LEAD
POISONING A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2004 by ICON Group International, Inc. Copyright 2004 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Lead Poisoning: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-84480-1 1. Lead Poisoning-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on lead poisoning. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.
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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.
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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes&Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health
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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON LEAD POISONING...................................................................................... 3 Overview........................................................................................................................................ 3 Federally Funded Research on Lead Poisoning.............................................................................. 3 The National Library of Medicine: PubMed ................................................................................ 61 CHAPTER 2. NUTRITION AND LEAD POISONING .......................................................................... 103 Overview.................................................................................................................................... 103 Finding Nutrition Studies on Lead Poisoning........................................................................... 103 Federal Resources on Nutrition ................................................................................................. 105 Additional Web Resources ......................................................................................................... 105 CHAPTER 3. DISSERTATIONS ON LEAD POISONING ..................................................................... 107 Overview.................................................................................................................................... 107 Dissertations on Lead Poisoning................................................................................................ 107 Keeping Current ........................................................................................................................ 109 CHAPTER 4. CLINICAL TRIALS AND LEAD POISONING ................................................................ 111 Overview.................................................................................................................................... 111 Recent Trials on Lead Poisoning................................................................................................ 111 Keeping Current on Clinical Trials ........................................................................................... 115 CHAPTER 5. BOOKS ON LEAD POISONING .................................................................................... 117 Overview.................................................................................................................................... 117 Book Summaries: Federal Agencies............................................................................................ 117 Book Summaries: Online Booksellers......................................................................................... 118 Chapters on Lead Poisoning....................................................................................................... 120 Directories.................................................................................................................................. 121 CHAPTER 6. MULTIMEDIA ON LEAD POISONING ......................................................................... 123 Overview.................................................................................................................................... 123 Video Recordings ....................................................................................................................... 123 CHAPTER 7. PERIODICALS AND NEWS ON LEAD POISONING ...................................................... 125 Overview.................................................................................................................................... 125 News Services and Press Releases.............................................................................................. 125 Academic Periodicals covering Lead Poisoning ......................................................................... 128 CHAPTER 8. RESEARCHING MEDICATIONS .................................................................................. 129 Overview.................................................................................................................................... 129 U.S. Pharmacopeia..................................................................................................................... 129 Commercial Databases ............................................................................................................... 130 Researching Orphan Drugs ....................................................................................................... 131 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 135 Overview.................................................................................................................................... 135 NIH Guidelines.......................................................................................................................... 135 NIH Databases........................................................................................................................... 137 Other Commercial Databases..................................................................................................... 139 APPENDIX B. PATIENT RESOURCES ............................................................................................... 141 Overview.................................................................................................................................... 141 Patient Guideline Sources.......................................................................................................... 141 Finding Associations.................................................................................................................. 148 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 151 Overview.................................................................................................................................... 151 Preparation................................................................................................................................. 151 Finding a Local Medical Library................................................................................................ 151 Medical Libraries in the U.S. and Canada ................................................................................. 151
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ONLINE GLOSSARIES................................................................................................................ 157 Online Dictionary Directories ................................................................................................... 160 LEAD POISONING DICTIONARY........................................................................................... 163 INDEX .............................................................................................................................................. 219
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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with lead poisoning is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about lead poisoning, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to lead poisoning, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on lead poisoning. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to lead poisoning, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on lead poisoning. The Editors
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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON LEAD POISONING Overview In this chapter, we will show you how to locate peer-reviewed references and studies on lead poisoning.
Federally Funded Research on Lead Poisoning The U.S. Government supports a variety of research studies relating to lead poisoning. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to lead poisoning. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore lead poisoning. The following is typical of the type of information found when searching the CRISP database for lead poisoning: •
Project Title: A SOCIAL NETWORK-BASED INTERVENTION TO REDUCE LEAD EXPOS Principal Investigator & Institution: Kegler, Michelle C.; Assistant Professor; Behavioral Scis & Hlth Educ; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2002; Project Start 30-SEP-1996; Project End 31-AUG-2005
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Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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Summary: (Taken from Applicant s Abstract) The purpose of this study is to test whether adding an inter-generational component to an existing social network-based lay health advisor intervention increases its effectiveness in mobilizing a Native American community to respond to heavy metal contamination from lead and zinc mining. Ottawa County Oklahoma, the site of the proposed research, was heavily mined for zinc and lead in the first half of this century. Mine tailings containing heavy metals are stored in piles up to 200 feet in height and cover 800 acres. Ottawa County is home to 8 Indian tribes and much of the mine waste is on tribal land. The proposed research builds on previous work with these tribes, by expanding to address cadmium in addition to lead, and by adding a youth component. Specifically, the study proposes to: a) integrate Native American youth groups with an existing lay health advisor program to form an inter- generational intervention; b) expand the existing lay health advisor intervention to address cadmium in addition to lead; c) use participatory research methods to involve tribal youth and adults in a residential particulate matter exposure study; d) assess the extent to which the intervention contributes to belief, attitude and behavior changes that will reduce heavy metal exposure and absorption in Native American children; e) assess whether the intervention contributes to changes in mean blood lead level of Native American children relative to white children; and f) assess the contribution of the intervention to creating changes in organizational, community, tribal and government (city, county, state, federal) capacity to address heavy metal contamination in Ottawa County, Oklahoma. The research design is a quasiexperimental pretest-post test design with a comparison group. Data collection methods for the outcome evaluation include a population-based blood lead screening of 400 Native American and white children (ages 1-6) and accompanying care giver interviews, organizational network interviews, and community leader surveys. In addition to assessing change at multiple levels, all instruments will assess key dimensions of community capacity (social capital, sense of community, community participation and civic, involvement) with an emphasis on capacity to respond to environmental health problems. Process evaluation methods include documentation of lay health advisory contacts and interviews with youth and adult volunteers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ADHESION AND REPULSION MOLECULES IN DEVELOPMENTAL NEUROTOXIC INJURY Principal Investigator & Institution: Reuhl, Kenneth R.; Univ of Med/Dent Nj-R W Johnson Med Sch Robert Wood Johnson Medical Sch Piscataway, Nj 08854 Timing: Fiscal Year 2002 Summary: (provided by applicant) The appropriate temporal and spatial expression of neural adhesion and repulsion molecules, membrane proteins which provide instructive guidance and support for neuron and neurite movement, is critical to normal brain develop disturbance of the synchronous expression and function of these molecules has adverse consequences ranging fro subtle learning disabilities to severe malformations. Exposure to toxic metals, particularly methylmercury known to result in behavioral disabilities in development and in deficient learning and processes in adults-possibly by the shared mechanism of disturbing brain morphogenesis. It is hypothesized that neurotoxic metals perturb brain development/morphogenesis by disrupting the coregulated expression and function of critical morphoregulatory adhesion and repulsion molecules. To elucidate the neurotoxic roles of these metals, four questions will be examined in hippocampus and cerebellum: 1) Does exposure to neurotoxic metals alter the expression of adhesion and repulsion molecules during stages of brain development,
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and thereby compromise morphogenesis? 2) Do selective transcriptional, translational or posttranslational processes mediate metal-induced changes adhesion and repulsion molecules? 3) What are the behavioral consequences of toxicant-disturbed adhesion and repulsion molecules? 4)Can the deleterious effects of toxic metals on morphoregulatory molecules be modified or ameliorated by intervention strategies? Complementary morphological, biochemical and behavioral assessments will be used to characterize the adverse of methylmercury or lead exposure on the adhesion molecules, NCAM L1, Ncadherin, and the Eph family of repulsion molecules in hippocampus (which remain plastic throughout life)and cerebellum (in which plasticity fades maturation). Consequences to both structural and behavioral development will be addressed in vivo, using ex vivo and in vitro models. Current clinical interventions for metal toxicity will be assessed for effects on molecules. As data are developed by the Exposure Assessment and Intervention and Clinical Science Projects, other candidate neurotoxic agents will similarly be studied for their effects on the adhesion and repulsion critical for normal develop. The long-term objective is to elucidate the mechanisms by which toxic metals an other xenobiotics alter neural pathway formation and synaptic regulation and how consequences of such exposures might be minimized. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: AGE, LEAD EXPOSURE, AND NEUROBEHAVIORAL DECLINE Principal Investigator & Institution: Stewart, Walter F.; Associate Professor; Epidemiology; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 01-SEP-1993; Project End 31-AUG-2004 Summary: (Adapted from applicant's abstract): This is the second resubmission of a competitive renewal application to continue studying the long-term CNS effects of past exposure to organic and inorganic lead. The primary goal of the original study was to determine if past exposure to a putative neurotoxicant was associated with a decline in cognitive function. A unique feature of the cohort we have studied is that none of the participants were occupationally exposed to lead at the time of enrollment. The average time since last exposure was 16 years. We found that past cumulative absorption of lead, measured as tibial lead, was associated with a decline in neurobehavioral test scores, with pronounced declines in tests of verbal and visual memory. Many of the effects were seen in tests that involved declarative new learning, which is known to require the hippocampus and related structures. These progressive changes, comparable to changes in learning and memory associated with aging, long after last occupational exposure to lead are unlikely to be explained by changes in CNS neurochemistry alone. Moreover, our findings are consistent with animal evidence suggesting that organic and inorganic lead can lead to cell death and selectively target areas of the limbic system and epidemiologic evidence that indicates impairment of visual and verbal memory from exposure to inorganic lead. As a logical next step, we propose to determine if there are structural (i.e., MRI based volumetric measures) correlates to the changes in cognitive function we have observed. These data will help determine if there are specific CNS target sites for lead in and will provide the foundation for understanding mechanisms that mediate the effect of adult lead exposure on CNS function, providing an important link between human observational studies and animal experimental studies. To this end we propose: 1. To determine if tibial lead is associated with changes in CNS structures (i.e., smaller brain volumes) suspected as targets of lead. 2. To determine if changes in CNS structures are either in the causal pathway of, or modify the relation between, tibial lead and changes in measures of cognitive function. These aims will be addressed in a three year study of 550 current study participants with past exposure to lead, 100
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individuals who participated as controls, and an additional 100 newly recruited subjects with past lead exposure. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ASTHMA AND LEAD PREVENTION IN CHICAGO PUBLIC HOUSING Principal Investigator & Institution: Knight, John Q.; Senior Program Associate; Safer Pest Control Project 25 E Washington St, Ste 1515 Chicago, Il 60602 Timing: Fiscal Year 2002; Project Start 15-SEP-2001; Project End 30-JUN-2005 Summary: (provided by applicant) African Americans, Puerto Ricans, and persons living in low income neighborhoods have at least five times the death rates from asthma as non- Hispanic whites. Many environmental variables have been shown to increase symptoms in persons predisposed to the disease, including exposure to cockroach allergens, furry/feathered pets, dust mites, rodents, endotoxins, and pesticide sprays. The purpose of the current study is to examine the effects of peer education and modification of the home environment on the incidence and severity of asthma, lead dust exposure, and lead poisoning in Chicago public housing residents over a four-year period. The project will build upon a network of community groups, healthcare providers, specialists, and Chicago Housing Authority (CHA) personnel committed to improving public health in Chicago public housing. A total of six peer educators will be recruited from Ogden Courts, Henry Homer, and Robert Taylor developments who will work with a total of 600 families with asthmatics from the three developments to assess and modify pest problems and other asthma triggers and lead hazards. A total of fifteen residents from the three developments will additionally be recruited to carry out small unit repairs (caulking and sealing of cracks and crevices) for cockroach and rodent management in all 600 units. The specific aim of this study is to reduce the incidence and severity of asthma and lead poisoning in Chicago Public Housing. Long-term objectives are to implement and formalize Integrated Pest Management (effective pest control while minimizing the use and hazards of pesticides) Authority-wide, to improve the self-sufficiency of CHA residents, and to enable CHA residents to direct environmental improvements in their own developments leading to better health. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ATTENTION DEFICIT DISORDER AND EXPOSURE TO LEAD Principal Investigator & Institution: Needleman, Herbert L.; Professor of Psychiatry and Pediatrics; Psychiatry; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2001; Project Start 01-APR-1990; Project End 31-MAY-2004 Summary: Attention Deficit Hyperactivity Disorder (ADHD) is the commonest psychiatric diagnosis in American children. Its etiology is unknown. We and others have shown that lead at low doses affects attention in children as measured by structured behavioral inventories e.g., reaction time under varying intervals of delay; and by teachers questionnaires. Behavioral and neurochemical studies in rodents and primates given lead support these findings. Whether lead is among the causes of clinical ADHD has not been investigated. This is a case control study of 250 ADHD subjects diagnosed at the Western Psychiatric Institute and Clinic and 250 appropriate controls. Hypotheses to be tested are that lead increases the risk for ADHD, and that lead exposure is associated with increased alcohol and substance use. A comprehensive assessment battery on the ADHD on the ADHD subjects evaluating behavior, cognition,
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use of alcohol and substances, health and socioeconomic factors has been collected. The comparison sample will be matched in range to the ADHD sample for the following variables: age within one year, gender, ethnicity, single versus two parent household, and parent education. Past history of lead exposure will be measured by K-like x-ray fluorescence, a technique that we have been using for 5 years. ADHD subjects and controls will be evaluated first by Mantel-Haenzel procedures for stratified data, and then by logistical regression, controlling for appropriate co-variates: age. sex, race, family status (e.g., two parents living in home, divorced, never married), family history of ADHD and other psychiatric disorders (SCID), parent education, socioeconomic status, family size, family alcohol use, and family conflict (Conflict Tactic Scale and Dyadic Adjustment Scale). Use of alcohol and substances will be shown to increase the risk for clinical ADHD, an estimation between lead and treatment outcome will be evaluated. If lead is shown to increase the risk for clinical ADHD, an estimation of the proportion of this common problem attributable to a lead would be identified, and an opportunity for authentic prevention of this segment made available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BEHAVIORAL TOXICITY OF LEAD--A PHARMACOLOGICAL ANALYSIS Principal Investigator & Institution: Cory-Slechta, Deborah; Professor; Environmental Medicine; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2002; Project Start 01-JAN-1990; Project End 30-JUN-2005 Summary: (Adapted from the Investigator's Abstract) Elevated lead (Pb) body burden still impacts almost 9% of U.S. children and >40% of children in some underdeveloped countries. Its association with cognitive deficits in children and in elderly men and women, and with delinquency and aggression, makes it a more pervasive public health problem than has generally been appreciated. Our neurochemical and behavioral studies over the past funding period show that chronic postweaning Pb appears to target the mesolimbic dopamine (DA) system, based on effects observed in its terminal projection region, the nucleus accumbens (NAC). NAC, however, is considered a limbicmotor interface, integrating information via glutamatergic projections from hippocampus and prefrontal cortex, two regions well known to mediate cognitive function. At the same time, Pb also produces a widespread inhibition of glutamatergic NMDA receptors. NMDA inhibition has been shown in prefrontal cortex and NAC to enhance activation of non-NMDA AMPA/kainate excitatory amino acid receptors. The proposed studies therefore test the hypothesis that Pb-induced behavioral impairments and neurochemical changes in mesolimbic systems actually derive from preferential AMP/kainate receptor activation of the glutamatergic projections from hippocampus and prefrontal cortex, to NAC. This hypothesis predicts that hippocampal and prefrontal glutamatergic projections to NAC should be critical in mediating behaviors known to be altered by Pb. Specific Aims 1 and 2 will thus determine whether disconnection of these projections also disrupts these behaviors, and whether preferential AMPAergic activation of these projections can mimic the behavioral toxicity of Pb in normal rats, using two behavioral baselines reliably altered by Pb: fixed interval performance and a repeated learning paradigm. Specific Aim 3 tests the associated prediction that AMPA antagonists in these projection regions should reverse these Pbinduced behavioral impairments. Specific Aim 4 seeks to determine whether preferential AMPAergic activation of these projections reproduces in normal rats the increases in evoked DA overflow in NAC associated with Pb, and if AMPA antagonists can reverse these increases in Pb-treated rats. To determine the extent to which these mechanisms
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generalize to human Pb exposure and whether they may be exacerbated by exposures earlier in development, Specific Aims 2 and 4 compare effects of preweaning, postweaning and continuous Pb exposures. These experiments will significantly advance our understanding of the control of complex operant cognitive behaviors by hippocampal and prefrontal projection circuits and the mechanisms by which Pb disrupts them. They will further define the comparative roles of NMDA and AMPA/kainate receptors in these projections and their interactions with DA systems, allowing rational behavioral and therapeutic approaches to mesolimbic system dysfunctions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BLOOD LEAD LEVELS AND DEVELOPMENT OF ASTHMA Principal Investigator & Institution: Joseph, Christine Lm.; Senior Staff Scientist; Biostatistics and Epidemiology; Case Western Reserve Univ-Henry Ford Hsc Research Administraion Cfp-046 Detroit, Mi 48202 Timing: Fiscal Year 2002; Project Start 01-APR-2001; Project End 31-MAR-2004 Summary: (Provided by Applicant) Despite progress made in the treatment and management of asthma, strategies for its prevention remain elusive. Likewise, lead poisoning remains a serious environmental health hazard for U.S. children. The two conditions have similar epidemiologic patterns. Both are prevalent among young children, elements in the physical environment heighten risk of disease, and residing in an urban environment increases the probability of exposure to relevant physical and socioeconomic risk factors. Recent published analyses have suggested a possible relationship between the two disorders. The objective of this study is to use automated data to examine relationships between blood lead levels (BLL) and development of asthma. The study population will be children greater than 2 years of age who have been continuously enrolled in the Henry Ford Health System (HFHS) managed care organization and for whom there is a BLL in the HFHS laboratory results database for 1995-1996. Asthma status will be determined using patient encounter and prescription claims databases. This information will be used to investigate the association of BLL and asthma prevalence at baseline, and to assess BLL as a predictor of development of asthma during a defined follow-up period. Results of this analysis will guide the design of future studies involving primary data collection. Benefits of this study include the ability to use available automated datasets to examine the association of BLL and occurrence of asthma in an ethnically and socioeconomically diverse population, adjusting for demographic variables and adjunct measures of socioeconomic status. Examination of the potential relationship between BLL and asthma is critical, as environmental lead would be a modifiable risk factor for asthma. In addition, information on this relationship can be instrumental in helping to uncover reasons for racial differences in asthma prevalence and gaining more information on ways to prevent or reduce the risk of asthma, especially among urban, minority children. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BONE LEAD STANDARDIZATION PROGRAM Principal Investigator & Institution: Parsons, Patrick J.; Research Scientist; Wadsworth Center Empire State Plaza Albany, Ny 12237 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-MAY-2007 Summary: (provided by applicant): The aim of this proposal is to create a Standardization Program for Bone Lead measurements (BLSP) obtained via reference
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methods and via in vivo X-Ray Fluorescence (XRF). The BLSP will fulfill current needs of the bone lead methodologies: lack of appropriate certified reference materials (RMs) and lack of traceability. The BLSP will also provide RMs for electrothermal atomic absorption spectrometry (AAS) and inductively coupled plasma-mass spectrometry (ICP-MS) and will conduct an interlaboratory validation study among laboratories using those methods. The program will also provide RMs for XRF, thereby providing traceability to SI units, and will conduct an interlaboratory validation study among laboratories using XRF for in vivo bone lead measurements. There are six goals: first to cross-validate AAS and ICP-MS in the Wadsworth Trace Elements Laboratory of the New York State Department of Health (NYS DOH); second to establish a national repository of RMs for bone lead measurement via AAS and ICP-MS traceable to NIST SRM 1486 Bone Meal and 1400 Bone Ash; third, to conduct an interlaboratory validation of AAS and/or ICP-MS for bone lead measurement. The fourth goal is to assemble a national repository of RMs for bone lead XRF by preparing two sets of wellcharacterized goat bone samples containing endogenous lead concentrations that encompass those found in human populations; the fifth goal is to conduct an in vitro XRF interlaboratory validation and comparison study using the two sets of goat bone samples. The first set of XRF RMs will be destroyed as part of the process of obtaining reference concentrations via AAS and ICP-MS for both surface and core bone that are traceable to SI units. The reference concentrations thus obtained will form the basis of the assessment of XRF accuracy. The second set of XRF RMs will be created and used for a second interlaboratory comparison and will be preserved for long-term use. The sixth and last goal is to conduct an in vivo XRF validation study using the euthanized members of the NYS DOH goat colony that will provide the RMs. XRF-measured in vivo concentrations will be compared to the reference concentrations obtained from AAS and ICP-MS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CELLULAR & MOLECULAR EFFECTS OF LEAD ON CHOND Principal Investigator & Institution: O'keefe, Regis J.; Professor; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2006 Summary: (provided by applicant): Lead exposure continues to be a major public health problem in the United States. Developing skeletal tissues are targets for Pb, however the molecular mechanisms of its effects have not been defined. The current proposal uses state- of-the-art molecular methods, combining both in vitro and in vivo approaches to investigate the following hypotheses: i) Pb alters the rate at which mesenchymal cells undergo chondrogenesis; ii) Pb alters the rate and organized pattern of chondrocyte differentiation in the growth plate; iii) these effects occur at low concentrations of Pb, consistent with levels observed in Pb-exposed children; and iv) that the effects are mediated by an alteration in specific signaling pathways in the target cells. These hypotheses will be investigated in three aims. In Specific Aim 1, the effect of Pb on chondrogenesis will be examined using mesenchymal cells isolated from stage E11.5 mouse limb buds. Preliminary data demonstrate that Pb enhances the rate of chondrogenesis and the signaling pathways involved in this effect will be identified. Specific Aim 2 investigates the effect of Pb on the rate of chondrocyte differentiation during the process of endochondral bone formation and uses a well-defined embryonic sternal chick chondrocyte cell culture model. This aim is based on strong preliminary data demonstrating important Pb effects on intracellular signaling, growth factor responsiveness, and chondrocyte differentiation. Specific Aim 3 uses an in vivo
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approach based on an ectopic bone formation model to investigate both chondrogenesis and chondrocyte differentiation in control and Pbexposed mice. This aim is based on preliminary data demonstrating morphological changes in the growth plate of Pb exposed animals as well as abnormal fracture healing in Pb exposed mice. The final aim will characterize the spatial and temporal alterations in gene expression that occur following Pb exposure and which result in abnormal bone formation and skeletal development. Thus, the proposal provides a comprehensive, hypothesis-based examination of the effect of Pb on endochondral bone formation using state-of-the-art molecular methods. The findings have important implications for the management of Pb exposed children and adults in the future. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: COMBINING K AND L XRF FOR IN VIVO LEAD IN BONE MEASURE Principal Investigator & Institution: Gardner, Robin P.; Nuclear Engineering; North Carolina State University Raleigh 2230 Stinson Drive Raleigh, Nc 27695 Timing: Fiscal Year 2002; Project Start 01-JAN-1995; Project End 31-MAY-2004 Summary: Chronic low-level lead poisoning is widespread, causing irreversible neurological problems in children. Assays of blood samples provide data on the amount of lead in circulation, but not on the accumulated lead concentration in the body - which is that contained in the skeleton. In vivo measurement of lead in the tibia by X-Ray fluorescence (XRF) is the present accepted method for determining lead in the skeleton. There are presently two XRF methods; one (the K XRF) uses the lead K X rays excited by the radioisotope source 109Cd while the other (the L XRF) uses the lead L X rays excited by the polarized X rays from an X-ray tube. Our previous research concentrated on improving the minimum detectable concentration (mdc) limits of both methods. This was accomplished by first developing a very comprehensive and accurate Monte Carlo model for simulating X-ray transport and the resulting spectra. It included L X rays, a detailed Compton scatter treatment, and polarized X rays. This model was then used to quantitatively determine errors in the two methods including variable skin covering thickness, variable and unknown sample position, and the presence of unknown lead concentration profiles in the bone. The Monte Carlo model was then used to investigate various methods of improving the minimum detectable lead limits. The primary improvement in both cases (a factor of about three in the reduction of statistical uncertainties) was found in using the entire spectral information rather than just the characteristic K and L peaks. The approach used is called the Monte Carlo - Library Least-Squares (MCLLS) approach. It is based on determining the elemental spectral libraries for any sample composition and analysis geometry by Monte Carlo simulation and then using these libraries in a linear least-squares analysis of the unknown sample spectrum for lead amount. An even more comprehensive and promising approach was identified and investigated in a very preliminary way. That approach is the combined use of the K and L methods by the MCLLS approach; thereby providing a direct basis for eliminating or at least minimizing the previously identified errors even more. The proposed method would use the radioisotope source 109Cd for excitation of both K and L X rays via the 88 keV gamma ray and silver K X rays, respectively. The major advantages of this approach are: (1) all the available spectral information is used in an optimum way, (2) one can determine if a lead concentration profile exists since the K and L X rays penetrate different bone thicknesses, and (3) the possibility exists that the spectral data taken can be used to eliminate the effect of unknown sample position variations and other patient-dependent variables that interfere with the lead
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measurement. The development and testing of this approach is the research proposed here. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: COMMUNITY ASSIST OF SOUTHERN ARIZONA Principal Investigator & Institution: Estrada, Ramon M.; Program Director; Child and Family Resources, Inc. 1040 N Alvernon Way Tucson, Az 85711 Timing: Fiscal Year 2002; Project Start 15-SEP-2001; Project End 30-JUN-2005 Summary: (provide by applicant) The long term objectives of the community-directed Community Assist of Southern Arizona (CASA) are to reduce the communities' exposures to environmental pollutants, link members of communities who are affected by adverse environmental conditions with healthcare providers, provide relevant and culturally sensitive information about environmental pollutants, promote a communitywide interest in the project, and act as a liaison between researchers and agencies and communities to help disseminate research results in an easy to understand format. The specific aim of this project is to expand the Child Health Champion Campaign (CHCC) in four ways: 1) to include all border regions of southern Arizona where Child & Family Resources, Inc. has an office (Nogales, Douglas, southern metropolitan Tucson, and Yuma; 2) to include additional information on mitigation measures and to assist with families' mitigation; 3) to expand the program to include additional environmental health areas of concern to the communities, in particular childhood lead poisoning; and 4) to further act as liaison between the community and researchers and government agencies. The two measurable goals of CASA are reduction in the number of visits to school nurses caused by respiratory illnesses and reduction in the number of childhood lead and arsenic poisoning cases reported by doctors and laboratories. The objectives which define the design and methods of the project are to finish laboratory analysis of items of concern for heavy metals; to develop survey instruments appropriate for each community; to conduct a minimum of 200 home visits in each community; complete mitigation in at least 75% of those homes requiring and desiring mitigation; to conduct six workshops for parents and children in each community; to develop at least one school program in each community; to present at least one radio broadcast in each community; of those identified with health problems, to assist at least 75% to obtain medical care; to conduct at least one workshop for farmacias and yerberias on the heavy metal content of home remedies; and to complete the evaluation of the project and the input of researchers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: COMMUNITY-BASED ENVIRONMENTAL*
PARTICIPATORY
RESEARCH
IN
Principal Investigator & Institution: Amaya, Maria A.; Wakefield Professor of Health Sciences; School of Nursing; University of Texas El Paso El Paso, Tx 79968 Timing: Fiscal Year 2002; Project Start 30-SEP-2001; Project End 31-JUL-2006 Summary: (provided by applicant): The objectives of the proposed study are to: 1) estimate the geographic distribution of environmental lead in El Paso and Juarez; 2) estimate the prevalence of elevated blood lead levels in the two cities; 3) differentiate chronic and acute lead exposures in children with elevated lead levels; 4) fractionate lead by etiological source in children; and 5) involve end- users to evaluate a scientifically based, culturally relevant prevention/intervention strategy. The study seeks to improve the capacity of the El Paso, Texas - Juarez, Mexico binational
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community to participate in research to identify the etiology of lead exposure among low-income Hispanic children. Project activities will increase the community's capacity to deliver environmental health intervention, prevention, and educational services in a binational setting through collaborative partnerships between academic institutions, community organizations, and stakeholders. Based on original research, the study joins environmental health scientists and community organization members in an interdisciplinary investigative team. This project will evaluate lead exposure and its adverse effect on the health of low-income Hispanic children on the U.S.-Mexico border. Environmental lead distribution will be estimated using data from indoor and outdoor sites. Nine hundred and thirteen blocks will be tested for outdoor lead levels in each city. In each block 40 random samples of soil will be analyzed using a portable X-ray fluorescence (XRF) lead analysis unit in public areas along streets, from playgrounds, schools, hospitals, etc. Indoor lead levels in water, soil, dust, and air will be tested in 4 households in 10 randomly selected blocks. An exposure assessment survey will be administered. High- household's risk will be defined as those exceeding EPA maximum household contaminant levels. Data will be statistically analyzed to produce binational maps of environmental lead distribution. Two hundred households will be randomly selected from high-risk blocks in each city (a total 400 households). One hundred and ninety-two children, ages 6 months to 11 years, will be recruited in each city. Blood lead levels will be analyzed using graphite furnace atomic absorption spectroscopy. Children with elevated lead levels (>10 ug/dL) will be tested to determine whether the exposure is chronic using K X-ray fluorescence spectroscopy of the tibia. The etiological source of lead in the blood will also be evaluated by inductively coupled plasma - mass spectroscopy (ICP-MS). Regression analysis will be conducted to model the relationships between blood and bone lead levels, environmental lead, and risk of exposure. Four community-based organizations (CBOs) will participate in the research process. A CBO liaison will build and coordinate a community-based partnership for education and outreach and overall capacity building. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CORE SURVEILLANCE MODEL PROGRAM IN CALIFORNIA Principal Investigator & Institution: Harrison, Robert J.; Public Health Institute Oakland, Ca 946074046 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 29-SEP-2004 Summary: The Occupational Health Branch (OHB) of the California Department of Health Services (CDHS) proposes to develop and implement a core state-based surveillance model program for the prevention of targeted workplace diseases, injuries and hazards. A multi disciplinary staff at the OHB currently conducts surveillance and investigation of multiple work-related diseases and injuries, including asthma, pesticide illness, carpal tunnel syndrome, selected fatal injuries and lead poisoning. In addition, we propose to add silicosis and selected nonfatal injuries as core surveillance activities. We propose several innovative approaches that will enhance our previous surveillance activities: (1) all conditions that are recommended as "core" public health activities by the State-NIOSH Surveillance Work Group will be placed under surveillance; (2) our surveillance model will use multiple data sources - including electronic reporting through a new Workers Compensation Information System - that can be replicated in other States; (3) our condition-specific surveillance systems will be integrated through a core surveillance database that can serve as a useful tool for targeting industries for indepth intervention activities; and (4) we will conduct a broad-based intervention in the construction industry based on multiple endpoint surveillance data. Our approach relies
