 165–171. 10. Padula, W.V. Neuro-Optometric Rehabilitation, Publ. by Optometric Extension Program Foundation, Inc., Santa Ana, CA, 1st ed., 1998. Chapt. 14, p. 194, Visual midline shift syndrome. 11. Connor, M., Padula, W. Visual rehabilitation of the neurologically involved person. In Functional Visual Behavior: A Therapist’s Guide to Evaluation and Treatment Options, Michele Gentile, Editor, The American Occupational Therapy Association, Inc., Bethesda, MD, Chapt. 9, pg. 295, 1997. 12. Trevarthen, C.B., Sperry, R.W. Perceptual unity of the ambient visual field in human commissurotomy patients. Brain, 1973, 96: 547–570.

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Firefighters and Carbon Monoxide Kevin J. Reilly, Jr., Frank Ricci, and David Cone

CONTENTS 28.1 Firefighter Fatalities Resulting From Suppression . . . . . . . . . . . . . . . . . . . . . . . . 28.2 Postfire and Overhaul . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28.3 Workplace/Industry Carbon Monoxide Standards . . . . . . . . . . . . . . . . . . . . . . . . 28.4 Investigation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28.5 Emergency Smoke Escape Devices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28.6 Emergency Department Screening . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28.7 Lethal Gas Combinations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28.8 Prevention and Awareness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28.9 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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Carbon monoxide (CO) is produced from the incomplete combustion of carbon-based fuels. It is found at every structure fire and is present most often when an appliance that uses combustion malfunctions. Firefighting as an occupation carries an extremely high risk of exposure to CO, owing to fire suppression, postfire overhaul, and response to routine CO alarm calls. Few other occupations involve the potential of such frequent exposure to CO. The fire department often provides the first emergency medical care to victims who have been exposed to CO, and is the first link in the emergency medical service (EMS) system. This chapter explores how CO impacts this profession and the civilians who are protected by it. We will bring to light some of the latest technology available for home and professional use, and will explore the gap between the medical community and the fire service. The first author of this chapter has written a recent review of this topic.1

28.1 FIREFIGHTER FATALITIES RESULTING FROM SUPPRESSION Smoke can have over 2000 toxic chemicals in it, yet after a review of 105 autopsies, the results usually indicate CO, hydrogen chloride, acrolein, soot, and hydrogen cyanide (HCN) as the leading contributing causes of death.2 In the 1990s, 63% of all nonheart attack deaths inside structure fires were the result of smoke inhalation.3 CO 643

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is considered one of the greatest threats in the fire service and is referred to as the “silent killer” in smoke.4 Even many professionals are surprised to learn that burns and crush injuries are overshadowed in number by smoke inhalation. In a National Fire Protection Association (NFPA) report that examined fire fatalities from 1978 to 1999, smoke inhalation was the leading cause of death for nonheart attacks each year. Physicians should be aware that a firefighter who has CO poisoning will likely have other toxic gases in his blood stream. Emergency department (ED) physicians should test for as many products of combustion as technology allows in smoke inhalation victims. Heart attacks account for over 44% of firefighter line-of-duty deaths. There are many contributing factors to these heart attacks, such as a pre-existing heart condition; however, the cumulative effect of chronic exposure to CO can act as a catalyst in initiating a heart attack. Oxygen is essential for the aerobic metabolism of the heart, and when oxygen transport is impeded by CO in the blood, the heart has to work harder to keep up, increasing the potential for a heart attack. Additional factors for firefighters are exhaustion from physically demanding work, and the added heat stress from their protective clothing. These deaths often occur at the fire station or when the firefighter returns home. While many firefighter deaths are due to the inherent nature of the profession, many can be avoided. Education about the hazards of CO and other products of combustion is key to helping reduce injuries and fatalities. In 2005 alone, smoke inhalation and respiratory distress accounted for 3390 injuries in the US fire service.5 Physicians do not routinely measure carboxyhemoglobin (COHb) in heart attack victims. In the case of firefighters, it is important that blood is analyzed for CO because of the toxic hazards associated with smoke exposure. When the blood sample of a heart attack victim is drawn post-CPR, the COHb value will be lower because the amount of 100% oxygen used on the patient during cardiopulmonary resuscitation (CPR). This should be considered when calculating the true peak level of COHb at the time the patient left the environment containing elevated CO concentration.

28.2 POSTFIRE AND OVERHAUL Overhaul is the process of opening up walls and ceilings of a structure to check for and extinguish hidden fire, in order to prevent rekindles. This stage of fire operations, when the building and its contents are still smoldering, often produces high levels of CO.2 As with any hazardous environment, in an area in which higher then allowable CO levels are suspected, it should be standard practice during overhaul to have a multigas meter in place to monitor the atmosphere. Being a by-product of combustion, CO is seldom found by itself, and multigas meters can be used to gauge the presence of other gases. For example, when a firefighter experiences watery eyes at a structure fire, acrolein is the likely cause. If the environment is ventilated, then metered, and found to be clear of CO, the firefighters should not experience watery eyes when they remove their SCBA (self-contained breathing apparatus) since the acrolein has been ventilated with the CO. Some fire department gas sensors only read CO. Firefighters must understand that if CO is found to be present, it is a likely indication of the presence of other toxic

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gases. Firefighters should wear a personal gas monitor (PGM), and continue to use breathing apparatus until CO readings in the area fall to within acceptable levels. Firefighters who smoke, fall into their own high-risk category. Pack-a-day smokers may have up to 5% COHb. These firefighters are more at risk for at least two reasons: (1) they are at a higher baseline COHb%, and (2) they are more likely to be asymptomatic from a CO exposure.

28.3 WORKPLACE/INDUSTRY CARBON MONOXIDE STANDARDS The standards for CO concentration are expressed in parts per million (ppm). There is a direct relationship between ppm and percent (1% = 10,000 ppm). See Chapter 35. Although the following standards are designed for industry, they play an important role in risk assessment for fire departments when CO has been stored or transported and is involved in a motor vehicle or industrial accident. The UN# for CO is 1016. It is usually transported as a cryogenic liquid. The current Occupational Safety and Health Administration (OSHA) permissible exposure limit (PEL) for CO is 50 ppm as an 8-h time-weighted average (TWA) [29 CFR 1910.1000∗ ]. The National Institute for Occupational Safety and Health (NIOSH) recommended exposure limit (REL) for CO is 35 ppm as an 8-h TWA and a ceiling limit (CL) of 200 ppm. The NIOSH recommended immediately dangerous to life and health concentration (IDLH) for CO is 1200 ppm. The IDLH is the concentration that results in death or irreversible health effects, or prevents escape from the contaminated environment within 30 min. The American Conference of Governmental and Industrial Hygienists (ACGIH) has adopted a threshold limit value (TLV) for CO of 25 ppm, as an 8-h TWA. For more information, see http://www.cdc.gov/Niosh/carbon2.html. Underwriters Laboratory standards for residential CO alarms are given in Table 28.1. CO alarms had to have a reset button. If the alarm sounded and the inhabitants of the building showed no sign of CO poisoning (nausea, vomiting, general body weakness, etc.), they were instructed to press the reset. If the alarm went off again, they were instructed to vacate the building and call an authority. The selectivity test criteria remained at previous levels. After October 1, 1998, UL 2034 listed CO alarms must measure and alarm when CO is: • 30 ppm for 30 days • 70 ppm for no more than 240 min before alarming (may alarm as early as 60 min) • 150 ppm for no more than 50 min before alarming (may alarm as early as 10 min) ∗ CFR 1910.1000 provides measurement standards for air contaminates and definitions found on an MSDS (Material Safety Data Sheet). The standards are law and fall under the jurisdiction of the US Department of Labor.

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TABLE 28.1 UL 2034. Carbon Monoxide Alarm Activation Standards 1992 and 1995. April 30, 1992, UL 2034 listed CO alarms had to measure and alarm when CO is • • • •

15 ppm for 8 h before alarming, or 100 ppm for no more than 90 min before alarming, or 200 ppm for no more than 35 min before alarming, or 400 ppm for no more than 15 min before alarming

After October 1995, UL 2034 listed CO alarms had to measure and alarm when CO is • 15 ppm for no less than 30 days, or • 100 ppm for no more than 90 min before alarming, or • 200 ppm for no more than 35 min before alarming, or • 400 ppm for no more than 15 min before alarming

• 400 ppm for no more than 15 min before alarming (may alarm as early as 4 min) and have a manual reset that will re-energize the alarm signal within 6 min if the CO concentration remains at 70 ppm or greater. Another significant change to the October 1, 1998 CO alarm listing was the addition to the instructions, stating that individuals with medical problems may consider using warning devices which provide audible and visual signals for CO concentrations under 30 ppm. UL 2034 information obtained from www.bacharach-training.com. CO-IDLH and PELs are based on the responses of healthy adults at resting ventilation. Elderly persons and infants are more susceptible to CO exposure. Specialized CO detectors are available and should be used in conjunction with these groups.

28.4 INVESTIGATION Structure fires are not the only situations where firefighters encounter CO, since the cause and presence of CO at a fire is known. Investigating situations where CO alarms are activated may be more hazardous, since locating the source of the CO can be difficult and time consuming (see Table 28.2). Interviewing building occupants about possible flu-like symptoms, asking what appliances were in use, and asking about any unusual odors may be helpful. CO is odorless, colorless, and tasteless, yet in the realm of CO alarm investigation, CO is not the only fire gas that is produced, and other gases can produce odors. Furnace malfunctions often produce aldehyde odors that can be compared to rotting fruit. An occupant who experiences watery eyes and notices a foul odor should exit the home and notify the fire department. Though the smell in the area and watery eyes may not be directly related to CO, they may be the result of lacrimators (an uncontrollable response to an irritant that causes release of tears) and may suggest that CO is also present and needs to be further investigated.

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TABLE 28.2 Common Investigative Tactics Associated with Finding the Source of a Carbon Monoxide Problem • • • • • •

Turn on all fuel-burning appliances Close all windows and doors to seal home as tightly as possible Set thermostat to activate heating unit Run hot water until the water heater turns on Start the gas clothes dryer (this device not only creates CO, it also vents air outside the home, which may create negative pressure inside and induce reverse stacking) Turn on house fans. This includes the kitchen and bathroom fan, as well as the electric clothes dryer and attic fan, if present. These may also contribute to negative pressure and reverse stacking

TABLE 28.3 Common Sources for the Generation of Carbon Monoxide in a Residence • Faulty furnace • Faulty water heater • Gas stove • Gas dryer • Fireplace • Attached garage • Driveway close to an open window or air conditioning unit • Heavy smoker (approximately 400 ppm in exhaled breath)

Locating the CO problem can be more difficult when a temporary source of CO is the cause. This might involve a car or lawn mower running near an open window or a heating ventilation and air conditioning (HVAC) intake unit (see Table 28.3). Water heaters or furnaces can be tricky too. It may be useful to turn up the thermostat to activate the furnace, or run hot water to activate the water heater. Meters are then used to check that the draft and flue pipes of these appliances are working properly. During any CO investigation, it is important to interview the occupants about what they were doing prior to the CO alarm activation. CO concentrations outside of buildings in urban areas might raise CO levels owing to heavy automotive traffic. Portable detection devices used by fire departments and utility companies have their limitations. Many meters may take as long as 5–7 min to achieve an accurate reading. It is important to be familiar with the operating instructions. Proper calibration is critical. The functions and limitations of gas meters vary between different manufacturers. A little known limitation can be within the sensors themselves. All CO sensors begin to degrade beyond the calibration range, typically after only 2 years. As with any tool, it is important to read the manufacturer’s directions and know the

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limitations of the instrument’s use. All meters must be zeroed (cleared) away from the monitoring site (i.e., before entering the area to be sampled) in order to establish a baseline. Technology provides us with additional devices to aid in a CO investigation. One such device is the data logger. Data loggers are effective when a CO investigation appears inconclusive. They can be left at the scene of a CO alarm to determine the CO level and time of that level. This aids in zeroing in on the source of the alarm activation. Data loggers today are compact and can store time stamped readings for prolonged periods of time. When retrieved, data loggers are uploaded to computer software that can determine the time of day an exposure occurs. For example, it may be used to explain why warming your car up in the garage in the morning will set the CO alarm off hours later, owing to the time it took the CO to migrate to the household CO detector. Traditionally, determining the level of CO exposure in people was limited to invasive blood testing in a hospital. In the field, first responders relied on symptom guesswork using complaints such as headache, fatigue/weakness, dizziness, and flulike symptoms to estimate CO exposure. Today, breath analyzers can be used in the field to estimate CO levels in the blood. CO breath analyzers measure the amount of CO in exhaled breath in ppm, suggesting a level of CO toxicity. Breath analyzers for CO have been available for many years, and were used earlier primarily for smoking intervention. Recently, EMS units have adopted CO breath analyzers in the field for their portability and ease of use. Many physicians continue to draw arterial blood samples to determine COHb levels, when venous blood or breath samples will do. Firefighters associate all invasive methods with pain and react with avoidance. Venous blood CO testing is just as effective as arterial for CO measurement. Firefighters would be more willing to be tested if venous blood instead of arterial blood is drawn. CO has a slightly lower molecular weight than air. The molecular weight of CO is approximately 28, while air has an average molecular weight of approximately 29. Reference materials may simplify this by assigning air an arbitrary number of one. Any substance with a value of less than one will float, and anything that has a value greater than one will sink. On this basis, CO has a value of 0.97 and this indicates that CO is slightly lighter than air. However, once CO is mixed with air it cannot spontaneously separate from it. The key physical characteristic here is that hot air rises and cold air falls. Accordingly, CO in air should be metered at three different levels. Unlike smoke detectors which are placed on ceilings, CO detectors should be placed on walls at head or chest level. CO may be found in closed spaces such as in closets and attics, necessitating removal by mechanical ventilation. Socioeconomic factors in urban areas play a part in the rise of CO emergencies. As heating costs go up, occupants have been found to attempt to heat their homes by running the gas stove, using kerosene heaters (illegal in most states), or bringing an outdoor grill inside. Besides the hazards of fire, accumulation of dangerous levels of CO is likely in all of these scenarios. In addition, absentee landlords may allow appliances to fall into disrepair with little regard for tenant safety. Illegally constructed apartments in basements can sometimes cause furnaces to be obstructed, preventing proper airflow (see Figure 28.1).

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CITY OF NEW HAVEN, CONNECTICUT DEPARTMENT OF FIRE SERVICE CARBON MONOXIDE INCIDENT CHECKLIST Alarm Number: _______________Date: _______________ Dispatch Time: _____________ Company: ____________________ Officer: _________________________________________

*

DID ANY PERSON OCCUPYING THE OCCUPANNCY DISPLAY AND SIGNS AND OR SYMPTOMS ASSOCIATED WITH CARBON MONOXIDE POISONING SUCH AS: YES NO Headache .

Nausea Dizziness Difficulty Breathing Altered Mental Status

. . .

. .

*

DID ANY PERSON DISPLAYING SIGNS AND OR SYMPTOMS FEEL BETTER WHEN HE EXITED THE OCCUPANCY? YES NO

*

DID ANY PERSON EXHIBIT THESE SIGNS AND OR SYMPTOMS BEFORE EXPOSURE TO THIS ENVORONMENT? YES NO .

*

ARE THERE ANY OCCUPANTS PRESENT THAT CAN BE CONSIDERED AS “AT RISK” PERSONS, SUCH AS: YES NO Individuals who are pregnant? . Children? . Persons with heart of respiratory disease? . Does anyone smoke in the occupancy? . Is there any fuel burning appliance present? If yes, List each _________________________________________________________________________________________________________ . . Was a fireplace and furnace in use at the same time? Is there any fireplaces, unvented heaters or coal/wood burning stoves in use at the time, if yes please explain. ______________________________________________________________________________________ Was an oven being used? Was an auto running in an attached garage? *

. .

THE FOLLOWING QUESTIONS REFER TO THE ALARM ACTIVATION:

What time did the CO Detector first sound? __________ am / pm Is the detectors’ sensor discolored? YES What was the highest digital alarm reading displayed? ______________________ Was the occupancy ventilated after the alarm activated Were all appliances shut off by the occupant or NHFD? Was a gas grill type unit used near the building? *

YES YES YES

NO

NO NO NO

LIST ALL READINGS DETECTED BY THE NHFD Initial entry: __________ Following ventilation: __________ Ventilation ceased: __________ Followup reading: __________ st nd Basement: __________ 1 Floor: __________ 2 Floor: __________ rd th th 3 Floor: __________ 4 Floor: __________ 5 Floor: __________

MEASUREMENTS OBTAINED PRIOR TO DEPARTING SCENE:

__________________________

FIGURE 28.1 investigations.

Sample form used by fire departments during carbon monoxide-related

Fire departments must not overlook basements and attics during their investigations, and have a fiduciary responsibility to summon the appropriate building officials when improper or illegal conditions are found. Some individuals bring themselves to the ED with CO poisoning, having bypassed the fire/EMS system. In these cases, the ED must ensure that this individual is not going home to a toxic environment.

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In urban areas, proper reporting may save the lives of others who may be housed in the same building. All ED’s should have a mechanism to ensure that the appropriate agencies are notified.

28.5 EMERGENCY SMOKE ESCAPE DEVICES There are no current testable North American standards in place for the use of emergency smoke escape devices commonly known as “smoke hoods”. However, the American National Standards Institute (ANSI) has a written standard ANSI-110 that is not yet in practice. It is important to know that the proposed standard is very similar to the existing European EN403 standard that has been in place since 1993. Although it is a European standard, the EN403 gas challenges are virtually the same as the proposed ANSI-110 standard. Until there is a recognized standard in the United States, the EN403 standard should be used as a reference when considering the purchase of a smoke hood, since some devices are of questionable value and may not offer the protection that they advertise. Several recognized International Standards specify the minimum requirements for single use emergency devices intended for use by persons escaping from fires. These include the European EN403: 2004—Respiratory protection devices for self-rescue/Filtering devices with hood for escape from fire. ANSI/ISEA 110:2003— the American National Standard for Air-Purifying Respiratory Protective Smoke Escape Devices, and the Australian/New Zealand Standard AS/NZS 1716: 2003— Respiratory Protective Devices. These standards, whether government mandated or voluntary, are vital to the safety of the end user and the integrity of the smoke hood industry. Standards represent a documented agreement, established by a consensus of subject matter experts and approved by a recognized body that provides rules, guidelines, or characteristics to ensure that materials, products, processes, and services are fit for their purpose. Adherence to these standards ensures governance by establishing processes and practices that promote and ensure integrity, compliance, and accountability. These performance standards serve as the benchmark for all new technologies and methods, defining the expected level of performance for all emergency smoke escape devices. Tables 28.4A and 28.4B summarize the Test Challenge and Breakthrough concentrations for determining smoke hood product performance. The breakthrough time shall not be less than 15 min when tested against the agents referenced in the tables.

28.6 EMERGENCY DEPARTMENT SCREENING Screening at the emergency department is essential in reflecting the true statistics associated with CO poisoning. It is common that an exposure goes undetected or misdiagnosed. As mentioned earlier in this chapter, there are alternatives for accurate blood screening, and venous blood sampling is just as effective for CO measurement as are ABG (arterial blood gas) measurements. Using a CO breath analyzer is an

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TABLE 28.4A Summary of “Test Challenge” of Smoke Hoods Test Challenge/Dose Concentrations (ppm) Gas

EN 403:2004

ANSI 110:2003 (1)*

AS/NZS 1716:2003

Carbon monoxide Hydrogen cyanide (2)* Hydrogen chloride Acrolein

2500 minimum 400 1000 100

3000 minimum 400 1000 100

2500 400 1000 100

Notes: (1)* = Also includes requirements for cyclohexane and sulfur dioxide; (2)* = International standards include cyanogen gas in the performance criteria for HCN.

TABLE 28.4B Summary of “Breakthrough Concentrations” When Testing Smoke Hoods Breakthrough (ppm) Gas

EN 403:2004

Carbon monoxide Hydrogen cyanide (2)∗ Hydrogen chloride Acrolein

200 (1)∗

ANSI 110:2003

AS/NZS 1716:2003

200 10 5 0.5

250 10 5 0.5

10 5 0.5

Notes: (1)∗ = Time weighted average in any single 5-min period; (2)∗ = Total concentration of HCN and C2 N2 shall not exceed 10 ppm at breakthrough.

excellent method for accurate, noninvasive COHb screening. A blood test can of course still be utilized to confirm a breath sample and screen for other toxic gases associated with smoke inhalation. One study found that 23.6% of patients presenting at a hospital with flu-like symptoms actually suffered from lower-level CO poisoning (see Reference 6, p. 178). Consequently, ED personnel, when interviewing patients with flu-like symptoms or other indicators of CO poisoning, should inquire about the condition of other household members as well, that is, take proper situational histories. Too often other household members whose symptoms are not as severe go unnoticed. This could lead to health problems as a result of low level chronic CO exposure.

28.7 LETHAL GAS COMBINATIONS Firefighters should be aware of the potential dangers associated with combinations of toxic gases. A CO reading of 200 ppm, although dangerous, would not by itself be

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considered immediately life threatening, but when combined with minimal amounts of HCN gas, could form a toxic environment that would be immediately hazardous. This may be found in postfire overhaul operations, after the main body of fire has been extinguished. It is well established that cyanide, primarily in the form of HCN, is an important and common component of fire smoke. While not as ubiquitous as CO, which can be found in every fire, cyanide “is to be expected in modern fires,”7 owing to the widespread use of synthetic materials that generate cyanide upon combustion. While animal studies have demonstrated that cyanide produced in fire can quickly be fatal, its true pathophysiologic role in humans in actual fires has been more difficult to study and quantify. Blood cyanide levels may be low in hot flash fires in which case heat and oxygen depletion are likely the primary causes of death, but may be high when the victim is away from the site of fire origin and is not subjected to intense heat and low oxygen levels.7 The evaluation of a number of fire fatality forensic databases revealed median cyanide levels ranging from 0.53 mg/L (database of fire deaths in Glasgow), to 1 mg/L (Dupont Plaza Hotel fire, Puerto Rico, 1986), to 3.14 mg/L (Paris database).7 In most of the databases examined, there was no correlation between cyanide and COHb levels, though other studies have found correlations, including an Australian study that found a mean COHb level of 40% and a mean cyanide level of 1.65 mg/L among 178 fire victims. The correlation coefficient was 0.34 (p < .001).8 From a physiologic perspective, it may be tempting to postulate that the combination of CO and cyanide exposure is more toxic than the simple sum of the two effects, but the data do not support this conclusion. It was found that subjecting rats simultaneously to the CO and HCN gas concentrations that individually produced incapacitation at 5 and 35 min (5706 ppm and 1902 ppm for CO, respectively, and 184 ppm and 64 ppm for HCN, respectively), resulted in incapacitation in only 2.6 and 11.1 min.9 It has been suggested that cyanide, by depressing respirations, may reduce or prevent the uptake of CO. This hypothesis is supported by observational data from fire databases, wherein certain fire victims had COHb levels well below lethal, yet very high blood cyanide levels.7 For example, data from a polyurethane mattress fire that killed 35 prison inmates in Argentina in 1990 showed COHb levels between 4% and 18%, but cyanide HCN levels ranging between 2.0 and 7.2 mg/L,10 well above levels felt to be lethal in humans. For obvious reasons, controlled experimental human data are lacking.

28.8 PREVENTION AND AWARENESS Chronically CO-exposed individuals can become asymptomatic over time. An example of this condition was found in a firefighter who smoked cigars. When a breath sample was taken from him it was discovered that he had a reading of 72 ppm (approximately 11.5% COHb), but he had no discernable symptoms. When this was brought to his attention he went for a medical check up and it was determined that he was in the early stage of heart disease. As a result he stopped smoking.

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It is important for firefighters to realize that firefighting as a profession has the highest rate of heart attack death of any occupation in the US. Regular medical examinations should be a top priority in the fire service. Being repeatedly exposed to hazardous environments increases the risk of numerous health problems. There is a need for a link between the medical community and the fire service to better understand the effects of CO. More studies need to be conducted in tandem with the fire service considering the frequency of exposure in this occupation.

28.9 CONCLUSIONS There are many variables to consider when it comes to understanding the effects of CO exposure. Acute CO exposure may not even register in the hemoglobin, which is why it is important for firefighters to monitor the environment in which they work. • Time is a critical factor to consider when conducting a CO investigation. • Gas sensors can have varied reaction times, some as long as 7 min or more to indicate a true ppm reading. • Air movement can create false positive readings in areas where too many personnel use a CO monitor. Use by only a limited number of personnel when investigating a CO alarm is important. CO is an elusive hazard that often goes undetected, both environmentally and physiologically. The development of affordable technology such as personal CO monitors and CO data-logging equipment has enabled more success in CO investigations. CO, also known as “The Great Imitator,” has many different faces. Symptoms emulating a flu-like condition, headache, or fatigue can make diagnosis of exposure tricky to recognize. However, with innovative technology such as a breath analyzer, there is now a noninvasive means to accurately determine CO levels in the blood. If there is COHb in the initial screening, a second test is necessary, since the COHb saturation can be ascending or descending. Given the vast number of variables associated with CO poisoning, it is important to recognize that true statistics of this common occurrence are attainable. Members of the medical community have a valuable resource in members in the fire service, whose exposure to CO is commonplace. Working together through further research and studies can produce positive results, which will benefit patients and save lives.

References 1. Reilly, K. Chronic CO poisoning in firefighters. Fire Engineering, 159, June, 2006; 110–114. 2. Jarbo, T. An examination of toxicity hazards associated with the burning of materials commonly encountered by firefighters, February, 1995. Report to the National Fire Academy Executive Fire Service Officer Program. 3. Fahy, R.F. NFPA. U.S. fire service fatalities in structure fires, 1977–2000, July, 2002. National Fire Protection Association, www.nfpa.org.

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Carbon Monoxide Poisoning 4. Alcora, R. Smoke inhalation and acute cyanide poisoning. JEMS, Supplement, Summer, 2004. 5. NFPA. National fire protection association research and reports on fire ground injuries, 1981 to 2005. 6. Montagna, F.C. Responding to Routine Emergencies, Fire Engineering, Penn Well Publishing Co., 1999, Tulsa, OK. 7. Alarie, Y. Toxicity of fire smoke. Crit. Rev. Toxicol., 2002; 32: 259–289. 8. Yeoh, M.J., Braitberg, G. Carbon monoxide and cyanide poisoning in fire related deaths in Victoria, Australia. J. Toxicol. Clin. Toxicol., 2004; 42: 855–863. 9. Chaturvedi, A.K., Sanders, D.C., Endecott, B.R., Ritter, R.M. Exposures to carbon monoxide, hydrogen cyanide and their mixtures: interrelationship between gas exposure concentration, time to incapacitation, carboxyhemoglobin and blood cyanide in rats. J. Appl. Toxicol., 1995; 15: 357–363. 10. Ferrari, L.A., Arado, M.G., Giannuzzi, L., Mastrantonio, G., Guatelli, M.A. Hydrogen cyanide and carbon monoxide in blood of convicted dead in a polyurethane combustion: a proposition for the data analysis. Forensic. Sci. Int., 2001; 121: 140–143.

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The Purpose and the Process of Litigation in a Carbon Monoxide Poisoning Case Stephen P. Willison

CONTENTS 29.1 The Purpose—Why Litigate? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.1.1 Why Litigation Works and How It Gets Abused . . . . . . . . . . . . . . . . . . 29.1.2 Keeping Focused on The Goal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.1.2.1 “Compensation” Does Not Mean “Profit” . . . . . . . . . . . . . . 29.1.2.2 The Secondary Goals Should be Just That—Secondary 29.1.3 The End Game and the Big Picture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.2 The Process—What to Expect and When to Expect it . . . . . . . . . . . . . . . . . . . . 29.2.1 Gathering Information. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.2.1.1 Filing Suit . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.2.1.2 The Discovery Process. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.2.1.3 Trial—Risks and Rewards . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.3 They Call it the Burden of Proof for a Reason . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.3.1 The Standard of Proof . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.3.2 Two Essential Elements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.3.2.1 Liability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.3.2.2 Damages . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.4 The Unique Problems of Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . 29.5 Your Life on Trial . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.6 An Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.6.1 Getting Help Managing the File . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.6.2 Trusting Everyone to Do the Job Assigned . . . . . . . . . . . . . . . . . . . . . . . . 29.6.2.1 The Attorney . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.6.2.2 Fact Witnesses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.6.2.3 Expert Witnesses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29.7 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

656 656 657 657 657 658 659 659 660 661 662 662 663 663 663 664 666 667 668 668 668 669 669 669 670

655

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If you are reading this chapter because you, or someone you care about, has recently suffered the effects of carbon monoxide (CO) poisoning, you are probably caught in a whirlwind of frustration, confusion, and anger. This chapter was invited by the editor to help you calmly and rationally sort out the pros and cons of pursuing litigation, and if you do pursue it, allow you to make some sense of what to expect. However, because every case is fact specific, this chapter should never be used to substitute for the advice of competent legal counsel. Instead, it will lay out for you the purpose and process of litigation so you can better understand the risks.

29.1 THE PURPOSE—WHY LITIGATE? Anyone considering litigation needs to honestly ask themselves, “why.” Your motives now will greatly influence whether you are satisfied with your decision at the end of the road. If you think it is easy, or you think it will solve your problems, let me save you some reading—a CO poisoning case may be the hardest thing you ever do, and you will still have all the same injuries when it is over. On the other hand, it can be a worthwhile experience if you can keep the right perspective.

29.1.1 WHY LITIGATION WORKS AND HOW IT GETS ABUSED In many ways, litigation is both the blessing and the curse of our society. It is the vehicle by which we hold other individuals and companies accountable for their actions. In fact, it is the only way that anyone other than the government can force another to change their ways or take responsibility for their misdeeds. Litigation is why untested products are typically not rushed to market. Litigation is why a manufacturer may choose more expensive, reliable materials over cheap and dangerous alternatives. Litigation is a significant part of why we can walk into stores, theatres and other public places with the confident assumption that under normal circumstances we will not get injured. At the same time, litigation has been significantly abused. Litigation is why the next miracle drug is currently not available. Litigation is why automobile insurance can sometimes cost more than the car. And litigation is why your ladder is covered with warning labels you probably have never read. The point is that litigation does expose problems in design, manufacturing, or training. More importantly, fear of litigation is what motivates a person or company to fix those problems rather than let them continue. However, because litigation frequently results in the payment of money, it is particularly susceptible to abuse. False allegations, exaggerated claims, and an entire cottage industry of people trained in how to help others cheat have created a counter movement of extraordinary efforts to prove every lawsuit illegitimate, every plaintiff a gold-digger, and every expert witness a liar. At the end of the day, we can only hope that truth prevails and the cheater (plaintiff or defendant) is stopped.

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29.1.2 KEEPING FOCUSED ON THE GOAL Assuming a legitimate cause of action where a plaintiff is actually hurt by someone’s actual misdeed, the primary goal of litigation is to restore to the plaintiff what someone else wrongfully took away. Sometimes litigation has additional benefits such as raising public awareness, getting a defendant to change its ways, or even produce some degree of punishment. Those secondary goals are very appealing, but in reality they are usually outside the realm of what you can make happen through the process. 29.1.2.1 “Compensation” Does Not Mean “Profit” So if the whole point is, “to restore to the plaintiff what someone else wrongfully took away” let’s start there. In legal circles, this is referred to as compensatory damages. In a perfect world, the person who did something wrong simply replaces what they took. In a situation where John Smith destroys your $100 bill, this calculation is easy. John must give you a replacement $100 bill. Calculating these damages become much more difficult, however, when we talk about the loss of someone’s life or abilities. No defendant can bring someone back from the dead. And while a defendant may be able to pay for certain types of treatment, he cannot erase the fact that you needed treatment in the first place. In those circumstances where the thing taken cannot be replaced, money is the substitute. Because money is the substitute, everything becomes complicated. When I was in law school I was shocked the first time I heard my professor say that a plaintiff is “a loser trying to get back to zero,” but it is a true statement. If you are a plaintiff, it is because you have already lost something. The best case scenario is where you are compensated in a way that gets you back to zero. Because you probably valued what you lost more than money, however, you will probably feel you have been left short. So please understand “compensation” does not mean “profit.” In fact, it probably does not even mean “restoration.” It is usually more along the lines of “something is better than nothing.” So why bother? Well, something really is better than nothing. If CO poisoning caused one of your loved ones to die, or left you injured, life is going to be hard enough. We tell our clients to think of it as a sugar coating on a bitter pill. If you have to live life with the kind of injury that causes you to get lost in your own grocery store, then you might as well be wearing a comfortable pair of shoes!1 29.1.2.2 The Secondary Goals Should be Just That—Secondary As we have discussed above, litigation can create change. It can call public attention to a problem. It can keep others from ending up like you. But those motivations, while very noble, can be risky. Defendants only change if they want to. Public attention only gets raised if the media is not obsessed with something different that week. And 1 Yes, a sense of humor makes even this seem easier.

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you probably would not save someone else unless one of those first two mechanisms work. So if you set out on the 2-year path of litigation, and run up all those expenses, strictly for the purpose of saving the world, those things you cannot control will drive you crazy. So what about raw meat? Is not there a way to punish the bad guy for what he did? Well in some states there is something called punitive damages. The goal of punitive damages is to punish very bad behavior. It has nothing to do with what the plaintiff lost. In fact, punitive damages can be awarded even if the actual loss to the plaintiff is minimal. Because these type of damages seek to punish a specific defendant, they are based on the net worth of that defendant. For example, a $1000 punitive award against a 19-year-old college student might be a crushing blow, but it would mean nothing to a Fortune 500 corporation. That is why we occasionally hear of jury verdicts in millions, or even billions of dollars. It is not because one life is worth more than another, but because a jury needed to get the attention of a very wealthy defendant. Although punitive damages make a great lead story in the news, it is punitive damages which are most frequently overturned on appeal or reduced by the trial judge. We can probably agree it may not be fair for someone who had only a minor loss, or participated in their own demise, to suddenly become a multimillionaire. At the same time, in a world where corporations frequently have billions of dollars of earnings per quarter, is it hard to imagine them being motivated by anything less. As a result, punitive damages are hard to prove and often restricted by various tort reform legislation. Some states have completely banned punitive damages. Others have limited how much can actually be received by the plaintiff. As a result, you should talk to your lawyer about them, but it is unwise to consider punitive damages at all in the process of determining whether or not to pursue litigation.

29.1.3 THE END GAME AND THE BIG PICTURE How you end up feeling about the entire litigation process is greatly dependent on what you considered when determining whether or not to file a suit. If you seek anything other than fair compensation, you will be disappointed. If you are motivated by greed, that will become clear and juries will likely become so offended they may refuse to compensate you at all for your loss. If you are motivated by revenge, you will never recover from the fact that the defendant went back to life as normal and you did not. If you seek anything beyond what is fair, you will find yourself more stressed, more worried, and more tempted to do and say things that you otherwise never considered. The only thing worse than being injured by someone else’s misdeed is voluntarily destroying your integrity to pursue some misguided goal. Knowing your motivation will also help you make decisions at the end of the case. With the advice of your lawyer, you will have to decide whether to try the case or settle, appeal or stop, hire another expert or go with what you have. A clear view of why you started will help you decide when to stop. The noble pursuit of secondary goals can cloud your vision when it comes to making that decision. More than one plaintiff has shouted, “Never! I will never let them off the hook until they change their ways or are out of business.” But remember, you cannot force other people to change. In most cases, the defendant denies responsibility

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even after signing a check. Occasionally you are left in a position where they go free entirely even when they acknowledge some fault. Then you have a bitter pill that is just more bitter. We can all hope to accomplish noble goals out of tragedy. We should all work toward that always. But you can advocate for change without litigation. In fact, you might be taken more seriously if you do not sue. On the other hand, you might be able to use the money you got from the defendant to do it. So separate everything but financial realities from your decision to pursue the litigation process. Get clear in your head that you either will or would not make a difference regardless of the litigation. Litigation can give you money, but often not satisfaction. How you live and what you do can give you satisfaction, but often not money. Your decision should be based on the likelihood of success, potential damages, and the ability to collect what you win—and nothing else. So if you are still interested, let’s discuss those details.

29.2 THE PROCESS—WHAT TO EXPECT AND WHEN TO EXPECT IT Every lawyer has his or her own strategy. What happens at each step of the way is a matter of individual strategy. Because my opponents will likely also read this book, we will not discuss my particular strategy here. It is also not the intent of this chapter to summarize 3 years of law school. But you should understand the basic components of the process.

29.2.1 GATHERING INFORMATION In the law, nothing exists without evidence. So after you come to grips with motivation, step one has got to be figuring out what you can prove. The rules of proof and evidence can be different from jurisdiction to jurisdiction (see other Willison chapter), so now is when you need the help of the lawyer who will have to prove it on the basis of the facts of your case. Death speaks for itself, but if you are claiming an injury, you have to decide if you can prove it. Can it be measured and viewed or do we have to take your word for it? If we have to take your word for it, are there things in your past that might make taking your word difficult? Are there witnesses who can testify about how you were before and after? Are there tests that can prove what you are talking about? Then you have to prove how the CO got to you in the first place. If it was a bad furnace, do you still have it? If you do not, is there any evidence of the problem still around, like a repair man, or a photo, or a fire department report? If you have that evidence, you better also find information about the people who authored it. Do you have enough information to find them 3 years from now if they move or change jobs? In fact, being able to locate witnesses is critically important. Someone other than you needs to record information about what they observed, with as much details as possible, as soon as possible. This can be in the form of a handwritten statement by the witness or other means of documenting that information. In addition, it is important

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you have the type of information you will need to find them later if they move. Never assume you will always be in touch with any person and someone will “never forget” the details of an event. Eventually, you will need some way to connect all of the information together to form the elements of your burden of proof. In many cases, this is done by the testimony of expert witnesses. Because of factors too numerous to list in this chapter, your attorney should be involved in that process. For the purpose of gathering important foundational information, expert witnesses should be brought into the loop as soon as it is practical. You and your legal counsel will also need to determine whether you have a right to sue. Statutes of limitations are laws which limit the amount of time in which you can file suit. Sometimes this time frame begins to run when you discover the problem. Other times and places it begins to run as soon as the incident occurs. For example, depending on your jurisdiction and the theory of liability, the statute of limitations may begin to run on the date you discovered that CO was entering your home, or it may have begun to run on the date that the appliance was improperly installed. In some circumstances, the statute of limitations may have expired before you ever found out there was a problem. In addition to statutes, the time frame for suing can be limited by contract or other means. If you do not have a right to sue the guilty party, you should not waste time, money, and energy on gathering information for the rest of the case. Finally, you have to determine whether your “guilty party” is collectable. If your CO poisoning was caused by a homeless person, for example, winning a one-million dollar judgment would only be worth the paper it is written on. Even small businesses may not be collectable unless they are adequately insured. While it may be unsettlingly pragmatic, it does not make sense to spend $50,000 in litigation expenses if you can only collect $20,000 from the defendant. It may feel unjust, but it is a necessary thing to consider before proceeding.

