Occupational and Environmental Lung Diseases: Diseases from Work, Home, Outdoor and Other Exposures

Occupational and Environmental Lung Diseases

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

Occupational and Environmental Lung Diseases Editors

Susan M. Tarlo Department of Medicine and Dalla Lana School of Public Health, University of Toronto, and Division of Respiratory Medicine, University Health Network, Toronto, Ontario, Canada

Paul Cullinan Occupational and Environmental Respiratory Disease, National Heart and Lung Institute (Imperial College), London, UK

Benoit Nemery Toxicology and Occupational Medicine, Department of Public Health, Faculty of Medicine, Catholic University of Leuven, Leuven, Belgium

This edition first published 2010, Ó 2010 John Wiley & Sons, Ltd Wiley-Blackwell is an imprint of John Wiley & Sons, formed by the merger of Wileys global Scientific, Technical and Medical business with Blackwell Publishing. Registered office: John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK Other Editorial Offices: 9600 Garsington Road, Oxford, OX4 2DQ, UK 111 River Street, Hoboken, NJ 07030-5774, USA For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com/wiley-blackwell The right of the author to be identified as the author of this work has been asserted in accordance with the Copyright, Designs and Patents Act 1988. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher. Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought. The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by physicians for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of fitness for a particular purpose. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the author shall be liable for any damages arising herefrom. Library of Congress Cataloging-in-Publication Data Occupational and environmental lung diseases : diseases from work, home, outdoor and other exposures/ [edited by] Susan M. Tarlo, Paul Cullinan, Benoit Nemery. p. cm. Includes index. Summary: ‘‘Documents both environmental and work-related causes of lung disease. Unlike other books on the subject, this new volume approaches occupational and environmental lung disease from the starting point of the patient who comes to the physician with respiratory symptoms. The authors recognize that potentially harmful exposures occur not only in the work environment, but also as a result of hobbies or other leisure activities, or from outdoor air pollution, and it is up the physician to identify whether a particular job or hobby is the cause of the patient’s respiratory symptoms. To help you arrive at a differential diagnosis, chapters in the book are arranged by job or exposure, and are divided into 5 sections: Personal environment. Home environment. Other indoor environments. Work environment. General environment. Each is written by an expert in the specific topic and provides pragmatic information for the practicing physician. This practical book is an invaluable resource that belongs close at hand for all physicians dealing with patients experiencing respiratory symptoms’’– Provided by publisher. ISBN 978-0-470-51594-5 (hardback) 1. Lungs–Diseases–Environmental aspects. 2. Occupational diseases. I. Tarlo, Susan M. II. Cullinan, Paul. III. Nemery, Benoit. RC756.O227 2010 616.20 4071–dc22 2010025645 ISBN: 978-0470-51594-5 A catalogue record for this book is available from the British Library. Set in 10.5/12.5 pt Minion-Regular by Thomson Digital, Noida, India Printed in Singapore by Markono Print Media Pte Ltd First Impression

2010

Contents Contributors Preface

xxiii

Introduction Paul Cullinan and Susan M. Tarlo Asthma Hypersensitivity pneumonitis (extrinsic allergic alveolitis) COPD Bronchiolitis Pneumoconiosis Lung cancer and mesothelioma Attribution Further reading Part I 1

2

xv

The personal environment

1 1 3 4 5 5 7 8 10 11

Cosmetics and personal care products in lung diseases Howard M. Kipen

13

1.1 1.2 1.3 1.4

Introduction: historical context of cosmetics and respiratory illness Epidemiological context Description of exposures Respiratory diseases associated with exposure to cosmetics and personal care products 1.5 Diagnosis and management of occupational asthma in hairdressers References Further reading

13 14 15

Passive smoking Maritta S. Jaakkola

23

2.1 Introduction 2.2 Exposure to second-hand smoke 2.3 Health effects of passive smoking in children 2.4 Health effects of passive smoking in adults 2.5 Diagnostic and management issues related to passive smoking 2.6 Prevention of SHS-related diseases References

23 24 27 33 39 40 41

17 19 21 21

vi

CONTENTS

3

Emissions related to cooking and heating Debbie Jarvis

45

3.1 Introduction 3.2 Description of exposures 3.3 Pollutants produced when using gas appliances in the home 3.4 Diseases associated with exposures References Further reading

45 46 46 50 54 54

Cleaning and other household products Jan-Paul Zock

55

4.1 Introduction 4.2 Description of exposures 4.3 Diseases associated with exposures 4.4 Diagnosis and management issues 4.5 Summary and conclusions References Further reading

55 56 61 65 67 67 67

Building materials and furnishing Jouni J.K. Jaakkola and Reginald Quansah

69

4

5

5.1

Introduction to building materials and furnishing as sources of indoor air pollution 5.2 Emission of formaldehyde from building and interior surface materials 5.3 Emissions of volatile organic compounds 5.4 Emission of phthalates from PVC building and interior surface materials 5.5 Damp buildings and emissions of biological particles 5.6 Specific diseases associated with exposures from building materials and furnishing 5.7 Diagnosis and management issues References Further reading 6

69 70 72 74 75 76 77 78 79

Mites, pets, fungi and rare allergens Frederic de Blay, Magdalena Posa, Gabrielle Pauli and Ashok Purohit

81

6.1 Introduction 6.2 Mites 6.3 Cat and dog allergens 6.4 Rodents and other pets 6.5 Cockroaches 6.6 Fungi (molds) 6.7 Rare allergens 6.8 Diagnosis and management issues Further reading

81 81 82 84 85 86 90 92 93

CONTENTS

7

Hobby pursuits Paul D. Blanc 7.1 Definitions and general approach 7.2 Arts, crafts, and related activities in the plastic arts 7.3 Hobbies and pastimes involving pets and other animals 7.4 Sports and the performing arts 7.5 Miscellaneous hobbies, pastimes and avocations 7.6 Specific diseases associated with hobby activities 7.7 Diagnosis and management Further reading

Part II 8

9

10

Other indoor environments

vii 95 95 96 99 100 102 104 104 105

107

Day-care and schools Eva Ro€nmark and Greta Smedje

109

8.1 Introduction 8.2 Description of exposures 8.3 Diseases associated with exposures in the school environment 8.4 Viral infections 8.5 Ventilation 8.6 Room temperature 8.7 Diagnosis and management issues 8.8 Summary 8.9 Recommendations Further reading

109 110 114 115 115 115 117 119 119 119

Secondhand smoke exposure and the health of hospitality workers Mark D. Eisner

121

9.1 Introduction 9.2 Exposure of hospitality workers to SHS 9.3 Diseases and health conditions associated with exposures 9.4 Diagnosis and management issues 9.5 Conclusions References

121 121 123 127 127 128

Health effects of environmental exposures while in automobiles Madeline A. Dillon and David B. Peden

129

10.1 Environmental exposures in automobiles 10.2 Air pollution exposure while driving in cars 10.3 Smoking exposure 10.4 Other exposures in cars 10.5 Diseases associated with exposures 10.6 Diagnosis and management issues 10.7 Helpful websites Further reading

129 130 132 132 133 134 135 135

viii 11

CONTENTS

Indoor sports Harman S. Paintal and Ware G. Kuschner

137

11.1 11.2 11.3

137 139

11.4 11.5 11.6 11.7 11.8 11.9 11.10 11.11 11.12 11.13 11.14 11.15 11.16

Part III 12

13

Introduction Ice sports and arenas Ice arena air pollution: exposures and practical hints when taking a history Indoor ice arena toxicant syndromes Standards, guidelines and public health considerations Cold air-exacerbated asthma and dyspnea Water sports Exposures Diseases and health effects Extrinsic allergic alveolitis (hypersensitivity pneumonitis) Infections Swimming-induced pulmonary edema Trauma Equestrian arenas and horseback riding Gymnastics, weightlifting, athletics (track and field) and rock wall climbing Further reading

139 140 143 144 144 145 147 149 151 151 152 152

The work environment

159

155 155

Agricultural environments and the food industry Jakob Hjort Bønløkke, Yvon Cormier and Torben Sigsgaard

161

12.1 Introduction 12.2 Agriculture and agribusiness 12.3 Case 1 12.4 Case 2 12.5 Symptoms not related to allergen exposure 12.6 Other agrobusiness 12.7 Seafood and meat processing 12.8 Case 3 12.9 Bakeries 12.10 Other food industry 12.11 International perspective References

161 161 166 166 167 169 170 172 172 173 174 175

Mining Robert L. Cowie

177

13.1 13.2 13.3 13.4 13.5 13.6

177 178 178 179 184 185

Introduction Population at risk The mine environment Pneumoconiosis Obstructive pulmonary disease Tuberculosis and nontuberculous mycobacterial diseases

CONTENTS

14

15

13.7 Malignant disease 13.8 Pleural disease 13.9 Connective tissue and renal diseases 13.10 Mining and tobacco smoking 13.11 Acute lung and airway inhalational injury 13.12 Trauma 13.13 Conclusion Further reading

185 186 186 187 188 189 189 189

Metal industry and related jobs (including welding) William S. Beckett

191

14.1 Introduction 14.2 Metals defined 14.3 Workplace hazards from metals 14.4 Metal industry processes 14.5 Pulmonary responses to metals 14.6 Beryllium: lung and systemic effects 14.7 Cobalt disease (hard metal pulmonary disease) 14.8 Welding-related lung disease Acknowledgment Further reading

191 191 192 192 193 195 197 197 201 201

Automobile maintenance, repair and refinishing Meredith H. Stowe and Carrie A. Redlich

203

15.1 15.2 15.3 15.4 15.5 15.6 15.7

203 204 204 205 205 209

Introduction – the industry Exposures from automobile maintenance and repair Exposures in auto body workshops Respiratory diseases in auto mechanics and repair workers Work-related asthma Other lung diseases in auto mechanics and repair workers Other nonpulmonary occupational diseases among auto repair workers Further reading 16

17

ix

210 210

Automotive industry Kenneth D. Rosenman

211

16.1 Introduction 16.2 Respiratory hazards and disease 16.3 Vehicle parts manufacturing Further reading

211 213 213 222

Wood and textile industries Kjell Tore
n

223

17.1 17.2 17.3

223 226 227

Wood industry The pulp and paper industry The textile industry

x

18

19

CONTENTS

17.4 Prevention References Further reading

231 231 231

Chemical, coatings and plastics industries Oyebode A. Taiwo and Carrie A. Redlich

233

18.1 18.2 18.3 18.4

Introduction and definitions Overview of the chemical, coatings and plastics industry Major types of paints, coatings and plastics Major respiratory disorders in chemical, coatings and plastics workers 18.5 Diagnosis and management Further reading

233 234 235

Work with electronics Sherwood Burge

247

19.1 19.2 19.3 19.4 19.5 19.6 19.7

247 247 248 248 249 249

Introduction The history of soldering Diseases in those exposed to soft soldering flux fumes Epidemiological context Definition of scope (and limitations) Exposures and processes in the electronics industry Practical hints (and pitfalls) when taking a history from patient 19.8 How to document exposure, including biomonitoring 19.9 Diseases associated with colophony and isocyanate exposure in the electronics industry 19.10 Diagnosis and management issues 19.11 Management and prevention 19.12 Medicolegal considerations and compensation 19.13 Public health issues 19.14 The spectrum of occupational diseases in electronics workers Further reading 20

241 244 245

249 251 252 254 256 256 257 257 258

The services industry George L. Delclos, Lea Ann Tullis and Arch I. Carson

259

20.1 20.2 20.3 20.4 20.5 20.6

259 260 265 266 268

Introduction Health diagnosing and treating occupations Personal care and service – cosmetology professionals Protective services Food preparation and serving-related occupations Building and grounds cleaning and maintenance occupations – janitors/cleaners 20.7 Conclusions Further reading

269 270 270

CONTENTS

21

22

23

24

xi

The construction industry Gary M. Liss, Edward L. Petsonk and Kenneth D. Linch

273

21.1 Introduction 21.2 Inhalation hazards in the construction industry 21.3 Diseases associated with exposures in construction work 21.4 Asthma and selected immunologic conditions 21.5 Occupational cancers 21.6 Other conditions Further reading

273 274 276 280 283 287 288

Police, firefighters and the military Aaron M. S. Thompson and Stefanos N. Kales

291

22.1 22.2

Introduction First responders: potential exposures common to police, firefighters and the military 22.3 Police 22.4 Firefighters 22.5 Military 22.6 Compensation Further reading

291

Office workers and teachers Jean M. Cox-Ganser, Ju-Hyeong Park and Kathleen Kreiss

313

23.1 Introduction 23.2 Exposures in office buildings and schools 23.3 Diseases associated with exposures 23.4 Diagnosis and management issues Further reading

313 316 330 333 336

Research workers Paul Cullinan

337

24.1 24.2 24.3 24.4 24.5 24.6 24.7

337 338 340 341 345 347

Introduction Respiratory hazards and diseases Respiratory sensitization: asthma and rhinitis Making a diagnosis of respiratory sensitization Management of respiratory sensitization in the research setting Respiratory disease arising from exposures to irritant substances Immediate effects of acute exposures to respiratory irritants at relatively high intensity 24.8 Management of the acute effects of high-dose irritant exposure 24.9 Longer-term effects of acute exposures at relatively high intensity 24.10 Nonasthmatic diseases 24.11 Asthma 24.12 Management of irritant-induced asthma 24.13 Other respiratory diseases in research workers 24.14 Other occupational diseases among research workers Further reading

292 302 303 306 309 310

348 350 350 350 351 352 353 354 354

xii 25

26

CONTENTS

Work in hyperbaric environments Mark Glover

357

25.1 Introduction 25.2 Respiratory hazards, diseases and their management 25.3 Further information Further reading

357 361 373 374

Effects of travel or work at high altitudes or low pressures Michael Bagshaw

377

26.1 Introduction 26.2 Physics of the high-altitude environment 26.3 Physiology of flight 26.4 Altitude illness Further reading

377 378 379 385 388

Part IV 27

28

29

The general environment

389

Natural sources – wildland fires and volcanoes Sverre Vedal

391

27.1 Introduction 27.2 Biomass burning 27.3 Volcanoes 27.4 Management/prevention Further reading

391 392 399 402 404

Traditional urban pollution Sam Parsia, Amee Patrawalla and William N. Rom

405

28.1 Introduction 28.2 Particulate matter 28.3 Sulfur oxides 28.4 Nitrogen oxides 28.5 Ozone 28.6 Air toxics References Further reading

405 407 411 413 415 417 418 418

Traffic-related urban air pollution Steven M. Lee and Mark W. Frampton

421

29.1 Introduction 29.2 History of traffic-related air pollution 29.3 Engines and emissions 29.4 Traffic-related air pollutants 29.5 Health effects of traffic-related air pollution 29.6 Conclusions References Further reading

421 422 425 428 430 439 440 442

CONTENTS

30

xiii

Outdoor sports  Kai-Hakon Carlsen

445

30.1 30.2 30.3

445 446

Introduction Epidemiological context Definition of exposures related to asthma and respiratory disorders in athletes – pathogenetic mechanisms 30.4 Diseases related to physical activity, training and competition in sports 30.5 Diagnostic considerations and medicolegal issues 30.6 Treatment of asthma and exercise-induced bronchoconstriction in athletes 30.7 International regulations for use of asthma drugs in sports 30.8 Controller treatment of EIA 30.9 Reliever treatment of EIA 30.10 Recommendations for the treatment of exercise induced asthma in athletes References Further reading Index

447 448 450 450 451 452 453 454 455 456 457

Contributors Michael Bagshaw

Jakob Hjort Bønløkke

Professor of Aviation Medicine King’s College London Visiting Professor Cranfield University WC2R 2LS, UK

Department of Environmental and Occupational Health Institute of Public Health Aarhus University Denmark

William S. Beckett

Sherwood Burge

Associate Professor of Medicine Harvard Medical School, Boston, MA Attending Physician, Medicine Mount Auburn Hospital 330 Mount Auburn St Cambridge, MA 02138, USA

Consultant Physician Occupational Lung Disease Unit Birmingham Heartlands Hospital Birmingham B9 5SS, UK

Paul D. Blanc Professor of Medicine and Endowed Chair Occupational and Environmental Medicine University of California, San Francisco Box 0924 San Francisco, CA 94143-0924, USA Fr
ed
eric de Blay Division of Pulmonology Asthma and Allergology Chest Diseases Department 1SB401 Hoˆpitaux Universitaires de Strasbourg BP426, 67091 Strasbourg Cedex, France

Kai-Ha˚kon Carlsen Professor of Paediatric Respiratory Medicine and Allergology University of Oslo Professor of Sports Medicine Norwegian School of Sport Sciences Oslo University Hospital, Rikshospitalet Department of Paediatrics NO 0027 Oslo, Norway Arch I. Carson Southwest Center for Occupational and Environmental Health Division of Environmental and Occupational Health Sciences The University of Texas School of Public Health Houston, Texas, USA

xvi

CONTRIBUTORS

Yvon Cormier

Madeline A. Dillon

Pulmonologist Institut Universitaire de Cardiologie et de Pneumologie de Qu
ebec (IUCPQ) Professor of Medicine Department of Medicine Universit
e Laval Qu
ebec, Canada

Center for Environmental Medicine Asthma and Lung Biology University of North Carolina Chapel Hill North Carolina, USA

Robert L. Cowie

Associate Professor of Medicine University of California, San Francisco San Francisco, CA 94143, USA

Professor of Medicine and of Community Health Sciences University of Calgary Director, Tuberculosis Services, Calgary Director, Calgary COPD and Asthma Program Respirologist, Alberta Health Services Health Research and Innovation Centre 3280 Hospital Drive NW Calgary, Alberta, T2N 4Z6, Canada Jean M. Cox-Ganser Division of Respiratory Disease Studies National Institute for Occupational Safety and Health Morgantown, West Virginia, USA Paul Cullinan Professor in Occupational and Environmental Respiratory Disease National Heart and Lung Institute (Imperial College), and Royal Brompton Hospital, London, UK George L. Delclos Professor Southwest Center for Occupational and Environmental Health The University of Texas School of Public Health Houston, Texas, USA

Mark D. Eisner

Mark W. Frampton Professor of Medicine and Environmental Medicine Pulmonary and Critical Care University of Rochester Medical Center 601 Elmwood Ave., Box 692 Rochester, NY, 14642-8692 585-275-4861, USA Mark Glover Medical Director Hyperbaric Medicine Unit St Richard’s Hospital Spitalfield Lane Chichester West Sussex PO19 6SE, UK Jouni J.K. Jaakkola Professor of Public Health Center for Environmental and Respiratory Health Research University of Oulu, Finland Professor of Environmental and Occupational Medicine Institute of Occupational and Environmental Medicine University of Birmingham UK

CONTRIBUTORS

xvii

Maritta S. Jaakkola

Kathleen Kreiss

Professor and Chief Physician of Respiratory Medicine Respiratory Medicine Unit Institute of Clinical Medicine University of Oulu and Oulu University Hospital P.O. Box 5000 90014 Oulu, Finland

Division of Respiratory Disease Studies National Institute for Occupational Safety and Health Morgantown, West Virginia, USA

Debbie Jarvis Respiratory Epidemiology and Public Health Group Emmanuel Kaye Building Manresa Road National Heart and Lung Institute Imperial College London SW3 6LR, UK Stefanos N. Kales Medical Director Employee & Industrial Medicine Cambridge Health Alliance Assistant Professor Harvard Medical School Director Occupational & Environmental Medicine Residency Harvard School of Public Health 1493 Cambridge Street Cambridge, MA 02139, USA Howard M. Kipen Professor and Interim Chair Department of Environmental and Occupational Medicine Acting Associate Director Environmental and Occupational Health Sciences Institute UMDNJ-Robert Wood Johnson Medical School 170 Frelinghuysen Road Piscataway, NJ 08854, USA

Ware G. Kuschner Associate Professor of Medicine Stanford University School of Medicine Division of Pulmonary and Critical Care Medicine United States Department of Veterans Affairs Palo Alto Health Care System 3801 Miranda Avenue, 111P Palo Alto, CA 94304, USA Steven M. Lee Pulmonary and Critical Care Medicine Southern California Permanente Medical Group Kaiser Permanente Fontana Medical Center 9985 Sierra Avenue, Fontana, CA 92335, USA Kenneth D. Linch Division of Respiratory Disease Studies Surveillance Branch National Institute for Occupational Safety and Health Morgantown, West Virginia, USA Gary M. Liss Assistant Professor Gage Occupational and Environmental Health Unit Dalla Lana School of Public Health University of Toronto (and Ontario Ministry of Labour) Toronto, Ontario, Canada

xviii

CONTRIBUTORS

Harman S. Paintal

David B. Peden

Clinical Assistant Professor of Medicine Stanford University School of Medicine Division of Pulmonary and Critical Care Medicine United States Department of Veterans Affairs Palo Alto Health Care System 3801 Miranda Avenue, 111P Palo Alto, CA 94304, USA

Center for Environmental Medicine Asthma and Lung Biology University of North Carolina Chapel Hill North Carolina, USA

Ju-Hyeong Park Division of Respiratory Disease Studies National Institute for Occupational Safety and Health Morgantown, West Virginia, USA

Edward L. Petsonk Professor of Medicine Section of Pulmonary and Critical Care Medicine West Virginia University School of Medicine PO Box 9166 Morgantown, West Virginia 26506, USA

Sam Parsia Assistant Professor Division of Pulmonary, Critical Care, and Sleep Medicine Department of Medicine New York University School of Medicine New York, NY, USA Amee Patrawalla Assistant Professor Division of Pulmonary and Critical Care Medicine University of Medicine and Dentistry of New Jersey New Jersey School of Medicine Newark, NJ, USA Gabrielle Pauli Division of Asthma and Allergy Chest Diseases Department University Hospital Strasbourg BP 426, 67091 Strasbourg Universit
e Strasbourg 4 rue Blaise Pascal 67000 Strasbourg, France

Magdalena Posa Division of Asthma and Allergy Chest Diseases Department University Hospital Strasbourg BP 426, 67091 Strasbourg Universit
e Strasbourg 4 rue Blaise Pascal 67000 Strasbourg, France Ashok Purohit Division of Asthma and Allergy Chest Diseases Department University Hospital Strasbourg BP 426, 67091 Strasbourg Universit
e Strasbourg 4 rue Blaise Pascal 67000 Strasbourg, France Reginald Quansah Institute of Occupational and Environmental Medicine University of Birmingham Birmingham, UK

CONTRIBUTORS

Carrie A. Redlich

Greta Smedje

Professor of Medicine Occupational and Environmental Medicine and Pulmonary & Critical Care Medicine Yale University School of Medicine New Haven, CT, USA

Department of Public Health and Clinical Medicine Occupational and Environmental Medicine Umea˚ University SE-901 85 Umea˚, Sweden

William N. Rom Sol and Judith Bergstein Professor of Medicine and Environmental Medicine Director Division of Pulmonary, Critical Care and Sleep Medicine Department of Medicine New York University School of Medicine 550 First Avenue New York, NY 10016, USA

Meredith H. Stowe

€nmark Eva Ro Associate Professor Department of Public Health and Clinical Medicine Occupational and Environmental Medicine Umea˚ University SE-901 85 Umea˚, Sweden Kenneth D. Rosenman Professor of Medicine Chief, Division of Occupational and Environmental Medicine College of Human Medicine Michigan State University 117 West Fee East Lansing MI 48824, USA Torben Sigsgaard Professor Department of Environmental and Occupational Health Institute of Public Health Aarhus University Denmark

xix

Associate Research Scientist Department of Medicine Yale Occupational and Environmental Medicine Lecturer Epidemiology and Public Health Yale University School of Medicine New Haven, CT 06510, USA Oyebode A. Taiwo Associate Professor of Medicine Director, Fellowship Training Occupational and Environmental Medicine Program Yale University School of Medicine 135 College Street, 3rd Floor New Haven, CT 06510-2483, USA Susan M. Tarlo Department of Medicine and Dalla Lana School of Public Health University of Toronto Division of Respiratory Medicine University Health Network Toronto, Ontario, Canada Aaron M. S. Thompson Occupational & Environmental Medicine Clinic St. Michael’s Hospital 30 Bond Street Toronto, Ontario M5B 1W8, Canada

xx

CONTRIBUTORS

Kjell Tor
en

Jan-Paul Zock

Professor/Senior Consultant of Clinical Allergology and Occupational Medicine Head Section of Occupational and Environmental Medicine University of Gothenburg Box 414, 405 30 Gothenburg, Sweden

Associate Research Professor Centre for Research in Environmental Epidemiology (CREAL) and Municipal Institute of Medical Research (IMIM-Hospital del Mar) Barcelona Biomedical Research Park (PRBB) Doctor Aiguader 88 08003 Barcelona, Spain

Lea Ann Tullis Southwest Center for Occupational and Environmental Health The University of Texas School of Public Health Houston, Texas, USA Sverre Vedal Professor of Environmental and Occupational Health Sciences University of Washington School of Public Health Adjunct Professor of Medicine University of Washington School of Medicine Seattle, WA, USA

Editors Susan M. Tarlo, MB BS, MRCP(UK), FRCP(C) Department of Medicine and Dalla Lana School of Public Health, University of Toronto, and Division of Respiratory Medicine, University Health Network, Toronto, Ontario, Canada Paul Cullinan, MD, FRCP Occupational and Environmental Respiratory Disease, National Heart and Lung Institute (Imperial College), London, UK Benoit Nemery, MD, PhD Toxicology and Occupational Medicine, Department of Public Health, Faculty of Medicine, Catholic University of Leuven, Leuven, Belgium

Preface This book was initially the concept of Dr Ben Nemery, who identified that no current textbooks approach the topic of Occupational and Environmental Lung Diseases from the starting point of the patient who comes to a physician with respiratory symptoms. Early in the clinical history the patient should be identified as having a particular job or ‘environmental’ exposure(s). A natural question then should be ‘Is this job (or other exposure or even hobby) the cause of the respiratory symptoms in this patient, and if so, what could be the differential diagnosis?’ The chapters in this book are therefore arranged by job or exposure(s) rather than by specific causative agents. Each is written by an expert in the specific topic and aims to provide pragmatic information for the practicing physician. The format of various chapters varies in keeping with the emphases considered to be most useful by the invited authors. In keeping with the aims of the book we have asked authors to provide practical information and to keep specific references to a minimum, but to include some key review articles that the reader may access for more detailed references if wished. With this format, the information presented represents the views of the author of each chapter, and there may be small differences expressed in different chapters. We also recognize that there is some degree of repetition in the book, but we felt it most useful to include this if it pertains to different jobs or exposures in different chapters. We recognize that potentially harmful exposures occur not only in work environments but also as part of hobbies or other leisure activities such as sports, and also from outdoor air pollutants; we have included sections on each of these. We have not included a chapter on the personal effects of tobacco products (since these effects are well recognized by all physicians), on the smoking of marijuana (for which there are far fewer published data) or on exposures to nanoparticles other than as outdoor ultrafine particulates (since the knowledge of their effects is currently very sparse). However we believe that most of the important exposures are addressed. We hope that this book will not be a reference guide on a bookshelf but will be a useful and much-used adjunct in the clinical setting, finding a place at your right hand. The editors

Introduction Paul Cullinan1 and Susan M. Tarlo2 1 2

Imperial College and Royal Brompton Hospital, London, UK University of Toronto and University Health Network, Toronto, Ontario, Canada

In this Introduction we aim to set the stage by giving a brief overview of the lung diseases that are alluded to in this book. While their details and those of the investigations used in their diagnosis may be familiar to the specialist respiratory physician, they may be more useful to review for other readers. Conversely, the discussion of disease attribution at the end of this chapter, which is probably familiar to occupational physicians, may be more useful for the pulmonary and primary care physician. We again wish to emphasize the importance of taking a detailed occupational and environmental history. Important in all patients, it is particularly so in those with respiratory symptoms, as can be clearly seen in the chapters that follow. There is a limited number of ways in which the lungs can respond to an environmental exposure, whether this is at work, home, outdoors or as part of a hobby. While the specific cause for the disease is important in diagnosis, and in allowing appropriate management to prevent further disease in the patient (and potentially in others), nevertheless, the pattern of disease can be similar from many different causes. The diagnosis of an occupational (and sometimes other environmental) disease may lead to disease-related compensation for the individual affected, but in particular should serve as a sentinal event, leading to appropriate consideration of co-workers who may also be at risk. Confirmation of an occupational disease, and where possible, identification of the cause can potentially lead to changes at work to protect others and reduce their risk of disease, and readers are encouraged to determine the appropriate steps locally to allow workplace interventions, e.g. by public health agencies or company physicians.

Asthma Asthma is a common condition that can start at any age. It affects between 5 and 10% of adults and can be caused or exacerbated by work or other environmental exposures, or Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

2

INTRODUCTION

may start incidentally and be provoked without a clear environmental trigger. It has been estimated that 10–15% of adult asthma may be attributed to occupation, and cohort studies have shown that up to 20% or more of working asthmatics can have exacerbations of their asthma due to exposures or conditions at work. Occupational asthma is defined as asthma that is caused by a specific exposure at work. It may be due to a demonstrated or presumed immunologic response to a work agent (sensitizer-induced occupational asthma), or can be due to a high-level irritantexposure (irritant-induced asthma, for which the most clear example is reactive airways dysfunction syndrome, RADS). Work-exacerbated asthma comprises unrelated asthma (preceding or with concurrent onset to work), which is worsened either on a sporadic or frequent basis by conditions at work. Both occupational and work-exacerbated asthma are included in the term ‘work-related asthma’. The features from the history which should increase suspicion of sensitizer-induced occupational asthma are primarily: (a) asthma beginning during a work period; (b) asthma symptoms improving on days or holidays away from work and/or worsening on work days; and (c) a known or presumed sensitizer exposure at work. Investigations for suspected occupational asthma include: objective confirmation of asthma with pulmonary function tests showing a significant bronchodilator response or positive methacholine or equivalent test of airway responsiveness; serial peak flow monitoring, with recordings of peak flow rates in triplicate at least four times a day during days at work and periods off work over several weeks, concurrently recording asthma symptoms and medications; repeat of methacholine or equivalent tests near the end of a work week and after 10 days or more off work to assess changes in PC20 related to work exposures; skin prick or in-vitro tests to identify specific IgE antibodies to a work sensitizer (when feasible); induced sputum cytology to identify changes in eosinophil and neutrophil counts during work period and off-work periods; and specific inhalation challenges with the suspected work substance (if needed and if available). Published guidelines, standards of care and consensus statements are available to provide more detail for investigations and interpretation of results. The best prognosis for sensitizer-induced occupational asthma occurs with early diagnosis and complete removal from further exposure to the sensitizer. Irritant-induced asthma resulting from a high-level, usually accidental exposure at work has different diagnostic features. The most definitive form, RADS, requires: absence of pre-existing airway disease; onset within 24 hours of high-level irritant exposure, usually leading to an urgent-care visit; objectively confirmed asthma by bronchodilator response or methacholine challenge; and asthma symptoms that persist for at least 3 months after the exposure. Somewhat more lax criteria may allow a diagnosis of irritant-induced asthma when RADS cannot be diagnosed. Work-exacerbated asthma is often diagnosed from history in a patient with preexisting asthma who has a transient exacerbation of asthma symptoms and/or increased need for asthma medications when there is an unusual exposure at work to conditions that may be expected to worsen asthma (e.g. construction in an office building or exposure to dusts or fumes). However, if work-related symptoms are frequent, then investigations as for sensitizer-induced occupational asthma should be performed. If the trigger for worsening of asthma is a specific workplace sensitizer, then management would be the same as for occupational asthma. If the trigger is a common allergen (such as dust mite) or a non-specific fume or dusts then

HYPERSENSITIVITY PNEUMONITIS (EXTRINSIC ALLERGIC ALVEOLITIS)

3

management may require adjustment of exposures, and/or optimization of pharmaceutical management.

Hypersensitivity pneumonitis (extrinsic allergic alveolitis) This is a hypersensitivity response in the small airways and alveoli involving production of IgG antibodies to the triggering antigen and also a cell-mediated immune response characterized by a lymphocytic alveolitis, non-caseating granulomas and interstitial foreign body granulomas, and can lead to eventual fibrosis. The triggering antigen is commonly an inhaled microbe which can be an atypical mycobacterium, fungus, a thermophilic actinomycete or a protozoa. Organic dusts such as soy dust or avian proteins, and some chemicals such as methylene diphenyl diisocyanate or phthalic anhydride, can also cause this response. The acute form has features similar to pneumonia, with fever, chills, cough, chest tightness (with or without wheezing), often with basal crackles and radiographic findings similar to pneumonia. Typically symptoms begin 4–8 hours after exposure to the inhaled antigen and clear within a few days, usually spontaneously. However they may be severe enough to cause hypoxia and require hospital admission with steroid treatment. Patients may require intubation and may be (unnecessarily) treated for pneumonia with unexpectedly fast recovery and recurrence when they are re-exposed again to the inciting agent. More chronic forms can occur with or without a preceding history of acute attacks. The presentation is then similar to that of idiopathic pulmonary fibrosis (IPF), with chronic cough, dyspnea, fatigue, weight loss and basal crackles. Chest radiograph may be normal or show changes similar to IPF, and the CT scan may show ground glass opacities and tree-in-bud appearance, or eventually may show changes of chronic interstitial fibrosis. The differential diagnosis also includes other causes of interstitial lung disease but bronchoalveolar lavage typically shows lymphocytosis, predominantly CD8 T cells, unlike findings in IPF or sarcoidosis. When feasible, a useful investigation for hypersensitivity pneumonitis (acute and occasionally chronic) is to look for serum precipitins identifying specific precipitating antibodies to the suspected antigen. Unfortunately there is a limited range of commercially available antigens for this test, and results can be positive in up to 50% of exposed asymptomatic individuals. Nevertheless, with a high pre-test probability of disease, this test can be very useful. Lacasse and colleagues have reported high diagnostic value for hypersensitivity pneumonitis from a combination among six features in patients with interstitial lung disease: known antigen exposure; positive precipitins; recurrent episodes of symptoms; timing 4–8 hours after exposure; inspiratory crackles on auscultation of the chest; and weight loss. Their study provided predictive values for various combinations of these tests and often prevents the need for more invasive diagnostic tests such as open lung biopsy or specific inhalation challenge, which can carry significant risk. Management as for those with occupational asthma requires complete avoidance of further exposure to the causative agent. Occasionally, when this is not possible for financial reasons, an air-supply respirator may prevent progressive changes, especially if exposure is occasional and for short periods.

4

INTRODUCTION

COPD ‘Chronic obstructive pulmonary disease’ is an awkward disease label, encompassing as it does a mix of symptoms (e.g. chronic sputum production), pathology (e.g. emphysema) and functional limitation (e.g. fixed airflow obstruction). Each of these may exist in isolation but their combination – especially in heavy smokers – is common. Indeed the link with cigarette smoking is so strong that the diagnosis of COPD is rare in nonsmokers; where it does occur in patients who have never smoked, an environmental cause – frequently occupational – is probable. For the same reason, establishing an environmental cause in a smoker is very difficult and generally, in the individual case, impossible. On a population level, however, it is estimated that 15% of the total burden of COPD is attributable to irritant exposures in the workplace often acting, probably, in synergy with cigarette smoking. Most current definitions of COPD rely heavily on the presence of irreversible airflow limitation measured by spirometry. Spirometry is a more challenging technique than is commonly recognized and requires considerable attention to detail; fortunately, guidelines for good practice are widely available. An ‘obstructive’ picture is one with a reduced FEV1/FVC ratio with or without a reduction in FEV1. There is no universal consensus as to what constitutes a ‘reduction’ in either of these measures but almost all authorities use some form of proportional comparison with expected values based on age and sex. Thus, for example, the Global Initiative on Obstructive Lung Disease advises that mild COPD exists where the measured FEV1/FVC ratio is less than 70% in the presence of a ‘normal’ (>80% predicted) FEV1. More severe disease is suggested by an FEV1/FVC ratio less than 70% and lower values of FEV1 such that measurements between 50 and 79% of the predicted value indicate ‘moderate’ COPD and lower values ‘severe’ or ‘very severe’ disease. There are innate problems with this approach. First, FEV1/FVC ratio declines with age and using a fixed ratio as the cutoff will tend to under-diagnose airflow limitation in the young and over-diagnose it in the elderly. FEV1 declines with age in both men and women but its variance does not; thus proportionate (‘% predicted’) methods of labeling ‘normality’ and ‘abnormality’ will lead to an over-diagnosis of obstruction in those with smaller absolute FEV1 values reflective of their age. A more meaningful approach would take advantage of the normal distribution of FEV1 at any age so that, for example, only spirometric values which lay two or more standard errors away from the predicted mean would be considered ‘abnormal’. This approach is not commonplace yet but is likely to become so in the near future. A second difficulty with purely spirometric approaches to the diagnosis of COPD arises in the situation – not uncommon in working populations – where an individual has an ‘abnormally’ large FVC but a ‘normal’ or mildly sub-normal FEV1; their spirometry will thus appear, at times wrongly, to be obstructed. Finally, single measurements of spirometry are representative only of the present and tell the clinician nothing about the past. Patients with apparently normal values may, a few years previously, have had higher values and thus be suffering an accelerated decline in lung function that cannot be detected without access to serial measurements. Most diagnostic algorithms for COPD include, in addition to the measurement of simple lung function, the presence of symptoms. These are typically of breathlessness (which may crudely be quantified) and/or of persistent sputum production (‘chronic

PNEUMOCONIOSIS

5

bronchitis’). Accompanying emphysema is sometimes apparent on a simple chest radiograph but is detectable with far greater sensitivity on CT scanning. Evidence of a reduction of oxygen uptake attributable to emphysema may be found through measurement of gas transfer (TLCO (DLco) and KCO) in the pulmonary function laboratory. The ‘fixed’ nature of the airflow obstruction in COPD is poorly responsive to pharmacological treatments but most physicians will advise a trial of inhaled bronchodilators with or without inhaled corticosteroids. Some patients respond well to oral corticosteroids but any improvement needs to be balanced against the likelihood of adverse ‘side effects’ of such treatment. The timely treatment of infective bacterial exacerbations is important as is prophylaxis with pneumococcal and annual influenza vaccination. Exercise – particularly if formalized as ‘pulmonary rehabilitation’ - is of proven benefit in improving function and reducing breathlessness, reflecting the systemic nature of disability in COPD.

Bronchiolitis COPD that arises from cigarette smoking typically affects both small and large airways; and, unfortunately, a great deal of damage can be inflicted on the former before symptoms develop and any changes on simple spirometry are apparent. Some rarer forms of pulmonary obstructive disease affect more specifically the smaller airways. Bronchioles are those distal airways that do not contain cartilage in their walls and have a diameter of less than 2–3 mm. Bronchiolar inflammation (‘bronchiolitis’) arises from a large number of causes which include the inhalation of irritant fumes, dusts or gases usually, but not necessarily, at high intensities. The eventual result may be ‘obliterative bronchiolitis’ (or ‘bronchiolitis obliterans’) in which there is irreversible occlusion of the small airways. In some cases the inflammatory response will include adjacent air spaces, a form of organizing pneumonia. Obliterative bronchiolitis presents with breathlessness and is easily mistaken for COPD. The distinction is generally made using high-resolution pulmonary CT scanning in which bronchiolitis can be detected by a mosaic pattern of oligaemia and by evidence of expiratory air trapping. In some cases, transbronchial or surgical biopsy is required. There is no clearly effective treatment for obstructive bronchiolitis but most physicians will offer a trial of treatment with oral and/or inhaled corticosteroids. Unless there is clear evidence of benefit, such treatments should not be prolonged.

Pneumoconiosis ‘Pneumoconiosis’ is yet another rather unsatisfactory respiratory disease label. Strictly it means nothing more than a disease of the lung caused by the deposition of dust but most specialists would restrict the term to conditions of diffuse, nonmalignant – sometimes fibrosing – parenchymal lung disease caused by occupational exposures to mineral dusts. Much, but not all, pneumoconiosis is apparent on chest radiography. The adjective ‘simple’ is used when the radiographic abnormalities are discrete and separated by areas of normal tissue; ‘complicated pneumoconiosis’

6

INTRODUCTION

(sometimes called ‘progressive massive fibrosis’) describes disease where the changes are confluent. There are corresponding degrees of breathlessness and lung function abnormality. Many airborne dusts that are inhaled at work remain in the lung but their effects are very variable, determined in large part by their innate toxicity and the kinetics of their excretion, but also by factors such as particle size, by co-exposures to other toxic substances, notably cigarette smoke, and by differences in individual susceptibility. Some mineral dusts or fumes – such as those from tin – cause little or no pulmonary damage but because they are highly radio-dense produce an alarmingly abnormal chest radiograph. Others – most infamously, asbestos – are innately fibrogenic while others (silica, coal dust, kaolin) cause disease by largely non-fibrogenic means. The pathological and radiological patterns of different types of pneumoconiosis are sometimes characteristic. Inhaled beryllium, for example, uniquely induces a pulmonary granulomatosis akin to idiopathic sarcoidosis; and cobalt, encountered in ‘hard’ metals, induces pulmonary fibrosis characterized by the presence of ‘giant cells’ in lung tissue or lavage specimens. In most cases the starting point in the diagnosis of a pneumoconiosis is – on a background of a history of occupational dust exposure – the presence of an abnormal chest radiograph. Again the patterns are often characteristic but a detailed description of each is beyond the scope of this book. Importantly, CT scanning of the lungs is a far more sensitive technology and will detect abnormalities that are not visible on a plain radiograph. The correlation between radiological abnormalities and functional limitation is imperfect. Minor degrees of (simple) pneumoconiosis, visible on a chest X-ray film, rarely give rise themselves to symptoms, changes in lung function or reductions in longevity. With more extensive disease, symptoms of breathlessness and cough develop and are accompanied by abnormalities in lung function. These latter are classically ‘restrictive’ with concomitant reductions in both FEV1 and FVC and an increased FEV1/FVC ratio. In practice these are often obscured by evidence also of ‘obstructive’ airflow limitation (generally from many years of cigarette smoking) so that a ‘mixed’ picture emerges. More sophisticated testing will often reveal deficiencies in gas transfer due to even minor pulmonary fibrosis or emphysema. Pneumoconiosis may be complicated by the development of other respiratory diseases. Silicosis, for example – and possibly even silica exposure alone – increases the risk of pulmonary tuberculosis, especially in settings where the latter is endemic. Coal workers’ pneumoconiosis, in those with sero-positive rheumatoid arthritis, may be complicated by the development of large, rounded ‘rheumatoid’ shadows in the midzones of the chest radiograph, so-called Caplan’s syndrome. Asbestosis, and perhaps asbestos exposure without evidence of pulmonary fibrosis, increases the risk of lung cancer in smokers and non-smokers, although the effect is much stronger in those who smoke. Any extensive pneumoconiosis – but most commonly asbestosis – may be complicated by the development of pulmonary hypertension, which is often the explanation of abrupt clinical deterioration. The management of pneumoconiosis is both limited and non-specific. The disease is generally of long latency and many patients will be retired from work at the time of their diagnosis. Those who are still working should be advised that further exposure is detrimental. Other treatment is entirely supportive; immunosuppressive therapies used

LUNG CANCER AND MESOTHELIOMA

7

in other forms of pulmonary fibrosis have no proven benefit in pneumoconiosis. In rare cases lung transplantation is offered.

Lung cancer and mesothelioma Most lung cancers arise in bronchial epithelial cells; squamous cell carcinomas account for about 40% of all male cases and about 30% of those in women. Most other types are either adenocarcinomas (20 and 40% respectively) or small cell carcinomas (20%). Rarer pulmonary tumors include ‘large cell’ and alveolar cell types. There is no clear evidence that the histological type correlates with etiology. Lung cancer tends to present ‘late’ and usually beyond a time when curative (surgical) treatment would be effective. Common presentations include a persistent cough, hemoptysis, pneumonia (a result of bronchial obstruction), pleural effusion or an abnormality on chest radiograph. The diagnosis is generally confirmed by a combination of cytological sputum examination, bronchoscopy with biopsy and more extensive radiology including, in some instances, the use of CT-PET scanning. The distribution of presentations and diagnostic methods is likely to change if there is increasing use of population-based screening for lung cancer. Except in those cases where complete resection is both appropriate and feasible, the treatment of lung cancer is not curative; it often includes the use of chemotherapy and radiotherapy alongside symptomatic treatment. Most cases of lung cancer occur in cigarette smokers which, as with COPD above, often makes it difficult to establish with any certainty an additional or alternative etiological explanation; this is particularly true in individual cases. Thus most of the evidence concerning other causes is derived from large-scale epidemiological studies – in almost all cases of occupationally exposed populations. There is very little evidence in relation to other ‘environmental’ exposures. An exception is mesothelioma, a highly malignant disease of the pleura. In almost all cases, this tumor arises as a result of exposure to asbestos, and particularly to amphibole types of asbestos (crocidolite, amosite and anthophyllite), with a latency of 30–40 years. In most cases the exposure is acquired at work (particular attention should be paid to occupations before the age of 30) but sometimes vicarious exposure – for example to the dusty overalls of a spouse or parent – is responsible. In many parts of the world – notably most of Europe, North America and Australasia – the import and use of asbestos have been banned since the early 1990s but the mineral is still used widely elsewhere. In countries where there has been no primary use for many years, most cases of mesothelioma arise in those who worked in the construction/refurbishment industry, their exposure being to asbestos used in buildings erected in the decades before any ban. This trend is predicted to continue, and indeed accelerate, for 10 years or more and, importantly, give rise to an increasing proportion of patients with mesothelioma who do not recall a clear history of asbestos exposure. As with other types of respiratory cancer, mesothelioma tends to present late and in a state of advanced growth. The median life expectancy after diagnosis is about 14 months; in some instances it is much longer, presumably reflecting disease that was ascertained at an earlier stage. There is no curative treatment for mesothelioma.

8

INTRODUCTION

Attribution Most patients are interested in the cause of their respiratory disease, a concern that is shared by many physicians and presumably all those who will use this book. Sometimes a cause is readily apparent; this is generally the case, for example, for infective and congenital respiratory diseases. In many other instances establishing etiology is less straightforward and, especially in the case of diseases that are common and at a population level have several important risk factors, it may in the individual case be essentially impossible. Thus, and uncomfortably for all concerned, the only honest answer to the question ‘is X responsible for my illness?’ has to be, in many cases, ‘I don’t know’. Such nihilism is not, however, always necessary and the prime purpose of this book is to help the physician determine, in a wide variety of circumstances, which diseases need to be considered, how they might be recognized or excluded, and how secure is the evidence that each may be attributed to an environmental exposure. Before embarking on a search for an environmental explanation, the wise doctor will have already considered the consequences of arriving at one; and the penalties of reaching the wrong one. For some respiratory diseases, both the consequences and any penalties are fairly trivial. The prescription of an antibiotic for acute bronchitis, for example, presumes a diagnosis of bacterial infection even if the physician knows that in most cases a viral cause is more probable. In the individual case – even if not at a global level – the issue matters little since most antibiotics are effective, cheap and safe and need not to be taken for very long; and most viral infections of the airways are self-limiting. Whether or not the infection is bacterial, most patients will rapidly and comfortably recover. In other cases, of course, the risk–benefit equation is more complex as is frequently the case when considering occupational or environmental issues. A diagnosis of occupational asthma, for example, generally leads to a change, and too often a loss, of employment. If the diagnosis is correct then this can be at least partly offset by the likelihood of improvement in the condition and its prognosis. It is not difficult to see, however, that a mistaken diagnosis can be disastrous and arguably worse than a missed diagnosis. Thus in this case the physician owes their patient a very high standard of certainty. A similar situation applies to diagnoses that demand an important change in lifestyle, such as the renovation of a damp home or a change in residence (or schooling) altogether. In other cases a lesser standard of proof may be acceptable. For example, it may matter little to the ex-baker who has decided that he will never again work in a bakery, whether or not his asthma was caused by his previous employment. The same may be the case for patients with other occupational diseases of long latency or for those who do not much mind abandoning a hobby or losing a pet; or even for those who have no intention of avoiding the exposure that is responsible for their disease. Balanced further against these considerations are often issues of compensation, whether sought through civil action or through the state. It is incumbent on all those who look after patients with occupational diseases at least that they be familiar with their local jurisdiction in this respect; and to remember that a weak diagnosis is likely to make a weak case in the courts. It is usually best to be honest and open, and it is our experience that most patients are perfectly happy to listen to and discuss such issues but that they may need time enough to do so. It is very rarely the case that such matters need to be decided in any hurry.

ATTRIBUTION

9

Figure I.1 A hierarchy of attribution in occupational lung diseases

Finally, we address the question of ‘certainty’. How certain is it possible to be when considering an environmental cause of respiratory disease? The simple answer is that it depends; the more complex answer is illustrated in Figure I.1, where we present a ‘hierarchy’ of attribution using occupational causes of lung disease as examples. .

At the top of the hierarchy we have placed ‘catastrophic’ events where an occupational exposure is followed rapidly by the onset of respiratory disease. Examples include asphyxiation or ‘toxic pneumonitis’ in the immediate aftermath of a heavy exposure to irritant fumes in the workplace. Here – on the basis of both the time relationship and the biological reasonability of the outcome – the establishment of cause and acute effect is secure, although effects may be worsened by pre-existing disease. If this seems obvious to the reader, we ask them to consider the question of other outcomes – such as asthma or ‘chemical sensitivity’ – following similar exposures, either of which could have other explanations.

.

Below this we place the few instances where it is possible, with a reasonable degree of certainty, to demonstrate a cause–effect relationship. The prime example here is occupational asthma where a casual relationship with a workplace exposure can usually be observed through the use of serial lung function measurement or specific provocation testing.

.

The third setting where attribution is generally possible at an individual level is where the disease is (relatively) specific to an occupation. While it is true that, as with most organs, the lung has a limited repertoire of reactions to adverse exposures, there is still a reasonably long list of ‘peculiar’ patterns of response. Many types of pneumoconiosis, pleural plaques in certain distributions and mesothelioma are examples of diseases that have both characteristic features and a very rare occurrence outside the occupational context. In these cases, attribution is relatively straightforward and can be achieved with a reasonable degree of certainty.

10

INTRODUCTION

.

The final two levels in the hierarchy describe situations where certainty is far less clear. The first, the ‘probabilistic’, refers to settings where the disease in question is both non-specific and has other important determinants but where there is consistent epidemiological evidence of a independent workplace risk. Where, under certain circumstances of exposure, this risk is more than doubled then it is possible to claim that, for a patient with such a level of exposure, it is more likely than not that, on average, their disease can be attributed to their occupation. Note that any greater degree of certainty is rarely possible and that certainty in the individual case is impossible. Examples in this category include COPD in coal miners with histories of extensive work underground, emphysema in those who have worked with cadmium fumes, and lung cancer in those with heavy exposure to asbestos.

.

In too many instances, there is insufficient epidemiological evidence to make even this level of certainty possible and here the clinician has nothing more to rely on than ‘analogy’. This is the case, for example, in most patients with COPD who have smoked but who also have a history of exposure at work to ‘dusts’ or ‘fumes’. While there is reasonable evidence that such exposures increase the rate of COPD at a population level, very few risk estimates are above 2, their relationship to smoking is unclear and there is very little information on specific exposures. Here attribution can only ever be weak at best.

In summary, the diagnosis of occupational lung disease can be challenging. Suspicion of an occupational cause should start with the primary care physician. Referral to an occupational lung specialist may be needed for complex cases but, for many cases, general internists, and especially other specialists such as respiratory physicians (pulmonologists), allergists and occupational medicine physicians can provide diagnosis and management.

Further reading Fishwick, D., Barber, C.M., Bradshaw, L.M., Harris-Roberts, J., Francis, M., Naylor, S., Ayres, J., Burge, P.S., Corne, J.M., Cullinan, P., Frank, T.L., Hendrick, D., Hoyle, J., Jaakkola, M., Newman-Taylor, A., Nicholson, P., Niven, R., Pickering, A., Rawbone, R., Stenton, C., Warburton, C.J., Curran, A.D. (2008) Standards of care for occupational asthma. Thorax 63: 240–250. Gibson, G.J., Geddes, D.M., Costabel, U., Sterk, P.J., Corrin, B. (2003) Respiratopry Medicine, 3rd edn. Saunders: London. Lacasse, Y., Selman, M., Costabel, U., Dalphin, J.C., Ando, M., Morell, F., Erkinjuntti-Pekkanen, R., Muller, N., Colby, T.V., Schuyler, M., Cormier, Y. (2003) Clinical diagnosis of hypersensitivity pneumonitis. Am. J. Respir. Crit. Care Med. 168: 952–958. Newman Taylor, A.J., Nicholson, P.J., Cullinan, P., Boyle, C., Burge, P.S. (2004) Guidelines for the Prevention, Identification and Management of Occupational Asthma: Evidence Review and Recommendations. British Occupational Health Research Foundation: London; available from: http:// www.bohrf.org.uk/downloads/asthevre.pdf Parkes, W.R. (1994) Occupational Lung Disorders, 3rd edn. Butterworth and Heinmann: Oxford. Tarlo, S.M., Balmes, J., Balkissoon, R., Beach, J., Beckett, W., Bernstein, D. et al. (2008) Diagnosis and management of work-related asthma. American College of Chest Physicians Consensus Statement. Chest 134: 1S–41S. The Global Initiative for Chronic Obstructive Lung Disease (GOLD); http://www.goldcopd.com/

Part I The personal environment

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

1 Cosmetics and personal care products in lung diseases Howard M. Kipen UMDNJ–Robert Wood Johnson Medical School, Piscataway, NJ, USA

1.1 Introduction: historical context of cosmetics and respiratory illness Cosmetics may be associated with respiratory illness through two different but overlapping mechanisms. One is via causation of pathological disease, most prominently related to allergen-mediated mucosal and airway responses. The second mechanism is through symptoms and illness behavior associated with odors from the cosmetics. The extent to which these symptoms may also interact with mucosal irritant properties of the agents makes differentiation between airway pathology and symptoms unrelated to airway pathology at times problematic. This chapter will describe the data supporting different disease mechanisms and appropriate clinical and preventive responses. A wide range of individuals, rather than typically ‘healthy workers’, regularly come into contact with personal care products such as soaps, perfumes and hair products. Many of these products are designed to announce their presence to those nearby (perfume odors), and they encompass a diverse array of chemical substances. Odordriven responses may be from the essential product, such as a perfume essence, or added material contained in a mix, such as fragrances added to a hairspray or after-shave. While behavioral effects of agents such as perfumes are intentional and legendary, the association of physical pulmonary conditions with cosmetic products was not reported until the late 1950s. Around 1960 a series of cases reporting a ‘storage disease’ (thesaurosis) or pneumonitis (‘hairspray lung’) were published. However a prevalent condition of the pulmonary parenchyma was never established (possibly due to various

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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changes in hairspray formulations) and all subsequent concern with respiratory effects of cosmetic and personal care agents has centered on the airways, particularly asthma. The first report of allergic occupational asthma in hairdressers is attributed to Jack Pepys [1] in 1976. The remainder of this chapter will consider both allergic airway disease from cosmetics and personal products and the more complex nonallergic responses to odors.

1.2 Epidemiological context 1.2.1 Occupational exposure to cosmetics and personal care products Data from the USA reveal the substantial size of the workforce involved in cosmetology. According to the US Bureau of Labor Statistics, barbers, cosmetologists and other personal appearance workers held about 790,000 US jobs in 2004. Of these, barbers, hairdressers, hairstylists and cosmetologists held 670,000 jobs; manicurists and pedicurists 60,000; skin care specialists 30,000; and shampooers 27,000. Because most of the relevant scientific literature pertains specifically to hairdressers, this term will be used for the remainder of the chapter. There is no available data on the number of individuals involved in the perfume industry. Although methods for ascertainment differ greatly between countries, the burden of airway disease in hairdressers has been quantitiated in many different nations. Methodologies of varying rigor, including some that are population-based, have documented apparent excesses of asthma and respiratory symptoms relative to the general population among hairdressers working in Sweden, France, Germany, Belgium, Norway, Turkey and Italy. A 2002 questionnaire study of all active Swedish hairdressers showed an asthma incidence rate ratio of 1.6 in never smokers, comparable to the effect of smoking alone in the same group. There was also a nonsignificant excess risk of asthma for self-reports of more frequent exposure to bleaching agents or hairsprays. Interestingly, there was no effect modification by reported atopy and no dose–response relationships for use of persulfates, at variance with much of the clinical data cited below that emphasize the role of persulfate exposure. Iwatsubo and colleagues [2] found no increased respiratory symptoms among hairdressing apprentices compared with office apprentices, but there was a significant decline in FEV1 and FEF25–75 (forced expratory flow), not linked to any specific hairdressing activities. Other studies from France are based on the voluntary national physician reporting program for occupational asthma (Observatoire National des Asthmes Professionels). French asthma incidence rates for hairdressers are 308/million, placing hairdressers at the third highest risk for occupational asthma after bakers and pastry makers (683/million) and car painters (326/million). In Belgium questionnaires completed by hairdressing students showed that 14.1% had already had asthma and 26.7% reported wheezing over the past 12 months. A 1996 study estimated that the burden of work-related asthma in Turkish hairdressers was 14.6%. In Italy about half of a group of hairdressers referred for work-related respiratory symptoms were found to have occupational asthma by specific inhalation challenge, along with a strong association with occupational rhinitis.

1.3 DESCRIPTION OF EXPOSURES

15

1.2.2 Non-occupational exposure to cosmetics and personal care products In a Danish nonoccupational population-based study that included methacholine challenge and skin prick testing it was found that there was no relationship between perfume-associated significant symptoms and atopy, serum ECP or FEV1. However, 42% of subjects reported ocular or airway symptoms from exposure to fragrance, and these 42% were 2.3 times as likely to have bronchial hyperreactivity (BHR) as those without symptoms, suggesting a link between fragrance responses and this defined physiological vulnerability. The fact that 30–40% of those who reported respiratory symptoms in this population-based study had a positive BHR test suggests the possible import of fragranceinduced symptoms, although physiological studies in vulnerable or symptomatic individuals, discussed below, suggest that these relationships are quite complex. Reported provocation of symptoms by environmental chemicals, prominently including perfumes and cosmetics, typically detected by odor, has been shown to be common, averaging about 10–20% of random samples with a range of 10–60% of more specific subpopulations, asthmatics being a prominent subgroup. A more extreme form of such reported sensitivity to chemicals is multiple chemical sensitivities (MCS) or idiopathic environmental intolerance (IEI). In this case the sensitivity to odors affects behavior and social interactions, becoming potentially disabling. No clear physiological abnormalities or explanations have been discovered. Although many clinicians and researchers favor psychological mechanisms for such odor-induced symptoms, there is substantial disagreement. Of particular interest to pulmonologists, individuals fitting the description of MCS seem to have a high rate of pulmonary symptoms. Although data come from clinical series, when compared with age- and sex-matched controls, MCS individuals reported on questionnaires from 1.5 to over 10 times the rate of upper and lower respiratory symptoms, and as suggested above, individuals with asthma report higher rates of provocation by cosmetics and personal care products.

1.3 Description of exposures 1.3.1 Major work processes Hairdressers, besides cutting and shampooing hair, are involved in permanent wave applications and rinsing, in applications of neutralizing agent, in preparing, applying and rinsing hair color, and in preparing, applying and rinsing hair bleaches. Mixing of bleaching powder takes 2–5 minutes per treatment, and it is thought that most exposure to persulfates occurs in this phase, often done in a back room of the salon, rather than during application in the salon per se.

1.3.2 Occupational exposures Hair dressers have three main classes of workplace exposures: 1.

para-phenylamine diamine based dyes, generally associated with delayed hypersensitivity contact dermatitis;

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CH 1 COSMETICS AND PERSONAL CARE PRODUCTS IN LUNG DISEASES

2. henna (vegetable dye), a rare cause of occupational asthma; and 3. lacquers and bleaching agents with persulfate salts, known to cause dermatitis, rhinitis and asthma. We focus on the latter for this respiratory disease text. There are three categories of hair-dye formulation used respectively for temporary, semi-permanent and permanent hair coloring. The latter are also known as oxidative dyes and are resistant to shampooing. The permanent dyes almost invariably contain ammonium, potassium and sodium persulfates. Persulfate salts are reactive, low-molecular weight compounds widely used in many industries, but particularly cosmetics. The persulfates (H2S2O8) are mixed with an oxidant (H2O2) immediately before use. Improved hair penetration is achieved with the addition of ammonia releasers such as ammonium chloride or ammonium phosphate. Permanent waving chemicals can be either alkaline or slightly acidic aqueous solutions. They contain thioglycolic acid or hydrogen peroxide, with ammonia added to enhance hair penetration. Thus, potent irritants/oxidants including ammonia, hydrogen peroxide (H2O2) and persulfates (H2S2O8) are commonly found in the hairdressing environment. Hair bleaching agents are generally felt to be the most common cause of occupational asthma in hairdressers; however not all studies report that duration of exposure was significantly greater in those who became sensitized. They are the leading causes implicated in specific occupational asthma reports from France and Italy.

1.3.3 Perfumes and nonoccupational exposures Perfumes are blends of odiferous ingredients made from a diluent (commonly ethanol) and mixtures of up to 3000 natural and synthetic fragrance ingredients including volatile oils and aldehydes, potential irritants and sensitizers. Because many of the ingredients are volatile, exposure is widespread, either intentionally or incidentally in proximity to users. Cleaning agents for home or commercial use are associated with asthma, and also contain perfume agents as well as cleaning agents that may be respiratory irritants or sensitizers.

1.3.4 Quantitation of exposures in hair salons In a Swedish study exposures to persulfates during mixing were associated with personal exposures of 35–150 mg persulfates/m3 and mixing area exposures ranged from 23–50 mg persulfates/m3. In a study of exposure in French salons, H2O2 showed mean personal exposure levels of 51 mg/m3, NH3 was 900 mg/m3 and persulfate was 190 mg/m3. These values are below applicable workplace standards, although many deficiencies in ventilation were noted in this study and would seem to be common in the industry.

1.4

EXPOSURE TO COSMETICS AND PERSONAL CARE PRODUCTS

17

1.3.5 Exposure history: practical advice and pitfalls It is important to understand the layout of a salon, including any separate rooms in which mixing of hair products takes place. Specific questions about windows or mechanical ventilation are important. Although ventilation in salons is often reported as substandard, in the rare instances when exposures have been measured, they have been typically less than applicable threshold limit values (TLV) (H2O2, NH3 and H2S2O8) on either side of the Atlantic. This may reflect that the salons studied were not completely representative of all salons. Of course, for individuals who have become sensitized, adherence to threshold limit values cannot be relied upon to prevent future reactions.

1.3.6 Documentation of exposure and biomonitoring Exposure monitoring in salons is not commonly performed, and measures of persistent body burden do not exist and are probably not appropriate to the natural history of the relevant conditions. Moscato [3] reports that, although some hairdressers with asthma have positive skin tests to persulfate, it is not a reliable test of sensitization, because many individuals with disease and apparent exposure have negative tests. As with other prominent causes of occupational asthma, especially for low molecular weight antigens, the available skin test is not clearly immunologically (IgE) mediated. One caveat is that anaphylaxis to persulfate skin testing has been reported.

1.4 Respiratory diseases associated with exposure to cosmetics and personal care products 1.4.1 Occupational asthma Occupational asthma in hairdressers is felt to arise most commonly from sensitization to persulfate salts, although there are case reports with henna as the sensitizer. Pulmonary function test changes and development of asthma are reported during apprenticeship, although latencies of up to 10–15 years appear in the literature. Most published descriptions of occupational asthma in hairdressers is of the allergic sensitization variant; however, there are a limited number of publications describing more immediate responses apparently independent of sensitization. The immunological basis of the sensitization has not been elucidated. One provocative study implicated hairsprays as triggers of pre-existing asthma. Schleuter and colleagues [4] studied immediate responses to hairspray in 1979. They reported a 10–20% decrease in mid flows in eight asthmatics, with no response in 13 healthy subjects to a 20 second spray of two hairsprays. The investigators attributed this bronchoconstriction response to the perfume content of the hairspray rather than the plasticizer, diethyl phthalate. However, this and other phthalates in indoor air from building products have been subsequently epidemiologically implicated in asthma induction, and they are still prevalent in hairspray at concentrations of up to 3%. Further examination of a potential role for phthalates in respiratory irritation and

18

CH 1 COSMETICS AND PERSONAL CARE PRODUCTS IN LUNG DISEASES

asthma is warranted, in both occupational and nonoccupational settings. For more information on the use of phthalates in cosmetics see: http://www.safecosmetics.org/ docUploads/NotTooPretty_r51.pdf

1.4.2 Responses to odors Cone and Shusterman [5] discussed the health effects of indoor odors. They emphasized variability in the human odor response, and that perfumes are a commonly reported exacerbating agent for asthma. The citation supporting the relationship between perfume and asthma derives from a commonly cited convenience sample of 60 asthmatics specifically recruited by Shim and Williams [6] with sensitivity to odors in mind. They documented that physiological responses to odor provocation could occur; and that atropine, beta agonists and cromolyn abrogated responses in three out of four subjects tested. However, subjects were not blind to test exposures and thus the response could have been perceptual rather than irritant. In fact, they raised the possibility of behavioral sensitization to odorants. The differentiation between irritant/ allergic airway effects as opposed to behaviorally or perceptually mediated effects is a recurring theme when considering the human (respiratory) response to cosmetics and personal care products. This differentiation is more frequently an issue in general environmental contexts rather than occupational contexts. Relationships have been documented in individuals among asthma symptoms, hay fever and chemical odorants. A number of well-controlled studies have shown that perfume stimuli induce respiratory symptoms in asthmatics but not always with accompanying physiological change. Millquist [7–9] exposed nonasthmatics, with a history of respiratory symptoms (but no airway obstruction) following nonspecific irritating stimuli, to perfume. She elicited respiratory symptoms (as well as hoarseness, eye irritation, headache and fatigue) without airway obstruction. The symptomatic responses persisted even after using a carbon filter to block odor. In a subsequent study of ocular exposure to perfume, she again elicited asthma symptoms, even in the absence of hyperventilation, as documented by stable end-tidal CO2. A sensory mechanism, possibly via the trigeminal nerve, was hypothesized, and this integrative approach is a promising avenue for further exploration of individual responses, as well as for therapy. Lastly, she exposed 10 asthmatics (all with provocative concentration for 20% fall in FEV1 < 2 mg/ml) to a commercial perfume and found no change in FEV1 compared with a saline exposure and no increase in symptoms. Similarly Opiekun et al. [10] studied mild and moderate asthmatics following a 30 minute controlled exposure to a prototypical fragranced air-sanitizing product. They found increased nasal symptoms, but there were no explanatory physiological changes in nasal mucosal swelling (measured by acoustic rhinometry), no ocular hyperemia, and no significant changes in FEV1 (other spirometric values were not reported) at 5 or 30 minutes after exposure. These investigations document that both asthmatics and nonasthmatics can respond to perfumes with respiratory symptoms, yet no significant bronchoconstriction. Making this determination between physiological airway responses and perceived respiratory distress can be challenging for the clinician. There are reports of those with immediate asthmatic (symptom) responses to perfume; however no analytic epidemiology addresses this issue per se. There is

1.5 OCCUPATIONAL ASTHMA IN HAIRDRESSERS

19

substantial literature on how professional cleaners/janitors and users of cleaning sprays have increased asthma morbidity; however this may be more associated with some of the cleaning agents as opposed to the scents and is addressed elsewhere in this book. Attempts to separate the effects of the alcohol vehicle from the active perfume ingredients have suggested that both may play a role in production of spirometric effects and symptoms, with more severe and atopic asthmatics showing greater responses to perfume challenge.

1.4.3 Unexplained symptoms and psychophysiological responses As suggested in Millquist’s work above, many individuals suffer from episodic respiratory symptoms, sometimes triggered by environmental exposures, but do not meet diagnostic criteria for asthma or other conditions: they do not have bronchospasm. Prominent among reported triggering exposures are cosmetics, with frequently described exposures including cosmetic counters at department stores, churches and office or classroom environments where coworkers use perfumes and other cosmetics. The limited epidemiology has been described above, but there are a number of pertinent clinical studies that have been carried out and suggest the importance of odor-triggered neural mechanisms as explanations for these symptoms. Van den Bergh suggested learned responses to odors of a Pavlovian nature that can be conditioned or deconditioned. A group in Toronto found that panic symptoms could be triggered by standardized stimuli much more readily in those with unexplained symptoms and suggested a relationship between unexplained symptoms, panic attacks and hyperventilation. Although this has not been studied in asthmatics, and does not directly concern perfume scents, it provides a potential mechanistic underpinning to understand individuals with complaints of respiratory distress attributed to scents, and suggests the design of behaviorally based therapeutic strategies where pathological pulmonary disease has been excluded.

1.5 Diagnosis and management of occupational asthma in hairdressers There are no randomized trials to guide diagnosis or management of occupational asthma in hairdressers. Diagnosis of occupational asthma in hairdressers is not always straightforward due to the lack of reliable markers of sensitization to persulfate salts as discussed above, but general methods have been reviewed [11]. Both immediate and delayed symptom responses are reported. Because an underlying IgE mechanism is not reliably demonstrated, immunological tests by skin prick or serum-specific IgE lack both sensitivity and specificity. Thus, reliable confirmation of clinical suspicion relies on specific inhalation challenge testing. Various techniques have been described, although such challenges are not in widespread use in many areas of the world, particularly the USA. Treatment of allergic occupational asthma is via standard protocols with avoidance of exposure at the top of the list. Once a diagnosis of occupational asthma in a hairdresser, usually to persulfate salts, has been made, exposure reduction or

20

CH 1 COSMETICS AND PERSONAL CARE PRODUCTS IN LUNG DISEASES

elimination is the most desirable therapeutic alternative. Use of respiratory protection is described but without apparent success, and improved hygiene of salons is often difficult to accomplish. In one study of eight cases, mean exposure duration prior to diagnosis was 15 years and mean duration of symptoms before diagnosis was 38 months, suggesting that improved surveillance could be a key to reducing morbidity.

1.5.1 Medical management of reactions to scented products Once physiological responses to environmental or occupational exposures have been excluded, a more difficult set of management challenges faces the practitioner. Pulmonary medications have little relevance unless there is comorbid asthma. Speech therapy or behavioral approaches may be useful for upper airway (vocal cord) dysfunction, which may be triggered by irritants and possibly nonirritating odors. Psychotherapy, anxiolytic medication, cognitive–behavioral therapy (CBT) and biofeedback have all been tried clinically, and have shown responses for individual cases in resolving respiratory and other symptoms associated with odiferous stimuli. More rigorous randomized trials have been conducted in broader groups of somatizing patients, and shown significant, 20–40%, improvement in symptoms and limitations, with courses of cognitive–behavioral therapy. Blind referrals to mental health practitioners are often ineffective. The referring pulmonologist must clearly communicate that organic lung disease has been excluded, freeing the mental health practitioner to concentrate on reducing symptomatic responses, possibly even in the face of continued exposure to moderate levels of nonsensitizing cosmetics. The ideal CBT takes place in the setting of a physician’s office, as some patients with these symptoms are reluctant to view their symptoms as psychological. It is sometimes useful to convey to the patient that they need to demonstrate the power of ‘mind over matter’, developing their mental strength to overcome as yet unidentified, but not lifethreatening, problems in their body.

1.5.2 Other illnesses Upper extremity musculoskeletal complaints are associated with work as a hairdresser, and can largely be addressed through client chairs that are adjustable in height. Use of nail cosmetics in nail salons is gaining increasing popularity worldwide. Although a number of irritant compounds are used, there are no reports of respiratory disease in the literature. Ethyl methacrylate, formerly used in artificial nail processing, has been linked to asthma. Its use is largely discontinued.

1.5.3 Medicolegal and compensation Individual countries and states vary in their system of compensation and requirements. In those places where specific inhalation challenge is a component of compensation evaluation, this bodes well for specific identification of cases, allowing for appropriate

FURTHER READING

21

compensation. In the USA, where specific challenge testing is not common, less direct evidence probably leads to less efficient, and likely more contentious, determinations.

1.5.4 Public health Some of the epidemiology has indicated an increased prevalence of asthma among hairdressing apprentices. In one study of hairdressers there was a mean of 38 months between symptom onset and diagnosis, accounting for fairly poor outcomes with persistent symptoms and a decline in FEV1, despite cessation of exposure. This emphasizes the importance of surveillance and early recognition of occupational disease if there is to be any confidence of avoiding long-term impairment. Development of nonsensitizing products for hair bleaching is clearly a goal.

References 1. Pepys, J., Hutchcroft, B.J., Breslin, A.B. (1976) Asthma due to inhaled chemical agents – persulphate salts and henna in hairdressers. Clin. Allergy 6(4): 399–404. 2. Iwatsubo, Y., Matrat, M., Brochard, P., Ameille, J., Choudat, D., Conso, F., Coulondre, D., Garnier, R., Hubert, C., Lauzier, F., Romano, M.C., Pairon, J.C. (2003) Healthy worker effect and changes in respiratory symptoms and lung function in hairdressing apprentices. Occup. Environ. Med. 60(11): 831–840. 3. Moscato, G., Pignatti, P., Yacoub, M.R., Romano, C., Spezia, S., Perfetti, L. (2005) Occupational asthma and occupational rhinitis in hairdressers. Chest 128(5): 3590–3598. 4. Schlueter, D.P., Soto, R.J., Baretta, E.D., Herrmann, A.A., Ostrander, L.E., Stewart, R.D. (1979) Airway response to hair spray in normal subjects and subjects with hyperreactive airways. Chest 75(5): 544–548. 5. Cone, J.E., Shusterman, D. (1991) Health effects of indoor odorants. Environ. Health Perspect. 95 53–59. 6. Shim, C., Williams, M.H. Jr. (1986) Effect of odors in asthma. Am. J. Med. 80(1): 18–22. 7. Millqvist, E., Bengtsson, U., L€ owhagen, O. (1999) Provocations with perfume in the eyes induce airway symptoms in patients with sensory hyperreactivity. Allergy 54(5): 495–499. 8. Millqvist, E., L€ owhagen, O. (1998) Methacholine provocations do not reveal sensitivity to strong scents. Ann. Allergy Asthma Immunol. 80(5): 381–384. 9. Millqvist, E., L€ owhagen, O. (1996) Placebo-controlled challenges with perfume in patients with asthma-like symptoms. Allergy 51(6): 434–439. 10. Opiekun, R.E., Smeets, M., Sulewski, M., Rogers, R., Prasad, N., Vedula, U., Dalton, P. (2003) Assessment of ocular and nasal irritation in asthmatics resulting from fragrance exposure. Clin. Exp. Allergy 33(9): 1256–1265. 11. Moscato, G., Galdi, E. (2006) Asthma and hairdressers. Curr. Opin. Allergy Clin. Immunol. 6(2): 91–95.

Further reading Albin, M., Rylander, L., Mikoczy, Z., Lillienberg, L., Dahlman H€ oglund, A., Brisman, J., Tor
en, K., Meding, B., Kronholm Diab, K., Nielsen, J. (2002) Incidence of asthma in female Swedish hairdressers. Occup. Environ. Med. 59(2): 119–123. Baur, X., Schneider, E.M., Wieners, D., Czuppon, A.B. (1999) Occupational asthma to perfume. Allergy 54(12): 1334–1335.

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Bornehag, C.G., Sundell, J., Weschler, C.J., Sigsgaard, T., Lundgren, B., Hasselgren, M., H€agerhedEngman, L. (2004) The association between asthma and allergic symptoms in children and phthalates in house dust: a nested case–control study. Environ. Health Perspect. 112(14): 1393–1397. Committee on the Assessment of Asthma Indoor Air (2000) Clearing the Air: Asthma and Indoor Air Exposures. Division of Health Promotion and Disease Prevention, Institute of Medicine: Washington, DC. Das-Munshi, J., Rubin, G.J., Wessely, S. (2007) Multiple chemical sensitivities: review. Curr. Opin. Otolaryngol. Head Neck Surg. 15(4): 274–280. Elberling, J., Linneberg, A., Dirksen, A., Johansen, J.D., Frølund, L., Madsen, F., Nielsen, N.H., Mosbech, H. (2005) Mucosal symptoms elicited by fragrance products in a population-based sample in relation to atopy and bronchial hyper-reactivity. Clin. Exp. Allergy 35(1): 75–81. Kipen, H.M., Fiedler, N., Lehrer, P. (1997) Multiple chemical sensitivity: a primer for pulmonologists. Clin. Pulmon. Med. 4(2): 76–83. Kumar, P., Caradonna-Graham, V.M., Gupta, S., Cai, X., Rao, P.N., Thompson, J. (1995) Inhalation challenge effects of perfume scent strips in patients with asthma. Ann. Allergy Asthma Immunol. 75 (5): 429–433. Mun˜oz, X., Cruz, M.J., Orriols, R., Torres, F., Espuga, M., Morell, F. (2004) Validation of specific inhalation challenge for the diagnosis of occupational asthma due to persulphate salts. Occup. Environ. Med. 61(10): 861–866. Mounier-Geyssant, E., Oury, V., Mouchot, L., Paris, C., Zmirou-Navier, D. (2006) Exposure of hairdressing apprentices to airborne hazardous substances. Environ. Health 5: 23. Tarlo, S.M., Poonai, N., Binkley, K., Antony, M.M., Swinson, R.P. (2002) Responses to panic induction procedures in subjects with multiple chemical sensitivity/idiopathic environmental intolerance: understanding the relationship with panic disorder. Environ Health Perspect. 110 (suppl. 4): 669–671.

2 Passive smoking Maritta S. Jaakkola University of Oulu and Oulu University Hospital, Oulu, Finland

2.1 Introduction Passive smoking is defined as exposure of a (nonsmoking) person to tobacco combustion products from smoking by others. Several synonyms are used in the literature, including involuntary smoking, exposure to environmental tobacco smoke (ETS) and exposure to second-hand smoke (SHS). SHS exposure has been recently recommended as the term to be used, for example by the Tobacco Free Initiative of the World Health Organization [1]. The term ETS was previously used widely, but it seems to have been introduced originally by the tobacco industry and it is recommended to be used less, as it can obscure the preventable nature of this exposure. The term ‘involuntary’ could imply that voluntary smoking would not be as bad for the health, so this term will also be used less in the future. Passive smoking is still common in homes, workplaces and public places in many countries, although in recent years there has been some progress, with increasing number of countries introducing smoke-free workplace legislation and other tobacco control measures. Some studies have suggested that smoke-free workplaces also reduce smoking at home, and thus lead to reduced passive smoking at home [2]. This may be explained by both increased awareness of the adverse health effects of passive smoking and the reduced active smoking detected in many studies as a consequence of the legislation. However, it is not possible to introduce legislation to protect directly those who are most vulnerable to the harmful effects of SHS exposure at home, i.e. infants, children and the elderly. To protect the health of these susceptible population groups, it is important to increase emphasis on educating people about the adverse effects of passive smoking, and to support smokers to quit or at least to behave in a way that does not expose others to tobacco smoke. In this work, healthcare personnel are among the key players.

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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CH 2 PASSIVE SMOKING

This chapter will first introduce definitions related to passive smoking and describe exposure to tobacco smoke, then review the current knowledge on health effects of SHS exposure in children and adults, and finally discuss clinical applications and preventive measures. In reviewing health effects, assessment of whether the relation between SHS exposure and the health condition is causal is based on the criteria usually used by the recent reviews. These include: (i) the number of studies that have been published on the topic and whether these studies come from different parts of the world; (ii) consistency of findings; (iii) validity of the studies, including control for confounding factors (i.e. other risk factors) and potential biases; (iv) evidence of an exposure–response relation (also called a dose–response relation); (v) evidence of biologically plausible mechanisms; and (vi) evidence of meaningful temporal relation. The best estimate of the effect is given based on recent meta-analyses, which have combined the results of studies published on the health outcome in question. If such a summary estimate is not available, the best effect estimate is given based on a recent, high-quality study.

2.2 Exposure to second-hand smoke 2.2.1 Definitions and constituents of tobacco smoke Second-hand smoke is composed of sidestream smoke (SS), which is formed from the burning of tobacco products and emitted directly into the environment from the smouldering end of the cigarette between puffs, and exhaled mainstream smoke (MS), which is first inhaled by the smoker before being released into the environment. Other smaller contributors to SHS include smoke that diffuses through the wrapper of the cigarette and smoke that escapes while the smoker inhales. SS is the principal constituent of SHS. Tobacco smoke is a mixture of thousands of chemicals released into the air as gases, vapors and particles [3]. Over 4000 individual constituents have been identified and these include more than 50 carcinogenic substances as well as many toxic and irritant compounds [4,5]. In addition, several compounds have adverse effects on reproduction. Many constituents are released in higher concentrations in SS than MS because of different burning conditions and less complete combustion of SS. Thus, SS contains higher concentrations of many harmful substances, but is usually then diluted into a larger volume (Table 2.1) [6]. The US National Toxicology Program estimated that at least 250 chemicals in SHS are known to be toxic or carcinogenic. In addition, it is possible that exposure to the mixture of different compounds in SHS is more harmful to health than exposure to any of the individual chemicals, as the compounds may have synergistic effects, i.e. they may have together a larger effect than would be expected from summing up the effects of individual compounds [7]. There is some evidence suggesting that evaporation of biologically less active components may cause aged sidestream smoke to be more toxic on a weight-for-weight basis. SHS exposure usually means passive smoking by nonsmokers. However, smokers are exposed to particularly high concentrations of sidestream smoke, because their own smoking is the major source of it and because they spend more time in smoky environments. Thus, SS may contribute to the adverse health effects detected in active

25

2.2 EXPOSURE TO SECOND-HAND SMOKE

Table 2.1 Emissions of selected tobacco smoke constituents in fresh, undiluted mainstream smoke (MS) and diluted sidestream smoke (SS) from nonfiltered cigarettes [6] Constituent

Amount in MS per cigarette

SS:MS ratio

12–48 mg 1.7 ng 4.6 ng 20–80 ng

5–10 30 2–4 13–30

12–23 mg 70–100 mg 60–100 mg 100–600 mg

2.5–4.7 0.1–50 8–15 4–10

Established carcinogensa Benzene 2-Naphthylamine 4-Aminobiphenyl Nickel Toxic or irritant Carbon monoxide Formaldehyde Acrolein Nitrogen oxides IARC category 1 ¼ carcinogenic to humans.

a

smokers, but as this has not been studied much, this chapter will focus on the health effects of passive smoking in nonsmoking populations, which have been studied extensively. It should be noted that a fetus can be exposed to tobacco smoke by either the mother’s active smoking during pregnancy or a nonsmoking mother’s exposure to SHS. Both of these influence the development of the fetus, as tobacco smoke constituents are transferred across the placenta, so both of them result in fetal passive smoking. This chapter will focus on fetal passive smoking from the mother’s SHS exposure during pregnancy.

2.2.2 Sources of SHS exposure For young children, smoking adults at home, especially the parents, form the principal source of SHS exposure. With increasing age, other places contribute as sources of SHS exposure: first day-care facilities and then school and many social environments. Among adults, home and workplace are the major sources of SHS exposure, because of the long time periods usually spent in these environments. However, some social environments, such as bars, restaurants and public transport, have been found to have particularly high concentrations of SHS. This chapter will focus on SHS exposure at home. It will briefly also mention SHS exposure at work, but other chapters will discuss SHS exposure in other environments.

2.2.3 Occurrence of SHS exposure The prevalence of SHS exposure varies considerably between countries and is influenced by the prevalence of active smoking, the traditions and behavioral cultures, the tobacco control legislation and the healthcare and educational systems. Multicenter studies from North America and Europe have measured cotinine in body fluids as an indicator of passive smoking and found that, in the 1980s, more than 80% of the

26

CH 2 PASSIVE SMOKING

nonsmoking populations were exposed to SHS. They also showed an alarming trend for the highest exposures to be detected in children and young adults. Today there is more variability in SHS exposure within Europe and between different states of the USA, as some countries and states have adopted smoke-free workplace and other forms of stricter tobacco control legislation, while others have not yet taken these preventive steps. For example, estimates of the prevalence of passive smoking of children from Europe have ranged from 7–15% in Finland and Sweden to 70–75% in Bulgaria and Poland. SHS still remains the most important preventable indoor exposure even in many high-income countries. The smoking epidemic in low-income countries seems unfortunately to continue, meaning that a high proportion of children in such countries are exposed to SHS. These children may be especially vulnerable to the harmful effects of SHS, as they may suffer also from malnutrition and may be exposed to other harmful compounds, for example from use of solid fuels that may act synergistically with SHS. WHO has databases on smoking prevalences and tobacco control legislations across the world (http://www.who.int/tobacco/global_data/en/index.html).

2.2.4 Measuring exposure to SHS Exposure to SHS can be assessed using different methods depending on the purposes of the measurements [7]. The most direct method to measure SHS exposure is to use personal monitors available for individual tobacco smoke components, such as nicotine or respirable suspended particles (RSP). However, this method requires a lot of labor, is rather expensive and only measures current exposure for a short interval. Individual tobacco smoke components can also be measured by fixed monitors in defined spaces. When combining the results of such measurements with information on time–activity patterns, an individual’s or a population’s exposure to SHS can be assessed. Again, this method only measures current exposure for a rather short interval, is expensive, and only measures exposure to specific compounds rather than to the entire mixture. However, such measurements may be useful, for example, when assessing the effectiveness of smoke-free workplace policy. Studies of health effects have most commonly applied questionnaires or diaries to assess SHS exposure. These methods have the advantages of being cheap and providing the possibility to measure long-term exposure which may be more relevant for many health effects [8]. Questionnaires can also inquire into past exposures. This is the relevant exposure, for example, when investigating lung cancer, as the relevant exposure has taken place at least 10 years earlier because of the long lag time. A potential problem related to questionnaires and diaries is whether people remember and report their exposures correctly. Many studies that have compared questionnaires with other exposure assessment methods suggest that questionnaires provide valid information, i.e. the majority of people report correctly whether they have been or have not been exposed to SHS, but that the exact quantification of exposure may not be very precise. However, it is still likely that people are able to recall rather well whether they have been exposed heavily or lightly. Another way to assess exposure to SHS is to measure biomarkers, i.e. compounds, their metabolites, hemoglobin or DNA adducts in biological samples, which are influenced by the uptake, metabolism and elimination mechanisms in addition to

2.3 HEALTH EFFECTS OF PASSIVE SMOKING IN CHILDREN

27

the exposure concentration. These may give relevant information about exposure to some target organs. The most commonly measured biomarker of tobacco smoke is cotinine in serum, saliva or urine. Cotinine is a major metabolite of nicotine. Its half-life is about 20 h, so it measures only recent exposure over the last 1–3 days. As a consequence of this, it may not be good assessment method for diseases for which long-term exposure is relevant. Hair nicotine concentration has been measured in some recent studies and seems to reflect exposure over the last 2 months. Some studies have also measured biomarkers of the carcinogenic substances, for example amino biphenyl hemoglobin adduct. Biomarkers are indicators for total exposure across different microenvironments, including home, workplace and social settings. For health effect studies, it has been recommended to use a combination of a questionnaire and some other method, if there are enough resources available.

2.3 Health effects of passive smoking in children Children are more susceptible to the adverse effects of SHS than adults for several reasons. Their respiratory system is not fully mature at birth and continues to develop both immunologically and physiologically. Children have higher breathing rate and inhale more air per body volume than adults, which results in higher exposure with a similar SHS concentration. In addition, children’s liver metabolism and other clearing mechanisms are not yet fully developed, so the harmful substances remain longer in the body. Some studies have suggested that children who were exposed to tobacco smoke in utero through either active or passive smoking by the pregnant mother are at greater risk for developing SHS-related diseases later, so tobacco smoke exposure in the very early phases of lung development may also make children more vulnerable later in life. This section will first discuss health effects related to SHS exposure from the mother’s passive smoking during pregnancy and then health effects related to the child’s passive smoking after birth. However, these exposures are highly correlated, as is maternal smoking during pregnancy and the child’s postnatal SHS exposure, so it has not been easy to disentangle the effects of these exposures.

2.3.1 Health effects of mother’s passive smoking during pregnancy Health effects related to mothers’ SHS exposure during pregnancy are summarized in Table 2.2. Lung function impairment Maternal smoking during pregnancy has been linked to reduced lung function in infants in many studies. According to recent reviews [5,9], there is also evidence of adverse effects of maternal passive smoking during pregnancy on the child’s lung function. However, as the number of studies looking at this question is limited, no definite conclusions concerning effects of mother’s SHS exposure during pregnancy on child’s lung function can be made.

28 Table 2.2

CH 2 PASSIVE SMOKING

Summary of health effects of mothers’ passive smoking during pregnancy

Condition

Best estimate of OR or RR

Reduced lung function Asthma Low birth weight Preterm delivery Other developmental effects

— — 1.2 1.57 —

95% Confidence interval

1.1–1.3 1.35–1.84

Reference

Causality (scale 0 to þþþ )a

[5] [9] [10] [11] [5]

þ þ þþþ þþ þ

0 ¼ no evidence of a relation between passive smoking and this condition; þ ¼ some evidence of a relation between passive smoking and condition; þ þ ¼ strong but not definitive evidence of a causal relation between passive smoking and condition; þ þ þ ¼ established causal relation between passive smoking and condition.

a

Asthma Maternal smoking during pregnancy has been strongly linked to the risk of childhood asthma [12], but again, the overall number of studies looking at the effects related to mother’s SHS exposure during pregnancy is limited [9]. Low birth weight Active smoking by the mother is a well-known cause of low birth weight (LBW). There is increasing literature also on nonsmoking mothers’ exposure to SHS and low birth weight [9,13]. Low birth weight has usually been defined as birth weight <2500 g either preterm or at full term (
37 weeks of gestation) birth. When LBW occurs at full term, it means that the fetal growth was reduced and the outcome is called small for gestational age (SGA). A review of this topic by US Surgeon General in 2006 [5] identified 43 cohort and three case–control studies on LBW or SGA. The most recent meta-analysis included 19 studies and gave a summary risk ratio of 1.2 (95% confidence interval, CI, 1.1–1.3), meaning a 20% excess risk in children of exposed mothers [10]. The average effect on birth weight was estimated as 28 g (41 to 16) in exposed infants compared with unexposed infants. The overall judgment based on recent reviews is that mothers’ passive smoking is causally linked to low birth weight of the infant [5,9,11,13]. This causal effect seems to be a consequence of reduced oxygen in the fetus, which is attributable to CO exposure from SHS and nicotine-induced vasoconstriction, leading to reduced blood flow of uterus, placenta and umbilical cord. Preterm delivery and other developmental effects The other pregnancy outcome that has been linked to mother’s passive smoking is preterm delivery, defined as <37 completed weeks of gestation [13]. The strongest evidence comes from a population-based Finnish study that found an OR of 1.30 (95% CI 0.30–5.58) for SHS exposure in the middle range and 6.12 (1.31–28.7) for the highest SHS exposure based on nonsmoking mother’s hair nicotine concentration [14]. The recent meta-analysis by California Environmental Protection Agency [11] gave a summary relative risk of 1.57 (1.35–1.84) for preterm delivery, meaning 57% excess risk in children of exposed mothers. However, not all studies have found consistent results, so more studies are needed before definite conclusions on causality of preterm delivery can be made. Other developmental effects that have been linked to mothers’ passive smoking include spontaneous abortion and perinatal death, congenital malformations and

29

2.3 HEALTH EFFECTS OF PASSIVE SMOKING IN CHILDREN

impaired neuropsychological and physical development, but because of limited evidence, no definite conclusions can be made concerning the strength of these relations [5]. Maternal SHS exposure has also been linked to increased persistent pulmonary hypertension of the newborn.

2.3.2 Health effects of passive smoking in childhood The first studies reporting a link between parental smoking and respiratory disease in children were published in the early 1970s. Since then abundant evidence on adverse health effects of SHS exposure in childhood has accumulated. This is summarized in Table 2.3. Acute lower respiratory illnesses More than 100 studies from different parts of the world have been published on parental smoking in infancy and early childhood and the risk of the child’s acute lower respiratory illness. These have consistently shown an increased risk of acute lower respiratory illnesses, including respiratory infections such as acute bronchitis, bronchiolitis, respiratory syncytial virus infections and pneumonia, and in some studies also symptoms of the lower respiratory tract [5,9,11]. There is evidence of an

Table 2.3

Summary of health effects of passive smoking in childhood

Condition

Best estimate of OR or RR

95% Confidence interval

Reference

Causality (scale 0– þþþ )a

Acute lower respiratory illness Acute otitis media Recurrent otitis media Chronic middle ear effusion Chronic wheeze Chronic cough Chronic phlegm Breathlessness Induction of asthma Exacerbation of asthma SIDS Childhood cancers Neurobehavioral disorders

1.59 1.38 1.37 1.33 1.26 1.35 1.35 1.31 1.32 — 1.94 — — Effect estimate (%b)

1.47–1.73 1.21–1.56 1.10–1.70 1.12–1.58 1.20–1.33 1.27–1.43 1.30–1.41 1.14–1.50 1.24–1.41

[5] [11] [5] [5] [5] [5] [5] [5] [11] [11] [15] [5] [11]

þþþ þþþ þþþ þþþ þþþ þþþ þþþ þþþ þþþ þþþ þþþ þ þ

[5] 1.15 0.32 4.76

1.56 to 0.75 0.71 to 0.08 6.35 to 3.18

þþþ

Lung function impairment FEV1 FVC MEFR

1.55–2.43

95% CI

0 ¼ no evidence of a relation between passive smoking and condition; þ ¼ some evidence of a relation between passive smoking and condition; þ þ ¼ strong but not definitive evidence of a causal relation between passive smoking and condition; þ þ þ ¼ established causal relation between passive smoking and condition. b Percentage difference of lung function in children exposed to SHS compared with unexposed children. a

30

CH 2 PASSIVE SMOKING

exposure–response relation, meaning that the risk of the disease increases with increasing amount of exposure, measured as the number of smoking parents and other household members or the number of cigarettes smoked at home. The most recent meta-analysis of these studies was conducted by the US Surgeon General [5] and gave a summary odds ratio of 1.59 (95% CI 1.47–1.73), suggesting an excess risk of 59% among children exposed to parental smoking. The risk related to mother’s smoking is higher (OR 1.72, 1.59–1.86) than that related to father’s smoking (OR 1.31, 1.19–1.43), but both maternal and paternal smoking increase significantly the child’s risk of getting lower respiratory illness. The higher risk from mother’s smoking could be explained by small children usually spending more time with their mother than with other adults, or by a synergistic effect between childhood maternal smoking and maternal smoking during pregnancy, as these often correlate. The risk from parental smoking seems to be highest in young children. For example in a meta-analysis by Li and co-workers [16], the summary RR was 1.71 (1.33–2.20) in children 0–2 years old. The smaller effect in older children has been explained by less time being spent in the presence of household smokers with increasing age as well as by maturation of the immune system of the child. In terms of biologically plausible mechanisms for the relation between passive smoking and lower respiratory illness, tobacco smoke is known to impair the immunological defense mechanisms as well as the function of airway cilia, both of which are likely to lead to increased susceptibility to infections. In addition, SHS has been shown to enhance bacterial adherence and disrupt respiratory epithelium, which is an important host defense barrier. In conclusion, all recent reviews have concluded that parental smoking is causally linked to increased acute lower respiratory illnesses, especially in young children [5,9,11]. Otitis media According to US Surgeon General’s Report in 2006 [5], 59 studies from different parts of the world have investigated the relation of parental smoking to middle ear disease in children. A causal association has been found with acute and recurrent otitis media as well as chronic middle ear effusion. The best estimates of relative risks from recent reviews are 1.38 (1.21–1.56) for acute otitis media and 1.37 (1.10–1.70) for recurrent otitis media in relation to either parent smoking, meaning 30–70% excess risk. The relative risk of chronic middle ear effusion is 1.33 (1.12–1.58). Potential mechanisms that underlie these relations include decreased mucociliary clearance leading to increased susceptibility to infections and Eustachian tube dysfunction due to mucosal swelling that can lead to accumulation of effusion in the middle ear [11]. Chronic respiratory symptoms Since the first studies on parental smoking and chronic respiratory symptoms in children were published in the early 1970s, a large number of studies on this topic from different parts of the world have been reported. The recent report by the US Surgeon General [5] included 88 studies in their quantitative overview. The summary relative risks related to either of the parents smoking were 1.26 (95% CI 1.20–1.33) for wheeze, 1.35 (1.27–1.43) for cough, 1.35 (1.30–1.41) for phlegm and 1.31 (1.14–1.50) for breathlessness, meaning 26–35% excess risk in children of smoking parents. All symptoms showed increasing risk with increasing number of parents smoking at home,

2.3 HEALTH EFFECTS OF PASSIVE SMOKING IN CHILDREN

31

suggesting exposure–response relation. Generally the risk was higher in relation to mother’s smoking, but father’s smoking was also related to significantly increased risk. All recent reviews have concluded that parental smoking is causally related to chronic respiratory symptoms in children [5,9,11]. Tobacco smoke contains many substances that can induce irritation and chronic inflammation in the airways, and these mechanisms are likely to underlie the observed relations with respiratory symptoms. Wheeze is a symptom of both respiratory infections and asthma in children, and so reflects disease mechanisms of these conditions, as reviewed separately. Asthma Induction of asthma. About 85 studies from different parts of the world have addressed the risk of developing asthma in childhood in relation to parents’ smoking. The most updated meta-analysis of these was conducted by the California Environmental Protection Agency [11] in 2005. Its meta-analysis was based on 29 studies and gave a summary RR for new-onset asthma of 1.32 (95% CI 1.24–1.41), meaning 32% excess risk in children whose parent(s) smoke. The risk was higher in preschool children (1.44, 1.04–1.99), but remained significantly increased also in older children. When the child was exposed to parental smoking both during pregnancy and after birth the risk was strongest, but significant increase in the risk was detected also in association with postnatal SHS exposure only. The risk of asthma increased with increasing duration of passive smoking, suggesting an exposure–response relation: RR was 1.22 (1.16–1.34) for 5 years of postnatal SHS exposure and 1.42 (1.28–1.70) for 10 years of such exposure. In addition to mechanisms that will be discussed in connection with adult asthma, in infants other mechanisms may play a role. These include impaired airway development during pregnancy and in infancy in those exposed to passive smoking and the influence of SHS on development of immunological responses, for example the balance between Th1 and Th2 cells [5]. Exacerbation of asthma. Several studies have shown that parental smoking is a causal factor for exacerbation of asthma in children with a pre-existing disease [11], in addition to increasing the risk of new asthma in previously healthy children. Different types of outcomes related to exacerbation of asthma have been studied, including the frequency and severity of asthma symptoms, use of asthma medications, school absenteeism, use of healthcare services, hospitalization and changes in lung function parameters, such as peak expiratory flow (PEF). In longitudinal studies, the effects of passive smoking have been detected most consistently on increased asthmatic symptoms, more and prolonged use of medication, and increased school absenteeism. Lung function impairment There are numerous cross-sectional and some longitudinal studies showing that parental smoking is linked to lung function deficits as well as to reduced growth of lung function in children. As discussed above, exposure during pregnancy seems to be of importance, but postnatal SHS exposure has also been shown to have significant adverse effect on lung function of children. The recent review by US Surgeon General [5] included 26 studies and measured the summary effect as percentage differences of lung function in children exposed to SHS compared with unexposed children. The effects were 1.15% (95% CI 1.56 to 0.75) on forced expiratory volume in 1 second

32

CH 2 PASSIVE SMOKING

(FEV1), 0.32% (0.71 to 0.08) on forced vital capacity (FVC), and 4.76% (6.34 to 3.18) on mid-expiratory flow rate (MEFR). Overall the results show small but significant adverse effect of childhood passive smoking on spirometric lung function, which is likely to persist into older ages. This effect has been judged by most recent reviews to be causal [5,11]. In addition, there is some evidence that passive smoking may lead to reduced diffusing capacity of the lungs [11]. Sudden infant death syndrome Sudden infant death syndrome (SIDS) is a sudden, unexpected and unexplained death of an infant before one year of age. A review from 1997 identified 39 studies that had investigated the risk of SIDS in relation to passive smoking after birth and gave a summary relative risk of 1.94 (95% CI 1.55–2.43), meaning 94% excess risk in infants exposed to SHS [15]. Most studies assessed exposure from mother’s smoking after birth and one-third of them controlled for maternal smoking during pregnancy (i.e. prenatal exposure). Also father’s smoking has been significantly linked to increased risk of SIDS. Several studies have shown evidence of exposure–response relation with the amount of SHS exposure. All recent reviews have concluded that there is a causal relation between parental smoking and SIDS [5,11]. Exposure to nicotine and toxicants in tobacco smoke has been shown to have neurotoxic effects, affecting neuroregulation of breathing and apnoeic spells. SHS exposure has been found to be associated with a change in the ventilatory and cardiac responses to hypoxia [5,11]. Childhood cancers Childhood cancers are relatively rare conditions. One cohort and some case–control studies have investigated the relations of childhood cancers to parental smoking. The strongest evidence links maternal smoking to overall childhood cancer risk. Of specific cancers, SHS exposure has been associated with leukemias, lymphomas and brain tumors. Few studies have distinguished the effects of postnatal exposure from exposure during pregnancy. Relevant exposure may have occurred already before conception, i.e. through mutations of male germ cells. In view of the rather small number of studies adjusting for other potentially important cancer risk factors, the relations between SHS exposure and childhood cancers have not been judged as causal and more studies on this topic are needed [5]. Neurobehavioral and other effects There is some evidence that children’s cognition and behavior are adversely affected by passive smoking [5,11]. A large study based on the third US National Health and Nutrition Examination Survey (NHANES III) showed a significant inverse relation between child’s serum cotinine level and performance on cognitive tests: decrements in cognitive scores were detected at higher cotinine levels, i.e. among those with more exposure to SHS. A large British study showed that children whose mother smoked had lower scores in a vocabulary test. However, not all studies have found such effects and more studies are needed before any definite conclusions can be made. Children’s passive smoking has also been linked in recent studies to significantly increased caries in young children and less favorable serum lipid profile in children up

33

2.4 HEALTH EFFECTS OF PASSIVE SMOKING IN ADULTS

to 15 years of age, including significantly lower levels of high-density lipoprotein cholesterol (HDL).

2.4 Health effects of passive smoking in adults The first studies linking passive smoking to adverse health effects in adults were from the early 1980s and focused mainly on lung cancer. More recently there has been increasing research also into nonmalignant effects of SHS exposure in adulthood. The evidence from adult studies is summarized in Table 2.4.

2.4.1 Lung cancer Lung cancer is the leading cause of cancer deaths in many countries and its main cause is active smoking. The first studies that linked passive smoking to lung cancer were published in 1981 and studied nonsmoking women who were exposed to a spouse’s smoking. Since then more than 50 case–control and cohort studies from different parts of the world have addressed the risk of lung cancer in relation to SHS exposure. The most recent meta-analysis of these studies was conducted by the US Surgeon General in 2006 [5]. It concluded that SHS from the spouse’s smoking as well as from exposure at

Table 2.4

Summary of health effects of passive smoking in adulthood

Condition

Best estimate of OR or RR

95% Confidence interval

Reference

Causality (scale 0– þþþ )a

Lung cancer Breast cancer Acute irritant symptoms Induction of asthma Exacerbation of asthma Wheezing Chronic phlegm Breathlessness Development of COPD Exacerbation of COPD Respiratory infections Ischemic heart disease (IHD) Exacerbation of IHD Stroke

1.29 1.25 — 1.97 — 1.99 1.69 1.44 1.55 — 2.5 1.27 — 1.82 Effect estimate (%b)

1.13–1.49 1.08–1.44

[5] [11] [17] [18] [11] [19] [19] [19] [20] [21] [22] [5] [5] [23]

þþþ þþ þþþ þþþ þþ þþþ þþþ þþþ þþ þ þ þþþ þþ þþ

[24]

þ

Lung function impairment FEV1

2.7

1.19–3.25 1.41–2.82 1.23–2.31 1.18–1.75 1.09–2.21 1.2–5.1 1.19–1.36 1.34–2.49 95% CI 4.1 to 1.2

0 ¼ no evidence of a relation between passive smoking and condition; þ ¼ some evidence of a relation between passive smoking and condition; þ þ ¼ strong but not definitive evidence of a causal relation between passive smoking and condition; þ þ þ ¼ established causal relation between passive smoking and condition. b Percentage difference of lung function in adults exposed to SHS compared with unexposed adults. a

34

CH 2 PASSIVE SMOKING

work are causally related to lung cancer in nonsmokers. Similar conclusions have been reached by earlier as well as two other recent reviews, one by the International Agency for Research on Cancer (IARC) [4] and the other by the California EPA [11]. The summary OR of lung cancer among nonsmokers ever exposed to spousal smoking was estimated at 1.29 (95% CI 1.13–1.49) among women and men combined, 1.22 (1.13–1.31) among women and 1.37 (1.05–1.79) among men [5]. The summary OR of lung cancer in relation to passive smoking at work was 1.22 (1.13–1.33). Thus, passive smoking at home and at work are both related to about 20–30% excess risk. There is abundant evidence of exposure–response relation between increasing SHS exposure at home and/or at work (measured as amount or duration of passive smoking) and increasing lung cancer risk. Longitudinal studies have provided evidence of meaningful temporal relation, i.e. SHS exposure has preceded development of lung cancer. Tobacco smoke is known to contain many carcinogenic substances. Biomarker studies have shown that nonsmokers exposed to SHS take up and metabolize carcinogenic substances of tobacco smoke and experience increased mutation burden compared with unexposed nonsmokers [5]. Many recent studies have addressed potential methodological problems that were related to the early studies, such as misclassification of disease or passive smoking status and potential influence of other risk factors, and have still provided results consistent with a causal effect of passive smoking on lung cancer. The effect of childhood passive smoking on lung cancer has also been investigated in some studies, but the results of these have been less consistent. A significant relation has been reported in studies from Asia, giving a summary relative risk of 1.59 (1.18–2.15) [5].

2.4.2 Breast and other cancers Recently several studies have also addressed the relation between passive smoking and breast cancer. The results of these have been somewhat inconsistent and recent reviews on this topic have provided variable conclusions. US Surgeon General [5] concluded that the evidence on the relation between passive smoking and breast cancer is suggestive of causality, while California EPA concluded [11] that the evidence supports a causal relation. Both reports pointed out that the relation between SHS exposure and breast cancer is stronger in premenopausal women. The meta-analysis conducted by California EPA gave a summary risk ratio of 1.25 (95% CI 1.08–1.44) for SHS exposure among women of all ages, while the RR for premenopausal women (<50 years old) was 1.68 (1.31–2.15). Other adult cancers that have been investigated in relation to passive smoking include nasal sinus and nasopharyngeal carcinomas. These cancers are less common than lung and breast cancer. The evidence is suggestive for nasal sinus cancer, but there are too few studies to make any conclusions concerning nasopharyngeal cancers.

2.4.3 Acute irritant symptoms SHS contains several substances that are irritant for mucosa. Many studies have shown that passive smoking causes acute irritant symptoms, first complaints of malodor and

2.4 HEALTH EFFECTS OF PASSIVE SMOKING IN ADULTS

35

eye irritation at lower SHS concentrations, then nose and throat irritation, excessive nasal secretions and cough at higher SHS concentrations [11]. These acute reactions have been confirmed by objective measurements, such as increased eye blink rate and nasal airway resistance [17]. Irritant symptoms are considered to be reversible after SHS exposure has ceased, but there are no follow-up studies of consequences of experiencing repeated acute symptoms from passive smoking. Atopic subjects seem to be more sensitive to SHS exposure than nonatopics.

2.4.4 Asthma There are several biological mechanisms by which SHS exposure could affect airways to cause asthma, chronic respiratory symptoms and chronic obstructive pulmonary disease [11,17]. SHS contains irritant substances that can induce mucus hypersecretion and inflammation in the airways. Long-term exposure can lead to chronic inflammation of the airways. Inflammatory cells release proteolytic enzymes and tobacco smoke inhibits antiproteases that protect against these enzymes. Tobacco smoke has been suggested to increase epithelial permeability to environmental allergens, which may explain the findings in animal studies and among children showing that SHS augments allergic reactions to some inhalable allergens. There is also some evidence that SHS exposure causes bronchoconstriction and increased microvascular leakage, both of which are features typical for asthma [5]. Although a large number of studies have been published on parental smoking and asthma in children, as reviewed above, the effects of SHS on asthma in adults have been studied less. However, in the recent years an increasing number of studies have addressed this question, strengthening the evidence considerably [2,11,17]. Induction of asthma To date altogether 14 studies from different parts of the world have investigated SHS exposure in relation to adult asthma, including three cohort, one incident case–control, two prevalent case–control, and eight cross-sectional studies [2,11,17]. These have shown rather consistently an increased risk of asthma in relation to adulthood passive smoking both at home and at work, the OR being 1.14–4.7, although not all studies detected statistically significant effects. Several studies showed evidence of exposureresponse relation with increasing SHS exposure, measured as hours of passive smoking per day, number of cigarettes the person was exposed to daily, duration of passive smoking or cumulative exposure over lifetime. Asthma has been defined in variable ways, most commonly based on the reporting of doctor-diagnosed asthma, but some studies have included clinical and lung function investigations to confirm the diagnosis with objective measures [18]. Recent studies have controlled for bias and confounding, and have shown evidence of a meaningful temporal relation, i.e. exposure has preceded the development of the disease. In conclusion, there is evidence of a causal relation between passive smoking and induction of asthma in adults [2,11]. The strongest evidence comes from the Finnish Environment and Asthma Study, which was a population-based case–control study of new adult-onset asthma [18]. The size of this study corresponded to a follow-up of approximately 100,000 adults for 5.8 years. The Finnish study estimated an OR of 1.97

36

CH 2 PASSIVE SMOKING

(95% CI 1.19–3.25) for SHS exposure at work and/or at home, meaning 97% excess risk in those who had been exposed to SHS during the previous 12 months. The evidence on the effect of childhood SHS exposure on adult asthma is less consistent, although a Norwegian 11-year follow-up study of adults suggested that maternal smoking during childhood significantly increases the risk of adult asthma, with an OR 1.9 (1.1–3.2) [25]. Exacerbation of asthma Individuals with asthma have chronic inflammation in their airways and may be particularly sensitive to SHS exposure. In community- and hospital-based surveys 69–78% of adult asthma patients report that passive smoking aggravates their symptoms [17,26]. To date nine studies have examined potential effects of passive smoking on exacerbation of pre-existing asthma in adults [11,17], including three longitudinal, one nested case–control and five cross-sectional studies. They were conducted mainly in Canada, India and the USA. These studies have shown that, in adults with asthma, SHS exposure at home and/or at work leads to increased respiratory symptoms, increased use of bronchodilator and steroid medication, reduced general health, increased healthcare utilization, such as emergency department visits and hospitalizations, increased bronchial hyperresponsiveness and reduced spirometric lung function. The NHANES III study found that adult asthmatics who experienced the highest SHS exposure based on serum cotinine levels had significantly lower lung function levels than those with low SHS exposure [27]. Some controlled chamber studies of SHS exposure and asthma have been published, showing somewhat inconsistent results, probably due to small sample sizes and variable exposure times [17]. Overall they suggest that there is a subpopulation of asthmatics who experience increased respiratory symptoms, decreased lung function and increased bronchial hyperresponsiveness in response to short-term SHS exposure. In summary, studies show rather consistently that SHS exposure affects adversely pre-existing asthma in adults. However, the evidence is still limited because of a small number of studies and because they have investigated very variable asthma outcomes.

2.4.5 Chronic respiratory symptoms Numerous studies from different parts of the world have been published on passive smoking and chronic respiratory symptoms in adults [2,11,17]. Early studies provided somewhat inconsistent results, but the more recent, often better quality, studies show rather consistently an increased risk of chronic respiratory symptoms in relation to SHS exposure at home and/or at work using both cross-sectional and longitudinal study design. The studies show evidence of exposure–response relations, i.e. increasing risk of symptoms with increasing passive smoking. Both asthma-type symptoms, i.e. wheezing, breathlessness and chest tightness, and bronchitis symptoms, i.e. cough and phlegm production, have been related to passive smoking. Three studies have shown significant decreases in upper and lower respiratory symptoms after state-wide or national smokefree workplace bans were introduced [2], suggesting that the effect of SHS on respiratory symptoms is reversible.

2.4 HEALTH EFFECTS OF PASSIVE SMOKING IN ADULTS

37

The recent reviews have concluded that SHS exposure is likely to play a causal role in chronic respiratory symptoms in adults. A large Swiss cross-sectional study reported an OR of 1.99 (95% CI 1.41–2.82) for wheezing, 1.69 (1.23–2.31) for phlegm production and 1.44 (1.18–1.75) for breathlessness [19].

2.4.6 Chronic obstructive pulmonary disease Development of COPD Chronic obstructive pulmonary disease (COPD) is a chronic disease that develops slowly over many years. It includes chronic bronchitis, characterized by chronic cough and phlegm production, emphysema, characterized by destruction of alveolar structures, and airflow obstruction that is largely irreversible. Studies on passive smoking in relation to chronic respiratory symptoms and lung function impairment reflect the early stages of COPD, while studies on diagnosed COPD investigate the advanced stages of this disease. To date five longitudinal, three case–control and a few cross-sectional studies have addressed the role of SHS exposure for COPD [2,17]. Most of the studies found an effect of SHS exposure at home on COPD, with OR 1.2–5.6. Some studies also showed increased risk in relation to workplace SHS exposure. There is some evidence of an exposure–response relation, when SHS exposure was measured as packs per day or years of passive smoking. The outcome has been defined in variable ways, often based on reported doctor diagnosis, but sometimes on diagnostic codes or lung function measurements. A recent population-based cross-sectional study included approximately 2000 adults 55–75 years of age from 48 US states [20]. It defined COPD as self-reported physician diagnosis of chronic bronchitis, emphysema or COPD. The OR observed in relation to the highest quartile of home exposure was 1.55 (95% CI 1.09–2.21) and of work exposure 1.36 (1.02–1.84), suggesting 55% and 36% excess risk, respectively. Recent reviews have concluded that there is limited but increasing evidence that SHS exposure is significantly related to the risk of COPD [2,5,17]. The mechanisms likely to underlie this are increased oxidant burden in the lungs and chronic airways inflammation caused by SHS exposure. Exacerbation of COPD Some studies, mainly from the USA, have investigated the impact of passive smoking on respiratory disease-related activity restrictions [21]. One study showed that respiratoryrelated activity restriction in the past 2 weeks increased by 1% per exposure to one cigarette per day at home. The other study showed increased risk of respiratory disease exacerbation in those exposed to SHS at home and/or at work, with an OR of 1.44 (95% CI 1.07–1.95).

2.4.7 Lung function impairment More than 20 studies, mainly cross-sectional by their study design, from different parts of the world have addressed the relation between passive smoking and lung function in adulthood, as reviewed by Jaakkola and Jaakkola [17] and California EPA [11]. Recent reviews concluded that SHS exposure is related to small, but measurable, decrements in

38

CH 2 PASSIVE SMOKING

spirometric lung function in adults. These effects seem to be dose-dependent, as they are observable mainly in countries and in occupations where SHS exposure levels are high. A meta-analysis published in 1999 included nine cross-sectional studies and found an average effect of 2.7% on FEV1 (95% CI –4.1% to 1.2%) [24]. Recent studies have suggested that patients with asthma are particularly susceptible to the adverse effects of SHS and consequently experience larger reductions in lung function than subjects with no pre-existing airways disease [11,27]. At least two studies have investigated the effects of SHS exposure reduction after introducing a smoke-free legislation [28,29]. Both of them showed a significant improvement in lung function levels, suggesting that the effects of SHS on lung function are partly reversible. However, more longitudinal studies are needed before making any definite conclusion on passive smoking and adult lung function.

2.4.8 Respiratory infections In contrast to the abundant evidence on parental smoking and respiratory infections in children, there are only a few studies of passive smoking and infections in adults. A population-based case–control study from the USA investigated the relation of SHS exposure to invasive pneumococcal disease, mainly pneumonia, in immunocompetent adults [22]. Among nonsmokers, the OR of pneumococcal infections was 2.5 (95% CI 1.2–5.1) in relation to passive smoking at home or outside home. An exposure– response relation was observed with the hours of daily passive smoking.

2.4.9 Cardiovascular diseases Cardiovascular diseases are the leading cause of death in many countries and active smoking is among the most important risk factors for them. Since the 1980s the relation of passive smoking to cardiovascular diseases has been investigated in many studies. Ischemic heart disease Induction of IHD. To date approximately 20 studies, including cohort and case–control studies, have been published on passive smoking and ischemic heart disease. These studies have shown that SHS exposure is consistently related to increased risk of ischemic heart disease (IHD) mortality (fatal myocardial infarction), morbidity (nonfatal events) and angina symptoms. Recent reports by California EPA [11] and US General Surgeon [5] concluded that IHD is causally related to SHS exposure. US Surgeon General estimated a summary OR to be 1.27 (95% CI 1.19–1.36), meaning 27% excess risk among nonsmokers exposed to passive smoking. Exposure to SHS at home and at work both have been linked to significantly increased risk of IHD and there is evidence of an exposure–response relation. In terms of mechanisms, experimental studies have shown that SHS can increase platelet adhesion and blood coagulability comparable to that seen in active smokers after consuming one to two cigarettes. SHS exposure has also been shown to cause endothelial dysfunction [5]. In human studies passive smoking has been related to thickened carotid artery intima-media, impaired endothelial function, and increased plasma fibrinogen levels [30]. The adverse effects of

2.5 DIAGNOSTIC AND MANAGEMENT ISSUES RELATED TO PASSIVE SMOKING

39

SHS on cardiovascular system may begin already in childhood, as children whose parents smoke have a less favorable lipid profile, including lower HDL levels. In animal studies, SHS exposure has been shown to cause atherosclerosis. The evidence of causality is further strengthened by some studies that have looked at morbidity or mortality from IHD before and after introduction of smoke-free legislation [2]. These have consistently shown decreases in IHD after the legislation came into effect. The most recent study was reported from Italy, where a legislation banning smoking in all indoor places came into effect in January 2005 [31]. In Rome, acute IHD events, including hospital admissions and out-of-hospital deaths, reduced significantly by 8–11% after the ban. Exacerbation of IHD. Passive smoking has been suggested to exacerbate IHD, with potentially fatal consequences, in addition to increasing the risk of developing IHD in previously healthy adults [5,21]. As little as 20 min of exposure to SHS leads to increased platelet adhesiveness and blood coagulability similar to that seen in active smokers. Experimental studies have demonstrated that, among patients with stable angina, SHS exposure increases heart rate, blood pressure and carboxy hemoglobin, reduces exercise capacity and increases arrhythmias. Stroke Although active smoking is a well-established risk factor for stroke, only a few studies have addressed potential effects of passive smoking on stroke. Based on some cohort, case–control and cross-sectional studies, there is evidence suggesting an increased risk of stroke in relation to SHS exposure at home or at work [2,5]. The best estimate of risk so far is from a case–control study from New Zealand, which assessed SHS exposure both at home and at work and showed an OR of 1.82 (95% CI 1.34–2.49) for nonfatal and fatal stroke, meaning 82% excess risk in those exposed to SHS [23].

2.5 Diagnostic and management issues related to passive smoking There is plenty of evidence that passive smoking plays a role for all acute and chronic respiratory diseases that are of major public health importance among children as well as adults. These include lower respiratory illnesses, otitis media and asthma in children, and lung cancer, asthma and COPD in adults. In adult populations, passive smoking has also been found to significantly affect cardiovascular diseases, which are major causes of death, and some evidence suggests that unfavorable lipid profiles are detected already in children whose parents smoke. Thus, the diseases linked to passive smoking are commonly encountered in general and hospital-based practices. In addition, SHS exposure has significant impact on the development of fetus, infants and children, affecting the maturation and development of their respiratory system. Passive smoking during pregnancy and in childhood has been shown to have long-term consequences for health. In the light of the evidence on

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impact of passive smoking on health, it can be concluded that SHS is the major preventable indoor exposure, which causes significant morbidity and mortality in the populations. In clinical practice, it is important to keep the role of passive smoking in mind and to always ask about exposure to tobacco smoke at home and at work when diagnosing the diseases reviewed in this chapter as well as when following up patients because of these diseases. In addition, health check-ups of children should always include questions about smoking at home, or at day-care if applicable. The diagnostic procedures for these common diseases follow the basic principles for their diagnostic tests in general and they are managed according to the state of the art guidelines with the addition of intervening to reduce/eliminate passive smoking if such exposure is reported. Other methods than interview to measure exposure to SHS were reviewed in this chapter in Section 2.2.4. Education and advice concerning the health impact of passive smoking given by health professionals is an important part of both primary and secondary prevention and management of diseases. It is complemented by preventive actions by the society, which include tobacco control legislation and educational programs on population level, but these do not substitute the efforts by healthcare professionals aimed at individual patients or families, or at small groups. In addition to SHS exposure influencing the induction of many diseases, passive smoking has been found to play a role for exacerbation of many common diseases, such as asthma, COPD and ischemic heart disease. Thus, the question on passive smoking should be brought up also in acute clinical situations, as it may be the exposure that underlies the sudden worsening of the condition. Passive smoking has also been suggested to affect the long-term prognosis of respiratory and cardio-vascular diseases, although more studies are needed to understand better the prognostic role of SHS. Thus, advising about passive smoking should be part of state-of-the-art clinical examinations and treatment of acute respiratory infections, chronic respiratory symptoms, exacerbations of asthma and COPD, reduced lung function and exacerbation of ischemic heart disease. The medico-legal considerations vary from country to country. For example, in Finland SHS is mentioned in the law as a causal (workplace) agent for cancer and pregnant mothers may receive special maternity benefits to be able to avoid passive smoking by their fetus. Potential compensation for occupational SHS-induced asthma depends on whether irritant-induced asthma from SHS is accepted as an occupational asthma and how firm evidence for its causal role for the disease in an individual can be provided.

2.6 Prevention of SHS-related diseases Prevention of passive smoking -related diseases should be among the top priorities of legislation, health policy, healthcare systems and practice of healthcare professionals. Tobacco-free workplace and public place legislation has been shown to be effective in reducing workplace SHS exposure of adult populations, and some studies have indicated that it also reduces SHS exposure outside work, probably because of reduction in active smoking and increase in awareness of the health risks related to

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passive smoking as a consequence of such legislation [2]. Thus, the legislation will also reduce children’s passive smoking at home. Health education, both at individual and population levels, should inform about the health risks related to passive smoking and include advice on how to avoid or at least reduce this exposure. Such education and advice should be provided in primary care and occupational health practices, schools, workplaces and hospitals. Increasing numbers of countries are including smoke-free workplaces and restaurants and bars in their tobacco control legislation and the experiences from these countries are good in terms of reducing SHS exposure, sustaining compliance with the law and improving the health of populations covered by the law [2]. In many countries the legislative efforts have been combined with media campaigns on the adverse health effects of SHS exposure and these seem to have influence, but it should be remembered that such campaigns are needed repeatedly. Increasing emphasis should be given to the role of healthcare professionals in reducing passive smoking-induced ill-health, as parents of children with diseases and diseased adults are likely to be more receptive for their advice. Physicians, nurses and other healthcare staff should recognize passive smoking of children as one of the major targets for education. Parents should be informed of the risks of passive smoking as early in pregnancy as possible, preferably already at the stage of planning the pregnancy. Smoking cessation programs should accompany the health education on passive smoking. Those not succeeding in stopping smoking should be encouraged to behave in such a way as to protect others from tobacco smoke exposure, especially pregnant women, children and the elderly. Such behaviors include smoking outdoors in areas not connected to indoor air systems. Tenant contracts could include conditions not allowing smoking indoors. All these measures combined should be effective in reducing the adverse health consequences of passive smoking.

References 1. World Health Organization. WHO Framework Convention on Tobacco Control (2003) http:// www.who.int/tobacco/framework/WHO_FCTC_english.pdf 2. Jaakkola, M.S., Jaakkola, J.J.K. (2006) Impact of smoke-free workplace legislation on exposures and health: possibilities for prevention. Eur. Respir. J. 28: 397–408. 3. Hoffman, D., Hoffman, I., El Bayoumy, K. (2001) The less harmful cigarette: a controversial issue, a tribute to Ernst L. Wynder. Chem. Res. Toxicol. 14: 767–790. 4. International Agency for Research on Cancer (2004) Tobacco Smoke and Involuntary Smoking. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vo. 83. IARC: Lyon; 1189–1413. 5. US Department of Health and Human Services (2006) The Health Consequences of Involuntary Exposure to Tobacco Smoke. A Report of the Surgeon General. US Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health: Atlanta, GA. 6. California Environmental Protection Agency (2005a) Proposed Identification of Environmental Tobacco Smoke as a Toxic Air Contaminant. Part A: Exposure Assessment. California EPA, Office of Environmental Health Hazard Assessment, Air Toxicology and Epidemiology Branch. 7. Jaakkola, M.S., Jaakkola, J.J.K. (1997) Assessment of exposure to environmental tobacco smoke. Eur. Respir. J. 10: (1997) 2384–2397.

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8. Jaakkola, M.S., Samet, J.M. (1999) Occupational exposure to environmental tobacco smoke and health risk assessment. Environ. Health Perspect. 107 (suppl. 6): 829–835. 9. Jaakkola, J.J.K., Jaakkola, M.S. (2002) Effects of environmental tobacco smoke on the respiratory health of children. Scand. J. Work Environ. Health; 28 (suppl. 2): 71–83. 10. Windham, G.C., Eaton, A., Hopkins, B. (1999) Evidence for an association between environmental tobacco smoke exposure and birthweight: a meta-analysis and new data. Paediatr. Perinat. Epidemiol. 13: 35–57. 11. California Environmental Protection Agency (2005b) Proposed Identification of Environmental Tobacco Smoke as a Toxic Air Contaminant. Part B: Health Effects Assessment for Environmental Tobacco Smoke. California EPA, Office of Environmental Health Hazard Assessment, Air Toxicology and Epidemiology Branch. 12. Jaakkola, J.J.K., Gissler, M. (2004) Maternal smoking in pregnancy, fetal development, and childhood asthma. Am. J. Public Health. 94: 136–140. 13. Lindbohm, M.-L., Sallmen, M., Taskinen, H. (2002) Effects of exposure to environmental tobacco smoke on reproductive health. Scand. J. Work Environ. Health 28 (suppl. 2): 84–96. 14. Jaakkola, J.J.K., Jaakkola, N., Zahlsen, K. (2001) Fetal growth and length of gestation in relation to prenatal exposure to environmental tobacco smoke assessed by hair nicotine concentration. Environ. Health Perspect. 109: 557–561. 15. Anderson, H.R., Cook, D.G. (1997) Passive smoking and sudden infant death syndrome: review of the epidemiological evidence. Thorax 52: 1003–1009. 16. Li, J.S., Peat, J.K., Xuan, W., Berry, G. (1999) Meta-analysis on the association between environmental tobacco smoke (ETS) exposure and the prevalence of lower respiratory tract infection in early childhood. Pediatr. Pulmonol. 27: 5–13. 17. Jaakkola MS, Jaakkola JJK. (2002b) Effects of environmental tobacco smoke on the respiratory health of adults. Scand J Work Environ Health; 28 Suppl 2: 52–70. 18. Jaakkola, M.S., Piipari, R., Jaakkola, N., Jaakkola, J.J.K. (2003) Environmental tobacco smoke and adult-onset asthma: a population-based incident case–control study. Am. J. Public Health 93: 2055–2060. 19. Leuenberger, P., Schwartz, J., Ackermann-Liebrich, U., Blaser, K., Bolognini, G., Bongard, J.P., et al. (1994) Passive smoking exposure in adults and chronic respiratory symptoms (SAPALDIA Study). Am. J. Respir. Crit. Care Med. 150: 1222–1228. 20. Eisner, M.D., Balmes, J., Katz, P.P., Trupin, L., Yelin, E.H., Blanc, P.D. (2005) Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease. Environ. Health. 4: 7–14. 21. Jaakkola MS. (2002) Environmental tobacco smoke and health in the elderly. Eur Respir J; 19: 172–181. 22. Nuorti, J.P., Butler, J.C., Farley, M.M., Harrison, L.H., McGeer, A., Kolczak, M.S., Breiman, R.F., the Active Bacterial Core Surveillance Team (2000) Cigarette smoking and invasive pneumococcal disease. New Engl. J. Med. 342: 681–689. 23. Bonita, R., Duncan, J., Truelsen, T., Jackson, R.T., Beaglehole, R. (1999) Passive as well as active smoking increases the risk of acute stroke. Tobacco Control 8: 156–160. 24. Carey, I.M., Cook, D.G., Strachan, D.P. (1999) The effect of environmental tobacco smoke on lung function in a longitudinal study of British adults. Epidemiology 10: 319–326. 25. Skorge, T.D., Eagan, T.M.L., Eide, G.E., Gulsvik, A., Bakke, P.S. (2005) The adult incidence of asthma and respiratory symptoms by passive smoking in utero or in childhood. Am. J. Respir. Crit. Care Med. 172: 61–66. 26. Tarlo, S.M., Broder, I., Corey, P.,et al. (2000) A case–control study of the role of cold symptoms and other historical triggering factors in asthma exacerbations. Can. Respir. J. 7: 42–48. 27. Eisner, M.D. (2002) Environmental tobacco smoke exposure and pulmonary function among adults in NHANES III: impact on the general population and adults with current asthma. Environ. Health Perspect. 110: 765–770. 28. Eisner, M.D., Smith, A.K., Blanc, P.D. (1998) Bartenders’ respiratory health after establishment of smoke-free bars and taverns. JAMA 280: 1909–1914.

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29. Menzies, D., Nair, A., Williamson, P.A., Schembri, S., Al-Khairalla, M.Z., Barnes, M., Fardon, T.C., McFarlane, L., Magee, G.J., Lipworth, B.J. (2006) Respiratory symptoms, pulmonary function, and markers of inflammation among bar workers before and after a legislative ban on smoking in public places. JAMA 296: 1742–1748. 30. Jousilahti, P., Helakorpi, S. (2002) Prevalence of exposure to environmental tobacco smoke at work and at home – 15-year trends in Finland. Scand. J. Work Environ. Health 28 (suppl. 2): 16–20. 31. Cesaroni, G., Forastiere, F., Agabiti, N., Valente, P., Zuccaro, P., Perucci, C.A. (2008) Effect of the Italian smoking ban on population rates of acute coronary events. Circulation 117: 1183–1188.

3 Emissions related to cooking and heating Debbie Jarvis Imperial College, London, UK

3.1 Introduction In most developed nations the majority of households cook and heat their homes with either electricity or natural gas. Wood, coal, peat, kerosene and town gas have been popular fuels in the not so distant past and remain the preferred option for some modern day householders. The use of each of these fuels in the home, except for electricity, has been reported to be associated with respiratory morbidity in children and adults in different parts of the world. In the less developed parts of the world, biomass remains a dominant indoor fuel source. Some have estimated that more than half the world’s population still relies on unprocessed biomass fuels (wood, crop residues and dung cakes) that are burnt in poorly ventilated homes using simple pits or rudimentary mud-formed cooking stoves. Emissions from these sources are recognized as a major cause of acute and chronic respiratory morbidity in children and adults living in these homes and are a major international public health concern. The World Health Organization is leading an international effort to reduce the health effects of biomass fuel usage. Regardless of what fuel is being burnt, exposure to the pollutants produced will vary with the amount of time spent in the affected area (which may depend on gender, climate or other socio-economic or cultural factors) and ventilation of the area (which may depend on local housing regulations, climate and cultural housing norms). These variations are likely to contribute to the inconsistent findings from research studies that have examined the association of health with exposure to pollutants from heating and cooking in the developed world. Although an association of a range of respiratory conditions with indoor pollution from cooking or heating is suspected, further evidence Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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is needed before a causal association can be proven. This is particularly the case for the health effects of the use of gas cooking and gas heating appliances and poses a dilemma for clinicians in developed nations. What should they say to patients who have respiratory complaints and who use indoor gas heating appliances? Should they advise a switch to electrical appliances? Furthermore, in the developed world, there has recently been a growth in the use of wood burning stoves. It is uncertain whether modern wood burning appliances may also be associated with increased indoor pollution and disease. The aim of this chapter is to provide a summary of current knowledge of the respiratory health effects of fuels used for heating and cooking, highlighting areas of certainty and areas of doubt. I will focus predominantly on the current modern day dilemma – whether to use gas or electricity – but will mention where relevant other common indoor fuels used in the developed nations.

3.2 Description of exposures The proportion of the population which uses gas for cooking and heating varies across the world. A main natural gas supply is absent in some countries (e.g. Norway), in some parts of some countries (e.g. rural areas) and in some types of housing stock (e.g. in modern blocks of flats). Where natural gas is absent, bottled gas may be available, stored either outside the home in large tanks or inside the home in bottles. The most common alternative fuel is electricity, but other fossil fuels such as kerosene, paraffin, coal, oil and peat as well as wood may be used, depending on local supply and local practice. All of these fossil fuels have one thing in common – as they combust, a range of gases and particulates are produced which may be harmful to respiratory health. Occupants of homes using these fuels will have higher exposure to pollutants if the appliance is faulty, the flue is blocked or the rooms in which they are used are poorly ventilated

3.3 Pollutants produced when using gas appliances in the home Combustion of fossil fuels and biomass in the home produces gases such as nitrogen dioxide, carbon monoxide, particles and other potentially toxic substances such as formaldehyde, volatile organic compounds and sulfur dioxide. We know much more about exposure to nitrogen dioxide in the home than most of the other pollutants. This is because relatively cheap and reliable passive samplers are available for measuring average levels of indoor nitrogen dioxide and have been used in large-scale studies. Because pollutants (including nitrogen dioxide) from fossil fuel combustion are present in the outdoor air, a proportion of the indoor levels may come from the outside, the proportion depending on the relative balance of indoor and outdoor sources.