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on the linking of surveillance data with intervention and prevention efforts to integrate occupational health into mainstream public health. The successes and lessons learned from these activities will be distilled to assist NIOSH in recommending a model for core occupational health surveillance that can be undertaken in other States. For each core condition under surveillance, we will conduct efficient case finding using existing NIOSH and/or CSTE case definitions, and employ standardized databases and coding systems to collect, analyze and report aggregate data to NIOSH. Using established guidelines for prioritizing cases for follow-up, we will perform hazard surveys and workplace investigations for purposes of targeted prevention activities. We will use a variety of means to disseminate our scientific findings and prevention recommendations, including the preparation of a surveillance annual report and articles for scientific publication. The project will develop and implement broad-based, industry-wide intervention activities that address simultaneously multiple health and safety hazards identified through the core surveillance system. Construction will be targeted as the focus of the intervention component, which will be identified, developed and implemented in a collaborative process with key stakeholders. We will evaluate aspects of this model core surveillance system including the function of endpointspecific surveillance systems, utility of the aggregate database for targeting industries and occupations, feasibility of replicating the model in other States, and process of working with stakeholders to develop and implement interventions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CORE SURVEILLANCE OF OCCUPATIIONAL HEALTH IN NEW YORK Principal Investigator & Institution: Gelberg, Kitty H.; Bureau of Occupational Health 547 River St Troy, Ny 12180 Timing: Fiscal Year 2002; Project Start 01-JUL-2001; Project End 30-JUN-2005 Summary: New York, with the assistance of the SENSOR and ABLES programs, has established a structure for occupational disease surveillance and follow-up in New York State. Provisions of the New York State (NYS) Public Health Law mandate the reporting of a number of occupational conditions in NYS. Since 1981, the New York State Department of Health, Bureau of Occupational Health (BOH) has operated a Heavy Metals Registry for the reporting of cases of lead, mercury, arsenic, and cadmium poisoning, and an Occupational Lung Disease Registry for the reporting of cases of work related lung disease. Since 1991, BOH has operated a Pesticide Poisoning Registry and receives reports from healthcare providers of suspected pesticide poisonings. While all of these registries are operational, the extent to which there is active surveillance, with aggressive case finding, ascertainment and follow-up, varies. There are a number of reasons for this variability, including differences in how the diseases are diagnosed and the different reporting sources for the various registries. Additional federal resources will permit us to build upon existing reporting laws and infrastructure and expand current surveillance efforts to help us achieve the NIOSH standards for a model core surveillance system for a range of significant occupational conditions. We propose to conduct general surveillance of existing databases available to the Department of Health such as death certificates and hospital discharge data to assist with documenting the magnitude of occupational injuries and illnesses in New York, and to identify trends and industries occupations at elevated risk. Focus will be primarily upon upgrading our Occupational Lung Disease Registry; however, we will also focus more attention on conducting educational outreach for all of our registries. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CORE--ANALYTICAL Principal Investigator & Institution: Wilson, m; Kennedy Krieger Research Institute, Inc. Baltimore, Md 21205 Timing: Fiscal Year 2002 Summary: The analytical core facilities have been developed to provide a strong central analytical core, with a variety of instrumentation for quantitative analysis, for use for all investigators in the program project. The core provides facilities and training that is used by each of the projects as required, for computerized image analysis of autoradiographic data such as gels, radioligand binding and in the situ hybridization, quantitative morphometric analysis of immunolabeled and conventionally stained tissue sections, and fluorescence ratio imaging. Three computerized image analysis systems are available for densitometric analysis for macro-autoradiographic specimens, a Zeiss Kontron KS400 Image Analysis System, which is used primarily for quantitative morphometric analysis of brightfield and fluorescence microscope images, and a Zeiss Attofluar Calcium Imaging System. A Fuji BAS 2500 Phosphor Imaging Scanner will be added to the MCID/M4 system to enhance the quantitative capabilities of the core; this scanner will be utilized by all of the proposed projects. Two darkrooms are also provided in the core A. Dr. Wilson, core leader, will assist investigator with the design and implementation of computer image analysis protocols and set policies for shared use of the facilities. Analysis of lead levels in the blood and tissue samples is provided through core A for all investigators, in the trace metals laboratory. Three methods of analysis are available; atomic absorption spectroscopy will be the primary method used by the program projects. Dr. Bressler, Associate Director of the trace metals laboratory, will provide oversight of protocols for lead administration and blood/tissue lead analysis. Core A will thus provide an important service, determination of lead levels, and provide access to state-of-the-art image analysis equipment that will be used for a wide variety of quantitative assessments by individual projects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CORE--COMMUNITY OUTREACH AND EDUCATION PROGRAM Principal Investigator & Institution: Peters, John M.; Professor and Director; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, Ca 90033 Timing: Fiscal Year 2002 Summary: The mission of the Center's Community Outreach and Education Program(COEP) is to increase the public understanding of the effects of the environment on human health and ways to reduce harmful exposures by linking the Center's research and its investigators with school, community, professional and policy making target populations, emphasizing underserved populations and children. The goals are to promote K-16 education about environmental health, provide education and technical expertise to community based organizations, contribute to public policy, facilitate communication between the Center investigators and the community, educate the professional community on environmental health, encourage environmental justice, and develop evaluation methods for judging the effectiveness of the COEP in working with the public and community organizations. The specific agenda of the COEP focuses on asthma, other respiratory diseases, lead, and cance Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CORE--COMMUNITY OUTREACH AND EDUCATION PROGRAM Principal Investigator & Institution: Trush, Michael A.; Professor; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: The goals of the Community Outreach and Education Program (COEP) at the Center in Urban environmental Health are to develop and conduct educational programs for community residents and specific target groups, to facilitate community based research that identifies environmental agents affecting health and addresses local community needs, and to facilitate intervention trials to alter behavior. To accomplish these goals the COEP has recently added a research technician and a community coordinator to an existing staff that includes a Director, Co-Director and Project Manager. The COEP focuses on three major health issues, including cancer, lead poisoning and pulmonary disease. These 0utreach goals are well-coordinated with and reflective of Center research themes. The major accomplishments include: 1) the development of a Resource Center for parents concerned about lead exposure in their children; 2) a cohesive educational program that includes a sustained teacher training institute, a course for doctoral and masters students on environmental outreach and a partnership with Maryland Public television to produce videos; and, 3) a series of assessments of indoor air quality in federal office buildings and schools. In many cases the projects were developed in response to concerns and requests from community groups, particularly those involving air quality evaluation. The COEP has a substantial level of interaction with community based organizations and has developed partnerships to facilitate research, gather information and data and to provide educational resources and programs. A notable collaboration with the South Baltimore Community Environmental Partnership was initiated in 1997. The COEP has become increasingly involved with the Partnership. The Center has contributed to the partnership by inviting speakers to an environmental symposium and providing funds to maintain the neighborhood office that serves as a meeting place for partnership activities. Seven communitybased prevention and education Centers are being established in minority communities and educational topics are being developed. The application also details participation of the COEP in community events such as health fairs and an Urban Earth Day, that raise awareness of environmental health issues and provide an opportunity to distribute pamphlets and informative materials. A significant accomplishment of the COEP was the hosting of a town meeting entitled: 'Baltimore Speaks Out About Environment and Health', in 1999. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CORE--EXPOSURE ASSESSMENT Principal Investigator & Institution: Wolff, Mary S.; Professor; Mount Sinai School of Medicine of Cuny New York, Ny 10029 Timing: Fiscal Year 2002 Summary: (Taken from application) The Exposure Assessment Core will provide analytical support for assessment of organochlorine (OC) exposures in two biomedical projects (10 and 11) and the CBPI. In Project 10, serum organochlorines will be measured in relation to Parkinson?s Disease and in Project 11 as a measure of fish consumption. For Project 7, body burden assessments for lead will include blood lead, ZPP and bone lead, representing multiple compartments for deposition of lead and widely variable rates of elimination. The Exposure Assessment Core will also work with all the research projects and the Genetic Analysis Core to integrate thematically new findings from the
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geological studies into the epidemiologic and basic science projects. The Core will provide advice on which environmentally important compounds should be measured in Projects 10, 11, 3 and the CBPI and molecular biology in Projects 6 and 9. Extensive quality control measures are implemented throughout to provide reliable exposure data and to maintain consistency between projects and over the years during which this research is undertaken. The proposed measures of exposure will provide an overall assessment of organic contaminants and lead that are present in New York harbor sediments, which are closely tied to the geologic Projects 8 (OCs) and 2 (lead). The Core leaders and technical staff are well recognized experts in the field of environmental exposure assessment for lead and organochlorines. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CORE--NEUROTOXICOLOGY DISEASES FACILITY
AND
NEURODEGENERATIVE
Principal Investigator & Institution: Mayeux, Richard P.; Professor of Neurology, Psychiatry and e; Columbia University Health Sciences New York, Ny 10032 Timing: Fiscal Year 2002 Summary: Research efforts in the Neurotoxicology/Neurodegenerative Disease Research Core will be under the direction of Dr. Richard Mayeux and will span clinical, epidemiological, and mechanistic studies of lead and mercury poisoning and neurodegenerative diseases including Parkinson s and Alzheimer?s disease. It is anticipated that Dr. Mayeux will form task-oriented working groups which will focus on specific problems within areas of interest. Members of the faculty, postdoctoral fellows and doctoral students will meet monthly to discuss topics of ongoing interest in one of the following areas: 1) gene-environment interactions in the neurodegenerative diseases of aging; 2) molecular mechanisms involved in the perturbation of iron metabolism as it relates to Parkinsonism; 3) genetic susceptibility to Parkinson s disease in first-degree relatives of both sporadic and familial cases and the pattern of inheritance; 4) the genetic bases of essential tremor and Alzheimer?s disease; 5) effects of lead on cognitive performance and development of children; 6) relationships between occupational exposure to mercury vapor and the risk of tremor, peripheral neuropathy, cerebellar dysfunction and measures of abnormal balance; 7) mercury exposure derived from amalgams in the mouth and possible associations with neurological dysfunction or neuropsychological deficits; 8) caloric intake, body mass index and the risk of neurodegenerative disease; 9) mitochondrial function in normal aging, Parkinson s and Alzheimer s disease; 10) occupational mercury exposure and the risk of memory and visuospatial ability and disturbed mood; 11) molecular mechanisms of lead neurotoxicity; 12) mechanisms of manganese-induced Parkinsonism; and 13) molecular mechanisms of MPTP. Task-oriented working groups will be composed of selected members of the research core, facilities cores and Center staff as needed. The framework in which these work groups will operate will be flexible and will address specific research concentrations dictated by the overall focus of the Center. The specific aims are as follows: 1) to stimulate and guide interdisciplnary research on neurodegenerative diseases; 2) to stimulate and guide research on neurotoxicology with an emphasis on the neurotoxicity of transition and heavy metals; 3) to expand mechanistic and epidemiologic studies among the elderly of Northern Manhattan and; 4) to extend research efforts concerning the interaction of genetic susceptibility markers and environmental exposures in Parkinson?s and Alzheimer?s Disease. It is anticipated that highlights of meetings held in the 12 research areas will be presented at the bi-weekly
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work-in-progress meetings and that these meetings will provide a vehicle for communication of progress to other members of the Center and outreach programs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CORE-NEUROTOXICOLOGY/NEURODEGENERATIVE DISEASE RESEARCH Principal Investigator & Institution: Graziano, Joesph H.; Columbia Univ New York Morningside 1210 Amsterdam Ave, Mc 2205 New York, Ny 10027 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: The developing nervous system is vulnerable to adverse effects due to exposures to a variety of substances in the environment, particularly metals and pesticides. At the same time, chronic exposure to low levels of neurotoxicants throughout life can lead to impaired neurologic functioning later in life, particularly in the elderly. As life expectancy increases, and the baby-boom generation approaches retirement age, neurodegenerative diseases such as IPD, Essential Tremor and Alzheimer's Disease will have a significant impact on quality of life, and will represent significant financial costs to the health care system. Collectively, the investigators in this research core are interested in understanding the extent to which, and mechanisms 295 whereby, populations exposed to known quantities of neurotoxicants suffer adverse consequences on the nervous system. The populations under investigation, which include birth cohorts in Yugoslavia and northern Manhattan, populations of adults and children chronically exposed to arsenic in drinking water in Bangladesh, and populations of the elderly in northern Manhattan, represent groups of individuals who have been remarkably well characterized for a variety of chemical exposures and other risk factors for adverse neurologic outcomes. At the same time, laboratory based scientists are exploring the mechanisms whereby the compounds of interest alter normal function. The overall goals of the Neurotoxicology/Neurodegenerative Disease Research Core are: I) to promote and facilitate interdisciplinary neuroscience-related research that will define the magnitude of effect of exposure to substances in the environment that are believed to be involved in the etiology of neurologic disease. These substances include metals (Pb, Mn, Fe and As), pesticides (chlorpyrifos, diazinon, propoxur, and others), 13- carboline alkaloids (harmane and harmine), and other factors; and 2) to unravel the cellular and molecular mechanisms whereby these substances exert their effects. The core is responsible for furthering the development of existing and new investigations of environmental exposures that affect the incidence and/or progression of diseases of the central and peripheral nervous systems. The Specific Aims currently under investigation include: 1) to define the cellular and molecular events involved in chemical models of Parkinsonism and in IPD, with the goal of defining those that are common to each; 2) to elucidate the environmental risk factors associated with the onset of IPD, Essential Tremor, and Alzheimer's Disease; 3) to examine, in both humans and animal models, the relationship between environmental Pb exposure and brain function, with particular interest in the possible mediating effects of Pb on thyroid hormone fate and transport; 4) to determine whether exposure to arsenic in drinking water is associated with adverse neuropsychologic effects in children, and polyneuropathy in adults; and 5) to develop biomarkers of prenatal pesticide exposure in humans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DEVELOPMENT OF COGNITIVE & SENSORY/MOTOR SKILLS BY METAL EXPOSURE Principal Investigator & Institution: Wagner, George; Univ of Med/Dent Nj-R W Johnson Med Sch Robert Wood Johnson Medical Sch Piscataway, Nj 08854 Timing: Fiscal Year 2002 Summary: (provide by applicant) Behavioral manifestations of developmental disorders may be characterized as "retardation" (a behavior fails to develop during a critical period), "regression" (a behavior develops at the right time but then is lost or exhibits a stunted rate of progression), or "intrusion" (appearance of behaviors aberrant in form or frequency). The period when symptoms appear may represent a time when environmental toxicants have accumulated in brain to critical levels or the deleterious effects of early exposure become manifest through perturbation of normal development of brain pathways. Furthermore, certain individuals may be more sensitive to toxicants because of a genetic (perhaps immune-related) predisposition. Within this framework, the hypothesis that toxicants are causally involved in developmental disorders lends itself well to testing. ln this proposal, a new paradigm for the study of toxicant-induced developmental disorders incorporating systematic assessment of retardation, regression and/or intrusions in male and female mice of three strains will be developed. This will include a characterization of the ontogeny of key behaviors under normal conditions: a) mid-air righting reflex and balance beam performance; b)water maze (hidden platform) and passive avoidance behavior; and c)water maze (visible platform), active avoidance, and stereotypic and self-injurious behavior. These behaviors have been linked to cerebellum, hippocampus, and striatum, brain areas known to be involved in developmental disorders and known to be targets of lead and methylmercury. The behavioral ontogeny will be linked to neural circuitry and synapse formation and the disruptive effects of low dose exposure to each toxicant on the development of each behavior will be assessed at three time points over full dose-response curves. Thus, the specific aims are: 1) characterize the normal development of these behaviors in these three strains of mice; 2) evaluate the effects of acute and chronic low dose-exposure to lead and methylmercury on these behaviors in each strain at each of three time points; 3) correlate the normal development with maturation of neural circuitry and synaptogenesis and the magnitude of toxicant-induced disruption of neurobehavioral development to morphological, neural circuitry, and neurochemical measures; and, 4) evaluate the outcome in the context of this new paradigm in the form of the following question: did toxicant exposure result in retardation, regression and/or intrusions in the neurobehavioral development of male or female mice of these strains? Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DIETARY SUPPLEMENTS & SUPPRESSION OF BONE RESORPTION & LEAD MOBILIZATION Principal Investigator & Institution: Hu, Horward; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2002 Summary: This project will take place in Mexico City, taking advantage of our current Superfund (SF)-supported project. Recent evidence indicates that there is a marked increase in the mobilization of lead from maternal bone stories into circulation during pregnancy and lactation. Furthermore, our SF data and the data of others indicate that this phenomenon carries a significant risk of fetal toxicity in the form of growth (decreased birth weight, head circumference, birth length) and subsequent cognitive
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development. These findings pose a major public health problem, even among societies with declining lead exposure, given the persistence of pockets of high lead exposure (including some communities living in proximity to hazardous waste) as well as the long residence team of lead in bone (years to decades). As suggested by our SF data and other studies, one possible strategy for suppressing the mobilization of metal bone lead stores during pregnancy is nutritional intervention. We propose to recruit a new sample of women of women in Mexico City who have relatively high bone lead levels and conduct a randomized, double-blinded, placebo-controlled trial of supplements containing calcium as a means of suppressing bone resorption and the resulting mobilization of lead from bone supplements containing calcium as a means of suppressing bone resorption and the resulting mobilization of lead from bone into plasma during pregnancy, and into breast milk during the postpartum period. We will take maternal measurements of (1) pre-pregnancy and postpartum-bone lead using our K-x-ray fluorescence technology; (2) bone resorption (by assaying (1) pre-pregnancy and postpartum bone lead using our K-x-ray fluorescence technology; (2) bone resorption (by assaying N-telopeptide of type I collagen in urine [urinary NTX]), (3) whole blood lead, and (4) plasma lead (using special collection techniques and measured by IDTIMSJ during pre-pregnancy, the first, second, third trimesters and at one and four months postpartum; and (5) breast milk lead levels are at one and four months postpartum. We will measure maternal plasma and breast milk lead levels as these are the most direct sources of fetal and infant lead exposures, and recent research suggests that maternal venous blood levels do not adequately reflect either of these parameters. We will test the hypothesis that supplements will significantly decrease urinary NTX, plasma lead, and breast milk lead levels. We will also explore the relationship plasma lead levels We will also explore the relationship of plasma lead levels to birth anthropometry measures. This research, if successful, may provide a means of preventing secondary toxicity from accumulated lead burdens among women of reproductive age. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DIFFERENTIAL PB TOXICITY IN NEURONS AND ASTROCYTES Principal Investigator & Institution: Audesirk, Gerald J.; Professor; Biology; University of Colorado at Denver P.O. Box 173364 Denver, Co 802173364 Timing: Fiscal Year 2002; Project Start 03-AUG-2001; Project End 30-JUN-2005 Summary: All humans carry much more Pb2+ than our distant ancestors, and our bodies probably do not possess adequate means for sequestering or excreting Pb2+ so that there are no deleterious effects on our physiology. Recent epidemiological data indicate that there are significant effects on children's IQ at blood lead levels well below the CDC action level of 10 mug/dl. The cellular substrate(s) of such subtle effects remain elusive. Lead exerts multiple deleterious effects on cells; at low concentrations, these effects are usually relatively small. A major premise of this application is that Pb2+ exposure is seldom high enough to cause major physiological dysfunction by itself. However, low levels of Pb2+ may alter cellular metabolism in ways that exacerbate the toxic effects of other insults, including everyday metabolism (e.g., generation of reactive oxygen species [ROS] by mitochondria) and pathological conditions (e.g., ischemia caused by stroke). This application is based on two hypotheses: (1) Low-level Pb2+ exposures stimulates the production and/or reduces clearance of ROS and/or reactive nitrogen species (RNS). Therefore, events that stimulate the formation or retard the clearance of ROS or RNS will cause more damage to cells that are also exposed to Pb2+. (2) Cells of the nervous system differ in their responses to Pb2+. Cells that have intrinsic resistance or that mount an adaptive response to Pb2+ (astrocytes) will suffer fewer
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Lead Poisoning
harmful effects when exposed to Pb2+. Cells with fewer defenses and/or that cannot mount an adaptive response to Pb2+ (neurons) wil be predisposed to damage from other insults. We further hypothesize that induction of heme oxygenase-1 (HO-1) in astrocytes confers protection against Pb2+; neurons, which do not induce HO-1 in response to Pb2+, lack this protection. We have the following specific aims: 1: To determine cell-specific effects of Pb2+ exposure on intracellular ROS and/or RNS, and on cellular damage from ROS/RNS. 2: To investigate whether Pb2+ exposure enhances cellular damage caused by other stresses. 3: To determine if Ho-1 provides protection against Pb2+-induced accumulation of ROS/RNS and against enhancement of cytotoxicity of other stresses of Pb2+/ 4: To determine if HO-1 expression by astrocytes provides protection to neurons from Pb2+-induced toxicity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EARLY DEVELOPMENT OF AUDITORY TEMPORAL PROCESSING Principal Investigator & Institution: Gray, Lincoln C.; Professor; Otolaryngology; University of Texas Hlth Sci Ctr Houston Box 20036 Houston, Tx 77225 Timing: Fiscal Year 2002; Project Start 30-SEP-2001; Project End 31-AUG-2005 Summary: (provided by applicant): This research will use an appropriate animal model to define the behavioral, physiological, and cellular changes that correlate with deficits in auditory temporal processing. We will test the hypothesis that one type of early insult (exposure to low levels of lead) but not another (exposure to loud sound) causes a deficit in hearing rapid changes in sound. Four observations from the literature predict that lead toxicity is a reasonable manipulation for investigating auditory temporal processing deficit. First, lead poisoning causes dyslexia. Second, children with dyslexia have auditory temporal and phonological processing deficits. Third, early exposure to low levels of lead in these animals causes an auditory temporal processing disorder. Fourth, the development of hearing in humans and these animals is remarkably parallel in many aspects, including auditory temporal processing. Signal detection analyses of unconditioned delays in the subjects' vocalizations will quantify the early development of forward, backward, and simultaneous masking, discrimination of speech and speechlike stimuli containing voice- and tone-onset-time cues. Several non-temporal controls (absolute thresholds, frequency and intensity discrimination) will prove the deficits are unique to rapidly changing sounds. Physiological recordings and immunohistochemistry of cells of the central auditory system will define possible mechanisms of the behavioral deficits. According to an important current hypothesis, difficulty processing the basic elements of language (phonemes) is due to a deficit in the perception of rapidly changing sounds. Basic questions about the early development of auditory temporal processing and the insults that can cause a decrement in these important abilities remain unanswered. This basic information will help us understand the effects of common environmental insults and perhaps the etiology of phonological processing deficits (associated with dyslexia in children) that affect between 5 percent and 17 percent of our children. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EARLY EXPOSURE TO LEAD AND ADULT ANTISOCIAL OUTCOME Principal Investigator & Institution: Ris, M Douglas.; Associate Professor; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2002
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Summary: (provided by applicant) Lead exposure and antisocial behavior are both major public health concerns. Recent research indicates that early exposure to environmental lead is associated with increased risk for delinquency. However, there is, as yet, no scientific evidence to indicate whether or not this increased risk extends into adulthood. Nor is there a clear understanding of what neurobehavioral factors mediate the relationship between lead and antisocial behavior. The investigators propose to assess the adult outcome of 280 participants in the Cincinnati Lead Study; a birth cohort whose development and exposure history have been exquisitely tracked for over 20 years. Outcome will be measured in three ways to insure accuracy and comprehensiveness. First, to assess criminal activities, Official Records will be accessed through County agencies and the National Crime Information Center. Second, to diagnose Antisocial Personality Disorder and Substance Use Disorder, a structured psychiatric interview will be performed. And third, self-report measures will be used, including the Self-Report of Delinquent Behavior, to measure various law- and normviolating behaviors. Neuropsychological measurements undertaken on the sample in late adolescence will be used to explore neurobehavioral mediating factors. Selfregulatory/executive abilities and academic skills are at risk in both the delinquent and lead exposed youth leading the investigators to propose these as critical mediational pathways. A better understanding of the remote behavioral effects of early lead exposure will allow the investigators to develop primary prevention methods (both environmental and cognitive/educational) that will alter the developmental trajectories of large numbers of lead-exposed youths. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EARLY INDICATORS OF LATER WORK LEVELS, DISEASE AND DEATH Principal Investigator & Institution: Fogel, Robert W.; National Bureau of Economic Research Cambridge, Ma 02138 Timing: Fiscal Year 2003; Project Start 30-SEP-1997; Project End 31-AUG-2006 Summary: (provided by applicant): The aims of this program project, as funded, are to: 1. investigate the impact of socioeconomic and biomedical insults during developmental, middle-life, and older ages on the onset of specific chronic diseases at middle and late ages, and on waiting time to death from specific causes in both white and black populations; 2. examine the effect of pensions and health on the demand for retirement and for independent living arrangements among black Union Army (UA) veterans; 3. Estimate what types of public health interventions have been most effective in lowering mortality, improving health in later life, and promoting exceptional longevity; 4. expand the range of biomedical and socioeconomic factors that can be considered in the life-cycle Union Army data set by linking it to the 1880 census, which provides health information, and by linking it to data on the epidemiological characteristics of cities and wards; 5. Create two new life-cycle samples, one for black UA veterans and one for men rejected for service from the UA; and 6. Maintain and improve the life-cycle sample of white UA veterans and encourage wider use through a sub-grants program. The supplement will enhance the program project by expanding the life-cycle data set of white UA veterans by creating a sample of brothers, allowing incorporation of a much richer set of covariates into the analysis. It will help us better understand what determines pension outcomes and provide valuable input for our analysis of the effects of pensions on black and white retirement rates and living arrangements. It will enhance the analysis of the predictors of later morbidity and mortality carried out under the parent grant by focusing on a specific devastating and
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Lead Poisoning
relatively common affliction--lead poisoning. Specifically, the aims of this supplemental application are to: 1. investigate the impact of observable familial factors on health and mortality across the life cycle and to estimate the social and environmental determinants of morbidity and longevity controlling for unobserved heterogeneity at the family level; 2. examine the social construction of disability in the past and the role of politics in past disability programs; 3. document the proportion of the population, by subgroups, with elevated lead levels and examine the effects of lead exposure on health, morbidity, mortality, and labor force participation; and 4. speed up the collection of the life-cycle sample of black Union Army veterans, expand the current public database to cover the beginning of the twentieth century, and create a life-cycle sample of brothers who served in the Union Army. Finally, we propose to expand the Administrative Core D commensurately to support the new scientific projects and the expanded Data Extension Core B. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EFFECTS OF LEAD ON CALCIUM-BINDING PROTEINS IN RATS Principal Investigator & Institution: Pevsner, Jonathan A.; Assistant Professor; Kennedy Krieger Research Institute, Inc. Baltimore, Md 21205 Timing: Fiscal Year 2003; Project Start 02-MAY-2003; Project End 31-MAR-2008 Summary: (provided by applicant): The major long-term objectives of the proposed research are [1] to test the hypothesis that lead interacts with calcium binding proteins of the C2 and annexin families, and [2] to identify genes and proteins of these calciumbinding families that are regulated following lead exposure of rats. Lead poisoning remains a pervasive problem in the United States, affecting at least 5% of all children. The proposed research is intended to elucidate molecular mechanisms underlying lead toxicity. Previous studies have demonstrated potent interactions between lead and proteins of the C2 domain family (e.g. protein kinase C and synaptotagmin) and annexins. Furthermore, lead exposure of cells has been shown to regulate the expression of genes encoding calcium-binding annexins. The four specific aims of this proposal are [1] to measure the interactions of lead with proteins of the C2 domain and annexin families, in order to determine the possible targets of lead. [2] To measure gene expression in the brain, kidney and liver of lead-exposed rats. This in vivo model may reveal whether lead exposure differentially regulates the expression of genes encoding calcium-binding proteins. [3] To extend gene expression studies to well characterized cell lines (astrocytes, PC12 cells, fibroblasts and normal rat kidney cells). These studies will complement gene expression measurements from the in vivo model. [4] To deposit gene expression data into a publicly accessible database. Together these studies may reveal which calcium binding proteins interact with lead, and which genes encoding calcium-binding proteins are regulated by lead exposure. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EFFECTS OF METALS ON PKC-NITRIC OXIDE SYNTHASEGLUTAMATE RECEPTOR IN THE BRAIN Principal Investigator & Institution: Rajanna, Bettaiya; Professor; Alcorn State University Lorman, Ms 39096 Timing: Fiscal Year 2002 Summary: Children exposed to Lead (Pb) show memory deficits associated with low levels of intelligence whereas, children and adults are equally sensitive to Methyl Mercury (CH3Hg). The biochemical basis of cognition has been shown to be dependent
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on proper functioning of two key enzymes in the hippocampus and the cerebellum namely the protein Kinase C (PKC) and Nitric Oxide Synthase (NOS). These enzymes are known to have multiple isoforms which are modulated by a number of endogenous and exogenous second messengers, neurotransmitters etc. The long term of our research is to delineate the role of PKC-NOS-NMDA complex to understand the mechanism of Pb and CH3HG induced neurotoxicity. The hypothesis to be tested in this proposal is that Pb and CH3Hg mediated developmental neurotoxicity. The hypothesis to be tested in this proposal is that Pb and CH3Hg mediated developmental neurotoxicity is dependent on single or multiple isoforms of PKC and NOS, and the regulation of glutamatergic neurotransmiss ion. The specific aims are: a) environmentally relevant Pb or CH3Hg exposure during the brain development results in changes of PKC and NOS and changes are isoform specific; b) The isoform specifics changes of PKC and NOS by perinatal and changes are isoform specific; b) The isoform specific changes of PKC and NOS by perinatal exposure of Pb and CH3Hg modulate the neurotransmitter pathways critical to cognitive functions; c) the changes in PKC and NOS isoforms, and NMDA receptors are related to the blood and tissue levels of Pb and Hg. The developing brains from rats of Post Natal Day (PND) 5,7, 10, 15, 21, 30, 45, 60 exposed to 1% Pb or 0.01% CH3Hg in deionized distilled drinking beginning at conception through 21 days after limiting will be used. We will study Pb and CH3Hg effects on: a) alpha-PKC, epsilonPKC and zeta-PKC, b) nNOS, iNOS, and eNOS; c) NMDA specific glutamate receptor, and d) correlate results from these studies with the levels of Pb and CH3Hg in the tissue and blood. At the completion of this project we expect to have provided new information on the mechanism of Pb and CH3Hg neurotoxicity. Furthermore we will have detailed the sensitivity of different isoforms of PKC and NOS to Pb and CH3Hg insult and their influence on the NMDA receptors. All research activities will be appropriately evaluated. A corollary influence of this research will be that Alcorn State University will gain a strong biomedical research base. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EFFICACY OF CHELATION THERAPY FOR LEAD INTOXICATION IN CHILDREN Principal Investigator & Institution: Schonfeld, David; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ENOS AND THE BLOOD LEAD-BLOOD PRESSURE RELATIONSHIP Principal Investigator & Institution: Lustberg, Mark; Epidemiology and Prev Medicine; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2002; Project Start 01-SEP-2002 Summary: Essential hypertension is a major cause of cardiovascular disease. Its etiologies are thought to involve both genetic and environmental factors. Elevated blood lead levels have been indicated as contributing factor in essential hypertension. It is unclear how lead exerts this effect. The purpose of this investigation is to consider endothelial nitric oxide synthase (eNOS) inhibition as a mechanism for this effect, using a population based approach and a recently reported Glu298Asp substitution polymorphism in eNOS. Specific Aims: 1) Describe the relation of the eNOS Glu298Asp polymorphism and blood pressure in this cohort. 2) Describe how the relation of lead
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Lead Poisoning
and blood pressure varies by the eNOS Glu298Asp polymorphism in this cohort. Methods: This will be a cross-sectional study of lead exposed workers and unexposed controls. Blood pressure and lead levels in these workers have been recorded, and blood samples have been taken. The blood samples will be genotyped for the Glu298Asp polymorphism. Linear regression models will be developed to examine the relation of lead and blood pressure in these workers. We will also consider stratified analyses, looking at odds ratios of hypertension. If eNOS is involved in lead induced increases in blood pressure, the lead-blood pressure relationship (the regression slopes or the odds ratios for hypertension) should different for individuals with and without Asp-variant eNOS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ENVIRONMENTAL & GENETIC RISK FACTORS FOR RENAL FUNCTION Principal Investigator & Institution: Weaver, Virginia M.; Environmental Health Sciences; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 01-MAR-1997; Project End 31-MAY-2007 Summary: (provided by applicant): End stage renal disease (ESRD) is associated with substantial morbidity and mortality. Strategies to prevent the renal function decline that can ultimately result in ESRD are essential. The impact of environmental exposures has received relatively little attention in this regard, despite the fact that exposures such as cadmium and lead are known renal toxicants that are stored long-term in the body and ubiquitous in humans. In fact, the lead and cadmium dose-effect curves for renal function remain uncertain for the low to moderate range of doses. The proposed study will investigate a broad set of causes of renal function decline, including lead, cadmium, blood pressure, diabetes, nephrotoxic medication use, genetic polymorphisms, and age. This application is a competing renewal application of the study "Exposure, dose, body burden, and health effects of lead" (Schwartz BS, PI) conducted from 1997-2001. It will build on data, from the large cohort of current and former lead workers and participants without occupational lead exposure in the originally funded grant. Study subjects have a wide range of lead exposure and dose measures and renal outcome data from three visits each over an average of 2.2 years. Analysis of existing data has already provided very important results, including longitudinal decline in renal function associated with lead dose measures; interaction between age and lead dose on renal function and renal function decline; interaction between ALAD genotype and lead dose on renal function; and associations of environmental level cadmium dose with elevated NAG in a subset of lead workers. However, in order to better understand the causes of renal function decline, cadmium dose must be characterized in all subjects, additional genotypes must be measured, and additional follow-up time is needed because of the slow rate of renal function decline. We propose to include 675 participants from the first study and enroll 225 new current or former lead workers over age 45 years, those at greater risk for renal function decline. We will obtain blood and tibia lead, genotyping, urinary cadmium, BUN, serum creatinine, measured and calculated creatinine clearances, NAG and RBP during 3 evaluations at yearly intervals. The specific aims are to determine: 1) if lead and cadmium dose are or continue to be associated with renal function at cross-section and longitudinally; 2) if there is effect modification by lead or cadmium dose, respectively, on associations between cadmium or lead dose and renal function decline; 3) if hypertension modifies the relations of lead or cadmium dose with renal function decline; and 4) whether polymorphisms in the genes for ALAD, VDR, ACE, and eNOS modify or continue to modify relations of lead and/or cadmium dose with renal
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outcomes. We believe the proposed work will allow a more complete understanding of the causes of renal function decline and lead to the development of public health interventions to prevent this considerable public health problem. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ENVIRONMENTAL NEURODEVELOPMENT
LEAD,
THYROID
FUNCTION
&
Principal Investigator & Institution: Factor-Litvak, Pam R.; Associate Professor; Epidemiology; Columbia University Health Sciences New York, Ny 10032 Timing: Fiscal Year 2002; Project Start 01-AUG-2001; Project End 31-JUL-2004 Summary: Severe deficiency of thyroid hormone during the prenatal and neonatal periods is associated with adverse neurodevelopmental outcomes in infancy and childhood. Maternal iodine deficiency during pregnancy leads to a lowered production of activated (i.e., iodinated) thyroid hormone (T3) and an increased risk of cretinism (with associated severe mental retardation) in the child. Congenital hypothyroidism and transient hypothyroidism of prematurity are associated with deficits in cognition during early life. In light of these observations, it is appropriate to ask whether sub-optimal maternal thyroid function, particularly during the first half of pregnancy when maternal contribution to fetal thyroid hormone is maximal, is associated with neurodevelopment of the child. Recent data suggest that children of mothers with 'low-normal' thyroid function are at risk for small deficits in cognition and increased reports of behavior problems. The overall goal of this project is to assess whether mild deficiencies in maternal thyroid function are associated with adverse neurodevelopment in the child, and, if so, to elucidate possible biologic mechanism. One possible mechanism is through damage to the choroid plexus, the site of production of the brain-specific transport protein for thyroid hormone. Animal studies suggest that the choroid plexus is damaged by exposure to environmental lead, raising the possibility that associations between lead exposure and cognition in the child arise through an effect of lead on transport of thyroid hormone to the brain. The proposed study draws on data from a prospective study designed to examine the associations between pre- and post-natal lead exposure and childhood development. The cohort comprises approximately 300 children, born in 1984-1985 in two towns in Kosovo, Yugoslavia who were followed through age 12. Sera are available to measure thyroid function in the mothers at midpregnancy and in the children at ages 4, 7 and 12. Outcomes, including cognition, motor function, behavior problems and anthropometric measurements, were measured repeatedly during infancy and childhood. This project will expand the findings of the Yugoslavia study to examine first, whether maternal thyroid function in the first half of pregnancy is associated with cognitive, behavioral and growth outcomes and second, whether the associations between Pb and these outcomes are mediated by exposure to thyroid hormone. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ERYTHROCYTE OVERBURDEN