29.2.1.1 Filing Suit Once you have come to the conclusion that you wish to pursue litigation, and have gathered enough information to be confident your attorney can prove your case in court, you must formally begin the lawsuit. This is done by filing a “complaint.” A complaint is typically a listing of factual allegations which, if proven true, would give you the right to recover from the named defendant. In your complaint, your attorney may list several defendants if the facts support it. In addition, you may have several different theories of liability against a particular defendant. In fact, most jurisdictions allow you to plead2 alternative (even inconsistent) theories. For example, you have the right to allege in Count I of your complaint that the defendant acted negligently and then in Count II of the complaint allege that

2 “Plead” or “Plea” are terms which refer to any allegation contained in a pleading. A “pleading” is typically defined as a complaint or an answer to a complaint.

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he acted intentionally. At trial, only one of them can be proven true, but by pleading them both you preserve your right to argue either one as further facts unfold. Once the defendant receives the complaint, they have an obligation to answer each allegation. By admitting, denying, or saying they do not know either way, you will immediately be able to see which issues will be the focus of your litigation. In addition, the defendant has a right to file “affirmative defenses.” These are assertions of certain legal theories which would get the defendant off the hook even if all the allegations in your complaint are true. For example, the defendant may allege that there was some other person who was responsible for the activities you allege in your complaint. The defendant may have immunity because of some sort of statute or contractual arrangement. They may also use affirmative defenses to point out deficiencies in your complaint. It is the purpose of the complaint, answer, and affirmative defenses to make sure that all parties involved in the litigation understand all of the reasons why the plaintiff believes the defendant is guilty and why the defendant believes that he is innocent. Assuming there is some disagreement after this phase, your case then moves into “discovery.” 29.2.1.2 The Discovery Process During the “discovery” phase, both sides get to find out the details of the other’s case. At this point, each side has the right to demand documents and information from the other. Each can interview witnesses under oath.3 A defendant can request releases for your medical information. You can request the design details of the product from the defendant corporation. In most jurisdictions, the purpose of discovery is to make sure that there are absolutely no surprises at trial. Both parties should fully understand the strongest portions of their opponent’s case before making a decision to actually put evidence in front of the jury. The discovery phase is by far the longest phase of the case. Parties may fight about whether they have a legal obligation to provide certain information. There may be delays in witness schedules, or the availability of attorneys. While the court always sets a deadline for discovery to be completed, it is not uncommon for one, or both parties to request an extension to find out more details about a specific issue. This discovery phase is also when several motions occur.4 This is how parties ask the judge to sort out which evidence will be allowed to be presented at trial and whether any portions of the complaint, or affirmative defenses, should be dismissed by the court. At some point before trial, the defendant will ask to have your case dismissed. This is done almost as a matter of routine. You should not take the defendant’s attempts to have your case dismissed as a sign of the strength or weakness of your case. In light of the risk of trial, you really cannot blame a defendant for trying. Although it should 3 Statements taken under oath during a lawsuit are called “depositions.” 4 A “motion” is any request to the court (usually by a party) to take some action, order someone else to act or clarify how the case will proceed.

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always be taken seriously, most judges prefer a case to be tried by a jury than thrown out on a technicality. Nonetheless, it is a judge’s job to not waste the court’s time if the plaintiff does not have the evidence required to meet their burden of proof. 29.2.1.3 Trial—Risks and Rewards At the end of this entire process is your trial. Either party may request to have the case tried by a jury. If both agree, it can be tried by a judge. Any trial is a risky proposition. While you may have all the evidence in the world, it is solely up to a handful of randomly chosen strangers to decide your fate. While you may have spent years wrestling with issues, they will only have a few days. While most jurors take their jobs very seriously, some are only interested in whatever path will get them back to their normal lives the quickest. In a situation such as a CO poisoning injury case, the quickest route home is to award zero. At the same time, juries are equally unpredictable for defendants. What may be perfectly reasonable in industry standards, may outrage the average citizen. Evidence that the defense team considers to be completely unbelievable may be accepted as absolute truth by the jury. And of course, the biggest thing working against defendants in many CO poisoning cases is the fact that every one of the jurors can imagine themselves in the same situation. Everyone has a furnace which could eventually go bad. Everyone has a car which may not be properly manufactured. Everyone is the customer of some utility company. The jury system is notoriously imperfect. At the same time, it is by far the best system on earth. It is precisely this unpredictability that causes even the most steadfast party to at least consider the possibility of settlement. Every party, plaintiff, or defendant must calculate the likelihood of the worst and the best case scenario. Research on previous verdicts in that jurisdiction can begin to narrow what is also the most likely scenario. All the variables such as the performance of witnesses, the availability of evidence, the randomness of jurors, and even the health and mood of the judge, attorneys, parties, witnesses, and jury can influence the outcome of a trial. Accordingly, most experienced trial attorneys will tell you that if they tried the same case ten times in the same county they would likely end up with at least two very different results. Many courts will require parties to participate in alternative dispute resolution prior to trial. This can be a form of mediation, arbitration, or even having the case evaluated by other attorneys from the jurisdiction. It is the goal of every court to get parties to negotiate an agreement rather than have a jury try the case. Nonetheless, it is every party’s right to choose to not negotiate. As a result, your entire case preparation should be focused on trying the case if you have to, but settling if you can.

29.3 THEY CALL IT THE BURDEN OF PROOF FOR A REASON Anyone who has ever watched a TV show about lawyers has heard the phrase “burden of proof.” What this means is that the plaintiff has the obligation to present admissible

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evidence sufficient to prove that the defendant is responsible. The plaintiff not only has to prove that they were injured, but what caused it, and who is responsible for that cause. The defendant never has to prove its innocence. In the circumstances of a CO poisoning case, this means the plaintiff has to prove all the details of how they came in contact with a substance that is completely invisible. If the defendant can convince the jury to not believe just one part of that story, they go free.

29.3.1 THE STANDARD OF PROOF The standard of proof refers to the degree of certainty to which the jury must be convinced before it can say the plaintiff has proved his/her case. In a civil case, such as a lawsuit over a CO poisoning injury, the standard is a “preponderance” of the evidence. That simply means that the plaintiff must prove that it is more likely than not that the proposition is correct. This is remarkably easier to prove than the criminal standard which is “beyond a reasonable doubt.” In a civil case, a jury can find in favor of the plaintiff even when they have reasonable doubt as long as it is the “most likely” cause. On the other hand, if the jury concludes that there are two equally plausible theories which may have caused the plaintiff’s injuries, the burden of proof has not been met and the plaintiff will lose.

29.3.2 TWO ESSENTIAL ELEMENTS In a nutshell, the elements of the burden of proof are liability and damages. Put in its most basic terms, liability is proving, with evidence, the answers to who, what, where, when, why, and how. If all that is proven, the plaintiff also has to show provable damages. 29.3.2.1 Liability The first element of any litigation is to prove liability. Basically, this means you have to prove who is legally responsible for your injury. To do that you must first know how you were injured. It is not enough to know that you have been exposed to CO. You must be able to prove where that exposure occurred, when that exposure occurred, and why you were exposed to CO. It is not enough to just know what caused your exposure, but we must also determine why that condition occurred. If the CO poisoning is a result of a cracked heat exchanger in the furnace in your home, it might be the result of a flaw in the manufacturing. However, it might be the result of a mistake made by a repairman. At the same time, it might be the fault of the homeowner because a repairman was never called to do the maintenance necessary on that machine. Once the where, when, and why questions are answered, you can then determine who is responsible for that exposure. In a negligence case, this often requires proof of whether someone has breached a duty they had to someone else. We all have a duty to act reasonably whenever we do something. This is the standard of a “reasonably prudent person.” If you drive a car, you must do it reasonably. If you do not, you will be

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held responsible for any unreasonable acts you commit with that car. This is a common duty we all have. At the same time there are other duties that are imposed on people. Some duties are imposed upon us by law. For example, laws in your state probably require a contractor to install a new water heater according to the manufacturer’s instructions. If the contractor chooses not to, he will likely be held responsible for anything resulting from his deviation from the instructions. Sometimes we volunteer for undertaking a duty by contract. For example, if a mechanic agrees to fix a problem in exchange for money, he has a duty to fix the problem. If he fails to fix that problem, or makes it worse, he will be responsible for that failure. Ultimately, liability is a combination of a number of factors which creates responsibility on behalf of one person to another. So you may know that you were injured by exposure to CO in the month of February in your home coming from a cracked heat exchanger on your furnace. You may know who manufactured that furnace, but if that furnace had a 10-year warranty, the manufacturer will not be liable for a heat exchanger which cracked in the 23rd year. At the same time, a service technician who failed to notice the crack in the heat exchanger when he performed a safety inspection might be liable for your exposure to CO even though he did not cause the crack to occur.5 29.3.2.2 Damages In order to have a right to bring a lawsuit, you must have suffered a loss. For the most part, the American civil legal system is set up to compensate for actual harm after it has occurred rather than prevention of what might happen. After you have answered the liability question, you still have to prove the “so what” and the “how much.” In a case of a CO poisoning lawsuit, it is not enough to prove that someone’s misconduct caused CO to leak into an area where you were at a particular time, you must be able to prove that it had some effect on you. If the problem was noticed immediately and you left the area before you suffered any symptoms, you likely have no basis to bring a lawsuit. 29.3.2.2.1 Proving the injury Proving that a death occurred as a result of CO poisoning is rather simple, if the appropriate tests were conducted to determine the cause of death. There are certain things that happen in the human body when it is exposed to lethal concentrations of CO which can be readily identified. Because the deceased person stopped breathing, we can also typically find very high levels of CO in the blood. In a case where a person does not die, but is injured, proof of CO poisoning becomes much more difficult. There is an overwhelming lack of understanding in the medical community about what CO does to human beings, other than cause death. This is a problem from a proof standpoint, because proving you have symptoms and proving you have been exposed to CO does not necessarily prove that one caused the other. If you suspect you

5 Of course, in that situation, he would only be responsible for the exposure to carbon monoxide after his inspection, not the carbon monoxide you were exposed to before he arrived.

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may have been injured by CO poisoning, you need to find someone in the medical field who understands CO. Let me be clear, this does not mean you should try to find a doctor to tell you, you have been injured by CO. There are doctors in this world who, for the right fee, will tell you anything you want to hear. Those doctors should be avoided at all costs. What you need to find is someone who understands CO who can truthfully and credibly tell you whether or not your symptoms have been caused by that exposure. You may go for years frustrating various uninformed medical professionals who can never determine why you are suffering from headaches and short-term memory loss before you find one that can scientifically explain to you, and eventually to a jury, the reason for your symptoms. But someone other than you will have to provide that connection. As with any toxin, the damage caused by CO is a function of time and dose. How long you are exposed to how much CO are important facts in determining whether your symptoms were caused by the problem. Even if we all agree on those numbers, there is disagreement in the medical-toxicology field about what CO poisoning can do. More importantly, what harm CO exposure actually causes can vary widely from person to person. Unfortunately, however, we do not often agree on either time or dose. By its very nature, the way CO interacts with the body causes it to disappear rather quickly. Having a blood test, even the next day, is often useless to determine the level of exposure. Because the common effects of CO poisoning are similar to many other medical conditions, the medical testimony might not go beyond the statements that your symptoms could have been caused by CO. If that is the case, it may be enough. In many jurisdictions, the jury is allowed to consider the totality of the evidence to conclude whether “more likely than not” you have suffered an injury as a result of your exposure. While there may be other plausible medical explanations for your symptoms, combining the testimony that it could have been caused by CO with the fact that you did not suffer those symptoms prior to exposure and the fact that these symptoms were noticed shortly after the exposure, may be sufficient to meet the burden of proof on injury. Again, this determination will be very specific to your case and dependent on the rules of evidence in your jurisdiction. 29.3.2.2.2 Economic damages Economic damages are those where we can more easily ascertain an amount of money to replace the loss. For example, if you miss work for six months, it is rather easy to calculate the amount of your lost wages. The reimbursement for the amount of money you spent on medical treatments is easy to calculate. It is somewhat more difficult in a situation where you can never work again and we must calculate the amount of what would have been your future earnings. In determining future economic damages experts need to calculate what would have been your career path. The likelihood of promotions, raises, and job changes must be considered together with the likelihood of lay-offs, demotions, and even other future injuries. Experts who are trained to utilize statistics and economic data can render reasonable opinions about what would have been. Of course, you can also see how defendants can find experts to point out that while every 20-year old intends to someday take over the company, only one of them actually will. More importantly,

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while we certainly have the data which allows us to calculate life and work expectancy we all know that some people live well beyond expectations and others tragically die too young. 29.3.2.2.3 Noneconomic damages The second type of compensatory damage is noneconomic. These damages are very real and important, but always subject to enormous debate. We can all agree in principal that injured people are entitled to recover for pain and suffering, but what is the value of a headache? If we can determine the value of a headache, how does that compare to the value of a migraine? How much should we compensate someone who can no longer engage in their favorite hobby? What is the value of one more day, or even one more hour, with a loved one? Is the life of a 5-year old worth more or less than the life of a 15-year old? In my experience, almost everyone who suffers one of these losses will tell you that there is no amount of money that can compensate them for their loss. This is the problem. While we cannot invent a number big enough to be adequate, the jury at trial will have to determine a number that is appropriate. It is important to remember that these damages are only supposed to compensate you for your loss. These damages are not for the purpose of punishing the defendant. Accordingly, these numbers should be the same whether it was a little old lady who harmed you or the largest corporation in the United States. Be prepared. Because this element of your loss is so uniquely personal, the defendant has the right to probe into some very private details to determine if they are valid. If you seek recovery for the loss of the companionship of your spouse, the defendant has the right to inquire about the quality of your marriage. If you claim you are depressed, the defendant will look deeply into your past to see if you were depressed before the exposure. If you seek damages for no longer being able to play golf, the defendant even has a right to speak to your golfing buddies to see if you actually enjoyed it or whether you were planning to give up the game. In the real world, however, your injury might make a bad marriage worse, people struggling with depression can go over the edge, and giving up golf should be on your terms, not someone else’s. In most jurisdictions, making a previous injury or condition worse is compensable. In fact, many times if the jury cannot sort out the difference before and after they will be allowed to award the entire value of the condition to you. As a result, you need to remember that it may be uncomfortable, but it is important if that is the type of loss you have suffered.

29.4 THE UNIQUE PROBLEMS OF CARBON MONOXIDE POISONING CO is odorless, tasteless, and colorless. It does not cause any of your senses to activate until you are already experiencing the symptoms of damage from exposure. In cases of acute exposure where someone has a dramatic reaction to a large dose of CO, like death or unconsciousness, it can be easy to pinpoint the time and place of exposure, but as you may have already read in other chapters of this book, CO poisoning can

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cause significant damage in much lower doses over long periods of time. Because nearly every home, car, place of work, and school has something capable of producing CO, long-term exposures can be very difficult to pin down to a particular place or time. That job is made even more difficult by the fact that any one of us could have multiple exposures to CO in various areas. Every time there is a new when or where it could have a dramatic impact on whether you will ever be able to prove liability for your exposure. The same characteristics which make CO difficult to catch inside the human body, make it even more difficult to catch in a room. Even in situations where lethal levels of CO exist in a room, the focus is, and should be, on the saving of the lives of individuals inside. That means first responders are trained to open doors and windows, shut off the fuel supply, and get affected people outside. Even rescue personnel are trained to evacuate the building when CO concentration reaches certain levels. As a result, we may be able to document that the CO concentration exceeded the emergency evacuation level, but we may never know whether it was double, triple, or a hundred times that level. This is a problem attorneys must face in CO litigation. Until CO detectors actually become accurate recorders of information, this will continue to be a problem.

29.5 YOUR LIFE ON TRIAL Whether the exposure to CO resulted in injury or death, any litigation will be about the impact on that life. As a result, the details of that life will be put on trial. The symptoms known to be caused by CO exposure are, unfortunately, also symptoms known to be caused by a number of other conditions. If you are alleging that you suffer from headaches or memory loss, the defendant has the right to examine your entire medical history to determine if there are other circumstances in your past which may have caused those symptoms. If you claim that since your exposure you have been having difficulty with math, the defendant has the right to take the deposition of your junior high math teacher. If you are claiming that the CO has caused you to lose control of your moods, you should plan on your ex-husband being called to testify about every time you were ever moody before the exposure. As difficult as all this may sound, those are reasonable tactics of legitimate defense attorneys. As we all know, however, some lawyers are neither legitimate nor reasonable. Some lawyers will do anything to win a case regardless of whether it is true, ethical, or fair. I have personally seen lawyers take one story from a Christmas party and turn it into allegations of alcoholism. I have seen pediatric records of colds and flu used to explain away the fact that a 50-year-old man has been coughing for 6 months. I have seen grieving parents accused of neglect. I have seen a loss of memory painted as a convenient lie. For every person who has ever received more than they deserved in litigation, there are likely far more who have walked away from a legitimate claim because they choose to no longer put up with the trouble. When deciding whether or not to proceed with your lawsuit you need to consider this fact. However, I have also found that

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being prepared for this ahead of time and knowing it will eventually come, helps my clients weather that storm. You need to have the courage to weather that storm. If you try to cover up any unfortunate fact, it will make everything worse. When there is a lot of money at risk, the defendants will eventually find all the information. You do not have to volunteer information, but if asked you cannot appear to be hiding anything. If you hide a doctor, a school, a military record, or any other fact, it will instantly look more important than what it is. It is always easier to explain away a bad fact than to undo the impression you are being dishonest. It is better for you to perform your best on every test and physical exam than to give the impression that you are someone who is exaggerating or malingering. In fact, if you come across as open and honest, any dirty tricks of a bad defense lawyer may work to your favor rather than his.

29.6 AN OVERVIEW 29.6.1 GETTING HELP MANAGING THE FILE One of the most common long-terms effects of exposure to CO is short-term memory problems. People with significant injuries often suffer from depression and CO poisoning can also cause emotional instability. These characteristics make the litigation process particularly difficult. You and your health care professionals need to do an accurate assessment of whether or not the exposed person is competent to carry on the tasks of daily living. For the litigation process especially, it is recommended that an unexposed person who is intimately familiar with the victim or victims, be called upon to work as your assistant in the litigation process. Because the litigation is about your life, it involves a seemingly never-ending process of gathering documents, information, names, phone numbers, and records. While you need this evidence to prove you have suffered an injury, the fact that you have suffered this type of injury will make gathering this stuff seem impossible. When you do a good job, the defendant will claim you are not injured. When you do a bad job, the defendant will claim you are trying to cover something up. All of that might be avoided by the appointment of someone to act on your behalf to gather information. This person must be in a position such that you do not mind sharing every intimate detail of your life. At the same time, you need to discuss with your attorney how best to handle that relationship so that you can preserve the privilege of your attorney/client communications. If used correctly, this assistant will dramatically reduce your stress.

29.6.2 TRUSTING EVERYONE TO DO THE JOB ASSIGNED Selecting your attorney is probably as important to the litigation process as choosing a physician is to having an accurate assessment of your health. Attorneys who understand CO poisoning are even more rare than health care professionals who understand it. Your town’s typical personal injury attorney does not have the experience necessary to handle the complexities of the case they must prove and the defense attorneys they will likely face. As a result, you should find whatever attorney you trust most

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and ask them to help you find the attorney who will be your lead counsel in the litigation. Once you find an attorney you can trust who is capable of handling this case, you need to trust that attorney with the entire process which includes your decision of whether or not to even pursue litigation. Let’s discuss some key roles in CO poisoning litigation. 29.6.2.1 The Attorney Although attorneys may be everyone’s favorite punch line of a joke, good attorneys make all the difference in a close trial. At the end of the day it is facts which win a case. Good attorneys cannot invent facts, but bad attorneys can fail to put them in front of the jury. Attorneys cannot change the testimony of witnesses, but good attorneys can know how to handle it, or even exclude it under certain circumstances. These types of trial decisions are enormously complex, based on a number of factors, and to some degree are a matter of personal style and experience. Accordingly, an attorney is kind of like the quarterback of a football team. They influence how things are presented to the jury and what particular parts of the case are emphasized or de-emphasized. You always have the right to ask your attorney to explain why decisions are being made. There needs to be open communication and a relationship of trust between a client and an attorney. 29.6.2.2 Fact Witnesses Most people who testify at a trial are there for the sole purpose of presenting facts. Aunt Millie will never be allowed to testify whether she thinks ABC Company ought to pay you for your injury. However, Aunt Millie may be able to testify about the differences she saw in you before or after the event. She could also testify about what she saw, heard, or read. The more fact witnesses are able to stick to just facts and personal observations, the less susceptible they are to being “beaten up” by the opposing attorney. It is the job of the attorney, not the witness, to argue which facts should be given the most emphasis and how they should be used in the litigation process. When fact witnesses try to do this they quickly loses credibility. 29.6.2.3 Expert Witnesses Unlike Aunt Millie, expert witnesses are allowed to give opinions at trial. These opinions must be based on factual evidence in the trial combined with their knowledge, experience and training. For example, an X-ray showing an arm bone with a line through it is a fact. A physician’s testimony that the line means that the arm is broken in that spot is an expert opinion. There are a number of rules affecting the scope and manner in which expert witnesses can testify (see the other Willison chapter). In a CO poisoning case, having expert witnesses explain complicated and technical matters is very helpful to a jury and ultimately critical to the litigation. Most people do not intuitively understand how toxins affect the brain. Experts are brought in to make things like this clear for a jury. If you try to do that for yourself, you will play into the defense strategy of looking like you are manufacturing a case for yourself.

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29.7 CONCLUSION The litigation process, and all that surrounds it, can be overwhelming to any individual, especially those struggling with the effects of being exposed to CO. One needs to consider and make many difficult decisions before beginning the journey involved in CO poisoning litigation. To begin with, your considerations should include the determination of goals and the finding of the right attorney to assist you in meeting those goals. As the process continues, one needs to gather the information of who, what, when, where, how, and why the exposure occurred and the person responsible for bringing those factors together. If sufficient evidence exists, the lawsuit can begin. Many people want to know how long it will take. That is impossible to answer. A case could settle at any point. If you go to trial, it depends on how busy the court is and how long discovery takes. In most places, you should plan on about 2 years from the time you file suit until you are actually in front of a jury. To the extremes, it will likely not be less than 1 year, nor more than 3 years. But that is just the trial. After trial, either party may appeal the decision. That can take another year or two. Then they might be able to appeal again to the Supreme Court of that jurisdiction. In the worst case scenario one of the Courts of Appeals might order the parties to go back and try the case all over again. As you can see, a negotiated settlement is almost always better than having your day in court. But you will never negotiate a decent settlement unless you are ready to take your day in court. We talked a lot about motivations at the beginning of this chapter. Let me end by bringing this full circle. Once you decide to litigate, the best way to survive the process is to forget about it. Move on with your life. By the time the complaint is filed your attorney should have most of the information he or she needs. You will be called upon from time to time to provide information, but your main roles will be to testify at a deposition and show up at trial. Over a 2-year period, you may have 30 days where you are personally involved. If you wake up every one of the other 700 days obsessed about the lawsuit, you will drive yourself (and everyone around you) crazy. The hardest part is to gather the information and make an informed decision about whether to sue. After you have crossed that bridge, let the process unfold while you live life. Remember, how you live and what you do brings satisfaction. Your litigation cannot serve that purpose.

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Offering Expert Opinions in a Carbon Monoxide Case Stephen P. Willison

CONTENTS 30.1 A Brief Introduction to the Rules of Engagement . . . . . . . . . . . . . . . . . . . . . . . . . 30.2 Roles—Who’s Who and What Do they Do. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30.2.1 Fact Witnesses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30.2.2 The Judge . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30.2.3 The Jury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30.3 Your Opinion—the Heart and Soul of Being an Expert Witness . . . . . . . . . 30.3.1 Are You Really an Expert? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30.3.2 Scope . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30.3.3 Basing Your Opinions on Reality . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30.3.4 Scientific Basis of Your Opinion—the Method Prevents the Madness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30.3.5 Putting It Together—Testifying About Your Opinions . . . . . . . . . . . 30.4 The Battle of Experts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30.5 Thinking Long Term . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30.6 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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Some trial attorneys tell jurors that a trial is like assembling pieces of a puzzle. If that analogy is true, then a good expert witness should be like the picture on the puzzle’s box. No one likes hearing about the “battle of experts.” After all, the law should be based on facts not opinions, right? But in reality, the typical juror often does not have the background or training necessary to understand the importance and relevance of many of the facts presented to them in a highly technical case. This is especially true in carbon monoxide (CO) litigation. Terms like “carboxyhemoglobin”, “523 ppm” and “lateralized cerebral dysfunction” can be critical pieces of the puzzle, but are useless to a jury unless they are educated about their meaning and place in the case. So, like the picture on a puzzle box, the expert witness takes those complicated pieces and helps the jury understand how they fit in and where they go, so the image of what happened begins to make sense. 671

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This chapter is not intended to be a substitute for law school or an outline of how to conduct a trial. It also is not intended to be specific to any field. Instead, it is intended to be a generalized guide for those asked to testify as an expert witness to understand their role in the process. It should encourage a better dialog between expert witnesses and trial counsel, not substitute for that dialog. There are many, many important issues in this area which cannot be covered without specific knowledge of your case or field.

30.1 A BRIEF INTRODUCTION TO THE RULES OF ENGAGEMENT Every court in the United States makes decisions about the admissibility of evidence on the basis of its Rules of Evidence. All federal courts share one set of rules called the Federal Rules of Evidence. However, each state has its own set of rules. While many states model their rules of evidence after the Federal Rules, almost all of them have some variations. As a result, there are 51 different sets of Rules of Evidence in this country. In addition to Rules of Evidence, every jurisdiction has its own set of Court Rules. While the Rules of Evidence determine whether a particular piece of information is admissible, Court Rules determine whether or not admissible evidence is actually admitted. Obviously, we cannot discuss, or even summarize, the thousands of variations. Because of its broad influence in almost every jurisdiction, an understanding of the Federal Rules of Evidence1 is a decent foundation for testimony in just about every court. Understanding the small variances in local rules, however, are critical to your specific case. For example, the Federal Rules of Evidence allow an expert witness’s opinion to be based on facts or data “perceived by or made known to the expert.”2 The Rules of Evidence in the State of Michigan, however, state that the facts or data upon which an expert bases his opinion “shall be in evidence.”3 So what is the difference? Everything. Imagine that a firefighter makes a statement to a local television station at the scene of an incident that they recorded carbon monoxide levels in excess of 1000 ppm. The next day, that firefighter retires and disappears. In addition, in his excitement over retirement, he failed to record that data into his notes. His statement to the media that the CO concentration was more than 1000 ppm is hearsay.4 Hearsay is not admissible.5 In a Federal Court (even a Federal Court in Michigan), an expert witness could still testify about opinions based upon that hearsay because it was a fact “made known to the expert.” In a State Court in Michigan, an expert witness could not testify to any opinion based on that hearsay because it would be on the basis of a fact not in evidence. 1 Sometimes abbreviated as F.R.E. 2 F.R.E. 703. 3 M.R.E. 703. 4 F.R.E. 801. 5 F.R.E. 802.

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This is why expert witnesses should not try to be lawyers. Each and every time you are asked to testify in a case, you should spend time with the attorney finding out about the rules of evidence, deadlines, disclosure rules, and everything else that may influence the admissibility of your opinions. In addition, it is critically important to understand what rulings have occurred in the particular case which may affect your testimony. A good working relationship between trial counsel and expert witnesses is a key factor to success. Just because you have testified as an expert a hundred times over does not mean you should make any assumptions about changes in the rules or differences between jurisdictions.

30.2 ROLES—WHO’S WHO AND WHAT DO THEY DO It is your job to help the jury make sense of the various facts that have been presented to them throughout the trial. However, you will not be the only person involved in the case. In all likelihood, you will not be the only “picture” presented to the jury as to what this “puzzle” should look like. Understanding how you fit into the litigation structure is important to your success.

30.2.1 FACT WITNESSES Obviously, there would not even be a litigation unless there was some substantial disagreement between the plaintiff and defendant. In a CO case, the plaintiff is likely trying to prove that the defendant is responsible for his or her injury or death. The defendant either reasonably or unreasonably denies responsibility for that injury. Plaintiffs, defendants, and all non expert witnesses are substantially limited as to the types of information they can offer in their testimony. As a group, these people are referred to as fact witnesses. Fact witnesses provide the pieces of the puzzle for which they have specific knowledge. Examples of fact testimony would include the following: • • • •

The alarm went off at 2:03 p.m. The CO meter read 364 ppm. The CO meter was last calibrated on January 15. The plaintiff was in the building when we arrived.

With few exceptions, fact testimony is limited to things that were seen, heard, or experienced by the witness himself. It can be verifiable, like the machine was calibrated on January 15. It can also be completely subjective like, “I had a headache.”

30.2.2 THE JUDGE In a civil trial with a jury, the role of the judge is simply to determine what evidence will and will not be presented to the jury. It is the judge’s job to know, interpret and enforce the Rules of Evidence we discussed earlier. While judges do not decide the facts of the case, they can greatly influence the outcome of the case by controlling what information the jury is allowed to consider.

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Judges are not perfect, but their position does deserve respect. Making objections, responding to opposing objections, and debating rules should be left to the lawyers and the judge only. Juries almost always like and trust the judge. If you are disrespectful to the judge in front of them in any way, they will likely start to mistrust you. Regardless of whether you agree, do whatever the judge tells you. Let the lawyers fight about it later.

30.2.3 THE JURY The jury ultimately decides what happened and who is responsible. In doing so, they are often given a questionnaire to fill out. Each jurisdiction has its own rules for how they can answer these questionnaires. However, most jurisdictions do not require a unanimous jury in a civil case. The members of the jury, more than anyone else, are the people who need to understand and believe your testimony. Although the substance of your opinions should never change, your method of delivery should be sensitive to your “audience”—the members of the jury. There is a temptation in a courtroom to want to appear smart. Impressing the lawyers, the judge, or other experts who may be in the courtroom might be gratifying, but your testimony will be useless if it is not understood by the jury. Even worse, your testimony will be harmful if your efforts to be “smart” are perceived by the jury as “smug.” It is far better for everyone in the room to think you are an idiot and the jury think you are the best witness at the trial, than for the opposite to be true. Typically, lawyers will have some basic information about jurors before you take the stand. Information like levels of education or professions might be useful, but also might be dangerous. Just because someone is educated does not mean they are smart. Just because someone dropped out of school and became a farmer does not mean they are not reading Plato and Socrates in the evening. Broader stereotypes are even worse. Information like age, gender, race, or perceived economic class is useless. You are not trying to convince a class of people, you are trying to convince a particular person. Body language feedback such as smiles, nods, even rolling eyes and scratching heads is generally a better indicator than education levels and economic status.

30.3 YOUR OPINION—THE HEART AND SOUL OF BEING AN EXPERT WITNESS There are two components to expert testimony. Like two wings on a bird, if either one is missing, your testimony cannot fly. First, you must be right. Second, you must have the ability to explain your opinion. Fortunately, these two things feed off each other. When you are right, it is easy to explain how you reached your conclusion. Moreover, when your opinion is formed with an understanding that you will have to explain it later, you have a higher likelihood of coming to the correct conclusion. Federal Rule of Evidence 702 controls whether expert testimony should be admitted. It states that: If scientific, technical or other specialized knowledge will assist the trier of fact to understand the evidence or to determine a fact in issue, a witness qualified as an expert

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by knowledge, skill, experience, training, or education may testify thereto in the form of an opinion or otherwise, if: 1. The testimony is based upon sufficient facts or data; 2. The testimony is the product of reliable principles and methods; and, 3. The witness has applied the principles and methods reliably to the facts of the case.

30.3.1 ARE YOU REALLY AN EXPERT? In a CO case, it is pretty easy to conclude that there are a number of things necessary to “assist the trier of fact to understand the evidence or to determine a fact in issue.” Given this fact, the first question that must be answered by the court is whether a particular witness, like you, is qualified to testify as an “expert” witness. As the rule states, an expert can be anyone who would assist the trier of fact by way of their knowledge, skill, experience, training, or education. You do not have to have a degree or license to be an “expert” witness. As an example, the US Supreme Court recognized that a perfume tester maybe an expert in identifying odors on the basis of years of experience and testing.6 Of course, you can also be an expert witness because you invented the product, have a doctorate degree or are a world renowned leader in your field. The point is, the judge and the jury has to have some understanding of why they should listen to you. We do not want technical cases influenced by “man on the street” opinions. As a result, you need to be prepared to present good reasons why you should be heard. You need to keep a list of any activities you have accomplished, studied, written, or taught that are relevant to the area in which you intend to testify as an expert. Every time you do something new, you should add it to your curriculum vitae immediately. To gain credibility, you should also stay current in your field. Just because you were the king of your field in 1972 does not mean that you are an expert in the twenty-first century. In addition, many jurisdictions require expert witnesses to produce a log of cases in which they have previously testified as an expert. While this is specific to each jurisdiction, the Federal Rules require the production of a list of any expert testimony in the past 4 years and any publications in the past 10 years.7 It is always permissible for an opposing attorney to make sure the jury is exposed to facts which may sway your testimony. For example, if you always testify that every product is safe, the jury should know. If you never treat patients, but only testify as an expert witness, the jury should know. These facts do not necessarily make your opinions invalid, but they do get factored into how much credibility your opinions will be given. You also have to be careful with what you call experience. Letting your ego run wild or making mountains out of molehills will destroy your credibility. Many physicians have tried to claim to be an expert in CO only to later reveal that the

6 Kumho Tire Company v Carmichael 119 S. Ct 1167, 1176 (1999). 7 F.R.C.V.P. 26(a)(2)(B).

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entire extent of their training and experience on CO involved reading one half of a chapter in one textbook, in one semester of medical school 20 years ago. Certainly, all physicians have training in how the body reacts to various conditions. Certainly, physicians should have a greater understanding than jurors on how even the rarest condition will affect a person. When they go the extra step of claiming to be an expert in carbon monoxide, however, they loose credibility quickly when the background training and experience is missing. Good attorneys do their research. I have seen experts have their careers destroyed because they bragged about degrees they did not earn and positions they did not hold. If you have published 100 papers on the topic about which you are going to testify, you should be prepared to be grilled with questions if even one of those papers is contrary to your current testimony. In fact, some defense attorneys and plaintiff attorneys keep databases on experts and share deposition transcripts. Never exaggerate your background because someone eventually will find it.

30.3.2 SCOPE You should understand the limits of your role in litigation. In all likelihood your job is not to provide the entire picture of the puzzle, but rather one portion of it. An expert’s testimony may or may not include a discussion of how his area of expertise plays out in the person’s life. Always remember—the further you get away from the solid footing of what you know, the more likely a skilled opposing counsel will make you look so silly the jury will discount even the core of your opinion. Sometimes you may be asked to give the ultimate opinion in a case. You may be the witness called to testify whether a product is safe, or whether a person is injured. When you serve in this role, your opinion should be based upon all the information you can get your hands on. Conversely, you may be asked to testify about a very specific point. For example, you may be asked to simply explain to the jury how CO can cause short-term memory loss. Perhaps other witnesses will be asked to testify whether it, in fact, happened. Your role might simply be to answer the hypothetical question. In this scenario, you may be able to testify based solely upon your background and experience without reviewing any portion of the case. Understanding your attorney’s expectation, and communicating your preferences to that attorney, is the best way to understand how to prepare for your expert testimony, defend your opinions, and satisfy your client.

30.3.3 BASING YOUR OPINIONS ON REALITY The Rules of Evidence require your testimony to have some bearing on the facts of the case. This means it not only has to be relevant8 but it also has to be based on sufficient facts or data. Most judges in most jurisdictions will not allow an expert witness to

8 “Relevant evidence” means evidence having any tendency to make the existence of any fact that is of consequence to the determination of the action more probable or less probable than it would be without the evidence. F.R.E. 401.

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testify about a medical diagnosis of a person they met 15 min before trial in the lobby of the courtroom. Your opinions must be based upon information gathered by first hand observation, facts in evidence, hypothetical scenarios, or other information which experts in your field reasonably rely upon.9 The most common attack on an expert’s opinion will come in the nature of the facts upon which it is based. For example, if an expert opinion is based upon the fact that a person was living in a home with a faulty furnace for two years, it would be critical to know whether that person actually spent time in the home or had been stationed overseas in the military for that entire period. Gathering information for the basis of your opinions is a critical part of the process. It can also be difficult. Not only is the nature of evidence in a CO case easily destroyed,10 there are financial considerations as to how much the client is willing to pay for the time it takes you to research these facts. Simply accepting someone else’s statement of the facts, although tempting, is a very thin basis for an expert opinion. Sometimes that is necessary for economic reasons. At the very least, you should review the documents or interview the witnesses who supplied the facts upon which your opinions are based. In addition, once you have these facts, you can more specifically inquire about areas that may discount those facts, such as previous treatments, other conditions, and so forth. When you are asked to render an opinion with limited background information, you should incorporate the scope of that information into your opinion. That way, if your opinion changes one way or another after the addition of facts, you have not lost any credibility.

30.3.4 SCIENTIFIC BASIS OF YOUR OPINION—THE METHOD PREVENTS THE MADNESS If you have ever worked as an expert, or even talked to anyone who has, you would no doubt have heard people talk about something called Daubert.11 Daubert is actually the plaintiff’s name in a Supreme Court case that set forth new standards for expert testimony in 1995. The history and implications of the Daubert decision and the cases which followed it are much too lengthy to be discussed in this chapter. However, a brief understanding of its history and its application today is important to any witness who may be an expert in a toxic exposure case. Prior to Daubert, the standard for expert testimony was that scientific evidence must be “generally accepted” in its field before it could be presented to a jury. Of course, this prevented the law from ever utilizing the latest technology or cutting edge research. As a result, the Supreme Court changed the standard from general acceptance to “scientifically valid.” That ruling has now been incorporated into the

9 Werth v Makita Electric Works Ltd. 950 F2nd 643, 648 (1991 CA 10th ), interpreting F.R.E. 703. 10 See “The Purpose and Process of Litigation in the Carbon Monoxide Case” in this book. 11 Dauber v Dow Pharmaceutical 509 U.S. 579 (1993).