3.3.1 Nitrogen dioxide The combustion of gas at high temperatures produces nitric oxide, which is oxidized to nitrogen dioxide, and other oxides of nitrogen including nitrous acid. Indoor

3.3

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nitric oxide levels, which are rarely measured, are usually low, although some experimental studies suggest they reach higher levels in poorly ventilated conditions. On the other hand, when a gas oven or hob is turned on, there is a sharp rise in nitrogen dioxide level, which diminishes slightly as the appliance heats up and gas burning becomes more efficient. High levels are maintained until the appliance is turned off and this is followed by a steady decay that depends largely, but not exclusively, on ventilation of the kitchen and circulation of air from the kitchen to other parts of the house. In studies that have continuously monitored nitrogen dioxide levels in areas near a gas cooker in use. the peaks measured have been recorded to be as high as 1100 mg/m3 (USA, late 1980s), 2500 mg/m3 (USA, late 1990s) and 3000 mg/m3 (UK, late 1980s). These values are far higher than those recorded by continuous monitoring of ambient air as part of the outdoor pollution monitoring programme in the UK and far higher than the World Health Organization’s short-term hourly guideline value for nitrogen dioxide in ambient air of 200 mg/m3. These peaks of exposure are rarely measured in large-scale health studies as continuous monitoring of indoor nitrogen dioxide involves cumbersome and expensive equipment. Passive sampling over a one to two week period generates an average value only and masks the peak levels that may have occurred. Some have argued that the use of passive samplers to quantify exposure to indoor nitrogen dioxide is unlikely to aid assessment of health effects of the use of gas appliances because of this problem and that all is needed is knowledge of the main types of fuel used in the homes. The use of gas for cooking increases not only the average kitchen level of nitrogen dioxide but also the average levels in other rooms (Figure 3.1) particularly if doors are left open between the kitchen and the rest of the house.

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NO2 level (µg/m3)

30 25 20 Gas Electricity

15 10 5 0 Spring Summer Autumn Kitchen

Winter

Spring Summer Autumn Living room

Winter

Spring Summer Autumn

Winter

Bedroom

Figure 3.1 Mean measured nitrogen dioxide level (mg/m3) in kitchen, living room and bedroom in English homes that use gas or electricity for cooking (drawn from data presented in: Berry et al. [1])

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There is some evidence that homes with gas ovens have higher nitrogen dioxide levels than those that only have gas hobs (or ranges). Indoor kitchen levels will be higher if there is a pilot light on the gas cooker, but this is not a common feature of gas cookers currently produced. It is not clear whether the use of particular types of gas (e.g. bottled gas) causes higher levels of nitrogen dioxide than the use of natural gas, although some studies in some parts of the world suggest this is the case. There are marked seasonal differences in indoor nitrogen dioxide level in homes that use gas, with lower levels in summer when windows and doors are more likely to be open to cool and ventilate the home. Summer is a time when less cooking is done and more cold food is eaten, so usage of gas ovens as well as gas heaters is less common, leading to lower levels of indoor pollutants. Kitchen ventilation by the use of ‘active aspiration devices’ has been found in some reports to be associated with lower levels of kitchen nitrogen dioxide when gas cookers are present, but this is not always the case. Indeed the most effective means of ventilating a kitchen is to open a door or window to the outside air, which should lead to much lower levels of all combustion pollutants in the kitchen.

3.3.2 Nitrous acid Nitrous acid (HONO) is present as a gas in indoor and outdoor air. In the indoor environment nitrous acid is produced both directly by gas combustion and indirectly by absorption of nitrogen dioxide and then release of nitrous acid from water-containing surfaces in the home. Nitrous acid levels in the outdoor air are substantially lower than indoor levels due to rapid photodissociation in sunlight and therefore indoor levels are a result of indoor combustion processes. Nitrous acid will interfere with accurate measurement of nitrogen dioxide by the most commonly used passive samplers. Some have suggested that the actual measured nitrogen dioxide level from these samplers should be ‘adjusted’ or ‘corrected’ for this interference. More importantly it has been proposed that adverse health outcomes that have been attributed to nitrogen dioxide (or to exposure to nitrogen dioxide-producing appliances such as gas stoves) could be confounded (or explained) by exposure to nitrous acid. It has been argued that the inconsistent results from studies that examine the association of indoor nitrogen dioxide with respiratory health may be explained by failure to measure this co-pollutant. Nitrous acid can be measured by a passive sampler but there is a dearth of studies in which both nitrous acid and nitrogen dioxide have been measured. As for indoor nitrogen dioxide, indoor nitrous acid levels are higher in gas-cooking homes, likely to be higher in homes with gas ovens rather than just gas hobs and follow a seasonal pattern.

3.3.3 Particles The act of cooking, particularly frying and the cooking of fatty foods, generates particles in the kitchen irrespective of the fuel used for cooking. However even if account is taken of this, the generation of particles when boiling water, stir frying, bacon frying, cake

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POLLUTANTS PRODUCED WHEN USING GAS APPLIANCES IN THE HOME

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baking, meat roasting and potato baking produces higher peak concentrations of ultrafine particles if conducted with a gas, rather than electric, appliance. A prolonged peak of ultrafine particles has been shown to be generated by cooking potatoes in a gas oven for 75 min, but the peaks decay, possibly due to particles coagulating into large conglomerates after release. Particles are generated by the use of a gas or electric cooker even if no cooking occurs. The particles generated by gas are smaller (15–40 nm diameter) than those generated by electric appliances, and are probably carbonaceous. There is very limited information available on the indoor particulate level that can be attributed to the use of gas for cooking or gas heaters and, as indoor particulate levels in living rooms and bedrooms are very much higher in homes with smokers, the public health effort has been directed towards this. In addition, concerns over penetration of outdoor particles generated by motor vehicles into the indoor environment has focused attention on this aspect of indoor particulate matter. However other fuels, such as wood and especially biomass, are likely to produce very high particulate levels in the indoor environment if not properly ventilated.

3.3.4 Damp Gas combustion produces water vapour, which can lead to high levels of humidity in homes. High humidity encourages the growth of house dust mites, molds and bacteria within the home.

3.3.5 Formaldehyde Combustion of natural gas and other fossil fuels will produce small quantities of formaldehyde, but the contribution of combustion sources probably adds only small amounts of formaldehyde in comparison to other indoor sources such as cosmetics, paints, coatings and insulation materials.

3.3.6 Sulfur dioxide Sulfur dioxide is produced by fossil fuel combustion, particularly the burning of oil and coal, but indoor sources are thought to contribute little to overall exposure to this gas.

3.3.7 Total personal exposure vs indoor levels Exposure to some of the pollutants produced by gas may occur in the outdoor environment due to other sources. Total personal exposure to nitrogen dioxide can be measured using passive samplers designed as badges to be clipped onto clothing and will depend on several factors including time activity patterns, ambient nitrogen

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dioxide levels and indoor nitrogen dioxide levels. For individuals who spend the majority of the day in the home, such as small children, housewives and the elderly, indoor sources are likely to be more important. In school children in the south of England, total nitrogen dioxide exposure was higher in those with a gas cooker or a pilot light on the gas cooker, those who lived with one or more smokers, and those who travelled to school by means other than a car. However these factors did not explain all of the variation in total personal exposure to nitrogen dioxide and the authors concluded that total personal exposure could only be determined by making direct measures and could not be imputed from questionnaire-derived information. In the absence of indoor gas appliances, outdoor levels of nitrogen dioxide, which can show marked variation between homes in a single geographic area depending on the levels of outdoor traffic, is the most important determinant of total personal exposure to nitrogen dioxide.

3.4 Diseases associated with exposures Respiratory morbidity has been associated with the use of gas appliances and levels of indoor nitrogen dioxide, but at present most would agree that there is insufficient evidence to confidently state that the reported associations are causal. Longitudinal studies, in which exposure is assessed prior to the development of disease, provide stronger evidence for casual links and some have shown health effects. However there are few randomized controlled trials that show whether reduction in exposure to gas appliances or indoor nitrogen dioxide leads to improvement in respiratory health. Many of the published cross-sectional studies have been criticized for inadequate adjustment for other household or socio-economic factors that may be important in disease aetiology and associated with high levels of gas use (confounders), and for failing to separate inception of disease from aggravation of existing disease. There are also concerns that many studies that have collected data and shown there is no association remain unpublished (publication bias). While recognizing these caveats, there is a considerable amount of information from laboratory studies, chamber exposure studies and epidemiological studies that support the hypothesis that exposure to gas appliances and pollutants from combustion of other fossil fuels is harmful to respiratory health. The following patterns of respiratory illness have been suggested to be important: (1) airway inflammation that is possibly related to oxidative damage and which may lead to symptoms of wheeze, cough and decrements in lung function; (2) increased susceptibility to airway infections, particularly in small children, that may lead to increased reports of lower respiratory tract symptoms such as cough and wheeze; (3) enhanced responses to inhaled allergen that are manifested as increased reporting of symptoms of cough and wheeze. These are manifested as increased rates of asthma and/or chronic obstructive pulmonary disease and as exacerbations of existing disease.

3.4 DISEASES ASSOCIATED WITH EXPOSURES

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3.4.1 Risk groups It is arguable whether some age groups are more vulnerable to these effects than others. Disentangling this is rather difficult because age is strongly related to exposure. For example, young children may spend more time in the home but are unlikely to be directly involved in any cooking activity, and older people may spend more time in the home but actually use their cooking appliances relatively little. However, there is a growing body of consistent evidence that young children living in homes with higher indoor nitrogen dioxide levels have more respiratory symptoms, possibly related to infections, and prolonged duration of infection if they become infected. Socio-economically disadvantaged people are likely to be at particular risk from the harmful effects of indoor combustion processes. This is because they are more likely to live in homes that are poorly ventilated, use appliances that are poorly maintained and use their appliances inappropriately (for example use gas cookers for heating). In the UK, improved legislation has meant that landlords are now obliged to maintain cooking and heating appliances, and the high-risk groups are now thought to be families and individuals living in private accommodation who have low levels of disposable income. Nitrogen dioxide is an oxidant gas. High exposure to oxidants causes oxidative stress within the lung, resulting in inflammatory changes, asthma and chronic obstructive pulmonary disease. High antioxidant intake through the eating of fresh fruit and vegetables is likely to protect against these effects, but protection is also offered by the presence of genes that regulate antioxidant activity. Information on the importance of these antioxidant genes is rapidly increasing and some individuals have been identified as being particularly susceptible to these oxidant exposures due to their genetic makeup. For example children in Mexico City with the GSTM1 null genotype have been shown to have significant ozone-related decrements in lung function on exposure. While considerably more work is needed, it is possible that some individuals will be more genetically susceptible to health effects from exposure to pollutants from indoor combustion.

3.4.2 Randomized controlled trials In the largest randomized controlled trial yet conducted to assess the health effects of reducing exposure to gas pollutants, the treatment arm involved replacement of unflued gas heaters in primary school classrooms to a flued gas heater or electric heaters. The nonintervention group continued to use the unflued gas heaters. Researchers then monitored the health of asthmatic children (n ¼ 45 in intervention and n ¼ 75 in nonintervention arm). Difficulty in breathing, chest tightness and daytime asthma attacks were reduced but no effect on lung function or bronchial reactivity was observed. This study provides early evidence that exposure to gas pollutants is harmful but does not identify which of the specific pollutants is the culprit. The levels of nitrogen dioxide levels in the intervention classroom were substantially lower than the levels in the nonintervention classroom (6 hourly mean 29.6 and 89.3 mg/m3 respectively).

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3.4.3 Nonrespiratory conditions Most of the regulations that govern the installation and use of gas appliances are there to protect the public from the harmful effects of exposure to carbon monoxide a colourless, odourless, tasteless, toxic gas that is produced by the incomplete combustion of the fossil fuels including gas. Each year about 500 people in the USA (50 in the UK) die from unintentional CO poisoning in the home. In the UK about 70% of these deaths are related to the use of gas appliances, the remainder resulting from the use of solid fuels in fixed heaters or stoves. Fatally high levels of carbon monoxide arise when air flow around the combustion process is limited (for example due to a blocked flue), the carbon monoxide disperses into the room and there is insufficient ventilation of the room for it to disperse further or to go outside. Carbon monoxide has a high affinity for haemoglobin, forming carboxyhaemoglobin and reducing the capacity of the blood to transport oxygen. This leads to symptoms of headache, dizziness, fatigue, nausea and vomiting which may then progress to altered consciousness, coma and death. Chronic exposure may lead to a wider range of symptoms including tiredness, lethargy, headaches, nausea, dizziness, personality changes, memory problems, Parkinsonian symptoms, visual loss and dementias.

3.4.4 Diagnosis and management As stated above, the level of evidence to support a change in exposure to gas pollutants as a treatment for asthma or COPD, or as a preventive action for the development of asthma, is very limited. Most of our knowledge comes from observational studies rather than randomized controlled trials. There is insufficient evidence to recommend that people with COPD, asthma or repeated infections should alter the type of fuel they use to heat or cook, but all patients should be made aware of current health advice regarding the use of the appliances they have. No harm can come from assessing an individual’s exposure to products of combustion at interview. From the evidence we have to date this assessment requires the following information (1) type of appliance; (2) whether the appliance has a flue, vent or chimney; (3) frequency of use; (4) amount of time spent near the appliance while it is in use; (5) ventilation practice – use of extractor fans that vent to the outside and the opening of doors and windows to the outside air and to other rooms while it is in use; (6) frequency with which appliance maintained and checked; (7) possibility that flue is blocked or not working properly.

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Any individuals using gas and fossil fuel to heat or cook in their home should be given the following advice: (1) always use your appliances for the purpose they were meant – for example do not use gas hobs for heating rooms, do not use outdoor barbequing equipment inside the home; (2) regularly check the flue and venting system of your appliance to ensure it is free from any obstruction and is not blocked; (3) always use a gas appliance in a well-ventilated room; (4) whenever possible, open a door or window to the outside air when cooking – this reduces not only exposure to the products of combustion but also to the pollutants from cooking; (5) install a carbon monoxide monitor in all rooms in which fossil fuel is burnt; (6) each year have your appliance checked by a qualified engineer.

3.4.5 Other fuels; the international public health initiative for indoor air quality The World Health Organization estimates that more than 3 billion people worldwide cook and/or heat their homes with biomass fuels. Biomass is a term meant to differentiate ‘recently dead’ biological fuels (e.g. dung and crops residues) from fossil fuels (such as oil and coal), but generally it is used rather imprecisely, and it may be used to include wood and charcoal. Global estimates of disease suggest that in 11 countries (Afghanistan, Angola, Bangladesh, Burkina Faso, China, the Democratic Republic of the Congo, Ethiopia, India, Nigeria, Pakistan and the United Republic of Tanzania) indoor air pollution due to biomass exposure is to blame for a total of 1.2 million deaths a year. Inside some homes it is estimated that the 24 hour mean level of particulates (PM10) in homes is as high as 1000 mg/m3, far in excess of any outdoor guideline level set by any nation (e.g. the USA sets outdoor particulate levels at 150 mg/m3). Lower respiratory tract infections, chronic obstructive pulmonary disease and lung cancer have been attributed to these exposures. Other health outcomes thought to be important are tuberculosis, cataract, oro-pharyngeal cancer and asthma. Without doubt the key driver of these health effects is ineffective removal of the products of combustion by the use of chimneys over the cooking area, coupled with overall poor household ventilation. Randomized controlled trials are underway to quantify the health benefits of changing the stoves and improving their ventilation. In the meantime the WHO is encouraging governments to find clean alternatives for their populations. Ironically gas is seen as one of these cleaner alternatives – even though, as discussed above, many would consider its use to also be harmful to health. Clearly, however, when compared with biomass, gas is a clean alternative. In China, coal is widely used as a household fuel and several studies have shown associations with lung cancer that cannot be explained by the lower socioeconomic status and increased smoking behavior in coal users.

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Physicians treating patients who may have lived in homes where biomass has been used as a fuel for cooking should be alert to the possibility that their patient’s disease may be attributed to past exposure to products of biomass combustion.

References 1. Berry, R.W., Brown, V.M., Coward, S., Crump, D.R. et al. (1996) Indoor air quality in homes: Part 2. Building Research Establishment Indoor Environment Study. Building Research Establishment Report.

Further reading Advisory Group on the Medical Aspects of Air Pollution Episodes (1993). Oxides of Nitrogen. Third Report. HMSO: London. Institute of Medicine (US) (2000) Committee on the Assessment of Asthma and Indoor Air, Institute of Medicine. Clearing the Air: Asthma and Indoor Air Exposures. National Academies Press: London. Jarvis, D. et al. (1998) European Community Respiratory Health Survey. The association of respiratory symptoms and lung function with the use of gas for cooking. Eur. Respir. J. 11: 651–658 The Environmental Protection Agency Website, http://www.epa.gov/iaq/index.html (accessed 16 June 2009). The WHO Indoor Air Pollution Website, http://www.who.int/indoorair/en/ (accessed 16 June 2009). World Health Organization (2003) Health Aspects of Air Pollution with Particulate Matter, Ozone and Nitrogen Dioxide. World Health Organization: Bonn. Zhang, J., Smith, K. (2007) Household air pollution from coal and biomass fuels in china: measurements, health impacts, and interventions. Environ. Health Persp. 115: 848.

4 Cleaning and other household products Jan-Paul Zock Municipal Institute of Medical Research (IMIM-Hospital del Mar) and Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain

4.1 Introduction Cleaning is a necessary activity to maintain the functionality, appearance and appropriate hygienic condition of our homes. In general this mainly involves the cleaning of surfaces, particularly floors, furniture, sanitary fittings and windows. This can be done by dusting, wiping, sweeping or vacuuming, but is usually done with the aid of (chemical) cleaning products. Apart from those used for the cleaning of surfaces, several other types of chemicals are applied in many households. The most common include laundry products, air fresheners and pesticides. Alkaline-based soaps have been used for centuries for general cleaning purposes. During the second half of the twentieth century, many cleaning products for specific purposes were introduced, increasingly containing synthetic chemicals including disinfectants, agents for surface care and other additives. To date most evidence on the adverse respiratory health effects of cleaning products comes from occupational studies. Professional cleaning is common, both as a job and as a major activity in many other occupations. Presumably also the majority of the general population is to some extent exposed to cleaning products and other household chemicals. Apart from housewives and househusbands, most people actively do some cleaning in their homes. Household members may also be passively exposed to volatile agents from cleaning products when present in the home during or shortly after the application of these products. This indicates that the potential health consequences of the use of cleaning and laundry products comprise an important public health issue. Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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The purpose of this chapter is to provide a concise overview of the most common cleaning agents and other household chemicals and to describe factors that determine respiratory exposure. The major acute respiratory effects and chronic respiratory disorders associated with these chemicals will be reviewed, and practical measures to reduce exposure to household chemicals will be discussed.

4.2 Description of exposures 4.2.1 Cleaning products Purposes Cleaning products are commonly used on a variety of surfaces and have four different, often supplemental, purposes. Obviously the main goal of using cleaning products is to facilitate the removal of surface contaminants. This is based on physical and chemical processes, including the dissolution of deposits of minerals, fat and inorganic salts by acid–base reactions or by the forming of complexes (‘micelles’). A second purpose is surface care – maintenance of the material and/or making it appear shiny. Thirdly, certain products aim at the disinfection of the surface. Finally, cleaning products may be used to introduce a pleasant smell, and perhaps even to mask an unpleasant smell. An overview of the most common cleaning products applied for surface cleaning in homes is given in Table 4.1. Several products can be used for different purposes, probably including situations where this is not recommended. Consumption The individual exposure to cleaning products depends on the frequency of use and the amount of product used on each occasion. The latter is likely to be extremely variable between individuals, between countries/cultures and between purposes and applications, and is in general difficult to estimate. Product labels typically contain instructions for use, including recommended amounts and grade of dilution. It is, however, not unusual for these products to be used in higher concentrations or larger amounts than necessary. This may be related to the deep-rooted though unfounded belief that cleaning is done better and/or more quickly this way. The frequency of use of cleaning products may vary significantly across geographical areas. In the framework of the second phase of the European Community Respiratory Health Survey (ECRHS II), study participants in 10 European countries were asked if they did the cleaning or washing in their own homes and, if so, how often they used each of a selected list of products. More than half of all study participants indicated that they carried out cleaning and washing at home, with large differences in the frequency of use of products such as bleach, ammonia, glass cleaning sprays and furniture sprays. The consumption of cleaning products at the population level can be estimated using the marketing reports of manufacturers. For hypochlorite bleach these confirmed the findings of the ECRHS that bleach use is more common in southern Europe than in Nordic countries. Following both methods, the highest use of bleach was reported for Spain, with a per capita consumption of 12 litres per person per year in the early 1990s. More than 90% of the Spanish ECRHS participants reported ever using bleach in their

Toilet bowl

Gas hob, electric cooker, oven, microwave oven Wash basin, bathtub, taps

Kitchen sink unit, extractor hood

Upholstered furniture

Furniture (wood, metal, plastic)

Glass (windows, mirrors, furniture)

Carpeted (textile) floors

Multi-use cleaners, floor cleaners, bleach

Hard floors (stone, tiles, marble, synthetic) Wooden floors

Scouring cream or powder, bleach, multi-use cleaners Multi-use cleaners, bleach, acids

Floor cleaners suitable for wood, floor waxes Foams, shampoos, sprays (solvent-based dry-cleaning agents) Ammonia, alcohol (methylated spirits), glass cleaners (often sprays), multi-use cleaners Furniture cleaners (often sprays), multi-use cleaners Foams, shampoos, sprays (solvent-based dry-cleaning agents) Scouring cream or powder, multi-use cleaners Degreasing sprays, multi-use cleaners

Products

Overview of the most common surface cleaning products

Type of surface

Table 4.1

Remove dirt spots and calcium stains, disinfection

Remove accumulated dust, fat and dirt, give shine Remove accumulated dust and dirt (stains), surface care Remove accumulated fat and dirt, give shine Remove accumulated fat and dirt, give shine Remove dirt spots and calcium stains

Remove accumulated dust and dirt, surface care, disinfection, give shine Remove accumulated dust and dirt, surface care, give shine Remove accumulated dust and dirt (stains), surface care Remove accumulated dust, fat and dirt, give shine

Purposes of use

Weekly

Weekly

Depends; from daily to monthly

Weekly

Less than once per month

Weekly

Less than once per week

Less than once per month

Weekly (waxing less often)

Weekly

Typical frequency of application

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homes, while almost 80% used bleach on a weekly basis. An increasing trend of aerosolized (spray) application has occurred over the last decade: over 1 billion household aerosols (the vast majority for cleaning) were produced in Europe in 2006. Chemical components Depending on the type of surface to be cleaned and the purposes of application, as outlined earlier, products contain a wide variety of chemical components. The most important are listed in Table 4.2. There are many qualitative and quantitative differences between products, but basically all contain a variety of substances from different chemical families. Few products contain (almost) exclusively one agent; an example is bleach which is basically an alkaline-buffered solution of sodium hypochlorite. The labels of household chemicals typically contain limited, ambiguous, nonquantitative information on chemical components. The information provided focuses on compulsory consumer information: whether the product is inflammable, corrosive and/or toxic. According to recently introduced European Union regulations, the ingredients of consumer products must be publicly available on the internet. In relation to this, the Human and Environmental Risk Assessment (HERA) on ingredients of European household cleaning products project is noteworthy (www.heraproject.com). This is a voluntary industry program to carry out human and environmental risk assessments on ingredients in household cleaning products. HERA is a European partnership established in 1999 between the formulators and manufacturers of household cleaning products and the suppliers and manufacturers of the raw chemical materials for the chemical industry. Table 4.2

Main chemical components of cleaning products

Type of agent

Aim or mechanism

Examples

Detergents (surfactants)

Lower surface tension of water

Complexing agents (water softeners) Alkaline agents

Acids

Dissolve and bind calcium and other cations; regulate the pH Dissolve fatty substances, disinfection, inhibit corrosion of metal surfaces Dissolve calcium

Fatty acid salts (soap), organic sulfonates Ethylene diamine tetraacetic acid, tripolyphosphates Silicates, carbonates sodium hydroxide, ammonia

Solvents Corrosion inhibitor Film formers, polishes

Dissolve fatty substances Protection of metal surfaces Surface care

Disinfectants

Destroy bacteria and other microorganisms

Preservatives

Avoid microbial growth during product storage Introduce pleasant smell

Perfumes, scents

Phosphoric-, acetic-, citric-, sulfamic-, hydrochloric acid Alcohols, glycol ethers Ethanol amines Wax, acryl polymers, polyethylene Hypochlorite (bleach), aldehydes, quaternary ammonium compounds Benzalkonium chloride, isothiazolinones, formaldehyde D-Limonene, terpenes (pinene)

Reproduced from Occupational and Environmental Medicine, Zock, J.P. 62: 581–584,
2005, with permission from BMJ Publishing Group Ltd.

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59

4.2.2 Determinants of respiratory exposure Respiratory exposure occurs due to evaporation of volatile components, especially enhanced when applied on large surfaces such as floors. The personal (effective) exposure will depend on the amount of cleaning product and the concentration of the active ingredients, temperature, humidity and ventilation, among others. The use of products in spray form (either propellant-based aerosols or bottle pump atomizers) facilitates inhalation of liquid aerosols containing both volatile and nonvolatile agents. A comprehensive overview of chemical exposures was provided by Nazaroff and Weschler [1], including both chemical ingredients and secondary pollutants created by chemical reactions with airborne oxidants or surface contaminants. There is relatively little data available to describe the exposure patterns associated with the use of different cleaning products, and there are few experimental studies on emissions and exposures, which mainly focused on volatile components after application of cleaning products. Most exposure studies were done under experimental conditions. Volatile chemicals under study included ammonia, ethanol, 2-butoxyethanol, terpenoids such as a-terpineol and limonene, among many others. Models have been developed to assess airborne exposure to volatiles from cleaning products. In a small study, personal exposure to ammonia and chlorine was measured continuously during common household cleaning activities. Peaks were identified and related to specific cleaning tasks and products. Finally, several studies have measured common volatile organic compounds that may originate from several sources, including household chemicals and furniture, carpets and building materials.

4.2.3 Acute inhalations Events involving acute inhalations of large quantities of chemicals (gases or fumes) have been frequently described, in both occupational and nonoccupational settings, including the household. In relation to cleaning products, these acute high-level exposures are mainly caused by inadequate mixtures of incompatible products, and to a lesser extent by spills or highly intensive contact with released airborne irritants. The most commonly reported mixtures include hypochlorite bleach with acids (e.g. phosphoric acid from toilet bowl cleaner; hydrochloric acid from decalcifiers), leading to a release of the strong airways-irritant chlorine. Mixing bleach with ammonia leads to the release of chloramines with irritant properties, predominantly the most volatile and less watersoluble trichloramine. The latter is also produced, albeit to a lesser extent, after mixing bleach with dishwashing liquid.

4.2.4 More information and data on exposures REACH is a new European Community Regulation on chemicals and their safe use (EC 1907/2006). It deals with the Registration, Evaluation, Authorization and Restriction of Chemical substances. The new law entered into force on 1 June 2007 (http://ec.europa. eu/environment/chemicals/reach/reach_intro.htm) and requires the coordination of the in-depth evaluation of potentially hazardous chemicals and the maintenance of a

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public database in which consumers and professionals can find hazard information. This can be particularly helpful when the chemical constituents are known (for example through the HERA project, as mentioned earlier). Another helpful database is the European Chemical Substances Information System (ESIS), which contains diverse information on chemicals (http://ecb.jrc.it/esis).

4.2.5 Other household chemicals Apart from cleaning products, several other chemical-based products are to some extent applied in many households. The most common include laundry products, air fresheners and pesticides, shoe care products and drain cleansing agents. Laundry products Washing powders (laundry detergents) typically contain soaps, decoloring agents, perfumes and enzymes. In detergent manufacturing workers, inhalatory exposure may cause enzyme sensitization, even with encapsulated enzymes. Respiratory exposure related to household use is generally considered to be low, in particular in liquid formulation. Apart from detergents, exposures from fabric softeners and refreshers and laundry bleaching agents may be relevant. Air fresheners Air fresheners with fragrances are commonly used in homes. There are various methods of application, including aerosols and plug-in air fresheners (with an electrical element) that guarantee a continuous release of airborne perfume. Apart from the perfumes (deodorizers), air fresheners contain a variety of volatile chemical compounds. The use of air freshening sprays in toilets and other confined spaces may lead to temporarily high airborne concentrations. Shoe polishes Shoe care products are used for material care (typically leather) and/or to make the surface impermeable or waterproof (impregnation of material by water and soil repellents). These products are available as creams, polishes and sprays (either aerosols or nonaerosolized atomizers). The latter may lead to relevant inhalation of volatile chemicals, including organic solvents, in particular when used in large quantities and/or in poorly ventilated spaces. Pesticides This is a large group of chemicals with the main purpose of killing a variety of unwanted organisms. Pesticides are typically used in the home to control mosquitoes, cockroaches, flies, fleas, ants and rodents. Some are used to treat (preventively or actively) pets like cats and dogs, or ornamental plants. Some specific products containing fungicides are used to treat surfaces like walls or ceilings of bathrooms that are infested with mold. Aerosolized applications are common and involve inhalatory exposure during and shortly after use. Pesticides may contain a variety of active ingredients such as organophosphates and carbamates, among others. Residual exposures may be relevant for a longer period.

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61

Drain cleansing agents Drain cleansing agents (sink decloggers) are highly corrosive chemicals that dissolve material obstructing a drain. They typically consist of caustic soda (almost 100% sodium hydroxide), although some are based on acids or other chemicals. Exposures are typically occasional and acute but may be massive in accidental situations.

4.3 Diseases associated with exposures 4.3.1 Populations at risk The active use of cleaning products and other household chemicals usually involves the highest exposures and users therefore form the main population at risk. In addition, other household members should be considered at risk due to passive exposure to chemicals from these products during or shortly after use. The most susceptible groups probably include children and those with chronic respiratory or allergic disorders. It has also been suggested that prenatal exposure related to the use of household chemicals by the mother during pregnancy may be relevant.

4.3.2 Asthma There is growing evidence that professional cleaning involves an increased risk of asthma. Epidemiological studies have identified specific professional cleaning products associated with asthma, including bleach and several sprays. Most of this evidence has been based on lower respiratory tract symptoms suggestive of asthma, and in fewer studies also on bronchial hyperresponsiveness. The mechanisms are largely unknown, but both irritant-induced asthma (due to either acute high-level or recurrent moderatelevel exposure to irritants) and sensitizer-induced asthma have been hypothesized. Most case studies on asthma in relation to cleaning products are related to acute inhalations, either on the job or in private households. Only very few studies have evaluated asthma and other respiratory health effects of common household use of cleaning products. Active users An analysis of the risk of asthma by occupational groups using participants from 12 countries of the ECRHS I showed that housewives had a 20–30% increased risk of asthma when compared with nonmanual workers. This was suggestive of an increased risk of either new-onset asthma and/or exacerbated asthma related to household work. In the follow-up study (ECRHS II), the frequency of use of specific cleaning products was assessed for those who did the cleaning in their homes. The incidence of asthma was higher among those who frequently used sprays (Table 4.3). This risk was predominantly found for the commonly used glass cleaning, furniture and air refreshing sprays. Cleaning products not applied in spray form were not associated with asthma in this study. In an asthma case–control study among domestic cleaning women in Spain, cleaning their own homes formed an important part of their exposure to cleaning products. The

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Table 4.3 Relationships between the use of household cleaning sprays and the incidence of asthma. European Community Respiratory Health Survey II, n ¼ 3484 participants doing the cleaning and/or washing in their homes and had no asthma at baseline Category

Frequency

New-onset asthma symptoms or medication, RR (95% CI)

New-onset wheeze when not having a cold, RR (95% CI)

New-onset asthma diagnosed by a physician, HR (95% CI)

Use of sprays <1 day/week 1 type of spray used
1 day/week 2 types of spray used
1 day/week
3 types of spray used
1 day/week p for linear trend

58%

1.00 (Referent)

1.00 (Referent)

1.00 (Referent)

26%

1.37 (0.99–1.90)

1.25 (0.92–1.69)

0.97 (0.53–1.77)

10%

1.45 (0.92–2.27)

1.63 (1.10–2.41)

1.47 (0.70–3.06)

6%

2.40 (1.47–3.91)

1.80 (1.11–2.94)

2.96 (1.33–6.56)

0.001

0.003

0.022

Relative risks or hazard ratios with 95% confidence intervals from log-binomial or Cox’s proportional hazards regression models, adjusted for sex, age, smoking status, cleaning job and study center. Reproduced with permission of the American Thoracic Society, Zock, J.P., Plana, E., Jarvis, D. et al. (2007) The use of household cleaning sprays and adult asthma: an international longitudinal study. Am. J. Respir. Crit. Care Med. 176: 735–741.
American Thoracic Society.

strongest independent risk factors for asthma in this study were frequent use of bleach and a history of acute inhalations related to cleaning products (predominantly due to mixing bleach with either acids or ammonia). A panel study among the cases of this study showed that frequent use of bleach, degreasing sprays and air fresheners were associated with an increase of symptoms on the day of exposure. This was suggestive of exacerbation of asthma due to exposure to household cleaning chemicals, but did not exclude the possibility of an earlier onset of asthma related to cleaning products as well. A study in the USA among asthmatic housewives confirmed that the use of cleaning products in the home produced short-term lower respiratory tract symptoms. This effect was not apparent in nonasthmatic individuals. Some chemicals may have allergy-promoting (adjuvant) effects and therefore may be indirectly related to allergic asthma. A systematic review concluded that it is unlikely that the use of cleaning agents should be considered to possess an important adjuvant effect in the general population. Several ingredients of cleaning products have been qualified as asthmagenic, such as sulfonates, ethanolamines and various perfumes such as pinene and limonene. Acute inhalations including reactive airways dysfunction syndrome Within the framework of the ECRHS II, acute inhalations during the 10-year period of follow-up were associated with new-onset asthma with bronchial hyperresponsiveness. Mixing of cleaning products accounted for 10% of all reported incidents, and was related to a 2.5-fold increased risk of asthma at follow-up. Consistently, in the case–control study among domestic cleaners mentioned earlier, 79% of the asthma cases reported a history of acute inhalations against 51% of the controls. This suggested that a relevant proportion of asthma cases among these cleaning women could be

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63

attributed to a history of acute inhalations. About two-thirds of the reported events were related to the mixing of two or more cleaning products, principally mixtures with bleach; others were incidents involving hydrochloric acid or ammonia. Data from poison control centers have shown increased airways responsiveness after massive irritant inhalations, particularly in those with persistent respiratory symptoms. Symptoms resolve quickly in most affected individuals; residual morbidity including persistently increased bronchial responsiveness is typically found in a minority. Analysis of hospital discharge data showed that household cleaning products were responsible for 24% of nonworkplace exposures leading to chemical-related respiratory disease. Reactive airways dysfunction syndrome (RADS) is an asthma-like disorder as it shares increased bronchial responsiveness and reversible airways obstruction with symptoms such as wheeze, cough and shortness of breath. It is produced after a onetime, massive exposure (acute inhalation). Cases of RADS related to cleaning products have been documented for mixing bleach with acids and for incidental high exposure to hydrofluoric acid due to intensive use of a cleaner. Other lung diseases Most epidemiological studies on respiratory effects of cleaning products have focused on asthma. However, the applied definition of asthma was often based on symptoms and hence did not exclude any overlap with conditions such as (chronic) bronchitis or perhaps bronchiolitis. Case reports are mostly related to incidental exposure to irritants from (the mixing of) cleaning products. Apart from asthma and RADS, other respiratory disorders have been reported in relation to acute inhalations. Adult respiratory distress syndrome (ARDS) was found in a patient after mixing bleach with acids (causing, presumably, a massive chlorine exposure). Toxic or chemical pneumonitis has been reported after a one-time high exposure to acids, chlorine and chloramines. Respiratory effects related to passive exposure The potential relevance of indirect exposure to cleaning chemicals in adults is illustrated by a case description of new-onset sensitizer-induced asthma due to a quaternary ammonium compound in a floor cleaner. Epidemiological studies in children have mainly focused on total chemical burden, assessed either by questionnaire or by measurement of volatile organic compounds. Analysis of data from the ALSPAC birth cohort study in the UK showed that a higher frequency of use of household chemicals by pregnant women was associated with a higher risk of wheeze in the offspring up to six years of age. The most common products included disinfectants, bleach, aerosols, air fresheners, window cleaners, solvents and pesticides. The observed respiratory health effect could also be associated with the use of household chemicals by the mother during the first years of life, since this was strongly correlated with prenatal use. A study among 234 Belgian children aged 10–13 years found that regular use of hypochlorite bleach in their homes was associated with less allergic sensitization to indoor allergens, but at the same time possibly with more symptoms of recurrent bronchitis and recurrent colds. The authors proposed that passive exposure to bleach may lead to respiratory symptoms through airway irritation, and that

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bleach may be efficient in inactivating indoor allergens and hence reduce potential allergic sensitization.

4.3.3 Respiratory health effects of other household chemicals In the ECRHS study on household cleaning sprays and asthma mentioned earlier, the use of air fresheners was among the sprays that were consistently associated with newonset asthma (Table 4.3). Very few studies have evaluated the respiratory effects of domestic use of pesticides. There is growing evidence that occupational exposure to pesticides may have adverse respiratory health effects and the professional use of pesticides has been associated with atopic asthma and with allergic rhinitis. Several active ingredients of pesticides may act as endocrine disruptors. It is unclear whether lower and/or less frequent exposures to pesticides in the home environment can negatively affect the immune and/or the respiratory systems. Apart from cleaning products, severe acute respiratory illness has been linked to incidental high exposures to chemicals from shoe sprays. A large number of cases with acute chemical pneumonitis or polymer-fume fever have been reported, probably related to several volatile hydrocarbons and fluoropolymers present in these sprays. Symptoms are mostly reversible, and may include cough, shortness of breath, chest tightness and fever. Chest radiographs may show alveolar or interstitial infiltrates. Acute inhalations due to the (incorrect) use of drain cleansing agents have been reported to lead to a variety of acute respiratory effects that commonly require medical attendance. Several studies evaluated the associations between asthma and levels of common volatile organic compounds (VOCs) that may originate from several sources, including household chemicals and furniture, carpets and building materials. Findings from available studies on associations between volatile organic compounds and asthma are summarized in a comprehensive review by Dales and Raizenne [2]. One study found that VOCs were associated with asthma in a case–control study among children less than three years of age, being apparent for most individual VOCs including benzene, toluene and ethylbenzene, among others. For more details on VOCs and their relation with respiratory diseases, see Chapter 5.

4.3.4 Non-respiratory endpoints Apart from inhalatory exposure, dermal exposure to cleaning products is important and skin disorders probably constitute the main nonrespiratory outcome related to cleaning products. Many agents are corrosive at high concentrations and irritative at lower concentrations. This involves a chemical hazard that may produce irritation of skin, eyes and mucous membranes of upper and lower airways, and even skin burns related to intensive and/or prolonged contact to high concentrations. Some chemical components of cleaning agents have carcinogenic or neurotoxic properties, and may act as endocrine disruptors or affect reproduction. Many household chemicals have acute toxicity after ingestion. Finally, it has been suggested that

4.4

DIAGNOSIS AND MANAGEMENT ISSUES

65

women frequently using air fresheners or other aerosols more often suffer from depression and headache, and possibly diarrhea. Intoxication (ingestion) Poisoning due to the ingestion of cleaning products is mainly related to suicide attempts and to accidents in small children. Poison control center data show that household products are most frequently ingested by children under 5 years of age. Domestic chemicals including cleaning products accounted for about 30% of all accidental ingestions by children. Hypochlorite bleach is a commonly reported product in relation to accidental ingestion and may lead to hospitalization. Hand dermatitis Skin contact principally affects the hands, and hence this is where dermal effects are mainly seen. Cleaning agents contain substances that degrease and break down the natural barriers of the skin. Exposure to water (wet work) changes the defense mechanisms of the skin barrier, and the skin is then easier to penetrate and more sensitive to other chemical substances. Probably the most common dermal disorder caused by cleaning products is irritant contact dermatitis with symptoms such as itching, redness, rough skin and vesicles on hands and (between) fingers. Allergic contact dermatitis may also be relevant. Some agents in cleaning products including preservatives and surface active agents may act as contact allergens. Several cleaning products contain high concentrations of skin irritants (such as acids or bases) and dermal effects after acute exposures have been described. For example, serious skin burns on hands and forearms were related to corrosive properties of caustic soda in an oven cleaner.

4.4 Diagnosis and management issues 4.4.1 Diagnostic issues Many of the observations described in this chapter point towards nonspecific respiratory effects of cleaning agents and other household chemicals, and in most cases the underlying mechanism remains to be clarified. This indicates a challenge for physicians when it comes to the recognition of respiratory diseases due to cleaning products and their correct diagnosis. When taking the medical history of a patient, it is important to focus on the time of onset of asthma and respiratory symptoms. If the patient has a history of asthma of say several years, the exacerbation of a pre-existing disease due to irritant exposures may be relevant. This is particularly evident when typical time patterns in exacerbations (symptoms) suggest a direct relation to exposures. Analogous to work-related asthma, even the recurrence of childhood-onset asthma that had apparently remitted may be considered. It is important to record a list of chemical products that the patient commonly uses in the household. This should include typical habits like diluting and mixing, and information about minor and major accidental inhalations should be obtained. This may be helpful to identify potential causes of the disease, and also to propose measures to prevent further exposures (see next page).

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It is even more difficult to diagnose a case of new-onset asthma or any other lung disease as being caused by specific cleaning products. This may be feasible when the patient shows specific sensitization to (components of) a cleaning product in a comparable way as a case of occupational asthma can be diagnosed. However, this is complex for a lung disease triggered by repeated exposure to irritants. Finally, in cases who have just suffered acute inhalations, standard clinical examination, blood cell counts and chest radiography are all helpful for diagnosis. It is strongly recommended to closely monitor the patient on a regular basis for a longer period. Repeated clinical examinations may include the severity of symptoms, use of treatment such as bronchodilators, characterization of the inflammatory pattern, spirometry and bronchial responsiveness testing.

4.4.2 Prevention of (further) exposure Reduction of respiratory exposure from cleaning products and other household chemicals is desirable to avoid future exacerbations and other respiratory health effects. The best prevention is probably complete avoidance of a certain product, but this may not always be practical. In addition, the specific cause of (exacerbations of) a respiratory condition is often not identified from the variety of cleaning agents that are used in the household. Therefore general recommendations should be given regarding education and other information, good housekeeping, reduction of hazardous chemicals, avoidance of exposure and personal protection. Clear and relevant safety information and education are extremely important in order to improve the awareness of hazards and the knowledge of simple ways to reduce risks. Prevention brochures about household chemical exposures have been developed and tested in target populations. Information should include how to store, dilute and use products; how to avoid incompatibilities with other products; accessibility to the supplier’s customer service system; how to properly dispose of unused products, waste and containers; and how to protect children and what to do in case of emergency. Before any application of cleaning products, the following issues may be considered: 1. Is it really necessary to use this strong/irritant product (ammonia, bleach, strong acids, degreasing sprays) or could it be replaced by other, less aggressive products? 2. If necessary, could it be used less frequently, and/or in smaller quantities? 3. Could it be used in another application form (glass cleaning sprays can often without inconvenience be replaced by glass cleaning liquids, and inhalatory exposure consequently reduced)? The mixing of cleaning products should always be avoided; even liquid multi-use cleaning products (e.g. for mopping floors) may contain bleach, and decalcifiers and toilet cleaners may contain acids. Surfaces should be rinsed after application of a cleaning product before using a second product (if necessary). During and after the use of cleaning products, windows should be opened whenever possible in order to increase the ventilation rate. Active users and other persons should avoid staying in the same room immediately after the application of strongly irritant

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cleaning agents. Respiratory protection can be recommended in cases of expected high airborne exposures to ammonia or other irritants by using a proper mask or a damp cloth. In order to avoid dermal effects such as contact dermatitis on the hands, the use of gloves can be recommended during wet work and/or when using chemical cleaning products. In addition, direct skin contact with cleaning products should be avoided, wet hands should be minimized and if wet dried thoroughly. Finally, an appropriate hand cream should be applied after use.

4.4.3 Public health issues The use of many household cleaning products and other domestic chemicals is very common, and therefore even a weak association or low relative risk of respiratory effect may have a large public health impact. The population burden of household chemicalrelated respiratory disease is difficult to estimate. Nevertheless, in the ECRHS it was estimated that, among people cleaning their homes, one in seven adult asthma cases could be attributed to common use of household sprays. This indicates a relevant contribution of household chemicals to the burden of asthma in adults.

4.5 Summary and conclusions Cleaning and other household products are commonly used and imply a large population at risk. Indirect exposure may be relevant as well, particularly for young children. Cleaning products contain a variety of chemical ingredients. Many of these are airway irritants and some have sensitizing properties. Inappropriate use and particularly mixing of incompatible products may lead to acute inhalations of strong irritants. This may result in long-term effects such as RADS. Recurrent exposure to airborne irritants from cleaning products may result in asthma-like chronic lower respiratory tract symptoms and perhaps bronchial hyperresponsiveness. Little is known about effect mechanisms, which makes accurate diagnosis difficult. Information and avoidance of strong chemical products may be helpful to reduce the respiratory burden related to household cleaners. Contact dermatitis on the hands is probably the most relevant nonrespiratory effect related to cleaning products.

References 1. Nazaroff, W.W., Weschler, C.J. (2004) Cleaning products and air fresheners: exposure to primary and secondary air pollutants. Atmos. Environ. 38: 2841–2865. 2. Dales, R., Raizenne, M. (2004) Residential exposure to volatile organic compounds and asthma. J. Asthma 41: 259–270.

Further reading Blanc, P.D. (2003) The role of household exposures in lung disease among women. Eur. Respir. Monogr. 25: 118–130.

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Wolkoff, P., Schneider, T., Kildeso, J. et al. (1998) Risk in cleaning: chemical and physical exposure. Sci. Total Environ. 215: 135–156. Zock, J.P. (2005) World at work: cleaners. Occup. Environ. Med. 62: 581–584. Zock, J.P., Plana, E., Jarvis, D. et al. (2007) The use of household cleaning sprays and adult asthma: an international longitudinal study. Am. J. Respir. Crit. Care Med. 176: 735–741.

5 Building materials and furnishing Jouni J.K. Jaakkola1 and Reginald Quansah2 1 2

University of Oulu, Finland and University of Birmingham, Birmingham, UK University of Birmingham, Birmingham, UK

5.1 Introduction to building materials and furnishing as sources of indoor air pollution The traditional design and construction of buildings is driven by functional, esthetic and economic values, but until recently little attention has been paid to the potential adverse health impact of indoor materials. This chapter describes how building materials and furniture partly determine indoor environmental conditions in homes and can be sources of emissions which may influence airways and respiratory health. Some of the available evidence comes from studies of other buildings such as office buildings, day-care centers and schools, but this evidence can be readily applied to homes. The determinants of indoor air quality can be divided into (1) outdoor sources, (2) the building envelope, (3) occupants and their activities, (4) physical indoor sources and (5) heating, ventilating and air conditioning. Building materials and furnishing naturally represent potential physical indoor sources of gaseous and particulate air pollution, which may have direct health effects. However, all the other determinants, except outdoor sources, may play a role in human exposure from building materials and furnishing. The building envelope, including the structures, openings and the type of ventilation system, influences the elimination of air pollutants from building materials and furnishing. Occupant activities and heating, ventilating and air conditioning influence indoor temperature, relative humidity and air exchange, which modify the relations between emissions and human exposure. Indoor temperature, relative humidity and their variation influence the emission rates of pollutants and their elimination. Dampness in materials may lead to microbial growth and mold problems and some microbes produce volatile organic compounds (VOCs). Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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5.2 Emission of formaldehyde from building and interior surface materials Formaldehyde (HCHO) is present in building materials (particleboard, fiber board and plywood), paintings and wall paints, glued wall papers, coatings, fabrics, fibers, draperies, carpets and insulation materials (Table 5.1). It is emitted more significantly from pressed wood products (particleboard, hardwood plywood panelling, medium density fiberboard) made using adhesives that contain urea-formaldehyde (UF) than those containing phenol-formaldehyde resins or conversion varnishes and latex paints. Experimental chamber studies have reported emission rates of different building materials including base coat floor finish (10, 800 mg/m2 h), pressed wood products (particleboard) (104–1580 mg/m2 h) and medium density fiber boards (210–264 mg/m2 h), most of which have been published by the WHO. Other sources of HCHO emissions include indoor ozone reactions with primary VOCs, or with fitted carpets or limonene, or with aliphatic hydrocarbons in photocopiers or laser printers. The first of these reactions is known experimentally to increase HCHO levels by a factor of 3. In a series of studies conducted in several European countries in the 1980s, HCHO concentrations between 72 and 3000 mg/m3 (0.06–2.50 ppm) were reported, with levels particularly high in houses containing particle board, UF insulation, glues for wall coverings or sealing-wax parquet flooring. Lower but significant concentrations have been reported more recently. For example, HCHO levels of <5–110 mg/m3 (0.004–0.090 ppm) were reported in selected Swedish homes, but in wooden houses, with wall-to-wall carpets and painted woods, the level of HCHO was above the Swedish limit value (100 mg/m3; 0.08 ppm). Lower concentrations (<3–72 mg/m3; 0.003–0.060 ppm) have also been noted in selected schools in Sweden and these were related to the fleece factor (area of fabrics in relation to room volume) and shelf factor (calculated as the length of open shelves in relation to room volume). Concentrations above 60 mg/m3 (>0.05 ppm) were also noted in newly painted living and bedrooms of children having new furniture and carpets as well as unflued gas heaters. In other studies the concentrations of HCHO were noted to decline with the age of the building [homes built in 2002, 123.5
70 mg/m3 (0.10
0.06 ppm), compared with those built in 1999 (83
36 mg/m3 or 0.069
0.03 ppm) and 1990–1998 (85
21 mg/m3 or 0.07
0.02 ppm)] and were higher in newly built houses containing computers and new furniture, and were significantly higher during summer than winter. In some schools that continue to use particleboard panels in Eastern Europe, HCHO concentrations above the 1987 WHO threshold value (0.05 ppm; 60 mg/m3) have been reported. Formaldehyde concentrations of 34.4
1.9 mg/m3 (0.03
0.002 ppm) have also been measured in kitchens, living rooms and bedrooms in France, and these levels were associated with temperature and the age of the floor coverings. Most people detect HCHO odour at concentrations of 49.1–490 mg/m3 (0.04–0.4 ppm). In the literature, upper airway irritation of the nose and throat is reported to occurred at concentrations in excess of 1227 mg/m3 (1.02 ppm) and lower airway effects characterized by cough, chest tightness and wheezing occurred at HCHO levels 2454 mg/m3 (2.05 ppm) [1].

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5.2 EMISSION OF FORMALDEHYDE

Table 5.1 A summary of major chemical emissions from building materials and interior finishes and possible respiratory health effectsTable 1 not mentioned? Building material and interior finishes source

Major chemical(s) emitted

Respiratory effects/symptoms

Textile wall materials

Naphthalene, methyl pyrrolidinone, styrene, aldehyde, phenol, formaldehyde, acrylonitrile, acetaldehyde, decane, tetradecane Propylene glycol, texanol, diethylene glycol monoethylene ether, diethyleneglycol monobutyl ether, dipropylene glycol monomethyl ether, ammonia, TXIBb, formaldehyde, butanol, aliphatic compounds (C8–C11) Toluene, xylene, white spirit, isobutanole, trimethyl benzene, n-nonane, n-decane, n-undecane Phthalate esters in dust (DEHP,b BBzPb), phthalate esters in air (DEHP, BBzP, DnBP), MEHP,a 2-butoxyethanol, 2-(2-butoxyethoxyl) ethanol, phenol, trimethyl benzene, TXIB, ammonia, acetic acid, hexanal, hexanoic acid, pentanoic acid, decane MEHP,a microbesb (Aspergillus veriscolor, Penicillium chrysogenum, Ulocladium botrytis, Fusarium culmorum, Cladosporium herbarum), MVOCsb (1-octen-3-ol, 2-ethyl-hexanol, dimethyl disulfide, 2-butanones, terpenes, 2-methyl furan, 3-methyl furan, 2-ethyl-1-hexanol, ammonia) Microbesb (A. veriscolor, P. chrysogenum, U. botrytis, F. culmorum, C. herbarum), MVOCsb (1-octen-3-ol, 2-ethylhexanol, dimethyl disulfide, 2-butanones, terpenes, 2-methyl furan, 3-methyl furan, 2-ethyl1-hexanol) Formaldehyde,b limonene, acetaldehyde, hexanal, pentanal, butylacetate, cyclohexanone

Mucosal irritation, allergic reaction

Painted indoor surface (with water-based paints)

Painted indoor surfaces (with solvent-based paints) PVC surface materials

Damp PVC flooring material

Damp interior finishes and building material like wall papers, woodchip etc. (excluding PVC materials)

Particleboard panels, furniture, cabinetry, shelving, wooden house, newly built house

Breathing difficulty, irritation of the eyes, nose and throat, nasal mucosal swelling, contact eczema, headache, wheezing, breathlessness,b asthma,b runny nose, hay fever Tiredness, eye irritation, nausea

Asthma,b allergic rhinitis,b eczema, wheezing, cough, phlegm, nasal congestion, bronchial hyper-reactivitya

Eye,b noseb and throatb irritation, cough,b wheezing,b asthma,b tiredness, headache, airway infections,b bronchial hyperreactivitya

Eye,b noseb and throatb irritation, cough,b wheezing,b asthma,b tiredness, headache, airway infections

Bronchial hyperresponsiveness, nose,b throatb and eyeb irritation, asthmab (continued)

72 Table 5.1

CH 5 BUILDING MATERIALS AND FURNISHING

(Continued )

Building material and interior finishes source

Major chemical(s) emitted

Respiratory effects/symptoms

Carpets, new linoleum flooring, new synthetic carpeting, new carpets, wall-to-wall carpets Interior surface polished with oil-based varnishesc

4-Phenylcyclohexene, vinyl acetate, styrene, dodecanol, acetaldehyde, formaldehyde

Runny nose, allergic rhinitis, asthma, wheezing, bronchial hyperresponsivesness Eye,b noseb and throatb irritation, coughb

Isobutanol, ethyl benzene, xylene, HCHOb

Note: items in column 1 reported to possibly cause respiratory health effects in column 3. a Expected respiratory health effects based on animal toxicity data. bEmissions reported to possibly cause respiratory health effects. cCould possibly cause respiratory health effects but nothing has been reported.

In mobile homes where UF glued particle board had been used for indoor panelling, high prevalences of nose and throat irritation and severe headache and tiredness were noted. Wall-to-wall carpets were also related to nocturnal breathlessness in Swedish adult populations. Eye irritation, headaches, nose and throat irritation and wheezing were also reported among children exposed to new synthetic carpet, wall covering, particleboard and furniture and recent painting. Among 88 children (cases) and 104 controls in Australia, a 10 mg/m3 (8.33ppb) increase in HCHO levels in living rooms and children’s bedrooms was associated with a 3% increase in risk of asthma, and HCHO levels >60 mg/m3 (0.05 ppm) were also related to a 39% increased risk of asthma in other case children. Several studies have also found strong associations between mucous membrane irritation and other respiratory problems among home occupants exposed to urea-formaldehyde foam insulation (UFFI). UFFI was used for housing insulation but was banned in many developed countries in the 1980s; variable but small levels of HCHO continue to be emitted depending on the age of building.

5.3 Emissions of volatile organic compounds There is no clear and widely acceptable definition for VOCs, but in the loose sense the term describes organic compounds with a boiling point range of 50–250 C (excluding pesticides) which would have an effect on air quality. The introduction of new building materials is changing the profile of VOC to include oxygenated compounds (e.g. carboxylic acids, alcohols, aldehyde and ketones) and chlorinated aromatic compounds of higher boiling points. Building materials, especially surface materials used on walls, floors and ceilings and interior finishes such as furniture, cabinets, carpet tiles and ceiling tiles, are major sources of primary VOC emissions (Table 5.1). Secondary emissions of VOCs formed through mechanisms such as reactions between ozone and aliphatic hydrocarbons (in photocopiers and laser printers), reactions between ozone and fitted carpets or limonene, microbiological emissions on damped surfaces (MVOCs), hydrolysis of wet PVC flooring materials or degradation of building and interior surface materials are also known. The most frequently reported VOCs include ethanol, limonene, carbonyls (aldehydes and ketones), aliphatic, cylic and aromatic hydrocarbons, methylene chloride, terpenes, glycols, acids and esters with their individual concentrations

5.3

EMISSIONS OF VOLATILE ORGANIC COMPOUNDS

73

varying from 5 to 50 mg/m3 (0.004–0.041 ppm), but higher concentrations have been found in newly built houses. Hodgson and Levin [2] for example, observed 3 times higher concentrations of acetaldehyde, propionaldehyde, benzaldehyde, a-pinene and D-limonene in newly built houses compared with existing houses. High concentrations of pentanal, a-pinene and D-limonene, 1,4-dichlorobenzene and dichloro-methane are also known in residential accommodations compared with offices because of the relatively large wood products to air volume ratio in the former. The total VOC (TVOC) concentrations measured in various dwellings in Europe are 250 mg/m3 (0.250 ppm) but lower concentrations are also known. Composite wood products and related products used for cabinet making and subfloors also emit aldehydes, terpenes and acetic acids and esters. Oil-based varnishes used as finishes on interior walls and ceilings also emit isobutanol, ethyl benzene, m,p,o-xylene and formaldehyde. Solvent-based paints with high VOC emissions are rapidly being replaced in developed countries by water-based substitutes with lower VOC emissions. The latter contain complex chemical compositions of butanols, 2,2,4-trimethyl-1,3-pentanediol diisobutyrate (TXIB), 2,2,4-trimethyl-1,3-pentanediol monobutyrate (texanol) and low concentrations of aliphatic hydrcarbons (C8–C11). In European studies the TVOC concentrations in dwellings with water-based paints have been around 413 mg/m3 (0.337 ppm). In one such study, TXIB was detected in 57% of living rooms and 60% of bedrooms. The maximum level of TXIB was about 373 mg/m3 (0.304 ppm) and that of tetanol was 50 mg/m3 (0.041 ppm). The indoor concentrations of the n-alkanes and butanol were 25 mg/m3 (0.020 ppm) and 10 mg/m3 (0.008 ppm), respectively, their concentrations being particularly high in newly built houses. Other studies have suggested that TXIB may have a strong affinity for dust particles and thus may interfere with the mucous membrane. Low geometric mean concentrations of acetaldehyde (10.7
1.8 mg/m3; 8.9
1.5 ppb), propionaldehyde (6.0
2.2 mg/m3; 5.0
1.8 ppb), pentaldehyde (8.9
2.7 mg/m3; 7.4
2.3 ppb) and hexanal (25.5
2.6 mg/m3; 21.3
2.2 ppb) were reported in recently refurnished rooms and kitchens with wall and floor coverings. Emissions of 2-ethyl-hexanol from wet PVC floor materials are also known. The growth of microbes of various genera in damp building and interior surface materials produces over 200 VOCs of microbial origin (MVOCs), but the most commonly reported of these include hydrocarbons (e.g. octane), alcohols (e.g. 2-methyl-1-propanol), sulfur compounds (e.g. dimethyl disulfide), ketones (e.g. 2-butanones), terpenes and terpene derivatives (e.g. geosmin), 2-methyl furan and 3-methyl furan. MVOC levels of 15–20 ng/m3 (0.012–0.016 ppb) have been reported, but concentrations of 423 ng/m3 (0.350 ppb) are also known. VOCs may affect the airways and induce inflammation and airway obstruction. VOC from water-based paint was shown to increase the prevalence of asthma 2-fold in Swedish healthy adults. Work-related symptoms of eye irritation, cough with sputum and itchy hands are common among users of water-based paints. Wheezing, asthmatic and respiratory symptoms are also known effects among users of solventbased paints, but among indoor occupants newly painted surfaces were associated with asthma and allergic symptoms. Measured concentrations of texanol (0.89 mg/m3; 0.70 ppb), TXIB (1.64 mg/m3) and MVOC (423 ng/m3; 0.350 ppb) were also related to nocturnal breathlessness and doctor-diagnosed asthma in 1014 pupils. Although

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this evidence is from observational studies, intervention studies have also suggested that wet PVC flooring, moist building problem and microbe growth on interior finishes and building material could also cause asthma in both children and adult populations.

5.4 Emission of phthalates from PVC building and interior surface materials Polyvinyl chloride (PVC) is a polymer and a major building material in which phthalates are used extensively as plasticizers to enhance its flexibility, viscosity, stability and other desirable physical properties. Plasticized PVC is used extensively indoors as wall and flooring coverings in kitchens, bathrooms and children’s playrooms and bedrooms because it is inexpensive and has easy-to-clean surfaces. Other indoor uses of plasticized PVC include roofing materials, shower curtains, electric cables, adhesives, synthetic leather, and so on. Because phthalate esters are not covalently bonded to the polymer with which they are mixed, they can migrate from PVC material and adhere to the surfaces of indoor particulate matter (PM) as well as house dust. Phthalate may also migrate to PM surfaces following wear and tear of PVC materials or during the use of other PVC products such as nail polishes. Di-ethyl-hexyl phthalate (DEHP) is the main phthalate ester found in house dust in a concentration range of 0.24–0.94 mg/g dust, but concentrations of other phthalates such as di-n-butyl phthalate (DPB) (0.13–0.69 mg/g dust) and n-butyl benzyl phthalate (BBzP) (0.22–0.75 mg/g dust) have been reported. In a nested case–control study, the mean geometric concentrations of BBzP were 0.237–0.224 mg/g dust and that of DEHP was 0.966 mg/g dust. BBzP was mostly emitted from PVC flooring material, whereas DEHP concentration was a result of emissions from PVC flooring in older buildings. These findings confirmed the results of an earlier study in which the indoor concentration of BBzP (0.208 mg/g dust) and DEHP (0.638 mg/g dust) was related to PVC flooring in children’s room. Several studies have measured urinary concentrations of phthalates and other biomarkers to understand the pharmacokinetics of individual phthalates or the extent of exposure to phthalates in a given population. In a new study in a population at Erlangen, Germany, 10% of the population had DEHP concentration levels above the tolerable daily intake (TDI) acceptable in the EU (37 mg/kg body weight/day) and 31% had values higher than the reference dose (RfD) of the US Environmental Protection Agency (20 mg/kg body weight/day). In a Japanese study phthalate esters were measured in kitchens of newly built houses. The levels of DEHP and particularly DBP were surprisingly high (6.18 mg/g dust). These concentrations were attributed to vinyl cloth used as ceiling coverings and vinyl paints. The authors suggested that exposure to phthalate esters through inhalation (7.8–15 mg/day) indoors is as important as ingested phthalate exposure in Japan (14.3 mg/day). Evidence of human hazards associated with phthalate exposure is very limited and most reports in the literature are based on animal studies. There is evidence of adverse effects such as increased weight, elevated enzyme levels and tumour development in rodents following administration of phthalates. Mono-2-ethylhexyl phthalate (MEPH) may modulate the immune response to allergen exposure in mice. At concentrations of 30 mg/m3 (0.024 ppm), calculated to be below the estimated level of human exposure to

5.5 DAMP BUILDINGS AND EMISSIONS OF BIOLOGICAL PARTICLES

75

indoor MEHP, no effect was observed, as evident in a recent review of 14 animal laboratory studies. In a recent systematic review and meta-analysis based on 27 studies, the risk of asthma and respiratory symptoms in the adult population was related to fumes emitted from PVC films in occupational settings. In the same review, the relation between PVC surface materials indoors and the risk of asthma (OR ¼ 1.55) and allergies was elevated (OR ¼ 1.33) among children. Scandinavian, German and Bulgarian studies have noted BBzP in house dust (from indoor PVC material) and this was associated with rhinitis and eczema, whereas DEHP was related to asthma. In other studies the presence of both moisture and wet PVC flooring material was significantly related to asthma and this was attributed to mono (2-ethylhexyl) phthalate (MEHP), a product of the primary hydrolysis of DEHP.

5.5 Damp buildings and emissions of biological particles Damp or moisture accumulates in building structures and/or interior finishes via leaks in roofs, windows or pipes; moisture from the ground penetrates into the building structure by capillary movement; moisture is created by humans and indoor activities such as cooking, bathing, respiration, humidifiers; and moisture may already be present in the building material from the time of construction. Damp may stimulate growth of microbes such as fungi, bacteria and in other situations protozoa, nematodes, mites and insects on material surfaces, thus defacing them and sometimes compromising the integrity of the material. Emissions of irritants and odorous substances from microbiological and chemical processes, e.g. HCHO and 2-ethyl-1hexyl-hexanol, on building structures and interior finishes following dampness are known. The minimal water activity to support fungi growth is 0.67–0.75. Equilibrium relative humidity, temperature and pH are also in the ranges 0.70–0.90, 8–60 C and 2–11, respectively. Several studies conducted in different parts of the world have shown that Aspergillus versicolor, Penicillum brevicompactum, P. chrysogenum and Cladosporum spp. are the most dominant species found on indoor surface materials and indoor ambient air. In wet rooms like bathrooms and kitchens (especially areas around the sink) Aureobasidium pullulans and Phoma exigua, Alternaria alternate, Cladosporium herbarum, C. sphaerospermum, Fusarium spp. and yeast have been identified on tiles, plasters and silicon caulking. Moist or damaged wallpapers such as woodchip, vinyl wallpapers, jute and cardboard containing cellulose may also support Acremonium strictum, Aspergillus niger, A. versicolor, Cladosporium herbarum, C. sphaerospermum, Epicoccum and yeast species. Stachybotrys chartarum, Aspergillus versicolo, Penicillum spinulosum and Streptomyces californicus have also been shown to grow on interior plasterboards at relative humidity 0.86–0.97. Some evidence exists that under limited nutrient conditions, some bacteria or fungi such as Streptomyces californicus can survive on the starch in plasterboards. Under favorable conditions microbes may produce mycotoxins such as alternariols, chaetoglobosin, mycophenolic acid, satratoxin and sterigmatocystins – each with potential dermatoxic, immunosuppressive and carcinogenic effects. Biologically active nonallergenic compounds, spores and cellular debris may also be liberated, e.g. during microbiological activity on damp surfaces, which could stay longer in the air traveling

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CH 5 BUILDING MATERIALS AND FURNISHING

through roofs, crevices and tiny cracks. The tiny fragments and spores could be carried by ultrasize particles and may enter the alveolar region when inhaled. The first signs of dampness on interior surfaces includes visible molds, damp stains, condensation on window panes and/or walls and moldy and musty smells. Early symptoms in indoor occupants such as tiredness and complaints of cold and other allergic symptoms such as eye, nose and throat problems have also been reported. There has been a series of reviews by various multidisciplinary groups in the US and Europe on this subject. The earlier review by the Nordic group of researchers (NORDDAMP) provided strong evidence that damp in buildings increases the risk of cough, wheeze and asthma and the effect estimates were in the range (ORs) 1.4–2.2, but the strength of association for symptoms such as tiredness, headache and airway infections was weak. These authors suggested that there exists a causal association between damp in building and adverse airway health effects. In the second review by a European group (EUROEXPO), which also included some members of the previous review, dampness in buildings and interior surfaces was related to health effects in non-atopics and atopics, but the causative agents, such as microbiological agents and organic chemicals from degraded building materials, were not conclusively identified. Moisture and microorganisms in buildings may affect health of indoor occupants through any one or more of the following ways: (i) allergic reactions (sensitization and immune response, i.e. asthma, allergic rhinitis or hypersensitivity reactions); (ii) infections (i.e. growth of the fungus in or on the body); and (iii) toxic responses. In a recent meta-analysis by Fisk and colleagues [3], a summary OR of 1.34–1.75 for several respiratory health problems was associated with building and indoor interior surface dampness and moldy conditions. About 30–50% of the increase in a variety of respiratory and asthma-related health problems were associated with building material damp or mold problems.

5.6 Specific diseases associated with exposures from building materials and furnishing Chemical and biological emissions from building materials may contain specific compounds which can cause the onset of new asthma as well as asthma-related symptoms among subjects who already have asthma. There is also some evidence that the risk of allergic rhinitis is related to emissions from building materials. Asthma is characterized by airway inflammation and airway obstruction, which is reversible either spontaneously or with treatment, and increased airways responsiveness to a variety of stimuli. The main mechanisms in its etiology are specific sensitisation involving type I immune reactions and inflammatory processes. In principle, dust particles from textile surface and furnishing materials could serve as specific allergens and contribute to the etiology of asthma, but to our knowledge no such cases have been reported. Long-term low-level exposure to formaldehyde has been shown to increase the risk of asthma. Fortunately the use of formaldehyde in particle boards and furniture has decreased dramatically since the 1970s. There is accumulating evidence that semi-volatile phthalates from PVC surface materials may increase the risk of asthma. A recent systematic review and meta-analysis by Jaakkola and Knight reported that results from epidemiologic studies provide consistent support. In addition, damp PVC materials may lead to degradation and emission of materials such as 2-ethyl-hexanol, which

5.7

DIAGNOSIS AND MANAGEMENT ISSUES

77

may contribute towards the risk of asthma. Finally, damp materials may promote microbial growth.

5.7 Diagnosis and management issues Diagnostic practice characteristic of occupational medicine can be applied to environmentally caused or environmental-related respiratory diseases. The following four areas of approach are applicable when suspecting indoor environmental causes: (1) a detailed history including both environmental and occupational exposures; (2) thorough physical examination; (3) pulmonary function testing; and (4) allergy testing. When examining a patient with new-onset asthma, special emphasis should be paid not only to existing exposures but also to recent changes in the home or work environment. A move to a new home or recent refurbishment during the past 1–2 years may have produced new, intensive exposures. New houses or apartments with synthetic materials, large painted surfaces and new furnishing and textiles may contain substantial sources of volatile organic compounds and phthalates whose emission rates are highest when the first occupants arrive. Refurbishment may include installation of new surface material, painting of large surfaces, use of various glues and putties and the opening of roofs, floors or ventilation ducts, which may contribute many types of potential respiratory sensitizers and irritants. Furthermore, changes in heating, ventilating and air conditioning systems may be directly or more often indirectly related to increase in exposures and their respiratory effects. In particular, a decrease in air changes will increase the concentration of all indoor airborne air pollutants. The start of use of heating systems after the summer or hot season may also introduce changes which may trigger asthmatic symptoms. The diagnosis of environmental asthma is based on both the report of intermittent respiratory symptoms and evidence of variable airway obstruction. Typical symptoms include wheezing, cough, phlegm, shortness of breath and chest tightness, and repeated bronchitis episodes. Symptoms in the eyes and upper respiratory tract may occur concomitantly with asthma-like symptoms when related to environmental factors. The relation of asthma to the home environment may follow several patterns: symptoms occur only at home, symptoms improve when away from home and symptoms improve after changing the home environment. Naturally the work environment may also contain exposures responsible for symptoms and/or the initiation of asthma and should receive systematic attention. With persistent exposure the symptoms may become chronic and any obvious time-relation to the home environment may be lost. Intermittent and home-related respiratory symptoms among other family members may also offer a clue to the role of building materials and furnishing as a cause of asthma or allergic rhinitis. Detection of wheezing on chest auscultation will be a helpful indicator of asthma, expiratory wheezing being typical. However, auscultation is frequently normal in mild asthma, being present only during respiratory infections or special exposure periods, e.g. the pollen season. Examination of the heart, upper airways and skin should also be included. Blocked nose and redness of eyes indicate allergic rhinitis and conjunctivitis. Dry, itchy eczema will indicate an atopic propensity. Spirometry for forced expiratory volume in one second (FEV1) and forced ventilatory capacity (FVC) are the best methods for assessing bronchial obstruction. Serial

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CH 5 BUILDING MATERIALS AND FURNISHING

recording of peak expiratory flow (PEF) over periods of days or weeks is the best way to document whether home or work environment plays a role in the etiology of asthma or symptoms. Pocket-size spirometers can similarly be used in serial measurements. A 20% or greater diurnal variation in PEF or FEV1 indicates asthma and repeated declines in lung function when at home provide strong evidence of the role of the home environment. Serial PEF measurements have become routine in diagnosis and treatment of occupational asthma, but they can be as beneficial in identifying causes of bronchial obstruction in the home or other microenvironments. The measurements should be conducted preferably four but at least twice a day. Allergy tests are useful in the early phase of asthma, because they may reveal important triggers of asthma and allergic rhinitis. Skin prick tests and allergen-specific IgE antibodies in serum are informative in assessing the role of specific inhalation allergen occurring in indoor and outdoor environments. Expert assessment of home environment for potential causes and triggers of asthma would be useful in both diagnosis and treatment of environmental asthma, but these types of services are not yet part of routine clinical practice. Removal of hypothesized causal agents is the best treatment. This can be achieved by removing suspicious building materials or furnishing from the home of the asthmatic or individual with home-related asthma-like symptoms. Sometimes moving to another home is the best solution. Drug treatment follows the usual pattern of asthma treatment. The most efficient means of primary prevention is through architecture and building engineering and the use of building materials with low chemical emissions is an important part of environmental management. Several macro-scale activities are likely to reduce population exposure from material emissions. Producers of building materials should develop and produce materials with lower emissions. Testing of new materials entering the market is a critical point, but can be difficult, because the amount of surface material used can vary in different microenvironments and emission rates depend on air change, temperature humidity and building structures. Special emphasis should be paid to materials covering large surfaces, such as walls and floors. Consumers should be informed about the emission rates of different materials and educated to demand ‘healthy’ materials, probably the most efficient way to influence the market. Classification of materials, paints and chemical would help consumers to choose their products and guide both builders and manufacturers. Finally the maintenance of buildings and heating, ventilation and air conditioning practices are important in the primary prevention of the harmful effects of emissions from building materials and furnishing.

References 1. Paustenbach, D., Alarie, Y., Kulle, T. et al. (1997) A recommended occupational exposure limit for formaldehyde based on irritation. J. Toxicol. Environ. Health 50(3): 217–263. 2. Hodgson AT, Bea J, McIlvaine JE. (2002) Sources of formaldehyde, other aldehydes and terpenes in a new manufactured house. Indoor Air 12: 235–242. 3. Fisk, W.J., Lei-Gomez, Q., Mendell, M.J. (2007) Meta-analyses of the associations of respiratory health effects with dampness and mold in homes. Indoor Air 17(4): 284–296.

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Further reading Afshari, A., Gunnarsen, L., Clausen, P.A. et al. (2004) Emission of phthalates from PVC and other materials. Indoor Air 14(2): 120–128. Bornehag, C.G., Blomquist, G., Gyntelberg, F., J€arvholm, B., Malmberg, P., Nordvall, L., Nielsen, A., Pershagen, G., Sundell, J. (2001) Dampness in buildings and health. Nordic interdisciplinary review of the scientific evidence on associations between exposure to “dampness” in buildings and health effects (NORDDAMP). Indoor Air 11(2): 72–86. Bornehag, C.G., Sundell, J., Bonini, S., Custovic, A., Malmberg, P., Skerfving, S., Sigsgaard, T., Verhoeff, A. (2004) EUROEXPO. Dampness in buildings as a risk factor for health effects, EUROEXPO: a multidisciplinary review of the literature (1998-2000) on dampness and mite exposure in buildings and health effects. Indoor Air 14(4): 243–257. Bornehag, C.G., Sundell, J., Weschler, C.J. et al. (2004) The association between asthma and allergic symptoms in children and phthalates in house dust: a nested case–control study. Environ. Health Perspect. 112(14): 1393–1397. Bornehag, C.G., Lundgren, B., Weschler, C.J. et al. (2005) Phthalates in indoor dust and their association with building characteristics. Environ. Health Perspect. 113(10): 1399–1404. Brown, V.M., Crump, D.R., Mann, H.S. (1995) Concentrations of volatile organic compounds and formaldehyde in five UK homes over a three year period. In J.J. Knight and R. Perry (eds), Volatile Organic Compounds in the Environment (pp. 289–301). Indoor Air International: London. COST Project 613. (1989) Formaldehyde emissions from wood based materials: guideline for the establishment of steady state concentrations in test chambers. Report No. 2. Prepared by Working Group 3 on behalf of the Community-COST Concertation Committee. Commission of the European Communities, Directorate-General for Science, Research and Development, Joint Research Centre, Ispra Establishment. EUR 121 96 EN. Hansen, M.K., Larsen, M., Cohr, K.H. (1987) Waterborne paints. A review of their chemistry and toxicology and the results of determinations made during their use. Scand. J. Work. Environ. Hlth 13(6): 473–485. Institute of Occupational Medicine (2004) Damp Indoor Spaces and Health. National Academy Press: Washington, DC. Jaakkola, M.S., Jaakkola, J.J.K. (2004) Indoor molds and asthma in adults. Adv. Appl. Microbiol. 55: 309–338. Jaakkola, J.J.K., Knight, T. (2008) The role of exposure to di(2-ethylhexyl) phthalate in the development of asthma and allergies. Environ. Hlth Perspect. 116: 845–853. Jaakkola, J.J.K., Oie, L., Nafstad, P. et al. (1999) Interior surface materials in the home and the development of bronchial obstruction in young children in Oslo. Norway. Am. J. Public Hlth 89(2): 188–192. Jaakkola, J.J.K., Parise, H., Kislitsin, V. et al. (2004) Asthma, wheezing, and allergies in Russian schoolchildren in relation to new surface materials in the home. Am. J. Public Hlth 94(4): 560–562. Jaakkola, J.J.K., Hwang, B.F., Jaakkola, N. (2005) Home dampness and molds, parental atopy, and asthma in childhood: a six-year population-based cohort study. Environ. Hlth Perspect. 113(3): 357–361. Jaakkola, J.J.K., Ieromnimon, A., Jaakkola, M.S. (2006) Interior surface materials and asthma in adults: a population-based incident case-control study. Am. J. Epidemiol. 164: 742–749. Jensen, L.K., Larsen, A., Mølhave, L. et al. (2001) Health evaluation of volatile organic compound (VOC) emissions from wood and wood-based materials. Arch. Environ. Hlth 56(5): 419–432. Katsoyiannis, A., Leva, P., Kotzias, D. (2008) VOC and carbonyl emissions from carpets: a comparative study using four types of environmental chambers. J. Hazard Mater. 152(2): 669–676. Marbury, M.C., Kriger, R.A. (1991) Formaldehyde. In J.M. Samet, J.D. Spengler (eds) Indoor Air Pollution: A HealthPerspective. Johns Hopkins Press: Baltimore, MD.

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Morrison, G.C., Nazaroff, W.W., Cano-Ruiz, J.A. et al. (1998) Indoor air quality impacts of ventilation ducts: ozone removal and emissions of volatile organic compounds. J. Air Waste Mgmt Assoc. 48(10): 941–952. Oie, L., Hersoug, L.G., Madsen, J.O. (1997) Residential exposure to plasticizers and its possible role in the pathogenesis of asthma. Environ. Hlth Perspect. 105(9): 972–978. Pasanen, A.L., Rautiala, S., Kasanen, J.P. et al. (2000) The relationship between measured moisture conditions and fungal concentrations in water-damaged building materials. Indoor Air 10(2): 111–120. Tuomi, T., Engstr€ om, B., Niemel€a, R., et al. (2000) Emission of ozone and organic volatiles from a selection of laser printers and photocopiers. Appl. Occup. Environ. Hyg. 15(8): 629–634. Weschler, C.J. (2004) Chemical reactions among indoor pollutants: what we’ve learned in the new millennium. Indoor Air 14(suppl. 7): 184–194. WHO, (1989) Formaldehyde. Environmental Health Criteria 89. World Health Organization, International Programme on Chemical Safety: Geneva. Wieslander, G., Norb€ack, D., Edling, C. (1994) Occupational exposure to water based paint and symptoms from the skin and eyes. Occup. Environ. Med. 51(3): 181–186. Wieslander, G., Norb€ack, D., Edling, C. (1997) Airway symptoms among house painters in relation to exposure to volatile organic compounds (VOCS) – a longitudinal study. Ann. Occup. Hyg. 41(2): 155–166. Wolkoff, P. (1999) How to measure and evaluate volatile organic compound emissions from building products. A perspective. Sci Total Environ. 227(2–3): 197–213.

6 Mites, pets, fungi and rare allergens Frederic de Blay, Magdalena Posa, Gabrielle Pauli and Ashok Purohit Hopitaux Universitaires de Strasbourg, France

6.1 Introduction Mites, pets, cockroaches and fungi are the main sources of indoor aeroallergens. More occasionally, rare allergens such as those from plants can induce sensitization and symptoms.

6.2 Mites House dust mites are arthropods belonging to the subphylum Chelicerata, class Arachnida, order Acari and suborder Astigmata. Other mites found in the Astigmata suborder include storage mites and scabies mites. Thirteen species of mites have been found in house dust, three of which are very common in homes around the world and are the major source of domestic allergens. Mite bodies and mite faeces are the source of mite allergens. The allergens associated with mite faeces are enzymes that originate from the mite’s digestive tract. Other mite allergens may originate from saliva, supra-coxal gland secretions (involved in water uptake) and enzymes associated with the moulting process.

6.2.1 Description of exposures The most common mite species are Dermatophagoides farinae, Dermatophagoides pteronyssinus and Euroglyphus maynei, which are all found in temperate climates.

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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In tropical and subtropical climates the storage mite, Blomia tropicalis, is also often found in house dust along with the other dust mites. In the USA and continental Europe, most homes are co-inhabited with D. farinae and D. pteronyssinus, but one species usually predominates. In Europe and in most other countries, D. pteronyssinus species is found more frequently than D. farinae; an exception is the inland part of Finland, where D. farinae predominates. In some parts of Europe, such as Reykjavik (Iceland), Uppsala (Sweden) and Albacete (Spain), very few domestic samples contain detectable levels of group 1 mite allergens. Mite allergens that are most often measured in the domestic environment are the major group 1 allergens: Der p 1, Dermatophagoides pteronyssinus 1 and Der f 1, Dermatophagoides farinae 1. Mattresses and mattress bases are the principal reservoir of mite allergens, but allergens are also found in dust from carpets, chairs, sofas and clothing. They may also be detected on soft toys and in dust from day-care centers and in various other public places such as cinemas, trains and buses.

6.2.2 Disease associated with exposure Prospective studies have demonstrated that early domestic exposure to mite allergens is a risk factor for the development of specific sensitization, and that such sensitization is a risk factor for decreased lung function at school age. In mite-free environments, mite-allergic asthmatics have lower levels of specific IgE to mite, reduced specific and nonspecific bronchial hyper responsiveness and a decrease in air trapping and airway inflammation. Patients with mite sensitization are rarely aware of a relationship between exposure and symptoms. Nevertheless, some of them describe rhinitis and/or asthma in contact with dust or in certain houses. The average time from exposure to the onset of symptoms is 30 min.

6.3 Cat and dog allergens 6.3.1 Description of exposure: qualitative aspects Cat allergens Fel d 1 (Felis domesticus1). More than 80% of patients who are allergic to cats display IgE reactivity to Fel d 1 which is produced by the sebaceous, salivary and anal glands of domestic cats. Different species can produce different levels of allergen; moreover, the production of Fel d 1 depends on the hormonal status of the cat; male cats –especially those non-neutered – produce more allergen than females. Fel d 2. Cat albumin (Fel d 2) is a minor allergen, sensitizing only about 15% of cat allergic patients. It is found in serum as well in epithelial extracts. Specific sensitization to cat albumin appears to be more common in patients with atopic dermatitis than in those with rhinitis. Fel d 3. Fel d 3 is a cystein protease inhibitor (cystatin) and another major allergen, sensitizing between 60 and 90% of cat allergic people.

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Fel d 4, a lipocalin, is also a major cat allergen with as many as 63% of cat allergic individuals having Fel d 4-specific IgE. Cat immunoglobulins. These allergens are present in both the serum and epithelial extracts from cats and are occasional causes of specific sensitization. Dog allergens Can f 1 and Can f 2. Like most – but not all – mammalian allergens, these are lipocalin proteins. About 80% of patients with an allergy to dogs display IgE reactivity to Can f 1 and Can f 2. Can f 1 is produced by tongue epithelial tissue whereas Can f 2 is predominantly produced by parotid glands and only to a lesser extent by the tongue. Neither allergen is produced by the skin but both may be present on hair and dander. No significant amounts of these allergens have been found in dog urine or faeces. As with cats, there may be some inter-breed differences; Can f 1, for example, seems to be produced less by Labradors than other dog breeds. Dog albumin (Can f 3) and immunoglobulin. Dog albumin and immunoglobulins are present in dog serum and in epithelial extracts but are minor allergens only, sensitizing just 5–30% of patients with dog allergies. Cross reacting allergens between cat and dog Patients very often display positive skin prick test responses to both cat and dog extracts and the question arises whether this reflects co-sensitization or cross sensitization. Since both cat and dog allergens (Can f 1 and 2 and Fel d 4) are lipocalins, some degree of cross-reactivity is plausible. The presence of a Fel d 1-like allergen in a dog extract has been demonstrated and may represent a target for the cross-reactive IgE antibodies present in the sera of 25% of cat- and dog-allergic patients; the clinical relevance of this allergen is unknown. Furthermore, albumin is an allergen present in both cat and dog secretions, although its clinical relevance too is still under discussion.

6.3.2 Description of exposure: qualitative aspects Cat allergens In many parts of the world, exposure to Fel d 1 is ubiquitous; the allergen has been found and measured in the dust of mattresses, carpets, sofas, classrooms, clinical waiting rooms (including those of allergists), the upholstery of buses, trains and cars, and shopping areas. Moreover, 40% of airborne Fel d 1 is associated with particles less than 5 mm and can be measured in undisturbed air. In school classrooms where there are pupils who are cat owners, the levels of airborne Fel d 1 may be higher than in houses without a pet cat. In a US national survey, 13% of homes had at least one pet cat (but not a dog); 9% of homes contained measurable levels of Fel d 1 with a geometric mean concentration of 4.73 mg/g of dust. Feld 1 concentrations were significantly higher in homes in the more western regions, and in households with higher incomes and with white residents of above-average educations. Fel d 1 levels measured in house dust appear to be sufficiently stable so that single measurements can be used with confidence in longitudinal epidemiologic studies.

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Dog allergens Can f 1 can be found not only in the dust from sofas, carpets and mattresses of homes housing dogs, but also in houses without a dog. As with cat allergens, it may be detected in the dust from classrooms, and in the upholstered seats of private cars, where levels are higher in cars whose owners keep dogs at home. Twenty-one per cent of US dwellings house at least one dog, but Can f 1 has been detected in up to 100% of US homes.

6.3.3 How to document exposure For mite, cat and dog allergens the gold standard of exposure measurement in dust or air is by the use of ELISA-based methods using monoclonal antibodies directed against the major allergens. For mite allergens, semi-quatitative home tests such as the Acarex test and Rapid test have been developed and show a good correlation with the ELISA methods.

6.3.4 Disease associated with exposure Cat sensitization rates in population based studies have varied from 36% in 17-year-old Finnish teenagers to 3% in German children aged 9–11. For dog, in the same age groups, the prevalence of sensitization varied from 19% in Finland to 2.6% in Munich. In patients attending allergy clinics, the sensitization rate for cat allergen, assessed by skin prick test, varied between 23 and 30% in Northern Europe, between 10 and 28% in central Europe and between 13 and 43 %, in southern Europe. Children who attended classes where more than 18% of pupils were cat owners reported significantly decreased PEF, more days with asthma symptoms, and increased use of medication after school started. Immediate bronchial responses to cat allergen appeared to be localized in large airways. The data on the effect on early pet ownership and indoor allergen exposure on the development of asthma in young children are conflicting. While several studies have shown that pet ownership during infancy decreased the risk of wheeze in later childhood, others have not found any association. However, most of the data show a trend of reduced risk for allergic disease in children exposed to animals early in life.

6.4 Rodents and other pets 6.4.1 Description of exposure: qualitative and quantitative aspects Measuring allergens in settled house dust and in domestic air suggests that, in some circumstances, levels of mouse allergens in indoor environments may be similar to those found in animal research facilities; in the USA, mouse allergens were detectable in 80% of dust samples collected in schools and in 100% of bedrooms in inner city homes; indeed, in a recent multicenter study performed in 75 different locations throughout the

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USA, 82% of randomly selected dwellings had measurable mouse allergen in house dust. Mouse allergen levels have consistently been found to be higher in kitchen dust than in bed dust. In contrast, concentrations of Mus m 1 and Rat n 1 (the major mouse and rat allergens, respectively) in Strasbourg (France) and in the UK seem to be far lower. The clinical significance of domestic rodent allergens (except in the case of pet animals) is unclear. Rabbits, guinea pigs and hamsters are also often kept as pets and each is a source of several important allergens present mainly in fur, but also in dander, urine and saliva. In an Italian multicenter study, 2.4% of children were sensitized to rabbit allergens, only half of whom had daily or episodic contact with these animals. Only 10% of the sensitized subjects – exclusively pet rabbit owners with asthma - were mono-sensitized.

6.4.2 Disease associated with exposure Rodents (especially rats and mice) are well-known as inducers of occupational respiratory symptoms in laboratory workers. In the domestic environment in the US, Mus m 1 and Rat n 1 were found in respectively 95 and 33% of the houses of inner-city children with asthma. Guinea pigs, to which the prevalence of symptoms is about 30% in occupational settings, are often kept as pets and can induce indoor asthma. Similarly, a report of 30 cases suggests that hamster ownership is associated with mild to severe asthma, sometimes requiring hospital admission and becoming evident about 15 months after the onset of hamster exposure. In a large population-based survey in Japan, pet hamster ownership appeared independently to increase the risk of respiratory symptoms. Severe asthma symptoms have been described in a patient washing a pet male ferret; specific IgE antibodies were detected against urinary proteins. Allergy to mink, a mammal from the same family as the ferret, has been described in occupational settings; keeping mink as pets is not unusual in certain countries. Household contact with chinchillas may lead to sensitization; allergic rhinitis and/or asthma in children and adults have been confirmed by nasal provocation testing.

6.5 Cockroaches 6.5.1 Introduction Cockroaches are common allergens in many countries especially in the warm parts of North America and Asia, but are infrequent causes of allergic diseases in Europe. Of the 69 species recorded from North America, 24 species are invasive. The most common pest species are: the German cockroach (Blattela germanica), the American cockroach (Periplaneta Americana), the oriental cockroach (Blatta orientalis), the brow-banded cockroach (Supella longipalpa) and the smoky-brow cockroach (Periplaneta fuliginosa). Several major cockroach allergens have been identified. In one study, twice as many cockroach allergic asthmatics had IgE antibodies against Bla g 2, compared with those

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against Bla g 1. An estimated 60–70% of cockroach-sensitive individuals have IgE antibodies to the allergens Bla g 4 and Bla g 5.

6.5.2 Description of exposure: qualitative and quantitative aspects In some countries, cockroaches are one of the most common insects encountered by homeowners, especially those living in low-income housing. Even low numbers of cockroaches can produce significant amounts of allergen, and after extermination and/or reduction of cockroach numbers, and even with aggressive cleaning, allergens can be measured in dust for longer than 6 months. The most aggressive pest management strategies seem significantly to reduce allergen levels but often not below the ‘disease threshold’ of 8 U/g of house dust.

6.5.3 Disease associated with exposure In some countries, exposure to cockroach allergens has an important role in asthma morbidity among inner city children. In inner cities in the USA, for example, more asthmatic children with cockroaches reported in their home were sensitized to cockroach allergens than those without exposure to cockroaches. In the same country, a study of urban, suburban and rural atopic patients found a higher prevalence of cockroach sensitivity among patients with a primary diagnosis of asthma (50%), than among those with a primary diagnosis of allergic rhinitis (30%). Exposure to cockroach allergens in early life has been associated with recurrent asthmatic wheezing in children with a family history of atopy. Exposure and sensitization to cockroach allergens increased rates of hospitalization, school absences and days with wheezing among asthmatic children. In European and other countries, sensitization to cockroaches appears to be less common; as is any associated morbidity. In France, for example, the prevalence among children of specific IgE antibodies to cockroach allergens seems to be below 5%. Importantly, evidence of specific sensitization can be influenced by co-sensitization with other house dust allergens such as mites, which have cross reacting allergens (glutathion transferase and tropomyosin) with cockroaches. Cockroaches present an additional, potential health problem; in a study of 80 cockroaches, around 70% were contaminated with Salmonella species, many of them resistant to antibacterial drugs.

6.6 Fungi (molds) Exposure of atopic children and adults to molds appears to be a risk factor for asthma. However, the fact that many studies have not been able to confirm an association points to the extreme difficulty of correctly assessing exposure to molds and, a fortiori, their allergens. Furthermore, although atopic individuals are at greater risk for asthma, the onset of cough and wheezing in atopic children and adults when exposed to molds might be not only the consequence of an allergic reaction but also an inflammatory

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response to the inhalation of mycotoxins and volatile organic substances liberated by molds.

6.6.1 Description of exposure: qualitative aspects Spores from several fungal species are important and near-ubiquitous1 sources of indoor and outdoor allergens. Of the many fungal species, the most clinically important are those derived from the deuteromycetes or fungi imperfecta (including Aspergillus fumigatus, Cladosporium herbarum, Penicillium chrysogenum, Alternaria alternata, Trichophyton rubrum and Candida albicans). All these species use airborne spore dispersal, and spores are often produced in concentrations exceeding those seen with pollens. In addition to spores, allergens may also be released from mycelia and yeast forms, and such sources are particularly relevant in fungi that cause conditions such as allergic bronchopulmonary aspergillosis and immediate and delayed-type dermal infections involving A. fumigatus, C. albicans, Trichophyton species and Malassezia furfur. The most clinically important fungal sources of aeroallergens are Aspergillus, Penicillium, Cladosporium and Alternaria species. The major allergens from Penicillium, Candida and Trichophyton species are proteases. Cross reacting allergens Usually, patients display positive skin prick tests to several mold extracts which probably reflects the presence of cross reactive allergens such as enolases that are present, for example, in Cladosporium herbarum, Aspergillus fumigatus, Penicillium chrysogenum and Alternaria alternata

6.6.2 Description of exposure: quantitative aspects Fungal growth indoors is influenced by various environmental factors, the most important of which is the availability of water. Water leaks, defective drainage, inadequate ventilation and moisture condensation resulting from faulty thermal insulation and heating, cooling and ventilation systems have been major contributors to moisture-related fungal problems in buildings. Prolonged high relative humidity has been shown to increase both dust and airborne fungal populations in indoor environments. The indoor environment may also become a secondary source of exposure if fungal spores colonize interior or building materials. Although indoor fungal levels tend to reflect the levels found outdoors, housing characteristics and occupants’ behavior can affect exposure levels considerably. Alternaria Alternaria spores are common aeroallergens in many regions of the world, especially in warm inland climates and in arid regions. Alternaria exposure is often assessed by 1

Molds have been found even in space stations.

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outdoor spore counts, because the most intense exposure is likely to occur outdoors. Nonetheless, fungal spores can enter a home from outside via ventilation or infiltration, or they can be carried in by occupants in their hair, skin, clothing or on their shoes as well as on their pets’ fur; the presence of a dog increases fungal populations in floor dust. In the dust of 831 houses in 75 locations throughout the USA, Alternaria antigen was detected in 95% of samples. Different factors may influence exposure to Alternaria; for example, antigen concentrations are significantly higher in homes that use dehumidifiers. The presence of a dehumidifier may be an indication of a persistent humidity or moisture problem, but dehumidifiers can also become reservoirs for fungi. Predictors of domestic Alternaria antigen concentrations vary by location because the activities of occupants and pets can affect each location in the home differently. Having carpeting in bedrooms predicts lower concentrations in beds, whereas kitchens with carpeting have significantly higher levels than kitchens without carpeting; frequent cooking may also result in higher temperature and humidity levels in kitchen. Furthermore, the presence of children predicts higher antigen levels in beds but not in floor or upholstery dusts. Less frequent cleaning contributes to higher Alternaria antigen levels in floor and upholstery dusts, especially in living rooms; correspondingly, levels in beds are lower if bedding is washed more frequently. Washing temperature (cold, warm, hot) does not seem to influence antigen levels. Other molds Aspergillus, Cladosporium and Penicillium levels in indoor environments are highest in the autumn, correlating with outdoor concentrations. Where indoor air levels are higher than those outside, this appears to be associated with home characteristics including damp (Cladosporium and Alternaria), the ownership of a pet cat (Aspergillus), cockroach infestation (Aspergillus) and a ‘musty’ smell (Penicillium).

6.6.3 How to document exposure The most frequent indoor molds are Aspergillus, Penicillium, Cladosporium and Alternaria. ELISA tests have been developed for measuring the major allergens of Alternaria (Alt a 1) and Aspergillus fumigatus (Asp f 1), but in most domestic environments, measurable levels are found in fewer than 10% of homes. It has been demonstrated that several common fungal species including Aspergillus and Alternaria release more allergen on germination than before germination and Asp f 1 can more often be measured in domestic air if its spores have germinated. However the clinical relevance of allergens associated with fungal germination remains to be resolved; ungerminated spores might be deposited in the favorable environment of warmth and moisture in the lung or nasal cavity, subsequently germinate and act as an additional source of allergen.

6.6.4 Disease associated with exposure In a European survey from the GA2LEN network, between 2.6 and 4% of patients in Northern Europe who were skin prick tested for inhalant allergens were found to be

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sensitized to Alternaria. Corresponding figures for central and southern Europe respectively were 1.7–16.4% and 10–20.5%. In general European population samples the prevalence is probably lower (1.1–5.1%). Among 4962 European subjects aged between 3 and 80 years and with rhinitis and asthma, 19% had a positive skin test at least to one mold; 15% of them were sensitized only to one or more molds (Alternaria 60%, Candida 33%, Trichophyton 4.6%) and not to other common aeroallergens. Among 4-year-old atopic children, the prevalence of a positive skin prick test to Alternaria alternata or Cladosporium herbarum was 6%. Exposure to Alternaria alternata may be a risk factor for asthma. In some studies the prevalence of current symptomatic asthma increased with increasing domestic Alternaria concentrations. In 414 children from seven urban American communities, all of them sensitized to molds, a correlation with indoor concentrations of Alternaria and Cladosporium has been reported. In centers with a higher prevalence of asthma, the prevalence of reported indoor mold exposure was also high. Asthma is the most common disease in children sensitized to molds. In a pediatric survey, at 4 years of age Alternaria and Cladosporium were the third most common causes of sensitization after house dust mite and grass pollen; and sensitization to molds correlated positively with a clinical diagnosis of asthma. An association between daily emergency department visits for asthma to the Children’s Hospital of Ontario, and daily concentrations of both pollen grains and fungal spores over a five-year period was found. The percentage increase associated with each group was 1.9% for deuteromycetes (Alternaria, Cladosporium, Penicillium, Aspergilus, Epicoccum). Mold exposure has also been associated with asthma symptoms and bronchial responsiveness, the effect being stronger in subjects sensitized to Cladosporium species. For children sensitized to Alternaria and heavily exposed to this mold there is a markedly increased risk of severe asthma. In a multicenter European epidemiological survey, data from people aged 20–44 with asthma and skin prick tests suggested that the severity of asthma was associated with sensitization to airborne molds rather than to pollens and cats. The frequency of sensitization to molds (Alternaria alternata or Cladosporium herbarum, or both) increased significantly with increasing asthma severity. Multiple mold reactions were also much commoner in the group with multiple admissions and the number of asthma admissions was related to the number and size of positive mold skin allergy tests and less strongly correlated to the number and size of non-mold allergy tests.

6.6.5 Other health effects Exposure to molds can cause human disease through several well-defined mechanisms including the generation of a harmful immune response, direct infection by the organism and toxic irritant effects from mold byproducts. In addition, many new mold-related illnesses have in recent years been hypothesized; many of these remain largely or completely unproven. Concerns about mold exposure and its effects are so common that all healthcare providers, particularly allergists and immunologists, are frequently faced with issues regarding both real and asserted mold-related illnesses.

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6.7 Rare allergens 6.7.1 Acarids Homes occasionally contain a large number of storage mites, such as Lepidoglyphus destructor, Tyrophagus putrescentiae and longior, Aleuroglyphus ovatus and Gohieria fusca. Sensitization rates to storage mites are highest in city dwellers; approximately 10% of the general population in Ohio (urban, suburban and rural) are sensitized to L. destructor and/or T. putrescentiae.

6.7.2 Insects House dust contains significant levels of silver fish (Lepisma saccharina) antigen, the clinical significance of which is unclear. Insects of the Coleopters order cause occupational sensitization in mill workers. In the indoor environment, cough and rhino-conjunctivitis during housekeeping were related to larvae of dermestidae (Attagenus pelio), a diagnosis of specific allergy being confirmed by epicutaneous tests, and specific IgE determination to larval proteins. A case of asthma has been reported, induced by dermestidae larvae present in wooden floors in a dwelling with stuffed animals on the wall. Environmental control measures such as scraping and disinfesting the wooden floor and covering it with a varnish, as well as removal of the stuffed animals, were sufficient to control the patient’s symptoms. Another example is allergic asthma to Psocus spp. (Pscoptera). These insects have been shown to proliferate in hemp fibers, which are sometimes used for house insulation. Other inhalant insect allergens have been described as outdoor agents responsible for epidemic asthma, possibly induced by crickets, locusts and moths (caddis fly). Some allergies to moths are related to hobbies: for instance, anglers may be in contact with different kinds of moths and their larvae. Other food products such as crustaceans or different worms and larvae can also lead to sensitization in fish hobbyists. In Japan, a higher frequency of IgE antibody responses to insects (moth, butterfly, caddis fly and chironomids) was found in patients with bronchial asthma; and air sampling revealed the presence of insect-related particles less than 10 mm in diameter.

6.7.3 Animal allergens Scaly animals such as lizards were assumed not to be allergenic. However, allergy to iguana has been reported and confirmed by skin tests and in vitro studies to iguana scales. Respiratory sensitization to avian allergens has also been described. The responsible allergens, especially Gal d 5, an alphalivetin, are implicated in bird egg syndrome.

6.7.4 Green algae Green algae (chlorella) grow under similar conditions to molds and can be found as indoor allergens. Sensitization to chlorella has been described in children (6% of

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outpatients in a study from Germany) and is mainly found among mold-sensitized patients. The clinical relevance, however, has not been clearly demonstrated.

6.7.5 Plant-derived allergens Among ornamental plants, Ficus spp., especially Ficus benjamina, was found to sensitize 6% of 395 outpatients in Sweden; among them 3% were symptomatic with perennial asthma, rhinitis or conjunctivitis. Specific Ficus allergens have been detected in house dust samples including those that are also present in natural rubber latex derived from a species of the same family (Hevea brasiliensis). Other latex plants, such as Euphorbia pulcherina and Araujia sericifera can induce immediate allergies in atopic patients. Other clinical cases of allergy to ornamental plants have been described, including allergy to the coffee plant, to papyrus (Cyperus alternifolius) and to Tradescantia albifloxia. Cut and dried flowers are potential allergenic sources but in the domestic setting seem to be less frequently a problem than they are for gardeners and florists.

6.7.6 Allergens introduced by stinging and biting Allergens introduced by stinging insects can induce allergic manifestations in the indoor environment. An example is given by fleas and especially cat fleas as well as by ground bugs. The European pigeon ‘soft tick’ (Argas reflexus) lives inside houses and is increasingly widespread due to growing pigeon colonies in urban areas. Bites by ticks usually occur at night and severe allergic reactions have been reported.

6.7.7 Airborne food allergens Exposure to airborne food allergens by handling and cooking can be induced by odors, fumes, vapors or sprays, which have a potential role in provoking clinical manifestations such as asthma, rhinitis and conjunctivitis in sensitized patients. Reactions induced by peeling vegetables such as raw potatoes, carrots and fresh asparagus are well-known, but the elicitation of asthma by the steam of cooking vegetables such as chick peas and lentils is also possible. The inhalation of steam when boiling fish or shrimps or other crustacean can also be an inadvertent exposure to allergens in the kitchen. Exposure to airborne allergens, even in low amounts, can induce moderate to severe symptoms in highly sensitized patients. Patients with peanut allergy may develop respiratory symptoms in closed environment such as an airplane cabin where peanut packages are opened. In assessing new or less well-known allergic etiologies, it is essential to document clinical cases by immunological tests. This requires expert laboratory support. The publication of well documented clinical cases increases the number of accessible and useful references in the literature, and will assist in the provision of evidence-based advice on the avoidance of relevant etiological factors that may lead to complete and definitive recovery.

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6.8 Diagnosis and management issues 6.8.1 Prevention There is no clear evidence that the primary prevention of allergic sensitization and/or disease by environmental allergen reduction in the home is effective. In contrast, there is valuable evidence relating to ‘tertiary preventive’ methods (the prevention of symptoms in allergic patients) for several allergens. Mite allergens Several studies have demonstrated a clinical benefit in mite-sensitive asthmatic children when global allergen avoidance has been performed; for example, symptoms in such children improve when they stay at altitudes of 1800 m or more. In contrast, three meta-analyses have underlined the absence of any consistent efficacy of methods of dust mite allergen exposure reduction and consequent clinical improvement. Major weaknesses in the published literature, however, make a definitive conclusion difficult. Cat allergens Two clinical studies, each using a vacuum cleaner with HEPA filter and an air cleaner in patients allergic to cat but who kept a cat at home, had contradictory findings. The first showed a benefit in terms of bronchial hyper responsiveness; the second showed no benefit. Cockroach allergens It is essential to identify the pest species; the use of commercial traps is further important in determining the extent and severity of the problem. Control strategies should include elimination of potential pest reservoirs and conduits and, when necessary, the application of insecticidal sprays, with minimal exposure to people and pets; a community action plan may be necessary. Post-treatment evaluations are essential. Global allergen avoidance Home visits by an Indoor Environment Medical counselor who has the time to measure, counsel and control compliance appears necessary. This new job has been validated by a multicenter study in France and two other larger studies in the USA. A randomized, controlled study included 937 children aged from 5 to 11 years with moderate to severe allergic asthma. After one year of global allergen avoidance using an indoor technician and different allergen reduction methods a significant decrease in allergen exposures was observed. This was associated with a 19% reduction in symptoms, a 13% reduction in emergency visits and a 20% reduction in school absenteeism. There was a correlation between clinical improvement and reductions in allergen exposures. The authors claimed that all the reduction methods were costeffective. Under such conditions, global avoidance must be regarded as part of the treatment of severely allergic asthma in children who are exposed to domestic allergens.

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Further reading Celedon, J., Milton, D., Ramsey, C. et al. (2007) Exposure to dust mite allergen and endotoxin in early life and asthma and atopy in childhood. J. Allergy Clin. Immunol. 120: 144–149. Chew, G., Rogers, C., Burge, H. et al. (2003) Dustborne and airborne fungal propagules represent different spectrum of fungi with differing relations to home characteristics. Allergy 58: 13–20. De Blay, F., Fourgaut, G., Hodelin, G. et al. (2003) Medical indoor environment counselor (MIEC) role in the compliance with advice on mite allergen avoidance and on mite allergen exposure. Allergy 58: 27–33. Gotzsche, P., Johansen, H. (2008) House dust mite control measures for asthma. Cochrane Database Syst. Rev. 2: CD001187. Review. Mahillon, V., Saussez, S., Michel, O. (2006) High incidence of sensitization to ornamental plants in allergic rhinitis. Allergy 61: 1138–1140. Morgan, W., Crain, E., Gruchalla, R. et al. (2004) Results of a home-based environmental intervention among urban children with asthma. New Engl. J. Med. 351: 1068–1080. Platt-Mills, T., Vaughan, J., Squillace, S. et al. (2001) Sensitization, asthma and modified Th2 response in children exposed to cat allergen: a population-based cross-sectional study. Lancet 357: 752–756. Rust, M.K., (2008) Cockroaches. In Public Health Significance of Urban Pests, Bonnefoy, X., Kampen, H., Sweeney K. (eds). WHO: Copenhagen; 53–84. Zock, J., Jarvis, D., Luczynskz, C. et al. (2002) Housing characteristics, reported mold exposure and asthma in the European Community Respiratory Health Survey. J. Allergy Clin. Immunol. 110: 285–292.

7 Hobby pursuits Paul D. Blanc University of California, San Francisco, CA, USA

7.1 Definitions and general approach Certain occupational/vocational activities are characterized variously as hobbies, pastimes, avocations or amateur undertakings. The respiratory health hazards arising out of these activities are heterogeneous, consistent with such a wide-ranging set of descriptors. For the sake of convenience, this group of pursuits will be referred to in this chapter collectively as ‘hobbies’, bearing in mind that no single word in current English usage adequately subsumes a full spectrum of activities that might be better captured by certain alternative terms. This is underscored by the differences in citations highlighted by a key word PubMed search using ‘pastime’ or ‘amateur’, as opposed to ‘hobby’, ‘hobbyist’ or ‘hobbies’. Hobby pursuits are often home-based (although not necessarily transpiring indoors) and small-scale. Nevertheless, hobbies can also take place in a workshop or another location removed from one’s residence or in an environment that is completely outdoors and, rather than being small in scope, can approach the scale of an industrial prototype operation. By implication if not by definition, hobby activities are either unsalaried or recompensed on a freelance basis, but they need not be sporadic or infrequent, as any dedicated hobbyist can testify. Most importantly, these practices, no matter how they are labeled or where and how often they take place, potentially carry substantive risk of illness or injury. Such effects can target many organs, even though the focus in this chapter is on respiratory tract endpoints. As the above indicates, it is important that hobby activities be considered as possible factors in respiratory disease causation or aggravation. Taking a hobby vocational history targeted to exposures and illnesses relevant to the respiratory tract may be considered either from the point of view of the type of activity involved, with its inherent risk factors, or from the disease endpoints that could be

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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associated with the hobby in question. Although there is an obvious rationale in clinical practice in working backwards from the disease or symptom complex at hand to potential exposures, from a conceptual point of view it may be more helpful to first consider hobbies grouped by their potential exposure characteristics.

7.2 Arts, crafts, and related activities in the plastic arts Activities that fall under this rubric are the most widely cited for their potential exposure risks relevant to occupational or environmental illness, even if objective evidence of adverse outcomes is limited to isolated case reports or, at most, fragmentary case series (Table 7.1). Nonetheless, it is obvious that certain substances that are employed in these hobby pursuits are so inherently dangerous that disease can potentially result, even if published documentation of such events is limited. Pigments used in painting, glazes employed in ceramics, and photographic emulsion salts share the potential for metal-related respiratory tract toxicity. Although lead is the most obvious metal toxic exposure arising from arts and crafts work, it is unlikely to be related to a disease presentation in which respiratory symptoms predominate (although shortness of breath could be a part of such a symptom complex in the event of severe anemia). Metal-associated sensitization leading to asthma or rhinitis is the most relevant respiratory disease mechanism for metals. Such sensitization is most clearly the case with asthma among photographers due to platinum salts. Because platinum printing is almost always done by photographers preparing their own impregnated emulsions, this work process allows for potential sensitization and repeated re-challenge. Indeed, this is a process that is not available commercially and thus is limited to the self-employed artist or hobbyist (as broadly defined here). In addition to platinum-caused asthma, palladium is a related metal used in specialist photographic processes that could result in sensitization. Cobalt and chromium are metals that are used in paint pigments and glazes that can also act as sensitizers, although documented cases have been limited to industrial applications of these substances. Vanadium, another metallic coloring agent, is linked to chronic bronchitis in occupational studies. This same group of crafts can certainly involve other exposures as well. Photographic work entails photographic developing chemicals that can act as respiratory sensitizers. Historically, photographically related printing techniques that entail intense light source exposure sometimes have employed carbon-arc sources that can generate rare earth exposures (a rare cause of pneumoconiosis). Ceramics work carries the potential for silica dust inhalation, particularly at stages in which dried, pre-fired pottery is manipulated. It is also important to clarify the nature and venting of an artisan’s kiln for firing. In addition to the potential evolution of irritant gas, certain firing techniques such as raku could generate particulate byproducts, a potential risk factor for chronic obstructive lung disease. Fiber-based crafts center on the spinning of thread, weaving or other techniques to create a fabricated textile piece, and dyeing. Handling certain raw textile materials is associated with respiratory allergic sensitization, in particular work with silks (cultivated and wild). In contrast, the chronic lung diseases associated with industrial scale cotton and linen dust are unlikely to be linked to work done by a ‘hobbyist’ in the

Sensitization; chronic obstruction Sensitization Anthrax Sensitization Sensitization Irritation EAA Fume fever Lung injury Silicosis Asbestos-related lung diseases Silicosis Sensitization Silicosis Sensitization Silicosis Asbestos-related lung diseases Asthma Sensitization

Fiber dust

Weaving vegetable fibers Weaving silk Weaving animal fibers Fiber dyeing Wood working Wood working Wood working Metal working Metal working Metal working Metal working Stone sculpting Jewelry making Jewelry making Glass making Glass making Glass making Glass etching Work with chemical polymerized in situ

Fiber dust Microbial contamination Synthetic dyes Wood dust Wood dust Lacquering Welding, cutting Welding, cutting Sand casting Asbestos Dust Solder flux Lost wax casting Metal pigments Silica Asbestos Hydrofluoric acid Reactive monomers

Sensitization Sensitization Sensitization Bronchitis Silicosis Irritation Sensitization

Metal salts (platinum; palladium) Developers; other chemicals Metallic glaze (chromium, cadmium) Metallic glaze (vanadium) Silica Kiln fumes Metallic pigments

Photography Photography Ceramics Ceramics Ceramics Ceramics Fine art painting

Possible respiratory tract effects

Possible relevant exposures

Most likely in fine art photography Could include photographic papers Usually applied as slurry, exposure when mixing As above More relevant to industrial ceramics Gases or particulates Aerosol generation is uncommon. Solvents may also be used in painting, but these are more likely to have other non-pulmonary effects (e.g. chemical hepatitis) Byssinosis is relevant to mass production or heavy cottage industry Wild and cultured silk Sporadic cases Fiber-reactive dyes in particular Selected exotic woods in particular Specific irritants poorly characterized Japanese pigment Galvanized metal Cadmium, phosgene More likely with larger scale foundry work Insulation materials (asbestos blankets) Risk with dry grinding, use of power equipment ‘Colophony asthma’ Abrasive grinding is another possible source Similar range of pigments as in glazes More relevant to industrial glass making Insulation materials (asbestos blankets) Irritant-induced asthma Possible whenever working with such materials

Special comments

Selected hobbies and other pastime activities with potential respiratory effects: arts, crafts and related plastic arts

Hobby, avocation or other pastime activity

Table 7.1

7.2 ARTS, CRAFTS, AND RELATED ACTIVITIES IN THE PLASTIC ARTS

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standard sense of the term. Nonetheless, it is important to remember that, in much of the world, fiber production is a cottage industry with home exposure the rule rather than the exception. This may be particularly relevant to certain syndromes, such as lung disease related to coconut husk fiber (coir) manipulation. Handling animal fibers, if imported through private unmonitored sources from anthrax-endemic areas, could lead to pulmonary infection. Dye handling is a route of potential respiratory sensitization, in particular through fiber-reactive dyes that are widely available to amateurs and professionals alike. Mention should be made of high couture fashion design and production as well, because this can involve exposure to exotic materials, including polymers with a strong propensity to cause asthma. Although this is hardly a ‘hobby’ undertaking, in principal it is an artisan-scale, prototype production process. Fine wood working (including cabinet making, musical instrument production and other closely related pursuits) typically employs a range of common and exotic woods far more heterogeneous than standard commercial carpentry. Many of these are wellrecognized respiratory tract sensitizers that can cause asthma and rhinitis (woods such as iroko, zebra wood and African cherry). Some woods also have irritant properties as well, although the medical literature on this subject is poor. In addition, woodworking can be glue and coating intensive, involving the use of acrylates, urethanes and epoxies with their inherent sensitizing risks. In Japanese lacquer making, extrinsic allergic alveolitis (EAA, also called hypersensitivity pneumonitis) has been associated with a mold-based pigment used to obtain a desirable black color. Although mold contamination of wood itself can also be a cause of EAA, this has been reported in industrial wood processing rather than fine crafts operations. There are a number of other highly specialized artistic pursuits that could involve recognized risk factors for lung disease. Metal-working (e.g. metal sculpting or artisan blacksmithing) that employs any welding, brazing or flame cutting technique could be linked to a range of adverse respiratory effects, including metal fume fever (welding galvanized material), cadmium pneumonitis (flame cutting sheet metal or previously soldered joints), phosgene acute lung injury (by causing the breakdown of chlorinated solvent through heat or ultra violet light, as could occur through work with freshly degreased metals), or irritant-induced asthma (for example, due to combustion byproducts). Historically, the use of asbestos insulation materials (gloves, aprons, blankets) has been common in such endeavors. Metal casting (which involves silica and other exposures) on a scale used for most sculpture is done in commercial foundries and is not carried out by individual artists working in small workshops. Sculpting in stone can generate considerable silica dust, even if done on a small scale, especially if performed using dry power equipment. Jewelry making can be linked to solder flux (colophony) exposure, a known cause of asthma, or silica, either through small-scale sand casting (e.g. ‘lost-wax’ process) or from abrasive wheel grinding dust exposure. Glass working can involve all of the pigments previously addressed above in relation to pigments and glazes in painting and ceramics; silica (especially in grinding or in sandblast etching); and hydrofluoric acid in certain etching techniques (as a risk of irritant-induced asthma). In addition, because of the heat sources used, glass-making has the same asbestos issues as metal-working. Over and above the ‘traditional’ media delineated above, in the twenty-first century, sculptors, jewelry-makers and other visual artists have access to a full range of synthetic chemicals, including solvents and specialty polymers, sometimes even

7.3

HOBBIES AND PASTIMES INVOLVING PETS AND OTHER ANIMALS

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industrial-strength products that would not normally be available to general consumers, but which could have adverse respiratory effects that are difficult to predict.

7.3 Hobbies and pastimes involving pets and other animals Keeping a common pet or even several pets is such a widespread activity that it is generally not considered a hobby or even a particular pastime, although taking a history of common pet ownership is certainly recommended in the evaluation of asthma triggers (both for cause of disease onset and aggravation of existing disease). Factors that tip the balance from ‘routine’ pet ownership to a hobby pursuit and that may increase the index of suspicion as an asthma trigger or expand the differential diagnosis to other conditions include the number of ‘pets’ kept and the location in which they are kept (increasing the exposure frequency and intensity), the type of animal involved (for example, avian as opposed to mammalian) and the activities involved in the hobby (for example, feeding pets using antigenic substances, grooming and cage cleaning or even sterilizing, or participating in competitive pet shows or other events). Bird keeping (pigeon-raising in particular) is the most well-studied and best documented pet-related hobby in the medical literature because of its causative role in EAA (bird-fancier’s lung and related terms) (Table 7.2). Pigeons are important because they are raised in numbers for sport (racing) and are frequently housed in close quarters (dove-cotes or coops are typically separate from human living quarters) where exposure levels are high (endemically with cleaning coops; with seasonal variation when pigeons molt in the fall). Single or only a few household birds can also be a potent risk factor for EAA, especially budgerigars (an Australian parakeet particularly popular in the UK), canaries, parrots and love birds. An important aspect of birds kept in the home is that ‘bystander’ illness can also occur among members of the household other than the pet-owner, thus asking about the hobbies of others is relevant, not simply the index Table 7.2 contact

Selected hobbies and other pastime activities with potential respiratory effects: animal

Hobby, avocation or other pastime activity

Possible relevant exposures

Possible respiratory tract effects

Special comments

Bird-keeping and breeding

Avian proteins

EAA

Pet birds

Infectious agents

Vertebrate pets Fish keeping and fishing

Antigens Fish food, bait, lures

Zoonotic pneumonia Sensitization Sensitization

‘Bystander’ illness noted as well as disease from feathers Especially psittacosis

Taxidermy Magician

Chemicals Stage animals

Irritant asthma Asthma, EAA

Need not be ‘furry’ Insect larva and other antigens; feather exposure can occur in making lures Also insect collectors Rabbits, doves

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case of disease. Moreover, exposure to feathers can also lead to disease; such exposures can be linked to hobbies other than bird-keeping, such as fabricating fishing lures. Pet birds can also be a source of avian-transmitted infectious diseases for which the lung is the target organ, most saliently psittacosis (ornithosis due to Chlamydophila psittaci, formerly Chlamydia psittaci). Rarely, avian transmission also has been implicated in pneumonia due to Q fever and has been suspected as a source of cryptoccocal infection. Counseling to avoid pet bird husbandry has been suggested for persons with immunocompromise related to drug treatment or underlying disease. Although bird-keeping is a risk factor for transmission to humans of H5NI influenza, to date this has been in an agricultural (occupational) context, not as a risk for hobbyists. As opposed to avian species, exposures to other animal species are linked principally to asthma as the main respiratory tract disease associated with hobby pursuits. Exotic pet-keeping is one such exposure scenario. It is unclear whether any of the species involved are particularly more allergenic than others, or rather it is simply the natural reporting bias that leads to the periodic appearance of case reports of unusual allergic sensitization cases presenting with asthma or rhinitis due to unusual pets. Certainly ‘furry’ animals are most commonly associated with asthma, although there are exceptional cases, for example, due to pet reptiles. Another exception is contact with various forms of insect larva, worms or crustaceans, an activity which appears to be a fairly potent route of sensitization reported among aquarium hobbyists (symptoms due to fish food) and sports fisherman (who become sensitized to the fish bait that they use). Beyond asthma (and related rhinitis), other respiratory tract illnesses attributable to non-avian animal-related hobbies are uncommon. For example, even though occupational causes of EAA are myriad, these are not typically relevant to hobby pursuits, bearing in mind that the occasional ‘gentleman farmer’, for whom agricultural activity is an avocation but not a source of income, can nonetheless contract ‘farmers lung’ due to contaminated silage. Moreover a systematic cataloging of all occupationally related zoonoses with potential respiratory manifestations, even though this could be potentially extended to any non-salaried avocation with the relevant animal contact, is beyond the scope of this review. Finally it is worth remembering that pet-associated hobbies can involve exposures to synthetic chemicals with potential adverse lung effects, not simply contact with antigens and infectious materials. Pesticides are one such example, although the associated toxic syndromes would be unlikely to present as primarily pulmonary processes. Taxidermy, which can be considered in this group, can involve exposure to preservative chemicals with respiratory irritant potential (as well as sensitizers – this can also be an issue with butterfly and other insect collectors).

7.4 Sports and the performing arts Sport activities and the performing arts typically would not be combined in the same category. From the perspective of potential respiratory complications, however, they do share certain key aspects in common. Both pursuits have major full-time professional cadres for whom occupational safety and health issues should be considered separately from hobby hazards, despite some obvious overlap (Table 7.3). Both pursuits are also

7.4

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Table 7.3 Selected hobbies and other pastime activities with potential respiratory effects: sports and performing arts Sport or performance activity

Possible relevant exposures

Possible respiratory tract effects

Special comments

Athletics

Exertion, cold air

Especially winter sports

Athletics Athletics

Acute trauma Upper extremity overuse

Swimming Mountaineering

Trinitrochlorine Altitude

Exercise-induced asthma Rib fractures Embolus from upper extremity thrombosis Irritant asthma Pulmonary edema

Diving Diving, swimming

Hyperbaric pressure Exercise in water

Barotrauma Pulmonary edema

Skating Performing arts

Nitrogen dioxide Exertion

Singers

Stress

Performing arts (stage) Performing arts (stage) Musicians (string)

Artificial fog/smoke Make-up Rosin

Lung injury Exercise-induced asthma Vocal cord dysfunction Irritation Sensitization Sensitization

Musicians (wind) Musician (drummer) Musician (wind, brass)

Reed or wood Microbes Intra-oral pressure

Sensitization Anthrax Upper airway disorders

Magician Performing arts (street) Magician Magician

Pyrotechnics Hydrocarbons Talc Latex

Sensitization Pneumonitis Talcosis Asthma

Rowers, golfers Paget–Schroetter syndrome; can occur in musicians as well Chlorinated pools Other high altitude sports as well Acute and chronic ‘Aqua-jogging’ also a risk factor Indoor rink resurfacing Dancers and others Other public speaking Glycols and mineral oils Lycopodium spores Ballet dancers also exposed Not only contact allergy Hide drums Velopharyngeal incompetence; laryngocele Lycopodium spores ‘Fire-eater’s lung’ From balloon handling From balloon handling

popular amateur activities involving large numbers of people. Also of note, both have physical demands and carry associated physical risks. Exercise-induced asthma is widely recognized as a common problem among amateur athletes, for example cyclists or runners. Winter sports may have the added stimulus of cold-air challenge. Swimming and related chlorinated pool-sports could carry the added risk of trinitrochlorine irritant exposure that could induce asthma or exacerbate pre-existing disease. In the performing arts, strenuous effort is also typical of disciplines ranging from dancing to circus performing. For both sports and the performing arts, symptoms may become manifest initially with these activities or asthma may predate the avocation (or even have been a factor in choosing the activity). Vocal cord dysfunction (VCD), which can symptomatically mimic asthma, is a related issue in athletics and in the performing arts. Mouth breathing in exercise can be a trigger for VCD episodes. In addition, the stress of competitive or public performance

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can play a role in the VCD syndrome. The latter can be a particularly prominent feature in performance that entails singing or public speaking. Physical trauma involving the chest is a factor to be considered and may be particularly relevant to certain avocation sports and other physical activities. Although this is not typically a diagnostic challenge, it may be in certain cases such as thoracic duct rupture with trivial or occult exercise-related injury. Understandably, certain sports are associated with particular patterns of trauma, such as stress fractures of the rib in rowers and golfers. Athletics-related pulmonary embolus due to upper vein thrombosis in the context of ‘overuse’ of the upper extremities (effort-related thrombosis of the upper extremity or Paget–Schroetter syndrome) is also an important consideration; this can also occur rarely in musicians in the context of upper-extremity overuse. Mountaineers and divers are also at notable risk for the pulmonary complications of low and high barometric pressure environments: high-altitude pulmonary edema in mountaineers and barotrauma and the pulmonary manifestations of decompression sickness in divers. Acute pulmonary edema has been associated with diving, swimming and, more recently, with aqua-jogging. Water swallowing during the swimming component of triathlon competition has been associated with leptospirosis, a multisystem infectious process with a prominent pulmonary component. Enthusiasts of indoor skating rinks can experience acute lung injury due to nitrogen dioxide overexposure from ice-resurfacing machine exhaust. There are also potential exposures that are peculiar to certain performing artists. Selected examples include: inhalation of ‘artificial’ stage fogs and smokes (mineral oil and glycols that can be respiratory irritants); use of stage make-up leading to respiratory sensitization (for example, Lycopodium derived from moss spores has a long history of use as a face powder and has been associated with asthma not only in industrial settings, but also among stage performers); allergy to rosin (used for musical instrument bows and for ballet shoes) and allergy to the mouthpiece (reed or wood) in wind instrument players (a cases of EAA has also been reported due to Candida mold contamination of a saxophone mouthpiece); and ethnic drummers who make their own drums can contract anthrax from contaminated animal hides. One might also expect that allergic sensitization to rabbits or doves used in tricks could lead to asthma or even EAA in performing magicians; latex used in masks or other disguises also could be a hazard of stage actors. A case of talc-related granulomatous lung disease also has been reported in an amateur magician (conjurer) due to the use of talc-contaminated balloons. Magic acts and stage pyrotechnics can also involve the use of Lycopodium spores because they can ignite rapidly when dispersed in air (this asthma-causing agent already noted above as used in stage make-up); ‘fire eater’s lung’ is a more serious complication of pyrotechnics related to street performance techniques that lead to acute hydrocarbon pneumonitis from aspirated material. Wind instrument and brass players can be at risk of upper airway disorders related to increased intraoral pressures, including velopharyngeal incompetence and laryngocele.

7.5 Miscellaneous hobbies, pastimes and avocations Given the variety of human passions, almost any activity can grow into an avid preoccupation, a phenomenon captured in Frank Stockton’s classic short story, the

7.5 MISCELLANEOUS HOBBIES, PASTIMES AND AVOCATIONS

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Table 7.4 Selected hobbies and other pastime activities with potential respiratory effects: miscellaneous avocations Hobby, avocation or other pastime activity Metal extraction (prospecting) Metal cleaning Model-making Cave exploring Hunting, camping, fishing Gambling Gardening Baking and pastry making

Possible relevant exposures

Possible respiratory tract effects

Mercury fume

Pneumonitis

Nitric acid fume Two-part glues Fungus Fungus

Pneumonitis Sensitization Histoplasmosis Blastomycosis

Second-hand smoke Plant antigens

Irritant asthma Sensitization

Cereal flours

Sensitization

Special comments

Heavy acute exposure required ‘Numismatist’s lung’ Acrylates, other glues ‘Spelunking’ From water sources Long-term cancer risk Pesticide exposure also possible Flours; enzymes less likely non-occupationally

Queen’s Museum, which tells the tale of a monarch’s world-class collection of ‘buttonholes’. Thus, it not surprising that medical literature is rich with case reports of various respiratory illnesses due to the predilections (and follies) of hobbyists and amateurs of every stripe and type (Table 7.4). By their vary nature, it is not possible to generalize about these cases, but a listing of some of the more notable associations is useful. Some examples include: acute lung injury due to mercury fume in amateur metal extractors such as gold prospectors (mercury fume exposure also occurs among antique clock and other mechanical device collectors–restorers, but since the material is not heated, the intensity of exposure is not sufficient to cause pneumonitis); acute lung injury from nitrogen dioxide from nitric acid–metal contact (reported as a case of ‘numismatist’s pneumonitis’; nitric acid is also used in metal plate etching for art); and asthma from acrylate (instant) glue in model-making (asthma and rhinitis from other reactive glues would also be an anticipated risk in model-making given its intensive use of glues and adhesives). Mold-related respiratory illness comprises a distinct subset of hobbyassociated disease. Pulmonary histoplasmosis is a particular risk among spelunkers (potholers) from exposure to the feces of infected bats. Camping, hunting and fishing have been linked to blastomycosis from water sources. An outbreak of coccidiomycosis was linked to participants in a model airplane competition in an endemic area; any leisure activity involving soil disruption where coccidiomycoses is found could lead to disease. Secondhand smoke exposure, with its intended respiratory risks, is certainly an ‘occupational’ hazard of gamblers. Gardeners are at risk of airway sensitization and potentially from agricultural chemicals (hothouse enthusiasts may have higher exposures). A hobbyist gardener is unlikely to have exposure to restricted agricultural chemicals such as paraquat, which can cause lung fibrosis. Finally, cooking, baking and pastry making are common tasks in salaried and unsalaried occupations, but are certainly also activities that rise to the level of avocation for many and can lead to respiratory sensitization to a number of materials (including, but not limited to, cereal flours).

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7.6 Specific diseases associated with hobby activities As the foregoing makes clear, although a wide spectrum of respiratory conditions can be linked to hobby activities, most of the associations are very uncommon. Nonetheless, it is possible to make some general comments on the pattern that emerges from the available data, even if the associations in question are almost entirely limited to scattered case reports or are suspected by analogy to known patterns of occupational exposure disease causation. Asthma and rhinitis, being allergic lower and upper airways responses that can be triggered by myriad potential sensitizers, comprise the largest component of hobbyassociated respiratory tract diseases. The potential for such problems exists within every one of the larger groups of activities reviewed above. Although most of the causal agents are naturally derived, high-molecular-weight sensitizers, some are lowmolecular-weight agents, in particular reactive glues and polymers that are employed in many hobby pursuits. In addition to allergic airways disease, exercise-induced asthma is relevant to sports and certain performing arts: pastime asthma exacerbation to cold-air pursuits such as winter sports, and the potential for irritant-induced asthma in hobbies involving contact with acrid fumes or gases. One of the most serious respiratory syndromes associated with hobby pursuits is EAA. Although this is dominated by bird-fancier’s disease through various scenarios, additional known triggers of EAA can be encountered through other scenarios, albeit rarely. The other severe lung syndrome of note, although rare through a hobbyist exposure scenario, is acute lung injury, which can be due to irritant inhalants or to selected toxic metal fumes. Both EAA and acute lung injury can be related to ‘bystander’ exposure in a household member who is not the hobbyist. The classic pneumoconioses are perhaps the least relevant to hobbies, although silica and talc exposure can occur with sporadic documentation of disease. Asbestos exposure scenarios in some hobby pursuits (at least historically) are very possible, especially in any pursuit that involves handling heat sources. Although such exposure is very unlikely to have been sustained and heavy enough to lead to asbestosis, pleural plaques and asbestos-related malignancy are reasonable considerations. Indeed, it is reasonable to presume that some cases of mesothelioma for which there is no clear-cut occupational exposure may be due to prior hobby-based asbestos use. Other lung conditions have narrow associations with very specific hobby and pastime activities, as noted in the preceding sections, with selected examples including pulmonary emboli (upper extremity over-use), hydrocarbon pneumonitis (street pyrotechnics), and fungal and zoonotic pneumonias (Tables 7.1–7.4).

7.7 Diagnosis and management The primary diagnostic dilemma in hobby-associated respiratory disease is considering a hobby/pastime/avocation/amateur pursuit among the potential differential etiologies. If the patient does not spontaneously volunteer a suspicion that a particular activity may be related to an illness, it is unlikely that the clinician will raise it first. Indeed, even if the issue is raised by the patient, it is often only the astute clinician who follows up on such a lead. There is no ‘template’ format for eliciting a hobby exposure history.