ISOZYME
BIOMARKERS
OF
LOW
LEAD
Principal Investigator & Institution: Lubin, Bertram H.; Director of Medical Research; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Lead Poisoning
Project Title: ETHICAL CHALLENGES IN LEAD POISONING PREVENTION RESEARCH Principal Investigator & Institution: Farfel, Mark R.; Health Policy and Management; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2006 Summary: (provided by applicant) Recent media attention on ethical, social, legal issues of CLP prevention research highlights the need for continuous and effective dialogue between communities and environmental health (EH) researchers about the aims, design, challenges, progress, and findings of research and ways to address these issues in the conduct and translation of research. The proposed project focuses on community involvement, capacity building, education, and empowerment in the context of CLP research conducted by the Kennedy Krieger Institute (KKI) and Johns Hopkins Bloomberg School of Public Health (JHBSPH). Specific aims are: 1) To build on existing infrastructure for sustained dialogue between EH researchers and community by creating a Community Board, building community capacity for research, and increasing researchers 'awareness of community values, priorities, knowledge; 2) to conduct with community involvement in-depth interviews, focus groups and surveys, assessing, community knowledge/attitudes/perceptions about EH research and CLP research in particular, EH researchers' knowledge/attitudes/perceptions about the community; and 3) to create educational materials with community related to EH research and CLP studies, including educational materials/programs for community related to four CLP studies; (b) developing educational materials/programs for researchers to address gaps in their knowledge and understanding of community, its needs, concerns, culture, and points of view about research; and (c) evaluating the process of developing and implementing the educational materials and their community impact. The project, targeted to the E. Baltimore Empowerment Zone, engages residents, community organizations, and individuals with expertise in bioethics, health education, community mediation, and the application of social marketing techniques to the development of innovative educational materials, to improve health and environmental justice. The investigators hypothesize that our approach can produce models for education of diverse communities and EH scientists. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EXPLAINING DISPARITIES IN COGNITIVE FUNCTION IN SENIORS Principal Investigator & Institution: Schwartz, Brian S.; Professor and Director; Environmental Health Sciences; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-AUG-2005 Summary: (Taken from the Investigator's Abstract) Cognitive function (CF) is central to daily functioning and quality of life. The life course trajectory in CF is known to vary by race/ethnicity and socioeconomic status (SES), and this variation involves a complex causal web. Unpacking this causal web has important political, social, and public health implications, and provides a foundation for prevention and for ensuring social equity. However, we have only a rudimentary understanding of the factors that mediate these disparities in CF. The causal web is complex and involves such diverse and possibly interrelated domains as genetic, social, behavioral, environmental, contextual factors, and individual vascular health. The direct and indirect contributions of these diverse factors must be considered in trying to explain variation by race/ethnicity and SES,
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moving beyond the traditional but somewhat limiting exploration of "gene-environment interactions" by more broadly defining the underpinnings of these disparities. Ubiquitous potential causes of a decline in CF in older adults include lead exposure, apolipoprotein E (ApoE) genotype, vascular risk factors (i.e., blood pressure), and health-compromising behaviors (e.g., inactivity and smoking). Importantly, a number of genes known to differ by race/ethnicity appear to influence the toxicokinetics or toxicity of lead, including those for the 8-aminolevulinic dehydratase (ALAD), vitamin D receptor (VDR), Na/K ATPase (NKATP), and ApoE genes. Disparities in CF must be examined using next-generation data and methods that allow the modeling of the causal structure of these multiple domains, and to see how and to what extent social, behavioral, and contextual factors are important mediators and moderators along an extended causal pathway. Only by testing this more complete model, will it be possible to fully explicate the complex multilevel associations that pattern everyday life. The goal of this research is to understand the direct and indirect influences of lead absorption, four specific genes, individual social and behavioral factors, contextual factors, and blood pressure in accounting for the associations of race/ethnicity and SES with CF and cognitive decline. The investigators propose a five-year prospective study of 900 urban residents, aged 50 to 70 years, randomly selected from specific geographic areas with variation in race/ethnicity and SES. All study subjects will have three visits at 16-month intervals, with measurement of cognitive function, blood pressure, tibial lead, patellar lead, individual social and behavioral factors, current and past contextual factors, and ALAD, VDR, NKATP, and ApoE genotypes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EXPOSURE ASSESSMENT AND INTERVENTION Principal Investigator & Institution: Lioy, Paul L.; Univ of Med/Dent Nj-R W Johnson Med Sch Robert Wood Johnson Medical Sch Piscataway, Nj 08854 Timing: Fiscal Year 2002 Summary: (provided by applicant) The exposure assessment and intervention project will provide quantitative data on the contact with body burden of neurotoxicants within children having neurological disorders and deficits. The investigators' hypotheses are that: 1) the unique behaviors of these children lead to high exposure to neurotoxicants found in their personal and residential environment, and 2) selected interventions can lead to reductions in exposure measured for neurologically impaired children. Each volunteer child will be selected from families that ate members ofthe community groups associated with this Center's application. The selection will be done in close collaboration with the Clinical Sciences Projects. The goal is to obtain the distribution of personal and micro-environmental exposure of these neurologically impaired children to neurotoxicants; including specific heavy metals, volatile organics, and pesticides that are present and have sources in the local ambient and residential and personal environments of the child. These results will be analyzed over time for each child by collecting exposure measurements at two different times. Once before and once after an intervention, the investigators will assess exposure over time scales coincident with the expression of disease endpoints, and examine reductions in exposure that can occur after completing the intervention and family training. An intervention will apply to the community groups and families, and they should also be valuable to the general public. In addition to the physical and chemical measurements of exposure within their environments and within their bodily fluids, they will be documenting the behavior of these children. The investigators will be using the innovative approaches developed by videotaping and augmented by the core research in this application. Throughout the
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Lead Poisoning
course of the study, the project will provide data that can be used to augment the neurotoxicants employed by the Basic Biological Sciences Projects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HAZARDOUS MATERIALS WORKER HEALTH AND SAFETY TRAINING Principal Investigator & Institution: Stafford, Erich J.; Center to Protect Workers Rights 8484 Georgia Ave, Ste 1000 Silver Spring, Md 20910 Timing: Fiscal Year 2002; Project Start 21-SEP-1992; Project End 31-AUG-2005 Summary: EPA Hazardous Waste Worker Training Program. The long-term objective of the Construction Consortium is to ensure that crafts workers who are called upon to work in EPA Superfund environments, have the skills, knowledge and confidence they need to protect their health and safety, and that of their co-workers, their families, their communities, and the environment. Our members perform a vast array of remediation and construction tasks at hazardous waste sites. With The Center to Protect Workers' Rights as the lead and coordinating organization, the consortium, which has recently grown to include ten international/national union members with the addition of the Electrical Workers, Plumbers and Pipefitters, and Bricklayers, has been providing effective training for our members who may work at EPA sites for the past nine years. In the first year of this grant the consortium will deliver 90 hazardous waste classes to 1,762 students and 133 hazardous waste refresher classes to 2,102 students. OSHA 10, scaffold user, and confined space classes will also be offered. Lead and asbestos worker courses will be delivered where specifically required by site contractors. The consortium, with its nationwide network of over 1,700 spacious and well equipped training centers, highly skilled national and local peer-trainers, containerized, craftspecific, and up-to-date training equipment, and centralized training support organization, can respond rapidly and effectively to requests for training from anywhere in the country. Consortium training is highly participatory, peer-led, and trade specific. Safety and health information is presented within a real-world context that readily transfers to the trainees' workplace environment. Problem solving exercises will guide trainees to help bring about health-related changes in their workplaces. Master trainers and program managers will work with training and evaluation experts to develop and improve training exercises, as well as classroom and web-based presentations. Extensive and rigorous trainer and master trainer preparation and enhancement programs will be coordinated by CPWR. It is a construction consortium objective to prepare a cadre of certified master trainers who can ensure the quality of their organizations' training well beyond the completion of this grant. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HEAVY METAL COMPOSITION OF SAMPLES
EXPOSURE--ELEMENTAL
AND
ISOTOPIC
Principal Investigator & Institution: Simpson, H J.; Mount Sinai School of Medicine of Cuny New York, Ny 10029 Timing: Fiscal Year 2002 Summary: (Taken from application) Large quantities of toxic metals remain dispersed in the environment where their distribution and fate are imperfectly characterized, especially near large urban centers where both emissions and population density are concentrated. Moreover, significant quantities of metals continue to be added to the environment, particularly to natural waters where they accumulate in sediments and, in
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cases such as Hg, can be accumulated by fish and thus reach human diets. A central aim of this project will be to better characterize current sources and transport mechanisms of Pb, Hg and other metals to the NY metropolitan area and Hudson River basin. We will continue to work in very close collaboration with ongoing research on chlorinated hydrocarbons. Our approach will be to reconstruct and extend temporal trends in contaminant levels, including Pb isotope compositions, through analysis of dated environmental samples (airborne particulate matter from filters, sediments core depth profiles and landfill ash deposits of known age) to assemble the history of development and use of municipal and non-municipal waste incinerators in New York City, and to compare our sediment-derived contaminant history to NYS DEC's database on contaminant levels in fish from several parts of the Hudson River basin. We will expand our use of urban lakes and park soils to characterize the temporal history and geographical extent of urban atmospheric deposition rates of metals. Data generated should allow us to investigate potential for human exposure to metals and chlorinated hydrocarbons from city parks and community gardens, to investigate human exposure pathways of chlorinated organics and Hg via fish consumption, and contribute to ongoing state and federal investigations of Superfund sites within the metropolitan area and Hudson River Basin. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HEAVY BIOMARKERS
METALS
IMPACT
USING
GENETIC
VARIATION
Principal Investigator & Institution: Walsh, Elizabeth J.; University of Texas El Paso El Paso, Tx 79968 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2007 Summary: (provided by applicant): It is well known that heavy metals can be detrimental to human health even at low concentrations. Traditionally, effects of heavy metals have been assayed singly, monitoring the effects of a particular metal or a suite of individual metals on model organisms. Rotifers have been used as model organisms for toxicity testing of water supplies because of their short life spans, high reproductive outputs, and ease of manipulation. These features make them ideal for rapid toxicological assessment. During the last 10 years, there has been a great deal of interest in the use of sublethal indicators of exposure and effects of environmental contaminants on health. One of the newest biomarkers being explored by environmental scientists is the use of genetic diversity to assess ecological health. Genetic diversity within a species normally is quite varied. This diversity is the basis for a large gene pool that allows populations of organisms to persist in the face of environmental change. The genetic integrity of populations is critical to their long-term survival. Recent studies have shown that genetic diversity is compromised in contaminated environments. The lack of species diversity in degraded environments has been documented for many years, but genetic diversity within a species also appears to be reduced. The goals of the proposed research are to determine whether exposure to heavy metals (Arsenic, copper and lead) can impact the genetic structure of a population over 20 generations, and how exposure impacts organisms' responses to secondary exposures. A model organism, the rotifer Plationus patulus, will be subjected to metal exposures over 20 generations. Genetic variation will be monitored in the initial population, at generations 5, 10 and 20. Amplified fragment length polymorphism will be used as the biomarker of genetic variation. This is a DNA fingerprinting technique that allows the calculation of genetic variation and a number of other population genetic statistics. Concentrations of all metals will be at environmentally relevant levels. Following metal exposure, animals
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Lead Poisoning
will be monitored for response to low pH, low food levels and a pesticide. Results obtained using organisms with rapid generational turnover times, such as rotifers, may give us some idea of what to expect when longer- lived species, including humans, are exposed to toxicants over generations. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HOPE PARTNERSHIP (HEALTH OBSERVANCES & PUBLIC EDUCATION) Principal Investigator & Institution: Gotsch, Audrey R.; Interim Deam; None; Univ of Med/Dent Nj-R W Johnson Med Sch Robert Wood Johnson Medical Sch Piscataway, Nj 08854 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): The UMDNJ-School of Public Health, through the Community Outreach and Education Program (COEP) at the Center for Environmental Health Sciences, a National Institute of Environmental Health Sciences (NIEHS) Center of Excellence at the Environmental and Occupational Health Sciences Institute (EOHSI), proposes to conduct the HOPE Partnership (Health Observances and Public Education), a five-year Phase I and II Development and Dissemination project. This program will help to improve public understanding of the biomedical and health-related sciences and the impact of research on human health, while determining the most effective outreach methods to achieve this goal. UMDNJ will direct this project in collaboration with seven COEPs based at Oregon State University, University of Arizona, University of North Carolina at Chapel Hill, University of Southern California, University of Texas M.D. Anderson Cancer Center, University of Wisconsin-Madison and Vanderbilt University. These COEPs have demonstrated their ability to collaborate to increase public understanding of the biomedical and health-related sciences through the SEPA project, entitled EH-STEP, supported through August 31, 2003. These diverse partners will ensure that the project is translatable nationwide. A public health science education model will be developed, implemented and evaluated. The model comprises six components: health observances, needs assessment, action mechanisms, public health science education materials, scientist involvement and program evaluation. Program components will capitalize on three established national health observances (Cancer Control Month, Asthma and Allergy Awareness Month and Lead Poisoning Prevention Week) to impact the target audiences (students, teacher, general public). A needs assessment will document the target audiences' perceptions, attitudes and knowledge of biomedical and health-related sciences. Utilizing the diverse experiences and expertise of this established network of NIEHS Centers and the needs assessment, the Health Observances & Public Education (HOPE) Partnership will develop public health science education materials that will be disseminated through action mechanisms: community forums, formal education, informal education, media, non-profit organizations and science centers/museums. Scientists will be involved throughout the initiative including the development of materials and the implementation of the action mechanisms. Formative and summative measures will be used to analyze all aspects, including overall project effectiveness. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HUMAN SPERM ZONA ACCEPTOR: ENVIRONMENTAL EFFECTS Principal Investigator & Institution: Benoff, Susan H.; Associate Professor; North Shore University Hospital 300 Community Dr Manhasset, Ny 11030
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Timing: Fiscal Year 2002; Project Start 01-JUL-1994; Project End 31-JUL-2006 Summary: (provided by applicant): We focus on developing an understanding of toxic metal action in the human testis. A male factor is present about 60% of infertile couples, but underlying molecular mechanisms are largely uncharacterized. Exciting results from our current work hints at one mechanism. Lead levels were elevated markedly in testes and seminal plasma (in 25% of males in four independent populations). High lead correlated with expression of particular potassium and calcium ion channel isofomis, with poor sperm-fertilization-potential biomarkers and low fertility by IVF, artificial insemination and coitus. A significant fraction of subjects studied longitudinally switched from high lead states to low lead states, with simultaneous conversion of biomarkers from infertile to fertile and switch in potassium channel isoform expression. This suggested lead epigerietically modified testicular gene expression (at the levels of transcription and mRNA splicing) and that potassium channel isoforms could be developed as biomarkers for lead exposure. A preliminary DNA microarray study of a lead-treated "lead-resistant" rat strain identified many lead-affected genes as being involved in calcium-mediated induction of apoptosis, including a potassium channel. Supported by current somatic cell apoptosis mechanisms, this prompted our hypothesis that lead exposures produce male infertility by altering calcium homeostatsis, and a related detailed mechanism of lead action. These will be tested in a lead-treated leadsensitive" rat strain and in humans. We will use microarrays to probe in rats for affected testicular genes with CAMP response elements and other genes involved in calcium/calmodulin-dependent protein kinase IV signaling. Controls include metal testing by atomic absorption, TUNEL estimates of apoptosis, cell type levels by histology and by cell-type-specific mRNA levels, and protein expression by Westerns. Comparison with the "lead-resistant" strain should identify lead-sensitivity" genes. We will probe for the same genes in a human clinical population, with similar controls. We will also probe for genes co-regulated with the potassium channel above. Results will test several specific steps in our proposed mechanism: verifying, negating or modifying it. Because microarrays cannot detect differential calcium channel splicing events correlated with lead effects upon human testes, this gene and other calcium transporters will be studied by immunocytochemistry, RT in situ PCR and real-time PCR. Outcome is test of hypothesis, and possible mechanism explaining infertility associated with low sperm counts or idiopathic male infertility, tools for diagnosis, and hope for treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IDENTIFYING RESIDENTIAL HAZARDS USING HOME TEST KITS Principal Investigator & Institution: Roda, Sandy; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2002 Summary: (provided by applicant) The primary purpose of this project is to establish a community-based approach to residential sampling to identify and reduce health risks from lead, pesticides and other environmental hazards. The investigators will partner locally with the Better Housing League and Baby's Milk Fund Clinics and nationally with the Alliance to End Childhood Lead Poisoning and the National Center for Lead Safe Housing. The first goal of this project is to test and validate tools for community members to assess levels of contaminants in their home environment. This goal will further our efforts to strengthen right-to-know laws by providing community members with tools to assess environmental contamination in their homes. It will also provide information about exposure assessment by occupants that may be useful for conducting large-scale epidemiologic studies. The second goal is to increase community awareness
32
Lead Poisoning
and involvement in understanding the role of environment in developmental disorders, hearing loss and school problems. The latter goal will be accomplished by establishing a resource center at the Better Housing League, continued advocacy to prevent morbidity and mortality due to residential hazards, and community outreach. The specific steps will be to: 1) Incorporate a pesticide wipe sampling test kit with the investigators' ongoing lead-sampling test kit pilot study; 2 ) Evaluate the accuracy of home sampling test kits for lead and pesticides in floor dust collected by community participants compared with repeat samples taken by trained, community workers; 3) Provide community-based organizations with knowledge and tools to assist community residents on how to identify and control residential hazards; 4) Disseminate data on the reliability of home sampling test kits and provide a tool for respondents to collect environmental samples for large, population-based studies; 5) Assist in the development of a Healthy Homes Resource Center to provide the community information on residential hazards at the Better Housing League. If successful, this community-based research project would provide tools for families and communities to identify environmental neurotoxins, and disseminate information by establishing a healthy homes resource center at the Better Housing League and nationally with the Alliance to End Childhood Lead Poisoning and National Center for Lead-Safe Housing. The results of this project would also stimulate community-wide prevention efforts and exposure assessment by participants in population-based studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IMMUNITY IN CHILDREN WITH EXPOSURE TO ENVIROMENTAL LEAD Principal Investigator & Institution: Lutz, Paula M.; Biological Sciences; University of Missouri Rolla 1 University of Missouri-Rolla Rolla, Mo 65401 Timing: Fiscal Year 2002; Project Start 15-JUL-1993; Project End 30-JUN-2004 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INNOVATION TOOLS FOR THE MOLECULAR DIAGNOSIS OF CANCER Principal Investigator & Institution: Henkens, Robert W.; Alderon Biosciences, Inc. 2810 Meridian Pky, Ste 152 Durham, Nc 27713 Timing: Fiscal Year 2004; Project Start 01-MAR-2004; Project End 28-FEB-2005 Summary: (provided by applicant): Current treatment of cancer patients relies on establishing an accurate diagnosis using a complex combination of clinical and histopathological data but in some instances accurate diagnosis is difficult or impossible because of atypical clinical or histopathological data. The National Cancer Institute has called for accurate, practical, and affordable tools for the diagnosis of cancer in both research and clinical applications. The detection, identification, and evaluation of the expression pattern of a particular mRNA across many RNA samples are becoming a powerful technique for cancer diagnosis. Molecular assay of gene expression can offer systematic human cancer information useful to make clinical judgments regarding the disease and appropriate treatments. Measurement of tumor gene expression signatures will be done with a book-sized electro-analytical instrument and a disposable 96-sensor array element. The proposed expression analysis system will perform sensitive and selective gene probe assays linked to signal amplification via electroactive enzyme labels. The anticipated Phase I result will be establishing the feasibility of this
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technology by accomplishing the measurable milestones of validated measurements (greater than 90% agreement with real-time PCR), capable of probing expression signatures with highly sensitive DNA sensors (milestone 10x current sensitivity of 60,000 molecules) in Electrochemical Sensor Plate assays for multiple genes or multiple samples that take less than 2 hours. Alderon Biosciences, Inc. is an innovator in the rapidly developing field of molecular detection systems and the company maintains a chemistry, biochemistry, cell culture, and engineering staff experienced with electrochemical instruments and biologically modified sensors. The company has successfully raised several million dollars in non-SBIR funding for product development, regulatory approval, and commercialization. These experiences have yielded several products including an FDA-approved in vitro-diagnostic device designed to screen children for lead poisoning. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INNOVATIVE BIOMONITORING FOR LEAD IN SALIVA Principal Investigator & Institution: Timchalk, Charles A.; Battelle Pacific Northwest Laboratories Box 999, 902 Battelle Blvd Richland, Wa 99352 Timing: Fiscal Year 2003; Project Start 19-JUN-2003; Project End 31-MAY-2007 Summary: (provided by applicant): This research project will establish a biomonitoring screen capability for lead (Pb) exposure utilizing a sensitive, non-invasive, portable micro-analytical system for real-time analysis of Pb that is excreted into saliva. In addition, a physiologically based pharmacokinetic model (PBPK) for Pb has been modified to incorporate a salivary gland compartment that will be utilized to quantitatively predict blood Pb concentration and total body burden based on the amount of Pb detected in saliva specimens. The utilization of saliva, coupled to real-time quantitation and PBPK modeling represents a novel approach having broad application for evaluating Pb exposures. In order to validate this approach there is a need to more fully understand the pharmacokinetics of Pb excretion in saliva under various physiological conditions and dose levels to ensure that the quantitation of Pb in saliva is an accurate predictor of "internal dose". To accomplish this goal a series of in vitro and in vivo studies will be conducted to evaluate the disposition and clearance of Pb in the blood, plasma, and saliva, and to evaluate salivary gland function following a prolonged Pb exposure. It is anticipated that these data will provide some understanding of the mechanism for saliva Pb clearance in the rat, and will be used to facilitate further development and refinement of the PBPK model to enable accurate prediction of blood Pb concentration, and body burden based on saliva Pb. The development of a predictive pharmacokinetic modeling approach with real-time saliva analysis represents a significant advancement over current biomonitoring screening strategies for Pb. It is reasonable to speculate that once this model system has been adequately validated it can readily be employed to screen sensitive populations (e.g. children) that are at greatest risk from chronic Pb exposure. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INTEGRATING ENVIRONMENTAL HEALTH SCIENCE IN RURAL SCHOOL Principal Investigator & Institution: Johnson, Larry; Veterinary Anatomy & Public Health; Texas A&M University System College Station, Tx 778433578 Timing: Fiscal Year 2002; Project Start 01-SEP-2000; Project End 31-AUG-2007
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Lead Poisoning
Summary: The long-term goal is to develop an engaging model for integrating environmental health science into math, English language arts, social studies, and science of rural grades 6-8. Rural is emphasized because of public concern for increased numbers of environmentally-related diseases in rural Texas (birth defects, lead poisoning, etc.). Rural schools are less likely than metropolitan schools to receive state of the art information on environmental health, but may need it most. Rural schools have less interaction with college professors that might influence their career choices. Middle school was chosen as it is the prime developmental period for social skills and is central to channeling young adolescents into the mainstream of American life by making vast improvements In their academic and personal competence (and resulting societal contribution). It is the most powerful venue to ensure our nation's leadership in math and science, but this period has received little education reform in recent years. Environmental health information and research experiences provided by faculty from the Center for Environmental and Rural Health will be integrated into the four disciplines by the College of Education and disseminated into rural settings via existing mass media distant learning methods and professional teacher development programs through the Texas Rural Systemic Initiative. The scientist-teacher approach will direct faculty human interface within public schools. The specific aims are: 1) to integrate existing environmental health materials/issues into engaging multimedia learning materials tailored for rural middle school students [develop integrated curricula (math, English, social studies, and science) transmitted to public schools via currently established and popular Internet Web sites]; 2) to provide professional teacher development programs [(develop/execute short courses for teams of teachers from the same school) that integrate implementing Web-based environmental health science curriculum units that enhance teachers' awareness of environmental health problems and solutions]; and 3) to provide a human interface and online interaction to establish partnerships among middle school and scientists directly (faculty, graduate students, and undergraduates visit and present environmental health issues and the excitement of conducting research to public school students directly or online). Through information on new discoveries and integration of local /rural environmental health themes, the knowledge that certain behaviors/situations increase risk of human disease and that basic research is needed to improve public health will be publicized. Important rural environmental health science themes integrated across disciplines will help reduce barriers to learning, improved enthusiasm and ownership for learning, and improved overall academic performance. A greater depth of understanding of how the environment interacts with individual age and susceptibility to impact human health through the proposed educational themes that arch disciplines will reduce the burden of human illness or dysfunction from environmental influences. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INTERACTION OF LEAD WITH ZINC FINGER PROTEINS Principal Investigator & Institution: Zawia, Nasser H.; Associate Professor; Biomedical Sciences; University of Rhode Island 70 Lower College Road, Suite 2 Kingston, Ri 028810811 Timing: Fiscal Year 2002; Project Start 01-MAR-1998; Project End 28-FEB-2004 Summary: (Adapted from the Investigator's Abstract) Exposure to lead is a significant environmental hazard facing children today. While the behavioral deficits due to lead exposure are known, the mechanisms that produce such permanent damage are not well understood. The underlying hypothesis of this research is based on the concept that long term adverse effects in cognitive processing, due to developmental exposure to lead,
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involve some alterations of gene function. Recent work in our lab has demonstrated that both transient and permanent alterations in cerebral mRNA levels occur in rats that are exposed to lead. This proposal seeks to elucidate the mechanisms through which lead may alter the regulation of gene expression. To accomplish this objective, both in vivo and in vitro models have been designed to examine the relationship between lead exposure and zinc finger transcription factors, which play key roles during growth and differentiation. These metalloproteins which regulate gene expression are likely targets for lead's action. The major aims of this work are to study the effects of lead exposure on the DNA binding properties of zinc finger proteins (zif268, SP1, and krox20) and to examine if their functional capacity of gene activation/deactivation is impaired by lead. Molecular techniques such as gel mobility shift assays, Northern and Western blotting, and tissue culture will be utilized in these studies. Understanding the mechanism of lead neurotoxicity with the models and experiments hitherto proposed will shed more light on metal toxicity and broaden our knowledge of the impact of heavy metals in the environment on our health. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LEAD (PB) EFFECTS ON NEUROENDOCRINE DEVELOPMENT Principal Investigator & Institution: Dees, W L.; Professor; Veterinary Anatomy & Public Health; Texas A&M University System College Station, Tx 778433578 Timing: Fiscal Year 2002; Project Start 01-MAR-1999; Project End 28-FEB-2004 Summary: Recent human and animal studies have suggested that the neuroendocrine axis is a specific target for low level lead (Pb) toxicity. Critical unanswered questions are when does the insult occur (prenatally or postnatally) and what is/are the specific mechanism(s) of action? It is known that the activation of hypothalamic N-methyl-Daspartic acid (NMDA) receptors will stimulate luteinizing hormone releasing hormone (LHRH) luteinizing hormone (LH) secretion and advance the onset of puberty. There is now convincing evidence that insulin-like growth factor I (IGF-I) and leptin are also involved in LHRH/LH secretion and the acquisition of puberty. The present investigation will utilize in vivo and in vitro techniques as well as molecular biology to determine what effect(s) low level Pb exposure in utero only, during lactation only, or in utero plus during lactation may have on the above substances and their respective influence on the neuroendocrine events of puberty. We will use four specific aims to assess: 1) The effects of Pb on the expression of specific proteins shown to be involved in the pubertal process, i.e. IGF-I and its type 1 receptor, leptin and its receptor, and the NMDA receptor. These results will be correlated with assessments of hypothalamic, pituitary and ovarian hormones, as well as with specific indices of growth and puberty; 2) the potential of Pb to block the ability of these proteins to induce or influence the timing of puberty; 3) the effects of Pb on IGF-1, as well as NMDA-receptor activated and leptin induced secretion of LH in vivo; and 4) the effects of Pb on IGF-1, as well as on NMDA-receptor activated and leptin- induced LH secretion in vitro. These studies are designed to obtain information which will allow us to better understand the critical time point(s) for Pb induced insult to occur and the detrimental effects and mechanism(s) of action of exposure to Pb during in utero and early postnatal development on growth and neuroendocrine regulation in the young female. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LEAD AND SKELETAL HEALTH IN BOSTON AREA WOMEN Principal Investigator & Institution: Rosen, Harold N.; Beth Israel Deaconess Medical Center St 1005 Boston, Ma 02215
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Lead Poisoning
Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LEAD EFFECTS ON SKELETAL STEM CELLS AND FRAC Principal Investigator & Institution: Schwarz, Edward M.; Associate Professor; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2006 Summary: (provided by the applicant): The unifying hypothesis of this Program Project is that Pb exposure causes osteoporosis, which at the cellular level is known to be the result of an imbalance between bone resorption and bone formation. This condition is also associated with defective skeletal repair, which represents a significant component of the disease, as it has been shown that ~24% of osteoporosis patients that sustain a hip fracture die from associated complications. Critical data in support of this theory are that animals feed Pb in their diet become osteoporotic. At present the mechanism of this Pb-induced osteoporosis and the effects of Pb on fracture healing are unknown. This project will test the hypotheses that 1) Pb-induced osteoporosis is caused by preferential inhibitory effects on bone stem cells (osteoblast >>osteoclast progenitors) and 2) this inhibition has significant effects on skeletal repair (fracture healing). To test this the investigators will utilize two different Pb exposure regimens: Chronic Pb exposure (adult mice continually fed Pb in their drinking water) and osteoporosis-induced exposure (adolescent mice are exposed to Pb during development to incorporate Pb into their bones following 2 month of a Pb free diet, to clear the systemic Pb, the mice are overiectomized to commence the osteoporosis-induced exposure). Utilizing these exposures regimens with the dosing of 0,200 or 500ppm of Pb in their drinking water, to achieve a blood Pb concentration of (<5, 15, and 40ug/dl respectively), the investigators will evaluate the effects of Pb on bone stem cells (Aim 1) and fracture healing (Aim 2). The effects of Pb exposure on osteoblast progenitor cells will be analyzed in nodule formation, alkaline phosphatase, and gene expression assays on primary bone marrow cells from mice. Effects on osteoclast progenitor cells will be evaluated in splenocyte CFU-M colony and osteoclastogenesis (TRAP) assays to determine osteoclast precursor frequency; and bone wafer resorption assays to evaluate effects on osteoclast activity. The effects of Pb exposure on fracture healing will be evaluated utilizing a stabilized tibia fracture model with quantitative radiology and histomorphometry at various time points after fracture. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LEAD EXPOSURE AND EMOTIONAL BEHAVIOR Principal Investigator & Institution: Delville, Yvon; Psychology; University of Texas Austin 101 E. 27Th/Po Box 7726 Austin, Tx 78712 Timing: Fiscal Year 2002; Project Start 01-FEB-2001; Project End 31-DEC-2003 Summary: (ADAPTED FROM APPLICANT'S ABSTRACT) During development, the nervous system is vulnerable to chemical agents present in the environment. For instance, children exposed to lead are at risk for cognitive and emotional problems contributing to lower IQ and antisocial behaviors. Today, the level of exposure to lead is still significant for children in urban, industrial and rural areas, and the intensity and frequency of violent acts performed by adolescents in America is particularly troubling. Various animal models are being developed to better understand the developmental effects of lead on cognition. However, little is known of the neurobiology underlying
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impairments in social and emotional behavior. The present studies were designed to test the effects of early exposure to lead on aggressive behavior and stress responsiveness in an animal model. Golden hamsters are ideal for these studies as their aggressive behavior has been well characterized. Furthermore, the neurobiology of aggression is also well understood in this species. The following topics are covered under the following studies. First, the proposed studies will determine the effects of exposure to various doses of lead on aggressive behavior and stress responsiveness in golden hamsters. These two topics will be studied together as they appear to be linked. Second, the proposed studies will tests the effects of lead exposure on the neurobiology underlying aggressive behavior and stress responsiveness, focussing particularly on the serotonin system. Third, the studies will test the effects of lead exposure on the neural systems controlling aggression and stress responsiveness. Together, these studies will provide a preclinical database that may contribute to a better understanding of risk factors and potential therapies in human populations. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LEAD EPIDEMIOLOGY
EXPOSURE,
GENETICS
AND
OSTEOPOROSIS
Principal Investigator & Institution: Korrick, Susan A.; Assistant Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002 Summary: The purpose of the study is to evaluate the possible health effects of lead stored in the skeleton. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LEAD EXPOSURE/DIETARY FACTORS IN CHILDREN'S ORAL HEALTH Principal Investigator & Institution: Burt, Brian A.; Professor and Director; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002 Summary: (Provided by the applicant): This study seeks to identify the relationships between lead levels, intake of dietary fats and sugars, and dental caries experience in disadvantaged African-American children, and to identify how these variables in the parent/caregiver relate to the child?s oral health status. The purpose is to identify areas for successful intervention toward reducing the disparities between those with the poorest oral health and their better-off peers. The population to be studied is children ages 0-5, and their primary caregivers, in the poorest 39 census tracts in Detroit. To be eligible, children must be equal or lower than 250 percentof the federal poverty line. Children and caregivers will be followed-up for 4 years. There will be 3 cycles of data collection over that time, in years 2, 4, and 6, so that for each family there are 2 years between data collection points. For adequate statistical power, the intent is to have the final data collection cycle include 833 children. Sampling, conducted by the Methodological Core (MC) for the center, has the study beginning with 994 adult caregivers for interview and 1,089 children for examination (two age-eligible children per family can be accepted). Each caregiver will complete a food frequency questionnaire (FF9) at home for him/herself and for the child(ren). The completed FFQs will be brought to the clinical examination, at which time an interviewer will review the FFQs with the caregiver. At this same appointment, both caregiver and child(ren) will receive a dental examination, and an FFQ for the child will be completed by interview.