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Rules of Evidence which requires that expert testimony must be “the product of reliable principles and methods.”12 In addition to broadening those standards, however, the court also instituted what is now referred to as the “gatekeeper” function of the trial court. The Supreme Court decided in Daubert, that the trial courts have a duty to analyze the proposed expert testimony before it is presented to a jury to determine whether it is the product of reliable principles and methods. Daubert specifically identified four types of data which may be looked at to determine this validity, but it is not an exhaustive list. Those factors are the following: 1. Whether it is a result of a reliable and repeatable methodology 2. Whether that methodology was subject to peer review or publication 3. The known or potential error rates and the standards of controlling the technique’s operation 4. Whether the methodology is generally accepted within the scientific community Eventually, this “gatekeeper function” was broadened to apply to even nonscientific expert testimony.13 Other cases have specified that this gatekeeper function can apply not only to a particular methodology used by an expert, but also to an entire field of study such as astrology.14 The federal courts have been very consistent and clear about the trial court’s duty to act as a “gatekeeper.” Unfortunately, the standards by which the gate should be kept have been very unclear. If a judge wants to keep evidence out, or allow evidence to come in, the decision surrounding the Daubert case seems to give him cover either way. The case law has been very clear that this should only be an analysis of the methodology, but sometimes it appears to hinge on whether the judge is personally convinced by the expert’s theories. There is no clear way to predict how a court will decide a Daubert challenge and, as a result, you should be prepared to explain the methodology by which you reached any opinion you hold in a case, and explain the research which proves that method is valid. Put another way, you need to be scientific about your work. If one were to analyze the historical basis upon which experts have been excluded from testimony for failing to meet the standard of “reliable principles and methods,” we would likely find that typically it is the result of the expert’s failure to explain the validation of the principles or methods utilized during the Daubert hearing rather than the actual failure of the principles and methods themselves. It very well may be, that after 20 years in your chosen field you can recognize certain situations very quickly, just by looking at them. If you ever testify that the basis of your opinion was “I could just tell by looking at it,” you will likely not 12 F.R.E. 702(2). 13 Kumho Tire Company v Carmichael 119 SCT 1167 (1999). 14 Id. at 1175.

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be allowed to testify as an expert witness. Instead, you need to explain those things you immediately recognized, the scientific research which supports the fact that those factors you observed are important, and then explain how putting those two things together lead to a conclusion, which other experts could repeat. There may be a disagreement as to whether or not a particular fact exists, but you should be able to support your conclusion that the existence of the fact has a scientific basis for being important. If you utilize a particular protocol, you should not only specify that protocol in your testimony, but identify each step of the process you used in reaching your conclusions. This is the best way to convince a judge you will not be wasting the jury’s time. Ironically, it is also the best way to convince a jury your conclusions are correct.

30.3.5 PUTTING IT TOGETHER—TESTIFYING ABOUT YOUR OPINIONS The strategies for testifying in a deposition or in front of a jury can be different depending on how your attorney wants to handle the discovery process. However, your goals should be the following: 1. State your opinion so plainly and clearly that even people who have never heard of your field can understand your conclusion. 2. Explain the reasons you arrived at your opinion in a manner that walks the listener through the process and in a way that any other conclusion would seem unreasonable. 3. State factors which you considered and ruled out only in the context of how they too support your opinion. If you spend too much time focusing on factors which were not present, the listener can become confused as to its relevancy or importance.15 The manner in which you testify is important. You do not want to come across arrogant. You do not want the jury to feel stupid. You also do not want to come across like some used car salesman desperate to have them buy what you are selling. Entire books have been written on what style and technique to use in a courtroom. Basically, they can all be summarized as this: use good manners. The entire courtroom setting revolves around the question/answer format. Your answers have to be responsive to the question asked. If you wander off into areas you want to discuss without being asked, the jury may wonder why you did not answer the question asked, and the attorney may be frustrated that you are not presenting information in the order he intended. 15 For example, if you ruled out MS as a cause of the plaintiff’s symptoms, you should not describe MS in detail without tying it back to the facts of this case. So your testimony should be, “MS can cause some of these symptoms, but it almost always presents with symptom A, which she does not have. Another symptom of MS is condition B, and the plaintiff also does not have that. The patient also has symptoms C, D and E and those are never associated with MS.”

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Some experts address every answer to the jury box. That can appear awkward because you are not having a conversation with the attorney asking the questions. At the same time, if the question is prefaced by “explain to us . . . ” you absolutely should take the opportunity to speak directly to the jury. You should work with your attorney at length before trial to make sure you both understand what important points will be covered and the order in which you will cover them. The best expert testimony will appear as an interesting conversation between lawyer and witness in which both provide information and explain difficult concepts.

30.4 THE BATTLE OF EXPERTS In most toxic exposure cases, you will also encounter an opposing expert in your field. Typically, your opponent will take one of two tactics: you are wrong or your opinions are incomplete. “Wrong” can take many different forms. They may allege you have misapplied scientific principles. They may claim you did not consider certain important facts. They may claim you have been fed wrong information. They may even claim you are being dishonest. The second strategy is to claim that you are improperly reaching a conclusion without sufficient information. This is what I refer to as the agnostic opinion. This testimony boils down to, “I don’t know and neither do you.” Because defendants do not have the burden of proof, this technique is almost exclusively used by defense experts. This strategy plays upon the jury’s desire to be sure. Experts employing this strategy will list off a litany of things that we are not aware of such as wind direction or other toxins the victim may have been exposed to, or the effects of that car accident the victim was in 20 years ago, and so forth. Believe it or not, there are people in this world who make significant incomes traveling around the country saying “I don’t know.” Accordingly, part of your role in the case may be to discredit the testimony of this opposing expert based on the facts of the case and the science of your profession. Ultimately, however, poking holes in an opposing expert’s testimony/opinion, is the job of the attorney. So, more specifically, your role may involve educating your attorney as to what the weakest places are in your opponent’s opinion. Your credibility is enhanced when you are cool under fire. Of course, this is easier to do when you are confident in your testimony. If opposing counsel makes outlandish comments, twists your testimony, or tries other silly tricks, solid science and civil respect will do far more to expose his weakness than any emotional reaction or wisecrack ever could. Skilled attorneys can sense when you might lose your cool. If they see the opportunity, they will be happy to make you unravel on the stand. Juries will forgive the bad behavior of attorneys much quicker than experts, because attorneys are not supposed to be neutral. At the same time, you should not be afraid to agree with opposing counsel when it is appropriate. Juries assume there is some legitimacy to both sides of the story. If you refuse to acknowledge any bad fact or concede any point, they may conclude

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the rest of your statements are embellished as well. Quite frankly, your testimony is highlighted when you can answer, “Yes,” “Yes,” “Yes,” “Yes,” “Absolutely not!” This technique also puts opposing counsel in the uncomfortable position of choosing to ask you “Why not?” (who knows what you will say) or moving on (he is afraid to let you talk—you must be right).

30.5 THINKING LONG TERM As mentioned above, your testimony is never about one case. If you intend to hold yourself out as an “expert” to be relied upon and trusted by juries, you must give “expert” advice. Telling clients what they want to hear will bring far more trouble than even the worst truth. Stretching the bounds of science to help this one case may haunt you the rest of your career. At the end of the day, expert witnesses live and die on their reputation and credibility. Both should be protected at all costs. This is important because when your opponent cannot tear apart your opinion, and cannot tear apart what your opinion is based upon, their only choice is to try to tear apart you. These attacks tend to fall into certain categories. Unfortunately, these attacks work because sometimes they are true. The most common personal attack when you testify is financial. This is particularly effective in blue collar areas or in communities with depressed economies. The easiest area of attack is your hourly rate. If a juror has a job which pays $15.00 per hour, he puts that money in his pocket. Accordingly, there can be an assumption that if you charge $150 per hour, you put ten times as much money in your pocket. Charging $500 per hour or more, therefore, might appear to be a way to make you look like you were “bought.” Assuming you are charging a fair rate for your services, you should not be embarrassed about the number. Embarrassment only adds credibility to the attack. To avoid that feeling, you should be prepared to explain your hourly rate. Perhaps you should explain that the fees are paid to a business, not you, and you need to pay other employees and rent and various expenses out of those fees. The ultimate response is that your client agreed to your rate before you had any information about the case. Clearly, the rate had nothing to do with the opinion. If it continues, the best counterattack to assaults on your fees, however, may be in the form of a simple economics lesson. Perhaps testifying as an expert witness is equal, or even less profitable, than the fees you can charge by performing other professional services. Perhaps the market has proven that your rates are reasonable because even at your hourly rate, you are offered more work than you could handle. On the other hand, perhaps you charge a higher hourly rate for expert services to intentionally make sure it does not end up becoming the only thing you do. Although it is certainly reasonable for an attorney or a jury to inquire about your level of compensation for the services provided, everyone, from every economic class, understands the awkwardness of being forced to talk about your personal finances in public. If it goes too far or becomes too personal, it is possible to garner some sympathy from the jury with an appropriate retort. For example, you might find an

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opportunity to say, “I think we have established that I have been successful in my field. Perhaps we could discuss the reasons for that.” Any counterattack, however, must be both fair and respectful. Another common attack is to try to twist your relationship with the client or the attorney. Again, if this is the 100th time you have testified in a case involving that attorney or client, there should be a legitimate reason for it. Be prepared to explain that reason. Do not be embarrassed. Perhaps the client keeps hiring you because you are the best in your field. Perhaps the client hires you because they trust they will get an honest assessment of the facts from you instead of what they want to hear. Perhaps you frequently work together because you are geographically close. The fact that you have worked with an attorney several times might make you more comfortable to be frank about your opinions and disagree on the assessment of some cases. Even if you never disagree with that attorney or client, it may simply be because the attorney is sophisticated enough to understand when it is necessary to hire an expert in your field. Personal attacks only work if they are true. If your opinions are honest and your fees are reasonable, you should have no problem explaining them in court. If you do have difficulty coming up with a reasonable explanation, perhaps you need to rethink how you operate. You must always make sure your decisions are based solely upon the facts of the case and sound science. Once it is proved that you lack integrity, your usefulness as an expert is over.

30.6 CONCLUSION Testifying as an expert witness can be an exciting and fulfilling experience. For many experts, it is an opportunity to be part of making a difference in how things are made and used. As with anything professional, however, it is important to keep your perspective. While you may develop opinions on what the outcome of the case should be, your role is to provide information and education to a jury. Avoiding the temptation to change from information source to “advocate” is the key to success and longevity as an expert witness.

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Injury Caused by Carbon Monoxide Poisoning: Defining Monetary Damages Steve Collard

CONTENTS 31.1 What is Health? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.2 Measuring Health . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.3 Quantifying Less-Than-Perfect Health . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.3.1 Years Lived with Disability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.3.2 Healthy Life Expectancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.3.3 Life-years Lost to Injury. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.4 From the Population to a Person . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.5 Disability and Major Activity: Working . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.6 Earning Capacity has Two Parts. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.7 Measuring One Person’s Loss of Capacity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.8 The Standard Vocational Interview. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.9 The Construct of Work. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.10 General Educational Development (GED) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.11 Specific Vocational Preparation (SVP). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.12 Diminishment of Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.13 Monetary Damages: The Five Steps in the Analysis of Loss of Earning Capacity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.14 Case Report . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.14.1 Mr. Jones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.14.2 Mrs. Betty Jones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.14.3 John Jones. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.14.4 Cathy Jones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31.15 Dedication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

684 684 687 687 687 689 690 692 693 694 695 696 697 697 699 699 703 703 714 717 721 723 723

683

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31.1 WHAT IS HEALTH? The well-being of an individual is a function of longevity and morbidity. Morbidity is defined as those nonlethal aspects of daily function and pain and suffering that affect people’s lives.1 A measurement device that uses only mortality rates understates the public health importance of conditions that result in proportionately more morbidity and disability. Mortality rates are useful in identifying conditions with the worst health outcomes, but conditions with low mortality rates may have a high burden of disease because of morbidity. Overall health of an individual is a function of self-perceived health, the ability to function, and existential/experiential symptoms and capabilities (see Figure 31.1).2 Awheelchair bound individual who competes in wheelchair basketball games or marathons would probably have a greater self-perceived health status than a wheelchair bound individual whose level of overall functioning is lower (see Table 31.1). Standardizing health measurement tools allows investigators insight in defining the effects of impairment causing disability on the individual in his or her environment.

31.2 MEASURING HEALTH In monitoring and determining the health of the population in the United States, in the early 1900s the leading causes of death were from infectious diseases. Today, the leading cause of death of persons age 1–44 are from injuries as a result of motor vehicle accidents.3 The overall health of a population was once measured as a function of the infant mortality rate. In 1993, Dr. Alan Lopez of the World Health Organization (WHO) prepared estimates of child-death by cause, which were consistent with the death totals provided by demographers at the World Bank. Concurrently, a World Bank effort was preparing consistent mathematical estimates for adult mortality by cause. Ensuring these consistencies was a major advance, and is a precondition for systematic attempts to measure disease burden.1 A goal of the WHO has been the gathering of timely and reliable health information, because the decisions related to spending billions of dollars annually require valid health statistics. From the community levels of health services to the national and international levels, information is gathered to determine the effectiveness of health strategies. These data help in monitoring the global epidemics, the potential pandemic H5N1 bird flu, and provide a continuous assessment of public health approaches to disease and injury prevention and control. The first nationwide surveillance system to measure the burden of any disease was implemented in 1950, when malaria surveillance was developed. The second and third national surveillance systems were implemented in 1955, due to shortages of the vaccine for polio and in 1957, influenza. Making a surveillance system that identifies and responds to health problems has led to the beginning of more scientific study of the morbidity and mortality from dozens of conditions. It is a challenge, which, given widespread use will lead to better decisions on spending health dollars that ensures a more equitable future health for everyone.

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Overall health

Self-perceived (self-rated) health

Abilityto function

Physical function

Mobility Daily activities

Social/role function With family and friends

Major life role

Recreation

Cognitive function

Existential/ experiential symptoms and capabilities

Pain

Energy/vitality

Emotional

Happiness/ mood Depression/ anxiety Self-image

Sensory

Vision

Hearing Memory

Problem solving

FIGURE 31.1 Concept of overall health.2

In 1988, by the World Bank, the Global Burden study began with Phase 1, called “Health Sector Priorities Review.” This was begun as an attempt to measure the significance to public health of individual diseases and what was known about the cost and effectiveness of relevant interventions for their control. The goals of this research were to, (1) include nonfatal diseases and injuries in the analysis of international health policy; (2) to decouple epidemiological assessment from advocacy so that estimates of the mortality or disability from a condition are developed as objectively as possible; and (3) to quantify the burden of disease in a manner that allows for cost-effective

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Mr. Smith's life expectancy would have been to age 77.7 had he not died due to carbon monoxide poisoning at age 50.

Mr. Smith was 50 years old at the time of his death.

Assuming survival, Mr. Smith would have continued working, benefitting society through his taxes and expenditures, and he would have continued providing services to his family and friends and chores and tasks for his household. The monetary losses to his estate exclude his personal consumption, however.

27.7 years of life lost

0

10

20

30

40

50

60

70

80

90

FIGURE 31.2 Life expectancy and years of life lost.

analysis.1 Dr. Christopher Murray of Harvard University introduced the term DALY (disability-adjusted life years) as a common measure of effectiveness for the review.1 The DALY is comprised of two components: The number of years of life lost (YLL) and years lived with disability (YLD). Years of life lost is the difference in years of the age at death owing to a specific cause from the cohort’s statistical life expectancy. A man who dies prematurely at age 50 would lose 27.7 years of expected life, because his life expectancy at age 50 is 77.7 years.1 (see Figure 31.2) Years lost to disability calculations take into account the severity of disability owing to a given disease as well as the average length of time the disability persists. The level of disability owing to a given condition is revealed as a disability weight. Disability weights range from 0.0 at perfect health to 1.0 for death.1 Murray and Lopez systematically reviewed published and unpublished data to estimate the incidence, prevalence, and duration of 483 disabling sequelae of 107 diseases and injuries. Internal consistencies were ensured using a software program that identified consistent parameters. The severity of disability in the YLD calculations was measured in a deliberate manner. First, panels of health professionals and disease experts in more than 100 diseases or injuries, were drawn from the WHO, the International Agency for Research in Cancer, the World Bank, the United States Centers for Disease Control and Prevention, and from numerous academic institutions. The professionals provided estimates (on the basis of published and unpublished studies) of the duration of the disease and of incidence, remission, case-fatality, prevalence, and the death rates. An average handicap was eventually derived for 22 indicator conditions. The different dimensions of a given nonfatal health outcome can be described as occurring under one of the indicator conditions, like

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physical manifestations (deafness or below-the-knee amputation, for example), neuropsychiatric manifestations (psychosis, depression), manifestations related to social or group interaction consequences (vitiligo), or pain manifestations (severe migraine, angina, or sore throat).1

31.3 QUANTIFYING LESS-THAN-PERFECT HEALTH 31.3.1 YEARS LIVED WITH DISABILITY The US Department of Health and Human Services (DHHS) publication # April 7, 1995 is titled “Years of Healthy Life.” In this publication, a definition of health and well-being is as follows: Symptoms of health and well-being usually involve the assessment of physical and psychological sensations, such as pain and feelings of anxiety, which are not directly observable. Physical functioning may be measured in terms of being confined to bed, couch, or chair due to health reasons, or in terms of health-related limitations in mobility. Social functioning may be measured in terms of an individual’s limitation in performing one’s usual social role, whether it is work, housework, or school. Health perceptions are assessed in terms of subjective evaluations of health and satisfaction with health. Social opportunity includes resilience and coping and can be measured in terms of social impact due to health. When symptoms and subjective complaints; mental, physical and social functioning; general health perceptions; and social opportunity are combined to describe health, the resulting multidimensional concept is generally referred to as Health-Related Quality of Life (HRQL).3

When the US DHHS implemented its Healthy People 2000, National Health Promotion and Disease Prevention Objectives for the Nation, one goal was increasing the span of healthy life. In 1987, the average life expectancy for the average 51 year old male was 25.1 years. In 2000, the number of years of life expectancy for same increased to 27.1 years, and most recent data published in 2006, based on 2003 data shows the life expectancy increase to 28.5 years for same.4 The DHHS’s Healthy People, 2010 program has two goals: (1) to increase the quality as well as the years of healthy life (YHL) of the US population; and, (2) to eliminate health disparities in the US population.

31.3.2 HEALTHY LIFE EXPECTANCY A table titled “Difference Between Healthy Life and Full Function Healthy Life at Single Years of Age by Race and Sex, United States, 1996” quantifies in terms of years the effect of morbidity on life expectancy.5 Researchers at the National Center for Health Statistics defined 30 health states on a scale of 1.0 (perfect health) to 0.10 (poor health). The 30 states consist of six stages of health combined with a self-perceived health scale of five categories. The five levels of self-perceived health are “excellent,” “very good,” “good,” “fair,” and “poor.” According to the values, a year of perfect health implies one full year of healthy life. Other health states result in less than one full year of healthy life.

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The six stages of health are as follows: 1. Not limited

2. Limited in other activities

• Not limited (includes unknowns) regardless of age; this category includes unknown role regardless of a person’s age • Limited in other activities regardless of age, or • Limitation in activity and 65–69 years of age but able to perform activities of daily living (ADLs) and able to perform instrumental activities of daily living (IADLs)

3. Limited in major activity

• 64 years of age and younger—limited in amount or kind of major activity • 65 years and older—major activity is considered to be ADL and IADL activities; therefore people in this age group cannot fall in this category

4. Unable to perform major activity

• 64 years of age and younger—Unable to perform major activity • 65 years and older—major activity is considered to be ADL and IADL activities; therefore people in this age group cannot fall in this category • 0–17 years of age—not applicable. Proxy respondents were used to obtain this information about children; unable to perform their major activity is the most severe functional limitation to which they can be assigned • 18–64 years of age—unable to perform routine needs without the help of other persons and unable to perform or limited in major activity • 65 years of age and older—unable to perform routine needs without the help of other persons.

5. IADL

6. ADL

• 0–4 years of age—not applicable. Proxy respondents were used to obtain this information about children; unable to perform their major activity is the most severe functional limitation to which they can be assigned • 5–64 years of age—unable to perform personal care needs without the help of other persons and unable to perform or limited in major activity • 65 years of age and older—unable to perform personal care needs without the help of other persons

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Using the National Health Interview Survey (NHIS), researchers categorize age groups, numbers of individuals within the groups, and the overall score for each health state. The resulting scores, by age groups, can then be applied to a life table onto the hypothetical cohorts in the life tables. A healthy life expectancy is less, when measured in terms of years, than a life expectancy, because of the mixture of perfect health and less-than-perfect health states found in the data.

31.3.3 LIFE-YEARS LOST TO INJURY The effect of preventive measures on increasing the overall health of our society is well known, but what is less well known is that the same type of measurement leading to preventing diseases is being applied by researchers in analyzing motor vehicle crashes to prevent injuries. Air bags and bicycle helmets are two examples of such research, the results of which mathematically can be confirmed as beneficial to society, and that citizens are probably going to remain healthier overall for using them than for not. The money being spent to prevent saves money over the long-term and increases postaccident quality of life outcomes. When a motor vehicle crash is reported, lots of information is gathered. Even before the law was passed requiring air bags, researchers with the National Highway Traffic Safety Administration knew that the devices would reduce loss of life and reduce the impact of head trauma (the combination of an air bag in addition to a lap and shoulder belt reduces the risk of serious head injury by 81%, compared with 60% reduction for belts alone).6 The authors of a study for the National Highway Traffic and Safety Administration titled “The Economic Impact of Motor Vehicle Crashes 2000” analyzed data from the National Automotive Sampling System Crashworthiness Data System. The economic cost of crashes includes costs for medical aspects, emergency services, vocational rehabilitation, market productivity, household productivity, insurance administration, workplace costs, legal costs, travel delay, property damage, and psychosocial impacts.6 A functional capacity index (FCI) was developed to standardize the loss of ability to perform different life functions, over the long-term, after sustaining injury in a motor vehicle crash. The FCI scale ranges from zero (being no loss of function) to one (full loss of function). The FCI measures across major activity (work, school, or homemaker), instrumental activities of daily living (IADLs) (getting around the home and community), and activities of daily living (ADLs) (feeding and self-care). Clinical validation studies confirm the FCI does measure functional outcome. To measure the long-term cost to society, the FCI for a given injury is multiplied times the person’s life expectancy, which results in a measure called life-years lost to injury (LLI). The LLI values for all kinds of injuries can be aggregated over a statistical population to measure the effect different types of injury have on society as a whole. For example, Tom, a 40 year old male, sustains back injury and cannot bend or lift as a result. The FCI for this injury is 0.49. This means that compared to a normal, healthy person’s level of function, Tom’s is reduced by 49%. At age 40,

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his life expectancy is 37 years. His resulting LLI is 18 years. Of his potential time living with unlimited functioning, half of his life functioning now is as a result of injury.

31.4 FROM THE POPULATION TO A PERSON Typically, the medical outcome of a patient is expressed in a percentage as an impairment rating. A zero impairment rating implies no limits, and as the impairment percentage rating goes up, the implication is that the degree of the severity of the condition is increased, and assumed difficulties in functioning are increased. Medical doctors routinely provide impairment ratings, but there is a transparent stretch of logic, usually, with connecting a quantity or diminished quantity of ability to function from an impairment rating. Occasionally, a functional capacity evaluation is done, which reveals the effect of the impairment on the person’s ability to perform a given function, and for the amount of time or tolerance for doing that particular task. In 1980, the International classification of impairments, diseases and handicaps (ICIDH) was developed as a part of a global health measurement system. With this, the positives and negatives of different medical treatments for similar sequelae could be more readily analyzed to help improve health care, in consideration to both overall costs and patient outcomes. After 9 years of international revision efforts coordinated by the WHO, the World Health Assembly on May 22, 2001, approved the International Classification of Functioning, Disability and Health,and its abbreviation of “ICF.” The ICIDH uses a linear progression to describe the framework of a nonfatal health outcome from disease (injury) to pathology to manifestation to impairment to disability to handicap. However, the new ICF is structured around the following broad components: 1. Body functions and structure 2. Activities (related to tasks and actions by an individual) and participation (involvement in a life situation) 3. Additional information on severity and environmental factors Functioning and disability are viewed as a complex interaction between the health condition of the individual and the contextual factors of the environment as well as personal factors. The picture produced by this combination of factors and dimensions is of “the person in his or her world.” The classification treats these dimensions as interactive and dynamic rather than linear or static. It allows for an assessment of the degree of disability, although it is not a measurement instrument. It is applicable to all people, whatever their health condition. The language of the ICF is neutral as to etiology, placing the emphasis on function rather than condition or disease. In Appendix 2 of the ICF Checklist for the examiner, there is a guide to help when interviewing the respondent to probe about problems in functioning and life

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activities, in terms of the distinction between capacity and performance. This guide is a good summary of the goal of a standard vocational interview: The first probe tries to get the respondent to focus on his or her capacity to do a task or action, and in particular to focus on limitations in capacity that are inherent or intrinsic features of the person themselves. These limitations should be direct manifestations of the respondent’s health state, without the assistance. By assistance we mean the help of another person, or assistance provided by an adapted or specially designed tool or vehicle, or any form of environmental modification to a room, home, workplace and so on. The level of capacity should be judged relative to that normally expected of the person, or the person’s capacity before they acquired their health condition. The second probe focuses on the respondent’s actual performance of a task or action in the person’s actual situation or surroundings, and elicits information about the effects of environmental barriers or facilitators. It is important to emphasize that you are only interested in the extent of difficulty the respondent has in doing things, assuming that they want to do them. Not doing something is irrelevant if the person chooses not to do it.7

The WHO defines disability as any restriction or lack (resulting from an impairment) of ability to perform an activity in the manner or within the range considered normal for a human being. The Americans with Disability Act adds the condition that the restriction or lack substantially limits the amount or kind of functioning. The NHIS defines Impairments as, Chronic or permanent defects, usually static in nature, that result from disease, injury or congenital malformation. Impairments represent decrease or loss of ability to perform various functions, particularly those of the musculoskeletal system and sense organs. Activity limitations are defined in terms of a person’s ability to perform a major activity. Major activities are defined differently for different age groups as follows: 1. 2. 3. 4.

For children under 5 years old, the major activity is ordinary play. For persons age 5–17, the major activity is attending school. For persons 18–69, the major activity is working or keeping house. For persons 70 and older, the major activity is self-care, without needing assistance in performance of ADLs or IADLs.

ADLs (self-care) usually include bathing, dressing, toileting, bed or chair transfer, feeding self, getting around the home, and continence. IADLs usually include performing customary household chores and tasks, handling money, getting around the community, shopping, using the telephone, and preparing meals. The NHIS defines Chronic Health Condition as a “condition that a respondent describes as having persisted for three or more months, or one that is on the NHIS list of conditions always classified as chronic, no matter how long the person has had the condition.” An “activity limitation” is defined as “being limited in an activity that a person would otherwise be expected to perform.” Activity restrictions are defined in terms of “bed-days,” “school-loss days,” “work-loss days,” and “cut-down days.”

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31.5 DISABILITY AND MAJOR ACTIVITY: WORKING The Department of Commerce, Bureau of the Census report called Labor Force Status and Other Characteristics of Persons With a Work Disability, Current Population Reports, Series P-23, Number 160, defines disability with a similar definition to the NHIS definition. Persons identified with a disability in the Current Population Survey (CPS) are defined as those having a health problem or disability which prevents them from working or which limits the kind or amount of work they can perform. Interestingly, the health state #3 from the NHIS (3) Limited in major activity

64 years of age and younger—limited in amount or kind of major activity.

is very similar to the CPS definition of work disability. The National Center for Health Statistics defined 30 health states. The derived health state value for an individual who reports excellent health but is limited in work is 0.81, with a health state value of 1.00 being equal to excellent health and no limits. The derived health state value for an individual who reports very good health but is limited in work is 0.74. The derived health state value for an individual who reports good health but is limited in work is 0.67. The derived health state value for an individual who reports fair health but is limited in work is 0.48. The derived health state value for an individual who reports poor health but is limited in work is 0.34. Since it is these health state values that are applied to the life expectancy data in computing healthy life expectancy, wouldn’t it be similarly appropriate to consider applying health state values to work life expectancy? The CPS is the primary source of information on labor force characteristics of the population of the United States. The sample is scientifically selected to represent the civilian noninstitutional population.8 The annual demographic survey, or March Supplement, provides the primary source of detailed information on the income and work experience of US workers by disability status, age, sex, and level of educational attainment. Two facts derived from the CPS data are (1) Persons meeting the definition of work disability on average earn less than nondisabled counterparts, regardless of age, education or gender; and (2) Persons meeting the definition of work-disability on average report lower participation and employment rates than nondisabled counterparts, regardless of age, education, or gender.8 In the CPS framework for work-disability, it is acknowledged that some respondents will report impairments, functional limitations, or disabilities in life activities other than work. This jibes with health state #2 from the NHIS

(2) Limited in other activities

Limited in other activities regardless of age, or Limitation in activity and 65–69 years of age but able to perform ADLs and able to perform IADLs

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The derived health state values are greater in this category across the board when compared to those in the #3 health state.

TABLE 31.1 Perceived Health Status Activity Limitation Not limited Limited-other Limited-major Unable-major Limited in IADL Limited in ADL

Excellent

Very Good

Good

Fair

Poor

1.00 0.87 0.81 0.68 0.57 0.47

0.92 0.79 0.74 0.62 0.51 0.41

0.84 0.72 0.67 0.55 0.45 0.36

0.63 0.52 0.48 0.38 0.29 0.21

0.47 0.38 0.34 0.25 0.17 0.10

Less-Than-Perfect-Health status can be measured as a burden of a condition on the individual level and when applicable as a function of reduced labor force participation and employment rates. Both measurements result in a loss of time, either in years lost to disability (YLDs) or reduced worklife expectancy. Disability weights and healthy life expectancy data provide empirical evidence supporting the observed evidence of the CPS. Work-disabled status is a health state that is more of a burden on the individual than perfect health and more likely to result in a shortened worklife. Compelling evidence supports using a diminished worklife probability in calculations determining loss of future earning capacity.

31.6 EARNING CAPACITY HAS TWO PARTS Earning capacity represents an individual’s ability or power to earn money. It’s that one figure that best represents the person’s lifetime ability. It may or may not be synonymous with actual earnings. In most instances, a mature worker experiences actual earnings that are congruent with earning capacity. A younger individual or somebody like a lawyer just passing the bar exam rarely has earning capacity defined by actual earnings. In such circumstance, a proxy, or substitute, representing the individual’s earning capacity can be used. Earning capacity is more commonly reduced, rather than destroyed, as a function of occupational disability. The occupationally disabled person’s age, education, previous work history, skill level, general learning ability, and severity of impairment combine to produce either a destruction or reduction of earning capacity. On the back of the Kool-Aid packet, the instructions state you’ll need a two-quart capacity pitcher. Earning capacity, conceptually, is similar to the Kool-Aid pitcherpicture, in that the amount of Kool-Aid in the pitcher doesn’t define the capacity of the pitcher, unless it is filled to the top.9 A mature worker like a 57-year-old legal assistant with 17 years in the same firm would probably have actual earnings that were representative of capacity.

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When occupational disability puts a crack in the Kool-Aid pitcher, the loss of capacity has two parts. The earning capacity on an annual basis is only one factor. The other issue that must be considered when defining loss of lifetime capacity to work and to earn money is called “worklife expectancy.” Worklife expectancy addresses the issues of being alive in the future, being a labor force participant in the future and being employed in the future. The government has annually collected data on the employment potential of disabled versus nondisabled persons, all other factors held constant, since 1981 through the CPS. The name of the study is The Labor Force Status and Other Characteristics of Individuals by Age, Education, Sex, and Disability status. The CPS provides the pulse-beat of who’s working in America by demographic characteristic. Employment rates are routinely stated on radio/TV news and in print media. In addition, studies and data which have corroborated these data are found in the Decennial Census and in the American Community Surveys. The various surveys early on had slightly different definitions of disability and sought different answers, but a recent trend has standardized the definitions. Quantifying less than perfect health with work disability status is an evolving construct and measurements should always be improved accordingly. The CPS time series data reveal that, just like nondisabled males with less than a high school diploma have a lower employment rate than nondisabled males with a high school diploma, who have lower employment rates than those college educated, the disabled, across the board, are less-frequent participants in the labor force and are less likely to find employment than the nondisabled counterpart, and have lower employment rates. While econometrical models which project future work life expectancy, like the Increment-Decrement Model, have an element of statistical validity, twostate (employed and unemployed) and three state (employed, unemployed and inactive) models fail to capture the diminishment of functioning over time as experienced by disabled workers. As the time-series CPS data show, those persons with disability departing the labor force at a greater rate than nondisabled counterparts, the increment–decrement models would reveal the same future work life for a disabled person if he or she were actually working at the time of measurement.

31.7 MEASURING ONE PERSON’S LOSS OF CAPACITY As Dr. Murray writes in the Global Burden of Disease, “. . . we believe it is preferable to make an informed estimate of disability due to a particular condition than to have no estimate at all. The absence of an estimate fosters the tacit assumption that there is no problem. For example, it may well be that the continued neglect of primary and secondary prevention and rehabilitation of disability is related to the lack of data on its magnitude, especially when compared to the information available about life lost due to premature mortality. Ex Cathedra statements without supporting empirical evidence do not contribute constructively to informed policy debate, and should be avoided.”1

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31.8 THE STANDARD VOCATIONAL INTERVIEW Trying to quantify the effects of impairment on one person’s ability to work and earn money in the future—in other words, trying to measure something that hasn’t happened—still can be an informed, reliable estimate. Using a standard vocational interview, a vocational-rehabilitation professional can reveal an individual’s demographic characteristics in his or her environment, as they existed before becoming impaired and with impairment. Basic demographic information of the client, like date of birth, race, gender, level of educational attainment, work history, skills and abilities are collected in the standard vocational interview, allowing the analyst to categorize the client. An important consideration is prior health status, or the existence of preexisting condition(s) which may or may not have limited the client’s ability to work and earn money. Investigating the client’s life through four domains, social, occupational, practical, and emotional-psychological in their preinjury and postinjury lives provides relevant information to the effect of the given impairments on this individual’s ability to function, in his or her environment. The SF-36 Health Survey was constructed for the Medical Outcomes Study to survey health status, and has been tested and validated extensively. Designed for use in clinical practice and research, health policy evaluations, and general population surveys, the SF-36 includes one multi-item scale that assesses eight health concepts: (1) limitations in physical activities because of health problems; (2) limitations in social activities because of physical or emotional problems; (3) limitations in usual role activities because of physical health problems; (4) bodily pain; (5) general mental health (psychological distress and well-being); (6) limitations in usual role activities because of emotional problems; (7) vitality (energy and fatigue); and (8) general health perceptions (see Table 31.2). The SF-36 is only a guide for the interviewer to delve into the client’s world through his or her social functioning, emotional/psychological functioning, practical functioning (household tasks, ADLs and IADLs), and occupational functioning. Questions are slightly modified in terms of functioning preinjury and postinjury.

TABLE 31.2 An SF-36 Data Set Scales

Mean

SD

Limitations in physical activities because of health problems Limitations in usual role activities because of physical health problems Limitations in social activities because of physical or emotional problems Energy/Fatigue/Vitality Emotional Well-being Social Functioning Pain General Health

70.61 52.97 55.78 52.15 70.38 78.77 70.77 56.99

27.42 40.76 40.71 22.39 21.97 25.43 25.46 21.11

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The first question of the SF-36 asks the same five-part self-perceived health question used in the standardized definition of overall health. The interviewer, however, needs to know the change in perceived health status, and would ask the client this question first in the context of pre-incident, and then ask about current perception, with impairments: 1. “In general, you would say that your overall health, prior to being exposed to CO poisoning, was either “excellent,” “very good,” “good,” “fair,” or “poor”? 2. “Now, as a result of being exposed to CO poisoning, how would you rate your overall health, “excellent,” “very good,” “good,” “fair,” or “poor”?

31.9 THE CONSTRUCT OF WORK Work is organized in a variety of ways. As a result of technological, economic, and sociological influences, nearly every job in the economy is performed slightly differently from any other job. Every job is also similar to a number of other jobs. In order to look at the millions of jobs in the US economy in an organized way, the Dictionary of Occupational Titles (DOT) groups jobs into “occupations” based on their similarities and defines the structure and content of all listed occupations. Occupational definitions are the result of comprehensive studies of how similar jobs are performed in establishments across the nation and are composites of data collected from diverse sources. The term “occupation,” as used in the DOT, refers to this collective description of a number of individual jobs performed, with minor variations, in many establishments.10 Worker functions are described as the ways in which a job requires a worker to function in relationship to data, people, and things, as expressed by mental, interpersonal, and physical worker actions. In the DOT, every job is assigned the three worker functions that best characterize the worker’s primary involvement with data, persons, and things. Data functions are an arrangement of different kinds of activities involving information, knowledge, or concepts. Some are broad in scope and some are narrow in scope. Components of data are synthesizing, coordinating, analyzing, compiling, computing, copying, and comparing. People functions are activities that have little or no hierarchical arrangement beyond the generalization that the least level is taking instructions/helping. Components of people are mentoring, negotiating, instructing, supervising, diverting, persuading, speaking-signaling, serving, and taking instructions-helping. Things functions can be divided into relationships on the basis of the worker’s involvement with either machines or equipment. Components of things are setting up, precision working, operating-controlling, driving-operating, manipulating, tending, feeding-off bearing, and handling. From the general guide of an interview, though, a more complete picture needs to be coordinated with the “worker characteristics components” applied to the more

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than 12,000 job titles in the DOT. The Selected Characteristics of Occupations (SCO) is a companion volume to the US Department of Labor’s DOT. Worker characteristics include job analysis components which reflect worker attributes needed to contribute to successful job performance. The seven worker characteristic components are as follows: • • • • • • •

General Educational Development (GED) Specific Vocational Preparation (SVP) Strength Physical demands Environmental conditions Temperaments Aptitudes

31.10 GENERAL EDUCATIONAL DEVELOPMENT (GED) This has three divisions, each with six levels: Reasoning development (applying common-sense understanding at the lowest level to applying logical or scientific thinking to a wide range of intellectual problems at the uppermost level), mathematical development, and language development. The six levels of Mathematical and Language Development are based on school curriculum taught in the United States, and the higher the assigned value is, equates to a higher level of education.