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The best approach may simply be to take a broad approach to the question by prompting the patient with several examples indicating the range subsumed by hobby pursuits and asking the patient, in an open-ended way, to describe any such activities that are relevant. Often the suspicion of a hobby-related exposure increases in the context of specific scenarios (adult-onset asthma with a distinct temporal pattern; EAA; zoonotic infection) in which obvious occupational or environmental causes have been excluded. Disease management should follow standard algorithms and stepwise protocols. In conditions for which ongoing exposure to the triggering agent is anticipated to be a stimulus for disease progression, especially EAA and allergic airway disease, elimination of further exposure is the intervention of choice. This may not be any easier with a devoted amateur than in the case of a paid job-related exposure upon which someone’s livelihood depends. Disease management should also emphasize primary prevention if others have potential exposure or if new safety measures would prevent future repetition of over-exposure (in the case of irritant inhalant acute events, for example). Finally, because the literature in this field is so sparse, sentinel case events should be documented and disseminated in order to better raise awareness of the potential respiratory hazards of hobby pursuits.

Further reading Butcher, J.D. (2006) Exercise-induced asthma in the competitive cold weather athlete. Curr. Sports Med. Rep. 5: 284–288. Duvall, K., Hinkamp, D. (eds) (2001) Health Hazards in the Arts. Occupational Medicine State of the Art Reviews, Vol. 16:4. Hanley & Belfus: Philadelphia, PA. Liu, S., Hayden, G.F. (2002) Maladies in musicians. South. Med. J. 95: 727–734. Mairesse, M., Ledent, C. (2002) [Allergy and fishing activities]. Allerg. Immunol. (Paris) 34: 245–247. Malo, J.-L., Chan-Yeung, M. (2006) Appendix: Agents causing occupational asthma with key references. In Bernstein, I.L., Chan-Yeung, M., Malo, J.-L., Bernstein D.I. (eds). Asthma in the Workplace and Related Conditions, 3rd edn. Taylor and Francis: New York; 825–866. McCann, M. (1979) Artist Beware. The Hazards and Precautions in Working with Art and Craft Materials. Watson-Guptill: New York. Sipsas, N.V., Kontoyiannnis, D.P. (2008) Occupational, lifestyle, diet, and invasive fungal infections. Infection; doi: 10.1007/s15010-008-8129-5. Wilson, J.J., Wilson, E.M. (2006) Practical management: vocal cord dysfunction in athletes. Clin. J. Sport Med. 16: 357–360. Winer-Muram, H.T., Rubin, S.A. (1991) Pet-associated lung diseases. J. Thorac. Imag. 6: 14–30.

Part II Other indoor environments

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

8 Day-care and schools €nmark and Greta Smedje Eva Ro 



Umea University, Umea, Sweden

8.1 Introduction Apart from homes, schools and day-care facilities are the most important indoor environments for children. Since (primary) school attendance is mandatory for children all over the world, schools – including their teachers and other employees – are probably the largest work places. Even in 1880, Professor Heyman in Sweden observed the importance of the school environment. Observing that childrens’ health improved after the school term had ended in the summer, he concluded that ‘poor school room air’ affected school children negatively. The school environment, including its buildings, varies considerably between and within countries and communities. For example, different climates may induce different environmental problems; high temperature may be a major problem in tropical countries, while the opposite may be relevant in countries with a cold climate. Outdoor pollutants, such as exhaust from traffic, may also be an indoor problem at schools. Furthermore, specific exposures occur in handicraft instruction and vocational schools. Asthma and other allergic diseases are by far the most common chronic noninfectious diseases among children and young adults. The worldwide prevalences of asthma, rhino-conjuntivitis and eczema among school children vary considerably. According to phase III of the International Study of Asthma and Allergy (ISAAC) performed in 2002–2003, the prevalence of asthma symptoms was highest and more than 20% in several countries in Latin and South America, in Australia, New Zealand and the UK. The reason for the increase in the prevalence of asthma and allergic diseases reported during the last five decades is unclear, but is probably related to changes in environmental and lifestyle factors. The indoor climate alone is probably not responsible for the prevalence increase, but is important at least in impairing those already diseased. Most

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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studies of indoor environment have focused on homes, and generally the school environment and its relation to respiratory diseases have not been extensively studied. Most studies of the school environment have been performed in Scandinavia, the USA and China. Several factors in the indoor environment of schools may cause respiratory symptoms, aggravate asthma and allergic diseases or facilitate the spread of infectious diseases. As in other buildings, high radon levels in school buildings may contribute to lung cancer. Thus, the school environment is of particular interest for many children and adults. This chapter summarizes the current knowledge about the school and daycare environment in relation to respiratory diseases.

8.2 Description of exposures Most of the critical exposures – such as damp, molds and bacteria, radon and environmental tobacco smoke – in premises for schools and day-care are not specific for these environments. However, for some factors, like dust, pet allergens and ventilation, the problem may be greater or different in schools and day-care compared with in homes.

8.2.1 Ventilation Well-balanced ventilation is fundamental in maintaining thermal comfort and high indoor air quality. The primary role of ventilation is to remove airborne pollutants and supply the building with clean air. Thus, the outdoor air quality is important for the indoor environment. The levels of most indoor pollutants are dependent on the amount of outdoor air supply. Recommendations of ventilation rate for school buildings differ between countries; for example it is around 8 l/s per person in Sweden and USA, and 3 l/s per person in Japan. Low classroom ventilation will result in elevated levels of carbon dioxide (CO2); indeed CO2 concentrations may be used as an indirect measure of ventilation rate, the correlation between the two being almost linear. In Sweden it is recommended that the level of CO2 not should exceed 1000 ppm; the corresponding value in Germany is 1500 ppm.Most schools worldwidedo not haveany mechanical ventilation, althoughit is common for instance in Scandinavian countries. Measurements of CO2 concentrations in schools have shown different levels. High concentrations have been found in schools in the UK (2100–5000 ppm), while lower levels were found in Denmark (500–1500 ppm). Generally, schools with natural ventilation have the higher levels. Ventilation by open windows during breaks is thus important. However, mechanical ventilation does not guarantee adequate ventilation. A study from Hong Kong found elevated levels of CO2 even in schools with air-conditioning or ceiling fans, indicating inadequate ventilation.

8.2.2 Indoor air humidity Indoor humidity is dependent on outdoor humidity, room ventilation, possible vapour built into the construction materials and emission from humans and their

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activities. Increased humidity may induce growth of molds and mites and increase emissions of volatile organic compounds (VOC). However, generally the total levels of VOC and mites are lower in schools than in offices and homes. Further, it has been shown that increased humidity may cause accumulation of indoor pet allergens.

8.2.3 Molds and bacteria Higher concentrations of airborne and settled microorganisms have been found in schools compared with offices. Concentrations in indoor air reflect the concentration of microorganisms in outdoor air, possible indoor sources and the effectiveness of the air filtration system. The proportion of Mycelia sterilia has been shown to be higher in schools than in homes, but the reason for this is not known. Actinomycetes species are common in buildings with dampness problems, but another major source of airborne bacteria is the occupants themselves.

8.2.4 Dust The concentration of settled dust is often higher in classrooms than in work places for adults. Higher concentrations have been found in rooms with textile carpets compared with rooms with smooth floors, and levels of dust are increased by the quantity of open shelves or other storage in the room. It is probable that most dust comes from indoor sources as the concentrations of particles, both less than 2.5 mm and less than 10 mm, are higher in classrooms than outdoors. Because of the childrens’ or students’ activities in classrooms and day-care facilities, the level of airborne particles is high. The correlation between the indoor and outdoor concentrations has been shown to be modest, apart from ultrafine particles which are primarily of outdoor origin. Better cleaning of classrooms and adequate ventilation reduces the amount of dust.

8.2.5 Allergens Despite pets being prohibited in most schools and day-care centers, allergens from cats and dogs are ubiquitous and found frequently in relatively high concentrations in schools worldwide. Pet allergens are transferred on the clothes and hair of pet owners from their homes to schools. The concentration of pet allergens in the classroom correlates well with the total number of pet owners in the class, and the concentrations are higher in classrooms with textile carpets than in rooms with smooth floors. The textiles act as reservoirs for allergens and dust. However, allergens from cats and dogs are easily found also in dust from smooth floors and desks. In total, the level of cat allergens is higher in schools than in homes without cats, but lower than in homes with cats (Figure 8.1). Cat allergen can be carried by very small particles, and these small particles can remain airborne for long time periods even if there is no air disturbance.

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µg of Fel d 1 per gram of dust

1000

100

87.5%

14.3%

5.7%

18.8%

12.5%

47.6%

24.3%

65.6%

0%

38.1%

70.0%

15.6%

10

1

0.1

Cat now (n=32)

Cat previously (n=21)

Homes

Cat never (n=70)

School desks & chairs (n=64)

Figure 8.1 Concentration of Fel d 1 in the dust from homes with and without cats as well as from school desks and chair samples in northern Sweden. Dashed lines represent the cut-offs between low and moderate (1 mg/g), and moderate and high (8 mg/g) allergen concentrations, respectively. Percentages indicate how many of the samples fall into each category. Reproduced with permission from the author: Perzanowski, M.S., Molecular epidemiology of allergen exposure, sensitization and   asthma in school children. Umea University Medical Dissertation, Umea, Sweden, 2003; ISBN 91-7305376-7

Thus, the activities in a classroom will result in high concentrations of cat allergens in the air during the whole day. Earlier studies regarding allergen exposures did not usually focus on pet allergens. A study from the USA reported lower allergen levels in schools compared with in homes but focussed on mite, pollen and molds. In Norway and the Netherlands, mite allergen levels in schools were found to be low, compared with in homes. Generally mite allergen can be found in textiles and not in dust from smooth floors. This was confirmed by a study performed in Sweden where no mite allergens were found in dust from the floor from schools and day-care centers, while low levels of mite allergens could be detected in textiles. A comparison between Northern Sweden and Virginia in the USA showed differences in allergen exposures at schools. In both Sweden and Virginia significant levels of cat and dog allergens were found. However, the levels of cat allergen were higher in Virginia while the levels of dog allergens were higher in Sweden. While no mite allergen was found in Sweden, mite allergens were detected in schools in Virginia, although the levels were lower than found in homes in Virginia. In China and Korea only low levels of furry pet allergen were found, probably reflecting a low prevalence of pet keeping at home. However, pet keeping is increasing in these countries and allergen exposures in schools may be an increasing problem in many parts of the world. Apart from allergens from domestic pets, allergens from more undesirable animals may also be present in school buildings, especially those from cockroaches but also from rats and mice. In inner-city schools in the USA, concentrations of cockroach allergens are similar to those found in local homes.

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Food allergens may also be present in schools. In many countries children bring their own packed meal which may be eaten in special areas or in the classroom. Allergens from eggs and fish have been shown to be present in Norwegian classrooms at levels only slightly lower than in homes. One American study investigated the presence of peanut allergens at school, but found no airborne peanut allergen (Ara h 1), nor was it found on desks. However, it is obvious that peanut allergens may occur, at least on surfaces due to contamination by hands. It is probable that methods for measuring environmental peanut allergens need to be improved.

8.2.6 Environmental tobacco smoke Throughout the world, there are initiatives to introduce policies to reduce smoking in public places, and in a large number of countries smoking is prohibited in schools and day-care facilities in front of the children. However, smoking may still be allowed in certain areas, and include smoking by both pupils and employees. Thus, exposure to environmental tobacco smoke (ETS), or ‘second hand smoking’, still occurs in schools in many countries. Common methods to estimate exposure to ETS are to measure nicotine in room air or cotinine (a nicotine metabolite) in saliva, blood or urine. Nicotine has been detected in the air of most schools, including those where smoking is prohibited, but the mean concentrations are lower than in most other public environments. A survey in Latin America found nicotine levels that ranged from <0.01–0.2 mg/m3; the concentration tended to be related to the prevalence of smoking in the country. In Western Europe, median nicotine concentration in schools varied from 0.01 mg/m3 in Sweden to 1 mg/m3 in Austria. This may be compared with nicotine levels in homes of daily smokers, which usually range from 0.1 to 10 mg/m3, with a mean around 1 mg/m3. An American prospective study followed infants during their first two years and measured cotinine in urine repeatedly. As expected, the strongest predictor of cotinine levels was having smoking parents. However, a significant and substantial contribution was also found from attending day-care away from home and frequency of smoking among day-care employees. In many infants, exposure to ETS from adults other than the parents resulted in cotinine levels that were higher than levels previously regarded as typical in children of smoking parents.

8.2.7 Radon The main source of excess levels of radon in buildings is entry of radon from soil through cracks in the floor. This flow arises because buildings are often at a slightly negative pressure in respect to their surroundings. Basement or ground floor rooms are chiefly affected. Some building materials, such as certain types of lightweight concrete, may also be a significant source of indoor radon. Many countries have target values for indoor radon concentrations. Several European countries have the same target value for domestic dwellings and workplaces. A common value is 400 Bq/m3. In other countries, there is a lower target value for

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schools than other types of workplaces. In several countries, including the USA, the target value for schools is 150 Bq/m3, but in other countries it is 200, 400 or even 1000 Bq/m3 Surveys of radon levels in schools have been conducted in different countries. In Ireland, 23% of schools had at least one room with an indoor concentration exceeding 200 Bq/m3. In Iran 15% of surveyed schools exceeded 400 Bq/m3 and in the USA 3% of schools had at least one room exceeding 150 Bq/m3. In day-care centers, the geometric mean was 44 Bq/m3 in Norway and 48 Bq/m3 in Slovenia. Recent data from Sweden indicate that 5% of schools and day-care centers have rooms with concentrations higher than 200 Bq/m3. Thus, in many countries there are schools and day-care centers with excessive radon levels.

8.2.8 Exposures in handicraft instruction and vocational schools In addition to the general exposures in day-care and schools described above, students and employees in handicraft teaching and vocational schools are exposed to the same agents as those working in the professions taught, and their health may be affected in a similar way. Examples are schools of agriculture, veterinary science, technical arts, woodwork, needlework, cosmetics and hair styling, textiles, baking and food preparation. Each of these is associated with specific respiratory hazards.

8.3 Diseases associated with exposures in the school environment Asthma is a common disease among children and all children have to attend school for several years. Despite this, it has been difficult to explore the effect of the school environment on the development of asthma and allergic diseases. The reasons are several. First, the incidence of asthma in early school age is around 1/100/year. This means that it is necessary to study large cohorts including several schools prospectively for several years. Secondly, as no school is exactly like another, objective exposure measurements are needed from all studied schools, which is costly. Furthermore, the home environment may be a confounding factor and should also be studied in the same manner. Thus, data regarding the school environment and development of allergic diseases are scarce. Regarding the environmental effects on subjects who already have developed asthma or other allergic diseases, the knowledge is somewhat better. Studies on school attendance give a uniform picture showing that subjects with asthma have more sick-leave from school compared with children without asthma. Further, children with asthma reported increased symptoms when attending school, and complaints were significantly related to the severity of the disease. Thus improvement of the school environment is important. Other respiratory diseases such as extrinsic allergic alveolitis (EEA) and pulmonary fibrosis may be related to exposures in vocational schools. However, these are mainly work-related problems and are described fully in Part III - the work environment.

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8.4 Viral infections Because of the relatively high person density, viral infections are common in day-care and schools, and epidemics of common colds and respiratory infections easily start. Good hygiene practices are essential. From other indoor environments, it has been shown that a low building ventilation rate may affect the spread of infectious disease, but there are few studies from schools investigating this factor.

8.5 Ventilation Among school employees, reduced nasal patency and an inflammatory biomarker response of the nasal mucosa have been related to low air exchange rate and old mechanical ventilation systems. An intervention study showed that pupils attending schools that got a new ventilation system had fewer asthmatic symptoms than pupils in other schools. The main cause is that poor ventilation in schools results in accumulation of several pollutants, both chemical and biological, in the air. These pollutants may induce respiratory or other allergic symptoms. It is known that VOC emitted from building materials and building occupants are often increased in indoor environments and particularly if the ventilation is poor. These substances have been associated with sensory irritation in the eyes and the nose. Recent studies from both schools and homes indicate that increased levels of VOC may also be associated with lower respiratory symptoms. Furthermore, poor design and maintenance of the ventilation system may result in microbial growth in filters and ducts that affects indoor air quality and health. High concentrations of CO2 have been related to tiredness, but there is no evidence that everyday levels of CO2, per se, have any impact on respiratory health. However, an American study found a 10–20% increase in student absence due to illness per 1000 ppm increase of concentration of CO2 in the classroom. Apart from installing a more effective ventilation system, a warning device showing when the CO2 level is too high with consequent advice to improve airing by opening windows has been shown to improve indoor air quality.

8.6 Room temperature While a cold winter climate may aggravate asthma symptoms, there is no evidence that average indoor temperatures have any impact on respiratory health, although they may present a comfort problem. Because of low ventilation rates and high person densities, schoolroom temperatures are often relatively high, at least during sunny periods.

8.6.1 Indoor humidity, dampness and molds Damp in the home has been identified as a risk factor for respiratory symptoms and asthma among both children and adults in several studies in different parts of the world, but the explanation is still unclear. It may be due to mold exposure, increased occurrence of dust mites, or emissions of chemical substances.

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Studies performed in schools show that attendance at a school with mold growth or problems with damp is related to an increased risk of respiratory symptoms, asthma medication use and asthma. A study from Denmark found that mold in dust was related to an increased prevalence of eye irritation, throat irritation and headache. Further, after remediation of a mold-damaged school, bronchitis and episodes of respiratory infections decreased among teachers.

8.6.2 Dust Subjects with asthma often report increased symptoms when exposed to dust. Dust contains a large number of different particles, including biological compounds such as allergens. A Danish study found that the inflammatory potential of the dust was related to its content of organic compounds, and dust collected from schools with more health complaints had a higher inflammatory potential than dust from other schools. Studies of respiratory health effects due to dust in the school are scarce, but children with asthma showed increased respiratory obstruction if they slept in a dusty room at home. The level of inflammatory markers in nasal lavage fluid was higher among school employees working in schools with increased levels of settled dust, and the prevalence of asthma among the children was higher. In contrast, studies from the Netherlands failed to show any correlation between the presence of textile carpets in schools (which may indicate higher dust levels) and expiratory peak flow variability among children with asthma. However, in a study among staff in schools and kindergartens, 50% of the employees complained of dust in the air.

8.6.3 Allergens from pets Avoidance of pets is an established and effective strategy to prevent allergic symptoms among subjects with a known allergy to pets. Nevertheless, in schools and day-care centers, children with pet allergy are often exposed to allergen levels that are high enough to evoke allergic symptoms such as asthma, rhino-conjuntivitis and eczema. Furthermore, levels may also be high enough to induce allergic sensitization among children. Most sensitized children have never lived in a home with a cat or dog, and schools and day-care centers are probably a major site of allergen exposure. Few studies report the clinical effects of allergen exposures at schools. However, pupils with asthma and furry pet allergy had impaired lung function and more respiratory symptoms in the first week of the school term, but only if they attended a class with many cat owners. Similarly, pupils with asthma and allergy to furry pets had increased bronchial hyperresponsiveness after exposure to the school environment.

8.6.4 Environmental tobacco smoke The adverse health effects from exposure to ETS in both adults and children are well-known. Major effects in children include an increased prevalence of lower respiratory tract illness and asthma. Thus, introducing and effectively implementing

8.7

DIAGNOSIS AND MANAGEMENT ISSUES

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policies against smoking in schools and day-care centers should be important measures, besides others, in reducing the negative health effects of smoking.

8.6.5 Radon Radon in buildings contributes to an excess risk of lung cancer. The risk is supposed to have a linear dose–response relation with no threshold. Several attempts have been made to calculate the radiation dose due to indoor exposure to radon, particularly in homes. The population’s mean annual effective dose typically is lower than 1 mSv; however, the range is very wide. Only a few studies have calculated the contribution from school attendance to this dose. An Irish study found that the mean radon concentration in schools was similar to that in domestic dwellings (93 and 89 Bq/ m3, respectively) and calculated an annual effective dose of 0.3 mSv from exposure in schools. A Greek study calculated an annual effective dose of 0.1 mSv for students and 0.2 mSv for teachers, based on a mean radon concentration of 35 Bq/m3. For risk management, and as no safe threshold level is shown, reducing the mean population dose as well as that in high-exposure individuals is equally important. A British study estimated the cost-effectiveness of radon remediation programs in different kinds of buildings and concluded that it is most cost-effective to conduct such programs in schools with high levels. Because of the high person density in schools, the cost per reduced Man–Sievert is much lower in schools than in homes.

8.7 Diagnosis and management issues For clinicians it is important to keep in mind that a patient’s reported symptoms may be related to the school environment. A detailed medical history is important in order to make a correct diagnosis. The next step is to consider which situations or environments could be the triggering factors. Skin prick testing or measurement of specific IgE are helpful in considering problems that may have an allergic mechanism. Serial peak expiratory flow measurements in subjects with asthma symptoms before and during attendance at school may be useful. Peak flow measurements are also helpful in judging the effectiveness of any intervention actions at school. Cooperation with the school’s health care providers is important. In addition, normal medical treatment following standard guidelines must be advised. Among schoolchildren, anaphylactic shock or similar severe reactions are primarily food-related. It has been shown that the outcome of such a reaction is worse if the onset is in school, probably because of substandard and/ or delayed care in the school setting. Thus education of pupils and school employees should be improved regarding the signs, symptoms, and measures to take.

8.7.1 Intervention trials at schools and day-care centers Allergen and dust intervention In some countries, schools may offer extra cleaning of classrooms for severely allergic children; however, this intervention has not been adequately evaluated. Although in

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office environments, intervention studies have shown positive effects of cleaning, very few intervention studies have been performed in schools and day-care centers; most report only changes in exposures, while the health effects are less studied. Studies from Sweden showed that the level of pet allergens at day-care centers could be reduced by intervention measures. In one of the studies, allergen levels were measured before and after extensive renovation, including installation of a new ventilation system. Old textiles including mattresses, pillowcases, curtains and sofas were removed and exchanged with new material. The cleaning routines were changed and the families and the school employees had to avoid direct and indirect contact with pets. Immediately after the renovation, the level of cat and dog allergen decreased dramatically, and the levels were still lower than before the intervention after one year. Another study compared the levels of pet allergens in ‘allergen avoidance’ and conventional day-care centers and found reduced levels of pet allergens in the former. Of importance in both these studies is that none of the families or the staff in the intervention centers were cat or dog owners. Another study evaluated the intervention effect on cat allergen levels with no restrictions regarding contacts with pets; several other actions were taken, including removal of upholstery and plants, replacement of bookshelves with cupboards and changes of the cleaning routines. Serial measurements of allergens were performed before and after these intervention measures. The study concluded that the allergen avoidance measures used did not reduce the levels of airborne cat allergens. However, the intervention was only partially successful in reducing the amount of dust-collecting fittings, and there was no increased cleaning of furniture (which has been shown to be correlated to the level of airborne particulates). An Australian intervention study aimed at creating a ‘low allergen school’ by limiting the amount of dust-collecting fittings, increasing air exchange and using a central vacuum cleaner demonstrated a cat allergen level that was about one-third of levels in control schools. The level of pet allergens in a classroom correlates strongly with the number of pet owners. Further, by introducing school uniforms and a ban on pet owning, the level of airborne cat allergen at schools can be reduced. Intervention studies including either or both of these factors typically have reduced allergen levels in school by around 90%, while other interventions have resulted in lower reductions, if any. In summary, the clinical effects of increased regular cleaning of classrooms are unclear. Intervention studies on exposure conclude that reducing incoming allergens is the most effective measure to reduce the allergen level in the school environment. This can be achieved by reducing the number of children and school employees who have pets at home or by the use of special school clothes that are not in use at home. Hygiene intervention A study in Finland investigated the effect of increased hygiene at day-care centers. The intervention lasted for 15 months and included several steps; the most important was increased hand hygiene by the use of an alcohol-based hand rub. Both the children and the personnel in the intervention centers had significantly fewer respiratory infections compared with the control centers, and the use of antimicrobials among the children decreased by 24%. A 12 year follow-up survey of the children who had participated in the study concluded, however, that that the decrease in infections did not affect the development of asthma or other allergic diseases in any direction.

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8.8 Summary Despite it being well-known that the environment in schools and day-care centers is not optimal, and that many children with allergic symptoms experience increased symptoms daily at their work place, the school, few studies have evaluated the health impact of the indoor environment at school. Today there is an increasing interest in the school environment in relation to health with an increasing number of national and international studies and campaigns. For instance, the US Environmental Protection Agency has developed an ‘Indoor Air Quality Tools for Schools’ program and the European Union is supporting research on ‘Health Effects of the School Environment’. A Swedish national position paper on how schools should deal with asthma and allergies was published in 2002. It stated that schools should bear the responsibility for their students’ health and substances that trigger allergic reactions and respiratory irritation should be kept to a minimum. Furthermore, the students should not exhibit symptoms, nor need to increase their medicines due to conditions at schools.

8.9 Recommendations In order to obtain an environment in schools and day-care centers that do not contribute to respiratory disease and are safe for those already affected, these recommendations are given: Keep the building ‘healthy’: .

fulfil ventilation standards;

.

maintain the building adequately;

.

prevent problems with damp and repair damage;

.

reduce high radon levels;

.

design the building and its fittings so that it is easily cleaned;

.

keep a high standard of cleaning, including textiles.

Take care of one another: .

avoid smoking;

.

avoid strong scents and spray products;

.

do not keep allergenic plants indoors;

.

discuss how to reduce the entry of pet allergens.

Further reading Allerman, L., Meyer, H.W., Poulsen, O.M., Nielsen, J.B., Gyntelberg, F. (2003) Inflammatory potential of dust from schools and building related symptoms. Occup. Environ. Med. 60(9): e5.

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Belanger, E., Kielb, C., Lin, S. (2006) Asthma hospitalization rates among children, and school building conditions, by New York State school districts, 1991–2001. J. Sch. Health 76(9): 408–413. Dunder, T., Tapiainen, T., Pokka, T., Uhari, M. (2007) Infections in child day care centers and later development of asthma, allergic rhinitis, and atopic dermatitis: prospective follow-up survey 12 years after controlled randomized hygiene intervention. Arch. Pediatr. Adolesc. Med. 161: 972–977. Godwin, C., Batterman, S. (2007) Indoor air in Michigan schools. Indoor Air 17: 109–121. Karlsson, A.S., Andersson, B., Renstr€ om, A., Svedmyr, J., Larsson, K., Borres, M.P. (2004) Airborne cat allergen reduction in classrooms that use special school clothing or ban pet ownership. J. Allergy Clin. Immunol. 113: 1172–1177. Lee, S.C., Chang, M. (2000) Indoor and outdoor air quality investigation at schools in Hong Kong. Chemosphere 41: 109–113. Meyer, H.W., Wurtz, H., Suadicani, P., Valbjorn, O., Sigsgaard, T., Gyntelberg, F. Members of a Working Group under the Danish Mould in Buildings Program (DAMIB) (2004). Molds in floor dust and building-related symptoms in adolescent school children. Indoor Air 14: 65–72. Mi, Y.H., Norb€ack, D., Tao, J., Mi, Y.L., Ferm, M. (2006) Current asthma and respiratory symptoms among pupils in Shanghai, China: influence of building ventilation, nitrogen dioxide, ozone, and formaldehyde in classrooms. Indoor Air 16: 454–464. Nebot, M., Lopez, M.J., Gorini, G., Neuberger, M., Axelsson, S., Pilali, M., Fonseca, C., Abdennbi, K., Hackshaw, A., Moshammer, H., Laurent, A.M., Salles, J., Georgouli, M., Fondelli, M.C., Serrahima, E., Centrich, F., Hammond, S.K. (2005) Environmental tobacco smoke exposure in public places of European cities. Tobacco Control 14: 60–63. Perzanowski, M.S., R€ onmark, E., Nold, B., Lundb€ack, B., Platts-Mills, T.A. (1999) Relevance of allergens from cats and dogs to asthma in the northernmost province of Sweden: schools as a major site of exposure. J. Allergy Clin. Immunol. 103: 1018–1024. R€ onmark, E., Perzanowski, M., Platts-Mills, T., Lundb€ack, B. (2002) Incidence rates and risk factors for asthma among school children: a 2-year follow-up report from the obstructive lung disease in Northern Sweden (OLIN) studies. Respir. Med. 96: 1006–1013. Smedje, G., Norb€ack, D. (2001) Irritants and allergens at school in relation to furnishings and cleaning. Indoor Air 11: 127–133. Synnott, H., Hanley, O., Fenton, D., Colgan, P.A. (2006) Radon in Irish schools: the results of a national survey. J. Radiol. Protect. 26: 85–96. Zhang, G., Spickett, J., Rumchey, K., Lee, A.H., Stick, S. (2006) Indoor environmental quality in a ‘low allergen’ school and three standard primary schools in Western Australia. Indoor Air 16(1): 74–80.

9 Secondhand smoke exposure and the health of hospitality workers Mark D. Eisner University of California, San Francisco, CA, USA

9.1 Introduction Hospitality workers comprise persons who work in bars, taverns, pubs, restaurants, cinemas, bowling alleys, casinos, bingo halls and other industries aimed at customer entertainment. Although these occupations do not generally involve unique exposures, hospitality workers have often been exposed to very high levels of second-hand smoke (SHS). Bar and tavern workers, in particular, have been exposed to SHS levels that are 4–6 times higher than in other workplaces [1]. Peak SHS exposures may reach extremely high levels, as much as 10 times the levels found in office workplaces or in the home. Consequently, hospitality workers may be particularly susceptible to the acute and chronic health effects of SHS exposure (Tables 9.1 and 9.2). A corollary is that they will accrue especially large health benefits from smoke-free workplaces.

9.2 Exposure of hospitality workers to SHS Numerous studies indicate that hospitality workers, particularly bar and tavern workers, are exposed to SHS in the workplace. Moreover, laws that prohibit smoking in hospitality workplaces are highly effective in reducing exposure. After the California workplace smoking ban went into effect, self-reported workplace exposure to SHS decreased from a median of 28 to 2 hours per week [2]. Total SHS exposure decreased from a median of 40 to 10 hours per week. Other studies have confirmed that hospitality workers experience markedly decreased SHS exposure after smoke-free workplaces are

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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Common respiratory tract and sensory symptoms after secondhand smoke exposure

Symptom class

Symptom

Sensory irritation symptom

Conjunctival injection or redness Conjunctival pruritis Tearing Rhinorrhea Nasal burning Nasal stuffiness Sore throat

Respiratory symptoms

Cough Cough with phlegm production Wheezing Dyspnea (at rest) Dyspnea (with exertion)

mandated, including self-reported exposure, measurement of cotinine (in saliva, urine or serum) and hair nicotine. Other studies have investigated the impact of smoke-free workplace laws on direct measurement of SHS constituents in the indoor environment. Investigators measured indoor PM2.5 levels in Irish pubs before and after the national smoking ban [3]. Before the ban, the average indoor level of PM2.5 was 35.5 mg/m3; after the ban the average level declined by 84% to 5.8 mg/m3. Of note, the post-ban PM2.5 level was the same as that in outdoor air, which is expected if there is no indoor point source of exposure (such as SHS). Indoor air levels of benzene, which is an established carcinogen, also decreased by 80%. Other studies have also shown that workplace smoking bans result in marked reduction in fine particles and carcinogens in the indoor air. Table 9.2

SHS exposure may cause chronic disease among hospitality workers

Disease category

Disease

Notes

Respiratory

Asthma induction Asthma exacerbation COPD induction COPD exacerbation Chronic respiratory symptoms

New cases in adulthood Among those with pre-existing disease New cases Among those with pre-existing disease Supported by effectiveness of smoke-free workplace laws on respiratory symptoms

Pulmonary function decline Cancer

Lung cancer Breast cancer in younger, pre-menopausal women Nasal sinus cancer

Causal effect Probable causal effect

Cardiovascular

Coronary heart disease induction

Causal effect 25–30% increased risk Causal effect Evidence is mounting, but remains controversial

Coronary heart disease mortality Stroke

Probable causal effect

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In sum, when smoking is permitted, hospitality workers are exposed to high levels of SHS, which includes potent respiratory irritants and carcinogens. Laws that ban workplace smoking are rapidly effective in reducing exposure of hospitality workers to these dangerous substances.

9.3 Diseases and health conditions associated with exposures 9.3.1 Respiratory and sensory irritation symptoms Nearly all persons exposed to SHS will develop sensory irritation symptoms, which comprise eye, nose or throat irritation (Table 9.1). Mucous membrane irritation causes the specific symptoms of itchiness, redness or tearing of the eyes, rhinorrhea, nasal stuffiness, pharyngeal irritation and pharyngeal pain. Many persons will also develop symptoms referable to irritation of the upper and lower respiratory tract. Common symptoms are cough, cough with sputum production, wheezing, chest congestion and dyspnea (Table 9.1). With persistent SHS exposure, chronic bronchitis may develop. The majority of hospitality workers who are exposed to SHS will experience sensory irritation and respiratory symptoms [2, 4].

9.3.2 Workplace smoking bans and respiratory health of hospitality workers In the state of California, smoking was banned in most workplaces effective 1 January 1996 and in all bars and taverns effective 1 January 1998. Using a case-crossover design, we studied the effects of the law, which prohibited tobacco smoking in bars and taverns, on the respiratory health of bartenders [2]. Based on a random sample of all bars and taverns in San Francisco, we interviewed and performed spirometry on 53 bartenders before and after the smoking ban. After prohibition of smoking, self-reported workplace SHS exposure sharply declined from a median of 28 to 2 hours per week. Thirty-nine (74%) of the 53 bartenders reported at least one respiratory symptom at baseline (including cough, dyspnea and wheezing), while only 17 (32%) were still symptomatic at follow-up. Of the 39 bartenders reporting baseline symptoms, 23 subjects (59%) no longer indicated any respiratory symptoms after prohibition of smoking (p < 0.001). In conditional logistic regression analysis, a 5 hours reduction of workplace ETS exposure was associated with a lower risk of respiratory symptoms at follow-up (OR 0.7; 95% CI 0.5–0.9), after controlling for upper respiratory infections and reduced personal cigarette smoking. The majority also reported sensory irritation symptoms (77%), which largely resolved after the smoke-free workplace law went into effect (19% at follow-up, reflecting a 78% reduction). After prohibition of workplace smoking, pulmonary function also rapidly improved. We observed an improvement in mean FVC (189 ml; 95% CI 82–296 ml) and mean FEV1 (39 ml; 95% CI 30–107 ml). Complete cessation of workplace SHS exposure was associated with an even greater pulmonary function improvement. Other studies from Scotland, Ireland, Norway and the USA, using a similar design, have shown a substantial decline in respiratory and sensory irritation symptoms

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among hospitality workers after their workplaces became smoke-free [2, 4]. In addition, pulmonary function has improved quickly after the smoking ban; this benefit has been observed up to 6 months after the smoking ban went into effect. It is important to note that both smokers and nonsmokers benefit from smoke-free workplace legislation; both experienced reduction in respiratory and sensory irritation symptoms. Other studies show that hospitality workers can experience a substantive decrement in pulmonary function after a single work shift in a smoky environment, suggesting that SHS has acute negative effects on airway tone and pulmonary function [4, 5]. In other studies, this cross-shift reduction of pulmonary function improved after a workplace smoking ban reduced SHS exposure. Studies demonstrating that smoke-free workplace legislation leads to rapid improvement in pulmonary function add to the general epidemiologic literature on the effects of SHS on lung function. These observations help clarify the previously published mixed results that are based mostly on cross-sectional or small studies that have lacked the prospective design, control for confounding or statistical power to definitively link SHS exposure to impaired pulmonary function. Taken together with a recent large prospective study, these hospitality worker studies strongly suggest a negative effect of SHS exposure on pulmonary function. Adults with asthma, because they have chronic airway inflammation, may be particularly susceptible to the respiratory health effects of SHS exposure. The Scottish smoking ban study showed that bar workers with asthma had a markedly greater improvement in pulmonary function than those without asthma after the smoking ban [4]. Bar workers with asthma enjoyed an average 10.1% predicted improvement in FEV1, compared with a 3.4% predicted increase among those without asthma. This was accompanied by a reduction in exhaled nitric oxide, a biomarker of airway inflammation and improved health-related quality of life. Consequently, hospitality workers with asthma have a substantially greater improvement in respiratory health after their workplaces become smoke-free.

9.3.3 SHS exposure and induction of obstructive lung disease In a population-based study of US adults, we examined the impact of cumulative lifetime SHS exposure and the risk of having chronic obstructive pulmonary disease (COPD). Higher lifetime SHS exposure, both at home and work, was associated with a greater risk of COPD, even after taking personal smoking history into account. On a population level, approximately 1 in 11 cases of COPD may be attributed, at least in part, to home SHS exposure; 1 in 15 cases may be attributable to workplace SHS exposure [6]. Other epidemiologic literature, albeit limited, also supports an association between SHS exposure and chronic bronchitis or obstructive pulmonary disease (which includes asthma) [7]. A study from Denmark found that hotel-restaurant workers were at elevated risk of COPD, although there was no direct control for personal smoking as a confounding factor [8]. In sum, hospitality workers, who are exposed to a high level of SHS at work and have a high lifetime smoking prevalence, are likely to be at increased risk of COPD.

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9.3.4 SHS exposure and the clinical course of established obstructive lung disease Because adults with asthma have chronic airway inflammation, they may be particularly susceptible to the effects of SHS exposure. Surprisingly, adults with asthma do not appear to selectively avoid SHS exposure. Studies show that SHS exposure is associated with increased asthma symptoms, rescue bronchodilator use, asthma severity and emergency department use and hospitalization for asthma exacerbation [9]. In addition, SHS exposure has been associated with decreased physical health status and health-related quality of life. In its recent review of the health effects of SHS exposure, the California Environmental Protection Agency concluded that SHS exposure is causally related to increased asthma severity among adults with asthma [9]. There is much less information about the effects of SHS exposure on persons with established COPD who no longer smoke. In a prospective population-based cohort study of adults with COPD, we previously studied the impact of directly measured SHS exposure on health outcomes [10]. The highest tertile of urine cotinine was longitudinally associated with greater dyspnea, worse COPD severity and poorer health status among adults with COPD. Although more work is needed, it appears that SHS exposure may indeed negatively affect the health of patients with COPD.

9.3.5 SHS and nonrespiratory health conditions among hospitality workers There are a number of serious diseases that are likely to be induced by SHS exposure. Although workplace SHS exposure has not been evaluated per se, there is no scientific reason to believe that the health effects would be any less than SHS exposure in other environments. In fact, workplace SHS exposure may be an even greater risk because of the high levels of exposure over a long time period experienced by hospitality workers. Concurrent exposure in some workplaces to vapors, dusts, gases or fumes could potentiate the harmful effects of SHS exposure. For example, carbon monoxide exposure from combustion associated with cooking could interact with SHS exposure to produce cardiovascular effects. Exposures to occupational dusts could interact synergistically with SHS to cause obstructive lung disease. In all likelihood, exposure to SHS in the hospitality workplace confers a particularly high risk for chronic disease (Table 9.2). The US Surgeon General, in a recent report on The Health Consequences of Involuntary Exposure to Tobacco Smoke, concluded that SHS is a cause of lung cancer and confers a 20–30% increased risk [11]. Perhaps this is not surprising, given that SHS contains more than 50 carcinogens. Hospitality workers, because they are exposed to high levels of SHS over a long time period, are probably at a particularly high risk of lung cancer, which has been supported by epidemiologic information. SHS exposure may also be a cause of breast cancer among younger, primarily premenopausal women, and sinus cancer, although recent authoritative reviews have disagreed about whether the evidence is sufficient to infer causality [9, 11] Evidence is also accumulating that SHS exposure is a cause of coronary heart disease. Even brief exposure to SHS may increase platelet activation/aggregation, endothelial dysfunction, oxidative stress and unfavorable lipid profile, which can predispose to coronary heart

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disease events. Investigators evaluated the impact of a smoke-free workplace law passed in Helena, Montana, which is a geographically isolated community with only one hospital for a large catchment area [12]. Presumably all patients hospitalized for acute myocardial infarction would be brought to this hospital. During the 6 month period when the law was enforced, the monthly incidence of hospitalization for acute myocardial infarction dropped by 40%. After suspension of the law, the incidence of myocardial infarction increased towards the baseline level. Although this is an ecological study design, it provides the strongest available evidence that smoke-free workplace legislation can reduce coronary heart disease events. Because hospitality workers are exposed to high levels of SHS, they could be especially vulnerable to the cardiovascular health effects of SHS exposure. Consequently, they may have an especially large benefit of smoke-free workplace laws. After reviewing all the available evidence, the US Surgeon General concluded that SHS exposure is a cause of premature mortality and shortens the lifespan. Smoke-free workplace legislation would be expected to prevent the adverse health effects of SHS exposure and to increase longevity.

9.3.6 Prevention: effectiveness of smoke-free workplaces in preventing SHS exposure Extensive evidence now indicates that banning smoking in the indoor work environment eliminates SHS exposure. Creating nonsmoking areas, installing ventilation systems or using air cleaners does not protect workers from SHS exposure [11]. A smoke-free workplace policy is the only effective method for eliminating SHS exposure. Because there is no known safe threshold for SHS exposure, complete elimination of workplace exposure must be achieved to prevent serious health consequences. Creation of smoke-free workplaces has another important public health benefit: a higher rate of smoking cessation among active smokers. Those who continue to smoke reduce their daily cigarette consumption. Shortly after the Irish smoke-free workplace legislation went into effect, a substantial proportion of smokers quit (15%) and many attributed their smoking cessation to the law. Smoke-free workplace laws, by reducing passive and active smoking, will lead to substantive health benefits for the population. Mandating smoke-free workplaces will decrease secondhand smoke exposure and will improve respiratory health, prevent chronic disease and extend life span. Important salutary health effects occur in as little as 1 month after cessation of SHS exposure. The comprehensive body of research documenting the serious adverse health effects of passive smoking provides a powerful rationale for prohibiting smoking in all workplaces.

9.3.7 Prevention: acceptance of smoke-free workplaces Smoke-free workplace laws are effective in reducing exposure only if compliance with the law is achieved. Potentially, achieving compliance could be particularly difficult in the hospitality industry. In fact, smoke-free workplace laws are effective in achieving compliance. Four years after the California ban on smoking in bars, compliance with the law was high: 99% of bars in restaurants and 76% of freestanding bars were

9.5 CONCLUSIONS

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smoke-free [13]. Near-perfect compliance has been reported in Boston, Ireland and New Zealand. A concern is often expressed that the general public will not accept smoke-free bars and restaurants. A series of international studies shows that most people do support smoke-free bars and restaurants. Moreover, opinions become increasingly positive following smoke-free legislation. Many bar and restaurant workers enjoy the benefits of working in a smoke-free environment. Adverse economic consequences are often cited: will smoke-free laws cause the hospitality industry to lose money? Fortunately, the answer is no. Using sales tax and other objective financial data, studies now conclusively demonstrate that bars, restaurants and hotels do not lose revenue after becoming smoke-free. In fact, some of these studies actually show a growth in income. In sum, smoke-free legislation is effective, accepted by the public and has no negative economic impact. It would appear to be a win–win situation for both health and business.

9.4 Diagnosis and management issues The practicing clinician may be faced with symptoms referable to the eyes (conjunctival injection, conjunctival pruritis or eye tearing), upper respiratory tract (rhinorrhea, nasal burning, nasal stuffiness or sore throat) or lower respiratory tract (cough, sputum production, dyspnea or wheezing). If the occupational history reveals a job in the hospitality sector, then SHS exposure must be suspected as a cause of these symptoms. A detailed history should be taken to assess for SHS exposure and its avoidance should be counseled. Even among active smokers, SHS exposure may have additional deleterious effects on the respiratory tract. In addition, any patient with obstructive lung disease, including asthma or COPD, should be assessed for SHS exposure. Because SHS exacerbates asthma, and may make COPD worse, counseling patients to avoid SHS exposure is an important part of clinical management. In particular, excessive use of short-acting bronchodilators may be a clue to ongoing SHS exposure. Although the most effective strategy for reducing SHS exposure is creating a smoke-free work environment, a change in job or job duties may be the only practical approach for an individual patient who works in the hospitality industry in the short term. Besides health conditions related to SHS exposure, hospitality workers may also be prone to health effects from other exposures. These may include alcohol dependence from alcohol consumption, hearing loss from excessive noise exposure, sleep disturbance from night-time shift work and violence. A careful occupational history should also elicit these and other potential exposures. A program of prevention can then be orchestrated with the patient and his or her employer.

9.5 Conclusions Hospitality workers are often exposed to very high levels of SHS over a long time period. Consequently, they are at risk of serious health consequences, ranging from chronic respiratory symptoms to lung cancer. Studies of smoke-free workplace legislation

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clearly document the rapid benefit of improved respiratory health. Long-term benefits are likely to include a lower risk of coronary heart disease, other cancers and obstructive lung disease burden. Smoke-free workplaces are effective, accepted and good for business. To improve the health of hospitality workers, and all exposed workers, a total global ban on smoking in workplaces and all public places is mandatory. Clinicians may be faced with respiratory and nonrespiratory health conditions that are caused or exacerbated by SHS exposure in the workplace. Consideration of SHS exposure in the differential diagnosis of upper and lower respiratory tract conditions is particularly important. Measures to reduce exposure, such as a change in job or job duties, may be an important step in the management of these patients. The ultimate solution, of course, is to create smoke-free workplaces to protect all workers from the health effects of SHS exposure.

References 1. Siegel, M. (1993) Involuntary smoking in the restaurant workplace. A review of employee exposure and health effects. JAMA 270(4): 490–493. 2. Eisner, M.D., Smith, A.K., Blanc, P.D. (1998) Bartenders’ respiratory health after establishment of smoke-free bars and taverns. JAMA 280(22): 1909–1914. 3. Goodman, P., Agnew, M., McCaffrey, M., Paul, G., Clancy, L. (2007) Effects of the Irish smoking ban on respiratory health of bar workers and air quality in Dublin pubs. Am. J. Respir. Crit. Care Med. 175(8): 840–845. 4. Menzies, D., Nair, A., Williamson, P.A. et al. (2006) Respiratory symptoms, pulmonary function, and markers of inflammation among bar workers before and after a legislative ban on smoking in public places. JAMA 296(14): 1742–1748. 5. Dimich-Ward, H., Lawason, J., Chan-Yeung, M. (1998) Work shift changes in lung function in bar workers exposed to environmental tobacco smoke. Am. J. Respir. Crit. Care Med. 157: A505. 6. Eisner, M.D., Balmes, J., Katz, P.P., Trupin, L., Yelin, E.H., Blanc, P.D. (2005) Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease. Environ. Health 4(1): 7. 7. Yin, P., Jiang, C.Q., Cheng, K.K. et al. (2007) Passive smoking exposure and risk of COPD among adults in China: the Guangzhou Biobank Cohort Study. Lancet 370(9589): 751–757. 8. Tuchsen, F., Hannerz, H. (2000) Social and occupational differences in chronic obstructive lung disease in Denmark 1981–1993. Am. J. Ind. Med. 37(3): 300–306. 9. Office of Environmental Health Hazard Assessment California Environmental Protection Agency (2005) Health Effects Assessment for Environmental Tobacco Smoke. Available from: ftp://ftp.arb. ca.gov/carbis/regact/ets2006/app3part%20b.pdf (accessed 27 March 2009). 10. Eisner, M.D., Balmes, J., Yelin, E.H. et al. (2006) Directly measured secondhand smoke exposure and COPD health outcomes. BMC Pulmon. Med. 6: 12. 11. US Department of Health and Human Services (2006) The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General. US Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health: Atlanta, GA. 12. Sargent, R.P., Shepard, R.M., Glantz, S.A. (2004) Reduced incidence of admissions for myocardial infarction associated with public smoking ban: before and after study. BMJ 328(7446): 977–980. 13. Weber, M.D., Bagwell, D.A., Fielding, J.E., Glantz, S.A. (2003) Long term compliance with California’s Smoke-Free Workplace Law among bars and restaurants in Los Angeles County. Tobacco Control 12(3): 269–273.

10 Health effects of environmental exposures while in automobiles Madeline A. Dillon and David B. Peden University of North Carolina, Chapel Hill, North Carolina, USA

10.1

Environmental exposures in automobiles

Cars and trucks are leading producers of air pollution worldwide. The number of cars in the world is estimated at 625 million and has been steadily increasing. The US Federal Highway Administration statistics estimate that 3.7 million cars have been added to roads each year since 1960, which is a 212% increase, putting the US total over 250 million. The time that people spend in cars is also increasing, with recent studies showing that most Americans spend an average of 90 minutes a day in cars. There are many occupations that require many hours in a vehicle, including truck drivers, bus drivers and police officers. Most people are unaware of the potential exposure to environmental pollution while they are driving and may even feel protected from the outside environment while inside a car. In the last 20 years, researchers have begun looking at the indoor environment of cars as a significant source of pollution exposure. Many studies have shown that driving in cars provides the highest level of exposure to particulate matter, volatile organic compounds, nitrogen compounds and carbon monoxide for most people. Several studies have shown that walking or biking in heavy traffic provides less exposure than driving a car in the same conditions. This exposure can adversely impact health and especially cause problems with the respiratory tract. Other exposures unique to the indoor environment of cars include smoking while driving, chemical out-gassing of volatile organic compounds from new cars and air bag deployment, which can all affect respiratory health.

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10.2 Air pollution exposure while driving in cars The pollution inside cars is a mix of gasoline and diesel exhaust and contains multiple noxious chemical substances in gaseous, aerosol and particulate form. Exposure is highest in heavy traffic, when driving behind vehicles that generate more exhaust, and in highly congested urban areas. Unfortunately, a car’s exterior and ventilation system do not protect passengers from exposure. Particulate matter (PM) is probably the most dangerous component of car exhaust that drivers and passengers are exposed to. PM is made up of liquids and solids suspended in the air and can range in size from 10 mm, identified as ‘coarse’ or PM10, to less than 2.5 mm, identified as ‘fine’ or PM2.5. PM is often the product of incomplete combustion and includes smoke, dust and soot. PM is breathed into the nasal, sinus and bronchial passages and can accumulate and calcify. Very fine PM can penetrate to the alveoli and can even be absorbed into the bloodstream. PM acts locally in the nose, throat and lungs as an irritant causing nasal congestion, sinusitis, throat irritation, coughing, wheezing, shortness of breath and chest discomfort. Several studies have shown that increased exposure to PM10 causes exacerbation of existing respiratory conditions, including asthma. A study done at Kaiser Permanente in Southern California showed that for every 10 mg/m3 increase in PM exposure, hospital admissions rose by 7% for patients with respiratory disease, 3.5% for patients with acute respiratory illnesses and 3% for patients with cardiovascular disease. A study by the California Environmental Protection Agency demonstrated an association of a 2.5% increase in emergency room visits and a 1% increase in mortality for people with pneumonia with every 10 mg/m3 increase in PM exposure level. The ‘Six Cities Study’ by the Harvard School of Public Health found that test subjects exposed to higher PM concentrations were 26% more likely to die prematurely than subjects exposed to lower concentrations. Air conditioning systems can remove between 40 and 75% of the largest PM, but remove only 2–15% of the dangerous particles less than 1 mm in diameter. Commercial air filters can decrease coarse PM by 90%, but only reduce the fine particles by 5%. A study from the University of Southern California and the California Air Resources Board collected data in Los Angeles in 2003 and determined that drivers were receiving 35–45% of diesel and ultrafine particle exposure during their commute (average 1.5 hours). Diesel trucks and hard accelerations were the main sources of this pollution. Volatile organic compounds (VOCs) are another significant component of air pollution emitted by cars. VOCs are produced by the combustion or evaporation of solvents, paints, glues and fossil fuels. VOCs are components of chemical reactions that create ozone/smog. The EPA has designated many VOCs hazardous air pollutants. Gasoline and diesel exhaust contains significant concentrations of dozens of VOCs. The most significant are benzene, 1,3-butadiene, xylenes, ethylbenzene, toluene and formaldehyde. Benzene and 1,3 butadiene are known carcinogens and formaldehyde is a suspected carcinogen. Inhaled benzene has been linked to leukemia and blood disorders in many studies, children being more susceptible. The World Health Organization has designated the acceptable level of benzene to be zero. There are no current links to the development of cancer secondary to exposure to benzene in vehicles, but it is felt that it contributes to the overall carcinogenic exposure. Short-term exposure to benzene may result in drowsiness, dizziness or headaches. Toluene acts on the central nervous system

10.2

AIR POLLUTION EXPOSURE WHILE DRIVING IN CARS

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and can cause short-term fatigue, sleepiness, headaches and nausea. Long-term exposure to inhaled benzene can decrease white blood cell numbers and immunoglobulin levels, causing susceptibility to infections, including influenza and the common cold. A 1991 study from the Harvard School of Public Health compared in-car VOC exposure, exposure on the roadside and exposure at a station away from the roadside. It found that exposures to the most significant VOCs (listed above) were the same in cars and in the air next to the car, but significantly higher than away from the roadside. Having the windows rolled up did not make any difference, although having the air conditioning on had a small impact on decreasing exposure. Another Harvard study found that exposure in cars was higher when compared with the exposure on the subway, while bicycling or walking. It also found that subjects’ commutes (average time 76 minutes) accounted for 21% of their benzene exposure. Carbon monoxide (CO) is a gas generated from incomplete combustion of hydrocarbons, such as gasoline and diesel fuel. Cars produce 60% of the CO in the USA. In high-density urban areas cars and trucks are the source of 95% of CO production. CO production is increased when engines are cold vs warm or if they are not properly maintained. CO rapidly dissipates in the air and is only detected in enclosed spaces or areas of very high traffic volume. CO is a poisonous gas that is odorless, colorless and tasteless. CO strongly binds to hemoglobin, thus reducing oxygen binding to hemoglobin and oxygen delivery to tissues. Symptoms of headaches, dizziness, disorientation, nausea and fatigue are common at low levels and are often mistaken for the flu. High-level exposure can result in death. Patients with underlying respiratory disease are at risk from CO exposure if they have an increased oxygen demand. This concept holds true for people with cardiac disease, children and the elderly. Many studies have shown that elevated CO levels are noted in cars while driving as compared with the ambient environment, even in heavy traffic areas. The California Air Resources Board conducted an extensive study of in-car CO exposure comparing different driving conditions, i.e. rush hour vs non-rush hour, freeway vs arterial and rural roads, in Los Angeles and Sacramento. The highest exposures were during rush hour on freeways in Los Angeles while the test vehicle was driving behind an out-of-tune truck or an older model sedan. Similar studies have been replicated internationally, specifically in Paris, the UK and Mexico City, which boasts the highest commuter CO exposure. Higher levels in general were found during evening commutes. In a Washington, DC study, this was felt to be secondary to many commuters receiving increased exposure when starting their cars in enclosed parking lots. Nitrogen oxides are also produced during combustion of fuel and contribute to ground-level ozone, acid rain and particulate matter. Nitrogen dioxide is the best studied nitrogen oxide species. Direct exposure to nitrogen oxide causes mucosal irritation of the eyes, nose, throat and lungs and can exacerbate respiratory conditions such as asthma and chronic obstructive pulmonary disease (COPD) secondary to penetration of fine particulate matter. Exposure to nitrous oxide compounds is also associated with decreased ability of the lungs to combat bacteria and viruses, leading to lung infections. Many studies show that nitrogen dioxide exposure is higher inside cars as compared with ambient or roadside monitoring. Ozone is not emitted by cars, but is a product of nitrogen oxide and VOCs reacting with sunlight. Relatively few studies have been done with regards to in-car exposure to ozone, but most show that ozone levels are lower in cars vs the ambient environment.

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10.3

Smoking exposure

There is no question that cigarette smoke exposure is harmful to smokers and those around them. This is backed up by the most recent US Surgeon General’s Report from 2006. Components of tobacco smoke can be readily measured in the air where someone is smoking, including small particles that can penetrate into the lung, carbon monoxide, nicotine and benzene. The concentrations of the smoke components depend upon the number of smokers and how much they are smoking, the size of the space where the smoking is taking place, the rate of exchange of air in the smokers’ environment with outdoor air, and the presence and efficiency of air cleaning devices. The exposure of nonsmokers depends on the proximity to smokers while smoking. Obviously, smoking in an enclosed space such as a car intensifies smoke exposure. For the smoker, the inherent risks of lung and cardiovascular disease are increased by the extra exposure to smoke confined in a vehicle. Mainstream smoke is the smoke that is inhaled through a burning cigarette/cigar by the smoker. Exhaled mainstream smoke is exhaled by the smoker and sidestream smoke is produced by the smoldering cigarette, both of which make up environmental tobacco exposure (ETS) or second-hand smoke (SHS). Recent studies have shown that SHS exposure while driving in cars is very high. Passengers in the back seat, who are often children, have higher exposure as the smoke tends to circulate and stay there. A study performed by the Harvard School of Public Health during 2005–2006 to evaluate SHS exposure and air quality in cars found unsafe levels of respired particulate matter and carbon monoxide for children. In 1992 the EPA classified SHS as a Class A carcinogen, characterized by strong epidemiologic evidence that it causes cancer. In children, SHS increases the risk of respiratory diseases including lower respiratory infections such as bronchitis and pneumonia, asthma and decreases overall lung function. There is also a link to the long-term risk of lung cancer that increases in a dose–response relationship. In a population-based, case–control study, household exposure to 25 or more smoker-years during childhood and adolescence doubled the risk of lung cancer, whereas exposure to fewer than 25 smoker-years did not increase the risk. An estimated 17% of lung cancer in nonsmokers is attributable to high levels of environmental smoke exposure during childhood and adolescence. There is a growing body of evidence that SHS exposure increases the risk of a child developing cardiovascular disease in adulthood, but requires further study. Adults exposed to SHS with underlying respiratory disease are more prone to exacerbations. There is evidence in adults as well, that the risk for lung cancer is increased with SHS exposure. The 2006 Surgeon General’s report included a meta-analysis including 52 studies, which showed that the relative risk of lung cancer among male and female nonsmokers who were ever exposed to SHS from a spouse was 1.21 (95% CI 1.13–1.30). The same report contained a meta-analysis of 25 studies of lung cancer and exposure to SHS in the workplace, which estimated a pooled relative risk of 1.22 (95% CI 1.13–1.33). The risk of cardiovascular disease is also increased by SHS exposure.

10.4

Other exposures in cars

Some patients may be sensitive to the phenomenon of ‘out-gassing’ from new cars, which is the release of VOCs from plastics, glues and solvents from the interior of cars.

10.5

DISEASES ASSOCIATED WITH EXPOSURES

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This is the ‘new car smell’. In several studies 40–60 VOCs were identified. The most significant were ethylbenzene, benzene, acetone, cyclohexanone, n-hexane, styrene, toluene, xylene and undecane. The total VOCs were twice as high as ambient VOCs levels. The level of VOCs decreases significantly with time and one study showed a 90% reduction in by 3 weeks, whereas another study showed a decrease of 60% by one month after manufacturing. If patients are sensitive to out-gassing, they will probably complain of headaches, fatigue, drowsiness and eye, nose and throat irritation. They should limit their exposure to new cars, but with time should be able to tolerate driving or riding in the car that caused problems. Airbag deployment and/or airbag rupture rarely cause serious lung injury, but there are case reports in the literature of reactive airway dysfunction syndrome (RADS) and asthmatic reactions related to sodium azide inhalation. Sodium azide reacts with potassium nitrite to produce a blast of nitrogen gas, which inflates the airbag. The gas then dissipates through tiny holes in the nylon fabric, deflating the bag. Sodium hydroxide and sodium carbonate are by-products of sodium azide combustion and released into the car. Sodium azide becomes hydroizoic acid, a volatile irritant, when mixed with water. RADS is characterized as chronic asthma-like symptoms developing within 24 h of exposure to an irritant. Patients often complain of cough, dyspnea and wheezing. A study by Gross et al. showed that asthma attacks could be precipitated by normal airbag deployment in some asthmatics. Car companies have obviously worked to make airbag deployment as safe as possible.

10.5

Diseases associated with exposures

As mentioned above, local irritation of the upper and lower airways can occur from PM and VOCs. Exacerbation of existing asthma, COPD and other respiratory diseases is effected by exposure to air pollution and smoking exposure in cars. The risk of lung cancer is increased in persons exposed to many years of SHS exposure, as is the risk of cardiovascular disease. In trying to infer health risks from environmental exposure in vehicles, many studies have been done evaluating professional drivers such as truck, bus and taxi drivers. Many of these studies show increased risk of diseases such as cancers and cardiovascular disease, but it is still difficult to make a causal link to in-vehicle pollution exposure based on these cohort studies, given the many other confounding factors of smoking, job stress and sedentary lifestyle. More studies need to be done to help us evaluate our risks. A large retrospective mortality study of American truck drivers from 1979 to 1990 found elevated proportional mortality rates for cardiovascular disease and lung cancer, especially among younger (less 55 years) long-haul truckers. Information about smoking habits was not available, but even after adjustment based on current rates of smoking, the authors propose that smoking habits are not fully responsible for the differences seen and exposure to diesel exhaust is likely to be a contributing factor. A study of over 2000 taxi drivers in Rome from 1950 to 1988 showed a lower overall mortality than expected, but an increase in diabetes and lung cancer. The risk of lung cancer was only seen in drivers enrolled in the later part of the study (from 1965 to 1975). It is unclear if occupational exposure accounted for this, but these drivers were probably exposed to heavier exposure. Myocardial infarction rates were increased in

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urban bus drivers in Sweden as compared with their rural counterparts, although no changes in cancer rates were seen. It is again difficult to attribute this strictly to environmental pollution exposure, but is reasonable to infer that the urban drivers have more exposure than the rural drivers. A study of urban bus drivers in New York City from the 1980s found that cardiovascular deaths and malignancy were elevated, especially cancer of the esophagus.

10.6 Diagnosis and management issues Diagnosing respiratory disease or cardiovascular disease related to in-vehicle exposure is difficult. Epidemiologic studies, as mentioned, show defined trends in increased disease, but there is actually little data that provides a causal link to in-vehicle exposure of pollution. We can infer that the known health hazards of the implicated chemicals and particulate matter also hold true during exposure in vehicles (Table 10.1). More evidence with regards to exposure to smoke while in a car shows it is directly correlated to increased disease. With any exposure, patients may be presenting with exacerbations of their underlying lung disease or new-onset disease. A medical history inquiring about how many hours they spend in a car may be important, including if they drive a vehicle for work. Discussing trends in their respiratory disease exacerbations with regards to time spent in a vehicle may also lead to clues. Having a patient find alternative transportation and seeing if this improves their symptoms may also help pinpoint vehicular exposure as a culprit. In general, physicians should counsel patients to reduce the amount of time spent driving in cars. Alternate forms of transportation including subways, trains, buses and even biking and walking diminish environmental exposure. Avoiding peak traffic times, especially evening rush hour, will also decrease exposure. Another key element to decreasing emission exposure is properly maintaining vehicles and driving more efficient cars that produce fewer emissions. Specific attention should be paid to the automobile air conditioning system, including routine maintenance and replacement of filters and hoses as needed. This is especially important as many automobiles now recommend use of the air conditioning year round as a means to control humidity. Additionally, exposure to particulates from the roadway and surrounding traffic may be decreased by keeping windows closed and using the air conditioning system. Exposure to exhaust can be minimized by attention to the muffler and exhaust system. Proper tuning of the vehicle will also increase combustion efficiency and decrease particulate, VOC and pas phase pollutant production. A patient who is a professional driver and is experiencing respiratory problems would need to be counseled about the risks their vocation may be causing to their health. The findings on SHS and disease have led to legislation for smoke-free indoor environments and education of parents concerning the effects of their smoking on their children’s health. Legislation is currently in place banning smoking in cars with children (usually under 16 or 18 years old) in Maine, Arkansas, Louisiana, California and Puerto Rico. Ten other states currently have bills under review. Nova Scotia became the first Canadian province to ban smoking with children in cars in April 2008 and has been followed by British Columbia and most recently Ontario.

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FURTHER READING

Table 10.1 Air pollution exposure Components of air pollution

Symptoms of exposure

Highest level of exposure

PM 2.5

Irritant effect upper and lower airways; wheezing, cough Exacerbation of asthma and lung disease Irritant effect upper and lower airways; wheezing, cough Exacerbation asthma and lung disease, increased respiratory disease Drowsiness, dizziness or headaches

Heavy traffic, urban areas

PM 10

VOCs CO

Nitrogen dioxide Ozone Cigarette smoke

Headaches, dizziness, disorientation, nausea and fatigue High exposure leads to death Irritation of the eyes, nose and throat Exacerbation of lung disease and increased risk of lung infections Cough; exacerbation of asthma and lung disease Irritation of upper and lower airways; cough Exacerbation of asthma and lung disease, increased ear infections in children Increased risk of lung cancer and cardiovascular disease

Heavy traffic, urban areas

In-car vs ambient environment ‘Out-gassing’ of cars Rush hour, evening hours

In-car vs ambient environment

Lower inside cars vs ambient environment For smoker SHS: in vehicle with person actively smoking; windows rolled up

More studies need to be performed in order to definitively link air pollution exposure in vehicles to increased disease, but the current data is certainly concerning. Legislation to decrease vehicle emissions and decrease the risk of SHS are also important avenues to decreasing exposure and safeguarding our health.

10.7

Helpful websites

.

http://www.epa.gov/air

.

www.surgeongeneral.gov/tobacco/

.

http://www.cdc.gov/niosh/

Further reading Alfredsson, L. et al. (1993) Incidence of Myocaridal infarction and mortality from specific causes among bus drivers in Sweden. Int. J. Epidemiol. 22(1): 57–61. Almeida, F. et al. (2006) Lung injury after airbag deployment: airbag lung. Injury Extra 37: 181–183.

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Borgia, P. et al. (1994) Mortality among taxi drivers in Rome: a cohort study. Am. J. Ind. Med. 25(4): 507–517. Chan, C.C. et al. (1991) Driver exposure to volatile organic compounds, CO, ozone, and NO2 under different driving conditions. Environ. Sci. Technol. 25: 964–972. Dockery, D. et al. (1993) An association between air pollution and mortality in six cities. New Engl. J. Med. 329: 1753. Hesterberg, T. et al. (2009) Non-cancer health effects of diesel exhaust: a critical assessment of recent human and animal toxicological literature. Crit. Rev. Toxicol. 39: 195–227. International Center for Technology Assessment (July (2000)) In-car air pollution, the hidden threat to automobile drivers. Available from: www.nanoaction.org. Janerich, D.T., Thompson, W.D., Varela, L.R. et al. (1990) Lung cancer and exposure to tobacco smoke in the household. New Engl. J. Med. 1990; 323: 632–636. Overton, S. et al. Identification of volatile organic compounds in a new automobile. Scientific Information services. Available from: www.sisweb.com. Rank, J. et al. (2001) Differences in cyclists and car drivers exposure to air pollution from traffic in the city of Copenhagen. Sci. Total Environ. 279: 131–136. Rees, V.W. et al. (2006) Measuring air quality to protect children from secondhand smoke in cars. Am. J. Prev. Med. 31(5): 363–368. Robinson, C.F. et al. (2005) Truck drivers and heart disease in the United States, 1979–1990. Am. J. Ind. Med. 47(2): 113–119. US Department of Health, Human Services (USDHHS) (2006) The Health Consequences of Involuntary Exposure to Tobacco Smoke: a Report of the Surgeon General. Centers for Disease Control and Prevention: Rockville, MD. Wilson, R. Sengler, J. et al. (1996) Particles in our Air: Concentraions and Health Effects. Harvard School of Public Health, Harvard University Press: Cambridge, MA, 1996.

11 Indoor sports Harman S. Paintal and Ware G. Kuschner Stanford University School of Medicine and United States Department of Veterans Affairs Palo Alto Health Care System, CA, USA

11.1 Introduction This chapter reviews hazardous respiratory exposures encountered during participation in, or proximity to, indoor sports and the diagnosis, management and prevention of the adverse health effects attributable to them. Respiratory risks vary across sports and across indoor venues (Table 11.1). Exposures and associated health risks are dependent upon multiple factors, including the activities and processes occurring within a venue, proximity to a toxicant point source and, in some circumstances, the ventilation characteristics of the venue. In contrast with exposed populations in most other hazardous environments, indoor sports participants are commonly engaged in vigorous athletic activity, significantly amplifying exposure dose and the associated risk of illness compared with sedentary individuals of comparable health status. Unsurprisingly, exposure assessment and diagnosis of illness attributable to activity in, or proximity to, an indoor sport can be challenging. Diagnostic and management strategies will necessarily differ across sports and across venues. Nevertheless, there are some general tenets and observations that apply to the indoor sports reviewed in this chapter and the respiratory health issues associated with them: .

Indoor sports participants, support staff and spectators experience ambient conditions and respiratory exposures they may not encounter elsewhere.

.

Physical activity increases aerobic activity and, by extension, minute ventilation, which amplifies airborne exposures and generally increases the risk of a toxicantrelated health effect.

.

The atmospheric microenvironment at the level of play in an indoor sports venue can be uniquely hazardous compared with other areas inside the venue, subjecting

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

138 Table 11.1

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Indoor sports, pulmonary exposures, and health effects

Sports

Pulmonary exposure

Health effects

Water sports Swimming Diving Water polo Synchronized swimming Hot tubs Jet pools Saunas

Disinfectants and by-products Organic and inorganic compounds Infectious agents Fluid shifts in body Blunt trauma

Ice sports Hockey Figure skating Speed skating Curling Equestrian

Carbon monoxide Nitrogen dioxide Cold air

Asthma Sensitizer-induced asthma (new onset) Acute irritant induced asthma (new onset) Exacerbation of pre-existing asthma Extrinsic allergic alveolitis Respiratory tract infections Pulmonary edema Pneumothorax Pulmonary contusion Central nervous system and cardiovascular system dysfunction Pneumonitis Asthma exacerbation

Gymnastics Weightlifting Rock climbing Athletics (track and field)

Sandy soils Clay Wood Crumb rubber Chip rubber Chalk dust Magnesium carbonate Calcium carbonate

Chronic bronchitis Asthma Cough Allergic rhinitis Cough Respiratory tract irritant effects

sport participants and ground-level support staff to heightened respiratory risk compared with that of individuals (e.g. spectators) who are not in close proximity to the area of play. .

Harmful exposures encountered during participation in indoor sports may go unrecognized because most health effects are nonspecific and because specific biomarkers of exposure and disease are generally not available in clinical practice (with the important exception of carbon monoxide intoxication).

.

Athletic impairment resulting from a harmful respiratory exposure encountered during participation in an indoor sport may not be easily appreciated because participants are generally otherwise healthy and have significant cardiopulmonary functional reserve. Accordingly, while low to moderate intensity exposures may adversely affect peak athletic performance, health effects may otherwise be ‘subclinical’, thereby eluding detection and prevention.

.

The use of masks or respirators is not a practical option under most circumstances for indoor sports participants, in contrast with occupational settings where the use of personal respiratory protection may be a prudent strategy to reduce exposure to airborne pollutants.

11.3

ICE ARENA AIR POLLUTION

139

.

Air contamination in indoor sports venues should be anticipated under standard operations. Appropriate engineering controls, ventilation and monitoring can reduce exposure and the associated risk of illness.

.

Very limited information is available about the long-term health effects of chronic, low-intensity exposures resulting from participation in indoor sports.

11.2

Ice sports and arenas

Over the past several decades, a spectrum of adverse health effects have been attributed to poor indoor air quality encountered in indoor ice arenas. Numerous contaminants and toxicants have been detected, the most important of which, carbon monoxide (CO) and nitrogen dioxide (NO2), are produced during ice resurfacing. Other compounds produced during ice resurfacing, including other oxides of nitrogen, aldehydes, volatile organic compounds and respirable-range particulate matter, may also contribute to disease. The total burden of illness and impairment (transient or chronic) attributable to poor indoor air quality in arenas is unknown, but may be quite significant. One analysis carried out in the late 1990s of 332 rinks in nine countries reported excess concentrations of NO2 in 40% of the rinks. Ice arenas are found throughout many communities worldwide, especially across Europe and North America. Multiple sports utilize indoor ice arenas, including ice hockey, figure skating, recreational ice skating, short track speed skating and curling. Ice hockey is among the world’s most popular sports with tens of millions of participants in youth and adult leagues worldwide. Since air quality monitoring in ice arenas varies across venues, if present at all, details about the scope of the problem and the public health impact of poor indoor air quality in indoor ice arenas cannot be precisely established. Moreover, since exposures to indoor ice arena air pollutants such as CO and NO2 typically produce nonspecific signs and symptoms and, because many of their health effects are typically short-lived and self-limited after the exposure abates, it is likely that a significant burden of disease attributable to poor ice arena air quality is not recognized.

11.3

Ice arena air pollution: exposures and practical hints when taking a history

Poor indoor air quality in ice arenas may result from a variety of environmental and engineering factors including ventilation system deficiencies, tobacco smoke, faulty heating systems, cleaning chemicals, refrigerants and mold contamination. A discussion of all possible point sources for poor indoor air quality is beyond the purview of this chapter. The principle focus of this section is ice resurfacing equipment exhaust, a major point source for pollutants in most arenas, and the health effects attributable to this exposure. Most ice resurfacers, including ‘Zamboni machines’, utilize combustion engines that operate with a fossil fuel (e.g. gasoline and propane) and produce exhaust with a mixture of hazardous compounds, including CO and oxides of nitrogen, especially

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NO2, as well as volatile organic compounds and respirable-range particulate matter. While there is nothing remarkable about the exhaust produced from ice resurfacing equipment, the machines present a special hazard in indoor ice arenas because they operate repeatedly, starting and stopping, in what is essentially a confined space. Just as running a motor vehicle inside of a closed garage can produce a hazardous exposure setting, the operation of ice resurfacing equipment inside a poorly ventilated arena can result in significant indoor air pollution. The concentration of compounds present in the exhaust of ice resurfacing equipment is partially a function of the temperature of the engine. CO production is greatest when an engine has been newly started and is running at a relatively low temperature. As the machine warms, CO production decreases while the production of oxides of nitrogen, including NO2, increases. Accordingly, concentrations of exhaust pollutants from ice resurfacing equipment inside an arena will, in part, depend upon on the frequency of equipment start–stop cycles and the duration that the engine runs during each cycle, as well as venue characteristics such as size and air exchange rate. The clinical syndromes attributable to ice arena air pollution are generally abrupt in onset and unfold over a relatively short time frame: minutes to hours. Health effects resulting from long-term exposure to low-level concentrations of airborne pollutants encountered in indoor ice arenas are not well established. While the relationships between chronic exposure to exhaust pollutants and cardiopulmonary and neurocognitive outcomes are of epidemiologic interest, it unlikely that a causal link between low-level indoor ice arena air pollution and a chronic health effect can be established with confidence at the level of the single individual. Operators of ice resurfacing equipment are at obvious risk of exposure to equipment exhaust as a consequence of their proximity to the point source and their repeated exposure to exhaust throughout their work shift. Athletes and sports participants are also at special risk because of the duration of exposure (i.e. time spent on the ice) and especially because of their increased ventilation and metabolic demands resulting from vigorous aerobic exercise. Confirmation of exposure to CO can be established through testing of peripheral blood specimens for carboxyhemoglobin in a clinical laboratory. In contrast, detection of exposure to most other toxic gases, including NO2, requires air sampling in the field by an industrial hygienist.

11.4 Indoor ice arena toxicant syndromes Diagnosis of an adverse health effect attributable to airborne pollutants in an indoor ice arena begins with the history. First, the clinician must suspect that an illness or symptom may be attributable to a toxic environmental exposure. Second, the clinician must act on the suspicion and gain data that supports or refutes the hypothesis. As is the case with other exposure settings and environmental illnesses, the patient may be the first person to consider a possible relationship between either a specific toxicant or exposure setting and the illness. In such instances, the process of establishing a diagnosis will be facilitated by the patient’s presenting complaint (e.g. ‘I am always the first person on the ice after the Zamboni machine finishes resurfacing because I like to take advantage of the excellent skating conditions, but I have noticed, lately, I develop

11.4

INDOOR ICE ARENA TOXICANT SYNDROMES

141

headaches and dizziness when I start skating which tend to get better on their own.’). Patient recognition of causation commonly occurs when there is an extreme exposure with a manifestly clear cause and effect relationship (e.g. a major mishap, accident or evident equipment malfunction), or a cluster of cases (e.g. multiple affected teammates) that point to etiology. In cases where causation is not obvious, the clinician will need to make the link between the exposure setting and possible etiologic toxicants and the disorder. Workers, athletes and spectators may be exposed to ice arena toxicants. Accordingly, the occupational history may elucidate causation for some affected individuals (i.e. employees who work in ice arenas, such as drivers of ice resurfacing machines) and, in turn, facilitate diagnosis of the illness. However, in others, an environmental history that considers hobbies, pastimes and athletic activities (i.e. participation in an ice sport) will be necessary to identify the exposure–disorder relationship. The major disorders attributable to ice arena air pollution are CO intoxication and NO2 pneumonitis. Strictly defined, carbon monoxide intoxication is not a disorder of the lungs. While the respiratory tract is the portal of entry for carbon monoxide, adverse health effects caused by carbon monoxide largely cause dysfunction of other organ systems. In contrast, the respiratory tract is both the route of exposure and the target organ in NO2 related illness.

11.4.1 Carbon monoxide Carbon monoxide is the gas most often reported as a cause of intoxication in indoor ice arenas. CO is a nonirritating, tasteless, odorless and colorless gas formed by hydrocarbon combustion and an important component of the exhaust of ice resurfacing equipment. CO diffuses readily across the alveolar–capillary interface and binds with avidity to hemoglobin, forming carboxyhemoglobin (COHb), which results in compromised oxygen transport and utilization. In addition to competing with oxygen for the heme moiety of hemoglobin, CO also compromises the ability of the other heme moieties with bound oxygen to offload oxygen to peripheral tissues. CO also interferes with peripheral oxygen utilization. These CO effects are independent of those on hemoglobin and oxygen delivery. The uptake of CO increases with exercise. Studies of CO concentrations in hockey players have found a linear relationship between COHb levels and exposure time and concentrations of ambient CO. Investigators found a 1.0% rise in COHb for each 10 parts per million (ppm) of ambient CO in an indoor arena during a 90 minute hockey game. Other investigators found a CO concentration of approximately 22 ppm raised COHb levels in hockey players to greater than 3% from a baseline of 1%, on average. Concentrations of CO exceeding 20 ppm in indoor ice arenas have been described in numerous reports. The United States Environmental Protection Agency National Ambient Air Quality Standard for CO is 9 ppm time weighted average over 8 h. The clinical findings of CO poisoning are nonspecific and vary based on severity of intoxication. COHb levels less than 2.5% are typically inconsequential. COHb concentrations between 2.5 and 10% may affect vision, manual dexterity and exercise tolerance. Concentrations greater than 20% can cause headaches, dizziness, malaise and nausea. Severe CO intoxication may result in seizures, coma and myocardial ischemia,

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and dysrhythmias. Severe intoxication in an indoor ice arena would only result from an unusual mishap such as the running (e.g. idling) of an ice resurfacing engine inside of a small confined space within the larger enclosed ice arena. Acute CO poisoning is first suspected on the basis of a suggestive history. Confirmation of intoxication requires a COHb level measured by co-oximetry of a blood gas sample. Moderate- to high-intensity exposures, especially in patients with underlying coronary artery disease, warrant further evaluation to assess for myocardial ischemia, including an electrocardiogram and measurement of cardiac enzymes. The most important interventions in the management of CO intoxication are removal of the affected individual from the CO source and institution of high-flow oxygen by face mask. The role of hyperbaric oxygen therapy remains controversial and is unlikely to be required to manage the low-level intoxication typically encountered in indoor ice arenas. Indeed, because symptoms of exposure (e.g. headaches and diminished exercise capacity) may be interpreted as a nuisance by the affected individual rather than a major health problem, an important consideration is the possibility of repeated low-level intoxication that goes undetected. Moreover, an affected individual (e.g. enthusiastic athlete) may not be receptive to counseling to avoid the potentially toxic environment. Suspicion of ice arena intoxication should prompt assessments of engineering controls at the venue.

11.4.2 Nitrogen dioxide Nitrogen dioxide is another gas that may be encountered in hazardous concentrations in indoor ice arenas, although disorders attributable to NO2 exposure have not been reported as commonly as CO intoxication. NO2 is a reddish-brown gas with a characteristic sharp, biting odor. The principle point source for NO2 is the internal combustion engine of an ice resurfacing machine. NO2 is heavier than most of the constituent gases in air and tends to remain close to the surface of the ice. NO2 causes respiratory tract injury that may range from mild irritation with minimal short-term clinical consequences to acute lung injury with significant symptoms and respiratory impairment. Chest tightness, wheezing, asthma flares and cough may be caused by NO2 inhalation. NO2 is relatively water-insoluble and therefore does not typically produce classic symptoms of irritation upon initial exposure. The lack of ‘warning symptoms’ can result in significant exposure over hours before any symptoms of injury develop. NO2 is a powerful oxidant and also slowly combines with water in the respiratory tract to produce nitric and nitrous acid which may contribute to lung injury. In one of the best described exposure incidents, an outbreak of NO2-induced respiratory illness occurred among players and spectators at two high school hockey games played at an indoor ice arena in Minnesota, USA. The source of the NO2 was the malfunctioning engine of the ice resurfacer. Affected individuals experienced acute onset of cough, hemoptysis and/or dyspnea during attendance or within 48 hours of attending a hockey game. In all, 116 cases were identified among hockey players, cheerleaders and band members who attended the two games. Members of two hockey teams had spirometry performed at 10 days and 2 months after exposure; no significant compromise in lung function was documented.

11.5

STANDARDS, GUIDELINES AND PUBLIC HEALTH CONSIDERATIONS

143

Swedish investigators reported two cases of toxic pneumonitis with delayed onset in hockey players due to NO2 exposure during an ice hockey game in an indoor arena. Signs and symptoms included cough, hemoptysis, dyspnea and reduced peak expiratory flow. The chest radiographs showed reticulo-nodular opacities in one player and patchy consolidation in the second player. Repeat chest radiographs obtained within one week of exposure were normal in both cases. It is unknown to what extent athletic performance may be adversely affected by ‘subclinical’ exposures to NO2 in indoor ice arenas. There is no specific therapy for NO2 pneumonitis. Bronchodilators are appropriate to treat airflow obstruction and inhaled corticosteroids may reduce airway inflammation. The role of systemic corticosteroids is not established, but should be considered with high-intensity exposures. Mixed exhaust exposures have also been linked with respiratory illness. Chronic cough and dyspnea were reported in ice hockey players after an acute exposure to a faulty ice resurfacer. In one report of 16 previously healthy hockey players, more than half complained of cough and dyspnea on exertion 6 months post-exposure. All had normal pulmonary function tests, exercise studies and chest computed tomographs. Additional testing using impulse oscillometry showed evidence of increased airway resistance and small airway disease. For concerns about ice arena toxicant exposure, emergent consultation with a medical toxicologist can be helpful. The United States Poison Control Network is available at ( þ 1) 800-222-1222, 24 hours a day, 7 days a week. This is the telephone number for every poison center in the United States. Calls to this number are automatically connected to one of 65 poison centers across the country. The World Health Organization’s list of international poison centers is available at www.who.int/ ipcs/poisons/centre/directory/en.

11.5

Standards, guidelines and public health considerations

Standards addressing air quality in indoor ice arenas have been developed and published. A Canadian agency has recommended average concentrations for CO and NO2 to be lower than those in work environments. The United States National Ambient Air Quality Standard for carbon monoxide is 9 ppm time-weighted average over 8 hours and 35 ppm over 1 hour, and for NO2 0.053 ppm (53 parts per billion, ppb) annual average. Additional Canadian guidelines for the operation of ice resurfacers with internal combustion engines include: (1) regular testing of ice resurfacer equipment emissions; (2) installation of monitors to measure the concentration of toxic gases at the opening of the exhaust pipe; (3) use of a catalytic purifier; (4) operation of resurfacers by an experienced operator to minimize time of equipment operation; (5) 90 minute intervals between resurfacing; (6) open rink doors during and after resurfacing; (6) air quality standards of 1 hour maximal allowable exposure to CO at 20 ppm and NO2 at 200 ppb; (7) regular monitoring of ambient air in indoor ice rinks; (7) installation of warning signs that describe the potential symptoms and hazards of CO and NO2 poisoning; (8) educational seminars for rink staff, coaches, parents and patrons of ice rinks; and (9) development of an emergency plan in the case of an intoxication incident.

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A potentially transformative engineering control has been the development of the electric ice resurfacing machine which does not emit exhaust fumes. As they are more costly than internal combustion models, replacement of internal combustion models with electric-powered ones may not be possible in many ice arenas, but if carried out would result in improved indoor air quality.

11.6 Cold air-exacerbated asthma and dyspnea Cold air can produce bronchoconstriction and provoke asthma exacerbations. Indeed, cold air challenges are used in some clinical pulmonary function laboratories to test for the presence of bronchial hyperresponsiveness, a hallmark of asthma. The combination of exposure to cold air and intense exercise contributes to dyspnea and provokes asthma in a significant minority of endurance athletes. The prevalence of asthma in elite athletes has been reported to be as high as 20%. Some individuals intolerant of intense exercise in cold air may avoid cold weather sports, resulting in a ‘healthy athlete effect’ and an underestimation of the total population affected by the co-exposures. Diagnosis of bronchoconstriction provoked by exercise in cold air may be facilitated by serial peak expiratory flow monitoring before, during and following exposure. The use of inhaled beta agonists before participation in cold weather sports is advisable for individuals with evidence of exercise-induced bronchoconstriction, and should be considered for athletes who experience dyspnea out of proportion to their exertion, or dyspnea that does not resolve with cessation of exercise. A trial of beta-2 agonist therapy may help to confirm the diagnosis of asthma, as well as offer relief to the sports participant. Importantly, not all dyspnea associated with exercise in cold air is due to bronchoconstriction. Reflex mechanisms in some individuals that reduce minute ventilation in response to cold air inhalation may contribute to dyspnea. Bronchodilators are not likely to be beneficial in these settings because bronchoconstriction is not a hallmark of the condition.

11.7 Water sports Swimming is a widely popular sport among people of all ages. In 2005 it was estimated that the number of Americans swimming for fitness was about 16 million. Learning how to swim is mandatory at the elementary school level in the UK and swimming is among the most popular forms of exercise among adults. Other competitive and recreational indoor water sports include water polo, springboard diving and synchronized swimming. Spas and fitness centers with hot water tubs, jet pools and saunas are additional indoor settings where the hazards of indoor water sports may be encountered. While the respiratory disorders associated with water sports are seen in both the indoor and outdoor setting, the indoor setting presents special risks. This is attributable to multiple factors including reduced ventilation, differences in pool maintenance requirements and micro-climates around indoor swimming arenas with higher temperature and humidity. The population at highest risk includes those who use such facilities with regularity, or workers such as lifeguards, trainers and cleaning and maintenance staff.

11.8

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EXPOSURES

Table 11.2 Primary disinfectants used in swimming pools Professional or large pools

Smaller pools, hot tubs, saunas

Domestic pools

Chlorinated compounds Chlorine gas Calcium and sodium hypochlorite Chlorinated isocyanurates Chlorine dioxide Bromochlorodimethylhydantoin Ozone gas Ultra-violet radiation

Bromine Liquid bromine Sodium bromide Sodium hypochlorite Lithium hypochlorite

Various combinations of bromide and hypochlorite Ultra-violet radiation Ozone gas Iodine

11.8

Exposures

The water in swimming pools, hot water tubs and spas has many organic and inorganic chemicals and contaminants. These may be present in water from the source, brought to the pool by swimmers and bathers, or introduced into the water intentionally by the staff for disinfection purposes (Table 11.2). The source water is usually drinking-quality water from the local municipality and contains organic materials like humic acid, disinfection by-products, lime and alkalis, phosphates and monochloramines. Swimmers and bathers introduce sweat, urine, lotions, cosmetics and soap residues into pool water which includes a variety of nitrogen-based compounds in the form of ammonia, urea, amino acids and creatinine (Table 11.3). The concentration of natural body products in the water, such as sweat or urine, is dependent on factors such as the amount of time and type of exertion while in water (for sweat and urine) and the demographic of bathers (with children passing more urine while in the water). Even though most of the nitrogen is excreted (or secreted) in Table 11.3 By-products of disinfection compounds commonly found in swimming pools Disinfectant

Disinfectant by-product

Chlorine

Trihalomethanes Haloacetic acids Haloacetonitriles Chlorate Chloramines Bromoform Chlorite Chlorate Bromate Aldehydes Ketones Bromoform Brominated acetic acids Bromal hydrate Bromate Bromamines

Bromine Chlorine dioxide Ozone

Bromochlorodimethylhydantoin

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the form of urea, swimming pools have a higher concentration of ammonia-based nitrates due to the reaction of various nitrogen compounds with chlorine-based products. A study using a model pool to simulate the fate of various natural compounds found that organic carbon, chloramines and trihalomethanes reached a steady state after 200–500 hours of operation and only nitrate-based compounds accumulated. The water in the pools requires continuous treatment, a process divided into filtration, coagulation, pH correction and disinfection. The choice of disinfectant is determined by factors like effectiveness, ease of handling and use, and ability to monitor levels of the chemicals employed. Chlorine-based products are the most widely used disinfectants since they have a residual effect after treatment. This is not the case with ozone or ultra-violet radiation, which kill microorganisms immediately, but need to be combined with chlorine- or bromine-based products for continual effect. Chlorinebased products include chlorine gas, sodium hypochlorite, calcium hypochlorite, lithium hypochlorite and chlorinated isocyanurates. Guidelines for acceptable ‘free’ (residual) chlorine levels vary by pool size and region, and it is generally recommended that levels for public pools be between 1 and 3 mg/l and those for public hot tubs may be slightly higher, but less than 5 mg/l. Concentrations higher than 5 mg/l may lead to higher incidence of mucous membrane irritation and should therefore be avoided. Higher chlorine levels (up to 20 mg/l) may be required infrequently to prevent biofilm buildup or to treat gross contamination. Chlorinated isocyanurates dissociate into free chlorine and cyanuric acid products and it is recommended that their level be kept below 117 mg/l. Chlorine dioxide disintegrates into chlorite and chlorate (and not into free chlorine, therefore it is not considered chlorine-based). Bromochlorodimethylhydantoin and a combination of sodium bromide and hypochlorite are both bromine based disinfectants used in indoor pool settings and their recommended levels are usually less than 2.0–2.5 mg/l. Ozone and ultraviolet radiation purify water as it passes through a treatment room without any residual disinfectant effect. The leakage of ozone (from the generators or tanks) is a serious concern given the highly irritating properties of the gas, and it is recommended that a separate de-ozonation process be included. The recommended concentration of ozone in air is less than 0.12 mg/m3. Disinfectants react with organic compounds excreted by bathers and form various by-products. Of all the chlorine-derived disinfection by-products found in the pools, trihalomethanes (THMs) such as chloroform and haloacetic acids like di-chloroacetic acid and trichloroacetic acid are present in the greatest concentrations. Inorganic bromine leads to the formation of brominated THMs. Both chlorine and bromine react with ammonia (from human source) to form haloamines like chloramines (monochloramine, dichloramine and nitrogen trichloride) and bromamines. Ozone reacts with organic matter to produce aldehydes and carboxylic acids. Studies have found a linear correlation between the number of people using the pool and the concentration of THMs. THMs are volatile in nature and are also found in the air above indoor pools. The concentration of THMs in the air is a function of their concentration in the water, the water temperature and the amount of splashing and surface disturbance. The concentration at different levels in the air depends on ventilation, building size and air circulation. Swimmers inhale these substances from just above the water’s surface, and the volume of air inhaled is a function of the intensity of effort and time spent in the

11.9

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pool. Inhalation is probably the major route of uptake of volatile components such as THMs One analysis of swimmers found that chlorinated swimming pool water lead to increased levels of THMs in both plasma and alveolar air, but the concentration in alveolar air rapidly fell after exiting the pool environment. This exposure becomes especially significant among lifeguards, coaches and pool maintenance staff. Exposure to volatile chloramines and bromamines (especially nitrogen trichloride and tribromide) can result in ocular and respiratory symptoms, particularly those related to irritation of mucous membranes (lacrimation, injection, cough, rhinorrhea, wheezing). The pulmonary symptoms are worse in patients with underlying bronchial asthma or increased bronchial hyperreactivity. Nitrogen chloride has an intense and unpleasant odor even at lower concentrations. The effect of exposure to chlorinated compounds is dependent upon the intensity (concentration) and duration of exposure. While high-intensity exposure can cause chemical burns, asthma, airway edema and chemical pneumonitis, lower-intensity exposures lead to lacrimation and nasopharyngeal irritation.

11.9

Diseases and health effects

The more common pulmonary disorders attributable to indoor water sports include: (1) asthma – exacerbations of pre-existing asthma and irritant-induced asthma; (2) extrinsic allergic alveolitis – also known as hypersensitivity pneumonitis; (3) nontuberculous mycobacterial infection (especially Mycobacterium avium and Mycobacterium intracellulare); (4) swimming-induced pulmonary edema; and (5) pulmonary contusion and pneumothorax.

11.9.1 Asthma In an unscientific survey of 220 participants at the interactive occupational grand round of the 1998 annual European Respiratory Society meeting in Geneva, about half the audience had either definitely or probably seen cases of swimming pool asthma. Most of these participants spent <10% of their practice time treating occupational lung disorders. Swimming pool cleaning staff are at special risk of respiratory tract injury and disease resulting from mishaps involving disinfectants, including mixing incompatibilities (e.g. bleach with ammonia or acids). A Dutch study collected samples from 38 swimming pool facilities and questionnaires from 624 workers at these facilities. They found a higher incidence of pulmonary atopy-related complaints among the workers compared with the general population. High levels of chloramine exposure correlated with greater frequency of pulmonary complaints. However, there are conflicting data that have resulted in children with asthma being encouraged to take up swimming because of the perceived benefit of breathing moist air. Elite swimmers have a higher incidence of bronchial hyperresponsiveness compared with the general population. Certain investigators have hypothesized that swimming in chlorinated pools potentiates lung damage and may be partly responsible for the increasing incidence of asthma in Western societies. This conclusion is based on the

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observation of elevated levels of serum pneumoproteins in children who frequently attend chlorinated swimming pools compared with controls. The elevated levels of serum pneumoproteins are believed to reflect increased alveolar–capillary permeability and early lung injury. The United States Centers for Disease Control and Prevention recently reported an analysis of a large number of guests at two separate hotels who were exposed to high levels of chloramine-like compounds near the indoor swimming pool area and experienced significant ocular and respiratory symptoms. Events such as these underscore the importance of staff training, proper ventilation and appropriate handling of compounds used for disinfection. Public health departments are encouraged to adhere to guidelines for cleaning and maintenance of swimming pools, to ensure ventilation and minimize exposure to volatile compounds, and to educate the public about proper pool hygiene. Exposure to certain chlorine-derived compounds or ozone can cause or exacerbate asthma. Asthma symptoms including cough, wheezing, chest tightness, dyspnea at rest or with exercise and reduced exercise capacity are usually temporally linked to either routine use of the pool or to exposures to high concentrations of chemicals (either unregulated or during shock treatment). Patients often feel better during days when they are not in the pool environment. The physical and laboratory findings in these patients may include wheezing, a prolonged expiratory phase, hypocapnea and hypoxemia on arterial blood gas measurement, especially during an exacerbation. Serial assessments of peak expiratory flow rate and pulmonary function testing are commonly part of the evaluation. Radiographs are often unremarkable, though hyperinflation may be seen in severe cases. If patients are symptomatic, but have nondiagnostic pulmonary function test results, bronchoprovocation testing with methacholine (methacholine challenge test) can provide important diagnostic information. Management consists of avoiding the pool and the surrounding environment if the symptoms are severe and debilitating. If it appears that a large number of users are developing similar symptoms, then the pool maintenance staff must test the water quality, ensure proper treatment of pools by using recommended practices, and also test air quality around the pool area with the objective that proper ventilation is maintained. Pharmacologic treatment is no different than that for other cases of asthma and includes corticosteroids and bronchodilators. Systemic corticosteroids may be used for severe exacerbations.

11.9.2 Acute irritant induced asthma The indoor pool environment presents the risk of an accidental high intensity exposure to water treatment chemicals. Such an exposure may cause severe respiratory tract irritation resulting in acute irritant-induced asthma. The hallmark features of irritantinduced asthma include a high-intensity exposure resulting in the abrupt onset of symptoms of increased airway reactivity, often within minutes of exposure. An important clinical reminder for physicians is that some patients manifest worsening symptoms after initial improvement or after a latency period of 6–12 hours after exposure. Therefore it is important to monitor individuals involved in major chemical

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spills and mishaps in a controlled setting for at least 24 hours. Acute irritant-induced asthma may improve over time or persist. It is necessary to prevent recurrent high intensity exposure to the offending agent. However, low-level exposure to the irritant agent is typically tolerated, so exposed individuals can typically return to the pool environment. Pharmacological management is similar to that for other presentations of asthma.

11.10

Extrinsic allergic alveolitis (hypersensitivity pneumonitis)

Extrinsic allergic alveolitis (EAA), also known as hypersensitivity pneumonitis, is an immunologic non-IgE mediated inflammatory lung disease that results from prior sensitization and subsequent exposure to specific organic and inorganic antigens in the atmosphere. It has been studied and investigated in both outdoor and indoor swimming pools, hot water tubs, spas and saunas. Factors associated with EAA include: (1) inadequate filtration and treatment of water harboring microorganisms either in a biofilm or as bacterial fragments; (2) higher temperature and humidity in such facilities, facilitating the growth of microorganisms; (3) intermittent use of the pool, tub or spa that promotes formation of biofilm; (4) spas generating water sprays and air bubbles that dissipate widely; (5) spray particle size in the respirable range (less than 10 mm in diameter); (6) prolonged and repeated exposures. Recent investigations examining local outbreaks found atypical mycobacterial species, especially Mycobacterium avium complex (Mycobacterium avium and Mycobacterium intracellulare), and endotoxins released into the air from various species of Pseudomonas, Stenotrophomonas maltophilia and Acinetobacter calcoaceticus were responsible for a large number of cases. Other bacteria implicated in cases of EAA associated with water include thermophilic actinomycetes, such as Faenia rectivirgula (Micropolyspora faeni or Saccharopolyspora rectivirgula) and Thermoactinomyces vulgaris. These organisms grow around pools, and also around air conditioners, humidifiers, ventilation systems and heaters. Free-living amoebae and nematodes found in contaminated water or ventilation systems may also cause EAA. EAA requires prior sensitization and therefore does not occur upon initial exposure. Affected individuals can present with acute symptoms within a few hours after second or subsequent exposure (acute EAA), while others may have a gradual progression of symptoms over a few weeks to months (subacute and chronic EAA). Patients usually present with symptoms of dry cough, exertional dyspnea and nonspecific constitutional symptoms of fever, headache, myalgias and loss of appetite leading to weight loss. Physical exam reveals diffuse end-inspiratory rales (‘crackles’). Computed tomography of the thorax shows poorly defined micro-nodules and diffuse

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ground glass opacities in predominantly upper and mid-lung zones. Pulmonary function testing often shows a restrictive ventilatory defect with a decrease in total lung capacity, residual volume, and reductions in the forced expiratory volume in one second (FEV1) and the forced vital capacity (FVC) with a preserved FEV1:FVC ratio. Reductions in diffusion capacity of carbon monoxide, hypoxemia and an increased alveolar–arterial oxygen difference are also commonly noted. Serum tests (via gel diffusion or immunoelectrophoresis) for detecting precipitating antibodies of the IgM, IgG or IgA class to the suspected antigens help in establishing evidence of exposure to specific antigens. Among patients undergoing bronchoscopy, bronchoalveolar lavage fluid analysis shows increased lymphocytes, plasma cells and a low CD4 þ /CD8 þ ratio. Lung biopsy often provides the definitive diagnosis, although it is not commonly employed in the acute form of the disease, especially with a history, physical exam, radiographs and other laboratory findings consistent with EAA. Patients with sub-acute or chronic EAA may need a lung biopsy to distinguish it from other forms of interstitial lung disease. Symptomatic relief can be attained with oxygen in some cases. Bronchodilators are usually ineffective. Systemic corticosteroids may be considered for periods varying from 1 to 6 months. They may be effective in the acute form of EAA, but they offer limited and inconsistent benefit in sub-acute and chronic EAA. The most important intervention for a case of water sports-induced EAA is avoidance of the exposure setting where the offending agent is encountered. The prognosis of hypersensitivity pneumonitis varies depending on the duration of clinical illness. While most patients with acute EAA recover without complications once the offending agent is removed, patients with both sub-acute and chronic forms of the disease may develop an indolent course with some patients developing persistent restrictive lung disease despite aggressive treatment. A few patients progress to fibrotic lung disease despite antigen avoidance along with treatment, and they have the worst prognosis. Engineering controls and other strategies to prevent EAA include: (1) maintenance of an effective sanitizer residual in every component of the pool; (2) use of automatic chemical feeders; (3) regular oxidation, shocking, and super-chlorination of water; (4) ensuring water circulation, especially where there is high swimmer/bather density per volume such as spas and hot tubs; (5) replacement of at least half the water in hot tubs daily; (6) complete draining of hot tubs and thorough cleaning of all surfaces and pipe-work weekly; (7) use of pool covers when not in use; (8) maintainance of the temperature of the pool water at 78
F. (9) room temperature always greater than the water temperature to minimize surface condensation; (10) maintainance of room relative humidity between 50 and 60% by installing dehumidifiers with heat transfer technology to minimize condensation;

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(11) treatment of all equipment after periods of nonoperation; (12) maintenance of strict standards for ventilation and air-filtration systems; (13) staff are qualified and trained to operate the recreational facility.

11.11

Infections

Most infectious agents associated with indoor water sports target the skin or nails, the gastrointestinal tract, central nervous system or the upper respiratory tract, including ears and sinuses. Common upper respiratory tract infectious agents include Staphylococcus aureus, Pseudomonas and Adenovirus. Infectious agents transmitted through water purification and transmitting systems (and also isolated in spas and hot tubs) that infect the lower respiratory tract and may cause pneumonia include Legionella, Pseudomonas, nontuberculous Mycobacteria (Mycobacterium avium, Mycobacterium intracellulare) and Staphylococcus aureus. A detailed description of the presenting symptoms, clinical signs, radiographic and laboratory findings, diagnostic criteria and treatment of respiratory tract infection, including pneumonia, is beyond the purview of this chapter. Most of these infectious agents can be controlled by following proper purification and treatment guidelines, as detailed elsewhere in this chapter. Prompt diagnosis and appropriate antimicrobial drugs are the cornerstones of effective management.

11.12

Swimming-induced pulmonary edema

Pulmonary edema induced by strenuous swimming is an uncommon occurrence but has been documented among young and healthy male subjects. This condition is thought to occur due to central blood pooling (related to immersion in water) accentuated by peripheral vasoconstriction after exposure to cold water. This increase in preload and afterload along with exercise-induced elevated pulmonary artery and pulmonary capillary pressures leads to altered Starling forces causing loss of integrity of the blood gas barrier. Swimming in a semi-supine position or with the help of fins tends to increase the incidence of swimming-induced pulmonary edema (SIPE). Severe dyspnea, productive cough and hemoptysis are the common symptoms associated with SIPE. Physical exam may demonstrate tachypnea, hypoxemia, basilar rales (crackles), elevated jugular venous pressures, restrictive lung function and pulmonary edema on chest radiographs. Recurrences have been known to occur; accordingly, affected swimmers should avoid strenuous water-based activities. Pulmonary edema has also been described after deep breath-hold diving. This is related to increased intrathoracic blood volume (and therefore increased pulmonary capillary transmural pressure) in conjunction with the decease in the total lung capacity seen with deep dives. The patients present with the aforementioned symptoms and signs of pulmonary edema. Diving in cold water carries additional risks for the reasons mentioned above. The treatment for both varieties of pulmonary edema consists of oxygen and diuretic therapy after ensuring there is no underlying cardiac ischemia.

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11.13 Trauma Most injuries related to indoor water sports involve the head, neck and spinal cord and occur during diving. Traumatic lung injury in indoor water sports is fairly rare. Among inexperienced divers attempting high platform dives, falling parallel or oblique to the surface of the water can result in fractures of the rib, pulmonary contusions and pneumothorax. Physicians should maintain a high index of suspicion in patients who present with localized chest pain (especially pleuritic) and dyspnea. Breath-holding techniques are used by divers and those performing synchronized swimming. These techniques lead to elevated intrathoracic pressure and can precipitate the development of pneumothoraces in patients with underlying bullous lung disease and those with prior history of pneumothoraces.

11.14 Equestrian arenas and horseback riding Some 4.6 million Americans are directly involved in the American equine industry, many of whom are exposed to the special environment of equine facilities on a regular basis. Employment as an instructor, trainer or handler and riding for sport represent opportunities for exposure to potentially hazardous respirable exposures. Recent investigations have demonstrated that the indoor equine environment can have an adverse effect on human respiratory health, as well as the health of horses. A spectrum of respiratory health effects are associated with the respiratory exposures encountered in the indoor equine environment. Demonstration of sensitization to horse allergens suggests allergic mechanisms may account for some of the health effects (i.e. asthma and allergic rhinitis) attributed to the indoor equine environment.

11.14.1 Organic and inorganic dusts Organic and inorganic materials are commonly encountered in the ambient air of equestrian facilities. Organic materials include horse dander and other animal proteins, vegetable matter (e.g. hay) and molds. Inorganic materials include particulates derived from the riding surfaces, ‘footing materials’, of arenas. Footing materials used in indoor horse arenas commonly include a blend of materials such as sandy soils, clay, wood, crumb rubber and chip rubber. Over time, all footing materials become pulverized by the hoof action of horses, generating a fine dust with respirable range particulates that become airborne. Dust exposure in indoor riding arenas can be significant, if dust suppression is not carried out on a regular (e.g. daily) basis.

11.14.2 Particulate health effects: general considerations A large body of epidemiologic literature has linked respirable-range ambient particulates with a spectrum of adverse acute and chronic cardiopulmonary effects, including upper respiratory tract irritant syndromes, asthma and chronic obstructive pulmonary disease decompensation, ischemic events, impaired lung development and premature mortality. Much of this research has focused on outdoor air pollution where the

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principle sources of particulates are fossil fuel combustion from motor vehicles and coal-fired power plants. The extent to which those findings are generalizable to other exposure settings and other classes of particulates, including organic and inorganic dusts encountered in indoor equestrian arenas, is not known. It is likely the physicochemical properties of the particulates are a determinant of toxicity, in addition to total particulate exposure dose. Nevertheless, in sufficiently intense doses, dust will be a nuisance exposure and a source of respiratory tract irritation for virtually anyone.

11.14.3 Allergy, asthma and airway symptoms Allergy to horse, including anaphylactic events, has been described in a limited number of reports. Case reports provide descriptions of sudden onset wheezing, sneezing, rhinorrhea, erythematous skin reactions, periorbital angiedemala and lip swelling in young children temporally associated with exposure to horses. In these cases, subsequent skin testing to horse dander demonstrated wheals consistent with an allergic response. Recurrent wheezing, rhinitis and sneezing triggered by repeated exposure to horse dander have also been described in other reports among children with asthma. Skin testing, exposure avoidance and standard asthma treatments provided evidence of a causal link between horse exposure and exacerbation of asthma in these cases. Sensitization to horse dander appears to be prevalent. In one analysis of allergic sensitization to horse allergens in an urban atopic population, more than 3% of studied subjects demonstrated allergic sensitization. Investigators suggested highly atopic individuals or those who were already sensitized to common pet dander should undergo skin prick testing and evaluation of serum specific IgE before beginning an activity involving regular direct horse contact and before entering environments containing horses such as stables, riding schools and race courses. In an analysis of 92 hippodrome workers (‘grooms’) that included a detailed questionnaire of respiratory and allergic symptoms, physical examination, skin prick tests and pulmonary function tests, sensitization to horse hair was detected in 13% compared with 4% in a control group. Among grooms compared with controls, there was a higher prevalence of asthma (14 vs 5%), allergic rhinitis (42 vs 18%), allergic conjunctivitis (35 vs 15%) and allergic skin diseases (33 vs 13%). Additionally, lung function was significantly worse among grooms. The authors concluded that occupational exposure to horse increases the sensitization to horse hair, induces asthma and allergic symptoms and also impairs lung function. In a cross-sectional analysis of 82 barn-exposed subjects and 74 control subjects, there was a significantly higher prevalence of self-reported respiratory symptoms in the barn-exposed group (50%) vs the control group (15%). Exposure to horse barns, smoking and family history of asthma or allergies was independent risk factors for respiratory symptoms. Those spending 10 hours week at an equine barn (n ¼ 59) were designated as having high exposure. The frequencies of non-nasal respiratory symptoms over the preceding 12 months were markedly greater in the high-exposure group vs the control group: dry cough (41 vs 8%), wheeze (19 vs 4%), chest tightness (25 vs 2%), productive cough (12 vs 2%), shortness of breath (19 vs 8%) and awakening at night with symptoms (20 vs 5%). In an adjusted model for multivariate analysis of exposure to horse barns as a risk factor for respiratory symptoms with age, gender,

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family history of asthma, family history of allergies and smoking retained in the model, high exposure to the horse barn yielded an odds ratio for self-report of at least one respiratory symptom in the past year of 8.9. The investigators also reported that 17% of the low-exposure group and 39% of the high-exposure group experienced nasal irritation symptoms compared with 12% of the control group. In another analysis of dust exposure and respiratory disorders among equestrians, 900 instructors and trainers were randomly selected from a North American riding database and mailed a self-administered questionnaire. Three-hundred and forty-eight (38%) returned the survey. The prevalence of symptoms of four respiratory conditions (chronic bronchitis, noninfectious rhinitis, asthma and pneumonia) was investigated in relation to variables that included job duties, dust exposures, smoking and other factors. The study found both nonsmoking and smoking equestrian instructors were more likely to develop symptoms of chronic bronchitis when the primary working facility was an indoor arena compared with an outdoor arena. Other groups have found the equine environment is associated with the development of organic dust toxic syndrome – a self-limited febrile illness that does not require prior exposure (sensitization), farmer’s lung (extrinsic allergic alveolitis), chronic bronchitis, dyspnea and asthma.

11.14.4 Dust suppression Dust suppression can be achieved through simple strategies that include the application of water onto footing materials and other dusts. A complication of water application is that sub-freezing conditions will result in a surface that is too hard for riding. Humectants that pull in water may also be applied to riding surfaces. Humectants have the advantage of maintaining a surface suitable for riding even in sub-freezing conditions. One analysis of the effects of dust suppression found that the quality of footing was a significant determinant of indoor dust level. Inorganic footing was associated with a 4-fold increase in total dust level compared with organic footing. Additionally, total dust levels were approximately 3 times higher during times of horse activity that was faster than a walk. In this study, respirable range particulates represented about half of the total dust during riding activity. Respirable range particulate concentrations during riding were greater than 10 times the United States Environmental Protection Agency National Ambient Air Quality Standard for particulate matter 10 mm in diameter, which is 150 mg/m3.

11.14.5 Diagnosis and management Dust type, burden of exposure, susceptibility factors, co-morbidities (e.g. underlying heart or lung disease) and co-exposures (e.g. cigarette smoking) probably play important roles in determining whether an exposed individual (rider or worker) will experience an adverse health effect from airborne equestrian dust. As is the case with most particulate-associated health effects, airway disorders including irritant effects, bronchitis and asthma exacerbations are among the most important conditions attributable to equestrian dust. Diagnosis is based largely on history. If available, skin

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testing and testing for serum-specific IgE may support diagnoses of allergic diseases, including asthma. Findings such as clinical improvement after dust avoidance support a causal link. Management includes encouraging the use of personal respiratory protection, especially among workers, and supporting the aggressive use of dust suppression in the arena.

11.15

Gymnastics, weightlifting, athletics (track and field) and rock wall climbing

Hand chalk is commonly used by athletes in sports that require a secure hand grip with an implement or structure. Gymnasts, weight lifters, throwers and climbers use chalk repeatedly to promote a secure grip with an apparatus (gymnastics), barbell (weightlifting), shot put (athletics/track and field), and the surface of stationary and mobile climbing walls (indoor rock climbing). Common practices associated with the application of hand chalk include blowing excess chalk from hands, especially in gymnastics. This has the potential to cause a ‘personal cloud’ of respirable-range chalk particulates. In the setting of vigorous athletic activity and increased minute ventilation, athletes may be exposed to a dose of chalk dust sufficient to cause irritant effects and, in susceptible individuals, exacerbate asthma. Minimizing exposure to airborne chalk dust, including minimizing the blowing of chalk dust from hands, stepping away from any personal cloud of dust generated from blowing, and avoidance of other athletes blowing chalk dust are prudent strategies to reduce the risk of an adverse respiratory response.

Further reading Ice sports and arenas Bougault, V., Turmel, J., St-Laurent, J., Bertrand, M., Boulet, L.P. (2009) Asthma, airway inflammation and epithelial damage in swimmers and cold-air athletes. Eur. Respir. J. 33: 740–746. Hedberg, K., Hedberg, C.W., Iber, C., White, K.E., Osterholm, M.T., Jones, D.B., Flink, J.R., MacDonald, K.L. (1989) An outbreak of nitrogen dioxide-induced respiratory illness among ice hockey players. JAMA 262: 3014–3017. Pelham, T.W., Holt, L.E., Moss, M.A. (2002) Exposure to carbon monoxide and nitrogen dioxide in enclosed ice arenas. Occup. Environ. Med. 59: 224–33. Salonen, R.O., Pennanen, A.S., Vahteristo, M., Korkeila, P., Alm, S., Randell, J.T. (2008) Health risk assessment of indoor air pollution in Finnish ice arenas. Environ. Int. 34: 51–57. Stensrud, T., Berntsen, S., Carlsen, K.H. (2007) Exercise capacity and exercise-induced bronchoconstriction (EIB) in a cold environment. Respir. Med. 101: 1529–1536. Weaver, L.K. (2009) Carbon monoxide poisoning. New Engl. J. Med. 360: 1217–1225.

Water sports Babu, R.V., Cardenas, V., Sharma, G. (2008) Acute respiratory distress syndrome from chlorine inhalation during a swimming pool accident: a case report and review of the literature. J. Intensive Care Med. 23: 275–280.

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Bernard, A., Carbonnelle, S., De Burbure, C., Michel, O., Nickmilder, M. (2006) Chlorinated pool attendance, atopy and the risk of asthma during childhood. Environ. Health Perspect. 114: 1567–1573. Bowen, A.B., Kile, J.C., Otto, C., Kazerouni, N., Austin, C., Blount, B.C., Wong, H.N., Beach, M.J., Fry, A.M. (2007) Outbreaks of short-incubation ocular and respiratory illness following exposure to indoor swimming pools. Environ. Health Perspect. 115: 267–271. Glazer, C.S., Martyny, J.W., Lee, B., Sanchez, T.L., Sells, T.M., Newman, L.S., Murphy, J., Heifets, L., Rose, C.S. (2007) Nontuberculous mycobacteria in aerosol droplets and bulk water samples from therapy pools and hot tubs. J. Occup. Environ. Hyg. 4: 831–840. Goodman, M., Hays, S. (2008) Asthma and swimming: a meta-analysis. J. Asthma 45: 639–647. Guidelines for Safe Recreational Waters (2006) Swimming Pools and Similar Recreational-Water Environments, Vol. 2. World Health Organization: Geneva; available from: http://www.who.int/ water_sanitation_health/bathing/bathing2/en/ (accessed 12 April 2010). Hanak, V., Kalra, S., Aksamit, T.R., Hartman, T.E., Tazelaar, H.D., Ryu, J.H. (2006) Hot tub lung: presenting features and clinical course of 21 patients. Respir. Med. 100: 610–615. Helenius, I., Rytil€a, P., Sarna, S., Lumme, A., Helenius, M., Remes, V., Haahtela, T. (2002) Effect of continuing or finishing high-level sports on airway inflammation, bronchial hyperresponsiveness, and asthma: a 5-year prospective follow-up study of 42 highly trained swimmers. J. Allergy Clin. Immunol. 109: 962–968. Jacobs, J.H., Spaan, S., van Rooy, G.B., Meliefste, C., Zaat, V.A., Rooyackers, J.M., Heederik, D. (2007) Exposure to trichloramine and respiratory symptoms in indoor swimming pool workers. Eur. Respir. J. 29: 690–698. Lindholm, P., Ekborn, A., Oberg, D., Gennser, M. (2008) Pulmonary edema and hemoptysis after breath-hold diving at residual volume. J. Appl. Physiol. 104: 912–917. Massin, N., Bohadana, A.B., Wild, P., H
ery, M., Toarmain, J.P., Hubert, G. (1998) Respiratory symptoms and bronchial responsiveness in lifeguards exposed to nitrogen trichloride in indoor swimming pools. Occup. Environ. Med. 55: 258–263. Nemery, B., Hoet, P.H., Nowak, D. (2002) Indoor swimming pools, water chlorination and respiratory health. Eur. Respir. J. 19: 790–793. Nickmilder, M., Bernard, A. (2007) Ecological association between childhood asthma and availability of indoor chlorinated swimming pools in Europe. Occup. Environ. Med. 64: 37–46. Pedersen, L., Lund, T.K., Mølgaard, E., Kharitonov, S.A., Barnes, P.J., Backer, V. (2009) The acute effect of swimming on airway inflammation in adolescent elite swimmers. J. Allergy Clin. Immunol. 123: 502–504. Pollock, N.W. (2008) Breath-hold diving: performance and safety. Diving. Hyperb. Med. 38: 79–86. Rickman, O., Ryu, J., Fiddler, M., Kalra, S. (2002) Hypersensitivity pneumonitis associated with mycobacterium avium complex and hot tub use. Mayo Clin. Proc. 77: 1233–1237. Rubin, B.D. (1999) The basics of competitive diving and its injuries. Clin. Sports Med. 18: 293–303. Thickett, K.M., McCoach, J.S., Gerber, J.M., Sadhra, S., Burge, P.S. (2002) Occupational asthma caused by chloramines in indoor swimming-pool air. Eur. Respir. J. 19: 827–832. Uyan, Z.S., Carraro, S., Piacentini, G., Baraldi, E. (2009) Swimming pool, respiratory health, and childhood asthma: should we change our beliefs? Pediatr. Pulmonol. 44: 31–37.

Indoor equestrian arenas and horseback riding Gallagher, L.M., Crane, J., Fitzharris, P., Bates, M.N. (2007) Occupational respiratory health of New Zealand horse trainers. Int. Arch. Occup. Environ. Health 80: 335–341.

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Mazan, M.R., Svatek, J., Maranda, L., Christiani, D., Ghio, A., Nadeau, J., Hoffman, A.M. (2009) Questionnaire assessment of airway disease symptoms in equine barn personnel. Occup. Med. Lond. 59: 220–225.

Gymnastics, weightlifting, athletics (track and field) and rock wall climbing Weinbruch, S., Dirsch, T., Ebert, M., Hofmann, H., Kandler, K. (2008) Dust exposure in indoor climbing halls. J. Environ. Monit. 10: 648–654.

Part III The work environment

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

12 Agricultural environments and the food industry Jakob Hjort Bønløkke1, Yvon Cormier2 and Torben Sigsgaard1 1

Aarhus University, Denmark Institut Universitaire de Cardiologie et de Pneumologie de Que´bec and Universite´ Laval, Que´bec, Canada

2

12.1 Introduction As a trade, food processing is tremendously diverse. Ranging from agriculture and fishing, to slaughtering and raw processing of foods to refined processing and cooking, the numerous and varied jobs offer countless types of potentially hazardous exposures. Exposure to airborne particles of organic material is the cause of a diversity of clinical conditions in all of the jobs within the group. Comprehensive reviews on the specific diseases related to farming are found in Linaker and Smedley [1] and in Schenker et al. [2]. Excellent reviews also exist in relation to bakery and seafood workers and to several of the other jobs within these trades. The history of disease related to crop, soil and animal contact is the oldest in the history of man’s occupational exposures. Descriptions of respiratory problems arising from such contact can be found in several ancient texts, many of which describe symptoms of readily recognizable conditions such as pneumonitis or chronic bronchitis, whereas asthma and rhinitis – the two respiratory conditions most widely associated with farming today – are less easily recognized. We do not know whether or not allergic reactions were less common in man’s long history of farming than they are today. Certainly this question has attracted much recent attention in relation to the ‘hygiene hypothesis’.

12.2

Agriculture and agribusiness

In Table 12.1 are listed the most common respiratory hazards in farming. Typical job types include: Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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Table 12.1 Possible respiratory hazards in agriculture Pollen and other seasonal allergens Organic dust from grain and other crops of microbial origin (molds, spores, bacteria, endotoxin and other toxins) Mites Animal (dander, urine, faeces) Inorganic dust (mainly silicates and other minerals from soil) Gases and fumes from slurry/manure and fertilizers – carbon dioxide, ammonia, hydrogen sulfide, methane from silage – nitrogen dioxide and carbon dioxide engine exhaust fumes welding fumes Chemicals pesticides (insecticides, herbicides, fungicides) disinfectants and cleaning agents paints Infectious agents (zoonoses)

.

field preparation and harvesting, mostly with machinery that creates dust, especially in dry weather;

.

maintenance of machines and buildings, resulting in exposure to diesel exhaust and different chemicals and dust;

.

application of and potential exposure to pesticides and other toxins;

.

handling of a great variety of crops with exposure to dust from these and from plant debris;

.

storage of crops and feedstuffs with potential exposure to molds and mites;

.

handling of animals with direct contact and exposure to their allergens in addition to infectious agents from them;

.

work in animal houses with exposure to complex mixes of bioaerosols and gases from feed, animals and manure;

.

storage and handling of manure and fertilizers with exposure to these in the form of aerosols or gases;

.

cleaning of animal houses with pressurized water, which liberates extremely high concentrations of humid aerosolized material of mostly organic origin.

Farmers as well as farm workers and farm dwellers are thus exposed to different kinds of dust throughout life. Depending on the type of farming, the region, climate and season, this exposure may be dominated by dry soil components (e.g. among crop farmers in dry climates during soil preparation and harvesting), by dusts from the crops themselves (e.g. from handling grain) or by the more humid bioaerosols containing dead and live microorganisms that are present in high concentrations in most animal houses. Farms are becoming ever larger and more specialized in most parts of the world. Most

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modern farmers specialize in producing only one or a few types of products rather than a range of different animals and crops on their farms. These changes in farming result in longer work periods with more uniform exposures (e.g. inside swine houses) and can result in much higher doses of airway irritants or allergens. On the other hand, larger operations will allow for more of the work to be performed by machines unsupervised by the farmer, potentially reducing the exposures. As single farming operations grow with more workers employed, groups of employees who are not traditionally considered farmers become exposed to the hazards of farming. Some of these workers have little knowledge about these hazards and may decline the use of respiratory protection if such protection is offered to them at all. Migrant farm workers, numerous in southern USA but common in farming almost anywhere in the world, are particularly vulnerable to the hazards of farming. They may be particularly prone to acute reactions such as reactive airways dysfunction syndrome (RADS), organic dust toxic syndrome (ODTS), hypersensitivity pneumonitis (HP), and to poisoning from inhalation or skin contact with pesticides. Nor does the seasonality of their work protect them from developing chronic diseases such as asthma or chronic bronchitis. City-dwellers, another group not commonly thought of as exposed to farming, make up an important workforce in the production of fruit, vegetables, and flowers, e.g. in greenhouses, because many of these operations are located close to towns. Farmers and farm workers commonly report respiratory symptoms such as wheeze, dyspnoea and cough. These symptoms are relatively nonspecific and can be caused by several occupational respiratory disorders, chronic as well as transient. However, persistent symptoms are not rare. Symptom prevalences from a study of 4.793 European farmers revealed prevalences of 3.3% for asthma, 14.9% for wheeze, 12.4% for chronic phlegm, 14.4% for nasal symptoms and 12.4% for toxic pneumonitis (ODTS). In California, prevalences of chronic symptoms or diseases in a farming population have been reported for persistent wheeze at 8.6%, for chronic bronchitis at 3.8%, for chronic cough at 4.2% and for asthma at 7.8%. In any type of farming, exposure to allergens is very common – see Table 12.3 for common examples. A farmer presenting with rhinorrhea, nasal congestion, nasal itching and sneeze, often accompanied by symptoms of conjunctivitis, is likely to have irritative or allergic rhinitis. As most farmers work outdoors in close contact with plants from spring to autumn, they are highly exposed to pollen with the potential of causing sensitization. Seasonality may be less pronounced in an allergic farmer than in other patients because farmers expose themselves perennially to feedstuff and animals, and because irritative reactions to diverse types of dust may maintain the nasal symptoms for prolonged periods. Indeed, irritative mechanisms probably explain the majority of upper airway and eye symptoms among farmers since such symptoms are very common (some studies suggest that more than 50% of farmers suffer from them), while allergic sensitization seems to be rarer than in the general population. Greenhouse workers, less affected by seasonal variations in exposure, are often in contact with plants with a large allergenic potential. In addition to dermatitis, conditions such as allergic rhinitis and asthma are common and are likely to cause many to change their occupation. In recent years different species of bacteria and small insects have been introduced in large numbers into greenhouses as alternative methods of combating plant disease. Sensitization to some of these species has been observed, but apparently only little illness has emerged from their use.

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Table 12.2 Some of the most common causes of hypersensitivity pneumonitis in agriculture and food processing (depending on climate) and the disease named thereafter Cause

Disease name

Moldy hay Moldy pressed sugarcane Moldy compost and mushrooms Moldy cork Contaminated barley Contaminated maple logs Contaminated redwood dust Contaminated wood pulp Cheese or cheese casings Greenhouse soil Mold on tobacco Mold on grapes Mold on peat moss Pigeon droppings Chicken feathers Oyster or mollusk shells

Farmer’s lung disease Bagassosis Mushroom picker’s disease Suberosis Malt worker’s disease Maple bark disease Sequoisis Wood pulp worker’s disease Cheese washer’s disease Greenhouse lung Tobacco worker’s disease Wine grower’s lung Peat moss lung Pigeon breeder’s disease Chicken breeder’s disease Shell lung

Much agricultural dust is so coarse that its penetration beyond the larynx is limited and symptoms arising from exposure may be restricted to the upper airways – including cough to ‘clear the throat’. Examples include allergic rhinitis caused by olive pollen in olive orchard workers, allergic rhinoconjunctivitis in greenhouse workers caused by exposure to predatory mites used as pest control agents and storage mites in farmers, allergic sensitization to horses accompanied by rhinitis and/or conjunctivitis in grooms and cow dander allergy and rhinitis in dairy farmers. The latter may illustrate the diversity of exposure even within the same type of farming as in Finland daily brushing of cows is common and they are kept indoor most of the year, causing respiratory allergies in a large proportion of dairy farmers. These allergies are not nearly as common in other countries with different farming traditions and climates. Farmer’s lung is a form of hypersensitivity pneumonitis, a respiratory disease caused by an exaggerated immune response to inhaled antigens; it was probably the first described occupational lung disease and typically occurs in dairy farmers exposed to dust that originates from poorly stored hay, straw, grain or similar plant material. Table 12.2 lists several of the most common types of exposures related with this disease. When any foliage is stored with a relatively high water content, i.e. above 15% humidity, heating occurs. This heating is initiated by an initial proliferation of lactobacteria, creating an ideal milieu for the growth of thermoactinomyces including Saccharopolyspora rectivirgula (SR) (formerly known as Micropolyspora faeni). When a farmer feeds this material to his animals in the following winter, when the barn’s ventilation is minimal, he or she is exposed to large quantities of dust containing dried antigens derived from this microorganism. This bioaerosol is generated not only by the direct handling of the material but also by shaking when the animals eat their feed. It is quite possible that a co-factor is needed to induce farmer’s lung disease. This co-factor could be endotoxin – abundantly present on farms – or a concomitant respiratory viral infection. Farmers’ lung can be acute with transient fever, chills and dyspnoea occurring

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Table 12.3 Some of the most common causes of allergic asthma in agriculture and food processing Animal-derived allergens cow dander (cow allergen Bos d 2) egg proteins (ovalbumin, conalbumin, lysozyme, ovomucoid) bird antigens (bird serum albumins Gal d 5) laboratory animal allergens (rat, mouse, guinea pig, rabbit, etc.) seafood and fish allergens (snow crab, Alaska king crab, lobster, shrimp, salmon, trout, etc.) Plant-derived allergens grain dust and cereal flours (wheat, rye, soya, barley, etc.) coffee beans and tea dust foods such as potato, onion, carrot, asparagus and several less common ones castor beans seeds (e.g. from onion, sunflower, sesame) garlic dust and other spices and herbs flowers (Lathyrus, Gypsophila, Freesia, Hyacinthus, and other common decorative flower species) vegetable gums (arabic gum, tragacanth and others and seed gums such as carob gum and guar gum) Parasites Anisakis simplex (in fish) Insects Mites (predatory mites in greenhouses and storage mites in grains) Molds and other microorganisms S. cerevisiae (yeast) Aspergillus (in bakers) Enzymes a-amylase (additive to baking flour) papain (in production of meat, juices, beer, etc.) pepsin (in production of liquors, cheese, cereals, etc.) pectinase (in fruit juice production) B-gluconase (additive to animal feed)

3–8 hours after exposure, or more indolent with progressive shortness of breath. Acute bouts usually heal completely while the more insidious form can lead to irreversible lung destruction in the form of fibrosis. The diagnosis is supported by the history of typical exposure and symptoms, restrictive lung function measurements, infiltrates on chest X-rays and high-resolution computed tomography (HRCT), and specific serum antibodies to the offending antigen. If the diagnosis is uncertain, a bronchoalveolar lavage should be obtained; a high number and percentage of lymphocytes in the bronchoalveolar lavage (BAL) fluid would clearly support the diagnosis while the absence of a lymphocytosis would rule out active HP. Although the confirmation of the diagnosis requires technology and expertise not readily available to the family physician, the first-line physician should through careful questioning and physical examination (bilateral inspiratory crackles) be able to suspect the diagnosis. The diagnosis is strongly supported by documented recurrence 3–8 hours after re-exposure to the farmer’s work environment. Farmer’s lung is a relatively rare disease. The current estimated prevalence in appropriately moist agricultural regions is less than one case per 1000 dairy farmers per year. A doctor working in a rural setting, even in such areas where the disease is

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prevalent, might see one or two cases in his or her lifetime. As for any ‘orphan disease’, the fewer cases a doctor sees, the less likely it is that he or she will think of the diagnosis. It is important therefore for any family physician to keep the diagnosis of HP (or farmer’s lung if the patient is a farmer) in mind. HP should be ruled out in any case presenting with recurrent febrile episodes or an interstitial lung disease. Even if asked about exposures, many farmers may not be aware of exposure to partly degraded hay or other animal feed because it is such a common situation on many farms and the antigens may have formed months before the farmer handled the material.

12.3 Case 1 A 65-year-old nonsmoking dairy farmer was brought to the hospital in respiratory distress. He had a high fever, inspiratory crackles and bilateral lung infiltrates. No detailed history was possible as the patient was intubated and mechanically ventilated with supplemental oxygen. He was given broad spectrum intravenous antibiotics. His condition rapidly improved and he was weaned off the respirator within 2 days and released from the hospital within 5 days of admission to continue oral antibiotics. Final diagnosis was bilateral pneumonia (no pathogens had been identified). The patient returned to the hospital a week later complaining of shortness of breath and chills. At this time a complete history revealed that he was a dairy farmer who had recently been using poorly conserved hay as bedding for his cows. The hay was so poor that he had used a chain saw to cut the bales into sections. The diagnosis of farmer’s lung was confirmed by serology, CT scan and BAL. His recovery was complete and, by changing his work environment, he was able to continue farming without recurrence. Care must be taken to differentiate farmer’s lung from an infectious process or inhalation fever such as ODTS. ODTS also occurs in dairy farmers but in this case the exposure to moldy bioaerosols is massive, e.g. when decapping a haylage silo. The response is limited to the airways but extends to the alveoli. It is caused by toxic material in the dust. ODTS is also called toxic pneumonitits and has previously been called mycotoxicosis. The latter name was changed when it became evident that the toxic material which causes it is most likely also derived from bacteria (e.g. endotoxins). This self-limiting syndrome is not an immune-mediated disease. As for farmer’s lung, the diagnosis of ODTS can usually be made simply by careful questioning and by remembering this possibility. There are no standardized diagnostic criteria; the diagnosis is only made by history and follow-up and by ruling out other diagnoses such as an infectious process and farmer’s lung. The dyspnoea, fever, cough and malaise appearing a few hours after exposure resemble HP but symptoms resolve spontaneously within 1–2 days. It is likely that more than one agent can give rise to the syndrome and that some of the mixes of agents present, e.g. in animal houses and stables, are more potent than single agents.

12.4 Case 2 A 42-year-old corn producer came to the hospital emergency room complaining of severe cough and chills since the evening before. His cough was unrelenting but he produced very little, blood-tinged sputum. Awaiting his turn to see the physician the

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receiving nurse obtained his vital signs. He had a fever of 39 C, his pulse was regular at a frequency of 140 beats/minute and his blood pressure was 140/94. A chest radiograph and spirometry were obtained, both of which were normal. Upon questioning the patient reported that he had been cleaning one of his corn silos the day before. He had spent 2 hours cleaning moldy grains of corn that remained on the edges of the otherwise empty silo. The doctor suspected an acute infectious bronchitis and was about to prescribe an antibiotic when the patient reported prior similar, although less severe, episodes after cleaning his silos in the past. With this additional information the doctor prescribed a cough suppression agent and aspirin. The patient was told he probably had ODTS and asked to return if the symptoms had not cleared within 24 hours. His recovery was uneventful, confirming that the diagnosis had probably been correct.