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The adult caregiver will be asked for a finger stick blood sample and a saliva aboutample (for lead assay); saliva samples will be sought from the children only at the exams in years 4 and 6. Participants will also be measured for height and weight at the first and later examinations. Data from these interviews, exams, and assays of the samples will be managed by the MC. For testing the hypotheses, the outcomes will be severe dental caries experience in the child, and exposures will be lead levels in child, and sugars and fats in the diets of child and caregiver. Other variables, such as the demographic information collected in other center studies and body mass index of the caregiver and child, will be included in the multivariate analyses to determine relative risk. Nested case-control studies, with several measures of caries as the outcomes, will also be conducted. The significance of this study will be that it will identify areas for intervention and produce a unique database from an African-American population. The child?s FFQ, to be developed for this study, will also be a valuable tool for other studies of child obesity and nutrition. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LEAD INDUCED CHANGES IN GLUTAMATE RECEPTORS & CORTICAL PLASTICITY Principal Investigator & Institution: Johnston, m; Kennedy Krieger Research Institute, Inc. Baltimore, Md 21205 Timing: Fiscal Year 2002 Summary: NMDA and metabotropic glutamate receptors have been shown to play a role in the activity-dependent formation of synaptic circuitry during critical periods of brain development. Lead interactions with glutamatergic signaling also have been demonstrated and these effects may alter synaptic connectivity and produce permanent impairments in the brain function. The proposed studies focus primarily on the use of a well- established model of cortical development, the somatosensory barrels, to test the hypothesis that lead-induced changes in the glutamate receptors alter activitydependent development of cortical circuitry. The proposed studies consist of (1) examination of the effects of low-level lead exposure on the temporal and spatial expression of glutamate receptor and glutamate receptor mRNA in the cortical barrel field, hippocampus and cerebellum; (2) examination of the effects of lead exposure during different periods of development on glutamate receptor expression in the barrel fields, hippocampus and cerebellum; and (3) examination of the effects of lead exposure on cortical barrel plasticity changes induced by neonatal whisker removal. To achieve the stated aims of this project, glutamate receptor expression will be evaluated by this project, glutamate receptor expression will be evaluated by immunohistochemistry, receptor autoradiography and in the situ hybridization. The overall goal of the project is to provide insight into the impact of lead on activity- dependent processes critical to normal brain development to test the stage for the design for rational intervention strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LEAD MOBILIZATION DURING PREGNANCY AND LACTATION Principal Investigator & Institution: Moline, Jacqueline; Assistant Professor; Mount Sinai School of Medicine of Cuny New York, Ny 10029 Timing: Fiscal Year 2002 Summary: (Taken from application) Evidence from case reports and studies of lead isotope ratios suggest that lead stored in the skeleton is mobilized during pregnancy
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and lactation, placing the mother and, in particular, the developing fetus and infant at risk of lead poisoning. The placenta is fully permeable to lead, and lead is present in breast milk. Calcium intake may protect against lead absorption. To investigate the hypothesis that skeletal lead is mobilized during pregnancy, and perhaps more importantly during lactation, we propose an intervention study with repeated measures of blood and bone lead in a population of women in Morelos, Mexico with high environmental lead exposure. Women will be randomized to receive calcium and vitamin supplements, calcium without vitamin supplements, or vitamin supplements alone. We will simultaneously follow a control group of non-pregnant women. We hypothesize that as lead is mobilized during pregnancy and lactation, maternal, fetal and infant blood-lead levels will increase, and maternal bone-lead levels will decrease. We will compare bone- and whole blood-lead levels prior to pregnancy with measurements obtained from the same women at two weeks, six months and twelve months postpartum. Bone-lead levels will be measured by X-Ray Fluorescence. We will examine molecular biomarkers of bone turnover to assess whether concurrent bone remodeling and lead mobilization occurs. We hypothesize that bone-lead levels will decrease during pregnancy, and further during lactation as a result of bone-lead mobilization. The control group of non-pregnancy women will allow us to compare the natural history of bone-lead changes in the absence of pregnancy and lactation. Bloodlead levels obtained in each child at the same time as the mother s postpartum evaluations will provide information about maternal transfer of circulating lead to the child. To assess gene-environment interactions, we will examine whether polymorphisms in ALA-D, the hemochromatosis gene and the Vitamin D receptor influence lead release from bone. We hypothesize that women receiving calcium supplements will have less lead mobilization and thus less transfer to their developing child. We will also assess whether calcium plus vitamin supplements is more protective than calcium alone. This study will be undertaken in Morelos, Mexico where the population has high environmental lead exposure, predominantly through the use of lead-glazed ceramics, and where women have high rates of breast-feeding. Thus we will be able to compare bone-lead mobilization during lactation with that which occurs during pregnancy. The investigation should provide important insights into the potential health effects of chronic environmental lead exposure to pregnant and lactating women, developing fetuses, and infants through breast feeding, as well as insights into approaches for prevention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LEAD OSTEOPOROSIS
TOXICITY
IN
THE
SKELETON
&
ITS
ROLE
IN
Principal Investigator & Institution: Puzas, J. Edward.; Donald and Mary Clark Professor of Ortho; Orthopaedics; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2006 Summary: (provided by applicant): This Program Project grant application seeks to define the mechanisms of Pb toxicity in the skeleton. The investigators have evidence that the adverse effects of this heavy metal on bone and cartilage function contribute to diseases such as osteoporosis and hinder osteoporotic fracture healing. The Program Project is made up of four projects, two of which are cellular and molecular in nature, one is animal-based and one is clinical. Two cores are also proposed, an Administrative Core and a Histopathology Core. Project 1: Molecular mechanism of lead's effect on osteoclasts and osteoblasts; this project will examine how Pb influences the key
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Lead Poisoning
regulatory genes controlling bone resorption and bone formation. Preliminary data have implicated osteoprotegrin (OPG), RANK ligand, and TRIP as the genes responsible. The project will have both in vitro and in vivo components. Project 2: Cellular and molecular effects of lead on chondrogenesis and cartilage differentiation; this research seeks to demonstrate that primordial regulators of chondrogenesis and cartilage differentiation; (i.e. the BMP's Indian hedgehog, PTHrP, etc.) are influenced in a complex way by Pb. Lead exposure leads to inappropriate skeletal development and predisposes affected individuals to osteoporosis. Project 3: Lead effects on skeletal stem cells and fracture healing; Project 3 will use an animal model to document that the findings in Project 1 and 2 are manifested in vivo. Additionally, this work will characterize the mechanism of the effect of Pb on hindering normal fracture healing. Project 4: Clinical diagnostic and therapeutic approaches to skeletal lead toxicity; this project extends the basic science investigations into a clinical trial. It seeks to determine if therapeutic approaches for osteoporosis are effective in Pb-containing skeletons and in controlling blood Pb levels. This Program Project will define novel molecular pathways to explain the adverse effects of Pb on bone and cartilage. The pathways will be examined and validated in animals, and ultimately the findings will be translated into clinical trials. This Program Project provides the opportunity to investigate the skeletal effects of Pb from "the bench" to the "bedside". It is unique in this regard. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LEAD TOXICITY--MIDBRAIN DOPAMINERGIC SYSTEM Principal Investigator & Institution: Pitts, David K.; Associate Professor; Pharmaceutical Sciences; Wayne State University 656 W. Kirby Detroit, Mi 48202 Timing: Fiscal Year 2002; Project Start 13-AUG-1999; Project End 31-JUL-2004 Summary: Substantial evidence indicates that lead (Pb) has a significant developmental impact on the midbrain dopaminergic (DA) system, and suggests that this system can be affected at low levels of exposure. Since the DA system is thought to play a role in cognition, attention, learning, and motor behavior, a role of the DA system in the neurotoxic effects of Pb is consistent with the neurological profile observed following childhood Pb exposure. Neurochemical reports have indicated that Pb alters DA turnover, DA release and the development of postsynaptic DA receptors. However, very little is known about the consequences of postnatal exposure on the dopaminergic system at the cellular level in vivo. The absence of any information concerning the effects of Pb on impulse generation in DA neurons or DA neuron viability represents a serious gap in our understanding of the impact of Pb on the DA system. The proposed experiments will examine the electrophysiological activity of the midbrain DAcontaining neurons and target neurons in the striatum and nucleus accumbens by using single-cell electrophysiological recording techniques. In addition, immunohistochemical techniques and specific behavioral assays will be used to examine the impact of Pb on DA neuron survival and the behaviors modulated by the DA system respectively. This approach will provide a thorough analysis of DA neuronal activity and provide the ability to correlate electrophysiological, immuno-histochemical and behavioral findings with blood and brain Pb levels. Two different exposure protocols will be used. In the pre-weaning protocol Pb will be provided to offspring via the milk of lactating dams that consume Pb-treated drinking water. In the post-weaning protocol Pb will be provided directly to weanlings via their drinking water. The overall hypothesis is that postnatal Pb exposure alters the electrophysiological activity and/or survival of midbrain DA neurons. The effects on the presynaptic component of the DA system (i.e., DA neurons) may then have an impact on the postsynaptic component, and
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this would be seen as changes in postsynaptic DA receptor responses and specific DArelated behaviors. Results obtained from these studies will be relevant to our understanding of the impact of low level Pb exposure on human brain development, and will provide more detailed insight into the neurological problems associated with such exposure at the cellular level. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LEAD, BLOOD PRESSURE, NEUROLOGIC AND RENAL FUNCTION IN 2 STUDY POPULATIONS Principal Investigator & Institution: Hu, Howard; Associate Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2002 Summary: The purpose of this project is to examine the relationship between lead exposure and hypertension, renal dysfunction and cognitive deficits in the Childhood Plumbism Follow-up Study, a group of middle-aged adults with a confirmed history of childhood lead poisoning, and the Neddleman/Bellinger tooth lead study, a cohort of young adults with either high or low tooth lead levels. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LEAD: ATTENTION, IMPULSIVITY, AND DOPAMINE Principal Investigator & Institution: Kiefer, Stephen W.; Psychology; Kansas State University 2 Fairchild Hall Manhattan, Ks 665061103 Timing: Fiscal Year 2002; Project Start 01-JUL-2000; Project End 30-JUN-2004 Summary: Although the hypothesis has repeatedly been posed that attention deficits underlie the cognitive impairments produced by Pb, no systematic examination of this assertion has been undertaken in either human cohorts of experimental animals. The current studies directly address in rats the hypothesis that impulsivity/aversion to delay, one of the three clinically- defined sympton domains of attention deficit disorder, may be a particular target of Pb, based on our comparative observations of Pb effects on a fixed ratio (FR) waiting for reward paradigm and a sustained attention task. On the FR wait paradigm, free food deliveries were available at increasing delays following the completion of an FR 50; any response during the waiting component reset the FR requirement. Mean waiting times of Pb-treated rats were 50 percent shorter than controls. While other explanations are feasible, these results could reflect an aversion to delay which was terminated by a response resetting the FR component. These same Pb exposures were without systematic effect in sustained attention task. Impulsivity, as measured in children using self-control procedures, is predicted by increased fixed interval (FI) response rates. Pb exposure reliably increases FI response rates in animal models. Thus, Pb exposure should likewise increase impulsivity in self-control procedures. This proposal seeks to further evaluate the effect of Pb on impulsivity, the role of aversion to delay in mediating it, and the importance of developmental period of exposure in such effects. Studies show that nucleus accumbens (NAC) dopamine (DA) systems modulate FI response rates. Thus, NAC DA should likewise modulate impulsivity if FI response rates are predictive of impulsivity. These studies will also determine the extent to which NAC DA systems modulate impulsivity in a self-control paradigm. Using combined behavioral/microinjection approaches, three hypotheses will be examined: 1) If Pb exposure produces impulsivity, it should increase the choice of small immediate rewards over larger but delayed rewards in self-control paradigm; 2) Delay aversion rather than alternative behavioral mechanisms accounts for the shorter
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Lead Poisoning
wait times of Pb-exposed rats on the FR wait paradigm; and 3) NAC DA activity will modulate levels of impulsivity. Collectively, these studies will i) enhance the understanding of impulsivity/delay aversion under both normal and Pb-exposed conditions; ii) provide a more precise basis for behavioral and chemical therapeutic strategies; iii) provide models to assess genetic or environmental risk factors in addition to Pb which can be directly extrapolated to pediatric cohorts. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LOW COST, ACCURATE, PORTABLE BLOOD LEAD ANALYZER Principal Investigator & Institution: Lewandowski, Jan J.; Director of Res. & Development; Biomec, Inc. 1771 E 30Th St Cleveland, Oh 44114 Timing: Fiscal Year 2002; Project Start 01-JUN-2002; Project End 30-MAY-2003 Summary: We will develop a low cost, accurate, portable blood lead analyzer. The device will utilize a unique miniature rotating microsample system, which can be incorporated into a fluidic chip. The electrochemistry of the system is equivalent to the performance of a typical rotating electrode but no moving mechanical parts are required. Anodic Stripping Voltammetry and Potential Stripping Analysis techniques will be evaluated. Based on preliminary data, it is expected that the device will be capable of providing blood lead determinations with the accuracy and sensitivity required by the CDC. Lead poisoning is the most common environmental health problem affecting children. The irreversible neurotoxic effects of childhood blood-lead at low concentrations, that do not cause immediate clinical symptoms, are now well documented. The present lack of inexpensive but accurate blood determination techniques prevents necessary widespread screening programs. Our device will be an order of magnitude cheaper than Atomic Absorption Spectroscopy systems and the blood lead analyses will be so inexpensive that widespread screening will be feasible. The proposed device can be easily adapted for determination of other toxic heavy metals such as mercury or cadmium. PROPOSED COMMERCIAL APPLICATIONS: The results of a cost-to-benefit analysis of blood level screening programs was presented in the CDC's report "Costs and benefits of Universal Screening Program for Elevated Lead Levels in 1 year old children". According to this document, the current average cost of blood lead screening is $60 per child. At this price the economic benefits of screening program exceed the costs of screening when the prevalence of the elevated blood level in the child population is 14% or greater. Our estimate is that the proposed device will reduce cost per assay to $10 or less. This will be accomplished by lowering of the direct cost of the assay and reducing the cost of sample withdrawal (finger piercing vs. venipuncture). Additionally the device will not require expensive, highly trained lab personnel to operate it. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LOW-LEVEL PRENATAL LEAD EXPOSURE AND RETINAL TOXICITY Principal Investigator & Institution: Fox, Donald A.; Professor; Basic Sciences; University of Houston 4800 Calhoun Rd Houston, Tx 77004 Timing: Fiscal Year 2003; Project Start 07-JUL-2003; Project End 31-MAY-2008 Summary: (provided by applicant): Lead is a pervasive and potent neurotoxicant that produces persistent, concentration-dependent retinal, visual-motor, auditory and cognitive deficits in man and animals following exposure during development and adulthood. Approximately 2 million young children in the USA have blood [Pb] equal
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to or >10 mu g/dL, the currently accepted "safe" level, and millions more have levels of 2.5-10 mu g/dL, which place them at risk for these adverse health effects. Postnatal blood [Pb] equal to or >20 mu g/dL produce SUBNORMAL rod-mediated electroretinograms (ERGs). In contrast, recent results reveal that 7-10 year old children with low-level (blood [Pb] from 4-14 mu g/dL) gestational and continuous postnatal lead exposure have unique SUPERNORMAL rodmediated ERGs characterized by increases in a-wave amplitude, b-wave amplitude and sensitivity. The overall objective of this research is to determine the sites and molecular mechanisms underlying ERG supernormality in children exposed to low-level lead during gestation. We developed a new rat model of lowlevel gestational lead exposure (blood [Pb] of 8-12 mu g/dL) that produces similar persistent supernormal rodmediated ERGs in adult rats. The proposed studies are designed to test the hypothesis that lead exposure during perinatal development produces ERG supernormality by altering the primary mechanism underlying the rod photoreceptor a-wave rod cGMP hydrolysis - and by altering the dopaminergic-modulated input underlying the b-wave amplitude and sensitivity. Specifically, we will determine whether perinatal lead exposure: 1) causes persistent supernormal ERG a- and b-waves by independent changes in rods and inner retinal neurons, respectively, 2) decreases the steady-state rate of rod cGMP hydrolysis by inhibiting the binding of any of the critical transcription factors to the rod cGMP phosphodiesterase beta-subunit promoter, and 3) produces TNF-alpha-mediated apoptotic cell death and dysfunction of dopaminergic retinal neurons resulting from the elevated retinal TNF-alpha levels measured following low-level perinatal lead exposure in rats. The results from these functional (ERG), biochemical, molecular and immunocytochemical studies will: 1) determine the mechanisms underlying the rodmediated ERG supernormality, 2) establish the critical period of retinal (neural) vulnerability during gestational development and 3) provide essential neurotoxicity data on low-levels of lead exposure that is of increasing scientific and regulatory concern. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MANIPULATION IONOPHORES
OF
LEAD
USING
CARBOXYLIC
ACID
Principal Investigator & Institution: Pfeiffer, Douglas R.; Professor; Molecular/Cellula/Biochemistry; Ohio State University 1960 Kenny Road Columbus, Oh 43210 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2006 Summary: (provided by applicant): The use of antibiotics in agricultural is often criticized because resistant strains of bacteria arise from the practice. There may be additional grounds for concern in the case of antibiotic ionophores, which are added to the feed of nearly all species that are employed by this industry. More specifically, these compounds are long know to be ionophores for physiological cations such as Na+, K+, and Ca2+, however, we have found that they are actually much more active and highly selective as ionophores for Pb2+. Since the compounds are known to carryover into the human diet, the prospect arises that the use of ionophores as feed additives impacts upon the pathophysiology of lead as a toxin in humans, as well as in the animals. The studies proposed here are designed to will test those possibilities from several perspectives. We will use rats as an animal model to determine it Pb2+ transporting ionophores increase or decrease lead absorption via the gut, when they are administered at levels that are typical of agricultural practices. We will also determine if Pb2+ transporting ionophores redistribute an existing lead burden between bone and soft
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Lead Poisoning
tissues and between individual soft tissues, including heart, brain, kidney, liver, and testis. We will furthermore determine if Pb2+ transporting ionophores improve access of previously accumulated lead to circulating chelators, and thereby shorten the otherwise lengthy duration of chelation therapy for lead intoxication. We will administer the ionophores to rats in feed and drinking water, respectively. Lead levels in organs, blood, urine and feces will be determined by electrothermal atomic absorption spectroscopy. Ionophore levels will be determined by HPLC using post-column derivatization with vanillin or fluorescent reagents. These animal studies will be complimented by a physical-chemical investigation of ionophore mediated Pb2+ transport in phospholipid vesicles and by an analogous investigation of Pb2+ transport in cultured cells. The physical-chemical studies emphasize spectroscopic and solution chemical methods. Taken in total, the proposed studies will reveal if the use of ionophores in agriculture might pose an unrecognized threat to the public health. They may furthermore identify improved methods for the treatment of lead intoxication. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISMS OF PB2T TOXICITY TO CEREBRAL MICROVESSELS Principal Investigator & Institution: Laterra, j; Kennedy Krieger Research Institute, Inc. Baltimore, Md 21205 Timing: Fiscal Year 2002 Summary: Brain microvasculature is one of the multiple sites that are susceptible to lead toxicity. Unfortunately, the mechanisms underlying this toxicity are unknown. Unfortunately, the mechanisms underlying this toxicity are unknown. It is wellestablished that microvessel development is regulated by numerous events, including local proteolysis, cell- extracellular matrix interactions, and angiogenic factors. The primary objective of this proposal is to determine whether Pb-induced microvessel toxicity results from the toxicant's effect on specific proteolytic pathways, microvesselmatrix interactions, or angiogenic factors such as cytokines. Both in the in vivo and in the vitro models will be used to address these objectives. Aim 1 will determine whether neonatal lead exposure alters rat brain microvessels or expression of BBB proteins. Immunohistochemical, biochemical and molecular biological methods will be used to examine microvessel formation and expression of BBB proteins such as gamma glutamyl transpeptidase, glucose transporter type-1, p- glycoprotein, transferrin receptor, and endothelial barrier antigen. Aim 2 will examine if lead alters the plasminogen activator (PA) and collagenase proteolytic pathways in the rat neonatal microvessels and in the in vitro astroglial-induced microvessel formation. Biochemical methods will be used to quantify changes in the proteolytic activity and of specific proteases and protease inhibitors. Changes of expression and distribution of specific proteases and protease inhibitors will be examined using immunohistochemistry, in the situ hybridization, and Northern blotting. Aim 3 will determine whether lead alters the expression of proteins which regulate interactions with the extracellular matrix. Effects of lead on laminin, collagen, proteoglycans, SPARC, thrombospondin and angiogenic cytokines associated with neonatal brain capillaries in the vitro glia-induced microvessels, will be determined. It is anticipated that these studies will expand our understanding of normal microvessel development and how these critical events are affected by lead. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MODULATION OF GROWTH FACTOR/ERK SIGNALING BY LEAD Principal Investigator & Institution: Reams, Romonia R.; Florida Agricultural and Mechanical Univ 400 Foote Hilyer Administration Center Tallahassee, Fl 32307
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Timing: Fiscal Year 2002 Summary: (provided by applicant): This proposal is directed at an area of research that has important ramifications for understanding the mechanism of signal transduction in the central nervous system and peripheral nervous system that ultimately leads to neurite outgrowth. An expected outcome of the proposed study is to determine that lead interferes with remodeling of neurites and synapses during development and learning. Once this knowledge is known, development of effective neuroprotective therapies for children exposed to lead can begin. Although the neurotoxicity of lead exposure is well documented, the cellular and molecular mechanisms underlying lead neurotoxicity have not been well defined. The applicants have investigated the effect of lead on nerve growth factor (NGF)-induced neurite outgrowth in PC12 cells and the role in this process of extracellular signal regulated protein kinase (ERK), a key component of NGF-induced differentiation. They found that exposure of cells to lead acetate (0 - 100 uM) resulted in enhanced NGF-induced neurite outgrowth and promoted formation of multiple neurites per cell in NGF-treated cells. The long-range goal of this application is to understand the causes of environmentally induced neurotoxicity. The objective of this proposal, which is the first step toward attaining this long-range goal, is to understand the molecular mechanism by which Pb enhances NGF-induced neurite outgrowth and ERK/MAPK activation. The exact mechanism by which Pb enhances ERK/MAPK activation is not known. The hypothesis of this proposal is that Pb enhances neurotrophin-induced neurite growth by interacting with one or more of the seven signaling components in the ERK/MAPK pathway and causes neurotrophin-induced neurite outgrowth. They will test this central hypothesis and attempt to accomplish the overall objective of this application by pursuing the following specific aims: (1) determine the molecular mechanism by which lead enhances NGF-induced ERK activation and neurite outgrowth in PC12 cells. Specifically, they will determine the ability of lead to activate the NGF receptor, I-kA, in the presence of NGF and its effects on downstream proteins Shc, Grb2, Sos, Ras, and Raf and ERK in PC12 cells. (2) Using dominant negative constructs, determine upstream and downstream effectors on ERK/MAPK kinase signaling as described in objective #1. (3) Using cDNA array technology, determine the effects of lead on NGF-induced activation of global gene expression. These aims will be accomplished using inhibitors and dominant negative constructs of the signaling components in the ERK/MAP kinase, SRC kinase, and PI 3kinase pathway to identify how ERK activation is induced by Pb in PC12 cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOHAWK CULTURE, BEHAVIOR, TOXICANT EXPOSURE AND HEALTH Principal Investigator & Institution: Schell, Lawrence M.; Professor and Associate Dean; Epidemiology; State University of New York at Albany 1400 Washington Ave Albany, Ny 12222 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2005 Summary: Considerable concern exists over possible effects on human physical and psychological development of endocrine disrupting environmental contaminants such as polychlorinated biphenyls (PCBs). Native American communities are particularly at risk owing to subsistence systems and a cultural ethos involving greater contact with the physical environment. The proposed study follows-up 220 Mohawk adolescents aged 17-21 years, who participated in a previous study when they were 10-16 years old. All adolescents are members of the Mohawk Nation at Akwesasne which is located on the St. Lawrence River, adjacent to hazardous waste sites where PCBs have contaminated
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Lead Poisoning
the local ecology. The investigation examines the interrelationship between Mohawk cultural identity, traditional Mohawk customs, behaviors related to toxicant exposure and current toxicant burden. Serum level of PCBs will be assessed by congener specific analysis. The study will determine 1) the relationship of congeners and their hydroxylated metabolites to thyroid function (thyroid hormone levels and anti-thyroid antibodies), and 2) psychosocial outcomes including school behavior and performance, hyperactivity, and adaptation to the community. Data gathered for the past study will be employed to assess variation in metabolism of PCBs, as well as how earlier measures of cognition and hyperactivity relate to 17 year old psychosocial outcomes. Variation in susceptibility to PCB effects will be determined by examining the effects of concurrent toxicant exposure (hexachlorobenzene, Mirex, dichlorodiphenyldichloroethene, lead), diet, and indicators of PCB metabolism, on the focal measures of adult functioning. The proposed study will clarify the causal pathways between culturally identifying behavior, PCB exposure and body burden, thyroid functioning, cognitive functioning, social behavior and school functioning while identifying activities that are important to maintain cultural identify and unrelated to exposure. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR NEUROTOXICITY
MECHANISMS
OF
INORGANIC
LEAD
Principal Investigator & Institution: Goldstein, Gary W.; President; Kennedy Krieger Research Institute, Inc. Baltimore, Md 21205 Timing: Fiscal Year 2002; Project Start 01-APR-1998; Project End 31-MAR-2004 Summary: This program project resubmission is geared to elucidate mechanisms by which lead exposure can interfere with the function of a child's brain. The present application has been reduced from the original five projects to four projects in the response to the review committee's suggestion. The remaining projects focus on two target sites in the developing brain which are affected by lead exposure. Projects 1 and 2 explore potential mechanisms by which lead light compromise the blood-brain-barrier. Projects 3 and 4 examine molecular events at the synapse that are altered by lead. More specifically, project 1, focuses on changes in the immediate early response gene expression, following leading exposure, particularly c-jun and c-fos. The basis for elevated c-fos mRNA levels are due to transcriptional or post-transcriptional mechanisms. The effects of Pb2+ on c-fos mRNA will also be examine din the glial endothelial cell culture. Each of these will be complemented by assay for alterations in the AP1 activity in the vitro: and lastly, the same effects of Pb2+ on c-fos mRNA and AP1 activity will be examined in the vivo. The goal of project 2 is to determine the effect of Pb2+ exposure in the neonate of rat brain microvessel growth and on the expression of blood- barrier proteins such as v-glutamyl transpeptidase, p-glycoprotein, or endothelial barrier antigen. Aims of this project will also investigate whether Pb2+ exposure affects proteolytic enzyme expression and activities that are associated with rat brain microvessel development, and whether exposure alters the level and distribution of proteins that mediate microvessel interaction with the extracellular matrix in the rat brain. Project 3 and 4 deal with molecular events in the synaptogenesis and potential interference by exposure to lead. In the project 3, the focus will be on the binding characteristics of Pb2+ to synaptotagmin and its biochemical and cell physiological consequences. This will be carried out in the vitro using PC12 cells and rat neurotransmitter releases. Lastly, the investigators will determine whether or not synaptotagmin deficient mice are less susceptible to lead-induce changes in the synaptic transmission than wild type. Project 4 will examine the hypothesis that glutamate
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receptors are a primary target of lead exposure during brain development. To this end, the investigator will ask whether exposure to Pb2+ alters the temporal or spacial distribution of glutamate receptors and/or their relative levels of expression in the fetal rat brains. The effects of lead exposure on glutamate receptor expression will be examined at different pre- and post-natal times. The effects of Pb2+ exposure of glutamate receptor will be analyzed in the barrel field, hippocampus, and cerebellum. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR MECHANISMS OF LEAD NEUROTOXICITY Principal Investigator & Institution: Pevsner, j; Kennedy Krieger Research Institute, Inc. Baltimore, Md 21205 Timing: Fiscal Year 2002 Summary: The long-term goal of this project is to understand fundamental molecular mechanisms by which lead mediates increased neurotransmitter release. Several lines of evidence support the thesis that lead interferes with the coordinated regulation of synaptic loading, vesicular movement, docking and fusion with presynaptic membranes. Recent biochemical data, employing in the vivo and in the vitro models, provides compelling evidence implicating lead-mediated perturbation of normal vesicular trafficking processes resulting in the inappropriate release of neurotransmitters in the neuromuscular in the inappropriate release of neurotransmitters in the neuromuscular junction, synaptosomes and in the permeabilized cell cultures. Preliminary data obtained in the response to previous review further strengthens the principal investigator's assertion that the effects of lead on ephaptic synaptic release of neurotransmitters may be mediated by binding to the regulatory protein synaptotagmin. However, the exact mechanism(s) of lead-induced spontaneous neurotransmitter release remain to be determined. The hypothesis that lead binds to synaptotagmin and, therefore, stimulates unscheduled release of neurotransmitters is addressed by three specific aims. Proposed experiments are aimed at understanding (1) the pharmacology of lead- binding to the calcium-dependent regulatory protein, synaptotagmin; (2) the role of lead-synaptotagmin complexes in the unscheduled neurotransmitter release; and (3) the alteration of lead-effects on proposed in the this revised submission may provide new insights into the role of lead in the perturbation of normal synaptic vesicular function. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MR ASSESSMENT OF BRAIN FUNCTION ALTERED BY LEAD EXPOSURE Principal Investigator & Institution: Cecil, Kim M.; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2002 Summary: (provided by applicant) Exposure to lead during pregnancy, infancy, and childhood increases the individual likelihood of impaired school performance, increased impulsiveness, aggression, and delinquent behavior. Disorders that result from exposure to environmental neurotoxicants are a complex web of interactions between genetic, neurochemical, biochemical, environmental and social factors that influence children during critical periods of development. To date, research in the area of human developmental neurotoxicology focuses primarily on global measures of sensory-motor development and cognition. However, human studies elucidating the biological basis for developmental and behavioral disorders due to environmental toxicant exposure are
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Lead Poisoning
lacking. Although gross brain structure appears normal, underlying problems must exist at a neural level. This project seeks to correlate childhood environmental lead exposure with changes in brain structure, neurochemistry and function assessed with magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS). Cortical and subcortical brain volumes will be determined with high resolution MRI. Neuronal and glial cell markers (N-acetyl aspartate, creatine, cholines and myo-inositol) will be measured using proton MRS. These structural and chemical measures will also be correlated with behavioral measures from the young adult participants of the Cincinnati Lead Study (CLS). These participants represent a unique and ideal study cohort of approximately 240 subjects with detailed histories of exposure and behavioral outcomes in lead exposed children monitored for approximately 20 years. As this cohort enters young adulthood, associations between childhood lead exposure and antisocial behaviors are emerging. While MRI and MRS provide structural and metabolic measures relevant to lead exposure, the significance to behavioral measures is limited. A pilot study (n=40) examining language, working memory and attention in combination with functional magnetic resonance imaging (fMRI) will also be performed to better investigate the correlation of functional and behavioral deficits. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NEONATAL LEAD EXPOSURE EFFECTS ON THE ADRENAL CORTEX FUNCTION Principal Investigator & Institution: Soliman, Karam F A.; 3m Distinguished Professor; Florida Agricultural and Mechanical Univ 400 Foote Hilyer Administration Center Tallahassee, Fl 32307 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NEUROBEHAVIORAL EFFECTS OF PREVALENT TOXICANTS IN CHILDREN Principal Investigator & Institution: Lanphear, Bruce P.; Professor; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2002 Summary: (provided by applicant) Epidemiologic and experimental data have established the adverse neurobehavioral effects of exposure in utero and during early childhood to numerous environmental toxicants, including lead, alcohol, mercury, PCB s, and environmental tobacco smoke (ETS). Still, the ideal biomarker for measuring in utero exposure to specific toxicants has not been established and the adverse effects of many potential neurotoxicants have not been rigorously tested. Fetal exposure is typically measured with self-reported surveys, maternal blood and urine, or cord blood. In contrast, meconium is a non-invasive method to simultaneously test for chronic exposures to numerous toxicants, but it is as yet unclear whether conventional biomarkers or meconium are more predictive of the adverse effects linked with specific toxicants. For lead exposure, emerging data indicate that our efforts should emphasize primary prevention, but the safety and efficacy of lead hazard controls are uncertain, especially for children with low blood lead concentrations. The investigators propose to conduct a longitudinal cohort study of 400 children, followed from less than 16 weeks gestation to 36 months of age, to examine the dose-response of low-level exposures (preand postnatal) to prevalent neurotoxicants with neurobehavioral outcomes and
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development disorders, such as conduct disorder, cognitive deficits, hearing loss and behaviors consistent with ADHD. The investigators will also conduct a nested, randomized controlled trial to test the efficacy of lead hazard controls or the development of adverse neurobehavioral effects. In Project 1 of University of California's Center Grant, the investigators will test the following hypotheses: 1) In utero exposures as measured by survey (alcohol and ETS), maternal and cord blood (lead, mercury, pesticides and ETS), and urine (pesticides) are less predictive of in utero effects of prevalent toxicants, such as cognition, behavioral problems, growth and hearing, compared with the same toxicants in meconium. 2) Postnatal exposures to pesticides, ETS and lead (at blood levels below 10 ug/dl) are associated with adverse neurobehavioral effects, growth delay and hearing loss in early childhood. 3) Children in the Lead Reduction Group will have blood lead levels that are 2.7 ug/dl (30%) or lower, significantly higher cognitive scores, less hearing loss, greater growth velocity, and fewer behavioral problems than the Control Group at 36 months of age. If funded, this project, combined with the specific aim of Project 2, to validate meconium as a marker of in utero exposure, will serve as a model to evaluate the adverse effects of exposures to multiple prevalent toxicants, validate meconium as a measure of in utero exposures to numerous toxicants, provide exposure and risk assessment data for residential pesticides, test an intervention for the primary prevention of subclinical lead toxicity, and test the efficacy of a lead hazard control on children?s blood lead concentration and neurobehavioral functioning. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NEUROCHEMICAL AND GENETIC MARKERS OF LEAD TOXICITY Principal Investigator & Institution: Wright, Robert O.; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-AUG-2005 Summary: (Taken from the Investigator's Abstract) This proposal will allow the candidate to gain knowledge and skills in environmental epidemiology under the direct supervision of a highly qualified sponsor, further enhancing his potential to develop into an independent investigator. The candidate is trained in pediatrics and medical toxicology, and he is presently studying for a Masters in Public Health degree in Quantitative Methods. In addition, he has spent the past two years at the Channing Laboratory working directly with the Metals Epidemiology Research Group. This collaboration has already resulted in the publication of two research papers on the relationship of iron stores to lead poisoning, which is a primary focus of this proposal. The first two years of this proposal will incorporate needed course work, seminars and experience in statistical analysis, molecular epidemiology and assessment of neurocognitive function. This will enable the Dr. Wright to undertake an intensive research experience in the latter three years of the proposal. The long-term goal of the candidate is to develop into an independent investigator in the field of environmental epidemiology, with specific expertise in neurodevelopmental assessment and molecular epidemiology. This proposal outlines his career development plan, which includes work with established experts in environmental health, neuro-epidemiology, neuroradiology, statistics, medical toxicology and population genetics. His development as a researcher will be enhanced both by course work at the Harvard School of Public Health and by directly working with the research team on projects involving neurotoxicology and molecular epidemiology. The overall scientific goal of this study is two-fold: 1) to determine whether elevated bone lead concentrations are associated with neurochemical changes in the frontal lobes and hippocampus of human subjects, and 2) to determine
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Lead Poisoning
whether hemochromatosis genotypes are associated with increased bone lead concentrations. This proposal will take advantage not only of the intellectual and laboratory resources described herein, but also the data and archived samples from the long-running, longitudinal Normative Aging Study (NAS) that form the basis of the sponsor's "Lead RO1" (ES 05257-08 Lead Biomarkers, Aging and Chronic Disease). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NEUROTOXICANT EFFECTS ON CELL CYCLE REGULATION OF NEUROGENESIS Principal Investigator & Institution: Cicco-Bloom, Emanuel Di.; Univ of Med/Dent Nj-R W Johnson Med Sch Robert Wood Johnson Medical Sch Piscataway, Nj 08854 Timing: Fiscal Year 2002 Summary: (provided by applicant) The investigators hypothesize that neurotoxic metals and teratogens disrupt neurogenesis in developing forebrain and hindbrain systems in vitro and in vivo, acting to inhibit proliferation by altering mitogenic growth factor receptors and cell cycles signaling pathways. There are increasing numbers of children who experience problems with learning, social interactions, and self-regulation, and exhibit difficulties with fine and gross motor control. Normal brain development depends on interactions among multiple factors including those from genetic, neurochemical, biochemical, social, and environmental sources. Significantly, recent studies indicate that environmental toxicants injure the developing brain, potentially contributing to cognitive and motor deficits. Toxicants affecting the brain, neurotoxicants, may act at multiple time windows, eliciting immediate stage-dependent effects in specific systems that influence subsequent ontogenetic processes as well. However, while negative effects of neurotoxicants on cell migration, differentiation, and survival have been well-characterized, little is known about the effects on the generation of neurons (neurgenesis) and underlying pathogenetic mechanisms. As child neurologists, the investigators frequently evaluate children for abnormal brain development in clinic, concerned about attention, learning, behavior, and autism spectrum disorders. Further, as a member of the Scientific Advisory Board of the National Alliance for Autism Research (NAAR), a community family advocacy organization, they provide targeted basic and clinical research support. This current proposal represents a new direction for basic research in the investigators laboratory, which has focused on defining mechanisms that control generation of distinct neuronal populations from dividing precursors. Previously, they examined both positive and negative regulators of precursor proliferation in the developing nervous system, defining growth factor and neuropeptide effects in culture and in vivo. Further, they employed neuronal populations in forebrain and hindbrain regions involved in learning, memory and motor functions in the fetus as well as the developing postnatal animal. Based on extensive studies, the investigators now turn attention to the effects of well-characterized neurotoxicants, including lead and mercury, and model teratogen, valproic acid, on neurogenesis in the embryo and the newborn, defining mediating mitogenic and cell cycle pathways and designing new model systems. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NMDA RECEPTOR FUNCTION IN LEAD NEUROTOXICITY Principal Investigator & Institution: Guilarte, Tomas R.; Professor; Environmental Health Sciences; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 01-DEC-1992; Project End 30-JUN-2008
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Summary: (provided by applicant): Despite significant efforts during the last three decades to reduce lead contamination of the environment, a significant number of children continue to be exposed to this potent and ubiquitous neurotoxicant. A recent report by the Surgeon General of the United States (Satcher, 2000) indicates that "lead poisoning poses one of the greatest environmental threats to children in America". It further states that the latest data show that in the United States, 1 in 20 children under the age of 6 have blood lead levels exceeding those considered to produce lasting deficits in cognitive function. Unfortunately, this problem is not going to disappear in the near future and we must devise new strategies to ameliorate or modify the devastating effects of lead on the central nervous system. The goal of the work proposed is to continue to elucidate the molecular mechanisms of lead-induced neurotoxicity. Our work has demonstrated that the N-methyI-D-Aspartate (NMDA)-type of glutamate excitatory amino acid receptors is a target for lead in the central nervous system. This is important because NMDA receptor function is essential for a number of physiological processes in the developing and mature brain. One of these processes is the acquisition and consolidation of learning and memory. We have shown that exposure to lead during development produces lasting changes in learning and memory in a rodent model of lead neurotoxicity. Further, the impairment in learning is associated with deficits in long-term potentiation in the hippocampus and alterations in NMDA receptor subunit genes and protein expression. Based on this new knowledge, we tested the hypothesis that environmental enrichment may alter the cognitive and molecular deficits induced by lead. Our studies show that environmental enrichment is able to reverse the cognitive and NMDA receptor deficits induced by developmental exposure to lead. This is an extremely important finding because it demonstrates that some of the lead-induced cognitive and molecular deficits are reversible. Further, environmental enrichment is an intervention that is applicable to children. The goal of our proposed studies is to further our understanding of the neurobiological substrates associated with lead-induced neurotoxicity and its reversibility by environmental enrichment. It is important to determine whether environmental enrichment is an intervention strategy that benefits children of any age and if the benefits are long lasting. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: OCCUPATIONAL LEAD EXPOSURE: RISK TO THE AGING WORKER Principal Investigator & Institution: Morrow, Lisa A.; Associate Professor; Psychiatry; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 29-SEP-2004 Summary: The National Institute for Occupational Safety and Health (NIOSH) has targeted several areas for research. Included in the topic areas of the National Occupational Research Agenda (NORA) is Special Populations at Risk, of which the aging worker is a focus. The present application is targeted to this agenda. The study proposes to test a large group of lead-exposed workers and non-exposed controls who were initially tested 15 to 17 years ago as part of a previously funded project. The prior assessment gathered information on neuropsychological function as well as occupational and medical history, including blood lead levels. These workers are currently age 38 to 77. Several studies have suggested that exposure to lead significantly increases the risk for the development of neurocognitive disorders in later years. There is also a significantly higher odds-ratio for having a diagnosis of neuropsychiatric disorder (e.g., depression) in pensioners who worked at jobs where exposure to lead was commonplace. These earlier studies are limited, however, by several deficiencies.