31.11 SPECIFIC VOCATIONAL PREPARATION (SVP) This is defined as the amount of time required by the typical worker to learn the techniques, acquire the information, and develop the facility needed for average performance in a specific job-worker situation. SVP includes vocational education, apprenticeship training, in-plant training, on-the-job training, and essential experience from other jobs on the career ladder. The 9-level scale of SVP is as follows: SVP 1: Short demonstration only SVP 2: Anything beyond a short demonstration up to and including 1 month SVP 3: Over 1 month up to and including 3 months SVP 4: Over 3 months up to and including 6 months SVP 5: Over 6 months up to and including 1 year SVP 6: Over 1 year up to and including 2 years SVP 7: Over 2 years up to and including 4 years SVP 8: Over 4 years up to and including 10 years SVP 9: Over 10 years

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The strength needed to perform a job is expressed by one of five terms over the period of the average work-day needed (constantly, frequently, occasionally, or not present). Sedentary Work, for example, requires that a worker be capable of exerting up to 10 pounds of force occasionally (activity exists up to 1/3 of the time) or a negligible amount of force frequently, to lift, carry, push, pull, or otherwise move objects, including the human body. Sedentary work involves sitting most of the time, but may involve walking or standing for brief periods of time. Jobs are sedentary if walking or standing is required only occasionally and all other sedentary criteria are met. Light Work, requires that a worker be capable of exerting up to 20 pounds of force occasionally, or up to 10 pounds of force frequently, (activity exists from 1/3 to 2/3 of the time) or a negligible amount of force constantly to move objects. Even though the weight lifted may be only a negligible amount, a job should be rated “light work”: • When it requires walking or standing to a significant degree • When it requires sitting most of the time but entails pushing or pulling of arm or leg controls • When the job requires working a production rate pace entailing the constant pushing pulling of materials even though the weight of those materials is negligible Medium Work requires that a worker be capable of exerting 20–50 pounds of force occasionally, or 10–25 pounds of force frequently, or greater than negligible up to 10 pounds of force constantly (activity exists 2/3 or more of the time) to move objects. Heavy Work requires a frequent lift, carry, push, pull of weight up to 50 pounds with an occasional lift, carry, push, pull of weight up to 100 pounds. Very Heavy Work requires exerting with lift, carry, push, or pull of weight in excess of 100 pounds occasionally, or in excess of 50 pounds frequently, or in excess of 20 pounds constantly. Physical demands analysis is a systematic way of describing the physical activities the job requires, over the period of the average work-day the activity is needed (constantly, frequently, occasionally, or not present). The physical demands in addition to strength are climbing, stooping, kneeling, crouching, crawling, reaching, handling, fingering, feeling, talking, hearing, tasting, and smelling, near acuity, far acuity, depth perception, accommodation, color vision, and field of vision. Environmental conditions are the surroundings in which a job is performed and consists of fourteen factors over the period of an average work-day needed (constantly, frequently, occasionally, or not present). It involves exposure to weather, extreme cold, extreme heat, wet and humid, noise intensity level (five levels), vibration, atmospheric conditions, proximity to moving parts, exposure to electrical shock, and working in high, exposed places. Temperaments are defined as the “personal traits” or the adaptability requirements made on the worker by a specific job situation. Eleven temperaments are A—working alone or in isolation from others; D—directing, controlling and planning activities of others; E—expressing personal feelings; I—influencing people in their opinions, attitudes, and judgments; J—making judgments and decisions;

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P—dealing with people; R—performing repetitive and continuous short-cycle work; S—performing effectively under stress; T—attaining precise set limits, tolerances, and standards; U—working under specific instructions; and V—performing a variety of tasks. A Standard vocational interview reveals the client in his or her environment. Utilizing the DOT and the SCO, the analyst is able to quantify with a reasonable degree of certainty that individual’s capacity to work. Within this framework, the analyst can ascertain the diminution of one individual’s capacity.

31.12 DIMINISHMENT OF FUNCTION Being limited in the amount or kind of work can usually be (but not always) observed within the construct of work delineated in the DOT. Occasionally, though, the standard vocational interview will reveal a client who has not missed a day of work, but it is revealed that the other three life domains are substantially impacted. It’s not reasonable to assume that a person with disability, who is giving all his life’s energy to occupational functioning, while his life’s energy toward functioning in the other three domains is diminished, will enjoy the same longevity in the labor force he potentially once had. While the client’s self-reported limitations provide a general overview for the analyst’s consideration, when combined with the medical provider’s, a more specific overview is derived. In physical injury situations, a medical provider like a physician with a specialty in rehabilitation medicine will assess and report through a functional capacity evaluation of the patient’s diminishment of functioning from preinjury levels, and will often opine on future medical care along with known outcomes from research which indicate the client will probably suffer exacerbations that will cause need for future interventions. These exacerbations and subsequent medical treatments will probably interrupt functioning in the four domains. In brain injury situations, a comprehensive neuropsychological evaluation can reveal specific losses which are easily correlated to worker functions described in the DOT. Frequently, the impact of injury affects physical, cognitive, and emotional-psychological functioning. As the individual describes a lower level of overall health due to loss of ability to function, along with pain, cognitive dysfunction or emotional-psychological distress, the normal effects of a human’s aging body will come abnormally sooner on a damaged body which is less prepared for the diminishment.

31.13 MONETARY DAMAGES: THE FIVE STEPS IN THE ANALYSIS OF LOSS OF EARNING CAPACITY Just as an attorney uses statutes as a framework for a given client’s circumstance, the analyst assessing loss of future earning capacity uses a five-step framework. The Five Steps are Step I: Preinjury earning capacity Step II: Preinjury work life expectancy

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Step III: Postinjury earning capacity Step IV: Postinjury work life expectancy Step V: Present value calculation Step I, the preinjury earning capacity, is the “size of the individual’s Kool-aid pitcher.” It is that dollar amount that best represents that person’s lifetime ability to earn money. It may or may not be the same as the person’s actual earnings. Typically, a mature worker in his mid-to-late 40s will be earning at capacity, but rarely will a younger worker’s actual earnings represent lifetime ability. A person’s earning capacity is a function of educational attainment, intelligence, skill, gender, and disability status. When actual earnings do not fairly represent earning capacity for the person, a substitution, or proxy can be used. Numerous data sources are available which reveal average annual earnings of persons by demographic characteristics or by job title. Computer software exists which can sort job titles from the DOT by skill level and intelligence level. The earning capacity of a child with average intelligence, for example, could be predicated upon the average annual earnings of similar persons with average intelligence. The preinjury worklife expectancy, Step II, is the number of years into the future we would reasonably expect the person to be alive, participating in the labor force, and employed. Consideration must be given to the person’s disability status in calculating preinjury worklife expectancy. The US Bureau of the Census, under the US Department of Commerce, collects population-related data. The Bureau of the Census’ CPS is conducted monthly. Since 1981, the March Supplement to the CPS has been collecting disability-related data. This information can be reviewed at the Department of Commerce’s Internet address HTTP://STATS.BLS.GOV/CPSAATAB.HTM. March surveys are a combination of the basic CPS and a Supplement which delves into work status and disability. Surveys are conducted by interviewers in approximately 57,000 households throughout over 700 sample areas which comprise nearly 2,000 counties, independent cities, and minor civil divisions. The sample is continually updated to account for new residential construction. The Labor Force Status and Other Characteristics of Persons With a WorkDisability: 1981–1988, Series P-23, No. 160, issued in July of 1989 notes the basic concept of disability and the relationship of the basic concept to the operational concept adopted for the March Surveys. A person has a disability if he or she has a limitation in the ability to perform one or more of the life activities expected of an individual within a social environment. The primary way for this concept to be operationalized in the March CPS is to ask whether any household member has a health problem or disability which prevents them from working or which limits the kind or amount of work they can do. Some of the persons who do not have a work disability do have impairments, functional limitations, or disabilities in life-activities other than work. The term “impairment” indicates a physiological, anatomical, cognitive loss or abnormality. The term “functional limitation” indicates a restriction in a physical functional activity (such as walking, reaching, or hearing), an emotional functional activity

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(maintaining satisfactory personal relationships), or a cognitive functional activity (solving problems). Persons with a given level of functional limitation may or may not have a work disability, depending on the individual environment and the reaction of the individual. An individual is considered to have a work-related disability if one or more of the following conditions are met: 1. Identified by the question, “Does anyone in this household have a health problem or disability which prevents them from working or which limits the kind or amount of work they can do?” 2. Identified by a question that asks, “Is there anyone in this household who ever retired or left a job for health reasons?” 3. Did not work in the survey week because of a long-term illness or disability which prevents performance of any kind of work?” 4. Did not work at all in previous year because ill or disabled. 5. Under 65 years of age and covered by Medicare. 6. Under 65 years of age and a recipient of Supplemental Security Income.” The data are represented in three categories (1) With no work disability; (2) With a work disability; and (3) With a severe disability. The categories are broken into age groups in ten-year increments from age 16 up to age 74 for both males and females, and by level of educational attainment (in four subgroups: less than a high school diploma, high school diploma, 13–15 years of education, and 16 or more years of education). What the data show are the participation in the labor force rates and employment rates by age, sex, education, and disability or nondisability status. Employment rates are calculated relative to those who are considered labor force participants (those who are either employed or actively seeking employment). Another nationally known household survey, the Survey of Income and Program Participation, has a compilation of employment rates by type and degree of disability status, but the population of this group is not representative of the overall general population. The decennial census and the American Community Survey additionally show diminished employment rates in different domains owing to the effect of disability. As noted above, category (2), those with a work disability, includes all six (1 to 6) conditions. Inspection of the data shows it is heavily weighted by the low participation rates for those in the labor force described in conditions “3” through “6” which comprise the data in category (3), with a severe disability. Analysis of the data in category (2) that remains after extracting the category (3) data reveals a subset of persons considered as category (4), with a moderate work disability. When considering future working status for all persons, the certainty of life should be reduced by the measurable probability of surviving. The chance a person could die is calculated using US DHHS, National Center for Health Statistics, Vital Statistics of the US Life Tables. A worklife expectancy considers the probability in the future of surviving, along with the probability of being a labor force participant, and the probability of being employed. A worklife expectancy for an individual in category (4), with a moderate

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work disability is less than a work life expectancy for a nondisabled cohort, regardless of that person’s age, sex, or years of education. The effects of work disability are greatest on those in the population with the least education, workers with less than a high school diploma. Two important facts exist for persons who meet the definition of occupational disability: On average, those persons earn less than nondisabled counterparts, and on average, those persons have lower participation and employment rates, and therefore have a reduced worklife expectancy. Step III, the postinjury earning capacity is typically, but not always, less than preinjury earning capacity. It could be congruent with preinjury capacity, but will never exceed it. If an individual with disability benefits with retraining which increases his postinjury earning capacity, clearly that individual had the capacity prior to injury to retrain as well. The difference is that the newly retrained person with disability could have been retrained before, without the burden of disability, and the analyst would now have to question if the disabled person with retraining would reach the compensation level of the nondisabled counterpart in the same occupation. Step IV, the postinjury worklife expectancy, like Step II, is the number of years into the future we would reasonably expect the person to be alive, participating in the labor force and employed. The CPS data would be used in conjunction with the analyst’s observation of the effect of the impairment on that individual in that individual’s environment to define the appropriate category of disability, moderately disabled, average disabled, or severely disabled. In some cases, the analyst might employ a continuum of employability as an opinion that the given individual in his or her specific environment might be somewhat better than the average for a given category. Step V, the present value calculation, considers the amount of money needed today, which in a prudent investment will replace the loss over time. Typically, courts of law require the analyst to reduce the loss to present value. This language, however, refers to the algebraic calculation of simplifying (reducing) a polynomial equation, and doesn’t necessarily imply that the present value will be less than the actual summation of the loss. Rather, the present value of a growing lump sum considers both future growth in relation to future interest accruing on the components, and the resulting figure could be equal to, greater, or less than the summed figure. In calculating the present value of a growing lump sum, the formula PV =




CF × {(1 + GROWTH RATE)/(1 + INTEREST RATE)}n

where CF represents the annual loss, cash flow, and n represents the exponent of time. As empirical evidence doesn’t relate the variables, from this formula three assumptions can be made as follows: (1) if it is assumed the rate of growth of wages will be greater than the assumed interest rate, the numerator is greater than the denominator, and the PV will require more money being invested today; (2) if it is assumed the denominator is greater than the numerator, the PV will require less money being

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invested today, and (3) if it is assumed that the growth rate equals the interest rate, one recognizes a number divided by itself is 1, and the present value is equal to the summation of the loss (also known as a total offset assumption).

31.14 CASE REPORT The Jones Family: Mr. Jones and his wife Betty, and their two children, John and Cathy Dear Mr. Attorney: You have asked me to perform analyses to measure the monetary losses, including loss of future earning capacity, for Mr. and Mrs. Jones, and their two minor children’s loss of adult future earning capacity, if any, as a result of impairments resulting from chronic carbon monoxide (CO) poisoning in 2005. In conducting the analyses, I interviewed the family on August 18 and 19, 2006. In addition, I reviewed the following information forwarded to me by your office: • • • • • • • • • • • •

Complaint Plaintiff’s answers to interrogatories Deposition transcripts of Mr. and Mrs. Jones Mr. Jones’ income tax returns for 2001–2005 John’s school records from middle school Cathy’s school records from elementary school Medical records from rehabilitation hospital Medical records from hospital Medical records from Dr. Maher Medical records from Dr. Paul Medical records from Dr. Gelbman Neuropsychological evaluation reports from R. Hoffman; PhD

31.14.1 MR. JONES The interview reveals the following for Mr. Jones: Mr. Jones’s date of birth is August 18, 1969. He is 37 years old. Mr. Jones was graduated from high school and attained a master of business administration degree from the University. Over his worklife, he has functioned as an investment analyst (DOT # 160.267-026), and had been promoted to partner, and his responsibilities included supervising 15 analysts and their assistants. This work is skilled (SVP = 8) in nature and sedentary in terms of physical demands, and requires a constant physical demand of near acuity (clarity of vision at 20 inches or less). The GED for reasoning, mathematics, and language are all at level 5, the second highest level. To perform the job successfully, the worker must possess above average aptitudes of (intelligence), verbal aptitude (the ability to understand meanings of words and ideas), numerical aptitude (the ability to perform basic arithmetic operations quickly and accurately), and clerical perception (the ability to perceive pertinent detail in verbal or tabular material).

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Carbon Monoxide Poisoning

His generalized work activities included the following12 : • Analyzing data or information—Identifying the underlying principles, reasons, or facts of information by breaking down information or data into separate parts. • Getting information—Observing, receiving, and otherwise obtaining information from all relevant sources. • Interacting with computers—Using computers and computer systems (including hardware and software) to program, write software, set up functions, enter data, or process information. • Processing information—Compiling, coding, categorizing, calculating, tabulating, auditing, or verifying information or data. • Communicating with supervisors, peers, or subordinates—Providing information to supervisors, coworkers, and subordinates by telephone, in written form, e-mail, or in person. Mr. Jones was a cub scout leader for his son, John’s group. They enjoyed camping and backpacking, and would frequently take their ski boat on camping trips to state parks outside of scout functions with Betty and Cathy. Mr. Jones and Betty enjoyed twice a year-long-weekend trips to Las Vegas, without the children. Mr. Jones performed all outside yard and car care work, did home repairs, kept the gutters clean, and maintained a vegetable and herb garden. In December 2004, the Jones family moved into a new home with natural gas fueling the forced air furnace and water heater. By spring, 2005, the entire family felt as if they had prolonged flu. Mr. Jones found it difficult to focus at work with his constant headaches. He began having difficulty following through on projects, and became easily frustrated with his coworkers and supervisors. His vision was blurry and he had difficulty reviewing the reams of paperwork he once easily reviewed and analyzed. He fell from the roof after a dizzy spell while cleaning the gutters, and fortunately, the shrubs below broke his fall enough to prevent serious injury from occurring. The family physician, Dr. Maher, suspected something besides the flu was affecting the family at this point, as all had similar complaints of lethargy, fatigue, headaches, cognitive dysfunction, and emotional outbursts, when none of this existed before they moved. After a thorough home inspection, an improperly installed ventilation system on the furnace was discovered, which was leaking directly beneath Mr. and Mrs. Jones’ bedroom. Dr. Maher referred Mr. Jones to a toxicologist, Dr. Smith, and a neurologist, Dr. Paul. The latter found Mr. Jones’ EEG (Electroencephalogram) and QEEG (Quantitative Electroencephalogram) to be abnormal. Dr. Smith referred the Jones family to R. Hoffman, Ph.D., for neuropsychological testing. Brain injury involves a change in the structure, physiology, and chemistry of the brain which is caused directly or indirectly by physical, chemical or force insult to brain tissue which results in a change in the way in which the brain acquires and processes information, and produces command signals.

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The results of testing for Mr. Jones revealed problems with word finding, memory, sequencing, multitrack thinking (i.e., multitasking) and differentiation abilities. The report continues with Mr. Jones’s attention and concentration abilities assessed at a level rated impaired, and memory and executive functioning in the impaired range. He also has deficits in abstract reasoning and in systematic thinking. Mr. Jones’s scores in the language domain were average. Executive function refers to the human brain’s ability to be aware of its environment, following through with tasks, self-motivation, self-correction and selfinitiation. Multitrack thinking and the speed at which thoughts are processed are considered executive function. Components of executive functioning include: • Word-finding (finding the word you want and speaking it in a reasonable length of time) • Sorting (the brain’s ability to separate truth from projection and its ability to retrieve information) • Discernment (the ability to be tactful or to keep social behavior appropriate) and details (the ability to notice small differences) • Sequencing (ability to perform tasks in a logical or productive progression) • Follow-through (ability to take an event all the way through to completion) • Multitrack thinking and differentiation (doing more than one thing at a time, thinking more than one thought at a time, or juggling several different thoughts or activities simultaneously, as required in adult thinking) Data functions are an arrangement of different kinds of activities involving information, knowledge or concepts. In Mr. Jones’s job as a supervisor/investment analyst, his data functioning involved both coordinating and analyzing prior to injury. In coordinating, one determines time, place and/or sequence of operations or activities on the basis of analysis of data; executing determinations or reporting on events. As the single point of contact for responsibility on a job, Mr. Jones wrote reports, met with supervisors and customers, and managed a team of coworkers and their assistants. In analyzing, one examines and evaluates data, and frequently presents alternate actions in relation to the evaluation. Because of his cognitive impairments, Mr. Jones has difficulty coordinating and analyzing at his prior level. As per people functioning, Mr. Jones’ level was supervising. Supervising is determining or interpreting work procedures for a group of workers, assigning specific duties to them, maintaining harmonious relations among them, and promoting efficiency. A variety of responsibilities are involved, such as training workers, evaluating workers’ performance, assisting workers in solving work problems, initiating and recommending personnel actions like hiring, firing, promoting, transferring or disciplining; and maintaining records of performance of these duties. Mr. Jones had to take advantage of short-term disability insurance. Eventually, he returned to working but at a much reduced level of functioning, performing at only a small percentage of his former ability, and at a lower rate of pay. Because of his prior success with the company (and a benevolent employer), a job was created especially

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706

for him that entailed only compiling information (data), and helping (people), and involved limited contact with coworkers he formerly supervised. Mr. Jones was administered the SF-36. He reports his current overall health as “fair.” He reports being limited a lot with vigorous activities, limited a little with moderate activities, and physical functioning causes his bodily pain to increase. He reports not accomplishing as much as he would have liked to, cut-down days, and missing numerous days from work when his headaches were severe. Mr. Jones’s life expectancy at age 37 is 40.0 years. His healthy life expectancy at age 37 is 35.9 years, but this does not consider the 19.2 years diminution of health he sustained as a result of CO poisoning. Prior to injury, Mr. Jones says that he enjoyed excellent overall health, and did not have a condition or impairment that limited the amount or kind of work he could do (see Figure 31.3). Mr. Jones’ social functioning is impacted by his chronic fatigue to the extent he cannot participate in the many activities he once enjoyed. He is trying with all his energy to function at work so he can keep a roof over the family. He knows, also, that the frequency and the type of leisure the family once enjoyed will not be as affordable, and this, too, is adding to his clinical depression. Emotional and psychological functioning, occupational functioning, practical functioning, and social functioning are the four life domains. Mr. Jones’ healthrelated quality of life is significantly below average, overall, as shown below through the results on the eight scales of his SF-36 (see Table 31.3). Although nonpecuniary damages like “pain and suffering,” and “loss of pleasure of life (hedonic damages)” have not traditionally been allowed in expert testimony, it seems that as disability becomes more quantifiable, courts will become more apt to consider that in life-years-lost to disability, time living with disability includes time not working as having a value.

An assumed worklife to age 67 is 30 years

13.9 years of worklife for the average disabled cohort

21.53 years of worklife probability for the average moderately disabled cohort

26.48 years of worklife probability for the average nondisabled cohort

0

5

10

15

20

25

30

FIGURE 31.3 Mr. Jones worklife expectancy.

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35

Injury Caused by Carbon Monoxide Poisoning: Defining Monetary Damages

707

TABLE 31.3 Mr. Jones’ SF-36 Data Set Scales Limitations in physical activities because of health problems Limitations in usual role activities because of physical health problems Limitations in social activities because of physical or emotional problems Energy/Fatigue/Vitality Emotional Well-being Social Functioning Pain General Health

Mean

SD

38.99

70.61

27.42

0

52.97

40.76

0

55.78

40.71

10 52 25 55 40

52.15 70.38 78.77 70.77 56.99

22.39 21.97 25.43 25.46 21.11

Two controversial aspects of hedonic damages calculations are the monetary value of a statistical human life, and the value of the life to the individual. What is the value of a statistical human life? Is life valued greater when an individual is young and reckless and has freedom to play and experiment, or when the individual is closer to the end of life, and each day has unique preciousness? Could an average jury decide the value of a statistical human’s life, and use the percentage of life-years lost to disability as the time metric? Different methods to quantify the value of a statistical life used by experts in Hedonic damages exist. When the value of a statistical life becomes mainstream/accepted, risk companies’actuaries will be better able to project funding needs for statistically projected losses. Until then, we will focus on the pecuniary damages. The five steps in analyzing Mr. Jones’loss of future earning capacity are as follows: Step 1, his preinjury earning capacity is reasonably represented by his actual earnings for 2005, $98,000 (For simplicity’s sake, fringe benefits are not considered as part of Mr. Jones’ total compensation/earning capacity); Step 2, Mr. Jones’ preinjury worklife expectancy is like a non-disabled male’s with a college degree, reduced by the likelihood of living and working from age 37 through age 74, or 26.48 years; Step 3, his postinjury earning capacity is reasonably represented by his annual rate of earnings in his new position, $55,000; Step 4, Mr. Jones’ postinjury worklife expectancy, at best, given the employer accommodations, is like an average moderately disabled male’s with a college degree, reduced by the likelihood of living and working from age 37 through age 74, or 21.53 years; and, Step 5, the present value calculation reveals a lifetime loss of future earning capacity in a range of $1,102,432–$1,410,772, using a range of an assumed net discount rate of 1.6% to a total offset assumption. A second analysis is conducted based on the assumption that Mr. Jones would lose his job for any reason, and would have to compete for comparable work with

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708

Carbon Monoxide Poisoning

non-disabled cohorts. Additionally, without the employer’s benevolence, Step 3, his postinjury earning capacity would be more like that of the average bookkeeper’s, or $30,000 per year. Clearly, his future employability becomes less likely under the given circumstance, so Step 4, Mr. Jones’ postinjury worklife expectancy would be more like an average disabled cohort’s, or 13.9 years. Step 5, the present value calculation for the second analysis reveals a lifetime loss of future earning capacity in the range of $1,722,092–$2,177,092, using a range of an assumed net discount rate of 1.6% to a total offset assumption. The following spreadsheet shows the underlying data and calculations for Mr. Jones’ loss of future earning capacity and his household services replacement costs. The numbers of life survivors in column C are from the most recent data from 2003 released in 2006, and the work probability data, E-H are a 10-year average, 1995–2004 (see Tables 31.4 and 31.5). Around the household, Mr. Jones is no longer able to fully perform chores and tasks as he once was. He cannot do the heavier, more physically demanding activities like yard work, and is advised to stay off the roof because he gets dizzy. Even when doing lighter demanding activities, he has to take frequent breaks, and he tries conserving his energy for work. From the National Human Activity Pattern survey conducted by the Environmental Protection Agency, Economic Demographers from Expectancy Data in Prairie Village, Kansas compiled numerous tables of categories of household members’ activities, outside the realm of occupational functioning.11 The statistical cohort of Mr. Jones, a married male working full-time with two dependent children in the household, averages 15.6 h per week of household production. Taking Mr. Jones’ self-reported activities from the standard vocational interview but using the average statistical cohort’s production rate assures the activities were performed while avoiding over-reporting the number of hours. Although the self report confirms that activities were done, instead of using as the baseline the self-reported amount of time spent performing activities, using the average cohort’s derived time spent performing activities makes a fairer baseline. Though we are not paid for doing household chores and tasks, there is a value for doing them. Even without the benefit of having the video of Mr. Jones’ “Truman Show,” and regardless of the quality of his work, this replacement value would be at least minimum wage, and could be as much as the opportunity cost of trading an extra hour of occupational functioning for household services functioning. Mean wages from Standard Occupational Classification codes as reported in Occupational Employment Statistics can be used as a proxy to assess an average hourly value of time spent by activity category. As Mr. Jones can no longer do half the activities he performed prior to injury, and the remaining activities take him twice as long to do as they used to, his estimated residual functioning is 25% of his preinjury level, implying 11.7 h per week need replacement. Using the national median replacement cost of $11.63 per h, approximately $136 per week would be needed. When the resulting $7076 per year figure is calculated over his formerly healthy life expectancy of 35.9 years, the present value of household services replacement costs are in a range of $192,651–$254,017 (see Table 31.6).

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B

Mr. Jones’ age

37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59

A

Number of Periods

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 96,045 95,852 95,648 95,424 95,182 94,916 94,627 94,321 93,984 93,629 93,228 92,799 92,342 91,848 91,318 90,756 90,154 89,540 88,851 88,142 87,340 86,569 85,678

Number of Life Survivors beginning at age 37

C

0.9980 0.9959 0.9935 0.9910 0.9882 0.9852 0.9821 0.9785 0.9748 0.9707 0.9662 0.9615 0.9563 0.9508 0.9449 0.9387 0.9323 0.9251 0.9177 0.9094 0.9013 0.8921 0.8820

Mr. Jones’ Probability of Life

D

0.857 0.857 0.857 0.857 0.857 0.857 0.857 0.857 0.85 0.85 0.85 0.85 0.85 0.85 0.85 0.85 0.85 0.85 0.594 0.594 0.594 0.594 0.594

Probability of working as Moderately Disabled

0.96 0.96 0.96 0.96 0.96 0.96 0.96 0.96 0.956 0.956 0.956 0.956 0.956 0.956 0.956 0.956 0.956 0.956 0.814 0.814 0.814 0.814 0.814

F

E Mr. Jones’ Probability of working as NonDisabled 0.542 0.542 0.542 0.542 0.542 0.542 0.542 0.542 0.556 0.556 0.556 0.556 0.556 0.556 0.556 0.556 0.556 0.556 0.354 0.354 0.354 0.354 0.354

Probability of working as Average, Disabled

G

0.129 0.129 0.129 0.129 0.129 0.129 0.129 0.129 0.123 0.123 0.123 0.123 0.123 0.123 0.123 0.123 0.123 0.123 0.099 0.099 0.099 0.099 0.099

Probability of working as Severely Disabled

H

0.958 0.956 0.954 0.951 0.949 0.946 0.943 0.939 0.932 0.928 0.924 0.919 0.914 0.909 0.903 0.897 0.891 0.884 0.747 0.740 0.734 0.726 0.718

Probability of Living and Working, Nondisabled

I

0.855 0.853 0.851 0.849 0.847 0.844 0.842 0.839 0.829 0.825 0.821 0.817 0.813 0.808 0.803 0.798 0.792 0.786 0.545 0.540 0.535 0.530 0.524

Probability of Living and Working, Moderately disabled

J

0.541 0.540 0.538 0.537 0.536 0.534 0.532 0.530 0.542 0.540 0.537 0.535 0.532 0.529 0.525 0.522 0.518 0.514 0.325 0.322 0.319 0.316 0.312

Probability of Living and Working, Average disabled

K

TABLE 31.4 Data and Calculations for Mr. Jones’ Loss of Future Earning Capacity and His Household Services Replacement Costs

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(Continued)

0.129 0.128 0.128 0.128 0.127 0.127 0.127 0.126 0.120 0.119 0.119 0.118 0.118 0.117 0.116 0.115 0.115 0.114 0.091 0.090 0.089 0.088 0.087

Probability of Living and Working, Severely disabled

L

Injury Caused by Carbon Monoxide Poisoning: Defining Monetary Damages 709

B

Mr. Jones’ age

60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76

A

Number of Periods

24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40

Table 31.4 (Continued)

84,710 83,640 82,549 81,324 80,050 78,674 77,222 75,675 74,010 72,257 70,359 68,359 66,286 64,037 61,682 59,223 56,590

Number of Life Survivors beginning at age 37

C

0.8709 0.8595 0.8467 0.8335 0.8191 0.8040 0.7879 0.7706 0.7523 0.7326 0.7117 0.6902 0.6667 0.6422 0.6166

Mr. Jones’ Probability of Life

D

0.814 0.814 0.814 0.814 0.814 0.454 0.454 0.454 0.454 0.454 0.278 0.278 0.278 0.278 0.278

Mr. Jones’ Probability of working as NonDisabled

E

0.594 0.594 0.594 0.594 0.594 0.231 0.231 0.231 0.231 0.231 0.174 0.174 0.174 0.174 0.174

Probability of working as Moderately Disabled

F

0.099 0.099 0.099 0.099 0.099 0.019 0.019 0.019 0.019 0.019 0 0 0 0 0

Probability of working as Severely Disabled

0.354 0.354 0.354 0.354 0.354 0.188 0.188 0.188 0.188 0.188 0.15 0.15 0.15 0.15 0.15

H

G Probability of working as Average Disabled, Nondisabled

0.517 0.511 0.503 0.495 0.487 0.186 0.182 0.178 0.174 0.169 0.124 0.120 0.116 0.112 0.107 21.53

26.48

Probability of Living & Working, Moderately disabled

J

0.709 0.700 0.689 0.678 0.667 0.365 0.358 0.350 0.342 0.333 0.198 0.192 0.185 0.179 0.171

Probability of Living & working Nondisabled

I

13.90

0.308 0.304 0.300 0.295 0.290 0.151 0.148 0.145 0.141 0.138 0.107 0.104 0.100 0.096 0.092

Probability of Living & Working, Average disabled

K

3.129

0.086 0.085 0.084 0.083 0.081 0.015 0.015 0.015 0.014 0.014 0.000 0.000 0.000 0.000 0.000

Probability of Living and Working, Severely disabled

L

710 Carbon Monoxide Poisoning

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$47,040 $46,940 $46,830 $46,712 $46,581 $46,439 $46,289 $46,124 $45,574 $45,379 $45,170 $44,948 $44,707 $44,449 $44,176 $43,883 $43,584 $43,249 $29,982 $29,709 $29,447 $29,144 $28,815

$93,891 $93,691 $93,472 $93,235 $92,974 $92,692 $92,392 $92,061 $91,331 $90,941 $90,523 $90,077 $89,594 $89,077 $88,529 $87,942 $87,343 $86,671 $73,208 $72,542 $71,902 $71,162 $70,358

N Postinjury EC $55,000 multiplied by J

M

Preinjury EC $98,000 multiplied by I $46,851 $46,751 $46,642 $46,523 $46,393 $46,252 $46,103 $45,938 $45,757 $45,562 $45,352 $45,129 $44,887 $44,628 $44,353 $44,059 $43,759 $43,423 $43,226 $42,833 $42,455 $42,018 $41,544

Difference in Pre–post expected Earnings

O

First Analysis

P

$47,366 $47,785 $48,198 $48,605 $49,002 $49,390 $49,772 $50,139 $50,492 $50,829 $51,152 $51,460 $51,747 $52,014 $52,263 $52,487 $52,703 $52,873 $53,213 $53,309 $53,420 $53,452 $53,429

Assuming Growth Rate at 1.1%

Q

$46,121 $45,306 $44,496 $43,691 $42,890 $42,094 $41,304 $40,515 $39,727 $38,941 $38,158 $37,378 $36,599 $35,821 $35,046 $34,271 $33,507 $32,732 $32,076 $31,289 $30,530 $29,745 $28,951

Assuming Discount Rate at 2.7%

R

$16,227 $16,193 $16,155 $16,114 $16,069 $16,020 $15,968 $15,911 $16,260 $16,191 $16,116 $16,037 $15,951 $15,859 $15,761 $15,657 $15,550 $15,431 $9,746 $9,657 $9,572 $9,474 $9,367

Postinjury EC $30,000 Multiplied by K

S

$77,664 $77,499 $77,317 $77,121 $76,905 $76,672 $76,424 $76,150 $75,071 $74,750 $74,406 $74,040 $73,643 $73,218 $72,767 $72,285 $71,792 $71,240 $63,462 $62,885 $62,330 $61,688 $60,991

Difference in Pre–post expected Earnings

T

$78,518 $79,213 $79,897 $80,571 $81,229 $81,873 $82,506 $83,115 $82,839 $83,391 $83,921 $84,426 $84,898 $85,336 $85,744 $86,112 $86,466 $86,745 $78,124 $78,265 $78,428 $78,475 $78,441

Assumed Growth Rate at 1.1%

Second Analysis

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(Continued)

$76,454 $75,103 $73,760 $72,426 $71,098 $69,778 $68,469 $67,161 $65,178 $63,888 $62,603 $61,324 $60,046 $58,769 $57,497 $56,226 $54,973 $53,701 $47,092 $45,937 $44,822 $43,670 $42,504

Assumed Discount Rate at 2.7%

U

TABLE 31.5 Data and Calculations for Mr. Jones’ Loss of Future Earning Capacity and His Household Services Replacement Costs (cont.)

Injury Caused by Carbon Monoxide Poisoning: Defining Monetary Damages 711

$28,451 $28,079 $27,663 $27,229 $26,761 $10,215 $10,010 $9,790 $9,558 $9,307 $6,811 $6,605 $6,381 $6,146 $5,901

$69,469 $68,563 $67,545 $66,487 $65,345 $35,773 $35,056 $34,285 $33,472 $32,594 $19,391 $18,803 $18,165 $17,497 $16,799

N Postinjury EC $65,000 multiplied by J

Preinjury EC $98,000 multiplied by I

M

Table 31.5 (Continued)

$41,019 $40,484 $39,883 $39,258 $38,583 $25,558 $25,046 $24,495 $23,914 $23,286 $12,579 $12,198 $11,784 $11,351 $10,898 $1,410,772

Difference in Prepost Expected Earnings

O

First Analysis

P

$53,335 $53,218 $53,005 $52,748 $52,412 $35,100 $34,775 $34,384 $33,938 $33,411 $18,247 $17,889 $17,472 $17,014 $16,516

Assuming Growth Rate at 1.1%

Q

$28,140 $27,340 $26,514 $25,692 $24,858 $16,209 $15,637 $15,055 $14,469 $13,870 $7,376 $7,041 $6,696 $6,349 $6,001 $1,102,432

Assuming Discount Rate at 2.7%

R

$9,248 $9,128 $8,992 $8,851 $8,699 $4,535 $4,444 $4,346 $4,243 $4,132 $3,203 $3,106 $3,000 $2,890 $2,775

Postinjury EC $30,000 Multiplied by K

S

$60,221 $59,435 $58,553 $57,636 $56,645 $31,238 $30,612 $29,939 $29,229 $28,462 $16,188 $15,697 $15,164 $14,607 $14,024 $2,177,971

Difference in Prepost Expected Earnings

T

$78,303 $78,131 $77,818 $77,441 $76,948 $42,901 $42,504 $42,026 $41,482 $40,837 $23,482 $23,020 $22,484 $21,895 $21,253

Assumed Growth Rate at 1.1%

Second Analysis

U

$41,313 $40,139 $38,927 $37,720 $36,494 $19,812 $19,112 $18,401 $17,685 $16,952 $9,492 $9,060 $8,617 $8,170 $7,722 $1,722,092

Assumed Discount Rate at 2.7%

712 Carbon Monoxide Poisoning

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TABLE 31.6 Household Services Analysis Household Services Analysis V Number of Periods in Full-functioning Life Expectancy 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 35.9

W Annual Replacement Cost $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $7,076 $6,368 $254,017

X

Y

Assumed Growth Rate at 1.1%

Assumed Discount Rate at 2.7%

$7,154 $7,232 $7,312 $7,392 $7,474 $7,556 $7,639 $7,723 $7,808 $7,894 $7,981 $8,068 $8,157 $8,247 $8,338 $8,429 $8,522 $8,616 $8,710 $8,806 $8,903 $9,001 $9,100 $9,200 $9,301 $9,404 $9,507 $9,612 $9,717 $9,824 $9,932 $10,042 $10,152 $10,264 $10,377 $9,442

$6,965 $6,857 $6,750 $6,645 $6,541 $6,440 $6,339 $6,240 $6,143 $6,048 $5,953 $5,861 $5,769 $5,679 $5,591 $5,504 $5,418 $5,334 $5,251 $5,169 $5,088 $5,009 $4,931 $4,854 $4,778 $4,704 $4,631 $4,559 $4,488 $4,418 $4,349 $4,281 $4,214 $4,149 $4,084 $3,618 $192,651

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Carbon Monoxide Poisoning

714

31.14.2 MRS. BETTY JONES The interview reveals that Mrs. Jones was born on October 12, 1961. She is a 35year-old woman who was graduated from high school, and subsequently attained an associate of science degree in accounting. As far as her worklife, Mrs. Jones states she began working at age 15, and occasionally worked two jobs concurrently, even while attending school full time. She worked part-time as a sales person (sales person, women’s apparel, DOT # 261.357-066), mostly because she liked wearing new fashions, and with her employee discount, the job basically supported her clothing wants. She functioned as a bookkeeper (DOT # 210.382-014) during her 2 years of college, and then after successfully completing on-the-job training, got a job as a claim examiner (DOT # 241.267-018) (see Figure 31.4). The work she’s performed is semiskilled to skilled in nature and sedentary to light in terms of physical demands. Her career path was voluntarily interrupted around the time her second child, Cathy, was born, but she had planned to return to work when Cathy began middle school, which would be calendar school year 2008–2009. A claim examiner needs above-average levels of general learning ability (intelligence), verbal aptitude, and clerical perception. Physical demands needed on a frequent basis include reaching, handling, fingering, talking, hearing, and near acuity. A claim examiner’s occupation-specific tasks include the following: • Adjust reserves and provide reserve recommendations to ensure reserving activities consistent with corporate policies. • Communicate with reinsurance brokers to obtain information necessary for processing claims. • Conduct detailed bill reviews to implement sound litigation management and expense control.