12.5

Symptoms not related to allergen exposure

A common disease entity among farmers is the ‘asthma-like syndrome’ with reported prevalences in some European farming populations of 20–50%. The syndrome resembles asthma as it can present with chest tightness, wheeze and dyspnea. Allergic reactions are absent. In contrast to the common worsening of asthma during a work week, the symptoms of asthma-like disease tend to improve as the working week progresses. Some allergic asthma may, occasionally, show the same pattern or in contrast may be worse on Saturdays after an entire week at work. In farming, such temporal patterns are usually very difficult to establish because work is rarely performed only on weekdays. Any episodic or persisting respiratory symptoms without systematic involvement are therefore evocative of asthma or asthma-like disease. Grain dust, ammonia and endotoxins have all been implicated in asthma-like disease – all of these exposures being common in animal houses. Endotoxins, ubiquitously present everywhere on farms and stemming from bacterial growth on feed, plant debris, in animal houses and elsewhere, have been associated not only with ODTS but also with worsening of asthma. Endotoxins are also commonly suspected of being at least partly responsible for asthma-like syndromes. In a current or former farm worker or farmer presenting with a history of persistent or recurring productive cough and dyspnoea, chronic bronchitis is not unlikely even in a nonsmoker. In nonsmoking farmers and workers in animal confinement buildings, chronic obstructive pulmonary disease (COPD) has been found in 17%, with 3% having severe disease. COPD appears to be more common in older farmers than in comparable nonfarming populations. Several agents within the farming environment can reach and cause inflammation of the conductive airways: they include organic and inorganic dust, gases and fumes. Alone none of these has been convincingly demonstrated as a sufficient cause of COPD, but endotoxin in animal confinement buildings has repeatedly been associated with accelerated loss of lung function and with COPD. An increased risk of chronic bronchitis has also been found among farmers who have experienced ODTS. In dry climates an association of chronic bronchitis with dust exposure has been put forward. Furthermore, exposures to welding fumes, exhaust and smoke from fires are not uncommon among farm workers and may add to the risk of chronic bronchitis. Thus, whether the presenting symptoms are wheeze, dyspnoea, cough, chest tightness, or are less specific, any farmer reporting historic episodes of respiratory problems may well have some degree of COPD.

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A farmer presenting with pulmonary fibrosis should be questioned about excessive exposure to dust from sand or soil or to the herbicide paraquat. Such inhalatory exposures are not uncommon during field work, but also occur when processing sugar beets, potatoes and grain or when burning straw etc., and can lead to fibrosis – an important diagnosis to consider in the dyspneic farmer. Irritants like ammonia or other gases, cleaning agents, or other chemicals are regularly handled on farms. Accidental high exposure to many such irritants can cause RADS. RADS is not easily missed due to the new onset of asthma-like symptoms very shortly after unusual episodes of exposures. It is debated how long RADS can persist. Distinguishing between whether persisting symptoms represent an underlying asthma or if one should accept an entity called persisting RADS may be purely academic since both diseases may be caused by exposures at farms (and other workplaces with chemical irritants) and require anti-asthmatic treatment. At lower concentrations, gases from decomposing organic material can become concentrated in silos and cause respiratory irritation. Usually a self-limiting condition, such an inflammatory reaction of the airways to high concentrations of noxious gases can turn into life-threatening lung oedema or cause a long-lasting RADS. Suffocation or near death is not uncommon in such silos or in manure pits or other enclosed or low-level spaces that may fill with hydrogen sulfide. Zoonoses are considered a rare cause of respiratory morbidity in farmers. Psittacosis, which is seen among poultry farmers due to their contact with infected birds, usually presents with nonproductive cough and other symptoms of a respiratory tract infection. Fever and other systemic symptoms will also be present. Bovine tuberculosis is well controlled in Europe and North America and infection of farmers has become rare. In some developing countries primary tuberculosis due to contact with cattle infected with Mycobacterium bovis remains a serious health problem. Fever may also be a symptom of Coxiella burnetii infection (Q fever) or other rare infectious diseases. Little is known about the prevalence of mild flu or cold-like viral infections transmitted from swine or other livestock. Such zoonoses may have become more prevalent because of higher density of animals in confinement buildings and because farm workers spend longer working hours inside these buildings. Farm workers, farmers and their relatives may if they present with airway infections or otitis, have been infected with multiresistant Staphylococcus aureus (MRSA), possibly transmitted from pigs. Such cases have been documented in recent years and are probably due to the frequent use of antibiotics not only for animal treatment but also as growth enhancers in most countries. Acute symptoms of bronchoconstriction can be caused by organophosphates and carbamates used as pesticides in farming. A chemical pneumonitis can result from exposure to the very commonly used herbicide glycophosphate. Chronic pulmonary disease is rarely caused by pesticide exposure alone, but pulmonary fibrosis may be the result of exposure to the herbicide paraquat. The overlapping respiratory conditions associated with farming are illustrated in Figure 12.1. Fractures, strains and wounds are inherent risks associated with farming due to the handling of machinery and large animals. Osteoarthritis of the lower back, hips or knees may emerge after years of heavy work in farming. Workloads of the intensity associated with arthritis have become uncommon in the industrialized farming of affluent nations, but remain familiar to farm workers elsewhere. Dermatitis can be the result of exposure to chemicals as well as due to allergic sensitization to plants or animals.

12.6

OTHER AGROBUSINESS

Asthma-like syndrome Chest tightness and cough on return to work

Organic dust toxic syndrome

169

Occupational asthma and aggravation of pre-existing asthma

Bronchitis Acute/subchronic Chronic

Upper airways inflammation: Mucous membrane irritation syndrome Sinusitis Allergic rhinitis

Pulmonary edema secondary to H2S

Figure 12.1 The spectrum of respiratory disease in swine confinement workers. Adapted with permission from von Essen and Dosman

Taking a job history or just trying to identify causal exposures in a farmer with airway symptoms can be complicated. This is due to the great variety of agents and processes (and their changing with seasons) and the fact that disease may be caused by microorganisms or impurities polluting other agents handled on the farm. By virtue of their natural origin, many relevant exposures are easily ignored by the patient and the doctor when scrutinizing suspected job functions. Often, because exposures are ‘natural’ and some degree of breathing difficulty considered normal, farmers will show a considerable lag time before consulting a physician. Enquiries back in time are therefore required. It is useful to note any agent encountered during the work processes of the farmer – even those at first appearing to be unlikely causes. A possible explanation for the lower prevalence of airway allergies among farmers is the fact that relief of symptoms may be impossible to find, thus forcing the farmer to change to another occupation not involving dust exposure. Rhinitis can occur following acute exposures to high concentrations of an irritant. In such a case it will usually be self-limiting. In most cases, however, rhinitis and other symptoms of upper airway and mucosal inflammation require lowering or cessation of exposure for extended periods in order to improve. Removing exposures or dramatically lowering them is usually required in order to improve the condition. In the agricultural setting this often proves very difficult because alternative jobs in the neighbourhood are scarce and the investments required for changing processes can be difficult to finance.

12.6

Other agrobusiness

Farmers and farm workers are not the only workers exposed to hazards from the allergens and dust present on crops. Across the many processes involved in ‘agribusiness’ there is

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potential for hazardous exposures, e.g. when handling or transporting grain, soybean or other crops, manure or ammonia, or even animals. In the industrialized farming of modern times, much of the handling of animals and grains, for example, is outsourced to transportation companies. Thus, drivers may be the persons with the highest exposures to dust from swine houses and other farming operations. Similarly, it is in grain elevators, where the loading and unloading of tons of different grains take place most of the year, that the highest dust exposures of workers have been observed. This is true for short-term peak exposures as well as long-term chronic exposures. The respiratory problems associated with this type of work are rhinitis, asthma, chronic bronchitis, HP and ODTS. For example, more than half of the grain handlers in the USA suffer from rhinitis. Besides these severe problems, nonspecific airway symptoms from both the lower and upper airways are common. Symptoms and diseases used to be experienced by the majority of grain handlers. Fortunately, many years of effort to reduce exposures and/or make the workers use respiratory protection has been successful in reducing the dust levels that grain elevator workers are exposed to. However, workers cannot avoid exposure to inorganic dust, mainly from soil, as well as organic components of which endotoxins, mycotoxins, glucans and fungal spores are considered responsible for most of the negative health effects. In the animal feed industry, in some cases allergens from crops have caused outbreaks of asthma. Soybean appears to be particularly hazardous in this respect. Thus, outbreaks of soybean allergy and severe asthma attacks have not only been reported in the animal feed industry itself but also among residents living in the proximity of such industrial operations. Perhaps the best-known example of this was in Barcelona in Spain. For several years, the cause of outbreaks of asthma attacks in the central parts of the city remained a mystery. It was only after many casualties that studies linked these outbreaks to the inhalation of soybean dust released during the unloading of soybeans into a silo used for storage in the harbour. After equipping the silo with properly working filters, soybean allergen levels decreased dramatically and the outbreaks of asthma ceased. Another cause of allergy in animal feed handlers is storage mites. Allergy to these is the cause of an important proportion of occupational asthma among grain handlers as well as among farmers. Among grain handlers, cross-shift declines in lung function are common. It seems likely that the workers with the greatest declines are those most prone to chronic loss of lung function, as is the case among swine farm workers. Common to the various animal feed operations is the potential for high exposures to dust. Depending on the types and components most prevalent in the dust, a variety of clinical airway diseases may result.

12.7 Seafood and meat processing In seafood processing, typical jobs include manual or mechanical cleaning, sorting, degutting, skinning and filleting of whitefish or cleaning, cracking, butchering and cooking of shellfish. Exposure to occasional splashes of water and substances from the outside of the animals is unavoidable. Because of the predominantly mechanical handling of most seafood species, exposure to aerosols of water and seafood parts from fast moving machines, from water-spraying nozzles or from water cutting or from sawing in frozen animals is extremely common; vapors from cooking and boiling are

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also common in some situations. The spices, brines and smoke used to conserve and add flavour to many seafood products may pose respiratory hazards if not handled properly. Other common jobs are fishmeal milling and bagging and other sorts of packing and canning. The use of high-pressure water in many cleaning jobs in the industry results in aerolization of seafood parts and cleaning agents. The seafood worker is, therefore, prone to develop different types of allergic respiratory disease (rhinoconjunctivitis, asthma and less commonly hypersensitivity pneumonitis). The proportion of workers that develop asthma depends on the species, the job tasks and the general working conditions. A seafood worker is likely to present airway symptoms only during specific seasons or periods. Many seafood species are processed only during a limited number of weeks or months every year during which the allergic reactions to them flourish. In the off-season most symptoms wane or disappear. A seafood worker with some pre-existing airways disease may well react with an increase in symptoms on every workday. The pattern of worsening can be mixed, as in Norwegian lobster production where bisulfites are commonly used as preservative agents, potentially causing specific reactions only in those who use the substance and nonspecific airway irritation in workers coincidentally standing nearby. The prevalence of occupational asthma associated with fish processing such as salmon has been reported to be 2–8%, while prevalences of almost 20% appear to be common in snow crab processing. The determinants of risk of allergy and asthma in seafood processing are poorly understood. Both crab and shrimp are mostly handled after boiling. Whereas crab is mostly handled manually, shrimp are mostly processed by aerosol-generating machinery. In contrast to crab, shrimp has not been associated with a significant asthma risk. Differences in allergenicity between species and/or unidentified differences in processing techniques may explain the differences in risk. However, any species of seafood must be considered capable of causing allergic respiratory disease if conditions are favourable. It is thus prudent to consider any seafood processing to be a potential cause of asthma. It is not unusual for seafood to be processed in small, poorly ventilated buildings not adapted for the number of diverse activities that take place or in the limited space on board fishing vessels. Much more common than the development of allergic reactions are, however, nonspecific breathing problems. Rhinitis or asthma-like symptoms often vary between days depending on the working conditions, e.g. due to the age of the fish processed, and usually recede if exposures are minimized. Ascribing the symptoms to colds is common but sometimes the employees are aware of conditions at work that seem to worsen their symptoms. Worsening of pre-existing allergic respiratory diseases is also likely to be very common. Allergic reactions cannot always be excluded despite negative skin prick test or serologic reactions to the seafood processed, as allergic reactions may develop to species that are only occasionally processed, to parasites in the seafood or to cleaning agents. Exhausts from diesel trucks used indoors or smoke from the smoking of fish are other potential respiratory hazards. Such fumes may contribute to asthma-like symptoms or worsening of pre-existing chronic bronchitis or other respiratory diseases. Jeebhay and colleagues have written an excellent review of allergic reactions in seafood processing [3]. Slaughterhouse workers are exposed to less mechanical handling and more manual butchering than seafood workers and, although they do develop respiratory allergies to

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dander and the like, they are rarely exposed to the high levels of bioaerosols generated by mechanical handling. A major exception is in the case of sawing in meat and bone. Similar to the seafood industry, meat workers may be exposed to vapors and fumes from smoking, diesel exhaust, flavouring, heating of plastic wrapping, etc. Since the first cases of ‘meat wrapper’s asthma’ were reported in 1973, sporadic reports of respiratory disease in workers exposed to heated polyvinyl chloride (PVC) products such as PVC film for the wrapping of food have been reported. The primary agent was originally reported to be phthalic anhydride, but this does not seem to be generally the case. Although PVC film has been partly replaced by polyethylene and other plastics or may be used with more care to avoid heating nowadays, irritative, allergenic and carcinogenic fumes from heated plastic may still be widespread in the food industry. Indeed, formaldehyde is released by heated wire cutting of polyethylene, the same cutting technique that causes problems with PVC products. Formaldehyde levels are usually well below levels of concern and respiratory problems caused by work in butchers and meat handling do not appear to be common. However, an excess of chronic bronchitis has been reported among female supermarket meat workers. It has been speculated that this could be due to prolonged exposure to vapors and fumes from meat wrapping and price labeling. In the meat industry, those who do develop allergic disease often have trouble in avoiding contact with the animal or product to which they react and may have to change their job.

12.8 Case 3 A 42-year-old woman without any history of allergic disease but with a life-long history of smoking consulted her family physician with complaints of cough, dyspnoea and wheeze. The symptoms had begun approximately one month earlier and were only present at or shortly after work. For two years she had been working in a fish filleting station in which she handled white fish, mostly plaice. Lung function tests after work in the doctor’s office were normal. No definite diagnosis was made and she continued to work in the same job. One month later, during an episode of coughing at work, the patient suddenly lost breath and felt pain in the right side of the thorax. A pneumothorax was detected, she was treated appropriately and kept off work for almost 2 months, during which her respiratory symptoms improved. On the very day of return to work, her respiratory difficulties reappeared, her peak expiratory flow fell from 400 to 200 L/min and eventually the diagnosis of occupational asthma was made. Serologic tests revealed increased levels of specific IgE to shrimp and plaice. It later transpired that, although her job had not changed prior to the occurrence of her symptoms, the quality of the fish had deteriorated in the months prior to her first attacks of asthma.

12.9 Bakeries The typical jobs in bakeries that cause respiratory hazards almost all include the handling of flour – from milling and handling of the flour over mixing it with other ingredients and making the dough to cleaning of the machines and the bakery. All of

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OTHER FOOD INDUSTRY

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these jobs can result in exposure to flour dust, sensitization and eventually respiratory allergies. In addition, bakers are often exposed to agents added to the flour, especially enzymes such as amylase. Spices may rarely be a cause of concern. Wheat is the dominant type of flour handled in most countries, but varying qualities of wheat as well as other types of flour may underlie differences in the risk of airway symptoms and development of allergies between bakeries in different areas of the world. To a large extent, the traditional manual handling has been replaced by mechanical handling and small bakeries have been replaced by factories in most westernized countries. Accordingly the majority of bakers and bakery workers work in industrialized or semi-industrialized settings in which exposures can be kept low if the work and cleaning are done carefully. Cleaner bakeries lead to lower exposures to grain flour dust as well as to added agents such as enzymes. Exposure to wheat allergen has generally decreased in many bakeries in recent years, as has the risk of occupational rhinitis and asthma. Still, however, bakers run the highest risk of occupational asthma with a prevalence around 10% and a prevalence of rhinitis around 20%. More than half of the bakers seeking compensation for work-related respiratory symptoms are sensitized to occupational allergens. The primary allergens in bakeries are components of wheat and rye flour proteins including enzymes, e.g. a-amylase. In some countries a surge of occupational allergies has appeared in supermarkets with small bakery sections. In westernized countries bakery sections for semi-manufactured bread are now widespread in supermarkets. Thus, exposure has been extended from beyond the traditional bakers and bakery workers. Cross-reactivity between wheat and grass can pose a diagnostic problem and it is recommended that serial peak flow measurements during and outside work periods or specific challenges be performed in order to confirm the diagnosis and give proper advice. Although there is a strong relationship between sensitization to occupational allergens and work disability, which has been confirmed in studies with specific challenges, nonspecific reactions and worsening of pre-existing asthma also occur in bakery workers.

12.10

Other food industry

Common to the production of a great variety of foods is the handling of spices. By nature spices and flavours are usually in the form of powder and may cause the release of large amounts of dust when handled. They are often handled manually even in large production facilities because they are used in small amounts compared with other ingredients that are handled mechanically. Accordingly, irritant or allergic reactions are not uncommon and may occur in response to virtually any natural spice or artificial flavour. A distinctive and serious problem has been identified in the popcorn industry in North America, where addition of flavours is more common than in Europe. Symptoms evocative of asthma or acute or chronic bronchitis are common, but may in reality reflect bronchiolitis obliterans and result in severe loss of lung function. Bronchiolitis obliterans, which is characterized by fixed airway obstruction with dry cough, dyspnea and wheeze, is easily missed even in occupations with exposures that are known as possible causative agents. An expiratory HRCT or a biopsy is required to confirm the

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diagnosis and without a suspicion of the disease the diagnosis may not be made. Mildly affected workers are likely to be diagnosed with asthma or COPD instead. Popcorn flavouring is associated with exposure to several volatile organic compounds and, although diacetyl has been identified as the probable cause, this compound may be but a proxy for one or more other compounds involved in the aetiology. A cluster of three cases of bronchiolitis obliterans in a chemical production plant in the Netherlands that produced diacetyl has strongly supported the suspicion of diacetyl as the causative agent. Vapors from cooking and boiling can often carry allergens or noxious fumes. Enzymes are not only used in bakeries but are manufactured and used in many jobs and may cause allergies. Encountering partly deteriorated foodstuff or moldy grains is not uncommon in a number of jobs, e.g. in breweries, where mold can cause HP. Handling of food packing can be a cause of exposure to several types of dust and fumes. In addition, biological material can be a problem even for those who work just with food containers and packaging. This was found in a Canadian study in which moldcontaminated bioaerosols from bottle recycling appeared to be responsible for lower respiratory symptoms such as cough, whereas dust from the broken glass was associated only with upper airway irritant symptoms.

12.11 International perspective In many economically less developed countries food production – from farming to processing – is performed with more traditional methods. This may result in less exposure due to less use of fast machinery and less work inside closed insulated buildings. Poorer working conditions and lack of access to respiratory protection, on the other hand, tend to cause high exposures. Especially when it comes to dust, the problems appear to be greater in poorer countries. As an example, grain dust unloading in developing countries is still performed under conditions that give rise to the extremely high dust levels that were observed, for example, in Canada a couple of decades ago. In dry and warm climates dusts from farming activities may themselves cause significant airway irritation. Reports indicate that prolonged exposure to poor and dusty working conditions results in chronic airway symptoms and maybe bronchitis. Poorer hygiene and storage conditions in less developed countries are bound to result in an increased risk of zoonoses, including airway infections. Severe reactions to mold toxins or the development of hypersensitive pneumonitis or allergic asthma are likely to occur as a result of degradation with mold growth on foodstuff. Respiratory symptoms are considered normal with many exposures to dust or aerosol in farming and other traditional trades where job types and the resulting exposures have changed little for generations. Many symptoms such as cough, wheeze and dyspnoea are considered annoying but not worrying because of this. Probably, many pathologic reactions to animals, crops and other foods escape the attention of doctors worldwide. Farming and food processing are considered ‘natural’ by most people and give rise to fewer worries about the health than do many modern or ‘chemical’ exposures. The increase in industrialization and size of farming operations appears to be universal and to steadily continue and to cause changes in exposures and patterns of disease. The same tendency to increase in size holds true only to a limited extent in the food industry as in

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recent years a surge in the number of micro-breweries, micro-coffee roasters and other high-quality productions has taken place in North America and Europe. With many such new, small and mixed food operations a huge potential for uncontrolled and unthought-of exposures among owners and employees has appeared – potentially causing allergic and other airway diseases in many previously unexposed people.

References 1. Linaker, C., Smedley, J. (2002) Respiratory illness in agricultural workers. Occup. Med. (Lond.) 52: 451–459. 2. Schenker, M., Christiani, D., Cormier, Y. et al. (1998) Respiratory health hazards in agriculture. Am. J. Respir. Crit Care Med. 158 (suppl): S1–S76. 3. Jeebhay, M.F., Robins, T.G., Lehrer, S.B. et al. (2001) Occupational seafood allergy: a review. Occup. Environ. Med. 58(9): 553–562.

13 Mining Robert L. Cowie University of Calgary and Alberta Health Services, Calgary, Alberta, Canada

13.1 Introduction The occupation of mining was one of the first to attract attention for its occupational diseases, with records going back to Roman times. In the tenth century miners were noted to be suffering from an illness called ‘bergsucht’ which was probably a composite illness caused by exposures to mercury, arsenic and silica and by hookworm infestation. The role of dust as a major factor in the illnesses of miners was recognized in the seventeenth century and was probably associated with the increase in respirable dust in the mines induced by the introduction of gunpowder and of primitive drilling apparatus in that century. As mines became deeper and explosives and drilling became more efficient towards the end of the nineteenth century, the effect of silica-containing dusts dominated and miners, especially those working at the rock face, became ill and died from acute silicosis and silico-tuberculosis. The life expectancy of a miner working at the rock face in mines with hard rock (quartz) was often no more than 5 years from the start of work. Since the latter half of the twentieth century, mines have been subject to regulations and laws which govern their environment and working conditions. Nevertheless in smaller mining operations and mines in industrializing countries, working conditions can be poor and the prevalence of occupational diseases high. When considering lung diseases in current or former mine workers, it is common to concentrate on mineral dust exposure such as silica, coal and asbestos, but the mine environment is complex and workers are exposed to contaminated water, gases, fumes and other particulates. This chapter deals with the topic of pneumoconiosis (mineral dust-induced lung fibrosis) and also the broad range of thoracic disorders and diseases which may be associated with mining.

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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13.2 Population at risk It is difficult to know how many people are currently employed as miners. Mining has progressively become more mechanized with a resultant reduction in the number employed in mines. Many national statistics provide data for the number of workers at risk from diseases such as silicosis and do not necessarily separate those who work in nonmining environments from those who work as miners. In the USA it has been estimated that 1.7 million workers are exposed to respirable silica in industries including mining, quarries, foundries, construction, concrete rehabilitation, masonry and agriculture. In the USA the number of coal miners has decreased from 130,000 to 100,000 over the last 20 years, while coal production has increased by 169 million to 1.15 billion tons per year. The world production of coal in 2007 was over 7 billion tons. Mines outside of USA are less mechanized and thus employ many more miners; for example, it is estimated that there are 6 million coal miners in China, which produces 2.8 billion tons of coal per year. Asbestos is still being mined, with approximately 2.4 million tons produced each year. The number of miners employed in asbestos mines is uncertain. In the USA, where asbestos mining has ceased, 1.3 million workers are currently exposed to asbestos in other occupations. In general, the number of those currently employed as miners is less relevant than the number who have worked in these occupations over the past several decades. Miningrelated occupational lung diseases, especially pneumoconioses, may first become apparent many years after cessation of exposure, and even if all mining were to stop immediately, there would be a substantial incidence of pneumoconioses and other mining-associated diseases for many decades.

13.3 The mine environment The mining environment is complex and is contributed to not only by the activities directly associated with mining, but also by a very large support system including access, ventilation, refrigeration, humidification, electrical supply and equipment, waste disposal and activities associated with exploration and development. Specific aspects of a mine environment vary according to the substance being mined and whether the mine is a surface or an underground mine. In general, underground mines have a more hazardous environment than surface mines, but substantial risks for exposure to dust and trauma exist for surface miners. Miners may be exposed not only to mineral dusts, notably crystalline silica, coal dust and asbestos, but also to general dust, diesel, radon, arsenic, mercury and other fumes and hazardous gases. Hazardous gases encountered in mining include nitrous oxides generated from explosions, welding and diesel, chlorine used for water treatment and gaseous products from other material, including cadmium, which can have a serious impact on the respiratory tract and the lungs. Microbiological agents including nontuberculous mycobacteria and parasites may be in the soil or carried into the mining environment by the water used to control dust. Mine living conditions, especially in industrializing countries, may include hostel living, which can be associated with the risk of transmissible diseases including tuberculosis, typhoid,

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meningococcal disease and pneumococcal pneumonia. Infection with HIV has become a major illness associated with mining where miners are migrant laborers separated from their families. The occupation of mining is also strongly associated with the risks of trauma and burns and of heat-associated disorders. Average geothermal gradients are 25 C per kilometer, which would translate into rock temperatures of 50 C in a modestly deep mine 1000 m below the surface. At these high rock temperatures failure of the ventilation and cooling system can cause heatrelated illnesses which may indirectly affect the respiratory tract through loss of consciousness, seizures and aspiration, while acute respiratory distress syndrome has been noted in some patients with heat stroke. Less obvious causes of illness in the mining environment include water borne diseases from the use of nonpotable water and poor toilet arrangements. Diseases in these categories include leptospirosis which can cause lung hemorrhage. Humidifier fever, which is thought to be caused by inhalation in a humidified environment of bacteria, endotoxins, fungi and protozoa in water, has not been reported in miners, but the environment is comparable with others where this disease has been prevalent. Similar exposures have also been related to hypersensitivity pneumonitis (extrinsic allergic alveolitis). Metalworking fluids, which may be aerosolized in the mining environment from drills and other machinery used in confined spaces, have also been associated with hypersensitivity pneumonitis and occupational asthma. Other materials used in mines, including methylene diphenyl diisocyanate (MDI) and other resins used in roof bolting systems, have the potential to cause occupational asthma and that diagnosis should be considered in a current or former miner with late-onset asthma. Cobalt, a component of tungsten carbide used for drills, is a recognized cause of occupational asthma and hypersensitivity pneumonitis, but is more likely to affect those who manufacture or sharpen drills than miners who use them. In general, although there are no clear data, it is appropriate to remain alert to the possibility of an association between mining and occupational asthma or hypersensitivity pneumonitis (extrinsic allergic alveolitis). Other specific respiratory illnesses associated with mining will be detailed.

13.4

Pneumoconiosis

The common pneumoconioses, silicosis, asbestosis and coal workers’ pneumoconiosis, are the best known of the occupational lung disorders associated with mining. These diseases are caused by the inhalation of respirable particles of crystalline silica (usually quartz), coal dust and asbestos fibers, and the resultant inflammatory and fibrotic reaction in the lung issue. Mine dust levels are generally well controlled at a level expected to be below that associated with pneumoconiosis, but these diseases still occur, although now they occur more frequently in nonmining settings. Even in mines where dust control levels are, on average, within the required threshold limits, new cases of pneumoconiosis continue to be reported and it has been estimated that 1% of career miners exposed to the NIOSH recommended exposure limit of 0.05 mg/m3 respirable crystalline silica, as a time-weighted average, for up to a 10 hour workday during a 40 hour working week will develop silicosis. In reality, because average dust levels can hide significantly higher exposures and because dust measuring may not be a true reflection of the working environment,

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outbreaks of pneumoconiosis are still reported. There are also some data to suggest individual susceptibility to the adverse effects of mineral dusts and a diagnosis of pneumoconiosis should not be rejected on the basis of work in an apparently wellcontrolled environment. In North America cases of pneumoconiosis in miners continue to be reported and in a recent report coal workers’ pneumoconiosis in young miners seems to be associated with work in small mines, which suggests that there might be an issue with dust control. Pneumoconiosis is often seen in older people who were exposed to mine dust at a time when dust control and recommended exposure limits were much less stringent. In those circumstances, even short periods of exposure such as pre-university or summer jobs might have produced sufficient lung dust burden. Pneumoconiosis may only become apparent years after cessation of exposure and occupational histories should not discount apparently remote work in mining. Working miners with pneumoconiosis should be encouraged to avoid further mineral dust exposure. In general, pneumoconiosis is defined and categorized by the chest radiograph. A high-resolution computerized tomogram (CT) of the chest can be used in cases of doubt, but the plain chest radiograph is usually used for surveillance and for diagnosis of pneumoconiosis. The International Labour Office produces a set of standard radiographs and an instruction manual that are widely used to establish and categorize pneumoconiosis in individuals with an appropriate occupational history.

13.4.1 Silicosis Silicosis is caused by the inhalation of dust containing crystalline silica, usually in the form of quartz. Quartz is found in many mines, notably gold mines but also in other mines including uranium, zinc, tin and copper mines and in coal mines where the coal seam is narrow and the grade of coal is high, as in anthracite. Silicosis in miners is nearly always the chronic and rarely the accelerated variety. Chronic silicosis usually becomes apparent after two or more decades of exposure, and is characterized by small nodular lung opacities which predominate in the upper lung zones (Figure 13.1). Hilar and mediastinal lymph node enlargement may not be obvious on the plain chest radiograph but is often noted on chest CT. Lymph node calcification of the eggshell variety may be present and is characteristic but not unique for silicosis. Accelerated silicosis will develop with more intense dust exposure of less than 15 years duration and also produces nodular opacities which are usually more uniformly distributed. Simple silicosis is silicosis which has not been complicated by the development of progressive massive fibrosis or by tuberculosis. Symptoms are often absent, although there may be a history of dyspnea, and there are no clinical signs associated with simple silicosis. Symptoms including dyspnea are usual in the presence of progressive massive fibrosis and the symptoms of tuberculosis do not differ from those of tuberculosis without silicosis. Uncommonly, systemic sclerosis occurs in association with exposure to silicacontaining dust with or without silicosis. More rarely, cases of vasculitis and of renal disease have been attributed to silica exposure.

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Figure 13.1 The chest radiograph (a) demonstrates an example of chronic silicosis with rounded opacities measuring between 3 mm (q) and 5 mm (r) with nodule profusion assessed by comparison with the ILO standard radiographs of 2 to 3 – 2/3 q/r. The apparently cystic lesion in the right upper mid zone was of concern regarding tuberculosis, but no suggestive lesion was seen on the CT, a representative example of which is seen in (b). The subject was assessed for tuberculosis. Sputum induced with nebulized 5% saline was negative on smear and culture for mycobacteria. Assessment for latent tuberculosis infection was done by a tuberculin skin test which measured 10 mm. This was thought to relate to his vaccination with Bacille Calmette–Guerin (BCG) as a schoolboy because an interferon g release assay was negative

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Silicosis is an indication of inadequate dust control and the discovery of a case places responsibility on the physician to notify the relevant authority in the interests of preventing others from similar exposure and to facilitate the identification of those who might already have been affected. Silicosis is a compensable disease in most jurisdictions. The presence of silicosis indicates a degree of pulmonary dysfunction which may, in part, be caused by silicosis, but may also reflect the effect of exposure to silica-containing dust to the airways with resultant obstructive pulmonary disease. Silicosis is also important as a signal of increased risk for tuberculosis, infection with nontuberculous mycobacteria and also for lung cancer. The first is the most remediable and a tuberculin skin test should be done and treatment for latent tuberculosis infection offered if the test is positive. Smoking enhances the risk associated with silicosis for obstructive lung disease, tuberculosis and for lung cancer, and smoking cessation advice should be a substantial component of the management of a smoker with silicosis. With rare exceptions, working miners with silicosis should be withdrawn from dusty work environments.

13.4.2 Asbestosis Asbestosis is lung fibrosis caused by exposure to asbestos fibers. The term is often incorrectly used to describe other asbestos-related lung and pleural diseases. Asbestosis is probably less often found in asbestos miners than in those who work with asbestos in asbestos mills and asbestos product manufacture. Asbestosis may occur from exposure to either amphibole (crocidolite, amosite) or serpentine (chrysotile) asbestos. In general the lung burden of asbestos fibers is very high in cases of asbestosis, usually of the order of 10 (for amphibole) to 30 (for chrysotile) million fibers per gram of dry lung tissue, and asbestosis generally occurs after many years of exposure, although rare cases of asbestosis after acute, short-duration exposure have been reported. Asbestosis should be distinguished from idiopathic pulmonary fibrosis but as both diseases have similar presentation with dyspnea as the dominant symptom, crackles audible at the lung bases, predominantly lower zone interstitial lung disease with fibrosis on X-ray and occasionally with finger clubbing, the distinction can be difficult. Confirmation of asbestos exposure from the history, the presence of calcified pleural plaques and pleural thickening, and the finding of asbestos (ferruginous) bodies in sputum or in bronchoalveolar lavage fluid will all assist in confirming a diagnosis of asbestosis. The pattern of pulmonary fibrosis initially centred around the bronchioles in asbestosis and the presence of asbestos bodies may help establish the diagnosis in open lung biopsy or autopsy samples. Asbestosis is associated with a predominantly restrictive pattern of lung dysfunction, but exposure to asbestos-containing dust may also cause airway disease with features of obstruction on lung function testing. It is strongly associated with lung cancer and especially so in ex- and current smokers. There is no evidence to suggest that tuberculosis or nontuberculous mycobacterial infections are more common in those with asbestosis. Progressive massive fibrosis is not associated with asbestosis. The occurrence of asbestosis should be reported to the relevant authority for the reasons indicated above under silicosis and to facilitate compensation for the affected

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person. Smoking cessation and, in the several countries where asbestos mining continues, avoidance of further asbestos exposure are important interventions in patients with asbestosis. There are currently no data to support routine screening for lung cancer or malignant mesothelioma in patients with asbestosis, although the risks of these malignancies are high and any suggestive new development such as chest pain, hemoptysis or new onset of clubbing should indicate further assessment. There is no evidence that any intervention alters the course of asbestosis, which will generally progress due to the ongoing influence of asbestos fibers already in the lung.

13.4.3 Coal workers’ pneumoconiosis Coal workers’ pneumoconiosis (CWP) is found predominantly in coal miners (as opposed to others who work with coal) and, although the population of coal miners has decreased with mechanization of coal mining, coal production continues to rise. Globally, coal is the dominant energy source for electricity production. The increase in mechanization has increased the levels of respirable coal dust and new cases of CWP continue to be reported. CWP is caused by exposure to coal and is usually characterized by small nodules, often less well defined than those of silicosis but also occurring predominantly in the upper lung zones. Coal is much less fibrogenic than silica and CWP becomes apparent only after very large lung dust burdens have been achieved. Workers with CWP may be asymptomatic and there are no characteristic clinical findings. The chest radiograph is insensitive to the diagnosis of CWP which even when advanced may show only small (<1.5 mm) nodules and lesser degrees of the disease might require high-resolution CT for confirmation. The presence of larger lung nodules often reflects associated silicosis, which may be seen in miners of high-grade coal, in mines where there is a high proportion of quartz bordering the coal seam and in miners who work in the haulage and development ends of the mine where drilling and roof-bolting produce silicacontaining dust. CWP may be complicated by the development of the large nodules of progressive massive fibrosis, which seems to be more common in certain areas and certain mines. In the absence of silicosis, the risk of tuberculosis is not increased in CWP, nor is there evidence of an increased risk for lung cancer. Coal miners with CWP may develop large nodules in their lungs associated with elevated levels of circulating rheumatoid factor – Caplan’s syndrome. This has also been reported in miners with silicosis but is more commonly associated with CWP. Exposure to coal dust has been shown to cause chronic bronchitis, which commonly affects coal miners, and chronic obstructive pulmonary disease (COPD). In this context, coal miners should be encouraged not to smoke. Cases of CWP should be reported to the relevant authority and CWP is generally compensable.

13.4.4 Other pneumoconioses Chronic beryllium disease is a distinctive, sarcoidosis-like lung disease which has not been described in miners who mine the ore, mainly beryl and bertrandite,

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from which beryllium is extracted. Dust in tin, iron and barium mines is not considered to be fibrogenic unless there is a high proportion of quartz in the mine ore. Miners in these mines may develop lung nodules but, respectively, stannosis, siderosis and baritosis are considered to be benign pneumoconioses with no recognized health consequences. The mining of nonasbestos silicates such as mica, kaolin and talc is not usually associated with pneumoconiosis. There may, however, be contamination with asbestos as in the case of the mica, vermiculite, mined in Montana, or with silica which may contaminate talc or kaolin. In the absence of contamination, interstitial fibrosis and the presence of nodules have been reported in talc and kaolin miners, but are rarely associated with complications such as progressive massive fibrosis. Many other pneumoconioses turn out to be silicosis in a newly described setting.

13.5 Obstructive pulmonary disease Obstructive pulmonary disease in miners was historically attributed to tobacco smoking, but it is now recognized that work in a dusty environment can cause chronic bronchitis and obstructive pulmonary disease. There is a nonspecific airway reaction to an environment characterized by dust, fumes and gases, and silica- and coal-containing dusts may be especially able to induce an airway response. Chronic bronchitis, simply defined as a chronic cough productive of sputum, occurs in many miners with figures ranging between 18 and 51% and, although this symptom is more common in miners who smoke, it is reported in up to 20% of nonsmoking miners. The characteristics of obstructive pulmonary disease in miners do not differ substantially from those of tobacco smoke-induced disease, and both emphysema and obstructive bronchitis are found in the occupational disease. In some studies, the effect of one year of exposure to mine dust has been considered comparable to one pack-year of cigarette smoking and this may be especially true in a mining environment where pneumoconiosis has been observed. It is likely that obstructive pulmonary disease occurs more commonly in a population of miners than does pneumoconiosis and, although the degree of obstruction is not, on average, severe, there will be those who will suffer severe obstruction as there will be others with minimal or no obstruction. In some jurisdictions, this effect of the mining environment is acknowledged and miners may be compensated for obstructive pulmonary disease. The case for occupational obstructive pulmonary disease is much easier to establish in those who have never smoked, but it should be possible, even in smokers, to calculate some attribution to the work environment. The management of occupational obstructive pulmonary disease is similar to that of usual COPD with advice to stop smoking, appropriate pharmaceutical and nonpharmaceutical management and consideration for the miner’s removal from the dusty working environment. A word of caution is necessary when assessing lung function in miners or ex-miners – miners, especially underground miners who work at the rock face, tend to be self-selected for their good physique and excellent lung function. This characteristic can obscure even significant loss of lung function when their lung function is compared with that of a standard reference population rather than with a working population of miners or with the subject’s own baseline measurements.

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Tuberculosis and nontuberculous mycobacterial diseases

Occupational exposure to silica-containing dust and, in particular, silicosis greatly increases the risks for mycobacterial disease. Whether miners develop tuberculosis or one of the nontuberculous mycobacterial (NTM) diseases is largely dependent upon the prevalence of tuberculosis in their general population. The risks for developing tuberculosis in miners exposed to silica dust who do not have radiologic evidence of silicosis are elevated above that of the general population and the risks rise further directly in proportion to the profusion of lung nodules in those with silicosis. It has been estimated that miners with category three nodule profusion silicosis have a risk for tuberculosis which is six times higher than that of miners from the same working population who do not have silicosis. The relevance of this observation is that treatment for latent tuberculosis infection (tuberculosis chemoprophylaxis) should be offered to silica-dust exposed miners, especially those with radiologic silicosis, with positive tuberculin skin tests or with positive interferon g release assays. The risks for extrapulmonary tuberculosis are also increased in these miners. Their risk for NTM diseases is increased and that diagnosis should be considered in populations where tuberculosis is uncommon and when radiologic features are atypical or there is a poor response to antituberculosis treatment. Mycobacterium kansasii and M. scrofulaceum are thought to be common NTMs in dusty environments. As noted below, tobacco smoking is associated with an additional risk for tuberculosis, which can be measured even in miners with silicosis The diagnosis of tuberculosis or of NTM lung disease is made using the same techniques which apply in general. The culture of mycobacteria from sputum, which may be induced by inhaling hypertonic saline or from bronchial washings, will generally establish a diagnosis of pulmonary tuberculosis or of NTM pulmonary disease. Appropriate samples should be obtained when extra-pulmonary tuberculosis is suspected. Care should be taken to exclude tuberculosis before offering treatment for latent tuberculosis infection.

13.7

Malignant disease

13.7.1 Lung cancer Crystalline silica and asbestos fibers are recognized carcinogens. Amphibole (crocidolite, tremolite and amosite) asbestos has greater carcinogenic potential than serpentine (chrysotile) asbestos. The risk for lung cancer in the absence of pneumoconiosis is recognized with asbestos exposure, but the relationship with silica dust exposure and lung cancer is less clear in the absence of silicosis. There is no association between coal workers’ pneumoconiosis and lung cancer and earlier reports of an association with stomach cancer have not been confirmed. A risk of lung cancer is recognized in uranium mining and relates to the associated exposure to radon. Radon exposure is thought to be the likely cause for the association between hematite mining and lung cancer whilst silica exposure may also contribute in that setting. There are data that suggest that other exposures in mining including diesel, nickel and arsenic may also contribute to an

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increased risk of malignant disease, notably lung cancer, in miners. Although beryllium and nickel are recognized carcinogens, it is not thought that miners are at risk for lung cancer from these agents.

13.7.2 Other malignancies Asbestos exposure is the established cause of malignant mesothelioma, which usually involves the pleura but may also arise in the peritoneum and, rarely, in the pericardium. Malignant mesothelioma has a long latency period with cases presenting four decades or more after asbestos exposure. Asbestos has been associated with cancer in other sites, including larynx, oesophagus, stomach, colon, pancreas, kidney and ovaries, but the data are either poor or, at best, inconclusive.

13.8 Pleural disease Although silicosis has been associated with pleural thickening and plaques, it is with asbestos that most pleural disorders are associated. Pleural plaques are the most common abnormality associated with asbestos mining (Figure 13.2). These areas of thickened parietal pleura are more common in the lower zones, especially the diaphragmatic pleura, and characteristically calcify. Pleural plaques may develop several years after relatively short periods of exposure and, when typical, are usually a reliable indication of previous exposure to asbestos. Pleural plaques carry the risks associated with exposure to asbestos, including pleural and pulmonary malignancies and pulmonary fibrosis. In addition to pleural plaques, which involve the parietal pleura, asbestos miners may develop pleurisy, which characteristically involves the visceral pleura and may be unilateral or bilateral. This visceral pleurisy may be associated with a pleural effusion which is generally exudative and often bloody. Pleural effusions often develop within two decades of exposure and need to be distinguished from other causes of pleural effusion, including mesothelioma. Visceral pleural asbestos disease is often manifest by pleural thickening and may be associated with so-called rounded atelectasis, which needs to be distinguished from other lung mass lesions including cancer.

13.9 Connective tissue and renal diseases The prevalence of connective tissue diseases is increased in miners with the risk for rheumatoid arthritis increased in coal miners with CWP and scleroderma in miners exposed to silica-containing dust. Other connective tissue disorders such as lupus erythematosis have been reported in accelerated and acute silicosis, which are now rarely reported in miners. There are several reports which support an association between silica exposure and silicosis with vasculitis and renal disease, notably with antineutrophil cytoplasmic autoantibody (ANCA).

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Figure 13.2 The chest radiograph (a) shows extensive calcified pleural plaques. On the CT (b) a calcified plaque can be seen extending two thirds of the way around the parietal pleura on the right and on the diaphragmatic pleura on the left. No interstitial disease (asbestosis) was apparent on the lung windows of the CT (not shown)

13.10

Mining and tobacco smoking

Silica-dust and asbestos exposure are associated with increased risk for lung cancer and this risk is enhanced by exposure to radon, which may occur in any underground

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mine. Miners who smoke are, at least additively, at increased risk for lung cancer. Work in any mine is associated with increased dust levels, which causes chronic bronchitis and measurable, dose-dependent COPD. This risk for COPD is greatly enhanced when miners are also tobacco smokers. It is less well-known that tobacco smoking increases the risk for tuberculosis in all miners, but this is especially relevant in miners exposed to silica-containing dust. For all of these reasons, smoking cessation programs should be widely available for miners and consideration should be given to strong incentive programs to encourage miners to stop smoking.

13.11 Acute lung and airway inhalational injury A variety of syndromes with acute lung inhalational injury have been reported from exposures in the mine environment. Fires underground can cause direct thermal injury to the upper and lower airway and major burns may also lead to the acute respiratory distress syndrome. Fires may cause carbon monoxide poisoning in miners and may release phosgene from the combustion of hydrocarbons. Other and often delayed respiratory syndromes occur in miners exposed to gases and fumes, including nitrous oxides, chlorine and cadmium. Cadmium fumes are reported in the mine environment as an example of many of the maintenance and development activities which are part of a working mine. Roof bolts in the mine haulage and other metal structures may be cadmium-coated and cutting or welding these can produce cadmium fumes. Inhalation of cadmium fumes induces an acute lung injury which may have a delayed onset of up to 24 hours and which can often be rapidly fatal. Nitrous fumes, notably nitrogen dioxide, are released after the use of explosives and also from welding and from diesel engines. These gases have an odor which should be detectable but the onset of symptoms may be delayed for up to 24 hours after exposure. The affected miner usually complains of dyspnea and coughing and a chest radiograph may show a picture of noncardiogenic pulmonary edema. Treatment includes oxygen and, often, corticosteroids. Recovery is common but a small proportion develops progressive and fatal respiratory failure. A proportion of those who recover from the initial illness later present with new onset dyspnea and coughing which might indicate the development of bronchiolitis. This was formerly called obliterative bronchiolitis but now has been separated into proliferative bronchiolitis and constrictive bronchiolitis. This third phase, which follows initial pulmonary edema and then recovery, may resolve or produce progressive disease. The role of corticosteroid therapy in determining the outcome is uncertain. Obliterative bronchiolitis from toxic fume exposure is not thought to occur without the initial acute illness. Chlorine would not ordinarily be associated with mining, but the treatment of mine water which is used for dust control and also for consumption may be associated with the release of chlorine gas in the mine. Chlorine gas may produce an illness similar to that caused by nitrogen dioxide but, being more soluble, is more likely to produce immediate and predominantly upper and central airway irritation and inflammation. Phosgene may be produced in mine fires when plastics have been subjected to high temperatures. The effect on the respiratory system is similar to that of nitrogen dioxide.

FURTHER READING

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Trauma

Trauma from rock falls and other injuries is common in mining. The lungs may be affected by direct chest trauma, which can cause a flail chest injury, lung contusion or pleural injury with a hemothorax or pneumothorax. Indirect lung injury by fat embolism after long bone fractures may be overlooked and can produce serious respiratory failure. In many instances in underground mines medical attention is delayed and the opportunity for additional trauma exists as injured miners need to be removed from difficult and often damaged areas of the mine and then transported several kilometers underground to the main access shaft.

13.13

Conclusion

The mine environment is complex and this is reflected in the wide range of lung and other diseases which might be observed in current and former miners. This chapter has provided a review of lung diseases in miners and readers are referred to some of the listed reference works for additional information and detail.

Further reading American Thoracic Society (1997) Adverse effects of crystalline silica exposure. Am. J. Respir. Crit. Care Med. 155(2): 761–765. American Thoracic Society (2003) Occupational contribution to the burden of airway disease. Am. J. Respir. Crit. Care Med. 167(5): 787–797. American Thoracic Society (2004) Diagnosis and initial management of nonmalignant diseases related to asbestos. Am. J. Respir. Crit. Care Med. 170(6): 691–715. Antao, V.C., Petsonk, E.L., Sokolow, L.Z., Wolfe, A.L., Pinheiro, G.A., Hale, J.M. et al. (2005) Rapidly progressive coal workers’ pneumoconiosis in the United States: geographic clustering and other factors. Occup. Environ. Med. 62(10): 670–674. Becklake, M.R. (1985) Chronic airflow limitation: its relationship to work in dusty occupations. Chest 88(4): 608–617. Blanc, P.D., Toren, K. (2007) Occupation in chronic obstructive pulmonary disease and chronic bronchitis: an update. Int. J. Tuberc. Lung Dis. 11(3): 251–257. Cowie, R.L., Mabena, S.K. (1991) Silicosis, chronic airflow limitation, and chronic bronchitis in South African gold miners. Am. Rev. Respir. Dis. 143(1): 80–84. Cowie, R.L., Murray, J., Becklake, M. (2010) Pneumoconioses and other mineral-dust-related diseases. In Murray and Nadel’s Textbook of Respiratory Medicine. 5th edn, (eds Mason, R.J., Broadus, V.C., Martin, T., King, T., Schraufnagel, D., Murray, J.F., Nadel, J.A). Philadelphia: Elsevier Saunders. International Labour Office (1997) Encyclopedia of Occupational Health and Safety. ( 4th edn). ILO: Geneva. International Labour Office (2003) Guidelines for the Use of the ILO International Classification of Radiographs of Pneumoconioses Ed 2000. ILO: Geneva. NIOSH (1995) Occupational Exposure to Respirable Coal Mine Dust. US Department of Health and Human Services, Public Health Services, Centers for Disease Control and Prevention: Cincinnati, OH.

14 Metal industry and related jobs (including welding) William S. Beckett Harvard Medical School and Mount Auburn Hospital, MA, USA

14.1 Introduction Work in metal industries results in exposures both to metals and to nonmetal materials. Respiratory effects of oil-containing solutions known as metal working fluids, which are widely used in shaping and cutting metals with tools, are discussed in detail in Chapter 16 by Rosenman, on the automobile industry.

14.2

Metals defined

Metals are elements. There are approximately 91 distinct metals in the periodic table. Each one may have a number of different valences and oxidation states. The different forms (i.e. oxidation states) may markedly affect metals’ effects on the lungs and other organs. Exposure in the workplace is usually to aerosols (small metal particles), and in some cases vapor, such as mercury, which is readily evaporated at room temperature. As elements, metals cannot be broken down or converted to other substances under usual conditions, so they are environmentally persistent. In usual practice, metals cannot be destroyed, but only moved from one place to another or combined into compounds. Mixtures made from two or more metals are alloys. Even after being burned, buried or recycled, metals can continue to affect the health of workers and the public. Metals can also be easily measured in workplace air by industrial hygienists, both by total weight and by particle size-specific fractions. Measurement of the concentration of certain metals in urine or blood may be a useful indicator of recent exposures, either environmental or occupational, and testing is Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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readily available from certified laboratories. Some metals which are less soluble in biological fluids are persistent in the lungs and other organs, and may be measured in biopsy or autopsy specimens.

14.3 Workplace hazards from metals While all substances are toxic to the lungs in sufficiently high doses, the large amounts of metals used widely in industry, and their dose–response toxicity, have identified beryllium and cobalt as frequent causes of serious occupational lung disease. Most metals are solid at room temperature and are converted to gas only at very high temperatures. When metal gas condenses in air, small particles of the metals combined with oxygen (metal oxide fume) result. Freshly formed fume particles are small enough to be inhaled and deposited in small airways and alveoli. Such small particles agglomerate rapidly in air to form larger particles. If the patient worked close to the source of fume formation, clinically significant amounts of metal may have been inhaled as fume particles. For this reason, an occupational exposure history of prolonged work with metals exposed to very high temperatures, or to very high mechanical forces, is suggestive of a workplace where larger amounts of metal inhalation may have occurred.

14.4 Metal industry processes Respiratory exposure to metals may occur in each of the common processes of the metal industry. Mining is the process of removing metals from their natural site of origin in the earth. The more significant risk of lung disease for metal miners may be from silica. Silica is the most common compound in the earth’s surface, and miners must often dig through silica-containing rock to extract the metal ore they seek. Inhaled crystalline silica may cause chronic mucous expectoration (chronic bronchitis), chronic airflow obstruction, nodular interstitial lung disease with pleural thickening, silicaproteinosis (a form of pulmonary alveolar proteinosis) and enlarged pulmonary and systemic lymph nodes. Silicosis predisposes to the development of active tuberculosis and also to lung cancer. Silica may also be a mixed exposure, with the metal ore being mined. Mixed dust pneumoconiosis closely resembles silicosis, but is distinguished by the predominance of nonsilica dust fibrotic lesions over silicotic nodules. This may occur in metal miners and others with mixed mineral dust exposure. Miners may also develop systemic medical toxicity from mercury, lead and manganese when exposures are of sufficient intensity and duration.

14.4.1 Metal ore processing Metal ores removed from the earth are often mixtures of the metal with other minerals which must be separated. Exposure to the metal itself, or to other metals present in the ore mined, may occur during these processes. Milling refers to the processing of metal ores (mixtures of metals with other minerals) to separate the component desired, and often involves mechanical crushing

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and heating the ore. Metal ore is separated from other mined minerals in a mill. Smelting is the process by which a metal is separated from its ore by using a chemical reducing agent to change the oxidation state of the metal. In a foundry metal is heated to a liquid form, and poured into a mold to form it into useful shapes. Silica sand is often used for this process and may be a hazardous source of silica dust exposure. Silica sand or other granular molding materials may contain a binder made with isocyanates or furans, which can cause respiratory sensitization and asthma. Forging deforms metal to a given size and shape using hot or cold processes. Grinding, polishing and buffing remove excess metal, or smooth and shape the metal surfaces, and may lead to inhalation exposures of materials used to accomplish these (such as grinding wheels) as well as the metal being shaped. Metal machining processes further shape the metal parts using a variety of cutting, drilling and surfacing tools, often with the use of metalworking fluids to cool and lubricate the process. These processes may produce an aerosol of metal particles and the aerosolized metalworking fluids may serve as a vehicle for metal particles or metal in solution, as well as their own inhalation effects. Electroplating produces a thin layer of metal on another surface by a process of electrical-chemical bonding of metal in a tank with metal salt solutions. Galvanization coats a thin layer of zinc oxide on steel either by an electroplating process or by dipping steel in molten zinc. Metals may also be applied to surfaces by the processes of combustion, detonation, plasma, and electric arc spraying, with resulting exposure to metal fume. Exposure to metals may also occur when products are scrapped, incinerated, reclaimed or recycled. Those performing these processes may have no way of knowing which metals they are exposed to. Inhalation exposure may occur in many intermediary processes using metals, and skin exposure may be important to the development of beryllium lung disease.

14.4.2 Steel structures, ship building, and shipbreaking Many large buildings and all ships are steel structures built to withstand extreme mechanical stress and a relentlessly oxidizing environment. Steel structures also include bridges, land-based liquid holding tanks, submarines, oil drilling platforms, airplanes and trains. Making such structures results in steel and other metal exposures both in producing the parts and in assembling them. Such structures are commonly built using welding and a variety of other assembly techniques. When these structures finish their useful life, they are torn down and the metal often cut apart for metal recycling using high-temperature torches. Exposures again occur in these processes, often in circumstances where the other constituents of the structures are unknown.

14.5

Pulmonary responses to metals

Metals cause a broad spectrum of common respiratory conditions – rhinosinusitis, nasal septal perforation, laryngeal disease, acute and chronic bronchitis, asthma, emphysema, pulmonary fibrosis, granulomatous lung disease (chronic beryllium disease) and lung cancer (Table 14.1). Most cases of metal-induced lung diseases are nonspecific (i.e. no pathological characteristics identifying them as occupationally

Airway hyperresponsiveness Loss of alveolar gas exhange surface area

Asthma

Other lung diseases

Lung cancer

Acute toxic pneumonitis

Pulmonary Fibrosis

Granulomatous interstitial lung disease (chronic beryllium disease), may include hilar/ mediastinal adenopathy, skin, liver disease

Lung parenchymal remodeling Acute lung injury

Nasal mucosal irritation Ischemic necrosis of nasal mucosa

Rhinosinusitis Nasal ulceration and nasal -septum perforation

Emphysema COPD

Pathophysiology

Lung disease

Table 14.1 Listing of selected metals and respiratory effects

Increased interstitial markings, lymph node enlargement

Increased interstitial markings Normal or interstitial infiltrates

Normal or hypodense

Normal or hyperinflation

Negative Negative

Chest radiograph

May be clinically indistinguishable from sarcoidosis without obtaining beryllium lymphocyte transformation test or lung tissue beryllium analysis

Not associated with occasional or minor exposure

Comment

Hexavalent chromium, beryllium Beryllium

Beryllium

Cobalt (hard metal)

Cadmium

Platinum salts Arsenic, chromic acid, chromates, copper dusts and mists Platinum, cobalt

Selected metals

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14.6

BERYLLIUM: LUNG AND SYSTEMIC EFFECTS

195

induced). Metal dust might be one of the environmental factors predisposing to the development of fibrosing alveolitis (usual interstitial pneumonia, idiopathic pulmonary fibrosis). There are also some metal-induced lung diseases which have distinctive characteristics (see chronic beryllium disease and giant cell interstitial pneumonia, below). Most metal particles can cause chronic bronchitis if particles small enough to penetrate to the large bronchi are inhaled with sufficiently intense and prolonged exposure. Clinically important toxicity to other organ systems may occur from metals which pass into the blood after being inhaled into the lungs. Lead affects peripheral nerves, brain and bone marrow; mercury affects peripheral nerves, brain and kidneys; cadmium is toxic particularly to kidneys; arsenic to the gastrointestinal system, peripheral nerves and skin; and manganese affects brain. Many metals, when inhaled in particle sizes small enough to be deposited and retained in the lungs, can cause dust macules, which are collections of dust and dustladen macrophages around small airways and vessels. If unaccompanied by a reaction of the lungs, these macules may be entirely asymptomatic, although they may create a pattern of densities on chest radiographs or other lung images. The prominence of lesions seen on chest radiograph is related in part to the radiodensity of the dust, so that some macules with no associated lung fibrosis but high intrinsic radiodensity can produce a strikingly abnormal radiograph with little or no functional loss. Inhaled barium dust is one such metal which produces this result. Other metals and dusts may cause significant loss of lung function with much less prominent chest radiograph abnormalities. Silica is associated with increased risk for collagen vascular disease. Use of complete pulmonary function testing, including spirometry, lung volumes and diffusing capacity, is the most accurate means of assessing residual lung function. Two specific metals and an important metal processes deserve special mention as causes of serious and sometimes characteristic lung disease.

14.6

Beryllium: lung and systemic effects

The metal beryllium is much lighter than aluminum, stiffer than steel, has a high melting point and will hold its shape over a wide temperature range. It may be used where there is need for a combination of good electrical conductivity, high strength, wear resistance, high fatigue strength and nonmagnetic and nonsparking properties. It has an unusual property of reflecting neutrons emitted from plutonium, which makes beryllium an essential component of nuclear weapons and nuclear reactors. Beryllium oxide is used to make light, strong industrial ceramic insulators. Beryllium is often alloyed with copper, aluminum and other metals. The metal has many applications in industrial and consumer product manufacturing. Selected common applications are electronic connectors, contact springs, switches, relays, metal diaphragms, friction wear parts, bushings and bearings, actuators, welding electrodes and plastic injection mold components. Major beryllium metal production facilities have existed in recent years in the USA, Khazakstan and China. Major manufacturing facilities for beryllium and berylliumalloys are located in the USA, Japan and France, and chronic beryllium disease has been

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well described in manufacturing workers. The beryllium metal, oxide and alloys produced are utilized worldwide in a large variety of applications including military and consumer electronics, cell phones and microprocessors to name only a few. Clinically significant exposure to beryllium may occur when processing beryllium alloy into consumer products (such as when drilling, grinding, or machining the alloy) or when recycling or reclaiming metals containing beryllium using a furnace to melt them. Exposure may also occur when welding beryllium metal using berylliumcontaining welding rods. When inhaled into the lungs beryllium can cause a chronic, T-cell mediated granulomatous disease involving lung, lymph nodes and sometimes skin, liver and other organs, that may have its clinical onset many years after first occupational exposure to beryllium dust. This usually slowly progressing condition is known as chronic beryllium disease (also known as berylliosis). A minority of workers exposed to beryllium develop chronic beryllium disease, and there is an important interaction between certain gene polymorphisms and exposure to the metal with regard to risk for disease. Because beryllium is expensive in comparison with other metals, recognized cases of beryllium disease have clustered around identified industrial facilities making beryllium metal or products from beryllium metal, nuclear weapons manufacturing facilities and operations recycling metal-containing electronic equipment. Because of the difficulty in diagnosis, it is difficult to estimate how many cases of beryllium disease occur annually. Investigators in Germany and Israel concluded that 13% of their patients with a previous diagnosis of sarcoidosis who were tested had chronic beryllium disease based on positive lymphocyte transformation tests for beryllium. However, worldwide use of beryllium has increased over time, suggesting that disease will continue to occur. Testing of exposed industrial groups with the beryllium lymphocyte transformation test can identify individuals with T-lymphocytes sensitized to beryllium even when they have no manifestations of disease. Clinical follow-up of these individuals over several years shows that some will go on to develop chronic beryllium disease, although it is not yet known whether all such individuals, or what proportion of those with sensitization, would develop disease with sufficient follow-up. Thus, asymptomatic individuals with positive beryllium lymphocyte transformation tests are at risk for developing chronic beryllium disease. For patients with progressive clinical disease, some experts recommend lifelong systemic corticosteroid therapy (e.g. prednisone, 0.5–0.6 mg/kg per day in divided doses) to prevent or slow progression of disease. Methotrexate has been used as a steroid-sparing agent. Controlled trials are not available to address the question of whether corticosteroid or methotrexate treatment improves prognosis or survival. Patients with chronic beryllium disease often present as adults with hilar or mediastinal adenopathy and patchy interstitial lung disease which is clinically recognized years after first exposure – a picture that usually cannot be distinguished from sarcoidosis based on standard clinical approaches. Lung biopsy shows noncaseating granulomas comparable to those of sarcoidosis. Patients with chronic beryllium disease often receive the diagnosis of sarcoidosis before the correct diganosis is made. Chronic beryllium disease can be distinguished by a history of beryllium exposure with an appropriate time interval of latency, and positive beryllium lymphocyte transformation tests of peripheral blood or bronchoalveolar lavage fluid. Clinical lymphocyte transformation testing is available from several reference laboratories in Europe and North

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America. Quantitation of the weight of beryllium metal per gram of ashed lung tissue from a large biopsy or autopsy specimen was used to confirm diagnosis before the availability of lymphocyte transformation testing. Inhalation of beryllium fume from heating the metal to high temperatures can cause severe or fatal acute toxic pneumonitis.

14.7

Cobalt disease (hard metal pulmonary disease)

Cobalt causes lung disease alone and when combined with tungsten in a preparation known as ‘hard metal’, composed of sintered tungsten carbide with cobalt. (Sintering is a process of combining metal powders under pressure into a hardened product.) Cobalt may cause occupational asthma or an acute or chronic interstitial lung disease which may have a distinct pathology originally described as giant cell interstitial pneumonitis. The onset of interstitial fibrotic lung disease may be while working with the metal, or with a period of latency after exposure. Pulmonary function testing may show a restrictive, obstructive or mixed pattern usually with reduced diffusing capacity. The course of the interstitial lung disease is variable, sometimes with early or late remission, although sometimes with progression to respiratory failure and death. As with beryllium disease, cases of hard metal or cobalt lung disease are sporadic among those exposed at work, but no gene polymorphisms associated with increased or decreased susceptibility have been identified.

14.8

Welding-related lung disease

Welding is defined as any process of joining pieces of metal that have been made soft or liquid by heat or pressure. The occupation of welder is a skilled and relatively highpaying one that is growing rapidly worldwide to meet the need for more large, strong, fabricated structures. Although welding techniques are numerous, many of them produce significant lung exposures, including the most common one, manual metal arc welding. Typically in this process the welder must closely watch the weld from a distance of only 50 cm (Figure 14.1), and thus can easily inhale the welding plume given off by the process. The eye protection necessary to prevent damage from light and particles is not sufficient to protect from inhalation exposures, and welders often do not wear separate respiratory protection. Inhalation of the gas and particle components of the welding plume is thus likely unless measures are taken to capture or divert the plume away from the welder’s breathing air. Spot welding is a mechanized process in which the period of welding is brief, and the operator of the welding machine may be at a greater distance from the source of the plume. The welding plume is a mixture of gases and metal fume the nature of which is related to the base metal being welded, the kind of welding consumables used, the presence of a shielding gas, and other variables (Table 14.2). Since welding is performed with a wide range of materials, the range of exposures to metals and other substances in the welding trade is very broad, and includes most of the metals mentioned in this chapter. The most common processes are performed with steel filler material on steel, and thus the most frequent inhalation exposure is to fine iron oxide

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Figure 14.1 Process of manual metal arc welding. Manual metal arc welding, the most widely used welding technology, uses an electric arc across an air gap between base metal (the material being joined together, here labeled ‘work’) and filler metal (the material used to make the electrode). The welder must usually visualize the process, through ultraviolet-filtering lenses to protect the eyes, from arm’s-length to assure the quality of the weld. The process creates the welding plume consisting of vaporized metal which rapidly forms fine metal-oxide fume particles, and gases. The largest metal component of the plume comes from the filler metal making up the welding ‘stick’ or filler ribbon, here labeled ‘electrode’. The components of the plume are usually multiple and complex. Heat from welding can convert nitrogen-containing materials coating the metal, or nitrogen in air, to nitrogen oxides, and ultraviolet light from the arc can convert oxygen to ozone. Exposures to these gases in enclosed spaces can be sufficient to cause acute lung injury. Local exhaust ventilation is usually needed to control exposures indoors. [Inset] To make a stronger weld without oxidation of the metal, welding processes exclude oxygen from the point of joining metal. Manual metal arc welding electrodes are coated with materials which create a gaseous shielding atmosphere as the electrode is consumed, keeping oxygen out. Droplets of molten metal from the electrode follow the path of electrons from electrode to the work (the arc stream) filling the weld with metal derived from the electrode

Table 14.2

Common inhalation exposures in manual metal arc weldinga

Nitrogen oxide Nitrogen dioxide Ozone Iron oxide Fluorides Nickel (in stainless steel) Chromium VI (hexavalent chromium, in stainless steel) Manganese a

Majority of metal fume comes from stick/electrode and not base metal.

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Table 14.3 Respiratory health effects of welding Acute Metal fume fever Toxic and hypersensitivity pneumonitis Infectious pneumonia (?) Chronic Chronic bronchitis Asthma Lung function changes Lung cancer

fume. Depending on the welding process and the ventilation conditions, the airborne exposures during welding can be very high, or very low. In an enclosed space, standards for particle exposures may be exceeded within a few minutes. Welders may also be exposed to metal particles when they grind the weld to smooth the surface, when they burn through paints and coatings containing metals (such as lead), or from bystander exposures to other processes. In the most common welding processes, metal exposure may come from the base metal, the metal coating on the work piece, the electrode and fluxes, but the majority of the metal inhalation exposure comes from the welding electrode or wire. It is thus important to know the constituents of the electrode (which are often complex) as well as of the base metal. Although most welders appear able to work in their profession without serious health effects, welders nonetheless may consult respiratory physicians. Respiratory health effects of welding are summarized in Table 14.3.

14.8.1 Metal fume fever The most frequent acute presentation of respiratory inhalation in welders may be metal fume fever, a systemic febrile response following inhalation of freshly generated zinc oxide fume, often resulting from welding galvanized (zinc coated) steel. The chest radiograph is clear in most instances, there is no oxygen desaturation, there may be an elevated white blood cell count and the welder recovers within hours. Antipyretics may speed resolution of fever.

14.8.2 Acute toxic pneumonitis More seriously, welders may present acutely with toxic pneumonitis from inhalation of cadmium, beryllium or manganese as well as nitrogen oxides, ozone, phosgene or phosphine. Clinically this may initially have the appearance of infectious pneumonia or acute lung injury (acute respiratory distress syndrome), with oxygen desaturation, pulmonary infiltrates and pleural effusions, elevated white blood count and even the need for mechanical ventilation. Fatal cases have been reported. Although untested in clinical trials, consideration may be given to acute treatment with systemic corticosteroids, as well as with oxygen and bronchodilators as needed.

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Limited studies also suggest that industrial workers exposed to metal particles, including welders, may be at higher risk for developing acute bacterial pneumonia, for which antibiotics are essential.

14.8.3 Chronic bronchitis The most frequent chronic respiratory condition in welders is chronic bronchitis, as defined by productive cough for four or more days of the week, three or more months per year, for two consecutive years. Most but not all studies of welders evaluating this have found an excess of chronic bronchitis in actively working welders compared with nonwelders, and higher rates of chronic bronchitis in smokers who weld than in smokers who do not weld. Some studies have also found higher rates of current cough among welders who do not meet the case definition for chronic bronchitis.

14.8.4 Asthma Asthma might occur in welders due to exposure to a specific sensitizing substance, a single severe acute exposure (reactive airways dysfunction syndrome or asthma without latency), and possibly (though this remains controversial) from chronic high-level irritant exposure. Given the large number of people employed as welders over the last century, the number of case reports of occupational asthma are strikingly few. Nonetheless, case reports confirmed by controlled specific inhalation challenge are convincing. A prospective study found that a higher rate of methacholine reactivity could be found in young shipyard welders than controls, adjusting for atopy, age and smoking status. Based on this finding, these authors estimated a 1% incidence of asthma among their shipyard welders in the UK.

14.8.5 Interstitial lung disease Very heavy and prolonged inhalation of iron oxide fume during welding has resulted in a nodular pneumoconiosis, welders’ siderosis, a general term for iron overloading in tissue which in this case involves lung. Radiographically, this appears as fine nodular lesions, and pathologically dust macules of iron oxide are found surrounding small airways and vessels. Case reports of welders with siderosis usually indicated they were asymptomatic, but dust macules can be associated with focal lesions and sometimes airflow obstruction. Follow-up studies of welders with siderosis who were removed from exposure have shown gradual clearing of the lesions on chest X-ray, associated with a gradual reduction of the amount of iron in the chest as measured magnetically. In welding facilities with adequate fume control programs, chest X-ray surveys do not find this abnormality, which was described more frequently in the first half of the twentieth century.

14.8.6 Lung cancer Because the metal fume produced by welding may contain substances known to cause lung cancer (particularly hexavalent chromium and nickel in stainless steel welding),

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there has been great interest in whether inhalation of welding fume increases the risk for lung cancer in welders. The question is made more complex by some studies which have shown higher rates of cigarette smoking in welders than in some other occupations, and by the historical association of asbestos exposure with welding in certain industries such as ship building. The International Agency on Research in Cancer (IARC) of the World Health Organization reviewed this topic in 1990, and concluded that ‘Welding fumes are possibly carcinogenic in humans’ (IARC category 2b). A meta-analysis of studies of welding and lung cancer in 1997 included additional studies, and concluded that there may be a causal relationship between exposure to stainless steel welding and lung cancer. Chronic inflammation and the production of oxidizing species have been proposed as mechanisms for lung carcinogenesis of welding fume.

14.8.7 Adverse effects on lung function Many studies of welders have been performed to determine whether they have lower lung function or lose lung function more rapidly than nonwelder control working groups. Many and perhaps most of these studies, often conducted in shipyards with environmental controls in place, have not demonstrated any adverse effects. Some other studies have shown small adverse effects on lung function in those with long exposures. Some studies show an interaction with cigarette smoke, in which those who smoke and weld have a significant loss of lung function with welding, while those who do not smoke and weld have a smaller or no effect of welding. These studies have little quantitative information on lifetime welding exposure, but it appears that good industrial hygiene measures in welding workplaces can prevent long-term adverse effects on lung function.

Acknowledgment This work was supported in part by ES-00131 and the New York State Occupational Health Clinics Network.

Further reading Antonini, J.M., Lewis, A.B., Roberts, J.R., Whaley, D.A. (2003) Pulmonary effects of welding fumes: review of worker and experimental animal studies. Am. J. Ind. Med. 43: 350–360. Beach, J.R., Dennis, J.H., Avery, A.J., Bromly, C.L., Ward, R.J., Walters, E.H., Stenton, S.C., Hendrick, D.J. (1996) An epidemiologic investigation of asthma in welders. Am. J. Respir. Crit. Care Med. 154: 1394. Burgess, W.A. (1995) Recognition of Health Hazards in Industry. A Review of Materials and Processes. 2nd edn. Wiley: New York. Honma, K., Abraham, J.L., Chiyotani, K. et al. (2004) Proposed criteria for mixed-dust pneumoconiosis: definition, descriptions, and guidelines for pathologic diagnosis and clinical correlation. Hum. Pathol. 35: 1515–1523. International Agency on Research in Cancer (1990) Chromium, Nickel, and Welding. Vol. 49; 447–525. Lauwerys, R.L., Hoet, P. (2001) Industrial Chemical Exposure. Guidelines for Biological Monitoring. 3rd edn. Lewis: Boca Raton, FL.

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Nemery, B., Verbeken, E.K., Demedts, M. (2001) Giant cell interstitial pneumonia (hard metal lung diseae, cobalt lung). Sem. Respir. Crit. Care Med. 22: 435–447. Palmer, K.T., Poole, J., Ayres, J.G., Mann, J., Burge, P.S., Coggon, D. (2003) Exposure to metal fume and infectious pneumonia. Am. J. Epidemiol. 157: 227–233 Sferlazza, S.J., Beckett, W.S. (1991) The respiratory health of welders: state of the art. Am. Rev. Respir. Dis. 143: 1134–1148. Sj€ ogren (1994) Occup. Environ. Med. 51: 33. Sjogren, B., Hansen, K.S., Kjuus, H., Persson, P.G. (1994) Exposure to stainless steel welding fumes and lung cancer: a meta analysis. Occup. Environ. Med. 51(5): 335–336.

Resources on the internet Occupational Respiratory Diseases. US National Institute for Occupational Safety and Health. September 1986. DHHS (NIOSH) publication no. 86-102. http://www.cdc.gov/niosh/86-102. html (accessed 1 January 2008). Particle analysis in environmental and biomedical samples. An illustrated description of the techniques of specialized particle analysis in environmental and biomedical samples, including in lung tissue, can be seen at: http://www.upstate.edu/pathenvi/index.shtml (accessed 1 January 2008).

15 Automobile maintenance, repair and refinishing Meredith H. Stowe and Carrie A. Redlich Yale University School of Medicine, New Haven, CT, USA

15.1

Introduction – the industry

The repair and maintenance of cars and trucks is a worldwide industry, as anywhere automobiles are driven there is a need for maintenance and repair workshops. Unlike the production of automobiles, repair and maintenance generally occurs in small workshops, even when incorporated into a car dealership. Relatively few epidemiology studies have been performed on this workforce, in part undoubtedly due to the typical workplace – small independently owned car maintenance and repair workshops. Workers in the larger workshops are usually more specialized, and these larger premises are more likely to have industrial hygiene controls and protective equipment. A different spectrum of exposures and occupational lung diseases is seen in the automobile maintenance and repair industry compared with the primary manufacturing of vehicles. Maintenance repair workshops may cover general engine repairs or specialize in certain repair work, such as radiators or transmissions. It is important to differentiate maintenance workshops from collision repair workshops or auto body repair workshops, which have additional unique exposures. Worker titles may assist in this distinction: a mechanic or service technician generally works on engines and mechanical repairs; auto body technicians may perform much of the same engine/mechanical work, but usually also do structural repairs and some painting. Painters are responsible for spray painting in body workshops. Smaller workshops may not have dedicated painters. Trucks and buses are usually maintained and repaired in separate facilities given differences in types of engines (diesel and biodiesel vs gasoline) and large scale. The types of respiratory hazards are similar, although spray painting large vehicles, especially if an appropriate sized spray booth is not available, can involve greater exposures. Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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15.2 Exposures from automobile maintenance and repair Exposures in car and truck engine repair and maintenance workshops are myriad and variable. Repair of clutches and brake linings can entail exposure to asbestos and solvents such as n-hexane which can cause peripheral neuropathy. Cases of mesothelioma have been reported among brake and car mechanics. Working on batteries may expose a worker to lead from the lead battery plates. Batteries also contain sulfuric acid. Radiator repair can also result in lead exposure, unless the radiator is lead-free. Welding, grinding and cutting metal engine parts can produce metal fumes, aerosols and particulates in the air. Other maintenance and repair work includes exposures to fuels, degreasers and various solvents. An engine running inside a workshop without sufficient ventilation can produce carbon monoxide and also diesel and gasoline exhaust fumes.

15.3 Exposures in auto body workshops In addition to the exposures in car maintenance workshops, auto body workers are also exposed to a number of other hazards. Grinding, sanding, cutting and occasionally sandblasting of metal parts occurs in auto body repair work, resulting in dust that can contain heavy metals, various particulates and potentially silica. Old paint may be removed with solvents such as methylene chloride, which along with n-hexane is neurotoxic, and is being replaced by less toxic solvents. Resin or putty such as ‘Bondo’, which typically contains a polyester resin, styrene, and talc, is commonly used as a plastic body part filler. Workers mix Bondo with a hardener, apply it to the damaged body part, and then sand it after it hardens, which can generate substantial irritant dust exposures. After cars are structurally repaired, the last step is to apply a new durable finish, comprising several layers of sprayed-on two-part polyurethane coating. These paints typically contain aliphatic diisocyanates, primarily polymeric hexamethylene diisocyanate (HDI) or isophorone diisocyanate (IPDI) dissolved in solvents such as acetone, toluene, xylene and methyl ethyl ketone. The isocyanate part is mixed with a B part containing the polyol, catalyst and other ingredients. Solvents are also used to wipe down a car prior to re-painting, usually hand-applied with a cloth or sprayed, and during clean-up. Several coats of primer and sealer are typically applied, followed by the color coat (basecoat) and finally the protective top coat (clear coat) is applied in several layers. The color coat usually does not contain isocyanate; the clear coat almost always contains isocyanate, which imparts the hard finish that is impervious to ultraviolet rays. Spray painting entails the highest risk of respiratory and skin exposure to isocyanates, but isocyanate exposures can occur with other job tasks and as a bystander. Skin exposure is particularly of concern with isocyanates, since such exposure probably is an effective route of sensitization. Skin exposure can occur from deposition of airborne exposures on skin, and also in settings where airborne exposures are generally well controlled, such as paint mixing, spills or contact with products that are not fully polymerized, such as compounding and polishing after the final paint coating, or from tasks that generate heat and thermal degradation products, such as sanding of coated parts. Skin exposure to isocyanate typically does not cause rashes or other warning symptoms that might reduce exposure.

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Auto body workshops are generally required to have a booth for spraying paint, but many still do not, or spray painting occurs outside the booth. Other ventilation systems for sanding, welding and mixing paint are also important, but may be absent, especially in smaller workshops. Personal protective equipment (PPE) whenever spraying paint should include an appropriate respirator, gloves and full skin covering – paint suit or long sleeves, head covering, as well as eye protection. For small paint jobs, workers may be less inclined to wear PPE. Gloves should be worn when using body filler, for all sanding, and when there is hand contact with fresh paints. Particulate filtered respirators are needed against dust and organic vapor filters should be used for solvent exposures. Appropriate respiratory and skin protection should also be worn for welding, grinding and cutting, and any other work with lead or solvents.

15.3.1 Spray-on truck-bed liners Following a worker’s death, the US National Institute for Occupational Safety and Health (NIOSH) issued an alert regarding the application of spray-on truck bed liners, a 2-part polyurethane coating product which is sprayed on the inside of truck beds. The liner coatings typically contain methylene diphenyl diisocyanate (MDI), an aromatic isocyanate that is commonly used to make polyurethane foams, coatings and adhesives for use in many industries. Although less volatile than HDI and TDI, similar precautions must be taken regarding use of ventilation and appropriate PPE especially when MDI is sprayed or heated.

15.4

Respiratory diseases in auto mechanics and repair workers

The most important occupational lung disease in automobile mechanics and auto body repair workers is work-related asthma, either exacerbation of pre-existing asthma secondary to the multiple irritant type exposures or new-onset asthma due to irritant, or more commonly, sensitizing agents. Non-asthmatic irritant and allergic responses, including upper airway irritation, eye symptoms and rhinitis are also common. By far the most common sensitizing agents in this industry are the isocyanates used in the polyurethane paints and truck-bed linings. Carbon monoxide poisoning can occur from idling vehicles. Less common diseases include acute pneumonitis, hypersensitivity pneumonitis and mesothelioma related to brake linings. There is limited data suggesting that chronic exposures may increase risk for chronic obstructive pulmonary disease (COPD) and interstitial lung diseases (Table 15.1).

15.5

Work-related asthma

Surveillance and epidemiologic studies have shown an increased risk of occupational asthma among workers in the auto repair industry, especially spray painters, and also among welders in general (Chapter 14). Workers in auto body workshops are at

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Table 15.1 Potential occupational lung diseases in automobile maintenance and repair

Automobile maintenance

Work process

Exposure

Possible Disease

Brake, clutch repair

Asbestos

Welding, grinding, cutting

Welding fumes (nickel, chromium, other metals) Lead, acids

Mesothelioma Asbestosis, plaques Asthma, metal fume fever, toxic pneumonitis

Battery work and radiator repair Run engine in workshop General Body repair and Repair/fill body parts refinishing Sanding

Spray-on truck bed liners

Carbon monoxide Exhaust fumes Fuel, degreasers, solvents Bondo, styrene, solvents Irritant dusts

Welding fumes, silica

Weld, cut, grind, sandblast metal parts Paint stripping Spray painting

Methylene chloride Isocyanates, solvents

Spraying coating

Isocyanate

Lead toxicity CO poisoning COPD Irritant upper/lower respiratory symptoms Neurological and irritant effects Upper/lower respiratory track irritation Work-exacerbated asthma Asthma, metal fume fever, silicosis, Interstitial lung disease, COPD Neurotoxicity Asthma, hypersensitivity pneumonitis Asthma, hypersensitivity pneumonitis

increased risk of work-exacerbated asthma and new-onset sensitizer asthma. Spray painters remain one of the work forces at highest risk of developing isocyanate asthma. As noted above, the primary sensitizing chemical used in the auto body workshops is isocyanates, primarily aliphatic isocyanates. Less common sensitizers include metals and other sensitizing chemicals such as diamines. Isocyanates may also cause allergic rhinitis, which typically precedes asthma, and less commonly allergic contact dermatitis and hypersensitivity pneumonitis. Once sensitized, exposure to extremely low levels, below regulatory or detectable levels, can lead to asthmatic responses, complicating recognition and prevention. Auto body welders, similar to other welders, can be exposed to a variety of metal fumes, particles and toxic thermal decomposition products depending on the base metal being welded, the metal coating on the work piece, the electrode and the fluxes (Chapter 14).

15.5.1 Diagnosis and management of asthma in auto repair workers The clinical presentation, diagnosis and management of work-related asthma in auto repair workers are similar to those in other industries. However, several features of the

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auto repair industry make recognition, diagnosis and prevention particularly challenging in these settings. New-onset occupational asthma can be particularly challenging to distinguish from work-exacerbation of pre-existing asthma. Auto repair worker exposures frequently begin at a young age, while still in school, or even as a child in familyowned businesses. Many such workers do similar work for their hobbies and on days off, and may not seek medical attention until they have had asthma for many years. The multiple exposures and variable tasks performed in automobile repair work complicate exposure assessment. As noted, in addition to isocyanates, numerous irritant dust exposures are generated during the diverse tasks involved in engine maintenance and auto body repair. Additionally the workshops typically are small, family-owned operations with less than 10 employees who perform multiple different tasks in the same general area, especially in those workshops that do not have dedicated paint booths. By-stander exposures from co-workers are common, and industrial hygiene controls and personal protective equipment are frequently inadequate. Most important in diagnosing work-related asthma in this population is a careful medical and occupational history. As with any worker suspected of work-related asthma based on the history, it is important to document that the patient has asthma vs another cause of such symptoms, such as upper airway irritation, hypersensitivity pneumonitis, or irritant-induced cough. This is usually done by documenting reversible airflow obstruction or airway hyper-responsiveness with spirometry and a bronchodilator response, or methacholine challenge testing as needed. However, with more chronic asthma and/or use of asthma medications, airway hyper-responsiveness may be more difficult to document. In taking the occupational and medical history on workers in this industry, clinicians should especially focus on the following: 1.

The nature of the upper and lower respiratory and skin symptoms – nasal and eye symptoms can precede asthmatic symptoms, such as wheezing, cough and shortness of breath. Cough can be the primary symptom, especially with isocyanate asthma. Fever and fatigue should also be asked about, as isocyanate asthma and hypersensitivity pneumonitis can be difficult to distinguish and can overlap. Rashes and skin exposure should also be inquired about, especially as skin exposure likely is an effective route of sensitization with isocyanates and potentially other sensitizers that cause asthma.

2.

The first onset of respiratory and allergic symptoms, and the first symptoms while working in this industry – onset of asthma may be years prior to current evaluation. A history of childhood asthma and allergies makes work-exacerbated asthma more likely.

3.

New sensitizer occupational asthma typically develops from several months up to several years after the onset of exposure, although the timing can be very variable, and workers may not be aware of changes in formulation of the paints and other products they work with.

4.

Timing of symptoms – delayed symptoms up to 6–10 hours after exposure (e.g. spray painting) are common with isocyanates, and should be specifically asked

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about, e.g. cough after work (e.g. in the evening if day shift). Such delayed symptoms can hinder recognition, especially when not accompanied by acute early asthmatic symptoms. Delayed symptoms can also help differentiate sensitizer from irritant responses, which typically occur more acutely after exposure, and also in response to a wider range of exposures. 5. Use of asthma and allergy medications, including changes in frequency of use. 6. Nonwork exposures such as pets, hobbies, environmental tobacco smoke and other home and environmental exposures. Important information about work the clinician should inquire about include: 1. Job title, years of employment and specific tasks (e.g. spray painting, welding, sanding, body filling) the worker performs and how often; 2. Whether or not there is a separate booth for spray painting, and whether or not spray painting also occurs on the workshop floor; the presence of overall ventilation, especially for dusty jobs such as sanding; 3. Whether or not the worker is near other workers, and what tasks other workers are performing given how common bystander exposures are in this industry; 4. The type of respiratory (cartridge, air supply, dust mask) and skin protective equipment (gloves, clothing) that is worn and how frequently; whether or not workers notice irritating dusts, fumes and vapors, and whether paints and other exposures get on their hands and skin. Material safety data sheets and/or labels should be obtained and reviewed to identify potential causative chemicals, in particular sensitizing agents, remembering that such information may be incomplete and/or inaccurate. In order to document whether the patient’s asthma is related to work, the clinician should ask in detail about the relationship of the patient’s symptoms to specific work exposures and tasks, focusing on: 1. The job the worker was doing when his/her symptoms first started, including the specific tasks and exposures – as asthma becomes more chronic the specific association with work can become less apparent; 2. Improvement away from work or other potential causative agent or triggers, or worsening with exposure – with more chronic asthma there may be little improvement away from work, especially with only 1–2 days off work; 3. Current asthma triggers at work and in general. Additional diagnostic tests beyond the occupational history that can further support an association between work exposures and sensitizer occupational asthma include IgE antibodies specific to the causative allergen and peak flow recordings at work and away from work. Unlike large molecular weight occupational allergens, IgE-specific immune responses to chemical asthmagens such as isocyanates may not be identified in affected workers, further complicating diagnosis and prevention. Peak flow recordings if they

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demonstrate work-related changes such as improvement away from work can be very helpful, but a few days away from work may not be sufficient to see changes, especially with more chronic asthmatics. With work-exacerbated asthma and irritant-induced asthma the association between work exposures and patient’s asthma is usually based on a careful occupational history. Disease management with work-related asthma in this industry should follow standard practice and treatment guidelines, also considering public health and preventive considerations. For example, if occupational asthma due to isocyanates is diagnosed, removal from further exposure is recommended, such as by job transfer away from exposure. With work-exacerbated asthma or irritant-induced asthma, reduction in irritant exposures and improved ventilation typically is effective. However, if asthma symptoms persist or worsen, additional treatment options should be considered. Whether other workers are similarly affected should also be considered.

15.6

Other lung diseases in auto mechanics and repair workers

15.6.1 COPD and interstitial lung disease The population-based epidemiology literature investigating occupational risk factors for COPD has demonstrated that workers exposed to various dusts, irritants, fumes and gases, such as welding fumes, vehicle exhaust fumes, particulates and chemical fumes, have an increased risk of COPD, but specific causative agents are not well defined. Limited epidemiologic studies of auto mechanics and auto body repair workers suggest that these workers may be at increased risk of COPD and accelerated loss of FEV1, beyond the sequellae of chronic asthma. Data on interstitial lung diseases in this industry is limited. Isocyanates can cause hypersensitivity pneumonitis, typically an acute or subacute presentation. Limited studies have identified increased risks of pulmonary fibrosis in workers exposed to welding, metals, transportation and dusty environments, but specific agents have been difficult to identify. Although brake workers are at risk of exposure to asbestos, cases of asbestos-related pleural disease and/or asbestosis related to auto repair work are uncommon, given relatively lower total levels of exposure compared with historic levels in other industries such as construction. Silica exposure is possible when old metal parts are sandblasted, but such sandblasting is less common and silicosis rarely reported in this industry. Workers who weld metal partsare atrisk of developingpulmonarydiseases seeninother welders, including asthma, metal fume fever and toxic pneumonitis (Chapter 14).

15.6.2 Cancer/mesothelioma Cases of mesothelioma have been reported in brake workers, typically beyond what might be expected, but limited epidemiologic studies have not consistently demonstrated an increased risk of mesothelioma or other cancers in brake workers, or other types of auto repair workers, potentially related to study size or other factors.

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15.7 Other nonpulmonary occupational diseases among auto repair workers The most important nonrespiratory occupational diseases in auto mechanics and auto repair workers include irritant and allergic contact dermatitis related to metals, solvents and irritants, lead toxicity from batteries and neurologic effects of solvents such as nhexane, methylene chloride and styrene.

Further reading Bello, D., Herrick, C.A., Smith, T.J., Woskie, S.R., Streicher, R.P., Cullen, M.R., Liu, Y., Redlich, C.A. (2007) Skin exposure to isocyanates: reasons for concern. Environ. Health Perspect. 115: 328–335. Chattopadhyay, B.P., Alam, J., Roychowdhury, A. (2003) Pulmonary function abnormalities associated with exposure to automobile exhaust in a diesel bus garage and roads. Lung 181(5): 291–302. Finkelstein, M.M. (2008) Asbestos fibre concentrations in the lungs of brake workers: Another look. Ann. Occup. Hygiene 52(6): 455–461. Gourdeau, P., Perent, M., Soulard, A. (1995) Exposure to carbon monoxide in garages: evaluation in car mechanics. Can. J. Public Health 86(6): 414–417. Newman Taylor, A.J., Nicholson, P.J., Cullinan, P., Boyle, C., Burge, P.S. (2004) Guidelines for the Prevention. Identification and Management of Occupational Asthma: Evidence Review and Recommendations. British Occupational Health Research Foundation: London. Available from: http://www.bohrf.org.uk/downloads/asthevre.pdf NIOSH. (2006) Preventing asthma and death from MDI exposure during spray-on truck bed liner and related applications NIOSH Alert, Cincinnatti, OH: DHHS (NIOSH). Pronk, A., Preller, L., Raulf-Heimsoth, M., Jonkers, I.C.L., Lammers, J.-W., Wouters, I.M., Doekes, G., Wisnewski, A.V., Heederik, D. (2007) Respiratory symptoms, sensitization, and exposure–response relationships in spray painters exposed to isocyanates. Am. J. Respir. Crit. Care Med. 176: 1090–1097. Pronk, A., Yu, F., Vlaanderen, J., Tielemans, E., Preller, L., Bobeldijk, I., Deddens, J.A., Latza, U., Baur, X., Heederik, D. (2006) Dermal, inhalation, and internal exposure to 1,6-HDI and its oligomers in car body repair shop workers and industrial spray painters. Occup. Environ. Med. 63(9): 624–631. Suplido, M.L., Ong, C.N. (2000) Lead exposure among small-scale battery recyclers, automobile radiator mechanics, and their children in Manila, the Phillipines. Environ. Res. 82(3): 231–238. Tarlo, S.M., Balmes, J., Balkissoon, R., Beach, J., Beckett, W., Bernstein, D., Blanc, P.D., Brooks, S.M., Cowl, C.T., Daroowalla, F., Harber, P., Lemiere, C., Liss, G.M., Pacheco, K.A., Redlich, C.A., Rowe, B., Heitzer, J. (2008) Diagnosis and management of work-related asthma: American College of Chest Physicians consensus statement. Chest 134: 1–41. Wisnewski, A.V. (2007) Developments in laboratory diagnostics for isocyanate asthma. Curr. Opin. Allergy Clin. Immunol. 7(2): 138–145. Zuskin, E., Mustajbegovic, J., Schachter, E.N. (1994) Respiratory symptoms and lung function in bus drivers and mechanics. Am. J. Ind. Med. 26(6): 771–783.

16 Automotive industry Kenneth D. Rosenman Michigan State University, East Lansing, MI, USA

16.1 Introduction The production of automobiles and trucks is a major worldwide industry. There are approximately 4 million auto and truck production workers worldwide with major growth in the industry occurring in Asian–Pacific countries. Historically vehicle production was vertically integrated within one company. That company would manufacture most of their own metal and plastic parts and then assemble them into vehicles. This business model has shifted in the last couple of decades, with in-house parts manufacture being spun off as independent companies so that now 75% of autoworkers work for companies that produce vehicle parts and 25% work for companies that assemble the final vehicles. Since vehicle production is a worldwide industry, the percentage of workers in vehicle assembly vs vehicle parts production in any given country varies. Of the 1 million autoworkers in the USA, 75% are in vehicle parts manufacturing facilities; in contrast, in Belgium almost 90% of vehicle workers work in assembly facilities. This distribution between vehicle assembly and parts manufacturing is important from the health care provider’s perspective. Vehicle parts manufacturing has significantly more respiratory hazards since it involves processes such as casting metal parts in foundries, machining metal parts, manufacturing foam products and extruding and injecting plastic into molds. In contrast, vehicle assembly requires a great deal of material handling as the various parts are assembled into the final vehicle. Accordingly the major health concern in vehicle assembly facilities involves musculoskeletal conditions. However, there are respiratory concerns in assembly facilities. Important activities in vehicle assembly that generate respiratory hazards are welding, painting and the use of adhesives. Another contrast between parts manufacture and assembly is that vehicle assembly facilities are more likely to be larger corporate entities: six corporations produce 75% of the world’s vehicle

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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production while just in the USA there are 5000–8000 vehicle parts manufacturers. This difference in corporate structure would suggest that the larger assembly facilities will have more expertise and resources to address health and safety issues than many of the smaller vehicle parts manufacturers. This chapter will examine the respiratory hazards in vehicle assembly and parts manufacturing. The respiratory hazards of car maintenance and repair are discussed in Chapter 15. Table 16.1 summarizes by vehicle manufacturing industry type (vehicle assembly vs vehicle part manufacturing) and activity (casting, welding, etc.) the possible exposures (isocyanate, silica, etc.) and the respiratory conditions (silicosis, asthma, etc.) that have been associated with these exposures in the vehicle manufacturing industry. Table 16.1 Work processes, exposures and respiratory conditions in the automotive manufacturing industry Vehicle parts manufacturing

Work process

Exposure

Respiratory condition

Metal parts

Casting

Silica Asbestos Benzo(a)pyrene

Chipping/grinding

Silica

Core/mold production

Silica Isocyanates

Machining

Metal working fluids

Forging/stamping

Drawing compounds

Asbestosis COPD Lung cancer Silicosis COPD Lung cancer Silicosis Asthma COPD Lung cancer Silicosis Asthma Hypersensitivity Pneumonitis Asthma Hypersensitivity pneumonitis

Polyurethane foam

Foam production for seats, arm rests, etc.

Isocyanates

Asthma

Plastic parts

Extrusion/injection molding

Styrene Polyvinyl chloride Polyethylene

Asthma Bronchitis

Carpeting/liners

Flocking

Nylon flock

Interstitial fibrosis

Body shop

Welding

Welding fumes NOx, ozone, particulates

Asthma COPD

Paint line Assembly

Painting Gluing

Isocyanates Isocyanates Epoxies

Asthma Asthma

Vehicle assembly

16.3

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Respiratory hazards and disease

Both obstructive and restrictive diseases occur from exposures in the vehicle manufacturing industry. With increased automation, substitution with alternative materials and better engineering and ventilation controls, restrictive lung disease such as asbestosis and silicosis have become less common. One restrictive lung disease in the vehicle manufacturing industry whose incidence is not decreasing is hypersensitivity pneumonitis. The increase in the use of water-based synthetic metal-working fluids has caused repeated outbreaks of hypersensitivity pneumonitis. The association between metal-working fluids (MWFs) and hypersensitivity pneumonitis was first recognized in the mid 1990s. Although the same microbial agent has been identified in the MWF in a number of the outbreaks from different facilities, this agent has not always been identified during outbreaks and it has also been identified in facilities without outbreaks. A lack of understanding of what are the other important factors that initiate these outbreaks has limited the ability to reduce the respiratory hazard from MWFs. Additionally, the introduction of new technology has caused recognition of a new restrictive lung condition, nylon flock disease. Most new cases of respiratory disease currently being identified in the vehicle production industry are obstructive: asthma, chronic obstructive pulmonary disease (COPD) and chronic bronchitis. The use of chemical sensitizers such as isocyanates, chronic exposure to irritants such as during welding and the occurrence of obstructive changes with repeated exposure to substances classically associated with restrictive disease such as silica are all causes for these obstructive lung conditions. Lung cancer is increased among foundry workers making vehicle parts. Historically, there has been exposure to three carcinogens in the foundry environment: asbestos, benzopyrene from the fumes of the molten metal and silica. There are studies reporting a cancer risk from exposure to natural (straight) metal-working fluids (mineral oils), with the best evidence of an association between MWFs and cancer being for laryngeal cancer and the nonrespiratory cancers of bladder, pancreas, rectal, scrotum and skin. Vehicle manufacturing workers, as other blue collar workers, generally have a higher prevalence of cigarette smoking than the general population. This increased prevalence of smoking in conjunction with workplace exposures such as silica or welding will increase the likelihood of lung cancer, COPD, chronic bronchitis and irritant symptoms more so then if the group only smoked cigarettes or only had the workplace exposures.

16.3

Vehicle parts manufacturing

16.3.1 Foundries Foundries produce metal parts by pouring molten metal into molds, which traditionally have been made from sand. In order to create internal cavities in the metal pieces being produced, cores made from sand are produced and placed in the mold prior to pouring in the molten metal. A common binder used in making sand cores is methylene

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Figure 16.1 An individual chipping and another grinding an engine block. Both workers are wearing respirators because air levels are above the permissible exposure levels

diisocyanate (MDI). After the metal hardens the mold and core must be removed and the metal smoothed. The activity of removing the mold and core is conducted in the ‘finishing’ or ‘clean’ room. Activities there include knocking off the sprue (hardened metal from where the pour goes into the mold), shake-out and chipping and grinding. Figure 16.1 shows a picture of an individual chipping and another grinding an engine block. Both workers are wearing respirators because air levels are above the allowable OSHA permissible exposure levels. During pouring, the molten metal heats the silica. Because heated silica is transformed into more fibrogenic forms, tridymite and cristobalite, and the removal of sand generates a large dispersion of particulates, the ‘cleaning’ area of a foundry is the location with the highest risk for silica exposure. Silica exposure is also significant in the mold and core areas and among any workers responsible for handling and cleaning up spilt sand. Asbestos exposure has occurred among workers maintaining furnaces, pipes and cupolas (the latter being the containers in which molten metal from furnaces are transferred to the molds). The workers who maintain and repair furnaces and pipes are in some facilities classified as ‘skilled trades’: insulators, electricians, plumbers and millwrights. Removal of fire bricks in furnaces and cupolas is a high-risk job for both asbestos and silica exposure. Furnaces are typically relined on a regular basis and, in the USA until the 1980s, workers on overtime from throughout the facility would on weekends and downtime throughout the year work in the furnaces chipping away the firebrick and asbestos insulation without adequate respiratory protection. There is substantial data that the mineral dusts, particularly silica, cause obstructive as well as restrictive disease. These obstructive changes are more prevalent in workers who also have smoked cigarettes. Silica exposure also increases the risk of active tuberculosis and silica is considered a risk factor, like diabetes or steroid use, when considering the indications for treating latent tuberculosis or the number of medications needed when treating active tuberculosis. Other conditions increased in silica-exposed workers are chronic renal failure and connective tissue diseases, particularly scleroderma and rheumatoid arthritis. Even in the absence of clinical disease, markers of connective

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disease including antinuclear antibody and rheumatoid factor are more prevalent in patients with silicosis. There are multiple methods for forming sand molds and cores. A common method involves the mixture of TEA gas (tetraethylamine) and MDI. Ruptured or disconnected hoses, causing acute exposure, are not uncommon in this work setting. Acute exposure after such a rupture or spill may cause an acute chemical pneumonitis. With recovery from the acute episode, the worker may be left with persistent shortness of breath and wheezing. On testing these patients may have a positive methacholine challenge test and meet the diagnostic criteria for reactive airway dysfunction syndrome. Exposure to TEA gas is associated with difficulty in vision, particularly being able to see at night. MDI is a common cause of sensitization and work-related asthma. This method is a ‘cold’ method. An alternative method is a hot process involving a phenolic–formaldehyde resin. Formaldehyde exposure from this process is a cause of work-related asthma. Alternative foundry processes, such as lost wax casting, or lost foam casting, that do not use silica or use less silica and do not use known sensitizers, have become more common in recent years. The risk of silicosis is also less in aluminum foundries. The International Agency for Research on Cancer has classified iron and steel founding as a group I human carcinogen: sufficient evidence of carcinogenicity in humans. Similar group I classifications have been given for asbestos, benzo(a)pyrene and silica, to which foundry workers have been commonly exposed. The US National Toxicology Program does not classify work processes such as foundries but has classified asbestos and silica as ‘known human carcinogens’ and benzo(a)pyrene as ‘reasonably anticipated to be a human carcinogen’. Asbestos and silica exposure in foundries is described above; benzo(a)pyrene is one of the polynuclear aromatic compounds produced with combustion and is formed when metal is heated, so that workers in the pouring areas of a foundry would have the potential for the greatest exposure.

16.3.2 Metal machining Metal pieces need to be cut, drilled, shaped and smoothed. In order to facilitate this machining, MWFs are used. These substances are commonly called ‘coolants’, but their primary properties are actually to remove metal particles, protect or treat the surface of the metal being machined and prolong the life of the machining equipment. Figure 16.2 shows a machining operation with an MWF being used. There are four types of metalworking fluids, straight (natural, mineral oil), emulsified, semi-synthetic and synthetic fluids. Straight fluid, as the name implies, is 100% mineral oil and generally is what was used prior to the 1970s. Water-based oils are now more commonly used; emulsified oil is an emulsion of mineral oil and water; semi-synthetic contains smaller amounts of mineral oil than the emulsified oils; and synthetic oils contain no mineral oils. Since these are water-based products, corrosion inhibitors as well as dyes and biocides to inhibit microbiological growth are found in the three types of nonstraight MWFs. Typically these fluids are collected in sumps around the machining operations and repeatedly reused in the machining process after the metal particles are filtered out. Specific personnel are designated to check the pH, assess the biological content and put in additives in response to the sampling results. Work around water-based MWFs is

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Figure 16.2 A machining operation with metal-working fluids being used

associated with a higher prevalence of respiratory symptoms, chronic bronchitis and doctor visits than work around the straight fluids. Individual components of waterbased metal-working fluids, such as ethanolamine compounds, have been shown by specific antigen bronchoprovocation testing to cause work-related asthma, while microbiological contamination of nonstraight MWFs has been associated with outbreaks of hypersensitivity pneumonitis. Historically there have been a few case reports of lipoid pneumonia among individuals working around straights MWFs. Current exposures are usually too well controlled to cause this condition. Another condition of historical interest is Pontiac fever, an influenza-like condition that was reported in an engine manufacturing plant using water-based MWFs. Patients had antibodies to a species of Legionella but no evidence of pneumonia. Although theoretically possible, there are no studies that indicate an increased risk of either upper respiratory infections or pneumonia among individuals who work with MWF contaminated with microbiological agents. Hypersensitivity pneumonitis (HP) from exposure to MWF was first reported in the mid 1990s in a facility that manufactured vehicle parts. A dozen or more outbreaks have subsequently been reported in the literature. The initial outbreak involved six patients. Antibodies to Pseudomonas were identified in the cases of this initial report. In subsequent outbreaks, Mycobacteria immunogenum has been the most common suspected etiologic microbiologic agent, although Mycobacteria immunogenum has been found in MWFs in facilities without cases of HP. Patients are usually nonsmokers, have symptoms of cough, dyspnea and fever, have ground glass opacification on their HRCT and have restrictive changes on spirometry and plethysmography and decreased diffusing capacity. Respiratory symptoms and radiograph changes will clear and pulmonary function changes will markedly improve over a period of months if the patient is removed from exposure soon after the onset of symptoms. If the patient is not removed from exposure, then fibrosis and increased respiratory symptoms are increasingly likely to occur as the exposure continues and the symptoms and radiographic changes are less likely to clear after removal from exposure. The sporadic nature of these outbreaks has remained perplexing. Are there truly outbreaks associated with overgrowth of certain microbiological species or are there endemic, ongoing cases that are

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misdiagnosed as atypical pneumonia? If during the time the patient is off work, changes are made to the worksite such as cleaning tanks, replacing all the MWF with new unused MWF or adding a biocide so that when the patient returns to work the causal biological agent is not present or is present in a much lower concentration, the fact that the patient was misdiagnosed with atypical pneumonia may never be recognized. Typically when an outbreak is identified, changes in the use of the metal work fluid as described above are instituted as well as improvements in ventilation controls. The actual workplace changes that cause the outbreak to end have not been identified since multiple interventions are typically instituted at the same time. Increased automation of machining with faster machines causing more aerosolization and increased used of water-based MWFs is the presumed reason why HP was not recognized in association with this work process until the 1990s. Microbial growth does not occur in straight oil and HP has not been reported in machining operations where only straight oils are used. The current US OSHA standard for oil mist of 5 mg/m3 is not sufficiently protective to prevent HP when emulsified or semi-synthetic MWFs are used nor relevant to machining operations involving synthetic MWFs. Work-related asthma has been identified in the same facilities where outbreaks of HP have been recognized. In a recent report of an outbreak of HP in an automotive engine manufacturing facility, work-related asthma was more common than HP. In the state of Michigan with its large vehicle manufacturing industry, MWFs are the second most common cause of work-related asthma. Case reports of work-related asthma documented by specific antigen bronchoprovocation testing have been reported with both used and unused emulsified MWF. Studies of cross-shift changes in FEV1 have reported the largest response among workers exposed to the semi-synthetic and synthetic MWFs. Amine compounds, which are common additives in the water-based MWFs, have also been documented by specific antigen bronchoprovocation testing to be the cause of work-related asthma. Routine elicitation from a patient concerning the onset of their respiratory symptoms and whether there is a temporal association with work is important for all adults with asthma. Studies have shown that such questioning is only documented in a minority of charts of adult asthmatics. Positive responses are important indicators of the need for further testing. A history of a temporal relationship is sensitive but nonspecific. Objective pulmonary testing is important to make the diagnosis of work-related asthma since medical restrictions or departure from work has serious socioeconomic consequences. Use of more specific testing and not relying on history alone is highly advised. Given the unavailability of specific antigen bronchoprovocation testing, which is the gold standard, other breathing tests using the patient’s actual workplace as the bronchoprovocation have been recommended.

16.3.3 Forging/stamping Similar to machining, MWFs, called drawing compounds, are used when cold rolled steel is stamped out into metal parts (stamping) or compressive force is used on heated metal to form metal parts to conform to the shape of dies (forging). Both processes use drawing compounds, since forging generally involves heated metal, and pyrolysis and volatization of the drawing compound are likely to increase the potential for exposure.

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The potential for the development of asthma and hypersensitivity pneumonitis in forging and stamping would be similar to machining.

16.3.4 Carpeting/liners In one process to make vehicle carpeting, and interior lining, short nylon, rayon or polyester fibers (flock) are glued to a cotton-polyester fabric substrate. In the early 1990s, outbreaks of interstitial disease were first noted in facilities making nylon flock. By 1998, 20 of 500 potentially exposed workers were reported with lung disease from four facilities in Canada and the USA. Symptoms were cough, both productive and nonproductive, two of the 20 cases had arthralgias, two had weight loss and eight had asthma. No temporal association was noted in the short term with work (i.e. improvement on the weekend), but with prolonged removal from work of weeks to months some individuals improved. These individuals had reoccurrence of their symptoms on return to work. Half of the reported cases had decreased total lung capacity and/or forced vital capacity, and 13 had decreased diffusing capacity. Although several of the cases had normal chest radiographs, their high resolution CT scan (HRCT) showed ground glass opacities with a peripheral predominance. A distinctive histology was described that showed ‘lymphocytic bronchiolitis and peribronchiolitis with lymphoid hyperplasia represented by lymphoid aggregates’. Transbronchial biopsies and/or bronchial lavage did not provide sufficient tissue in relation to the pulmonary lobular architecture for diagnosis. There is one reported case of interstitial fibrosis occurring in this industry outside of North America – a case report from Spain, after exposure to polyethylene flock.

16.3.5 Polyurethane foam Isocyanates are commonly used in vehicle parts manufacture to make seat cushions, inner padding such as arm rests and bumpers and fascias. Figure 16.3 shows an auto

Figure 16.3 An auto part being made from MDI. The hoses bring the MDI and the catalyst, an amine compound, into the mold where the two chemicals mix in the mold. The chemicals react and assume the shape of the mold and then the worker removes the product from the mold

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part being made from MDI. The hoses bring the MDI and the catalyst, an amine compound, into the mold where the two chemicals mix in the mold. The chemicals react and assume the shape of the mold and then the worker removes the product from the mold. Across all types of industries, isocyanates are the most common etiologic agents of occupational asthma. The most common type of isocyanate used has been changing over time. MDI and more recently polymeric forms of the isocyanates are being used more frequently than toluene diisocyanate (TDI). A health benefit of this switch is that MDI and the polymeric foams are less volatile and human exposure should be decreased. However, the generation of heat in some of the processes involving isocyanates and limited data that respiratory sensitization can occur after skin exposure have meant that sensitization to isocyanates remains an ongoing issue. Clearly workers in the area where the isocyanate is mixed with the catalyst are at potential risk. Generally day-to-day exposure measured by the 8-hour time-weighted average of exposure is below the regulatory standard, which is in the thousandth of a part per million. However, spills and leaks and clean-up of these spills without proper protective equipment causes increased exposure that has been associated with the onset of isocyanate-induced asthma. For example, the US National Institute for Occupational Safety and Health recommends air-supplied respirators when cleaning up isocyanate spills. Studies on skin exposure show the potential for skin exposure even after mixture of the amine catalyst and the isocyanate during the time the material is ‘curing’. The diagnosis of work-related asthma from isocyanates is similar to the diagnosis of work-related asthma from other chemicals and the health care provider should not rely on the history alone to make the diagnosis. A temporal association of symptoms during the day or at night after work with improvement on weekends and vacations is a sensitive but nonspecific finding. Unfortunately, however, this sensitive screening for work-related asthma is overlooked. It has been consistently reported that physicians fail to document and presumably fail to ask about their patient’s work and whether their patient’s symptoms are associated with work. Collecting pulmonary function testing in conjunction with the patient’s work allows the clinician to perform a natural challenge test, given the general unavailability of a laboratory which will perform specific antigen bronchoprovocation testing. With chronic exposure the patient may have lost the temporal pattern or the patient may be on long-term leave from the facility. In these situations return to the workplace after a prolonged absence and documenting changes in spirometry or peak flows may be useful to confirm the clinical history. There are both IgE and IgG antibody testing for hexamethyldiisocyanate (HDI), MDI and TDI available from commercial laboratories. IgE has a low sensitivity (10–15% range) and IgG as a marker of exposure has a low specificity for disease. Research is underway for better assays and a limited number of research laboratories may have a test with better sensitivity and specificity parameters. A positive specific antigen bronchoprovocation test to an isocyanate has been reported in patients with a negative methacholine challenge test. This has occurred in individuals who are no longer being exposed to isocyanates. The absence of a positive methacholine challenge in a patient currently exposed to isocyanates is highly suggestive that the patient has an alternative diagnosis such as irritative symptoms, or vocal cord dysfunction but not asthma.

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Case reports of HP have also been reported after acute exposure to an isocyanate. HP is much less common than asthma after isocyanate exposure.

16.3.6 Plastic Plastic has been substituted for many metal parts that historically were used in vehicles. The ability to manufacture strong but relatively cheap plastics, and their lighter weight in comparison to metal, which improves fuel economy, have all led to this switch. The two common manufacturing processes for plastic parts are injection molding and extrusion. In injection molding, plastic granules or powders are heated to fluid, which is then forced into a metal mold where it hardens and assumes the shape of the product. In extrusion, heating softens the plastic and then the softened plastic is forced through a die and on cooling assumes the shape of the die. Since heat is involved in both processes, plastic fumes may be released into the air. In most facilities multiple injection molding or extrusion machines will be in the same room. A machine may be dedicated to a particular plastic; more often the same machine is used for multiple different types of plastic and the machine needs to be ‘purged’ when the plastic is switched. The highest exposures occur during purging. During purging, the machine is superheated and residual plastic in the machine is burnt off. With multiple machines in the same area a worker may be exposed to fumes from purging even though the machine they are operating is not being purged. Identification of the plastic used in the machine when the patient has respiratory problems is important in evaluating the cause of the patient’s respiratory problem. Some plastics contain ingredients that have caused sensitization and work-related asthma. These include styrene and formaldehyde, and a single case report with a positive specific antigen bronchoprovocation test for polypropylene. In addition to determining the type of plastic and eliciting a temporal relationship between the patient’s respiratory symptoms and particular work exposures, it is important to determine the patient’s medical condition before deciding whether and if medical restrictions are indicated. Patients can develop asthma, have aggravation of existing asthma or COPD, bronchial irritation or polymer fume fever. Spirometry with determination of hyper-responsiveness by pre/post bronchodilator or methacholine challenge as indicated by the FEV1 results on baseline spirometry with lung volumes and diffusing capacity are typically needed to reach a clinical diagnosis before delving into the even more complicated area of documenting causality. Clearly patients cannot have work-related asthma if they do not have asthma. Similarly medical restrictions will be different for a patient having irritative symptoms than for a patient with work-related asthma. A self-limited condition associated with manufacturing plastic parts is ‘polymer fume fever’ after exposure to polyvinyl chloride or polytetrafluoroethelyene. Here an individual will develop flu-like symptoms in the evening after work with fever, headache, chills and myalgia that typically resolves in 24–48 h. Symptoms typically occur on return to work when the individual has not been exposed for a period of time, i.e. after a vacation, and will not reoccur the rest of the week. The condition is similar to metal fume fever from exposure to zinc oxide fumes given off when galvanized (zinc coated) metal is burnt or cut.

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16.3.7 Vehicle assembly Generally healthcare providers involved with assembly workers need to address musculoskeletal issues, and respiratory conditions are relatively uncommon. However, the parts of the assembly facility where the greatest potential for respiratory exposures exist are in the body shop and on the paint line, including the touch up area.

16.3.8 Body shop In a typical car over a thousand welds are necessary to assemble the vehicle. Worldwide, in modern facilities the vast majority of welds are performed by robots with individual workers placing and removing various parts in position for the robot welding. In less automated facilities thousands of workers may be performing welding. This work is performed in the ‘body shop’ where hundreds of robots will be performing welding. The area is typically noisy from the manipulation of so many metal parts and the movement of these metal parts along the line. Workers are required to wear hearing protection and special gloves to reduce cuts from handling the sharp metal pieces. Even though the workers in an automated body shop are not doing the actual welding, they are in close proximity to where the welding is performed and are potentially exposed to welding fumes. In limited areas workers themselves continue to perform spot welding. There are approximately 80 different types of welding. Electric arc and resistance welding are the most common types used in the vehicle assembly facility. Ozone and nitrogen oxide and particulates are produced during the welding. Studies of workers in vehicular ‘body shops’ have reported increased respiratory symptoms. There is good documentation that stainless steel welding with exposure and sensitization to chromium causes work-related asthma. Although welding in the vehicle manufacturing industry is not done on stainless steel, workers in this industry develop new-onset asthma. Although not documented by specific antigen testing or work-related pulmonary function testing, welding is the fifth most common cause of work-related asthma (90% new onset) reported by physicians to the SENSOR surveillance program in Michigan, a state with a large vehicle manufacturing industry.

16.3.9 Paint line Vehicular paint or a clear protective coat sprayed over the paint usually contains the isocyanate HDI, a well-recognized cause of work-related asthma. Vehicular painting is performed in assembly facilities and in many facilities is well contained, with separate ventilation and exhaust systems from the rest of the assembly operations. Historically, such ventilation controls will not have been as extensive. The paint area has a limited number of workers who wear airline respirators and complete skin protection or the spraying of the paint or clear coat is performed by robots, thus markedly reducing the likelihood of exposure to workers on the paint line. Limited access to the paint line by non-paint line workers is the other factor limiting exposure. One reason access is limited to the paint areas in addition to health concerns is the concern about the offgassing of perfumes, colognes and shampoo that are worn by individuals which affect

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the bonding of the paint to the vehicles. The potential for adverse health effects is greatest either during spills, leaks and maintenance or when touch-up work is performed as compared with routine operations. The levels of protective equipment provided and work practices during spills, leaks, maintenance and touch-up activity are important factors affecting the level of risk. Cars that are damaged after painting during handling will have touch-up painting performed. This touch-up is performed in a similar manner to procedures used in auto body shops (Chapter 15). Potential exposure to the isocyanates both via inhalation and skin will be greater in this work situation, although the number of employees in an assembly plant involved with touch-up is small.

16.3.10 Assembly During assembly some of the adhesives used may contain chemicals that cause asthma, isocyanates and/or epoxies. For example, an isocyanate adhesive is used to attached the front and rear windows in a car. Exposure, however, is limited as the adhesive has a low volatility and is applied by a robot which limits the potential for skin exposure during routine work. Inadequate protection during clean-up of spills or leaks or during maintenance will determine if there is exposure potential for developing asthma.

Further reading Antonini, J.M., Lewis, A.B., Roberts, J.R., Whaley, D.A. (2003) Pulmonary effects of welding fumes: review of worker and experimental animal studies. Am. J. Ind. Med. 43: 350–360. Beach, J., Rowe, B.H., Blitz, S., Crumley, E., Hooton, N., Russell, K., Spooner, C., Klassen, T. (2005) Evidence report/technology assessment no. 129. (prepared by the University of Alberta Evidencebased Practice Center, under contract no. 290-02-0023). AHRQ publication no. 06-E003-2. Agency for Healthcare Research and Quality: Rockville, MD. Available from: http://www.ncbi. nlm.nih.gov/books/bv.fcgi?rid¼hstat1b.chapter.25934 (accessed 3 March 2008). Eschenbacher, W.L., Kreiss, K., Lougheed, M.D., Pransky, G.S., Day, B., Castellan, R.M. (1999) Nylon flock-associated interstitial lung disease. Am. J. Respir. Crit. Care Med. 159: 2003–2008. Hnizdo, E., Vallyathan, V. (2003) Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence. Occup. Environ. Med. 60: 237–243. Nicholson, P.J., Cullinan, P., Taylor, A.J., Burge, P.S., Boyle, C. (2005) Evidence based guidelines for the prevention, identification, and management of occupational asthma. Occup. Environ. Med. 62: 290–299. Robertson, W., Robertson, A.S., Burge, C.B.S.G., Moore, V.C., Jaakkola, M.S., Dawkins, P.A., Burd, M., Rawbone, R., Gardner, I., Kinoulty, M., Crook, B., Evans, G.S., Harris-Roberts, J., Rice, S., Burge, P.S. (2007) Clinical investigation of an outbreak of alveolitis and asthma in a car engine manufacturing plant. Thorax 62: 981–990. Tarlo, S.M., Balmes, J., Balkissoon, R. et al. (2008) Diagnosis and management of work-related asthma. American College of Chest Physicians Consensus Statement. Chest 134 (suppl.): 1S–41S.

17 Wood and textile industries Kjell Tor
en University of Gothenburg, Gothenburg, Sweden

17.1

Wood industry

17.1.1 Description of the industry The term ‘wood industry’ is used to describe those industrial processes that use trees as their raw material. One branch of the industry includes forestry, sawmills, building and construction (including pre-fabrication of detached and semi-detached houses, as well as on-site construction work), furniture manufacture and board production. Woodwork teachers are an often overlooked group subject to the exposures common to these sectors. Another important branch includes those industries that extract cellulose from wood pulp; that is, pulp and paper mills. The final products of these mills are a wide variety of paper products including different kinds of paper boards. The majority of the trees harvested throughout the world are used for sawn lumber, while most of the rest are used by the pulp and paper industry. However, a minor fraction is used for fuel, a fraction that will increase in the future. Similarly, the production of ethanol from wood – for use as fuel – is likely to be increasingly important. The largest forested areas in the world are in Russia, Brazil, Canada, the USA and China, while the largest exporters of forest products are Canada, the USA, Finland and Sweden. The major forest export products from Canada, Finland and Sweden are pulp and paper. The wide spectrum of industries and production technologies implies a number of different occupational exposures, the most obvious being wood dust. In Sweden in the late 1990s 6.4% of men and 0.5% of women of working age reported occupational exposure to wood dust.

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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Table 17.1 The most important occupations, exposures and respiratory diseases in forestry, sawmills, the construction industry and furniture manufacture (including vocational schools) Occupations

Exposures

Diseases/symptoms

Lumberjacks

Irritant symptoms

Sawmill workers

Wood dust, terpenes Exhausts Wood dust, terpenes

Cabinet-makers

Molds Wood dust

Carpenters Woodwork teachers

Glues Paints, solvents Wood dust

Impaired lung function Irritant symptoms Allergic alveolitis Asthma Sino-nasal cancer Asthma Asthma Rhinitis

17.1.2 Forestry, sawmills, the construction industry and furniture manufacture (including vocational schools) Workers in these sectors are exposed to a variety of substances that increase the risk for respiratory diseases. The major exposures of respiratory relevance are wood dust, volatile chemicals such as terpenes, airborne microorganisms and formaldehyde. In addition, workers are often exposed to noise, vibration and poor ergonomic conditions. The most important occupations, exposures and respiratory diseases are listed in Table 17.1. When taking a patient’s history, the most important question to ask is whether the workplace is dusty. Is there dust on the floors, walls and benches? If the patient is a sawmill worker, he (most workers in this industry are men) should also be asked whether he has observed mold at the workplace. In some special cases personal sampling of dust can be of value. If there is mold at the workplace, spores can be collected by impaction onto glass slides, by impaction in liquid (impingers) or on filters.

17.1.3 Diseases associated with work in primary and secondary woodworking industries Occupational asthma Occupational asthma due to sensitization to different varieties of wood is well described. The best-known type is asthma due to western red cedar (Thuja plicata), although many other common tree species such as eastern white cedar (Thuja occidentalis), ash, cedar of Lebanon, mahogany, birch and teak have also been reported to induce occupational asthma. Sensitization properties have been found to vary by species, and so it is thought that the sensitization is due to naturally occurring substances that vary between the species. For example, the causative agent in western red cedar and eastern white cedar asthma has been identified as plicatic acid. It is not clear whether exposures to softwood from coniferous species such as pines, spruces and firs increases the risk of asthma. Several studies of workers exposed to these

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kinds of dust have shown an increased prevalence of respiratory symptoms, but no clearly increased risk for asthma. The clinical investigation of a wood-working patient with suspected occupational asthma is similar to other occupational asthma investigations. However, the clinican should be aware that such a patient may be exposed to other agents that can cause respiratory disease. Some of these occupations require frequent handling of paints, glues and varnishes containing reactive chemicals such as diisocyanates and acrylates. The standard adhesive used by carpenters and other woodworkers is based on urea–formaldehyde, and formaldehyde is released during heating. Exposure to formaldehyde may exacerbate asthma. Extrinsic allergic alveolitis (hypersensitivity pneumonitis) Extrinsic allergic alveolitis (hypersensitivity pneumonitis) has been described among sawmill workers and wood trimmers in Northern Europe, the USA and Canada. The antigens responsible for these diseases are molds growing in the wood dust or in the bark of the logs. The main species are Cryptostroma corticale in maple strippers’ disease, Alternaria spp. in sawmills and Aspergillus spp. and Thermoactinomyces vulgaris in moldy wood chips. In Sweden in the 1970s, there was an outbreak of allergic alveolitis among wood trimmers due to the fact that unsawn wood was stored under warm and damp conditions, promoting the growth of Rhizopus spp. and Penicillium spp. Outbreaks of maple bark disease occurred among workers peeling off moldy bark from maple logs. Patients with allergic alveolitis often present with febrile influenza-like reactions with cough, chest tightness, malaise and chills. These symptoms start 4–8 hours after the beginning of the exposure, and disappear during the following night. If the exposure continues the symptoms will recur. In the typical case there will be bilateral crackles on chest auscultation. In addition to this acute form of allergic alveolitis, there may also be a subacute form characterized by progressively increasing dyspnea and dry cough. A chronic form is mainly characterized by the development of pulmonary fibrosis. The two latter forms result from long-standing, chronic exposure to the causative agents. When faced with a patient of working age presenting with a febrile illness as described above, it is wise to consider the possibility of allergic alveolitis. Key questions that should be asked are the patient’s occupation and whether he or she has handled moldy material; note that the latter may have occurred in nonoccupational settings, for instance while burning woodchips in a domestic boiler. A patient with suspected allergic alveolitis should be investigated with pulmonary function tests, chest X-ray or CT and sometimes also bronchoscopy. An occupational hygiene investigation is often helpful. IgG antibodies may appear after repeated exposures to airborne fungal spores. Specific IgG antibodies to Saccharopolyspora, Aspergillus, Penicillium and Rhizopus have been used as markers of exposure in studies of farmers and workers from sawmills. Clinically, such analyses can be useful for establishing that an exposure has occurred; however, the presence of specific IgG is only a marker of exposure and is not a sign of the disease. Chronic bronchitis Wood dust and volatile chemicals have irritant properties which may cause inflammation in the upper airway, as well as increasing the risk for chronic bronchitis. Exposure

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to wood dust is associated with acute effects on lung function, as well perhaps as longterm effects, such as development of chronic airways obstruction. An increased risk for rhinitis has been described among woodwork teachers. Cancer The International Agency for Cancer Research has classified wood dust as a group I human carcinogen. There are several studies showing a very high risk for sino-nasal adenocarcinoma among workers exposed to dust from hardwoods, such as oak, mahogany and beech. There is probably also an increased risk for sino-nasal cancer after exposure to softwood, but studies are less conclusive.

17.2 The pulp and paper industry The production of paper from fiber originates from China, where paper from rags and grass was produced as early as 100 AD. Rags were the main source of fiber for paper production until middle of 1800s. In the early years of the Industrial Revolution there was an increasing demand for paper; however, paper production was greatly hampered by the lack of raw material, as rags were the only existing fiber source. In the middle of the 1850s, the fiber supply shifted as several different methods were developed to extract pulp from wood. This was a major breakthrough of great importance for further scientific and industrial development. The main methods were mechanical (abrasion), acidic (sulfite) or alkaline (sulfate or Kraft). Today the use of recycled paper has increased. In some parts of the word bagass (the remains of sugar cane after the extraction of raw sugar) is used for pulp production. The main producers of pulp are the USA, Canada, China and Sweden. The fibers used to make paper are often bleached; this was originally achieved by a combination of sunlight and acid. The use of chlorine became widespread during the 1800s, and chlorine was later replaced with chlorine dioxide. Many nonchlorine bleaching methods have since been developed, including bleaching based on peroxides, oxygen, ozone and peracetic acid. Pulp originating from the sulfite process is lighter and generally easier to bleach; hence, for environmental reasons, the use of sulfite fibers for paper production has increased. The extracted fibers are used for paper production; the most common products are newsprint, printing and writing paper and soft paper products (toilet paper and napkins). The final product contains many additives; while toilet papers and newsprint have a high proportion of fibers (80%), the additive content of printing papers may be as high as 50%. Possible additives include kaolin, talc and different kinds of glues and whiteners. Asbestos was also used as a filler in some paper products. The most important occupations and exposures are shown in Table 17.2.

17.2.1 Diseases associated with work in pulp and paper industry The most important diseases associated with work in pulp and paper industry are shown in Table 17.2. Exposure to chlorine and chlorine dioxide used for bleaching increases the risk for asthma. Exposure levels tend to be low under normal conditions

17.3

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Table 17.2 The most important occupations, exposures and respiratory diseases among pulp and paper mill workers Occupations Process operators Sulfate mills Sulfite mills Mechanical mills Bleachery workers

Paper-machine workers

Maintenance workers

Exposures

Diseases/symptoms

Reduced sulfur compounds Sulfur dioxide Wood dust Terpenes Chlorine dioxide Ozone Peracetic acid Paper dust Kaolin Talc Asbestos Reduced sulfur compounds Sulfur dioxide Wood dust Terpenes

Asphyxia Asthma, chronic bronchitis Lymphomas Asthma Asthma Rhinitis Chronic bronchitis Malignant mesotheliomas Lung cancer

but can become much higher during accidents and process disturbances. These exposure accidents are probably the main inducers of asthma among bleachery workers. Ozone was quite recently introduced as an environmentally friendly way of bleaching pulp. However, the process is very unstable, and studies from Sweden have shown that bleachery workers exposed to ozone develop asthma and pulmonary function impairment. The risk is linked to the number of peak exposures to ozone. The highest levels of paper dust are found in soft paper mills, where the proportion of recycled paper is high (up to 80%). The fibers used in recycled paper are shorter than virgin fibers, and so are more likely to escape from the paper during processing. High levels (often over 10 mg/m3) of total (paper) dust have been measured in such mills. Dose-dependent impairment of lung function has been demonstrated in such environments, as well as an increased risk of obstructive airway diseases. In other paper mills, producing printing papers or newsprint, the dust levels are much lower, and no lung function impairment or increased risk for asthma has been described. Asbestos has been used, and still is used in some countries, for insulation purposes in pulp and paper mills; maintenance workers in particular have an increased risk for lung cancer and mesotheliomas. An increased risk for lymphoma has also been noted among pulp mill workers. The causative agents in this case may be soluble components in the wood.

17.3

The textile industry

17.3.1 General background The textile industry includes a wide range of different processes, such as spinning, weaving, knitting and the production of yarn. It includes also the dyeing of yarn and

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Table 17.3 The most important occupations, exposures and diseases in the textile industry Occupations

Exposures

Diseases

Yarn manufacturing Wool production

Dust, bleaching chemicals Bacteria (anthrax), dust and bleach

Silk industry Synthetic fibers Dyeing Spinning and weaving

Natural silk, bacteria Fiber dust Sensitizing dyes, acids and alkalis Dust, microorganisms and endotoxins

Asthma Byssinosis Inhalation fever Asthma Bronchiolitis obliterans Asthma Byssinosis Inhalation fever

fabrics. Originally the textile industry was based on natural fibers from silk, cotton and wool, but the use of synthetic fibers is increasing: in 2004, more than 50% of the worldwide fiber supply to the textile industry was synthetic. Work in the textile industry has long been acknowledged as hazardous. With the increased mechanization of the industry by means of the flying shuttle, the spinning jenny and the water frame spinner, production increased and factories became larger, resulting in higher levels of dusts, endotoxins and microorganisms. In the 1800s there were several descriptions of epidemic outbreaks of mill fever, byssinosis and asthma. This pattern of respiratory diseases is still recognizable in the textile industry, but in recent years diseases such as bronchiolitis obliterans and lung fibrosis have been described. The different processes and main exposures are described in Table 17.3. In addition to respiratory hazards, textile industry workers are exposed to repetitive work which may cause shoulder and neck disorders. Exposure to carbon disulfide in factories producing rayon fibers has clearly been linked to an increased risk to ischemic heart disease.

17.3.2 Diseases associated with work in the textile industry Byssinosis Respiratory diseases have always been one of the most important ailments among textile industry workers. The most common is byssinosis, an acute or chronic lung disease among workers exposed to organic dust, usually derived from cotton, hemp or flax. Byssinosis-like syndromes have also been demonstrated among workers exposed to other kinds of organic dust, for instance agricultural workers. The most important exposure today is cotton dust: about 300,000 workers in the USA are exposed to cotton dust, but in recent years there has been a steep decline in cotton dust-induced lung disease in the USA. The prevalence of byssinosis in cotton workers in industrially developed countries is now just a few percent. This is in sharp contrast to the conditions in low- and middle-income countries where the prevalence is much higher. In countries like Indonesia, India and Sudan, byssinosis has been reported to affect 30–50% of the workforce. The prevalence of byssinosis in Turkish cotton processing workers was reported to be 14% [1]. The clinical manifestations are chest tightness, dyspnea and coughing. The symptoms begin on Monday and abate in the evening; this distinguishes byssinosis from occupational asthma, where the symptoms tend to increase over the working week. If

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Table 17.4 Severity classification of byssinosis Symptom

Grade

No chest tightness or dyspnea on Mondays Cough and sometimes chest tightness on Mondays Chest tightness and/or dyspnea on Mondays (only) Chest tightness and/or dyspnea on all workdays

0 0.5 1.0 2.0

the worker is away from exposure for a longer period, the symptoms tend to be more severe when re-exposure occurs. If exposure continues over the weekend, the Monday symptoms will not appear. Pulmonary function is also affected in two different ways due to exposure to organic dust. The first effect is chronic and is characterized by reduced FEV1 as well as reduced FEV1:FVC. The reduction is dependent on the cumulative exposure to dust; that is, both dust concentration and duration of exposure. The second effect is an acute one, characterized by increasing obstruction over a work shift where there is exposure to cotton dust. The cross-shift decrement is more severe after an absence from exposure for more than 2 days. In the 1940s and 1950s extensive studies of respiratory diseases were performed in the British textile industry by Schilling and colleagues. Based on these studies, a grading scheme for byssinosis was proposed, and the value of this classification has been confirmed by others (Table 17.4). The causative agent is probably some part of the plant (cotton) or some contaminants associated with the plant. The contaminants could be microorganisms and/or their constituents, mainly endotoxins from Gram-negative bacteria. Experiments with water-soluble extracts from cotton bracts (the leaves below the cotton ball) have confirmed their ability to induce obstruction and inflammation in the airways. However, experimental cardroom studies have strongly suggested that endotoxin is an etiologic factor in the acute respiratory reaction to cotton dust. Inhalation fever Inhalation fever is a syndrome characterized by fever, cough, chills and malaise. It occurs soon after the start of work. The symptoms disappear after a few days’ work, but return if the worker starts to work again after an absence from work. Chest tightness does not appear to be associated with inhalation fever. The chest radiograph and pulmonary function are normal. The mechanism behind inhalation fever is considered to be a nonspecific activation of alveolar macrophages and systematic releases of pyrogenic factors, such as TNF-a and interleukin-6. Inhalation fever occurs in many occupations, such as welders, metal workers and workers handling different polymers. It is also associated with textile manufacturing; the causative factor in this industry is probably endotoxin produced by Gram-negative bacteria in the cotton. Such fever syndromes occur most frequently with the use of lowquality raw cotton. Inhalation fever is also known as mill-fever, mattress-maker’s fever and weaver’s cough. The alternative name ODTS (organic dust toxic syndrome) has been proposed; however, the syndrome shares clinical features with other inhalation fevers, such as metal fume fever or polymer fever, and the term ‘inhalation fever’ is to be preferred.