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First, they relied on weak markers of exposure - surrogates such as job titles or interviews. Second, in many cases structured and standardized tests of neuropsychiatric function were either not employed or when used, the testing was cursory. Finally, important confounders (e.g., alcohol) were either superficially estimated or ignored. This study proposes to re-evaluate lead-exposed workers and controls (105 subjects in each group) and to stratify workers into three age bands. All subjects will complete a battery of neuropsychological tests and psychiatric measures. In addition, lead exposure will be assessed with X-ray fluorescence to estimate cumulative exposure over the lifetime. Current blood lead levels will also be ascertained. The present application will determine whether long-term occupational lead exposure (as defined by bone lead levels) is associated with greater neuropsychiatric and cognitive morbidity in the aging worker. This is a revision of 1 R01 OH03891-01 Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: POISONING
ONE-STEP
RAPID
SCREENING
FOR
CHILDHOOD
LEAD
Principal Investigator & Institution: O'daly, John P.; Alderon Biosciences, Inc. 2810 Meridian Pky, Ste 152 Durham, Nc 27713 Timing: Fiscal Year 2003; Project Start 20-JUN-2003; Project End 31-DEC-2004 Summary: (provided by applicant): The CDC states that lead poisoning is the number one environmental health problem affecting children in the US because it affects one of every six at-risk children and it is acknowledged to be a source of cognitive and behavioral impairment. Only 25% of the at-risk US children are tested. Atomic absorption instruments do 80% of blood lead tests in the US, but this technology is not likely to become substantially more accessible because it is limited to sophisticated labs and requires skilled operators. The objective of this proposed multi-phase project is to develop new capillary electrochemical blood lead testing technology that will satisfy the economic, performance, and logistical needs of at-risk populations. We will configure a sensor that will accept unmeasured, untreated sample and an assay that will produce a quantitative blood lead result in 3-8 minutes. The market need for a one-step, CLIA waived blood lead system will increase the amount of lead testing done and ultimately lower the cost per result to < $3. We will also work to improve electrochemical blood lead analysis performance and extend the dynamic response range to meet U.S. and worldwide needs. We will incorporate instrument and sensor features that would allow users to test unmeasured and untreated whole blood and obtain an accurate, precise result. The expected result of the overall project will be technology that will allow substantially more lead testing in the United States and worldwide. Within the guidelines of permissible levels of childhood blood lead levels there are as many as 10 million children at risk, but only 2.5 million are tested. Atomic absorption instruments do 2 million of these tests. Atomic absorption does such a decidedly disproportionate share of this testing because it costs $1 to $3 per reportable result, while point-of-care electrochemical tests cost $4 to $6 per reportable result. Atomic absorption cannot easily increase the number of blood lead tests done because it is logistically inaccessible to 80% of the US target population and nearly 100% of the target international population. The genuine potential in the US blood lead market (7.5 million tests) lies with cost-effective and rapid electrochemical measurement. The proposed high-performance, low-cost technology will be extremely competitive for the $7.5 million available US market and the potentially much larger international market. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: OUPATIONAL SURVEILLANCE MODULES FOR PREVENTION Principal Investigator & Institution: Bonauto, David; Washington State Dept Lab/Indust of Labor and Industries Olympia, Wa 98504 Timing: Fiscal Year 2002; Project Start 01-JUL-2001; Project End 30-JUN-2005 Summary: Through surveillance of several National Occupational Research Agenda (NORA), Healthy People, and Washington State Department of Labor and Industries priority conditions including occupational asthma (OA), adult lead poisoning, musculoskeletal disorders of the upper extremity, low back disorders, dermatitis, hospitalized burns, traumatic head and brain injuries (THBI) as well as assaults, the Safety and Health Assessment and Research for Prevention (SHARP) program will demonstrate the application of a comprehensive, occupational surveillance program. Through demonstration of the proposed surveillance program, SHARP will create a systematic model for adoption by other states. To allow for adaptability, SHARP proposes development of a modular approach which demonstrates several approaches to outcome based surveillance, hazard based surveillance, and subsequent prevention activities. The proposed project will address the following aims: 1) Conduct a survey of state based occupational surveillance programs to determine currently employed approaches to surveillance and prevention, program capabilities, and program opinion leaders. 2) Demonstrate a modular approach to occupational surveillance. This modular approach should encompass the use of different data sources for priority conditions selected by an individual program. 3) Develop modules for the creation, dissemination, and evaluation of prevention efforts. 4) Conduct an employer/employee survey to further identify etiologic agents or practices in one identified industry. 5) Develop an Internet based library of surveillance modules and prevention materials. 6) Produce and disseminate three surveillance reports for WA State priority conditions per year. 7) Produce and disseminate two prevention reports to employers or employees per year. Through the proposed project, SHARP will demonstrate the utilization of several data sources for the surveillance of occupational diseases and hazards. Further, SHARP will demonstrate the analysis of such data, the creation of simple public health interventions using surveillance data, the implementation of interventions, and the evaluation of interventions using surveillance data. Finally, SHARP will produce a web accessible library of materials detailing the methodology of the various components of the surveillance program including prevention materials that may be modified and disseminated in other states. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PORPHOBILINOGEN SYNTHASE FAMILY Principal Investigator & Institution: Jaffe, Eileen K.; Member; Institute for Cancer Research Philadelphia, Pa 19111 Timing: Fiscal Year 2002; Project Start 01-APR-1991; Project End 30-JUN-2004 Summary: (Adapted from Applicant's Abstract) The porphobilinogen synthases (PBGS's) are ancient proteins, essential to nearly all cellular organisms. They catalyze the first common step in tetrapyrrole biosynthesis (i.e., porphyrin, chlorophyll, vitamin B12, etc.), which is the condensation of two molecules of 5-aminolevulinic acid to form porphobilinogen. To date, only one reaction intermediate is known for this complex reaction. All PBGS's are metalloenzymes and metal ion usage has suffered a unique phylogenetic switch between Zn(II) and Mg(II). Human PBGS is the primary target for lead poisoning and the less frequent of two alleles is reported to predispose humans toward this environmental disease. The proposed studies address various aspects of the
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PBGS's. The first specific aim uses a novel "designer gene" approach to produce and purify 100 mg quantities of human and pea PBGS because human PBGS uses Zn(II) and pea PBGS uses Mg(II). The second aim is to characterize the PBGS derived from two common human alleles and determine the molecular basis for their apparent Pb(II)related differences. This aim includes a thorough kinetic and biochemical characterization of the human proteins, including 13C NMR and collaborative EXAFS and Raman spectroscopies and X-ray crystallography. The Raman data are complementary to the 13C NMR data on active site ligands. The third aim uses mutagenesis in conjunction with kinetics, metal and substrate binding studies, and magnetic resonance techniques, plus collaborative techniques to probe structure/function relationships in PBGS. The mutations will allow us to characterize the yet unknown intermediates in the PBGS-catalyzed reaction. Some mutations probe individual functions of the two active site Zn(II) of human PBGS and others probe the structural basis for half-sites reactivity in these homo-octameric proteins. The fourth aim focuses on the intriguing phylogenetic switch between the catalytically essential Zn(II) vs. Mg(II). Studies are directed at pea PBGS and also probe an allosteric Mg(II), absent in mammalian PBGS but present in plant and many microbial PBGS. The sum of the proposed studies is expected to yield new and important information on the mechanism of lead poisoning, on the intermediate in the PBGS catalyzed reaction, on the possible roles of both Zn(II) and Mg(II) in enzyme catalysis, on the structural basis for half sites reactivity, and on the phylogenetic differences between PBGSs. Because PBGS is an essential enzyme with distinct variations between species, we envision that a thorough understanding of the phylogenetic differences will form the basis for the rational design of a new class of organism-specific drugs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF GENOMIC IMPRINTING IN DEVELOPMENTAL NEUROTOXICI* Principal Investigator & Institution: Silbergeld, Ellen K.; Professor; Environmental Health Sciences; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 15-MAR-2002; Project End 31-JAN-2004 Summary: (provided by applicant) The developing organism is in many ways highly sensitive to exogenous influences on development. For these reasons, there is a priority to identify developmental toxicants and especially to understand their mechanisms of action since this can assist us in developing science-based methods of hazard identification and prioritization. The least well understood class of developmental toxicants are agents that can affect the development of offspring consequent to preconception exposure of one or both parents, especially the male. Relatively few agents that may affect offspring development consequent to preconception paternal exposures have been identified, as compared to the number of agents identified as developmental toxicants associated with in utero exposures via the mother. Research in this area has been hampered by a lack of mechanistic understanding as to how preconception exposures of the male could affect the development of offspring during embryogenesis and into post-natal life. Recent advances in fundamental biology of development now make it appropriate to propose and test new hypotheses on the interaction of acquired risks with the molecular developmental program. Of particular relevance to this proposal is the new understanding of the importance of paternal or maternal-specific contributions to the genome of the zygote and the phenotype of the offspring. The overall goal of this project is to investigate the role of genomic imprinting as a mechanism of developmental neurotoxicity, associated with preconception
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exposure of paternal germ cells. The objectives are as follows: 1. To apply molecular methods to study parental specific allelic expression of imprinted genes in the zygote, following paternal preconception exposures to a model developmental neurotixicant. 2. To utilize high throughput methods to examine patterns of DNA methylation in candidate genes in sperm and zygote in order to detect the presence of male-mediated effects on imprinted genes involved in early development. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF IERG ACTIVATION IN THE LEAD ENCEPHALOPATHY Principal Investigator & Institution: Goldstein, g; Kennedy Krieger Research Institute, Inc. Baltimore, Md 21205 Timing: Fiscal Year 2002 Summary: The biochemical and molecular biological mechanisms responsible for cerebral micro-vasculopathy following acute lead toxicity remain poorly-defined. Increasing evidence points to a role for protein kinase C (PKC), an enzyme that regulates many cellular processes such as growth and differentiation. The proposed experiments were designed to test the hypothesis that lead activation of PKC interferes with the cascade of PKC-mediated processes that regulated protein phosphorylation, gene expression, and microvascular cell behavior. The goals of the current proposal are to determine the mechanism by which lead increased expression of c-fos in the vitro and in the vivo. In the aim 1 the investigators will determine if lead increases mRNA levels of immediate early response genes(IERGs) by enhancing gene transcription or slowing mRNA degradation. If transcriptional events are implicated than lead-sensitive c-fos transcriptional regulatory elements will be determined. Aim 2 will determine if lead induced increases in the IERG proteins and AP-1 activity can regulate the expression of other important genes. Aim 3 was designed to determine if lead alters IERG expression in the vivo. The fundamental goal of the experiments is to define the biochemical and molecular mechanisms essential to a more complete understanding of lead toxicity within the central nervous system. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SPECTROSCOPIC PROBES OF LEAD/PROTEIN INTERACTIONS Principal Investigator & Institution: Godwin, Hilary A.; Associate Professor; Anthropology; Northwestern University 633 Clark Street Evanston, Il 60208 Timing: Fiscal Year 2002; Project Start 01-AUG-1999; Project End 31-JUL-2004 Summary: (Adapted from Applicant's Abstract) Despite the fact that lead poisoning affects almost one in twenty young children in the US, the mechanism of lead poisoning is not understood at the molecular level. Recent advances in neurobiology and human genetics have pinpointed two proteins that are likely targets for lead in vivo: synaptotagmin (Syt) and delta-aminolevulinic acid dehydratase (ALAD). The goals of the proposed research are to elucidate the mechanisms by which lead inactivates these critical metalloproteins. Specifically, the aims of this study are: 1: To determine whether Pb+2 blocks Ca+2 from binding Syt. 2: To determine whether calcium mediates the activity of Syt by causing a change in the association state of the C2 domains and whether Pb+2 interferes with this process. 3: To determine how lead interferes with formation of the synaptotagmin-syntaxin complex by testing whether Pb+2 destabilizes syntaxin and by determining the metal-dependence of the association between Syt and Syn. 4: To determine whether the metal-binding properties of ALAD1 and ALAD2 account for the phenotypes observed for the two isoforms. By studying lead's
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interactions and effects on each of these proteins we seek to gain a broad understanding of the mechanisms of lead toxicity. Furthermore, the studies proposed herein will provide the foundation for future studies by providing methodologies for studying lead-protein interactions that can then be extended to new protein targets as they are identified. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE EFFECTS OF RETAINED LEAD BULLETS ON BODY LEAD BURDEN Principal Investigator & Institution: Rothenberg, Stephen J.; Anesthesiology; Charles R. Drew University of Med & Sci 1621 E 120Th St Los Angeles, Ca 90059 Timing: Fiscal Year 2002; Project Start 01-AUG-2000; Project End 31-JUL-2003 Summary: Numerous case reports have demonstrated lead poisoning with potentially fatal consequences can result from retained lead projectiles following firearm injuries. To assess the impact of retained projectiles on subsequent lead exposure, one cannot rely on self-selected cases presenting with symptoms of lead intoxication. The long-term goal of this project is to reduce the morbidity associated with body lead burden as a result of retained bullets from firearm injuries. The proposed investigation seeks to identify risk factors of elevated blood lead levels for individuals with retained lead bullets, establish appropriate protocols for lead testing, develop indications for bullet removal and provide guidelines for the appropriate management of fragments not removed. The study design included follow-up of 300 patients with retained lead bullets/bullet fragments presenting for acute care of firearm injury at large publicly owned Level 1 Trauma Center. A baseline blood level is measured as soon after patient stabilization as possible and repeated at intervals of 3, 6 and 12 months. Medical history regarding prior firearms injuries and other retained projectiles is taken, along with a screening and risk factor questionnaire to determine other sources of lead (occupational/recreational) to which the patient might have been or at present be exposed. The patient will have K- shell X ray florescence determination of bone lead in the tibia and calcaneus in order to determine past lead exposure not revealed by medical history and risk factor questionnairer. Multivariate models of blood level are made for each patient visit using risk factor and bone lead concentration data. Determinations will be made if changes in blood lead, adjusted for risk factors and bone lead concentration, from one 3 month period to the next can be significantly predicted by the coded location and fragmentation data of projectiles and presence or absence of fractures. The variables of location, fragmentation, fracture and total time during which the projectile was retained in the body will be tested using logistic regression. This will determine odds ratios of elevated lead at various concentrations (greater than 15 mug/dL, greater than 25 mug/dL, greater than 40 mug/dL, etc.) due to these factors. Data will also be analyzed in the framework of the general linear model (GML), with a repeated measure design. Principal interest will be in increasing trend of blood level as a function of fragmentation location, fracture and duration variables. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: THE POLITICAL ECONOMY OF PUBLIC HEALTH, 1870-1940 Principal Investigator & Institution: Troesken, Werner; National Bureau of Economic Research Cambridge, Ma 02138 Timing: Fiscal Year 2002
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Summary: (provided by applicant): Focusing on the nineteenth and early twentieth century, this project explores the effects of public health programs in American cities and towns on morbidity, mortality, and labor force participation. In particular, the project has four specific aims. The first aim is to measure the effect of public health programs (e.g., the construction of water and sewerage systems) on health and labor force participation among Union army veterans. The second aim is to assess the impact of long-term lead exposure on health and labor force participation. We will examine, for example, the health effects of occupational exposure and the use of lead water mains by American cities. The third aim is to assess the distributional effects of public health programs. For example, did cities install fewer water and sewer mains in poor neighborhoods, particularly in African-American neighborhoods, than in wealthy neighborhoods? The fourth aim is to measure the effectiveness of alternative institutions (e.g., households, private enterprises, or government authorities) in promoting public health. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE ROLE OF METALS IN OSTEOARTHRITIS Principal Investigator & Institution: Jordan, Joanne M.; Associate Professor; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2007 Summary: Symptomatic osteoarthritis (OA) of the knee and hip is common, the leading cause of disability and diminished quality of life among those 65 years of age and older, and responsible for a large proportion of the costs associated with joint replacement surgery and other direct and indirect health costs(I-10). As the population in the United States ages, this problem can only be expected to increase(9). Despite the high personal and societal costs of knee and hip OA, few modifiable risk factors for its occurrence or progression have been identified (11; 12). Heavy metals are ubiquitous, and exposure through drinking water, contaminated food, pesticides, and other means, is widespread in our society(13-18). This proposal introduces chronic metal exposures as novel, potentially modifiable risk factors for thc incidence and progression of knee and hip OA and its consequences. The study population is the Johnston County Osteoarthritis Project, an ongoing longitudinal study of OA in African-Americans and Caucasians in a rural county of North Carolina. The research plan adds the collection of additional biological specimens, namely whole blood and toenails, to the already funded examinations of the cohort to establish a resource for current and future examinations of multiple metals in OA and OA-related outcomes. Whole blood will be analyzed for lead at the Centers for Disease Control and Prevention, and toenails will be analyzed for mercury and selenium by instrtmaental neutron activation analysis at the University of Missouri-Columbia Research Reactor Center. Multiple logistic regression will be used to test associations between these metals and incidence and progression of radiographic knee and hip OA, knee and hip symptoms, and disability. By dovetailing this proposal with the funded cohort, costs are minimized, and efficiency and utility maximized. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: THIRTY YEAR FOLLOW-UP OF NEGLECTED CHILDREN Principal Investigator & Institution: Widom, Cathy S.; Professor; Psychiatry; Univ of Med/Dent Nj Newark Newark, Nj 07103 Timing: Fiscal Year 2002; Project Start 14-SEP-2000; Project End 30-JUN-2005
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Summary: This is a sample of 543 documented cases of child neglect followed 30 years later. All cases were less than 11 years of age at the time the neglect/ abuse was documented. Neglect cases will be compared to cares of documented sexual abuse (N= 96) and documented physical abuse (N = 110) and a matched comparison group (N = 520). Assessments will include: (a) health status and health risk behavior; (b) economic productivity; (c) neighborhood hazards/ toxins; and (d) past and present service utilization and access to care. This study will also develop a self-report measure of neglect and assess correspondence of memories of neglect with documented history of neglect. Similar measures were developed in past research with this sample with regard to self report of childhood sexual and physical abuse. Some preliminary analyses from previous studies of this population have documented relatively high levels of health concerns, exposure to subsequent traumatic life events (e.g., rape) leading to PTSD, and relatively low SES. Within each domain of inquiry, several specific hypotheses are noted. Measures are drawn from previous epidemiological survey research, including the National Health Interview Survey, the Behavioral Risk Factor Surveillance Survey, and the Social Support measure from the Vietnam Veterans Readjustment Study. Some established questionnaires will be administered to participants to measures self esteem, locus of control, stressful life events, coping, and depression. Some limited neurobehavioral assessments will be completed, as well. Neighborhood characteristics will be assessed from census data on poverty, as well as by asking participants to describe their neighborhood during an interview. Economic productivity will be assessed using information about income, public assistance, size of home, etc. Plans are in place for a medical screening that will include immunological functioning and HIV status. The analysis plans were detailed and appropriate. Group comparisons will be made using MANOVAs with covariance, as necessary. Power analyses indicate adequate sample size, especially since the CSA and CPA groups will be aggregated for many of the analyses. Hierarchical multiple regressions are planned, as well as hierarchical linear modeling. Strategies for dealing with missing data are described. The investigators make appropriate cautions against over generalizing the results since current definitions and practices for documenting child abuse and neglect differ from those used 30 years ago. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TOXIC METAL COMPLEXATION BY DE NOVO DESIGNED PEPTIDES Principal Investigator & Institution: Pecoraro, Vincent L.; Professor; Chemistry; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2003; Project Start 09-JUN-2003; Project End 31-MAR-2008 Summary: (provided by applicant): Heavy metal poisoning by elements such as mercury, lead, cadmium, and arsenic is a significant human health problem. Understanding the interaction of heavy metals with proteins is essential for defining the mechanism of toxicity, developing ways to minimize human exposure and to provide therapeutic regimens for removal of toxic ions. Our goals are (1) to develop peptide systems that provide a groundwork for the understanding of metalloregulatory proteins and metallochaperones, (2) to develop peptidic systems that can efficiently and selectively sequester heavy metal ions from aqueous solutions, and (3) to understand the thermodynamics and kinetics of metal binding to these designed peptides. To achieve these goals we will use a de novo peptide system based on the three-stranded coiled coil peptide aggregate motif that encapsulates with high affinity single heavy metal ions and
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provides spectroscopic models of mercury, cadmium and arsenic binding sites in biological systems. We will generate high resolution structures of this peptide system in the presence and absence of these heavy metals, elucidate the kinetic and thermodynamic mechanisms of heavy metal encapsulation, and expand the array of characterized systems to transition metal ions Fe(II), Cu(I), Ni(II), Co(II) and Zn(II). We will also extend the original design to include single chain peptides that encapsulate heavy metals and coiled coils that provide different coordination environments than the original design and those that encapsulate more than one heavy metal ion. These studies will expand the foundation of knowledge that has been laid by the scientific community investigating metallopeptide design, metalloregulatory proteins and heavy metal detoxification. These objectives will develop insight into the interplay between metal coordination and apopeptide structure in defining the overall metallopeptide fold, an important aspect of metallopeptide design. Also, development of highly efficient and specific heavy metal sequestering peptides could, ultimately, provide a viable and biodegradable means of removing heavy metals from contaminated water. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TOXICOGENOMICS OF LEAD, MERCURY, AND CADMIUM Principal Investigator & Institution: Ruden, Douglas M.; Environmental Health Sciences; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 15-MAR-2002; Project End 31-JAN-2004 Summary: Human activity has resulted in the environmental distribution of many toxic substances, among them the heavy metals that are spread throughout our biosphere. In addition to acute toxic effects in the humans exposed to heavy metals there are more insidious effects of chronic exposure on the development of all organisms. The resulting altered developmental processes produce in human children symptoms such as hyperactivity, changes in sensory function, and changes in cognitive abilities (IQ). Drosophila is a promising model organism to study the effects of heavy metal exposure during development because of (1) the sophisticated understanding of its genetics, and the ease of manipulating its genome; (2) availability of behavioral and morphological assays sensitive to small doses of toxins. Both human and Drosophila cells are thought to induce expression of protective genes upon exposure to certain toxicants. The hypothesis of this proposal is that over-expressing some of the "protective genes" induced by heavy metals will make flies resistant to the behavioral and developmental alterations caused by heavy metal exposure, and conversely, that knocking out some of these genes might make flies more sensitive to heavy metal exposure. To test this hypothesis, Aim 1 is to expose the larvae to environmentally relevant doses of lead, mercury, and cadmium, and to provide data on their effects on cognition, locomotion and synaptic function. Aim 2 is to perform DNA microarray analysis heavy metalexposed larvae (exposure will be to NOAEL, LOAEL, and LD50, as determined in the Aim 1, and determine what subsets of genes are most affected, either positively or negatively. Aim 3 is to upregulate, by conditional overexpression, or down regulate, by using existing mutations, the genes with the most significant changes in expression and to determine the effects of the test chemicals on cognition, locomotion, and synaptic function of these genetically altered flies. Results of these studies will identify candidates for the most important genes that are altered during heavy metal exposure in humans, and could well lead to bioassays or treatments for heavy metal exposure at or below NOAEL and LOAEL values. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Lead Poisoning
Project Title: TOXICOLOGY OF METAL INDUCED IMMUNOPATHOLOGY Principal Investigator & Institution: Lawrence, David A.; Lab Chief & Professor; Wadsworth Center Empire State Plaza Albany, Ny 12237 Timing: Fiscal Year 2001; Project Start 01-JUN-1998; Project End 31-MAY-2004 Summary: (Adapted from the investigator's abstract). The long-term goal of this project is to determine the mechanism(s) by which an environmental agent such as lead (Pb) interplays with genetics to influence the onset of an autoimmune disease such as Systemic Lupus Erythematosus (SLE). Susceptibility to SLE is known to be under complex polygenic control and is thought to be influenced by environmental agents capable of modulating the immune system of individuals with a genetic liability. The goal of this proposal is to pursue the hypothesis that environmental toxicants contribute to the triggering and exacerbation of SLE. The focus will be on the effects of Pb on susceptibility to SLE by taking advantage of a new model in New Zealand Mixed (NZM) strains of mice. These recombinant inbred strains were derived from the parental strains of the classic NZB x NZW Fl hybrid female SLE model; the mixtures of susceptibility genes, inherited from the ancestral genomes by recombination and segregation, contribute to phenotypic differences of nephritis, CNS lupus, and other autoimmune phenotypes. The NZM strains, therefore, offer a new way of looking at the effects of the environment on triggering or exacerbating SLE in a closely related set of lupus-prone, H-2 identical strains. The novel advantage is that some NZM strains with partial or low penetrance of autoimmunity may be more informative than mice at the extremes of susceptibility or resistance. The Specific Aims are: (1) determine the effects of Pb exposure on the time course, severity, morphogenesis, and immunopathology of autoimmune immune-complex-mediated nephritis and CNS pathology in selected NZM strains with high, partial, and low penetrance. (2) ascertain effects of Pb on manifestations of B-cell autoimmunity to include strain-specific patterns of anti-dsDNA and anti-chromatin autoantibody profiles, Coombs' positivity (anti-erythrocyte autoantibodies), anti-phospholipid, and B-cell hyperactivity. (3) assess T-cell activation and cytokine profiles (IL-2 and IFNg vs IL-4 and IL-5) and accessory cytokine levels (IL1, IL-6 and TNFa) and 4 evaluate the involvement of hormonal patterns in disease modulation. The proposed research will provide basic information on the effects of Pb on SLE susceptibility in individuals with variable numbers of threshold liability genes, in identifying SLE genes, and a general understanding of the extent to which environmental factors may influence autoimmunity and autoimmune disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TREATMENT OF LEAD EXPOSED CHILDREN FOLLOW UP Principal Investigator & Institution: Bornschein, Robert L.; Professor; Environmental Health; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2002; Project Start 01-AUG-1999; Project End 28-FEB-2004 Summary: The Treatment of Lead-Exposed Children (TLC) clinical trial was carried out in four large urban pediatric departments. The study was designed to test the hypothesis that children with moderate blood lead concentrations who were treated with succimer would have higher scores than placebo treated children on a range of tests measuring cognitive and behavioral development three years after treatment. TLC randomized 384 children to placebo and 396 to succimer between August 1994, and January, 1997. Recognizing that the most important effects of early lead exposure are difficult to assess prior to school age, TLC-Plus is designed to assess the long-term developmental benefits of oral chelation therapy with succimer. The study's principal
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aim is to determine whether succimer is effective in ameliorating the adverse impact of early lead toxicity on neuropsychological functioning behavior and social adjustment. A state of the art, efficient assessment battery will be administered to TLC-Plus subjects at all Clinical Centers in two sessions following their seventh birthday. At this age, a wider and more differentiated range of abilities can be examined, scores on psychometric measures are more precise and reliable, and early academic performance and social functioning outside of the home environment can be evaluated. Assessments of psychometric, psycho educational, social-adaptive, and neurological functioning will be made Instruments tapping these domains will be administered to TLC subjects when they attain 7 and 7.5 years of age. Intent-to-treat data analyses will examine the impact of treatment on these domains using analysis of covariance and repeated measures methods. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TREATMENT OF LEAD IN CHILDREN Principal Investigator & Institution: Schwarz, Donald; Children's Hospital of Philadelphia 34Th St and Civic Ctr Blvd Philadelphia, Pa 19104 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.3 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with lead poisoning, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “lead poisoning” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for lead poisoning (hyperlinks lead to article summaries): •
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A case of lead poisoning due to snooker chalk. Author(s): Dargan PI, Evans PH, House IM, Jones AL. Source: Archives of Disease in Childhood. 2000 December; 83(6): 519-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11087293
PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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A community-developed, community-based lead poisoning prevention program: Lead Awareness North Philly Style. Author(s): Rothman NL, Lourie R, Gaughan J, White N. Source: Holistic Nursing Practice. 1999 October; 14(1): 47-58. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12119980
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A comparison of two dosing regimens of succimer in children with chronic lead poisoning. Author(s): Farrar HC, McLeane LR, Wallace M, White K, Watson J. Source: Journal of Clinical Pharmacology. 1999 February; 39(2): 180-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11563411
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A global approach to childhood lead poisoning prevention. Author(s): Meyer PA, McGeehin MA, Falk H. Source: International Journal of Hygiene and Environmental Health. 2003 August; 206(45): 363-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12971691
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A molecular epidemiological study of childhood lead poisoning in lead-polluted environment. Author(s): Zheng Y, Leng S, Song W, Wang Y, Niu Y, Zhang W, Yan H, Liu Y, Huang Q, Wu Y. Source: Zhonghua Liu Xing Bing Xue Za Zhi. 2002 June; 23(3): 175-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12411083
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A presumptive case of lead poisoning in a brass-worker's child. Author(s): Sathaye AU, Javadekar BB. Source: J Indian Med Assoc. 2000 August; 98(8): 457-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11294328
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A randomized trial of calcium supplementation for childhood lead poisoning. Author(s): Markowitz ME, Sinnett M, Rosen JF. Source: Pediatrics. 2004 January; 113(1 Pt 1): E34-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14702492
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A simple fluorometric assay of protoporphyrin in erythrocytes (EPP) as a screening test for lead poisoning. Author(s): Orfanos AP, Murphey WH, Guthrie R. Source: The Journal of Laboratory and Clinical Medicine. 1977 March; 89(3): 659-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=839124
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Acute lead poisoning in children. Author(s): Greaves SJ. Source: N Z Med J. 1978 May 24; 87(612): 366. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=276719
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Acute lead poisoning: an unusual cause of hepatitis. Author(s): Beattie AD, Mullin PJ, Baxter RH, Moore MR. Source: Scott Med J. 1979 October; 24(4): 318-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=555820
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Acute pediatric lead poisoning: combined whole bowel irrigation, succimer therapy, and endoscopic removal of ingested lead pellets. Author(s): Clifton JC 2nd, Sigg T, Burda AM, Leikin JB, Smith CJ, Sandler RH. Source: Pediatric Emergency Care. 2002 June; 18(3): 200-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12066009
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Adult lead poisoning from a herbal medicine. Author(s): Ibrahim AS, Latif AH. Source: Saudi Med J. 2002 May; 23(5): 591-3. Erratum In: Saudi Med J 2002 July; 23(7): 879. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12070589
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Adverse effects of reduced-dose d-penicillamine in children with mild-to-moderate lead poisoning. Author(s): Shannon MW, Townsend MK. Source: The Annals of Pharmacotherapy. 2000 January; 34(1): 15-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10669180
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Advisability of colonoscopy in the management of ingested lead poisoning. Author(s): Gleason WA Jr. Source: Archives of Pediatrics & Adolescent Medicine. 1998 December; 152(12): 1247. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9856441
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Alterations in the activity of enzymes of haem biosynthesis in lead poisoning and acute hepatic prophyria. Author(s): Campbell BC, Brodie MJ, Thompson GG, Meredith PA, Moore MR, Goldberg A. Source: Clin Sci Mol Med. 1977 October; 53(4): 335-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=913057
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An artificial gene for human porphobilinogen synthase allows comparison of an allelic variation implicated in susceptibility to lead poisoning. Author(s): Jaffe EK, Volin M, Bronson-Mullins CR, Dunbrack RL Jr, Kervinen J, Martins J, Quinlan JF Jr, Sazinsky MH, Steinhouse EM, Yeung AT. Source: The Journal of Biological Chemistry. 2000 January 28; 275(4): 2619-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10644722
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An unusual case of lead poisoning in an infant: nursing-associated plumbism. Author(s): Kokori H, Giannakopoulou CH, Hatzidaki E, Athanaselis S, Tsatsakis A, Sbyrakis S. Source: The Journal of Laboratory and Clinical Medicine. 1999 November; 134(5): 522-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10560946
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Assessing lay health advisor activity in an intervention to prevent lead poisoning in Native American children. Author(s): Kegler MC, Stern R, Whitecrow-Ollis S, Malcoe LH. Source: Health Promotion Practice. 2003 April; 4(2): 189-96. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14610989
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Assessment of cleaning to control lead dust in homes of children with moderate lead poisoning: treatment of lead-exposed children trial. Author(s): Ettinger AS, Bornschein RL, Farfel M, Campbell C, Ragan NB, Rhoads GG, Brophy M, Wilkens S, Dockery DW. Source: Environmental Health Perspectives. 2002 December; 110(12): A773-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12460817
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Association between iron deficiency and low-level lead poisoning in an urban primary care clinic. Author(s): Wright RO, Shannon MW, Wright RJ, Hu H. Source: American Journal of Public Health. 1999 July; 89(7): 1049-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10394314
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Bal therapy in human lead poisoning. Author(s): Flora SJ, Singh S, Tandon SK. Source: Indian Journal of Medical Sciences. 1985 August; 39(8): 187-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4065937
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BAL, EDTA, DMSA and DMPS in the treatment of lead poisoning in children. Author(s): Chisolm JJ Jr. Source: Journal of Toxicology. Clinical Toxicology. 1992; 30(4): 493-504. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1331490
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Behavioural change associated with chronic lead poisoning in working dogs. Author(s): Nicholls TJ, Handson PD. Source: The Veterinary Record. 1983 June 25; 112(26): 607. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6879989
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Biomedical communication and the reaction to the Queensland childhood lead poisoning cases elsewhere in the world. Author(s): Burnham JC. Source: Medical History. 1999 April; 43(2): 155-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10885137
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Bite the bullet: lead poisoning after ingestion of 206 lead bullets. Author(s): McNutt TK, Chambers-Emerson J, Dethlefsen M, Shah R. Source: Vet Hum Toxicol. 2001 October; 43(5): 288-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11577935
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Blood lead levels and risk factors for lead poisoning among children in a Mexican smelting community. Author(s): Albalak R, McElroy RH, Noonan G, Buchanan S, Jones RL, Flanders WD, Gotway-Crawford C, Kim D, Dignam T, Daley WR, Jarrett J, Eduardo E, McGeehin MA. Source: Archives of Environmental Health. 2003 March; 58(3): 172-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14535578
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Blood lead levels and risk factors for lead poisoning among children in Jakarta, Indonesia. Author(s): Albalak R, Noonan G, Buchanan S, Flanders WD, Gotway-Crawford C, Kim D, Jones RL, Sulaiman R, Blumenthal W, Tan R, Curtis G, McGeehin MA. Source: The Science of the Total Environment. 2003 January 1; 301(1-3): 75-85. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12493187
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Breaking the childhood lead poisoning cycle--a program for community casefinding and self-help. Author(s): Challop R, McCabe E, Reece R. Source: American Journal of Public Health. 1972 May; 62(5): 655-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5024290
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Bullet appendicitis. A new form of lead poisoning. Author(s): Rydell WB Jr. Source: Rocky Mt Med J. 1970 March; 67(3): 48-50. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5418821
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Bullets, lead poisoning and thyrotoxicosis. Author(s): Cagin CR, Diloy-Puray M, Westerman MP. Source: Annals of Internal Medicine. 1978 October; 89(4): 509-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=697230
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Can antioxidants be beneficial in the treatment of lead poisoning? Author(s): Gurer H, Ercal N. Source: Free Radical Biology & Medicine. 2000 November 15; 29(10): 927-45. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11084283
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Cerebellar calcification: a possible marker of lead poisoning. Author(s): Tonge JI, Burry AF, Saal JR. Source: Pathology. 1977 October; 9(4): 289-300. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=201908
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Childhood lead poisoning from paint chips: a continuing problem. Author(s): Su M, Barrueto F Jr, Hoffman RS. Source: Journal of Urban Health : Bulletin of the New York Academy of Medicine. 2002 December; 79(4): 491-501. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12468669
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Childhood lead poisoning in Arkansas. Author(s): Blackwood RR. Source: J Ark Med Soc. 1977 June; 74(1): 77-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=141444
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Childhood lead poisoning in North Carolina: experience in Wilmington. Author(s): Gehlbach SH, West B, Morris J, Summey E, Reynolds FR. Source: N C Med J. 1977 July; 38(7): 383-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=267807
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Childhood lead poisoning investigations: evaluating a portable instrument for testing soil lead. Author(s): Reames G, Lance LL. Source: Journal of Environmental Health. 2002 April; 64(8): 9-13, 25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11930816
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Childhood Lead Poisoning Prevention Program Memphis and Shelby County Health Department. Author(s): Madlock YS, Bradley E. Source: Tenn Med. 2002 October; 95(10): 418-20. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12369542
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Childhood lead poisoning. Author(s): Piomelli S. Source: Pediatric Clinics of North America. 2002 December; 49(6): 1285-304, Vii. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12580366
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Childhood lead poisoning: a re-evaluation. Author(s): David OJ, Clark J, Hoffman S. Source: Archives of Environmental Health. 1979 March-April; 34(2): 106-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=434930
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Choosing area based socioeconomic measures to monitor social inequalities in low birth weight and childhood lead poisoning: The Public Health Disparities Geocoding Project (US). Author(s): Krieger N, Chen JT, Waterman PD, Soobader MJ, Subramanian SV, Carson R. Source: Journal of Epidemiology and Community Health. 2003 March; 57(3): 186-99. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12594195
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Chronic lead poisoning: induced psychosis in an adult? Author(s): Kohlmeier RE. Source: The American Journal of Forensic Medicine and Pathology : Official Publication of the National Association of Medical Examiners. 2002 March; 23(1): 101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11953505
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Clinical lead poisoning in England: an analysis of routine sources of data. Author(s): Elliott P, Arnold R, Barltrop D, Thornton I, House IM, Henry JA. Source: Occupational and Environmental Medicine. 1999 December; 56(12): 820-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10658538
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Clinician follow-up of children screened for lead poisoning. Author(s): Markowitz M, Rosen JF, Clemente I. Source: American Journal of Public Health. 1999 July; 89(7): 1088-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10394321
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Collaborating with private sector physicians: the example of childhood lead poisoning prevention. Author(s): Schlenker TL. Source: Journal of Public Health Management and Practice : Jphmp. 1999 November; 5(6): 35-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10662062
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Community-based screening for childhood lead poisoning. Identification of risk factors and susceptible populations in Duluth. Author(s): Bronson MA, Tilden RL, Renier CM. Source: Minn Med. 1999 January; 82(1): 25-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10073066
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Constipation causing lead poisoning? Author(s): Hodge D, Puntis JW. Source: Journal of Pediatric Gastroenterology and Nutrition. 1999 November; 29(5): 6079. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10554134
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Correlation between clinical indicators of lead poisoning and oxidative stress parameters in controls and lead-exposed workers. Author(s): Gurer-Orhan H, Sabir HU, Ozgunes H. Source: Toxicology. 2004 February 15; 195(2-3): 147-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14751670
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Cost-effectiveness analysis of lead poisoning screening strategies following the 1997 guidelines of the Centers for Disease Control and Prevention. Author(s): Kemper AR, Bordley WC, Downs SM. Source: Archives of Pediatrics & Adolescent Medicine. 1998 December; 152(12): 1202-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9856430
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Costs and benefits of enforcing housing policies to prevent childhood lead poisoning. Author(s): Brown MJ. Source: Medical Decision Making : an International Journal of the Society for Medical Decision Making. 2002 November-December; 22(6): 482-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12458978
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Cottage industry lead poisoning: this time, no paprika. Author(s): Laszloffy M, Kakosy T, Hudak A, Naray M. Source: Journal of Toxicology. Clinical Toxicology. 1999; 37(1): 117-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10078170
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Deaths related to lead poisoning in the United States, 1979-1998. Author(s): Kaufmann RB, Staes CJ, Matte TD. Source: Environmental Research. 2003 February; 91(2): 78-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12584008
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Decreasing childhood lead poisoning in New York City: 1970-1998. Author(s): Klitzman S, Leighton J. Source: Journal of Urban Health : Bulletin of the New York Academy of Medicine. 1999 December; 76(4): 542-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10609601