Betty’s life expectancy at age 35 is 46.4 years

Betty’s full functioning life expectancy would be 39.7 years

Betty’s health-adjusted life expectancyis 29.7 years, meaningout of her 46.4 year life expectancy, 64% is with burden of disability

0

5

10

15

20

25

30

35

40

45

FIGURE 31.4 Betty’s Jones life and healthy life.

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• Confer with legal counsel on claims requiring litigation. • Contact and/or interview claimants, doctors, medical specialists, or employers to get additional information. • Enter claim payments, reserves and new claims on the computer system, inputting concise yet sufficient file documentation. • Examine claims investigated by insurance adjusters, further investigating questionable claims to determine whether to authorize payments. • Investigate, evaluate and settle claims, applying technical knowledge and human relations skills to effect fair and prompt disposal of cases and to contribute to a reduced loss ratio. • Maintain claim files, such as records of settled claims and an inventory of claims requiring detailed analysis. • Pay and process claims within designated authority level. • Prepare reports to be submitted to company’s data processing department. • Present cases and participate in their discussion at claim committee meetings. • Report overpayments, underpayments, and other irregularities. • Resolve complex, severe exposure claims, using high service oriented file handling. • Supervise claims adjusters to ensure that adjusters have followed proper methods. • Verify and analyze data used in settling claims to ensure that claims are valid and that settlements are made according to company practices and procedures. Mrs. Jones’ free time as a homemaker/mother was probably busier than it was during her college-working days, as she wore all the different hats, juggled all the changing schedules and planned the leisure activities, all things considered, for the family. Like Mr. Jones, Mrs. Jones and Cathy were den mother and brownie for a local troop, and they shared lots of time doing many activities. Mrs. Jones reports she was able to keep an impeccably clean home. She regularly visited the farmer’s market for fresh vegetables, in addition to the tomatoes and peppers and herbs she grew at home. She kept roses and changed seasonal flowers in her flower beds. She was in a ladies bowling league on Tuesday nights, and visited her mother at least once per week. Dr. Paul found abnormal findings on Mrs. Jones’ EEG and QEEG. He suspected Mrs. Jones’ bilateral hand tremors and chronic pain were due to damage in her cerebellum, and had her evaluated by a neurologist specializing in motion and movement disorders. Dr. Hoffman did neuropsychological testing. The results of testing for Mrs. Jones revealed problems with discernment (the ability to be tactful or to keep social behavior appropriate), and details (the ability to notice small differences); and multitrack thinking and differentiation (doing more than one thing at a time, thinking more than one thought at a time, or juggling several different thoughts or activities simultaneously, as required in adult thinking, i.e., multitasking) abilities. She is very depressed, and he is doing counseling and cognitive retraining. She states they tried giving her numerous psychotropic

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medications, but she had negative reactions to each one, and they all put her in a fog. Mrs. Jones was referred to Dr. Craig, a Physiatrist specializing in Rehabilitation Medicine. Dr. Craig performed numerous physical capacities tests, and provides a reliable and valid measurement of Mrs. Jones’ physical functioning. Additionally, Dr. Craig delineates the future medical care and affiliated costs which Mrs. Jones will probably need in the future, based on his knowledge of outcomes for persons in the similar condition. Consistency is noted when comparing the notes from the standard vocational interview to Dr. Craig’s functional capacity evaluation. Mrs. Jones has a significant loss of ability to do things like reaching (extending her hands and arms), handling (seizing, holding, grasping, turning, or otherwise working with hand or hands. Fingers are involved only to the extent that they are an extension of the hand, such as to turn on a switch or shift gears), and fingering (picking, pinching, or otherwise working primarily with fingers rather than with the whole hand or arm, as with handling) due to chronic joint pain, tremors and muscle fatigue. She is unable to lift, carry, or push/pull significant weight without causing her pain to increase and minor activities exhaust her energy. A Home Health Aide assists Mrs. Jones with performing her ADLs and IADLs, and performs the food shopping, food-preparation and cooking. A housekeeper comes in twice per week and maintains the laundry and housecleaning. Dr. Craig opines she will need this assistance for life. Prior to CO Poisoning, Mrs. Jones’ states her overall health was Excellent. Her Life expectancy at age 35 is 46.4 years, and her Full-Functioning Life Expectancy at age 35 is 39.7 years; however, this doesn’t consider the negative health impact CO poisoning has on her present overall health (see Figure 31.5). At present, Mrs. Jones rates her overall health as good, but she is limited in terms of performing her ADLs. The results of her SF-36 are below (see Table 31.7). Mrs. Jones had the capacity to work and earn money like a Claim Examiner before her exposure to CO Poisoning, and could have returned to doing it at any time. The Five Steps analyzing Mrs. Jones’ loss of future earning capacity are as follows: Step 1, her preinjury earning capacity is reasonably represented by the actual earnings that accrues to Claim Examiners, or $41,670; Step 2, Mrs. Jones’ preinjury worklife expectancy is like a nondisabled female’s with 13–15 years of education, reduced by the likelihood of living and working from age 35 through age 74, or 24.19 years; For Step 3, her postinjury earning capacity, and Step 4, her postinjury worklife expectancy it is assumed Mrs. Jones is 100% occupationally disabled as a result of a combination of impairments, including exertional and nonexertional limitations; and, Step 5, the present value calculation reveals a lifetime loss of future earning capacity in a range of $792,809–$1,008,179, using a range of an assumed net discount rate of 1.6% to a total offset assumption. Mr. Cooley’s Life Care Plan delineates the cost for Mrs. Jones’ future medical care ($8,750 per year) and home care/assistance needs ($41,184 per year). When these figures are calculated through Mrs. Jones’ Life Expectancy, she will need between $1,740,402 and $2,168,321, stated in terms of present value.

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When these figures are added to her loss of future earning capacity, her combined losses are in a range of $2,533,212–$3,176,500, stated in terms of present value (see Table 31.8). Betty’s worklife expectancy chart

Betty’s assumed worklife toage 67 is 33 years

A severely disabled cohort of Betty’s would have a future worklife of 2.63 years. An average disabled cohort would have a 9.27 year worklife expectancy

An average disabled cohort would have a 9.27 year worklife expectancy

At age 35, Betty’s nondisabled worklife expectancy is 24.19 years

0

5

10

15

20

25

30

35

FIGURE 31.5 Betty Jones’ worklife expectancy chart.

TABLE 31.7 Mrs. Jones’ SF-36 Data Set Scales Limitations in physical activities because of health problems Limitations in usual role activities because of physical health problems Limitations in social activities because of physical or emotional problems Energy/Fatigue/Vitality Emotional Well-being Social Functioning Pain General Health

33.3

Mean 70.61

SD 27.42

0

52.97

40.76

0

55.78

40.71

10 52 25 32.5 40

52.15 70.38 78.77 70.77 56.99

22.39 21.97 25.43 25.46 21.11

31.14.3 JOHN JONES John Jones celebrated his 12th birthday on August 21, 2006. Dr. Hoffman’s neuropsychological evaluation of John’s abilities reveals that, as a result of CO poisoning, he has a postinjury level of intelligence that is one standard deviation below his

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B

Mr. Jones’ Age

35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54

A

Number of Periods

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 98,073 97,977 97,875 97,763 97,644 97,512 97,364 97,204 97,030 96,848 96,642 96,424 96,184 95,933 95,666 95,375 95,064 94,730 94,367 93,992

Number of Life Survivors Beginning At age 35

C D

0.9990 0.9980 0.9968 0.9956 0.9943 0.9928 0.9911 0.9894 0.9875 0.9854 0.9832 0.9807 0.9782 0.9755 0.9725 0.9693 0.9659 0.9622 0.9584 0.9541

Mr. Jones’ Probability of Life

TABLE 31.8 Loss of Future Earnings Data

0.818 0.818 0.818 0.818 0.818 0.818 0.818 0.818 0.818 0.818 0.844 0.844 0.844 0.844 0.844 0.844 0.844 0.844 0.844 0.844

Mr. Jones’ Probability of Work as Non disabled

E

0.653 0.653 0.653 0.653 0.653 0.653 0.653 0.653 0.653 0.653 0.676 0.676 0.676 0.676 0.676 0.676 0.676 0.676 0.676 0.676

Probability of work Moderately Disabled

F

0.354 0.354 0.354 0.354 0.354 0.354 0.354 0.354 0.354 0.354 0.319 0.319 0.319 0.319 0.319 0.319 0.319 0.319 0.319 0.319

Probability of Work Average Disabled

G

0.13 0.13 0.13 0.13 0.13 0.13 0.13 0.13 0.13 0.13 0.084 0.084 0.084 0.084 0.084 0.084 0.084 0.084 0.084 0.084

Probability of work Severely Disabled

H

0.817 0.816 0.815 0.814 0.813 0.812 0.811 0.809 0.808 0.806 0.830 0.828 0.826 0.823 0.821 0.818 0.815 0.812 0.809 0.805

Probability of Living and Working, Nondisabled

I

J

0.652 0.652 0.651 0.650 0.649 0.648 0.647 0.646 0.645 0.643 0.665 0.663 0.661 0.659 0.657 0.655 0.653 0.650 0.648 0.645

Probability of Living and Working, Moderately Disabled

K

0.354 0.353 0.353 0.352 0.352 0.351 0.351 0.350 0.350 0.349 0.314 0.313 0.312 0.311 0.310 0.309 0.308 0.307 0.306 0.304

Probability of Living and Working, Average Disabled

0.130 0.130 0.130 0.129 0.129 0.129 0.129 0.129 0.128 0.128 0.083 0.082 0.082 0.082 0.082 0.081 0.081 0.081 0.081 0.080

Probability of Living and Working, Severely Disabled

L

718 Carbon Monoxide Poisoning

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21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 46.4

55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81.4 93,569 93,124 92,615 92,108 91,508 90,858 90,133 89,398 88,562 87,674 86,692 85,658 84,553 83,351 82,062 80,693 79,169 77,579 75,860 74,033 72,070 0.9495 0.9443 0.9392 0.9331 0.9264 0.9190 0.9116 0.9030 0.8940 0.8840 0.8734 0.8622 0.8499 0.8368 0.8228 0.8072 0.7910 0.7735 0.7549 0.7349 0.669 0.669 0.669 0.669 0.669 0.669 0.669 0.669 0.669 0.669 0.275 0.275 0.275 0.275 0.275 0.145 0.145 0.145 0.145 0.145 0.476 0.476 0.476 0.476 0.476 0.476 0.476 0.476 0.476 0.476 0.181 0.181 0.181 0.181 0.181 0.084 0.084 0.084 0.084 0.084 0.201 0.201 0.201 0.201 0.201 0.201 0.201 0.201 0.201 0.201 0.131 0.131 0.131 0.131 0.131 0.067 0.067 0.067 0.067 0.067 0.055 0.055 0.055 0.055 0.055 0.055 0.055 0.055 0.055 0.055 0.005 0.005 0.005 0.005 0.005 0 0 0 0 0 0.452 0.450 0.447 0.444 0.441 0.437 0.434 0.430 0.426 0.421 0.158 0.156 0.154 0.151 0.149 0.068 0.066 0.065 0.063 0.062 18.52

0.635 0.632 0.628 0.624 0.620 0.615 0.610 0.604 0.598 0.591 0.240 0.237 0.234 0.230 0.226 0.117 0.115 0.112 0.109 0.107 24.19

9.27

0.191 0.190 0.189 0.188 0.186 0.185 0.183 0.182 0.180 0.178 0.114 0.113 0.111 0.110 0.108 0.054 0.053 0.052 0.051 0.049

2.63

0.052 0.052 0.052 0.051 0.051 0.051 0.050 0.050 0.049 0.049 0.004 0.004 0.004 0.004 0.004 0.000 0.000 0.000 0.000 0.000

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720

preinjury level, as was found on standardized school tests. The Perdue Pegboard test reveals he has a one standard deviation decrease in his ability to manipulate small pegs, diminishing his handling and fingering ability. John’s Life Expectancy is 63.5 years at age 12. His Full-functioning Healthy Life Expectancy would have been 56.8 years, but for the CO Poisoning. His DisabilityAdjusted Life Expectancy, considering his overall health is very good, but he is obviously limited in his major activity, work, as an adult, compared to what he could have done, 74%, is 46.99 years. Thus, 16.51 years are lost to disability (see Figure 31.6). Step 1, John’s preinjury adult earning capacity is like that of an average nondisabled male with at least 1–3 years of college and at most a college degree, or approximately $69,937 per year; Step 2, John’s preinjury worklife expectancy, beginning at age 18 and reduced through age 74 by the probabilities of Life and Working for nondisabled males with at least 1–3 years of college and at most a college degree, is 40.83 years; (see Figure 31.7) Step 3, John’s postinjury adult earning capacity is at least like that of an average disabled male with a high school diploma, and at most like that of an average disabled male with 1–3 years of college, which is approximately $40,771 per year; Step 4, John’s postinjury worklife expectancy beginning at age 18 and reduced through age 74 by the probabilities of life and working for disabled males with at least a high school diploma and at most, disabled males with one to three years of college, or 32.24 years; Step 5, John’s loss of future earning capacity is in a range of $1,035,692– $1,541,334, stated in terms of present value.

From age 12, 26% of John’s life expectancy, or 16.51 years is with burden of disability

John’s full-functioning, healthy life expectancy is 56.8 years

John’s life expectancy at age 12 is 63.5 years

0

10

20

30

40

50

60

FIGURE 31.6 John’s life and health-adjusted life expectancy.

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An average nondisabled cohort of John’s has a 40.83 year worklife probability

An average moderately disabled cohort of John’s has a 32.24 year worklife probability

An assumed worklife from age 18 to retirement age 67 is 50

0

10

20

30

40

50

60

FIGURE 31.7 John’s worklife chart.

31.14.4 CATHY JONES Cathy Jones celebrated her 9th birthday on September 8, 2006. Dr. Hoffman’s neuropsychological evaluation of Cathy’s abilities reveals that, as a result of the CO poisoning, she has not sustained a cognitive decline in functioning. However, the Perdue Pegboard test reveals she has a one standard deviation decrease in her ability to manipulate small pegs, diminishing her handling and fingering ability. Cathy’s Life Expectancy is 71.7 years at age 9. Her Full-functioning Healthy Life Expectancy would have been 63.5 years, but for the CO poisoning. Her DisabilityAdjusted Life Expectancy, considering her overall health is very good, but she is obviously limited in her major activity, work, as an adult, compared to what she could have done, 74%, is 53.06 years. Thus, 18.64 years of Cathy’s life are lost to disability.(see Figure 31.8) Step 1, Cathy’s preinjury adult earning capacity is like that of an average nondisabled female with at least 1–3 years of college and at most a college degree, or approximately $46,128 per year; Step 2, Cathy’s preinjury worklife expectancy, beginning at age 18 and reduced through age 74 by the probabilities of life and working for nondisabled females with at least 1–3 years of college and at most a college degree, is 37.37 years;(see Figure 31.9) Step 3, Cathy’s postinjury adult earning capacity is at least like that of an average disabled female with 1–3 years of college, and at most like that of an average disabled female with a collage degree, which is approximately $39,884 per year; Step 4, Cathy’s postinjury worklife expectancy beginning at age 18 and reduced through age 74 by the probabilities of life and working for moderately disabled females with at least a 1–3 years of college and at most a college degree, or 30.47 years;

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18.64 years, or 26 %of cathy’s life is lived with the burden of disability

Cathy’s full-functioning healthy life expectancy would have been 63.5 years

Cathy’s statistical life expectancy at age 9 is 71.7 years

0

10

20

30

40

50

60

70

80

FIGURE 31.8 Cathy Jones’ life and health-adjusted life expectancies.

Cathy’s statistical worklife probability as average moderately disabled is 30.47 years

Cathy’s statistical worklife probability as nondisabled is 37.37 years

The period from Cathy’s 18th year to a retirement age 67 years later is 50 years

0

10

20

30

40

50

60

FIGURE 31.9 Cathy Jones’ worklife chart.

Step 5, Cathy’s loss of future earning capacity is in a range of $341,096–$508,492, stated in terms of present value. Social Scientists are reminded of the poem by John Saxe, The Six Blind Men of Indostan, who each, after inspecting a different body part of an elephant, described the elephant differently from his own, limited perspective. Disability, as a Gestalt, has aspects from the health economist, mental and physical health-care providers,

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social workers, and occupational-rehabilitational professionals. By better understanding the “healthy elephant,” social scientists can continue improving quality of care provided and hopefully ensuring a better quality of life outcome for persons with disability.

31.15 DEDICATION This chapter is dedicated to the memory of Don Vogenthaler, Rh.D. A mentor, friend and colleague for more than a decade, Don’s dedication to assisting survivors of traumatic brain injury was inspiring and lead me to become actively involved with facilitating the recovery of survivors in a similar group. Don was a caring advocate for the many wrongfully-injured persons he touched throughout his career. He is greatly missed, although his endeavors will continue with at least this analyst, and with the readers, if they, too are challenged to care.

References 1. Murray, C.J. and Lopez, A.D.,Global Burden of Disease and Injury, Copyright 1996, World Health Organization, NY and Geneva. 2. Fryback, D.G., “Methodological Issues in Measuring Health Status and Health-related Quality of Life for Population Measures: A Brief Overview of the “HALY” Family of Measures”, Appendix C, Summarizing Population Health - Directions for the Development and Application of Population Metrics, National Academy Press, Washington DC, 1998. 3. Pennifer Erickson, Ronald Wilson, and Ildy Shannon. “Years of Healthy Life”, U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Health Statistics, www.health.gov/healthypeople, April, 1995. 4. National Center for Health Statistics, United States Abridged Life Tables, vital stats 1987, 2000 and 2003. 5. Expectancy data, Economic Demographers, Shawnee Mission, Kansas, “Difference between expected life and full function healthy life at single years of age. . .” 6. The Economic Impact of Motor Vehicle Crashes, 2000, U.S. Department of TransportationNational Highway Traffic Safety Administration, May, 2002. 7. International Classification of Functioning, World Health Organization, 2001. 8. Department of Commerce, Bureau of the Census report Labor Force Status and Other Characteristics of Persons With a Work Disability, Current Population Reports, Series P-23, Number 160. 9. This descriptive analogy quoted with permission from Dr. Donald Vogenthaler, a dear friend and mentor. 10. United States Department of Labor Office of Administrative Law Judges Law Library, http://www.oalj.dol.gov/PUBLIC/DOT/REFERENCES/DOTPARTS.HTM 11. Expectancy Data, The Dollar Value of a Day: 1999 Dollar Valuation. Shawnee Mission, KS, 2001, Table 1, Average Hours of Activities in a Week by Persons Employed Full-time. 12. Occupation Information Network, O-Net Online, http://online.onetcenter.org/link/ summary/13-2051.00

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32

My Carbon Monoxide Poisoning: A Victim’s Story Joseph A. Cramer

I’m Joe—an everyday guy. I’m six foot two, 200 pounds give or take, and chunk up a bit in the winter. A real family guy, a loyal friend, and trusting. I work and play hard. I had thinning hair by age 30, brown eyes,and calloused hands. When the chips are down I’m there with a hand to help. After a beer or two I can join the guys in a round of jokes, but I know when to go home. I have stories to tell about every age—from running away from home at age 5 and walking around Lake Michigan at age 20. From being smitten with my 9th-grade teacher and giving up on becoming a priest, to learning what it was like when all hell breaks loose in my marriage. Working hard to provide the good life. A good husband and a good father. Hunting and fishing, especially fishing were mainstays of my leisure time if I wasn’t occupied fawning over my family, teaching my kids the proper way to squash ants. I loved racing sports cars, watching “Wild World of Sports” on TV, and watching my family have fun. Little things were important. Walking the dog every morning, riding a bicycle, spending time with my kids on Saturday mornings, and surprising my wife with flowers. I worked hard so I could do all of that. Nothing meant anything without my family alongside. That is me, nothing more, nothing less. That all went away for 2 years after carbon monoxide (CO) poisoning. I had worked at an auto care facility for almost 2 years. Occasionally, when the doors were closed for long periods because of cold weather, the air inside grew stagnant and had an odd smell. On most workdays, by early afternoon I would feel rather silly and laugh at most anything —funny or not. Other employees were affected similarly, but not to the same degree. I was a bit of a workaholic and spent long hours at the facility. On those days, by the time I arrived home however, I’d developed a splitting headache and usually had a terrible temper, which was not at all my usual temperament (nor had I ever suffered from headaches to any noticeable degree). Starting in the fall of 1977 my symptoms became more frequent and more severe. So much so, that my wife brought it to my attention because I was starting to shout at her and the kids once in a while for little or no reason. We still didn’t relate it to work as it got worse and worse. I was working 5.5 or 6 days a week, 12–16 h a day 725

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and I was inhaling fumes all the while. Never having enough time to clear my system of the poison, it was taking its toll, little by little it had become chronic. As friends and relatives started coming over less and less because of my appalling behavior, it never entered my mind that it could possibly be CO poisoning at work. I knew the building was equipped with an air makeup system for just such possibilities. My family wanted to know what was happening. It was like I was becoming a different person right before their eyes. It seemed that no matter how hard I breathed, I couldn’t get enough oxygen into my lungs. I constantly forgot why I was in a particular place and what I was supposed to do. My cognitive skills began to diminish to an almost ridiculous level of understanding. My body was slowly falling asleep, sort of like when you hit your funny bone on your elbow, and I started to feel numb all the time—not just at work. I thought that soon it would go away. It didn’t. And I didn’t know how to stop it. On the final day, the last thing I can remember is somebody putting a locker where I didn’t think it belonged. I freaked out and tried to smash it with a hammer. I didn’t know what was happening to me, but it was a bad thing and I tried to fight it somehow. Next I started to yell at a customer; I even swore at him and I never did those sorts of things. I had been working about 18 h, nonstop, that day. My tongue started to swell and I couldn’t talk right. There was no oxygen, nothing was working, and I had to find a way to put air in my lungs—I had to keep fighting! I asked a fellow employee to help me, but I don’t think he understood what I was asking. I swore at him, too, just before he grabbed me. Although I have no personal memory of it, it’s been explained to me that at this point in time I was driven home by a couple of fellow employees. They left me there with my wife and children. My wife, Sandy, called our doctor and for the next 24 h it remained a mystery as to what was happening to me and what course to take. Finally I was asked to speak to the doctor. My tongue was swollen and I spoke gibberish. He ventured a guess that perhaps I had CO poisoning and had my wife bring me to the hospital for tests where his hypothesis was confirmed. My mind was a goo of mishmash and lightning flashes. My head hurt so badly it felt like it would explode. I pushed on my temples as hard as I could to try and stop the pain. A lady was talking to me in a loud voice, but I couldn’t understand what she was saying. I looked at her but it appeared like she was a long way off in a long dark tunnel. There was a little boy by her feet. I tried to talk to her and tell her about my head breaking apart. The words didn’t come out of my mouth in the way I was thinking them. My tongue was still swollen and wouldn’t do what I wanted it to. Everything slowly went dark and I couldn’t see anymore although my eyes were open. There was more noise and someone cried. Now I felt odd, very odd. Nothing hurt. Actually I felt nothing at all. I was floating. My feet weren’t touching anything. I felt I must be flying in the air, but I couldn’t see where I was. I didn’t know where I was or even if I was anywhere at all … I wasn’t real anymore … Nothing was real … It was a dream … . I couldn’t breath … I thought I must be dead … . Everything was gone… It was like I’d never been born .… There was nothing! I am lying down and a woman in a white dress was trying to jab a needle into my wrist. I explained that it hurt terribly, but she didn’t appear to hear me and kept

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jabbing. My whole body felt like it was made of cement and attempts at movement were useless. My head hurt even more and I tried to sleep. Noises woke me up sometimes and I found them extremely annoying. Someone gave me a pill and a drink and soon my head stopped hurting and I fell asleep again. There were people around me sometimes, but I had no idea who they were. A man in a light gray suit woke me up and asked my name. I couldn’t tell him. He said I was Joe. That name sounded OK to me. He told a lady I could go home and I went with her. We didn’t talk much, but she asked a lot of questions I couldn’t answer. I felt myself getting upset. When we got to her house, she gave me a pill and I took it with a glass of water. After a while my mouth got very dry, but I was not upset. I didn’t know how to think or speak understandably. It had been explained to my wife, Sandy that even after 24 h there still remained almost a lethal amount of CO in my blood, but the symptoms should go away after a few days of rest. (editor’s note: This often does not occur, as you will see in this instance). My memory was almost entirely gone except for a few basics. I did start talking understandably when my tongue began working again, but much of it was nonsense; speaking about lights and sounds no one else could see or hear, but gradually evolving into an acceptable type of communication, though it could still certainly not be called articulate. That took a great deal longer. That’s what I’ve been told, but can only vaguely remember. It was a truly frightening time for my family. I had no feelings other than placid and annoyance. I took trips to various doctors and received several tests including a CAT scan along with more blood tests. If I remember correctly, perhaps an electrocardiogram or something of that nature with electrodes glued all over my head and upper torso. They didn’t show much, if anything at all that we were told of. There was really nothing that could be done, they told me. I was given a drug called “Elavil” to keep me calm. I took as many as four aspirin at a time, as many as five times a day to numb the headache, but that also made my ears ring. Medical doctors treated me; however they could and after a few weeks seemed to be both surprised and disappointed that my memory had not returned. As time went on, it seemed as though some in the medical field thought I was being stubborn by not getting better—that I was actually refusing to improve by my own choice. In the very beginning of this ordeal, some of my behavior was nothing short of juvenile. I couldn’t pass a refrigerator without putting my hand into the freezer. It was fascinating to feel the cold on my hand and wonder where it came from. I also wondered where everything went when I flushed the toilet. Crude perhaps, but interesting. Sandy kept telling me to stay away from the stove because I’d burn myself. I watched her light matches and blow them out. Eventually, I lit one myself and burned my hand to see what it felt like. It hurt like hell! The following is my wife Sandy’s comments about that period in my life: “I opened the door and two guys that Joe worked with told me that Joe wasn’t acting right and they couldn’t control him. They thought they’d better bring him home till he got better. Then they left. I looked at Joe and his eyes were blank, as if he didn’t know where he was. I was scared. I didn’t see the guy that went to work the day before. (He’d worked all night and most of that day —about 18 h). I held the door open and he came in, his

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eyes began to dart all over the place. He was acting mean. I backed away, he moved in quick movements, grabbing things as if to keep his balance. Going from room to room looking quickly and moving to the next. I asked him what was going on. He looked at me and his mouth opened but no words came out, only sounds I’d never heard before. I backed away again. I thought, “Who was this?” Joe kept moving all around; when he saw himself in the mirror he kept sticking his tongue out and scraping it on his teeth. When our son went up to him and started to talk Joe yelled odd sounds and moved his legs toward him, making him run away crying. It was horrible. I didn’t know what to do. Then suddenly Joe became calm and quiet, acting exhausted. I led him to the bed and he lay down and went to sleep. I was still scared but felt that when he woke up it would be all right. I didn’t sleep at all that night. My home didn’t feel safe anymore. Joe had always protected us. Not that night. The next morning Joe woke up and held his pants like a little kid, looking around. I took him to the bathroom and he went. He didn’t seem able to talk, made odd sounds, eyes still looked glazed and distant, darting back and forth, still exhausted. He looked weird and disoriented. He wasn’t better. I called our family doctor and did my best to tell him what was going on. He asked to talk to Joe. I gave Joe the phone. He made noises into the phone and dropped it. I picked it up and the doctor asked me where Joe had been when this happened. I told him and he said to call the poison control center and get to the hospital for tests. I called a babysitter for the kids and when she got there I managed to get Joe in the car and drove to the hospital. (I cannot remember exactly how I got Joe to do all this). Blood was drawn for tests and a doctor told me Joe had enough Carbon monoxide in his body to kill most people. He said that within a day or so he’d be back to being himself. I’m not sure, but I think they gave Joe a shot. Then he became irritable and they gave him a pill. He calmed down and I took him home. I kept asking Joe questions but he didn’t answer. It was like he didn’t understand me, but at least he was calm and not mean. The next few weeks it was just, give him pills to keep him calm and try to teach him to talk. He could eat and went to the bathroom but that was about it. When he began to speak in a couple days it was about lights at first and I couldn’t see them. Then we could talk but it was like being with a little kid. He didn’t know anything. He was mean sometimes, sometimes not. He certainly didn’t get better in a few days. When we went back to my family doctor he told me to start teaching Joe about his life and then he would get better. It took 2 years.” For lists of changes and symptoms that occurred after the CO poisoning, see Appendix 1. The first weeks were filled with one new learning experience after another, and not all of them nice. My son, Stephen was playing with a toy matchbox car and I stepped on it. It hurt. I screamed at Stephen, grabbed the car and smashed it with a hammer until it was flat, Stephen crying all the time. It happened so quickly, it took Sandy by surprise and she couldn’t stop me. The damage was already done. Another lesson—I was a very different and had to be watched more closely. It was frightening for my entire family. What would happen next? She took me back to the doctor. My general practitioner suggested that I walk and ride a bicycle to build up my lung capacity and keep pumping oxygen into my system. It would also keep me

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occupied and I’d have less chance of becoming upset. Walking was not difficult, but my kids went with me so I wouldn’t get lost. I had no memory of my neighborhood and if the house was not within sight I was apt to go in any direction. Riding a bicycle proved to be a much greater challenge. Although I had been an avid cyclist all of my life, my sense of balance was gone and had to be developed because whenever I got on the bike it would fall over before I’d get it started. It looked rather ridiculous—my being a full-grown adult and all, falling over on a bike. When I finally accomplished the balance to an acceptable level, there arose another small detail we hadn’t considered. I still had no sense of direction or location and got lost the first trip. After that I rode with a note pinned to my pocket reading, “If found please contact …” with a phone number to reach my wife, Sandy and a small explanation of my predicament. For a reason beyond my understanding, if I was gone for more than a few hours I could often be found somewhere close to the house I was born in—most often sitting on the curb in front of it. How I managed to find my way there was a mystery. Because I was not responding to medical treatment or perhaps the lack of any medical treatment available, I was sent to a psychiatrist. He asked me all kinds of confusing questions I didn’t understand and couldn’t answer. He asked me how I felt a lot of times. I had no idea. The meetings went like that. I really don’t remember what we talked about. I just know it annoyed me (I can distinctly remember swearing at him inside my head, perhaps even out loud) and after several visits I was told that perhaps this refusing to remember was due to a difficulty I had with my parents, more specifically my mother. Now, that was just plain crazy. Even I knew it wasn’t that. I never went back to him. It was as though there was no possible way that CO poisoning could cause what I was going through. (Editor’s note—This is such a common response of physicians) I was continually examined and treated, but with disbelief about my situation. Apparently, there were no effective tests or procedures available. Sandy explained later that she felt as if everyone was simply guessing. When she spoke with our G.P., he pretty much confirmed her feeling. I wasn’t going to change. Even Sandy was getting depressed. Where do we go from here? By the following fall, when the snow came, I had been told what it was but the sight and feel of it was an unforgettable experience, almost as if I walked outside into a different world—all cold and clean and fluffy. I played in it like a little child. Stephen and Brenda and I got along well playing in the snow like that. They taught me how to slide and throw snowballs and build a snowman. We needed that type of activity together badly. It was like being on a huge, cold cloud. I didn’t like the shoveling so much, however, the snow did teach me that recreation was cathartic, so we played whenever we could. The specter of my unpredictable reactions always loomed around the next corner, however. During one snowstorm my neighbor suggested I use his snow blower to clear my driveway and sidewalk. Fine, it sounded good to me. He got it started and off I went. I pushed it into a snow pile too fast and stopped the engine. I pulled and prodded and could not get it going. With the wind blowing snow down my neck and my ears feeling all prickly with frost bite I wound up on my neighbors front porch accusing him of tricking me with a broken snow blower. He wouldn’t come

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out the door, but talked me through getting the thing started again. I finished but I was also half-frozen and irritated. When I went into the house, my son Stephen, was all excited and wanted to go out and play in the snow. I scolded him and told him to quit bothering me. Devastated, he began to cry and ran to his bedroom. I chased him down the hallway yelling all the way until he slammed the door. I’d done it again. I saw what I had done and went down into the basement to be alone and make sure I stayed away from everybody for a while. When the next summer came, Sandy and I spent a couple of weekends away without the kids; they stayed at Grandma’s house. The first was spent canoeing with close friends on a river in Northern Michigan called the Pine. We figure’d I wouldn’t get lost because the river only goes one way. It went rather well actually except for a couple things. I was teased a lot by everyone there, because I stepped into the river at a stop to cool-off and darn near drowned in 8 ft of water. It was muddy and I couldn’t see how deep it was. “Still water runs deep,” they said. OK, lesson learned. At the end of the trip, Sandy and I arrived first and stood on the bridge waiting for the other canoes. The water under the bridge was quite still. When the canoes came around the bend with our friends, I dove off the bridge to swim out to them. BANG! I hit my head on the bottom. The water was only a couple feet deep. I’m lucky I didn’t break my neck, although I did crack a couple vertebrae and bit the end of my tongue off. Another lesson learned: “Not all still water runs deep.” Later in the summer, another friend had a birthday celebration at his cottage, also in Northern Michigan and invited us to join his weekend party. We had a great time. No tense moments that I recall. I woke up Sunday morning and got into the car to go to church about 5 miles away. I left and didn’t come back for over 4 h. I got lost and never did make it to church. I finally got back by stopping at a grocery store to ask for help and as luck would have it, the owner knew where the party was and led me back. Now that was good for a few laughs and thankfully I didn’t panic. The following 2 years seemed to be an effort in futility; with many useless attempts to find a medical solution. Outside of our own learning activities, nothing seemed to help. After over a year, I went to a holistically inclined doctor, an osteopath recommended by an acquaintance. He took my case under his wing because he found it interesting. I don’t even think he charged me. After he examined and tested me, his opinion was that my brain was or had been swollen just like my tongue had been. It was his diagnosis that the effects were similar to those following a stroke because of the lack of oxygen. Also, because of the length of time since the accident, he didn’t believe there was any drug or therapy that could help other than to keep me calm like Elavil was doing. Only time and the body’s natural ability to heal would make a difference. He suggested I follow a specific diet free of impurities and continue to exercise as much as possible. He recommended that I hone my cognitive skills by working out word and math puzzles so my brain could create new pathways. Other than that, I’d pretty much have to learn to live with what I had. I began the puzzles with a passion. In the beginning it was hilarious. I couldn’t solve a thing and had to ask someone for every answer. It was the strangest thing. Here we knew I had a vocabulary somewhere in my head because I could talk. I had perfected swearing, almost to a fine art. But ask me a question about a word or number problem and I drew a blank. My thinking process was all screwed up.