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Anthrax or woolsorter’s disease Anthrax is a potentially lethal infectious disease caused by Bacillus anthracis, a Grampositive spore-forming bacterium [2]. It is highly contagious, but the pathway is from animals to humans; there are no known cases of human to human transmission. It was early observed that woolsorters were at increased risk for anthrax and Thackrah reported in 1832 that 20% of the workforce was affected by a severe respiratory disease, which was probably anthrax. Handling of wool was early suspected as the cause of the disease, but it was only when Robert Koch and Louis Pasteur discovered B. anthracis that the mode of transmission was detected. The main source of infection was dried blood in the fleeces, not from sheep but from goats, and camels. In the industrialized world the disease has almost disappeared as an occupational disease and during the last 20 years just 14 cases have been reported [3]. However, anthrax is still common in parts of Africa and Latin America and eastern Europe. From eastern Turkey (Anatolia) 85 cases were reported, and about half of them were probably of occupational origin [4] Asthma, chronic bronchiolitis and interstitial lung disease Occupational asthma caused by sensitization to reactive dyes has been described among textile dyers and workers producing reactive dyes. Workers processing raw silk are exposed to a fine dust derived from the gum that binds the strands secreted by the silkworms. Studies from Russia and China have reported a high prevalence of occupational asthma among these workers. However, it is not clear whether exposure to textile dust in general increases the risk for asthma. Several studies of workers exposed to textile dust have shown an increased prevalence of respiratory symptoms, but no increased risk of asthma. Chronic bronchitis (recurrent cough with phlegm) is common among textile workers, and is caused by exposure to dust. Several cases of bronchiolitis obliterans have occurred among workers exposed to paint that has been sprayed on textiles. The most famous outbreak was in Spain in 1990s in the Ardystil plant in Alcoy: the so-called Ardystil syndrome. The causative exposure was polyamide-amine polymers in the paint, and the reason for the toxic reaction was the use of spraying as the mode of paint application. This mode of application is still used and new cases may show up. Any occupational pulmonary physician must place the patient’s occupation very high on the suspect list when a new case of bronchiolitis obliterans is seen in a patient of working age. Interstitial lung disease has been observed among workers exposed to microfibers or flock; this is known as flock worker’s lung. The flocking industry produces fleeced fabric for use in the production of upholstery, clothing, carpets and similar items. Flock consists mainly of synthetic short fibers, often of nylon, rayon or polypropylene. Flock manufacturers cut these materials into a powder of short fibers, measuring 0.5–5.0 mm. Exposed workers develop an interstitial lung disease with cough, dyspnea and radiographic evidence of interstitial fibrosis. The histopathological pattern is bronchiolar with peribronchiolar lymphocytic inflammation and lymphoid hyperplasia. Lung function tests show a restrictive pattern. Cases have been reported from Canada, the USA and Turkey, but the syndrome/disease is probably under-recognized. Another interstitial lung disease that occurs in textile industry is silicosis: Turkish physicians have recently reported 35 cases of silicosis among young males working with jet sandblasting of denim jeans.

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Malignant diseases Lung cancer and mesotheliomas have been described among employees of asbestos textile plants. However, in the 1970s a reduced risk for lung cancer was described among male cotton workers in Georgia, USA. This unexpected inverse observation has been reproduced in several studies with adequate control for confounders such as smoking. Experimental and epidemiological studies indicate that endotoxin is the most plausible candidate for the protective factor.

17.4

Prevention

Most of the diseases occurring among wood workers, pulp and paper mill workers and textile workers are preventable. Some specific respiratory diseases such as allergic alveolitis, inhalation fever and byssinosis are almost all (in close to 100% of cases) caused by occupational exposures. The burden of illness due to occupation is approximately 15–20% for asthma and chronic obstructive pulmonary disease. These figures imply that primary prevention action of choice is control of the occupational exposure by reducing or eliminating the levels at workplace. This can be accomplished by removal or substitution of hazardous substances, improved ventilation, the modification of production techniques or by automation of the process. If these efforts fail, personal protection could be used. Protective equipment may also be useful during very short tasks, such as maintenance tasks, where more general efforts are not feasible.

References 1. Altin, R., Ozkurt, S., FisekC¸i, F., Cimrin, A.H., Zencir, M., Savinc, C. (2002) Prevalence of byssinosis and respiratory symptoms among cotton mill workers. Respiration 69: 52–56. 2. Sternbach, G. (2003) The history of anthrax. J. Emerg. Med. 24: 463–467. 3. Metcalfe, N. (2004) The history of woolsorter’s disease: A Yorkshire beginning with an international furure. Occup. Med. 54: 489–493. ¨ ., Bilici, A., Bilgili, S.G., Evirgen, O ¨ . (2008) 4. Karahogacil, M.K., Akdeniz, N., Akdeniz, H., C¸alka, O Cutaneous antrax in eastern Turkey: a review of 85 cases. Clin. Exp. Dermatol. 33: 406–411.

Further reading Balmes, J., Becklake, M., Blanc, P., Henneberger, P., Kreiss, K., Mapp, C., Milton, D., Schwartz, D., Tor
en, K., Viegi, G. (2003) American Thoracic Society Statement: Occupational contribution to the burden of airway disease. Am. J. Respir. Crit. Care Med. 167: 787–797. Blanc, P.D. (2007) How Everyday Products Make People Sick. Toxins at Home and in the Workplace. University of California Press: Berkeley, CA. Camus, Ph., Nemery, B. (1998) A novel cause for bronchiolitis obliterans organizing pneumonia: exposure to paint aerosols in textile workshops. Eur. Respir. J. 11: 259–262. Chan-Yeung, M., Malo, J.-L. (2006) Western red cedar (Thuja plicata) and other wood dusts. In Asthma in the Workplace, 3rd edn, Bernstein, I.L., Chan-Yeung, M., Malo, J.-L., Bernstein, D.I. (eds). Taylor&Francis: New York.

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Cimrin, A., Sigsgaard, T., Nemery, B. (2006) Sandblasting jeans kills young people. Eur. Respir. J. 28: 885–886. Eduard, W. (2006) The Nordic Expert Group for Criteria Documentation of Health Risk from Chemicals. 139. Fungal Spores. Arbete och H€alsa; 21. Hendrick, D.J., Burge, P.S., Beckett, W.S., Churg, A. (2002) Occupational Disorders of the Lung. Recognition, Management and Prevention. Saunders: London. Kern, D.G., Crausman, R.S., Durand, K.T.H., Nayer, A., Kuhn, C. (1998) Flock worker’s lung: Chronic interstitial lung disease in the nylon flocking industry. Ann. Intern. Med. 129: 261–272.

18 Chemical, coatings and plastics industries Oyebode A. Taiwo and Carrie A. Redlich Yale University School of Medicine, New Haven, CT, USA

18.1

Introduction and definitions

The overall objective of the chemical industry is to convert raw materials such as oil, gas, minerals and metals into industrial chemicals and eventually numerous consumer products (Figure 18.1). Coatings and plastics are diverse, overlapping and rapidly growing sectors of the chemical industry, and comprise the majority of the chemistry industry’s output worldwide. Coatings include a range of products such as paints, primers, varnishes and other products that protect, decorate, and/or add functionality to the surface or object being covered, such as waterproofing or protection against corrosion. Plastics refer to synthetic or semi-synthetic polymeric materials that can be made into many different types of products, including hard and soft plastic products. Although the chemical, coatings and plastics industries encompass a wide array of different production processes, substances and products, they share some common features, exposures and respiratory risks. Primary production of coatings and plastics, the focus of this chapter, typically occurs in larger-scale chemical plants. Coating and plastic chemicals frequently then undergo additional formulation and processing in other industries, which may include final production stages, or the formulated plastic or coating may have its final application by an end-user, such as a foam applicator or spray painter. Thus exposure to coatings and plastics can occur in many other settings, such as the automotive (Chapter 16), wood and textile (Chaper 17), service (Chapter 20), construction (Chapter 21) and mining industries (Chapter 13), and the home environment during home improvement projects and hobbies (Chapers 5 and 7). Many of

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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RAW MATERIALS (minerals, metals, oils, natural gas)

Base Organic and Inorganic Chemicals (coal tar, acids, alkalis, salts)

INTERMEDIATES (catalysts, resins, solvents)

FINISHED CHEMICAL PRODUCTS (Plastics, paints, drugs, cosmetics)

Figure 18.1 Main components of the chemical industry

the base chemicals used to produce coatings and plastics (e.g. acids, solvents, pigments) are used in other major sectors of the chemical industry, such as agricultural and food industries (Chapter 12) and electronics (Chapter 19). This chapter is intended to help practicing clinicians understand the types of work exposures and hazards that occur in the primary chemical, coatings and plastics industries and help them recognize the respiratory disorders that can occur in workers involved in these major chemical sectors. Given the widespread use of coatings and plastics, and growing concerns regarding potential health effects, practitioners need to be familiar with major types of plastics and coatings being produced, and their potential adverse health effects. The major sectors of the chemical industry and the overall processes and potential exposures involved in the production of coatings and plastics are described first, followed by specific commonly used plastics and associated respiratory diseases. Finally an approach to diagnosis and management of workers in the chemical coating and plastics industries is summarized.

18.2 Overview of the chemical, coatings and plastics industry The chemical industry is a large, diverse and expanding industry, with the biggest area of growth in southeast Asia. Over a million workers are currently employed in the manufacture of chemicals in the USA and over 3 million workers are employed in this sector in the European Union. Recent changes in the chemical industry, including

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Table 18.1 Chemical plants: typical components and potential hazards Component

Selected potential hazards

Process units – reactors/distillation towers/heat exchanges/pumps Storage facilities – tanks Loading/unloading facilities

Routine and accidental release chemicals, maintenance equipment Accidents, explosions Accidental exposures loading and unloading chemicals Heat generation, asbestos for insulating boilers, thermal degradation products Leaks, explosions Novel chemical products Air, soil and water contamination Transportation accidents

Power sources – boilers/incinerators Warehouses – storage Analytical laboratories Waste treatment areas Transportation – railcars, tank trucks

the shift in production from traditional mainly European and American countries to Asia, Latin America and eastern European countries and the development of new production technologies, may lead to new or previously unrecognized respiratory hazards. Typical modern chemical plants are large, automated facilities that share certain common types of facilities, equipment and hazards (Table 18.1). These typically include: large tanks for chemical storage; loading and unloading facilities; power sources; storage areas; cooling towers; control rooms; process equipment; and nearby transportation facilities. There is potential for exposures during maintenance and repair of equipment, and from accidental leaks, explosions and fires. Flexible batch-production chemical plants are being built that can produce a greater number and volume of chemicals in smaller size facilities. The growth in the number and productivity of such chemical plants, combined with financial pressures to reduce costs and lax health and safety regulations, can create greater opportunities for exposure to hazardous chemicals.

18.3

Major types of paints, coatings and plastics

Paint and coating manufacturing facilities produce a large array of paints, varnishes, inks, adhesives, and specialty coatings that preserve, protect and decorate products. These include house paints, automotive finishes, appliance finishes, metallic paints and paints used for graphics and artwork. Plastics refer to a wide range of synthetic or semi-synthetic polymerization materials or products. With advances in plastic technology and increasingly diverse uses, plastic materials are one of the fastest growing components of the chemical industry worldwide. The production of plastics involves three main steps: (1) the synthesis of plastic polymers; (2) mixing and compounding of various additives to the resin materials; and (3) conversion of the compounded polymer into different products. Common uses are in packaging and numerous consumer products, and increasingly in building and construction. Plastic materials have replaced glass, wood and metal in many industrial and commercial purposes.

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Major types of plastics and coatings, their uses and chemicals used in their production are briefly discussed below, to provide clinicians with an overview of these diverse products and potential workplace exposures.

18.3.1 Acrylics The acrylics are a group of plastics containing polymerized acrylate esters produced from acrylic monomers such as methyl methacrylate. The polymerized acrylics are used to produce glass substitutes (plexiglass), dentures, surgical prostheses, adhesives, paints and other products. The acrylic monomers are known respiratory tract irritants and sensitizing agents. Occupational asthma has been reported with several different acrylate monomers, typically in end-user settings, rather than in primary production of the acrylic components.

18.3.2 Acrylonitrile Acrylonitrile is an important monomer in the manufacturing of synthetic polymers such as acrylic fibers. Acrylonitrile is also copolymerized with butadiene and/or styrene to form the major synthetic rubbers in use. Acrylonitrile is an irritant to the mucous membranes and skin. Acrylonitrile is metabolized to form cyanide, which is further metabolized to thiocyanates. Therefore, acute toxicity may initially cause symptoms of headaches, lightheadedness and fatigue and rarely progresses to asphyxia and death.

18.3.3 Epoxy resins Epoxy resin products are polymers formed through the reaction of uncured epoxide resins (monomers or oligomers) with a curing agent or catalyst. The uncured resin typically consists of epichlorohydrin, diluents, fillers and pigments. Diluents include glycidyl ethers of bisphenol A and various solvents. Fillers such as sand, clay or fiberglass add bulk. Common curing agents or hardeners include acid anhydrides, amines and polyamides. Major applications of epoxy resins include adhesives, laminating materials, coatings, electronics manufacturing and composite tools. Epoxy resins, similar to polyurethanes, are frequently cured where the final product is used, resulting in potentially greater exposures among end-users than among producers or formulators. Workers using epoxy resin-based paints have showed higher incidence of cough, dyspnea and cross work shift declines in FEV1 compared with unexposed workers. The most common respiratory problem reported among workers who produce epoxy resins has been asthma, with most cases attributed to the hardening or curing agents, such as acid anhydrides, discussed further below. Exposures most commonly occur when the epoxy resin chemicals are combined and mixed or during curing, which can generate heat and fumes. Epichlorohydrin and glycidyl ethers used to form epoxy resins such as bisphenol A epoxy are irritants at high levels, and also sensitizers, and can cause allergic contact dermatitis in exposed workers, with asthma less commonly reported.

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18.3.4 Acid anhydrides Acid anhydrides such as phthalic anhydride, trimellitic anhydride and maleic anhydride are low-molecular weight reactive chemicals used primarily as curing or hardening agents for epoxy resins. Such reactive curing agents are also used in the production of other resins, plastics, polyesters, polyurethanes and coatings, and the production of dyes, insecticides and other products. Acid anhydrides, although best known as sensitizers, can cause severe irritation of the upper and lower airways, presenting as epistaxis or diffuse pneumonitis. Acid anhydrides can cause several respiratory syndromes felt to be largely immunemediated, most commonly occupational asthma and rhinitis. The chemicals can react with proteins such as albumin to form antigenic complexes, and induce acid– anhydride–albumin specific immune responses. Specific IgE is usually detected in workers with asthma due to trimellitic anhydride. Exposure to acid anhydrides can also cause a hypersensitivity pneumonitis-like syndrome that has similarities to the inhalation fevers, and that has been termed late trimellitic flu. Workers present with myalgias, fever and respiratory symptoms following a work shift. An immunogenic origin for this syndrome is likely; however, direct toxicity of the acid anhydride is also possible, as well as interactions with co-exposures. Inhalation of high levels of trimellitic anhydride has also been reported to cause a rare syndrome characterized by hemoptysis, pulmonary infiltrates, hypoxia and anemia called pulmonary disease–anemia syndrome. Lung biopsies have shown diffuse alveolar hemorrhage and edema, but the mechanism of this syndrome remains unclear.

18.3.5 Other curing agents Amines like dimethylethanolamine, piperazine and ethylenediamine are used predominantly as curing agents for resins. Some amines like hexamine are also used in the rubber industry as an accelerator. Amines can be respiratory tract irritants and also sensitizers causing occupational asthma.

18.3.6 Formaldehyde–amino resins Formaldehyde, a reactive colorless aldehyde gas produced from methanol, is a central chemical used in the synthesis of many chemical compounds, including resins, produced by the combination of formaldehyde with melamine, urea or phenol. These resins are used in numerous applications such as foam insulation, adhesives and binders and in the production of plywood, particleboard, furniture, molded plastic, paper production and textiles. Formaldehyde also has antimicrobial properties and is used in cosmetics, formalin embalming fluid and disinfectants (Chapters 1, 4 and 20). Occupational exposures are most common in secondary exposure settings such as particleboard mills, paper or textile finishing, or disinfection or embalming, rather than primary chemical production (Chapter 17).

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Formaldehyde has a pungent odor and is highly irritating to the nasal and upper airways. Less commonly formaldehyde exposure can lead to asthma, and rarely inhalation of very high levels can cause chemical pneumonitis and pulmonary edema. Asthmatic-type allergic sensitization to formaldehyde has been reported, but is not common. There is little data on the pulmonary effects of long-term formaldehyde exposures. The other major health concern regarding formaldehyde is carcinogenicity. The International Agency for Cancer Research has concluded that formaldehyde is a human carcinogen, with the strongest evidence for nasopharyngeal cancer among workers exposed to formaldehyde.

18.3.7 Fluoropolymers Fluoropolymers comprise a growing class of polymer materials that contain fluorine, such as polytetrafluoroethylene (PTFE), known as Teflon coating. They combine high chemical resistance with low friction, making them useful coating materials for wires, cables, metal parts and nonstick cookware. Inhalation of the thermal decomposition of fluorocarbon polymers such as PTFE can cause polymer fume fever, similar to other inhalation fevers such as metal fume fever (see below). Exposures can occur in a variety of settings, such as welding of coated parts or among production workers who smoke, presumably from heat decomposition of cigarettes contaminated with the polymer.

18.3.8 Polyethylene Polyethylene is an important thermoplastic polymer produced from polymerization reactions involving the monomer ethylene, accounting for over 30% of the plastics produced in the USA. High-density polyethylene is used in the manufacture of containers, machine parts, toys and housewares, while low-density polyethylene is used for coatings, garbage bags and food packaging. The thermal decomposition products of polyethylene can include carbon dioxide, formaldehyde and acrolein, potent respiratory irritants. Asthma has been reported among workers heating polyethylene film as part of food-wrapping activity. Ethylene gas is one of the most extensively produced organic compounds worldwide, used in the production of polyethylene polymers, and other common chemicals, such as ethylene oxide (a potential sensitizer), polyvinyl chloride and trichloroethylene. Historically ethylene was used as a surgical anesthetic. It can act as an asphyxiant, displacing oxygen, and can be fatal at very high concentrations.

18.3.9 Polypropylene Polypropylene is a plastic characterized by relative strength, heat resistance and durability, formed from the monomer propylene. It is used in molded products such as pipes and packaging, in fibrous forms to make clothing and carpeting, and as sheets to produce office supplies such as folders. Propylene is a simple asphyxiant and can

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produce symptoms of hypoxia after high accidental exposures. The thermal decomposition products of polypropylene include respiratory irritants like acrolein and formaldehyde.

18.3.10 Polystyrene Polystyrene is a polymer used to produce a wide range of rubber and plastic polymers. One of its most common uses is in the production of polystyrene foam for packaging material and food products such as plates and disposable food containers. Polystyrene is made from polymerization of the aromatic monomer styrene. Reported adverse health effects related to polystyrene production have focused largely on the irritating effects of styrene on the upper airways. Styrene has also been suggested to be a possible sensitizer.

18.3.11 Polyvinyl chloride Polyvinyl chloride (PVC) is produced by the polymerization of vinyl chloride monomer, with various plasticizers, such as phthalates and other additives. PVC is widely used in products such as plumbing pipes, cable coatings, construction composites (e.g. vinyl siding, flooring, roofing), packaging materials, housewares, electronic accessories and automotive parts. Inhalation of PVC dust and fumes has been associated with nonmalignant respiratory diseases, including pneumoconiosis and asthma. Diffuse irregular nodular densities on chest X-ray and mild restrictive and obstructive changes in pulmonary function have been reported in workers exposed to high PVC dust levels in PVC manufacturing plants. Histologic evaluation of lung tissue from a few workers who developed pneumoconiosis has shown histiocytes, multinucleated giant cells, foreign body granulomas and fibrosis. The risk of respiratory diseases in workers exposed to PVC dust appears to be low in current operations. Heat degradation products of PVC products can also cause respiratory irritation and probably asthma. Similar to polyethylene, ‘meat-wrappers’ asthma has been reported in workers who package food with PVC wrapping material that is heated. PVC degradation products include hydrogen chloride and various irritants, and possibly sensitizers such as phthalic anhydrides, but asthmatic responses are most likely due to the irritant exposures. There have been concerns that plasticizers and other chemicals added to PVC such as diethylhexyl phthalate may leach out of consumer products such as soft PVC toys or off-gas from home vinyl products such as flooring, but there is little data demonstrating associated health effects.

18.3.12 Polyurethanes – diisocyanates Diisocyanates are primarily used in the production of polyurethane products, including rigid and flexible foams, coatings and paints, elastomers, adhesives and sealants The major commercial diisocyanates (commonly referred to as ‘isocyanates’) are

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toluene diisocyanates (TDI), methylene diphenyl diisocyanates (MDI) and hexamethylene diisocyanate (HDI), all of which can cause isocyanate asthma. Polyurethane products are used in numerous industries, including automotive, construction, furniture, paints and coatings, sports equipment and medical applications. Diisocyanates used in polyurethane production should be distinguished from monoisocyanates such as methyl isocyanate, which contain one NCO, are not cross-linking agents and are produced for limited applications, such as pesticides. Methyl isocyanate, a potent volatile irritant, was the chemical released from a pesticide factory in Bhopal India in 1984, one of the worst recorded industrial accidents. Numerous residents living around the factory died, probably from toxic pneumonitis and pulmonary edema. Careful long-term follow-up has been difficult, but persistent respiratory symptoms, airflow obstruction and restrictive lung changes have been reported in survivors. Isocyanates are well-known sensitizers and remain one of the most common causes of occupational asthma in industrialized countries, despite efforts to reduce airborne exposures. Most reported cases occur in end-use settings, such as spraying or when heated, rather than the primary production of isocyanates or the formulation of different polyurethane systems. In addition to respiratory exposure, skin exposure to isocyanates may also contribute to sensitization and risk for asthma. Opportunities for skin exposure are common during polyurethane production and application, such as spills, contact with contaminated equipment or direct contact with uncured or partially cured polyurethane products. Once sensitized, exposure to very low airborne levels of isocyanates, below regulatory standards, can lead to asthmatic symptoms. Preventive efforts should target respiratory and skin exposure. Isocyanates, typically following higher respiratory exposures, can also cause hypersensitivity pneumonitis, which can overlap with asthma in the same patient. At high concentrations isocyanates can be airway irritants. Finished cured polyurethane products, as with other plastics, are considered inert and nonhazardous. However, full curing can take longer than is apparent (tack-free), providing opportunities for unexpected exposure, especially skin exposure from handling recently made polyurethane products or coatings. Processes that generate heat such as drilling or cutting cured polyurethane materials, or fires, can generate toxic mixtures of thermal degradation products, including monoisocyanates such as methyl isocyanate and diisocyanate monomers.

18.3.13 Reactive dyes/diazonium salts Reactive dyes are used to dye various materials, including plastics such as polyesters and nylon. The dyes contain a chromophore (the dye), and a reactive group such as vinylsulfonyl that can bind with the plastic. Diazonium compounds or salts are intermediates in the organic synthesis of reactive dyes. Reactive dyes and diazonium salts can be potent sensitizers and can cause allergic contact dermatitis and asthma. They can be difficult to identify as the causative agent, as they typically are a tiny fraction of the final product, one of many chemical substances added during production, and may not be listed on MSDS sheets or labels. They may also be used in only certain batches or production areas, making exposures more sporadic.

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Table 18.2 Selected respiratory diseases related to exposures in the chemical coating and plastics industries Respiratory disorder

Selected agents (known or suspected)

Upper airway irritation

Numerous irritant gases, fumes, dusts, particulates (e.g. ammonia, formaldehyde, hydrogen chloride, phosgene)

Asthma Sensitizer Irritant (RADS) Acute/subacute inhalational injury Toxic pneumonitis Polymer fume fever Ardystil syndrome Bronchiolitis obliterans Hypersensitivity pneumonitis Interstitial lung disease

18.4

Isocyanates, anhydrides (e.g. trimellitic anhydride), reactive dyes Irritant gases, fumes (chlorine, formaldehyde, ammonia, sulfur dioxide)

Irritant gases, fumes (phosgene, nitrogen oxides, sulfur dioxide, smoke, thermal degradation products, mixed exposures Thermal degradation fluoropolymers (polytetrafluoroethylene) Polymer textile paint (Acramin) Nitrogen dioxide, diacetyl, sulfur dioxide Isocyanates, anhydrides Polyvinyl chloride dust Nylon flock (Flock workers lung) Asbestos (old insulation)

Major respiratory disorders in chemical, coatings and plastics workers

Workers in the chemical, coating and plastics industries can be exposed to numerous chemicals, materials, work processes and hazards, and thus a full spectrum of occupational lung diseases can occur (Table 18.2). Acute inhalational injuries and allergic lung diseases are the most commonly recognized work-related respiratory tract illnesses in these workers. The major respiratory problems that can occur are described below. The primary nonrespiratory occupational health problems in chemical, coating and plastics facilities, in addition to acute injuries, tend to be contact dermatitis, noiseinduced hearing loss and musculoskeletal problems.

18.4.1 Acute inhalation injury and sequelae Exposure to a numerous chemicals used within the chemicals and plastics industry can cause a spectrum of acute inhalation injuries to the upper and lower airways (Table 18.2). These include mucosal irritation, bronchitis, irritant-induced asthma, toxic pneumonitis and pulmonary edema. The nature and extent of the injury depends primarily on the chemical agent(s) and the extent of exposure, for more severe injuries typically an accidental event. The different inhalation injury syndromes can overlap, especially as exposures are commonly mixed. In general, gases that are highly soluble in water (e.g. ammonia, chlorine and hydrochloric acid) affect primarily the upper respiratory tract, causing mucosal and eye irritation, laryngitis, bronchitis and less

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commonly reactive airways dysfunction syndrome or irritant-induced asthma. Such water-soluble irritant gases typically have good warning properties, so that exposures are more likely to be noticed and avoided than exposures to gases that have low water solubility (e.g. phosgene, nitrogen oxides). The later typically cause less mucosal irritation and are more likely to reach the lung parenchyma and cause chemical pneumonitis and possibly pulmonary edema. Thermal degradation products of plastics and coatings can be particularly toxic and unpredictable. In addition to well-known toxic gases, including some that are chemical asphyxiants (e.g. hydrogen cyanide), poorly characterized mixtures of chemical fumes, gases and particulates can be released from burning plastics and coatings. Polymer fume fever, a flu-like clinical syndrome similar to metal fume fever, can occur in workers exposed to fluorine-containing polymers such as polytetrafluoroethylene (Teflon coating) that have been over-heated. Symptoms of fever, chills, cough and dyspnea typically develop following exposure. The condition can vary in severity, probably depending on the type of pyrolysis products generated and the magnitude of exposure. Although typically self-limiting, cases that more resemble acute chemical pneumonitis, with pulmonary edema, have been reported, as well as also more longterm sequelae. Most workers appear to recover following acute inhalation injury, whether the injury involved more the upper airways or the lung parenchyma, with improvement in symptoms and lung function over a period typically of weeks to months. However, a spectrum of lung abnormalities can persist, but current knowledge is based largely on case series and reports, and extrapolation from animal studies, rather than systematic long- term follow-up. The most common longer-term pulmonary effect noted following acute inhalational injuries is asthmatic-type symptoms. It is likely that a spectrum of airway changes can persist after acute and subacute inhalational injuries, that include irritant-induced asthma, reactive upper airways dysfunction syndrome and gastroesophageal reflux disease. Bronchiolitis obliterans and/or bronchiolitis obliterans organizing pneumonia (BOOP) have been reported following several chemical exposures, including sulfur dioxide, nitrogen dioxide and plastic thermal decomposition products. Several outbreaks of unusual respiratory diseases have been reported among factory workers exposed to a variety of polymeric substances and/or chemicals. Respiratory BOOP-like disease was documented in textile workers spraying polymeric paints (Ardystil syndrome). Bronchiolitis obliterans has recently been recognized in popcorn and chemical workers exposed to diacetyl, a chemical that provides butter flavor (popcorn lung). An unusual form of interstitial lung disease (flock workers lung) has been reported in workers who process synthetic polymeric flocks. Ground glass opacities and micronodules have been reported on thin-section CT scan and pathology has shown lymphocytic bronchiolitis and peribronchiolitis with lymphoid hyperplasia. These outbreaks, although different disease entities, highlight challenges in recognizing and preventing occupational lung diseases in workers who produce and process chemicals, coatings and plastics. In most instances, earlier cases had occurred but gone unrecognized and further evaluation of other workers revealed unrecognized disease. The outbreaks involved exposures that were presumed to be inert or previously

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Table 18.3 Selected sensitizing agents in the chemical and plastics industry Sensitizing agent

End products

Isocyanates (TDI, MDI, HDI) Acid anhydrides Reactive dyes and diazonium salts

Polyurethane foams, coatings, paints Paints, vanishes and reinforced plastics Dyes or intermediates for coloration of cellulose and other fibers, plastics Curing agents for plastic resins, dyes

Amines (ethylenediamines, ethanolamines, piperazine) Acrylates Azodicarbonamide, azobisformamide

Glass substitutes, dentures, surgical prosthesis Plastics

unsuspected based on prior toxicity testing. These occupational diseases also highlight the complexity of exposures in the chemical, coating and plastics industries, including new substances substituting for older ones, mixed exposures and manipulation of inert products (e.g. cutting or sanding) generating toxic exposures.

18.4.2 Allergic diseases – occupational asthma A number of chemicals used in the production of chemical coatings and plastics are known sensitizers that can cause occupational asthma, including isocyanates, amines, anhydrides and reactive dyes (Table 18.3). Such exposures may also cause allergic rhinitis and less commonly hypersensitivity pneumonitis. Dose–response relationships for allergenic chemicals are typically not well-defined, and once sensitized, exposure to extremely low levels can lead to asthmatic responses, complicating recognition and prevention. Surveillance and epidemiologic studies have shown an increased risk of occupational asthma among workers in the primary chemical and plastics industries, and among end-users such as spray painters and floor layers. Such data also show that isocyanates remain the most commonly identified chemical cause of occupational asthma worldwide, despite reduced airborne exposures with the use of less volatile formulations and better hygiene practices. Skin may be an additional route of exposure, especially for chemical asthmagens, and contribute to sensitization and asthma.

18.4.3 Chronic exposures/lung diseases The pulmonary consequences of more chronic long-term exposures in chemical, coating and plastics workers have not been adequately evaluated. Epidemiologic studies of relevant occupational cohorts are limited and have mostly focused on cancer risks, with few longitudinal studies evaluating impact on pulmonary status. The populationbased epidemiology literature investigating occupational risk factors for chronic obstructive pulmonary disease (COPD) has demonstrated that workers in industries such as plastics, textile and automotive repair have an increased risk of COPD, suggesting possible chronic effects of work exposure in such settings, but specific causative agents are not well-defined.

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Data on interstitial lung diseases in chemical, coating and plastics workers are even more limited, similar to the epidemiology literature in general on interstitial lung diseases, most of which are ‘idiopathic’. Few chemicals and processes have been associated with interstitial lung diseases (Table 18.1) such as PVC dust or flock worker lung, noted above. Isocyanates and anhydrides can cause hypersensitivity pneumonitis, with almost all reported cases reflecting acute or subacute rather than chronic hypersensitivity pneumonititis.

18.4.4 Cancer A limited number of chemicals used to produce coatings and plastics have been shown to be carcinogenic in humans, such as vinyl chloride and chloromethyl ethers, although for several others data is controversial or inconclusive, such as formaldehyde, bisphenol A, epichlorohydrin and styrene. Spray painters have been identified as an occupation at increased risk of cancer, but the specific exposures not identified. Chemical plants, especially older ones, may contain asbestos insulation around furnaces, pipes and other structural areas.

18.5 Diagnosis and management The possibility that the workplace may be a contributing factor should be considered in any patient who works in the chemical, coating and plastic industries and presents with new or worsening respiratory complaints, especially new asthma or allergies. Most important is for the clinician to take a careful occupational history, even if the worker does not attribute his/her respiratory symptoms to work. Medical evaluation should follow standard practices, typically first clarifying the pulmonary or nonpulmonary disorder(s) present, such as asthma. Onset of symptoms, temporal relationships of symptoms to work, days off work, and any process changes at work should be inquired about, focusing in particular on when the symptoms first started. Nonpulmonary symptoms may provide important information, such as skin rashes or neurologic symptoms. Since chemical allergies and asthma are of particular concern, history of asthma, allergies, dermatitis and eczema should be determined. Whether co-workers have had similar problems should also be determined. Information regarding work exposures is most commonly obtained from a careful occupational history, including description of the process and workplace, known exposures, time periods worked and use of personal protective equipment. Material safety data sheets and/or labels should be reviewed to identify potential causative chemicals, remembering that such information may be incomplete and/or inaccurate. Nonoccupational exposures and smoking history should also be clarified. Additional tests that can confirm association between work exposures and the patient’s disease, such as immunologic assays, peak flow recordings, should be considered, following standard guidelines for diagnosis. For patients who present with acute inhalational injuries following a specific defined accidental exposure event at work, such as an accidental spill or fire, the critical task is for the clinician to best determine the nature and extent of the toxic exposures and

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anticipate and treat delayed or prolonged health effects. Follow-up with careful assessment of lung function is important. Disease management should follow standard practice and treatment guidelines, also considering public health and preventive considerations. For example, if occupational asthma due to a sensitizer is diagnosed, avoiding further exposure is recommended (including skin exposure), ideally by modifications in the workplace, or a job transfer away from exposure with medical protection. Surveillance of other workers to detect similarly affected workers should be considered, as well as preventive measures to reduce exposures.

Further reading Atis, S., Tutluoglu, B., Levent, E. et al. (2005) The respiratory effects of occupational polypropylene flock exposure. Eur. Respir. J. 25: 110–117. Bernstein, I.L., Chan-Yeung, M., Malo, J.L. et al.. (eds) (2006) Asthma in the Workplace and Related Conditions, 3rd edn. Taylor & Francis: New York. Blomqvist, A., Duzakin-Nystedt, M., Ohlson, C.G. et al. (2005) Airways symptoms, immunological response and exposure in powder painting. Int. Arch. Occup. Environ. Health 78: 123–131. Camus, P., Nemery, B. (1998) A novel cause for bronchiolitis obliterans organizing pneumonia: exposure to paint aerosols in textile workshops. Eur. Respir. J. 11: 259–262. Eckardt, R.E. (1976) Occupational and environmental health hazards in the plastics industry. Environ. Health Perspect. 17: 103–106. Grammer, L.C., Shaughnessy, M.A., Zeiss, C.R. et al. (1997) Review of trimellitic anhydride (TMA) induced respiratory response. Allergy Asthma Proc. 18: 235–237. Malo, J., Hae-Sim, P., Bernstein, I. (2006) Other chemical substances causing occupational asthma. In Bernstein, I.L., Chan-Yeung, M., Malo, J.L. et al.. (eds) (2006) Asthma in the Workplace and Related Conditions, 3rd edn. Taylor & Francis: New York. Markowitz, S. (2005) Chemicals in the plastics, synthetic textile, and rubber industry. In Textbook of Clinical and Environmental Medicine, Rosenstock, L. et al.. (eds). Elsevier Saunders: Philadelphia, PA. Nemery, B. (1996) Late consequences of accidental exposure to inhaled irritants: RADS and the Bhopal disaster. Eur. Respir. J. 9: 1973–1976. Redlich, C.A., Bello, D., Wisnewski, A.V. (2007) Health effects of isocyanates. In Environmental and Occupational Medicine, Rom, W.N. (eds). Lippincott-Raven: Philadelphia, PA. Shusterman, D.J. (1993) Polymer fume fever and other fluorocarbon pyrolysis-related syndromes. Occup. Med. 8: 519–531. Studnicka, M.J., Menzinger, G., Drlicek, M. et al. (1995) Pneumoconiosis and systemic sclerosis following 10 years of exposure to polyvinyl chloride dust. Thorax 50: 583–585; discussion 589.

19 Work with electronics Sherwood Burge Birmingham Heartlands Hospital, Birmingham, UK

19.1 Introduction The most common respiratory problems in the electronics industry are caused by inhaling fluxes used for soldering.

19.2

The history of soldering

Soldering has taken place since ancient times. The first written account is in 77AD in Pliny’s Naturalis Historica. He describes the soldering of copper with cadmea (zinc oxide) with lead resin (probably colophonian) or white lead (tin). At that time, the resin was produced from a number of different species of pine and birch, one of which was the colophon pine. Between 800 and 1100 AD the Mappae Clavicula, a written set of workshop instructions, included one form of solder cream whose recipe translates ‘take two parts of axle grease and a third of resin, mix with an equal quantity of tin filings, heat as you know how and a joint will be made’. In about 1125 a monk known as Theophilus wrote a first-hand account of soldering in the jointing of tin which, after heating the tin, involved smearing it round with the resin of a fir tree. In 1360 Bartholomew Granville wrote an encyclopaedic book called De Proprietatibus Rerum, which states that the jointing of metals ‘may not be foundered without tallow and rosen’. Soft soldering is therefore very ancient. Colophony has been recommended as a flux at least since 1150 and has been the standard flux for the electronics industry since the 1930s. Activators are now added routinely to the colophony to hasten its action. Since

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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about 1980 there have been attempts to replace the colophony in soldering fluxes with a number of other materials, many of which are less easy to use.

19.3 Diseases in those exposed to soft soldering flux fumes Pliny notes that colophony is yellower than ‘the rest but if ground up turns white; it has a rather oppressive scent and consequently the perfumers do not make use of it’. There is then no mention of health hazards until, in 1967, an outbreak of respiratory disease amongst coil winders and tinners in an electronics factory in Monkstown, Northern Ireland. Thirty-nine women and one man in a factory employing 700 were affected with breathlessness and cough. The attacks occurred at work and at night in bed, and were associated with fever and sweating. Polyurethane-coated wire had recently been introduced for coil winding and isocyanates were detected in the fume. The outbreak was attributed to isocyanate sensitization without further investigation; the workers were also exposed to colophony fumes. The first bronchial provocation testing for isocyanates in electronics workers was in 1972, when isocyanates were shown to be the cause in a solderer and wirer and a supervisor working in an electronics factory. The occupational exposure standard for colophony exposure was based on a study by Christy in 1973 following respiratory problems in an American telephone factory where 25 people were restricted from working in the soldering area because of upper respiratory irritation. The exposure standard first proposed 5 years earlier was developed following the exposure of 18 asymptomatic volunteers to heated colophony fumes for periods of 15 minutes and was based on the level required for irritation to the eyes, nose and throat. As an assay on resin acids was not available, the aldehyde content of the fume, expressed as formaldehyde, was initially set as the item to be measured (to make the measurement in mg/m3 a molecular weight of the aldehyde needed to be used; formaldehyde is the lowest molecular weight aldehyde and was used for convenience). This caused great confusion, leading to the belief that formaldehyde was the agent responsible for the adverse reactions to colophony, rather than the resin acid content of the fume, as subsequently demonstrated. Occupational asthma due to colophony fumes was first reported in 1976 from Moscow and London, both with positive bronchial provocation tests to the colophony based fluxes. All patients were wirers and solderers in different factories. There are a number of other soldering fluxes that have (rarely) caused occupational asthma. They include dodecanediotic acid, polyether alcohol–polypropylene glycol and adipic acid. Corrosive fluxes containing zinc and ammonium chloride have caused asthma; however, these are usually used for plumbing rather than electronics as their residues are corrosive and need washing off after soldering.

19.4 Epidemiological context There are many millions employed in the electronics industry worldwide. Basic manufacture involving large workforces, such as soldering operations, has moved from high-income countries to low-income countries. Most of the literature is from

19.7

PRACTICAL HINTS (AND PITFALLS) WHEN TAKING A HISTORY FROM PATIENT

249

the former but it is likely that adverse health consequences are at least as frequent in lower-income countries.

19.5

Definition of scope (and limitations)

This chapter concentrates on occupational asthma. The main causes in the electronics industry are colophony and to a lesser extent isocyanates and acrylates, often used for encapsulation. Recent work on indium alveolitis is included; as far as is known, this is arare disease and doesnot fit easily into the usualclassification ofinterstitial lung diseases. There is little information on other respiratory hazards in the electronics industry.

19.6

Exposures and processes in the electronics industry

Printed circuit board manufacture includes resin bonding, impregnation, laminating, photomasking and etching, cutting and drilling, marking and testing. During preparation, boards may be cleaned with persulfate salts, recognized as potential respiratory sensitizing agents. Once prepared, the circuit boards are then assembled with components which need to be soldered into the printed circuits. This process may be enclosed in automatic flow solder machines, or may involve hand soldering, particularly when rectifying faulty connections. The solder flux fumes are the major hazard, but rectification may involve using a soldering iron to burn through a surface coating, which if encapsulated by polyurethanes may liberate isocyanates. The board is then ready for assembly into the final product. Semiconductor wafer manufacture is where circuits are etched onto silicon wafers. Processes include crystal purification and growth, wafer preparation, epitaxy1 and oxidation, photolithography, doping and type conversion, metallization, interconnections and packaging. This is followed by the assembly of the semiconductors including die separation and bonding, wire bonding, encapsulation, marking and testing. The encapsulation process may involve isocyanates, acrylates or epoxy resins, possible causes of occupational asthma (Table 19.1).

19.7

Practical hints (and pitfalls) when taking a history from patient

.

Colophony is often called rosin. It is the same material that stringed musical instrument players put on their bows to increase friction, and it used to be used in older adhesive dressings. Resin is a less specific term which includes colophony.

.

Many workers exposed to solder flux fumes get their exposure as bystanders rather than by performing soldering themselves. Some surveys have found the prevalence of occupational asthma to be as high in bystanders as in those soldering.

1 Epitaxy is the growth of the crystals of one mineral on the crystal face of another mineral, so that the crystalline substrates of both minerals have the same structural orientation.

Indium

liquid-crystal and plasma display manufacture

Interstitial lung disease with bullae

Sarcoid-like interstitial lung disease

Beryllium

Beryllium Copper machining

Breathless, pneumothorax, no crackles, occasional clubbing

Breathless, no signs in chest. Occasional dermatitis

HRCT Full Lung function Serum Indium levels

CXR, HRCT, BAL, Beryllium lymphocyte proliferation assay (fresh blood)

Serial measurements of peak flow Specific challenge IgE to isocyanate conjugates (20% only positive in occupational asthma)

Chest tightness or breathlessness with improvement on days away from work

Occupational asthma Occupational rhinitis

Isocyanates (from polyurethane coated wires or encapsulation) Epoxy resins and anhydrides Acrylates Colophony

Encapsulator, rectifier Surface coater

Serial measurements of peak flow Specific challenge if flux unusual

Chest tightness or breathlessness with improvement on days away from work

Occupational asthma Occupational rhinitis (Allergic alveolitis, rare)

Colophony most common

Solderer Bystander to soldering by others

Main investigations

Symptoms/signs

Respiratory effects

Possible relevant exposures

Job

Table 19.1 Shows a list of jobs and possible exposures and respiratory health outcomes

250 CH 19 WORK WITH ELECTRONICS

19.8

HOW TO DOCUMENT EXPOSURE, INCLUDING BIOMONITORING

251

.

Hazard labels on solder are often concerned with its lead content. The usual electronic solder is a mixture of tin and lead, neither of which is volatile at soldering temperatures of 250–350  C; lead poisoning is not a problem in electronics workers. The volatile products come from the fluxes which are needed to exclude oxygen from the heated metals to be joined and to assist the flow of the solder.

.

Not all electronic solders contain colophony, and not all colophony-free fluxes are completely free of colophony.

.

Workers using colophony-free soldering fluxes may still be exposed to colophony when de-soldering equipment (during repairs) which was originally soldered with colophony fluxes.

.

Exposure to isocyanates may occur when polyurethane coated wires are soldered, or soldering takes place through polyurethane encapsulation during repair work.

19.8

How to document exposure, including biomonitoring

Exposure to electronic soldering fluxes is usually fairly obvious, as a fume is required for successful soldering. Sometimes the soldering is automated and enclosed; exposure is then possible during breakdowns, or if extracted fume is recirculated into the work environment. Exposure standards are based on the total resin acid content of the fume, which requires gas chromatography and flame ionization detection. In the UK the workplace exposure limit is currently 0.05 mg/m3 and a 15 minute time-weighted average of 0.15 mg/m3 for short-term exposures. Biological monitoring is not in general use and is usually unnecessary, but it is possible in urine collected at the end of a shift. Analysis requires hydrolysing aliquots of urine at 90 C for 1 hour with concentrated hydrochloric acid, followed by extraction into diethyl ether and evaporated under nitrogen. The residue is then derived using methylformamide dimethylacetal and analysed by gas chromatography with mass spectrometric detection using positive electron impact ionization and selected ion monitoring. An 8 hour exposure at the workplace exposure limit of 0.05 mg/m3 equates to a post-shift urinary dihydroabietic acid level of 2.8 mmol/mol creatinine (95% CI 2.2–3.4). A level below 3.0 mmol/mol creatinine has been suggested as a possible biological standard. Local exhaust ventilation is difficult to achieve with hand soldering. The ideal is probably extraction at the tip of the soldering iron. This, however, makes delicate soldering more difficult, and may cool the soldering tip. Once extracted the resins cool and solidify in fine tubing, blocking the extract. Larger printed circuit boards may obstruct the duct orifice of bench-mounted extraction. Some ducted extracts pass through filters and return the air to the work environment, rather than extract to atmosphere. The filters need to be in good condition to avoid spreading the soldering fume over the rest of the workforce. Exposure to isocyanates is nearly always far from obvious. There is usually nothing to see, nothing to smell and often ignorance about the possible presence of isocyanates in the air. Continuous reading monitors are available for monitoring isocyanate levels in air, but sensitization can occur when exposure is well below the exposure standard. Biological monitoring is possible by measuring isocyanate-derived diamines in the urine in post-shift samples; few laboratories offer such an analysis.

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19.9 Diseases associated with colophony and isocyanate exposure in the electronics industry 19.9.1 Irritant reactions The first occupational exposure limit for colophony was based on its irritant effect on previously unexposed volunteers. Some 30% reported irritation to the eyes, nose and throat at a concentration of 0.07 mg/m3 (measured as the aldehyde content in the fume expressed as formaldehyde) and 5% reported irritation at 0.05 mg/m3. These concentrations are higher than have been measured in any of the electronics factories described in epidemiological studies and led to the widespread use of electronics soldering fluxes containing colophony without local exhaust extraction until the early 1980s. Nevertheless irritant-induced eye, nose, throat and airway disease is possible at high levels of exposure in the workplace.

19.9.2 Occupational rhinitis Occupational rhinitis is common and usually precedes occupational asthma (if occupational asthma is going to develop). It improves on days away from work.

19.9.3 Occupational asthma Most occupational asthma due to colophony is likely to be due to sensitization as there is a latent interval between exposure and first symptoms. Only a small proportion of the workforce is affected and sensitized workers can react to very low concentrations of colophony. Having said this, colophony fumes are more irritating than some other causes of occupational asthma such as isocyanates and they probably cause irritant reactions in those with bad asthma at concentrations that may be encountered in poorly controlled workplaces. In the 1970s when electronics components were bigger and soldering was largely uncontrolled, the mean latent interval from first exposure to first symptom was 4 years, although the variation was very wide. There was a peak within the first year of exposure and the longest recorded was 23 years. This latent interval is longer than that seen with isocyanates in the exposures at the same time. Once sensitization had occurred, the most common reaction was for deterioration to be progressive throughout the working week with the last working day worse than the first, and with recovery starting within 1 or 2 days away from work. About 25% had equivalent deterioration each work day. Since exposures have been reduced, the progressive deterioration pattern has been less common and the equivalent deterioration pattern more common. There are some individuals who take more than 2 days to recover and do not notice improvement over a 2 day weekend away from work. Colophony is a biological product derived from the sap of pine trees and varies in constituents depending on the source of the pine tree, but positive specific challenge testing has been shown to all the main types of colophony. The fluxes also contain activators which differ between manufacturers and, many of them being amines, may contribute to an irritant effect of the fume.

19.9

COLOPHONY AND ISOCYANATE EXPOSURE IN THE ELECTRONICS INDUSTRY Colophony Methyl Colophony

2.6 2.4

FEV1 liters

253

2.2 2 1.8 1.6 1.4 1.2 -1

0

1

2

3

4

5

6

7

8

9

10

11

hours after exposure

Figure 19.1 Specific challenge tests to colophony in an electronics worker with bystander exposure to colophony flux-cored solder showing a dual immediate and late asthmatic reaction. Methylation of the colophony using a similar exposure nearly abolished the reaction

Differential challenge tests to different adducts of colophony showed reduced reactions to a methyl ester of colophony, suggesting that the carboxyl groups are important in allergen recognition (Figure 19.1). A cross-sectional study of electronics solderers and assemblers in 1978 showed that 22% of shop floor workers had work-related wheeze or dyspnea and that symptoms were as common in bystanders as in those soldering (exposure measurements were also similar). Work-related symptoms were more common in smokers than in nonsmokers. A case–control study of workers in the same factory showed an increased risk of work-related asthmatic symptoms in atopics, although the correlation was weak and there was no significant effect with a family history of allergic disease. A similar study carried out in a factory manufacturing flux core solder where the colophony was heated to 140 C and decomposition of the resin acids was unlikely showed similar results, suggesting that the resin acids themselves are the likely cause of the occupational asthma.

19.9.4 Interstitial lung diseases There have been occasional reports of extrinsic allergic alveolitis caused by colophony at a time when local exhaust ventilation was not being used for soldering operations. The cases were described before high-resolution CT scans and bronchoalveolar lavage; each had fever and muscle aches on occupational exposure and alveolar reactions, with a fall in transfer coefficient (KCO) following colophony challenges. Beryllium is occasionally found in electronics, often as a beryllium copper alloy. Beryllium can cause a granulomatous disease, chronic beryllium disease (CBD), which is very similar to sarcoidosis (some regard it as a cause of sarcoidosis). CBD can be caused by very low exposures to inhaled (or implanted through the skin) beryllium and is associated with a positive beryllium lymphocyte proliferation test. It is very rare in the electronics industry. High levels of indium–tin oxide exposure have also been associated with an interstitial lung disease in manufacturers of liquid-crystal and plasma display panels,

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where the powders of indium oxide and tin oxide are mixed, pulverized, pressed and sintered before surface grinding and sawing. The CT scans of affected workers showed a mixture of mosaic attenuation, ground glass opacities and areas of emphysema. The workers had no relevant symptoms, no crackles on auscultation, but in some cases had finger clubbing. The total lung capacity and DLCO decreased with increasing exposure, but were generally above predicted values. Their mean serum indium levels were 7.9 mg/l, higher in those with a longer duration of exposure, and also in those who had left employment, suggesting a long half-life. Indium in the air of the working environment ranged from 0.01 to 0.05 mg/m3, with similar levels in other areas with surface grinding. Two workers from the same factory had previously been identified with interstitial lung disease. One died of bilateral pneumothoraces 4 years after diagnosis; his serum indium was 290 mg/l. The other presented with breathlessness and had a serum indium of 51 mg/l. A lung biopsy showed unusual histology not conforming to the more usual classification of interstitial lung diseases. There was proliferation of centrilobular peribronchial fibrous tissue with huge numbers of cholesterol clefts, and giant cells with brown pigment containing indium. There was also an alveolitis with indiumcontaining macrophages and macroscopic subpleural emphysema. Following removal from exposure, his disease was static.

19.10 Diagnosis and management issues The diagnosis of occupational asthma starts in two ways, either in a worker who has new symptoms or declining FEV1 detected during routine workplace surveillance, or in a worker who presents clinically with symptoms of new or deteriorating asthma. Both should be asked whether symptoms improve on days away from work or on holiday. In the context of workers exposed to soldering flux fumes, occupational asthma can be confirmed in more than half. Those undergoing regular surveillance should be seen within a context where the first step is to confirm or exclude occupational asthma (the reason that surveillance is undertaken). Those seen clinically need the clinician to think of work as a cause for symptoms. If this is not considered, there may be a delay in diagnosis and reduced chance of cure. Objective confirmation of the diagnosis is required. There are no satisfactory immunological tests for solder fluxes to aid diagnosis. Confirmation of occupational asthma is done differently in different countries. The most direct method is to monitor lung function at and way from work. Before and after work measurements are not recommended as they are compounded by the effects of spontaneous diurnal variation which results in morning and day shift workers often having their worst lung function shortly before starting work, minimizing any work-related deterioration, which is often delayed to the period after work. The best method is to monitor peak flow and/or FEV1 every 2 hours over three work-weeks and days off. Computer analysis using the Oasys software has a specificity of 94% and sensitivity of 79% compared with specific challenge tests, better than any other validated method, and specifically validated in electronics workers. Records are liable to fabrication, which can be largely overcome using data-logging meters. Figure 19.2 shows an Oasys plot in an electronics worker with occupational asthma.

19.10

DIAGNOSIS AND MANAGEMENT ISSUES

255

Figure 19.2 An Oasys plot of 2 hourly peak flow measurements in an electronics worker who remained well for the first 10 years until she developed symptoms of occupational asthma. Her original job involved soldering with colophony fluxes and encapsulation with a polyurethane resin (with isocyanate exposure). The peak flow above was made after relocation away from the encapsulation process when she had bystander exposure to the soldering fume. The plot shows: (Top panel) Daily diurnal variation expressed as percentage predicted. The horizontal lines are at 20% and 50% and the variation often exceeds 20%. (Middle panel) Upper dotted line, daily maximum peak expiratory flow (PEF), solid middle line, daily mean and lower dotted line daily minimum PEF. Days at work have a shaded background, days away from work a clear background. The dashed horizontal line is the predicted PEF. (Lower panel) The day and date, the number of readings/day (usually 7–9) and the hours worked. The record shows deterioration on workdays which is usually progressively worse as the working week continues, and improvement on days away from work, which is often better on the second day off than the first. Fewer hours were worked on Fridays, perhaps accounting for the reduced reactions on some Fridays. The record confirms occupational asthma, but on its own does not identify the cause. Repeating this in areas with different exposures can help identify the precise cause

Tests of nonspecific reactivity can be normal at the time of diagnosis of colophony asthma in about 30% of those with positive specific challenges when the test of airway responsiveness is performed after 2 days off work. It can also be measured after a period of exposure and after 2 weeks away from exposure but this method has not been specifically validated in electronics workers. Specific challenge testing to solder flux fumes can reproduce the exposures at work, using the same flux and soldering temperature as at work (Figure 19.3). There is no good external comparator for specific challenge tests and it is not easy to reproduce the levels of exposure encountered at work, which are rarely measured regularly. The sensitivity of specific challenge was 100% and specificity 67% in one study using the independent outcome of continuing work exposure for a further year without deterioration as a measure of no serious occupational asthma and the need to leave work with subsequent improvement as an outcome for occupational asthma. This could be interpreted as tolerance to exposure in the workplace to exposure levels which may have been lower than in the challenge chamber. Specific challenges with isocyanates, with a ceiling value of 0.02 ppm in the challenge chamber, showed a sensitivity of 82% and a specificity of 100% using similar outcome

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FEV1 liters

4 3.5 3 Colophony

2.5

colophony free solder 2

Colophony flux solder

1.5 -5

10

25

40

55

70

85

100 115 130 145 160

minutes after exposure

Figure 19.3 Specific challenge test in an electronics worker soldering with the flux-cored solder used in her workplace for 2.5 minutes. There was an immediate asthmatic reaction. When colophonyfree flux-cored solder was used for 5 minutes there was no significant reaction. The reaction was reproduced by dipping the soldering iron into colophony alone and taking 10 breaths, showing that the colophony component of the flux was the cause of her asthma

variables, suggesting that some exposures at work were higher than those used in the challenge chamber. Unfortunately no test is perfect.

19.11 Management and prevention The miniturization of electronics has reduced colophony exposure. Other jointing methods without soldering are probably the best method for control. The soldering operation must generate fume to be effective unless carried out in an inert atmosphere, as one action of the fume is to exclude oxygen from the joint to prevent oxidation. Colophony-free fluxes are available, but most are slower and more difficult to use and may occasionally cause occupational asthma themselves. Local exhaust extraction should always be used for hand soldering, but is often difficult to position well. Extraction systems also often return the extracted air after filtration to the workplace. It is easy for this to go wrong when filters fail or are not maintained adequately. Soldering operations are often spread around a factory at different stages of the assembly process, making it difficult to relocate workers away from bystander exposure. There is one study comparing workers who were relocated to reduced colophony exposure compared with those removed completely. Few became asymptomatic, but nonspecific reactivity returned to normal in half of those completely removed from exposure and in 1/8 of those with reduced exposure (who had less severe disease at presentation).

19.12 Medicolegal considerations and compensation Occupational asthma due to colophony, isocyanates or acrylates is compensated in most countries. Few systems, however, leave the sensitized worker with useful employment. The aim of compensation for nondisabling diseases should be to support

19.14

THE SPECTRUM OF OCCUPATIONAL DISEASES IN ELECTRONICS WORKERS

257

Table 19.2 Reports of occupational disease in electronics workers in the UK (from THOR, the UK voluntary reporting scheme for occupational respiratory diseases) 1996–2006 Reports Occupational asthma Inhalation accidents Contact dermatitis Musculoskeletal (upper arm) Anxiety/depression Hearing loss

574 114 1868 1896 351 158

a sensitized worker during retraining. Even then a newly trained skilled worker usually starts again at the bottom of the employment hierarchy.

19.13

Public health issues

Colophony is made by bleeding pine trees. The spirit fraction is turpentine, the resin colophony. Colophony exposure can be measured in the air in pinewoods. There are no recorded cases of colophony sensitization from outdoor wood exposure alone, but some workers with colophony asthma from soldering fluxes are worse in pine woods. Isocyanate exposure enough to provoke asthma in a highly sensitized worker can occur from contact with isocyanate-exposed workers outside the workplace (this has not been described with colophony, where extreme sensitivity is unusual).

19.14

The spectrum of occupational diseases in electronics workers

The SWORD (Surveillance of Work-related and Occupational Respiratory Diseases) scheme in the UK is a voluntary reporting scheme for occupational lung disease. Notification does not result in any compensation; the clinician reports cases that are thought to be due to work ‘on the balance of probabilities’, i.e. the chance of an

Number

200 150 100 50

g di n W el

er nt /la cq u

an d as se s G

Pa i

fu

m es

re si n ox y Ep

Is oc ya na te s

C

ol op ho ny

0

Figure 19.4 Reported causes of occupational asthma in the electronics industry in the UK (data from SWORD).

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CH 19 WORK WITH ELECTRONICS

occupational cause is >50%. This is combined with occupational physicians reporting all occupational diseases. The two databases are combined in THOR (The Health and Occupation Reporting Network) together with other specialty reporting schemes. Reports are grouped by industry. Electronics is included in Standard Industrial Classification (SIC) 29–33, which includes the manufacture of office machinery and computers, electrical machinery, radio, television and communication equipment, medical, precision and optical instruments, watches and clocks. The number of reports of occupational disease between 1996 and 2006 are shown in Table 19.2. Figure 19.4 shows the agents reported to SWORD as the most likely cause of occupational asthma in electronics workers. The reported causes for occupational asthma are shown in Figure 19.4.

Further reading Baldwin, P.E.J., Cain, J.R., Fletcher, R., Jones, K., Warren, N. (2007) Dehydroabietic acid as a biomarker for exposure to colophony. Occup. Med. 57: 362–366. Burge, P.S. (1984) Occupational asthma: rhinitis and alveolitis due to colophony. Clin. Immunol. Allergy 4: 55–81. Burge, P.S., Pantin, C.F.A., Newton, D.T., Gannon, P.F.G., Bright, P., Belcher, J., McCoach, J., Baldwin, D.R., Burge, C.B.S.G. and the Midlands Thoracic Society Research Group (1999) Development of an expert system for the interpretation of serial peak expiratory flow measurements in the diagnosis of occupational asthma. Occup. Environ. Med. 56: 758–764. Elms, J., Fishwick, D., Robinson, E., Burge, S., Huggins, V., Barber, C., Williams, N., Curran, A. (2005) Specific IgE to colophony? Occup. Med. 55: 234–237. Homma, S., Miyamoto, A., Sakamoto, S., Kishi, K., Motoi, N., Yoshimura, K. (2005) Pulmonary fibrosis in an individual occupationally exposed to inhaled indium–tin oxide. Eur. Respir. J. 25: 200–204. Koh, D., Chan, G., Yap, E. (2004) World at work: the electronics industry. Occup. Environ. Med. 61: 180–183. Nicholson, P.J., Cullinan, P., Newman Taylor, A.J., Burge, P.S., Boyle, C. (2005) Evidence based guidelines for the prevention, identification, and management of occupational asthma. Occup. Environ. Med. 62: 290–299. Pengelly, M.I., Groves, J.A., Foster, R.D., Ellwood, P.A., Wagg, R.M. (1994) Development of a method for measuring exposure to resin acids in solder fume. Ann. Occup. Hyg. 38: 765–776.

Websites http://www.occupationalasthma.com/– this website has a full list of references on electronics workers and asthma, and most other causes of occupational asthma. It has downloads and instructions for diagnosing occupational asthma from serial measurements of peak flow (or FEV1). It has a question and answer section, both of which you can contribute to. http://www.hse.gov. – this is part of the UK Health and Safety Executive site on occupational asthma and is mainly for workers giving general advice. The following links from the same site access a worker information booklet ‘Solder fume and you’ – http://www.hse.gov. – and a method for estimating colophony in air – http://www.hse.gov. http://www.ilo.org/safework_bookshelf/english/ – this is a link to the electronics industry section of the ILO encycopedia. It lists the general processes involved.

20 The services industry George L. Delclos, Lea Ann Tullis and Arch I. Carson The University of Texas School of Public Health, Houston, Texas, USA

20.1 Introduction If one considers the primary sector of economic activity to consist of those jobs and industries dealing with the extraction of raw materials (e.g. mining, fishing, agriculture), and the secondary sector centering on manufacturing of goods, services industries are often considered to represent the ‘tertiary’ sector. Typically, in the most economically developed countries, over half of the working population labors in service-related businesses. In the United States, service-based workers outnumber workers in manufacturing by about 8 to 1. Services industries are numerous, and classification schemes defining what constitutes a service-related occupation can vary by country or region. For the purposes of this chapter, the industries and occupations targeted include those as defined in the 2002 North American Industry Classification System (Table 20.1). Although this chapter describes occupational respiratory diseases reported in recent years as having an association with specific service-related jobs, the review may not be all-inclusive, as exposures vary depending on a number of factors, including geographic location, worker demographics and the existence and effectiveness of regulatory controls. In addition, exposures could exist within an occupation that may not as yet have been identified or recognized as potentially hazardous.

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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Occupations in the services industries

Occupational group and description Health diagnosing and treating occupations: professionals caring for people and animals; office settings mostly with a lower degree of physical labor; exposures vary greatly

Healthcare support: individuals supporting the healthcare professionals (i.e. physicians, dentists, nurses); settings vary from offices to hospitals and homes; degree of physical labor and exposures also vary greatly Personal care and service: individuals involved in caring for people and animals; settings, degree of physical labor and exposures vary greatly

Protective services: individuals involved in ensuring the safety and security of the public; settings can be dangerous and typically involve a high degree of physical labor; exposures vary greatly Food preparation and serving related occupations: individuals involved in the preparation, and serving of food; settings can vary and typically involve a high degree of physical labor; exposures vary greatly Building and grounds cleaning and maintenance occupations: individuals involved in cleaning and maintaining buildings and grounds; typically involves a high degree of physical labor; exposures vary greatly

Occupations Audiologists, chiropractors, dentists, dietitians and nutritionists, occupational therapists, optometrists, pharmacists, physical therapists, physician assistants, physicians and surgeons, podiatrists, radiation therapists, recreational therapists, registered nurses, respiratory therapists, speech-language pathologists and veterinarians Dental assistants, massage therapists, medical assistants, medical transcriptionists, nursing aides, psychiatric aides, and home health aides, occupational therapist assistants and aides, pharmacy aides, physical therapist assistants and aides Animal care and service workers, barbers, cosmetologists and other personal appearance workers, childcare workers, fitness workers, flight attendants, gaming services occupations, personal and home care aides and recreation workers Correctional officers, fire fighting occupations, police and detectives, private detectives and investigators, and security guards and gaming surveillance officers Chefs, cooks and food preparation workers, and food and beverage serving and related workers

Building cleaning workers, grounds maintenance workers, and pest control workers

Modified from the US Department of Labor Bureau of Labor Statistics Occupational Outlook Handbook, 2007 (based on the 2002 North American Industry Classification System, NAICS).

20.2 Health diagnosing and treating occupations 20.2.1 Hospital-based healthcare professionals and support personnel Healthcare workers (HCWs) comprise approximately 8% of the US workforce and roughly half of the top 30 fastest growing occupations. Hospitals and other inpatient healthcare settings house potential exposures that cover the full spectrum of workplace hazards, including biological, physical, chemical, radiation agents and psychosocial risk factors. In the 1990s, particular attention centered on respiratory issues in HCWs,

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partly due to increased concerns over occupational latex allergy that emerged following a significant increase in the use of latex-containing personal protective equipment, such as powdered gloves, to counter the risks of nosocomial and occupationally acquired infection. Putative respiratory hazards in healthcare environments go beyond latex, and include disinfectants/sterilants (e.g. glutaraldehyde, formaldehyde), pharmaceuticals (e.g. psyllium, various antibiotics, platinum-containing antineoplastic agents), sensitizing metals (e.g. dental alloys), methacrylates, aerosolized medications (e.g. pentamidine, ribavirin), general cleaning agents and infectious agents. Respiratory health effects consist primarily of upper and lower airway irritative and allergic syndromes, and occupational infections. Airways disease Different countries have reported work-related asthma among physicians, respiratory therapists, workers in endoscopy units and radiology departments, nurses and general HCWs. The agents most often associated with these reported asthma cases include latex, cleaning products and poor indoor air quality. Physician-diagnosed asthma developing after entry into the profession appears to especially affect nurses and respiratory therapists, and is significantly associated with medical instrument cleaning, exposure to general cleaning products, use of powdered latex gloves and the administration of aerosolized medications. Sensitization to latex products can vary in type. At least 13 botanical proteins present in the rubber tree and in the finished products have been characterized as potential sources of type I allergy. Type I hypersensitivity results in an immediate reaction in the form of localized urticaria and erythema at the site of the exposure; this can be evidenced with careful skin prick tests. Immediate systemic reactions can also occur, including a diffuse rash, conjunctivitis, rhinitis, bronchospasm and, rarely, hypotension, anaphylaxis and death. Latex gloves, particularly when powdered, have been linked to these type I reactions. Bound by cornstarch powder during the manufacturing process, the latex proteins can be aerosolized through the handling, donning and removal of powdered latex gloves. Type IV hypersensitivity reactions have also been observed in association with latex glove use, although whether this is due to the latex proteins themselves is debatable. In sensitized individuals, type IV delayed hypersensitivity manifests 6–72 hours postexposure, causing contact allergic dermatitis. However, in most cases, these delayed reactions are attributable to additives used in the manufacturing process of rubber gloves rather than to the latex proteins themselves. Allergy can be confirmed through patch skin testing for these additives. There is evidence that latex control policies implemented in hospitals over the past several years are having a beneficial impact. In 1997, in response to increasing reports of latex allergic reactions, hospitals in the USA were advised to reduce unnecessary use of powdered latex gloves. Although overall sales in the USA continued to increase, the total protein and powder content in latex gloves decreased markedly. A subsequent decrease in numbers of reported cases of latex allergy has been observed, underscoring the effectiveness of substitution of powdered latex gloves by low-latex alternatives and other workplace control measures. Glutaraldehyde is commonly used in endoscopy units for cold sterilization, particularly for disinfecting heat-sensitive equipment, including fiberoptic endoscopes,

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dialysis instruments and surgical instruments; it is also used as a tissue fixative in pathology laboratories or for developing radiographs, and can act as both a respiratory irritant and sensitizer. Instrument cleaning products linked to sensitization and occupational asthma may also include enzyme-containing products, such as subtilisins (detergent protease enzymes). Chronic bronchitis, nasal symptoms, and the onset of ‘multiple chemical sensitivity’ have been reported in workers using glutaraldehyde, as have higher prevalences of headache, fatigue and irritation of skin, eyes and throat than among those without this exposure. Moreover, glutaraldehyde has also been linked to the occurrence of occupational asthma, especially among respiratory therapists and nurses who routinely sterilize endoscopes with this compound. Many health and safety authorities have recommended implementation of controls, including enclosure and automation of cold sterilization procedures, and substitution of glutaraldehyde with less toxic alternatives. In many hospitals, glutaraldehyde is being replaced with orthophthalaldehyde, also a high-level disinfectant and presumably less of a sensitizer. Ethylene oxide gas has been widely used to sterilize heat-labile medical equipment in central supply and sterilizing units. Overexposures typically occur with use of faulty equipment, poor work practices or when gas tanks are changed out. Acute inhalation of high concentrations of ethylene oxide can produce both upper and lower respiratory tract irritation, including bronchospasm and, in rare cases, reactive airways dysfunction syndrome (RADS) or sensitization. In addition, this gas has neurotoxic properties, leading to central nervous system effects, including headache, nausea and loss of coordination. Concerns regarding the effects of chronic exposure to ethylene oxide have mostly centered on neurotoxicity (peripheral neuropathy) and carcinogenicity, as it is considered a Class I (i.e. definite) human carcinogen by the International Agency for Research on Cancer. Modern hospitals have implemented control measures for ethylene oxide use, including area detection monitors, enclosure systems, use of self-contained breathing apparatuses to manage leaks and substitution of ethylene oxide with alternate sterilization methods, such as hydrogen peroxide gas plasma. Both occupational and work-aggravated asthma among radiographers also occurs. The process of ‘wet’ radiography involves the use of X-rays to create an image on a film surface by the reduction of silver halide crystals to elemental silver. During film development, reducing agents such as hydroquinone are used to enlarge and stabilize the image followed by fixing agents that are used to dissolve the unused halides. Automated film processing machines use higher temperatures, typically in the range of 28–35  C, to achieve shorter developing times. These machines use hardening agents such as glutaraldehyde within the developer solution and hot air to dry and fix the film. Film developing in confined, less well ventilated spaces, such as in some mobile radiography units, may enhance exposure opportunities. Additionally, radiographers are potentially exposed to glycols, acetic acid, sodium sulfite, sulfur dioxide, ammonium chloride, silver compounds and other chemicals that may cause or exacerbate asthma. With the increasing shift from traditional film developing to digital radiography, however, it is likely that cases of airway syndromes in radiographers will decrease in coming years. Cases of RADS and persistent symptoms of bronchial hyper-responsiveness have been described in HCWs following exposure to acute chemical spills, such as glacial acetic acid. In the UK, numbers of reported inhalation accidents among health service staff have been found to be high, mostly due to anesthetic gases and cleaning agents. It is

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less well established whether chronic low-level exposure to irritants can lead to asthma, although certainly airborne irritants can trigger asthma exacerbations. In summary, workers in healthcare settings are at an increased risk of both upper airway syndromes and asthma, both immunologically and nonimmunologically induced. Despite this, important gaps in knowledge remain with respect to better risk characterization of at-risk HCW subgroups, identification and assessment of specific agents within the broad exposure categories mentioned herein, monitoring of trends in asthma rates over time, estimation of the impact of asthma on work patterns and productivity among healthcare workers, and effectiveness of preventive measures. Respiratory infections Transmission of tuberculosis, one of the oldest occupational diseases linked to work in healthcare settings, remains a threat to HCWs, especially in developing nations. Risk of occupationally acquired tuberculosis is greater in certain healthcare settings, including those with a high proportion of patients from correctional facilities, indigent populations and/or HIV infection. In addition, risk preferentially affects selected HCW subgroups (e.g. pulmonary physicians, nurses and respiratory therapists) and those persons performing or involved in cough-inducing procedures (e.g. administration of nebulized medications, bronchoscopy or intubation). In the mid-1980s and early 1990s, cases of multidrug-resistant tuberculosis were reported among HCWs in the USA, mostly in nursing home settings and correctional facilities, and primarily occurring in HIV-infected HCWs. In response to the emerging threat, in 1994 the Centers for Disease Control and Prevention issued guidelines for preventing the transmission of tuberculosis in healthcare settings. The focus of the 1994 guidelines was on assessment of risk in a given facility, followed by implementation of environmental, administrative and personal protection controls commensurate with that risk. These guidelines were widely adopted in the country, with a resulting decrease in outbreaks of tuberculosis in healthcare settings, lowered transmission rates between patients and workers, and a decline in multidrug-resistant tuberculosis. By 2004, the national tuberculosis rate was the lowest on record, reflected by fewer reports of occupationally acquired active tuberculosis and decreasing rates of tuberculin skin test conversions on periodic surveillance exams among HCWs. Revised guidelines were published in 2005, emphasizing measures to maintain the success achieved and to eliminate remaining threats to HCWs, mostly from patients or persons with as yet undiagnosed active infection. Notwithstanding these improved trends, multidrugresistant tuberculosis among HCWs remains a threat in developing and rapidly industrializing nations, where background rates of both tuberculosis and HIV infection may be high and access to the same control measures used in developed countries is often limited. Other occupationally acquired bacterial infections presenting a risk to HCWs and that are well documented in the literature include infections caused by Neisseria meningitidis, Bordetella pertussis and Legionella. Among viral diseases of concern are measles, varicella and influenza; effective vaccines exist for all of these, and should routinely be offered during preplacement and routine surveillance evaluations of workers in healthcare settings. Recommendations for prophylaxis and control of these infections are regularly updated and published by the US Centers for Disease Control and Prevention (www.cdc.gov).

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20.2.2 Dental personnel Dental personnel, including dentists, dental assistants, dental nurses and dental hygienists, are potentially exposed to a variety of allergens, and there is limited evidence that the incidence of occupational respiratory disease among dental professionals has increased in recent years. Among the exposures are methacrylates, used in bonding agents and resins; natural rubber latex proteins in gloves, accelerators and antidegradants in natural and synthetic rubber gloves; and glutaraldehyde in disinfectants. Methacrylates (including methyl methacrylate, 2-hydroxyethyl methacrylate, 2-hydroxypropyl methacrylate, ethylene glycol dimethacrylate and triethylene glycol dimethacrylate) are established type IV contact allergens. Exposure to these compounds has been linked to the development of allergic contact dermatis (pulpitis of fingertips, or dermatitis of the face caused by airborne methacrylates) as well as to respiratory hypersensitivity. Daily use of methacrylates has been related to an increased risk of adult-onset asthma, nasal symptoms and work-related cough or phlegm. Exposure–response relationships between increasing years of exposure to methacrylates and risk of nasal symptoms, hoarseness, dyspnea and wheezing with dyspnea have been observed. It is unclear whether a history of atopy or pre-existing allergic contact dermatitis predisposes to subsequent development of respiratory hypersensitivity to these compounds. Other potential allergens include the various metals in restorations and dental appliances, as well as miscellaneous antimicrobials and preservatives. Occupational exposures to these agents, for the most part, produce type I or type IV allergic reactions, although IgE-independent occupational asthma and protein-based contact urticaria are also possible. Latex-induced allergic reactions are well described in dental personnel but, as is the case for other HCWs, the prevalence of type I natural rubber latex allergy is likely to be declining, partly due to increased recognition and the introduction of stricter controls in natural rubber latex product manufacturing, resulting in gloves with a lower protein content and the implementation of latex control policies in workplaces where latex end products are used.

20.2.3 Professionals caring for animals In the veterinary professions, possible respiratory exposures include hair, dandruff, feathers, latex, mites, organic dust, disinfectants and ammonia. The incidence of occupational illness and injury claims in veterinary personnel can be up to 3 times greater than among general practitioners of medicine, and nearly a quarter of the claims are for respiratory and contact allergic reactions. Besides animal-related allergies, other respiratory illnesses reported include latex allergy, alveolitis and toxic respiratory disease. Swine veterinarians have unique exposures in addition to those listed above. Working in swine confinement units is associated with exposure to toxic gases, endotoxin, ammonia and dust. High prevalences of work-related upper and lower respiratory symptoms occur, together with an association between abnormal pulmonary function and increased number of hours working in the barns.

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In research animal laboratory workers, both allergic and irritant upper airway symptoms, skin rashes and, to a lesser extent, asthma are common. Allergic reactions are usually through type I IgE-associated hypersensitivity caused by dermal or respiratory exposure to animal allergens found primarily in dander and secretions present in urine and saliva. The prevalence of allergic symptoms to laboratory animals may be high, affecting up to or over 40% of these professionals over a lifetime; around 8% at any given time have positive skin prick tests to laboratory animal antigens, and 18% have positive nonspecific bronchial challenge tests. Dose–response relationships between allergy and weekly hours of exposure to laboratory animals and number of different animal species handled have been observed as well. Preventive measures should emphasize and favor engineering controls, including local exhaust ventilation, frequent bedding changes and use of dustless bedding, over personal protective equipment.

20.3

Personal care and service – cosmetology professionals

Cosmetology professionals, including barbers, hairdressers and manicurists, are potentially exposed to various sensitizing and irritating chemicals. Sensitizing agents include persulfate salts contained in hair bleaches, reactive dyes, epilating substances, antiseptics, formaldehyde, henna, fungi and latex. Irritants include cosmetic agents, reactive dyes, epilating substances, antiseptics, perfumes, shampoos and hair creams/ gels. Task-related risk factors for the development of respiratory disease involve performing more chemical applications, hair styling, shaving and honing of razors, and application of artificial nails. The potential for significant exposures can be enhanced by the work environment characteristics of many hairstyling and nail salons, such as small square footage and inadequate ventilation. Professionals in the cosmetology industry are more than 3 times more likely to leave their profession due to concerns for their health, most notably hand eczema or asthma. The most common adverse respiratory effects encountered are upper and lower airway syndromes, including rhinitis with or without eye symptoms, dry or productive cough, dyspnea, wheezing, asthma and chronic bronchitis. With respect to asthma in cosmetology professionals, up to 40% can develop their asthma after entry into the profession. Among the causes of occupational asthma are persulfate salts in hair bleaches and henna, used in organic hair dyes and for temporary tattoos. Moreover, asthma exacerbations commonly occur during shaving and honing of razors, and hairstyling, including use of hair lacquers and permanent wave solutions. There is also some evidence of adverse effects on lung function among hairdressers, and reports of parenchymal lung disease, including alveolitis, lung granulomatosis associated with exposure to polyvinylpyrrolidone in hair lacquers and idiopathic pulmonary fibrosis, a chronic diffuse interstitial lung disease of unknown cause characterized pathologically by inflammation and fibrosis of the lung parenchyma, which occurs at higher rates in this occupational group. Nail salons (which can be part of a hair salon or stand-alone facilities) have other potentially unique exposures. Artificial nails contain varying combinations of acrylics, gel, fiberglass and porcelain, and are applied to the natural nails using glues such as ethyl cyanoacrylates. Much of the work is performed in the vicinity of the manicurist’s

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breathing zone, and tasks include not only application of chemicals, but sculpting and shaping of the nails to assure a proper fit. Consequently, nail stylists are potentially exposed to both respirable chemicals and dusts. Among the chemicals are acetone, formaldehyde, methylene chloride, methyl ethyl ketone, toluene and xylene. Standalone nail salons have proliferated in the USA over the past couple of decades, and are often small in size, with poor ventilation and crowded conditions, all of which can favor exposure to harmful levels of these chemicals. Prior to 1974, methyl methacrylate was also found in nail products, but was ultimately banned by the US Food and Drug Administration. Ethyl methacrylate, however, is still used and, as was the case with its predecessor, can cause contact dermatitis, asthma exacerbations and allergic conjunctivitis and rhinitis. With respect to lung malignancy, there is little evidence of an increased risk in cosmetology professionals.

20.4 Protective services 20.4.1 Police Traffic police constitute a sector of the police force that may be at increased risk of occupationally related respiratory disease, yet studies are few. However, such an association is plausible. In urban areas, vehicular pollution significantly contributes to the degradation of air quality. Traffic generates volatile organic compounds, suspended particulate matter, oxides of sulfur, oxides of nitrogen and carbon monoxide, and contributes to the production of ozone via secondary photochemical reactions. Several respiratory effects from exposure to air pollutants can occur following exposure to these contaminated air environments, ranging from nonspecific respiratory symptoms such as acute and chronic respiratory tract irritation, cough and dyspnea, to aggravation of asthma, chronic obstructive pulmonary disease and other chronic respiratory disorders. This is likely to occur most often in developing countries, where very high levels of air pollution can occur in urban settings on a regular basis.

20.4.2 Firefighters The main causes of fatalities among firefighters include sudden cardiac death, typically from myocardial infarction or arrhythmias, followed by motor vehicle accidents and asphyxiation for volunteer and career firefighters, respectively. Toxic gases, rather than heat and flame, are the most common agents of death in a fire. This has been well established since the Cleveland Clinic and Boston Coconut Grove fires of 1929 and 1943, respectively. In both incidents, large numbers of people perished, and yet few were actually burned. During a fire incident, firefighters are potentially exposed to a number of agents capable of causing acute respiratory illness, including asphyxiating gases and aerosols, acrolein, benzene, carbon monoxide, formaldehyde, glutaraldehyde, hydrogen cyanide, nitrogen dioxide, particulates, sulfur dioxide, smoke and other nonspecific combustion and pyrolysis products. Plastics pyrolysis products contain many of the same toxic and reactive species found in ‘fresh’ smoke, as well as particulates capable of

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acting as carriers of other toxic gases deep into the lung. Personal sampling in firefighters has found carbon monoxide and acrolein to be present at dangerous levels in a large proportion of fires. In more than 50% of fires, acrolein exposures can be at or above occupational short-term exposure limits; concentrations over immediately dangerous to life and health level can occur in up to 10% of incidents. Acrolein can cause rapid development of pulmonary edema at concentrations as low as 10 ppm. In addition to immediate life-threatening respiratory injury associated with acute smoke inhalation, other respiratory complaints among firefighters, despite wearing self-contained breathing apparatuses (SCBAs) or other forms of respiratory protection, are common. Among these are new-onset asthma and chronic respiratory symptoms, including dyspnea, nasal catarrh, sinusitis and hoarseness. With respect to long-term decline in lung function, there is less evidence of an adverse effect, with the literature providing conflicting results. Firefighters in full gear carry a large amount of extra weight, due to their SCBAs, slicker gear, boots, helmets and tools, which can affect both the cardiovascular and respiratory systems by increasing both cardiac work and the work of breathing. Heavier respirators (e.g. a 35 pound SCBA) will result in an increased heart rate and cardiac output for a lesser level of physical demand, and a decrease in maximum work performance. Moreover, thermal stress is added by increases in the temperature of exhaled air inside the mask. This heat load is further aggravated by working in a hot environment, wearing impermeable protective clothing that limits the ability of the body to dissipate heat, and/or engaging in high levels of physical exertion that generate additional body heat. The amount of thermal stress can reach dangerous levels, leading to heat exhaustion, which is not uncommon in firefighters. ‘Overhaul’ is the process whereby firefighters search for and extinguish possible sources of reignition; respiratory protection may not always be worn during this task, thus exposing firefighters to increased concentrations of combustion products, producing both transient declines in spirometric lung function as well as increases in various biomarkers of lung permeability, such as serum Clara cell protein 16 and surfactant-associated protein A levels. The aftermath of the September 11 World Trade Center disaster resulted in a large humanitarian rescue and recovery effort that lasted for months. Among those most involved in these operations were New York City firefighters and policemen. Exposures to smoke, dust and chemical mixtures were of much higher magnitude than previously recorded. Air sampling performed at the time demonstrated a predominance of coarse particulate dusts (95%), containing cement, glass, asbestos, lead, polycyclic aromatic hydrocarbons, polychlorinated furans, dioxins and polychlorinated biphenyls; the high alkalinity (pH > 9.0) of the dust was another important feature. Arrival time at Ground Zero and job title (special operations command firefighters vs other responding firefighters) were associated with increased levels of various chemical metabolites in biological specimens. Inflammatory changes in sputum of the firefighters were also documented. There has been close surveillance, with periodic medical evaluations, of firefighters, police and other rescue and recovery workers over the past several years. Large proportions of these workers, in some cases approaching 70%, have reported persistent upper and lower respiratory symptoms, appearing within the first several weeks of exposure. Declines in lung function, increased bronchial hyper-responsiveness, reactive upper airways dysfunction, gastroesophageal reflux and some cases of

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parenchymal inflammatory disease, as well as cases of new-onset asthma, suggestive of irritant-induced asthma, have been reported as well. Risk factors predicting abnormal lung function included initial arrival time at the site, duration at the site, and presence of persistent respiratory symptoms. Interestingly, a few studies have examined possible associations between firefighting and sarcoidosis, although the biological plausibility of such an association is not well established. Nonetheless, in 1985, the New York City Fire Department began a surveillance program for biopsy-proven sarcoidosis. By 1998, the average annual incidence of pulmonary sarcoidosis was 12.9 cases per 100,000 among firefighters, compared with no cases among a comparison group of emergency medical services healthcare workers. Following the collapse of the World Trade Center towers, the incidence of sarcoidosis and ‘sarcoid-like’ granulomatous pulmonary disease increased in the subsequent first (86/105) and fourth (22/105) years, in comparison an average incidence of 15/105 in the 15 preceding years. There is no consistent evidence that firefighters are at an increased risk of developing cancer.

20.5 Food preparation and serving-related occupations 20.5.1 Bakers Baker’s asthma is one of the best known and described forms of occupational asthma, and one of the leading causes in countries where this type of information is tracked. It is an IgE-associated reaction in which demonstration of sensitization to bakery allergens is a central component of the diagnosis, together with documentation of work-related symptoms and lung function variability. The most common causal agents for baker’s asthma are found in wheat, rye and barley flour, and enzymes, primarily fungal alphaamylase. Sensitization among bakers increases with duration in the trade, from around 4% after one year in the apprenticeship to 9% after two years. In developed nations, changes in the location of traditional bakeries may be affecting the distribution of disease. Thus, in recent years, stand-alone bakeries have been replaced by bakeries inside supermarkets and larger establishments. In coming years, it will be important to see if this change affects the pattern of baker’s asthma and allows the implementation of appropriate workplace controls.

20.5.2 Bar and restaurant workers Eating and drinking establishment workers are exposed to high levels of second-hand smoke, up to 2-fold higher than those in office settings, while levels in bars can be over 6-fold higher. Increasingly, smoking ordinances and bans are being implemented in public places in many countries. However, restaurants and bars are exempted in some countries. Despite concerns by establishment owners that smoking bans would adversely affect their business, this has mainly been found only in tobacco industryfunded studies. Instead, there is good evidence that smoking bans have led to significant reductions of exposure to environmental tobacco smoke. In as little as one year after

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implementing a ban, improvements in forced vital capacity and peak expiratory flow values, together with a decrease in nonspecific respiratory symptoms (e.g. daily cough, phlegm production, rhinorrhea and throat soreness) have been observed.

20.6

Building and grounds cleaning and maintenance occupations – janitors/cleaners

Janitors and professional cleaners, in both domestic and industrial settings, form a large part of the workforce in most countries. In 2006, approximately 5.4 million persons were employed in the USA in cleaning and building service occupations, with another 746,000 working in private home service-related occupations, i.e. approximately 3% of the total workforce. This is likely to be an underestimate since many workers employed in private households may be undocumented. Distribution by gender is quite different, with males representing slightly over 50% of those working in commercial and industrial settings, whereas women make up 95% of those employed in private households. Wages are low, and access to healthcare is limited. Cleaners perform various tasks, including cleaning surfaces, toilets, carpets and sinks, stripping and waxing floors, and washing windows. These tasks usually involve use of different cleaning products, sometimes in combination. Active components in cleaning products include solvents (e.g. acetone, ammonia, ethanol and pine oil), alkalis (especially bleach), surfactants (e.g. quaternary ammonium chlorides), builders (e.g. sodium EDTA and acetic acid), enzymes (e.g. amylase and proteinase) and disinfectants (e.g. glutaraldehyde, and dialkyl and dimethyl ammonium chlorides). Most are volatilized during cleaning tasks, reaching the breathing zone of unprotected workers, and include both respiratory irritants and sensitizers. Method of application is likely to be important with regards to airborne exposure potential, e.g. sprays vs application with a cloth onto a surface. Inhalation of inappropriately mixed cleaning agents (e.g. bleach and ammonia) can be particularly hazardous, and constitute a common cause of emergency center visits and calls to poison centers. Furthermore, cleaners are also exposed to allergen-containing dusts present on furniture, carpets and in the general air environment of the physical locations where they work. The potential adverse respiratory health effects of work exposure in the cleaning professions have only recently been recognized, especially asthma. The evidence base linking work with cleaning products as a risk factor for asthma is now fairly substantial, largely stemming from population-based surveys and case–control studies from Europe and the USA. As compared with workers who do not routinely use cleaning products, the odds of asthma in cleaners ranges from 1.8 to 2.5 times greater, increasing further among those who reported cleaning kitchens, polishing furniture and using oven sprays and polishes. Both upper and lower respiratory tract symptoms occur commonly in association with specific cleaning tasks, including dusting, vacuuming and cleaning bathrooms and kitchens. Symptoms include sneezing, runny nose, nasal congestion, nasal burning, dry cough, productive cough, wheeze, chest tightness and dyspnea. Among the chemical products producing such symptoms are diluted bleach, degreasing sprays, ammonia and air fresheners. Findings of an increased prevalence of new-onset asthma and symptoms of bronchial hyper-responsiveness among HCWs, such as nurses, who are more likely to adopt

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a bystander role, suggest that not only professionals who directly apply cleaning products are at risk of respiratory airway disease. Additionally, when one factors in the millions of unpaid spouses who clean in their own homes, exposure to cleaning products as a risk factor for both upper and lower airway syndromes may prove to be substantial.

20.7 Conclusions As a nation develops economically, service-based industries employ an increasing proportion of its workers. In the most developed countries, this proportion easily exceeds 50%. Specific occupations in the services sector are at risk of exposures leading to adverse respiratory effects, mostly involving the upper and/or lower airways. Among the at-risk occupations are healthcare professionals, persons caring for animals, traffic police and firefighters, bakery workers, employees in restaurants and bars, and professional cleaners. Although in many cases causes are well established and have led to implementation of controls, the presence of numerous chemicals with sensitizing or irritant potential (e.g. cleaners), lack of resources (e.g. tuberculosis among healthcare workers in developing countries), changes in traditional work locations (e.g. bakeries) and unanticipated exposure incidents (e.g. the September 11 attack on the World Trade Center) indicate that risks continue to exist in this sector, warranting heightened vigilance.

Further reading Arif, A.A., Delclos, G.L., Whitehead, L.W. et al. (2003) Occupational exposures associated with work-related asthma and work-related wheezing among U.S. workers. Am. J. Ind. Med. 44: 368–376. Brant, A. (2007) Baker’s asthma. Curr. Opin. Allergy Clin. Immunol. 7: 152–155. Buyantseva, L.V., Tulchinsky, M., Kapalka, G.M. et al. (2007) Evolution of lower respiratory symptoms in New York police officers after 9/11: a prospective longitudinal study. J. Occup. Environ. Med. 49: 310–317. Delclos, G.L., Gimeno, D., Arif, A.A. et al. (2007) Occupational risk factors and asthma among health care professionals. Am. J. Respir. Crit. Care Med. 175: 667–675. Hamann, C.P., Rodgers, P.A., Sullivan, K.M. (2004) Occupational allergens in dentistry. Current Opin. Allergy Clin. Immunol. 4: 403–409. Kogevinas, M., Zock, J.P., Jarvis, D. et al. (2007) Exposure to substances in the workplace and newonset asthma, an international prospective population-based study (ECRHS-II). Lancet 370: 336–341. National Institute for Occupational Safety and Health (NIOSH) (1999) Controlling Chemical Hazards During the Application of Artificial Fingernails. US DHHS, publication no. 99–112. Nienhaus, A., Skudlik, C., Seidler, A. (2005) Work-related accidents and occupational diseases in veterinarians and their staff. Int. Arch. Occup. Environ. Health 78: 230–238. Skogstad, M., KjI`rheim, K., Fladseth, G. et al. (2006) Cross shift changes in lung function among bar and restaurant workers before and after implementation of a smoking ban. Occup. Environ. Med. 63: 482–487. US Census Bureau (2002) North American Industry Classification System (NAICS); http.//www. census.gov/epcd/naics02/index.html (accessed 15 November 2007).

FURTHER READING

271

US Centers for Disease Control and Prevention (2005) Guidelines for preventing the transmission of Mycobacterium tuberculosis in health-care settings, 2005. Morbid. Mortal. Wkly Rep. 54 (no. RR-17). US Department of Health and Human Services (1997) NIOSH Alert. Preventing Allergic Reactions to Natural Rubber Latex in the Workplace. DHHS (NIOSH) publication no. 97-135. US Department of Health and Human Services (2001) NIOSH Alert. Glutaraldehyde. Occupational Hazards in Hospitals. DHHS (NIOSH) publication no. 2001-115.

21 The construction industry Gary M. Liss1, Edward L. Petsonk2†and Kenneth D. Linch3z 1

University of Toronto (and Ontario Ministry of Labour), Toronto, Ontario, Canada West Virginia University School of Medicine, Morgantown, West Virginia, USA 3 National Institute for Occupational Safety and Health, Morgantown, West Virginia, USA 2

21.1 Introduction Construction of domestic and commercial structures as well as roads and other public works is performed in virtually all societies. In 2007, 7.8 million workers were employed in the construction sector in the USA, representing 5–6% of total nonfarm employment (source: US Bureau of Labor Statistics, Current Employment Statistics Survey). Occupational health issues, including respiratory disorders, among construction workers are often quite challenging. The great variation in work processes and tasks, as well as the continually changing workplace settings often impede the ability of managers and workers to anticipate, document and prevent hazardous exposures. The multiplicity of potential respiratory hazards associated with construction jobs guarantees that many physicians will be challenged to manage respiratory diseases among construction workers and to assess the significance of job exposures on disease occurrence in the clinical findings. In this section, we discuss the types of exposures to respiratory hazards that may be encountered in the construction setting and the potential health effects, including (1) nonmalignant conditions; (2) malignancies; and (3) immunologic conditions, with an emphasis on asthma.

†

Formerly Senior Medical Officer, Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health. z Formerly Engineer/Industrial Hygienist. Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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21.2 Inhalation hazards in the construction industry 21.2.1 Introduction The scope of construction projects ranges from simple, small-scale jobs such as building a deck or patio at a single family home, to massive and complex undertakings such as construction of dams, highways, power plants and office towers. Because of the nature of construction, workers in this industry may experience a diversity of worksite exposures. While a limited number of companies have hundreds or even thousands of employees, construction enterprises are typically small, often employing 75 or fewer individuals, with limited resources to address workplace safety and health. Work settings are frequently nonstandardized and changeable, and to maintain employment, workers often must change jobs and employers as some projects are completed and others are started. On the other hand, there are also large construction companies that can employ several thousand workers. Adjacent construction activities can result in exposures to substances that are unrelated to the worker’s particular job tasks. Considering these factors, as well as the almost daily changes in weather and work locations, the evaluation and control of hazardous airborne exposures for a construction worker are uniquely challenging.

21.2.2 The hazards Construction respiratory hazards can be grouped into three main categories: particulates (including fumes), gases and vapors, and sensitizers. This chapter summarizes some of the most commonly recognized hazards in construction work. Exposure to welding fumes can be encountered on construction sites with potential for acute and chronic lung effects, and metal fume fever; however, welding is covered elsewhere in this book (Chapter 14) and is not considered further here. Paints are frequently present during construction activities but the health effects of exposure to paints are covered elsewhere (Chapter 18). Building materials used in construction are often obtained in the region of the project, to reduce transportation costs of these often bulky and dense materials. The content of masonry, stone and other building materials is thus often determined by the locally available raw materials. To better anticipate potential workplace respiratory hazards, occupational physicians should become familiar with the mineralogy (and particularly the content of free silica and asbestiform fibers) of the materials commonly used for construction in their region. Other exposures often encountered are wood dust and asbestos in removing old pipe fittings in renovations and demolition construction work. Respirable particles These include silicates, crystalline silica, fibers, fumes, fungal and mold spores, and wood. .

Silicates – in the construction industry, silicates are often associated with the soil in which the construction activity is taking place. Silicates in the form of clay are commonly encountered during earth works, but may not pose much of a respiratory

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275

hazard if they remain damp. Portland cement dust, which may be released during some construction work, is composed largely of calcium silicates, aluminates and alumino-ferrites, but may also contain hexavalent chromium. .

Crystalline silica – the form of crystalline silica most commonly associated with construction is quartz. Quartz is a major component of the earth’s crust and is found in many types of rock, especially sandstone and granite. Respiratory hazard ensues when quartz or other forms of crystalline silica (cristobalite, tridymite) are mechanically disturbed and rendered into respirable-sized particles. Construction sand can be 80–99% quartz, depending on the source. Masonry is generally obtained from natural mineral sources, which also often contain quartz. Mortar for building masonry structures generally consists of silica sand combined with Portland cement and water. Concrete is a mixture of cement, water and appropriately sized mineral aggregate. The aggregate comprises a controlled mixture of sized rock, gravel and sand. The combination of masonry, concrete and steel re-enforcement is prized the world over for its strength, longevity and low maintenance. Hazardous exposures to respirable crystalline silica are possible whenever particulates are generated through disturbance of rock, concrete, mortar or masonry, during new construction, renovation or demolition. Proper engineering controls must be used to prevent dust from becoming airborne.

.

Fibers – for occupational health purposes, particles with a length-to-diameter ratio of 3 : 1 or greater are considered to be fibers. Respirable fibers are less than 1.3 mm in diameter and can be up to 200 mm long. Fibers may either be man-made (fibrous glass, mineral wool and refractory ceramic fibers) or naturally occurring, such as asbestos. Asbestos is the term used for a special group of naturally occurring silicate minerals. There are several forms of asbestos; the most common is chrysotile, a fibrous form of serpentine. When disturbed, asbestos breaks into respirable filaments. In the USA, Europe and elsewhere, because of restrictions on its use (29CFR 1910.1001 OSHA, 40CFR61 and 40CFR763 EPA, Commission Directive 1999/77/EC), asbestos is generally only encountered in the construction industry during renovations and demolition of industrial and commercial structures in which it was used for thermal insulation. Fibrous glass is used for thermal and acoustic insulation, in the form of flexible blankets or rigid boards, and is also used in bathroom fixtures such as tubs, sinks and shower stalls. Fibrous glass may also be added to particular types of concrete and mortar for its strength and thermal properties. Mineral wools have applications similar to those of fibrous glass. Refractory ceramic fibers are spun from molten kaolin clay, silica and minor amounts of oxides. Because of their thermal insulation properties, refractory ceramic fiber products are used to insulate furnaces, stoves and chimneys, and to protect industrial equipment from high temperatures.

.

Fumes – fumes encountered in the construction industry include metals from welding/torch cutting, products of combustion including diesel and other fuels, and hot asphalt (see http://www.osha.gov/SLTC/weldingcuttingbrazing/chemicals. html).

.

Fungi and molds – contaminated drywall, carpet, wood or other surfaces may be encountered especially during renovation and demolition. Varieties of aspergillus,

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plasmopara viticola, dictyostelium discoideum, tricoderma koningii, slime molds and other fungi and molds may be present. .

Wood – beech and oak are confirmed human carcinogens. Birch, mahogany, teak and walnut are suspected human carcinogens. A number of commercially important tree species are also known or suspected to induce respiratory sensitization (see Appendix D of 2006 ACGIH TLV, p. 84). Sawing or other contact with wood that has been treated to retard deterioration may result in worker exposures to oxides of chromium, copper and arsenic. Chromated copper arsenate, acid copper chromate, ammoniacal copper arsenate and ammoniacal copper zinc arsenate are or were common compounds used in wood treatment.

Gases Gaseous exposures during construction work may include oxygen, ozone, oxides of nitrogen and acetylene used in welding and oxy-acetylene cutting of metals. Chemical vapors Chemical vapors may be present from evaporation of solvents, paints, laquers, fuels and oils associated with heavy construction equipment or from off-gassing of construction materials such as carpeting and plywood. Sensitizers and asthmagens Diisocyanates are important sensitizers often encountered in the construction industry and may be components of adhesives, epoxies, paints and spray thermal insulation. Other sensitizing exposures include chromium and nickel compounds (for welders and cutters); resins (electricians); soldering fumes and welding fumes (welders); wood dust and formaldehyde (construction carpenters); water-based paints with azidine and lacquers with formaldehyde and microbiocides (painters and lacquerers); chromiumcontaining cement dust and epoxy adhesives (bricklayers and tile setters); and methylmethacrylates (reinforced concrete layers). Numerous other man-made and naturally occurring substances are classified as asthmagens (see AOEC website list: http://www.aoec.org/tools.htm).

21.3 Diseases associated with exposures in construction work 21.3.1 Chronic obstructive pulmonary disease and the pneumoconioses Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation that is not fully reversible. Predominant pathological features of COPD are emphysema, small airways disease and chronic bronchitis. The association between occupational exposures to dusts, gases and fumes and COPD was firmly established through a series of systematic epidemiological investigations. In 2002, the American Thoracic Society estimated that, based on the available epidemiologic evidence, about 15% of all cases of

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277

COPD in the US population were attributable to occupational exposures. Nevertheless, because COPD is also associated with tobacco smoking, which is prevalent among construction workers and other blue collar populations, the role of occupational exposures in the etiology of COPD is often neglected. Depending on the specific work processes and the effectiveness of dust control activities, construction workers can potentially be exposed to relatively high levels of fibrogenic mineral dusts (e.g. asbestos and silica), causing pneumoconiosis, and non- or weakly-fibrogenic dusts, which can also be associated with adverse lung effects (e.g. emery, graphite, gypsum, marble, mica, plaster of Paris, Portland cement, silicon, soapstone). Other harmful exposures in construction that can increase the risk of chronic airflow limitation include irritant gases and fumes (e.g. welding, painting, blasting fumes, combustion exhaust, asphalt, adhesives, sealants, hydrochloric acid), man-made mineral fibers and organic dust (e.g. wood). Airflow limitation in construction workers may thus be related to mineral dust-induced pneumoconiosis and nonfibrotic changes in airways associatedwithexposures todusts,gasesandfumes.Theeffectsofeachoftheseagentsmay be aggravated in some exposed individuals by associated mycobacterial lung infections. Although the adverseeffects of manyofthese agentshas been establishedin epidemiologic studies conducted across a wide spectrum of industrial workers, epidemiologic research carried out among construction workers has helped to ascertain the potential of the above agents for causing respiratory mortality and morbidity in these workers.

COPD Mortality Studies Taken together, studies carried out among construction workers in different countries have shown a clear pattern of elevated respiratory disease mortality, although there is variation in the strength of the association with construction employment; the differences may in part be explained by differing construction techniques, materials, and dust control programs. In the USA, surveillance data indicate that the number of deaths from asbestosis and silicosis is highest in workers who report they have worked primarily in the construction industry. Asbestosis deaths represented about one-third of all pneumoconiosis mortality during the 10-year period from 1990 to 1999 and the annual number of asbestosis deaths among US residents continues to increase. Occupations with the highest adjusted proportional mortality rate (PMR) from asbestosis are insulation workers, boilermakers, plumbers, pipe-fitters, plasterers, electricians, welders, brick and stone masons, crane and tower machine operators, and carpenters. Reports of deaths from silicosis in the USA declined from 1968 to 1999; in recent years the construction industry has accounted for 13.4% of all deaths from silicosis. Occupations with elevated PMR from silicosis included machine operators and construction labourers. US surveillance data also demonstrate elevated COPD mortality in the construction industry (Table 21.1). Occupations with elevated mortality included a number of construction trades: excavation and loading machine operators, followed by drywall installers, painters, construction and maintenance, carpenters and construction labourers. Smoking can potentiate the effect of construction exposures on COPD. A mortality study of California construction workers found an elevated adjusted standardized mortality ratio (SMR) for COPD, but SMRs for other unhealthy lifestyle-related causes of death were also significantly elevated.

Increase in unhealthy lifestylerelated causes of death Exposure to inorganic dust Exposure to inorganic dust Exposure to gases and irritants Exposure to fumes Only mortality from cancer was elevated

SMR ¼ 1.2 (0.89–1.58) white workers SMR ¼ 1.5 (0.74–2.65) black workers HR ¼ 1.10 (1.06–1.14) all workers HR ¼ 2.30 (1.07–4.96) never smokers HR ¼ 3.9 (2.50–5.94) never smokers HR ¼ 4.4 (2.80–7.04) never smokers SMR ¼ 77 (56–102)

COPD

NMRD ¼ non-malignant respiratory disease

Thuret, A. et al. (2007) J. Occup. Environ. Med. 49: 546–556 (N ¼ 12,788)

Risk higher in construction trades, excavation, machine operators

PMR ¼ 1.19 (1.16–1.23)

COPD

Work-related Lung Disease Surveillance Report 2002 (2003) US Department of Health and Human Services, Public Health Service, CDC/NIOSH. Burkhart, G. et al. (1993) Am. J. Ind. Med. 24: 413–425. Bergdahl, I.A. et al. (2004) Eur. Respir. J. 23: 402–406 (N ¼ 317,629)

NMRD

COPD

Comment

Finding

Outcome

Mortality studies

Table 21.1 Summary of epidemiologic findings: mortality studies among construction workers

278 CH 21 THE CONSTRUCTION INDUSTRY

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DISEASES ASSOCIATED WITH EXPOSURES IN CONSTRUCTION WORK

279

In a mortality study of 317,629 Swedish male construction workers, followed from 1971 to 1999, the COPD mortality hazard ratio was higher among never smokers for exposure to inorganic dust (hazard ratio, HR ¼ 2.30, 1.07–4.96), gases and irritants (HR ¼ 3.85, 2.50–5.94) and fumes (HR ¼ 4.44, 2.80–7.04). On the other hand, in a mortality study of a cohort of 12,788 French construction workers, followed up from 1974 to 1999, SMR was primarily increased for cancers of the digestive and respiratory system.

COPD Morbidity Studies Several large epidemiologic studies have shown associations between deficits in ventilatory lung function and construction work. A US population-based study found elevated adjusted odds ratio for COPD (based on spirometry criteria) for persons who reported their longest held job to be in the construction industry, in comparison to those who reported their longest held job as office workers, although the increase was not statistically significant (OR ¼ 1.3, 95% CI 0.8–2.3). COPD morbidity was observed to be significantly increased among nonsmoking construction trade labourers, and in African-Americans and Mexican-Americans construction workers. Among Norwegian tunnel workers with exposures to both respirable dust and quartz (mean exposures 1.2–3.6 and 0.019–0.044 mg/m3, respectively), FEV1 was significantly decreased and was also further reduced in association with blasting fumes. Among Dutch concrete workers the prevalence of COPD (based on spirometry) was 7% vs 3% in a comparable control group of nonexposed workers. The workers demonstrated significant deficits of lung function (FEV1/FVC and MMEF) in association with average concentrations of 0.8 mg/m3 respirable concrete dust and 0.06 mg/m3 respirable silica. Among Dutch construction workers, lung function was significantly lower in comparison to a reference population, after adjusting for age and pack-years smoked; chest radiological changes (profusion category 1/1 or greater predominantly irregular opacities) were associated with a further increased risk of airflow limitation. Increased risks of airflow obstruction have also been observed among construction painters, arc welders and construction insulators. Elevated risks of chronic bronchitis have been reported among construction workers exposed to spray-painting, asbestos, man-made mineral fibers, metal fumes, arc welding operations, and heavy construction and tunnel operations.

Conclusion Considerable epidemiologic evidence supports a causal link between the development of COPD (including the health outcomes of airflow limitation, chronic bronchitis and emphysema) and occupational exposures in construction work, broadly defined as gases, vapors, dusts and fumes. When a clinician evaluates the effect of occupational exposure in an individual, the available epidemiologic evidence needs to be considered together with the individual’s occupational exposure history, as well as the magnitude of any other risk factors for respiratory disease, such as tobacco smoking. It is difficult to precisely quantify the relative contributions of smoking and occupational exposures in an individual worker. However, the epidemiologic evidence makes it clear that inhalation exposures that are routinely encountered in construction work can cause

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and contribute to the development of obstructive lung disease, and simply because a construction worker has been an active smoker does not mean that occupational factors did not play an important role in the development of his or her lung disease. The literature cited above emphasizes the importance of prevention of COPD in construction workers through the application of best practices for exposure control. Evaluation of individual occupational exposures should be done and, whenever possible, hazardous exposures should be reduced or eliminated through substitution of less hazardous materials or engineering controls (e.g. process enclosure, workplace ventilation). Administrative controls and revised work practices may also help limit hazardous occupational exposures. Finally, comprehensive programs for application of personal protective equipment (e.g. respirators) should be recommended when other measures are infeasible or insufficient by themselves. In addition, construction workers exposed to conditions and agents that have been associated with significant adverse respiratory health effects should be monitored for their respiratory health, using standardized respiratory questionnaires and lung function testing. In individuals whose respiratory health monitoring results suggest adverse effects, interventions should be initiated. Periodic discussions with individual workers about their lung function test results (level of lung function or the rate of lung function decline) can help to guide decisions and may improve adherence to actions directed at preventing further excessive lung function loss. Additional steps to decrease inhalation of noxious particulates and gases are usually the most important interventions. Among smokers, complete smoking cessation may be required to halt excessive lung function decline. The potential for additive effects of smoking and occupational exposure on excessive decline in lung function should be explained to individuals who smoke and are exposed to occupational respiratory hazards. Weight gain also contributes to lung function decline, due to loss of fitness and reductions in total lung capacity. Management commitment to an integrated worksite health and safety program provides a key foundation for success in maintaining a healthy workforce. Programs are likely to be more effective when they address workers’ concerns about health risks on the job as well as wellness issues. Smoking (for example) should be addressed in the broader context of a comprehensive worksite health and safety policy. Intervention at the individual level is then more likely to be successful.

21.4 Asthma and selected immunologic conditions This section focuses largely on asthma and follows with brief consideration of some other immune-mediated respiratory conditions that may occur among construction workers, such as hypersensitivity pneumonitis and beryllium disease.

21.4.1 Asthma Although there has been considerable attention given to dust diseases and cancer outcomes in construction, investigation of work-related asthma in this sector has been

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281

neglected. As discussed above, both airborne sensitizing and irritating agents can be encountered in the construction environment. Population-based studies A number of studies have been published from a range of countries and with various outcome definitions. Most but not all studies found construction workers to be at increased risk of asthma. It should be emphasized that workers may experience newonset occupational asthma (OA) from job-related exposure to sensitizers. However, individuals with pre-existing asthma may experience worsening of their asthma at work associated with exposures to nonspecific dust or irritants, a condition termed work-aggravated asthma (WAA). WAA occurs in approximately 1 in 4 working adult asthmatics, and is associated with a diminished quality of life. Construction work often involves exposures to agents and conditions associated with WAA such as chemicals, including cleaning products, paints and solvents; dust; second-hand cigarette smoke; gases, fumes, odours or smoke; exertion; very cold air; and hot, humid or polluted outdoor air. Investigators have estimated the prevalence rate of various reported respiratory conditions based on a national probability sample of construction workers from data collected for the 1988 National Health Interview Survey. Prevalence rates of respiratory conditions among (white) men who indicated they had experience in the construction industry were compared with those found among other workers who participated in the survey. Asthma was reported less frequently by construction workers than by the other workers. The authors felt that, since sensitized individuals or those having a significant response to workplace irritants (perhaps work-aggravated or workexacerbated asthma) ‘may voluntarily leave the construction workforce, additional research should investigate the potential role of health-related employment migration in reducing the rate of asthma reported by construction workers’. This possible explanation regarding survivor bias/dropout should be borne in mind (that is, relative risks for asthma morbidity in the construction industry may be underestimated). Specific occupations The incidence of asthma among male workers in the construction industry in Finland was examined as a follow-up to a population-based study. The study was a comprehensive registry-based nationwide follow-up (cohort) study, and thus provided relatively rigorous evidence. The authors determined asthma incidence for men without preexisting asthma employed in the construction trade and a comparison group employed in administrative work, for the interval from 1986 to 1998. Follow-up was conducted using two national registries (Medication Reimbursement Register and the Finnish Register of Occupational Diseases). Significantly increased risks for asthma onset were demonstrated for a number of construction occupations, as shown in Table 21.2. Among those with the highest risks were painters and lacquerers and insulation workers, where isocyanates may be used. Of interest, only 2% of the cases of asthma among construction workers had been recognized as OA (i.e. through the Finnish national compensation process), suggesting a lack of recognition or reluctance to file claims. In a separate report, Vandenplas et al. described two cases of OA in construction (wood-roof maintenance) workers. Of note, both affected individuals were sensitized to a prepolymer, but not the monomer of toluene diisocyanate (TDI). The risk for sensitization to newer oligomer forms of isocyanates has been of increasing concern.

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Table 21.2 Epidemiologic study of the risk of asthma in construction worka Occupation

Administrative, managerial and clerical work Motor vehicle drivers Sheet metal workers Plumbers Welders and flame cutters Construction carpenters Cabinet makers and joiners Painters and lacquerers Bricklayers and tile setters Concrete shutterers and finishers Insulation workers Assisting building workers

N

Population

Incidence rate per 1000 workers per year

Relative risk (95% CI)

1,275

79,087

1.23

1.00 (referent)

114 70 193 56 406 18 182 82 33 51 325

3992 3166 6502 1664 16,546 737 6319 2818 1067 1950 12,348

2.15 1.62 2.20 2.53 1.77 1.85 2.10 2.09 2.17 1.96 1.92

1.71 1.59 1.90 2.34 1.51 1.77 1.75 1.83 1.67 1.78 1.65

(1.41–2.07) (1.25–2.02) (1.63–2.21) (1.79–3.06) (1.35–1.68) (1.11–2.82) (1.50–2.04) (1.46–2.28) (1.19–2.37) (1.34–2.35) (1.11–2.38)

a

Table adapted from Karjalainen, A., Martikainen, R., Oksa, P., Saarinen, K., Uitti, J. (2002) Incidence of asthma among Finnish construction workers. J. Occup. Environ. Med. 44: 752–757.

Exposure to isocyanates during construction activities Studies from Canada, the USA and France have identified the potential for exposure to methylene diphenyl diisocyanate (MDI), a commonly used type of isocyanate, during construction activities, including during the process of insulating buildings with sprayed polyurethane foam. Concentrations exceeding established limits were observed for both indoor and outdoor sprayers. Both the applicator and assistants could be exposed. In a recent study which measured both monomer and oligomeric MDI, the average monomer concentration exceeded the permissible exposure limit (ceiling) at distances ranging up to 6–12 m. The current ACGIH TLV of 0.005 ppm is one-quarter of the PEL. The aerosol particle size measurements indicated a mean respirable fraction of 20%, while approximately two-thirds of the total mass of the airborne particles in the spray foam aerosol were greater than 3.5 mm in diameter. Recent investigations have linked skin contact with isocyanates to respiratory sensitization, implying that exposures to larger ‘nonrespirable’ particles may also be biologically relevant.

21.4.2 Other immunologic conditions Beryllium A large survey was undertaken to screen for beryllium disease among 3842 current and former construction workers at Department of Energy (DOE) nuclear sites in the USA. Screening with a beryllium blood lymphocyte proliferation test (BeLPT) was offered to all current workers as well as many who had left employment years before the examination took place. The findings indicated that only a minority of workers had any awareness of the presence of beryllium (Be), let alone knowledge of potential work tasks or locations in which exposure to Be could have taken place. About onethird reported exposure to beryllium; overall 2.2% had at least one abnormal BeLPT

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283

and 1.4% were also abnormal on a second test. Having worked in a building with potential beryllium exposure (i.e. where beryllium activities had taken place) was a strong and significant predictor for an abnormal BeLPT (odds ratio 3.4, 95% CI 1.3–8.8). A small number of participants (five) were diagnosed with chronic beryllium disease (CBD), a rate that was lower than the expected prevalence in other more highly exposed populations, where the rate of CBD among those sensitized to beryllium has been reported occasionally as high as 50%. The Be exposure among these construction workers was different (probably lower) than in production facilities; however, coupled with the BeLPT findings, this study indicates that significant exposures can occur among construction workers, most likely during maintenance, repairs, renovation or demolition in facilities where beryllium was used. Hypersensitivity pneumonitis Hypersensitivity pneumonitis (HP) is a lung disorder which occurs in a small proportion of individuals exposed to organic dusts, and may also be triggered by commonly encountered workplace chemicals such as isocyanates. There are few reports of HP specifically occurring in construction workers; however, the possibility should be kept in mind. There is a likelihood of exposure to hazards for HP and a related disorder, organic dust toxic syndrome, during demolition and renovation of old or abandoned structures, especially in agricultural environments, such as grain storage bins. Hypersensitivity pneumonitis has been recognized in the construction industry in Spain among stucco makers and plasterers exposed to Esparto grass. Esparto grass is a plant widely distributed in the south of Europe and North Africa, used in the manufacturing of clothing and especially as supporting material for plaster plaques and molds in the building industry. Cases of HP have been reported in individuals who have demonstrated precipitating antibodies to one of several workplace agents, including Aspergillus fumigatus, thermophilic microorganisms and Esparto extract. In fact, in Spain, Esparto is one of the most frequently identified agents causing HP.

21.5

Occupational cancers

21.5.1 Epidemiologic studies of cancer Many (but not all) published studies of male construction workers from North America and Europe have documented an increased risk of several specific malignancies (Table 21.3). The observation of an excess risk for lung cancer has been a particularly consistent finding, and the risks observed in construction have in general remained significantly elevated after controlling for the effects of tobacco smoking. For many cancer hazards found in the construction work environment, increased risks for both adenocarcinoma and squamous lung cancer histologies have been observed. Significant increases in proportionate mortality have also been observed for cancers of the nasopharynx and larynx among male construction workers. Increased risks have also been observed for upper gastrointestinal cancers, particularly adenocarcinoma. An elevated overall risk of cancer-related mortality has also been observed in some but not all studies of construction workers. Fewer investigations have been reported among female construction workers and few studies are available from Asia or South America,

2.3–4.8

SMR OR OR PMR IRR

IRR

IRR

OR OR

RR RR

OR

SMR

SMR

SMR

All cancer Bone sarcoma Bone sarcoma Buccal cavity Esophageal adenocarcinoma Gastric (cardia)

Gastric

Laryngeal Larynx and hypopharynx

Laryngeal (squamous) Lip cancer

Lung

Lung

Lung

Lung

0.88

1.12–1.37

0.70–0.83

1.4

1.7 1.7

2.42 2.61

1.3–1.5

0.89 2.93 4.25 1.43 3.8–4.5

Statistic

Malignancy

Valuea

Asphalt workers

Heavy equipment operators, Diesel Truck drivers, Diesel

All construction

All construction (asbestos, wood) Construction work (sunlight)

Cement, high exposed Concrete workers

All construction Construction workers Carpenters, joiners All construction Construction (high exposed, asbestos and cement) Construction (high exposed, asphalt fumes, wood dust) Cement, quartz, diesel

Implicated job/agent

Table 21.3 Epidemiologic studies of the risk of malignancy in construction work

Arndt, V. et al. (2004) Occup. Environ. Med. 61: 419–425.Cohort Merletti, F. et al. (2006) Int. J. Cancer 118: 721–27. CC, Smk Adj Merletti, F. et al. (2006) Int. J. Cancer 118: 721–727. CC, Smk Adj Wang, E. et al. (1999) Appl. Occl. Environ. Hyg. 14: 45–58. Cohort Jansson, C. et al. (2005) Cancer Causes Control 16: 755–764. Cohort, Smk Adj Jansson, C. et al. (2005) Cancer Causes Control 16: 755–764. Cohort, Smk Adj Sjodahl, K. et al. (2007) Int. J. Cancer 120: 2013–2018. Cohort, Smk Adj Dietz, A. et al. (2004) Int. J. Cancer 108: 907–911. CC, Smk Adj Boffetta, P. et al. (2003) Cancer Causes Control 14: 203–212. CC, Smk Adj Brown, L.M. et al. (1988) Cancer Res. 48: 1960–1964. CC, Smk Adj Nordby, K.C. et al. (2004) Cancer Causes Control 15: 619–626. Cohort, no exp-resp Richiardi, L. et al. (2004) Cancer Causes Control 15: 285–294. CC, Smk Adj Jarvholm, B. et al. (2003) Occup. Environ. Med. 60: 516–520. Cohort, Smk Adj Reduced cancer risk with use of closed cabs Jarvholm, B. et al. (2003) Occup. Environ. Med. 60: 516–520. Cohort, Smk Adj Bergdahl, I.A. et al. (2003) Am. J. Ind. Med. 43: 104–108 (exposures and cancer incidence lower after 1965)

Reference and commentsb

284 CH 21 THE CONSTRUCTION INDUSTRY

1.3

IRR

PMR OR OR

Pharynx Sino-nasal (adenocarcinoma) Sino-nasal (squamous)

b

1.34 5.8 3.7–8.1

All construction Carpenters (wood) Construction, carpenters

Diesel exhaust exposed

All construction Wood dust exposed, (mainly carpenters) Sunlight (high exposed)

Silica, concrete

For most studies, only male construction workers were included. CC indicates case–control design; Smk Adj indicates study adjusted for tobacco smoking.

a

2–3.4

RR

Malignant melanoma (head, eye, neck) Myeloma

1.13 1.5–3.6

PMR OR

Lung Lung (all cell types)

1.4–2.5

OR

Lung (nonadenocarcinoma)

Lee, W.J. et al. (2003) Int. J. Cancer 107: 134–138. Cohort, Smk Adj, no exp-response Wang, E. et al. (1999) Appl. Occl. Environ. Hyg. 14: 45–58. Cohort Luce, D. et al. (1992) Am. J. Ind. Med. 21: 163–175. Smk Adj Luce, D. et al. (1992) Am. J. Ind. Med. 21: 163–175. CC, Smk Adj

Siemiatycki, J. et al. (1989) Am. J. Ind. Med. 16: 547–567. CC, Smk Adj Wang, E. et al. (1999) Appl. Occl. Environ. Hyg. 14: 45–58. Cohort Barcenas, C.H. et al. (2005) Am. J. Ind. Med. 47: 349–357. 05, CC, Smk Adj (light smokers included as nonsmokers) Hakansson, N. et al. (2001) Epidemiology 12: 552–573. Cohort

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285

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but several of these studies have observed an increased risk of cancer mortality among these construction workers. Lung cancer hazards have been recognized from various construction exposures, including asbestos, silica and certain man-made vitreous fibers (particularly refractory ceramic fibers), as well as insulation materials made from asbestos-contaminated vermiculite. Important exposures to these materials have occurred in new construction, and although application ofthese materialshasbeenrestricted,potential hazards continue during repair, renovation and demolition of various structures. Other potentially carcinogenic exposures have been identified in construction workplaces. Workplace exposures to cement dusts, whose hazardous constituents can include silica and asbestos, as well as hexavalent chromium, have been documented as a cancer risk. Other cancer hazards that have been reported in specific construction environments include arsenic, found in treated wood products, beryllium and nickel compounds. Diesel exhaust exposure in construction has been documented to result in airborne levels of polycyclic aromatic hydrocarbons (PAHs, recognized lung carcinogens) that can exceed recommended levels. There is some evidence that use of air-conditioned cabs on diesel equipment is protective. Asphalt fumes in road construction and roofing tars can also result in exposures to PAHs, and fumes from solvents used in various processes may includeexposurestotoxins tothelymphatic andhematologicsystems.Exposures tofumes containing cadmium, nickel and chromium have been documented in welders. Formaldehyde is used in many adhesives and coatings, and potentially important exposures have been documented in construction settings. Construction, repair and demolition projects in the nuclear industry can entail significant exposures to ionizing radiation. Despite the complexity of the construction work environment and the difficulty in documenting exposures for individuals in construction work, epidemiologic studies in this industry have related several exposures to particular cancer risks. Some studies among construction workers who have high levels of exposure to solar radiation have demonstrated elevated rates of skin cancers, including squamous carcinoma of the lip, and malignant melanoma of the face and eye. Lung cancer in construction workers has been associated with exposures to asbestos and cadmium, while laryngeal cancer and malignant mesothelioma have been related to exposure to asbestos fibers. Studies of wood dust exposures among carpenters and special trades construction workers have associated inhalation of these dusts with cancers of the nose and sinus mucosae. The evidence of carcinogenicity of hardwoods is judged to be stronger than for soft woods, although both exposures have been implicated. There is also some evidence that inhalation of wood dusts may result in other cancers, including lung cancer and bone sarcomas.

21.5.2 Neoplasms in construction workers: diagnosis and management issues The clinician may not infrequently encounter a malignant neoplasm arising in an individual who has worked in the construction industry. The contribution of the workplace to the etiology must be considered, and is often a challenging issue. As described elsewhere in this chapter, depending on the specific tasks and processes, construction work can involve exposure to several agents and dusts which are recognized carcinogens. Because of the nature of construction work, exposures are often

21.6

OTHER CONDITIONS

287

extremely variable between tasks and projects, and few data are available to document the frequency, duration and levels of exposure to most workplace hazards in construction. Additionally, construction settings are often arrayed such that significant exposures can result from adjacent activities (such as cutting, grinding, welding, insulating, etc.), and individuals experiencing such ‘bystander’ exposures may be unaware of the risk or the need for protection. When evaluating a construction worker with a malignancy, the clinician may be presented with a formidable challenge in documenting the worker’s history of exposure to potential carcinogens. It may be necessary to review in considerable detail the projects and tasks in which the patient participated or was a significant bystander, querying specifically about carcinogens that are potentially present during specific types of construction. Table 21.3 catalogs a number of major studies which have assessed the association of construction work with cancer.

21.5.3 Cancer in construction workers: summary Attribution of causality is challenging for a cancer patient with prior reported exposures to carcinogens in construction work. Similar to other occupational exposures, the probability of a work-related malignancy increases with the intensity, frequency and duration of reported exposures. Conversely, the likelihood that a tumor is causally related to exposure decreases when the latency period is atypical (i.e. unusually long or short), if there is documentation of the effective application of exposure controls and when there are substantial exposures to competing causes such as tobacco smoking. In some individuals, the etiology can be presumptively confirmed by the demonstration in tissues of the agent and/or response (e.g. lung cancer in a worker who has been diagnosed with asbestosis or silicosis, or in a patient whose sputum cytology or lung tissue has demonstrated asbestos fibers or ferruginous bodies). At times, the specific cell-type of the tumor is an important factor (e.g. mesothelioma is presumed occupational in an individual with prior workplace asbestos exposure). Diagnosis and management of malignancy attributed to exposures in construction work is, in general, not different from the treatment of similar cancers in other settings, although concurrent occupational diseases may complicate treatment or obviate curative resection.

21.6

Other conditions

Construction workers may also develop respiratory infections and irritant effects related to exposures. For completeness, it should be noted that construction work presents a greatly increased risk of trauma due to injuries on the job.

21.6.1 Infections Construction workers involved in excavation in tropical or subtropical areas may be at risk for nocardia, particularly if they have risk factors for deficient cell-mediated

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immunity such as immunosuppressive therapy or lymphoma. When soil is disturbed during road work and other construction activities in endemic regions, workers may be exposed to fungal spores and thereby be placed at risk for developing certain fungal lung infections. Histoplasmosis (often associated with bird droppings) and coccidioidomycosis commonly occur in individuals with normal immune systems. Construction workers with silicosis are at increased risk for tuberculosis and nontuberculous mycobacterial infections. Legionnaires’ disease has been related to construction activities involving excavation as well as work in proximity to water cooling towers.

21.6.2 Irritant effects Depending on the agent and intensity of exposures, construction workers can experience upper respiratory tract mucous membrane irritation, bronchitis, bronchiectasis and acute respiratory distress syndrome. Painters and other construction workers may experience mucous membrane and lower respiratory tract irritation associated with multiple dust exposures as well as inorganic and organic chemicals such as hydrochloric acid and organic solvents, including components of paints, varnishes or lacquers such as methyl ethyl ketone, acetone and n-butyl lactate.

Further reading Balmes, J., Becklake, M., Blanc, P. et al. (2003) American Thoracic Society Statement: Occupational contribution to the burden of airway disease. Am. J. Respir. Crit. Care Med. 167: 787–797. Gamboa, P.M., Urbaneja, F., Olaizola, I., Boyra, J.A., Gonzalez, G., Antepara, I., Urrutia, I., Jauregui, I., Sanz, M.L. (2005) Specific IgG to Thermoacynomices vulgaris, Micropolyspora faeni, and Aspergillus fumigatus in building workers exposed to Esparto grass (plasterers) and in patients with espartoinduced hypersensitivity pneumonitis. J. Invest. Allerg. Clin. Immunol. 15: 17–21. Hnizdo, E., Kennedy, S.M., Blanc, P., Toren, K., Bernstein, I.L., Chan-Yeung, M. (2006) Chronic airway disease due to occupational exposure. In Asthma in the Workplace, Bernstein, I.L., ChanYeung, M., Malo, J.L., Bernstein, D.L. (eds). Taylor and Francis: New York. Karjalainen, A., Kurppa, K., Martikainen, R., Klaukka, T., Karlalainen, J. (2001) Work is related to a substantial portion of adult-onset asthma incidence in the Finnish population. Am. J. Respir. Crit. Care Med. 164: 565–568. Karjalainen, A., Martikainen, R., Oksa, P., Saarinen, K., Uitti, J. (2002) Incidence of asthma among Finnish construction workers. J. Occup. Environ. Med. 44: 752–757. Kogevinas, M., Anto, J.M., Sunyer, J., Tobias, A., Kromhout, H., Burney, P. and the European Community Respiratory Health Survey Study Group. (1999) Occupational asthma in Europe and other industrialised areas: a population-based study. Lancet 353: 1750–1754. Le Moual, N., Kennedy, S.M., Kauffmann, F. (2004) Occupational exposures and asthma in 14,000 adults from the general population. Am. J. Epidemiol. 160: 1108–1116. Ringen, K. et al.. (eds) (1995) Special issue. Occupational Medicine State of the Art Reviews, Construction Safety and Health 10(2). Sorenson, G., Barbeau, E.M., Stoddard, A.M., Hunt, M.K., Goldman, R., Smith, A., Brennan, A.A., Wallace, L. (2007) Tools for health: the efficacy of a tailored intervention targeted for construction laborers. Cancer Causes Control 18: 51–59.

FURTHER READING

289

Sullivan, P.A., Bang, K.M., Hearl, F.J., Wagner, G.R. (1995) Respiratory disease risks in the construction industry. Occup. Med. State Art Rev. 10 (2): 313–334. TLVs and BEIs Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents & Biological Exposure Indices. ACGIH : Cincinnati, OH. US Department of Heath and Human Services Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health (2004) A Summary of Health Hazard Evaluations: Issues Related to occupational Exposure to Isocyanates, 1989–2002. DHHS (NIOSH) publication no. 2004-116. Vermeulen, R., Heederik, D., Kromhout, H., Smit, H.A. (2002) Respiratory symptoms and occupation: a cross-sectional study of the general population. Environ. Hlth 1(5): 1–7.

22 Police, firefighters and the military Aaron M. S. Thompson1 and Stefanos N. Kales2 1 2

St. Michael’s Hospital, Toronto, Ontario, Canada Harvard Medical School and Harvard School of Public Health, MA, USA

22.1 Introduction Police, firefighters and military personnel may be exposed to pulmonary toxins and irritants, placing them at risk for the development of acute and chronic respiratory disease. While each profession is distinct, potential exposures overlap significantly. The first section of this chapter addresses potential exposures for all three professions in their capacity as first responders. The remainder of the chapter considers exposures more unique to each of the three professions. Sources for each exposure are discussed along with relevant historical aspects. Pathophysiological mechanisms are addressed in conjunction with clinical presentation. Primary prevention is discussed in varying detail, although due to the uncontrolled nature of the environments in which police, firefighters and military personnel work, administrative and engineering controls are often not possible and personal protective equipment (PPE) may be the sole preventative measure. Secondary prevention, in the form of medical surveillance, is touched upon where relevant. Treatment and prognosis are also described.