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Delayed primary dentition in a case of congenital lead poisoning. Author(s): Pearl M, Roland NM. Source: Asdc J Dent Child. 1980 July-August; 47(4): 269-71. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6938538
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Deleading dilemma: pitfall in the management of childhood lead poisoning. Author(s): Rey-Alvarez S, Menke-Hargrave T. Source: Pediatrics. 1987 February; 79(2): 214-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2433676
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Determination of numbers of lead-exposed American children as a function of lead source: integrated summary of a report to the U.S. Congress on childhood lead poisoning. Author(s): Mushak P, Crocetti AF. Source: Environmental Research. 1989 December; 50(2): 210-29. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2684625
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Determination of numbers of lead-exposed U.S. children by areas of the United States: an integrated summary of a report to the U.S. Congress on childhood lead poisoning. Author(s): Crocetti AF, Mushak P, Schwartz J. Source: Environmental Health Perspectives. 1990 November; 89: 109-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2088736
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Determination of numbers of lead-exposed women of childbearing age and pregnant women: an integrated summary of a report to the U.S. Congress on childhood lead poisoning. Author(s): Crocetti AF, Mushak P, Schwartz J. Source: Environmental Health Perspectives. 1990 November; 89: 121-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2088737
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Developing a system to monitor and track childhood blood lead levels. Tennessee Childhood Lead Poisoning Prevention Program. Author(s): Cook J, Younger S. Source: Tenn Med. 2002 October; 95(10): 409. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12369539
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Diagnosing lead poisoning. Author(s): Loefler IJ. Source: The New England Journal of Medicine. 1999 February 18; 340(7): 569. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10026057
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Diagnosing lead poisoning. Author(s): Abramowicz M. Source: The New England Journal of Medicine. 1999 February 18; 340(7): 569. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10026056
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Diagnosing lead poisoning. Author(s): Lawrence C. Source: The New England Journal of Medicine. 1999 February 18; 340(7): 568; Author Reply 569. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10026054
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Diagnosing lead poisoning. Author(s): Adler L, Muller D. Source: The New England Journal of Medicine. 1999 February 18; 340(7): 568; Author Reply 569. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10026053
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Diagnosis and treatment of chronic lead poisoning in CAPD patients. Author(s): Kessler M, Durand PY, Hestin D, Gamberoni J, Chanliau J. Source: Adv Perit Dial. 1993; 9: 143-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8105909
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Diagnosis of lead poisoning. Author(s): Wynchank S, Selby P, Ehrlich R, Todd AC. Source: Presse Medicale (Paris, France : 1983). 1994 November 19; 23(36): 1670. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7899297
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Diagnostic parameters for detecting early lead poisoning. Author(s): Lu CM, Wang HC, Chien TC, Miao HF. Source: Chinese Medical Journal. 1978 September; 4(5): 403-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=102500
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Did Hippocrates describe lead poisoning? Author(s): Waldron T. Source: Lancet. 1978 December 16; 2(8103): 1315. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=82824
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Dietary calcium intakes of urban children at risk of lead poisoning. Author(s): Bruening K, Kemp FW, Simone N, Holding Y, Louria DB, Bogden JD. Source: Environmental Health Perspectives. 1999 June; 107(6): 431-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10339442
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Difficult cases of lead poisoning. Author(s): Fischbein A, Wallace J. Source: Lancet. 1982 January 16; 1(8264): 170. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6119547
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Distribution of non-heme porphyrin content of individual erythrocytes by fluorescence image cytometry and its application to lead poisoning. Author(s): Sassaroli M, daCosta R, Vaananen H, Eisinger J. Source: Cytometry : the Journal of the Society for Analytical Cytology. 1992; 13(4): 33945. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1526194
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Does lead poisoning occur in Canadian children? Author(s): Tenenbein M. Source: Cmaj : Canadian Medical Association Journal = Journal De L'association Medicale Canadienne. 1990 January 1; 142(1): 40-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1688398
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Education a key to reducing the risk of lead poisoning. Author(s): May RB. Source: Rn. 1994 October; 57(10): 9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7973385
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Effect of bias in hematofluorometer measurements of protoporphyrin in screening programs for lead poisoning. Author(s): Mitchell DG, Doran D. Source: Clinical Chemistry. 1985 March; 31(3): 386-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3971558
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Effects of calcium disodium versenate (CaNa2EDTA) chelation in moderate childhood lead poisoning. Author(s): Markowitz ME, Bijur PE, Ruff H, Rosen JF. Source: Pediatrics. 1993 August; 92(2): 265-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8337028
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Efficacy and toxicity of D-penicillamine in low-level lead poisoning. Author(s): Shannon M, Graef J, Lovejoy FH Jr. Source: The Journal of Pediatrics. 1988 May; 112(5): 799-804. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3361395
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Electrophysiologic study in acute lead poisoning. Author(s): Wong VC, Ng TH, Yeung CY. Source: Pediatric Neurology. 1991 March-April; 7(2): 133-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2059254
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Electrophysiological study of subjects occupationally exposed to lead and with low levels of lead poisoning. Author(s): Bordo BM, Filippini G, Massetto N, Musicco M, Boeri R. Source: Scand J Work Environ Health. 1982; 8 Suppl 1: 142-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7100841
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Environmental lead poisoning in three Montreal women of Asian Indian origin. Author(s): Lecours S, Osterman J, Lacasse Y, Melnychuk D, Gelinas J. Source: Can Dis Wkly Rep. 1989 September 2; 15(35): 177-9. English, French. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2791074
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Environmental pollutants and disease in American children: estimates of morbidity, mortality, and costs for lead poisoning, asthma, cancer, and developmental disabilities. Author(s): Landrigan PJ, Schechter CB, Lipton JM, Fahs MC, Schwartz J. Source: Environmental Health Perspectives. 2002 July; 110(7): 721-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12117650
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Eosinophilia, lead poisoning and Toxacaris canis infection in children. Author(s): Rosenblatt JS, Porter J, Marcus S. Source: Vet Hum Toxicol. 1991 October; 33(5): 495-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1746146
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EPA faults classic lead poisoning study. A review questions a study linking lead in teeth with low IQ scores; EPA finds other grounds for regulation. Author(s): Marshall E. Source: Science. 1983 November 25; 222(4626): 906-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6688887
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Epidemic outbreak of acute lead poisoning. Author(s): Carton JA, Maradona JA, Arribas JM. Source: Archives of Internal Medicine. 1985 July; 145(7): 1334-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4015291
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Epidemiological aspects of occupational lead poisoning. Author(s): Landrigan PJ, Baker EL Jr. Source: J Uoeh. 1983 March 20; 5 Suppl: 145-55. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6679665
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Erythrocyte protoporphyrin screening for lead poisoning in Bedouin children. A study from Kuwait. Author(s): Shaltout AA, Guthrie R, Moussa M, Kandil H, Hassan MF, Dosari L, Hunt CJ, Fernando NP. Source: Journal of Tropical Pediatrics. 1989 April; 35(2): 87-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2786086
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Erythroid karyorrhexis in the peripheral blood smear in severe arsenic poisoning: a comparison with lead poisoning. Author(s): Eichner ER. Source: American Journal of Clinical Pathology. 1984 April; 81(4): 533-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6702757
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Evaluation of erythrocyte protoporphyrin and zinc protoporphyrin as micro screening procedures for lead poisoning detection. Author(s): Bush B, Doran DR, Jackson KW. Source: Annals of Clinical Biochemistry. 1982 March; 19(Pt 2): 71-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7073218
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Evaluation of the current risk of lead poisoning in the ceramics industry. Author(s): De Rosa E, Toffolo D, Sigon M, Brighenti F, Gori GP, Bartolucci GB. Source: Scand J Work Environ Health. 1983 December; 9(6): 463-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6673104
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Evolution of the management and prevention of childhood lead poisoning: dependence of advances in public health on technological advances in the determination of lead and related biochemical indicators of its toxicity. Author(s): Chisolm JJ Jr. Source: Environmental Research. 2001 June; 86(2): 111-21. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11437457
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Exaggerated threat of childhood lead poisoning in California--epidemic by edict. Author(s): Schoen EJ. Source: The Western Journal of Medicine. 1992 October; 157(4): 470. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1462556
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Experience in controlling lead poisoning in the People's Republic of China. Author(s): Gu XQ. Source: Scand J Work Environ Health. 1985; 11 Suppl 4: 16-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3832430
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Experience with D-penicillamine in treating lead poisoning. Author(s): Marcus SM. Source: Vet Hum Toxicol. 1982 February; 24(1): 18-20. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7058627
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Failure of the urinary delta-aminolevulinic acid test to detect pediatric lead poisoning. Author(s): Blanksma LA, Sachs HK, Murray EF, O'Connell MJ. Source: American Journal of Clinical Pathology. 1970 June; 53(6): 956-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5515391
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Fallacies in the diagnosis of chronic lead poisoning in industry. Author(s): Corrigan CE. Source: Manit Med Rev. 1967 December; 47(10): 559-60. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6080581
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Familial lead poisoning from contaminated wine. Author(s): Loi F, Battista G, Malentacchi GM, Paradiso C, Pompella A, Rubegni M, Federico A. Source: Italian Journal of Neurological Sciences. 1981 August; 2(3): 283-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7341551
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Family operational co-factors in the epidemiology of childhood lead poisoning. Author(s): Stark AD, Meigs JW, Fitch RA, DeLouise ER. Source: Archives of Environmental Health. 1978 September-October; 33(5): 222-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=708115
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Fast hemoglobin in lead poisoning. Author(s): Charache S, Weatherall DJ. Source: Blood. 1966 September; 28(3): 377-86. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5918470
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Feasibility and effectiveness of screening for childhood lead poisoning in private medical practice. Author(s): Schlenker TL, Fritz CJ, Murphy A, Shepeard S. Source: Archives of Pediatrics & Adolescent Medicine. 1994 July; 148(7): 761-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8019635
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Federally-assisted screening projects for childhood lead poisoning control: the first three years (July 1972-June 1975). Author(s): Hopkins DR, Houk VN. Source: American Journal of Public Health. 1976 May; 66(5): 485-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1275126
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Fluorometric assay of erythrocyte protoporphyrin: simple screening test for lead poisoning and iron deficiency. Author(s): Paton TJ, Cembrowski GS. Source: Can Med Assoc J. 1982 November 1; 127(9): 860-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7139505
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Free erythrocyte protoporphyrin (FEP) and zinc protoporphyrin (ZnP) as biological parameters for lead poisoning. Author(s): Harada K, Miura H. Source: International Archives of Occupational and Environmental Health. 1984; 53(4): 365-77. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6715060
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Free erythrocyte protoporphyrin and zinc protoporphyrin measurements compared as primary screening methods for detection of lead poisoning. Author(s): Kaul B, Slavin G, Davidow B. Source: Clinical Chemistry. 1983 August; 29(8): 1467-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6872205
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Free radicals involvement in neurological porphyrias and lead poisoning. Author(s): Monteiro HP, Bechara EJ, Abdalla DS. Source: Molecular and Cellular Biochemistry. 1991 April 24; 103(1): 73-83. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1857346
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Further cases of lead poisoning from wine. Author(s): Perrelli G, Capellaro E, Pira E, Maina G, Vergnano P. Source: American Journal of Industrial Medicine. 1984; 5(5): 377-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6720696
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Further observations on the mechanical fragility of the red cell in lead poisoning. Author(s): De Kretser AJ, Waldron HA. Source: Br J Ind Med. 1965 October; 22(4): 315-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5836573
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Gasoline sniffing and lead poisoning in a child. Author(s): Chessare JB, Wodarcyk K. Source: American Family Physician. 1988 July; 38(1): 181-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3394603
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Gasoline sniffing and lead poisoning. Author(s): Moss MA, Cooper PJ. Source: Acta Pharmacol Toxicol (Copenh). 1986; 59 Suppl 7: 48-51. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3776613
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Gasoline sniffing and tetraethyl lead poisoning in children. Author(s): Boeckx RL, Postl B, Coodin FJ. Source: Pediatrics. 1977 August; 60(2): 140-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=887326
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Gasoline sniffing, lead poisoning, and myoclonus. Author(s): Hansen KS, Sharp FR. Source: Jama : the Journal of the American Medical Association. 1978 September 22; 240(13): 1375-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=682330
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Genetic susceptibility to lead poisoning. Author(s): Onalaja AO, Claudio L. Source: Environmental Health Perspectives. 2000 March; 108 Suppl 1: 23-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10698721
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Gingival pigmentation as the sole presenting sign of chronic lead poisoning in a mentally retarded adult. Author(s): Lockhart PB. Source: Oral Surg Oral Med Oral Pathol. 1981 August; 52(2): 143-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6943483
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GIS and decision making for public health agencies: childhood lead poisoning and welfare reform. Author(s): Hanchette CL. Source: Journal of Public Health Management and Practice : Jphmp. 1999 July; 5(4): 41-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10538413
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Great debate on environmental lead poisoning in the U.S.A.: a historical analysis. Author(s): Kim OJ, Cho SI, Hwang SI. Source: Uisahak. 1999; 8(1): 69-77. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11624465
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Greta and Azarcon: a survey of episodic lead poisoning from a folk remedy. Author(s): Trotter RT 2nd. Source: Hum Organ. 1985 Spring; 44(1): 64-72. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10270259
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Hair and blood as substrates for screening children for lead poisoning. Author(s): Esteban E, Rubin CH, Jones RL, Noonan G. Source: Archives of Environmental Health. 1999 November-December; 54(6): 436-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10634234
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Hazards of 'deleading' homes of children with lead poisoning. Author(s): Amitai Y, Graef JW, Brown MJ, Gerstle RS, Kahn N, Cochrane PE. Source: Am J Dis Child. 1987 July; 141(7): 758-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2438931
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Health education, public policy and disease prevention: a case history of the New York City Coalition to End Lead Poisoning. Author(s): Freudenberg N, Golub M. Source: Health Educ Q. 1987 Winter; 14(4): 387-401. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3319970
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Health effects of lead at low exposure levels. Expert consensus and rationale for lowering the definition of childhood lead poisoning. Author(s): Rosen JF. Source: Am J Dis Child. 1992 November; 146(11): 1278-81. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1415061
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Height and weight following lead poisoning in childhood. Author(s): Sachs HK, Moel DI. Source: Am J Dis Child. 1989 July; 143(7): 820-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2741854
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Hematologic and biochemical studies in a case of lead poisoning. Author(s): Berk PD, Tschudy DP, Shepley LA, Waggoner JG, Berlin NI. Source: The American Journal of Medicine. 1970 January; 48(1): 137-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4984424
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Hemolytic anemia associated with lead poisoning from shotgun pellets and the response to Succimer treatment. Author(s): Aly MH, Kim HC, Renner SW, Boyarsky A, Kosmin M, Paglia DE. Source: American Journal of Hematology. 1993 December; 44(4): 280-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8238001
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Hepatitis caused by acute lead poisoning. Author(s): Beattie AD. Source: Med Chir Dig. 1981; 10(4): 309-10. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7300483
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Hidden threats: lead poisoning from unusual sources. Author(s): Jones TF, Moore WL, Craig AS, Reasons RL, Schaffner W. Source: Pediatrics. 1999 November; 104(5 Pt 2): 1223-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10545579
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High incidence of lead poisoning revealed by erythrocyte protoporphyrin (EPP) screening in Arabian children. Author(s): Shaltout AA, Ghawaby MM, Hassan MF, Hunt MC, Fernando N, Devarajan LV, Kollberg H, Guthrie R. Source: Annals of Tropical Paediatrics. 1985 December; 5(4): 207-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2418770
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Home abatement and blood lead changes in children with class III lead poisoning. Author(s): Swindell SL, Charney E, Brown MJ, Delaney J. Source: Clinical Pediatrics. 1994 September; 33(9): 536-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8001322
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How to diagnose and treat lead poisoning in children. Author(s): Browder A. Source: Med Times. 1972 October; 100(10): 203-4 Passim. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5073971
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Identification of children at risk for lead poisoning: an evaluation of routine pediatric blood lead screening in an HMO-insured population. Author(s): Haan MN, Gerson M, Zishka BA. Source: Pediatrics. 1996 January; 97(1): 79-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8545230
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In the air that they breathe. Lead poisoning remains a major health hazard for America's children. Author(s): Spake A, Couzin J. Source: U.S. News & World Report. 1999 December 20; 127(24): 54-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10724814
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Incidence of lead poisoning in young children from inner-city, suburban, and rural communities. Author(s): Rifai N, Cohen G, Wolf M, Cohen L, Faser C, Savory J, DePalma L. Source: Therapeutic Drug Monitoring. 1993 April; 15(2): 71-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8389068
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Increased lead absorption and lead poisoning from a retained bullet. Author(s): Fiorica V, Brinker JE. Source: J Okla State Med Assoc. 1989 February; 82(2): 63-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2926538
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Increased lead poisoning diagnoses may precede possible eradication of problem. Author(s): Zylke JW. Source: Jama : the Journal of the American Medical Association. 1991 July 17; 266(3): 316-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1647467
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Index of suspicion. Case 1. Toxocara canis and Ascaris infection with lead poisoning] Author(s): Kidd J, Batisky DL. Source: Pediatrics in Review / American Academy of Pediatrics. 1995 November; 16(11): 433, 434. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8539194
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Industrial lead poisoning and the family physician. Author(s): Christophers AJ. Source: Aust Fam Physician. 1977 September; 6(9): 1084-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=911267
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Influence of documented lead poisoning on environmental modification programs in Newark, New Jersey. Author(s): Foster JD, Louria DB, Stinson L. Source: Archives of Environmental Health. 1979 September-October; 34(5): 368-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=496435
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Influence of nutrient intake on blood lead levels of young children at risk for lead poisoning. Author(s): Gallicchio L, Scherer RW, Sexton M. Source: Environmental Health Perspectives. 2002 December; 110(12): A767-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12460816
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Inorganic lead poisoning in an adult. Author(s): Spaedy S, Schubert TT. Source: The American Journal of Gastroenterology. 1988 May; 83(5): 581-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3364417
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Intercurrent infection in lead poisoning. Author(s): Sachs HK. Source: Am J Dis Child. 1978 March; 132(3): 315-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=629250
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International environmental health for the pediatrician: case study of lead poisoning. Author(s): Falk H. Source: Pediatrics. 2003 July; 112(1 Pt 2): 259-64. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12837919
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Intracranial vascular calcifications, glioblastoma multiforme, and lead poisoning. Author(s): Teo JG, Goh KY, Ahuja A, Ng HK, Poon WS. Source: Ajnr. American Journal of Neuroradiology. 1997 March; 18(3): 576-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9090426
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Intramuscular administration of iron during long-term chelation therapy with 2,3dimercaptosuccinic acid in a man with severe lead poisoning. Author(s): Haust HL, Inwood M, Spence JD, Poon HC, Peter F. Source: Clinical Biochemistry. 1989 June; 22(3): 189-96. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2544323
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IQ following treatment of lead poisoning: a patient-sibling comparison. Author(s): Sachs HK, Krall V, McCaughran DA, Rozenfeld IH, Yongsmith N, Growe G, Lazar BS, Novar L, O'Connell L, Rayson B. Source: The Journal of Pediatrics. 1978 September; 93(3): 428-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=99504
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Is eye cosmetic a source of lead poisoning? Author(s): Nir A, Tamir A, Zelnik N, Iancu TC. Source: Isr J Med Sci. 1992 July; 28(7): 417-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1506164
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Is lead poisoning still a problem? Author(s): Chisolm JJ Jr. Source: Clinical Chemistry. 1977 February; 23(2 Pt. 1): 252-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=832387
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Is screening for lead poisoning justified? Author(s): Denham AC, Collins LJ. Source: The Journal of Family Practice. 2003 September; 52(9): 722-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12967549
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Isotope ratios and the source of lead in lead poisoning. Author(s): Manton WI. Source: Journal of Toxicology. Clinical Toxicology. 1998; 36(7): 705-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9865238
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It takes awareness and vigilance to stop lead poisoning. Author(s): Sokoloski M. Source: Rn. 1993 August; 56(8): 10-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8362180
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Lead poisoning -- plumbeous alcoholic hepatopathy and amino-levulinedehydrathasis enzymes. Author(s): Huberman E, Astolfi E, Gotelli C, Vasquez Leon E. Source: Vet Hum Toxicol. 1979; 21 Suppl: 222-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=574333
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Lead poisoning and brain tumors in children: a report of 2 cases. Author(s): Schreier HA, Sherry N, Shaughnessy E. Source: Annals of Neurology. 1977 June; 1(6): 599-600. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=883776
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Lead poisoning from a gunshot wound. Report of a case and review of the literature. Author(s): Dillman RO, Crumb CK, Lidsky MJ. Source: The American Journal of Medicine. 1979 March; 66(3): 509-14. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=373435
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Lead poisoning from aphrodisiacs: potential hazard in immigrants. Author(s): Brearley RL, Forsythe AM. Source: British Medical Journal. 1978 December 23-30; 2(6154): 1748-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=737477
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Lead poisoning from cosmetics. Author(s): Waldron HA. Source: Lancet. 1979 November 17; 2(8151): 1070-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=91802
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Lead poisoning from sniffing gasoline. Author(s): Coodin FJ, Boeckx R. Source: The New England Journal of Medicine. 1978 February 9; 298(6): 347. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=622102
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Lead poisoning in a group of demolition workers. Author(s): Campbell BC, Baird AW. Source: Br J Ind Med. 1977 November; 34(4): 298-304. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=412513
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Lead poisoning in adults. Author(s): Ayoola EA. Source: Niger Med J. 1979 February; 9(2): 185-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=543257
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Lead poisoning in children in Madras city. Author(s): Santhanakrishnan BR, Bai TP. Source: Indian Pediatrics. 1978 June; 15(6): 469-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=721262
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Lead poisoning in children. Author(s): Alli BA. Source: Journal of the National Medical Association. 1977 November; 69(11): 797-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=752732
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Lead poisoning in children--what price shall we pay? Author(s): Lin-Fu JS. Source: Children Today. 1979 January-February; 8(1): 9-13, 36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=436547
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Lead poisoning in South Carolina. Author(s): Whitlock NH, Reigart JR, Priester LE. Source: J S C Med Assoc. 1977 August; 73(8): 378-80. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=268471
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Lead poisoning treated with haemodialysis. Author(s): Pedersen RS. Source: Scandinavian Journal of Urology and Nephrology. 1978; 12(2): 189-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=99808
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Lead poisoning without encephalopathy. Effect of early diagnosis on neurologic and psychologic salvage. Author(s): Sachs HK, McCaughran DA, Krall V, Rozenfeld IH, Yongsmith N. Source: Am J Dis Child. 1979 August; 133(8): 786-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=463833
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Lead poisoning. Author(s): Pincus D, Saccar CV. Source: American Family Physician. 1979 June; 19(6): 120-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=110123
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Lead poisoning. Author(s): McCabe EB. Source: The New England Journal of Medicine. 1978 June 1; 298(22): 1261-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=651972
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Lead poisoning. A comprehensive review and report of a case. Author(s): Gordon NC, Brown S, Khosla VM, Hansen LS. Source: Oral Surg Oral Med Oral Pathol. 1979 June; 47(6): 500-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=108646
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Lead poisoning. Further observations on erythrocyte pyrimidine-nucleotidase deficiency and intracellular accumulation of pyrimidine nucleotides. Author(s): Paglia DE, Valentine WN, Fink K. Source: The Journal of Clinical Investigation. 1977 December; 60(6): 1362-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=915002
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Lead poisoning: a veterinary responsibility? Author(s): McLeavey BJ. Source: New Zealand Veterinary Journal. 1979 October; 27(10): 199. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=295098
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Lead-contaminated health food. Association with lead poisoning and leukemia. Author(s): Crosby WH. Source: Jama : the Journal of the American Medical Association. 1977 June 13; 237(24): 2627-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=266087
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Management of childhood lead poisoning. Author(s): Piomelli S, Rosen JF, Chisolm JJ Jr, Graef JW. Source: The Journal of Pediatrics. 1984 October; 105(4): 523-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6481529
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Management of childhood lead poisoning: a survey. Author(s): Glotzer DE, Bauchner H. Source: Pediatrics. 1992 April; 89(4 Pt 1): 614-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1313555
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Management of childhood lead poisoning: clinical impact and cost-effectiveness. Author(s): Glotzer DE, Freedberg KA, Bauchner H. Source: Medical Decision Making : an International Journal of the Society for Medical Decision Making. 1995 January-March; 15(1): 13-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7898292
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Management of childhood lead poisoning: strategies for chelation. Author(s): Glotzer DE. Source: Pediatric Annals. 1994 November; 23(11): 606-12, 615. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7838613
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Management of lead poisoning from ingested fishing sinkers. Author(s): Mowad E, Haddad I, Gemmel DJ. Source: Archives of Pediatrics & Adolescent Medicine. 1998 May; 152(5): 485-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9605033
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Mapping for prevention: GIS models for directing childhood lead poisoning prevention programs. Author(s): Miranda ML, Dolinoy DC, Overstreet MA. Source: Environmental Health Perspectives. 2002 September; 110(9): 947-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12204831
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Maternal perceptions of lead poisoning in children with normal and elevated lead levels. Author(s): Anderson RL, Whitwell JK, Snyder SA, Besunder JB. Source: Journal of Pediatric Health Care : Official Publication of National Association of Pediatric Nurse Associates & Practitioners. 1999 March-April; 13(2): 62-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10382466
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Maternal-fetal lead poisoning from a 15-year-old bullet. Author(s): Raymond LW, Ford MD, Porter WG, Saxe JS, Ullrich CG. Source: J Matern Fetal Neonatal Med. 2002 January;11(1):63-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12380612
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Measurement of free erythrocyte protoporphyrin in blood collected on filter paper as a screening test to detect lead poisoning in children. Author(s): Davidow B, Slavin G, Piomelli S. Source: Ann Clin Lab Sci. 1976 May-June; 6(3): 209-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=942180
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Meso-2,3-dimercaptosuccinic acid in the diagnosis and treatment of lead poisoning. Author(s): Bentur Y, Brook JG, Behar R, Taitelman U. Source: Journal of Toxicology. Clinical Toxicology. 1987; 25(1-2): 39-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3035204
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Methods for reducing lead exposure in young children and other risk groups: an integrated summary of a report to the U.S. Congress on childhood lead poisoning. Author(s): Mushak P, Crocetti AF. Source: Environmental Health Perspectives. 1990 November; 89: 125-35. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2088738
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Mixed urinary incontinence secondary to lead poisoning. Author(s): Crewalk JA, Shenot PJ, Rivas DA, Chancellor MB. Source: The Journal of Urology. 1996 June; 155(6): 2029. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8618319
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Moderate lead poisoning: trends in blood lead levels in unchelated children. Author(s): Markowitz ME, Bijur PE, Ruff HA, Balbi K, Rosen JF. Source: Environmental Health Perspectives. 1996 September; 104(9): 968-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8899376
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Molecular characterization of the human delta-aminolevulinate dehydratase 2 (ALAD2) allele: implications for molecular screening of individuals for genetic susceptibility to lead poisoning. Author(s): Wetmur JG, Kaya AH, Plewinska M, Desnick RJ. Source: American Journal of Human Genetics. 1991 October; 49(4): 757-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1716854
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Moonshine, lead poisoning, and pragmatism. Author(s): Kirkland LR. Source: Archives of Internal Medicine. 1994 February 14; 154(3): 348, 351. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8297205
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Mouthing activities and their relationship to lead poisoning. Author(s): Marcus SM, Damaso-Diaz R, Ziering R. Source: J Med Soc N J. 1978 November; 75(12): 837-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=280697
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Multiple system involvement in chronic lead poisoning. Author(s): Marcus SM. Source: Vet Hum Toxicol. 1981 December; 23(6): 424-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7336566
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Mythology of lead poisoning. Author(s): Banner W Jr, Vuignier BI, Pappas JB. Source: Pediatrics. 1993 January; 91(1): 161-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8416491
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Mythology of lead poisoning. Author(s): Lakatos L. Source: Pediatrics. 1993 January; 91(1): 160; Author Reply 161. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8416490
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Myths & facts. about lead poisoning. Author(s): Quillen T. Source: Nursing. 1993 August; 23(8): 26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8361686
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Need for the lead mobilization test in children with lead poisoning. Author(s): Markowitz ME, Rosen JF. Source: The Journal of Pediatrics. 1991 August; 119(2): 305-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1907320
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Neonatal lead poisoning from maternal pica behavior during pregnancy. Author(s): Hamilton S, Rothenberg SJ, Khan FA, Manalo M, Norris KC. Source: Journal of the National Medical Association. 2001 September; 93(9): 317-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11560285
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Neonatal lead poisoning. An unusual clinical manifestation. Author(s): Sensirivatana R, Supachadhiwong O, Phancharoen S, Mitrakul C. Source: Clinical Pediatrics. 1983 August; 22(8): 582-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6407798
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Nephropathy in chronic lead poisoning. Author(s): Lilis R, Gavrilescu N, Nestorescu B, Dumitriu C, Roventa A. Source: Br J Ind Med. 1968 July; 25(3): 196-202. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5663423
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Nephropathy in chronic lead poisoning. Author(s): Morgan JM, Hartley MW, Miller RE. Source: Archives of Internal Medicine. 1966 July; 118(1): 17-29. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5940188
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Neurologic concepts of lead poisoning in children. Author(s): Goldstein GW. Source: Pediatric Annals. 1992 June; 21(6): 384-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1620563
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Neurological picture of lead poisoning. Author(s): Feldman RG. Source: Acta Neurologica Scandinavica. Supplementum. 1982; 92: 185-99. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6962651
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Neuropsychological assessment after lead poisoning without encephalopathy. Author(s): Sachs HK, Krall V, Drayton MA. Source: Percept Mot Skills. 1982 June; 54(3 Pt 2): 1283-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7110870
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Neuropsychological manifestations of lead poisoning. Author(s): Millichap JG. Source: Imj Ill Med J. 1975 February; 147(2): 170-1. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=236223
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New developments in pediatric lead poisoning. Author(s): Schonfeld DJ. Source: Current Opinion in Pediatrics. 1993 October; 5(5): 537-44. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8287076
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New screening guidelines for lead poisoning. Author(s): Fritz CJ. Source: The Nurse Practitioner. 1991 July; 16(7): 14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1870760
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New sources add to lead poisoning concerns. Author(s): Benevich T. Source: Jama : the Journal of the American Medical Association. 1990 February 9; 263(6): 790-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2296136
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Newark's fight against childhood lead poisoning. Author(s): Parker C. Source: Urban Health. 1979 September; 8(7): 37-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10243750
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Notes on modern aspects of neurotoxicosis in chronic industrial lead poisoning. Author(s): Ursan G, Suciu I. Source: J Hyg Epidemiol Microbiol Immunol. 1965; 9(4): 409-20. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5893704
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Nutritional factors in lead poisoning. Author(s): Abdulla M. Source: Nutrition Reviews. 1982 August; 40(8): 255-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7133568
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Occult lead poisoning. Author(s): Brown S, Ede R. Source: Br J Hosp Med. 1995 May 3-16; 53(9): 469. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7613722
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Occupational and environmental lead poisoning: case study of a battery recycling smelter in Taiwan. Author(s): Wang JD, Soong WT, Chao KY, Hwang YH, Jang CS. Source: J Toxicol Sci. 1998 July; 23 Suppl 2: 241-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9760474
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Occupational health and child lead poisoning: mutual interests and special problems. Author(s): King BG, Schaplowsky AF, McCabe EB. Source: American Journal of Public Health. 1972 August; 62(8): 1056-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5046444
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Occupational lead poisoning among silver jewellery workers. Author(s): Kachru DN, Tandon SK, Misra UK, Nag D. Source: Indian Journal of Medical Sciences. 1989 April; 43(4): 89-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2767754
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Occupational lead poisoning in Ohio: surveillance using workers' compensation data. Author(s): Seligman PJ, Halperin WE, Mullan RJ, Frazier TM. Source: American Journal of Public Health. 1986 November; 76(11): 1299-302. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2945445
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Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels. Author(s): Baker EL Jr, Landrigan PJ, Barbour AG, Cox DH, Folland DS, Ligo RN, Throckmorton J. Source: Br J Ind Med. 1979 November; 36(4): 314-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=508643
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Occupational lead poisoning, animal deaths, and environmental contamination at a scrap smelter. Author(s): Levine RJ, Moore RM, McLaren GD, Barthel WF, Landrigan PJ. Source: American Journal of Public Health. 1976 June; 66(6): 548-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=937600
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Occupational lead poisoning. Author(s): Sokas RK, Schwartz E, Wesdock JC. Source: American Family Physician. 1998 October 1; 58(5): 1077, 1083. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9787276
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Occupational lead poisoning. Author(s): Bennett L, Bennett A. Source: American Family Physician. 1998 October 1; 58(5): 1070, 1077; Author Reply 1083. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9787275
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Occupational lead poisoning. Author(s): Staudinger KC, Roth VS. Source: American Family Physician. 1998 February 15; 57(4): 719-26, 731-2. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9490995
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Occupational lead poisoning. Author(s): Neale TJ, Bailey RR. Source: N Z Med J. 1976 December 8; 84(577): 458. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1071163
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Occupational lead poisoning. 2. Chemical signs of the absorption of lead. Author(s): Kehoe RA. Source: J Occup Med. 1972 May; 14(5): 390-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5029146
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Occupational lead poisoning: can it be eliminated? Author(s): Kaufman JD, Burt J, Silverstein B. Source: American Journal of Industrial Medicine. 1994 November; 26(5): 703-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7832217
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Occupational lead poisoning: who should conduct surveillance and training? Author(s): Keogh JP, Gordon J. Source: American Journal of Industrial Medicine. 1994 November; 26(5): 713-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7832218
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Ohio APNs: lead poisoning knowledge and practices. Author(s): Choate DW, Polivka BJ. Source: Journal of the American Academy of Nurse Practitioners. 2000 December; 12(12): 503-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11930596
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One century of studies on lead poisoning in papers published in La Medicina del Lavoro. Author(s): Alessio L, Cortesi I, Materzanini P, Barenghi M. Source: American Journal of Industrial Medicine. 2000 September; 38(3): 361-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10940977
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Oral chelators for childhood lead poisoning. Author(s): Liebelt EL, Shannon MW. Source: Pediatric Annals. 1994 November; 23(11): 616-9, 623-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7838614
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Oral penicillamine therapy for chronic lead poisoning in children. Author(s): Vitale LF, Rosalinas-Bailon A, Folland D, Brennan JF, McCormick B. Source: The Journal of Pediatrics. 1973 December; 83(6): 1041-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4757518
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Osteosclerotic metaphyseal dysplasia: a skeletal dysplasia that may mimic lead poisoning in a child with hypotonia and seizures. Author(s): Mennel EA, John SD. Source: Pediatric Radiology. 2003 January; 33(1): 11-4. Epub 2002 September 18. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12497229
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Oxidative stress in acute intermittent porphyria and lead poisoning may be triggered by 5-aminolevulinic acid. Author(s): Bechara EJ. Source: Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Medicas E Biologicas / Sociedade Brasileira De Biofisica. [et Al.]. 1996 July; 29(7): 841-51. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9070373
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Pain in abdomen--do not forget lead poisoning. Author(s): Sood A, Midha V, Sood N. Source: Indian J Gastroenterol. 2002 November-December; 21(6): 225-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12546173
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Pediatric lead poisoning: is there a threshold? Author(s): Landrigan PJ. Source: Public Health Reports (Washington, D.C. : 1974). 2000 November-December; 115(6): 530-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11354335
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Pediatric management problems. Lead poisoning. Author(s): Agruss JC; Rush University College of Nursing, Department of Community and Mental Health Nursing, Chicago, IL., USA. Source: Pediatric Nursing. 2001 November-December; 27(6): 611-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12024536
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Physicians play an important role in helping to eliminate childhood lead poisoning. Author(s): Tillman UJ. Source: Del Med J. 2000 August; 72(8): 357-60. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10984979
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Pre-1950s housing in Tennessee counties puts children at risk for lead poisoning. Author(s): Stultz E, Weatherby N, Owusu A, Weaver A. Source: Tenn Med. 2002 October; 95(10): 425-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12369544
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Preventing childhood lead poisoning in Tennessee. Author(s): Yarbrough M, Holmes M. Source: Tenn Med. 1996 November; 89(11): 415-6, 418. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8942281
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Preventing childhood lead poisoning: screening practices in the United States. Author(s): Kattapong VJ, Garbarino KM, Duncan PM, Carney JK. Source: Pediatrics. 1997 July; 100(1): 161. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9229714
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Preventing childhood lead poisoning: the challenge of change. Author(s): Jackson RJ, Cummins SK, Tips NM, Rosenblum LS. Source: American Journal of Preventive Medicine. 1998 April; 14(3 Suppl): 84-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9566943
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Preventing lead poisoning and its consequences. Author(s): Fisher AM, Vessey JA. Source: Pediatric Nursing. 1998 July-August; 24(4): 348-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9849268
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Preventing lead poisoning in children. Author(s): Silbergeld EK. Source: Annual Review of Public Health. 1997; 18: 187-210. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9143717
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Prevention of childhood lead poisoning. Author(s): Campbell C, Osterhoudt KC. Source: Current Opinion in Pediatrics. 2000 October; 12(5): 428-37. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11021406