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This doctor also believed I should find a job working with people for a while in order to work on my social skills along with my regular work of detailing cars. A close friend, Virgil helped get me a job selling sports cars at the same place he worked and he also briefed me on many things such as driving a car and reading and understanding maps so I didn’t get lost. It took no time at all to learn the driving part. I had a real knack for that. Then I could drive a car back and forth to work instead of my bicycle. My boss, Dave was a real comedian and introduced me to being the brunt of jokes, constantly. He said he’d never had a retarded salesman before. The laughing was good, Dave helped me learn to laugh. Some other people had treated me as though I was retarded and avoided me. Dave said it out loud and treated me like a friend. I had a strong attraction to sports cars (I had driven and raced them in the past), so working in car sales was a real plus. I was earning money and learning how to interact with other people when my mind shut off. Eventually, however, I left the car lot to continue my own business full time. Dave had allowed me to clean cars in his service department at night, but that was not enough. I couldn’t get over the fear of anxiety attacks in front of people. When I described the anxiety problem to one of my doctors, he suggested I should carry a paper bag in my pocket and when the attack came on to put the bag over my mouth and keep breathing my own air until it was over. I think I tried it three or four times. It lessened the reaction, but I still believed I was going to die. After a while I forgot about the bag. In looking back, I realize that leaving the car lot, very much against my wife’s better judgement, was not such a good idea because for a while the anxiety attacks and depression increased until I had other employees around me again. The socializing had been way more important than I’d accepted. It kept my mind working where as physical labor, although therapeutic in its own way, came almost automatically, instinctively. While working one night, I didn’t take any Elavil, got upset and threw a buffer through a 6 in. thick plasterboard wall from my shop into the next. The owner of the other shop came over carrying the buffer and with a smile on his face said, “Didn’t take your med’s did ya?” His attitude helped me through the moment. Reminded me of Dave. Meanwhile my wife was left with the responsibility of rebuilding me as a person. Daily, she showed me pictures and told me stories of the past. In the beginning many of these sessions were not very nice at all because of my volatile temperament. I’d become angry and aggressive when told of certain things or places, but there was no warning ahead of time, it wasn’t always the same things and, of course, I had no understanding or explanation for it. When visiting my mother’s house on some occasions I’d get irritable and refuse to walk into the front yard (my father had died in my arms in the front yard, but I had no memory of it then, just an uneasy feeling) and still other times I strolled across the yard without hesitation. Slowly I was able to develop an alter memory based on what she told me along with a rather flimsy grasp of feelings I gathered from watching the reaction of others to situations. I was an excellent mimic. Sandy and my kids, Brenda and Stephen all helped me with reading, so I eventually gained knowledge that way. It wasn’t the reading so much as the understanding of what I had read. Stephen was only four and five during that time, but he knew or

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sensed there was something wrong with his dad, so he sat on my lap and recited words from stories he had memorized and turned pages for me. Kids are amazing sometimes. Those people that I came into contact with either believed I was ill and tried to understand or didn’t believe it, and thought I should have gotten over it within a few days. The signs of my illness were not physical, and were therefore, perhaps not acceptable. So many times I’d try to hide my problem by being a jerk. Sandy was led to believe and later explained to me that the overall general consensus, even in the medical community (even though I feel they did what they could) was that the effects, whatever they may be, should be over with in a matter of days or weeks. But still the problems continued. Worst of it all, was the swearing and my being an obnoxious jerk. I knew I was not reacting very well to a lot of situations, but didn’t know how to stop it. Occasionally, I’d panic when it seemed my mind wasn’t working at all. An example of it was one day I was sitting behind my desk in my office, which is 12 ft. long and 8 ft. wide. I needed to go out the door for some reason (it was on the other side of my desk). I couldn’t see anything else in the room, only my desk and the door. What to do? I climbed over the desk instead of simply walking around it. I had to get out. Nothing else mattered. If it happened when I was around other people I would try to find a place to be alone until it passed. A bathroom maybe or just going outside. I had to escape, otherwise at times, I’d get so upset I’d throw up. That would mess me up for a few days, every time. I hated that. There was this constant impulse that I had to fight off anything that was unknown to me. I had little ability to defend myself with words, but I realized early on that I had a strong physical ability. Subduing that impulse to be physical was not my easiest task. Although I was an excellent student and learned quickly and could function in many capacities, there seemed to be a problem in that I could not differentiate between my own thoughts and what I had heard from others. As an example; my brother told me the story of how he had caught a huge fish and the fight it put up, how long it was and how much it weighed. A short time later, I described the identical story to a mutual friend, only now it was my fish. I believed it in my heart and could not remember the previous conversation with my brother. I continued to develop my extreme habit of swearing and cursing along with yelling for little or no reason. I especially did not cope well when a conversation would speed up and I wasn’t allowed enough time to organize my thoughts and match them to what I had learned. There were those times when I’d get upset and throw things, too. Thank God, it was never at a person. I never physically hurt anyone. All of these things were a complete turn around from my natural personality. I fought with severe bouts of depression, wishing I were dead, and also almost crippling events of anxiety—highlighted by the feeling of being suffocated, without enough oxygen no matter how hard I breathed. I worked entire days alone, locked up in my shop, keeping myself away from other people including my family. I knew I was “different,” and was afraid I would hurt someone or their feelings, or that my mind would grow blank, or any of a dozen other fears that would crop up at any time. I did not know how to react to many

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common situations, including the death of my brother-in-law. I was completely lost in feelings I couldn’t name or describe. Whatever they were they made me want to disappear from the situation and never come back. More Elavil and aspirin did not help. I decided not to go to a psychiatrist again because I didn’t feel he believed me the first time. On a friends suggestion, I finally went to a priest and speaking with him did help. At the very least it got me through the crisis at the time. Being in or around a church had a calming affect on me. At the funeral I saw those around me, his wife and children, siblings and parents, suffering loss. I wasn’t aware of how to make it better, but I felt the need to do something. I was completely at a loss of what to do, so I said almost nothing. I felt I was responsible for their anguish, and I had caused so many other problems because I wasn’t normal. I have to say that redeveloping a relationship with my wife in some ways was a real treat. Laying on a blanket in the back yard after dark and the kids were in bed, looking at the stars and listening to Sandy’s stories of back when I was a good guy both as a father and a husband was wonderful. I had always been there for my family—teaching our children the important things of life and helping with their skills like making things, fishing, child’s games and, the all-important art of squishing ants with your thumb. I would take my family everywhere with me, even to work. I loved being with my family. She told me all of these things and more (it helped me like who I had been, but I also grew to dislike, very much, who I had become). I had difficulty with mathematics and completely lost my ability to understand music or play a guitar, both of which I had done quite well before the accident. The order of musical notes simply did not make sense to me. My daughter, Brenda helped me tremendously with the math part—sitting for long stretches on the living room couch correcting me and making sure I grasped a calculation and then moving on. She was 12 at the time. I honestly don’t know how it would have gone without the help of my family. Not nearly as well though, I think. The accident apparently came about because of the air make up unit at the car care facility not functioning properly, if at all. Most of the difficulties I experienced in the beginning such as equilibrium, body numbness, eye focus, speaking, and dexterity gradually diminished over a period of 6 months to where they were almost unnoticeable. Life as a family member and business owner was difficult but manageable because of the intense efforts of my family and friends who taught me who I was. The feelings and understanding that went with the knowledge were nowhere near where they should have been, though. It was merely survival, not a walk in the park. I fell deeper into depression over my continuous fits of anger and inability to do anything right. Then towards the middle of the 2nd year, I experienced a sort of awakening. All of the learning efforts sort of began to come together. It started with my venturing out of the shop in search of customers. We were about to go broke because there wasn’t much business just walking through the door. It was the middle of January and we had no money for bills, or food, or gas for the car. It was a dark time. I walked to work one morning in a blowing snowstorm feeling very depressed. Sandy and I had talked the night before about maybe losing our home and everything else we had. She wondered where we would go. I promised her I’d find a way to work it out. Instead of going into the shop I went to the bus stop and took a bus to a car lot

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about 8 miles away. I asked the manager if he had any cars to detail. He said no, so I walked to the next car lot and asked the same question. No again. I walked 6 miles through the snowstorm from car lot to car lot until around dinnertime a manager said I must be crazy to be walking around like that. I said I probably was crazy, but I could clean cars like nobody’s business. He gave me a car and I cleaned it. When he saw how well I did, he sent me a bunch more. I didn’t sleep for 72 h, but I cleaned enough cars to get us out of trouble. When I saw Sandy’s face as I gave her the money it changed me. I’d finally done something good and I wanted to see that face again. Something clicked! The next day I hired my sister-in-law, Karen to help me with the business and watch over me. She understood my problems and also needed a job. It worked. If I lost focus or became depressed, she’d find ways to snap me out of it. A joke or word of advice, a cup of her lousy coffee, or a call to Sandy—whatever it took. Even without the long-term memory, I began to excel as a person and a businessman. Life took a new turn. I learned to ask a question if I didn’t understand something. Bit by bit I gained confidence in myself. My disability became less and less obvious. I began to experience happiness, a real emotion. It beat the heck out of depression, too. Life was better at work and at home, especially for my family. A problem arose when workmen’s compensation refused to pay for the doctor bills and tests any longer. The effects of CO poisoning were not supposed to last that long; therefore, I was technically better and required no further treatment. Nothing had worked so far anyway. I hired an attorney, an excellent attorney, and he jumped into the case with both feet. When we had the hearing, he told me to be quiet and let him talk. Although I wasn’t understanding what was happening, I sat quietly. Afterwards I fired him. When I first went to him, I explained that all I wanted was for the company to pay my doctor and hospital bills. I felt I had made that clear. When we went to the hearing he told the attorneys and the judge we were demanding hundreds of thousands of dollars for this and that and suffering and stuff like that. Sandy and I had already discussed that issue and she was certain we didn’t believe in that sort of thing. We just wanted the bills paid. After firing my attorney, I called the company’s attorney and they paid the bills that same day. We chose not to pursue it any further. I signed a waiver and it was done. We were now on our own. Agree or not agree, it’s our way. The memory problems lasted over 2 years, until midspring of the second year. I was driving home from work in the late afternoon and got stuck in a traffic jam caused by an accident. The weather was pleasant so the windows were down and a breeze flowed into the car and brought with it the smell of lilacs from a grove located alongside the road. My eyesight became blurred as if I was looking into a TV screen when the station goes off the air and I saw, as if it was actually happening, my old house when I was 11 years old, filled with lilacs that I had brought from a field. After my head cleared, I continued home and told Sandy about it. She didn’t know what it meant, so I called my mother and she explained that when I was 11, my uncle, her brother had died and she went to church to pray for him. When she got home I had filled the entire house with lilacs because I didn’t want her to cry. A few weeks later, I was in a store shopping for onions and the smell triggered another memory of picking onions with my brother and father when I was about

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five or so. The memories were so extreme that I had to sit right down on the floor of the grocery store—the clerk thought I was dying or something. It became manageable in a short time and I went home, leaving the clerk to wonder what happened to the crazy guy. My mind was no longer paralyzed. Over the next few months it happened often and with more frequency. Eventually my memory became closer to normal, and in some ways greatly enhanced. That was over 26 years ago. During that ordeal there is no doubt in my mind that all of the puzzles and riddles I attempted to solve created unique pathways in my brain function patterns causing my perspectives to be altered in a sometimes indelicate fashion. Occasionally, when a problem is brought up during normal conversation, I have to refrain from giving my input even when asked. My perspectives are no longer necessarily what people want to hear. I don’t judge them; they are simply there and I can’t control them. I don’t often share those extreme thoughts except with those I am closest to. Those perspectives refine, in my mind, the issues I hear into a specific black and white area with no gray in between. At other times, in my mind, a sentence I speak or hear becomes broken up and moved around and forms an entirely different meaning. I am surprised I’m telling you about them now, but I feel it’s important to say. There are always consequences we cannot change. Those perspectives still cause me concern. I doubt they would have been there normally. I’m still learning to keep my mouth shut and deal with them, one at a time. As it is, I’ve used that perspective to my advantage for 26 years by conducting an annual treasure hunt made up of riddles to celebrate the return of my memory and help create awareness of the danger of CO and the reality of amnesia. It’s been quite successful with over 40,000 participants at times. I do what I can with what I’ve got and where I am. There are still gaps. I still cannot play a guitar or understand much about music (that may be my gift to the world). Yet, even now from time to time, I will reach a point in a conversation and draw a complete blank. It still comes on without provocation or warning, but happens less every year and doesn’t last long, usually. I’ve learned to deal with it and I don’t usually panic over it. The swearing and temper took a long time to go away much to the dismay of my family and friends and me when I’d realize what I was doing. They had become a habit I guess. I’m a pretty calm person now, but believe me, I had to do a lot of apologizing for a few years. And the anxiety attacks kept up for about 4 years. They’ve been gone ever since. Because I have seen the consequences of behavioral problems with swearing and temper, for the last 18 years I’ve attempted to spend time whenever I can with people that are alone and without friends because of those same problems. I visit, play cards, and listen to their swearing and temper tantrums, leave and come back another day. Sometimes I call and simply listen to them talk of their problems. I offer odd jobs when I can to some that are able, but out of work. We talk then. I visit as many as I can on Thanksgiving morning, and bring them some sort of little gifts, usually some stupid toy for laughs, a few donuts, and a bottle of wine or juice and we play cards and share a few stories. My hope is it makes a difference in their lives and gives them a sense of worth. I’ve been there and understand that sometimes that’s as good as it gets. But I can remember the loneliness that invaded my very soul when I’d drive others away with my words or actions. It was the people that stayed that gave me life.

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My life has been altered in many ways because of the CO poisoning, but except for the 2 years of horror to me and my family while my memory was gone, is as close to normal as one might expect. Is it a burden any longer? No, I really don’t think so. We laugh, we cry, we have problems and dilemmas, we find solutions and move on. The most incredible outcome of all of this is I now have emotions. For better or worse, they are my greatest gift. There are still occasions when something will trigger a memory from long ago and that in turn will trigger an emotion. Happy, sad, angry, melancholy, what have you. It’s a treasure I did not have for a long, long time. My memory has become much keener than before and I seem to remember my past in much finer detail than most others. I am most grateful for that. I do think rather slowly for whatever reason. Some common ordinary situations I respond to out of habit, but if it’s not something I deal with almost daily I can take a considerable amount of time to form an opinion. It would be interesting to find out what’s going on in there where the thinking is done. And, I’m not at all good at swearing any more (except of course … well, we’ll leave it at that). I do have a decent sense of humor, too. That’s a good thing. Just in case I screw up. That’s what happened when I didn’t die from carbon monoxide poisoning.

APPENDIX 1. CHANGES/SYMPTOMS AFTER THE CO POISONING, JOSEPH A. CRAMER Before I was brought home Silly, I’d laugh at almost anything Headache Argumentative/confrontational Uncontrollable, unpredictable aggressively violent behavior Speech difficulties, talking incoherently Eyes glazed Heavy breathing Immediately upon being brought home Angry, mean, out of control Screamed and hollered at everyone Repeatedly looked in the mirror at my tongue, uttering something about it being thick Talking was difficult and unintelligible Spoke about lights and sparks Couldn’t feel anything, numb Uncooperative, didn’t appear to understand anything Calmed down, looked exhausted, Went to the hospital after 24 h

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Unable to answer questions, became frustrated when asked (Given a pill to calm me down) No memory, did not respond to familiar surroundings or people Inability to explain or describe anything Arterial blood gases (ABG) indicated CO poisoning at an extreme level Sedated and sent home with my wife At home after the hospital Behaved erratically, sometimes almost comatose, sometimes overactive Wandered aimlessly, enthralled with normal things, appeared to be learning Depressed and anxious, erratic behavior continued Elavil began to take effect and behavior became calm Little sense of balance, wobbled or fell when I closed my eyes After 3 days I could talk more understandably, childish sentences After about 2 weeks at home Began to learn about his surroundings Knew enough to ask questions Smiled, but for no reason Walked in a straight line instead of wandering Got lost if not in sight of home After about 4 weeks at home Knew how to read and to make sense of what I read Rode a bicycle without falling over Learning became easier No long-term memory During the time of my memory loss Angered easily Swore constantly Depressed Anxiety I knew how to work and play, but didn’t know why until it was explained Indecisive Cognitive skills absent Math and music skill deficits

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Personality remained opposite (i.e., different) I felt as though I was being controlled by another person but I couldn’t see him How I have changed since before the CO poisoning Cannot understand music or play a guitar (I could play quite well before) Can now remember minute details from the past, which I couldn’t before Extremely sensitive to odors and lack of fresh air Don’t deal well with others in control Have an overdeveloped sense of responsibility toward others, that is, extremely empathetic Slower thinker—I have to consider all perspectives Difficulty with crowds and close places Editor’s note: This is Joe’s story. Be aware that everyone does not respond in the same way to CO poisoning. Some people are more sensitive to CO and some more tolerant. For some the damage may be more serious cognitive-memory deficits, while for others it may be greater psychiatric or sensory-motor deficits, and yet for others it may be constant miserable physical symptoms and gross neurologic effects. Most CO victims sustain none, or at the most, very small decrements in long-term memory, unlike Joe. Also for most CO victims, damage in the cognitive-memory area is irreversible. It is clear from his story, that Joe was luckier than most CO poisoning victim’s in terms of eventual recovery of most of his functionality. It is this very strong recovery by Joe that has allowed him to present his story for you to hear.

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33 Noninvasive Measurement of Blood

Carboxyhemoglobin with Pulse CO-Oximetry Neil B. Hampson

CONTENTS 33.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33.2 New Pulse CO-Oximetry Equipment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33.3 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

739 740 743 743

33.1 INTRODUCTION Carbon monoxide (CO) poisoning causes symptoms that range from headache, nausea, vomiting, and dizziness to loss of consciousness, pulmonary and cardiac failure, and even death. Since the milder symptoms of CO poisoning are nonspecific, patients may be misdiagnosed with conditions such as viral illness, food poisoning, or motion sickness, depending upon the circumstances of the exposure. Diagnosis of CO poisoning requires both clinical awareness and biological confirmation of exposure. Among the many mechanisms of toxicity of CO,1−5 its effect on hemoglobin has been known for over a century. When inhaled, CO binds to hemoglobin in red blood cells transiting the pulmonary capillaries, forming carboxyhemoglobin (COHb). Because CO binds to hemoglobin in sites normally used to transport oxygen, the result is a decrease in the oxygen content of arterial blood and an associated reduction in peripheral oxygen delivery. Since CO binds to hemoglobin much more avidly than oxygen, COHb remains in the circulation for hours and is a biomarker that can be measured to document recent exposure to CO. Until recently, determination of an individual’s COHb level required drawing a blood sample and measuring it in a laboratory with a benchtop COoximeter or estimating it by measuring exhaled CO.6 Laboratory CO-oximeters use multiple wavelengths to spectrophotometrically distinguish and quantify the various hemoglobin species present (oxy-, deoxy-, carboxy- and methemoglobin). 739

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33.2 NEW PULSE CO-OXIMETRY EQUIPMENT Pulse oximetry is a technique widely utilized for the immediate evaluation of a patient’s oxygenation status. The technology provides an instantaneous, noninvasive, in vivo estimate of arterial hemoglobin saturation with oxygen. Conventional pulse oximeters transmit two wavelengths of light through tissue (typically 660 and 940 nm), measuring changes in absorbance at each wavelength over time and calculating the functional saturation of hemoglobin with oxygen (SpO2 ). When arterial hemoglobin is partially saturated with CO, pulse oximetry measurements have been shown to overrepresent true arterial fractional hemoglobin saturation with oxygen in both animals7 and humans.8 COHb and O2 Hb have similar absorption characteristics at 660 nm, but not at 940 nm (Figure 33.1). As a result, pulse oximeters measure COHb similarly to O2 Hb. Although some have suggested that the two species are measured identically, this is not true and the difference becomes apparent at high COHb levels.8 A new pulse CO-oximeter, developed by Masimo Corporation9 (see Addendum), utilizes eight wavelengths of light and is able for the first time to provide a noninvasive measurement of COHb (“SpCO”) in seconds, in addition to conventional oximeter variables SpO2 and pulse rate. The accuracy of the device has been demonstrated by the manufacturers up to 40% SpCO, with a range of ± 3% around the measurement (Figure 33.2).9 Because the instrument is relatively new, only a few independent studies of it are available. In a series of 31 patients reporting to a pulmonary function laboratory for testing, arterial blood analysis by laboratory CO-oximetry confirmed the stated

Extinction coefficient

10

Methemoglobin

1

Oxyhemoglobin Reduced hemoglobin

.1

Carboxyhemoglobin .01 600

640

680

720

760

800

840

880

920

960

1000

Wavelength (nm)

FIGURE 33.1 Absorption spectra of four hemoglobin species.

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Noninvasive Measurement of Blood Carboxyhemoglobin with Pulse CO-Oximetry 741 Test results for Masimo Rad-57 versus blood sample 40.0

Masimo Rad-57 SpCO (%)

35.0 30.0 25.0 20.0 15.0 10.0 5.0 0.0 0.0

5.0

10.0 15.0 20.0 25.0 30.0 35.0 40.0

Reference HbCO from blood sample (%)

FIGURE 33.2 Pulse CO-oximetry SpCO measurements versus simultaneous laboratory COoximetry COHb levels in normal volunteers (From Masimo Corporation website. Rad-57 Pulse CO-oximeter. Available at: http://www.masimo.com/rad-57/index.htm. Accessed: September 26, 2005.)

accuracy of the device.10 However, the range for COHb in that population was only 0.8–9.3%. In a clinical laboratory study, ten volunteers breathed 500 ppm CO until COHb was raised to 15%.11 SpCO correlated with CO-oximeter COHb with a precision of 2.19%. The pulse CO-oximeter has also been used to measure baseline COHb levels in patients presenting to another pulmonary function laboratory for assessment of pulmonary diffusing capacity (DLCO).12 The SpCO value obtained was then utilized to “correct” the measured DLCO when severity of impairment was graded by the interpreting physician. In another study, the pulse CO-oximeter was utilized in an ambulatory research setting to measure the blood COHb levels of smokers and nonsmokers exposed to second-hand cigarette smoke.13 In a case report, the device was used to continuously monitor COHb during treatment of a victim of CO poisoning resulting from smoke inhalation.14 At an actual initial COHb of 35%, the SpCO was 39%. After 150 min of normobaric 100% oxygen, the COHb was 5% with an SpCO of 6%. This same group has since reported on using the device to screen patients presenting to their emergency department (ED).15 Over 1700 patients had SpCO measured at triage. Not surprisingly, they found that self-reported smokers exhibited higher SpCO readings than nonsmokers (5.3% ± 3.8% versus 2.9% ± 2.7; p < .00001). More importantly, they identified three cases of unsuspected CO poisoning that were confirmed through laboratory analysis. In all clinical studies to date, the device has been found to be convenient and easy to use. It is felt that the 40,000 cases of CO poisoning diagnosed each year in US EDs underestimate the actual incidence and that many more cases are either not seen in an ED or are not diagnosed when seen.16 Because clinicians have traditionally only

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ordered blood measurement of COHb when the condition was suspected, it is likely that there has been a tendency to measure COHb in the more symptomatic patient or in those whose exposure history was known. EDs, emergency medical support (EMS) providers and other first-responders will begin using the new pulse CO-oximeter soon. Since EMS providers and paramedics commonly use a pulse-oximeter to measure SpO2 at the scene, one can predict that many instances of elevated SpCO will be discovered among patients without a classic history or recognized exposure to CO. A suggested triage and management plan for patients with elevated SpCO levels has recently been published to address this issue (Figure 33.3).17 Furthermore, many hospitals have not had the ability to measure COHb until now. One recent study of a four-state region found that less than one-half of the acute care hospitals had laboratory CO-oximetry available.18 This is due to the expense of the instrument, as suggested by the fact that hospitals without CO-oximeters tend to be located in smaller communities. Since pulse CO-oximeters are significantly less expensive, their availability will undoubtedly contribute to increased diagnosis of CO poisoning. Even though most hospitals without CO-oximetry report that they currently send blood samples to other laboratories for COHb measurement, the attendant delay appears to affect timeliness of diagnosis and management. In the same study, over 90% of CO-poisoned patients referred to a regional hyperbaric oxygen treatment facility came from hospitals able to measure COHb. Since hyperbaric treatment is Measure SpCO

0–3%

>3%

No further medical evaluation of SpCO needed

Loss of consciousness or neurological impairment or SpCO > 25%?

Yes

Transport on 100% oxygen for ED evaluation. Consider transport to hospital with hyperbaric chamber

No

SpCO > 12%

SpCO < 12%

Transport on 100% oxygen for ED evaluation

Symptoms of CO exposure? * Yes

No

Transport on 100% oxygen for ED evaluation

No further medical evaluation of SpCO needed. Determine source of CO if nonsmoker

FIGURE 33.3 Algorithm for individuals possibly exposed to carbon monoxide, on the basis of pulse CO-oximetry SpCO measurement (From: Hampson, N.B., Weaver, L.K. Noninvasive CO measurement by first). Responders: A suggested management algorithm. J. Emerg. Med. Serv. 2006, 24(suppl.): 10–12. * Common symptoms of CO exposure include nausea, vomiting, headache, dizziness, weakness, and loss of consciousness.

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felt to be more effective when administered early,19 rapid identification of poisoned individuals is of great importance.

33.3 CONCLUSION The new pulse CO-oximeter represents a major advance in field and ED screening of individuals for CO exposure and poisoning. Because many of these will initially be discovered to have an elevated SpCO level by first-responders, it is important that triage and management protocols be available. As use of the device increases in all venues, the number of individuals diagnosed with CO poisoning each year is likely to increase dramatically.

References 1. Piantadosi CA. Carbon monoxide intoxication. In: Vincent JL, ed. Update in Intensive Care and Emergency Medicine. New York, NY: Springer-Verlag NY Inc; 1990; 460–471. 2. Zhang J, Piantadosi CA. Mitochondrial oxidative stress after carbon monoxide hypoxia in the rat brain. J. Clin. Invest. 1991; 90: 1193–1199. 3. Thom SR. Carbon monoxide-mediated brain lipid peroxidation in the rat. J. Appl. Physiol. 1990; 68: 997–1003. 4. Thom SR. Leukocytes in carbon monoxide-mediated brain oxidative injury. Toxicol. Appl. Pharmacol. 1993; 123: 234–247. 5. Thom SR, Bhopale VM, Fisher D, Zhang J, Gimotty P. Delayed neuropathology after carbon monoxide poisoning is immune-mediated. Proc. Natl. Acad. Sci. USA. 2004; 101: 13660–13665. 6. Cunnington AJ, Hormbrey P. Breath analysis to detect recent exposure to carbon monoxide. Postgrad. Med. J. 2002; 78: 233–237. 7. Barker SJ, Tremper KK. The effect of carbon monoxide inhalation on pulse oximetry and transcutaneous PO2 . Anesthesiology 1987; 66: 677–679. 8. Hampson NB. Pulse oximetry in severe carbon monoxide poisoning. Chest 1998; 114: 1036–1041. 9. Masimo Corporation website. Rad-57 Pulse CO-oximeter. Available at: http://www.masimo.com/rad-57/index.htm. Accessed September 26, 2005. 10. Mottram CD, Hanson LJ, Scanlon PD. Comparison of the Masimo Rad57 pulse oximeter with SpCO technology against laboratory CO-oximeter using arterial Blood. Resp. Care 2005; 50: 1471. 11. Barker SJ, Curry J, Morgan S. Measurement of COHb and MetHb by pulse oximetry: A human volunteer study. Anesthesiology 2006; in press. 12. Mahoney AM, Stimpson CL, Scott KL, Hampson NB. Noninvasive measurement of carboxyhemoglobin levels for adjustment of diffusion capacity measured during pulmonary function testing. Am. J. Respir. Crit. Care Med. 2006; 3: A720. 13. Hampson NB, Ecker ED, Scott KL. Use of a noninvasive pulse CO-oximeter to measure blood carboxyhemoglobin levels in bingo players. Resp. Care 2006; 51: 758–760. 14. Plante T, Harris D, Monti J, Tubbs R, Jay GD. Carbon monoxide poisoning detected and monitored continuously and noninvasively: A case report. Resp. Care 2005; 50: 1480.

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Carbon Monoxide Poisoning 15. Chee KJ, Suner S, Partridge RA, Sucov A, Jay GD. Noninvasive carboxyhemoglobin monitoring: Screening emergency department patients for carbon monoxide exposure. Acad. Emerg. Med. 2006; 13 (Suppl. 1): 179. 16. Hampson NB. Emergency department visits for carbon monoxide poisoning. J. Emerg. Med. 1998; 16: 695–698. 17. Hampson NB, Weaver LK. Noninvasive CO measurement by first responders: A suggested management algorithm. J. Emerg. Med. Serv. 2006; 24 (Suppl.): 10–12. 18. Hampson NB, Scott KL, Zmaeff JL. Carboxyhemoglobin measurement by hospitals: Implications for the diagnosis of carbon monoxide poisoning. J. Emerg. Med. 2006; 31: 13–16. 19. Hampson NB, Mathieu D, Piantadosi CA, Thom SR, Weaver L. Carbon monoxide poisoning: Interpretation of randomized clinical trials and unresolved treatment issues. Undersea Hyperb. Med. 2001; 28: 157–164.

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34

Chronic Carbon Monoxide Exposure: How Much Do We Know About it?—an Update Alastair W.M. Hay

CONTENTS References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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Editor’s Note: This chapter was invited as an update on the study of chronic carbon monoxide (CO) poisoning published by the CO Support group in the late 1990s (Hay et al., 2000).1 Exposure to CO and the health consequences for those exposed acutely and severely are well documented.2−5 However, the effects of chronic exposure to CO gas are far less well known and less frequently the subject of research. This short treatment reviews new developments on the subject and thoughts about our study a decade out. It was nearly 70 years ago that the first report on the effects of repeated exposure to sublethal concentrations of CO was reported.6 In his study of 97 individuals, Beck recorded the fact that his subjects had been exposed to CO over periods ranging from several months up to 18 years. Seven principal symptoms were reported by the subjects he examined, all over 40 years of age. These included headaches, vertigo, nervousness, palpitations, and neuro-muscular pain (see Reference 7). It is not unusual to see these same symptoms in individuals who have been acutely poisoned by CO. Regrettably when poisoning with CO is discussed, it is invariably assumed that the exposure has only been acute. Perceptions about exposures to CO are changing, but slowly. In the past the view prevalent amongst clinicians was that unless exposure to CO rendered an individual unconscious, the consequences for that person’s health were minimal. All that might be required was fresh air, or if poisoning was severe a whiff of pure oxygen. But the 745

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evidence indicates that exposure to concentrations of CO, insufficient to render a person unconscious, will damage the brain and result in neurological sequelae.8,9 Chronic exposure to CO has now also been reported to result in damage to the brain,10,11 some of which appears after a delay. In his fine review of the literature, Weaver states that “lower-level CO exposures can cause headache, malaise, and fatigue and can result in cognitive difficulties and personality changes.”12 If acute CO exposure will cause neurological sequelae in individuals, then the consequences of repeated exposure to CO may be of even more consequence. In the vast majority of published studies, carboxyhemoglobin (COHb) saturations are not known. For individuals chronically exposed to CO, there is even less likelihood of some measurement of COHb being made. Their absence has frequently frustrated victims who have attempted to discover the cause of their continuing ill health. More problematic still, for those chronically exposed to CO, is the lack of awareness in the medical profession that such exposures can have serious consequences for health. To address some of the gaps in what was known about the effects of chronic CO exposure, we conducted a questionnaire study on 77 individuals, who were known to have been exposed to CO, over periods ranging from several days to more than 20 years.1,13 The results were reported separately for two groups who were chronically exposed, a cohort of 65 people who never suffered loss of consciousness (LOC), and a group of 12 people who did. For those who had LOC there was a period leading up to the episode in which they collapsed when they had been exposed to lower, and invariably, increasing concentrations of CO. Sixty years after Beck6 reported the consequences of chronic exposure to CO, the situation has not changed much in the United Kingdom. Although there is increasing recognition of the risks from CO with some 30 deaths occurring annually in the United Kingdom, there is less concern about the effects of chronic exposure. The results of our survey indicated that there was a continuing and unrecognized problem associated with chronic exposure to CO. Most physicians did not recognize the symptoms of CO poisoning, and in consequence, did not diagnose it. Many individuals suffered for years as a result of their exposure to the gas, and our survey indicated that many people continued to suffer symptoms years after the exposure had stopped. Many respondents to our questionnaire indicated that they had experienced a wide range of symptoms for up to 2 years after exposure ended.1,13 One weakness of our study was in relation to the evidence about the duration of symptoms during exposure to CO. Most respondents complained of a range of symptoms, and some stated that they had had these symptoms for many years. Without any objective evidence of actual exposure to CO, it was difficult to be certain that individuals who complained that they had experienced these symptoms for, say, 20 years prior to CO exposure being discovered, were, in fact, suffering the effects solely of CO exposure. But this is true for many individuals who are exposed to CO. Given that the symptoms of exposure are nonspecific and similar to those of an infection, although long-lived, clinicians invariably look for a viral or bacterial cause. Unique to our survey, we were able to ascertain that the majority of respondents had been exposed to CO because the problem had been identified (i.e., discovered) by gas engineers/technicians inspecting gas fires (i.e., heaters), central heating boilers,

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and the flues and chimneys which vent the exhaust gases into the atmosphere. Physicians were the least likely group to identify the problem. In the majority of the cases reported in our study,1,13 it was a gas engineer who condemned a fireplace or a flue as dangerous, and as the source of CO exposure. We thus had confirmation for the vast majority of our respondents, that they were indeed exposed to CO. However, we were unable to say how much of the gas they inhaled, or what their likely COHb saturations might have been. For many, COHb concentrations were likely to have been over 20%, given the reports of headaches, however, we could not be certain of the range, nor their duration. For the subjects who suffered LOC as a result of their exposure, the evidence suggests that their COHb concentrations would have been 40% or greater.2,14 In his report on the investigation of clinical symptoms in 97 people repeatedly subjected to sublethal concentrations of CO over periods ranging from several months up to 18 years, Beck6 noted the symptoms cited above. In addition, his subjects also complained of nervous and mental symptoms, including feelings of depression, restlessness, anxiety, and fears. Also reported were experiences of introspection, emotional upheaval, mental retardation with memory defects, and confusion. For a further discussion of these symptoms, see Penney, 2000.7 Feelings of weakness and an inability to walk properly were mentioned by some. Drowsiness and insomnia were recorded frequently, and approximately one-third of patients complained of paresthesia (“bugs walking on the skin”), chiefly in the extremity. In the 97 individuals concerned, 7 complained of speech defects, but the exact nature of the defects is not specified. Disturbances of the vasomotor system were also reported, and these resulted in morbid flushing, local sweating, cold extremities (thermoregulatory dysfunction); and a purplish congestion of the hands and feet. The principal neuromuscular complaint was a pain which was either felt as a dull pain, or as acutely spasmodic in nature. A dull aching pain often occurred in the back, shoulders, epigastrium, lower abdomen, and chest. Of 97 patients, 10 complained of dysuria. Beck would have no difficulty recognizing the spectrum of symptoms in the cohort of our study.1,13 Complaints by the respondents to our questionnaire, indicate a spectrum of symptoms all too similar to those reported by Beck’s own patients. It was clear to us that the problem had not disappeared. Myers et al.10 document seven cases where the evidence indicates chronic exposure to CO occurred. For a further discussion of these symptoms, see Penney, 2000.7 Symptoms similar to those reported by Beck6 are described as well as the results of neuropsychological testing of all the subjects. These tests demonstrate damage to the brain sufficient to cause serious distress to the subjects. Their assessment led the authors to suggest that chronic CO exposure should be suspected if a virus-like illness persists with a significant neuropsychiatric overlay and a history of some form of “gas” exposure. Sick cohabitants, visitors, or pets (and pets dead) are also significant in the view of the authors.10 The authors note that the CO Neuropsychometric Screening Battery (CONSB) which was developed for assessing the effects of acute exposure, is of little value for the assessment of those with chronic poisoning. A far better approach is a detailed neuropsychological evaluation that includes visual, spatial, motor, intellectual, and perceptual testing. They note that with hyperbaric oxygen treatment (HBOT) functional ability is improved, but by a mechanism which is not

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understood. Psychiatric difficulties also tend to persist in chronically exposed patients, but are treatable with psychotherapy and medications for anxiety and depression.10 Similar cases are reported in two other publications,11,15 one of which reports the outcomes of magnetic resonance imaging in the assessment of brain damage in four patients chronically-exposed to CO.15 The author reports that magnetic resonance imaging (MRI) scans are often within normal limits despite clinical and neuropsychological evidence of intellectual impairment. Another report16 documents the case of a crane driver at a smelter, who developed permanent symptoms after 20 years of exposure to CO. Also reported are the effects of exposure from a faulty oilfired central heating system, and the long lasting symptoms in four members of one family. The authors also note that symptoms of chronic CO poisoning which include headache, dizziness, and tiredness, usually disappear after some weeks or months in people who have been exposed, but that in some individuals they become permanent. Infants are also at risk from chronic CO exposure. The case of a three-and-a-half year old girl who was exposed repeatedly to CO has been described.17 The child was admitted to a hospital when a month old, discharged after she improved, readmitted at 2 months when her mother noted she had breathing difficulties which were so severe that the father had to administer mouth-to-mouth breaths. After treatment, the child was again discharged with the mother receiving advice on treatment for apnea. At 3 months of age she was readmitted again with respiratory distress. Areview of her blood results revealed slightly elevated COHb, prompting an investigation of the home environment where it was found that the mother had been using a kerosene heater in the house. On questioning it was apparent that other members of the household and visitors too had experienced headaches which resolved when they left the house. Two interesting biochemical findings were revealed when the child was hospitalized: serum potassium and lactic acid levels were elevated, both of which resolved spontaneously. The failure to recognize CO as the cause of symptoms in the cohort which we studied,1,13 meant that few of our subjects received treatment that was of much benefit. Only one-third of the patients who experienced LOC as a result of their CO exposure received HBOT in our cohort. Two of the subjects who were never unconscious, but were chronically exposed to CO, also received HBOT over a period of time after their exposure to CO was recognized. Medical treatment of the symptoms in patients chronically exposed to CO and those who were unconscious, following what would appear to have been a prolonged exposure period prior to their collapse, was far from satisfactory. Our interviewees complained of continuing pain. There is an urgent need to identify treatment protocols, in addition to the psychological, for subjects suffering from the effects of CO poisoning. As well as the need for more effective treatment, there is a more pressing requirement which is the need to help health care professionals recognize patients who are exposed to CO. It is important to explain to the medical community that although many individuals who are acutely exposed to CO may recover relatively quickly from their ordeal, there are some who will experience continuing illhealth for a long period of time. For those who are chronically exposed, recovery will be slow and prolonged. Crucially, there is now evidence that HBOT may improve the functionality of those chronically exposed to CO.10

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Our data indicate that many of those chronically exposed to CO were likely to have had COHb saturations in excess of 20%. Some individuals are likely to be at considerable risk if they are repeatedly exposed to CO at those and even to lesser COHb levels. Those who are physiologically stressed either by exercise or through medical conditions are likely to be susceptible to lower levels of CO. In individuals where there is any impairment of oxygen transport to the brain, there is likely to be increased susceptibility to increased CO. This group includes those with atherosclerotic lesions, noninsulin diabetes, and cerebral microvascular pathology.18 Women experiencing complications in pregnancy such as pre-eclampsia where there is cerebral vasoconstriction that fails to respond to the normal stimuli that cause vasodilation, could be at risk. And the elderly where there may already be a degree of vascular compromise (as in Alzheimer’s) could be more sensitive to elevated CO. The effect of CO exposure in individuals also taking various medications (particularly of a psychoactive nature) or who are abusing drugs, is unknown. The effects in some of these individuals, however could be anticipated because of CO’s effects on the brain.18 Of no lesser importance is the risk to the developing fetus. With evidence suggesting that exposures to CO of 150–200 ppm, leading to COHb saturations of 15–25%, cause birth weight reductions, delayed behavioral development, and disrupted cognitive function in laboratory animal species19 the risk for the human fetus is all too clear. Evidence from studies on smoking implicate CO at lower concentrations as one agent responsible for lower birth weight babies, however cigarette smoke contains numerous other agents which may also contribute to the effect and which make the role of CO more difficult to disentangle in these circumstances.18 The fascinating studies of low birth weight in over 100,000 live births in Los Angeles correlated with ambient CO concentrations at or below the US Environmental Protection Agency (US EPA) threshold limit standard of 9 ppm, suggest that the developing fetus may be exquisitely sensitive to chronic CO exposure.20 The manner in which the source of CO was identified in our cohort bears further examination. Apart from the small role which the medical profession played in the diagnosis of the problem, it was evident that regular servicing of appliances will not always guarantee that individuals escape poisoning by CO. For over 40% of the respondents in both our chronically exposed group, and in the group of LOC subjects, regular servicing of an appliance did not identify that there was a problem with it. The problem occurred after the equipment was serviced. How long after the servicing the problem appeared was not known. It was also apparent from the returns to the questionnaire, that many appliances were not serviced routinely. The best advice that can be given to individuals to prevent exposure to CO, is to ensure that all fuel-using appliances are serviced regularly, and that they ensure that the flues or chimneys which vent exhaust gases to the atmosphere, are cleaned regularly—at least once a year. Use of CO detectors and alarms provides a third tier of protection. Ultimately, however, equipment should be designed so that it will cease operation when there is any risk of significant concentrations of CO building up in the living space. It is not sufficient to have equipment turn off simply if there is a failure of adequate oxygen to ensure complete combustion. Devices that monitor excessive CO production could be wired to shut-down heating appliances.