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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22.2 First responders: potential exposures common to police, firefighters and the military Police, firefighters and military personnel act as first responders to threats involving public safety and security. Potential exposures include acute chemical emergencies (chemical weapons and hazardous materials), biological hazards and fire smoke. The World Trade Center (WTC) disaster on 11 September 2001 exposed emergency response personnel to a novel and complex mixture of smoke and hazardous dusts. A large proportion of first responders to the WTC disaster developed a variety of respiratory problems, some of which are unique to this population. As such, respiratory disease in WTC responders is considered as a distinct topic in this chapter.

22.2.1 Chemical weapons and hazardous materials Exposure to chemical weapons may occur during terrorist attacks or warfare. Chemical warfare agents include crowd control agents, chlorine, sulfur mustard (SM), phosgene and nerve agents. Hazardous material exposure can result from industrial disasters, recreational mishaps and natural catastrophes. Hazardous materials incidents involve a wide variety of chemical hazards, with clandestine drug laboratories posing unique risks. Most chemical weapons and hazardous material incidents involve exposure to strong irritants. The clinical effects of exposure are dependant on concentration, duration of exposure, the water content of exposed tissues and individual characteristics of the exposed victim. Agents with high water solubility (crowd control agents, chlorine, ammonia) predominantly affect exposed mucous membranes and upper airways, while those with lower water solubility (SM, phosgene) penetrate to the small airways and alveoli. Table 22.1 delineates these exposures by source, water solubility and mechanism of toxicity. The basic management of acute chemical exposures involves cessation of exposure and aggressive supportive measures as needed. The former is accomplished by early decontamination (ideally prior to hospital transport). Clothing removal eliminates 85–90% of trapped chemical substances, and should be followed by soap and water decontamination. Clinical signs of severe chemical injury include altered mental status, cardio-respiratory manifestations, unconsciousness and convulsions. Initial supportive care should focus on airway patency, ventilation and circulation, while surveying the patient for burns, trauma and other injuries. Chemical weapons Crowd control agents are a unique form of chemical weapon to which first responders, and police in particular, are exposed. The most commonly used crowd control agents are o-chlorobenzylidene malononitrile (CS), chloroacetophenone (CN) and dibenzoxazepine (CR). While colloquially referred to as ‘tear gas’, these agents are actually aerosolized powders. Eye and upper airway symptoms typically occur within 30 seconds of exposure and persist for up to 30 minutes post-exposure. Severe exposure may cause laryngospasm and bronchospasm, especially in persons with pre-existing respiratory disease such as asthma or bronchitis. Effects are usually self-limited, although they may persist longer in cases of high exposure (such as in enclosed spaces) or in individuals

Fire smoke (inorganic combustion, melamine nylon, silk and wool) Hazardous materials incidents Fire smoke (combustion of retardant materials containing bromine, and fluorinated resins and films) Fire smoke (combustion of chlorinated acrylics, polyvinyl chloride, and fire retardant materials) Fire smoke (combustion of compounds containing sulfur)

Ammonia

Crowd control agents Chemical weapons

Fire smoke (combustion of cellulosics and polyolefins)

Chemical weapons Hazardous materials incidents

Chemical weapons

Tear gas (CS, CN, CR)b

Acrolein

Chlorine derivatives

SM (mustard gas)

SOx

Hydrogen chloride

Halogenated acids

Source

Toxic inhalant

Acid formation

Acid Formation

High solubility

High solubility

Moderate solubility

Moderate solubility

Moderate solubility

High solubility

Alkylation

Acid formation

Cytotoxic

Alkylation

Acid formation Oxidation

Alkali formation

High solubility

High solubility

Mechanism of Injury

Characteristics

Table 22.1 Respiratory irritants and toxicants; sources, solubility and mechanisms of injurya

damage heavy exposure

damage heavy exposure

damage heavy exposure

Epithelial damage Increased membrane permeability Irritation of nerve fibers Pain via bradykinin release Blistering of exposed mucous membranes and upper airways in severe cases Histopathological effects in the bronchi and/or trachea include exfoliation, edema, inflammation, vascular congestion and hemorrhagic necrosis Epithelial damage primarily to the upper airway Heavy exposures may result in toxic pneumonitis and pulmonary edema Impaired cell homeostasis Epithelial cell death (desquamation of the airway epithelium) (continued)

Tissue liquefaction Predominant upper airway Lower airway damage with Epithelial damage Predominant upper airway Lower airway damage with Epithelial damage Predominant upper airway Lower airway damage with

Pathology

22.2 FIRST RESPONDERS

293

b

Sensitizer

Cholinesterase inhibition

Absorbed in respiratory tract, dermally and via the gut

Cellular asphyxiant

Cellular asphyxiant

Acylation Acid formation

Oxidation

Mechanism of Injury

Absorbed in respiratory tract

Diffuses into blood

Diffuses into blood

Low solubility

Low solubility

Characteristics

Airway hypersecretion Bronchoconstriction Thoracic weakness Decreased respiratory drive

Epithelial damage Increased membrane permeability Irritation of nerve fibers Increased capillary permeability leading to progressive pulmonary edema Epithelial damage secondary to HCl formation is secondary and relevant only with severe exposures No significant pulmonary injury Decreased respiratory drive at high doses No significant pulmonary injury Decreased respiratory drive at high doses Upper airway inflammatory response

Pathology

International Programme on Chemical Safety (IPCS). INCHEM. Concise International Chemical Assessment Documents (CICADs). CS, o-chlorobenzylidene malononitrile; CN, chloroacetophenone (CN); CR, dibenzoxazepine.

a

Nerve agents, organophosphorus and carbamate pesticides

Isocyanates

Carbon monoxide

Hydrogen cyanide

Acrylonitrile, nylon, polyurethane paper, silk and wool Fire smoke (incomplete combustion of hydrocarbons) Fire smoke (combustion of urethane and isocyanate polymers) Hazardous materials incidents Chemical weapons Hazardous materials incidents

Fire smoke (combustion of cellulose nitrites and fabrics) Hazardous materials incidents Chlorinated acrylics, polyvinyl chloride, and fire retardanttreated materials

NOx

Phosgene

Source

Toxic inhalant

Table 22.1 (Continued)

294 CH 22 POLICE, FIREFIGHTERS AND THE MILITARY

22.2

FIRST RESPONDERS

295

with underlying lung disease. In general, long-term prognosis is excellent; however, reactive airways dysfunction syndrome (RADS) and other sequelae have been reported in select cases. Chlorine gas, an irritant with intermediate solubility, was first used as a weapon in World War I in the Second Battle of Ypres, on 22 April 1915. Its use in World War I as a chemical weapon declined with the advent of phosgene and SM. Today, chlorine is ubiquitous as both an industrial chemical and disinfectant. Among hazardous materials incidents, accidental releases of chlorine compounds are second only to those involving ammonia. Chlorine gas causes upper and lower airway damage via its conversion to hydrochloric and hypochlorous acids. Low concentrations are scrubbed out in the upper airways, while higher exposures (>50 ppm) penetrate more deeply, causing acute lung injury and potential long-term respiratory complications. Even with severe exposures, mortality is low and long-term prognosis is good. Pulmonary symptoms usually resolve within 1–2 months, although there have been case reports of persistent obstructive disease, restrictive disease and RADS. Smokers and those with chronic chlorine exposure are most susceptible to persistent respiratory sequelae. Treatment is supportive (bronchodilators and steroids in severe cases). Nebulized sodium bicarbonate may be of benefit in select cases. SM, the most widely used chemical weapon in the past century, is a vesicant or ‘blistering’ agent known as mustard. SM predominantly causes skin and eye injuries, but can also affect the conducting airways and adjacent alveoli. The mechanism of action of SM involves DNA and protein alkylation, causing cell death. The result is desquamation of the airway epithelium and a generalized inflammatory response. Mortality rates are low, although subsequent morbidity (eye, skin and respiratory) is common and often significant. Long-term respiratory complications from SM exposure include interstitial fibrosis, chronic obstructive pulmonary disease (COPD), bronchiectasis and bronchiolitis obliterans. Bronchiectasis and pulmonary fibrosis are usually confined to the lower lobes. Victims can also develop an SM-induced asthma. Treatment is supportive, including antibiotics for superinfection and selective use of steroids to prevent progression of fibrosis. Phosgene (carbonyl chloride) was the most lethal chemical weapon used in World War I, causing an estimated 80% of poison gas deaths. Today, phosgene is a widely used industrial chemical. Its low water solubility allows it to penetrate to the distal respiratory units of the lung parenchyma. Phosgene causes diffuse injury by directly damaging cellular elements of the respiratory tract and triggering a cytokine-induced inflammatory cascade. Moderate to high exposures (>3 ppm) cause a triphasic response. The initial ‘reflex’ phase occurs when sensory receptors initiate a vagal reflex which leads to rapid shallow breathing. An asymptomatic second ‘latent’ phase characterized by increased pulmonary capillary permeability may then ensue after a period of up to 30 hours. In severe cases, victims progress to a third phase: adult respiratory distress syndrome. Radiographic evidence of early pulmonary edema may begin as early as 7–8 hours post-exposure, showing blurred enlargement of the hila and ill-defined patches or strip shadows in the central portions of the lung. Treatment is supportive, often requiring positive airway pressure ventilation. Diuretics should be avoided as pulmonary edema is due to capillary leak, which can lead to a relative vascular hypovolemia. While no specific antidote for phosgene exposure exists, steroids and ibuprofen have been used with some success. The long-term prognosis is generally good

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for victims surviving the initial stages of disease, although an obstructive pattern compatible with chronic bronchitis, emphysema or RADS on pulmonary function testing may persist for months to years. The chemical weapons sarin, soman, tabun and VX are organophosphorous compounds often referred to as ‘nerve agents’ because they inhibit acetylcholinesterase, resulting in cholinergic overstimulation. Cholinergic overstimulation presents with muscarinic and nicotinic effects. Muscarinic symptoms include profuse exocrine secretions, miosis, headache and eye pain. Nicotinic symptoms include skeletal muscle weakness, fasciculations and paralysis. While primarily systemic toxins, mortality from nerve agent exposure usually results from respiratory compromise due to hypersecretions, bronchoconstriction, thoracic weakness and decreased respiratory drive. Treatment is predicated upon diagnosing the clinical cholinergic toxidrome. Measuring erythrocyte and serum cholinesterase levels is confirmatory, although results are not available rapidly enough to be useful, and treatment should not be delayed for purposes of laboratory confirmation. Supportive treatment consists of supplemental oxygen, suctioning of secretions and, in severe cases, mechanical ventilation. Benzodiazepines are used as anticonvulsants, and are the only effective anticonvulsant drugs in the context of nerve agent poisoning. Two specific antidotes exist: (1) atropine competitively blocks the action of acetylcholine at muscarinic receptors; (2) pralidoxime and other ‘oximes’ reactivate acetylcholinesterase and work at nicotinic, muscarinic and central nervous system receptors. Hazardous materials Hazardous materials comprise a wide range of physical, chemical and biological hazards in a variety of settings. Most hazardous material incidents do not result in chemical exposure victims. Incidents that do result in casualties usually involve irritants such as chlorine derivatives, ammonia, phosgene and other corrosive substances. The mechanisms of injury, clinical presentation, treatment and prognosis are the same as described for irritant chemical weapons. In events involving fires and explosions, thermal injury and exposure to fire smoke can also cause significant injury. Fire smoke is discussed below. Organophosphorous and carbamate pesticides may also be released during chemical accidents. These substances are cholinesterase inhibitors with effects analogous to those of the nerve agent chemical weapons. The resulting cholinergic toxidrome and its treatment are similar to those described for nerve agents. The major difference between cholinesterase-inhibiting pesticides and weaponized nerve agents is the time course of symptoms. Pesticides tend to have a slower onset but longer duration of action. As such, supportive care for cholinesterase-inhibiting pesticide exposure is usually longer, and the cumulative dosage of atropine required greater, than is required for exposure to the weaponized nerve agents. A unique set of toxins encountered by first responders and law enforcement personnel are those produced in clandestine drug laboratories. Potential exposures include lead oxide, aluminum hydroxide, mercury vapor, iodine, phosphine, yellow phosphorus, hydrogen chloride and anhydrous ammonia. While some of these agents have the potential to cause serious systemic toxicity, respiratory irritation is the most common acute symptom and long-term sequelae may include persistent cough, wheeze, breathlessness, bronchitis, chest colds, pneumonia, chronic bronchitis and emphysema.

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FIRST RESPONDERS

297

Primary prevention for personnel responding to chemical weapons or hazardous materials releases requires provision and instruction in the use of appropriate PPE. Administrative controls include written protocols addressing the order in which responders enter buildings and the PPE they should wear. Secondary prevention should include periodic medical assessments, including spirometry. In the event of phosgene, SM or chlorine gas exposure, patients should have ongoing medical surveillance to ensure optimization of therapy in cases of residual airway hyperreactivity, and to rule out the development of pulmonary fibrosis. Existing evidence indicates that hazardous material (HAZMAT) procedures and personal protective equipment are effective, with the literature reporting that HAZMAT responders do not lose pulmonary function at an accelerated rate compared with their non-HAZMAT firefighting counterparts.

22.2.2 Biological weapons Bacterial pathogens can be disseminated as aerosols for use in biological warfare or acts of terrorism. Biological agents with the potential to be weaponized include bacteria, viruses and biologically derived toxins. Although the pathological endpoints for most biological weapons are systemic, victims may present with isolated respiratory symptoms. The United States Centers for Disease Control and Prevention (CDC) has identified, and placed in priority order according to likelihood of weaponization, those biological agents thought to pose a risk for use as biological weapons. Category A represents agents considered to be of highest priority (agents already weaponized or with high likelihood to be weaponized in the future), while Category C represents agents of low priority (emerging diseases or agents that may be weaponized in the future). The essentials for diagnosis and management of the primary potential biological weapons of interest (respiratory anthrax, plague, tularemia, brucellosis, glanders and Q fever) are summarized in Table 22.2. Suspected infection with any of these agents requires immediate work-up because rapid diagnosis is vital to enable identification of index cases, manage potential outbreaks and prevent further exposures. An in-depth discussion of these specific biological agents is beyond the scope of this chapter, although some general aspects of presentation regarding each is worth mention. Anthrax has been of greatest concern to date, with documented attacks having already occurred. Anthrax presents with a biphasic course, and distinguishes itself from influenza and other viral illnesses because of early dyspnea, gastrointestinal upset, lack of rhinorrhea and sore throat. Mediastinal widening on chest imaging is characteristic. Pneumonic plague is the least common form of plague, after bubonic and primary septicemic plague. Pneumonic plague initially presents as a flu-like illness. The presence of a bubo, an erythematous swollen and tender lymph node, is characteristic of infection. Recognized and appropriately treated, the prognosis for pneumonic plague is good, although multidrug resistant strains exist so susceptibility testing is recommended. Pneumonic tularemia is characterized by marked respiratory symptoms, with most victims developing prominent lymphadenopathy and a nonspecific secondary rash in select cases. Pleuritic chest pain and fever may also be noted upon presentation.

Infectious agent/toxin

Bacillus anthracis

Yersinia pestis

Francisella tularensis

Coxiella burnetii

Disease

Anthrax

Pneumonic plague

Pneumonic tularemia

Q fever

B

A

A

A

CDC priority

Table 22.2 Bioterrorism agents

14–21 days

2–5 days (up to 21)

3–4 days (up to 10)

2–5 days

Incubation period Biphasic. Early (4–6 days post exposure): nonproductive cough, low-grade fever, malaise, gastrointestinal symptoms. Late: dyspnea at rest, stridor, dry cough and high fevers Progressive course. Early (2–4 days post exposure): cough, chest pain, hemotysis. Late: fulminant pneumonia and respiratory failure Progressive course; dyspnea, minimally productive cough, pleuritic chest pain, and fever Atypical pneumonia. Most individuals asymptomatic; 25% present with pleuritic chest pain

Clinical presentation

Body fluid culture (blood, lymph node aspirate, sputum, cerebrospinal fluid) Serologyb,c

Presence of a bubo; an erythematous swollen and tender lymph node

Elevated liver enzymes  hepatosplenomegaly (one-third of patients). 50% patients abnormal CXR.

Serologyc

Blood culture

Mediastinal widening on CXR

Prominent lymphadenopathy

Diagnosis

Characteristic finding(s)

Streptomycin, gentamicin, tetracyclines or chloramphenicol

Streptomycin

Inactivated vaccine Limited availability Poor efficacy Live attenuated vaccine Limited availability Inactivated vaccined

Doxycycline

Ciprofloxacin or doxycycline

Antibiotic susceptibilitya

Acellular Vaccine Limited availability

Vaccine

298 CH 22 POLICE, FIREFIGHTERS AND THE MILITARY

Brucella abortus Brucella canis Brucella melitensis Brucella suis Burkholderia mallei

B

B

1–14 days

5–60 days

Atypical pneumonia, pulmonary abscesses and pleural effusions

Influenza-like illness; 20% present with cough and pleuritic chest pain. Acute pneumonia unusual

Splenomegaly, generalized papular/ pustular eruptions

Elevated liver enzymes  hepatosplenomegaly, anemia, thrombocytopenia

b

Resistance may occur; consult current recommendations prior to use. Tularaemia serologic tests may cross-react with Salmonella, Brucella, Yersinia and Legionella species. c Blood culture difficult/unreliable means of diagnosis. d Do not give to previously infected individuals. Pre-vaccination screening.

a

Glanders

Brucellosis

Tissue gram stain and culturec

Serology and/or blood culture

Doxycycline and rifampin or doxycycline and streptomycin

Amoxicillin and clavulanate, doxycycline, or trimethoprim and sulfamethoxazole

None currently available for humans

Not currently available

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Acute Q fever may present as an atypical pneumonia. Most individuals with Q fever are asymptomatic; only 50% show radiographic evidence of pneumonia and only 25% develop pleuritic chest pain. Elevated liver enzymes with or without evidence of hepatosplenomegaly are seen in up to one-third of cases. Diagnosis is based on serology. Brucellosis in humans is caused by four different species of Brucella. Brucella suis was the first biological agent weaponized by the USA in 1954. Brucella has a long incubation period of 2–4 weeks. Most symptoms are systemic (general malaise and gastrointestinal); only 20% of patients present with cough and pleuritic chest pain, and acute pneumonia is unusual. Glanders is caused by Burkholderia mallei bacteria, which exists primarily in horses. Inhalational exposure may cause pneumonia, pulmonary abscesses and pleural effusions. Progression to septicemia can be fatal in 7–10 days. Human infection with B. mallei is extremely rare and the diagnosis should prompt suspicion of a malicious source of the infection. Staphylococcal enterotoxin B, Clostridium perfringens-toxin and ricin are biotoxins with the potential to be weaponized. Staphylococcal enterotoxin B causes a syndrome of fever, nausea and diarrhea. Clostridium perfringens-toxin, if aerosolized, can result in acute lung injury. Ricin intoxication, although usually manifesting with gastrointestinal hemorrhage after ingestion or muscle necrosis after intramuscular injection, can also cause acute pulmonary disease after inhalation. In summary, while most potential biological warfare agents produce systemic infections, pulmonary manifestations may be significant. Respirator selection is complicated and differs depending on the agent’s physical characteristics, concentration, infectious dose and mode of dispersion. Use of a self-contained breathing apparatus (SCBA) is recommended for responders to a suspected bioaerosol attack, while a high efficiency particulate (HEPA) filter equipped respirator is usually adequate for bioaerosols disseminated by letter or package. Many biological and chemical warfare agents can be absorbed dermally, so full contact precautions and facilities and training for rapid and effective decontamination are necessary.

22.2.3 Other respiratory infections First responders come into direct contact with the general public in uncontrolled environments, which predisposes them to respiratory infections. Police frequently interact with people living in shelters or on the street and incarcerated criminals, and transport persons who are in custody. Firefighters may be exposed during provision of emergency medical services. Military personnel live in close quarters and, while deployed overseas for humanitarian or combat duties, are exposed to populations affected by social disruption, poor hygiene and crowded conditions. Common viral infections are the most prevalent respiratory infections to which police, firefighters and military personnel are exposed placing them increased risk of upper respiratory tract infections (URTIs). Tuberculosis (TB) and emerging respiratory infections, such as severe acute respiratory syndrome (SARS) and avian influenza, are also significant concerns. URTIs, although rarely serious health threats, can significantly impact operational capabilities, accounting for a large proportion of absenteeism and adversely affecting emergency preparedness. Emergency personnel may also spread infections to susceptible

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persons in the communities they serve. An additional concern is that infection may debilitate first responders in general, making them more susceptible to other, more severe, forms of disease. For example, it has been postulated that increased rates of influenza may explain the higher rates of on-duty coronary heart disease deaths in firefighters during the winter months. Preventative immunizations should be aggressively promoted, in particular for influenza and pertussis. Self-reporting of symptoms, frequent hand washing and general hygiene measures must also be encouraged. Tuberculosis remains a common disease with inner city, incarcerated and developing world populations having the highest risk. Increased conversion rates have been demonstrated in military personnel involved in humanitarian and refugee operations, and it is expected that police and firefighters are also at increased risk due to their contact with institutionalized and marginalized populations. Primary prevention in cases of known or suspected contact with infected persons requires National Institute for Occupational Safety and Health (NIOSH) approved HEPA respirators with filters classified as N95 being the minimum acceptable level. A complete respirator protection program requiring periodic fit testing should be in place. Secondary prevention should include screening first responders for TB, timely reporting of cases, initiation of isoniazid or other approved chemoprophylaxis for converters in accordance with existing guidelines and ensuring compliance with therapy. First responders are also called upon to deal with outbreaks of novel infectious disease. The most prominent recent example was the SARS outbreak of 2003. During an outbreak, first responders may transport infected individuals or help to enforce quarantine requirements. Provision and training in the use of respiratory protection is vital. While there is now compelling evidence that SARS is transmitted by contact or droplet transmission, cases were documented of healthcare workers who contracted the disease despite droplet precautions. Thus, properly fit tested N95 respirators in conjunction with universal precautions are recommended in the event of the reemergence of SARS or an avian influenza outbreak.

22.2.4 World trade center disaster and occupational lung disease On 11 September 2001, the collapse of the WTC intensely exposed an unprecedented number of emergency response personnel to a complex mixture of smoke and hazardous dusts. RADS, ‘WTC cough’, new-onset asthma, gastroesophageal reflux disease and sarcoidosis have all been linked to exposures occurring in workers involved in the immediate response and clean-up of the disaster. A detailed exposure assessment for first responders to the WTC disaster is difficult, although studies on the subject report an aggregate consisting of polycyclic aromatic hydrocarbons, polychlorinated biphenyls, organochlorine pesticides, vermiculite, plaster, synthetic foam, asbestos, glass fibers and fragments, calcium sulfate (gypsum) and calcium carbonate (calcite). The exact mechanisms of WTC dust toxicity remain unresolved, but the alkaline and corrosive nature of the dust seems to have caused acute upper respiratory tract irritative symptoms and persistent hyper-reactivity with airway dysfunction. It has also been postulated that inflammation was triggered by high exposure to fine and ultrafine particulate matter.

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‘WTC cough’ refers to complaints of a severe, persistent, nonasthmatic cough and dyspnea in exposed individuals in the months following the WTC disaster. The case definition specifies symptoms that are debilitating enough to require affected individuals to have taken at least 4 weeks of medical leave and onset of symptoms to have occurred within 6 months of exposure. A dose–response relationship has been observed in affected individuals. New-onset asthma has also been observed in first responders to the WTC disaster, with a dose–response relationship suggested by the finding that responders exposed to the initial cloud of dust and debris were more than twice as likely to report newly diagnosed asthma compared with unexposed individuals. Gastroesophageal reflux disease (GERD) has been closely associated with WTC cough with the majority of firefighters with ‘WTC cough’ also reporting new onset GERD. Interesting, a dose–response relationship has also been demonstrated with earlier arrival to the scene being predictive of more severe disease. The etiology and significance of this is not completely understood, although GERD is known to both cause and aggravate respiratory symptoms such as laryngitis, asthma and chronic cough. Sarcoid-like granulomatous pulmonary disease has been recognized in New York City firefighters. This association is discussed further below.

22.3 Police Police are not routinely exposed to respiratory hazards, although significant exposures may occur while responding to vehicular accidents, natural disasters and crime scenes. Crowd control agents also pose respiratory risks, as can chemicals used in forensic investigation.

22.3.1 Epidemiology of respiratory disease in police workers Epidemiologic studies reveal the prevalence of lung disease in police to be lower than that of the general population. Notable exceptions are an increased prevalence of occupational asthma in police working in forensic identification, and the potential for increased risk of respiratory infections resulting from frequent contact with the general public and high-risk populations. Concern has also been expressed over the potential health effects of exposure to vehicular exhaust in police working in traffic-related positions.

22.3.2 Respiratory exposures in police workers Occupational asthma has been reported in police forensics workers. Forensic identification involves a wide variety of chemicals, primarily irritants, and certain known sensitizers. Police involved in forensic identification have been found to have a significantly higher prevalence of respiratory symptoms compared with matched

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Table 22.3 Respiratory diseases associated with police work Disease

Associated exposures

Infection

Community acquired infections Tuberculosis Cyanoacrylate (used in forensics) Elevated rates of tobacco smoking Chemicals used in forensics (e.g. Gentian Violet)

Asthma Lung cancer

controls working in other fields. Cyanoacrylate, a known sensitizer, is used to uncover fingerprints and has been postulated as the most likely cause of occupational asthma in this population. Primary prevention for forensics workers should include respiratory protection and periodic health assessments with spirometry. In cases where sensitization has occurred, removal from the exposure and continued medical surveillance should be conducted to prevent the development of persistent bronchial hyperreactivity. Police officers may be exposed to TB as a result of their frequent dealings with atrisk populations such as current and former prisoners, the homeless and intravenous drug users. Although it is widely recognized as a potential occupational hazard, the literature does not offer much insight regarding the incidence and prevalence of TB in police. Similar to healthcare workers, secondary prevention using annual TB skin testing is recommended for police officers who have frequent contact with at risk populations. Several studies have examined whether police workers who frequently perform traffic-related duties are at increased risk for respiratory disease. The literature does not suggest increased respiratory symptoms in most police workers exposed to vehicular exhaust, except perhaps in exceptional circumstances. The only study of note that demonstrated significant effects involved heavily exposed officers in Bangkok. These officers reported significantly more cough and had lower FEV1 measurements than their occupationally nontraffic-exposed controls.

22.3.3 Respiratory cancer in police workers Slightly elevated rates of lung cancer have been reported in police, although these results have been attributed to greater cigarette smoking in this population. Forensic work involves the use of some known chemical carcinogens, but evidence of increased cancer among police working in forensics doing fingerprint work is lacking. Vehicular exhaust has not been linked to an increased risk of respiratory cancer among police workers (Table 22.3).

22.4

Firefighters

The act of firefighting consists of four stages: break-in/breach of the burning structure; rescue operations; fire suppression; and overhaul and salvage. Overhaul and salvage

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involve firefighters checking the structure to ensure the fire is entirely extinguished and assessment of structural integrity. During fires, firefighters are exposed to a variety of pulmonary toxicants. The highest exposures occur during the initial stages of firefighting, although it is standard practice for firefighters to wear a self-contained breathing apparatus during these initial stages. During overhaul and salvage activities, respiratory protection is often not worn due to the perception that the toxicants have dissipated. In actual fact, the risks of airborne toxicant exposure remain elevated throughout these stages of firefighting.

22.4.1 Epidemiology of respiratory disease in firefighters Historically, firefighters have shown increased rates of airway hyper-reactivity/asthma and, to a lesser extent, decreased ventilatory function (FVC, FEV1). Improved sophistication and compliance with SCBAs has lowered the risk for decreased ventilatory capacity in firefighters to a level similar to the general public, and significant impairment now appears to be limited to those with a long service history. In contrast to persistent ventilatory dysfunction, epidemiological surveys continue to show firefighters to have high rates of occupational asthma. The SENSOR program in California, a surveillance initiative recording prevalence of work-related asthma, found firefighters to have the second highest rate among considered occupations (the highest rates were observed in correctional officers). Airway hyper-responsiveness in firefighters may be acute or chronic. Acutely, firefighters may show airway hyper-responsiveness for up to 24 hours post-exposure to fire smoke. Particularly severe exposures can result in cases of chronic airway hyper-reactivity. Sarcoidosis is more prevalent among firefighters then in the general population. Prior to 11 September 2001, the point prevalence for sarcoidosis in New York City firefighters (FDNY) was 7–13 times greater than their healthcare worker counterparts. The WTC disaster led to a further increase in the incidence of sarcoidosis among FDNY rescue workers. The etiology of these sarcoidosis cases has not been resolved, but is suspected to involve a complex gene–environment interaction. Plausible environmental factors include infections, allergens and aerosolized toxins. Using police officers as controls, firefighters have historically had increased rates of nonmalignant respiratory disease mortality with an estimated relative risk ratio of 1.4–2.0. Improved respiratory protection and a lower incidence of structure fires appear to be lowering these standardized mortality ratios. Wildland firefighters are a distinct group of firefighters, and tend to have an increased risk of pulmonary sequelae compared with their structural firefighting counterparts. This discrepancy is probably the result of decreased use/level of respiratory protection in these workers.

22.4.2 Respiratory exposures in firefighters Firefighters are exposed to toxicants in fire smoke and pulverized structural elements of buildings including metals (lead, antimony, cadmium, uranium), mineral dusts, and other chemical substances (Table 22.4).

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Table 22.4 Respiratory diseases associated with firefighters Disease

Associated exposures

Airway hyper-reactivity/ asthma Chronic obstructive and/or restrictive impairment Sarcoidosis

Irritants in fire smoke: ammonia, halogenated acids, hydrogen chloride, sulfur dioxide, acrolein, oxides of nitrogen and phosgene Irritants in fire smoke: ammonia, halogenated acids, hydrogen chloride, sulfur dioxide, acrolein, oxides of nitrogen and phosgene Unknown: hypothesized to result from complex interaction of genetic predisposition and exposures (including mineral/metal dusts) WTC dust mixtures

Fire smoke Approximately 1–5% of North American firefighters’ professional time is spent fighting fires. The majority of US firefighters’ work involves the provision of emergency medical services or is nonemergency-related. Despite this, fire smoke remains one of the most significant occupational hazards facing firefighters. Fire smoke is a complex mixture of particulate matter and toxic gases whose exact composition depends on the materials being burned, the rate and temperature of burning, and ambient oxygen levels. Smoke inhalation causes bronchopulmonary injury via four primary mechanisms: (1) hypoxic gas inhalation/oxygen deficiency; (2) thermal injury; (3) inhalation of systemic toxins/asphyxiants; and (4) inhalation of bronchopulmonary irritants. Hypoxic gas inhalation, while acutely debilitating, does not usually directly damage the airways or pulmonary parenchyma. Thermal injury can acutely cause tracheobronchitis/ bronchiolitis and, in severe cases, asphyxiation due to laryngeal edema. Injury is usually confined to the supraglottic airways because heat exchange is rapid in the naso- and oropharynx. The exception to this is exposure to hot gases or steam which, having a greater thermal capacity than dry air, penetrate to the intrathoracic airways at temperatures high enough to cause injury. In most cases, inhalational thermal injuries occur in the hours to days following exposure with good recovery thereafter. Stricture formation in the larynx and/or trachea may occur in severe cases. Carbon monoxide, cyanide gas and methemoglobin-forming materials may also be components of fire smoke. These agents cause tissue hypoxia with little or no direct respiratory irritation. Sequelae from chemical asphyxiant poisoning are primarily neurological and cardiac. Carbon monoxide, produced from incomplete combustion of carbonaceous materials, binds hemoglobin and cardiac myoglobin, and disrupts cytochrome oxidase. Cyanide, produced from the combustion of plastics, polyurethane, wool, silk, nylon, nitrites and rubber, binds cytochrome oxidase, blocking aerobic metabolism. Methemoglobin-forming materials enter the blood stream and oxidize ferrohemoglobin to methemoglobin. The list of potential methemoglobinforming compounds is extensive; nitrites are the most frequently encountered. The most common irritants in smoke are ammonia, halogenated acids, hydrogen chloride and sulfur dioxide (high water solubility); acrolein (moderate water solubility); and oxides of nitrogen and phosgene (low water solubility). The mechanism of injury for each irritant may differ (Table 22.1), although with sufficient exposure all can lead to inflammation and necrosis of the lung parenchyma. Acute complications

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include bronchopneumonia, atelectasis, pleural effusion, pulmonary embolism and pneumothorax. Chronically, airway hyper-reactivity/RADS may occur. In summary, most episodes of smoke inhalation do not result in lung injury, although subclinical transient declines in pulmonary function may occur. Severe exposures can result in respiratory compromise due to the combined effects of thermal injury and bronchopulmonary irritants. In patients surviving the initial complications of inhalational injury, there is usually no chronic respiratory impairment, although cases of increased airway hyper-reactivity/RADS have been documented. Chronic exposure to smoke may predispose to the development of airway hyper-reactivity. Prospective studies involving younger cohorts of firefighters have not demonstrated any decline in ventilatory function due to chronic smoke inhalation. Decreased pulmonary function tends to be marginal, with smoking history playing the predominant role in most cases. Metals Exposure to aerosolized metals may result from the burning of painted surfaces, such as materials coated with leaded paint, and firefighters have been shown to have blood lead levels slightly above that of the general population, although frank heavy metal toxicity is rarely an issue. Mineral dusts Firefighters may be exposed to minerals including asbestos and silica from the pulverization of structural materials after a building collapses, and fire smoke may act as a vehicle for these exposures. The malignant and nonmalignant pulmonary diseases associated with exposure to mineral fibers, including asbestos and silica, are well described. While a theoretical risk of asbestos and silica related disease exists, the literature does not document increased rates of such diseases in firefighters. Nonetheless, firefighters are potentially exposed to these minerals and respiratory protection, even during overhaul, is strongly recommended.

22.4.3 Respiratory cancer in firefighters Asbestos exposure represents a potential carcinogenic risk for firefighters, as do some heavy metals (cadmium, hexavalent chromium) and chemicals (polyaromatic hydrocarbons, benzene, diesel exhaust). Meta-analyses suggest statistically increased risks of some site specific cancers among firefighters including bladder, central nervous system, colorectal, non-Hodgkin lymphoma, prostate and testicular cancer. Notably, studies to date have not shown an increased risk of respiratory cancers among firefighters.

22.5 Military Military personnel work in both combat and noncombat situations. Noncombat situations include humanitarian missions and emergency disaster assistance. Military duties vary depending on post and may involve rigorous training, maintenance work

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and repair, administrative duties and weapons/equipment testing. Terrorism, chemical warfare and emergency disaster assistance may expose military personnel to the hazards discussed in the section on first responders. This section will focus on respiratory hazards unique to military personnel, including zinc chloride (smoke bomb) inhalational injury, blast injury to the lung (BLI), asthma/vocal cord dysfunction (VCD) and respiratory infections to which military personnel are at risk.

22.5.1 Epidemiology of respiratory disease in military personnel Military personnel have increased rates of respiratory infections. The observed increase is largely representative of overseas deployments in general, although further increases are observed during combat operations. Higher rates of other select pulmonary diseases have also been reported in military personnel, including asthma, VCD, acute eosinophilic pneumonia and lung cancer. Military personal may also be presumed to be at increased risk of inhalational injury from exposure to smoke bombs (zinc chloride) and BLI.

22.5.2 Respiratory exposures in military personnel Smoke bombs are used by the military as an obscurant during training and in combat conditions. The primary pulmonary toxin in smoke bombs is a corrosive zinc chloride aerosol. Documented complications from exposure include upper airway obstruction, bronchospasm, consolidation and acute lung injury. Pathological examination reveals pulmonary edema, pneumonitis, diffuse alveolar damage with alveolar obliteration and, in severe cases, pulmonary fibrosis. Treatment is supportive using ventilatory support and judicious use of steroids. Smoke bomb inhalation may also induce methemoglobinemia, resulting in a functional anemia. Prognosis is generally good, with initial spirometric dysfunction tending to resolve gradually over time in most cases. Blast injuries affect gas-containing organs and include BLI, ruptured tympanic membranes and intestinal blast injury. In BLI, the blast wave acutely elevates intrathoracic pressure, tearing the alveolar septae, resulting in alveolar hemorrhage, pulmonary edema and the formation of alveolovenous fistulae. Air embolism is a wellrecognized complication and one of the primary causes of immediate death in BLI. Clinically, the triad of respiratory distress, hypoxia and progressive ‘butterfly’ or ‘batwing’ pulmonary infiltrates is characteristic of BLI. Treatment is supportive. Mechanical ventilation should be used with caution due to the risk of pneumothroax and air emboli via alveolovenous fistulae. High-frequency ventilation and nitric oxide may reduce ventilation pressures and improve oxygenation. Survivors of the initial pulmonary sequelae tend to have a good prognosis. During recovery, a restrictive pattern may be seen on pulmonary function testing, which usually returns to baseline over time. Asthma is a significant disease for military personnel because of its impact on the ability of affected individuals to perform duties. For this reason, in many countries the diagnosis is grounds for exclusion from service. There is some evidence of increased

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rates of asthma among military personnel, which may reflect occupational exposures or, more likely, case finding of previously undiagnosed exercise-induced asthma during detailed medical pre-placement and surveillance exams. VCD should be included in the differential diagnosis of asthma, as military personnel may be at increased risk for VCD due to stressors associated with training and combat. VCD should be considered in cases of suspected asthma that present atypically or fail to respond to standard therapy. Further evidence for VCD is provided by spirometry, which may show attenuation of the inspiratory flow volume loop. The gold standard for diagnosis is laryngoscopic demonstration of paradoxical vocal cord movements during an acute attack. Treatment options include patient education, speech therapy and psychological counselling/cognitive behavioral therapy. Military personnel are at risk of both domestically acquired respiratory infections, as well as infections somewhat unique to military deployments and working conditions. Military camps are prone to epidemics of influenza, Mycoplasma species, pneumococcus, meningococci and adenovirus. Group A streptococci (GAS) pneumonia, uncommon in the general population, has also been found to have a higher incidence among military personnel, and personnel serving overseas have higher than expected rates of Q fever. Crowded living conditions and exposure to populations with increased prevalence of infection are likely to be the most important predisposing factors. New research suggests depressed immune function associated with overexertion during training exercises may also be a contributing factor. A higher than expected incidence of acute eosinophilic pneumonia (AEP) among military personnel deployed to Iraq and surrounding areas has also been observed. Acute eosinophilic pneumonia is a rare disorder, distinguished from chronic eosinophilic pneumonia by a lack of previous asthma, no protracted history of symptoms prior to presentation and rapid progression to respiratory failure. AEP is characterized by diffuse infiltrates on chest radiograph and pulmonary eosinophilia. The causative agent in cases of AEP in military personnel in Iraq has not been identified. Postulated causes include parasitic infections, certain medications and new-onset smoking. Tobacco use in the military deserves special mention, because smoking rates in military personnel significantly exceed those of the general population. Proposed explanations for the high prevalence of smoking in military personnel (reported as being over 50% in active personnel) include stress, boredom, lower education level, lower economic status, group living conditions, the encouragement of conformity in an environment with high rates of smoking and the availability of cigarettes at discounted cost. The literature does not suggest military personnel to have an overall increased rate of nonmalignant smoking-related disease, but increased rates of smoking-related cancers have been observed.

22.5.3 Respiratory cancer in military personnel Rates of malignant respiratory tumors in VA hospitals are double that of the general population, with the majority of these cancers being linked to smoking. It is hypothetically possible that some of these cancers might be related to other exposures including

22.6

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309

Table 22.5 Respiratory diseases associated with military personnel Disease

Associated exposures

Infections

Influenza Group A strep Tuberculosis Pneumococcus Meningococci Adenovirus Q fever Elevated rates new onset tobacco smoking Query dust exposure Zinc chloride (smoke bomb) inhalation Blast lung injury (tends to resolve)

Acute eosinophilic pneumonia Acute lung insults with potential chronic obstructive and/or restrictive impairment Lung cancer Mesothelioma

Elevated rates of tobacco smoking Asbestos exposure from ship-building, insulation and use of fire retardant materials

nuclear weapons testing, chemical weapons, propellants used for missiles or substances aerosolized from combustion sources such as oil-well fires, vehicular exhaust and tent heaters. Studies on the subject have considered military personnel in general, as well as specific cohorts such as those involved in nuclear weapons tests and nurses who served in Vietnam, but have not drawn any conclusive links to occupational exposure when smoking is controlled for in the analyses. The exception is mesothelioma. Increased rates of mesothelioma have been demonstrated in war veterans and navy personnel due to asbestos exposure from ship-building and insulation and the use of fire-retardant materials. Increased incidences of mesothelioma have also been documented in military personnel secondary to the assembly and/or use of gas masks in the 1940s, which contained 20% crocidolite in their filters (Table 22.5).

22.6

Compensation

Most US States and Canadian Provinces have presumptive disability provisions that apply to fire fighters and police officers. These laws tend to cover the development of heart and lung disease. Depending on the country, province or state in question, presumption laws may include lung diseases such as COPD, infectious diseases such as tuberculosis and respiratory cancers. In the case of firefighters, lung cancer is rarely included, although amendments in some locales have recently made this addition. Volunteer police and firefighters may also be covered by such legislation depending on the locality in which they work. The International Association of Fire Fighters maintains a database of the current presumptive disability provisions for fire fighters in the USA and Canada (Table 22.6). Compensation for military personnel usually functions within a separate system outside that of civilian workers’ compensation. In the USA, for example, military and Veterans Administration (VA) programs administer such services. In general,

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Websites/organizations and suggested reading Websites and organizations

Websites/organizations

.

The International Association of Firefighters: http://www.iaff.org/

. National Institute of Safety and Health; Fire Fighter Fatality Investigation

and Prevention Program: http://www.cdc.gov/niosh/fire/ World Health Organization (2001) Health Aspects of Chemical and Biological Weapons: Report of a WHO Group of Consultants. Projected 2nd edn. World Health Organization: Geneva; available at: http://www. who.int/emc/pdfs/BIOWEAPONS_FULL_TEXT2.pdf . US Department of Health and Human Services; World Trade Center Health Resources: http://www.hhs.gov/wtc/reports/ responderworkers.html .

Further reading

. Trottier, A., Brown, J. (1995) Occupational medicine for policing. J. Clin.

Forens. Med. 2(2): 105–110. Scannell, C.H., Balmes, J.R. (1995) Pulmonary effects of firefighting. Occup. Med. 10(4): 789–801. . Zajtchuk, R., Bellamy, R.F. (eds) (1997) Textbook of Military Medicine. Office of the Surgeon General, Walter Reed Army Medical Center: Washington, DC; available at: https://ccc.apgea.army.mil/sarea/ products/textbook/Web_Version/ .

compensation provided via the military/VA payment schemes tends to be as good or better with respect to payments and provision of services when compared with civilian workers’ compensation programs.

Further reading First responders Banauch, G.I., Dhala, A., Prezant, D.J. (2005) Pulmonary disease in rescue workers at the World Trade Center site. Curr. Opin. Pulmon. Med. 11 (2): 160. Greenfield, R.A., Brown, B.R., Hutchins, J.B., Iandolo, J.J., Jackson, R., Slater, L.N., Bronze, M.S. (2002) Microbiological, biological, and chemical weapons of warfare and terrorism. Am. J. Med. Sci. 323 (6): 326. Kales, S.N., Christiani, D.C. (2004) Acute chemical emergencies. New Engl. J. Med. 350 (8): 800. Urbanetti, J. (1997) Toxic inhalation injury. In Medical Aspects of Chemical and Biological Warfare, Zajtchuk, R., Bellamy, R.F. (eds). Office of the Surgeon General, US Department of the Army: Washington, DC; 1997; 247–270.

Police Burgess, J.L., Kovalchick, D.F., Siegel, E.M., Hysong, T.A., McCurdy, S.A. (2002) Medical surveillance of clandestine drug laboratory investigators. J. Occup. Environ. Med. 44(2): 184. Trottier, A., Brown, J. (1995) Occupational medicine for policing. J. Clin. Forens. Med. 2(2): 105–110. Trottier, A., Brown, J., Wells, G. (1994) Respiratory symptoms among forensic identification workers. J. Clin. Forens. Med. 1(3): 129–132.

FURTHER READING

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Firefighters Alarie, Y. (2002) Toxicity of fire smoke. Crit. Rev. Toxicol. 32(4): 259. Prezant, D.J., Dhala, A., Goldstein, A., Janus, D., Ortiz, F., Aldrich, T.K., Kelly, K.J. (1999) The incidence, prevalence, and severity of sarcoidosis in New York City firefighters. Chest 116(5): 1183–1193. Scannell, C.H., Balmes, J.R. (1995) Pulmonary effects of firefighting. Occup. Med. 10(4): 789–801.

Military Allen, M.B., Crisp, A., Snook, N., Page, R.L. (1992) ‘Smoke-bomb’ pneumonitis. Respir. Med. 86(2): 165–166. Avidan, V., Hersch, M., Armon, Y., Spira, R., Aharoni, D., Reissman, P., Schecter, W.P. (2005) Blast lung injury: clinical manifestations, treatment, and outcome. Am. J. Surg. 190(6): 927–931. Gray, G.C., Callahan, J.D., Hawksworth, A.W., Fisher, C.A., Gaydos, J.C. (1999) Respiratory diseases among U.S. military personnel: countering emerging threats. Emerging Infect. Dis. 5(3): 379.

23 Office workers and teachers* Jean M. Cox-Ganser, Ju-Hyeong Park and Kathleen Kreiss National Institute for Occupational Safety and Health, Morgantown, West Virginia, USA

23.1 Introduction 23.1.1 History In contrast to blue collar industrial workers, white collar workers (including office workers and teachers) are often thought to work in nonhazardous environments. In fact, a long history exists of concerns for office and school worker health in relation to large buildings that require mechanical ventilation and air conditioning. In the early decades of the twentieth century, ventilation standards were developed to provide for control of body odor in indoor environments where large numbers of people congregated. As early as the 1920s, ventilation parameters were established to control transmission of infectious diseases. Public interest in indoor environmental quality arose in the late 1970s after changes in building environments and their ventilation occurred in the wake of the energy crisis in the USA. Office workers in diverse parts of the USA had symptoms of headache, mucous membrane irritation and difficulty concentrating in tight temporal association with occupancy of their work buildings. The public health response to investigation was stymied when industrial hygienists failed to measure any contaminant at levels exceeding industrial health standards. Some public health professionals attributed widespread complaints in particular buildings to mass psychogenic illness, although the type of symptoms and endemic nature of complaints did not meet criteria for hysteria. European investigators took an epidemiologic approach and established building-related risk factors for the common symptoms of mucous membrane irritation and discomfort. These included air conditioning, extent


The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the National Institute for Occupational Safety and Health.

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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of carpet and fleecy materials such as textile-covered partitions and chairs, open shelving with paper in the indoor environment, housekeeping and eventually outdoor air ventilation rate and ventilation maintenance practices, among others. Indoor air quality consultants incorporated these observations into their recommendations for ventilation rates and maintenance, and the complaints of nonspecific sick building syndrome symptoms alone decreased in the 1990s. In their place, however, the proportion of building-related chest symptoms have increased relentlessly, at least as reflected in the number of worker requests for health hazard evaluations (http:// www.cdc.gov/niosh/hhe/HHEprogram.html) for indoor air quality concerns submitted to the US National Institute for Occupational Safety and Health (NIOSH). These chest symptoms often arise in buildings with a history of dampness. As this chapter will explore, abundant evidence now exists that indicates environments in offices and schools can lead to asthma, hypersensitivity pneumonitis, rhinosinusitis and perhaps even sarcoidosis. In addition, the traditional tools of industrial exposure assessment of chemicals, particulates, bioaerosols and ventilation have roles in understanding the emerging hazards of offices and schools.

23.1.2 Epidemiologic context In the USA almost 70% of the workforce is employed in nonindustrial, indoor settings. Office and administrative support occupations accounted for an estimated 20 million workers in the US census in 2000, and management, business and financial operations occupations accounted for an additional 16.6 million. In 2006, the US census bureau estimated that there were 6.8 million school teachers. Schools also employ nonteaching staff with work environments similar to those of teachers. In keeping with the historical view that office workers have few occupational risks, this group is commonly used as the comparison group in analyses looking for occupational risk of respiratory conditions. Population-based information on health risks to office workers is meager. A study of middle-aged professional women in France documented that, in comparison to work in naturally ventilated buildings, work in buildings with heating, ventilation and air-conditioning (HVAC) systems was associated with an increased risk for annual visits to otorhinolaryngologists, as well as sickness absences. These observations hint that occupational respiratory disease occurs in the indoor environment and may present in pulmonary and occupational medicine practices. Using office workers as a comparison group, an analysis of 20,991 US adults, 18 years of age and older who participated in the 2001 National Health Interview survey, found that workers in elementary and secondary schools and colleges had an increased risk for asthma. It is of interest that from 1990 to 1999, US secondary school teachers had excess proportionate mortality from asthma as compared with the expected based on all occupations. In state-based reporting of physician-diagnosed work-related asthma (WRA) from 1993 to 1995, 1101 cases were identified in California, Massachusetts, Michigan and New Jersey. Indoor air pollutants (including those arising from poor ventilation, pesticides, dusts and dirt, molds, environmental tobacco smoke, paint odors and other nonspecific building odors) were reported as a cause of both new-onset and work-aggravated asthma in all four states and represented the most frequent

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putative cause. Nonindustrial workers reportedly affected by indoor air pollutants included teachers, office workers, nurses, secretaries, librarians, computer operators and programmers, technicians and clerks. A subsequent analysis of 2995 WRA cases reported between 1993 and 2000 from the same four states found that 265 (9%) WRA cases were employed in educational services, of which 69% (182/265) were new-onset asthma. Indoor air pollutants, mold, dusts and cleaning products were the most frequently reported agents. There is some evidence that respiratory conditions other than asthma are found in excess in teachers. Teachers had excess work-related eye, nose and throat symptoms, wheezing and five or more episodes of cold or flu in the past year over other working women. Some of these health effects may have been related to exposure to children with infectious conditions. A large case–control study of sarcoidosis in the USA started in the mid 1990s (the ACCESS study) found that elementary and secondary school teachers were at an elevated risk for sarcoidosis.

23.1.3 Scope and limitations In this chapter, we concentrate on indoor environmental quality and conditions that are commonly associated with office worker and teacher concerns with respect to respiratory disorders (Table 23.1). Chief among these are dampness-related exposures and conditions. In our experience with worker requests for assistance with indoor quality

Table 23.1 Indoor environmental conditions pertinent to respiratory diseases Environmental condition or contaminant

Asthma

Respiratory symptoms

Hypersensitivity pneumonitis

Infection

Dampness Renovation-related exposures Inadequate ventilation Contaminated ventilation system Legionella-contaminated cooling towers, water supply, or water features Disruption of contaminated bird/bat roosts Art/science/shop supplies in schools Pesticides Chemical emissions from building materials or furnishings Entrainment of vehicle exhaust Carbonless copy paper Paper dust Allergens (dust mite, cat, cockroach), antigens Cleaning Agents

   

   

 

a a 

a

b c

  

  

   

   





Opportunistic infections particularly in immuno-compromised individuals. Legionnaire’s disease, Pontiac fever. c Histoplasmosis. b





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CH 23 OFFICE WORKERS AND TEACHERS

issues, renovation-associated symptoms are commonly reported by office workers and teachers. Finally work activities in office buildings and schools generate a host of exposures which may be implicated in occupational respiratory disease. In this chapter we do not cover environmental tobacco smoke, cosmetic fragrances, asbestos, man-made fibers and indoor exposures to radon gas.

23.2 Exposures in office buildings and schools 23.2.1 Overview There are a variety of environmental conditions leading to microbial, chemical and particulate contamination associated with work-related respiratory conditions in office workers and teachers (Table 23.1). In describing the contaminants, their sources and exposure pathways, we concentrate on issues related to building dampness, ventilation systems and renovation activities. Damp building conditions can result from both external and internal sources of water (Figure 23.1). External leaks can occur through roofs, windows, exterior walls and foundations. Internal leaks occur when building water-pipe or plumbing systems fail. Condensation and high humidity are also sources of building dampness. Many design and maintenance issues in office buildings and schools can lead to dampness problems, e.g. flat roofs, curtain walls, either no moisture barriers for walls or foundations or incorrect placement and installation of the moisture barriers, poor installation of insulation, flashing and caulking of windows and roofs, incorrect grading around the building foundation, lack of maintenance of mechanical ventilation systems, and inattention to repair of the building. Damp building conditions can result in both biological and chemical exposures to occupants.

INTERNAL LEAKS Plumbing heating/cooling pipes Fire sprinkler system LEAKS THROUGH BUILDING ENVELOPE

CONDENSATION PROBLEMS

HVAC DRAINAGE PAN MALFUNCTION

HIGH HUMIDITY INSIDE BUILDING

DAMPNESS

Damp conditions promote

BIOLOGICAL CONTAMINANTS Mold, bacteria, dust mite and cockroach allergens

Figure 23.1

RELEASE OF CHEMICALS FROM WET BUILDING MATERIALS AND FURNISHINGS e.g. formaldehyde, phthalates

Conditions leading to damp buildings and resulting contaminants

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Table 23.2 Types of contaminants circulated by ventilation systems throughout a building &

Entrainment of contaminants from outside the building * Vehicle exhausts * Building exhausts (toilets, boiler room, kitchen, laboratories) * Cooling tower mists contaminated with Legionnella bacteria * Soil contaminated with Histoplasma mold (from roosting birds/bats) & Contaminants with an internal building source * Colds/flu viruses from occupants * Microbial agents from contaminated building materials or furnishing * Particulates from paper, printers, copiers, carbonless copy papers * Chemicals emitted from building materials, furnishings and equipment * Chemicals emitted from art and laboratory sources * Ventilation system contamination as a source of exposure (microbial contamination of wet drain pans, filters, internal duct liners, condensate drain tubes) * Housekeeping chemicals and deodorizers

Heating, ventilation and air-conditioning systems are meant to supply adequate outside air to building occupants as well as conditioning the air (such as heating, cooling, humidity control and particulate filtration). For office buildings and schools, outside air ventilation rates are usually adequate to dilute body odors but are not in general set to dilute other possible air contaminants. There are a range of recommended minimum ventilation rates per person depending on the type of facility and room function. Contaminants from outside the building may be entrained into the HVAC via air intakes and can lead to poor indoor air quality (Table 23.2). Diesel school buses may park and idle their engines close to school buildings, leading to diesel exhaust exposures inside the schools. Commonly, outside air intakes on roofs are too close to building exhaust vents such as those from the bathrooms, boiler room, kitchens or laboratories. The HVAC system itself may become contaminated and circulate these contaminants throughout the building. In such situations, increasing ventilation rates can increase occupants’ exposures. When the building (other than the HVAC system) has internal sources of microbial, chemical or particulate contamination, the HVAC may increase occupant exposures by circulating these contaminants throughout the building. The spreading of influenza viruses within office buildings and schools is of special importance with the possibility of pandemics. In our studies of indoor environmental quality we have found that renovation activities in general or remediation activities related to dampness and mold are frequently carried out without relocation of the building occupants and without adequate containment, thus leading to occupant exposures (Table 23.3). Some of the exposures are construction dusts, volatile organic compounds (VOCs) from solvents, paints and glues, and microbial agents from contaminated materials. In both office buildings and schools, day-to-day work activities such as handling of paper, the use of carbonless copy paper, printing and copying can generate particulate and VOC exposures (Table 23.4). Housekeeping practices can resuspend carpet dust which may have accumulated microbial particulates and detergent dust. Pest management practices can lead to pesticide exposures, and chemicals used in art, craft and laboratory classes can cause exposures.

318 Table 23.3

CH 23 OFFICE WORKERS AND TEACHERS

Exposures related to renovation and remediation activities

Activity

Types of exposures Biological

Deconstruction Removal of existing walls, ceilings, carpeting, flooring, insulation

Construction Soil disturbance Dry wall construction

Mold/bacteria from contaminated materials

Particulate Construction dusts Carpet dusts Dusts from area above ceiling Asbestos Man-made fibers Lead from old paint

Chemical Chemicals adsorbed onto construction dusts

Mold/bacteria Alkaline construction dusts Construction dusts Man-made fibers

Ceiling replacement

VOCsa from paint, solvents VOCs from glues, carpets

Painting Carpet installation a

Volatile organic compounds.

23.2.2 Dampness and associated exposures The little information available on the proportion of office or school buildings in the USA that have dampness problems, or the severity of such conditions, indicates that the problem is widespread. From a large study of US office buildings not known to have indoor air quality complaints in the 1990s, it was found that 85% of 100 buildings had incurred some past water damage, while 43% of the buildings had current water

Table 23.4

Exposures related to work activities in office buildings and schools

Activity

Types of exposure Biological

Handling paper products Printing Copying Carbonless copy paper use Carpet and surface cleaning Pest management Art/craft/laboratory class Pets in classrooms a

Volatile organic compounds.

Particulate

Chemical

Paper dusts

Microbial agents, allergens

Toner particulates Dusts Carpet dust

VOCsa VOCs VOCs Cleaning agents Pesticides Chemical supplies

Microbial agents, allergens

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damage. In 1995, the Government Accounting Office reported that about 30% of schools in the USA needed repairs to plumbing, roofs or external walls, windows and doors. Individual buildings can become damp indoor environments through being poorly designed, poorly built, poorly maintained or poorly run. Since the late 1990s, three influential literature reviews (two from Europe and one from the USA) have concluded that living, working or going to school in damp indoor environments poses a respiratory health threat. Despite the absence of a standardized way to describe levels of dampness in buildings, studies have shown an increasing risk for respiratory symptoms in occupants with increases in the number of signs of dampness, water incursions and water damaged materials, both as reported by occupants or as scored by researchers. A NIOSH study of college employees demonstrated that exposure to dampness, as estimated by weighting the dampness score of individual rooms by employees’ time spent in the specific rooms, was a good predictor of employees’ respiratory illnesses. The dampness scores were calculated based on the extent of water stains, visible mold, mold odor and moisture observed by industrial hygienists in seven room components (walls, ceiling, floor, windows, ventilation system, furniture and pipes). A Finnish research group has also developed a moisture damage index based on a study of homes. The index was based on the location of damage, type of damage, duration, type of damaged material and size of damaged area, as measured by civil engineers. They also demonstrated that this index was correlated with health symptoms. Dampness itself cannot be a cause of respiratory disease, and there is still uncertainty about the causal agents of respiratory problems related to dampness. However, there is growing epidemiological evidence of associations between respiratory health effects and microbial contaminants derived from mold and bacteria, allergens from dust mites and cockroaches, and chemical agents released from wetted building materials and furnishings. Molds Growth of molds in a building is directly related to dampness. If mold odors occur, whether or not there is visible mold, it is not necessary to do air sampling for mold spores. Rather, appropriate remediation to mitigate sources of water or moisture should be carried out. Remediation guidelines for moldy environments can be found in the following web page of US Department of Labor: http://www.osha.gov/dts/shib/ shib101003.html. Traditional air sampling for molds is highly variable. The results from such methods may not accurately indicate either a patient’s exposure or risk of illness. Air sampling methods using culture media or sticky slides collect small amounts of air due to potential overloading of mold spores on the media or slides. Thus, they are not likely to capture the inherently large temporal and spatial variability of airborne mold concentrations unless many samples are collected at different times at the same location and also at multiple locations simultaneously. The culture method only supports growth of viable spores which may represent as little as 1% of the total mold. Despite these limitations, many environmental consultants still rely on air sampling methods as described above in investigating damp/moldy environments. Many research groups use measurements of mold in floor, chair or other surface dust, which may better represent historical exposure to mold. Although the dust

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measurement does not directly represent inhalation exposure, research findings have demonstrated that dust measurements are useful in epidemiologic associations of health effects and mold in damp indoor environments. Several research groups have also used measurements of ergosterol (a principal sterol in the fungal membrane) in environmental samples for exposure assessment of mold. Although ergosterol does not provide information on mold species, it may be a useful method to assess exposure to total fungal biomass since it measures both viable and nonviable spores and fungal fragments. Additionally, measurements of (1 ! 3)-b-D-glucan (a major carbohydrate constituent of fungal cell walls), extracellular polysaccharide (a carbohydrate in fungal cell walls) of Penicillium and Aspergillus species and microbial volatile organic compounds (MVOCs), and PCR (polymerase chain reaction) analysis of fungal DNA or RNA have been explored for mold exposure assessment. Table 23.5 shows evidence of associations between physician-diagnosed asthma or respiratory symptoms and molds from recent studies. Currently, there are no standards for what level or what species of molds constitute a health risk. Thus, there are no known safe levels of exposure. For example, all molds have the potential to be allergenic, but there is a lack of knowledge on the antigens or allergens found in the vast majority of molds. Existing recommendations for what constitutes low or high levels of microbial contamination are not consistent and are not based on exposure–health response relationships. Approaches recommended by the American Industrial Hygiene Association are to use the ratio of counts of indoor to outdoor fungi as a measure of possible indoor fungal contamination (ratios greater than one indicate possible problems); the use of rank order of fungal species indoors compared with outdoors to suggest indoor sources of microbial amplification. There is also a new approach to identify buildings with mold contamination, developed at the US Environmental Protection Agency, which uses PCR analysis of fungal species in dust to calculate a relative moldiness index value based on typical fungal species found in water-damaged and nonwater-damaged buildings. A recent NIOSH study of a water-damaged office building indicated that water-loving (hydrophilic) fungi in dust were associated with respiratory health effects in office workers. A list of fungal species that have been associated with damp building conditions is given in Table 23.6. Bacteria Some bacteria have been associated with damp indoor environments. These include Gram-negative bacteria, actinomycetes and nontuberculous mycobacteria. A 2006 Finnish study of visibly damaged building materials from 34 water-damaged buildings found actinomycetes in 24% of 75 samples at concentrations ranging from less than 45 to 8.0  106 colony forming units per gram (CFU/g) of dust and mycobacteria in 23% of 88 samples at concentrations ranging from 60 to 2.0  107 CFU/g. A variety of species of mycobacteria were found in the water-damaged materials and the proportion of samples positive for mycobacteria increased with increasing concentrations of fungi. Endotoxin is the biologically active lipopolysaccharide found in cell walls of Gramnegative bacteria, and has been associated with asthma and respiratory symptoms. Endotoxin is ubiquitous because Gram-negative bacteria are present everywhere. To determine exposure to environmental endotoxin, biological activity of lipopolysaccharide, expressed in endotoxin units (EU), is measured using an extract of the blood of

Doctor-diagnosed post-occupancy asthmae Doctor-diagnosed asthma or asthma symptomse Work-related:f Wheeze Chest-tightness Shortness of breath Cough Doctor-diagnosed asthmag Nocturnal breathlessnessg Daytime breathlessnessg Wheezeg Upper respiratory symptoms (sore/dry throat, sinus congestion, cough, sneezing)

Office workers Case–control studya

2.0 (fd) 1.9 (fd) 2.4 (fd) 1.7 (fd) 0.94 (a) 0.84 (a) 0.94 (a) 0.93 (a) 1.4 (cd)

1.6 (fd) 1.7 (cd) 1.7 (fd) 1.6 (cd)

Total fungi (Hyd/fd) (Hyd/cd) (Hyd/fd) (Hyd/cd)

— — — — — — — — 1.4 (Asp,Zyg/cd) 1.1 (Bot,Pen,Ulo/cd) 1.1 (Bot,Dre/fd)

2.2 1.9 1.8 1.6

Specific fungi

— — — — — — — — —

1.4 (Erg/fd) 1.6 (Erg/cd) 1.6 (Erg/fd) 1.5 (Erg/cd)

Fungal biomass

Odds ratios

2.5 (fd) 2.2 (fd) 1.9 (fd) 1.3 (fd) — — — — —

1.4 (fd) 1.2 (cd) 1.5 (fd) 1.1 (cd)

Endotoxin

— — — — 0.97 (a) 0.92 (a) 0.97 (a) 0.99 (a) —

— — —

Total bacteria

— — — — 2.1 (a) 5.2 (a) 1.8 (a) 1.4 (a) —

— — —

MVOC

Odds ratios in bold are significant at p  0.05. Underlined odds ratios are marginally significant at 0.05 < p  0.10. Abbreviations for microbial agents: a ¼ airborne, fd ¼ floor dust, cd ¼ chair dust, erg ¼ ergosterol, MVOC ¼ microbial volatile organic compound. Abbreviations for specific fungi: hyd ¼ hydrophilic fungi, Asp ¼ Aspergillus spp., Zyg ¼ Zygomycetes, Bot ¼ Botrytis spp., Pen ¼ Penicillium spp., Ulo ¼ Ulocladium spp., Dre ¼ Drechslera spp. a Park, J.H., Cox-Ganser, J.M., Kreiss, K., White, S.K., Rao C.Y. (2008) Hydrophilic fungi and ergosterol associated with respiratory illness in a water-damaged building. Environ. Health Perspect. 116(1): 45–50. b Park, J.H., Cox-Ganser, J., Rao, C., Kreiss, K. (2006) Fungal and endotoxin measurements in dust associated with respiratory symptoms in a water-damaged office building. Indoor Air 16(3): 192–203. c Kim, J.L., Elfman, L., Mi, Y., Wieslander, G., Smedje, G., Norb€ack, D. (2007) Indoor molds, bacteria, microbial volatile organic compounds and plasticizers in schools – associations with asthma and respiratory symptoms in pupils. Indoor Air 17(2): 153–163. d Chao, H.J., Schwartz, J., Milton, D.K., Burge, H.A. (2003) The work environment and workers’ health in four large office buildings. Environ. Health Perspect. 111(9): 1242–1248. e ORs are for IQR (interquartile range) increase (CFU/g dust) in exposure; f ORs are for highest tertile compared with lowest tertile exposure group; g ORs are for each 102/m3 increase of bacteria or mold, and 1 mg/m3 increase of total MVOC.

Elementary school students Cross-sectional studyc Office workers Longitudinal studyd

Office workers Case–control studyb

Respiratory effects

Study

Table 23.5 Recent epidemiological studies investigating an association between microbial agents and asthma and respiratory symptoms in offices or schools

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CH 23 OFFICE WORKERS AND TEACHERS

Table 23.6 Identification of the species of fungi from samples may indicate the dampness conditions of buildings (AIHA, Field Guide for the Determination of Biological Contaminants in Environmental Samples, 2005) Chronic wet conditions

Alternating wet and dry conditions

Acremonium strictum Alternaria alternata Aspergillus niger Botrytis cinerea Chaetomium globosum Doratomyces spp. Gliocladium roseum Graphium spp. Mucor racemosus Phoma spp. Rhizopus spp. Sistotrema brinkmanii Stachybotrys chartarum Trichoderma spp. Verticillium spp. Yeasts

Aspergillus fumigatus A. ochraceus Cladosporium spp. Epicoccum nigrum Fusarium oxysporum F. solani Paecilomyces variotii Penicillium aurantiogriseum P. brevicompactum P. chrysogenum P. commune P. viridicatum Scopuariopsis brevicaularis S. candida Ulocladium chartarum

Limulus (the horseshoe crab). In normal conditions with no internal bacterial contamination, the indoor air level of endotoxin should not be higher than outdoors. Typically, the outdoor air endotoxin level changes significantly across seasons, showing higher levels in the growing season (around 1–3 EU/m3), due to aerosolized Gramnegative bacteria from leaves, than during winter (around 0.2 EU/m3). No health-based standard for endotoxin levels exists. However, the American Conference of Governmental Industrial Hygienists (ACGIH) (Bioaerosols: Assessment and Control) proposed that appropriate action should be taken when the level of endotoxin in the indoor environment (in the presence of respiratory symptoms) is at least 10 times higher than background outdoor levels. Similar to mold sampling, the traditional minutes-long bacterial air sampling methods using culture media may give results that represent less than 1% of the total bacterial flora present. Thus, this method may significantly underestimate exposure to environmental bacteria. Bacterial biomass measurement using muramic acid (a sugar in the peptidoglycan layer of Gram-positive and -negative bacterial cell walls) has also been developed for exposure assessment of environmental bacteria. There are few studies which have investigated airborne bacterial levels in office and school buildings. A research study reported that the level of indoor airborne bacteria was 105 CFU/m3 in office building environments.

23.2.3 Chemicals released from building materials/furnishings and growing microbes Volatile organic compounds are defined as organic compounds with boiling points in the range of 50–250 C. In indoor environments of schools and offices, there are many

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sources of VOCs, such as building materials (especially in new buildings), furniture, plastics, floor wax, cleaning agents, occupants and photocopiers. There are several thousand VOCs, and over 900 VOCs have been identified in indoor environments. Acetone, aliphatic hydrocarbons (hexane, octane, decane, etc.), aromatic hydrocarbons (toluene, xylene, benzene, etc.), chlorinated solvents (methylene chloride, trichloroethane, etc.), n-butyl acetate, dichlorobenzene, 4-phenylcyclohexene and terpenes are among the most commonly found VOCs. Since measurement and identification of an individual VOC with very low concentration is expensive, total VOCs are frequently measured. There is no standard for total VOCs in the USA and Canada, nor are consensus guidelines available from the American Society of Heating, Refrigerating, and Air Conditioning Engineers (ASHRAE). Microbial volatile organic compounds can be produced while microorganisms, especially mold, actively grow in damp building materials. In laboratory studies, more than 200 VOCs have been recognized as having microbial origins. Recently, the American Industrial Hygiene Association’s Field Guideline for the Determination of Biological Contaminants in Environmental Samples identified 14 compounds as potential MVOCs (3-methyl furan, 1-butanol, 3-methyl-1-butanol, 3-methyl-2butanol, 2-pentanol, 2-hexanone, 2-heptanone, 3-octanone, 3-octanol, 1-octen-3-ol, 2-octen-1-ol, 2-nonanone, borneol and geosmin), which were consistently detected by more than three authors in field surveys. Unique musty, earthy, mushroom-like or mold odors in damp/mold buildings are due to several MVOCs (e.g. geosmin, 2-methyl-iso-borneol or 8-carbon MVOCs). Many researchers in epidemiological studies have successfully used mold odor as a useful predictor for adverse health effects in damp indoor environments. However, no MVOC measurements have been shown to be predictive of health risk. Formaldehyde, a well-known irritant and sensitizer, is a colorless gas and can be recognized by pungent odor at a concentration higher than 0.2 parts per million (ppm). Building materials and furnishings (e.g. particle board, carpets and fabrics), cleaning agents and adhesives can release formaldehyde. Irritant effects have been found to occur when formaldehyde is present at levels above 0.1 ppm. Studies in schools have reported levels generally at 0.05 ppm or less, but some concentrations above the irritancy threshold were found. A study of Italian office workers with symptoms of irritation while working in newly renovated offices, found levels of formaldehyde from 0.07 to 0.4 ppm. The ACGIH classified formaldehyde as a ‘suspected human carcinogen’ with a ceiling threshold limit value of 0.3 ppm. NIOSH also identified formaldehyde as a potential occupational carcinogen and recommended a time-weighted average (up to a 10 hour workday and a 40 hour working week) exposure limit of 0.016 ppm and a 15 minute-average ceiling limit of 0.1 ppm. Phthalates are plasticizers added to polyvinyl chloride (PVC) products to keep them pliable, as well as to a number of other products such as paints, glues, cleaners and cosmetics. They are ubiquitous in the environment. There are public concerns about the health effects of phthalates, since they may act as endocrine disruptors and can affect the reproductive system. Recent research on children in homes and schools has indicated that phthalates and other plasticizers and their breakdown products are associated with respiratory symptoms, asthma, rhinitis and eczema. Moisture can lead to increased release and breakdown of plasticizers from PVC-containing building materials such as floor tiles and carpet backing; thus increased exposure to phthalates in

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CH 23 OFFICE WORKERS AND TEACHERS

damp, water-damaged schools and offices may be a concern. More research is needed to understand exposure–response relationships between phthalates and respiratory health effects.

23.2.4 Animal allergens A 2000 Institute of Medicine (IOM) report on asthma and indoor air exposures found sufficient evidence of a causal relationship between the development of asthma and house dust mite, limited or suggestive evidence of an association between the development of asthma and exposure to cockroach in preschool-aged children, and insufficient evidence to make a conclusion on the development of asthma and exposure to cockroach (in people other than preschool-aged children), cat, dog or rodents. In regards to exacerbation of asthma, the IOM committee found sufficient evidence of a causal relationship with exposure to cat, cockroach and house dust mite, sufficient evidence of an association with exposure to dog, and insufficient evidence to make a conclusion regarding exposure to rodents. Dust mites thrive in warm moist places, and keeping relative humidity below 50% is a recommendation for reducing dust mites and their allergen levels. The dust-mites commonly found in indoor environments such as homes, schools and office buildings are Dermatophagoides farinae (Der f) and Dermatophagoides pteronyssinus (Der p). Their Group 1 allergens, Der f 1 and Der p 1, are often assessed for associations with allergy and asthma. There is a dose–response relationship between sensitization and exposure to dust mite allergen. Research on children has indicated that exposure to 2 mg/g or more of Der p 1 allergens in dust increases the risk of sensitization (as measured by positive skin tests or presence of IgE antibodies), and the development of asthma, although there is some evidence that sensitization can occur at lower levels. Exposure to 10 mg/g Der p 1 or more in dust increases the risk of asthma symptoms in mite-allergic people, but the relationship is not clear. Concentrations of Der f 1 and Der p 1 found in office building and school building dusts are usually lower than the levels found in dust from homes. Furthermore, the opportunity for exposure to dust-mite allergens may be lower in nonresidential buildings since allergens are contained in particles of mite feces which do not remain suspended in the air for long if disturbed. In homes, bedding is a major source of mite allergen exposure. Cat allergens are ubiquitous, being found in homes with and without cats and in many types of public buildings, including schools and office buildings. They are sticky and are carried into buildings on clothing. There is a proposed threshold of 8 mg/g of the major cat allergen Fel d 1 for sensitization, while a level of 1 mg/g has been reported to elicit asthma symptoms in sensitized people. The allergens are carried on a range of particle sizes, but are often on small particles that can remain airborne for long periods of time after dust has been disturbed. There are many species of cockroaches, but the German cockroach Blattella germanica (Bla g) is commonly found in homes and schools, and to a more limited extend in office buildings. Its major allergens Bla g 2 and Bla g 1 have been widely used to assess exposure to cockroaches in relation to asthma. The proposed threshold levels of cockroach exposure is 2 units per gram (U/g) allergen in dust for an increased risk of sensitization and 8 U/g of allergen in dust for asthma symptoms. Cockroach allergens

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are usually carried on larger particles and thus do not remain suspended in the air for long after disturbance of dust. Most work on exposures to indoor animal allergens has been done in homes, and the levels of allergens in office buildings and schools are generally lower than residential exposures. Nevertheless, for some proportion of the samples, animal allergen levels in dust at or above threshold levels for sensitization and symptoms (proposed for residential settings) do occur in office buildings and schools. Furthermore, dust mite and cat allergens can accumulate in carpets and upholstered furniture. A 2005 review of indoor allergens in settled dust in schools concluded that from a clinical perspective the school environment is important for allergic occupants, especially if attempts have been made to reduce allergen exposures in their home environment. Examples of levels of dust mite, cat and cockroach allergens that have been found in offices and schools are given in Table 23.7.

23.2.5 Ventilation In the early 2000s, the European Commission funded a working group of scientists who were expert in indoor environmental quality and ventilation issues (EUROVEN) to review the literature on ventilation and health. The EUROVEN group came to the following conclusions in relation to office buildings and schools. There are associations between ventilation and comfort, health, sick leave and productivity in office workers. For office buildings, outdoor air supply rates of less than 25 l/s per person lead to increased sick building syndrome symptoms, increased sick leave and decreased productivity (there is little information for schools currently). Poor maintenance of HVAC systems contributes to increases in building-related symptoms. Ventilation rates should be designed to reduce all indoor pollution sources, not just human odor. Finally the EUROVEN group concluded that more work was needed on ventilation and health issues, particularly in schools. A review of the published literature up to 1999 on indoor air quality, ventilation and health symptoms in schools in the USA, Canada and Europe found indications that ventilation was inadequate in many classrooms, and often did not meet the minimum existing ASHRAE guidelines. A 2007 review on the role of ventilation in airborne transmission of infectious disease concluded that there is strong evidence for an association between ventilation in buildings and the spread of infectious diseases (e.g. measles, tuberculosis, chickenpox, influenza, smallpox and SARS). There is currently not enough known to set ventilation requirements for schools, offices and other indoor environments that would reduce such transmission. A useful website on ventilation issues for indoor environmental quality is http://eetd.lbl.gov/IED/viaq/.

23.2.6 Legionella Legionella is a genus of Gram-negative bacteria that are ubiquitous in water, are chlorine-resistant and can contaminate building water systems. Legionella bacteria grow well in stagnant, warm water (32–45  C). They form biofilms which can coat the interior surfaces of water systems and make elimination difficult. When inhaled or aspirated, Legionella can cause pneumonia or a less severe form of flu-like illness termed

Offices Molhave et al. (2000) Atmos. Environ. 34: 4767–4779; pooled floor dust from 7 Danish office buildings with no known problems Perfetti et al. (2004) Sci. Total Environ. 328: 15–21; dust from floors and upholstered chairs of 160 Italian offices and archives Macher et al. (2005) Indoor Air 15(suppl. 9): 82–88; floor dust from 92 large nonproblem US office buildings Schools Sarpong et al. (1997) J. Allergy Clin. Immunol. 99: 486–492; floor dust from 4 US urban primary schools

Study/setting

Not measured

—

0.8%

2.0%

—

0.4%

0.6%

3.7%

0.8%

0.6%

5%

Median Der p1e ¼ 0.08 Median Der f1e ¼ 0.09

Median Der p1g ¼ 0.05 Median Der f1g ¼ 0.04

—

% >10 mg/gb

—

% >2 mg/ga

0.16 (single measurement)

mg/g

Dust mite allergen in dust

Not measured

Median Fel d1h ¼ 0.43

Median Fel d1f ¼ 0.03

0.33 (single measurement)

mg/g

—

0.8%

0.0%

—

% >8 mg/gc

Cat allergen in dust

Table 23.7 Studies investigating levels of dust mite, cat and cockroach allergens in dust in offices or schools

—

22%

3.7%

—

% >1 mg/gd

Median Bla g 1i ¼ 2.6 25% >10 U/g

3/160 (2%) samples above limit of detection, maximum Bla g 2 ¼ 25 U/g Not measured

Not measured

Cockroach allergen in dust U/g

326 CH 23 OFFICE WORKERS AND TEACHERS

Median Der f1 ¼ 1.13

Median Der p1 ¼ 4.46

Not measured

—

—

—

—

Geometric mean Fel d1 ¼ 2.2 (carpet) Geometric mean Fel d1 ¼ 0.33 (no carpet) Median range Fel d1 ¼ 0.02–0.4

b

Threshold level for sensitization to dust mites and the development of asthma. Major risk factor for the development of acute asthma in mite-allergic individuals. c Threshold level for sensitization to cat allergen and the development of asthma. d Threshold level for symptoms. e Detectable Der p 1 levels found in 54% of workplaces and detectable Der f1 levels found in 55% of workplaces. f Detectable Fel d 1 levels found in 54% of workplaces. g Detectable Der p 1 levels found in 70% of workplaces and detectable Der f1 levels found in 63% of workplaces. h Detectable Fel d 1 levels found in 99% of workplaces. i Detectable Bla g1 levels found in 69% of samples of dust from schools. j Sensitization threshold levels for dust mite, cat and cockroach allergens were exceeded in many schoolrooms.

a

Patchett et al. (1997) J. Allergy Clin. Immunol. 100: 755–759; floor dust from 11 classrooms in 9 New Zealand primary schools Abramson et al. (2006) J. Sch. Health 76(6): 246–249;41 US schoolsj (results are for the lower grade carpeted rooms of Birmingham schools in spring). —

—

Bla g2 found in all schools and rooms. Median range Bla g2 ¼ 0.08–0.28

Not measured

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Pontiac fever. These bacteria, when present, can become aerosolized from cooling towers or humidifiers and be spread throughout a building via the ventilation system. L. pneumophila serogroup 1 is the main causative agent of disease. The dose of L. pneumophila needed to cause disease is not known. In the USA there are currently no federal or state guidelines for monitoring Legionella or regulations specifying exposure limits. The US Occupational Health and Safety Administration (OSHA) recommends testing for the presence of Legionella in water samples. Although dose– response relationships are not understood, and there is still discussion among experts as to the usefulness of regular water testing in the absence of disease, there are action levels recommended by US OSHA. Action level 1 involves prompt cleaning and/or biocide treatment of the system with levels of 100 colony forming units per milliliter (CFU/ml) in cooling tower water, 10 CFU/ml in domestic water, or 1 CFU/ml in humidifier water. Action level 2 involves immediate cleaning and/or biocide treatment, as well as taking prompt steps to prevent employee exposure, with levels of 1000 CFU/ml in cooling tower water, 100 CFU/ml in domestic water or 10 CFU/ml in humidifier water. The European Working Group for Legionella infections has also published action levels following Legionella sampling, which are based on levels of 1 and 10 CFU/ml. The Centers for Disease Control and Prevention (CDC) has a topic site for Legionella: http://www.cdc.gov/legionella/. The European working group has a website: http:// www.ewgli.org/index.htm.

23.2.7 Histoplasma capsulatum Histoplasma capsulatum is a mold which grows in soils throughout the world. In the USA, the proportion of people infected by H. capsulatum is higher in central and eastern states, especially along the Ohio and Mississippi river valleys where Histoplasma is endemic. The dose of spores needed to cause disease is not known, and the level of response to exposure varies among people, depending on age, susceptibility to the infection and likely the number of spores inhaled. Prior infection with Histoplasma can induce immunity and lessen responses to future infections. This mold is not generally associated with damp indoor environments but with soils rich in bird and bat droppings. Thus if birds or bats roost in or around buildings where spores from contaminated soils become carried into the occupied spaces, people in the building are at risk for infection and development of histoplasmosis. Reports exist of histoplasmosis occurring due to Histoplasma spores entering office and school buildings through HVAC air intakes after surrounding soil had been disturbed by construction activities or by rototilling. Environmental samples can be tested for the presence of Histoplasma using a PCR technique. Further information can be found at http://www.cdc.gov/ niosh/docs/2005-109/.

23.2.8 Work-process-related exposures Carbonless copy paper, copier and printer fumes and paper dust Carbonless copy paper (CCP) was introduced in the early 1950s, and within 10 years office workers were complaining of health effects. Irritation of the skin, eyes and upper

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respiratory system were common and cases of allergic contact dermatitis and some systemic effects were reported. In 2000 NIOSH published a hazard review which concluded that there was enough evidence to support exposure to carbonless copy paper or its components as a cause of symptoms of irritation and dermatitis. Symptoms of irritation in office workers have also been linked to exposure to copier and printer fumes. Newer research has provided evidence that adult-onset asthma in office workers may be associated with exposure to CCP as well as to paper dust, but not with exposure to copier and printer fumes. It is possible that components of CCP may cause sensitization, but this has not been well studied. Dose–response relationships are not understood for these exposures.

Pesticides Although there are no published data on the health effects of pesticides in office workers, information on pesticide exposure in schools is pertinent to the office environment. Exposure to pesticides in schools is associated with acute heath effects in both school children and school employees, including respiratory symptoms and aggravation of asthma. Analysis of surveillance data in the USA from 1998 to 2002 indicated an incidence rate of 27.3 cases per million employee full-time equivalents for acute illnesses associated with pesticide exposure in school employees. The incidence rate for the school children was 7.4 cases per million. Exposure to insecticides accounted for 35% of the cases, followed by disinfectants (32%), repellents (13%) and herbicides (11%). Almost 70% of the illness cases were associated with pesticides used at schools as opposed to drift from pesticides used on nearby land. Respiratory effects were reported in 49% of the cases. In the USA there are no federal regulations limiting exposure to pesticides in schools. Some states have regulations regarding the use of pesticides in schools. Useful websites are http://www.cdc.gov/niosh/docs/2007-150/ and http://www .beyondpesticides.org/children/asthma/AsthmaBrochureCited.pdf.

Cleaning agents There is no direct information on health effects of cleaning agents in office workers and teachers, but exposure to cleaning agents is associated with asthma onset and exacerbation in professional cleaners and in healthcare professionals. Furthermore, a recent population-based study in Europe showed that the use of spray cleaners and air fresheners in the home was associated with adult-onset asthma. Although more work is needed to understand the mechanisms by which various cleaning agents cause asthma, certain constituents, such as benzylkonium chloride and the ethanolamines, have been shown in the literature to be sensitizers. There is little information as to dose–response relationships. Certainly cleaning agents may act as irritants and trigger asthma symptoms, especially if cleaning concentrate products are inadvertently used in stronger concentrations than recommended, or components like ammonia and bleach are mixed together.

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Table 23.8 Indoor-related exposures associated with asthma Source

Example or agent

Dampness

Mold or mold-associated products Bacteria Endotoxin Phthalates Dust mites and their feces Cockroaches Cat allergen Phthalates Pesticides, e.g. pyrethrums Cleaning agents, e.g. amines Paints, glues from renovation Carbonless copy paper emissions Formaldehyde and other emissions from furnishings and building materials Alkaline dusts, e.g. drywall remodeling Toner cartridge products Paper-related dusts, e.g. from damp environments

Living creatures

Chemicals

Particulates

23.3 Diseases associated with exposures 23.3.1 Asthma Asthma is a common disease with both environmental etiologies and genetic propensities. Occupational asthma induced by workplace sensitizers can be cured if the inciting sensitizer is identified early in the disease course and the patient can be removed from exposure. The challenge for the practicing physician is to identify the plausibility of potential asthmagen exposure in the patient’s work environment so that the patient management maximizes cure or at least prevention of further inflammatory injury and remodeling of the airways to a permanent asthmatic phenotype. In office workers and teachers, the etiologic candidates for asthma are many (Table 23.8). Chief among the contributors to asthma in office and school workers is dampnessassociated exposures. The specific antigens, allergens and mechanisms remain undetermined. However, the epidemiologic evidence for asthma risk in relation to both residential and indoor workplace water damage is incontrovertible. In the residential setting, investigators in Europe and North America have found increased risk of wheeze, cough, nasal and throat symptoms, and asthma symptoms in sensitized persons associated with exposure to damp indoor environments. Some evidence exists for dyspnea, lower respiratory illness in otherwise-healthy children, and asthma development in association with damp indoor environments. Since the IOM review of literature published in 2004, additional evidence has mounted that some water-damaged buildings are associated with considerable increases in asthma incidence, consistent with adult-onset asthma being caused by exposures in such damp buildings. With respect to offices and schools in North America, no general population-based studies of building occupants exist with which to describe population-based frequency of asthma in relation to such buildings and damp building-related risk factors.

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Nevertheless, within particular damp buildings, risks as high as 7.5-fold increases in adult asthma onset have been documented post-occupancy, as compared with preoccupancy, with many additional co-workers having building-related respiratory symptoms for which they have not sought care or been diagnosed with asthma. A quarter of employees in some damp buildings have new-onset physician-diagnosed asthma. The complex microbial and chemical exposures arising in damp buildings makes identification of a specific verifiable etiology unlikely, even within a particular building subject to extensive environmental characterization. In the absence of an environmental measurement of risk for asthma, a shift in physician and public health paradigm is required. Protection of the asthmatic patient with symptoms arising in a damp building requires exposure cessation. In the short run, this may require restriction from the implicated work area. In the long run, exposure cessation requires remediation of the conditions leading to water incursion from the outside or leaks from indoor sources, as well as replacement of water-damaged materials in a way that precludes further dissemination of microbially contaminated sources. Public health agencies responding to indoor air quality concerns in relation to asthma can consider affected persons as sentinels of risk to co-workers and hence a public health problem. Asthma in office workers and teachers associated with animal allergens come to public health attention less commonly. Chemical causes of asthma in offices and schools are often recognized by patients in association with symptom exacerbation with respect to odors or indoor activities. Lower respiratory symptoms and asthma can be associated with particulates in indoor air. In a series of 80 buildings with indoor air quality complaints investigated by NIOSH, dry wall renovations within the previous 3 weeks was associated with building-related respiratory symptoms. Whether the renovation-associated symptoms are a marker for previous water damage and bioaerosol exposure or alkaline dust from dry wall remains in question. Particulates from copy rooms are sometimes associated with asthma and such work areas merit exhaust ventilation rather than contributing particulate load to the recirculated air as is common in modern buildings. Finally, office workers frequently complain of exacerbation of their building-related asthma symptoms when working with papers moved from previously water-damaged environments to new work environments. Whether such papers with high surface area carry contaminated dust or were sources of bioaerosol amplification in previous damp environments remains unclear, but such anecdotes recur in many building settings.

23.3.2 Hypersensitivity pneumonitis In contrast to building-related asthma, which is a newly recognized phenomenon, this granulomatous interstitial pneumonitis, also known as allergic alveolitis, has been recognized in relation to indoor nonindustrial environments for decades. Early publications of outbreaks usually implicated microbial dissemination from humidification and ventilation systems, although the specific organism(s) were rarely identified. Rather, the epidemiologic distribution of affected persons and resolution with remedial measures for the implicated sources were the basis of attribution to a building component. In fact, serum precipitins were often interpreted as identifying specific microbial etiology, but such immunologic findings are markers of exposure and not disease. Indeed, the precipitins may be markers of exposure to another agent which is correlated with the etiologic agent rather than the etiologic agent itself. The inability of

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some hypersensitivity pneumonitis cases to reoccupy implicated environments after remediation and cleaning is well established. Ventilation- and humidifier-related hypersensitivity pneumonitis may have decreased with recognition of the need for design changes and maintenance of cleanliness in these systems. More recent publications have implicated damp indoor environments in causing hypersensitivity pneumonitis. Buildings with long-standing water damage from roof leaks, other building envelope water incursion, plumbing leaks and below-grade moisture problems have all had reported clusters of hypersensitivity pneumonitis. Unlike asthma, hypersensitivity pneumonitis is rare in the general population, and even one case with building-related symptoms justifies public health investigation. In the presence of a building-related hypersensitivity pneumonitis case, there is usually a spectrum of other building-related respiratory symptoms and diseases among coworkers. Employee-reported physician-diagnosed asthma is frequently elevated in comparison to the general population. Cough, chest tightness, wheezing and shortness of breath without reported physician diagnoses are also often present in excess. In some damp buildings, clusters of sarcoidosis have occurred. Although pulmonary sarcoidosis might be misdiagnosed hypersensitivity pneumonitis, extra-pulmonary sarcoidosis cases have also been seen in case clusters. Specific etiologies for sarcoidosis in building-related clusters are under investigation.

23.3.3 Rhinitis/sinusitis For three decades, nasal and throat symptoms have been attributed to indoor environments when they occur in tight temporal association with ‘sick buildings’. These nonspecific symptoms did not generate much scientific investigation with objective tests in the era in which ‘sick building syndrome’ was considered subjective and difficult to study. More recently, interest has increased in these upper respiratory tract symptoms because of the robust information coming from study of damp residential environments associated with such symptoms, in which skepticism about secondary gain in the work environment is not a factor. A substantial body of information exists linking asthma exacerbation to upper respiratory tract symptoms. Indeed, the vast majority of occupational asthma cases have work-related rhinitis. In the occupational setting of increased building-related asthma risk, physicians have been impressed that rhino-sinusitis frequently precedes development of asthma with a work-related pattern. To date, little research exists to document the degree of risk of longitudinal progression of building-related rhinosinusitis to asthma. Correlations between symptoms or objective measures of rhinosinusitis and environmental measurements are also in their research infancy. To this end, measurements of nasal peak flow, acoustic rhinometry and nasal markers of inflammation and infection can be adapted to field epidemiology settings to establish a scientific basis for clinical understanding and management.

23.3.4 Other illnesses associated with office and school environments The exposure section above addresses some of the environmental risks in office and school settings associated with the illnesses listed in Table 23.1. These do not require

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Table 23.9 Other illness associated with indoor-related exposures Condition

Example or agent

Environmental contribution

Legionnaire’s disease Histoplasmosis Tuberculosis Communicable virus infection Cough

Legionella pneumophila Histoplasma capsulatum Mycobacterim tuberculosis Influenza, rhinovirus Detergent dust

Contaminated water Disruption bird/bat roosts Ventilation Ventilation Poorly diluted carpet shampoo

further description here, since they may not present to the clinician as building-related or work-related. Nevertheless, their occurrence may trigger a reporting requirement to public health authorities, e.g. legionellosis. Noncommunicable infections often have environmental sources in specific office or school environments. Historically, legionellosis occurred as a result of entrainment of contaminated cooling tower effluents in ventilation systems. Histoplasmosis has occurred in employees exposed to construction dusts from outdoor work, particularly when topsoil with bird droppings is disturbed. Ventilation effects on communicable respiratory infections is an active area of investigation pertinent to pandemic planning and studies of workforce productivity affected by the short-term absenteeism associated with communicable viral respiratory disease. Finally, specific irritant syndromes, such as respiratory irritation due to carpet residual of inadequately diluted carpet shampoo, are discovered by tight temporal association with building occupancy (Table 23.9).

23.4

Diagnosis and management issues

23.4.1 Diagnosis Eliciting a history of symptoms in temporal relation to occupying the work environment is the most critical step in identifying those with building-related asthma, hypersensitivity pneumonitis and rhinitis/sinusitis. Unlike sick building syndrome, which remits when employees exit an implicated building, the temporal pattern of building-related asthma and hypersensitivity pneumonitis is generally more subtle. Examples are occurrence on the evenings of work days in comparison to evenings on the weekend; progressive deterioration over the working week; and remission with sickness absence. Certainly cases can be missed in the history of work-relatedness, particularly for subacute hypersensitivity pneumonitis and sinusitis complicated by infection. Nevertheless, even in these situations, exploration of improvement with prolonged work absence, e.g. over summer holidays in teachers, can be suggestive of a work-related pattern. Exploring whether similar illness is reported by co-workers is also useful. Certainly, report of environmental risk factors, as described above, should increase the clinician’s efforts to explore potential work-relatedness. In 2004, the Center for Indoor Environments and Health of the University of Connecticut Health Center published a document: ‘Guidance for Clinicians on the Recognition and Management of Health Effects Related to Mold Exposure and Moisture Indoors’. This document includes suggestions for taking a patient history

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in relation to work-related dampness exposures. This document can be accessed at: http://www.oehc.uchc.edu/clinser/MOLD%20GUIDE.pdf. For other respiratory illness related to offices and schools, e.g. noncommunicable infections, there is no history of work-relatedness, and the patient may have little insight into environmental risks for such illnesses, e.g. contaminated water systems or construction activities. Although some evidence exists for increased transmission of common respiratory infections as a function of ventilation rate and crowding in office workers and teachers, physicians may not be aware of these risks. The tools for making a diagnosis of any of these diseases in office workers and teachers are the same as for any patients. Physical examination, spirometry, bronchodilator responsiveness, bronchial hyperreactivity, diffusing capacity, radiology, bronchoalveolar lavage, transbronchial biopsy and other tests are applied in order to narrow the differential diagnosis. The major additions to consider in documenting work-relatedness include symptom and medication logs in relation to work hours and tasks; serial peak flow or hand-held spirometry logs over several weeks to examine a work-related pattern of obstruction or restriction; serial bronchial reactivity tests before and after prolonged work absence; and serial exercise capacity with a focus on respiratory parameters and gas exchange for interstitial disease. Most clinicians do not have the option of specific inhalation challenge to document reactivity to single allergens or antigens, as this test is performed by few referral hospitals. In any case, for most building-related illness, specific single etiologies are unlikely and uncharacterized. Precipitin testing has not been useful in most outbreak situations, in part because relevant antigens may not be commercially available for the complex exposures present in the environments of damp buildings.

23.4.2 Management Building-related respiratory diseases are best managed by exposure cessation. Indeed, for building-related asthma diagnosed early in its course, removal from exposure can be curative. With prolonged symptomatic exposure and steroid dependency, buildingrelated asthma may not remit with removal from exposure, as is the case with most etiologies of occupational asthma. The challenge for patient and clinician is how to achieve exposure cessation to the implicated environment. Medical restriction from a damp building may threaten continued employment. If water damage is limited to part of a building, a trial of relocation within the building or to another part of the enterprise may be justified. These concerns are common to all occupational lung diseases. The pharmacologic treatment of the disease is identical to that of other patients without work-related etiology. In the intermediate and long term, remediation of the environmental conditions resulting in work-related respiratory disease is critical both for individual patients and for prevention of disease in coworkers. Such intervention is a decision beyond the control of most office and school staff, being a prerogative of management or building owner. Notification of the responsible parties of occupational disease is critical, but patients may request that the clinician not do so, for fear of job loss or retribution. In such instances, involvement of public health investigators can protect patient confidentiality where it might otherwise be threatened.

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23.4.3 Medicolegal considerations The provisions for work-related illness compensation vary from country to country and state to state in the USA. Some jurisdictions require etiology to be established by objective tests, specific inhalation challenge or occurrence in a previously recognized industrial setting with specific listed chemical exposure. Other jurisdictions are less restrictive in diagnostic criteria. In general, however, workers’ compensation is an adversarial process for occupational respiratory disease in comparison to work-related traumatic injury, and many patients have their cases denied until they appeal with expert legal and clinical resources. With building-related illness, in particular, the science of the health impact of damp indoor spaces is new enough that compensation systems have little experience with these claims. In the USA, the litigation surrounding alleged health effects of mold has spawned an aggressive defense medicolegal coalition against such claims in residential tortes, insurance proceedings and workers’ compensation.

23.4.4 Public health issues Occupational respiratory illness in educational staff and office workers is a sentinel for co-workers at risk. Apart from occupational physicians employed by a specific business entity, few clinicians have the time or resources to follow back an index case to a working population. However, a clinician can ‘activate’ public health investigation by reporting suspected cases. Public health agencies can bring together multidisciplinary teams to aid in the screening of co-workers and in ascertaining remediable causes of dampness, recommending interventions and even evaluating the effectiveness of interventions. This model of public health preventive action triggered by case reporting is an ideal. In reality, many public health agencies are understaffed, financially stretched and have little experience with occupational disease, either in industrial or nonindustrial environments. The reporting of asthma or hypersensitivity pneumonitis should be to state epidemiologists or physicians, who can recognize the public health implications and request additional resources, for example from federal occupational health agencies. One pitfall is contacting federal or state labor agencies which are regulatory in mission. No permissible exposure limits exist in most jurisdictions for agents associated with dampness. Without regulations to enforce, compliance officers are at a loss to help. In the USA, the research and service agency with expertise in building-related respiratory disease is NIOSH, which is part of the CDC. This agency investigates building-related health concerns in response to requests from three employees (who need not be personally affected), labor unions or managers. In addition, the agency has frequently provided consultation or on-site technical assistance to state and local public health agencies requesting its assistance. As an emerging public health issue, dampness in indoor spaces is currently an emphasis area for both research and service. Similar efforts exist in occupational and public health agencies in other countries such as Canada, Finland and Sweden. Since regulations regarding indoor environmental quality are largely absent in the USA, patients often remain powerless in getting adverse conditions fixed. In schools, parental concern for student health risk and performance can lead to a logical alliance

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with staff with similar health concerns. In office workers, motivating remediation is a difficult task, since the expense can be considerable, and public health investigation of specific employee populations to develop data for priority setting and policy is a rarity. With the increasing evidence of work-related disability in relation to these nonindustrial settings, perhaps societal consensus can be shifted toward both primary prevention of dampness problems and prompt remediation when necessary.

Further reading Daisy, J.M., Angell, W.J., Apte, M.G. (2003) Indoor air quality, ventilation and health symptoms in schools: an analysis of existing information. Indoor Air 13: 53–64. Guidance for Clinicians on the Recognition and Management of Health Effects Related to Mold Exposure and Moisture Indoors (30 September 2004) Published by the Center for Indoor Environments and Health at University of Connecticut Health Center with support from a grant by the US EPA. Available online at: http://www.oehc.uchc.edu/clinser/MOLD%20GUIDE.pdf. Institute of Medicine of the National Academies of Science (2004) Damp Indoor Spaces and Health. National Academies Press: Washington, DC. Institute of Medicine of the National Academies of Science (2000) Clearing the Air: Asthma and Indoor Exposures. National Academies Press: Washington, DC. Li, Y., Leung, G.M., Tang, J.W., Yang, X., Chao, C.Y.H., Lin, J.Z., Lu, J.W., Nielsen, P.V., Niu, J., Qian, H., Sleigh, A.C., Su, H.-J. J., Sundell, J., Wong, T.W., Yu, P.L. (2007) Role of ventilation in airborne transmission of infectious agents in the building environment – a multidisciplinary systematic review. Indoor Air 17 (1): 2–18. Mudarri, D. and Fisk, W.J. (2007) Public health and economic impact of dampness and mold. Indoor Air 17: 226–235. The IAQ Scientific Findings Resource Bank. Contains summary information and down loadable papers on the relationship of IEQ with people’s health and work performance. This site was developed in conjunction by Lawrence Berkeley National Laboratory in collaboration with the US Environmental Protection Agency; available from: http://eetd.lbl.gov/ied/sfrb/.

24 Research workers Paul Cullinan Imperial College and Royal Brompton Hospital, London, UK

24.1 Introduction The exposures encountered by research workers are as numerous and varied as the research they do. Thus the term ‘research worker’ is a broad one and encompasses a very wide range of individuals with an unusually wide range of potentially hazardous exposures. Moreover, at least in economically developed countries, the total population of research workers is large. Many researchers will be working in universities or other places of higher education – in some cities these are major employers with many thousands of research staff. Others will be employed in the research departments of the commercial sector, often in the pharmaceutical or biotechnology fields; again these workforces are often large although there is an increasing trend, particularly in the biotechnology sector, towards small companies employing just a few research staff. The term ‘research worker’ might also be applied to those who work in developmental or quality control laboratories within industry. In this context, any meaningful clinical assessment of a potentially ‘occupational’ lung disease will require close attention to particular exposures relating both to materials that are used in primary research and those that represent finished products. In many cases such exposures will be obvious; these include, for example, research work with laboratory animals, the use of chemicals widely recognized to cause respiratory irritation and the wearing of latex gloves. Other exposures will be more obscure and will require careful questioning and/or consultation of reference information obtainable either through an employer or directly from the producers or suppliers of chemical agents. Research workers are, in general, highly educated and highly motivated. They will have a better understanding of their work than will their clinician; at the same time they may have a mildly cavalier attitude to the hazards associated with their work, especially

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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if they have been involved in it for many years. Many will be reluctant, at least initially, to consider an occupational etiology for their disease and more reluctant still to consider leaving or changing their work; this poses special difficulties for those who have developed an occupational hypersensitivity. On the other hand their levels of education – and the relatively liberal environments where they work – mean that career options are often wider than for those who work in industry. Most institutes of higher education and most large companies involved heavily in research will have a well organized system of occupational healthcare including regular health surveillance. Thus their employees are, in this respect, relatively well supported. Furthermore, most research settings are carefully regulated and most research processes are on a fairly limited scale. For these reasons, researchenvironment exposures – with some exceptions, notably those relating to laboratory animals – tend to be considerably less intense than those encountered on the shop floor.

24.2 Respiratory hazards and diseases The most important occupational respiratory diseases in this workforce are those characterized by (variable) airflow limitation (Figure 24.1). Asthma and rhinitis may airborne exposures in research setting

sensitizing sensitising agent

irritant chemical

high low molecular molecular mass mass

high dose

lower dose - repeated

acute

new asthma and/or rhinitis

provocation of pre-existing asthma

toxic damage to airways: nose pharynx trachea bronchi toxic pneumonitis pulmonary oedema edema

? new asthma and/or rhinitis

chronic

asthma (RADS*) OB* OB* COP* other interstitial lung disease

Figure 24.1 Overview of occupational respiratory disease in a research setting; RADS
¼ reactive airways dysfunction syndrome; OB
¼ obliterative bronchiolitis; COP ¼ (cryptogenic) organizing pneumonia

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339

be induced through sensitization to a workplace agent or, less commonly, by exposure to a toxic dose of a respiratory irritant. Other respiratory diseases arising from research work are far less common. Acute exposures to high doses of respiratory irritants (‘inhalation accidents’) can give rise to toxic damage to the upper and lower airways and even to the gas-exchanging parts of the lung. Irritant exposures of sufficient intensity to cause severe disease appear, fortunately, to be rare in the laboratory. Various forms of interstitial lung disease including hypersensitivity pneumonitis have been attributed to chemical and biological exposures, but again rarely in research workers. More rarely still, in this context, exposures in the laboratory have been considered as contributory to some cases of lung cancer. In each case of occupational respiratory disease in a research worker it is helpful to establish precisely the causative agent; and where appropriate to distinguish disease that has arisen de novo as a result of an exposure at work from pre-existing disease that has been provoked by one or more such exposures. Most commonly the need for this distinction arises in cases of work-related asthma. In the strict sense, ‘occupational asthma’ is that which has been induced by a sensitizing or irritant agent in the workplace, while ‘workexacerbated asthma’is that fromanother (nonoccupational) cause that is provoked by one or more exposures at work (Figure 24.2). Such a distinction may not be easy but has important diagnostic, management, prognostic, employment and legal implications. Most of the common occupational respiratory diseases in research workers are of short – or relatively short – latency. Thus the adverse outcomes of inhalation accidents are generally immediate, with even the longer term sequelae becoming apparent within a few months. The risks of respiratory sensitization are highest within the first few years of first exposure. It is generally easier to establish (or otherwise) an occupational etiology for a disease that is of relatively brief latency. On the other hand they tend to give rise to important employment and related consequences that may be more prominent than for diseases, such as many pneumoconioses, whose onset is only apparent many decades later. high molecular mass (protein)

respiratory sensitizing agent

new (‘occupational’) asthma

low molecular mass (chemical – R42)

high (‘toxic’) dose single exposure

respiratory irritant (airborne)

new (‘occupational’) asthma low dose repeat exposures

high/low dose repeat exposures

provocation of pre-existing asthma

Figure 24.2 Asthma and occupational exposures at work. Note that those with pre-existing asthma can also become sensitized to a workplace agent and develop worsened asthma as a consequence. ‘R42’ is a chemical hazard identification for a recognised respiratory sensitising agent

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24.3 Respiratory sensitization: asthma and rhinitis Asthma and rhinitis may readily be induced as immunological reactions to an airborne sensitizing agent in the research workplace. There are many such agents, generally categorized as of high or low molecular mass. The former group is composed largely of proteins, the latter of reactive chemicals. Some groups of research workers are exposed to high concentrations of well recognized respiratory sensitizing agents in the course of their work; examples are given in Table 24.1. The most common are high-molecularmass proteins, particularly but not exclusively those found in the excreta and/or secreta of laboratory animals. Less commonly, researchers may develop respiratory sensitization to an inhaled drug or other reactive chemical. The list in Table 24.1 is by no means exhaustive and any case of asthma or rhinitis arising in a laboratory worker should prompt a search for an occupational etilogy – especially where there is exposure to an airborne protein, any one of which is probably capable of inducing asthma. Laboratory animal allergy in those who carry out in-vivo animal research is common, with a prevalence of around 15% and an annual incidence of about 5% among those with regular exposure. The risks are higher in those with highest exposure and in those with other atopic disease such as hayfever or cat allergy. Most cases now arise from contact with mice, reflecting the increased use of this species in medical and Table 24.1 Respiratory sensitizing agents – and the relative frequency with which they cause disease – encountered by research workers Agent (examples) Laboratory animal proteins Mice Rats Guinea pigs Hamsters Ferrets Dogs Cats Primates Locusts, grasshoppers Drosophila spp. (fruit fly) Mealworms Butterflies, moths Cockroaches Serum albumen (bovine, mouse, etc.) Animal feedstuff (corncob, etc.) Pollen (grass, oil seed rape, sunflower, etc.) Latex Molds (Aspergillus spp., Dictyostelium, etc.) Enzymes (papain, pancreatin, xylanase, bromelin, etc.) Egg white Drugs (piperazine, penicillins, morphine, cimetidine, etc.) Cleaning agents (glutaraldehyde, benzyl ammonium chloride, etc.) Other chemicals (ninhydrin, iso-nonayl oxybenzene sulfonate, etc.)

Relative frequency of published cases þþþ þþþ þþþ þþ þ þþ þ þ þþ þþ þ þ þ þ þ þ þþ þ þ þ þ þ þ

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MAKING A DIAGNOSIS OF RESPIRATORY SENSITIZATION

341

pharmaceutical research. Other commonly implicated species are rats, guinea pigs and larger mammals such as dogs (Table 24.1). Sensitization to primates appears to be rare. The major allergens in small mammals are found in their urine and are easily transmitted to the pelt and to bedding material and thus, when dried, become airborne. Direct handling of whole animals, anesthetized or otherwise, and changing bedding (cage cleaning) are common causes of respiratory exposure. Many animal research workers will have only intermittent exposure relating to the timing of their experiments; those tasked with animal husbandry are likely to have higher and more consistent exposures. Chemicals that are recognized to induce respiratory sensitization should carry a specific label, generally to be found on the relevant safety data sheet. Currently their label is ‘R42’ (‘may cause sensitization by inhalation’); with the soon to be enacted ‘Globally Harmonized System’ for chemical classification this will become ‘H334’. Lists – albeit incomplete – of biological and chemical agents that have been reported to cause occupational respiratory sensitization are available in print (see Further Reading) or via the web (www.asmanet.com, www.asthme.csst.qc.ca, www.eaaci.net). Additionally there is increasing interest in the structural characteristics that distinguish (inorganic) chemicals that are capable of inducing respiratory sensitization. Quantitative structure–activity relationship analysis of such chemical is becoming increasingly sophisticated and appears to have near-perfect negative predictive value. Access to analysis of this sort and appropriate interpretation is freely available on the web and may prove helpful when considering the etiological role of an unfamiliar chemical (http:// homepages.ed.ac.uk/jjarvis/research/hazassess/hazassess.html).

24.4

Making a diagnosis of respiratory sensitization

The clinical manifestations of laboratory animal allergy are well recognized and are instructive. They probably apply to most other causes of respiratory sensitization among research workers: .

Most cases arise within two years of first exposure, a reflection of the responsible immune process and of innate individual susceptibility. It is unusual for a laboratory animal researcher to develop disease after many years of similar work. Beware, however, the researcher who has been employed for many years but has recently started work with a different species or process, and the researcher who has elected previously to deny the presence of work-related symptoms.

.

For much the same reasons, laboratory animal allergy does not generally manifest within the first few months of exposure. This period of latency is an important clinical clue to the distinction of ‘occupational’ asthma from the exacerbation of asthma due to another cause.

.

Symptoms of asthma due to animal sensitization are universally accompanied by nasal and eye symptoms similar to those that characterize hayfever. Thus the absence of eye and nose symptoms at work makes a diagnosis of laboratory animal asthma improbable.

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.

Both lower and upper respiratory symptoms are related to exposures at work in as much as they are provoked by being at work and are, at least in early cases, relieved when away from work. Immediate (‘early’) symptoms may be accompanied by those that occurlater(‘delayed’),perhapswhileathomeafterwork.Thiscangiverisetosome diagnostic confusion. In more chronic cases there may be relatively little – or no – relief when away from work, a reflection of ongoing bronchial and nasal hyper-reactivity.

.

Similarly, hyper-reactivity as a result of immunological sensitization may also give rise to symptoms on contact with nonspecific and nonoccupational irritant exposures such as perfumes or cold air; again this may confuse the clinical picture.

.

Laboratory animal asthma – and most cases of laboratory animal rhinoconjunctivitis – is almost always accompanied by evidence of specific immunological sensitization. This is characterized by the production of specific IgE antibodies and is detectable by skin prick testing with appropriate allergens or by measurement of specific IgE antibodies in serum. Suitable reagants for many animal species are available commercially but in more unsusual cases it may be necessary to communicate directly with an experienced laboratory. For small mammals, testing with urinary antigens is more sensitive than testing with epithelial extracts. Skin prick testing should include the use of positive and negative control solutions; the latter is especially important to avoid false positive findings.

.

Once sensitized, patients with laboratory animal allergen may be exquisitely sensitive to even very small concentrations of airborne allergen. This is reflective of the hypersensitive immunology that gives rise to the disease; it can make management of an individual case very difficult.

The diagnostic process in research workers suspected of laboratory animal allergy reflects the manifestations and processes listed above. History taking requires careful attention to the nature and duration of appropriate exposures. It is helpful especially to enquire: .

What exactly is their occupational contact with animals in terms of direct handling of live, anesthetized or dead animals? Are they handling only harvested tissues? For how long and how frequently do they have such contact? Does their work include cleaning cages or the handling of bedding or foodstuffs? In occasional cases sensitization arises not from animal proteins but from biological material used as feed.

.

How often are they in the animal facility without direct animal contact? Is their animal work only within the animal house or do they also carry out experiments in other laboratories?

.

How close and how often are they working to and with others who handle animals? Similarly, is this only within the animal house or does it occur in other settings?

.

Do they wear latex gloves when working with animals? Where powdered gloves are (or have been) used, then these may be responsible for immune sensitization (latex allergy) rather than the animal species which they are used to handle.

.

Do they wear protective respiratory equipment when working with animals? How often do they wear it – and how often is it serviced? Are simple half-face masks

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MAKING A DIAGNOSIS OF RESPIRATORY SENSITIZATION

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re-used and in any case do they fit properly? Some animal research facilities require the use of powered full-face ventilators; if used routinely and properly, these are extremely effective in reducing exposures to airborne allergens. .

What has been their previous experience with laboratory animal work – including as an undergraduate? Do they – or have they in the past – kept similar animals as pets at home? Pet rats, for example, are remarkably adept at inducing sensitization in their domestic owners.

While it is possible to measure air levels of, and personal exposures to, animal allergens within the laboratory the methodology is complicated, poorly standardized and seldom if ever useful in clinical practice. In the same way as above, a careful account of the character, latency and timing of symptoms is crucial. Here, helpful information includes: .

A history enquiring into previous respiratory allergy – even if quiescent at the time of starting work. It is of course perfectly possible to acquire an occupational asthma or rhinitis on the back of a prior history of such allergic disease; disentangling the two can be difficult.

.

The timing of first symptoms at work. Those that begin very shortly after starting a new job are likely to reflect the provocation of pre-existing disease or asymptomatic bronchial hyper-reactivity. Those that start several months later are more likely to reflect immune sensitization.

.

The use of asthma or nasal treatments and an assessment of the degree of control of any pre-existing condition.

.

The co-existence of work-related nasal and lower respiratory symptoms and their relative timing of onset. Classically in laboratory animal allergy rhinitis is reported before the onset of asthma symptoms.

.

The current temporal relationship between symptoms and work. Recall that any improvement away from work may be less obvious if symptoms have been present for a long time.

.

The current temporal relationship between symptoms and specific tasks at work. Advantage can be taken of the often very variable daily schedule of many research workers. Note that patients with bronchial hyper-reactivity may relate their symptoms to irritant exposures at work. Most respiratory irritants do not induce specific sensitization and reactions to them may reflect an immunologically induced bronchial hyper-reactivity to another agent.

It is unwise to make a diagnosis of animal allergy on the basis of a history alone; such a practice will inevitably give rise to false positive diagnoses. In the presence of a characteristic history from an animal research worker with appropriate exposure, the next step is the establishment or otherwise of specific sensitization using, as above, either skin prick testing or measurement of serum specific IgE antibodies – or preferably both. The absence of an identifiable IgE response – assuming this has been done rigorously – should prompt serious consideration of an alternative diagnosis.

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24.5

MANAGEMENT OF RESPIRATORY SENSITIZATION IN THE RESEARCH SETTING

345

Conversely the presence of IgE sensitization alone is insufficient to make a diagnosis of laboratory animal asthma since there clearly exists a state of ‘asymptomatic sensitization’. Even with an appropriate history and with evidence of IgE sensitization, most clinicians will search for further evidence of an occupational etiology. This is most easily done through measurements of peak expiratory flow serially at home and work; the sensitivity and specificity of this diagnostic approach is considerably enhanced (to about 75 and 90% respectively) if measurements are made more than four times a day for a period of at least a month. By plotting daily mean, maximum and minimum values and comparing these between periods at home and at work it is generally possible to establish – or disprove – a functional relationship with work (Figure 24.3a). Asthma and rhinitis that arise from other high molecular mass allergens in the research setting (Table 24.1) have features that are essentially identical to those described above and should be investigated in the same way. Respiratory sensitization to a low molecular mass chemical agent typically shares most of the same clinical characteristics but there are a few important differences: .

Recourse to technical information on the chemical(s) in question is often necessary – especially where they are not widely recognized as being capable of inducing respiratory sensitization. Examination of the relevant safety data sheets (and in particular for R42 or H334 codes) may be helpful.

.

Rhinitis may be less common.

.

Very few such chemical agents elicit an identifiable specific IgE response. This can make diagnosis more difficult and, where there are suitable facilities, often gives rise to the necessity for specific provocation testing under controlled conditions. Here specialist and experienced advice is essential.

.

For some chemical sensitizing agents it is possible, using validated methods, to make measurements in air including in the breathing zone. These are unlikely to be helpful in diagnosis but may be useful in guiding management.

24.5

Management of respiratory sensitization in the research setting

The first step in the effective management of an established case of laboratory animal allergy – or indeed other respiratory hypersensitivity – lies in a firm diagnosis, a clear 3 Figure 24.3 (a) Serial peak flow record in research worker with prior sensitization to rat urinary proteins. Days at work are depicted by shaded columns, those away from work by unshaded columns. On each day only the mean (solid line), maximum (squares) and minimum (circles) values of six daily readings are shown. There is clear evidence of a fall in peak flow and increased diurnal variability (see boxes) when the patient is at work. Note: during this record the patient had no direct contact with rats and nor did he enter a room where rats were being held. The changes in peak flow and his accompanying symptoms of asthma were caused by very low exposures encountered in the corridors adjacent to rat-containment rooms (see also Figure 24.4). Only by complete avoidance of the workplace was he able to abolish his symptoms – and record a flat peak flow record (b)

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understanding of the responsible species (agent) and a good working knowledge of the workplace (Figure 24.4) and available options. In this setting, a false positive diagnosis can be disastrous since it is likely to give rise to needless and often major professional disruption for the patient with little likelihood of clinical improvement. Where a firm diagnosis has been reached then management relies primarily on avoidance of further exposure to the causative antigen in the knowledge that even very small exposures may give rise to continuing bronchial inflammation and symptoms. It

animal facility changing room

lab

lab

lab

species 1

species 2

species 1

barrier system

office

stock holding rooms

designated laboratory

departmental offices and laboratories

office

office

office

office histology room store 34

office lift

toilet

Figure 24.4 Schematic diagram of research laboratories and office space with adjacency to animal holding facility. Animal experiments may be carried out within the animal facility laboratories or in other ‘designated’ laboratories. Staff may move freely between different areas. Thus animal allergens may contaminate a wide area – potentially all the rooms and corridors shown here, not only those where animals are present. This is important to understand when managing hypersensitivity

24.6

RESPIRATORY DISEASE ARISING FROM EXPOSURES TO IRRITANT SUBSTANCES

347

is believed, with reasonable evidence, that continuing exposure to the causative agent at intensities sufficient to cause ongoing symptoms is harmful to prognosis and diminishes the chances of eventual recovery. On the other hand, if further such exposure can be avoided then there is almost always a major reduction in symptoms and a high probability of eventual cure. Avoidance of exposure will naturally require a major re-consideration – and sometimes even abandonment – of a career. Research workers are especially reluctant in this respect and many will choose to continue with their work. In such cases, expert advice on reducing exposure and on the use of protective respiratory equipment is helpful. Even with great care in this respect, symptoms may persist, causing considerable management difficulties (Figure 24.3b). Animal workers sensitized to, for example, rats may question whether they can safely work with another species, say mice. This strategy is seldom successful for very long, although those who move to work with a very different species – say, in this case, dogs – appear to fare well. In the face of continuing exposure, phamacological treatment with antihistamines and standard asthma/rhinitis regimens can be helpful but rarely gives rise to complete or lasting disease control. There is very limited evidence that treatment with an inhaled corticosteroid may hasten recovery in those who have avoided further exposure. All patients with occupational respiratory sensitization should be advised that continuing exposure is probably detrimental to their prognosis. Knowledgeable advice on statutory compensation – available in many countries – should be provided. Evidence-based guidelines on the diagnosis and management of occupational asthma – including laboratory animal allergy – has been published by the British Occupational Research Foundation (see Further Reading). Using a question-andanswer format it is a handy and practical tool.

24.6

Respiratory disease arising from exposures to irritant substances

Respiratory disease in research workers may also arise from exposures to agents that are irritating to the upper and/or lower respiratory tract. This is an area where some (potential) outcomes are well understood and characterized but others are far less so and can give rise to considerable controversy. It should be emphasized that in most research settings exposures to respiratory irritants are unlikely to give rise to any new disease. As with potentially sensitizing agents, those that are irritant and may be encountered in the laboratory are many and varied. They include irritant gases such as chlorine and ammonia, organic chemicals such as acetic acid, formaldehyde and numerous solvents, metals and metallic compounds such as oxides or halides of zinc or cadmium and complex mixtures such as smoke from fires or the pyrolytic products of burning plastics. High-intensity exposures to irritants in a research setting are inevitably unpredictable or accidental and seem, fortunately, to be rare. Repeated exposures at lower intensities are far more common.

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In this context some issues are relatively clear: .

Acute exposures to high intensities of respiratory irritants can induce – with relative ease – acute nasal, oro-pharyngeal or lower respiratory diseases. These include cough, hoarseness, tracheo-bronchitis, pulmonary edema, adult respiratory distress syndrome and very occasionally death; further details are given below.

.

Similarly, high-concentration exposures over a very short-time period can induce persistent respiratory disease. Examples include bronchiolitis obliterans and/or organizing pneumonia, bronchiectasis and an asthma-like syndrome; these too are described in more detail below.

.

The mechanisms under consideration here are not those of immunological sensitization but those of toxic injury, inflammation and consequent repair processes.

.

In such cases – especially those of self-limiting or unusual disease – attribution of cause and effect is usually on the basis of the temporal association between an extraordinary event and the apparent onset of new disease.

.

Lower and sometimes repeated exposures to respiratory irritants – not uncommon in research laboratories, for example – can readily exacerbate pre-existing asthma. In general this is easily managed by careful attention to the reduction of such exposures and to pharmacological asthma control.

Other issues are far less clearly understood: .

In some circumstances, less intense exposures over longer time periods (‘sub-acute’ exposures) can give rise to respiratory disease. This is much more difficult to determine, especially in an individual case, and often requires the identification and epidemiological investigation of a number of similarly exposed cases. This is more likely to occur where the disease phenotype is uncommon or unusually severe. Outbreaks of such disease have not yet been reported among research workers but have been recognized in several industrial settings, giving rise to ‘new’ diseases such as ‘nylon-flock workers’ lung and ‘Ardistyl’ lung.

.

The question of whether repeated, ‘low-dose’ exposures to respiratory irritants can give rise to novel asthma is contentious – and of considerable importance to the research community where such exposures are probably not uncommon. Difficulties arise – particularly in individual cases – because asthma is a common disease in the (research) population and naturally follows a course of remission and relapse. The firm attribution of apparently new disease to ‘not-so-sudden’ irritant exposures in an individual case is essentially impossible.

24.7 Immediate effects of acute exposures to respiratory irritants at relatively high intensity Unusually, in clinical practice the starting point in this setting is generally not in the investigation of disease (‘effect’) but in the consideration of an ‘event’ and its possible

24.7

ACUTE EXPOSURES TO RESPIRATORY IRRITANTS AT RELATIVELY HIGH INTENSITY

349

Table 24.2 Selection of respiratory irritants that may be encountered in the laboratory with a measure of their relative water solubility and reported outcomes after acute, intense exposure. All, at high enough does, can cause ‘toxic pneumonitis’ Water solubility

Reported effects Acute

Ammonia Acetic acid Hydrogen chloride Sulfur dioxide Chlorine Oxides of nitrogen Ozone Zinc oxide

High High High High Medium Low Low

Long-term

Acute upper airway irritation

Irritant-induced asthma

Interstitial lung disease

þþþ þþþ þþþ þþþ þþ þ / þ / þ /

þ þþ

þ

þþ þþ þ

þ þþ

sequelae. This highlights the importance of understanding in considerable detail the nature of the apparently initiating incident and in particular the agent(s) involved and the probable intensity of exposure(s). The likely outcomes – and the likelihood of a particular outcome – of any particular exposure are thus more predictable. Almost any irritant gas, chemical, metallic compound or other irritant agent may be encountered by research workers in the course of their job; a list of some of these is provided in Table 24.2. High-intensity exposures in the research setting are stochastic and follow equipment failure or are due to human error. Some agents are well recognized as noxious to the respiratory tract; others are less commonly encountered and both their chemistry and likely toxic effects less well understood. Gaseous respiratory irritants are often classified by their solubility in water which, to some extent, determines the site of any lung injury consequent on their inhalation. Highly soluble compounds such as ammonia, hydrogen chloride or sulfur dioxide immediately induce upper airway and ocular symptoms; chlorine, of intermediate solubility in water, has a similar effect. Because these effects are of very brief latency and are perceived as very unpleasant, exposed persons generally seek an early escape. Lower respiratory effects are less common with such agents unless exposures are intense enough to overwhelm upper airway absorption. Other irritant gases – notably ozone, oxides of nitrogen and phosgene – are far less soluble in water. They rarely give rise to immediate upper airway symptoms but if inhaled in sufficient quantities can induce terminal bronchial and alveolar disease. Other important characteristics of gaseous and other irritants include their pH and whether they are reactive oxygen species, and the presence and size of any particulate matter. Together with solubility and dose these determine, respectively, the mechanism and site of damage consequent on their inhalation. The range of potential outcomes from high-does irritant exposure is broad and includes disease in: 1. The upper airways – a burning sensation in the eyes, nose and throat is common in exposure to respiratory irritants; it is often accompanied by eye watering, sneezing,

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nasal discharge, hoarseness and, prominently, a cough. There may be evidence of corneal, conjunctival, oropharyngeal and dermal burns or ulceration. Very heavy exposures can cause upper airway obstruction due to edema and/or laryngeal spasm. This may require emergency treatment. 2. The large and small airways – acute pain, breathlessness, chest tightness and wheeze may each or all follow an inhalational injury. Again, exceptionally heavy exposures can cause epithelial sloughing and airway obstruction. 3. The alveoli – so-called ‘pneumonitis’ may result from inhalation of poorly soluble irritants or from very heavy exposure to those of higher solubility. Depending on the intensity of the insult, the features of ‘toxic’ or ‘chemical’ pneumonitis include increasing breathlessness, sputum (typically frothy-pink), bilateral radiographic shadowing (consistent with pulmonary edema) and the development of respiratory failure. These may not develop for as long as 72 hours after exposure; later complications may include adult respiratory distress syndrome and infection.

24.8 Management of the acute effects of high-dose irritant exposure Upper airway damage following exposure to a respiratory irritant is generally selflimiting but may require attention to burned or ulcerated areas in order to prevent their infection. There are no specific treatments for lower airway and alveolar damage, their management being essentially supportive and conservative, sometimes requiring intensive care. Because the effects of respiratory irritants (at high concentrations) may be delayed, careful observation for a period of up to 48 hours (or longer) may be necessary. Where there is a suggestion of widespread epithelial damage it is probably wise to administer oxygen sparingly. While corticosteroids are often used there is no convincing evidence for their efficacy in reducing immediate or long-term morbidity. Appropriate treatment with antibiotics is important.

24.9 Longer-term effects of acute exposures at relatively high intensity It must be stressed that most exposures to respiratory irritants do not induce any identifiable long-term respiratory disease. Recovery may, however, be delayed by the psychological effects of what can be a very traumatic experience.

24.10 Nonasthmatic diseases Intense exposures – usually acute but in some cases repeated (sub-acute) – giving rise to severe ‘pneumonitis’ may be followed by evidence of increasing and irreversible small airways obstruction. Obliterative bronchiolitis of this type may be accompanied by early inspiratory crackles on auscultation of the chest and by evidence of gas trapping (high

24.11

ASTHMA

351

residual volume) on pulmonary function testing. While chest radiography is usually normal, expiratory CT scanning will also suggest a mosaic pattern of gas trapping. Histological confirmation is rarely required but typically will confirm the obliteration of small airways with granulation tissue and fibrosis. Other, nonasthmatic sequelae of an inhalational injury include organizing pneumonia; this appears to be rare but has been best described following the inhalation of oxides of nitrogen at high intensities. Other interstitial lung diseases have been described after irritant inhalation but most often in small case series or by single case reports and their true frequency – and indeed relation to the incident – is unknown.

24.11

Asthma

Relatively high-intensity, acute exposures to respiratory irritants may also be followed by asthma – or at least a disease that shares many clinical features of asthma. Originally known as ‘reactive airways dysfunction syndrome’ (RADS) this was first described in 1985 in a series of 10 cases where very heavy respiratory exposures on a single occasion to toxic compounds (including fire smoke) were followed by the apparently new development of bronchial hyper-reactivity, variable airflow obstruction and symptoms of asthma. The criteria for establishing a diagnosis of RADS – as first set out – are shown in Table 24.3. Subsequently the question has arisen as to whether lower dose, perhaps repeated, exposures to respiratory irritants can similarly give rise to RADS – or, as it is more often termed now, irritant-induced asthma. This is a controversial area and the available literature, most of it epidemiological, is not consistent. Perhaps the most common consequence of an inhalational accident is a constellation of asthma-like symptoms in the absence of any detectable deficit in lung function, or increase in airflow variability or bronchial reactivity. In these cases symptoms of cough, chest tightness of breathlessness may be provoked by exposure to a very wide variety of commonly encountered irritants such as household aerosols, cleaning materials, perfumes, wet paint and petrol fumes. Accompanying symptoms such as fatigue and headache produce a picture of ‘multiple chemical sensitivity’. Alternatively, or in addition, a vocal chord dysfunction may develop. These outcomes are not necessarily

Table 24.3 The original criteria for a diagnosis of reactive airways dysfunction syndrome (RADS) – after Brooks, S., Weiss, M.A., Bernstein, I.L. (1985) Reactive airways dysfunction syndrome: persistent asthma syndrome after high-level irritant exposure. Chest 88: 376–384 Onset after a single, toxic exposure Onset within 24 hours of the exposure Symptoms consistent with asthma Evidence of subsequent airflow obstruction Evidence of subsequent nonspecific bronchial hyper-reactivity (metacholine or histamine challenge test) Documented absence of prior respiratory symptoms Other pulmonary disease excluded Nonsmoker

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relatable to any pre-incident psychological features but may be color by persisting anxiety.

24.12 Management of irritant-induced asthma For patients, and the clinicians of patients, with (suspected) irritant-induced respiratory disease, a common point of focus is the causative relationship between the inhalational incident and their disease. This may especially be so when a claim for personal injury is being made through the civil courts. While this is obviously important, it is not always possible to establish causation with any satisfactory degree of certainty. In some, perhaps many, cases an ultimately fruitless focus on etiology may hinder recovery. In any case it is important to establish with great care and as far as possible the details of the incident and those of the immediate clinical aftermath. Information on the nature of the released chemicals should be collected. Direct measures of exposure intensity are rarely available but estimates can be made from the quantity of released material, the nature of the environment in which the incident took place and the duration of exposure. Inthe research setting,mostincidents willtake place indoors; information onthe distance of the incident from the patient, the size of the room where it took place and the presence of any ventilation is helpful. In outdoor incidents, the prevailing weather (especially wind direction) may be an important determinant of exposure. A record of immediate responses – such as the use of protective equipment – and of immediate symptoms – such as burning of the eyes or nose – should be made. It is also helpful to establish whether colleagues were also exposed and, where possible, what has been their experience. Early measurements of lung function are valuable; as a minimum these should include measurement of basic spirometry but an early assessment of bronchial reactivity and, in some cases, of lung volumes and diffusion capacity is often helpful. It is generally appropriate to maintain clinical follow-up of patients with persistent symptoms until a clear prognosis and management can be established. This may require several years. Repeated measurements of lung function (often including bronchial reactivity), at judicious intervals, are advisable. As always with such measurements, their results are informative about the current state of the patient – but not of the past. Thus it is important, especially when considering etiology, to make an enquiry into the existence of any pre-incident measurements. In the research environment these are quite commonly made and retained by occupational health services. Irritant-induced asthma should be treated with usual asthma protocols but appears to respond less favorably to standard pharmacotherapies. On the whole, severe asthma is uncommon but any symptoms may be difficult to treat. The ultimate prognosis is uncertain but is probably dependent on the severity of the initiating incident and on age – and perhaps on psychological issues also. As always, and as in particular with work-related disease, careful attention to continuing work ‘fitness’ is important. In almost all cases, provided that there is minimal risk of a further incident, an early return to work is both appropriate and helpful. This should be organized in close liaison with the occupational health service. Organizing pneumonia – with or without obliterative bronchiolitis – may respond well to systemic steroids. Other types of interstitial lung disease and obliterative

24.13

OTHER RESPIRATORY DISEASES IN RESEARCH WORKERS

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bronchiolitis itself are, in this context, essentially untreatable. Very severe cases may need to be considered for lung transplantation.

24.13

Other respiratory diseases in research workers

24.13.1 Pulmonary infection Research workers who handle infectious material or work with infected animals or patients may themselves develop respiratory infection. Inhaled viral, bacterial, mycobacterial and even protozoal agents may be responsible. The diagnosis of such infections requires a low threshold of suspicion and a careful enquiry into potentially relevant exposures. Their management is by standard chemotherapy and the eradication of any further exposure to the infecting agent.