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Prevention of lead poisoning in construction workers: a new public health approach. Author(s): Vork KL, Hammond SK, Sparer J, Cullen MR. Source: American Journal of Industrial Medicine. 2001 March; 39(3): 243-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11241557
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Primary prevention of childhood lead poisoning through community outreach. Author(s): Schlenker TL, Baxmann R, McAvoy P, Bartkowski J, Murphy A. Source: Wmj. 2001; 100(8): 48-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12685297
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Primary prevention of childhood lead poisoning--the only solution. Author(s): Rosen JF, Mushak P. Source: The New England Journal of Medicine. 2001 May 10; 344(19): 1470-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11346814
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Primary prevention of lead poisoning in children. Author(s): Buttery CM. Source: American Family Physician. 2001 August 15; 64(4): 564, 567, 570. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11529257
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Prophylactic chelation therapy in occupational lead poisoning: a review. Author(s): Bridbord K, Blejer HP. Source: American Industrial Hygiene Association Journal. 1977 October; 38(10): 536-42. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=411363
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Prospective economic evaluation of lead poisoning prevention programs. Author(s): Broudy DW, Swint JM, Lairson DR. Source: Journal of Community Health. 1979 Summer; 4(4): 291-301. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=112125
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Protecting children from lead poisoning and building healthy communities. Author(s): Ryan D, Levy B, Levy BS, Pollack S, Walker B Jr. Source: American Journal of Public Health. 1999 June; 89(6): 822-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10358669
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Public policy and child lead poisoning: implementation of Title X. Author(s): Knestrick J, Milstead JA. Source: Pediatric Nursing. 1998 January-February; 24(1): 37-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9555443
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Racism and lead poisoning. Author(s): Weintraub M. Source: American Journal of Public Health. 1997 November; 87(11): 1871-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9366653
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Radiological case of the month. Lead poisoning. Author(s): Narchi H. Source: Archives of Pediatrics & Adolescent Medicine. 2000 January; 154(1): 83-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10632257
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Radiological diagnosis of inorganic lead poisoning. Author(s): Rovira M, Calvet X, Ros E, Nogue S, Navarro S. Source: Journal of Clinical Gastroenterology. 1989 August; 11(4): 469-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2760438
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Rapid, sensitive micro blood lead analysis: a mass screening technique for lead poisoning. Author(s): Verebey K, Eng YM, Davidow B, Ramon A. Source: Journal of Analytical Toxicology. 1991 September-October; 15(5): 237-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1960972
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Recognizing lead poisoning in adults. Author(s): Keogh JP. Source: Archives of Internal Medicine. 1984 October; 144(10): 1944-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6486978
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Recognizing, treating, and preventing lead poisoning. Author(s): Markiewicz T. Source: The American Journal of Nursing. 1993 October; 93(10): 59-62, 64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8213948
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Recommendations for assessing children's lead exposure and screening for lead poisoning. Author(s): Hoffman RE. Source: Colo Med. 1992 August; 89(8): 260-1. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1451389
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Recommended diagnostic criteria for occupational chronic lead poisoning. Author(s): Sun JB, Wang JP. Source: Biomed Environ Sci. 1995 December; 8(4): 318-29. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8719173
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Recurrent cerebellar dysfunction as related to chronic gasoline sniffing in an adolescent girl. Lead poisoning from “leaded” gasoline as an attendent complication. Author(s): Young RS, Grzyb SE, Crismon L. Source: Clinical Pediatrics. 1977 August; 16(8): 706-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=872480
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Recurrent lead poisoning in a child with immobilization osteoporosis. Author(s): Shannon M, Lindy H, Anast C, Graef J. Source: Vet Hum Toxicol. 1988 December; 30(6): 586-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3149814
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Red-cell pyrimidine 5'-nucleotidase and lead poisoning. Author(s): Buc HA, Kaplan JC. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1978 July 1; 87(1): 49-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=668145
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Reducing bone lead content by chelation treatment in chronic lead poisoning: an in vivo X-ray fluorescence and bone biopsy study. Author(s): Batuman V, Wedeen RP, Bogden JD, Balestra DJ, Jones K, Schidlovsky G. Source: Environmental Research. 1989 February; 48(1): 70-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2492468
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Re-emergence of lead poisoning from contaminated flour in a West Bank Palestinian village. Author(s): Richter E, El-Sharif N, Fischbein A, Konijn A, Gorodetsky R, El-Sharif H, Kaul B, Hershko C, Grauer F, Foner H, Al-Baba A, Dweik Z, Lihsounat M. Source: International Journal of Occupational and Environmental Health : Official Journal of the International Commission on Occupational Health. 2000 July-September; 6(3): 183-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10926721
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Renal function 9 to 17 years after childhood lead poisoning. Author(s): Moel DI, Sachs HK, Cohn RA, Drayton MA. Source: The Journal of Pediatrics. 1985 May; 106(5): 729-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3998912
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Repeated surveillance of lead poisoning among children. Author(s): Silvany-Neto AM, Carvalho FM, Chaves ME, Brandao AM, Tavares TM. Source: The Science of the Total Environment. 1989 January; 78: 179-86. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2717920
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Residual cognitive deficits 50 years after lead poisoning during childhood. Author(s): White RF, Diamond R, Proctor S, Morey C, Hu H. Source: Br J Ind Med. 1993 July; 50(7): 613-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8343422
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Risk of lead poisoning in abused and neglected children. Author(s): Flaherty EG. Source: Clinical Pediatrics. 1995 March; 34(3): 128-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7774138
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Risk of pediatric lead poisoning from nonenvironmental exposures: gun ownership. Author(s): Gellert GA, Meyers HB, Yeung A. Source: Am J Dis Child. 1993 July; 147(7): 720-2. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8322739
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Round and round it goes: the epidemiology of childhood lead poisoning, 1950-1990. Author(s): Berney B. Source: The Milbank Quarterly. 1993; 71(1): 3-39. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8450821
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Rural residents' knowledge of lead poisoning prevention. Author(s): Polivka BJ. Source: Journal of Community Health. 1999 October; 24(5): 393-408. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10555927
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Screen Medicaid children for lead poisoning when they are most at risk. Author(s): Dynes R. Source: Del Med J. 1999 January; 71(1): 21. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10024756
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Selective screening for lead poisoning in an urban teaching practice. Author(s): Froom J, Boisseau V, Sherman A. Source: The Journal of Family Practice. 1979 July; 9(1): 65-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=448321
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Severe congenital lead poisoning in a preterm infant due to a herbal remedy. Author(s): Tait PA, Vora A, James S, Fitzgerald DJ, Pester BA. Source: The Medical Journal of Australia. 2002 August 19; 177(4): 193-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12175323
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Severe gastrointestinal symptoms due to lead poisoning from Indian traditional medicine. Author(s): van Vonderen MG, Klinkenberg-Knol EC, Craanen ME, Touw DJ, Meuwissen SG, De Smet PA. Source: The American Journal of Gastroenterology. 2000 June; 95(6): 1591-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10894609
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Severe lead poisoning in pregnancy. Author(s): Shannon M. Source: Ambulatory Pediatrics : the Official Journal of the Ambulatory Pediatric Association. 2003 January-February; 3(1): 37-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12540252
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Should the Centers for Disease Control and Prevention's childhood lead poisoning intervention level be lowered? Author(s): Bernard SM. Source: American Journal of Public Health. 2003 August; 93(8): 1253-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12893607
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Should we screen for lead poisoning after 36 months of age? Experience in the inner city. Author(s): Karp R, Abramson J, Clark-Golden M, Mehta S, Daniele RM, Homel P, Deutsch J. Source: Ambulatory Pediatrics : the Official Journal of the Ambulatory Pediatric Association. 2001 September-October; 1(5): 256-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11888411
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Some clinical aspects of industrial lead poisoning. Author(s): Martin KS, Wicks AC. Source: Cent Afr J Med. 1977 March; 23(3): 53-5. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=851994
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Succimer in symptomatic lead poisoning. Author(s): Kalra V, Dua T, Kumar V, Kaul B. Source: Indian Pediatrics. 2002 June; 39(6): 580-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12084955
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Sulphydryl compounds in lead poisoning. Author(s): Candura F, Franco G, Malamani T, Scalisi L. Source: Lancet. 1979 February 10; 1(8111): 330. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=84986
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Surma and lead poisoning. Author(s): Bakhshi SS. Source: British Medical Journal. 1978 October 21; 2(6145): 1159. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=709279
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Surma and lead poisoning. Author(s): Ali AR, Smales OR, Aslam M. Source: British Medical Journal. 1978 September 30; 2(6142): 915-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=709125
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Symptomatic lead poisoning in infancy: a prospective case analysis. Author(s): Dietrich KN, Berger OG, Bhattacharya A. Source: The Journal of Pediatrics. 2000 October; 137(4): 568-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11035840
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Tetraethyl lead poisoning from gasoline sniffing. Author(s): Robinson RO. Source: Jama : the Journal of the American Medical Association. 1978 September 22; 240(13): 1373-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=682329
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The battle against occupational lead poisoning in Finland. Experiences during the 15year period 1964--1978. Author(s): Hernberg S, Tola S. Source: Scand J Work Environ Health. 1979 December; 5(4): 336-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=538424
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The control and prevention of pediatric lead poisoning in East Orange, New Jersey. Author(s): Margulis HL. Source: Journal of Environmental Health. 1977 March-April; 39(5): 362-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10235755
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The effects of industrial lead poisoning on cytochrome P450 mediated phenazone (antipyrine) hydroxylation. Author(s): Meredith PA, Campbell BC, Moore MR, Goldberg A. Source: European Journal of Clinical Pharmacology. 1977 November 14; 12(3): 235-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=412677
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The hematofluorometer in screening for lead poisoning. Author(s): Marcus SM, Ziering R. Source: J Med Soc N J. 1979 February; 76(2): 97-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=284156
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The risk of lead poisoning in battery chargers and the possible hazard of their occupation on the environment. Author(s): Asogwa SE. Source: Niger Med J. 1979 February; 9(2): 189-93. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=543258
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The summer disease. An integrative model of the seasonality aspects of childhood lead poisoning. Author(s): Hunter JM. Source: Social Science & Medicine (1982). 1977 November; 11(14-16): 691-703. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=563625
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The summer disease. Some field evidence on seasonality in childhood lead poisoning. Author(s): Hunter JM. Source: Social Science & Medicine (1982). 1978 June; 12(2D): 85-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=568313
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Treatment of lead poisoning by 2,3-dimercaptosuccinic acid. Author(s): Friedheim E, Graziano JH, Popovac D, Dragovic D, Kaul B. Source: Lancet. 1978 December 9; 2(8102): 1234-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=82738
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Treatment of lead poisoning with an immobilized chelator comparison with conventional therapy. Author(s): Ambrus CM, Anthone S, Stadler A, Cameron MS, Wells K, Stadler I, Ambrus JL Jr. Source: Res Commun Mol Pathol Pharmacol. 2001; 110(3-4): 253-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12760492
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Unexpected presentations--four cases of lead poisoning. Author(s): Mathew J, Mathew T, Kannan R, Satheesh S, Sundararaman T, Sethuraman KR. Source: J Assoc Physicians India. 2002 September; 50: 1172-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12516703
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Unsuspected sources of lead poisoning. Author(s): Rice C, Lilis R, Fischbein A, Selikoff IJ. Source: The New England Journal of Medicine. 1977 June 16; 296(24): 1416. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=859557
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Update on lead poisoning in a Nicaraguan community. Author(s): Morales Bonilla C, Mauss EA. Source: American Journal of Public Health. 2003 March; 93(3): 362-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12604468
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Urinary excretion pattern of triethyllead, diethyllead and inorganic lead in the tetraethyllead poisoning. Author(s): Yamamura Y, Arai F, Yamauchi H. Source: Ind Health. 1981; 19(2): 125-31. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7263301
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Use of 2,3-dimercaptopropane-1-sulfonate in treatment of lead poisoning in children. Author(s): Chisolm JJ Jr, Thomas DJ. Source: The Journal of Pharmacology and Experimental Therapeutics. 1985 December; 235(3): 665-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4078728
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Use of capitated reimbursement to provide comprehensive management of childhood lead poisoning. Author(s): Davoli CT. Source: American Journal of Public Health. 1997 December; 87(12): 2056-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9431306
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Use of geographic information system technology to aid Health Department decision making about childhood lead poisoning prevention activities. Author(s): Reissman DB, Staley F, Curtis GB, Kaufmann RB. Source: Environmental Health Perspectives. 2001 January; 109(1): 89-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11171530
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Use of the Centers for Disease Control and Prevention childhood lead poisoning risk questionnaire to predict blood lead elevations in pregnant women. Author(s): Gemmel DJ. Source: Obstetrics and Gynecology. 1996 July; 88(1): 159-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8684754
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Use of the Centers for Disease Control and Prevention childhood lead poisoning risk questionnaire to predict blood lead elevations in pregnant women. Author(s): Stefanak MA, Bourguet CC, Benzies-Styka T. Source: Obstetrics and Gynecology. 1996 February; 87(2): 209-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8559525
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Using unstimulated urinary lead excretion to assess the need for chelation in the treatment of lead poisoning. Author(s): Berger OG, Gregg DJ, Succop PA. Source: The Journal of Pediatrics. 1990 January; 116(1): 46-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2104929
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Vinyl miniblinds and childhood lead poisoning. Author(s): West R. Source: Archives of Pediatrics & Adolescent Medicine. 1998 May; 152(5): 512-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9605041
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Warnings unheeded: a history of child lead poisoning. Author(s): Rabin R. Source: American Journal of Public Health. 1989 December; 79(12): 1668-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2683817
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What do parents know about lead poisoning? The Chicago Lead Knowledge Test. Pediatric Practice Research Group. Author(s): Mehta S, Binns HJ. Source: Archives of Pediatrics & Adolescent Medicine. 1998 December; 152(12): 1213-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9856432
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What happens in lead poisoning? Author(s): Lee WR. Source: Journal of the Royal College of Physicians of London. 1981 January; 15(1): 48-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7463387
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Wisconsin children at risk for lead poisoning. Author(s): LaFlash S, Joosse-Coons M, Havlena J, Anderson HA. Source: Wmj. 2000 November; 99(8): 18-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11149252
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Zinc protoporphyrin (ZPP): a simple, sensitive fluorometric screening test for lead poisoning. Author(s): Lamola AA, Joselow M, Yamane T. Source: Clinical Chemistry. 1975 January; 21(1): 93-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1116283
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Zinc protoporphyrin determination: a rapid screening test for the detection of lead poisoning. Author(s): Fischbein A, Eisinger J, Blumberg WE. Source: The Mount Sinai Journal of Medicine, New York. 1976 May-June; 43(3): 294-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1084474
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Zinc protoporphyrin level in blood determined by a portable hematofluorometer: a screening device for lead poisoning. Author(s): Blumberg WE, Eisinger J, Lamola AA, Zuckerman DM. Source: The Journal of Laboratory and Clinical Medicine. 1977 April; 89(4): 712-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=557519
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CHAPTER 2. NUTRITION AND LEAD POISONING Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and lead poisoning.
Finding Nutrition Studies on Lead Poisoning The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.4 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “lead poisoning” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
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Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
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The following information is typical of that found when using the “Full IBIDS Database” to search for “lead poisoning” (or a synonym): •
A comparison of calcium disodium ethylene diamine tetra-acetate (CaEDTA) by oral and subcutaneous routes as a treatment of lead poisoning in dogs. Source: Hamir, A.N. Sullivan, N.D. Handson, P.D. Barr, S. J-Small-Anim-Pract. Gloucestershire : British Small Animal Veterinary Association. January 1986. volume 27 (1) page 39-43. 0020-4510
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Adult lead poisoning from an Asian remedy for menstrual cramps--Connecticut, 1997. Source: Anonymous MMWR-Morb-Mortal-Wkly-Repage 1999 January 22; 48(2): 27-9 0149-2195
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Childhood lead poisoning associated with tamarind candy and folk remedies-California, 1999-2000. Source: Anonymous MMWR-Morb-Mortal-Wkly-Repage 2002 August 9; 51(31): 684-6 0149-2195
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Detecting lead poisoning in children of affluent parents. Source: Nutr-Health. New York : Columbia University, Institute of Human Nutrition. March 1986. volume 12 (3) page 1. 0270-6588
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Lead poisoning and parasitism in a flock of mute swans (Cygnus olor) in Scotland. Author(s): Avian Health Unit, SAC Veterinary Services, Auchincruive, Ayr. Source: Pennycott, T W Vet-Rec. 1998 January 3; 142(1): 13-7 0042-4900
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Lead poisoning following ingestion of homemade beverage stored in a ceramic jug-New York. Source: Anonymous MMWR-Morb-Mortal-Wkly-Repage 1989 June 2; 38(21): 379-80 0149-2195
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Lead poisoning, haem synthesis and 5-aminolaevulinic acid dehydratase. Author(s): Dept of Molecular Genetics, Institute of Ophthalmology, London, UK.
[email protected] Source: Warren, M J Cooper, J B Wood, S P Shoolingin Jordan, P M Trends-Biochem-Sci. 1998 June; 23(6): 217-21 0968-0004
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Lead poisoning: a disease for the next millennium. Author(s): Albert Einstein College of Medicine, Bronx, New York, USA. Source: Markowitz, M Curr-Probl-Pediatr. 2000 Mar; 30(3): 62-70 0045-9380
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The diagnostic significance of free erythrocyte protoporphyrin and the FEP/hemoglobin ratio in plumbism. Source: RajkuMarch, S Geibel, V Devanagondi, B Kaul, B Brown, A K N-Y-State-J-Med. 1987 October; 87(10): 542-5 0028-7628
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The role of iron therapy in childhood plumbism. Author(s): Rhode Island Hospital, Providence 02903, USA.
[email protected] Source: Wright, R O Curr-Opin-Pediatr. 1999 June; 11(3): 255-8 1040-8703
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Three patients with lead poisoning following use of a Chinese herbal pill. Author(s): Department of Medicine and Geriatrics, Tuen Mun Hospital, Tsing Chung Koon Road, Tuen Mun, Hong Kong. Source: Auyeung, T W Chang, K K F To, C H Mak, A Szeto, M L Hong-Kong-Med-J. 2002 February; 8(1): 60-2 1024-2708
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Ultrastructural aspects of the small intestinal lead toxicology. Part II. The small intestine goblet cells of rats during lead poisoning. Author(s): Department of Electron Microscopy, Silesian Academy of Medicine, Katowice, Poland. Source: Tomczok, J Grzybek, H Sliwa, W Panz, B Exp-Pathol. 1988; 35(2): 93-100 02321513
Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
The following is a specific Web list relating to lead poisoning; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
Minerals Calcium Source: Integrative Medicine Communications; www.drkoop.com
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CHAPTER 3. DISSERTATIONS ON LEAD POISONING Overview In this chapter, we will give you a bibliography on recent dissertations relating to lead poisoning. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “lead poisoning” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on lead poisoning, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Lead Poisoning ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to lead poisoning. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •
A Descriptive Study of the Special Education Status of School Children Diagnosed As Having Lead Poisoning by West, Maryanne, EDD from Boston University, 1989, 116 pages http://wwwlib.umi.com/dissertations/fullcit/8918013
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An Examination of the Environmental and Psychological Correlates of Lead Poisoning in Young Children by Conrad, Mary Katherine, PhD from The University of Wisconsin - Milwaukee, 1980, 187 pages http://wwwlib.umi.com/dissertations/fullcit/8024953
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Effects of Asymptomatic Lead Poisoning of Psychoneurological Functioning of School-age Urban Children: A Follow-Up Study. by Duva, Nicholas Anthony, PhD from Fordham University, 1977, 89 pages http://wwwlib.umi.com/dissertations/fullcit/7714863
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Health Education Programming among Federally Assisted Lead Poisoning Prevention Projects in 1973. by Roulhac, Edgar Edwin, PhD from Southern Illinois University at Carbondale, 1974, 188 pages http://wwwlib.umi.com/dissertations/fullcit/7500137
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Lead Poisoning Prevention: An Analysis of the Intergovernmental Paradigm of Response Using a Case Study of Camden, New Jersey by Rice Kuennen, Stacey; PhD from University of Delaware, 1999, 252 pages http://wwwlib.umi.com/dissertations/fullcit/9948256
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Lead Screening Initiatives in Hillsborough County, Florida: A Detailed Analysis of Lead Poisoning in Children under Six by Marino, Karma Dawn; PhD from University of South Florida, 2003, 159 pages http://wwwlib.umi.com/dissertations/fullcit/3079996
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Learning and Behavioral Functioning of Low Income, Black Preschoolers with Asymptomatic Lead Poisoning. by Mac Isaac, David Sean, PhD from Fordham University, 1976, 94 pages http://wwwlib.umi.com/dissertations/fullcit/7625778
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Tennessee Healthcare Provider Childhood Lead Poisoning Attitude, Belief, and Practice Survey by Lowry, Karen Adele Rasnake; PhD from The University of Tennessee, 2002, 161 pages http://wwwlib.umi.com/dissertations/fullcit/3075552
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The Effects of a Family-Based Educational Intervention on the Prevention of Lead Poisoning in Children by Wasserman, Loraine Royce; EdD from Florida International University, 2002, 140 pages http://wwwlib.umi.com/dissertations/fullcit/3059791
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The Effects of Parental Education on Preventing Childhood Lead Poisoning in Inner City Cleveland, Ohio by Omidpanah, Parvis, PhD from Walden University, 1998, 249 pages http://wwwlib.umi.com/dissertations/fullcit/9840093
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The Geographic Modeling of Lead Poisoning Risk in North Carolina by Hanchette, Carol L., PhD from The University of North Carolina at Chapel Hill, 1998, 155 pages http://wwwlib.umi.com/dissertations/fullcit/9902471
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The Influence of Diet on the Pathogenesis of Lead Poisoning in Waterfowl by Irwin, James C; PhD from University of Guelph (Canada), 1978 http://wwwlib.umi.com/dissertations/fullcit/NK37420
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The Silenced Epidemic: A Social History of Lead Poisoning in the United States since 1900 by Warren, Christian, PhD from Brandeis University, 1997, 476 pages http://wwwlib.umi.com/dissertations/fullcit/9729362
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Towards Voice: Urban Mothers of Color and Their Children's Threat of Low-level Lead Poisoning (Lead Burdening) in Camden, New Jersey by Hill-Jackson, Valerie Lynn; EdD from Saint Joseph's University, 2003, 305 pages http://wwwlib.umi.com/dissertations/fullcit/3083142
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Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 4. CLINICAL TRIALS AND LEAD POISONING Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning lead poisoning.
Recent Trials on Lead Poisoning The following is a list of recent trials dedicated to lead poisoning.5 Further information on a trial is available at the Web site indicated. •
Effect of environmental exposures on the egg fertilizing ability of human sperm Condition(s): Male Infertility; Testicular Diseases; Urologic and Male Genital Diseases; Lead Poisoning Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Environmental Health Sciences (NIEHS) Purpose - Excerpt: Our data indicate that environmental exposure to the heavy metal lead are more widespread than currently appreciated and that such exposures are associated with the production of human male subfertility. Lead's effects are observed in male partners of infertile couples attending an IVF clinical, in men acting as semen donors in an artificial insemination program and in men representative of the general public. Our goal is to identify the mechanism(s) underlying lead's anti-fertility action. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00012480
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Environmental Contaminants and Infant Development Condition(s): Mercury Poisoning; Lead Poisoning Study Status: This study is currently recruiting patients.
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These are listed at www.ClinicalTrials.gov.
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Sponsor(s): National Institute of Environmental Health Sciences (NIEHS); Indian and Northern Affairs, Canada; Health, Canada; Danish Institute for Public Health Purpose - Excerpt: This study is designed to examine the effects of prenatal exposure to environmental contaminants on cognitive and behavioral development and physical growth in two groups of Inuit infants-one in Northern Quebec; the other in Greenland. Study Type: Observational Contact(s): Joseph L Jacobson, Ph.D. 313-577-2802
[email protected] Web Site: http://clinicaltrials.gov/ct/show/NCT00013858 •
Bone Lead Levels and College Achievement Scores Condition(s): Lead Poisoning Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Environmental Health Sciences (NIEHS) Purpose - Excerpt: This project studies the relationship between lead exposure and academic achievement in college students. Most studies of the neurobehavioral effects of lead have focused on performances at the low end of the distribution. There is evidence that lead affects outcome across the entire distribution. This is a retrospective cohort study of subjects whose cognitive function is adequate to gain admission to college. We will use x-ray fluorescence to measure bone lead concentrations in undergraduate college students and test the hypothesis that achievement scores are related to early lead exposure. Early lead exposure has been shown to have measurable effects on academic performance and neurobehavioral outcomes at 18 years of age. Should an effect be found in this study, the spectrum of lead toxicity would be expanded to include subjects with above average function. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00014885
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Early Exposure to Lead and Adolescent Development Condition(s): Lead Poisoning Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Environmental Health Sciences (NIEHS) Purpose - Excerpt: This prospective cohort study examines the role of prenatal and early postnatal lead exposure on the neuropsychological status and social adjustment of adolescents enrolled in the Cincinnati Lead Study. We are examining the relationship between moderate exposure to lead and neuropsychological deficits, difficulties in peer relationships, personality disturbances and juvenile delinquency. This birth cohort of approximately 300 subjects has been followed since 1980 with regularly scheduled assessments of blood lead concentrations, health history, social and hereditary factors, and neurobehavioral development. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00011674
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Exposure, Dose, Body Burden and Health Effects of Lead Condition(s): Lead Poisoning Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Environmental Health Sciences (NIEHS) Purpose - Excerpt: This is a study of the effects that lead has on the health of the central nervous system (for example, memory), peripheral nervous system (for example, sensation and strength in the hands and fingers), kidneys, blood pressure, and the blood forming system. A total of 803 lead workers and 135 persons without occupational lead exposure are being studied in South Korea. Lead in the body is being assessed by measurement of blood lead, chelatable lead (an estimate of lead in the tissues), and lead in bone. Subjects are tested three times each over three years. Several genetic factors are also being assessed for the role they play in the health effects of lead. These genes are known to differ among individuals. We are interested to know whether different forms of the same genes can modify the effect lead has on health. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00013819
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Lead Mobilization & Bone Turnover in Pregnancy/Lactation Condition(s): Lead Poisoning Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Environmental Health Sciences (NIEHS) Purpose - Excerpt: We are examining the role of maternal bone lead turnover during pregnancy and lactation as a potential source of lead exposure for the fetus and the infant (via breast milk). A cohort, ascertained at entry to care, consists of >1000 women to be followed through pregnancy. In the postpartum subjects are recruited for a nested case control study to assess the influence of lactation on maternal bone density, maternal blood lead and breast milk lead. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00011726
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Lead, Endocrine Disruption and Reproductive Outcomes Condition(s): Lead Poisoning; Infertility Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Environmental Health Sciences (NIEHS) Purpose - Excerpt: This prospective cohort study of 400 lead exposed and 400 non-lead exposed women and their husbands assesses endocrine dysfunction and adverse reproductive outcomes. Residing in two study areas in Shenyang, China, the women are married, 20 and 34 years of age, never smokers, have obtained permission to have a child, and have attempted to become pregnant over the course of the study. Lead exposure is defined by lead levels in blood samples collected at the baseline survey (both women and their husbands), first and second trimesters, and at delivery (both maternal and cord blood). Endocrine dysfunction is monitored by urinary hormone metabolites including follicle-stimulating hormone (FSH), luteinizing hormone (LH),
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estrone conjugates (E1C), and pregnanediol-3-glucuronide (PdG). Reproductive endpoints include menstrual disturbance, time to conception, spontaneous abortion, preterm delivery, and low birth weight. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00023101 •
Social Network Based Intervention to Reduce Lead Exposure among Native American Children Condition(s): Lead Poisoning Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Environmental Health Sciences (NIEHS) Purpose - Excerpt: The purpose of this study is to examine whether adding an intergenerational component to an existing social network-based lay health advisor intervention increases its effectiveness in mobilizing a Native American community to respond to heavy metal contamination from lead and zinc mining. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00011661
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Does Lead Burden alter Neuropsychological Development? Condition(s): Lead Poisoning Study Status: This study is completed. Sponsor(s): National Center for Research Resources (NCRR); HRSA/Maternal and Child Health Bureau Purpose - Excerpt: Inner city children are at an increased risk for lead overburden. This in turn affects cognitive functioning. However, the underlying neuropsychological effects of lead overburden and its age-specific effects have not been well delineated. This study is part of a larger study on the effects of lead overburden on the development of attention and memory. The larger study is using a multi-model approach to study the effects of lead overburden on these effects including the event-related potential (ERP), electrophysiologic measures of attention and memory are studied. Every eight months, for a total of three sessions the subjects will complete ERP measures of attention and memory which require them to watch various computer images while wearing scalp electrodes recording from 11 sites. It is this test that we are going to be doing on CRC. There will be 30 lead overburdened children recruited from the larger study for participation in the ERP studies on CRC. These 30 children will be matched with 30 children without lead overburden. This portion of the study is important in providing an index of physiological functioning to be used along with behaviorally based measures of attention and memory, and for providing information about the different measures. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000104
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Randomized Study of Succimer (Dimercaptosuccinic Acid) on Growth of LeadPoisoned Children Condition(s): Lead Poisoning Study Status: This study is completed. Sponsor(s): National Institute of Child Health and Human Development (NICHD); Children's Hospital Columbus Purpose - Excerpt: Objectives: Compare growth of lead-poisoned children receiving succimer (dimercaptosuccinic acid; DMSA) plus standard treatment to those receiving standard treatment only. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004838
Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “lead poisoning” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: •
For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/
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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html
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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/
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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm
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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm
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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm
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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp
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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm
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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/
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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm
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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm
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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm
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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm
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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm
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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials
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CHAPTER 5. BOOKS ON LEAD POISONING Overview This chapter provides bibliographic book references relating to lead poisoning. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on lead poisoning include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “lead poisoning” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on lead poisoning: •
Dr. Carl Robinson's basic baby care: A guide for new parents for the first year Source: Oakland, CA: New Harbinger. 1998. 204 pp. Contact: Available from New Harbinger Publications, 5674 Shattuck Avenue, Oakland, CA 94609. $10.95. Summary: This book is written to help first-time parents take care of their infants in the first year. Chapters cover these topics: before the baby is born; at the hospital; the basics of babyproofing the house, traveling with the baby, and day care; health care and medical concerns; feeding the baby; common physical concerns such as fevers and lead poisoning; and parenthood issues such as working together to take care of the baby, coping with stress, expressing anger, and substance and child abuse. The book is aimed at African Americans. It contains a list of resources and a detailed index.
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Beyond the Health Room Contact: Council of Chief State School Officers, HIV/School Health Project, 1 Massachusetts Ave NW Ste 700, Washington, DC, 20001-1431, (202) 408-5505, http://www.ccsso.org. Summary: This monograph examines the need for schools to improve their health education programs. It begins with a section on putting health programs in context, looking at the relationship between health and learning capability, the health status of children and adolescents in the United States, and the role of schools in meeting health needs. The second section turns to children's health needs, starting off with an examination of adolescent sexual behavior that emphasizes Human immunodeficiency virus (HIV) infection and Acquired immunodeficiency syndrome (AIDS), Sexually transmitted diseases (STD's), and pregnancy. The section also studies alcohol, tobacco, and substance abuse; chronic and infectious diseases; nutrition and lead poisoning; child abuse and neglect; violence and injuries; and suicide. The monograph's third section describes the characteristics and components of comprehensive school health programs, including instruction, services, environment, coordination, the relationship between school health programs and community services, and assessment of programs. The fourth and final section focuses on HIV and AIDS. It considers what children and adolescents need to know, what training and information teachers need, cultural factors in learning, and peer education.
Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “lead poisoning” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “lead poisoning” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “lead poisoning” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
Childhood lead poisoning : older homes, silent hazard : hearing before the Subcommittee on Public Health of the Committee on Health, Education, Labor, and Pensions, United States Senate, One Hundred Sixth Congress, first session. November 15, 1999 (Lewiston, ME.) (SuDoc Y 4.L 11/4:S.HRG.106-313); ISBN: 0160601444; http://www.amazon.com/exec/obidos/ASIN/0160601444/icongroupinterna
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Getting the Lead Out: The Complete Resource on How to Prevent and Cope With Lead Poisoning by Irene Kessel, et al; ISBN: 0306455250; http://www.amazon.com/exec/obidos/ASIN/0306455250/icongroupinterna
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Lead and Lead Poisoning Antiquity by Jerome O. Nriagu; ISBN: 047108767X; http://www.amazon.com/exec/obidos/ASIN/047108767X/icongroupinterna
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Lead poisoning and your children (SuDoc EP 1.2:L 46/16) by U.S. Environmental Protection Agency; ISBN: B00010CTOY; http://www.amazon.com/exec/obidos/ASIN/B00010CTOY/icongroupinterna
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Lead poisoning federal health care programs are not effectively reaching at-risk children : report to the ranking minority member, Committee on Government Reform, House of Representatives (SuDoc GA 1.13:HEHS-99-18) by U.S. General Accounting Office; ISBN: B000110EHW; http://www.amazon.com/exec/obidos/ASIN/B000110EHW/icongroupinterna
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Lead poisoning in animal models : papers; ISBN: 0842272682; http://www.amazon.com/exec/obidos/ASIN/0842272682/icongroupinterna
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Lead Poisoning Prevention: A Directory of State Contacts 1995-96 by Doug Farquhar (Compiler); ISBN: 1555164307; http://www.amazon.com/exec/obidos/ASIN/1555164307/icongroupinterna
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Lead Poisoning Prevention: Directory of State Contacts, 1994 by Doug Farquhar, Linda South; ISBN: 1555164285; http://www.amazon.com/exec/obidos/ASIN/1555164285/icongroupinterna
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Lead Poisoning: 25 True Stories from the Wrong End of a Gun by Chris Pfouts, Chris Pfouts; ISBN: 0873646207; http://www.amazon.com/exec/obidos/ASIN/0873646207/icongroupinterna
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Lead Poisoning: A Selected Bibliography (Public Administrations Series, No 2518) by Robert W. Lockerby; ISBN: 1555909787; http://www.amazon.com/exec/obidos/ASIN/1555909787/icongroupinterna
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Preventing lead poisoning in young children : a statement (SuDoc HE 20.7302:L 46/2/991) by U.S. Dept of Health and Human Services; ISBN: B000108114; http://www.amazon.com/exec/obidos/ASIN/B000108114/icongroupinterna
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Report of a committee under the chairmanship of Sir Brian Windeyer appointed to inquire into lead poisonings at the RTZ Smelter at Avonmouth; ISBN: 0101504209; http://www.amazon.com/exec/obidos/ASIN/0101504209/icongroupinterna
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Request for assistance in preventing lead poisoning in construction workers (SuDoc HE 20.7123:L 46) by U.S. Dept of Health and Human Services; ISBN: B00010V21U; http://www.amazon.com/exec/obidos/ASIN/B00010V21U/icongroupinterna
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Screening young children for lead poisoning : guidance for state and local public health officials (SuDoc HE 20.7002:98012295) by U.S. Dept of Health and Human Services; ISBN: B00010URQQ; http://www.amazon.com/exec/obidos/ASIN/B00010URQQ/icongroupinterna
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Screening Young Children for Lead Poisoning: Guidance for State and Local Public Health Officials by Richard J. Jackson (Editor); ISBN: 0788178032; http://www.amazon.com/exec/obidos/ASIN/0788178032/icongroupinterna
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Steel Shot and Lead Poisoning in Waterfowl: An Annotated Bibliography of Research, 1976-1983 (National Wildlife Federation Scientific and Technical,) by J. Scott Feierabend; ISBN: 091218650X; http://www.amazon.com/exec/obidos/ASIN/091218650X/icongroupinterna
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The Lead Poisoning of America's School Children: An Action Plan by Dick Amann; ISBN: 0917194217; http://www.amazon.com/exec/obidos/ASIN/0917194217/icongroupinterna
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Chapters on Lead Poisoning In order to find chapters that specifically relate to lead poisoning, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and lead poisoning using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “lead poisoning” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on lead poisoning: •
Acquired and Developmental Disturbances of the Teeth and Associated Oral Structures Source: in McDonald, R.E. and Avery, D.A., eds. Dentistry for the Child and Adolescent. 7th ed. St. Louis, MO: Mosby, Inc. 2000. p. 105-150. Contact: Available from Harcourt Health Sciences. 11830 Westline Industrial Drive, St. Louis, MO 63146. (800) 325-4177. Fax (800) 874-6418. Website: www.harcourthealth.com. PRICE: $72.00 plus shipping and handling. ISBN: 0815190174. Summary: This chapter on acquired and developmental disturbances of the teeth and associated oral structures is from a textbook on dentistry for the child and adolescent that is designed to help undergraduate dental students and postdoctoral pediatric dentistry students provide comprehensive oral health care for infants, children, teenagers, and individuals with various disabilities. This chapter covers alveolar abscess; cellulitis (a diffuse infection of the soft tissues); developmental anomalies of the teeth, including odontoma (a tumor arising from a tooth germ), fusion of the teeth, germination, and dens in dente (dens invaginatus, tooth within a tooth); early exfoliation (shedding) of primary teeth, including that due to hypophosphatasia, familial fibrous dysplasia (cherubism), acrodynia, hypophosphatemia (rickets), cyclic neutropenia, and other disorders; enamel hypoplasia (less than normal growth of the enamel), including that due to nutritional deficiencies, to brain injury and neurologic defects, nephrotic syndrome, allergies, chronic pediatric lead poisoning, local infection and trauma, repaired cleft lip and palate, X radiation, rubella embryopathy, and fluoride (fluorosis); the use of enamel microabrasion to remove superficial enamel discolorations; preeruptive 'caries' (defects of the developing permanent teeth); inherited dentin defects, including dentinogenesis imperfecta and dentin dysplasia; amelogenesis imperfecta; enamel and dentin aplasia (lack of enamel and dentin); taurodontism; agenesis of teeth, including adontia (complete failure of the teeth to develop), hypodontia (oligodontia, a condition where only a few teeth develop), and ectodermal dysplasias; intrinsic discoloration of teeth, in erythroblastosois fetalis, porphyria, cystic fibrosis, tetracycline therapy, and their treatment with bleaching; micrognathia (small jaw); anomalies of the tongue, including macroglossia (large tongue), ankyloglossia (tongue tie), fissured tongue, geographic tongue, coated tongue, white strawberry tongue, black hairy tongue, indentation of the tongue margin (crenation), median rhomboid glossitis, and trauma to the tongue; and abnormal labial frenum and frenectomy. For each condition, the authors describe etiology, symptoms, diagnosis, and treatment options. 51 figures. 100 references.