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For more on equipment self-monitoring of CO, see the chapter by Drs. Galatsis and Wlodarski (Chapt. 10). Adoption of this kind of technology would prevent excessive production of CO in heating devices and thus reduce the dangers of CO exposure to users. It is only through continuing discussion with victims of CO poisoning, the medical community, and the fuel industry which provides the much needed heating for our homes, that the problem of exposure to CO whether acute, or chronic, will be solved. Much remains to be done to understand the effect of CO on the brain and other organs, what it may do in vulnerable individuals and what treatments might ameliorate its effects.

References 1. Hay, A.W.M., Jaffer, S., Davis, D. Chronic carbon monoxide exposure: The CO Support study. In Carbon Monoxide Toxicity, D.G. Penney, ed., CRC Press, NY, 2000, Chapt. 19, pp. 419–437. 2. World Health Organisation. Carbon Monoxide. Environmental Health Criteria, No. 13. Geneva, 1979. 3. Lowe-Ponsford, F.L., Henry, J.A. Clinical aspects of carbon monoxide poisoning. Adverse drug reaction. Acute Poisoning Review, Oxford University Press, Oxford, U.K. 1989, 8, 217–240. 4. Smith, J.S., Brandon, S. Morbidity from acute carbon monoxide poisoning at three year follow up. Brit. Med. J., 1, 318, 1973. 5. Garland, H., Pierce, J. Neurological complications of carbon monoxide poisoning. Quart. J. Med., New series 36, 144, 445, 1967. 6. Beck, H.G. Carbon monoxide asphyxiation: a neglected clinical problem. JAMA, 107, 1025, 1936. 7. Penney, D.G. Chronic carbon monoxide poisoning. In Carbon Monoxide Toxicity, D.G. Penney, ed., CRC Press, NY, 2000, Chapt. 18, pp. 393–418. 8. Chambers, C., Hopkins, R.O. Weaver, L.K. Cognitive and affective outcomes compared dichotomously in patients with acute carbon monoxide poisoning. Undersea Hyperbaric Med., 48, 2006. 9. Hopkins, R.O. Neurocognitive and affective sequelae of carbon monoxide poisoning In Carbon Monoxide Poisoning, D.G. Penney, ed., CRC-St. Francis Press, 2007, Chapt. 22. 10. Myers, R.A., Defazio, A., Kelly, M.P. Chronic carbon monoxide exposure: a clinical syndrome detected by neuropsychological tests. J. Clin. Psych., 54, 555, 1998. 11. Knobeloch, L., Jackson, R. Recognition of chronic carbon monoxide poisoning. Wisconsin Med. J., 98,26, 1999. 12. Weaver, L.K. Environmental emergencies. Carbon monoxide poisoning. Crit. Care Clin., 15, 297–320, 1999. 13. Hay, A.W.M., Jaffer, S., Davis, D. Carbon Monoxide Support. Effects of chronic exposure to CO:Aresearch study conducted by CO Support. Technical Paper. October, 1997. 47 pp, appendices. 14. Winter, E.M., Miller, J.N. Carbon Monoxide Poisoning. JAMA, 236, 1502, 1976. 15. Prockop, L.D., Carbon monoxide brain toxicity: clinical, magnetic resonance imaging, magnetic resonance spectroscopy, and neuropsychological effects in 9 people. J. Neuroimag. 15, 144, 2005.

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16. Tvedt, B., Kjuus, H., Kronisk CO-Forgiftning. Eruken av. Generator gass under den annen verdenskrig og nyere forskning. [Chronic CO poisoning. Use of generator gas during the Second World War and recent research]. Tidsskrift for Den NorskeLageforening, 117, 2454, 1997. 17. Foster, M., Goodwin, S.R., Williams, C., Loefflerj. Recurrent acute life-threatening events and lactic acidosis caused by chronic carbon monoxide poisoning in an infant. Pediatrics, 104, 34, 1999. 18. Raub, J.A., Benignus, V. Carbon monoxide and the nervous system. Neurosci. Biobehav. Rev. 26, 925, 2002. 19. Penney, D.G. Effects of carbon monoxide exposure on developing animals and humans. In Carbon Monoxide, D.G. Penney, ed., CRC Press, NY, 1996, Chapt. 6, pp. 109–144. 20. Ritz, B., Yu, F. The effect of ambient carbon monoxide on low birth weight among children born in Southern California between 1989 and 1993. Environ. Health Perspectives, 107, 17–25, 1999.

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35

Essential Reference Tables, Graphs, and Other Data David G. Penney

CONTENTS 35.1 Physical Characteristics of Carbon Monoxide . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35.2 History of Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35.3 Carbon Monoxide Concentration Inhaled and Blood CO Saturation . . . . 35.4 Carbon Monoxide Wash-Out Rate, Peter Tikuisis, Ph.D. . . . . . . . . . . . . . . . . . 35.5 Scientific Methodology in Clinical Toxicology . . . . . . . . . . . . . . . . . . . . . . . . . . . 35.6 Hyperbaric Oxygen Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

753 754 755 759 763 764 764

35.1 PHYSICAL CHARACTERISTICS OF CARBON MONOXIDE TABLE 35.1 Physical Characteristics of Carbon Monoxide Molecular weight Critical point Melting point Boiling point Specific gravity relative to air Density At 0◦ C, 760 mm Hg At 20◦ C At 25◦ C, 760 mm Hg At 37◦ C Explosive limits in air Solubilitya At 0◦ C At 25◦ C Conversion factors At 0◦ C, 760 mm Hg At 25◦ C, 760 mm Hg

28.01 −145◦ C at 43.5 atm −207◦ C −192◦ C 0.968 1.25 g/L 3.54 mL per 100 mL 2.32 mL per 100 mL 1.25 g/L 2.14 mL per 100 mL 12.5–74.2% (by volume) 3.54 mL/100 mL water 2.14 mL/100 mL water 1 mg/m3 = 0.800 ppm 1 ppm = 1.250 mg/m3 1 mg/m3 = 0.874 ppm 1 ppm = 1.145 mg/m3

a Volume of CO indicated is at 0◦ C, 760 mm Hg. Source: Adapted from Criteria for a Recommended Standard … Occupational Exposure to Carbon Monoxide, 1972. U.S. Department of Health, Education and Welfare; Maynard and Waller, In Air Pollution and Health, Academic Press 1999; www.coheadquarters.com/CO1.htm.

753

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35.2 HISTORY OF CARBON MONOXIDE POISONING

TABLE 35.2 Benchmarks in the History of Carbon Monoxide Poisoning (Jain, 1990)4 Aristotle, third century BC Cicero (106–43 BC) Rome Paracelsus (1493–1541) Van Helmont (1577–1644) Rammazzini (1633–1714) Clayton (1688) Priestly (1772) Harmant (1775), France Murdock (1792), England (1794), Prussia Cruickshank (1800) LeBlanc (1842) Chenot (1854) Claude Bernard (1857), France Hoppe (1857), Germany Linus and Limousin (1868) Haldane (1895) Saint-Martin and Nicloux (1898) Mosso (1901) Warburg (1926) End and Long (1942) Migeote (1949) Smith and Sharp (1960) 1980s/1990s

“Coal fumes lead to heavy head and death” Coal fumes were used for suicide and execution Wrote the first treatise on diseases of miners Experimented on himself with “woodgas” from a pot of charcoal and nearly died Wrote De Morbis Arteficum (Diseases of miners). Pointed out the danger of gases from burning coal Distilled coal gas from coal Described a combustible gas that burned with a blue flame (carbon monoxide) First clinical description of coal gas poisoning Proposed the use of coal gas for illumination First regulations for protection against coal gas poisoning Showed that carbon monoxide is an oxide which can be converted to CO2 by exploding it with oxygen Identified CO as the toxic substance in coal gas First explanation of the mode of action of CO Showed that CO produces hypoxia by reversible combination with hemoglobin Showed that CO changes the color of blood to bright red First to try oxygen therapy for CO poisoning Showed that rats survived CO poisoning when placed in oxygen at 2 atm pressure First demonstration of endogenous CO Suggested the use of hyperbaric oxygen for CO poisoning CO shown to depress respiratory chain enzymes Treated CO poisoning in experimental animals using HBO Detection of CO in the atmosphere First clinical use of HBO in CO poisoning Introduction of CO detector/alarms in living/work spaces, catalytic converters required on motor vehicles

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35.3 CARBON MONOXIDE CONCENTRATION INHALED AND BLOOD CO SATURATION

TABLE 35.3 Carboxyhemoglobin Equilibrium at a Barometric Pressure of 1 atm. CO Inhaled (ppm)

COHb Saturation (%)

1 3 5 7 9

0.49 0.81 1.14 1.46 1.78

10 30 50 70 90

1.94 5.03 7.92 10.65 13.22

100 300 500 700 900

14.45

1,000 3,000 5,000 7,000 9,000

62.41 83.26 89.23 92.06 93.72

10,000∗ 30,000 50,000 70,000 90,000

94.31 98.03 98.81 99.15 99.33

100,000 300,000 500,000 700,000 900,000

45.40 53.77 59.91

99.40 99.80 99.88 99.91 99.93

* 10,000 ppm = 1%.

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10,000 5,00 ppm 3,0 0 ppm 00 p 2, 00 pm 0 pp m

Blood COHb (%)

756

t=

pm

t=

% 2.0 ∝6

p 0 m 50 1, 0 pp ppm m 20 ,000 0 pp ppm , 1 1 80 600 ppm 500 ppm 400 m 300 pp m 200 pp

20

10

t=∝

b COH 49.4% Hb .8% CO t = ∝ 44 Hb .4% CO t = ∝ 39 Hb .4% CO t = ∝ 32 t = ∝ 22.6% COHb

Equilibrium value CO in inspired air

100 ppm

1

Hb CO 6.5% 5 ∝

2

at t = 14.0%COHb

3

4

5

Exposure time (h)

FIGURE 35.1 Uptake of carbon monoxide by humans under resting conditions. COHb saturation after “infinite” exposure time (steady state conditions) is shown on each line. (Redrawn plot of Forbes, W.H., Sargent, F., Roughton, F.J.W., Am. J. Physiol, 143, 594–608, 1945.)

%

%

12 0.

% 20

15

0.

0.

0.30%

0.50%

1.0%

t=

% 2.0 ∝6

Hb CO t

5% 56. =∝

Hb CO

9.4% t = ∝4

COHb

4.8% t = ∝4 t = ∝3

%

OHb

C 9.4%

10

0.

t = ∝3

8%

0

0.

6% 0.0 % 5 0.0 0.04% 0.03%

t=∝ 32.8%

COHb

t=∝ 22.6%

OHb

C 2.8%

t=∝ 14.0%

t = ∝24.6% COHb

e at t = ∝24.6%

Equilibrium valu

0.02%

COHb

ired air 0.01% CO in insp

Minutes of exposure according to scales given below 250 200

200

REST PULSE 70 L.T. ACT. PULSE 80

200 150

100 30

40

50

60

70

80

90

LT WORK PULSE 110

in

m 10

20

HD WORK PULSE 135

FIGURE 35.2 Uptake of carbon monoxide by humans at various levels of activity-rates of ventilation (From Forbes, W.H., Sargent, F., Roughton, F.J.W., Am. J. Physiol, 143, 594–608, 1945.)

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20 18 16

% CO Hb (increase)

14

t = ∝14.0% CO

100

Hb

12 10 8

t = ∝7.6% CO Hb

50

6

40

4

30 25

2

20 15 10

Pulse 70 0 0 6 l/min Pulse 80 0 10 l/min Pulse 110 20 l/min 0 Pulse 135 30 l/min

t = ∝6.1% CO Hb t = ∝4.7% CO Hb t = ∝3.9% CO Hb t = ∝3.2% CO Hb t = ∝2.4% CO Hb t = ∝1.6% CO Hb

1 2 3 4 5 6 7 8 9 10 11 1213 14 15 16 17 181920 21 2223 24 1

2 1

3

4

5

2 1

3 2

6

7 4 3

8

9 5

10 11 12 13 6

4

7 5

Rest Light activity

14 15 8 6

9 7

Walking Hard work

Time (h)

FIGURE 35.3 Uptake of carbon monoxide at air concentrations up to 100 ppm and various levels of activity—from Maynard, R.L., Waller, R., In Air Pollution and Health, Academic Press 1999 (Redrawn from data of Forbes, Sargent, and Roughton, 1945)

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758 1000 800 600 500 de

Se

400

ar

nt

300

LW H W

CO concentration in air (ppm)

y

200

100 80 60 50 40 30 20

10 10

20

30

40

60

80

100

200

300 400 500

Duration of exposure (min)

FIGURE 35.4 Length of time to achieve 5% carboxyhemoglobin (COHb) by humans engaged in light and heavy work (From Criteria for a Recommended Standard … Occupational Exposure to Carbon Monoxide, 1972. U.S. Department of Health, Education and Welfare.) “Light work” is VA = 18 L/min; DL = 40 ml/min/mm Hg. “Heavy work” is VA = 30 L/min; DL = 60 ml/min/mm Hg.

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35.4 CARBON MONOXIDE WASH-OUT RATE, PETER TIKUISIS, PH.D. Assumptions: • • • •

Predictions based on CFK model M = 218 (Haldane ratio) Vco = 0.007 mL STPD·min−1 Wt = 70 kg, blood volume = 5500 mL, total hemoglobin concentration = 0.154 g·mL−1 blood • DLCO = 20, 25, 30 mL STPD·min−1 ·Torr−1 for Rest, 2 × Rest, and 3 × Rest, respectively • VA = 6, 12, 18 mL STPD·min−1 for Rest, 2 × Rest, and 3 × Rest, respectively • COHb start = 25%

TABLE 35.4 Depletion Factor; Hyperbaric Condition = 1580 mmHg (2 × Normobaric) O2 level → Activity →

21% Normobaric Rest

2 × Rest

100% Normobaric

3 × Rest

Time (min) 0 10 20 30 40 50 60 90 120 150 180 210 240 270 300 330 360 390 420 450 480 510 540 570 600

Rest

2 × Rest

100% Hyperbaric Rest

Depletion Factor (%) 0 2 4 6 8 10 11 17 21 26 30 34 38 42 45 48 51 54 57 59 62 64 66 68 70

0 3 7 10 13 16 19 27 34 41 47 52 57 61 65 68 71 74 77 79 81 83 85 86 87

0 5 9 14 18 21 25 35 44 52 58 64 69 73 76 80 82 85 87 88 90 91 92 93 94

0 12 23 33 41 49 55 70 80 86 91 94 96 97 98 99 99 99 99 100 100 100 100 100 100

0 18 33 45 55 63 70 83 91 95 97 98 99 99 100 100 100 100 100 100 100 100 100 100 100

0 22 39 53 63 71 78 89 95 98 99 99 100 100 100 100 100 100 100 100 100 100 100 100 100

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TABLE 35.5 Remaining Factor (= 100–Depletion Factor); Hyperbaric Condition = 1580 mmHg (2 × Normobaric) O2 level → Activity →

21% Normobaric Rest

2 × Rest

Time (min) 0 10 20 30 40 50 60 90 120 150 180 210 240 270 300 330 360 390 420 450 480 510 540 570 600

100% Normobaric

3 × Rest

Rest

2 × Rest

100% Hyperbaric Rest

Remaining Factor (%) 100 98 96 94 92 90 89 83 79 74 70 66 62 58 55 52 49 46 43 41 38 36 34 32 30

100 97 93 90 87 84 81 73 66 59 53 48 43 39 35 32 29 26 23 21 19 17 15 14 13

100 95 91 86 82 79 75 65 56 48 42 36 31 27 24 20 18 15 13 12 10 9 8 7 6

100 88 77 67 59 51 45 30 20 14 9 6 4 3 2 1 1 1 1 0 0 0 0 0 0

100 82 67 55 45 37 30 17 9 5 3 2 1 1 0 0 0 0 0 0 0 0 0 0 0

100 78 61 47 37 29 22 11 5 2 1 1 0 0 0 0 0 0 0 0 0 0 0 0 0

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TABLE 35.6 Multiplication Factor (= 100/Remaining Factor)—to be Applied Against a Measured Value at Some Time After Start of Washout to Determine Initial Value; Hyperbaric Condition = 1580 mmHg (2 × Normobaric) O2 level → Activity →

21% Normobaric Rest

2 × Rest

Time (min) 0 10 20 30 40 50 60 90 120 150 180 210 240 270 300 330 360 390 420 450 480 510 540 570 600

100% Normobaric

3 × Rest

Rest

2 × Rest

100% Hyperbaric Rest

Remaining Factor (%) 1.00 1.02 1.04 1.06 1.09 1.11 1.12 1.20 1.27 1.35 1.43 1.52 1.61 1.72 1.82 1.92 2.04 2.17 2.33 2.44 2.63 2.78 2.94 3.13 3.33

1.00 1.03 1.08 1.11 1.15 1.19 1.23 1.37 1.52 1.69 1.89 2.08 2.33 2.56 2.86 3.13 3.45 3.85 4.35 4.76 5.26 5.88 6.67 7.14 7.69

1.00 1.05 1.10 1.16 1.22 1.27 1.33 1.54 1.79 2.08 2.38 2.78 3.23 3.70 4.17 5.00 5.56 6.67 7.69 8.33 10.00 11.11 12.50 14.29 16.67

1.00 1.14 1.30 1.49 1.69 1.96 2.22 3.33 5.00 7.14 11.11 16.67 25.00 33.33 50.00

1.00 1.22 1.49 1.82 2.22 2.70 3.33 5.88 11.11 20.00 33.33 50.00

1.00 1.28 1.64 2.13 2.70 3.45 4.55 9.09 20.00 50.00

Narrative: The factors listed in the above table will yield the initial %COHb when multiplied by the %COHb measured at a specific time after the end of an exposure to CO. For example, if the measured COHb = 15% at 3 h after an exposure to CO has ended, then the initial value = 1.43 × 15% = 21.5% for a resting individual breathing air. Note that these values are approximate and are out-of-range or suspect if the resultant initial COHb exceeds 50%. Further Note: The last caveat arises because errors in measurement at low values of COHb can cause wide variations the initial values (e.g., if measured COHb = 5 ± 2% at 2 h on 100% O2 at rest, then the initial value can range from 5 × 3 = 15% to 5 × 7 = 35%. The effect worsens as the multiplication factor increases. Note: For additional information see Tikuisis, P. Modelling the uptake and elimination of carbon monoxide. In: Carbon Monoxide. Penney DG (ed), CRC Press, Boca Raton, FL, 1996, pp 45–67:

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762 Ambient PCO

CO body stores Exogenous

Alveolar PCO

Endogenous COMB 1.5 mL

COHB 8 mLCO Production Hgb Catab Other

0.3 mL/h

0.2%/h

CO–X <0.5mL

Metabolism

CO→CO2

0.1 mL/h Intravascular

Extravascular

FIGURE 35.5 Carbon monoxide body stores—(From James F. Coburn, Ann. NY Acad. Sci 174, 11–22, 1970.)

% Hb O2 100 90 80 70 75

50 25 10 0 %

COHb

60 50 40 30 20 10 10

20

30

40

50

60

70

80

90

P O2 mm Hg.

FIGURE 35.6 Shift of the oxyhemoglobin dissociation curve in the presence of COHb— (From Rogers, M.C., Helfaer, M.A. Handbook of Pediatric Intensive Care., 1999.

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35.5 SCIENTIFIC METHODOLOGY IN CLINICAL TOXICOLOGY Criteria for the Occupational and/or Environmental-Relatedness of Disease: “Sir Bradford-Hill’s criteria for causation were developed for use in the field of occupational medicine, but have been widely applied in other fields.9,10,11 These criteria serve as a general guide, and are not meant to be an inflexible list. Not all criteria must be fulfilled to establish scientific causation. The key criteria required to establish causation are commonly, (1) temporal relationship, (2) specificity, (3) biological plausibility, and (4) coherence. The US Supreme Court in its Daubert decision12 addresses this issue and concludes that the expert has to provide scientific opinion on the basis of methods and techniques generally used, and relying on peer reviewed publications for testability of his opinion that causation is more likely than not owing to the toxicant in question (>50% probability). The expert does not necessarily need to rely on epidemiology or scientific certainty, or provide scientific proof, but rather to follow the guidelines applied by the US Supreme Court Daubert decision. The expert must know the accepted methods to establish causation as described in the scientific and medical literature and established originally by Sir Bradford-Hill.” (from: OEM Meducation Fact Sheet 3)

TABLE 35.7 Scientific Methodology in Clinical Toxicology 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Gather the facts—history, interview, and so forth Do the facts fit the literature?—consistency with past knowledge Exclude improbable/unlikely causes—use differential diagnosis Temporal relationship—EFFECT follows CAUSE, not the other way around Is the effect occurring in only one individual, or has it occurred to several people simultaneously? immediate, nonselective, latent period Consistency and unbiasedness of findings—self-report and other-report Dose-reponses—specific relationship of toxin strength to response of biological system Strength of association—frequency that factor is found in “disease”; correlation coefficient Specificity—only one factor is isolated and stimulates the condition Coherence—do the facts fit the picture? Biological plausibility

Source: Adapted from Sir-Bradford-Hill, Proc. Royal Soc. Med., 9, 295–300, 1966; Bradford-Hill, A., Proc. Royal Soc. Med., 58, 295, 1966; Rom, W.N., In Textbook of Environmental and Occupational Medicine, 1992.

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35.6 HYPERBARIC OXYGEN THERAPY

TABLE 35.8 Disorders Approved for Hyperbaric Oxygen Therapy • • • • • • • • • • • •

Decompression illness Air embolism Clostridial myonecrosis Osteomyelitis Acute traumatic ischemias (compartment syndrome) Skin grafts and flaps (compromised) Radiation tissue damage Smoke inhalation CARBON MONOXIDE POISONING Cyanide poisoning Thermal burns Anemia caused by excessive blood loss

Source: From Rogers, M.C., Helfaer, M.A., Handbook of Pediatric Intensive Care. Lippincott Williams & Wilkins, Philadelphia, PA, 1999.

References 1. Criteria for a Recommended Standard … Occupational Exposure to Carbon Monoxide, 1972. U.S. Department of Health, Education and Welfare. 2. Maynard, R.L., Waller, R. Carbon monoxide. In Air Pollution and Health, Academic Press, NY, Chapt. 33, 1999. 3. Available at: www.coheadquarters.com/CO1.htm. 4. Jain, K.K. Carbon Monoxide Poisoning. Warren H. Green, Inc., St. Louis, MO, p. 377, 1990. 5. Forbes, W.H., Sargent, F., Roughton, F.J.W. The rate of carbon monoxide uptake by normal men. Am. J. Physiol., 143, 594–608, 1945. 6. Tikuisis, P. Modelling the uptake and elimination of carbon monoxide. In: carbon monoxide. D.G. Penney, Ed., CRC Press, Boca Raton, FL, 1996, pgs. 45–67. 7. Coburn, J.F. The carbon monoxide body stores. Ann. NY Acad. Sci., 174, 11–22, 1970. 8. Rogers, M.C., Helfaer, M.A. Handbook of Pediatric Intensive Care. Lippincott Williams & Wilkins, Philadelphia, PA, 1999, p. 156. 9. Bradford-Hill, A. The environment and disease: association or causation? Presidents Address. Proc. Royal Soc. Med., 9, 295–300, 1965. 10. Bradford-Hill, A. Criteria for causation in occupational and/or environmental-related disease. Proc. Royal Soc. Med., 58, 295, 1966. 11. Rom, W.N. Causation. In Textbook of Environmental and Occupational Medicine, 2nd ed., 1992, Little, Brown, Boston, MA. 12. Daubert versus Merrill Dow Pharmaceuticals—509 U.S. 579, 113 Supreme Court 2786, 1993.

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Index Note: Page numbers in italics refer to figures and tables

A Absorption, 141, 204 Academic testing, 523 Activities of Daily Living (ADL), 419, 485, 504, 593, 607, 632, 689, 691 Activity limitation, 691 Activity restrictions, 691 Acute CO poisoning, 346, 348, 350, 351, 355, 360, 391, 458–459, 460, 462, 463, 464, 482, 538, 653, 746; see also Poisoning HBO therapy for, 382, 484–485 basic science overview, 395–398 effects, 394–395 human evidence, 398 Affective disorders, in CO-poisoned patients depression and anxiety, 487–488 Kluver–Bucy syndrome, 488 obsessive-compulsive disorder, 488 Airbag deployment, 30 Air-free CO measurement, 52–53, 103, 104–106 Air movement, 201, 653 Air Pollutants Exposure Model (APEX), 14 Air quality control region (AQCR), 7, 9 Ala Moana Shopping Center motor vehicle exhaust in, 22 Alarm, CO, 120, 215, 217, 251, 271–274, 280, 315, 749 domestic CO alarms, 253–263 UL standards, 646 effectiveness, in marine environment, 183–184 onboard, failure of, 190 Allopurinol, 351–352 Ambient visual system, 621, 622, 626 American Boat and Yacht Council (ABYC), 158, 187 American College of Emergency Medicine, 398 American College of Emergency Physicians, 380 American Community Survey, 694, 701 American Conference of Governmental and Industrial Hygienists (ACGIH), 32

occupational exposure standards, for CO, 291, 645 American Gas Association (AGA), 138 American Industrial Hygiene Association (AIHA), 292 American Insurance Association, 218 American Lung Association, 252 American National Standards Institute (ANSI), 44, 90, 93, 102, 103, 118, 138, 148 ANSI-110, 650 ANSI 119.2, 60, 66 ANSI Z21.1, 54, 102–103, 112, 115, 120, 127 ANSI Z21.47, 148 standards, for warning labels ANSI 535.2, 207 ANSI A13.1, 208 workplace area warnings and labeling, 211–213 American Society for Testing and Materials (ASTM) workplace area warnings and labeling, 211–213 American Society of Heating, Refrigeration, and Air Conditioning Engineers (ASHRAE), 48, 54 Amyl nitrite, 357 Anatomical imaging findings CT, 323, 352, 358, 359, 384, 449, 458–459, 472, 473, 485, 486, 571 MRI, 323, 356, 358, 359, 384, 449, 450, 452, 459, 461, 462, 463, 472, 473, 485, 486, 497, 506, 570, 571, 610, 635, 748 Anthony Farr and Stacy Beckett Boating Safety Act (2004), 182 Anxiety, in CO-poisoned patients, 487–488, 516, 625, 637, 731 Apoptosis, 347–348 Aripiprazole, 361 As-measured CO measurement, 103–106 Assembly Bill (AB) 2222, 182 Audit trail, 297

765

8417:

“8417_c036” — 2007/9/11 — 18:55 — page 765 — #1

Index

766

Australian Medical Association (AMA), 265, 266 Automobile air quality monitor (AQM), 254, 263–265, 264 commuter exposure, 12–13, 26 Auxiliary power generators, 62–64

B Back drafting, 64–65 in fireplace flue, 66 of flue gases, 83 Barbecue Industry Association, 18 Battle of experts, 680–681 Benzodiazepine, 361 Boating Accident Report Database (BARD), 160 Boat-related CO poisoning, 164–165, 177–180; see also Nonfatal boat-related CO poisoning medical characteristics for, 164–166 Brain-derived neuropeptides, 355 Brain injury, 514, 603, 704; see also Mild traumatic brain injury; Traumatic brain injury in children mechanism, 478 structural brain injury, evidence of, 571 Brain SPECT imaging, 450–451 after CO poisoning, 457 chronic lower-level CO exposure, findings of, 464 delayed CO-induced encephalopathy, findings of, 464–471 neuroimaging modalities, 458 anatomical imaging findings, 458–459 functional imaging findings, 460–463 Breath analyzer, 648, 650–651, 648, 653 British Gas, 281–282 Bromocriptine, 361 BS EN 50291, 252 Building Officials and Code Administrators International, Inc. (BOCA), 139 Building Performance Institute (BPI), 118, 120 Buoyancy, of CO, 200–201 Burden of proof, 662–666 damages, 664 economic damages, 665–666 on injury, 664–665 noneconomic damages, 666 liability, 663–664 standard of proof, 663 Butane, 50, 141, 142, 143, 202 boiling point, 141–142

8417:

C Cabin cruisers, 170–171, 177–178 California Air Resources Board (CARB), 181, 292 Canadian Gas Association (CGA), 44 Canadian Standards Association (CSA), 138 Carbogen, 343, 356 Carbon monoxide (CO), 6, 130, 144, 251, 313, 437; see also individual entries accumulation, within an enclosure, 87–90 rate of dissipation, 89–90 concentration inhaled and blood co-saturation, 755–758 as drowning risk factor, 165–166 in human body, 334, 664, 667 poisoned patients, case study for, 606–611 ADL, 419, 485, 504, 593, 607, 632, 689, 691 LCP issues care providers/residential care, 610 complications, 611 diagnostic studies, 610 laboratory, 610 medical care, 609 medication, 610 recreation, 610 therapeutic modalities, 609 transportation, 610 outcome, 608–609 TSA, 607–608 Carbon Monoxide Headquarters (COHQ), 285–286 goals, 285–286 Carbon Monoxide Neuropsychological Screening Battery (CONSB), 357, 359, 403, 503, 504, 747 Carboxyhemoglobin (COHb), 159, 164–166, 273, 289, 317, 321, 343, 480, 484, 644, 746, 747, 748, 749 in blood, noninvasive measurement of with pulse co-oximetry, 739 levels, 290 half-life, 294 measurement limitations, in marine environment, 164 Caspase-1, 348 Catecholamine, 347, 353 Central furnaces, 135–136, 140, 148 Cerebrolysin, 355 Certified Life Care Planners (CLCP), 606 Charcoal briquets, CO poisoning from, 18 grills, 18, 19 Chemical properties of CO, 67–68 of LP-gas, 52

“8417_c036” — 2007/9/11 — 18:55 — page 766 — #2

Index

767

Children brain injury in mechanism, 478 structural brain injury, evidence of, 571 CO toxicity in, see Toxicity treatment, for CO poisoning, 360–361 Chimney dynamics, 82–83 Chronic CO exposure, 571, 573, 577, 585–586, see also Exposure update on study, 745–750 Chronic CO poisoning, 320, 443–446, 464, 472, 497, 551; see also Poisoning case study educational history, 540–541 exposure information, 540 initial testing, 541–542 neuropsychological re-evaluation, 542–545 patient demographics, 540 persisting physical symptoms, 541 characteristics, 443 cognitive sequelae, 498–502 demographics, 552–553 discovery of problem, 445–446 emotional and affective sequelae, 498–502 Helffenstein study battery, of neuropsychological tests, 508 MMPI-2, 531–536 neuropsychological testing outcome, 516 norms, 509 persisting symptoms, reported, 511–516 reported symptoms, during chronic CO exposure, 509–511 sample and exposure data, 506 vocational outcomes, 536–538 incidence, 497–498 misdiagnosing, 446 physical sequelae, 498–502 self-report questionnaires, 558–564 source, 551–552 symptomatic evaluation data, 553–558 utilizing neuropsychological assessment, 502–506 Chronic Health Condition, 691 City Technology, 253 CO sensor, 261–262, 262 Clean Air Act (CAA), 7, 8, 9, 14, 30, 181, 189, 246 Clinical effectiveness, of HBO therapy, 378–382 negative trials, 378–379 positive trials, 379–382 Clinical treatment, for CO poisoning, 341, 619 approach to patient with CO poisoning, 355–361 children, 360–361

8417:

during pregnancy, 360 neuroimaging studies, 358–360 historical perspective, 342–344 management of sequelae, 361–362 mechanisms, of CO toxicity, 344–348 neuroprotective treatments allopurinol, 351–352 brain-derived neuropeptides, 355 HBO therapy, 348–351 hypothermia, 355, 425 insulin, 352–354 NAC, 351–352 NBO, 321–322, 348, 349, 350, 356, 379–380, 396, 397, 400, 401, 406 NMDA receptor antagonists, 347, 354, 376 visual system functioning, 620–622 VMSS, 620 case study, 634–640 clinical testing, 624–625 symptoms, 622–624 treatment, 625–626 with yoked prism, 626 rehabilitative and supplementary considerations, 626–633 Clothes dryers, 65–66, 135 CO-caused morbidity, 241–243 recent national studies of nonfatal CO poisoning, 242–243 CO-caused mortality, 236–240 studies, 237–240 Cognitive issues, of CO poisoning, 593–595, 595 case study, 606–611 executive dysfunction, 594 sensory-motor dysfunction, 594 short-term memory dysfunction, 594 vision and information processing dysfunction, 595 Cognitive sequelae, CO poisoning, 478 DNS, 481–482 functional imaging, 486 HBO effect on, 484–485 lower level, 483–484 markers, severity and outcome, 484 neuroimaging findings, comparison, 485–486 PNS, 481–482 Cognitive therapy, 626 CO Hot Pot™ , 110–111, 112–115, 125 Combustion, 68, 131–132 CO as product of, 199–200 initiate and perpetuate basic requirements to, 68–69 principles, 143–144 complete combustion, products of, 143–144

“8417_c036” — 2007/9/11 — 18:55 — page 767 — #3

Index

768

Combustion (Continued) incomplete combustion, products of, 144 Community exposure standards and guidelines, for CO, 291–292, 293 Commuter exposures, 25–31 airbag deployment, 30 defective exhaust systems, 26–29 drive-up facilities, 29–30 motor vehicle emission control program, 30–31 parking garages, 29 service stations, 29 Compensatory damages, 657 Complete combustion, products of, 143–144 Computed tomography (CT), 323, 352, 358, 359, 384, 449, 458–459, 472, 473, 485, 486, 571 Consumer products, 204–205 CO-related accidents investigation case study, 151–154 root cause, 148–151 CO level estimation, 151 determination, 151 follow-up inspections, 149–151 initial discovery, 149 CORGI, 282 Coronary artery disease, 8 COSTAR® , P-1, 210 Council of American Building Officials (CABO), 139 Council on Environmental Quality (CEQ), 11, 12, 13 CSA 6-19-01, 252 CSA Star, 138 Current Population Survey (CPS), 692, 693, 694, 700 Custom and practice, of CO safety information, 224, 226–227, 228 Cytochrome c, 343, 344, 345, 359, 478

Hyperbaric Oxygen” (SR Thom), 402–404 Department of Commerce, Bureau of the Census, 692, 700 Department of Environment, 277, 281 Department of Trade and Industry, 281–282 Depression, in CO-poisoned patients, 8, 319, 355, 392, 409, 487–488, 515 Descriptive characteristics, of marine CO poisoning, 161–163 Detectors, CO, 251, 305, 749 as preventive medicine Chicago experience, 307–308 clinical implication, 308 current and future directions, 309–310 effectiveness, 308–309 initial standard setting, 306–307 technology, 306 effectiveness, in marine environment, 183–184 Differential diagnosis, 296 Diffuse axonal injury (DAI), 572 Diffusion capacity for CO (DLCO), 741 Digit Symbol Incidental Memory Test, 502 Dilution, 201–202 Dipyridamole, 343 Direct vent system, 137 Disability, 691, 700 estimating, 694 and functioning, 690 and working, 692–693 Disability-adjusted life years (DALY), 686 Dissipation, 89–90, 204 Dizocilpine, see MK-801 Domestic water heater, 65 “Do no harm”, 214 Draft diverter, 132–133 safety problems, 133 Drive-up facilities, 29–30 Drowsiness, 747

D

E

Dantrolene, 361 Data functions, 696, 705 Data loggers, 14, 15, 648 “Death Zone”, 171 Decennial Census, 694, 701 Defective exhaust systems, 26, 29 Delayed administration, of HBO therapy, 383 Delayed neurological sequelae (DNS), 349, 358, 359, 361, 375, 384, 396, 403, 413, 414, 423, 458, 462, 481–482, 486 “Delayed Neuropsychologic Sequelae after Carbon Monoxide Poisoning: Prevention by Treatment With

Earning capacity, 605, 693–694 loss, analysis of, 699–703 loss of future, 703–723 Echocardiogram (ECHO), 345 Eco-Balls, 272 Econometric models, 694 Economic Demographers from Expectancy Data, 708 Elavil, 727 Electrocardiogram (EKG), 290, 345, 356, 396 Electrochemical gas sensors, 253, 261–263 Electroencephalogram (EEG), 349, 350, 358, 402, 461, 486, 630, 635, 704

8417:

“8417_c036” — 2007/9/11 — 18:55 — page 768 — #4

Index

769

Electronic ignition system, 134 Emergency department (ED), 644, 649–650, 651, 741–742 screening, 650 Emergency medical service, 187, 643, 649, 742 Emergency medical support, 742 Emergency medical technicians (EMTs), 295 Emergency smoke escape devices, 650 Emission from gas ranges, 99–128 trends, 8–10 Emotional and behavioral issues, of CO poisoning, 596–598 case study, 606–611 Emotional and psychological functioning, 706 EN403 standard, 650 Engineering control research and development, 184–187 Environmental conditions, 698 “Environmental health gap”, 243 Ethane, 142, 202 Ethical and philosophical reasons, for safety information, 214–216, 217, 218 Excess air combustion, 69, 71–72, 103, 104, 105, 143, 144, 314 Excess fuel combustion, 69, 72 Exchange transfusion, 343 Excitatory amino acids (EAA), 347–348, 354, 376 Executive functioning, 538, 572, 585, 705 miscellaneous tests, 529–530 Exit velocity, in CO producing equipment, 202–203 Expert opinions, in CO case battle of experts, 680–681 components, 674 expert witnesses, 674–680 fact witnesses, 673 judge, 673–674 jury, 674 Expert witnesses, 288, 289, 660, 669, 671, 672–673, 674, 675–676 long-term thinking, 681–682 opinions, on reality, 676–677 scientific basis, 677–679 scope, 676 testifying, strategies for, 679–680 Exposure, 54, 289 chronic CO exposure update on study, 745–750 COHb levels, 290 community exposure standards and guidelines, for CO, 291–292, 293 commuter exposures, 25–31 airbag deployment, 30