24.13.2 Beryllium sensitization and chronic beryllium disease Research workers in electronics and communications may, in the course of their work, be exposed to airborne particles of beryllium. Copper–beryllium alloys, for example, are commonly used in electrical components. Exposure is generally during grinding or other mechanical handling. In sensitive subjects, inhalation of beryllium can induce an asymptomatic state of beryllium sensitization that is detectable on lymphocyte transformation testing – an investigation available only in a few, specialized laboratories. While there is no evidence that beryllium sensitization alone has any short or longterm adverse consequences, further exposure to beryllium (unlikely in laboratory conditions) may cause chronic beryllium disease, a pulmonary condition that is clinically similar to sarcoidosis.

24.13.3 Lung cancer There is a long list of occupationally encountered agents that have been related, epidemiologically, to lung cancer. They include asbestos, arsenic, polycyclic hydrocarbons, chromates, beryllium, sulfuric acid mist, chloromethyl ethers, nickel compounds and tetrachlorodibenzene–para-dioxin. Laboratory exposures to any of these are very unlikely to be sufficiently high to induce carcinogenesis and in any case establishment of cause and effect at an individual level would be very difficult. However there are a few case reports of lung cancers in research staff that have been attributed, at least in part, to exposures they encountered at work.

24.13.4 Work with nanoparticles The use of artificial nanostructures in the research environment, as in a wider industrial context, will increase substantially. Such structures are very varied and include particles of solid, tubular and fibrous forms all of which, due to their size, are readily inhalable

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and have the potential for deposition deep within the lungs. There has been extensive research – not all of it encouraging – into their toxicity and there are considerable concerns around the hazards they may pose. The magnitude of any real risks to human respiratory health are as yet unknown.

24.14 Other occupational diseases among research workers Given the vast range of research it is unsurprising that those engaged in it face a large variety of other, nonrespiratory hazards. These are generally unconnected with the respiratory diseases described above. The most important of them include: 1. Infection, most probably following ‘needle-stick’ injuries, with blood-borne viruses such as hepatitis B. 2. Physical hazards such as those from lasers, from extremes of temperature (including hot and cold burns), from electrical equipment and from spilt liquids (falls). 3. Chemical splashes to eyes and skin. 4. Eye and musculo-skeletal strain from prolonged use of visual display equipment. 5. Radiation-induced diseases. Most research institutions will have high-quality health and safety management programmes that render the actual risks of most of the above low.

Further reading 1. For a referenced list of known respiratory sensitizing agents: Bernstein, I.L., Chan-Yeung, M., Malo, J.L., Bernstein, D.(eds) (2006) Asthma in the Workplace, 3rd edn. Taylor & Francis: New York; 415–435 and 825–866. 2. Similar material, albeit less complete, is available for free on the following websites: . www.occupationalasthma.com . www.asmanet.com . www.asthme.csst.qc.ca . www.eaaci.net 3. For those who wish to investigate for themselves the likely sensitizing potential of an inorganic chemical, free software and interpretation is available through: http://www.medicine.manchester. ac.uk/coeh/research/asthma/. The original paper is published as: Jarvis, J., Seed, M.J., Elton, R., Sawyer, L., Agius, R. (2005) Relationship between chemical structure and the occupational asthma hazard of low molecular weight organic compounds. Occup. Environ. Med. 62(4): 243–250. 4. For evidence-based guidance, based on a systematic literature review, on the diagnosis and management (and prevention) of occupational asthma including that arising in the research setting: Newman Taylor, A.J., Nicholson, P.J., Cullinan, P., Boyle, C., Burge, P.S. (2004) Guidelines for the Prevention, Identification and Management of Occupational Asthma: Evidence Review and Recommendations. British Occupational Health Research Foundation: London; available from: http://www.bohrf.org.uk/downloads/asthevre.pdf.

FURTHER READING

5.

6.

7.

8.

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Tarlo, S.M., Balkissoon, R., Beach, J., Beckett, W., Bernstein, D. et al. (2008). Diagnosis and management of work-related asthma, American College of Chest Physicians Consensus Statement. Chest 134: 1S–41S. A good summary of laboratory animal allergy is included in the following book chapter: Gordon, S., Bush, R.K., Newman Taylor, A.J. (2006) Laboratory animal, insect, fish and shellfish allergy. In Bernstein, I.L., Chan-Yeung, M., Malo, J.L., Bernstein, D. (eds), Asthma in the Workplace, 3rd edn. Taylor & Francis: New York; 415–435. Excellent summaries of irritant-induced respiratory disease are available in two chapters from the same book: Nemery B. (2002) Toxic pneumonitis: chemical agents. In Occupational Disorders of the Lung, Hendrick, D.J., Burge, P.S., Beckett, W.S., Churg, A. (eds). W.B. Saunders: London; 201–220. Schwartz, D.A. (2002) Toxic tracheitis, bronchitis and bronchiolitis. In Occupational Disorders of the Lung, Hendrick, D.J., Burge, P.S., Beckett, W.S., Churg, A. (eds). W.B. Saunders: London; 93–104. The original description of RADS: Brooks, S., Weiss, M.A., Bernstein, I.L. (1985) Reactive airways dysfunction syndrome: persistent asthma syndrome after high-level irritant exposure. Chest 88: 376–384. For a good study of the usual outcomes of inhalation accidents see: Sallie, B., McDonald, C. (1996) Inhalation accidents reported to the SWORD surveillance project 1990–1993. Ann. Occup. Hyg. 40: 211–221.

25 Work in hyperbaric environments Mark Glover St Richard’s Hospital, Chichester, West Sussex, UK

25.1 Introduction This chapter summarizes issues of both direct and indirect relevance to the respiratory tract that are encountered when exposed to environmental pressure raised above that found at sea level (normobaric). Raised (hyperbaric) environmental pressure is achieved either by diving in a fluid or by entering dry pressurized environments such as underground works and recompression chambers. Humans have been exposed to elevated pressures for subsistence, work or pleasure ever since the first person dived underwater. Over many thousands of years breath-hold diving developed from a means to collect food for survival into profitable, if hazardous, industries which harvested food and other desirable natural items and salvaged lost valuables from shallow waters. Man’s desire to go deeper for longer was realized in the sixteenth century through the use of diving bells. These upturned air-filled vessels could be lowered underwater and the diver could enter to take a breath of air without needing to return to the surface. Various methods of delivering breathing gases to individual divers have since been developed and are broadly divided into those that are self-contained and those that are supplied via hoses. Each of these categories is further divided into equipment that recycles exhaled breath for re-inhalation and equipment that does not. As early as the seventeenth century well-intentioned and innovative individuals built precursors to modern hyperbaric chambers. Patients sitting inside these vessels were exposed to minimally raised or lowered pressure in an attempt to treat a range of diseases. In the nineteenth century, mining and building works proliferated and became increasingly ambitious. Ingress of water was a problem for underground works near to an expanse of water, and also for a caisson sitting on a sea or river bed. Increased

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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pressure was used to minimize this problem. The miners, tunnelers and caisson workers who worked in these conditions were also subjected to elevated pressure, but without immersion. These techniques are still used today. Working breath-hold divers exist to the present day. There is now also a welldeveloped competitive sport based on breath-hold diving, although increasingly elaborate equipment, from suits and fins to weights and buoyancy devices, is required to allow the boundaries to be pushed ever further. The current record for depth on a single breath-hold is in excess of 200 meters. Most recreational divers breathe compressed air, via a demand valve, supplied from a cylinder worn by the diver in an assembly known as self-contained underwater breathing apparatus (SCUBA). The diver’s exhaled air is released into the surrounding water. Equipment using this principle is known as ‘open circuit’. See Figure 25.1. Other gases mixed with oxygen are used for breathing by commercial divers and by ‘technical divers’ amongst the recreational fraternity when they wish to dive deeper than the usual recreational range. It is not unusual for breathing gas to be delivered to commercial divers by hose from the surface or from a bell with the advantage of greater endurance and assured communication with the surface but the disadvantage of limited mobility. Another form of underwater breathing apparatus allows the diver to rebreathe exhaled gas once it is scrubbed clean of carbon dioxide and the oxygen is replaced. These ‘rebreathers’ minimize wastage of expired gas. The advantage of greater gas economy comes at the cost of greater complexity and a requirement for more extensive maintenance and training. As depth and ambient pressure increase, the inhaled gas is compressed more, so that a greater ‘surface equivalent’ volume of gas is wasted in each breath in an open-circuit system. Rebreathers avoid this depth-related increase in gas consumption. In ‘closed’ rebreathers no gas escapes from the system when at a steady depth. ‘Semi-closed’ sets produce a constant stream of excess gas, but in volumes that are generally much less than from an ‘open-circuit system’ (Figures 25.2–25.4).

Figure 25.1 Open-circuit SCUBA. 1, Compressed gas. 2, First stage reduces gas pressure to a few bars above ambient. 3, Second stage delivers gas to diver at ambient pressure. 4, Exhaled gas bubbles disperse in water

25.1

INTRODUCTION

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Figure 25.2 Closed circuit oxygen rebreather. 1, Oxygen added to counterlung either manually or by a demand valve mechanism. 2, Relief valve to allow expanding gas to escape from counterlung on ascent. 3, Mouthpiece – one-way valves ensure that gas goes only in one direction in the circuit. 4, Exhaled gas passes through a carbon dioxide absorbent before returning to the counterlung

Figure 25.3 Semi-closed circuit rebreather. 1, Reducer delivers a constant mass of gas per unit time to the counterlung throughout dive and at all depths; proportion of oxygen is calculated to avoid hypoxia and hyperoxia between surface and maximum intended depth; rate is calculated to accommodate expected oxygen consumption; extra gas added either manually or automatically to make up for volume lost on descent. 2, Relief valve to allow gas to escape from counterlung 3, Mouthpiece – one-way valves ensure that gas goes only in one direction in the circuit. 4, Exhaled gas passes through a carbon dioxide absorbent before returning to the counterlung

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Figure 25.4 Automated closed circuit mixed gas rebreather. 1, Sensors monitor oxygen levels in the circuit and oxygen or mixture is added to the counterlung to maintain oxygen at the desired level; nonautomated versions require the diver to add the required gas; extra gas added either manually or automatically to make up for volume lost on descent. 2, Relief valve to allow expanding gas to escape from counterlung on ascent. 3, Mouthpiece – one way valves ensure that gas goes only in one direction in the circuit. 4, Exhaled gas passes through a carbon dioxide absorbent before returning to the counterlung

For deep, long dives commercial divers can remain at pressure for weeks at a time, traveling between working depth and the surface in a pressurized diving bell. Shifts of some 6–8 hours are spent working in the water with rest periods in a dry, pressurized chamber facility on-board a diving support vessel. This is known as saturation diving (Figure 25.5).

Figure 25.5 Hyperbaric exposures. 1, Tunnel. 2, SCUBA. 3, Surface supply. 4, Bell. 5, Saturation

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Hyperbaric chambers are now used to treat decompression illness (DCI) and a range of other conditions which, for therapeutic effect, require inspired partial pressures of oxygen greater than those that can be achieved at sea level. Commercial and recreational divers are exposed to both raised pressure and immersion. Tunnelers, caisson workers and hyperbaric chamber staff are, in general, exposed solely to raised pressure. Surface-oriented working divers return to normobaric conditions after each dive. The depth and duration of the dive dictate the rate at which they may ascend. These divers are transported to and from their worksite in the water either by their own propulsion, by small powered vehicles, or lowered in a basket or in a bell which can be fully closed or partially enclosed. Tunnelers and hyperbaric chamber workers enter enclosed spaces which are compressed to allow them to work in a pressurized environment and then decompressed to allow them to return to normal atmospheric pressures. In the UK the annual fatal accident rate for all diving at work activities is estimated at 6–7 per 100,000. There are approximately three cases of DCI each year in the offshore sector. This can be compared with the UK recreational sector in which, among perhaps 100,000 divers, there are approximately 16 fatalities and 200–250 cases of DCI per year – and with compressed air work which is associated with some 25 cases of DCI (in approximately 2000 workers) per year. An exposure is quantified primarily by the mixture(s) of gases breathed, the ambient pressure and duration for which each is breathed and whether the individual is immersed. Pressure is typically expressed as a depth in diving, increasing by approximately 100 kPa for each descent of 10 m (or 33 feet) in seawater. In compressed air work pressure is typically measured in bars of overpressure above atmospheric (1 bar is approximately 100 kPa). The permitted overpressure is usually limited to 3.5 bars in the UK. There is a considerable amount of information beyond basic quantification of the exposure that can be collected to assist in diagnosis and management of pressure-related disorders. This information, and its significance, is summarized in Tables 25.1 and 25.2. Exposures are typically recorded in the individual’s personal logbook and, in the case of commercial exposures, in the records kept by the employer. Each entry will usually describe pressure/depth, duration, environmental conditions, breathing equipment, gas(es) and decompression schedule used plus a note of any adverse incidents.

25.2

Respiratory hazards, diseases and their management

25.2.1 Acute pulmonary effects of immersion Water is much denser than air. Differential pressures applied to the body are negligible in air. They become significant in water to the extent that effort of ventilation may be noticeably affected unless the mouth is at the same depth as the lungs. The pressure also neutralizes gravitational pooling of blood in dependent limbs, redistributing blood to the thorax, increasing right heart filling, inducing an immersion diuresis and reducing lung capacity. This redistribution is potentiated by cold so, while head-out immersion in thermoneutral water at 35 C reduces vital capacity by 5%, it will fall by 10% in water at 20 C.

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Table 25.1 Points to explore in the history of an individual with symptoms and signs attributed to exposure to raised environmental pressure – details regarding the exposure Item

Significance

Occupation/pastimes

Useful for identifying any relevant additional exposures, e.g. respiratory sensitizers For example, surface-orientated, saturation, dry, immersed Immersion pulmonary edema, saltwater aspiration syndrome and near-drowning require immersion Immersion increases the risk of cerebral oxygen toxicity For example, SCUBA, open-circuit or rebreather, semi-closed, fully-closed Resistive load or large dead space in any diving equipment and absorbent failure or one-way valve malfunction in a rebreather are potential causes of hypercapnia Elevated PICO2 increases risk of cerebral oxygen toxicity Potential for diver to consume oxygen faster than it is delivered in a semi-closed rebreather can cause dilution hypoxia or hypoxia of ascent Potential for exhaled inert gas to accumulate in a closed-circuit pure oxygen rebreather leading to risk of dilution hypoxia or hypoxia of ascent It is possible to rupture the respiratory tract with forceful exhalation against resistance or by overpressurizing the breathing circuit Hyperventilation before a breath-hold dive increases the risk of hypoxia For example, temperature, visibility, current, surface conditions Immersion pulmonary edema typically occurs in divers in cold water or who have been working hard, such as swimming against a current, exercise, shivering This might not be an illness induced by immersion or pressure. Remember to ask about other potential exposures, e.g. breathing gas contaminants, dust, hydrocarbon fumes, welding fumes, underwater blast, and their relationship to the onset of symptoms Anxiety is a risk factor for cerebral oxygen toxicity These data are required to calculate decompression obligation. Post-incident gas analysis data might be available CNS oxygen toxicity unlikely to occur in a dry chamber at PIO2 below 200 kPa CNS oxygen toxicity can occur if PIO2 exceeds approximately 140 kPa while immersed. A hyperoxic seizure can lead to drowning, near-drowning, aspiration or an uncontrolled ascent with closed glottis causing pulmonary barotraumas  DCI Pulmonary oxygen toxicity can occur if PIO2 exceeds 50 kPa. Units of Pulmonary Toxic Dose can be calculated to assess potential Acute hypoxia can occur if PIO2 falls below 15 kPa A depressurization from a depth of 1 m or greater in water can cause rupture by pulmonary overinflation. A dive on air or another oxygen nitrogen mixture at a depth of 30 m or deeper increases risk of hypercapnia in a CO2 retainer

Type of exposure

Equipment

Other environmental information

Timing and nature of untoward incidents

Depths/durations/inspired gas mixtures

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Table 25.1 (Continued) Item Gas consumption

Rapid or uncontrolled ascents Omitted decompression stops Method used to calculate decompression Activities during dive

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Significance Voluntary hypoventilation in order to conserve open circuit gas supply is a risk factor for hypercapnia It is possible to rupture the respiratory tract with a maximal inhalation; this might be an important mechanism in the rupture of lungs in divers who ‘skip-breathe’, deliberately holding themselves in prolonged inspiration in an attempt to reduce gas consumption Risk factor for pulmonary barotrauma and for DCI Risk factor for DCI For example, decompression table, computer, instinct Allows potential for omitted decompression to be assessed Hypercapnia typically occurs in divers who have been working hard at depth Working hard is a risk factor for cerebral oxygen toxicity

25.2.2 Pulmonary oxygen toxicity Atelectasis can occur when breathing a high fraction of oxygen in normobaric and hyperbaric conditions. Breathing oxygen at partial pressures greater than 50 kPa can cause additional pathological changes of inflammation spreading from the carina, suppression of surfactant production and eventual fibrosis of respiratory epithelium. The greater partial pressures of oxygen achievable in hyperbaric environments accelerate the pathological process. Symptoms and signs range from an isolated sensation of airway irritation through crackles and wheezes, fever, thick secretions and bronchial breathing, to respiratory failure due to impaired gas exchange across inflamed respiratory epithelium. Lung volumes, flows, compliance and gas transfer all deteriorate, and the earliest changes usually precede symptoms. Large, rapidly reversing flow changes are more likely to be due to bronchoconstriction mediated vagally following a direct toxic effect of oxygen on the central nervous system. Management of pulmonary oxygen toxicity Clinical findings and results of investigations will depend on the severity of the condition. Sometimes bilateral opacities are seen on chest X-ray. Treatment requires the inspired partial pressure of oxygen to be reduced to 50 kPa or lower. Most changes apart from fibrosis are reversible and symptoms will start to improve within 2 hours. They are expected to resolve within 3 days of cessation of exposure, although an upper respiratory tract infection soon after the exposure can provoke symptom recurrence. Lung function improves rapidly at first, but a complete return to normal can take several weeks. It is possible to predict the likely pulmonary consequences of an oxygen exposure using the concept of units of pulmonary toxic dose (UPTD). The relationship between UPTDs and clinically measurable variables is non-linear (see Figures 25.6 and 25.7) and there is considerable inter-individual variation. Oxygen toxicity is prevented by limiting duration and/or magnitude of exposure. Saturation divers, for instance, often spend several weeks at pressure and breathe

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Table 25.2 Points to explore in the history of an individual with symptoms and signs attributed to exposure to raised environmental pressure – post-exposure details Item

Significance

Flying or other altitude exposure after dive

Risk factor for DCI, impact decreases the longer the delay after diving. Recommended delay can be up to 48 hours depending on type of diving Working hard after a dive increases the number of circulating bubbles and is believed to be a risk factor for DCI DCI, pulmonary barotrauma of ascent and hypoxia of ascent can arise only once decompression has begun Signs and symptoms of pulmonary oxygen toxicity, DCI, pulmonary barotraumas, immersion pulmonary edema, saltwater aspiration syndrome and neardrowning persist for some time beyond acute provocative exposure. Signs and symptoms of hypoxia typically do not. The respiratory symptoms of hypercapnia will resolve rapidly on termination of the exposure but a throbbing headache typically persists DCI can occur during decompression in saturation diving. In most other circumstances 50% of DCI cases will manifest within 1 hour of surfacing and 90% within 6 hours The initial symptoms of arterial gas embolism typically present during the ascent or within the first 10 minutes after surfacing. Hemiplegia, hemiparesis and reduced level of consciousness commonly occur. It is not unusual for the condition to improve then relapse later In view of the indiscriminate nature of the bubbles, it is not unusual to have a number of manifestations, for them to appear at different times and to evolve in different ways For example, normobaric oxygen, fluids, recompression Although normobaric oxygen is an important first aid measure it can mask symptoms and signs of DCI which then appear when the treatment is discontinued Remember that a response to recompression does not necessarily confirm a diagnosis of DCI and that a failure to respond does not necessarily exclude DCI Remember that other disorders can present coincidentally Pyrexia is thought to be a risk factor for cerebral oxygen toxicity

Activities after dive Timing, severity, nature, rate of onset and subsequent evolution of manifestations

Response to treatment

Past medical history, including any previous diving illness

oxygen at partial pressures of around 50 kPa without clinically important deterioration in lung function. Tolerable exposure will depend on necessity. If a patient with serious DCI required aggressive hyperbaric oxygen therapy, it would be reasonable to allow some reversible lung changes in order to maximize resolution of a functionally important neurological deficit. The wide variation in individual susceptibility means that a decision on the amount of oxygen administered is often empirical, being guided by the response of the patient.

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Figure 25.6 Units of pulmonary toxic dose accumulated per minute plotted against inspired partial pressure of oxygen

25.2.3 Decompression illness At raised environmental pressure gas accumulates in the tissues in increasing quantities until, eventually, a dynamic equilibrium is reached. At this point equal amounts of gas diffuse into and out of the tissues and they are ‘saturated’ at that pressure. An increase in ambient pressure will encourage more gas to dissolve. A decrease will cause excess gas to be released. The amount of gas that needs to be safely eliminated from each tissue during the return to surface pressure, and hence the decompression schedule required, will depend on the pressure and duration of the exposure. If the tissues are all saturated, however, no more gas will accumulate and the required decompression schedule will

Figure 25.7

Change in vital capacity plotted against units of pulmonary toxic dose

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Table 25.3 Decompression obligations of different durations of exposure at approximately 3.5 bar above atmospheric pressure. All from the 6th revision of the US Navy Diving Manual except asterisked entry which is from UK Blackpool tables for compressed air workers Gas breathed

Time at pressure

Time required to depressurize

Air Air Air  Oxygen in helium, PIO2 < 130 kPa Oxygen in helium, PIO2 < 130 kPa Oxygen in helium, PIO2 < 48 kPa and >44 kPa

10 minutes 40 minutes 4 hours 15 10 minutes 40 minutes Saturation – potentially unlimited

4 minutes 56 minutes 344 minutes 35 minutes 78 minutes 2700 minutes

not change thereafter. This is the basis of saturation diving. See Table 25.3 for some representative decompression times. Decompression illness is caused by gas bubbles that can arise in the body in two ways. Gas can ‘escape’ from ruptured lungs, enter the pulmonary veins, return to the left side of the heart and then be distributed around the body causing arterial gas embolism. Alternatively, as the excess gas dissolved in tissues at pressure is liberated (or ‘evolved’) on depressurization, it can form bubbles. Bubbles usually accumulate intravascularly but can be extravascular if the decompression is of sufficient rate and magnitude. It is not unusual for bubbles to appear in venous blood on decompression. Moderate quantities are harmlessly trapped in the alveolar capillaries where the gas they contain diffuses out rapidly and is exhaled. The filtered blood then returns to the left heart. A right–left circulatory shunt, such as a patent foramen ovale or a pulmonary arteriovenous shunt, can potentially allow venous gas emboli to bypass the pulmonary ‘filter’. If the filtering capacity of the lungs is overwhelmed, bubbles can spill over into the systemic circulation or even compromise the lungs’ abilities to exchange gas. In more severe cases, the pulmonary circulation can be threatened. Inert gases such as nitrogen and helium are the primary sources of ‘evolved’ bubbles. Oxygen is constantly consumed by aerobic metabolism. Carbon dioxide is highly soluble, is buffered extensively and diffuses rapidly. As a result, oxygen and carbon dioxide are believed to contribute insignificantly to ‘evolved’ gas disease in normal circumstances. A higher fraction of inert gas in the breathing mixture will, therefore, increase the decompression obligation for a given pressure exposure. Bubbles can block vessels from inside (as arterial emboli or by venous congestion) or outside, causing ischemia, they can tear apart structures and cause bleeding, they can damage vascular endothelium and can act as foreign bodies which trigger pathological reactions such as inflammation and activation of clotting mechanisms. Decompression illness can manifest in many ways. Bubbles do not necessarily respect normal anatomical boundaries and patchy or multi-system presentations are not uncommon. It is a dynamic disease. Manifestations can be progressive, static, relapsing, resolved or spontaneously improving and their evolution can change. The disease can range in severity from trivial and self-limiting to disabling or life-threatening. Cardiopulmonary manifestations are rare but range from cough or mild dyspnea, through shortness of breath, chest pain, hemoptysis, cyanosis and edema, to frank

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cardiopulmonary arrest. This extreme is associated with very severe decompression stress such as explosive decompression to altitude and is, fortunately, seen only very rarely. Neurological symptoms are common and can range from subjective sensory alteration through subtly impaired higher mental function to loss of consciousness, motor weakness, incoordination and sphincter dysfunction. Limb pain is also common, typically beginning as an ill-defined pain which settles in one or more large limb joints. Girdle pain, which has a distribution along one or more thoracolumbar dermatomes, is often a herald of more severe decompression illness. Cutaneous decompression illness ranges from pruritis through erythema, papular rash to skin marbling due to ischemia. The marbling, known as cutis marmorata, is often painful and tender and, if it presents acutely, is usually considered an indicator of severe decompression stress and a precursor of more serious symptoms. DCI can cause enlarged or painful lymph nodes and/or swelling of the area drained by the affected lymph vessels. Constitutional manifestations are those that cannot be readily associated with any one organ system and include malaise, loss of appetite, nausea, vomiting, headache and inappropriate fatigue. Management of decompression illness The first step is prompt diagnosis. Bear in mind that:

1.

decompression illness can mimic many other conditions and vice versa;

2.

pressure exposures can cause problems other than decompression illness, some unique to the hyperbaric environment and some found in other circumstances; and

3.

there might be other medical conditions in addition to decompression illness; a traumatic incident with a riveting tool or an acute myocardial infarction might, for example, prompt the diver to make a rapid return to the surface.

First aid treatment for decompression illness is the same as for most other conditions. Airway, breathing and circulation take priority. Oxygen should be given at as high an inspired fraction as possible. Hypovolemia is common, caused by immersion diuresis, vomiting and/or bubble-mediated endothelial damage. Restore circulating volume by oral or intravenous administration of fluid, as appropriate. Avoid intravenous glucose if there are any neurological manifestations. In the event of prolonged immobility, consider thromboprophylaxis. The definitive treatment for decompression illness is recompression. Many cases caused by surface-oriented diving are treated at 284 kPa breathing 100% oxygen following a ‘standard recompression therapy’ schedule that returns to surface pressure in slow steps over 4 hours and 45 minutes. Other schedules are used and the choice depends on circumstances and the response to the initial recompression. Outcome of recompression therapy depends primarily on the severity of the illness prior to treatment. Typically, approximately 50 % require only one treatment to achieve complete resolution and 70% require one or more treatments. The remainding 30% are left with residual symptoms ranging in severity from minor sensory symptoms to profound neurological deficit. In the event of ‘undeserved’ decompression illness where decompression was adequate yet sufficient inert gas accumulated to create venous gas emboli, it is

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appropriate to screen the individual for right–left shunt using bubble-contrast echocardiography prior to a return to hyperbaric exposures.

25.2.4 Pulmonary barotrauma of descent Although thoracic blood shift compensates for loss of gas volume and the lungs can tolerate compression far beyond residual volume, extreme exposures will cause damage leading to edema and hemoptysis.

25.2.5 Pulmonary barotrauma of ascent Pressure-related change in volume in gas-filled spaces in or next to the body can inflict mechanical damage known as barotrauma. Injury can be avoided if the spaces are ventilated and gas can pass in and out as it expands and contracts. Studies have shown that fresh cadaveric lungs rupture if overpressurized by approximately 9 kPa. If the chest is bound, hence limiting lung expansion, rupture occurs at 14 kPa overpressure and the damage occurs at different sites compared with when the chest is not bound. A similar overpressure could be generated by an ascent in water of the order of 1 m in a fully inflated, obstructed lung segment or in lungs held at full capacity against a closed glottis. Gas can escape from the respiratory tract, including extrapulmonary sites, resulting in one or more of pneumothorax, pneumomediastinum, subcutaneous emphysema, pulmonary interstitial disruption and arterial gas embolism. Management of pulmonary barotrauma of ascent Symptoms and signs are the same as those of lung injury and rupture by other mechanisms. First aid management of symptomatic cases is directed at care of airway, breathing and circulation and administration of high fraction inspired oxygen. Arterial gas embolism is a form of decompression illness and requires recompression. A pneumothorax is managed in the same way as one caused by trauma or that has occurred spontaneously. Pneumomediastina are often asymptomatic, can present solely with voice change, and only 50% are visible on a P-A chest X-ray. High fraction inspired oxygen, rest and observation are often required in symptomatic cases. In studies of submarine escape trainees, victims of pulmonary barotrauma are more likely to have a low forced vital capacity. Reduced compliance and lack of support from the chest wall are two theoretical reasons offered to explain this finding. A low expiratory ratio (FEV1/FVC), however, has not been shown to be a risk factor. This might be because candidates with significant obstructive defects are likely to have been disqualified from submarine escape training. Nevertheless, a low forced vital capacity (less than 80% of predicted), peak expiratory flow (less than 80% of predicted) or low expiratory ratio (less than 70%) deserves investigation to exclude airway narrowing or gas trapping prior to hyperbaric exposures. Further investigation is indicated following pulmonary barotrauma of ascent or following a decompression illness consistent with arterial gas embolism even if there were no lung symptoms. Gas trapping, fixed or reversible airway narrowing or any other predisposition to pulmonary rupture or overinflation should be excluded.

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High-resolution CT may be required if there is any uncertainty. Even if no abnormality is found, sufficient time should be allowed for the respiratory tract to heal; recommended periods typically vary between one and three months.

25.2.6 Barotrauma of other structures Other targets of barotrauma of descent include the middle and external ear, paranasal sinuses, carious teeth, whole body and soft tissues under dry suit or mask. Barotrauma of ascent can affect the middle ear, paranasal sinuses, gastro-intestinal tract and carious teeth. Bleeding from sinuses or from the Eustachian tube following a barotraumatic injury can present as hemoptysis and can usually be distinguished from pulmonary barotrauma by examining the ear, nose and throat to establish the most likely source of bleeding.

25.2.7 Hypoxia Hypoxia is less likely to occur in a pressurized environment as the partial pressure of oxygen is elevated in proportion to the ambient absolute pressure. It can, however, occur if the wrong gas mixture is selected, if the wrong procedure is adopted when using rebreather equipment and in breath-hold diving. As the inspired partial pressure of oxygen falls progressively below 20 kPa, mental and physical function deteriorate in the same manner as from hypoxia in other circumstances. The clinical picture and the rapidity of onset depend on the rate of oxygen depletion and the final partial pressure reached. Consciousness will be prolonged if PACO2 is elevated, causing cerebral vasodilatation and enhancing brain perfusion.

25.2.8 Hypoxia of ascent If a mixture of gases is compressed, the partial pressure of each component gas increases in proportion to the total pressure. As the gas is depressurized, such as when a diver returns to the surface, the partial pressure of each component gas falls. In normal circumstances the rising partial pressure of carbon dioxide, rather than the drop in oxygen, will force a breath-hold diver to take a breath. As the diver surfaces the partial pressure of oxygen falls, but usually not far enough to compromise consciousness. Hyperventilation before a dive reduces the PACO2. This delays the hypercapnic stimulus to take a breath and loss of consciousness on ascent due to hypoxia can potentially result in fatality. This can even occur in a relatively shallow swimming pool.

25.2.9 Dilution hypoxia A fault in equipment design or set up can allow a diver to consume oxygen faster than it is delivered to a semi-closed rebreather circuit. The fraction of oxygen falls but, because

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diluent inert gas remains in the circuit, the diver has limited warning of any problem until the inspired partial pressure of oxygen is dangerously low. The diver can either lose consciousness at depth or as the partial pressure of oxygen drops further during the ascent. Management of hypoxia Treatment of hypoxia is administration of oxygen in addition to basic supportive measures. Hypoxia is prevented by maintaining inspired partial pressure of oxygen at a minimum of 15 kPa, and ideally above 20 kPa. Inert gas diffuses out of tissues when 100% oxygen is breathed. Divers using closed-circuit oxygen rebreathers avoid dilution hypoxia by flushing the breathing circuit with oxygen early in the dive to ensure that the inert gas does not accumulate. Divers using semi-closed rebreathers anticipate how hard they will be working and ensure that their oxygen delivery will be sufficient to avoid dilution hypoxia; they also flush the breathing circuit with fresh gas prior to ascent to avoid hypoxia of ascent.

25.2.10 Immersion pulmonary edema Some divers develop pulmonary edema while immersed and in the absence of any obvious aspiration or pulmonary or cardiac abnormality. The diver complains of cough, sometimes productive of blood and/or frothy sputum. Syncope has also been reported but not chest pain. Typically the immersion has involved either cold water or strenuous exercise. Investigation of individuals who have suffered from immersion pulmonary edema has revealed that they have higher peripheral vascular resistance and an atypical dramatic further rise in response to cold challenge. It is thought that the balance between pulmonary capillary pressure and plasma oncotic pressure is disrupted by hemodynamic changes associated with immersion plus either cold-induced systemic vascular resistance or increased cardiac output on exercise. Excessive rehydration and inspiratory resistance from airway narrowing or faulty equipment have also been suggested as potential additional factors. Management of immersion pulmonary edema Exclude other causes of acute pulmonary edema. Symptoms typically resolve within hoursbut thirdheartsounds,basalcrackles andX-raychanges consistentwithpulmonary edema might be found earlier. Treatment is rest and oxygen. The edema usually resolves within hours although diuretics may be required in more severe cases. Some 1.1% of respondents reported symptoms suggestive of pulmonary edema in one survey of divers. Some have experienced recurrent episodes and should be advised against diving.

25.2.11 Saltwater aspiration syndrome Aspiration of small amounts of salt water can induce a cough, sometimes productive, and with frothy hemoptysis in a minority, immediately after a dive. The diver then develops more respiratory symptoms, typically dyspnea, cough and retrosternal discomfort with wheeze on chest examination and patchy consolidation in a proportion

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of chest X-rays. These symptoms develop rapidly in severe cases and after a latent period of 1–2 hours in milder cases. In addition, systemic features of pyrexia, rigors, anorexia, nausea and vomiting, headaches, malaise, aches and even impaired consciousness may occur. Management of saltwater aspiration syndrome This occurs less frequently now as diving equipment has improved, reducing the risk of aspiration. Investigation is required to exclude any other cause of the symptoms. White cells can be elevated, PAO2 is often low and PACO2 low or normal. Respiratory symptoms are treated with oxygen and the systemic symptoms often respond to warming. Most cases resolve within 6–24 hours.

25.2.12 Drowning and near-drowning Despite the many illnesses unique to diving, the most common end-point in fatal incidents is drowning. The clinical features, diagnosis and management of drowning and near-drowning are not unique to hyperbaric exposure and are not dealt with in this chapter.

25.2.13 Hypercapnia Hypercapnia is an important complication and a limiting factor in hyperbaric environments. Experienced divers often hypoventilate involuntarily. The reason for this is not fully understood. Gas density increases in proportion to ambient pressure and breathing equipment introduces extra resistance, so work of breathing, oxygen consumption and carbon dioxide production all increase in hyperbaric conditions. Oxygen is typically delivered at higher than normal partial pressures so it is seldom limiting. It has been suggested that the body adapts to this situation by tolerating a higher PACO2 in order to minimize the work of breathing. Hyperoxia might have an additional effect of reducing basal ventilatory drive and response to exercise. The denser gas also directly affects the ventilation of the lungs such that physiological dead space increases and maximal voluntary ventilation decreases. As a result, carbon dioxide elimination becomes more critical than oxygen delivery when working hard at pressure. Apart from its direct toxic effects, which are well recognized in other clinical situations and are not listed here, high levels of carbon dioxide have other relevant consequences. Vasodilatation accelerates heat loss from superficial vessels in a cold environment and might accelerate delivery of inert gas to tissues. The carbon dioxide also potentiates the narcotic effects of inert gases such as nitrogen and lowers the threshold for cerebral oxygen toxicity. Management of hypercapnia Symptoms and signs are seldom sufficiently unique to make a diagnosis, although a persistent throbbing headache is traditionally associated with hypercapnia. Dependent on the precise cause, aim to reduce the inspired partial pressure of carbon dioxide, reduce its endogenous production and/or increase its elimination. Changing to a

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non-contaminated gas (including fresh air at the surface), increasing ventilatory rate and tidal volume, reducing activity and moving to a shallower depth are options that will be appropriate, according to the circumstances. Preventive measures include ensuring that: 1. the breathing gas is not contaminated; 2. activity is limited to safe levels; 3. equipment complies with breathing standards; 4. absorbent is packed to avoid settling or formation of low-resistance ‘channels’; 5. equipment is functioning correctly. Less dense gas mixtures instead of air, such as heliox (oxygen in helium) or trimix (oxygen in a mixture of helium and nitrogen) can also minimize the density-related problems. A small population hypoventilates and develops hypercapnia even when diving in moderately raised pressures. Other than monitoring their physiological response while diving, it is difficult to identify these individuals. Although they often have a reduced ventilatory response to PICO2 or a raised end-breath-hold PACO2, these measurements lack sufficient specificity and sensitivity for effective screening. A smaller proportion of non-divers also have this tendency. Although these carbon dioxide retainers are economical with gas consumption and have little or no dyspnea, they are not protected from the indirect effects of hypercapnia mentioned above. Also, they are not immune to hypercapnic narcosis and will receive little dyspnoeic warning of rising PICO2 in the event of equipment malfunction. Use of a less dense mixture, such as oxygen-in-helium, also reduces the tendency to retain carbon dioxide in this group.

25.2.14 Central nervous system toxicity Symptoms that are commonly attributed to oxygen toxicity are visual disturbances, tinnitus, irritability and dizziness. Appearance of any of these symptoms often heralds a generalized seizure if the inspired partial pressure of oxygen is not reduced promptly. The seizure can also occur without warning. Management of central nervous system toxicity Details of management will depend on whether the symptoms occur in a dry environment or while diving. Reduce the inspired partial pressure of oxygen if at all possible and safe to do so. Avoid depressurization until the seizure has resolved as the glottis can be closed during the tonic phase, predisposing to pulmonary barotrauma. Keep the casualty safe from harm during the seizure, which is usually short-lived. The post-ictal phase can be prolonged. In a hyperbaric chamber, patients often breathe air between periods on high-oxygen therapeutic gas in order to reduce the risk of toxicity. While diving, the risk is reduced by keeping the inspired partial pressure within a safe range, typically below 140–160 kPa depending on circumstances and level of activity.

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FURTHER INFORMATION

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25.2.15 High pressure neurological syndrome Dives to great depths typically use mixtures which contain a large fraction of helium. Such dives are associated with a disorder characterized predominantly by dysfunction of the central nervous system, known as the high pressure neurological syndrome (HPNS). At depths in excess of 300 m divers complain of dyspnea which is worse on inspiration. The symptoms are lessened by the addition of nitrogen to the breathing mixture, despite the fact that this makes the gas denser and increases the work of breathing. Nitrogen can be used to counter some of the other effects of HPNS so the symptoms are probably due to neurological interference with the control of breathing rather than a direct effect upon the lungs. The effects resolve on depressurization.

25.2.16 Long-term pulmonary effects Divers tend to have larger lung volumes than expected. Suggested reasons for this include divers being a self-selecting fit population and respiratory muscle training from breathing dense gas against resistance in the diving equipment. Forced vital capacity (FVC) tends to be enlarged proportionately more than FEV1, which gives many divers a lower FEV1/FVC expiratory ratio. Mid and late expiratory flows have also been found to be lower in divers, with some evidence of a relationship with length of diving career, and this might be an indication of small airway changes. In addition, lung volumes appear to decline at a faster rate than expected in some longitudinal studies of divers. Diffusing capacity is impaired after a saturation dive, possibly due to low grade oxygen toxicity and bubble damage, but it is thought that this recovers gradually following the exposure. Despite these findings, no structural changes have been demonstrated on imaging and the no clinically relevant consequences have been found.

25.2.17 Respiratory aspects of fitness for hyperbaric exposure In general, normal pulmonary function is required for hyperbaric exposures. Impaired gas flow could predispose to barotraumatic injury. Depending on severity, deficient gas exchange will restrict the candidate’s ability to cope with the respiratory demands of the hyperbaric environment, the work routinely required within it or emergency actions that might arise. The British Thoracic Society has produced very useful Guidelines on Respiratory Aspects of Fitness for Diving.

25.3

Further information

Further information on activities involving hyperbaric exposures can be obtained from: Regulatory bodies .

UK Health and Safety Executive: http://www.hse.gov.uk/

.

Occupational Safety and Health Administration: www.osha.gov

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Advisory bodies .

Compressed Air Working Group: http://www.britishtunnelling.org.uk/groups_ safety.php

.

European Diving Technology Committee: http://www.edtc.org

.

European Committee for Hyperbaric Medicine: http://www.echm.org

.

International Maritime Contractors Association: www.imca-int.com

.

Diving Medical Advisory Committee: http://www.dmac-diving.org

Recreational diving organizations .

UK Sport Diving Medical Committee: http://www.uksdmc.co.uk/

.

British Sub-Aqua Club: http://www.bsac.com

.

Professional Association of Diving Instructors: http://www.padi.com

.

Divers Alert Network: http://www.diversalertnetwork.org

Diving and hyperbaric medicine societies .

European Underwater and Baromedical Society: http://www.eubs.org

.

British Hyperbaric Association: http://www.hyperbaric.org.uk

.

Undersea and Hyperbaric Medical Society: http://www.uhms.org

.

South Pacific Underwater Medicine Society: http://www.spums.org.au

Sources of scientific information .

Rubicon Research Repository: http://archive.rubicon-foundation.org/

Further reading Textbook specifically dedicated to the effects of hyperbaric exposure on the lung: Lundgren, C.E.G., Miller, J.N. (eds) (1999) The Lung at Depth. Marcel Dekker: New York.

General textbooks of diving medicine Brubakk, A., Neuman, T. (eds) (2003) Bennett and Elliott’s Physiology and Medicine of Diving, 5th edn. London: Saunders. Edmonds, C., Lowry, C., Pennefather, J., Walker, R. (eds) (2002) Diving and Subaquatic Medicine, 4th edn. Arnold: London.

Relevant studies and case reports Benton, P., Woodfine, J., Westwood, P. (1996) Arterial gas embolism following a 1-meter ascent during helicopter escape training: a case report. Aviat. Space Environ. Med. 67: 63–64.

FURTHER READING

375

Brooks, G.J., Pethybridge, R.J., Pearson, R.R. (1988) Lung function reference values for FEV1, FVC, FEV1/FVC ratio and FEF (75–85) derived from the results of screening 3,788 Royal Navy submariners and submarine candidates by spirometry. Paper 13 in Conference Papers of the XIVth Annual Meeting of the EUBS, Aberdeen, 5–9 September 1988. Slade, J.B., Hattori, T. et al. (2001) Pulmonary edema associated with scuba diving: case reports and review. Chest 120: 1686–1694. Wilmshurst, P.T., Nuri, M., Crowther, A. et al. (1989) Cold-induced pulmonary oedema in scuba divers and swimmers and subsequent development of hypertension. Lancet i: 62–65.

Medical standards British Thoracic Society (2003) Guidelines on respiratory aspects of fitness for diving. Thorax 58: 3–13.

Regulations Diving at Work Regulations (1997) Available from: http://www.opsi.gov.uk/SI/si1997/19972776.htm (accessed 4 December 2009). Work in Compressed Air Regulations (1996) Available from: http://www.opsi.gov.uk/SI/si1996/ Uksi_19961656_en_1.htm (accessed 4 December 2009).

Miscellaneous HSE Diving Health and Safety Strategy to 2010. UK Health and Safety Executive. Offshore Injury, Ill Health and Incident Statistics 2007/2008. HID Statistics Report. HSR 2008 – 1. Date of Issue: December 2008. Health and Safety Executive. United States Navy Diving Manual. Available from: http://www.supsalv.org/pdf/DiveMan_rev6.pdf (accessed 4 December 2009).

26 Effects of travel or work at high altitudes or low pressures Michael Bagshaw King’s College London and Cranfield University, UK

26.1 Introduction Exposure to high altitude implies exposure to low ambient pressure as a consequence of the physics of the atmosphere. The exposure can occur gradually, as in mountaineering or high hill walking, or relatively quickly, as in ascent by aeroplane or balloon. Exposure to gradual terrestrial ascent above about 3000 m puts the susceptible individual at risk of developing altitude illness, a collective term encompassing the major conditions caused directly by hypobaric hypoxia. These include acute mountain sickness and high-altitude pulmonary edema. Rapid ascent in the atmosphere above about 3000 m on the other hand, as may occur in an aeroplane, gives rise to hypoxic hypoxia (the term given to hypoxia due to insufficient oxygen reaching the blood and a low partial pressure of oxygen in arterial blood), to which all individuals are susceptible. The clinical features of the acute phases of altitude illness are different from those observed in aviation-related hypoxic hypoxia, with differences in diagnosis and treatment. A high incidence of acute mountain sickness has been reported in tourists flying to high-altitude cities such as Lhasa (3658 m), Leh (3514 m), La Paz (3625 m) and Cuzco (3415 m), so a simple distinction between mountain sickness and aviation hypoxia is not necessarily straightforward. Occupations exposed to high altitude include mountaineers and mountain guides, with their associated professions, and professional aircrew and frequent business flyers.

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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26.2 Physics of the high-altitude environment At sea level the atmosphere exerts a pressure of about 760 mmHg (101 kPa); it is variably moist, has a temperature that ranges from
60 to þ 60 C, and moves at wind speeds from 0 to 160 km/h. With increasing altitude, the temperature, pressure and water content of the atmosphere fall and wind speeds increase.

26.2.1 Atmospheric pressure Total gas pressure falls with altitude in a regular manner, halving every 18,000 ft (5500 m; it remains the convention in aviation to use ft for altitude). The oxygen percentage of the atmosphere (20.93%) is constant to very high altitudes, so the same curve can be used to obtain the ambient oxygen pressure by rescaling the ordinate. The oxygen pressure of physiological importance is that which exists in ambient air when it is warmed and wetted on entering the bronchial tree. This raises water vapor pressure to about 47 mmHg, regardless of the total gas pressure outside. The oxygen pressure in moist inspired gas (PiO2) fully saturated with water vapor at 37 C is given by the relationship: PiO2 ¼ FiO2 ðPB
47Þ

where PB is barometric pressure and FiO2, the fractional concentration of oxygen in the inspirate, is 0.2093.

26.2.2 Atmospheric temperature The atmospheric temperature falls at a rate of 1.98 C/1000 ft (300 m) from the standard sea level temperature of 15 C, to the tropopause [the border between the lower level, the troposphere, and the higher level or stratosphere; 40,000 ft (12,200 m)]. It remains stable at
56 C up to about 80,000 ft (24,400 m) and then rises to almost body temperature at about 150,000 ft (46,000 m), but by then air density is so low that its temperature is unimportant.

26.2.3 Atmospheric ozone Atmospheric ozone at high altitude is formed by ultraviolet irradiation of diatomic oxygen molecules which dissociate into atoms. At very high altitudes all oxygen exists in the monatomic form. Lower down, some of this monatomic oxygen combines with oxygen molecules to form the triatomic gas ozone, with concentrations up to 10 ppm. The ozonosphere normally exists between 40,000 and 140,000 ft (12,200 and 42,700 m). Below 40,000 ft (12,200 m) the irradiation is normally too weak for significant amounts of ozone to form in this manner (although it is formed by reactions between hydrocarbons and nitrogen oxides in the presence of sunlight and contributes to tropospheric air pollution). Concentrations of ozone of 1 ppm at sea level can cause

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379

lung irritation. However, modern passenger jet aircraft are fitted with catalytic converters in the environmental control system which break down the ozone before it enters the pressurized cabin.

26.2.4 Cosmic radiation Aircraft occupants are exposed to elevated levels of cosmic radiation of galactic and solar origin. At jet aircraft operating altitudes, galactic cosmic radiation is 2.5–5 times more intense in polar regions than near the equator. The Earth’s surface is shielded from cosmic radiation by the atmosphere, the ambient radiation increasing with altitude by approximately 15% for each increase of around 2000 ft (dependent on latitude). Cosmic radiation doses The effect of ionizing radiation depends not only on the dose absorbed, but also on the type and energy of the radiation and the tissues involved. These factors are taken into account in arriving at the dose equivalent, measured in Sieverts (Sv). However doses of cosmic radiation are so low that figures are usually quoted in microsieverts (mSv) or millisieverts (mSv). Calculated and measured doses for aircrew and frequent flyers are well within the occupational exposure limits recommended by the International Commission on Radiological Protection. Health risks of cosmic radiation Whilst it is accepted that there is no level of ionizing radiation exposure below which effects do not occur, current epidemiological evidence indicates that the probability of airline crew members or passengers suffering any abnormality or disease as a result of exposure to cosmic radiation is very low.

26.3

Physiology of flight

The physiological effects of flight are distinguished from those of terrestrial high altitude because exposures are relatively rapid, brief and not cumulative. Flyers do not adapt to the hypoxic environment, unlike inhabitants of terrestrial high altitudes. However, the aircraft can be a means of transporting an individual to a high-altitude destination.

26.3.1 Hypoxia Although ambient oxygen pressure is related exponentially to altitude, falling progressively with ascent from the surface of the Earth, the pressure of oxygen to be found in the lungs does not have the same relationship. That pressure is determined by two equations. The alveolar ventilation equation states that alveolar CO2 pressure (PaCO2) depends only on CO2 excretion (CO2) and alveolar ventilation (Va), so: PaCO2 ¼ kðCO2 =Va Þ

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CH 26 EFFECTS OF TRAVEL OR WORK AT HIGH ALTITUDES OR LOW PRESSURES

where k is a constant. The alveolar air equation states that, since at any one time there is a fixed trading ratio (R) between oxygen uptake and CO2 excretion (R ¼ CO2/O2), alveolar oxygen pressure (PaO2) can be calculated from the moist inspired oxygen pressure (PiO2 ) and alveolar PCO2, so: PaO2 ¼ PiO2 *
ðPaCO2 =RÞ

Progressive hypoxia leads to a mild hyperventilation (i.e. a rise in Va and fall in PaCO2). When arterialized blood leaves a healthy lung, the oxygen pressure is some 10 mmHg less than that in the alveoli, due to uneven matching of ventilation to perfusion, some anatomical shunting and an almost nominal obstacle to diffusion. In resting individuals, the alveolar–arterial oxygen gradient does not change much with altitude, although the relative importance of the factors contributing to it alter considerably as explained below, so subtracting a further 10–15 mmHg describes the relationship between arterial oxygen pressure and altitude. The most important change is the loss of pressure driving oxygen from the alveoli to blood, as the fall in alveolar PO2 is much greater than that in mixed venous PO2 (because of the shape of the oxygen dissociation curve, Figure 26.1). As a result the alveolar– venous gradient for oxygen diffusion is reduced and equilibration is slower than at ground level. When people ascend to altitude in a matter of minutes, rather than over several days, they react to hypoxia by an increase in blood flow and a modest hyperventilation, limiting the effects of hypoxia. Individuals abruptly exposed to altitudes of 10,000 ft (3000 m) and above suffer mental and physical effects, and this is the ceiling above which aviators are provided with oxygen. To allow a margin of safety, the maximum certified cabin altitude in civilian passenger aircraft is 8000 ft (2440 m), at which barometric pressure is 565 mmHg and arterial oxygen pressure is around 55 mmHg (Figure 26.1), and venous oxygen pressures have fallen by only by 1–2 mmHg. Even at this altitude, there is a decrease in performance. The latest generation passenger aircraft are manufactured from newer materials that are lighter and stronger, allowing a lower cabin altitude to be maintained at higher aircraft altitudes. Two physiological features of

Figure 26.1 The oxyhemoglobin dissociation curve

26.3

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Table 26.1 The time of useful consciousness following the sudden loss of oxygen supply for a healthy individual at rest and moderately active, both for a progressive decompression and a rapid decompression Altitude (ft)

20,000 25,000 30,000 35,000 40,000 43,000

Progressive decompression

Progressive decompression

Rapid decompression

Seated at rest

Moderately active

Seated at rest

20 min 5 min 1.5 min 45 s 25 s 18 s

10 min 3 min 45–60 s 30 s 18 s 12 s

5 min 2–2.5 min 60 s 25 s 12–15 s 12–15 s

altitude hypoxia are important for safety in aviation. The first is the total lack of awareness of cerebral impairment. The second is that there is a ‘time of useful consciousness’, which describes how rapidly consciousness is lost, thus dictating how quickly the condition must be recognized and corrective action taken. The time of useful consciousness is the interval after the onset of hypoxia during which an individual can carry out some purposeful activity. The general relationship between this time interval and the altitude of sudden exposure is shown in Table 26.1. This diminishes from about 4 min at 25,000 ft (7620 m) to a minimum of roughly 15 s, which is reached at around 40,000 ft (12,200 m). This represents the sum of the 7 s or so required for blood to travel from the lungs to the brain and the time needed for the brain to utilize the oxygen already dissolved in its substance. Loss of useful consciousness is sensitive to many other factors, such as the degree of hyperventilation and the acceleration to which the individual is exposed at the time. Hyperventilation causes cerebral vasoconstriction, and positive headwards acceleration opposes the upward flow of blood to the brain. Sometimes deterioration in consciousness is quickened by vasovagal syncope, but more often there is tachycardia as consciousness is lost. Exertion also quickens loss of consciousness, because blood transits quickly through the lungs, leaving insufficient time for oxygen equilibration. The minimum cabin pressure of 565 mmHg (75.1 kPa; 8000 ft, 2440 m) in commercial passenger aircraft, will bring a healthy individual’s arterial PO2 along the plateau of the oxyhemoglobin dissociation curve until just at the top of the steep part (Figure 26.1), still saturated. At ground level, people with respiratory disease may have an adequate arterial oxygen saturation with arterial oxygen pressures as low as 55–60 mmHg. As they ascend to 8000 ft (2440 m), their arterial PO2 will fall further and may result in respiratory failure. If their hypoxemia at ground level is due to a mismatch of ventilation to perfusion, as is usually the case, the drop in arterial PO2 will not be as extensive as in healthy people (about 40 mmHg), but if it is due to diffusion defect associated with desaturation on exertion, as in some fibrotic conditions, it may be greater.

26.3.2 Treatment of acute hypoxic hypoxia In either event, hypoxic hypoxia can be reversed completely by the administration of oxygen, 30% oxygen at 8000 ft (2440 m) being equivalent to breathing air at ground

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CH 26 EFFECTS OF TRAVEL OR WORK AT HIGH ALTITUDES OR LOW PRESSURES

level. Given prior notice, most airlines can provide a personal oxygen supply for any passenger, although there may be a charge. (The altitudes of the patient’s destination and transit points en route should also be considered.) The administration of oxygen to an acutely hypoxic individual almost invariably results in a rapid and complete recovery, as is also the case if environmental pressure is increased so that the alveolar oxygen tension is restored towards its normal level. The only persistent symptom tends to be a generalized headache, and only then if the exposure to hypoxia was prolonged. In some individuals, however, sudden restoration of the alveolar oxygen tension to normal may cause a transient worsening of the severity of symptoms and signs of hypoxia for up to a minute. This oxygen paradox is usually mild and is manifest only by flushing of the face and hands and perhaps deterioration in performance of complex tasks over the immediate period following restoration of the oxygen supply. Occasionally oxygen administration may produce a severe paradox, with the appearance of clonic spasms and even loss of consciousness. The mechanisms responsible for the phenomenon are unclear and it is a rare occurrence. It may be the result of generalized hypotension associated with marked hypocapnia.

26.3.3 Aircraft oxygen equipment and pressure cabins Aircraft operating below 10,000 ft (3000 m) do not require oxygen equipment. Many sophisticated light aircraft which can cruise above 10,000 ft do not have pressurized cabins, so oxygen equipment must be provided, usually consisting of a gas bottle, simple regulator, tubing and nasal speculae or a mask for each occupant. Other aircraft that fly higher usually have reinforced cabins capable of holding a high differential pressure between inside and out. These are the high-differential type, seen in passenger and transport aircraft generally, and the low-differential variety found in military high-performance aircraft. The former, holding a high transmural pressure, maintain cabin pressure above 565 mmHg (8000 ft, 2440 m). They provide an environment in which the occupants breathe cabin air. However, it is possible rarely that the pressurization system can fail, allowing the cabin pressure to fall to the external ambient value. Thus an emergency oxygen supply is available for passengers and crew. The aircraft environmental control system automatically manages the internal cabin environment, providing healthy and comfortable surroundings for all occupants. There are regulatory requirements for minimum cabin air pressure, maximum levels of carbon monoxide, carbon dioxide and ozone, and minimum ventilation flow rates. The cabin air must also be free from harmful or hazardous concentrations of gases or vapors. The cabin air supply is bled from the outside air entering the aircraft engine, or may be supplied from the outside air via electrically driven compressors. It is then passed through the air-conditioning packs and mixed with filtered recirculated air before distribution to the cabin. The system provides approximately 20 cubic feet (566 liters) of air per minute per passenger, of which about 50% is recirculated air (compared with up to 80% recirculated in buildings and other forms of public transport), giving a complete cabin air exchange every 2–3 min. These high ventilatory flow rates maintain normal pressurization, as well as temperature control and the removal of odours and carbon dioxide. The high flow

26.3

PHYSIOLOGY OF FLIGHT

383

Figure 26.2 Cabin air circulation and distribution

rates also ensure that the volume of oxygen far exceeds the requirements of the aircraft occupants (0.34 l/min at rest and 0.85 l/min when walking). The air is distributed to the cabin via overhead ducts and grills running the length of the cabin. The airflow circulates around the cabin rather than along the cabin and is continuously extracted through vents at floor level, as shown in Figure 26.2. The recirculated air is passed through high efficiency particulate air (HEPA) filters, giving 99.99% efficiency in the removal of physical contaminants such as microbial particles. Aircraft cabin air has been demonstrated to be bacteriologically cleaner than the air in buildings, trains or buses. Although clean, the aircraft cabin air remains dry. During the flight, moisture is derived from the metabolism and activities of the cabin occupants as well as from the galleys and washrooms, giving a maximum relative humidity in the order of 10–20%. These levels are associated with surface drying of skin, mucous membranes and cornea which may cause discomfort. Normal homeostatic mechanisms prevent dehydration and no harm to health has been demonstrated, although pharyngeal drying can stimulate the cough reflex. A high-differential cabin pressure limits the vehicle’s range and manoeuvrability and increases the risk of catastrophic damage if the fuselage is punctured. Thus military high-performance aircraft are fitted with low-differential cabins, which prevent cabin pressure falling below 280 mmHg (37.2 kPa) (equivalent to a pressure altitude of 25,000 ft, 7620 m). At this level decompression illness becomes a potential hazard (see below). In such aircraft, oxygen equipment is used routinely.

26.3.4 Mechanical effects of pressure change In civilian passenger and transport aircraft the climb to cruise altitude takes about 30 min and involves a maximum fall of about 200 mmHg (26.6 kPa) in cabin pressure

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CH 26 EFFECTS OF TRAVEL OR WORK AT HIGH ALTITUDES OR LOW PRESSURES

(to the equivalent of 8000 ft, 2440 m). Descent to land takes much the same time. Body fluids and tissues generally are virtually incompressible and do not alter shape to any important extent when such pressures changes are applied. The same is true of cavities such as the lungs, gut, middle ear and facial sinuses that contain air, provided that they can vent easily. Gas-containing spaces that cannot vent easily behave differently. The thoraco-abdominal wall can develop transmural pressures of þ100 mmHg or so briefly, but is normally flaccid and has a transmural pressure of a few millimeters of mercury. Gas within will usually be at a pressure very close to that outside, and must follow Boyle’s law. Ascent from ground level (760 mmHg) to 8000 ft (2440 m) (565 mmHg) will expand a given volume of trapped gas in a completely pliable container by about 35%. This may cause slightly uncomfortable gut distension in healthy people but it is not an important problem. Even very diseased lungs can vent themselves over a minute or so. In consequence, the risk of lung rupture in normal flight is extremely small. The cavity of the middle ear vents easily, but sometimes fails to fill because the lower part of the Eustachian tube behaves as a non-return valve, especially when it is inflamed. As a result, the cavity equilibrates quite easily on ascent but may not refill on descent, and the ear-drum bows inwards, causing pain that can be severe (otic barotrauma).

26.3.5 Altitude-induced decompression illness If ambient pressure falls quickly to less than half its original value, the gas dissolved in blood and tissue fluids may come out of solution precipitously, forming bubbles and obstructing flow in small blood vessels. The time symptoms take to develop varies widely between individuals and shortens markedly as the altitude of exposure rises. Symptoms usually resolve quickly after a descent of a few thousand feet and rarely persist after descent to ground level, breathing oxygen. Should they persist, treatment should involve recompression in a specialist unit (as discussed in the Chapter 25, Work in Hyperbaric Environments). Atmospheric pressure halves at 18,000 ft and decompression illness occurs rarely, if at all, below this altitude. It is very rare below 25,000 ft (7600m) and therefore is normally of no concern at normal passenger aircraft cabin altitudes, although the risk continues to be significant in some military flights. However, it does occasionally occur in those passengers who have been exposed to a hyperbaric environment prior to flight, such as divers and tunnel workers. Sub-aqua divers are advised to allow a minimum of 12 h to elapse between diving and flight, or 24 h if the dive required decompression stops.

26.3.6 Hyperventilation In the aviation environment it is generally recognized that hyperventilation is a common condition, often related to anxiety or emotional stress. Studies have shown that a large proportion of aircrew under training hyperventilate, as do experienced aircrew when confronted with an unusual event or in-flight emergency. A 2009 study raised concerns about the prevalence of unrecognized hyperventilation amongst airline pilots and the potential risk to flight safety. Symptoms can include light-headedness, headache, feelings

26.4

ALTITUDE ILLNESS

385

Figure 26.3 The hyperventilation syndrome

of unreality and anxiety, paresthesiae, visual disturbances, palpitations, cognitive impairment, loss of concentration and, in extreme cases, muscular tetany and paralysis. Whereas in general medicine, the hyperventilation syndrome may not always be readily recognized as a clinical entity, falling as it does between physiology, psychiatry, psychology and medicine, the condition of hyperventilation is readily accepted in aviation medicine. However, diagnosis can be difficult in the absence of a simple measurement. The physiological diagnosis of hyperventilation is breathing in excess of metabolic requirements, thus implying arterial hypocapnia and an abnormally high respiratory drive. However, in chronic cases PCO2 can be profoundly affected by the total physiological inputs to respiration and the conscious state of the individual. There can be a tendency to hyperventilate, even though the resting PCO2 is normal. There are a number of factors which may perpetuate hyperventilation (Figure 26.3). Apart from renal compensation, there appear to be physiological mechanisms resetting the PCO2 to a lower level independent of chemoreceptor setting. Habit may be a perpetuating mechanism, as may be misattribution of symptoms of hypocapnia (symptoms not dissimilar to those of carbon monoxide toxicity). The interaction of factors contributing to chronic hyperventilation remains uncertain.

26.4

Altitude illness

This is a collective term including the major conditions resulting directly from terrestrial hypobaric hypoxia, namely acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE) and high-altitude cerebral edema (HACE). It is thought that AMS and HACE probably represent different ends of a severity spectrum, sharing a common pathophysiology.

26.4.1 Acute mountain sickness Away from aviation, AMS is the commonest type of altitude illness. Although relatively benign, its presence indicates that acclimatization is incomplete and the traveler is at

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CH 26 EFFECTS OF TRAVEL OR WORK AT HIGH ALTITUDES OR LOW PRESSURES

risk of developing life-threatening altitude illness (HACE or HAPE) if ascent is continued with symptoms. Important risk factors include the altitude attained and the rate of ascent, as well as individual susceptibility. Some individuals readily develop AMS on ascent to high altitude while others are able to ascend rapidly without problems; approximately 25% of visitors who ascend rapidly to 3000–4000 m in Colorado experience AMS and 50% of trekkers in Nepal develop AMS when hiking above 4000 m over 5 days. Exertion may be a risk factor for AMS, but lack of physical fitness is not. There is no relationship with age, although females seem to have a higher incidence than males. Characteristic symptoms include the development of headache, accompanied by some or all of nausea, vomiting, anorexia, lassitude and dizziness, typically starting a few hours after arriving at altitude. Physical signs are non-specific, but often include an apathetic disinterested facial expression. Localized crackles may be heard in the lung fields and peripheral and periorbital edema may be observed. Vital signs are usually normal. Pathophysiology AMS is likely to be due to mild cerebral edema and is thus part of the spectrum of HACE. The symptoms and signs involve the central nervous system and neuroimaging studies have demonstrated brain swelling in AMS. However, brain swelling has also been demonstrated on ascent to high altitude in the absence of AMS, indicating individual susceptibility. Prevention The following guidelines are recommended for travelers ascending to high altitude:

1. Avoid abrupt ascent to greater than 3000 m, limiting the ascent rate to 300–400 m per day. 2. Spend at least one night at an intermediate elevation (1500–2500 m) to aid acclimatization. 3. If rapid ascent to greater than 3000 m is unavoidable (e.g. flying to La Paz or Lhasa), allow sufficient time for acclimatization before ascending higher. Consider drug prophylaxis. 4. Follow any recommended established safe itinerary for a given destination. 5. If previous experience indicates individual susceptibility to AMS, ascend at a rate slower than recommended in the itinerary. 6. Allow for unplanned rest days when planning the itinerary. 7. Be aware and watchful for symptoms of AMS and take immediate action. Drug prophylaxis Susceptible individuals may benefit from drug prophylaxis, but the use of drugs for other travelers remains controversial. Acetazolamide is the drug of choice for prevention of AMS, its effectiveness having been demonstrated in several placebo-controlled trials. The standard dosage is 250 mg twice daily, or a single daily dose of the 500 mg

26.4

ALTITUDE ILLNESS

387

slow-release formulation. For prophylaxis, acetazolamide should be started 1 day before ascent and continued until 2 days after the maximum altitude is reached. Side effects are mild and may include paresthesiae, diuresis, change in taste, nausea, drowsiness and headache. Should hypersensitivity occur, the less effective alternative of dexamethasone 4 mg 8-hourly may be used. Aspirin has been used prophylactically to prevent highaltitude headache. Treatment Unlike the hypoxic hypoxia encountered in aviation, where administration of oxygen is immediately effective, descent is the definitive treatment for all forms of terrestrial altitude illness. In the presence of symptoms of AMS, descent should be immediate if there is any suggestion of cerebral or pulmonary edema, as deterioration can occur rapidly. Oxygen relieves the symptoms of AMS, but the optimal therapy includes descent of 500–1000 m. Portable hyperbaric chambers made from fabric bags are carried on some high-altitude expeditions for emergency use.

26.4.2 High-altitude pulmonary edema HAPE is a potentially life-threatening form of non-cardiogenic pulmonary edema which may occur at altitudes above 2500 m. When compared with AMS it is relatively uncommon, although for susceptible individuals the recurrence rate is 60–70% at about the same altitude. In these individuals HAPE is precipitated by rapid ascent, strenuous exercise and cold. Recent inflammatory illness such as a viral infection increases the risk. HAPE is frequently preceded by symptoms of AMS, with the main symptoms being breathlessness and cough. Dyspnea on exertion progresses to orthopnea and breathlessness at rest. The initially dry cough may progress to the production of white then pink frothy sputum associated with gurgling in the chest and chest pain. Physical signs may include sinus tachycardia, low-grade pyrexia, tachypnea, central cyanosis and localized inspiratory crackles. Cerebral edema may also occur in severe cases. Where medical facilities are available, chest radiography may show patchy pulmonary edema and arterial blood gases confirm pronounced hypoxia. Untreated the mortality is up to 50%, emphasizing the importance of early recognition and treatment. Pathophysiology The mechanism of HAPE is uncertain, although it has been shown that pulmonary hypertension precedes the formation of pulmonary edema. It may result from uneven pulmonary vasoconstriction throughout the vascular bed, leading to pulmonary overperfusion in susceptible individuals. Another hypothesis suggests that inflammation in the presence of hypoxia may be the cause of pulmonary capillary leakage in some cases. Prevention Individuals with known susceptibility to HAPE should understand that it is a lifethreatening condition. They should avoid hasty ascent and gain altitude only slowly.

1. Above 2500 m, ascent up to 350 m per day in sleeping altitude may take place in the absence of symptoms of AMS.

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2. If symptoms of AMS persist for more than a day, descend. 3. Avoid vigorous exercise during acclimatization. Drug prophylaxis Drug prophylaxis is effective in individuals susceptible to HAPE. The drug of choice is nifedipine MR 20 mg orally 8-hourly and should be continued until the subject descends to an acclimatized altitude or below 3000 m. Nifedipine will not prevent AMS. Advice should be sought from a physician experienced in high-altitude medicine (not necessarily the same specialty as aviation medicine). Treatment The treatment of HAPE is urgent, with the aim of improving oxygenation and reducing pulmonary artery pressure. The patient should be sat up, kept warm and administered oxygen, with an immediate descent of at least 1000 m. Nifedipine can be given sublingually and a portable hyperbaric bag should be used to facilitate descent when available. If an oxygen saturation >90% can be achieved with no more than 4 liters oxygen per minute, then immediate descent may be avoided. Diuretics, nitrates, opiates and alcohol should be avoided.

26.4.3 Other altitude-related respiratory conditions Dry cough and sore throat are common occurrences at terrestrial high altitude, with 42% of trekkers to Mount Everest developing cough and 39% sore throat. This is likely to be the result of increased ventilation, breathing cold dry air, and increased cough receptor sensitivity. Occupants of pressurized aircraft cabins frequently report the development of coughs and colds. There is no evidence of an increased risk of respiratory infection during airline travel, the cabin air being microbiologically clean due to HEPA filtration. The cabin air is dry, which may lead to pharyngeal drying and stimulation of the cough reflex.

Further reading Aviation medicine Davis, J.R., Johnson, R., Stepanek, J., Fogarty, J.A. (eds) (2008) Fundamentals of Aerospace Medicine, 4th edn. Philadelphia, PA: Lippincott Williams & Wilkins. Rainford, D.J., Gradwell, D.P. (eds) (2006) Ernsting’s Aviation Medicine, 4th edn. London: Hodder Arnold.

Terrestrial altitude illness Murdoch, D.R., Pollard, A.J., Gibbs, J.S.R. (2001) Altitude and expedition medicine. In Principles and Practice of Travel Medicine, Zuckerman, J., Zuckerman, A.J. (ed.). Chichester: Wiley; 247–260.

Part IV The general environment

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

27 Natural sources – wildland fires and volcanoes Sverre Vedal University of Washington, Seattle, WA, USA

27.1 Introduction The distinction between natural sources of air pollution and other emission sources is not a clear one. We do not typically speak of ‘unnatural’ sources as distinct from ‘natural’ sources, but rather of anthropogenic (i.e. man-made) sources and natural sources. While most often ‘anthropogenic’ refers to pollution made up of products of combustion, crustal and other types of dust generated by human activities are also in a sense man-made and could be considered anthropogenic, although that is not common usage. It is important to understand that designating a source of air pollution as natural provides no assurance that these natural emissions are not harmful to health. Emissions from natural sources, as will be described in this chapter, contain components that are well known to be toxic. The following specific types of pollution from natural sources will be considered in this chapter: smoke from wildfires, including forest, bush and grass fires; smoke from agricultural burning; and volcanic emissions. Smoke from agricultural burning, while not strictly natural, is included here to the extent that it provides insight into wildfire emissions and their effects. Biomass smoke will be used here to refer to smoke from wildland (forest and bush) fires and agricultural burning. Inhalation burn injuries or effects due to carbon monoxide intoxication will not be covered here. Much is known about the health effects of individual components that make up biomass smoke and volcanic emissions. Much less is known about the effects of exposure to biomass smoke or volcanic emission in general, or about the contributions of the individual components in the respective pollutant mixes in producing these effects. Information from many sources will be used and integrated here in summarizing the health effects evidence. Some insight can be gained from knowing the individual Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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components and concentrations that are present in these emissions. Toxicological studies employing exposures to emissions can provide insights into pathophysiological mechanisms and can serve to shore up plausibility of suspected effects. Ultimately, findings from experimental and epidemiological (observational) human studies are needed to understand the effects that actually result from these exposures. The study designs employed in the human studies will be briefly identified as they are encountered in this chapter, as will some of their strengths and shortcomings that influence how we interpret findings based on them. This chapter begins with a review of biomass smoke exposure and its effects, followed by a review of volcanic emissions exposure and effects. Each review will conclude with a brief summary. A final section will address prevention of exposures and patient management. A small list of recommended readings is included at the end. Many of the studies referred to in this chapter review are referenced in those readings.

27.2 Biomass burning Exposure to smoke from wood and other biomass burning has been commonplace throughout human history. While smoke from forest wildfires is the most dramatic example of biomass smoke, bush and grass fires and controlled agricultural burns are also important outdoor sources of smoke exposure. The most prevalent source of biomass smoke exposure is indoor burning, with exposures resulting from personal wood burning for heating or biomass burning for cooking, or from neighborhood smoke resulting from residential burning. Effects of these more prevalent exposures will not be reviewed here, apart from brief mention in the context of extreme exposures below.

27.2.1 Extreme biomass smoke exposures Health effects resulting from extreme exposures can serve to suggest effects that might potentially occur with more commonplace exposures. It should be kept in mind, however, that more commonplace exposures may never in fact have such severe effects. Case reports involving intense exposures to products of wood combustion indoors have strongly indicated that these exposures have the potential to cause interstitial lung disease and asthma. ‘Hut lung’ has been used to describe cases of interstitial lung disease caused by chronic exposure to high levels of biomass smoke. Case–control studies of women in developing countries have provided good evidence that long-term exposure to the high concentrations of pollutants generated from burning biomass for cooking can produce chronic obstructive pulmonary disease (COPD) and associated pulmonary hypertension that can be as severe as those due to cigarette smoking. There is also evidence that these exposures in developing countries can cause lung cancer and increase the risk of active tuberculosis.

27.2.2 Forest fires Forest wildfires are either caused naturally, most often from lightning strikes, or are started by people either accidentally or intentionally. In the USA, from 15,000 to

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20,000 km2 (or 0.2% of the total land area) are burned each year. In Indonesia in 1997 and 1998, approximately 100,000 km2 burned. Smoke from forest fires often does not drift to areas where people will be exposed. When exposure does occur, it is most often on a small scale in small rural communities involving relatively few people. On occasion, especially with very large fires, smoke can drift over large urban areas exposing a large number of people to varying degrees and over varying periods of time. While the health impacts of smoke exposure on an individual are not obviously influenced by the size of the community affected, except perhaps through the potentially modifying effects of background urban air pollution, the ability to adequately study these impacts, and in particular the most adverse impacts such as mortality, is only possible when large numbers of people are exposed. Opportunities for studying these more severe effects are consequently limited. Population density is increasing in areas prone to forest fires, such as in southern California, which is increasing the likelihood of significant population exposures. The apparent increased occurrence of large forest fires, possibly related to global climate change, and certainly related to the practice of using burning to clear large areas of forest, is also enhancing prospects for increased exposure. Wood smoke constituents and exposures Forest fire smoke, as is typical of smoke from any combustion process, especially an inefficient one, is a complex mixture of particles and hundreds of chemical compounds. Most of the particles are in the inhalable size range (PM10), by both number and by mass, and most of those are in the fine inhalable (PM2.5) size fraction. By far the largest numbers of particles are in the submicrometer size range. Particles this small settle poorly and can be transported in the air over several hundreds of kilometers before depositing. The particles are carbonaceous and include both elemental carbon (essentially soot) and organic carbon compounds. Gaseous compounds in wood smoke include carbon monoxide (CO), nitrogen oxides and a host of hydrocarbons. Many of the hydrocarbons are potent respiratory irritants, such as acrolein, and many, including formaldehyde, benzene, and polycyclic aromatic hydrocarbons (PAHs), are either known or strongly suspected to be carcinogens. The relative proportions of the various compounds present in smoke both in the particulate and vapor phase is highly dependent on the type of wood burned and its water content, and the burning conditions such as whether a fire is smoldering or flaming. Less efficient burning, such as with a smoldering fire, produces less oxidized compounds. Exposures to wildfire smoke are extremely variable, as would be expected, with the primary determinant being proximity to the fire. Particulate concentrations measured in areas where people are exposed can vary by more than two orders of magnitude. In close proximity, PM10 concentrations can reach several milligrams per cubic meter (i.e. thousands of micrograms per cubic meter), while dispersed smoke in urban areas may result in increases above background concentrations of only a few micrograms per cubic meter. CO can reach lethal concentrations immediately next to a fire and in smoke-filled spaces, but elevations in CO concentrations can also be barely detectable when smoke is dispersed. Only a minority of forest fires result in significant nonoccupational (‘environmental’) smoke exposure, and a much smaller number result in large populations being

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exposed. As a group, firefighters receive the highest concentrations and the longest durations of smoke exposure. Of the many constituents of wood smoke, personal concentrations of PM in firefighters when fighting fires are consistently the most elevated relative to occupational or ambient air standards. Personal peak concentrations over 1 mg/m3 are regularly measured in firefighters. Because of the intense physical activity entailed in fighting fires, lung doses for a given air concentration would be expected to be considerably higher in these workers than in the relatively sedentary. See the section on wildland firefighters on the next page. Wood smoke health effects In Table 27.1, health effects are listed that might be expected on the basis of the constituents present in wood smoke. Later, in Table 27.2, a summary of the evidence that these expected effects actually result from exposure to wood smoke is presented, ordered from least to most adverse effects. There is little controversy that exposure to wood smoke causes symptoms of irritation such as eye burning, throat soreness and cough. Anyone who has been exposed to wood smoke can personally relate experiencing these symptoms. It is reasonable to expect that individuals with underlying cardiopulmonary disorders, and even some without underlying illnesses, would be more sensitive to wood smoke effects and therefore experience more deleterious effects from wood smoke exposure than merely symptoms of irritation. Findings from properly conducted epidemiological and experimental health effects studies provide the basis for optimal recommendations for preventive measures and medical management. The 2003 wildfires in Southern California provided an opportunity to study effects in a large population. Recently, the effects on children already enrolled in a large cohort study were reported. Children in this cohort experienced more respiratory symptoms with smoke exposure. Asthmatic children were not singled out as being more likely to experience worsened symptoms than children without asthma. Doctor visits prompted by symptoms were increased in those who reported more smoke exposure, but not in those living in areas with higher concentrations of PM mostly from wood smoke. Increased doctor visits for respiratory complaints were also seen during the 2003 wildfires in southern British Columbia. The increase in doctor visits was limited to the one of the two cities studied that experienced the highest PM concentrations, suggesting that a certain level of exposure may be required to trigger doctor visits. Table 27.1

Constituents and potential health effects of wood smoke

Component

Health concerns

Particulate matter (PM)

Wide ranging effects from respiratory symptoms to cardiopulmonary morbidity and mortality; effects of both short- and long-term exposure Acute hypoxia; myocardial ischemia in coronary artery disease at low concentrations Pulmonary edema at high concentrations; possible airways effects at low concentrations Mucous membrane and respiratory irritant Carcinogen (leukemia) Probable lung carcinogens (e.g. benzo[a]pyrene)

Carbon monoxide (CO) Nitrogen oxides Acrolein Benzene Polycyclic aromatic hydrocarbons (PAHs)

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Table 27.2 Evidence for health effects of biomass smoke exposure Health outcome

State of evidence

Irritant symptoms Impaired lung function Increased hospital visits Lung cancer

Definite Suggestive in wildland firefighters Best evidence for asthma With indoor biomass burning in developing countries; possible from occupational exposure in the sugar cane industry Possible, but evidence for an acute effect is mixed

Increased mortality

Earlier studies in California and Florida identified increases in emergency room visits for respiratory conditions in relation to wildfires. Increased hospitalizations were also reported during the Southeast Asia wildfires of 1997 and 1998. Because of the wealth of evidence regarding short-term PM exposure effects on mortality, there would naturally be concern that wood smoke-related increases in PM have similar effects. Also, if hospitalizations are increased from smoke exposure, one might expect that some very susceptible persons would be even more severely affected. The evidence for mortality effects is mixed, however. Findings of studies of the Southeast Asia wildfires were inconsistent, but indicated that effects on mortality may have occurred. No effects on mortality were identified in a recent study of two episodes in which smoke from a wildfire drifted briefly over Denver, Colorado. There is little information on acute cardiovascular effects of wood smoke exposure, effects expected in light of the cardiovascular effects of PM. No increase in cardiovascular doctor visits was seen in the 2003 southern British Columbia fires. One controlled, human exposure study using wood smoke generated from a wood stove has been performed to date. The most compelling finding was an exposure-related increase in serum amyloid A, an acute-phase reactant that reflects increased systemic inflammation and is a risk factor for atherosclerosis. There were no meaningful effects in this experimental study on coagulation factors, exhaled nitric oxide or an indicator of oxidative stress. Wildland firefighters The dramatically higher exposures to wildfire smoke experienced by firefighters would indicate that studies of smoke-related health effects in wildland firefighters might be ideal for identifying worst case scenarios. Unfortunately, some challenges encountered in studying firefighters have limited their usefulness in this regard. The physical demands of firefighting require a relatively healthy workforce. Studies in which no effects are identified can therefore be generalized to only a subset of the exposed population. Effects that are identified might be expected to underestimate effects experienced in a less healthy general population in settings of comparable exposure, but these settings would be unusual. Finally, the locations and rough terrain where firefighting activities are often performed limit the ability to assess exposure. Use of respiratory protection (respirators) by wildfire firefighters to reduce exposure is variable. The most effective protection is provided by atmosphere-supplying respirators, such as self-contained breathing apparatuses, but these are largely impractical. The least effective is the bandana, which provides only minimal protection against particles and essentially no protection against gases, but is nevertheless commonly used. Air filter

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masks that are more effective than bandanas against respirable particles are variably used. Powered air-purifying respirators are more effective than filter masks, but these are little used. Firefighter exposures to smoke occur both while fighting fires using some type of respiratory protection that is most often inadequate to protect against the many components of smoke, and while in the vicinity of fires when respiratory protection is not used. Study designs have therefore most often relied on indirect and crude measures of exposure such as a workshift in pre- and post-workshift studies, and a fire season in pre- and post-season studies. Cross-season studies have shown increased symptom reporting, lower level of lung function and increased bronchial responsiveness after a firefighting season compared with those before the season. The rare cross-shift study has shown mean decreases in level of lung function over a workshift. One cross-sectional study of wildland firefighters done before the fire season was aimed at identifying effects of long-term smoke exposure. Levels in measures of lung airway function in this study were lower than those in control workers. Workers with more years of exposure, surprisingly, were not more severely affected than those with less exposure. Assessing exposure–response relationships in cross-sectional studies such as this is hampered by the healthy worker effect in which the more healthy workers tend to preferentially continue working. This could make it appear that those who have worked the longest, and had the largest cumulative exposure, are actually healthier. In spite of the challenges in interpreting and applying findings from firefighter studies, evidence favors both short-term and long-term respiratory effects from the sometimes extreme exposures that this work entails. Evidence from toxicology Toxicological studies serve not only to investigate mechanisms underlying effects of smoke exposure, but to enhance the plausibility of epidemiological findings. Very high dose, acute inhalational studies, although relevant in indicating the types of effects that could occur with smoke inhalation, do not offer much insight into effects at the levels of exposure investigated in most epidemiological studies. Some lower dose studies have been done, however. Animal studies in which carboxyhemoglobin levels did not exceed 20% have demonstrated alterations in pulmonary immune defense mechanisms, specifically in macrophage function, and reduction in pulmonary clearance of bacteria. No pulmonary inflammation, as reflected by increased pulmonary inflammatory cell infiltration or increased lung cytokines, is typically observed at those levels of exposure. There is evidence for reduced lung antioxidant activity, however. There is also some evidence of smoke-induced exacerbation of allergen allergic responses, such as increased allergen-specific serum IgE and increased pulmonary eosinophils, which may be relevant to the epidemiological observations regarding smoke exposure and asthma. Forest fire smoke instilled in rat lungs produces little inflammation compared with other combustion sources. Little evidence for cardiac effects or lung tumors has been found in relevant toxicological studies of wood smoke exposure. Wood smoke is mutagenic, however. Although somewhat dependent on burning conditions and type of wood burned, the potency of wood smoke in initiating skin tumors, a test of general tumor producing potential, is less than gasoline or diesel exhaust, but greater than cigarette smoke, which is typically less potent than other combustion sources.

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397

27.2.3 Bush and grass fires and agricultural burning Bush and grass fires, and agricultural fires, most of which involve burning of agricultural straw and stubble, can be reasonably discussed together. Increases in PM, CO and volatile organic compounds have been measured in relation to these types of burning, as they have for forest fires. Unlike for forest fires, it is not unusual for smoke from these fires to drift over large urban areas, thereby providing an opportunity to investigate effects in population studies. A series of relatively small studies from Sydney, Australia largely showed no effects of bush fire smoke on respiratory emergency room visits or on level of lung function in asthmatic children. In contrast, in a larger time series study in Darwin, an association between PM concentration and asthma emergency visits was detected during a period of near-continuous bushfires. Time series studies, in which daily measures of smoke are related to daily counts of health events such as hospitalizations or deaths, are often used to study smoke effects. These studies are relatively easy to carry out as long as the relevant smoke data and counts of health endpoints are available. Interpretation of time series studies in assessing smoke effects relies on being able to identify burning-related pollutant concentrations or time periods. PM concentrations are often used as a measure of smoke exposure, which is reasonable if PM in the specific study setting is composed largely of wood smoke PM. Number of acres burned has been used as a surrogate measure of agricultural burning in some time series studies. Emergency room visits for asthma have been associated with burn acreage in California and eastern Washington State. In Winnipeg, Canada, most of a cohort of subjects with mild to moderate airways obstruction reported increased respiratory symptoms with exposure to smoke from straw and stubble burning in surrounding fields; over one-third of this presumably susceptible cohort noted no increase in symptoms. Recently, relatively low concentrations of smoke from agricultural stubble burning in eastern Washington State did not affect either level of lung function or exhaled nitric oxide in asthmatics. In rural Iran, however, rice stubble burning was associated with measures of worsened asthma control. Also, rice stubble burning in Japan has been associated with increased asthma emergency visits and hospitalization in children. One experimental human exposure study using controlled burning of rice stubble has been performed, and included only subjects with allergic rhinitis. No increase in inflammatory cells was seen in broncho-alveolar lavage fluid. Effects of sugar cane burning have also been studied. Time series studies have suggested effects on intensity of hospital emergency nebulizer use in Brazil and, more recently, on asthma hospitalizations. Asthma hospital visits in Louisiana are higher in the sugar cane burning season. There has been concern that occupational exposure in the sugar cane industry causes lung cancer and mesothelioma, specifically exposure to the amorphous silica fibers in sugar cane smoke. Evidence was determined to be inadequate for judging the carcinogenicity of sugar cane work in the IARC assessment on this in 1997, in spite of reports of increased lung cancer risk from several case–control studies. A subsequent case–control study from India also identified increased risk of lung cancer. Although anecdotal cases of mesothelioma have been reported in sugar cane workers, case–control studies have not supported this anecdotal impression.

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27.2.4 Biomass burning summary There are many challenges to rigorously studying health effects associated with exposure to smoke from forest fires, bush fires and agricultural burning. One of the greatest challenges is adequately estimating exposure to smoke. Exposure misclassification is likely to be substantial when surrogate measures such as burning season and burn acreage are used. Even when concentrations of smoke pollutants such as PM are used, substantial spatial variability in concentrations is likely to be present, with attendant exposure misclassification. Also, when PM concentrations are not dramatically elevated during burning periods, PM may include significant contributions from nonburning sources. This limits the ability to attribute observed PM effects to burninggenerated PM specifically, especially in time series studies that attempt to relate shortterm concentration changes with changes in health. Use of PM measures that are specific for biomass burning would address this limitation, but specific measures have not been used in epidemiological studies. In one commonly used study design, a measure of morbidity over a specified time period, hospital visits for asthma in September or October, for example, is compared across other time periods of the year. This design is particularly prone to bias due to seasonal trends in disease morbidity that may coincide with the burning season. The near-universal increase of asthma morbidity in the fall of each year, for example, often coincides with periods of burning. If these short-term temporal trends in the data cannot be accounted for, the more credible comparisons may be with morbidity measures at the same time period from other years when no burning occurred, such as was done in studying the wildfire smoke effects from the 2003 southern British Columbia fires described above. In spite of these challenges in adequately estimating exposure and in using appropriate study designs, it is clear that exposure to smoke from biomass burning has health impacts. The types of impacts produced are known with varying degrees of certainty (Table 27.2). Some are known to occur only in specific exposure settings, but might be suspected in other settings as well. Regardless of the type of biomass burned, smoke produces symptoms of mucous membrane and airway irritation. There is good evidence that people exposed to smoke are more likely to seek medical attention manifested either as increased doctor visits, emergency room visits or hospitalizations; this evidence is particularly strong for asthmatics. It is not clear that effects on asthma are due to worsened airways inflammation; there is little suggestion from experimental studies that relevant exposures result in airways inflammation, although some data suggest enhancement of allergic responses. Whether smoke exposure increases mortality is controversial at this point. Clearly intense acute smoke inhalation can be lethal. Also, arguing from the example of PM and its effects on mortality, unless PM in smoke is considerably less toxic than other sources of PM, smoke-induced mortality would be expected. Based on studies to date of large populations exposed to smoke, however, no firm conclusion regarding mortality is possible. Similarly, there is yet little evidence for cardiovascular effects of wood smoke exposure. However, based on the burgeoning amount of information on the cardiovascular effects of PM, cardiovascular effects of smoke would be anticipated. The human experimental finding of smoke-induced increase in serum amyloid A, an inflammatory marker and risk factor for atherosclerosis, supports the possibility of vascular effects.

27.3

27.3

VOLCANOES

399

Volcanoes

Volcanic eruptions, exposures to volcanic emissions and their attendant health impacts have occurred repeatedly throughout human history. Reportedly, the most significant air pollution event related to a volcanic eruption in Europe in recent times was due to the eruption of Laki in Iceland in 1783. The resulting degradation in air quality in Europe during the summer months of 1783 was such that there was a distinct odor, visibility was reduced, effects on vegetation were apparent and human health impacts, consisting of irritation symptoms and respiratory illness, were reported. In North America, the Mt St Helens eruption in 1980 was important in focusing attention on the health effects of emissions from volcanic eruptions. Rather than producing discrete air pollution episodes, volcanic emissions sometimes contribute to further degradation of already poor air quality, such as the contributions of emissions from Popocatepetl or the Miyake Island volcano on Mexico City’s and Tokyo’s air quality, respectively. In some cases, concern is focused more on gaseous volcanic emissions vented from a relatively quiescent volcano or due to soil gas in the vicinity of a volcano (‘degassing’), rather than eruptive emissions.

27.3.1 Composition of volcanic emissions Emissions from volcanic eruptions contain pollutants in the particulate, vapor and gaseous phases. Emissions of air pollutants from volcanoes that occur between eruptions include similar pollutants. Gaseous pollutants include carbon monoxide, carbon dioxide, sulfur dioxide, hydrogen sulfide and radon. These can be present as gases in a volcanic eruption or produced in volcanic venting or degassing; degassing refers to the noneruptive emission of volatile compounds from volcanic magma in volcanic craters or through the ground. Acidic fumes (from condensed vapor) composed of hydrochloric acid, hydrofluoric acid and sulfuric acid can also be emitted primarily or formed secondarily from gaseous emissions. Volcanic ash consists of particles of varying size, ranging from larger particles that settle quickly and are not inhalable, to fine inhalable particles. Inhalable particles (PM10) typically make up the largest number of particles but less than half of the particle (PM) mass. Fine inhalable PM (PM2.5) in volcanic ash, as distinct from typical urban ambient PM2.5, usually makes up only a small proportion of the PM mass. Silica is a prominent component of ash, especially in the inhalable fraction, but its contribution to total mass varies according to the type of volcanic activity. Crystalline silica, the form of concern in relation to silicosis, makes up much less of the mass. Volcanic PM also includes secondary compounds such as sulfate and various acid aerosols that form in the atmosphere after being emitted, although these can also be part of the primary emission mix. Heavy metals such as lead and mercury are also common particle components. It is important to realize that not all volcanoes emit the same mix of pollutants in similar proportions, and that the same volcano may emit a different pollutant mix at different times. Health effects, to the extent that they are related to the composition of the emissions, would also be expected to be variable.

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A large range of exposures to volcanic pollutants is expected based largely on marked differences in proximity of populations to volcanic emission plumes. It is estimated that at least 500 million people in the world today (8%) live in areas where they could be exposed to emissions from volcanoes known to have been active in human times. Volcanic emissions from the often long periods between eruptions affect a much smaller subset of this population.

27.3.2 Health effects Health effects due to exposure to volcanic ash have been investigated using both observational and experimental approaches. There was a flurry of interest in the health effects of volcanic ash following the Mt St Helens eruption in southern Washington State in 1980. Short-term effects included increased emergency and hospital visits for respiratory symptoms and asthma. Pre-existing respiratory disease was a risk factor for adverse effects. Short-term ocular symptoms were also common. In vitro toxicology studies generally found toxicity similar to that of ‘low-toxicity’ minerals. Inhalational animal studies showed conflicting results, but those done using more realistic, although still high, concentrations of ash showed little toxicity. The ash was clearly less toxic than crystalline silica. Other series of health studies have been carried out in relation to the Mt Sakurajima volcano in Japan and the Soufriere Hills volcano in Montserrat in the West Indies. Regular and frequent eruptions of the Mt Sakurajima volcano have chronically exposed the local population to volcanic emissions and ash since 1955. While no cases of silicosis have been detected, there is a slightly increased prevalence of respiratory symptoms related to exposure. Level of lung function in area loggers has not been associated with exposure. Eruptions of the Soufriere Hills volcano have resulted in frequent ash exposures of the resident population since 1995. Most of the crystalline silica in ash from this volcano is cristobalite, a particularly fibrogenic form. Prevalence of respiratory symptoms in children is higher in those from higher exposure areas of Montserrat. Inhalational studies using the Soufriere Hills ash in rats have shown more lung inflammation than with inert dust, but toxicity is considerably less than that of quartz. While no chest radiographic evidence of pneumoconiosis in island residents has been found, the latency period from onset of exposure is obviously short. Exposure to volcanic gases also has the potential to be harmful. CO2 from volcanoes may be concentrated in high enough concentrations to cause asphyxiation. This can occur as a result of the sudden release of a CO2 cloud or from accumulation of CO2 in low-elevation areas where air circulation is limited, even at times when a volcano is quiescent. The evidence for deaths due to CO2 asphyxiation is largely indirect, being typically based on reports of large numbers of deaths in a defined area not due to other apparent causes, such as occurred around Lake Nyos in the Cameroon in 1986, and on some case reports. These reports are nevertheless compelling. Hydrogen sulfide is another potential cause of asphyxiation from concentrated volcanic or geothermal releases. Like CO2, H2S can concentrate in low-elevation areas. If concentrations are high enough, the fraction of inspired oxygen could be critically reduced, leading to asphyxia. Unlike CO2, H2S in these situations probably causes its

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effects not by asphyxiation but by blocking the mitochondrial cytochrome chain, much like cyanide. Also, because H2S is lipid-soluble, effects are often localized to the central nervous system with manifestations of loss of consciousness or respiratory arrest. In those who survive exposure to high H2S concentrations, the clinical presentation could be one of pulmonary edema, adult respiratory distress syndrome or pneumonia. While the pneumonia is probably a chemical pneumonitis, bacterial pneumonia should be suspected if pneumonia develops several days after the incident. At low concentrations, H2S is a potent irritant to mucous membranes and the respiratory tract. The sulfurous rotten egg odor of H2S is apparent at much lower concentrations than produce irritant symptoms. There has also been concern about effects of long-term exposure to much lower concentrations of H2S and other reduced sulfur compounds. The evidence is most convincing for neurological and psychological sequelae of long-term H2S exposure and for increased reported respiratory symptoms. As concerns other respiratory effects of H2S exposure, most evidence indicates no effect on level of lung function; evidence for increased respiratory hospitalizations and lung cancer is sporadic and inconsistent. An ecological study from Rotorua, New Zealand, a city affected by H2S emissions from a geothermal field, found evidence for neurological and respiratory hospitalization rates being increased in higher exposure areas, although there was also a suggestion that cardiovascular hospitalization rates were also increased. As in all ecological studies, because no data on individuals was available, there is concern that the observed associations could have other explanations than exposure to H2S. Sulfur dioxide exposure can also be harmful, especially at high concentrations, where it is well known to cause bronchoconstriction in asthmatics. The evidence that high concentrations of volcanic SO2 specifically have been harmful is limited. As with other gases and fumes, it is has been difficult to implicate SO2 as the harmful component of what is often a mix of gases and fumes. However, episodes of degassing of SO2 have reportedly caused a small number of deaths in asthmatics. Volcanic acid fumes and acid aerosols, some generated from SO2, could potentially also contribute to adverse health effects, but evidence implicating them specifically is lacking.

27.3.3 Volcanic emissions summary Both volcanic ash and gases from volcanic eruptions and degassing can cause effects on health. Exposure to ash most certainly causes ocular and respiratory symptoms and causes symptomatic individuals to seek medical care, especially those with pre-existing respiratory conditions such as asthma. Whether more severe effects of volcanic ash occur is controversial. Of particular concern is whether those chronically exposed to airborne ash are at risk of silicosis. While there have been no documented cases of silicosis caused by volcanic ash, silicosis is a theoretical possibility when risk is assessed on the basis of concentrations of crystalline silica and years of exposure. The health impacts of volcanic gases specifically appear to be due largely to the rare episodes in which very high concentrations cause death by asphyxiation, poisoning or severe exacerbation of asthma. While chronic exposure to gases is of concern, apart perhaps for neuropsychological sequelae of H2S exposure, the evidence for effects from long-term exposure to volcanic gases is weak (Table 27.3).

402 Table 27.3

CH 27 NATURAL SOURCES – WILDLAND FIRES AND VOLCANOES

Volcanic emissions and anticipated severity of respiratory health effects

Emission component

Respiratory health effect Respiratory symptoms

Reduced level of lung function

Respiratory hospitalization

Respiratory mortality

Ash

Good evidence

None

Good evidence, especially if preexisting lung disease From asphyxiation and its sequelae

Little evidence, but plausible

CO2

Little evidence as a result of long-term exposure None

H2S

Potent respiratory irritant; odor threshold much lower than irritant threshold In asthma

Unlikely

From asphyxiation or poisoning and sequelae

Acutely in asthma

Plausible in asthma

SO2

From asphyxiation and its sequelae From asphyxiation or poisoning and sequelae

Suspected in case reports of asthma

27.4 Management/prevention 27.4.1 Biomass smoke exposure There are many instances where a diagnosis of a respiratory disease in an individual, or even an exacerbation of underlying disease, cannot be unequivocally attributed to smoke exposure. Exceptions include dramatic cases where the temporal association firmly establishes the causal connection, or where a diagnostic procedure such as broncho-alveolar lavage detects evidence of high-level particle exposure in the context of clinical disease, such as interstitial lung disease. In the common situation where such certainty is not possible, it is prudent to keep an open mind about the likelihood that, failing other explanations, smoke exposure is responsible for symptoms or illness. Since there are no treatment approaches for respiratory conditions that are specific to the exposures described in this chapter, except possibly for the case of H2S intoxication (see below), general recommendations for management of these conditions should be followed. Preventive measures should be considered, especially if the underlying condition is sufficiently severe that worsening would cause distress or prompt clinical intervention. General preventive measures include pharmacologic measures; exposure specific preventive measures typically aim to reduce or eliminate exposure. In patients with asthma or COPD, it is important to encourage compliance with maintenance medications and to review action plans of incrementally more aggressive treatment and management based on symptoms or personally monitored level of lung function. In

27.4

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fragile patients exposed to smoke, it may be prudent to increase medication dosage or frequency above the maintenance level before symptoms or lung function worsens. Because particles smaller that 1 mm in diameter gain ready access indoors, staying indoors will not provide much protection from these fine particles. When doors and windows are closed, larger particles, many of which still reach distal parts of the bronchial tree as well as the alveoli, do not gain ready access indoors. Irritant symptoms, to the extent they are caused by larger particles, can be lessened or prevented by keeping indoors. Running air conditioning or using the fan on home heating systems that have some filtration function can also be helpful. The effectiveness of portable air cleaners in lowering indoor concentrations of PM from wood smoke has been debated. The effectiveness of portable high efficiency particulate air (HEPA) cleaners and electrostatic precipitators was investigated recently in two studies, one in relation to forest fires in the Okanagan Valley in southern British Columbia in 2003, and the other in relation to the Hayman fire near Denver, Colorado in 2002. Somewhat surprisingly, in both studies use of air cleaners resulted in substantial reductions in indoor PM concentrations. In a California study, people who used portable HEPA filters longer had fewer symptoms. Air cleaning devices are therefore recommended. These should be appropriate for the size of the room in which they are used. Personal protective equipment, such as an N95 mask that has been fit tested, theoretically should also provide some degree of protection against fine PM. The effectiveness of such well-fitted masks in relevant exposure settings has not been formally tested, however. In the California study above, mask use was deemed ineffective, but fit testing was not performed. It is very difficult to determine whether and when to evacuate residents exposed to smoke for health reasons, particularly those with underlying cardiopulmonary disease. Health surveillance data are seldom timely or definitive enough to be helpful. Guidelines to assist in making evacuation decisions have been formulated, such as those contained in the Forest Fire Emergency Action Guidelines of the Manitoba Emergency Plan (http://www.gov.mb.ca/emo/index.html) from the Province of Manitoba in Canada.

27.4.2 Exposure to volcanic emissions Because of the temporal association, the diagnosis of respiratory conditions related to volcanic eruptions is relatively straightforward. Also, for the most part, management of these respiratory conditions is not dictated by the nature of the exposure. Exceptions include patients presenting with conditions potentially due to exposure to high concentrations of gases. In those who survive these exposures, the nature of the exposure may not be immediately apparent, thereby making the diagnosis difficult. Medical practitioners working in areas close to volcanic or geothermal activity should be familiar with situations in which exposure to gases occurs and to suspect exposure when presented with suggestive symptoms. For example, in these settings, SO2 exposure should be considered when faced with worsening asthma. Pulmonary edema may be the presenting picture following extreme CO2 or H2S exposure if asphyxiation or poisoning was not severe enough to be lethal. It is often suggested that patients exposed acutely to high concentrations of H2S should be treated with the cyanide antidote kit that uses

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nitrites to produce methemoglobin to bind H2S, forming sulfhemoglobin. This treatment is controversial in H2S poisoning and has even been suggested to be potentially harmful as a result of sulfhemoglobinemia, further reducing blood oxygen-carrying capacity. In the aftermath of the Mt St Helens eruption, attention was given to the preparedness of medical facilities in adequately managing the sudden increase in patient load following volcanic eruptions in areas at risk. While outside the scope of this chapter, one of the lessons learned from Mt St Helens and other dramatic volcanic eruptions is that planners are well-advised to develop emergency plans to deal with the abruptly increased demand for appropriate care. Practicing physicians and other health care professionals in these areas can and should play important roles in the planning process.

Further reading Biomass fires Naeher, L.P., Brauer, M., Lipsett, M., Zelikoff, J.T., Simpson, C.D., Koenig, J.Q., Smith, K.R. (2007) Woodsmoke health effects: a review. Inhal. Toxicol. 19: 67–106.

Volcanoes Hansell, A., Oppenheimer, C. (2004) Health hazards from volcanic gases: a systematic literature review. Arch. Environ. Hlth 59: 628–639. Horwell C.J., Baxter P.J. (2006) The respiratory health hazards of volcanic ash: a review for volcanic risk mitigation. Bull. Volcanol. 69: 1–24.

28 Traditional urban pollution Sam Parsia1, Amee Patrawalla2 and William N. Rom1 1 2

New York University School of Medicine, New York, NY, USA New Jersey School of Medicine, Newark, NJ, USA

28.1 Introduction The twentieth century was marked by a rapid increase in industrial processes involving consumption of fossil fuels, particularly in the years following the Second World War. The pollutants generated by coal-fired power plants, steel mills, smelters and fertilizer plants became increasingly prevalent in the ambient air of developed regions of the world, particularly Europe and the USA. Even before the Second World War, air pollution was becoming an increasingly recognized reality. The first health crisis directly attributable to air pollution occurred in the Meuse Valley in Belgium in December 1930, where hundreds became ill and approximately 60 people (10 times the mortality rate) died during a 3 day period. The cause of this episode was a perfect combination of geography, weather and heavy industrial activity that resulted in a stagnant air mass containing high concentrations of toxic pollutants that settled over the towns of Huy and Liege. In the USA, a cloud of smog was visible over the Los Angeles skyline by the mid 1940s, and the coal-fueled Midwestern industrial boom filled the skies of the populous Eastern seaboard with airborne pollutants. A weather pattern similar to that seen in the Meuse valley occurred over the small town of Donora, Pennsylvania in 1948, once again concentrating the pollutants from nearby factories and causing widespread respiratory symptoms and 20 deaths (6 times the mortality rate). Although both the events in Liege and Donora received intense political and media attention in their respective countries at the time of each occurrence, the event that probably receives the most attention in environmental health literature is the London Fog of December 1952. During a four day period of December 1952, a dense, pollutantladen fog settled over the city and was blamed for about 3000 excessive deaths during the following weeks. Recent investigators have applied more contemporary modeling Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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techniques to public health records from the period and have raised the estimated death toll to as many as 12,000 excess deaths. Even taking the historical figure of 3000 deaths, the astounding number of deaths from this episode is considered by many to be the first major stimulus to the study and reduction of air pollution. Despite the many lessons learned from these historic environmental disasters, the rapidly developing countries of Asia, the Middle East and Latin America will probably suffer similar episodes given their large reliance on traditional energy sources and industrial practices to build their economies. In today’s global society, countries that have already learned from such disasters should help develop methods of industry that allow for sustainable growth, without a return to the smoggy days of London, Liege and Donora. The following will include a description of the major components of traditional sources of air pollution, a current understanding of the health effects of each component, and a brief summary of current policy issues. Common patient questions are addressed below (Table 28.1).

Table 28.1 Selected issues for patients with respiratory disease Question

Answer

When is the best time to exercise outdoors?

In cities, air pollution from ozone is generally lowest early mornings before rush-hour traffic, so exercise at that time, not close to a highway At a population level, by legislation to reduce air pollutants At a personal level, reduce use of gasoline or diesel, and limit outdoor activities during high pollution episodes By reducing outdoor exposure, by reducing exposure to relevant allergens and other asthma triggers and by optimizing asthma control with prescribed medications Ozone concentrations can also be high in rural areas with natural sources of NOx contributing to ozone in the summer months. No studies to date have shown overall improved outcomes among those who have moved to rural areas For patients with cardiovascular disease or COPD, there also is no current evidence to support a move to a more rural setting which may have less air pollution but also may have less availability of healthcare resources The generally relatively small risks of air pollution effects need to be balanced against the known beneficial effects of exercise for children, and there are currently no recommendations to restrict outdoor exercise for children except at times of extreme air pollution episodes The answer to this remains unclear but smoking, cooking with biomass fuel and occupational exposures remain the most important causes of COPD

How can exposure to air pollution be minimized?

How can the effects of air pollution on asthma exacerbations be prevented?

Should a patient with lung disease avoid living in a city?

Should outdoor play be restricted for children in cities?

How much COPD can be blamed on outdoor air pollution?

28.2

28.2

PARTICULATE MATTER

407

Particulate matter

28.2.1 Characteristics of PM Particulate matter (PM) includes air particles from many different sources and of various sizes. Total suspended particles are composed of particles up to 40 mm in diameter. PM10 refers to particles up to 10 mm in diameter and are those which can be inhaled past the upper airways. PM is further delineated into PM10-2.5 and PM2.5, the latter of which are fine particles up to 2.5 mm in diameter. Ultrafine particles are those which have a diameter less than 0.1 mm. Other important characteristics of PM are the contributing source and its various components. PM can be directly produced by combustive sources such as coal-fired power plants, or can be formed in the atmosphere as a result of the combination of gases from motor vehicles, industries and natural sources. Direct sources of PM in the traditional urban environment include coal- and oil-fired power plants and industry. The actual composition of PM2.5 varies tremendously based on both region and season. In a study of composition of PM2.5 over 187 counties in the USA, only seven of the 52 compounds analyzed accounted for 1% or more of the yearly or seasonal average of total PM2.5 mass. These included ammonium, elemental carbon, organic carbon matter, nitrate, sodium, silicon and sulfates and made up 79–85% of the total PM2.5 mass. PM and its effects vary based on source, region and season, which are also linked to particle size and composition.

28.2.2 Animal experiments Many efforts to develop a simple and consistent animal model of particle induced health effects have been made with variable success. The development of techniques to concentrate ambient particles at both New York University and Harvard School of Public Health in the 1990s has made standardized exposures easier to achieve, and have advanced this line of research immeasurably. These techniques allow investigators to collect ambient air and concentrate the particles without necessarily altering the distribution of sizes and chemical composition of the pollutants. Results of experiments employing materials obtained via these concentrators in closed chamber animal experiments follow. Effects on the respiratory system Early experiments compared normal rats with those exposed to 250 ppm SO2/day for 6 weeks as a method of inducing chronic bronchitis. The rats were then exposed to either concentrated ambient particles (CAPs) or filtered air 5 hours per day for three consecutive days and assessed for measures of pulmonary function and inflammation. The ambient air particle mass on each day was 7.1, 19.1 and 18.6 mg/m3 and after concentration via the Harvard/EPA Ambient Particle Concentrator levels of 205.5, 733.3 and 606.7 mg/m3 were achieved in the exposure chamber. After exposure, the chronic bronchitis rats interestingly had significant increases in both tidal volume and peak expiratory flow, whereas normal rats had increased tidal volume over baseline. Bronchoalveloar lavage showed no difference in total cell counts, but a shift in the

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cellular differential towards neutrophilic inflammation and increased fluid protein content was observed. Similar experiments in normal dogs showed no statistically significant differences in bronchoalveloar lavage cellularity, but a nonsignificant trend towards increased neutrophils. Exposure to CAPs, collected from a community in southwestern Detroit with known high levels of air pollution showed no demonstrable airway inflammation in healthy rats; however, ovalbumin-sensitized rats did have significant, although variable inflammatory responses after five consecutive days of exposure. Finally, no differences were found in pulmonary immune responses in rats exposed to CAPs collected in New York City; however, there was a significant elevation in blood polymorphonuclear leukocytes. Effects on the cardiovascular system Acute exposure (4 weeks) to PM10 has been shown to enhance progression of atherosclerotic lesions in rabbits with inherited hyperlipidemia. A longer term (6 month) study of apolipoprotein E knockout mice (ApoE
/
) who were exposed to concentrated PM2.5 for 6 hours per day, 5 days per week also showed increased atherosclerosis, particularly when fed a high-fat diet. These mice were also found to have alterations in vasomotor tone, heart-rate fluctuation and vascular inflammation. These effects also seem to translate into worse clinical outcomes in models of myocardial infarction, as dogs exposed to CAPs developed a significantly greater degree of ST segment elevation after coronary artery occlusion.

28.2.3 Health effects of PM in humans Short-term health effects of PM The influence of particulate air pollution on short-term health effects has been largely examined through time-series studies, which generally relate daily PM levels to various indicators of disease. Several multi-city, time-series studies have been performed, including a 90-city study in the USA, the National Morbidity, Mortality and Air Pollution Study (NMMAPS). In this study, multiple pollutants were examined and PM10 levels were found to be associated with an increase in mortality, with the largest effect size seen in the northeast region. Nationally, for every 10 mg/m3 increase in PM10, a 0.2% increase in mortality with a 1-day lag was detected. In addition, there was a 0.3% increase in cardiopulmonary-specific mortality, for every 10 mg/m3 rise in PM10. Hospital admissions for cardiovascular disease and COPD among elderly in 14 cities from NMMAPS were also correlated with PM10 levels. The multi-city European project, APHEA (Air Pollution and Health: a European Approach), has also studied the short-term effects of particulate air pollution. In the initial study, black smoke (representing PM < 4 mm) and PM10 were correlated with daily mortality in 12 European cities. A 50 mm3 increase in black smoke and PM10 was associated with respective 3 and 2% rises in mortality in western European cities. A more comprehensive study, APHEA2, included 29 European cities and measured health outcome and particulate levels over 5 years, beginning in 1990. Similar to NMMAPS, APHEA2 correlated a 0.6% increase in daily mortality with a 10 mg/m3 rise in PM10 and black smoke. Larger effects sizes were noted among elderly, and in cities with higher NO2 and warmer climates.

28.2

PARTICULATE MATTER

409

Long-term health effects of PM Health effects of chronic air pollution in traditional urban areas were investigated in a study comparing three counties in Utah, each with a major city. Two of the counties, Utah and Cache Counties, were similar, in terms of demographics, religion and minimal tobacco use, until a steel mill was built in Provo (Utah County) in the 1940s. Salt Lake County, which included the third city, was notably more characteristic of a US city. Smoking, for example, was twice as common in Salt Lake County. Approximately 45% of PM10 levels in Utah County were produced by the Provo steel mill. From 1960 to 1970, respiratory cancer death rates doubled in Utah County, in contrast to Cache County, where they were relatively unchanged, and continued to increase in subsequent decades. Long-term air pollution, which increased substantially in Provo and was largely attributed to the steel mill, was associated with increased mortality and morbidity from both respiratory cancers and nonmalignant pulmonary disease. Temporary cessation of operations at the Utah County steel mill in 1986 led to decreased PM10 levels, and was associated with fewer county-wide hospital admissions for respiratory illnesses [1]. Fine particulate matter and mortality More specific health effects of fine particulate matter have also been studied. The effects of long-term air pollution and PM2.5 were studied in the cohort from the Harvard Six Cities Study, which included roughly 8100 adults from Watertown, MA, Harriman and Kingston, TN, St Louis, MO, Steubenville, OH, Portage, WI and Topeka, KS, areas with differing degrees of air pollution. Central air pollution and individual health data were collected from the mid-1970s to 1991. Overall mortality in this cohort study was most strongly linked with fine (PM2.5), inhalable particulate matter, especially sulfates, with relative rate ratios of 1.26–1.27 across the range of pollution found in these cities. Specific causes of death linked to air pollution in this study included lung cancer and cardio-respiratory illness [2]. An association between PM2.5 and mortality was also found as part of the Cancer Prevention Study II, where data on 1.2 million people across the USA was prospectively collected. Overall, PM2.5 levels decreased in the USA from 1979 to 2000, which was the span over which air pollution data was collected. Whether assessed at the start or end of the study, air pollution as reflected by PM2.5 levels was linked with all-cause, cardiorespiratory and lung cancer deaths. For a 10 mg/m3 increase in PM2.5, there was a relative risk of 1.06 (95% CI 1.02–1.11), 1.09 (95% CI 1.03–1.16) and 1.14 (95% CI 1.04–1.23) for all-cause, cardio-pulmonary and lung cancer mortality, respectively [3]. In a follow-up study of the Harvard Six Cities cohort, all-cause, cardiopulmonary and lung cancer mortality were again found to parallel PM2.5 levels [4]. As seen in CPSII, PM2.5 levels decreased in all six cities, with greatest reduction in the most polluted cities. For every 10 mg/m3 decrease in PM2.5 seen in the follow-up period, there was a reduction in all-cause mortality (RR ¼ 0.73; 95% CI 0.57–0.95). This was seen for cardio-respiratory mortality, but not for lung cancer deaths. This follow-up study reiterated the association between PM2.5 levels and mortality, and also suggests that health effects of air pollution can be attenuated [4]. Fine particulate matter and morbidity PM2.5 has also been studied in terms of morbidity among both adults and children. Hospital admissions in a Medicare population were recently reviewed in conjunction

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with available PM2.5 levels in 204 US counties to examine the short-term effects of air pollution on cardiopulmonary morbidity. Daily variations in PM2.5 were linked to change in hospital admission rates for heart failure, COPD, respiratory tract infections, cerebrovascular disease, peripheral vascular disease, ischemic heart disease and heart rhythms. Hospitalization rates for up to 2 days of lag time after the measured PM2.5 level were examined. Cardiovascular hospitalizations were most likely on day 0 (except for ischemic heart disease), whereas there was more variability in timing of hospitalization for respiratory illnesses. For every 10 mg/m3 increase in PM2.5, there was a 1.28% higher risk of same-day hospitalization due to heart failure. The authors calculated that annual admissions for heart failure would drop by 3156, in these 204 counties, if PM2.5 was reduced by 10 mg/m3. Hospitalizations for respiratory tract infections and COPD would be reduced by 2085 and 990, respectively [5]. Some regional variation was also seen, with greater cardiovascular effect size seen in Eastern counties. Fine PM and cardiovascular morbidity Cardiovascular health effects include reduced heart rate variability as a risk factor for mortality, especially in elderly subjects. Diminished heart rate variability was linked with higher PM2.5 levels in a small, elderly population in Utah. More recently, a study of the cardiovascular effects of long-term air pollution in a large cohort of postmenopausal women without pre-existing heart disease was published (Women’s Health Initiative Observational Study). An adjusted hazard ratio of 1.24% (95% CI 1.09–1.41) for time to first cardiovascular event, including cerebrovascular events, was associated with a 10 mg/m3 increase in PM2.5. Other pollutants were measured, but were not significantly linked to cardiac morbidity. The strongest findings were for mortality endpoints, and especially for death due to definite coronary heart disease. Higher hazard ratios for mortality endpoints were found than in previous cohort studies which included men, which may reflect greater vulnerability of women in terms of air pollution or differences in methodology of the studies. Theories that have been offered to help explain the effect of air pollution on cardiovascular disease include accelerated atherosclerosis, change in autonomic control and increased inflammation. Fine PM and respiratory morbidity Clinical studies assessing the association of PM2.5 on respiratory morbidity have also been performed. Populations with pre-existing illnesses seem to be at greater risk of negative effects of air pollution. In APHEA2, a 10 mg/m3 rise in PM10 levels was correlated with an increase in respiratory admissions, including children and adults with acute asthma and COPD, by approximately 1%. In another study, children with asthma were given personal exposure monitors and followed for 2 week periods. FEV1 (percentage predicted) was found to be negatively associated with the level of personal, fine PM exposure. Nonmobile measurements of PM were also recorded and associated with pulmonary function, but more weakly than personal PM levels. In addition, personal PM had a larger effect in atopic boys with susceptibility to indoor allergens. Children with more severe asthma also seem to be more susceptible to effects of particulate air pollution, in a study of schoolchildren in Denver, Colorado. PM2.5 levels were found to be highest in the morning hours when children were traveling to school. Higher morning PM2.5 levels resulted in greater use of bronchodilators at school, also suggesting rapid onset of symptoms. This relationship was also more pronounced in

28.3

SULFUR OXIDES

411

children with severe asthma. In addition, urinary leukotriene E4 was measured during the school day and was associated with morning PM2.5 levels. Another personal monitor study in Seattle, Washington examined lung function effects of particulate air pollution in children with asthma and adults with COPD. Decrease in FEV1 was associated with PM2.5 measurement at a central location, after a 1-day lag, in patients with COPD, although it did not correlate with personal levels. In asthmatic children not on antiinflammatory medications, PM2.5 was associated with declines in MMEF, FEV1 and PEF. While some change in lung function was seen overall, the correlation was stronger in asthmatics not on anti-inflammatory medications, lending support to possible PM triggering of inflammatory mechanisms [6]. Elevated exhaled nitric oxide was associated with PM2.5 levels in these same children in an earlier report, further highlighting the potential inflammatory effects of air pollution. While further categorizing the respiratory effects of air pollution, these studies also point out that use of daily averages of PM levels may not be sufficient to fully understand the health effects of particulate air pollution. Associations between respiratory illness and particulate air pollution have been further strengthened by studies involving experimental exposures to PM in humans, which help define underlying mechanisms for disease causation. In one study, healthy volunteers were exposed to CAPS (concentrated ambient particles 0.1–2.5 mm in size) for 2 hours. Final exposure concentrations ranged from 23.1 to 311.1 mg/m3, and were dependent on variation in outside particulate levels. There were no differences in pulmonary function testing or symptoms between those exposed to CAPS versus filtered air controls. However, increases in cellularity and neutrophil counts of bronchoalveolar lavage fluid were seen after CAPS exposure as compared with filtered air. In addition, bronchoalveolar lavage fluid neutrophils appeared to increase in a dose-dependent manner, highlighting a possible inflammatory pathway of particulate air pollution induced illnesses. In recent literature, particulate air pollution has been increasingly associated with adverse health effects. As reviewed, there is evidence for both increased mortality and cardio-respiratory morbidity linked to PM exposure. While earlier studies focused on short-term mortality risk, the current body of research supports an increased chance of long-term consequences as well. There has also been focus on highly susceptible populations, such as those with chronic respiratory illnesses as well as the elderly. Work on elucidating the pathogenesis of PM-associated cardiovascular and respiratory morbidity has also progressed. In the USA, the National Ambient Air Quality Standards (NAAQS) for PM were slightly lowered in 2006 on the basis of growing evidence for adverse PM-related health effects. Adverse health outcomes have been seen even at low PM concentrations in recent time-series studies and many argue, in fact, that PM NAAQS are not stringent enough.

28.3

Sulfur oxides

28.3.1 Characteristics of sulfur oxides Sulfur is a major component of fossil fuel sources such as coal and oil, as well as several common metal ores such as iron, zinc, and copper. Combustion of these materials leads to the formation of the gas sulfur dioxide, which may dissolve in water vapor to form

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acidic aerosols that eventually fall to the earth in the form of acid rain. These acidic byproducts of sulfur combustion primarily concentrate in lakes and streams, often resulting in a decrease in pH significant enough to reduce, or in some cases eliminate natural aquatic wildlife populations. Sulfur dioxide may also combine with other particles in the air to form sulfate particulate matter, which contributes to visual pollution, particularly in summer months when it forms a milky, white haze in the afternoon. While ambient SO2 concentrations are highest close to the source of production (coal-fired power plants, petroleum refineries, smelters), sulfate particles can have an impact relatively far away since their small size lends to long distance transport. Intercontinental transport of SO2 and other toxic emissions promises to be an important policy issue for years to come.

28.3.2 Acute health effects Sulfur dioxide is rapidly absorbed by mucosal surfaces of the nasopharynx and upper airway. It is readily soluble in epithelial lining fluid, forming acidic species that result in cellular damage. Although this rapid upper airway absorption protects the lower airways from the irritant effect, the increase in minute ventilation and tidal volume during exercise overcomes its absorptive capacity, often resulting in lower airway effects. Acute exposure to sulfur dioxide can result in a variety of symptoms, most commonly dyspnea, cough, and exacerbation of chronic cardio-pulmonary disease. Controlled chamber experiments, which allow for measurements of the specific effects of SO2, have demonstrated a spectrum of responses in healthy individuals, from no effect to marked bronchoconstriction. The asthmatic population is generally more susceptible, but in these controlled settings without the additive effects of other pollutants, the effects are generally reversible in minutes to hours. The minimum concentration required to demonstrate a decline in lung function in normal is approximately 1000 ppb (2860 mg/m3), whereas asthmatics may have significant reductions in lung function at as low as 400 ppb (1144 mg/m3). For reasons mentioned above, the effects of SO2 may be augmented by exercise, and in one study an interaction was found when SO2 was administered with cold dry air.

28.3.3 Effects of chronic exposure The effects of long-term exposures to SO2 are less clear, and there is controversy in the literature as to its negative effect independent of sulfate and nonsulfate PM. As part of the APHEA project, a 3% increase in daily mortality was shown with an increase in SO2 by 50 mg/m3 (95% CI 2–4%) that was independent of PM10. However, six other studies that resulted from APHEA data failed to replicate these findings. Several Chinese investigators have been able to demonstrate an effect of SO2 on morbidity and mortality independent of total suspended particles in a variety of locations in China, which may reflect a difference in population susceptibility or unique characteristics of industrial emissions in the region. Since PM2.5 may be the more specific causal agent in PMrelated disease, further data on SO2 effects independent of PM2.5 would be valuable in establishing an independent effect. One such analysis of data from Chongqinq, China

28.4

NITROGEN OXIDES

413

did show independent increases in relative risk of respiratory and cardiovascular mortality independent of PM2.5. Overall, SO2 should be viewed as an airway irritant with several demonstrated acute, negative effects on respiratory symptoms and physiology, while its long-term effects on morbidity and mortality remain a topic for investigation.

28.3.4 Regulatory actions Worldwide sulfur emissions peaked in 1989, and have declined since then, although they remain well above those at the beginning of last century. Initial efforts to decrease the local levels of SO2 involved mandating the construction of tall (in some cases 500 feet high) smokestacks so that SO2 would disperse over a greater area and reduce the effects on the local population. While this policy was successful in reducing the human impact of SO2, the generation of PM remained unabated until policy to decrease the total amount of sulfur emissions produced was enacted. The first Clean Air Act was passed by the UK during the 1950s after recognizing the health impacts of the London Smog, and the USA followed suit in 1963 with subsequent modifications, most notably in 1970 with the establishment of the Environmental Protection Agency (EPA). The most recent revision of the Clean Air Act in 1990 included a specific Acid Rain Program that implemented a ‘cap and trade’ system whereby individual power plants were given an allowance of emissions per unit of energy when compared with a historical standard. If this allowance is then exceeded, additional emissions ‘credits’ may be bought or traded for on the open market. This policy was hailed as an approach to air pollution control that allowed for some flexibility within the industry to reduce emissions without necessarily forcing the immediate closure of older plants that would be costly to update to cleaner technologies. As a result of the initial phase of the Acid Rain Program, SO2 emissions in the USA declined by 17% between 1990 and 1998, and Phase II of the program promises further reductions in years to come. As mentioned previously, concerns about industrialization in Asia and other parts of the developing world temper optimism about a true reduction in sulfur emissions globally, since many of the improvements made in developed countries could easily be nullified by increased emissions worldwide.

28.4

Nitrogen oxides

28.4.1 Characteristics of nitrogen oxides Although there are many known sources of nitrogen oxides in rural settings related to nitrogenous fertilizers and manure management, traditional urban sources (excluding vehicular) arise primarily from combustion of fossil fuels such as coal and oil for electricity production, with a lesser contribution by sewage treatment plants. Fossil fuelrelated power generation initially leads to release of nitrogen oxide, which can be further oxidized to nitrogen dioxide in the atmosphere. Nitrogen dioxode is a colorless, odorless gas, whereas nitrogen oxide has an odor and a reddish-brown color that contributes to visible pollution independent of associated particulates. The combination of these and other oxidized nitrogen species are typically referred to as NOx. As will

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be described in subsequent sections, the primary health effects of NOx species are ozone formation via interactions with volatile organic compounds in the presence of sunlight. In addition, NOx contributes to acid rain along with sulfur oxides, and has effects on water systems independent of pH by upsetting the balance of nutrients required by aquatic plants and animals. This process of excess nitrogen deposition is termed eutrophication, and can result in algae overgrowth that eventually depletes oxygen from the body of water creating a ‘dead’ zone. Nitrous oxide (N2O), a lesser component of NOx, persists in the atmosphere for approximately 120 years and is thought to be a significant contributor to global warming.

28.4.2 Acute health effects In terms of direct health effects of nitrogen oxides, NO2 has widely recognized effects from known occupational exposures (silo-filler’s disease), during which a highly concentrated exposure leads to severe respiratory symptoms and adult respiratory distress syndrome. In the case of ambient pollution, however, studies vary in their ability to demonstrate or refute the specific role of NOx in human disease due to the large populations required and potential confounding from other pollutants. Controlled experiments that simulate levels commonly observed in the atmosphere have shown no effect in healthy subjects at NO2 concentrations up to 0.60 ppm, but asthmatics were demonstrated to have a decrease in FEV1 during exercise and cold air inhalation after exposure to NO2 at 0.30 ppm.

28.4.3 Effects of chronic exposure Large-scale population based studies are less conclusive, although several are suggestive. A retrospective analysis of hospital asthma admissions in Hong Kong found the relative risk of admission was 1.028 (95% CI 1.021–1.034) for every 10 mg/m3 rise in NO2 concentration. Similar findings were obtained in a study that included controls for four types of pollen, as well as the more usual PM, SO2 and ozone. Increases in viral respiratory tract infections have been observed in asthmatic children, and patients over the age of 65, and there is some in-vitro data to suggest altered host response to infection with respiratory syncytial virus. In terms of mortality, although some found no association with increased mortality from NO2 independent of PM, several others found positive associations with statistically significant increases in total mortality 0.30% (95% CI 0.25–0.35%), cardiovascular disease mortality 0.41% (95% CI 0.34–0.49%), and respiratory mortality 0.34% (95%CI 0.17–0.51%) for every 10 mg/m3 increase in NO2 in an analysis of APHEA-2 data [7]. A cohort study of 4800 German women living in North Rhine–Wesphalia found that both total and cardiopulmonary mortality correlated with a rise in the NO2 interquartile range by 16 mg/m3, when adjusted for smoking and socioeconomic status [8].

28.4.4 Regulatory actions As in the case of sulfur oxides, levels of nitrogen oxides have been decreasing in the USA and Europe as the result of legislation. Data from the UK National Atmospheric

28.5

OZONE

415

Emissions Inventory show energy generating emissions declined by approximately 45% between 1990 and 2003, and US EPA data show a 30% decline over a similar period. These data do not take into account reductions due to a decrease in industrial activity in developed countries, but also fail to note the impact of increased industrialization in Asia. In summary, nitrogen oxides in concentrations commonly observed in the atmosphere are likely contributors to cardiopulmonary morbidity in susceptible populations; however, definite mortality associations remain to be fully elucidated (Table 28.2).

28.5

Ozone

28.5.1 Characteristics of ozone Ozone is not a directly emitted pollutant, but rather is generated by the interaction of multiple pollutants in the atmosphere in the presence of sunlight. Volatile organic compounds emitted by industry, solvents and motor vehicles (gasoline), combine in the atmosphere with nitrogen oxides (NOx) generated by combustion of coal and other fossil fuels to form atmospheric ozone (O3). This interaction was first noted by A.J. HagenSmit, a Dutch chemist working at the California Institute of Technology in the 1940s, during a period of intense smog in the Los Angeles area. Although ozone serves as protection from UV radiation when it naturally forms high in the stratosphere (15–35 km above sea level), high concentrations near the Earth’s surface are associated with adverse health effects. Ozone levels typically peak during summer afternoons given the longer duration of sunlight, and susceptible individuals should be encouraged to stay indoors as much as possible during these periods.

28.5.2 Acute health effects Ozone has a potent oxidizing and direct toxic effect on cell membranes that leads to the generation of intracellular peroxides and free radicals. In vitro studies show that O3 is able to deactivate alpha1-antitrypsin, which could theoretically increase susceptibility to emphysema. In terms of acute effects in humans, as with other pollutants, the response is variable and largely depends on individual susceptibility. A heterogeneous sample of asthmatics and nonasthmatics will demonstrate a significant drop in FEV1 after controlled ozone exposure in only 10–20% of subjects, while others have mild or even no effect from the exposure. Contrary to these findings, an hourly decrease in lung function was shown in 10 healthy volunteers who were exposed to 120 ppb of O3 for 6.6 hours while performing 5 hours of moderate exertion (similar to outdoor labor). These findings were subsequently replicated using lower concentrations of ozone, with 80 ppb being the lowest concentration to show a significant effect. Studies of inflammatory mediators in bronchoalveolar lavage as well as nasal airway lavage, have shown increases in neutrophils, immunoglobulins, elastase and a variety of other markers of inflammation. Airway responses to allergen can also be enhanced by preceding ozone exposure.

Interaction of VOCs, nitrogen oxides and sunlight VOCs derived from vehicle exhaust, industry, solvents

Vehicle exhaust Combustion of fossil fuels Sewage treatment plants Fertilizers and manure in rural settings Coal burning plants and other fossil fuel use such as smelters Coal-fired power plants, diesel and other vehicle exhaust, industry, natural sources

Ozone

NOx

VOC, volatile organic compounds.

Carbon monoxide Traffic exhaust fumes

Particulate pollution

SO2

Main sources

Pollutant

Bronchoconstriction in asthmatics (with exercise) Possible increased mortality separate from particle effects Association with firing of defibrillators Cardiovacular and COPD hospitalization

Asthmatics Athletes Elderly Those with cardiovascular risk factors or cardiovascular disease Possibly women Asthmatics and those with COPD

Elderly Those with cardiovascular risk factors or cardiovascular disease

Cardiovascular mortality All-cause death, including lung cancer and cardiorespiratory deaths Asthma emergency visits Cardiac events

Chest tightness, difficulty in full inspiration, airflow limitation, asthma exacerbation, increased airway inflammation, increased response to allergen, increased emergency visits and hospitalization for asthma, possibly increased risk of onset of asthma Significant effect on mortality separate from particle effects Increased risk of respiratory viral illness in children Airflow limitation in asthmatics (with exercise) Unclear if increases in cardiorespiratory mortality separate from particle effects

Genetically susceptible individuals Asthmatics Children Endurance athletes

Children

Health effects

Susceptible populations

Table 28.2 Summary of health effects of outdoor air pollutants (dependent on exposure concentrations and susceptibility of population)

416 CH 28 TRADITIONAL URBAN POLLUTION

28.6

AIR TOXICS

417

28.5.3 Chronic health effects Studies correlating increases in environmental ozone and health indicators are numerous and fairly consistently demonstrate adverse effects. The Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society of 1996 included several statements regarding ambient ozone resulting in increases in respiratory symptoms, emergency room visits and hospitalizations for exacerbations of asthma and other respiratory diseases, as well as some of the physiological and molecular effects mentioned above. This statement was in part fueled by studies by multiple groups studying air pollution in general that found effects of ozone independent of particulates, SO2 and other pollutants. Despite these findings, policy makers in the USA at times cite ‘scientific uncertainty’ regarding the negative health effects of ozone when pressed to impose stricter standards on ambient ozone levels.