8417:

defective exhaust systems, 26–29 drive-up facilities, 29–30 motor vehicle emission control program, 30–31 parking garages, 29 service stations, 29 duration assessment, 292, 294 methylene chloride exposure, 31–32 nonoccupational exposure, 31 occupational exposure, 32 microenvironmental exposures, 17 commuter exposures, 25–31 occupational exposures, 20–22 recreational exposures, 23–25 residential exposures, 17–20 shopping center exposures, 22 NAAQS, guidelines of, 7–8 occupational exposure standards and guidelines, 291 OSHA and industry standards for, 54 types, 440

F Fact witnesses, 669 opinion, in CO case, 673 Failure modes, of gas appliances, 146–148 False alarms, 307–308 Fatal exposures, 19–20 Faulty heating equipment, 19 Federal Rules of Evidence (FRE), 672, 674–675, 702 Figaro, 253 Firefighters and CO emergency department screening, 650 emergency smoke escape devices, 650 fatalities from suppression, 643–644 investigation, 646–650 lethal gas combinations, 651–652 overhaul and postfire, 644–645 prevention and awareness, 652–653 workplace/industry CO standards, 645–646 Fireplaces, 66 FiS, 253 SB series sensor, 255, 256, 257–258 Fixed-site monitoring (FSM) stations, 8, 9, 12, 13 Flame rollout switch, 134 Flue gases, 82 back drafting, 83 Fluid Attenuation Inversion Recovery (FLAIR), 459, 571 Flu symptoms, 319, 446, 498, 505, 634, 646 Focal visual system, 621, 622 Food and Drug Administration (FDA), 221, 222, 357

“8417_c036” — 2007/9/11 — 18:55 — page 769 — #5

Index

770

Fuel, 68–69 burning devices, 44, 60 combustion, 44, 72 fuel gases, 140–143 input adjustments, 140 Fume hoods, 64 Functional capacity evaluation (FCE), 600–601, 690, 699, 716 Functional capacity index (FCI), 689 Functional imaging findings, 460 fMRI, 461 MRS, 359, 449, 450, 461–462, 472, 482 PET, 358, 359, 385, 449, 450, 460–461, 472, 473, 486, 504 SPECT, 323, 345, 358, 359, 385, 449, 450, 451, 452, 453, 457, 459, 460, 461, 462–463, 464–471, 472, 473, 486, 497, 538, 539–540 Functional limitation, 700–701 Functional Magnetic Resonance Imaging (fMRI), 461

G Gamma aminobutyric acid (GABA), 353 Gas appliance certification, 138 design, 130–131 failure modes, 146–148 heating/gas appliance system, 145–146 industry, 130 installation requirements, 138 manufacturer’s installation instructions in, 139–140 safety devices, 134–135 types, 135–138 Gas burners combustion equations, 50–53 Gas flow, 72–73 Gasoline engine, 53–54, 209 Gas refrigerators, 65 Gas sensors, 653 Gas Research Institute, 102, 108, 111–112 Gas Research Institute of Des Plaines, 108, 122 Gawey-Apgar, S., 628–630 “Gel cell” detectors, 306 General educational development (GED), 697 Generator tailpipe exhaust, 83–85 Glasgow Coma Scale (GCS), 164, 166, 384 Glen Canyon National Recreation Area (GCNRA), 158, 159, 160, 165 Glen Canyon NPS decision logic, for patient triage, 188 Gliosis, 347 Glutamate, 347, 354, 376

8417:

Gracey, J.M., 627 “The Great Imitator”, 653 Gulf of Mexico CO poisoning, 169

H Haber’s Law, 292 Hall, T.O., 627–628 Halstead–Reitan tests, 522 Health, 684–690 less-than-perfect health, quantifying healthy life expectancy, 687–689 life-years lost to injury, 689–690 years lived with disability, 687 measuring, 684–687 stages, 688 Health and Safety Executive (HSE) department, 282–284 Health Care Financing Administrations (HCFA), 422 Health-Realted Quality of Life (HRQL), 687 Healthy life expectancy, 687–689 Healthy People 2010, 243, 687 Heating, ventilation, and air conditioning (HVAC) system, 252, 253, 263, 647 Heating/gas appliance system, 145–146 combustion and ventilation air supply, 146 fuel supply, 146 service personnel, 146 venting system, 146 Heating value, of gas, 143 Heavy work, 698 Hedonic damage calculations, controversial aspects of, 707 Helffenstein, D.A., 632–633 Helffenstein study battery, of neuropsychological tests, 508 MMPI-2, 531–536 neuropsychological testing outcome academic testing, 523, 525 executive function test, 529–530 Halstead–Reitan tests, 522, 523, 524 index score, 516–518 information processing speed, 527–528 IQ tests, 518–522 language comprehension, 530–531 memory testing, 522–523, 524, 525 motor skills, 528–529 visual–visual perceptual testing, 525–527 norms, 509 persisting symptoms, reported, 511–516 cognitive symptoms, 512, 515 physical symptoms, 511, 513 psychological/behavioral symptoms, 513, 515–516 visual symptoms, 512, 513–515

“8417_c036” — 2007/9/11 — 18:55 — page 770 — #6

Index

771

reported symptoms, during CO exposure, 509–511 sample and exposure data admission criteria, 506–507 CO exposure level, 507 duration and frequency of exposure, 507–508 sample demographics, 507 source and location exposure, 507 time since exposure, 508 vocational outcomes, 536–538 Helmholtz resonance, 81 Heme iron, 458 oxygenase, 347 proteins, 345, 376 Hibachis, 19 High limit control, 134 History of CO poisoning, 754 Houseboats, 171–174, 178–179 Household cooking gas appliances, 135 Household Cooking Gas Appliances (ANSI Z21.1-1993), 102–103, 112, 127 Human exposure to CO concentrations, 10–17 Hydrocarbon gas, 31, 43, 51, 53, 141, 142, 143, 144; see also Butane; Natural gas; Propane Hydrogen cyanide (HCN), 643, 652 Hydrogen peroxide, 343 Hydroxycobalamin, 357 “Hyperbaric or Normobaric Oxygen for Acute Carbon Monoxide Poisoning: a Randomised Controlled Clinical Trial” (CD Scheinkestel), 406–412 Hyperbaric oxygen (HBO) therapy, 241–242, 295–296, 321–322, 344, 348–351, 375, 400, 401, 406, 482, 764 for acute CO poisoning, 391, 393 basic science overview, 395–398 effects, 394–395 human evidence, 398 clinical effectiveness, 378–382 negative trials, 378–379 positive trials, 379–382 CO effects, at cellular level, 376–377 delayed administration, 383 functional ability, 747, 748 future directions, 384–385 indications, 382–383 during pregnancy preposed indications, 359, 360 repeated treatment, 384 “Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning” (LK Weaver), 412–420 Hypothermia, 355, 425

8417:

Hypoxic hypoxia, 316–317 Hypoxic ischemia, 344

I Immediately Dangerous to Life and Health (IDLH), 291, 645 Impairment rating, 690 Impairments, 691, 700 Incomplete combustion, products of, 144 Increment–Decrement Model, 694 Index score, 508, 516–518 Induced draft system, 137–138 Industrial products and processes, 205 Information website, CO, 274–277 Infra-red (IR) sensors, 253, 256–261 Injury by CO poisoning case report, 703 diminshment of function, 699 disability and working, 692–693 earning capacity, 693–694 general educational development, 697 health, 684–690 less-than-perfect health, quantifying, 687–690 measuring, 684–687 stages, 688 monetary damages earning capacity loss, analysis of, 699–703 from population to person, 690–691 specific vocational preparation, 697–699 standard vocational interview, 695–696 work construct, 696–697 Insomnia, 747 Inspection and maintenance (I/M) programs, 9 Institute for Environment and Health, 497 Instrumental activities of daily living (IADLs), 689, 691 Insulin, 352–354 International Academy of Life Care Planners (IALCP), 605 International Agency for Research in Cancer, 686 International Association of Plumbing and Mechanical Officials (IAPMO), 139 International BoatBuilders Exposition, 187 International Classification of Diseases (ICD), 236 codes, for CO poisoning, 237 International Classification of Functioning, Disability and Health (ICF), 690–691 International classification of impairments, diseases and handicaps (ICIDH), 690 International Code Council, Inc. (ICC), 139

“8417_c036” — 2007/9/11 — 18:55 — page 771 — #7

Index

772

International Conference of Building Officials (ICBO), 139 Investigation of CO poisoning, 287 case study, 297–299 duration assessment, 292, 294 exposure level COHb levels, 290 community exposure standards and guidelines, 291–292 occupational exposure standards and guidelines, 291 factors, 296 signs and symptoms, 288–289 treatment, 295

J Job coach, 601 Judge opinion, in CO case, 673–674 Jury, 662, 663, 665, 666 opinion, in CO case, 674

K Karg Field Protocol, 118 development, 108–121 oven bake burners, field testing, 115–121 range top burners field testing, 109–112 laboratory testing, 112–115 for measuring CO emissions, from gas ranges burning testing, preparation for, 124–125 failed burner, 126 oven bake burner testing, 125–126 range top burner testing, 125 safety, during emission testing, 124 visual inspection and customer education oven inspection, 123–124 range top inspection, 122–123 objectives, 102 Ketamine, 354 Kidde, 253 Kluver–Bucy syndrome, 488 Kool Aid packet, 693–694

L Labeling, 206; see also Safety information, for CO custom and practice, 224, 226–227, 228 design, 207–209

8417:

ethical and philosophical reasons, 214–216, 217, 218 litigation-driven safety information, 227–230 need, 216–219 regulations, 219–224, 225 voluntary standards, 219, 220, 221 workplace area labeling, 211–213 The Labor Force Status and Other Characteristics of Individuals by Age, Education Sex, and Disability status, 694 Lake Cumberland CO poisoning, 174, 178 Lake George Inlet CO poisoning, 170 Lake Havasu CO poisoning, 179–180 Lake Minnetonka CO poisoning, 169 Lake of the Ozarks CO poisoning, 174 Lake Powell CO poisoning, 158, 159, 160, 161, 165–166, 168–169, 171, 173–174, 177, 178, 179, 180, 183, 184, 189 Large vehicle propulsion engines, 62 Leakage location, into an enclosure, 90 smoke testing, 91 considerations, 91–92 negative pressure testing, 92 positive pressure testing, 92 typical smoke testing, 93–96 Lees-Haley Fake Bad Scale (FBS), 546–547 Less-severe CO poisoning, 483–484, 565 Less-than-perfect health, 693 quantifying, 687 healthy life expectancy, 687–689 life-years lost to injury, 689–690 years lived with disability, 687 Lethal gas combinations, 651–652 Lidocaine, 343 Life Care Plan (LCP), for CO-poisoned patients, 605–606 case study, 609–611 care providers/residential care, 610 complications, 611 diagnostic studies, 610 laboratory, 610 medical care, 609 medication, 610 recreation, 610 therapeutic modalities, 609 transportation, 610 development, 606 Life-years lost to injury (LLI), 689–690 Light work, 698 Lipid peroxidation, 288, 346–347, 351, 376, 377 Liquefied petroleum (LP) butane, 50, 141, 142, 143, 202 propane, 50, 52, 123, 124, 141, 142, 143, 199, 202, 540

“8417_c036” — 2007/9/11 — 18:55 — page 772 — #8

Index

773

Litigation, in CO poisoning assistant in process, 668 attorney, 668–669 burden of proof, 662 damages, 664–666 liability, 663–664 standard of proof, 663 expert witness, 669 fact witness, 669 gathering information process, 659 discovery phase, 661–662 filing suit, 660–661 trial–risks and rewards, 662 life on trial, 667–668 problems, 666–667 purpose goal, 657–658 motivation, 658–659 work and abused, 656 Litigation-driven safety information, 227–230 Long-term community adjustment themes for CO-poisoned patients, 603–605 Lopez, Alan, 684, 686 Loss of consciousness (LOC), 3, 166, 359, 395, 397, 480, 484, 488, 501, 746, 747 Low-pressure boilers, 136–137 LP-gas physical and chemical properties, 52 vapor pressures, 53

M Magnetic resonance imaging (MRI), 323, 356, 358, 359, 384, 449, 450, 452, 459, 461, 462, 463, 472, 473, 485, 486, 497, 506, 570, 571, 610, 635, 748 Magnetic resonance spectroscopy (MRS), 359, 449, 450, 461–462, 472, 482 Malonylaldehyde, 346 “Managing Carbon Monoxide Poisoning with Hyperbaric Oxygen” (JC Raphael), 405–406 Manufacturer’s installation instructions, in gas appliances, 139–140 proper fuel input adjustments, 140 Marine CO detector evaluation, 183–184 Marine CO poisoning, 157 airborne CO concentrations, on and near boats, 175–180 evaluation criteria, 176 investigation methods, 175 Lake Havasu study, 179–180 cabin cruisers, 170–171, 177–178 descriptive characteristics, 161–163 future directions, 188–190 houseboats, 171–174, 178–179

8417:

identification, 159–161 case identification, 161 at Lake Powell, 160, 161 at nationwide, 160–161 medical characteristics, 164–166 prevention efforts, 180–188 ski boats, 166–169, 177 Masimo Corporation, 740 Masimo Rad-57, 446–448 Masimo Rainbow SET™ , 447 Masimo SET® , 447, 448 McKenna, P., 630–632 Mckenzie, Lord, 283 Medical characteristics, of marine CO poisoning, 164–166 boat-related CO poisoning, 164–165 CO, as drowning risk factor, 165–166 COHb measurement limitations, 164 nonfatal boat-related CO poisoning, 166 Medicare Services Advisory Committee of the Department of Health and Aged Care, 399 Medium work, 698 Memory impairment, 361, 480–481, 585 Memory testing, 522–523 Methane, 70, 141, 142, 202, 314 Methylene chloride exposure, 31–32 nonoccupational exposure, 31 occupational exposure, 32 Microchemical (MiCS), 253, 254–155 Micro-Electro-Mechanical Systems, 255 Microenvironmental exposures, 17 commuter exposures, 25–31 airbag deployment, 30 defective exhaust systems, 26–29 drive-up facilities, 29–30 motor vehicle emission control program, 30–31 parking garages, 29 service stations, 29 occupational exposures, 20–22 recreational exposures, 23–25 residential exposures, 17–20 fatal exposures, 19–20 nonfatal exposures, 18–19 shopping center exposures, 22 Migration, 200–202 Mild poisoning, 289 Mild traumatic brain injury (MTBI), 628, 629, 630; see also Brain injury; Traumatic brain injury Minnesota Multiphasic Personality Inventory (MMPI-2), 506, 531–536, 546, 547 Minnesota Multiphasic Personality Inventory-Adolescent (MMPI-A), 531 Mirage software464

“8417_c036” — 2007/9/11 — 18:55 — page 773 — #9

Index

774

Misconceptions, CO detection, 313, 314, 315 miscellaneous, 322–323 physiology, 316–317 presence, 313 properties, 313, 314 symptoms, of CO poisoning, 318–320 treatment and outcome, 320–322 MK-801, 354 Mobile homes, of CO accidents statistics, 59 codes and standards, 59–60 fuel-fired appliances combustion process, 68–69 excess air combustion, 71–72 excess fuel combustion, 72 physical and chemical properties, 67–68 thermochemical equations, 69–71 Moderate poisoning, 289 Monetary damages earning capacity loss, analysis of, 699–703 Monox, 253 Morbidity, 241–242, 471, 478, 488–489, 684 limitations, 245–246 More severe CO poisoning, 565 Mortality, 236, 246, 377, 684 limitations, 244–245 national CO mortality, studies of, 237–240 Motor homes, of CO, 60 interior devices clothes dryers, 65–66 domestic water heaters, 65 fireplaces, 66 gas refrigerators, 65 oil-fired space heaters, 65 ovens, 64–65 ranges, 64 internal combustion engines, 61 auxiliary power generators, 62–64 large vehicle propulsion engines, 62 Motor vehicle emission control program, 30–31 exhaust, in Ala Moana Shopping Center, 22 exhaust gas, 265–267 Multiple Cause-of-Death Mortality Database, 236 Murray, Christopher, 686, 694 Myelin basic protein (MBP), 346–347, 377, 397, 478, 570 Myleoperoxidase, 346 Myoglobin binding, 345

N NAAQS Exposure Model (NEM), 14 N-acetyl-aspartate (NAA), 453, 461

8417:

N-acetylcysteine (NAC), 351–352 National air monitoring stations (NAMS), 9 National Ambient Air Quality Standards (NAAQS), 9, 10, 14, 15, 18, 19, 20, 26, 33 guidelines, 7–8 National Association of State Boating Law Administrators (NASBLA), 182 National Case Listing, 161 National Center for Environmental Health, 237, 238 Air Pollution and Respiratory Health Branch, 237 National Center for Health Statistics (NCHS), 19, 236, 241, 305, 687, 692 Vital Statistics of the US Life Tables, 701 National Center for Injury Prevention and Control (NCIPC), 236, 238 National Council of State and Territorial Epidemiologist (CSTE), 243–246 National Electronic Injury Surveillance System (NEISS), 240, 241, 243 National Fire Protection Association (NFPA), 44, 90, 93, 644 NFPA 54, 139, 140, 150 NFPA 501 c, 59, 60 National Health Interview Survey (NHIS), 689, 691, 692 National Highway Traffic Safety Administration, 689 National Hospital Ambulatory Medical Care Survey (NHAMCS), 241, 242 National Hospital Discharge Survey 2002, 246 National Human Activity Pattern Survey (NHAPS) study, 17, 18, 20, 22, 25, 32, 33, 708 National Institute for Occupational Safety and Health (NIOSH), 3, 20, 54, 160, 179, 218, 220, 291 ceiling limit (CL), 645 immediately dangerous to life and health concentration (IDLH), 645 recommended exposure limit (REL), 645 National Marine Manufacturers Association (NMMA), 183, 216 National Oceanographic and Atmospheric Administration (NOAA), 78 National Park Service (NPS), 158, 159, 160, 178, 187, 188 National surveillance system, for CO, 243–246, 684 case definitions, 243–244, 244 morbidity limitations, 245–246 mortality limitations, 244–245 National Vital Statistics System (NVSS), 236, 237, 239, 240, 245, 246

“8417_c036” — 2007/9/11 — 18:55 — page 774 — #10

Index

775

National Workgroup on Carbon Monoxide Surveillance, 243, 244 Natural gas, 100, 109, 123–124, 130, 140, 142, 143, 145, 199, 200, 314 boiling point, 141 NEISS All Injury Program (NEISS-AIP), 241, 242 Neuroimaging after CO exposure, 449 location and symmetry of lesions in brain regions, 450–451 sequential studies, 450 modalities, 458 anatomical imaging findings CT, 458–459 MRI, 459 functional imaging findings, 460 fMRI, 461 MRS, 461–462 PET, 460–461 SPECT findings, in CO poisoning, 462–463 studies, 358–360 Neuro-otological treatment, 626 Neuroprotective treatments, for CO poisoning allopurinol, 351–352 brain-derived neuropeptides, 355 HBO therapy, 348–351 hypothermia, 355, 425 insulin, 352–354 NAC, 351–352 NBO, 321–322, 348, 349, 350, 356, 379–380, 396, 397, 400, 401, 406 NMDA receptor antagonists, 347, 354, 376 Neuropsychological re-evaluation circumstances, 542 results, 543–545 self-reported symptoms, 542–543 test scores comparison, 543 Neuropsychological testing, for chronic CO poisoning, 502–506 academic testing, 523, 525 executive function test, 529–530 Halstead–Reitan tests, 522, 523, 524 index score, 516–518 information processing speed, 527–528 IQ tests, 518–522 language comprehension, 530–531 memory testing, 522–523, 524, 525 motor skills, 528–529 proper fuel input adjustments, 140 visual–visual perceptual testing, 525–527 Neuropsychological treatment, 626 Nitric oxide synthase (NOS) inhibitor, 347, 348 Nitrogen, 143

8417:

N-methyl-d-aspartate (NMDA) receptor antagonists, 347, 354, 376 “Non-Comatose Patients with Acute Carbon Monoxide Poisoning: Hyperbaric or Normobaric Oxygenation?” (JL Ducasse), 401–402 Nondispersive infrared reference (NDIR), 9, 13, 306 Nonfatal boat-related CO poisoning, 166; see also Boat-related CO poisoning Nonfatal exposures, 18–19 Nonoccupational exposure methylene chloride, 31 Nor-binaltrophimine, 361 Normobaric oxygen (NBO), 321–322, 348, 349, 350, 356, 379–380, 396, 397, 400, 401, 406 NPS Emergency Medical Services (EMS), 158, 160, 643, 648, 742 medical management, innovations in, 187–188

O Obsessive–compulsive disorder, 488 Occupation, 696 Occupational Employment Statistics, 708 Occupational exposure, 32 microenvironmental, 20–22 standards and guidelines, for CO, 291 Occupational functioning, 706 Occupational Health and Safety Administration (OSHA), 3, 44, 54, 222, 226, 252, 291 permissible exposure limit (PEL), 645 Office of Air Quality Planning and Standards (OAQPS), 9 Ohio survey, 100–101, 102, 126 Oil-fired space heaters, 65 Optical gas sensors, see Infra-red sensors Oven, 64–65 Oven bake burners, 123 emissions, measurement of, 125–126 field testing, 115–121 Overhaul and postfire, 644–645 Oxidative stress, 347–348, 377, 478 Oxygen, 644 Oxygen depletion sensor (ODS), 44, 45, 215, 217–218 application, to small burners, 48–50 Oxygen therapy, 342–344

P Paresthesia, 747 Parking garages, 29

“8417_c036” — 2007/9/11 — 18:55 — page 775 — #11

Index

776

Parkinsonism, 361 Pearson Assessment website, 546, 547 People functions, 696 Perdue Pegboard test, 720, 721 Peroxynitrite, 346 Perry Lake CO poisoning, 173 Persistent neurocognitive sequelae (PNS), 358, 359, 400, 413, 414, 464, 481–482 Personal exposure monitors (PEMs), 13 Personal gas monitor (PGM), 645 Pew Environmental Health Commission, 243 Phenyl-n-tert-butyl-nitrone (PBN), 351 Physiatry pain management, 626 Physical characteristics of CO, 67–68, 753 Physical demands, 698, 714 Physical issues, of CO poisoning, 595–596 case study, 606–611 Pilot flame, 45, 68–69, 134 Poisoning acute, see Acute CO poisoning boat-related CO poisoning, 164–165, 177–180 case study, 606–611, 725 chronic, see Chronic CO poisoning cognitive issues, 593–595, 595 case study, 606–611 executive dysfunction, 594 sensory-motor dysfunction, 594 short-term memory dysfunction, 594 vision and information processing dysfunction, 595 cognitive sequelae, 478 DNS, 481–482 functional imaging, 486 HBO effect on, 484–485 lower level, 483–484 markers, severity and outcome, 484 neuroimaging findings, comparison, 485–486 PNS, 481–482 combustion theory application air flow around and through enclosures, 77 back drafting of flue gases, 83 chimney and flue dynamics, 82–83 cyclical inflow and outflow of enclosure, 81 deflector, 80 exhaust gas flow, 72–73 flow through bent or displaced exhaust pipes, 85–86 generator tailpipe exhaust, 83–85 Helmholtz resonance, 81 living quarters, inflow and outflow, 82 missing exhaust system, 86 scoop, 80 stagnation pressure, 75–76

8417:

thermal pressure, 76 total pressure, 73–75 ventilator opening, 80 wind rose, 78 diagnosis, 437, 444 chronic CO poisoning, 443–446 Masimo Rad-57, 446–448 problems, 438, 439–442, 443 situation history, 440 emotional and behavioral issues, 596–598 history, 754 investigation, see Investigation of CO poisoning marine, see Marine CO poisoning nonfatal boat-related CO poisoning, 166 sequelae management, 361–362 Portable monitors, 11 Positron Emission Tomography (PET), 358, 359, 385, 449, 450, 460–461, 472, 473, 486, 504 Postinjury worklife expectancy, 702 Post-Traumatic Vision Syndrome (PTVS), 514 Practical functioning, 706 Pregnant patients treatment, for CO poisoning, 360 Preinjury earning capacity, 700 Preinjury worklife expectancy, 700 Present value calculation, 702 Prevention efforts, for marine CO poisoning, 180–188 boat manufacturing/recall authority USCG regulations for, 180–181 CO detector/alarms case-based data, 183 evaluation, 183–184 engineering control research and development, 184–187 marine engine emissions, EPA regulation for, 181–182 NPS EMS medical management, 187–188 state legislative action, 182 Probabilistic NEM for CO (pNEM/CO), 14, 15, 17 Procaine hydrochloride, 343 Propane, 50, 52, 123, 124, 130, 142, 143, 199, 202, 540 boiling point, 141 Proper fuel input adjustments, 140 Psychiatry treatment, 626 Public health surveillance, for CO, 233, 234–236 CO-caused morbidity, 241–243 CO-caused mortality, 236–240 components, 235 national surveillance system, 243–246, 684

“8417_c036” — 2007/9/11 — 18:55 — page 776 — #12

Index

777

Public perceptions, about CO, 325 best action, 336–338 electric generator use, 327–329 emitting devices, 339 exhaust gas danger, conditions affecting, 332–333 experienced CO poisoning, 338–339 greater hazards, 334–335 propane radiant heater use, 329–330 property, 338 recreational powerboat safety, 331–332 safe use indoors, 333 time duration, in body, 338 worst poison, 335–336 Pulse CO-oximetry equipment, 446–448, 740–743 Pulse oximetry, 740 Punitive damages, 658 Pyridoxalated hemoglobin-polyoxyethylene conjugate (PHP), 343

postacute multidisciplinary treatment planning, 599–600 tools, for community reintegration, 600 FCE, 600–601 supported employment, 601 work hardening, 601 Rehabilitation counselor, 592–593, 595, 596, 597, 598, 599, 600, 601, 602, 603, 607, 608–609 Rehabilitation evaluation, for CO-poisoned patients, 592–593 case study, 606–611 Residential exposures, 17–20 fatal exposures, 19–20 nonfatal exposures, 18–19 Room air ventilation, for humans oxygen uptake estimation, for setting, 45–47 Room heaters, 136 Rules of Evidence, 672–673

S

Q Quantitative Electroencephalogram (QEEG), 349, 704 Quantitative Magnetic Resonance Imaging (QMRI), 358, 459, 463, 497 Quantum Group, 253, 258, 263 biomimetic CO gas sensor, 258–259, 260, 261

R “Randomized Prospective Study Comparing the Effect of HBO Versus 12 h NBO in Noncomatose CO Poisoned Patients: Results of the Interim Analysis” (D. Mathieu), 404–405 Range top burners emission, measurement of, 125 field testing, 109–112 inspection, 122–123 laboratory testing, 112–115 Reactive oxygen species (ROS), 346, 347, 348, 349, 458 Recreational exposures, 23–25 at indoor sporting events, 24–25 on vehicles, 23 Regulations, for CO safety information, 219–224, 225 Rehabilitation counseling, for CO-poisoned patients, 598–599 job development and prevocational planning, 602

8417:

Safe Practices for Boat-Towed Watersports Act, 182 Safety and monitoring devices, 44–45 Safety information, for CO, 206; see also Labeling; Warning custom and practice, 224, 226–227, 228 ethical and philosophical reasons, 214–216, 217, 218 litigation-driven safety information, 227–230 need, 216–219 regulations, 219–224, 225 voluntary standards, 219, 220, 221 written instructional information on, 209–211 Saxe, John, 722 Scientific methodology, in clinical toxicology, 763 Sedentary work, 698 Segami Corporation, 464 Selected Characteristics of Occupations (SCO), 697, 699 Select Serotonin Re-uptake Inhibitor (SSRI), 516, 636 Self-contained breathing apparatus (SCBA), 3, 317, 644 Semiconducting metal oxide (SMO) gas sensors, 253, 254–256 Sensor systems, 263–265 Sensor technologies, for CO gas detection, 253–263, 263 electrochemical gas sensors, 253, 261–263 optical gas sensors, 253, 256–261 SMO gas sensors, 253, 254–256

“8417_c036” — 2007/9/11 — 18:55 — page 777 — #13

Index

778

Sequential neuroimaging studies, 450 Service stations, 29 Severe poisoning, 289, 309, 397 SF-36 Health Survey, 695–696 Shasta Lake CO poisoning, 171 Shopping center exposures, 22 Signal Extraction Technology (SET)® , 446; see also Masimo Rainbow SET™ ; Masimo SET® Simulation of Human Activity and Pollutant Exposure (SHAPE), 14, 15 Single photon emission computed tomography (SPECT), 323, 345, 358, 359, 385, 449, 450, 451, 452, 453, 486, 497, 538, 539–540 brain imaging, 457, 459, 460, 461, 462–463, 472, 473 for delayed CO-induced encephalopathy, 464–471 Single-zone mass balance model, 106–108 Ski boats, 166–169, 177 Small engine exhaust gases CO accumulation from, 53–54 Smoke alarm, 273, 274 “Smoke kills” campaign, 273 Smoke testing, 91 considerations, 91–92 negative pressure testing, 92 positive pressure testing, 92 typical smoke testing, 93–96 Social functioning, 706 Socioeconomic factors, in urban areas, 648 Sodium nitrite, 357 Sources, of CO common investigative tactics, for location, 647 consumer products, 204–205 generation in residence, 647 industrial products and processes, 205 Southern Building Code Congress International, Inc. (SBCCI), 139 Space heating appliances central furnaces, 135–136 low-pressure boilers, 136–137 room heaters, 136 wall furnaces, 136 water heaters, 137 special design appliances, 137–138 SpCO, 740, 741 Special design appliances, 137–138 Specific gravity, of gas, 142–143 Specific vocational preparation (SVP), 697–699 Stagnation pressure, 75–76 Standard Occupational Classification codes, 708

8417:

Standard of proof, 663 Standard vocational interview,695–696, 699 State and local air monitoring stations (SLAMS), 9 State and Territorial Injury Prevention Directors Association (STIPDA), 244 Stockdale, S., 630 Suicide(s), 471 car exhaust as means of, 265–267, 392 Supervising process, 705 Supported employment, 601 Surveillance system, to health problems, 684 Survey of Income and Program Participation, 701

T Teak surfing, 168, 169, 177, 182, 190, 331 Tedlar™ bags, 12, 23 Temperaments, 698–699 Thermal pressure, 76 Thermochemical equations, 69–71 Thermocouple, 44, 45, 48, 49, 134 Things functions, 696 Tiarks, Frank, 275 Time, 653 Total pressure, 73–75 Toxic Exposure Surveillance System (TESS), 241, 242 Toxicity in children brain injury mechanism, 570–571 structural brain injury, evidence of, 571 case study, 577–586 development effects age as critical variable, 574–575 developmental neuropsychological approach, 575–576 pediatric vulnerability, 573–574 neurobehavioral symptoms, 571–572 symptoms, 569–570 white matter injury, 572 mechanisms of, 344–348 apoptosis, 347–348 hypoxic ischemia, 344 lipid peroxidation, 346–347 myoglobin binding, 345 oxidative stress, 347–348 vascular oxidative stress, 346 Tracer gas model for predicting CO accumulation in small structures, 47–48 Transferable Skills Analysis (TSA), 607–608 Traumatic brain injury (TBI), 572, 603, 604, 605; see also Brain injury; Mild traumatic brain injury

“8417_c036” — 2007/9/11 — 18:55 — page 778 — #14

Index

779

“Trial of Normobaric and Hyperbaric Oxygen for Acute Carbon Monoxide Intoxication” (JC Raphael), 400–401 Tsongas protocol, 116, 118, 120

U U-50488H, 361–362 UL 2034, 184, 252, 305–306, 307, 309, 645–646 Underwater and Hyperbaric Medical Society (UHMS), 380, 384, 419 Underwriters Laboratory (UL), 44, 305–306 CO warning label, 221 UL 2034, 184, 252, 305–306, 307, 309, 645–646 United States Centers for Disease Control and Prevention, 6, 160, 161, 236, 237, 239, 240, 241, 242, 243, 329, 686 United States Coast Guard (USCG), 158, 159, 160, 161, 177, 185, 187 boat manufacturing/recall authority, regulation for, 180–181 United States Consumer Product Safety Commission (CPSC), 19, 44, 100, 108, 180, 218, 222, 225, 240, 241, 243, 252, 305, 306 CO deaths, estimates of, 145 United States Department of Energy (DOE) program, 100–101, 108, 110, 122 United States Department of Health, 277–280, 399 United States Department of Health and Human Services (DHHS), US, 422, 687, 701 United States Environmental Protection Agency (EPA), 3, 6, 7, 8, 9, 10, 14, 15, 33, 54, 154, 181, 189, 218, 239, 292, 315, 334, 708, 749 marine engine emissions, regulation for, 181–182 United States Public Health Service, 227 USCG Office of Boating Safety Recreational Boating Product Assurance Division, 180, 183, 184

V Vascular oxidative stress, 346, 458 Ventilation, for humans requirements, in small structures, 48 room air ventilation oxygen uptake estimation, for setting, 45–47 Venting system, 131–133, 146 draft diverter, 132–133

8417:

safety problems, 133 failure modes, 147 Vent safety shutoff system, 134–135 Very heavy work, 698 Visual Midline Shift Syndrome (VMSS), 620 case study, 634–640 clinical testing, 624–625 symptoms, 622–624 treatment, 625–626 with yoked prism, 626 rehabilitative and supplementary considerations, 626–633 Visual system function, 620–622 Visual–visual perceptual testing, 525–527 Vocational outcomes, 536–538 Voluntary standards, for CO warnings, 219, 220, 221

W Wall furnaces, 136 Warning, 206; see also Safety information, for CO custom and practice, 224, 226–227, 228 design, 207–209 layout, 208 ethical and philosophical reasons, 214–216, 217, 218 litigation-driven safety information, 227–230 need, 216–219 regulations, 219–224, 225 voluntary standards, 219, 220, 221 written instructional information, 209–211 workplace area warnings, 211–213 Wash-out rate, of CO, 759–762 Water Fuse, 272 Water heater, 137 chronic CO poisoning due to, 505, 540 domestic water heater, 65 Web-based Injury Statistics Query and Reporting System (WISQARS), 236 Wide-ranging Online Data for Epidemiologic Research (WONDER), 236 Wind rose, 78, 79 Work construct, 696–697 Worker characteristics components, 696–697 Worker functions, 696 Work hardening, 601 Working Group on Motor Vehicle Exhaust Suicide, 266

“8417_c036” — 2007/9/11 — 18:55 — page 779 — #15

Index

780

Worklife expectancy, 694 Workplace area warnings and labeling general OSHA warning signage, 211–212 industry warning criteria, 213 specific OSHA exposure warning signage, 212–213 Workplace/industry CO standards, 645–646 Work-related disability, 701 World Bank, 684, 685, 686 World Health Assembly, 690 World Health Organization (WHO), 3, 236, 252, 619, 684, 686, 690, 691 guidelines, for CO, 8 Written instructional information, on safety information, 209–211

X Xanthine oxidase inhibitor, see Allopurinol

Y Years lived with disability (YLD), 686, 687 Years of life lost (YLL), 686 Yoked prism therapy, 620 for VMSS, 626, 638, 639, 640 rehabilitative and supplementary considerations, 626–633

Z Z21/83 Committee, 138, 148 Zero impairment rating, 690 Ziprasidone, 361

8417: “8417_c036” — 2007/9/11 — 18:55 — page 780 — #16

SY

CK-BRAIN

03/27/06

Baseline data versus adult normals I +4

Right lateral view

Anterior view

Superior view

Left lateral view

Posterior view

Interactive view-no cerebelhm

+3

+2

-2

-3

-4 -5

COLOR FIGURE 20.1 A SPECT scan of cortical function after carbon monoxide poisoning. The color scale (left side) displays normal perfusion in gray, subnormal perfusion in green and blue, and hyperperfusion in red. In other cases hypoperfusion is found in the frontal areas. Thus, the abnormalities found vary from one patient to another. (Credit to J. Michael Uszler)

8417: “8417_c037” — 2007/9/12 — 14:33 — page 1 — #1

Finding No. 1(cont.): Toxic injury from carbon monoxide poisoning

Normal

"CO poisoned"

COLOR FIGURE 21.2 Example of diffuse neuronal injury two years after acute carbon monoxide poisoning.

Mild

Medium

Severe

COLOR FIGURE 21.3 SPECT scans of three patients with mild, medium and severe cognitive defects two years after acute carbon monoxide poisoning.

8417: “8417_c037” — 2007/9/12 — 14:33 — page 2 — #2

Adult male

Adult female

COLOR FIGURE 21.4 SPECT scans of male and female patients two years following acute carbon monoxide poisoning with identical carboxyhemoglobin levels (34.5% vs. 34.9%)

LC

RL

IG

TM

BAW

SP

BRW

COLOR FIGURE 21.5 Superior, transverse views of SPECT perfusion findings in isolated lentiform nuclei of seven patients, two years following acute carbon monoxide poisoning. Yellow areas in the color plates are areas of abnormally decreased perfusion.

8417: “8417_c037” — 2007/9/12 — 14:33 — page 3 — #3

ROI label Caudate nucleus—Left

975

Caudate nucleus—Right

975

Right lateral view

Left lateral view

# Elts

Volume

Maximum Minimum

0.3 %

71.1 %

26.9 %

0.3 % 74.1 % Anterior view

37.9 %

Posterior view

Mean 42.6 %

Standard deviation 9.3 %

52.9 % 7.7 % Superior view

Interactive view

COLOR FIGURE 21.6 Six SPECT isolation views of caudate nuclei of a patient two years following acute carbon monoxide poisoning. All areas other than red in the color plates represent areas of abnormally decreased perfusion.

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