28.5.4 Effects on human mortality Many large-scale, population-based studies have attempted to show a relationship between ambient ozone levels and mortality. Recent data demonstrated a significant association between short-term changes in ozone and noninjury related mortality across 95 US urban centers utilizing databases developed for the National Morbidity, Mortality, and Air Pollution Study. A 10 ppb increase in ozone levels showed a 0.52% increase in daily mortality (95% posterior interval [PI] 0.27–0.77%), and a 0.64% increase in cardiovascular and respiratory mortality (95% PI 0.31–0.98%) in the subsequent week. Similar conclusions were drawn in a study of 23 European cities (APHEA), where increases of 0.45% of cardiovascular deaths and 1.13% of respiratory deaths were observed during summer months following increases in ozone concentrations. In addition, several meta-analyses support these hypotheses as well. As with sulfur oxides, the potential for confounding by PM is omnipresent; however, results indicate a robust effect independent of PM10 or PM2.5.

28.6

Air toxics

28.6.1 Benzene Potential sources of exposure include exhaust from vehicles, solvents used in manufacturing plants and hazardous waste areas. Health effects of benzene are probably the result of its metabolites, including benzoquinone, benzene oxide and muconaldehyde. While it has been recognized as a carcinogen for hematologic malignancy in occupational settings, correlation between exposure level and hematologic risk has also been variable. Several nonoccupational studies have linked childhood leukemia with residence near petroleum industries and gas stations, which may point to the effects of ambient benzene exposure. Little is known about other effects of benzene at the low exposure levels found in outdoor air.

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28.6.2 Other exposures Outdoor air may also contain other pollutants that can affect the lung. Examples include chemicals from industrial sources in the area. Cases of sensitization have been reported from beryllium and diisocyanates in the neighborhood around companies using these. Asbestos fibers are in the air in urban settings at low levels, but in areas close to asbestos mines there have been increased risks of mesothelioma reported (although it may be difficult to separate the effects of outdoor exposure from second-hand indoor exposure from family members who worked in the mines).

References 1. Pope, C.A. (1991) Respiratory hospital admissions associated with PM10 pollution in Utah, Salt Lake, and Cache Valleys. Arch. Environ. Hlth 46: 90–97. 2. Dockery, D.W., Pope, C.A., Xu, X. et al. (1993) An association between air pollution and mortality in six U.S. cities. New Engl. J. Med. 329: 1753–1759. 3. Pope, C.A., Burnett, R.T., Thun, M.J. et al. (2002) Lung cancer, cardiopulmonary mortality and long-term exposure to fine particulate air pollution. J. Am. Med. Assoc. 287: 1132–1141. 4. Laden, F., Schwartz, J., Speizer, F.E., Dockery, D.W. (2006) Reduction in fine particulate air pollution and mortality. Am. J. Respir. Crit. Care Med. 173: 667–672. 5. Dominici, F., Peng, R.D., Bell, M.L. et al. (2006) Fine particulate air pollution and hospital admission for cardiovascular and respiratory diseases. J. Am. Med. Assoc. 295: 1127–1134. 6. Trenga, C.A., Sullivan, J.H., Schildcrout, J.S. et al. (2006) Effect of particulate air pollution on lung function in adult and pediatric subjects in a Seattle panel study. Chest 129: 1614–1622. 7. Samoli, E., Aga, E., Touloumi, G. et al. (2006) Short-term effects of nitrogen dioxide on mortality: an analysis within the APHEA project. Eur. Respir. J. 27: 1129–1138. 8. Gehring, U., Heinrich, J., Kramer, U. et al. (2006) Long-term exposure to ambient air pollution and cardiopulmonary mortality in women. Epidemiology 17: 545–551.

Further reading Balmes, J.R., Fanucchi, M.V., Rom, W.N. (2007) Ozone, a malady for all ages. Am. J. Respir. Crit. Care Med. 176: 107–108. Bernstein, J.A., Alexis, N., Barnes, C., Bernstein, I.L., Bernstein, J.A., Nel, A., Peden, D., Diaz-Sanchez, D., Tarlo, S.M., Williams, P.B. (2004) Health effects of air pollution. J. Allergy Clin. Immunol. 114: 1116–1123. Chen, T.M., Shofer, S., Gokhale, J., Kuschner, W.G. (2007) Outdoor air pollution: overview and historical perspective. Am. J. Med. Sci. 333: 230–234. Committee of the Environmental Occupational Health Assembly of the American Thoracic Society (1996) Health effects of outdoor air pollution. Am. J. Respir. Crit. Care Med. 153: 3–50. Committee of the Environmental Occupational Health Assembly of the American Thoracic Society (1996) Health effects of outdoor air pollution Part 2. Am. J. Respir. Crit. Care Med. 153: 477–498. Delfino, R.J., Sioutas, C., Malik, S. (2005) Potential role of ultrafine particles in associations between airborne particle mass and cardiovascular health. Environ. Health Perspect. 113: 934–946. Gryparis, A., Forsberg, B., Katsouyanni, K. et al. (2004) Acute effects of ozone on mortality from the ‘Air Pollution and Health: A European Approach’ Project. Am. J. Respir. Crit. Care Med. 170: 1080–1087.

FURTHER READING

419

Schwartz, J., Zanobetti, A., Bateson, T. (2003) Morbidity and mortality among elderly residents of cities with daily PM measurements In Revised Analyses of Time-Series Studies of Air Pollution and Health. Special Report Health Effects Institute Boston, MA. Vedal, S. (2002) Update on the health effects of outdoor air pollution. Clin. Chest Med. 23: 763–775, vi. Viegi, G., Maio, S., Pistelli, F., Baldacci, S., Carrozzi, L. (2006) Epidemiology of chronic obstructive pulmonary disease: health effects of air pollution. Respirology 11: 523–532.

29 Traffic-related urban air pollution Steven M. Lee1 and Mark W. Frampton2 1 2

Kaiser Permanente Fontana Medical Center, Fontana, CA, USA University of Rochester Medical Center, Rochester, NY, USA

29.1 Introduction There is widespread recognition that pollution of the air we breathe, by cumulative products of human activity, adversely affects health. Studies of air pollution find evidence for health effects at ever-lower ambient concentrations, leading to continual tightening of air quality standards in developed countries. While these developed countries work to minimize emissions in order to improve air quality, many developing countries are experiencing massive increases in air pollution as a result of economic growth in the absence of emissions controls. Studies over the last two decades show that current pollution levels in cities around the world worsen the burden of lung and heart disease, increase mortality and may affect fetal and newborn growth and development. Traffic-related emissions represent a major contribution to the burden of ambient air pollution. The role that traffic pollution plays in air pollution health effects, relative to other emission sources such as industry and power generation, remains uncertain. However, the public health impact of traffic-related air pollution is not inconsequential. K€ unzli et al. [1] studied the overall public health impact of traffic-related air pollution in three European countries: Austria, France and Switzerland. While the individual risk for a significant health related impact of air pollution was small, the public health impact was significant. In the three countries, more than 40,000 deaths (6% of total mortality) were attributable to increases in particulate air pollution, with about 20,000 deaths attributable to traffic-related pollution. The costs associated with the increased mortality and morbidity amounted to 1.7% of the gross domestic product, a cost exceeding that for traffic accidents [2]. Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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Considerable effort is being expended to reduce engine emissions, with some notable success. However, the potential benefits of reduced emissions are often negated by the increased number of vehicles on the road, increased miles traveled by those vehicles, and the persistence of older, high-emitting vehicles. It is anticipated that traffic-related emissions, and their health effects, will increase most dramatically in developing countries. The growth of vehicle sales in Asia is likely to far outstrip that of the rest of the world in the coming decades. Emission and pollution controls have not received a major priority in many developing countries, and thus marked increases in trafficrelated emissions are expected. The goal of this chapter is to provide a perspective on our current understanding of the health hazards associated with exposure to traffic related air pollution. We will begin with a historical overview, describe the nature of traffic emissions, review current evidence that traffic emissions adversely affect health and finally identify key knowledge gaps and future approaches to the problem.

29.2 History of traffic-related air pollution Traffic-related air pollution started with the invention and widespread use of gasoline and diesel-powered motor vehicles. Automobiles were first developed in the nineteenth century, and were predominately powered by steam or electric engines. In 1876, Nicolaus Otto developed the first practical four-stroke internal combustion engine, and used it to power a motorcycle. Gottlieb Daimler constructed the first fourwheel automobile powered by a gasoline engine in 1886. Rudolf Diesel, who was born in Paris, discovered that fuel could be ignited in an engine without a spark. He was granted a patent in 1898 for the first diesel engine. Mass production of gasolinepowered automobiles was underway by the early 1900s, with Henry Ford pioneering assembly-line mass production, and making the automobile available to the masses. The increasing use of the automobile meant that people no longer had to live and work in the city. The past 50 years has seen a steady migration out of cities to the suburbs as improved roadways made this practical, especially in the USA. Commuting to work has contributed to an increased dependence on motor vehicle transport and marked increases in miles traveled. The numbers of cars on the road is increasing in many parts of the world. Automobile traffic in Europe is increasing much more rapidly than other modes of transportation (Figure 29.1). China is experiencing an explosion in the number of automobiles (Figure 29.2), with the number of registered vehicles increasing from about 600,000 in the year 2000, to 3.8 million in 2005. As the number of motor vehicles and the number of miles they travel increases around the world, vehicle emissions will be a growing international concern. The realization that traffic-related emissions have adverse health effects is a fairly recent phenomenon. Historical air pollution events in the Meuse Valley in Belgium in 1930, Donora, Pennsylvania in 1948, and London, UK in 1952 demonstrated unequivocally that air pollution can kill. The London Fog episode ranks as one of the worst natural disasters in history. During four days of stagnant air and temperature inversion over London, concentrations of particulate matter and sulfur dioxide soared, and more than 4000 people died. These episodes made it starkly clear that air pollution was more

29.2

HISTORY OF TRAFFIC-RELATED AIR POLLUTION

423

Figure 29.1 Volume of passenger transport in the 15 countries belonging to the EU before May 2004, in 1990, 1998 and 2010 (projection). From World Health Organization [34], reproduced by permission of World Health Organization

than just a nuisance, and spurred efforts to control emissions and establish air pollution standards, including the passage of the Clean Air Act by the US Congress in 1970. The pollution causing these historical air pollution episodes predominantly represented emissions from industrial processes and coal burning for home heating, not traffic. In developed nations, such ‘point source’ emissions have decreased, in part through improved emission control technology and air pollution regulation, but also as

Figure 29.2 New car registrations in China, 1998–2005. From: http://www1.eere.energy.gov/ vehiclesandfuels/facts/2006_fcvt_fotw438.html, accessed 2 April 2008

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a consequence of outsourcing of industrial production and changing home heating from coal burning to natural gas and electric. In contrast, traffic emissions continue to increase. Today, in developed countries, most human exposure to outdoor air pollution comes from traffic. Traffic has long been acknowledged as a major contributor to air pollution in major US cities. Table 29.1 summarizes the efforts and milestones in controlling traffic related pollution in the USA. Deterioration of air quality in Los Angeles and other cities in the 1950s and 1960s, and the growing recognition of health risks associated with air pollution, spurred the US Congress to pass sweeping air pollution legislation in 1970. The Clean Air Act established the new US Environmental Protection Agency (EPA) and promulgated an aggressive plan to reduce automobile emissions. The subsequent story of efforts to reduce traffic related air pollution is one of success mixed with compromise and delay. For example, the Clean Air Act emissions standards targeted for 1975 were

Table 29.1

A brief history of US traffic air pollution control measures

Year

Action

1970

Congress passes Clean Air Act US Environmental Protection Agency (EPA) established EPA directed to set ‘National Ambient Air Quality Standards’ for six pollutants A 90% reduction in emissions from new automobiles required by 1975 Congress delays the hydrocarbon and carbon monoxide standards until 1978 Corporate Average Fuel Economy (CAFE) program: more stringent fuel economy standards Catalytic converters introduced Unleaded gasoline introduced Congress amends Clean Air Act Hydrocarbon, carbon monoxide and nitrogen oxides standards delayed again New cars meet amended Clean Air Act standards for the first time EPA lowers the amount of lead allowed in gasoline Inspection and Maintenance programs established EPA adopts stringent diesel emission standards Phase-out of leaded gasoline is completed EPA sets fuel volatility limits aimed at reducing evaporative emissions EPA limits diesel fuel sulfur content Congress amends Clean Air Act: further reductions in emissions, gives EPA authority to regulate nonroad vehicles Oxygenated gasoline introduced in cities with high carbon monoxide levels EPA regulations target marine engines Emission standards for diesel-powered locomotives Emission standards for nonroad diesel engines Reduced emission standards for new large marine diesel engines Reduced emission standards for SUVs and light-duty trucks Plans to reduce sulfur in on-road diesel fuel by 97% by mid-2006 EPA identifies 21 mobile source hazardous pollutants (air toxics) and regulates toxic emissions Japanese electric–gasoline hybrid cars hit market

1974

1975 1977 1981 1982 1983 1985 1986 1989 1990 1990 1992 1996 1997 1998 1999 2000

2001

Modified from: http://www.epa.gov/otaq/invntory/overview/solutions/milestones.htm.

29.3

ENGINES AND EMISSIONS

425

Table 29.2 Strategies for reducing motor vehicle emissions More stringent regulation of vehicle emissions Technological advances in engine design Inspection and maintenance of vehicles Reduced sulfur in fuels Increased fuel prices Reduction in miles traveled: Carpooling Increased use of public transport City planning

not actually met until 1981. Nevertheless, regulatory efforts overall have been successful in reducing vehicle emissions in the nearly 40 years since the passage of the Clean Air Act. However, much of the benefits related to reduced vehicle emissions have been negated by increased numbers of vehicles and miles traveled. Table 29.2 lists approaches to limiting vehicular travel and emissons.

29.3

Engines and emissions

29.3.1 Combustion engines In order to understand traffic emissions, we must first learn about the various types of combustion engines. Modern combustion engines are internal or external. Diesel and gasoline engines, the two major sources of traffic-related air pollution, are both internal combustion engines. External combustion engines include steam and Stirling engines. Since they do not contribute significantly to traffic-related air pollution, we will not discuss them further in this chapter. Internal combustion engines have been widely used to power modern vehicles, including almost all automobiles, trucks, motorcycles, boats and aircraft. Their advantages include high power-to-weight ratios and excellent fuel energy density. In internal combustion engines, the combustion of fuel and oxidizer occurs in a combustion chamber (a closed system). Thus, gases are generated at high temperature and pressure and are permitted to expand. This expansion of hot gases applies force to the solid parts of the engine, such as pistons and rotors. Figure 29.3 shows a representative design of an internal combustion engine. A commonly used internal combustion engine is the diesel engine. In this type of engine, combustion is initiated by the process of self-ignition of the fuel, which is injected after the air is compressed in the combustion chamber. A diesel engine is more efficient than a gasoline engine of equivalent power, resulting in lower fuel consumption. This greater efficiency leads to production of less carbon dioxide (CO2) and carbon monoxide (CO) per unit distance, compared with the gasoline engine. The second type of internal combustion engine is the gasoline (petrol) engine. In gasoline engines, the fuel and air are pre-mixed before the compression stroke, and combustion is ignited with a spark plug. Gasoline alone has a tendency to ignite early when used in high compression internal combustion engines, so additives are almost always used to retard ignition. Lead was historically used as an additive, but fell out of

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Figure 29.3 Internal combustion engine. The cross section shows one cylinder of a four-stroke internal-combustion engine. In the first stroke (shown), a cam (left) compresses a valve spring, opening the intake valve to admit the fuel-air mixture to the cylinder. Both valves then close, the mixture is compressed by the piston, and current is sent to the spark plug. Ignited by the spark plug, the burning mixture forces the piston down, producing power to turn the crankshaft and run the car. Another cam (right) opens the exhaust valve and the burned exhaust gases exit. From MerriamWebster’s Collegiate Encyclopedia,
2000 by Merriam-Webster Inc. Reproduced by permission of Merriam-Webster. Available from: http://www.britannica.com/eb/art-66070/Cross-sectionshowing-one-cylinder-of-a-four-stroke-internal (accessed 28 April 2008)

favor and was removed in the 1980s, because of the discovery of its adverse environmental and health effects. Lead has been replaced by other additives, such as methylcyclopentadienyl manganese tricarbonyl (MMT), aromatic hydrocarbons, ethers and alcohol (ethanol or methanol).

29.3.2 Engine emissions In this section, we will discuss some of the potential environmental issues created by diesel and gasoline engines. Diesel engines can contribute to traffic air pollution, because the exhaust contains large numbers of ultrafine particles containing elemental and organic carbon – so-called ‘black soot’. This may increase the risk for asthma and cancer. Diesel exhaust also includes gaseous pollutants such as nitrogen oxides (NOx), which contribute to the photochemical production of ozone. Because of the potential health risks associated with diesel exhaust, the EPA has enforced the 2008 Locomotive and Marine Diesel Rule, which mandated that all new diesel engines sold in the USA, starting on 1 January 2007, must meet more stringent emission standards with

29.3

ENGINES AND EMISSIONS

Figure 29.4

427

Clean diesel technology.

particulate matter (PM) reductions of about 90% and NOx reductions of about 80%, compared with engines meeting the previous standards. As a result of this regulation, the newer diesel engines have been designed with addition of some of the following features: (1) a diesel particulate filter to filter out PM from the exhaust system; (2) diesel oxidation catalysts to break down pollutants into harmless gases; (3) exhaust gas recirculation, selective catalytic reduction, and NOx absorber technologies to reduce NOx emissions; (4) utilization of ultra-low sulfur diesel fuel; and (5) a new combustion chamber to maximize power output, fuel efficiency and reduce combustion emissions (Figure 29.4). However, because diesel engines generally have a long road life, years must pass for the new emission reductions to have a beneficial effect. Like diesel engines, gasoline engines are also important sources of air pollution. Lead additive in gasoline is an important example. Although leaded gasoline was eliminated in the USA in 1986, vehicles running on leaded gasoline prior to that time released a significant amount of lead into the atmosphere, with the potential for adverse health effects, including reduced cognitive abilities, lethargy, impaired hearing acuity, hyperactivity, hypertension, abdominal symptoms, impaired hemoglobin synthesis, male infertility and developmental delay in children. Combustion of unleaded gasoline can still lead to air pollution with the release of many compounds, such as CO, CO2, NOx, hydrocarbon (HC) and PM. Furthermore, gasoline vapors evaporating from the tank react in the sunlight to produce photochemical smog in the atmosphere.

29.3.3 Emission patterns The emissions from road transport can be categorized into four main classes: (1) hot emissions; (2) cold-start emissions; (3) emissions from fuel evaporation; and (4) nonexhaust PM emissions. In this section, we will discuss each of the four emission patterns in detail.

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Hot exhaust emissions are those that occur when the engine has warmed up to its normal operating temperature. Parameters that affect hot emissions include: mean vehicle speed, driving dynamics, vehicle type, fuel and road type. For instance, high vehicle speed demands higher power output, which can in turn increase emissions. On the other hand, when automobiles travel at slow speeds in city traffic, the frequent stopand-go conditions, with increased frequency and intensity of vehicle acceleration and deceleration, can also enhance emissions. Cold-start emissions are pollutants generated immediately after engine start-up, before reaching normal operating temperature. A vehicle engine generally emits at a higher rate when it is cold than when it has warmed up to the designed operating temperature. For this reason, a decrease in ambient temperature will increase cold-start exhaust emissions. Other dependent parameters for cold-start emission include vehicle technology and distance traveled when the engine is cold. Cold-start emission of pollutants is concentrated mainly in urban areas, where the average trip distance is short, and car engines are turned on and off at high frequency. This leads to relatively high emissions per distance driven, compared with long-distance driving on roads outside of urban areas. Emissions also originate from evaporative losses, which consist of diurnal loss, hot soak loss and running loss. The diurnal rise in ambient temperature increases the volatility of the fuel and expansion of vapor in the tank. Hot soak loss is the evaporation of fuel when the hot engine is turned off, arising from the transfer of heat from the engine and hot exhaust to the fuel system where fuel is no longer flowing. Running loss occurs when the vehicle is in motion. Evaporative losses depend on the ambient temperature variation, fuel volatility, and mean trip distance. Emissions are also generated from nonexhaust sources through wear on vehicle components, such as tires, brakes and clutch, and through road abrasion. The above emissions often consist of PM with a diameter of 3–10 mm, with primary composition of metals, organic materials, rubber and silicon compounds. Some brake pads, linings and clutches may still contain asbestos, even though there has been significant international effort to ban the use of asbestos in all industries, including automobile manufacturing, due to the potential health hazards of asbestos exposure. Some countries, such as China, Russia, India, Kazakhstan, Ukraine, Thailand, Brazil and Iran, remain large consumers of asbestos, and produce asbestos-containing automobile parts. Asbestos is currently banned in the European Union, Japan and Australia. However, it has been reported that many Japanese automakers continued to use asbestos-containing components in new automobiles from 1996 to 2005. In the USA, the industrial use of asbestos has not been completely eliminated. In 1989, the EPA issued the Asbestos Ban and Phase Out Rule, but this was subsequently overturned in 1991. Asbestos use continues in the production of some automobile parts in the USA. In addition, some vehicles imported into the USA have asbestos-containing components.

29.4 Traffic-related air pollutants The main pollutants emitted from traffic include: PM, elemental carbon (EC), carbon monoxide (CO), carbon dioxide (CO2), nitrogen oxides (NOx), sulfur dioxide (SO2)

29.4

TRAFFIC-RELATED AIR POLLUTANTS

429

and polycyclic aromatic hydrocarbons (PAH). Carbon monoxide, nitrogen dioxide (NO2), benzene and black smoke are often used as indicators of traffic-related air pollution. We will discuss some of the above pollutants in detail.

29.4.1 Particulate matter Particulate matter is now recognized as one of the most important traffic air pollutants, because of its significant effects on human health. Ambient PM consists of a heterogeneous mixture of solid and liquid particles suspended in air, continually varying in size and chemical composition in space and time. Particulate matter can be characterized by source, size and chemical composition, and comes from both natural and anthropogenic sources. Natural sources include wind-borne soil, sea spray and emissions of organic compounds from vegetation. Anthropogenic sources include combustion of fuel, vehicle exhaust, mining, agriculture, industry and power generation. Figure 29.5 shows the particle size distribution of typical roadway aerosol. Particles smaller than 10 mm (PM10) are considered ‘respirable’, because they have a greater likelihood than larger particles to gain access to the lower respiratory tract. PM10 is further categorized as: (1) coarse particles diameter (between 2.5 and 10 mm); (2) fine particles (PM2.5, or diameter less than 2.5 mm); and (3) ultrafine particles (PM0.1, with diameter less than 0.1 mm). Larger (coarse and fine) particles dominate ambient particle mass concentrations, while smaller particles (ultrafine) dominate ambient particle number concentrations. Particles with diameter less than 1 mm usually have ambient particle concentrations ranging from 100 to 100,000 particles/cm3, while those larger than 1 mm may have concentration less than 10 particles/cm3. In other words, ultrafine particles have a high ambient particle number concentration, but low mass concentration.

Figure 29.5 Typical engine exhaust particle size distribution, showing weighting by both particle mass and number. From Kittelson D. (1998) Engines and nanoparticles: a review. J. Aerosol Sci. 29: 575–588. Reproduced by permission of Elsevier

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Particulate matter from different sources has different chemical compositions. For example, tailpipe exhaust emissions of PM consist of a mixture of EC, organic compounds, sulfur and trace heavy metals. Nonexhaust PM from wearing of tires contains many carbonaceous compounds, while brake wear releases PM rich in heavy metals. In addition, PM can be formed in the atmosphere by conversion from gaseous precursors, such as NOx, SO2, ammonia (NH3) and volatile organic compounds.

29.4.2 Other traffic pollutants In addition to PM, gases also contribute to traffic-related air pollution. CO is produced from incomplete combustion of carbon-containing fuels, which occurs in the engine operation of motor vehicles. Given the current low ambient concentrations in the USA, CO serves more as an indicator of combustion-related pollution, rather than a direct toxicant. However, in certain circumstances (such as an insufficiently ventilated parking structure or on a busy highway), CO can attain concentrations sufficient to increase the risk for cardiac ischemia in persons with atherosclerotic coronary artery disease. Sulfur dioxide is primarily considered a point source emission, related to the burning of sulfur-containing coal in power plants and industry. However, the combustion of sulfur-containing fuels in diesel engines also produces SO2. Sulfur dioxide is a highly soluble gas. On contact with water, as in the respiratory tract lining fluid, it forms sulfurous acid, a strong irritant to eyes, mucous membranes and skin. People with asthma may experience acute reductions in lung function following even very brief exposures to SO2. In general, traffic is not considered a major contributor to ambient levels of SO2 in the USA. The formation of NOx results mainly from combustion of fossil fuels in motor vehicles. Most toxicological and epidemiological studies have focused on NO2 rather than other NOx chemical species, because it is the most abundant, stable and toxic form of NOx in the atmosphere, it is one of the air pollutants regulated by ambient air quality standards, and it plays a major role in the generation of ozone. Polycyclic aromatic hydrocarbons are a group of organic chemical compounds that contain two or more aromatic benzene rings fused together. Today, vehicle emissions are the primary sources of PAH in most urban areas, although wood burning may be an important source in some areas, such as Scandinavia and Eastern Europe. Some PAHs, such as benzene, are carcinogenic. The particulate fraction of PAH is usually of greater concern, since it contains the majority of the carcinogenic compounds and can be transported over long distances. A major review of mobile-source air toxics, which include PAHs, was recently published [3].

29.5 Health effects of traffic-related air pollution Many epidemiological studies have shown an association between human exposure to ambient air pollutions and increased mortality and morbidity. However, limited epidemiological studies have focused on the effects of traffic-related air pollution on human health. There are two reasons for this: (1) federal and state air monitoring

29.5

HEALTH EFFECTS OF TRAFFIC-RELATED AIR POLLUTION

431

programs are typically set up to measure pollutants at regional, but not local levels; and (2) regional monitoring stations typically do not measure all types of pollutants, such as ultrafine particles (UFP), that are increased near highways. However, it is important to investigate how near-highway exposure affects the health status of people living near busy roads. Several studies have demonstrated higher rates of respiratory symptoms, elevated risk for development of asthma, lung cancer, increased cardiopulmonary mortality and reduced lung function in people living near major roads. In the following sections, we will review some of the epidemiological studies examining the relationship between traffic-related air pollution and human health, by organ system.

29.5.1 Pulmonary diseases Pediatric pulmonary morbidity Evidence is fairly strong that near-highway exposures present increased risk for respiratory symptoms and diseases in pediatric populations. Studies that used larger geographic frames have generally found no association between traffic-related pollution and asthma prevalence. However, recent studies that have used narrower definitions of proximity to traffic and focused on major highways have found statistically significant association between the prevalence of asthma or wheezing and residence close to busy roadways [4]. In the following sections, we will discuss some of the recent studies of highway exposure and childhood respiratory morbidity. The risk for wheezing has been found to be elevated among children living near busy roads. In a case–control study of 6147 primary school children (aged 4–11 years) and a random cross-sectional sample of 3709 secondary school children (aged 11–16 years) in the UK, Venn et al. [5] found the following results: among children living within 150 m of a main road, the risk of wheezing per 30 m increment in road proximity increased by an odds ratio (OR) of 1.08 (95% confidence interval, CI, 1.00–1.16) in primary school children, and 1.16 (95% CI 1.02–1.32) in secondary school children. In addition to wheezing, morning cough has been found to be a common association with traffic-related pollution among children. In a cross sectional study between 1995 and 1996 of 5421 children (aged 5–11 years) living in a 1 km2 grid in Dresden, Germany, with monitoring of air pollution from streets, Hirsch et al. [6] showed that an increase in the exposure to benzene of 1 mg/m3 air was associated with an increased prevalence of morning cough (adjusted OR, aOR, 1.15; 95% CI 1.04–1.27) and bronchitis (based on physician’s clinical diagnosis) (OR 1.11; 95% CI 1.03–1.19). Similar associations were observed between cough and exposures to NO2 and CO. Studies have also investigated the association between traffic-related pollution and asthma. For example, English et al. [7] examined the locations of residences of 5996 children (age
14) who lived in San Diego county with the diagnosis of asthma in 1993, and compared them with a random control series of nonrespiratory diagnoses (n ¼ 2284). The investigators found that, among children with the diagnosis of asthma, there was an increase in the number of medical visits associated with higher traffic flow. Similarly, Morgenstern et al. [8] studied the association between individual exposure to traffic-related air pollutants and allergic diseases (including asthma) in a prospective birth cohort study on 2860 children at the age of 4 and 3061 at the age of 6 in Munich,

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Germany in 2005. The study used individual estimated exposure levels derived from geographical information system (GIS) based modeling. The investigators found that the distance to the nearest main road and long-term exposure to particulate matter were positively associated with asthmatic bronchitis (OR 1.56; 95% CI 1.03–2.37), hay fever, eczema and allergic sensitization. In addition, it has been found that traffic-related air pollution is linked to diminished lung development in children. In a longitudinal study of 1759 children (average age of 10 years) in southern California beginning in 1993, Gauderman et al. [9] found that over the 8-year period of follow-up, deficits in the growth of FEV1 were associated with exposure to NO2 (p ¼ 0.005), acid vapor (p ¼ 0.004), PM2.5 (p ¼ 0.04) and elemental carbon (p ¼ 0.007). Traffic-related air pollution has also been found to cause short-term reductions in lung function. In a 2-week panel study of 19 children (aged 9–17 years) in southern California in the autumn of 1999 and spring of 2000, Delfino et al. [10] examined the relationship between temporal changes in subjects’ FEV1 and their continuous PM exposure (measured by nephelometer), as well as 24-hour average of gravimetric PM mass measured at home and central sites. The investigators found an inverse association between subjects’ FEV1 and their PM exposure. In sum, there is epidemiological evidence that traffic-related air pollution is associated with increased risk for wheezing, morning cough, prevalence or exacerbation of asthma, and diminished lung growth in children. Nonetheless, it should be noted that many of the epidemiological studies on pediatric populations used a cross-sectional design, which may not distinguish whether the traffic exposure precedes or follows the respiratory symptoms or diseases, since exposure and morbidity are measured at the same time. Such studies should be interpreted with caution. Adult pulmonary morbidity The majority of epidemiological studies on the relationship between traffic-related air pollution and pulmonary diseases have been conducted with children, and the data on adults are more limited and less consistent. While some studies have found an increased prevalence of asthma in adults exposed to traffic-related pollution, other studies did not find such positive associations. However, recent studies by McCreanor et al. [11] provide strong evidence for acute adverse effects of diesel exposure in people with asthma. A possible explanation for the inconsistency among studies on asthma prevalence is study methodology: cross-sectional studies vs case–control studies vs survey of respiratory symptoms and demographics. None of the methods used in the above studies is considered ideal for examining the causal relationship between traffic exposure and respiratory morbidity. Over the years, there has been growing interest in the association between asthma and exposure to diesel exhaust, which is one of the major contributors to traffic-related air pollution. Since it is difficult to isolate diesel exhaust from other components of traffic air pollution, many studies have used surrogates of diesel exhaust (such as elemental carbon, black smoke, ultrafine particles or proximity to roadway) to measure exposure to diesel. In general, the epidemiological data on the association of diesel exhaust (or its surrogates) with causation or worsening of asthma has been inconsistent [12]. However, two studies are worth mentioning and are described below.

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One published study suggested that diesel exhaust exposure caused asthma in three workers [13]. Three workers developed asthma following excessive exposure to diesel exhaust while riding immediately behind the lead engines of caboose-less trains. In this report, asthma was diagnosed by respiratory symptoms, pulmonary function tests and measurement of bronchial hyper-responsiveness. All three workers went on to develop persistent asthma. McCreanor et al. [11] probably provided the strongest evidence thus far to support the association of diesel exposure with worsening of asthma. They conducted a randomized, cross-over study in 2003–2005 to investigate the effects of short-term exposure to diesel traffic in adults with either mild or moderate asthma. In the study, each of the 60 participants walked for 2 hours on Oxford Street in the center of London (heavy diesel traffic with higher exposure to PM2.5, UFP, EC, and NO2) and in Hyde Park (away from major roadways, lower pollutant exposure). The investigators found that walking on Oxford Street significantly reduced subjects’ FEV1 (up to 6.1%; p ¼ 0.04) and FVC (up to 5.4%; p ¼ 0.01) in comparison with Hyde Park (Figure 29.6). In addition to allergic pulmonary disease, several adult studies have observed a link between nonallergic respiratory symptoms and near highway exposure. For example, Nitta et al. [14] used a standard questionnaire among approximately 5000 adult subjects in Japan in 1993 to investigate the effect of automobile exhaust on respiratory symptoms. The study showed that exposure to automobile exhaust may be associated with an increased risk of respiratory symptoms, such as chronic cough, chronic sputum production and chronic dyspnea. The ORs for the respiratory symptoms ranged from 0.76 to 2.75 [14]. More recently, in a cross-sectional study which investigated questionnaire-derived data on street type at home in relation to respiratory health in Germany in 1998, Heinrich et al.[15] found that living near busy roads was statistically significantly associated with chronic bronchitis (OR 1.36; 95% CI 1.01–1.83). Studies using exposure models have also sought an association between transportrelated pollution and nonallergic respiratory morbidity in adults. Buckeridge et al. [16] developed an exposure model using GIS to estimate the average daily exposure to PM2.5.

Figure 29.6 Mean percentage changes in FEV1 (A) and FVC (B) in asthmatics during and after exposure on Oxford Street and in Hyde Park. Asterisks denote p < 0.05 for the difference in values between Oxford Street and Hyde Park exposures. I bars represent 95% CI. From McCreanor et al. [11]. Reproduced by permission of Massachusetts Medical Society. Copyright
2007 Massachusetts Medical Society. All rights reserved

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The modeled exposure to transport-related air pollution was associated with bronchitis, chronic obstructive pulmonary disease, pneumonia and hospital admission. In sum, the epidemiological data examining the association between asthma prevalence and traffic exposure has been limited and inconsistent. However, increasing evidence suggests that exposure to traffic-related air pollutants, especially diesel exhaust, worsens existing asthma. Studies also suggest that traffic-related air pollution is related to increased risks for respiratory symptoms in nonasthmatics, such as chronic cough, sputum production and dyspnea. Whether traffic exposure contributes to the causes of asthma, or increases allergen sensitization, has not been convincingly established.

29.5.2 Cardiovascular diseases Growing evidence has supported an association between exposure to traffic-related air pollution and increased risk for cardiovascular morbidity and mortality [4, 17]. Many epidemiological and controlled exposure studies have paid special attention to PM, although CO, SO2, NO2 and EC have also been studied. Although not particularly focused on near-highway pollution exposure, two large prospective cohort studies, namely the Six-Cities Study [18] and the American Cancer Society Study [19], provided the groundwork for subsequent research on the association between fine PM and cardiovascular diseases. Both studies found a strong correlation between increased levels of exposure to ambient PM and annual average mortality from cardiopulmonary causes. The epidemiology of other air pollutants has been studied as well. Although not specifically focused on traffic-related air pollution, several time-series studies showed that exposures to black smoke, NO2, CO and SO2 were associated with increased hospital admissions for cardiovascular diseases [20]. In addition, there has also been growing evidence that living close to high traffic roads is associated with increased prevalence of coronary heart disease (CHD). For example, in a population-based, prospective cohort study involving 3399 subjects, using data from the German Heinz Nixdorf Recall Study, Hoffmann et al. [21] showed that the OR for prevalence of CHD at high traffic exposure was significantly elevated at 1.62 (95% CI 1.12–2.34) and rose to 1.85 (95% CI 1.21–2.84) after adjusting for cardiovascular risk factors and background air pollution. With the same population data base from the German Heinz Nixdorf Recall Study, Hoffmann et al. [22] conducted another prospective cohort study from 2000 to 2003, involving 4494 participants (aged 45–74 years), to investigate the association of longterm residential traffic exposure with the degree of coronary artery calcification, which is an indirect measure of coronary atherosclerosis – the main mechanism of CHD. The investigators found that participants living 50, 51–100 and 101–200 m away from major roads had OR of 1.63 (95% CI 1.14–2.33), 1.34 (95% CI 1.00–1.79) and 1.08 (95% CI 0.85–1.39), respectively, for a high coronary artery calcification (above age- and genderspecific 75th percentile). The study indicated that long-term residential exposure to traffic-related air pollution is associated with increased coronary atherosclerosis. In recent years, there has been growing interest in scrutinizing the association between the onset of myocardial infarction and exposure to traffic-related pollution. In

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a case-crossover analysis of 772 subjects with myocardial infarction (MI) in the greater Boston area between 1995 and 1996 as part of Determinants of Myocardial Infarction Onset Study, Peters et al. [23] found that the risk of MI increased in association with elevated concentrations of PM2.5 both in the previous 2 hour period (OR 1.48; 95% CI 1.09–2.02) and the day before the onset of MI (OR 1.69; 95% CI 1.13–2.34). In a subsequent case-crossover study, Peters et al. [24] identified 691 subjects, from the Cooperative Health Research in the Region of Augsburg Myocardial Infarction Registry for the period from 1999 to 2001, who survived for at least 24 hours after the onset of MI and for whom the date and time of MI were known. An association was found between exposure to traffic and risk for onset of MI within 1 hour afterward (OR 2.92; 95% CI 2.22–3.83; p < 0.001; Figure 29.7). After adjusting for the levels of exertion, the risk for MI was slightly lower, but still significant (OR 2.73; 95% CI 2.06–3.61; p < 0.001). In addition, the study also showed that there was an association between the time spent on public transportation and the onset of MI 1 hour later. On the day of the MI, of all hours the subjects spent in traffic, 72% were spent in a car, 16% on a bicycle, 10% on public transportation and 2% on a motorcycle [24]. The Peters studies overall showed that increased traffic exposure is associated with higher risk of MI. The mechanisms by which traffic exposure induces cardiovascular events remain unclear. However, a growing body of evidence indicates that exposure to PM alters vascular endothelial function. Endothelial dysfunction is now considered to be an early marker of cardiovascular risk. In human clinical studies, 1 hour exposures to freshly generated diesel exhaust, with a PM concentration of 300 mg/m3, impaired vasodilatory responses in the forearm in healthy subjects [25]. In patients with previous myocardial infarction, 2 hour exposures to 300 mg/m3 diesel exhaust increased cardiac ischemia during exercise, and impaired acute endothelial release of plasminogen activator, a response that favors coagulation [26]. Pulmonary vascular function may also be affected by pollutant exposure. Inhalation of 50 mg/m3 carbon ultrafine particles for 2 hours, with intermittent exercise, altered peripheral blood leukocyte phenotype [27] and reduced the pulmonary diffusing capacity for carbon monoxide [28], findings which are consistent with effects on pulmonary vascular function. Inhalation of UFP also reduced forearm reactive hyperemia, a measure of systemic vascular

Figure 29.7 Time spent in traffic during 72 hours preceding the onset of myocardial infarction. Percentages are the proportions of subjects with exposure during the hour in question. From Peters et al. [24]. Reproduced by the permission of Massachusetts Medical Society. Copyright
2004 Massachusetts Medical Society. All rights reserved

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responsiveness, and reduced plasma nitrate levels, findings consistent with reduced NO availability and subtle systemic vascular effects of UFP exposure [29]. In addition to endothelial dysfunction, reduced heart rate variability (HRV) has also been found to be a risk factor for cardiovascular events [30]. Adar et al. [31] were able to show that heart rate variability is reduced with exposure to traffic-related pollution. In the study, 44 nonsmoking seniors (aged 60 years; some with cardiac risk factors and coronary heart disease) were asked to participate in four 2 hour trips to downtown St Louis between March and June of 2002, aboard a diesel-powered bus. The investigators found that exposure to PM2.5 and black carbon was associated with reduced HRV. However, other studies [32] did not find reduced HRV in association with in-vehicle pollution (see below). Riediker et al. [32] showed that short-term exposure to PM2.5 among healthy young subjects can lead to elevated serum inflammatory makers, which are also risk factors for coronary heart disease [33]. In the Riediker et al. study, nine young (average age 27.3 years) healthy nonsmoking male North Carolina Highway Patrol troopers were monitored on four consecutive days while working a 3 p.m. to midnight shift and riding in gasoline-powered patrol cars. It was found that in-vehicle PM2.5 (average of 24 mg/m3) was associated with increased C-reactive protein (32%), von Willebrand factor (12%), neutrophils (6%) and red blood cell indices (1%). In addition, the investigators found increased HRV associated with in-vehicle PM2.5 exposure, a finding that differs from the negative association observed by Adar et al. [31]. The differing findings regarding HRV may be due to differences in age, cardiovascular fitness, or prevalence of heart diseases among the subjects in the two studies. In sum, epidemiological and clinical studies have increasingly demonstrated an association between traffic-related air pollution and increased risk for cardiovascular diseases and events. Several cohort and time series studies have shown that trafficrelated air pollutants, such as PM, CO, SO2, NO2 and EC, are linked to increased cardiovascular mortality and morbidity. In addition, recent evidence indicates that increased traffic exposure and concentration of traffic-related air pollutants are associated with increased risk for myocardial infarction. While the exact mechanism by which traffic exposure induces cardiovascular events remains unclear, some controlled exposure studies have found that traffic-related air pollution may increase markers of cardiovascular risk, such as reduced HRV and increased inflammatory markers. Human clinical studies have also indicated that exposures to diesel exhaust and ultrafine PM can alter vascular function – a potential mechanism by which traffic pollutants could induce cardiovascular effects. However, the specific pollutants or other traffic-related factors that are responsible for the epidemiological associations have not been conclusively identified.

29.5.3 Reproductive diseases Obstetric outcomes Epidemiological studies have indicated associations between ambient air pollution and adverse pregnancy outcomes, such as decreased fetal growth, congenital birth defects, low birth weight, preterm birth, stillbirth and post-neonatal infant mortality [34, 35].

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However, very few studies have specifically investigated the role of traffic-related air pollution in these effects. In addition, the currently available studies have inconsistent results. We will discuss some of the studies in the following sections. Wilhelm and Ritz [36] conducted an epidemiologic case–control study of 50,933 infants to examine whether maternal residential proximity to heavy-traffic roadways influenced the occurrence of low birth weight and preterm birth in Los Angeles County between 1994 and 1996. Traffic exposure was weakly associated with preterm birth (relative risk, RR 1.08; 95% CI 1.01–1.15), but not low birth weight. The study by Ha et al. [37], on the other hand, did find a positive, but weak, association between low birth weight and mothers’ exposure to CO and NO2 (markers of traffic-related air pollution) during pregnancy (gestational age 37–44 weeks) in South Korea from 1996 to 1997. The adjusted RR (aRR) for low birth weight was 1.08 (95% CI 1.04–1.12) for an interquartile increase in CO concentration during the first trimester. The aRR was 1.07 (95% CI 1.03–1.11) for NO2. There is limited evidence for associations between intrauterine growth retardation (IUGR) and traffic-related air pollution. However, several studies, not particularly focused on traffic exposure, did find positive relationships between PM and IUGR. For example, in the research project entitled ‘Teplice Program’, conducted in the Czech Republic to evaluate the impact of air pollution on all hospitalized pregnancies in two districts (Teplice and Prachatice), Sram et al. [35] found significant associations between intrauterine growth retardation and PM10 levels > 40 mg/m3 in the first trimester (OR for 40–50 mg/m3 ¼ 1.6; OR for >50 mg/m3 ¼ 1.9). Some data suggest that health consequences of traffic-related air pollution may persist beyond birth and infancy, and influence cognitive and intellectual development in children. For example, Suglia et al. [38] studied a prospective birth cohort of 202 children in Boston from 1986 to 2001 (mean age 9.7 years), to examine the association between cognitive development and exposure to black carbon (BC) (considered in this study to be a marker of traffic pollution). BC exposure was associated with decreases in matrices (4.0; 95% CI 7.6 to 0.5) and composite intelligence quotient (3.4; 95% CI 6.6 to 0.3) scores of the Kaufman Brief Intelligence Test, and with decreases on visual subscale (5.4; 95% CI 8.9 to 1.9) and general index (3.9; 95% CI 7.5 to 0.3) of the Wide Range Assessment of Memory and Learning. The exact mechanism by which BC and other traffic-related pollutants affect neurocognitive development in children is not clear at this point. Elder et al. [39] proposed that ultrafine and fine particles can translocate from the lungs to other organs such as the brain via the circulation, or directly from the nose to the brain via the olfactory nerve. This has been observed in animal studies [40]. Overall, the data on the association between traffic exposure and adverse pregnancy outcomes has been weak and inconsistent. Further research is needed in this area. Although limited, some data do suggest a possible association between traffic exposure and impaired cognitive and intellectual development among children. Male fertility Traffic-related air pollution may adversely affect male fertility, although the number of studies that have examined this relationship is small. De Rosa et al. [41] investigated the impact of traffic-related air pollution on semen quality. The study was conducted in Italy from 2000 to 2002, and involved 85 men employed at motorway tollgates and

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85 age-matched men living in the same area. Sperm counts were within the normal range in both groups. However, sperm motility and function were significantly lower in the tollgate workers than the control subjects. In addition to traffic-related pollution, urban industrial air pollution has been found to be associated with male reproductive disorders. Selevan et al. [42] conducted a comparative study of sperm quality and quantity between young men living in Teplice, Czech Republic (a highly industrialized area with seasonally elevated levels of air pollutions) and those living in Prachatice (a rural district with relatively clean air). The sperm concentrations and total counts were not associated with district of residence or period of elevated air pollutions. However, periods of elevated air pollution in Teplice were strongly associated with decrease in sperm motility and fewer sperm with normal morphology and chromatin.

29.5.4 Cancer Epidemiological studies have long pointed out the association of cancer with exposure to ambient air pollution. Some of these studies have specifically focused on trafficrelated air pollution. Lung cancer is by far the most studied malignancy that has been found to be associated with air pollution. As part of the Cancer Prevention II Study, Pope et al. [19] collected vital status and causes of death for approximately 1.2 million adults in 1982. The results of the study showed that each 10 mg/m3 increase in fine particulate air pollution was associated with 8% increased risk of mortality due to lung cancer (aRR 1.08; 95% CI 1.01–1.16). Several Scandinavian studies, which used NO2 or benzene as indicators of transportrelated air pollution, showed increased risk for developing lung cancer with exposure to traffic-related pollution. For example, in a population-based case–control study among men aged 40–75 between 1950 and 1990 in Stockholm County, Sweden, Nyberg et al. [43] found that average traffic-related NO2 exposure over 30 years was associated with increased risk for lung cancer, with RR of 1.2 (95% CI 0.8–1.6), adjusted for tobacco smoking, socioeconomic status, residential radon and occupational exposures. In addition, many studies have found increased risks of developing lung cancer among professional drivers, such as truck, bus and taxi drivers. Hansen et al. [44] conducted a case–control study in Denmark between 1970 and 1989 on 2251 male professional drivers with primary lung cancer. The OR for lung cancer, adjusted for socioeconomic status, was 1.6 (95% CI 1.2–2.2) among taxi drivers (who were considered to be exposed to the highest concentrations of vehicle exhaust fumes); 1.3 (95% CI 1.2–1.5) among bus and truck drivers; and 1.4 (95% CI 1.3–1.5) for unspecified drivers. Professional drivers may be at risk of developing lung cancer because of their higher exposure to potential carcinogens, such as diesel exhaust. Steenland et al. [45] conducted an exposure–response analysis of diesel exhaust and lung cancers among workers in the trucking industry in the period 1949–1990. It was found that a male truck driver exposed to 5 mg/m3 of EC would have a lifetime (through age 75) excess risk of lung cancer of 1.6% (95% CI 0.4–3.1) above a background risk of 5%. Professional drivers may also have increased risk of developing malignancies other than lung cancer. In the National Bladder Cancer Study, a population-based,

29.6

CONCLUSIONS

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case–control study conducted in 10 areas of the USA in 1977–1978, 1909 white male bladder cancer patients and 3569 controls were interviewed. The study indicated that male truck drivers have a statistically significant (50%) increase in risk of bladder cancer. In addition, a significant trend toward increasing risk of bladder cancer with increased duration of truck driving was observed [46]. Moreover, in a retrospective cohort study of 18,174 bus drivers or tramway employees in Copenhagen, Denmark in the period 1900–1994, bus drivers and tramway employees had an increased risk for all malignancies, compared with the expected cancer rates among general population (standardized incidence ratio 1.24; 95% CI 1.19–1.30). These malignancies included lung, laryngeal, pharyngeal, kidney, bladder cancer, rectal, liver and skin cancers [47]. While the association between traffic-related air pollution and risk of malignancy (especially lung cancer) has been better defined in adults, such association has been found to be less consistent among children. Raaschou-Nielsen and Reynolds [48] reviewed the epidemiological literature up to 2006 regarding association between traffic-related air pollution and childhood cancer. The authors found four case–control studies that provided positive evidence and three case–control studies with negative evidence. The four case–control studies that provided positive evidence were relatively small and had some methodological limitations. In conclusion, the evidence for an association between traffic-related air pollution and childhood cancer is weak and limited.

29.6

Conclusions

It is now well-established that combustion-related air pollution, especially PM, is associated with increased morbidity and mortality from pulmonary, cardiovascular and malignant disease. There is evidence that traffic-related emissions contribute to those relationships. In the USA and other developed countries, efforts to reduce motor vehicle emissions have been successful. However, public health benefits from those reductions have largely been negated by increases in numbers of vehicles and miles traveled. Traffic-related emissions include PM, NOx, CO and PAH. EC, CO and NOx may be markers of toxic traffic-related emissions, but may also contribute to health effects on their own. The most convincing relationship with health effects has been found for PM. However, other traffic-related emissions and stressors may contribute to traffic-related health effects. The complex mix of diesel exhaust deserves a special consideration, because growing evidence links diesel exposure with worsening of asthma, and possibly the causation of allergic-related disease. Considerable evidence suggests that exposure to diesel exhaust and particulate matter contribute to cardiovascular dysfunction and disease. There are persistent questions and issues related to the impact of traffic on health. For example, what are the components most responsible for traffic related health effects? What are the mechanisms involved? How do we most effectively minimize health impacts of traffic without stifling economic development and individual freedom? PM traffic emissions are perhaps at the top of the list of causative agents. However, PM is a complex mix, and there is no established consensus as to the components of PM most responsible. We may never completely understand the specific chemical species or characteristics that explain all traffic-related health effects. Smoking-related health

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effects represent an example and precedent for this difficulty. The toxicology and health effects of smoking have been clearly and irrefutably established, and yet we still do not know what specific agents in cigarette smoke are most responsible. Traffic-related pollution is a major public health issue. The world is facing exponential growth in the number of vehicles and miles traveled, particularly in developing countries. This means more roads and more people living near roads, and thus increased exposure. In developed countries, technological and engineering advances are reducing vehicle emissions. We need to achieve the goal of zero emissions, which is a promise of fuel cell vehicles, and these advances need to be extended to developing countries. However, also needed are strategies to reduce the need for transport, increase the use of low-emitting public transport and replace older, polluting vehicles with newer and cleaner technology. Continued progress in understanding the mechanisms by which traffic affects health will allow us to target specific kinds of emissions or engines that are most responsible.

References 1. K€ unzli, N., Kaiser, R., Medina, S. et al. (2000) Public-health impact of outdoor and traffic-related air pollution: a European assessment. Lancet 356: 795–801. 2. London, S.J., Romieu, I. (2000) Health costs due to outdoor air pollution by traffic. Lancet 356 (9232): 782–783. 3. HEI. Air Toxics Review Panel (2007) Mobile-Source Air Toxics: A Critical Review of the Literature on Exposure and Hlth Effects. Health Effects Institute: Boston, MA. 4. Brugge, D., Durant, J.L., Rioux, C. (2007) Near-highway pollutants in motor vehicle exhaust: a review of epidemiologic evidence of cardiac and pulmonary health risks. Environ. Hlth: Global Access Sci. Source 6: 23. 5. Venn, A.J., Lewis, S.A., Cooper, M. et al. (2001) Living near a main road and the risk of wheezing illness in children. Am. J. Respir. Crit. Care Med. 164(12): 2177–2180. 6. Hirsch, T., Weiland, S.K., von Mutius, E. et al. (1999) Inner city air pollution and respiratory health and atopy in children. Eur. Respir. J. 14(3): 669–677. 7. English, P., Neutra, R., Scalf, R. et al. (1999) Examining associations between childhood asthma and traffic flow using a geographic information system. Environ. Hlth Perspect. 107(9): 761–767. 8. Morgenstern, V., Zutavern, A., Cyrys, J. et al. (2008) Atopic diseases, allergic sensitisation and exposure to traffic-related air pollution in children. Am. J. Respir. Crit. Care Med.; doi: 10.1164/ rccm.200701-036OC. 9. Gauderman, W.J., Avol, E., Gilliland, F. et al. (2004) The effect of air pollution on lung development from 10 to 18 years of age. New Engl. J. Med. 351(11): 1057–1067. 10. Delfino, R.J., Quintana, P.J., Floro, J. et al. (2004) Association of FEV1 in asthmatic children with personal and microenvironmental exposure to airborne particulate matter. Environ. Hlth Perspect. 112(8): 932–941. 11. McCreanor, J., Cullinan, P., Nieuwenhuijsen, M.J. et al. (2007) Respiratory effects of exposure to diesel traffic in persons with asthma. New Engl. J. Med. 357(23): 2348–2358. 12. Delfino, R.J. (2002) Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research. Environ. Hlth Perspect. 110(suppl. 4): 573–589. 13. Wade, J.F. III, Newman, L.S. (1993) Diesel asthma. Reactive airways disease following overexposure to locomotive exhaust. J. Occup. Med. 35(2): 149–154. 14. Nitta, H., Sato, T., Nakai, S. et al. (1993) Respiratory health associated with exposure to automobile exhaust. I. Results of cross-sectional studies in 1979, 1982, and 1983. Arch. Environ. Hlth 48(1): 53–58.

REFERENCES

441

15. Heinrich, J., Topp, R., Gehring, U. et al. (2005) Traffic at residential address, respiratory health, and atopy in adults: the National German Health Survey 1998. Environ. Res. 98(2): 240–249. 16. Buckeridge, D.L., Glazier, R., Harvey, B.J. et al. (2002) Effect of motor vehicle emissions on respiratory health in an urban area. Environ. Hlth Perspect. 110(3): 293–300. 17. Godleski, J.J. (2006) Responses of the heart to ambient particle inhalation. Clin. Occup. Environ. Med. 5(4): 849–864. 18. Dockery, D.W., Pope, C.A. III, Xu, X. et al. (1993) An association between air pollution and mortality in six US. cities. New Engl. J. Med. 329(24): 1753–1759. 19. Pope, C.A. III, Burnett, R.T., Thun, M.J. et al. (2002) Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA 287(9): 1132–1141. 20. Brunekreef, B. (2006) Traffic and the heart. Eur. Heart J. 27(22): 2621–2622. 21. Hoffmann, B., Moebus, S., Stang, A. et al. (2006) Residence close to high traffic and prevalence of coronary heart disease. Eur. Heart J. 27(22): 2696–2702. 22. Hoffmann, B., Moebus, S., Mohlenkamp, S. et al. (2007) Residential exposure to traffic is associated with coronary atherosclerosis. Circulation 116(5): 489–496. 23. Peters, A., Dockery, D.W., Muller, J.E. et al. (2001) Increased particulate air pollution and the triggering of myocardial infarction. Circulation 10(23): 2810–2815. 24. Peters, A., von Klot, S., Heier, M. et al. (2004) Exposure to traffic and the onset of myocardial infarction. New Engl. J. Med. 351(17): 1721–1730. 25. Mills, N.L., Tornqvist, H., Robinson, S.D. et al. (2005) Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis. Circulation 112(25): 3930–3936. 26. Mills, N.L., T€ ornqvist, H., Gonzalez, M.C. et al. (2007) Ischemic and thrombotic effects of dilute diesel exhaust inhalation in men with coronary heart disease. New Engl. J. Med. 357: 1075–1082. 27. Frampton, M.W., Stewart, J.C., Oberd€ orster, G. et al. (2006) Inhalation of carbon ultrafine particles alters blood leukocyte expression of adhesion molecules in humans. Environ. Hlth Perspect. 114: 51–58. 28. Pietropaoli, A.P., Frampton, M.W., Hyde, R.W. et al. (2004) Pulmonary function, diffusing capacity and inflammation in healthy and asthmatic subjects exposed to ultrafine particles. Inhal. Toxicol. 16(suppl. 1): 59–72. 29. Shah, A.P., Pietropaoli, A.P., Frasier, L.M. et al. (2008) Effect of inhaled carbon ultrafine particles on reactive hyperemia in healthy human subjects. Environ. Hlth Perspect. 116: 375–380. 30. Godleski, J.J., Verrier, R.L., Koutrakis, P. et al. (2000) Mechanisms of morbidity and mortality from exposure to ambient air particles. Res. Rep. Hlth Effects Inst. 91: 5–88. 31. Adar, S.D., Gold, D.R., Coull, B.A. et al. (2007) Focused exposures to airborne traffic particles and heart rate variability in the elderly. Epidemiology 18(1): 95–103. 32. Riediker, M., Cascio, W.E., Griggs, T.R. et al. (2004) Particulate matter exposure in cars is associated with cardiovascular effects in healthy young men. Am. J. Respir. Crit. Care Med. 169(8): 934–940. 33. Pai, J.K., Pischon, T., Ma, J. et al. (2004) Inflammatory markers and the risk of coronary heart disease in men and women. New Engl. J. Med. 351(25): 2599–2610. 34. World Health Organization Health Effects of Transport-related Air Pollution, Krzyzanowski, M., Kuna-Dibbert, B., Schneider, J., (2005) (eds). World Health Organization: Copenhagen. 35. Sram, R.J., Binkova, B., Rossner, P. et al. (1999) Adverse reproductive outcomes from exposure to environmental mutagens. Mutat. Res. 428(1–2): 203–215. 36. Wilhelm, M., Ritz, B. (2003) Residential proximity to traffic and adverse birth outcomes in Los Angeles county, California 1994–1996. Environ. Hlth Perspect. 111(2): 207–216. 37. Ha, E.H., Hong, Y.C., Lee, B.E. et al. (2001) Is air pollution a risk factor for low birth weight in Seoul? Epidemiology 12(6): 643–648. 38. Suglia, S.F., Gryparis, A., Wright, R.O. et al. (2008) Association of black carbon with cognition among children in a prospective birth cohort study. Am. J. Epidemiol. 167(3): 280–286. 39. Elder, A., Gelein, R., Silva, V. et al. (2006) Translocation of inhaled ultrafine manganese oxide particles to the central nervous system. Environ. Hlth Perspect. 114(8): 1172–1178.

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40. Oberdorster, G., Sharp, Z., Atudorei, V. et al. (2004) Translocation of inhaled ultrafine particles to the brain. Inhal. Toxicol. 16(6–7): 437–445. 41. De Rosa, M., Zarrilli, S., Paesano, L. et al. (2003) Traffic pollutants affect fertility in men. Hum. Reprod. 18(5): 1055–1061. 42. Selevan, S.G., Borkovec, L., Slott, V.L. et al. (2000) Semen quality and reproductive health of young Czech men exposed to seasonal air pollution. Environ. Hlth Perspect. 108(9): 887–894. 43. Nyberg, F., Gustavsson, P., Jarup, L. et al. (2000) Urban air pollution and lung cancer in Stockholm. Epidemiology 11(5): 487–495. 44. Hansen, J., Raaschou-Nielsen, O., Olsen, J.H. (1998) Increased risk of lung cancer among different types of professional drivers in Denmark. Occup. Environ. Med. 55(2): 115–118. 45. Steenland, K., Deddens, J., Stayner, L. (1998) Diesel exhaust and lung cancer in the trucking industry: exposure–response analyses and risk assessment. Am. J. Ind. Med. 34(3): 220–228. 46. Silverman, D.T., Hoover, R.N., Mason, T.J. et al. (1986) Motor exhaust-related occupations and bladder cancer. Cancer Res. 46(4 Pt 2): 2113–2116. 47. Soll-Johanning, H., Bach, E., Olsen, J.H. et al. (1998) Cancer incidence in urban bus drivers and tramway employees: a retrospective cohort study. Occup. Environ. Med. 55(9): 594–598. 48. Raaschou-Nielsen, O., Reynolds, P. (2006) Air pollution and childhood cancer: a review of the epidemiological literature. Int. J. Cancer 118(12): 2920–2929.

Further reading [Anonymous] (2008) Automobile history – the history of cars and engines. [Homepage of Anonymous Ask.com] [Online]. Available from: http://inventors.about.com/od/cstartinventions/a/ Car_History.htm (accessed 3 July 2010). Brook, R.D., Franklin, B., Cascio, W. et al. (2004) Air pollution and cardiovascular disease: a statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association. Circulation 109(21): 2655–2671. Davis, D. (2004) When Smoke Ran Like Water: Tales of Environmental Deception and the Battle against Pollution. Basic Books: New York. Environmental Protection Agency (2002) Health Assessment Document for Diesel Engine Exhaust. Prepared by the National Center for Environmental Assessment. EPA/600/8-90/057F. Environmental Protection Agency (2007) Regulatory Announcement: EPA Proposal for More Stringent Emissions Standards for Locomotives and Marine Compression-ignition Engines. Available from: http://www.epa.gov (accessed 28 April 2008). Environmental Protection Agency (2007) An Introduction to Indoor Air Quality. Lead (Pb). Available from: http://www.epa.gov/iaq/lead.html (accessed 28 April 2008). Environmental Protection Agency (2007) Current Best Practices for Preventing Asbestos Exposure Among Brake and Clutch Repair Workers. Available from: http://www.epa.gov (accessed 28 April 2008). Environmental Protection Agency (2008) Asbestos Ban and Phase Out. Available from: http://www. epa.gov (accessed 29 April 2008). Jakobsson, R., Gustavsson, P., Lundberg, I., Increased risk of lung cancer among male professional drivers in urban but not rural areas of Sweden. Occup. Environ. Med. (1997) 54(3): 189–193. Janssen, N.A., Brunekreef, B., van Vliet, P. et al. (2003) The relationship between air pollution from heavy traffic and allergic sensitization, bronchial hyperresponsiveness, and respiratory symptoms in Dutch schoolchildren. Environ. Hlth Perspect. 111(12): 1512–1518. Jarvholm, B., Silverman, D. (2003) Lung cancer in heavy equipment operators and truck drivers with diesel exhaust exposure in the construction industry. Occup. Environ. Medicine. 60(7): 516–520. Joumard, R., S
eri
e, E (2008) Modelling of Cold Start Emissions for Passenger Cars. INRETS report, LTE 9931, Bron, France, 86. Available from: www.inrets.fr/infos/cost319/index.html (accessed 28 April 2008).

FURTHER READING

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Kabir, Z., Bennett, K., Clancy, L. (2007) Lung cancer and urban air-pollution in Dublin: a temporal association? Irish Med. J. 100(2): 367–369. Kim, J.J., Smorodinsky, S., Lipsett, M. et al. (2004) Traffic-related air pollution near busy roads: the East Bay Children’s Respiratory Health Study. Am. J. Respir. Crit. Care Med. 170(5): 520–526. Langholz, B., Ebi, K.L., Thomas, D.C. et al. (2002) Traffic density and the risk of childhood leukemia in a Los Angeles case–control study. Ann. Epidemiol. 12(7): (2002) 482–487. Lanphear, B.P., Hornung, R., Khoury, J. et al. (2005) Low-level environmental lead exposure and children’s intellectual function: an international pooled analysis. Environ. Hlth Perspect. 113(7): 894–899. Lanphear, B.P., Hornung, R., Khoury, J. et al. (2005) Low-level environmental lead exposure and children’s intellectual function: an international pooled analysis. Environ. Hlth Perspect. 113(7): 894–899. Le Tertre, A., Quenel, P., Eilstein, D. et al. (2002) Short-term effects of air pollution on mortality in nine French cities: a quantitative summary. Archiv. Environ. Hlth 57(4): 311–319. Lin, M.C., Chiu, H.F., Yu, H.S. et al. (2001) Increased risk of preterm delivery in areas with air pollution from a petroleum refinery plant in Taiwan. J. Toxicol. Environ. Hlth Pt A 64(8): (2001) 637–644. Livingstone, A.E., Shaddick, G., Grundy, C. et al. (1996) Do people living near inner city main roads have more asthma needing treatment? Case control study. BMJ 312(7032): 676–677. UNECE/EMEP (2004) Task Force on Emissions Inventories and Projections. EMEP/CORINAIR Emission Inventory Guidebook, 3rd edn. European Environment Agency: Copenhagen. Wilkins, E.T. (1954) Air pollution aspects of the London fog of December 1952. Q. J. R. Meteorol. Soc. 80(344): 267–271.

30 Outdoor sports


Kai-Hakon Carlsen University of Oslo, Norwegian School of Sport Sciences and Oslo University Hospital, Rikshospitalet, Oslo, Norway

30.1 Introduction Exercise-induced asthma and exercise-related respiratory problems are important for both the asthmatic child and adolescent, as well as for actively competing athletes. For the asthmatic child it is important both for their self-perception and development that they undertake and enjoy physical activity; indeed it may even be a means of mastering their asthma. However, the present chapter will be limited to matters relevant to the competing athlete. Asthma and allergy represent increasing problems for the actively competing athlete with an increasing prevalence of exercise-induced asthma (EIA) or exercise-induced bronchoconstriction (EIB) reported, especially among elite endurance athletes [1–3]. Exercise-induced asthma and exercise-induced bronchoconstriction are terms used to describe the transient narrowing of the airways that follows vigorous exercise. The term EIA is used to describe symptoms and signs of asthma provoked by exercise and EIB for the reduction in lung function which may be demonstrated after an exercise test or a naturally occurring exercise. In 1989 it was reported for the first time that high-level endurance training by adolescent swimmers increased nonspecific bronchial hyper-responsiveness (BHR) to histamine depending on the intensity of the physical training. Nine years later the finding of inflammatory changes in bronchial biopsies from young skiers was reported from Trondheim. The effect of intensive physical activity may be enhanced by untoward environmental conditions during the activity, such as cold ambient temperatures for winter sports and organic chlorine products from indoor swimming pools in swimmers. It should also be emphasized that the present day heavy training and intense physical activity during competitions reached by elite athletes due to their extremely high level of physical fitness and maximum oxygen uptake (V’O2max), make it Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

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increasingly difficult to discriminate between physiological and pathological limitations to maximum exercise.

30.2 Epidemiological context Sixty-seven of 597 American Olympic Athletes (who collectively won 41 medals) for the Los Angeles 1984 summer Olympic Games suffered from EIA or asthma. This was followed by reports of high prevalences of asthma from later Olympic Games; in 1996 an asthma prevalence of 45% was reported in cyclists and mountain bikers compared with none in divers and weightlifters. However, these reports were almost all questionnairebased without attempts objectively to verify the presence of EIB by exercise tests or other means. Later, the prevalence of BHR to metacholine (49%) in 100 competitive athletes of various sports was compared with that of sedentary subjects (28%). The prevalence of BHR varied in athletes performing their sports in cold air, dry air, humid air or combinations of these. Subsequently, reports on the use of inhaled drugs after applications for their use in the three latest Olympic Games suggested that 5.2% of all participating athletes used inhaled b2-agonists in the Winter Olympic Games in 2002 and 4.2% in the Summer Olympics in 2004. From data collected over the three latest Summer Olympic Games, in Atlanta 1996, Sydney 2000 and Athens 2004, it appears that the use of inhaled b2-agonists is highest in endurance sports, with cycling top (15.4% of all competitors), followed by the triathlon and by swimming.

30.2.1 Winter sports In 1993, it was reported that 23 of 42 elite cross country skiers had a combination of BHR and asthma symptoms compared with only one of 23 referents. This was followed by reports of high prevalences in Norwegian and Swedish skiers, in competitive figure skaters, in elite cold-weather athletes and among participants in the 1998 American Olympic National team for winter sports, including gold medalists.

30.2.2 Summer sports BHR to methacholine (PD20-methacholine < 16.3 mmol) was found in 35.5% of the Norwegian national female soccer team, and 56% of Canadian professional football players had a positive bronchodilator test (increase in FEV1  12%) to inhaled salbutamol [4]. Among American track and field athletes, 10% of men and 23% of women suffered from EIB after a national competitive event with higher incidences after long-distance events. Helenius and Haahtela in a series of studies on Finnish elite track and field athletes reported physician diagnosed asthma in 17% of long-distance runners, 8% of speed and power athletes and 3% of controls. They also reported total asthma (current asthma, physician diagnosed asthma or BHR) in 23% of the athletes compared with 4% of the controls, current asthma in 14% compared with 2% among controls and a positive skin prick test in 48% of the athletes compared with 36% among controls. Among swimmers

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DEFINITION OF EXPOSURES RELATED TO ASTHMA AND RESPIRATORY DISORDERS IN ATHLETES 447

they found a high prevalence of BHR (48%) to histamine. Employing the objective criteria for diagnosing asthma and/or bronchial hyper-responsiveness as ruled by the IOC, Medical Comission, Dickinson reported prevalences among UK participants in the Olympic Games in 2000 and 2004 to be 21.2 and 20.7%, respectively, with a positive bronchoprovocation or bronchodilator test. Thus it can be concluded that elite athletes, especially active in endurance sports, have a high prevalence of asthma and bronchial hyper-responsiveness. We will enquire if this is due to type of physical activity in itself, or due to environmental exposures during the performance of sports. In relationship to individual sports, there is limited evidence and it is necessary to combine knowledge based upon different types of sports performed in different environments in order to reach an understanding about the relevant pathogenetic mechanisms.

30.3

Definition of exposures related to asthma and respiratory disorders in athletes – pathogenetic mechanisms

Exposures may be related to the environmental conditions under which the sport is performed, or to particular aspects of the type of sport itself. These exposures may have a direct relationship to the pathogenetic mechanisms at work in causing asthma and related problems in many athletes in particular types of sport. As above, asthma and bronchial responsiveness develop more frequently in endurance sports than in speed and power sports and sports related to esthetic performance. In particular these sports have in common prolonged and increased ventilation during training and competition. This was recently shown experimentally in an Italian study of training mice, with signs of wearing in the mucous membranes after exercising compared with nonexercising mice. Another animal study of competing Alaskan sled dogs participating in a 1100 mile endurance race demonstrated intraluminal debris by bronchoscopy 12–24 hours after completing the race with higher numbers of macrophages and neutrophils in bronchoalveolar lavage as compared with control, nonracing dogs. Table 30.1 shows which environmental exposures may be important for the different types of sports. Best described are the conditions for cross-country skiers, in which the environmental exposure factor is believed to be the repetitive inhalation of cold air, and swimmers with inhalation of chlorine and organic chlorine products like trichloramine. An increase in bronchial responsiveness correlating with exercise intensity in both asthmatic and healthy elite competitive adolescent swimmers after 3000 m swimming in an indoor swimming pool represents the first description of change in bronchial responsiveness related to sports. The exposure combined heavy endurance swimming with inhalation of chlorine and organic chlorine products. Subsequently, young competitive skiers were found to have lymphoid aggregates in their bronchial mucosa and signs of bronchial remodeling (tenascin) in bronchial biopsies in addition to increased responsiveness to cold air in contrast to healthy, somewhat older medical students who were not particularly physically active. A mixed type of eosinophilic and neutrophilic inflammation was found in elite swimmers, ice-hockey players and

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Table 30.1 Environmental exposures important for the development of athma and bronchial hyperresponsiveness in some selected endurance sports Type of sports

Primary exposure

Secondary exposure

Cross country skiing; biathlon Swimming

Increased ventilation during training/competition Increased ventilation during training/competition Increased ventilation during training/competition Increased ventilation during training/competition Increased ventilation during training/competition

Cold air inhalation

Cycling Long-distance running; marathon Speed skating, figure skating, ice-hockey

Exposure to chlorine and organic chlorine products Environmental pollution, NOx Environmental pollution, NOx from accompanying cars Ultrafine particles from icing machines

cross-country skiers; the environmental exposures differed between these groups of athletes (Table 30.1). Swimmers with exercise-induced bronchial symptoms had significantly higher sputum eosinophil counts than symptom-free swimmers. The inflammation may be due to repeated thermal, mechanical or osmotic airway trauma resulting in a healing or remodeling process, and seems to be directly associated with heavy training since discontinuing high-level exercise was effective in reducing eosinophilic airway inflammation in a five-year follow-up study of competitive swimmers. There appears to be a relationship between neutrophilia in induced sputum and endurance training in swimmers, training and competing outdoors, and nonasthmatic middle-aged amateur marathon runners. In young competitive rowers an increased number of cells in sputum was found after an all-out rowing test with a change in cell dominance from neutrophils to bronchial epithelial cells. By use of induced sputum, comparing asthmatic subjects with and without EIB, it has been reported that injury to the airway epithelium, overexpression of cysteinyl leukotrienes, relative underproduction of prostaglandin E(2), and greater airway eosinophilia are distinctive immunopathologic features of asthma with EIB. The response may differ between different types of sports, being dependent upon the environment in which the sport takes place. Further research is needed in this field to fully understand these processes.

30.4 Diseases related to physical activity, training and competition in sports Physical activity may cause several different conditions in the respiratory tract. Exerciseinduced asthma is most important, occurring most often in asthmatics who are not taking inhaled steroids. EIA will typically occur shortly after exercise with bronchial obstruction occurring within a few minutes after exercise or after reducing the intensity of exercise. The dyspnoea will typically be expiratory and with audible wheeze on auscultation. Other respiratory conditions are also related to physical activity and sports, representing the important differential diagnoses to EIA and EIB in an athlete. Studies

30.4

DISEASES RELATED TO PHYSICAL ACTIVITY, TRAINING AND COMPETITION IN SPORTS 449

have demonstrated that most of the elite athletes referred for respiratory problems do not suffer from asthma or exercise-induced asthma, but rather from some of the differential diagnostic conditions. One frequent differential diagnosis is exercise-induced inspiratory stridor or exercise-induced vocal chord dysfunction. The symptoms consist of inspiratory stridor occurring during maximum exercise, and ceasing when exercise is terminated unless hyperventilation is maintained by the patient. In such cases, there are audible inspiratory sounds from the laryngeal area, and bronchodilators or other asthma medication will not help. This condition most often occurs in young well-trained athletic girls from approximately 15 years of age. Symptoms only occur during maximum exercise. The symptoms are probably due to the relatively small crosssectional area of the laryngeal orifice, which may be even further reduced by the negative pressure created by the strong inspiratory flow during heavy exercise. One possible differential diagnosis to this syndrome is paradoxical movement of the vocal chords with adduction during inspiration, sometimes occurring without exercise. The diagnosis of vocal chord dysfunction/exercise induced inspiratory stridor can be made clinically and confirmed and differentiated by direct fibreoptic laryngoscopy during exercise. Swimming-induced pulmonary edema is another differential diagnosis to EIA. Swimming-induced pulmonary edema occurs in well-trained swimmers after a heavy swimming session. The condition was reported in 70 previously healthy swimmers, who developed typical symptoms of pulmonary edema together with a restrictive pattern in pulmonary function, remaining for up to one week after the swimming incident. In addition, other chronic disorders including heart diseases as well as other chronic respiratory diseases may impact upon physical performance and represent a possible differential diagnosis to exercise-induced asthma. Over- and underweight may also influence the diagnosis, but rarely concerns athletes. Poor physical fitness or overtraining may represent other possible differential diagnoses to EIA. This is especially so when physical fitness and exercise performance are not up to the expectations of the athletes – or their trainers or parents. A lack of success in sports is often attributed to asthma even if this is not actually the case. Finally, exercise-induced arterial hypoxemia occurs in many athletes, especially in those who are highly trained. It is thought to be due to limitations in diffusion and ventilation–perfusion inequality during exercise. In the healthy lung, the former (limited diffusion) is thought to be due to a rapid red blood cell transit time through the pulmonary capillary bed. Physical training improves muscle strength and endurance, with increased ionotrophic and chronotrophic capacities of the cardiovascular system but no such effects occur in the respiratory tract. Ventilatory requirement rises with no alteration in the capacity of the airways and the lungs to produce higher flow rates or higher tidal volumes, and there is little or no change in the pressure-generating capability of inspiratory muscles. The result is exercise-induced arterial hypoxemia which may occur in up to 50% of highly trained athletes. This reduction in arterial oxygen saturation may be confused with EIA. Thus several differential diagnoses to EIA exist. Whatever the cause for the respiratory difficulties, it is important to make a thorough examination and rule out possible differential diagnoses as this has important implications for treatment.

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30.5 Diagnostic considerations and medicolegal issues The following procedure is recommended in the examination of the athlete with respiratory problems. The diagnostic criteria are identical to those of the usual asthmatic patient. However, due to criteria set by the Medical Commission of the IOC, certain modifications must be made. The following diagnostic procedure is recommended. 1. Careful case history with a focus on exercise-related symptoms or other symptoms of asthma and possible allergic disease. 2. Clinical examination with a focus on possible signs of bronchial obstruction. 3. Lung function, in particular maximum expiratory flow volume loops with assessment of reversibility to an inhaled b2-agonist like salbutamol. 4. Assessment of bronchial responsiveness, either by direct or indirect methods: (a) bronchial provocation with metacholine (or histamine); (b) exercise test standardised for assessing EIB; (c) other tests of indirect bronchial responsiveness such as the eucapnic hyperventilation test, inhalation of cold dry air, AMP inhalation, mannitol inhalation or exercise field testing. 5. Exercise test with maximum intensity to diagnose possible exercise-induced vocal chord dysfunction. Other specific examinations may become necessary dependent on findings and symptoms. The choice of diagnostic procedure depends on laboratory facilities, on case history and the medical regulations in the different countries. More than one test may be necessary. To satisfy the criteria of the IOC Medical Commission and obtain permission to use inhaled b2-agonists in relationship to Olympics and other forms of competitive sports, a positive test related to point 3 or 4 above is necessary.

30.6 Treatment of asthma and exercise-induced bronchoconstriction in athletes The treatment of asthma is extensively covered in international guidelines. While they consider most aspects of asthma, few address the specific situation in the athlete, particularly regarding the use of reliever and controller treatment. When choosing treatment for athletes compared with the ordinary asthma patient, some additional factors should be considered. For the top athlete it is important not only to control symptoms of asthma and prevent progression, but it becomes equally important to stop disease processes to reduce their impact upon sports performance, often performed under extraordinary circumstances. Therefore, the prescribed treatment should have an optimal effect upon asthma, but the possibility of potential side effects should be carefully considered. Larsson et al. [4] have published a systematic review of the treatment of athletes and EIB, including only randomized double-blind placebocontrolled or drug-comparison studies with eight subjects or more.

30.7

INTERNATIONAL REGULATIONS FOR USE OF ASTHMA DRUGS IN SPORTS

451

Treatment of EIB has been extensively studied in asthmatic subjects over the last 30 years, but only occasionally in athletes with EIB. Thus, it is not fully known whether athletes with EIB or ‘sports-asthma’ respond similarly to subjects with classical allergic or nonallergic asthma; at present, however, there is no evidence supporting different treatment for EIB in asthmatic athletes and nonathletes. The same principles as for asthma management in general may be applicable to EIA, combining the judicious use of controller (anti inflammatory) and reliever (premedication before exercise and treatment of symptoms) therapies.

30.7

International regulations for use of asthma drugs in sports

In order to be allowed to use the most common asthma drugs in relationship to international competitive sports, it is necessary to obtain permission to do so from the World Anti-Doping Association (WADA) or IOC, Medical Commission (IOC-MC). For participation in Olympic Games IOC-MC gives the necessary permissions; WADA is responsible for other international competitive sports. Although IOC-MC set up restrictionsfortheuseofinhaledb2-agonistsasearlyas1993,thesehavesinceandrepeatedlybeen modified.Itisnecessarytomakeanapplication before acompetition; the asthmaticathlete in need of asthma medication such as inhaled steroids and inhaled b2-agonists may apply for a therapeutic use exemption (TUE). The latest update on the rules and application forms for a TUE can be found on the WADA website: http://www.wada-ama.org. Furthermore, WADA has published their own recommendation as regards athletes and asthma; this too which can be found on their website: http://www.wada-ama.org/ rtecontent/document/Asthma_en.pdf. Before each Olympic Games, the IOC-MC publishes the updated regulations for the coming Olympic Games. These can be found on the IOC-MC website: http://www .olympic.org/PageFiles/61597/Olympic_Movement_Medical_Code_eng.pdf. IOC-MC requires a positive bronchodilator test, a positive metacholine bronchial provocation test, with necessary results required specified on their website, or a positive exercise challenge test, a positive test of eucapnic voluntary hyperventilation or most recently a positive mannitol test. WADA has employed the following rules according to the latest 2009 update: .

Topical steroids – there are presently no restrictions for topical use on skin, nose and eye.

.

For the use of inhaled corticosteroids there is no longer a need for application for approval before competitions. Only a self-declaration about the use of inhaled steroids in case of doping control is required.

.

An application for a TUE is still needed for inhaled b2-agonists. Inhaled b2-agonists are also not permitted out-of competition. For the use of inhaled b2-agonists WADA has now declared: ‘It is preferred to leave to the professional judgment of the physician the medical conditions under which these drugs are to be prescribed’ (Explanatory Notes, 2006). The team manager and team doctor are also responsible when an athlete is caught in doping. A concentration of urinary salbutamol

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1000 ng/l is considered an adverse analytical finding regardless of the granting of any form of TUE. The doping rules are usually modified every year, and the physician treating athletes with respiratory diseases should know these rules, keep updated and apply them to any prescribed medication in order not to cause problems for the competing athlete.

30.8 Controller treatment of EIA It should be emphasized that in general the ordinary international guidelines for asthma should be followed. However, specific concerns for the athlete have been mentioned above.

30.8.1 Inhaled corticosteroids Optimal treatment of asthma aiming at reducing BHR and maintaining control of disease activity is important for mastering EIA and enabling the athlete to participate freely in physical training, sports activity and competitions. Anti-inflammatory treatment by inhaled corticosteroids is currently the most important and effective management in these respects. Even after a week of regular treatment with inhaled budesonide in children, EIA improves significantly, but to obtain a significant reduction also in the fall of MEF25-75, further treatment of 3–4 weeks is necessary. Attenuation in exercise-induced decrease in FEV1 is also seen only after 1 week of therapy with inhaled ciclesonide at doses greater than 40 mg. However, maximal attenuation in exercise response continues to increase at doses greater than or equal to 200 mg, even after 3 weeks of therapy. Inhaled corticosteroids improve EIA more rapidly than BHR, measured by methacholine bronchial provocation. After 2–3 months of treatment with inhaled corticosteroids in children, the anticipated improvement of EIA is reached [5], whereas ongoing improvement of methacholine-induced bronchial responsiveness can be observed for up to 22 months. In children with mild asthma, a low dose of inhaled corticosteroids significantly improved EIA over a 3 month treatment period. Few studies on the effect of inhaled corticosteroids on asthma and BHR have been performed in athletes, and no studies in top athletes. In a study of 25 young competitive skiers with asthma-like symptoms or bronchial hyper-responsiveness who were attending a specialist high-school, each was prescribed budesonide 400 mg twice daily or placebo over a period of 10–32 weeks in the competitive season. No effect upon cellular inflammation in the bronchial mucosa or tenascin expression in the mucosal basement membranes from bronchial biopsies nor any cellular differences in BAL fluid were found between those taking active or placebo treatments; moreover there was no differential effect on BHR. However, with few subjects in each group, and with only five subjects with reported BHR, the study may have been underpowered. Inhaled corticosteroids have both systemic and local side effects that should be taken into account in the relationship between sports and EIB. Of particular concern are

30.9

RELIEVER TREATMENT OF EIA

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adrenal suppression, growth retardation in children and adolescents and reduction in bone density. Adrenal suppression is rare, but known to occur by use of high doses of inhaled corticosteroids. Because of adrenal suppression by high doses of inhaled steroids, hypoglycaemic convulsions have been reported in several patients being admitted to hospital. Reduction in bone mineral density has been noted as another possible systemic side effect of inhaled corticosteroids. Although rare, this possibility should be considered, especially when treating asthmatic women practising endurance sports since female marathon runners have been noted to be at particular risk for osteoporosis.

30.8.2 Leukotriene antagonists Leukotriene antagonists (LA) reduce EIA. In adults, a single dose of LA protects significantly better against EIA than placebo, and 2 days of treatment with a leukotriene synthesis inhibitor (zileuton) causes a 40% protection against EIA. Two days of use of montelukast, an alternative leukotriene receptor antagonist, significantly reduces EIA both in children and adults. Comparison studies with the long-acting inhaled b2-agonist, salmeterol, demonstrated that the protection against EIA obtained by montelukast after 3 days, remains unchanged after 8 weeks of treatment in adults, whereas tolerance to salmeterol develops after this time. In athletes there are few studies on the effect of montelukast on EIB. Whereas, in a randomized placebo-controlled cross over study of 16 ice-hockey players with EIB, no effects on asthma-like symptoms, BHR, exhaled nitric oxide and sputum cell parameters were found, in most, but not all of 11 physically active subjects with EIB, montelukast seemed to protect against EIB and lung function reduction after eucapnic hyperventilation. A Norwegian double-blind randomized crossover study in 16 adults with EIB demonstrated that montelukast improved their physical performance (running time, and Borg score for exhaustion), without altering gas exchange parameters. It may be concluded that montelukast has a protective effect upon most athletes with EIB, but not in all.

30.9

Reliever treatment of EIA

30.9.1 Treatment before exercise b2-Agonists The class of drugs most studied in this respect, and demonstrated to be effective against EIB, is the inhaled b2-agonists. By the 1970s it was established that orally administered b2-agonists offer poor protection against EIB compared with the same inhaled drug. Inhaled b2-agonists have an almost immediate effect upon EIB, with a maximum effect 20 minutes after inhalation. The effect may still be observed 3 hours after inhalation, but disappears after 4 hours. In a direct comparison of the shortacting inhaled b2-agonist salbutamol with the long-acting salmeterol, the latter appears to be to be active against EIB from 30 minutes to 6.5 hours after inhalation,

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whereas salbutamol is as effective as salmeterol 30 minutes after, but less so from 2.5 to 6.5 hours after inhalation. Formoterol, another long-acting inhaled b2-agonist, has a similar long-lasting protective effect on EIB, but with the added benefit of an onset of protective effect as rapid as salbutamol or terbutaline. Even if the inhaled b2-agonists protect against EIB, they do not completely abolish it, as exemplified by one study with a maximum reduction in FEV1 after exercise of 18–19% after inhaled salmeterol compared with 30% after placebo. It has been observed that, after regular use of long-acting inhaled b2-agonists, the protective effect on EIB is somewhat reduced, a development referred to as tolerance. Tolerance develops after 4–8 weeks of regular treatment with salmeterol; whether it has any general clinical significance is uncertain, but this cannot be ruled out in athletes. However, use of the drugs three times a week or less does not seem to result in any tolerance. When prescribing asthma drugs for the athlete, the problem with the development of tolerance should be considered, but it is not widely recognized that it is not prevented by inhaled corticosteroids. Secondly, a systematic review suggested an increased risk of severe cardiovascular side effects in patients taking long-acting inhaled b2-agonists on a regular basis. Thirdly, the FDA issued in November 2005 an alert against the regular use of inhaled long-acting b2-agonists; it is recommended that long-acting b2-agonists should not be prescribed without simultaneously giving inhaled steroids. Ipratropium bromide Ipratropium bromide may be effective against EIA in some but seldom the majority of patients. An additional protective bronchodilator effect may be obtained when ipratropium bromide is added to an inhaled b2-agonist. Whereas ipratropium bromide improves lung function both before and after exercise in asthmatic men as compared with nonasthmatic men, it has no effect upon cardio-respiratory or cardiovascular parameters of performance after a step-wise cycle exercise test. No restrictions apply to ipratropium bromide in relationship to sports.

30.10 Recommendations for the treatment of exercise induced asthma in athletes Many of the above recommendations have been incoporated into a statement from the Joint Task Force of the European Respiratory Society and the European Academy of Allergy and Clinical Immunology for asthma, allergy and sports. Treatment of EIA should follow the general guidelines for treating asthma. Reports of symptoms of EIA and other chronic respiratory symptoms in athletes should be verified by objective diagnosis by standardized exercise test or other measures of direct or indirect BHR, as there are several important differential diagnoses to EIA. 1. EIA without other clinical manifestations of asthma may be best controlled by the use of short-acting inhaled b2-agonists taken 10–15 minutes before exercise.

REFERENCES

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2.

EIA combined with other asthma symptoms may best be controlled by antiinflammatory treatment either alone or in combination with reliever treatment. Inhaled corticosteroids in low to moderate doses are the preferred treatment. It should be noted that, according to the latest modification of the rules given by WADA (from Januray 2009), it is not necessary to make an application for the use of inhaled steroids related to sports activity, but rather give a self-declaration about the use in case of a doping control.

3.

In certain circumstances leukotriene antagonists alone may be tried, but should be clearly followed up for assessment of treatment effect.

4.

Without full control with inhaled corticosteroids add either: (a) short-acting inhaled b2-agonists before exercise or (b)

long-acting inhaled b2-agonists may be tried;

(c)

a leukotriene antagonist can be tried in addition to inhaled corticosteroids.

Be aware of the possibility of developing tolerance to inhaled b2-agonists used on a regular basis, and the reports of nonresponse in some to patients to leukotriene antagonists. 5.

In some patients the combination of inhaled corticosteroids, long-acting inhaled b2-agonists and leukotriene antagonists may be needed to control exercise related symptoms.

6.

Sodium cromoglycate or nedocromil sodium or ipratropium bromide may be tried for EIA after individual assessment, either alone or in addition to other treatments.

To be noted: a lack of response to treatment may be due to misdiagnosis and require reassessment of the diagnosis of EIA. Another cause of lack of response is the possible lack of compliance with treatment. This should be taken into consideration as well as inhaler technique.

References 1. Larsson, K., Ohlsen, P., Larsson, L., Malmberg, P., Rydstrom, P.O., Ulriksen, H. (1993) High prevalence of asthma in cross country skiers. BMJ 307: 1326–1329. 2. Heir, T., Oseid, S. (1994) Self-reported asthma and exercise-induced asthma symptoms in highlevel competitive cross-country skiers. Scand. J. Med. Sci. Sports 4: 128–133. 3. Helenius, I.J., Tikkanen, H.O., Haahtela, T. (1998) Occurrence of exercise induced bronchospasm in elite runners: dependence on atopy and exposure to cold air and pollen. Br. J. Sports Med. 32: 125–129. 4. Ross, R.G. (2000) The prevalence of reversible airway obstruction in professional football players. Med. Sci. Sports Exerc. 32: 1985–1989. 5. Waalkens, H.J., van Essen-Zandvliet, E.E., Gerritsen, J., Duiverman, E.J.K.K., Knol, K. (1993) The effect of an inhaled corticosteroid (budesonide) on exercise- induced asthma in children. Dutch CNSLD Study Group. Eur. Respir. J. 6: 652–656.

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Further reading Anonymous (2006) Global Strategy for Asthma Mangement and Prevention. Available from: http:// www.ginasthma.com/Guidelineitem.asp??l1¼2&l2¼1&intId¼60. Bernard, A., Carbonnelle, S., Michel, O., Higuet, S., De Burbure, C., Buchet, J.P., Hermans, C., Dumont, X., Doyle, I. (2003) Lung hyperpermeability and asthma prevalence in schoolchildren: unexpected associations with the attendance at indoor chlorinated swimming pools. Occup. Environ. Med. 60(6): 385–394. Carlsen, K.H. (2005) Evidence-based recommendations for the diagnosis of exercise-induced asthma in athletes. In Diagnosis, Prevention and Treatment of Exercise-Related Asthma, Respiratory and allergic Disorders in Sports, Carlsen, K.H., Delgado, L., Del Giacco, S.,(eds). European Respiratory Journals: Sheffield; 102–104. Carlsen, K.H., Anderson, S.D., Bjermer, L., Bonini, S., Brusasco, V., Canonica, W., Cummiskey, J., Delgado, L., Giacco Del, S., Drobnic, F., Haahtela, T., Larsson, K., Palange, P., Popov, T., van Cauwenberge, P. (2008) Exercise-induced asthma, respiratory and allergic disorders in elite athletes: epidemiology, mechanisms and diagnosis: part I of the report from the Joint Task Force of the European Respiratory Society (ERS) and the European Academy of Allergy and Clinical Immunology (EAACI) in cooperation with GA2LEN. Allergy 63(4): 387–403. Carlsen, K.H., Anderson, S.D., Bjermer, L., Bonini, S., Brusasco, V., Canonica, W., Cummiskey, J., Delgado, L., Giacco Del, S., Drobnic, F., Haahtela, T., Larsson, K., Palange, P., Popov, T., van Cauwenberge, P. (2008) Treatment of exercise induced asthma, respiratory and allergic disorders in sports and the relationship to doping: Part II of the report from the Joint Task Force of European Respiratory Society (ERS) and European Academy of Allergy and Clinical Immunology (EAACI) in cooperation with GA2LEN. Allergy 63(5): 492–505. Drobnic, F., Haahtela, T. (2005) The role of the environment and climate in relation to outdoor and indoor sports. In Diagnosis, Prevention and Treatment of Exercise-Related Asthma, Respiratory and allergic Disorders in Sports, Carlsen, K.H., Delgado, L., Del Giacco, S. (eds). European Respiratory Journals: Sheffield; 35–47. Drobnic, F., Freixa, A., Casan, P., Sanchis, J., Guardino, X. (1996) Assessment of chlorine exposure in swimmers during training. Med. Sci. Sports Exerc. 28(2): 271–274. Fitch, K.D. (2006) b2-Agonists at the Olympic Games. Clin. Rev. Allergy Immunol. 31(2–3): 259–268. Helenius, I., Haahtela, T. (2000) Allergy and asthma in elite summer sport athletes. J. Allergy Clin. Immunol. 106(3): 444–452. Lagerkvist, B.J., Bernard, A., Blomberg, A., Bergstrom, E., Forsberg, B., Holmstrom, K., Karp, K., Lundstrom, N.G., Segerstedt, B., Svensson, M., Nordberg, G. (2004) Pulmonary epithelial integrity in children: relationship to ambient ozone exposure and swimming pool attendance. Environ. Hlth Perspect. 112(17): 1768–1771. Larsson, K., Carlsen, K.H., Bonini, S. (2005) Anti-asthmatic drugs: treatment of athletes and exerciseinduced bronchoconstriction. In Diagnosis, Prevention and Treatment of Exercise-Related Asthma, Respiratory and allergic Disorders in Sports, Carlsen, K.H., Delgado, L., Del Giacco, S. (eds). European Respiratory Journals: Sheffield; 73–88. World Anti Doping Agency (2009) Medical Information to Support the Decisions of TUECs Asthma. Available from: www.wada-ama.org/rtecontent/document/Asthma_en.pdf

Index Numbers in italics refer to Figures Numbers in bold refer to Tables acarids, 81–2, 90 acrolein, 25, 293, 393, 394 firefighters, 266–7, 305 acrylates, 225, 243, 249, 250, 256 acrylics, 236 acrylonitrile, 236 acute eosinophilic pneumonia (AEP), 307, 308, 309 acute inhalational injury, 188, 241, 241–3 acute irritant symptoms, 33, 34–5 acute lower respiratory illness, 29, 29–30, 39 acute lung injury, 98, 102, 103, 104 acute mountain sickness (AMS), 377, 385–7, 388 acute pulmonary effects of immersion, 361 adult respiratory distress syndrome (ARDS), 63, 350, 401 agribusiness, 161–6, 169–70 agriculture, 161–75 burning, 391–2, 397, 398 non-allergen symptoms, 167–9 air-bag deployment, 129, 133 air conditioning in cars, 130–1, 134 air fresheners, 55, 60–5, 329 airways disease, 261–3 alcohols, 57, 58, 73, 426 Alternaria, 87–9, 225 altitude sickness, 377, 385–8 amines, 237, 243, 243, 252 ammonia, 16, 264, 293, 295, 305, 430 agriculture, 162, 167, 168 cleaning products, 56, 57, 58, 59, 62–3, 66–7, 269 research workers, 347, 349, 349, 353

ammonium chloride, 16, 248, 262 anhydrides, 236, 237, 241, 243, 243, 244, 250 animals, 82–5, 88, 90, 324–5, 331, 407–8 agriculture, 162, 162–4, 165, 166–8, 169, 170, 174 hobby pursuits, 99, 99–100 research workers, 337–8, 340, 340–3, 344–5, 345–6, 346, 347 veterinarians, 264–5, 270 see also cats; dogs; horses; rodents anthrax, 97, 98, 101, 102, 228, 230 biological weapons, 297, 298 anti-neutrophil cytoplasmic autoantibody (ANCA), 186 antenatal exposure see pregnancy ardystil syndrome, 241, 242 arsenic, 194, 195 arts and crafts, 96, 98–9 asbestos, 10, 182–3, 241, 244, 418, 428 automobile industry, 212, 213–5 automobile maintenance and repair, 204, 206, 209 construction, 274, 275, 279, 284, 286 firefighters, 306 hobby pursuits, 97, 98, 104 mining, 177–9, 182–3, 184–6 pulp and paper, 227, 227 asbestosis, 104, 179, 182–3, 206, 209 automobile industry, 212, 213 construction, 277, 287 Aspergillus, 87–8, 89, 225, 275, 283 asthma, 1–2, 91, 92, 243, 252 agriculture, 161, 163, 165, 167–8, 169, 170 attribution, 8, 9, 9

Occupational and Environmental Lung Diseases Edited by Susan M. Tarlo, Paul Cullinan and Benoit Nemery © 2010 John Wiley & Sons, Ltd. ISBN: 978-0-470-51594-5

458

INDEX

asthma (Continued ) automobile industry, 212, 213, 216–22 automobile maintenance and repair, 205–9 automobile pollution, 426, 430–3, 433, 434, 439 bakery, 14, 173 biomass smoke, 392, 394, 395, 396–8, 402 buildings and furnishing, 71–2, 72–3, 75–8 chemical weapons, 292, 295 chemicals and coatings, 236–40, 241, 241–5 children, 29, 31, 39 cleaning products, 16, 19, 61–3, 64, 65–7 cockroaches, 85–6 construction, 273, 276, 280–2, 282 cooking and heating emissions, 50, 51, 52, 53 cosmetics, 14–6, 17–21 day-care and schools, 109–10, 114–9 drugs allowed in sport, 451–5 electronics industry, 248–9, 250, 251–7 exercise-induced, 101, 101, 104, 445–6, 448–9, 451–5 firefighters, 266–8, 304, 305 food industry, 171, 172, 173–4 fungi and moulds, 86, 89 hairdressers, 17, 19 hobby pursuits, 96, 97, 98–105 horses, 152, 153–5 hospitality workers, 122, 124, 125, 127 indoor sports, 138, 142, 144, 147–9, 152–5 insects, 90 inside of automobiles, 130–3, 135 metal industry, 193, 194, 197, 199, 200 military, 307–8 mining, 179 mites, 82, 92 offices and schools, 314–5, 315, 320, 321, 323–4, 329–35 outdoor sports, 445–7, 448, 448–55 passive smoking, 28, 31, 33, 35–6, 38–40 pets, 84, 85, 99 police, 266, 302, 303 pulp and paper, 226, 227, 227 research workers, 338–9, 340–1, 342–8, 349, 351, 351–3 service industries, 261–5, 266–9 smoking in pregnancy, 28, 28 textile industry, 228, 228, 230

urban pollution, 406, 410–2, 414–5, 416, 417 volcanic emissions, 401, 403 wood industry, 224, 224–5 World Trade Centre disaster, 301–2 atelectasis, 363 atmospheric pressure, 378 atmospheric temperature, 378 athletes, 446–7, 448, 448–9, 450, 453–5 indoor meetings, 138, 155 attribution, 7–10 automobiles, 109, 129–30, 211–22 environment exposure inside, 129–35 maintenance and repair, 203–10 new car registrations in China, 423 urban pollution, 406, 407, 416, 417, 421–40 US traffic pollution controls, 424 volume of passenger transport, 423 avian influenza, 300, 301 aviation, 377–85, 387, 388 oxygen equipment, 382–3 physiology, 379–85 azobisformamide, 243 azodicarbonamide, 243 bagassosis, 164 bakery, 103, 103, 161, 165, 172–4, 268, 270 asthma, 14, 173 bars and restaurants 121–8, 268–9, 270 barium, 195 benzene, 64, 417 biomass smoke, 393, 394 inside automobiles, 130–1, 132, 133 second hand smoke 25, 122, 132 traffic pollution, 427, 430, 431, 438 benzopyrene, 212, 213, 215 beryllium, 192, 193, 194, 195–7, 199, 353 construction, 282–3, 286 electronics industry, 250, 253 mining, 183–4, 186 urban pollution, 418 see also chronic beryllium disease (CBD) beta-agonists, 18, 453–4, 455 biological hazards, 292, 296, 297, 298–9, 300 biomass fuels, 45, 46, 49, 53–4, 406 biomass smoke, 391–2, 394, 395, 396–8, 402–3 biomonitoring, 251 bird egg syndrome, 90 bird fancier’s lung, 99, 104

459

INDEX

birds, 90, 99, 99–100, 104, 164, 165, 168 blast injury to the lung (BLI), 307 blastomycosis, 103, 103 bone sarcomas, 284, 286 breast cancer, 33, 34, 122, 125 bromine, 145, 146 bromochlorodimethylhydantoin, 145, 146 bronchial hyper-responsiveness or hyperreactivity (BHR), 262, 433 animals, 82, 92, 116 buildings and furnishing, 71–2 cleaning products, 61, 62, 67, 269 cold air exacerbated, 144 firefighters, 267 hairdressers, 15 indoor water sports, 147 outdoor sports, 445–7, 448, 452, 454 research workers, 342, 343, 351, 351 bronchiectasis, 288, 295, 348 bronchiolitis, 5, 9, 29, 63, 188 bronchiolitis obliterans, 5, 241, 242, 295 food industry, 173–4 research workers, 338, 348, 350–1, 352–3 textile industry, 228, 228, 230 bronchiolitis obliterans organizing pneumonia (BOOP), 242 bronchitis, 77, 116, 200, 227, 230, 241 agriculture, 161, 163, 167, 169, 170, 174 automobile industry, 212, 213, 216 chemical weapons, 292, 296 cleaning products, 63 construction, 276, 279, 288 food industry, 171, 173 hobby pursuits, 96, 97 indoor equestrian sports, 138, 154 metal industry, 192, 193, 195, 199, 200 mining, 183, 184, 188 research workers, 348 second hand smoke, 29, 36, 37, 123, 124, 132 service industries, 262, 265 traffic pollution, 431–2, 433–4 urban pollution, 407 brucellosis, 297, 299, 300 buildings and furnishing, 69–78 agriculture, 162, 168 day-care and schools, 109–10, 113, 115, 117, 119 offices, 315, 316–30 buildings and grounds cleaning, 260, 269–70

bush and grass fires, 391, 397, 398 byssinosis, 228, 228–9, 229, 231 cadmium, 9, 10, 286, 347 metal industry, 194, 195, 199 mining, 178, 188 cadmium pneumonitis, 98 calcium carbonate, 138 Caplan’s syndrome, 183 carbamates, 60, 168 carbon dioxide, 110, 115, 162, 379–80 hyperbaric environment, 358, 359, 362, 366, 369, 371–2 traffic pollution, 425, 427, 428 volcanic emissions, 399, 400, 402, 403 carbon monoxide, 52, 53, 125, 188, 294 automobile maintenance and repair, 204, 205, 206 biomass smoke, 393, 394, 397 firefighters, 166–7, 305 indoor sports, 138, 138, 139–42, 143 inside automobiles, 129, 131, 132, 135 traffic pollution, 425, 427, 428–30, 434–5, 437, 439 volcanic emissions, 399 carbonless copy paper, 315, 317, 317, 318, 328–9, 330 cardiovascular disease, 38–9, 40, 132, 133–4, 135 particulate matter, 410, 413, 416 traffic pollution, 434–5, 435, 436, 439 carpeting for cars, 212, 218 cats, 82–4, 88, 89, 92 day-care and schools, 111, 112, 112, 116, 118 fleas, 91 offices, 324–5, 326–7, 330 research workers, 340, 340 central nervous system toxicity, 372 ceramics, 96, 97 cheese washer’s disease, 164 chemical industry, 233–45 components, 234, 235 potential hazards, 235 chemical weapons, 292, 293–4, 295–7, 309 chicken breeder’s disease, 164 children, 27–33, 84–5, 92, 394 buildings and furnishing, 70–2, 73–5 cancers, 29, 32 cleaning products, 61, 63–7 cooking and heating, 45, 50, 51

460

INDEX

children (Continued ) day-care and schools, 109–19 fungi and moulds, 86, 88, 89 green algae, 90–1 indoor sports, 145, 147–8, 153 inside automobiles, 131, 132, 134, 135 mites, 82, 92 outdoor sports, 445, 452 passive smoking, 23–4, 25–6, 27–33, 39–41 traffic pollution, 431–2, 437 urban pollution, 406, 410–1, 416 chloramines, 63 chlorine, 188, 226, 292, 293, 295, 297 cleaning products, 59, 63 research workers, 347, 349, 349 swimming, 145, 146, 147–8, 445, 447, 448 chlorine dioxide, 145, 146, 226, 227 chromium, 198, 200, 275, 276, 286 chronic beryllium disease (CBD), 183–4, 253, 353 construction, 280, 282–3 chronic obstructive lung disease, 96, 97 chronic obstructive pulmonary disease (COPD), 3–5, 194 agriculture, 167 attribution, 9, 10 automobile industry, 212, 213, 221 automobile maintenance and repair, 205, 206, 209 biomass smoke, 392, 402 chemical weapons, 295 chemicals and coatings, 243 construction, 276–7, 278, 279, 280 cooking and heating, 50–3 firefighters, 305, 309 food industry, 174 indoor equestrian sports, 152 inside of automobiles, 131, 133 mining, 183, 184, 188 second hand smoke, 33, 37, 39–40, 122, 124–5, 127 traffic police, 266 traffic pollution, 434 urban pollution, 406, 408, 410–1, 416 wood and textile industries, 231 circuit boards, 249 clean diesel technology, 427 cleaning products, 55–67, 168, 171, 172 day-care and schools, 117–8, 119 healthcare workers, 261–2 janitors, 269–70

offices, 315, 315, 317, 318, 323, 329, 330 research workers, 340, 351 swimming pools and hot tubs, 148, 150 coal, 53, 405, 407, 411–3, 415, 416, 423–4 coal mining, 9, 10, 177, 178, 183 coal worker’s pneumoconiosis (CWP), 179, 183, 185, 186 coatings, 233–40, 241, 241–5 cobalt, 192, 194, 197 coccidiomycosis, 103 cockroaches, 85–6, 92, 112, 340 offices, 317, 319, 324–5, 326–7, 330 cold-start emissions, 427, 428 colophony (rosin), 247–8, 249, 250, 249–57 combustion engines, 425–6, 426 compensation, 8, 40, 256, 335 firefighters and police, 309 hairdressers, 20–1 military, 309–10 mining, 182, 183, 184 research workers, 347, 352 connective tissue disease, 186, 214–5 cooking, 45–54, 91, 125, 392 food industry, 161, 170, 174 coronary heart disease, 122, 125–6, 128 cosmetics, 13–21, 234, 237, 265–6 cosmetology, 265–6 cosmic radiation, 379 cotinine, 27, 32, 113, 122, 125 cows, 164, 165, 166, 168 crowd control agents, 292, 293, 302 cyanoacrylate, 303, 303 cycling, 446, 448 damp, 49, 87–8, 111 buildings, 69, 71, 72–7 day-care and schools, 110–1, 115–6, 119 offices, 314–24, 330, 330–2, 336 decompression illness (DCI), 361, 362–3, 364, 364–8, 384 altitude induced, 383, 384 dental personnel, 264 diazonium salts, 240, 243 diffuse pneumonitis, 237 diisocyanates, 225, 239–40, 276, 418 disinfectants, 162, 264 cleaning products, 55, 56, 57, 58, 63 indoor water sports, 138, 145, 145–8 diving, 357–8, 359–60, 360–1, 362–3, 363–74, 384 saturation, 360, 360, 363–4

INDEX

dogs, 83–4, 88, 324, 408 day-care and schools, 111, 112, 116, 118 research workers, 340, 341, 347 drain cleansing agents, 60, 61 drug laboratories, 296 dyes and dyeing, 227, 228, 230, 240, 241, 243, 243 electroplating, 193 electronics industry, 247–57 elemental carbon (EC), 428, 430, 434, 439 emissions in buildings, 69, 70, 71–2, 72–6, 77–8 emissions from fuel evaporation, 427, 428 emphysema, 10, 37, 254, 296 construction, 276, 279 metal industry, 193, 194 endotoxins, 264 agriculture, 167, 170 offices, 320, 321, 322, 330 textile industry, 228, 229, 231 epoxies, 212, 222, 276 epoxy resins, 236, 237, 249, 250, 257 epistaxis, 237 equestrian sports, 138, 152–5 ethanolamines, 62 ethyl methacrylate, 20 ethylene, 238 ethylene oxide, 262 exercise-induced arterial hypoxemia, 449 exercise-induced bronchoconstriction (EIB), 445–6, 448, 450–4 extrinsic allergic alveolitis (EAA) see hypersensitivity pneumonitis (HP) farmer’s lung disease 100, 154, 164, 164–6 fertilizers, 162, 162 fire-eater’s lung, 101, 102 fibrous glass, 275 fire smoke, 266–8, 292, 293–4, 296, 304, 305, 305–6 from biomass, 391–2, 394, 395, 396–8, 402–3 research workers, 347, 351 firefighters, 266–8, 270, 291, 303–4, 305, 305–6, 309 biomass smoke, 394, 395, 395–6 first responders, 292, 296, 300–1 World Trade Center, 301–2 fishing, 99, 100, 103, 103, 161, 170–2 insect allergens, 90

461 flock worker’s lung, 230, 241, 242 floor cleaners, 57 fluorides, 198 fluoropolymers, 64, 238, 241 food allergens, 91, 113 food industry, 161, 164, 165, 170–5 food preparations, 260, 268–9 forest fires, 391, 392–6, 398 forging/stamping, 212, 217 formaldehyde, 25, 130, 172, 237–8, 244, 393 automobile industry, 215, 221 buildings and furnishing, 71, 70–2, 76 construction, 276, 286 cooking and heating, 46, 49 cosmetology, 265–6 electronics industry, 248, 252 firefighters, 266 offices, 323, 330 research workers, 347 wood industry, 224–5 formaldehyde–amino resins, 237–8 foundries, 213, 214, 214–15 fume fever, 97, 98 fungi and moulds, 49, 87–8, 225, 265, 319–20, 321, 322 agriculture, 162, 162, 164, 165, 166–7, 170, 174 buildings and furnishing, 69, 76 construction, 274, 275–6, 288 day-care and schools, 110, 111, 112, 115–16 hobby pursuits, 98, 103, 104 indoor equestrian sports, 152 indoor ice sports, 139 offices, 314–5, 317, 318, 319–23, 328, 330 pesticides, 60 research workers, 340 furniture makers, 223, 224 galvanization, 193 gas, 45, 46–50, 51–3 gastrophageal reflux disease (GERD), 301–2 giant cell interstitial pneumonitis, 197 glanders, 297, 299, 300 glass cleaners, 56, 57, 61, 63, 66 glass making, 97, 98 glutaraldehyde, 261–2, 264, 266 glycophosphate, 168 grass pollen, 89 green algae (chlorella), 90–1

462

INDEX

greenhouse lung, 164 gymnastics, 138, 155 hairdressing, 13–21, 265–6 hairspray lung, 13 halogenated acids, 293, 305 hard metal pulmonary disease, 197 hay fever, 18, 71, 340, 341, 432 hazardous materials, 292, 293–4, 295, 296–7 health diagnosing and treating occupations, 260, 260–5, 270 healthcare workers, 260, 260–3, 264, 269–70 heating, 45–54, 69, 77–8, 87 hemoptysis, 142, 143, 151 hemothorax, 189 henna, 16, 17, 265 HERA, 58, 60 herbicide, 168 hexamethyldiisocyanate (HDI), 219, 221, 240, 243 high altitude, 377–8, 379 high altitude cerebral edema (HACE), 385, 386, 387 high altitude pulmonary edema (HAPE), 377, 385–8 high density lipoprotein cholesterol (HDL), 33, 39 high pressure neurological syndrome (HPNS), 373 Histoplasma from bird and bat droppings, 315, 317, 328, 333 histoplasmosis, 103, 103, 328, 333, 333 horses, 138, 152–5, 164 hospitality workers, 121–8, 268–9, 270 hot emissions, 427, 428 hut lung, 392 hydrocarbon pneumonitis, 102, 104 hydrocarbons, 64, 131, 141, 393, 426, 427 buildings and furnishing, 70, 72, 73 polycyclic aromatic, 286, 393, 394, 429, 430, 439 hydrochloric acid, 63 hydrofluoric acid, 63, 98 hydrogen chloride, 293, 305, 349, 349 hydrogen cyanide, 294 hydrogen peroxide, 16 hydrogen sulphide 162, 168, 402 volcanic emissions, 399, 400–1, 402, 403–4 hygiene, 118, 161 hypercapnia, 362–3, 364, 371–2

hypersensitivity pneumonitis (HP; aka extrinsic allergic alveolitis (EAA)), 3 agriculture, 163, 164, 164, 166, 170, 174 automobile industry, 212, 213, 216–7, 219 automobile maintenance and repair, 205, 206, 206–7 chemicals and coatings, 237, 240, 241, 243, 244 construction, 280, 283 electronics industry, 250, 253 food industry, 171, 174 hobby pursuits, 98, 99, 99, 100, 102, 104–5 indoor equestrian sports, 154 indoor water sports, 138, 147, 149–51 mining, 179 offices, 314, 315, 331–2, 333 research workers, 339 schools, 114 welding, 199 wood industry, 224, 225, 231 hyperventilation, 380–1, 384–5, 385 hypocapnia, 148 hypoxemia, 148, 150 hypoxia hyperbaric, 359, 362, 364, 369–70 hypobaric, 377–81, 385–8 hypoxic, 377, 387, 379–82 ice sports, 447, 448, 453 indoor, 138, 139–44 toxicant syndromes, 140–3 idiopathic environmental intolerance (IEI), 15 immersion pulmonary edema, 362, 364, 370 indoor humidity, 110–1, 115–6 see also damp indium, 250, 253 indium alveolitis, 249 infections, 115, 131, 135, 151, 287–8 cooking and heating, 51, 52 military, 307–8, 309, 309 office workers and teachers, 315, 315, 333, 333–4 passive smoking, 29, 33, 38 police, 303, 309 research workers, 350, 353, 354 upper respiratory tract, 151, 300–1 inhalation fever, 228, 229, 231 inhaled corticosteroids for asthma, 452–3, 455

INDEX

463

insects, 90, 91, 163, 165, 340 see also cockroaches insulation, 276, 279, 281, 282, 282, 286 interstitial fibrosis, 212, 295 interstitial lung disease, 200, 241, 244, 230 automobile maintenance and repair, 205, 206, 209 biomass smoke, 392, 402 electronics industry, 249, 250, 253 research workers, 349, 351, 352 ipratropium bromide, 454, 455 iron oxide, 197, 198, 199, 200 ischaemic heart disease (IHD), 33, 38–9, 40 isocyanates, 252–4, 282, 294 automobile industry, 212, 213, 218–9, 221–2 automobile maintenance and repair, 204–9 chemicals and coatings, 239–40, 241, 243, 243–4 construction, 281, 282, 283 electronics industry, 248–51, 255, 256–7, 257

military, 307, 308, 309 mining, 182–3, 185–6, 187 police, 303, 303 pulp and paper, 227, 227 radon in schools, 110 research workers, 339, 353 second hand smoke, 26, 33, 33–4, 39, 122, 125, 127 smoking in automobiles, 132, 133, 135 textile industry, 231 urban pollution, 409 volcanic emissions, 401 welding, 199, 200–1 lung and pulmonary fibrosis, 103, 114, 225, 228 agriculture 165, 168 automobile maintenance and repair, 209 chemical weapons, 295, 297 hairdressers, 265 metal industry, 193, 194, 195 military, 307 mining, 177, 180, 182, 186 lung injury from sports, 142

jewelry, 97, 98

magicians, 99, 101, 102 magnesium carbonate, 138 male fertility, 437–8 mainstream smoke, 24, 25, 132 malt worker’s disease, 164 manganese, 195, 198, 199 manure, 162, 162, 168, 170 maple bark disease, 164 meat processing, 170, 172 meat wrapper’s asthma, 172, 239 mercury, 191, 195, 399 mesothelioma, 6–7, 9, 9, 186, 397, 418 brake linings, 204, 205, 206, 209 construction, 286, 287 military, 309, 309 pulp and paper, 227, 227 textile industry, 231 metal fume fever, 199, 199, 220, 238, 242 automobile maintenance and repair, 206, 209 metal machining, 212, 215–17 metal working, 97, 98, 191–201 metal-working fluids, 191, 193, 213, 215, 216, 216–17 methacrylates, 264, 266, 276 methane, 162 methyl colophony, 253

laryngocele, 101, 102 latex, 261, 264, 265 research workers, 337, 340, 342 laundry products, 55, 60 lead, 195, 199, 306, 425–6, 427 automobile maintenance and repair, 204, 206, 210 volcanic emissions, 399 legionella, 315, 317, 325, 328, 333, 333 Legionnaire’s disease, 333 leptospirosis, 102, 179 leukotriene antagonists, 453, 455 limonene, 62, 70, 72, 73 low birth weight, 28, 28, 436–7 lumberjacks, 224 lung cancer, 6–7, 10, 133–4, 244 automobile industry, 212, 213 automobile maintenance and repair, 204–5, 206, 209 automobile pollution, 426, 431, 438–9 biomass smoke, 392, 395, 396, 397 construction, 283, 284–5, 286–7 cooking and heating, 53 firefighters, 306, 309 metal industry, 193, 194

464

INDEX

methyl isocyanate, 240 methyl methacrylates, 266, 276 methylene diisocyanate (MDI), 240, 243, 282 automobile industry, 213–4, 218, 218–9 microbes and microorganisms, 115, 320, 321 agriculture, 162, 162–4, 165 automobile industry, 216–7 buildings and furnishing, 69, 71, 72–3, 75–7 indoor water sports, 146, 147, 149 offices, 316, 316–23, 325, 328, 330 textile industry, 228, 229 wood industry, 224 military, 291, 306–9, 310, 384 first responders, 292, 296, 300–1 mites, 81–2, 86, 90, 92 agriculture, 162, 162, 164, 165, 170 day-care and schools, 111, 112, 115 offices, 317, 319, 324–5, 326–7, 330 morbidity, 279, 409–13 traffic pollution, 430, 431–4, 436, 439 mortality, 409, 412–3, 414, 417, 421 construction, 277, 278, 279 traffic pollution, 430–1, 434, 436, 439 moulds see fungi and moulds mountaineering, 377 mushroom picker’s disease, 164 mycotoxicosis, 166 mycotoxins, 170 nasal sinus cancer, 34, 122, 125 nasal septal perforation, 193, 194 nasopharyngeal cancer, 34, 238, 283 near-drowning, 362, 364, 371 nerve agents, 292, 294, 296 neurobehavioral disorders, 29, 32–3 nickel, 25, 198, 200, 276, 286 nicotine, 113, 132 second hand smoke, 26, 27, 28, 32, 122 nitric oxide exhalation, 124 nitrogen chloride, 147 nitrogen dioxide, 188, 198, 241, 242, 266 agriculture, 162 cooking and heating, 46–8, 49–51 hobby pursuits, 103 ice-skating, 102, 138, 139–41, 142–3 inside automobiles, 131, 135 traffic pollution, 429, 434, 437–9 urban pollution, 408, 413, 414 nitrogen oxides, 25, 212, 266, 276, 448 automobile pollution, 426–7, 428, 430

biomass smoke, 393, 394 fire smoke, 294, 305 inside automobiles, 131 research workers, 349, 349, 351 urban pollution, 406, 413–5, 416 welding, 198, 198, 199 nonexhaust emissions, 427, 428 nontuberculosis mycobacterial (NTM) disease, 179, 185, 320 indoor water sports, 147, 151 numismatist’s lung, 103, 103 nylon flock disease, 212, 213, 218, 348 obstructive pulmonary disease (OPD), 184 organic dust toxic syndrome (ODTS), 154, 283 agriculture, 163, 166, 167, 169, 170 organophosphates, 60, 168 organizing pneumonia, 348, 351, 352 otitis, 29, 30, 39, 168 out-gassing from new cars, 132–3, 135 oxygen toxicity, 362, 363–4, 364, 365 oxyhemoglobin dissociation curve, 380, 380 ozone, 72, 212, 276, 426, 430 atmospheric, 378–9 indoor water sports, 145, 146, 148 inside automobiles, 131, 135 pulp and paper, 226, 227, 227 research workers, 349, 349 traffic police, 266 urban pollution, 406, 414, 415, 416, 417 welding 198, 198, 199 Paget–Schroetter syndrome, 101, 102 paints, 233, 234, 235–6, 241, 243, 243–4 agriculture, 162 automobiles, 14, 203–5, 206, 207–8, 211, 212, 221–2 buildings and furnishing, 70–2, 71, 77–8 construction, 276, 279, 281, 282, 288 electronics industry, 257 hobby pursuits, 96, 97 offices, 318, 330 wood industry, 224, 225 para-phenylamine diamine, 15 paraquat, 168 particleboard, 70, 71, 76 particulate matter (PM), 48–9, 152–3, 274–6, 407–11, 416, 429 agriculture, 161

INDEX

automobile industry, 49, 212, 215 automobile maintenance and repair, 204, 206 biomass smoke, 393–4, 394, 395–8, 402–3 buildings and furnishing, 74, 76 construction, 274–6, 280, 282 cooking and heating, 46, 48, 53 firefighters, 266–7 indoor sports, 139–40, 152–3, 154 inside automobiles, 129–30, 131–4, 135 offices, 315, 316–7, 318, 330, 331 research workers, 349, 353–4 traffic police, 266 traffic pollution, 422, 426–9, 429, 430–1, 434–6, 439 urban pollution, 407–11, 412–4, 416, 417 volcanic emissions, 399, 402 World Trade Center, 301 passive smoking see second hand smoke peat moss lung, 164 pediatric pulmonary morbidity, 431–2 performing arts, 100, 101, 101–2, 104 perfumes, 13, 16, 18–9 cleaning products, 58, 60, 62 personal care and service, 260, 265–6 persulfates, 15–7, 19–20, 249, 265 pesticides, 55, 60, 63–4, 100, 103 agriculture, 162, 162, 163, 168 hazardous materials, 294, 296 offices, 314, 315, 318, 329, 330 pets, 82–5, 88, 99, 99–100 day-care and schools, 110–1, 118–9, 318 phosgene, 98, 188, 199, 305, 349 chemical weapons, 292, 294, 295–7 phosphine, 199 photography, 96, 97 phthalates, 17–8, 239, 323–4, 330 buildings and furnishing, 71, 74–5, 77 pigeon breeder’s disease, 164 pinene, 62 plague, 297, 298 plant allergens, 91, 165 plastics, 96, 98–9, 233–45 automobile industry, 212, 221 platinum, 194 pleural plaques, 9, 104, 182, 186, 187 pneumoconiosis, 5–6, 179–84, 192, 339 attribution, 9, 9 construction, 276–7 hobby pursuits, 96, 104

465 mining, 177, 178, 179–84 PVC, 239 pneumomediastinum, 368 pneumonia, 151, 154, 296, 325, 401, 434 agriculture, 166 automobile industry, 216–7 passive smoking, 29, 38, 132 welding, 199, 199–200 pneumonitis, 13, 101, 215, 238, 307, 401 agriculture, 161, 163, 168 cleaning products, 63, 64 hobby pursuits, 103, 103 indoor sports, 138, 141, 143, 147 pneumothorax, 172, 189, 250, 368 water sports, 138, 147, 152 police, 291, 302–3, 303, 304, 309 first responders, 292, 296, 300–1 traffic duty, 266, 270, 302, 303 pollen, 162, 163, 164, 340 polycyclic aromatic hydrocarbons (PAHs), 286, 393, 394 traffic pollution, 429, 430, 439 polyethylene, 212, 238, 239 polymer fume fever, 64, 220, 238, 241, 242 polypropylene, 238–9 polystyrene, 239 polytetrafluoroethylene (PTFE), 238, 242 polyurethane, 212, 218–9, 239–40, 243, 282 electronics industry, 248, 249, 251, 255 polyvinyl chloride (PVC), 29, 212, 239, 241, 244 buildings and furnishing, 71, 72–7 food industry, 172 offices, 323 Pontiac fever, 328 pregnancy, 28, 421, 436–7 cleaning products, 61, 63 passive smoking, 25, 27–9, 30–2, 39–41 preterm delivery, 28, 28–9, 436–7 protective services, 260, 266–8 psittacosis, 99, 100, 168 public health, 21, 257, 405–18 cleaning products, 67 indoor ice arenas, 143–4 offices, 331, 334, 335–6 smoke-free workplaces, 126–7 pulmonary barotrauma, 362–3, 364, 368–9, 372 pulmonary contusion, 138, 147 pulmonary disease–anemia syndrome, 237

466

INDEX

pulmonary edema, 238, 240, 241–2, 295 agriculture, 168, 169 firefighters, 267 military, 307 research workers, 338, 348 sports, 101, 102, 138, 147, 151, 449 volcanic emissions, 401, 403 pulmonary embolus, 101, 102, 104 pulmonary fibrosis see lung fibrosis pulmonary hypertension, 392 pulp and paper industry, 223, 226–7, 227, 231 Q fever, 168, 297, 298, 300, 309 radiographers, 262 radon, 110, 113–4, 117, 119, 399 mining, 178, 185, 186 REACH, 59–60 reactive airway dysfunction syndrome (RADS), 241, 242, 262 agriculture, 163, 168 airbag deployment, 133 chemical weapons, 295–6 cleaning products, 62–3, 67 firefighters, 267, 306 research workers, 338, 351, 351 World Trade Center, 301 rebreathers, 358, 359, 360, 362, 369–70 renal diseases, 186 reproduction, 24, 64, 436–8 rhinitis, 82, 86, 89, 91, 171, 261, 265 agriculture, 161, 163, 164, 169, 169, 170 automobile maintenance and repair, 205, 206 bakery, 172 buildings and furnishing, 71–2, 75, 77–8 coatings and plastics, 237, 243 day-care and schools, 109, 116 electronics industry, 250, 251 hairdressers, 14, 16 hobby pursuits, 96, 98, 100, 103, 104 indoor sports, 138, 152, 153, 154 office workers and teachers, 323, 332, 333 pesticides, 64 pets, 82, 85, 100 pulp and paper, 227 research workers, 338, 338, 340–1, 343, 345, 347 wood industry, 224 rhinorrhea, 147, 153, 163 rhinosinusitis, 193, 194, 314, 332, 333

rock wall climbing, 138, 155 rodents, 84–5, 112, 324, 407–8 research workers, 340, 341, 343, 344–5, 347 saltwater aspiration syndrome, 362, 364, 370–1 sarcoidosis, 253, 268, 301–2, 304, 305 office workers and teachers, 314–5, 332 sawmills, 223, 224 SCUBA diving, 358, 358, 360, 362 seafood, 161, 164, 165, 170–2 second hand smoke, 23–41, 139 automobiles, 132, 134, 135, 135 children, 23–4, 25–6, 27–33, 39–41 day-care and schools, 110, 113, 116–7, 119 hobby pursuits, 103, 103 hospitality workers, 121–8 workplace smoking bans, 123–4 sensory irritation symptoms, 122, 123–4 sequoisis, 164 severe acute respiratory syndrome (SARS), 300, 301 shell lung, 164 ship building and breaking, 193 shoe care products, 60, 64 siderosis, 200 sidestream smoke, 24, 25, 132 silica, 192, 193, 195, 306 automobile industry, 212, 213, 214, 215 automobile maintenance and repair, 204, 209 construction, 274, 275, 279, 285, 286 mining, 177–80, 182–6, 188 volcanic emissions, 399, 400, 401 silicates, 274–5 silicosis, 97, 192, 230 automobile industry, 212, 213, 215 construction, 277, 287, 288 mining, 177, 179, 180, 181, 182, 183–6 volcanic emissions, 399, 400, 401 silver fish, 90 sino-nasal cancer, 224, 226, 285 sinusitis, 332, 333 skiing, 446, 447, 448, 448 smelting, 193 smoking 14, 23–41, 132, 268–9, 439–40 automobile industry, 213 construction workers, 277, 278, 279–80, 283, 287 COPD, 4, 5, 10

467

INDEX

firefighters, 306 indoor equestrian sports, 153–4 inside automobiles, 129–30, 132–5, 135 military, 308, 309 miners, 182–3, 184, 185, 187–8 police, 303 urban pollution, 406 welders, 200–1 workplace bans, 123–4 see also second hand smoke sodium azide, 133 soldering, 247–8, 249–56, 276 spices, 173 spinning and weaving, 96, 97, 227, 228 steel, 193 stings and bites, 91 stone sculpting, 97, 98 stroke, 33, 39 styrene, 212, 220, 239 suberosis, 164 sudden infant death syndrome (SIDS), 29, 32 sulphates, 409, 412 sulfite mills, 226, 227 sulfonates, 55, 62 sulfur dioxide, 46, 49, 227, 241, 242, 262 firefighters, 266, 305 research workers, 349, 349 traffic pollution, 428, 430, 434 urban pollution, 412–3, 414, 416, 417 volcanic emissions, 399, 401, 402, 403 sulfur mustard (SM), 292, 293, 295, 297 sulfur oxides, 266, 293, 411–3, 414, 417 swimming, 145, 146, 147–8, 445–7, 448, 448–9 swimming-induced pulmonary edema (SIPE) 151 talcosis, 101, 102 taxidermy, 99, 100 teargas, 292, 293 Teflon coating, 238, 242 temperature, 115–6, 378 terpenes, 224, 224, 227 textiles, 96, 97, 98, 227–31 thesaurosis, 13 thiocyanates, 236 thioglycolic acid, 16 ticks, 91 time of useful consciousness, 381, 381 tobacco worker’s disease, 164 toluene, 64, 130–1

toluene diisocyanate (TDI), 219, 240, 243, 281 toxic pneumonitis, 9, 166, 194 automobile maintenance and repair, 205, 206, 209 chemicals and coatings, 240, 241, 241–2 research workers, 338, 349, 350 welding, 199, 199–200, 209 trauma, 178, 179, 189, 287 trihalomethanes (THMs), 146–7 truck-bed liners, 205, 206 tuberculosis, 53, 214, 288, 333, 392 agriculture, 168 healthcare workers, 263 military, 300, 301, 309, 309 mining, 177–8, 180, 181, 182, 185, 188 police, 300, 301, 303, 303, 309 tularaemia, 297, 298 underground workers, 357–8, 360, 361 upper respiratory tract infections (URTI), 151, 300–1 urban pollution, 405–18, 421–40 vehicle assembly, 211–2, 212, 221, 222 velopharyngeal incompetence, 101, 102 ventilation, 137, 265, 448 automobile industry, 213, 217, 221 automobile maintenance and repair, 204–5, 208 barns, 164 buildings, 69, 77–8 cleaning products, 59, 66 cooking and heating, 45–9, 51, 52, 53 day-care and schools, 110, 111, 115, 118, 119 electronics industry, 252 fungi and moulds, 87–8 hairdressers, 16–7 ice sports, 139–40 inside automobiles, 130 mining, 178–9 offices, 313–6, 317, 325, 328, 331, 333, 333–4 second hand smoke, 126 water sports, 144, 146, 148, 149, 151 welding, 199 wood and textile industries, 231 veterinarians, 264–5, 270

468 vocal cord dysfunction (VCD), 101, 101–2, 351 military, 307–8 outdoor sports, 449, 450 volatile organic compounds (VOCs), 72–4, 87 biomass smoke, 397 buildings and furnishing, 69, 70, 72–4, 77, 115 cleaning products, 64 day-care and schools, 111, 115 indoor ice sports, 139–40 inside automobiles, 129, 130–1, 132–3, 134, 135 offices, 317, 318, 320, 321, 322–3 traffic, 266, 430 urban pollution, 415, 416 volcanic emissions, 391–2, 399–401, 402, 403–4 weaving and spinning, 96, 97, 227, 228 weightlifting, 138, 155 welding, 197, 198, 199–201, 221, 257

INDEX

automobile industry, 211, 212, 213, 221 automobile maintenance, 204–5, 206, 207, 209 construction, 275, 276, 279, 282 wine grower’s lung, 164 wood, 223, 224, 224–6, 231 construction, 274, 276, 282, 285, 286 forest fires, 391, 392–6, 398 hobby pursuits, 97, 98 wood pulp worker’s disease, 164 woodwork teachers, 223, 224, 226 wool, 228 woolsorter’s disease, 230 World Trade Center, 267–8, 270, 301–2, 304, 305 cough, 301–2 zinc, 199, 220, 248, 347 zinc chloride (smoke bombs), 207 zinc oxide, 347, 349 zoonoses, 162, 168, 174 zoonotic pneumonia, 99, 104, 105