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Trauma Source: in Gerber, S.E. Etiology and Prevention of Communicative Disorders. 2nd ed. San Diego, CA: Singular Publishing Group, Inc. 1998. p. 129-145. Contact: Available from Singular Publishing Group, Inc. 401 West 'A' Street, Suite 325, San Diego, CA 92101-7904. (800) 521-8545 or (619) 238-6777. Fax (800) 774-8398 or (619) 238-6789. E-mail:
[email protected]. Website: www.singpub.com. PRICE: $65.00 plus shipping and handling. ISBN: 1565939476. Summary: This chapter on trauma is from a textbook that focuses on the primary and secondary prevention of communicative disorders. The author discusses three kinds of trauma that may contribute to communication disorders: mechanical trauma, chemical trauma, and burns. The author stresses that it is important to observe that traumata appear in children at rates different from those in adults. Topics include head injuries, temporal bone fracture, child abuse, facial injuries, laryngeal injuries, lead poisoning, chemical injuries, and thermal injuries. For each type of trauma, the author outlines recommended prevention strategies. The chapter concludes with a glossary of terms and a reference list. 3 figures. 5 tables. 53 references.
Directories In addition to the references and resources discussed earlier in this chapter, a number of directories relating to lead poisoning have been published that consolidate information across various sources. The Combined Health Information Database lists the following, which you may wish to consult in your local medical library:6 •
Directory of state and local lead poisoning prevention advocates Source: Washington, DC: Alliance to End Childhood Lead Poisoning. 1995. 122 pp. Contact: Available from Alliance to End Childhood Lead Poisoning, 227 Massachusetts Avenue, N.E., Suite 200, Washington, DC 20002. Telephone: (202) 543-1147 / fax: (202) 543-4466 / e-mail:
[email protected] / Web site: http://www.aeclp.org/. $16.00 plus $2.00 shipping and handling; prepayment required. Summary: This directory lists non-governmental groups at the state and local levels that advocate the prevention of lead poisoning. A preface explains the purpose of the directory; each entry provides contact information, indicates the group's areas of expertise, provides their mission statement, and notes affiliations, the size of the membership, and geographic focus. Entries are arranged by state, and indexes list the contacts' names and the organizations included; a list of national and regional resources is also provided.
6
You will need to limit your search to “Directory” and “lead poisoning” using the "Detailed Search" option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find directories, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Select your preferred language and the format option “Directory.” Type “lead poisoning” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months.
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CHAPTER 6. MULTIMEDIA ON LEAD POISONING Overview In this chapter, we show you how to keep current on multimedia sources of information on lead poisoning. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.
Video Recordings An excellent source of multimedia information on lead poisoning is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “lead poisoning” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “lead poisoning” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on lead poisoning: •
Protecting your child from lead poisoning. (Rev. ed.) Source: Providence, RI: Women's and Infants Hospital of Rhode Island. 1995. 1 videotape (12 minutes, VHS 1/2 inch). Contact: Available from Providence Ambulatory Health Care Foundation, 469 Angell Street, Providence, RI 02906-4490. Telephone: (401) 444-0400 / fax: (401) 444-0421. Summary: This videotape for parents discusses what lead is, how it makes people sick, the need for testing young children for lead, information about the tests, symptoms some children with lead poisoning have, and how to protect children from lead poisoning. The video was originally published in 1989. It is available in English, Cambodian, Hmong, Laotian, Spanish, Portuguese, and Vietnamese. [Funded by the Maternal and Child Health Bureau].
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CHAPTER 7. POISONING
PERIODICALS
AND
NEWS
ON
LEAD
Overview In this chapter, we suggest a number of news sources and present various periodicals that cover lead poisoning.
News Services and Press Releases One of the simplest ways of tracking press releases on lead poisoning is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing. PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “lead poisoning” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance. Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to lead poisoning. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “lead poisoning” (or synonyms). The following was recently listed in this archive for lead poisoning: •
Calcium supplements of no use for lead poisoning in well-nourished children Source: Reuters Industry Breifing Date: January 13, 2004
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•
Calcium not useful for lead poisoning if diet good Source: Reuters Health eLine Date: January 13, 2004
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Lead poisoning does not increase likelihood of asthma Source: Reuters Medical News Date: September 16, 2002
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Imported candy source of kids' lead poisoning-CDC Source: Reuters Health eLine Date: August 08, 2002
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CDC report highlights often-overlooked sources of lead poisoning Source: Reuters Medical News Date: August 08, 2002
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Experts say anti-lead poisoning efforts fall short Source: Reuters Health eLine Date: November 14, 2001
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Refugee children at risk of lead poisoning Source: Reuters Health eLine Date: July 03, 2001
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Entering foster care, lead poisoning linked Source: Reuters Health eLine Date: May 14, 2001
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Lead poisoning seen in Chinese children Source: Reuters Health eLine Date: February 06, 2001
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Poverty-stricken children hit hard by lead poisoning Source: Reuters Health eLine Date: December 22, 2000
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Lead poisoning still a risk for children living in poverty Source: Reuters Medical News Date: December 22, 2000
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Pool chalk can be source of lead poisoning Source: Reuters Health eLine Date: November 30, 2000
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Child suffers lead poisoning from imported "vitamin" Source: Reuters Health eLine Date: September 05, 2000
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International adoptees at risk for lead poisoning Source: Reuters Health eLine Date: February 11, 2000
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Housing policy reduces lead poisoning in children Source: Reuters Health eLine Date: November 26, 1999
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Reduction of lead poisoning in children may be due to Massachusetts housing policy Source: Reuters Medical News Date: November 02, 1999
Periodicals and News
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Teen marksmen may be at risk for lead poisoning Source: Reuters Health eLine Date: September 09, 1999
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Asian menstrual remedy tied to lead poisoning Source: Reuters Health eLine Date: January 22, 1999
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Costs of lead poisoning screening strategies vary with tested populations Source: Reuters Medical News Date: December 28, 1998
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FDA Approves Portable Lead Poisoning Kit Source: Reuters Medical News Date: September 12, 1997
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CDC: New Strategy On Prevention Of Lead Poisoning In Children Needed Source: Reuters Medical News Date: February 21, 1997
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The NIH Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “lead poisoning” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or
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you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “lead poisoning” (or synonyms). If you know the name of a company that is relevant to lead poisoning, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/. BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “lead poisoning” (or synonyms).
Academic Periodicals covering Lead Poisoning Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to lead poisoning. In addition to these sources, you can search for articles covering lead poisoning that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 8. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for lead poisoning. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with lead poisoning. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The
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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to lead poisoning: Paraldehyde •
Systemic - U.S. Brands: Paral http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202440.html
Penicillamine •
Systemic - U.S. Brands: Cuprimine; Depen http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202445.html
Succimer •
Systemic - U.S. Brands: Chemet http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202664.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/. PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee.
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Researching Orphan Drugs Although the list of orphan drugs is revised on a daily basis, you can quickly research orphan drugs that might be applicable to lead poisoning by using the database managed by the National Organization for Rare Disorders, Inc. (NORD), at http://www.rarediseases.org/. Scroll down the page, and on the left toolbar, click on “Orphan Drug Designation Database.” On this page (http://www.rarediseases.org/search/noddsearch.html), type “lead poisoning” (or synonyms) into the search box, and click “Submit Query.” When you receive your results, note that not all of the drugs may be relevant, as some may have been withdrawn from orphan status. Write down or print out the name of each drug and the relevant contact information. From there, visit the Pharmacopeia Web site and type the name of each orphan drug into the search box at http://www.nlm.nih.gov/medlineplus/druginformation.html. You may need to contact the sponsor or NORD for further information. NORD conducts “early access programs for investigational new drugs (IND) under the Food and Drug Administration’s (FDA’s) approval ‘Treatment INDs’ programs which allow for a limited number of individuals to receive investigational drugs before FDA marketing approval.” If the orphan product about which you are seeking information is approved for marketing, information on side effects can be found on the product’s label. If the product is not approved, you may need to contact the sponsor. The following is a list of orphan drugs currently listed in the NORD Orphan Drug Designation Database for lead poisoning: •
Succimer (trade name: Chemet capsules) http://www.rarediseases.org/nord/search/nodd_full?code=164
If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute7: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
•
National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
•
National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
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National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
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National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
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National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
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National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
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National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
7
These publications are typically written by one or more of the various NIH Institutes.
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•
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
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National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
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National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
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National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
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National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
•
National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
•
Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
•
Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.8 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:9 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
•
HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
•
NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
•
Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
•
Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
•
Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
•
Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
•
Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
•
Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
•
Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
•
MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
8
Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 9 See http://www.nlm.nih.gov/databases/databases.html.
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•
Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
•
Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html
The NLM Gateway10 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.11 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “lead poisoning” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total
Items Found 9404 330 804 8 66 10612
HSTAT12 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.13 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.14 Simply search by “lead poisoning” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
10
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
11
The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 12 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 13 14
The HSTAT URL is http://hstat.nlm.nih.gov/.
Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations.
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Coffee Break: Tutorials for Biologists15 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.16 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.17 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
•
Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
15 Adapted 16
from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.
The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 17 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on lead poisoning can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.
Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to lead poisoning. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly. The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below. Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to lead poisoning. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “lead poisoning”:
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Other guides Environmental Health http://www.nlm.nih.gov/medlineplus/environmentalhealth.html Household Poisons http://www.nlm.nih.gov/medlineplus/householdpoisons.html
Within the health topic page dedicated to lead poisoning, the following was listed: •
General/Overviews FAQ - Lead Poisoning Source: Environmental Protection Agency http://www.epa.gov/region02/faq/lead_p.htm Lead Source: Agency for Toxic Substances and Disease Registry http://www.atsdr.cdc.gov/tfacts13.html Lead Source: National Center for Environmental Health http://www.cdc.gov/exposurereport/leadfactsheet.htm Lead in Paint, Dust and Soil Source: Environmental Protection Agency http://www.epa.gov/opptintr/lead/leadinfo.htm Public Health Statement for Lead Source: Agency for Toxic Substances and Disease Registry http://www.atsdr.cdc.gov/toxprofiles/phs13.html Tox Town Source: National Library of Medicine http://toxtown.nlm.nih.gov/
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Diagnosis/Symptoms Lead Test Source: American Association for Clinical Chemistry http://www.labtestsonline.org/understanding/analytes/lead/test.html
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Nutrition Fight Lead Poisoning with a Healthy Diet http://www.epa.gov/lead/nutrition.pdf
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Specific Conditions/Aspects Don't Use Solder that Contains Lead for Work on Drinking Water Systems Source: Consumer Product Safety Commission http://www.cpsc.gov/cpscpub/pubs/5056.html
Patient Resources 143 How Lead Affects the Way We Live & Breathe Source: Environmental Protection Agency, Office of Air Quality Planning and Standards http://www.epa.gov/air/urbanair/lead/index.html Kohl, Kajal, Al-Kahl, or Surma: By Any Name, a Source of Lead Poisoning Source: Center for Food Safety and Applied Nutrition http://www.cfsan.fda.gov/%7Edms/cos-kohl.html Lead (in the Workplace) Source: Occupational Safety and Health Administration http://www.osha-slc.gov/SLTC/lead/index.html Lead in Drinking Water in Schools and Day Care Centers Source: Environmental Protection Agency, Office of Water http://www.epa.gov/safewater/lead/schoolanddccs.htm Sources of Indoor Air Pollution - Lead Source: Environmental Protection Agency http://www.epa.gov/iaq/lead.html •
Children About Lead Hazards Source: National Center for Healthy Housing http://www.centerforhealthyhousing.org/1012/html/about_lead_hazards.html Adventures of the Lead Busters Club Source: National Institute of Environmental Health Sciences http://www.niehs.nih.gov/kids/leadbusters/home.htm Know Where Lead Might be Hiding Source: National Institute of Environmental Health Sciences http://www.niehs.nih.gov/kids/leadhouse.htm Lead Poisoning Kids' Page Source: National Institute of Environmental Health Sciences http://www.niehs.nih.gov/kids/lead.htm
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From the National Institutes of Health Lead and Your Health: Lead Is All Around Us Source: National Institute of Environmental Health Sciences http://www.niehs.nih.gov/oc/factsheets/lyh/lyh.htm
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Law and Policy Identifying Lead Hazards in Residential Properties http://www.epa.gov/lead/403FS01.pdf Lead in Paint, Dust and Soil: Rules and Regulations Source: Environmental Protection Agency, Office of Prevention, Pesticides and Toxic Substances http://www.epa.gov/lead/regulation.htm
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New EPA Rule to Protect Children from Lead Poisoning Source: Environmental Protection Agency http://www.epa.gov/reg3wcmd/leadpoisoning.htm •
Lists of Print Publications National Lead Information Center: Document Request Form Source: Environmental Protection Agency http://www.epa.gov/lead/nlicdocs.htm
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Organizations Environmental Protection Agency http://www.epa.gov/ National Center for Healthy Housing http://www.centerforhealthyhousing.org/ National Institute of Environmental Health Sciences http://www.niehs.nih.gov/ Office of Healthy Homes and Lead Hazard Control Source: Dept. of Housing and Urban Development http://www.hud.gov/offices/lead/
•
Prevention/Screening Actions You Can Take to Reduce Lead in Drinking Water Source: Environmental Protection Agency http://www.epa.gov/safewater/Pubs/lead1.html CPSC Warns About Hazards of “Do lt Yourself” Removal of Lead Based Paint: Safety Alert Source: Consumer Product Safety Commission http://www.cpsc.gov/cpscpub/pubs/5055.html FDA Warns Consumers about Use of “Litargirio” - Traditional Remedy That Contains Dangerous Levels of Lead Source: Food and Drug Administration http://www.fda.gov/bbs/topics/ANSWERS/2003/ANS01253.html Humans and Lead Fishing Sinkers Source: Environmental Protection Agency, Office of Water http://www.epa.gov/owowwtr1/fish/humans.html Is Lead a Problem in My Home? Source: American Industrial Hygiene Association http://www.aiha.org/ConsultantsConsumers/html/OOlead.htm Protect Your Family from Lead in Your Home http://www.hud.gov/offices/lead/outreach/leapame.pdf Reducing Lead Hazards When Remodeling Your Home http://www.epa.gov/lead/rrpamph.pdf Testing Your Home for Lead in Paint, Dust, and Soil http://www.epa.gov/lead/leadtest.pdf
Patient Resources 145 What You Should Know About Lead Based Paint in Your Home: Safety Alert Source: Consumer Product Safety Commission http://www.cpsc.gov/cpscpub/pubs/5054.html •
Research Detecting Lead Using DNA Source: National Institute of General Medical Sciences http://www.nigms.nih.gov/news/releases/brief_lu.html Drug Treatment of Lead-exposed Children Does Not Improve Psychological Test Scores Source: National Institute of Environmental Health Sciences http://www.nih.gov/news/pr/may2001/niehs-09.htm Lead Exposure: A Top Indicator of Delinquency Source: National Institute of Environmental Health Sciences http://www.niehs.nih.gov/oc/crntnws/2003mar/lead.htm Very Low Lead Levels Linked with IQ Deficits, According to NEJM Study Source: National Institute of Environmental Health Sciences http://www.niehs.nih.gov/oc/news/leadiq.htm
You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on lead poisoning. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: •
Bright Futures for families: Lead poisoning.still an environmental problem for children and families Source: Washington, DC: National Parent Consortium. 2000. 8 pp. Contact: Available from National Maternal and Child Health Clearinghouse, 2070 Chain Bridge Road, Suite 450, Vienna, VA 22182-2536. Telephone: (703) 356-1964 or (888) 4344MCH / fax: (703) 821-2098 / e-mail:
[email protected] / Web site: http://www.nmchc.org. Available at no charge. Summary: This booklet shows parents how to prevent lead poisoning in their children. A list of additional resources is included. [Funded by the Maternal and Child Health Bureau].
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Nutrition and childhood lead poisoning prevention: A quick reference guide for health providers Source: Arlington, VA: National Center for Education in Maternal and Child Health. 1994. 2 pp. Contact: Available from National Maternal and Child Health Clearinghouse, 2070 Chain Bridge Road, Suite 450, Vienna, VA 22182-2536. Telephone: (703) 356-1964 or (888) 4344MCH / fax: (703) 821-2098 / e-mail:
[email protected] / Web site: http://www.nmchc.org. Available at no charge. Summary: This fact sheet discusses how nutrition is related to the prevention of childhood lead poisoning, and nutritional recommendations health providers should make to the parents of young children. It is accompanied by a 2-page bibliography on nutrition and lead. [Funded by the Maternal and Child Health Bureau].
•
Childhood lead poisoning prevention: Strategies and resources Source: Washington, DC: Children's Safety Network, CSR. 1997. 12 pp. Contact: Available from Librarian, National Center for Education in Maternal and Child Health, 2000 15th Street, North, Suite 701, Arlington, VA 22201-2617. Telephone: (703) 524-7802 / fax: (703) 524- 9335 / e-mail:
[email protected] / Web site: http://www.ncemch.org. Available for loan. Summary: This newsletter-style publication discusses the problem of childhood lead poisoning, sources of the problem, and solutions, focusing on state health departments. It also discusses what parents can do, gives contacts for information, and includes references. [Funded by the Maternal and Child Health Bureau].
•
Nutrition and lead: Healthy eating helps protect your child from lead poisoning Source: [Little Rock, AR]: Division of Nutrition Services, Arkansas Department of Health. 1996. 2 pp. Contact: Available from Wanda Lung'aho, Arkansas Department of Health, 4815 West Markham Street, Little Rock, AR 72205. Telephone: (501) 661-2807. Single copies available at no charge. Summary: This pamphlet for parents describes the symptoms of lead poisoning, explains how healthy eating can help prevent lead poisoning and lower lead levels, and lists the foods that can help protect children from lead poisoning. A sample menu is provided. Healthfinder™
Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database:
Patient Resources 147 •
Childhood Lead Poisoning Prevention Program - Centers for Disease Control and Prevention Summary: Childhood lead poisoning remains a major preventable environmental health problem in the United States. The goal of CDC is to eliminate childhood lead poisoning as a major public health problem. Source: National Center for Environmental Health, Centers for Disease Control and Prevention http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=1062
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Lead Poisoning Prevention Outreach Program -- National Safety Council Source: National Safety Council http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=3248
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Lead Poisoning Prevention Programs - Office of Pollution Prevention and Toxics/EPA Summary: The information contained on this site is designed to give you access to all aspects of the Federal lead poisoning prevention program, with a special focus on the efforts within EPA's Office of Source: U.S. Environmental Protection Agency http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=3009
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Lead Poisoning Videos Summary: Order forms for the Children's Television Workshop videos are available upon request. Source: U.S. Environmental Protection Agency http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=3012
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Ten Tips to Protect Children from Pesticide and Lead Poisonings Around the Home Source: Office of Pesticide Programs, Office of Prevention, Pesticides and Toxic Substances/EPA http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2991 The NIH Search Utility
The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to lead poisoning. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html.
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Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/specific.htm
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Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
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Med Help International: http://www.medhelp.org/HealthTopics/A.html
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Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
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Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
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WebMDHealth: http://my.webmd.com/health_topics
Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to lead poisoning. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with lead poisoning. The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about lead poisoning. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “lead poisoning” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given
Patient Resources 149 the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “lead poisoning”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “lead poisoning” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “lead poisoning” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.18
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
18
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)19: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
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Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
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Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
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California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
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California: Gateway Health Library (Sutter Gould Medical Foundation)
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California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
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California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
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California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
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California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
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California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
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Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
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Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
19
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
Finding Medical Libraries 153
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Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
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Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
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Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
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Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
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Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
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Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
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Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
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Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
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Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
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Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
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Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
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Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
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Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
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Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
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Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
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Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
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Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
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Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
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Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
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Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
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Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
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Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
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Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
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Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
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Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
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Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
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Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
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Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
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Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
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Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
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Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
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Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
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National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
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National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
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National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
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MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
•
Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
•
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
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Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
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Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on lead poisoning: •
Basic Guidelines for Lead Poisoning Erythropoietic protoporphyria Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001208.htm Lead poisoning Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002473.htm Lead poisoning disease Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001653.htm Malabsorption Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000299.htm
•
Signs & Symptoms for Lead Poisoning Abdominal cramping Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003120.htm
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Abdominal cramps Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003120.htm Abdominal pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003120.htm Agitation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003212.htm Anemia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000560.htm Arthralgia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003261.htm Coma Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003202.htm Confusion Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003205.htm Constipation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003125.htm Convulsions Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003200.htm Decreased appetite Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003121.htm Diarrhea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003126.htm Fatigue Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm Hallucinations Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003258.htm Headache Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003024.htm High blood pressure Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003082.htm Hyperactivity Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003256.htm Incoordination Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003198.htm
Online Glossaries 159 Irritability Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003214.htm Joint pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003261.htm Lethargy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm Loss of appetite Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003121.htm Metallic taste Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003050.htm Muscle soreness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003178.htm Myalgia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003178.htm Paralysis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003190.htm Paresthesias Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003206.htm Seizures Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003200.htm Sleeping difficulty Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003210.htm Staggering gait Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003199.htm Vomiting Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003117.htm Weakness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003174.htm Weight loss Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003107.htm •
Diagnostics and Tests for Lead Poisoning Abdominal film Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003815.htm Bone marrow biopsy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003934.htm
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Gastric lavage Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003882.htm HCT Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003646.htm Peripheral smear Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003665.htm Protoporphyrin levels Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003372.htm Serum lead Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003360.htm X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003337.htm •
Background Topics for Lead Poisoning Acute Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002215.htm Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Lead poisoning Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002473.htm Long bones Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002249.htm Renal Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002289.htm Safety Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001931.htm Solder Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002822.htm
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
•
MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
Online Glossaries 161 •
Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
•
Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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LEAD POISONING DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Abscess: A localized, circumscribed collection of pus. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acrodynia: A condition occurring in infants, marked by swollen, bluish red hands and feet and disordered digestion, followed by multiple arthritis and muscular weakness. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adipocytes: Fat-storing cells found mostly in the abdominal cavity and subcutaneous tissue. Fat is usually stored in the form of tryglycerides. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction
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between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Agenesis: Lack of complete or normal development; congenital absence of an organ or part. [NIH]
Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Alexia: The inability to recognize or comprehend written or printed words. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alkaline: Having the reactions of an alkali. [EU] Alkaline Phosphatase: An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1. [NIH] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allergens: Antigen-type substances (hypersensitivity, immediate). [NIH]
that
produce
immediate
hypersensitivity
Allo: A female hormone. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Alveolar Process: The thickest and spongiest part of the maxilla and mandible hollowed out into deep cavities for the teeth. [NIH] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Ameliorated: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amelogenesis Imperfecta: Either hereditary enamel hypoplasia or hypocalcification. [NIH] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (-
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COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Aminolevulinic Acid: A compound produced from succinyl-CoA and glycine as an intermediate in heme synthesis. [NIH] Amniotic Fluid: Amniotic cavity fluid which is produced by the amnion and fetal lungs and kidneys. [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH] Ampulla: A sac-like enlargement of a canal or duct. [NIH] Amygdala: Almond-shaped group of basal nuclei anterior to the inferior horn of the lateral ventricle of the brain, within the temporal lobe. The amygdala is part of the limbic system. [NIH]
Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Analytes: A component of a test sample the presence of which has to be demonstrated. The term "analyte" includes where appropriate formed from the analyte during the analyses. [NIH]
Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Annexins: Family of calcium- and phospholipid-binding proteins which are structurally related and exhibit immunological cross-reactivity. Each member contains four homologous 70 kD repeats. The annexins are differentially distributed in vertebrate tissues (and lower eukaryotes) and appear to be involved in membrane fusion and signal transduction. [NIH] Anomalies: Birth defects; abnormalities. [NIH] Anthropometric measurements: Measurements of human body height, weight, and size of component parts, including skinfold measurement. Used to study and compare the relative proportions under normal and abnormal conditions. [NIH] Anthropometry: The technique that deals with the measurement of the size, weight, and proportions of the human or other primate body. [NIH]
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Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Anticonvulsant: An agent that prevents or relieves convulsions. [EU] Antidote: A remedy for counteracting a poison. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Anti-infective: An agent that so acts. [EU] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antineoplastic Agents: Substances that inhibit or prevent the proliferation of neoplasms. [NIH]
Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Aplasia: Lack of development of an organ or tissue, or of the cellular products from an organ or tissue. [EU] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Appendicitis: Acute inflammation of the vermiform appendix. [NIH] Aqueous: Having to do with water. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU]
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Arteries: The vessels carrying blood away from the heart. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Articular: Of or pertaining to a joint. [EU] Asbestos: Fibrous incombustible mineral composed of magnesium and calcium silicates with or without other elements. It is relatively inert chemically and used in thermal insulation and fireproofing. Inhalation of dust causes asbestosis and later lung and gastrointestinal neoplasms. [NIH] Asbestosis: A lung disorder caused by constant inhalation of asbestos particles. [NIH] Aspartate: A synthetic amino acid. [NIH] Aspartic: The naturally occurring substance is L-aspartic acid. One of the acidic-amino-acids is obtained by the hydrolysis of proteins. [NIH] Aspartic Acid: One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astringents: Agents, usually topical, that cause the contraction of tissues for the control of bleeding or secretions. [NIH] Astrocytes: The largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the blood brain barrier. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with microglia) respond to injury. Astrocytes have high- affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitter, but their role in signaling (as in many other functions) is not well understood. [NIH] Astrocytoma: A tumor that begins in the brain or spinal cord in small, star-shaped cells called astrocytes. [NIH] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Auditory: Pertaining to the sense of hearing. [EU] Autoantibodies: Antibodies that react with self-antigens (autoantigens) of the organism that produced them. [NIH] Autoantigens: Endogenous tissue constituents that have the ability to interact with autoantibodies and cause an immune response. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by autoimmune diseases. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous
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systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Autoradiography: A process in which radioactive material within an object produces an image when it is in close proximity to a radiation sensitive emulsion. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Pigments: Pigments that give a characteristic color to bile including: bilirubin, biliverdine, and bilicyanin. [NIH] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Bioassays: Determination of the relative effective strength of a substance (as a vitamin, hormone, or drug) by comparing its effect on a test organism with that of a standard preparation. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic
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engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Bladder: The organ that stores urine. [NIH] Blastocyst: The mammalian embryo in the post-morula stage in which a fluid-filled cavity, enclosed primarily by trophoblast, contains an inner cell mass which becomes the embryonic disc. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Body Burden: The total amount of a chemical, metal or radioactive substance present at any time after absorption in the body of man or animal. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH] Bone Density: The amount of mineral per square centimeter of bone. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by photon absorptiometry or x-ray computed tomography. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone Marrow Cells: Cells contained in the bone marrow including fat cells, stromal cells, megakaryocytes, and the immediate precursors of most blood cells. [NIH] Bone Remodeling: The continuous turnover of bone matrix and mineral that involves first, an increase in resorption (osteoclastic activity) and later, reactive bone formation (osteoblastic activity). The process of bone remodeling takes place in the adult skeleton at discrete foci. The process ensures the mechanical integrity of the skeleton throughout life and plays an important role in calcium homeostasis. An imbalance in the regulation of bone remodeling's two contrasting events, bone resorption and bone formation, results in many of the metabolic bone diseases, such as osteoporosis. [NIH] Bone Resorption: Bone loss due to osteoclastic activity. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the
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blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Brain Injuries: Acute and chronic injuries to the brain, including the cerebral hemispheres, cerebellum, and brain stem. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with diffuse axonal injury or coma, posttraumatic. Localized injuries may be associated with neurobehavioral manifestations; hemiparesis, or other focal neurologic deficits. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]
Breakdown: A physical, metal, or nervous collapse. [NIH] Breast Feeding: The nursing of an infant at the mother's breast. [NIH] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Burns: Injuries to tissues caused by contact with heat, steam, chemicals (burns, chemical), electricity (burns, electric), or the like. [NIH] Burns, Electric: Burns produced by contact with electric current or from a sudden discharge of electricity. [NIH] Cadmium: An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to cadmium poisoning. [NIH] Cadmium Compounds: Inorganic compounds that contain cadmium as an integral part of the molecule. [NIH] Cadmium Poisoning: Poisoning occurring after exposure to cadmium compounds or fumes. It may cause gastrointestinal syndromes, anemia, or pneumonitis. [NIH] Calcaneus: The largest of the tarsal bones and is situated at the lower and back part of the foot forming the heel. [NIH] Calcification: Deposits of calcium in the tissues of the breast. Calcification in the breast can be seen on a mammogram, but cannot be detected by touch. There are two types of breast calcification, macrocalcification and microcalcification. Macrocalcifications are large deposits and are usually not related to cancer. Microcalcifications are specks of calcium that may be found in an area of rapidly dividing cells. Many microcalcifications clustered together may be a sign of cancer. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium-Binding Proteins: Proteins to which calcium ions are bound. They can act as transport proteins, regulator proteins or activator proteins. [NIH] Callus: A callosity or hard, thick skin; the bone-like reparative substance that is formed round the edges and fragments of broken bone. [NIH] Calmodulin: A heat-stable, low-molecular-weight activator protein found mainly in the
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brain and heart. The binding of calcium ions to this protein allows this protein to bind to cyclic nucleotide phosphodiesterases and to adenyl cyclase with subsequent activation. Thereby this protein modulates cyclic AMP and cyclic GMP levels. [NIH] Caloric intake: Refers to the number of calories (energy content) consumed. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carcinogen: Any substance that causes cancer. [NIH] Carcinogenic: Producing carcinoma. [EU] Cardiac: Having to do with the heart. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Career Choice: Selection of a type of occupation or profession. [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Carpal Tunnel Syndrome: A median nerve injury inside the carpal tunnel that results in symptoms of pain, numbness, tingling, clumsiness, and a lack of sweating, which can be caused by work with certain hand and wrist postures. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group. [NIH] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Cathode: An electrode, usually an incandescent filament of tungsten, which emits electrons in an X-ray tube. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] Caudate Nucleus: Elongated gray mass of the neostriatum located adjacent to the lateral ventricle of the brain. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU]
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Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cellular metabolism: The sum of all chemical changes that take place in a cell through which energy and basic components are provided for essential processes, including the synthesis of new molecules and the breakdown and removal of others. [NIH] Cellulitis: An acute, diffuse, and suppurative inflammation of loose connective tissue, particularly the deep subcutaneous tissues, and sometimes muscle, which is most commonly seen as a result of infection of a wound, ulcer, or other skin lesions. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Centrifugation: A method of separating organelles or large molecules that relies upon differential sedimentation through a preformed density gradient under the influence of a gravitational field generated in a centrifuge. [NIH] Cerebellar: Pertaining to the cerebellum. [EU] Cerebellar Diseases: Diseases that affect the structure or function of the cerebellum. Cardinal manifestations of cerebellar dysfunction include dysmetria, gait ataxia, and muscle hypotonia. [NIH] Cerebellum: Part of the metencephalon that lies in the posterior cranial fossa behind the brain stem. It is concerned with the coordination of movement. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral hemispheres: The two halves of the cerebrum, the part of the brain that controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. The right hemisphere controls muscle movement on the left side of the body, and the left hemisphere controls muscle movement on the right side of the body. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also
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controls speech, emotions, reading, writing, and learning. [NIH] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Chelation: Combination with a metal in complexes in which the metal is part of a ring. [EU] Chelation Therapy: Therapy of heavy metal poisoning using agents which sequester the metal from organs or tissues and bind it firmly within the ring structure of a new compound which can be eliminated from the body. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Cherubism: A fibro-osseous hereditary disease of the jaws. The swollen jaws and raised eyes give a cherubic appearance; multiple radiolucencies are evident upon radiographic examination. [NIH] Chlorophyll: Porphyrin derivatives containing magnesium that act to convert light energy in photosynthetic organisms. [NIH] Chlorpyrifos: An organothiophosphate cholinesterase inhibitor that is used as an insecticide and as an acaricide. [NIH] Chondrogenesis: The formation of cartilage. This process is directed by chondrocytes which continually divide and lay down matrix during development. It is sometimes a precursor to osteogenesis. [NIH] Choroid: The thin, highly vascular membrane covering most of the posterior of the eye between the retina and sclera. [NIH] Choroid Plexus: A villous structure of tangled masses of blood vessels contained within the third, lateral, and fourth ventricles of the brain. It regulates part of the production and composition of cerebrospinal fluid. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]
Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH]
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Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cognition: Intellectual or mental process whereby an organism becomes aware of or obtains knowledge. [NIH] Cohort Studies: Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics. [NIH] Coitus: Sexual intercourse. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Colonoscopy: Endoscopic examination, therapy or surgery of the luminal surface of the colon. [NIH] Communication Disorders: Disorders of verbal and nonverbal communication caused by receptive or expressive language disorders, cognitive dysfunction (e.g., mental retardation), psychiatric conditions, and hearing disorders. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH]
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Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Cone: One of the special retinal receptor elements which are presumed to be primarily concerned with perception of light and color stimuli when the eye is adapted to light. [NIH] Congenita: Displacement, subluxation, or malposition of the crystalline lens. [NIH] Conjugated: Acting or operating as if joined; simultaneous. [EU] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consolidation: The healing process of a bone fracture. [NIH] Constriction: The act of constricting. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Contamination: The soiling or pollution by inferior material, as by the introduction of organisms into a wound, or sewage into a stream. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Control group: In a clinical trial, the group that does not receive the new treatment being studied. This group is compared to the group that receives the new treatment, to see if the new treatment works. [NIH] Conventional therapy: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional treatment. [NIH] Conventional treatment: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional therapy. [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Creatine: An amino acid that occurs in vertebrate tissues and in urine. In muscle tissue, creatine generally occurs as phosphocreatine. Creatine is excreted as creatinine in the urine. [NIH]
Creatinine: A compound that is excreted from the body in urine. Creatinine levels are
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measured to monitor kidney function. [NIH] Creatinine clearance: A test that measures how efficiently the kidneys remove creatinine and other wastes from the blood. Low creatinine clearance indicates impaired kidney function. [NIH] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Cross-Sectional Studies: Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with longitudinal studies which are followed over a period of time. [NIH] Cues: Signals for an action; that specific portion of a perceptual field or pattern of stimuli to which a subject has learned to respond. [NIH] Cultured cells: Animal or human cells that are grown in the laboratory. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytotoxic: Cell-killing. [NIH] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] Data Collection: Systematic gathering of data for a particular purpose from various sources, including questionnaires, interviews, observation, existing records, and electronic devices. The process is usually preliminary to statistical analysis of the data. [NIH] Databases, Bibliographic: Extensive collections, reputedly complete, of references and citations to books, articles, publications, etc., generally on a single subject or specialized subject area. Databases can operate through automated files, libraries, or computer disks. The concept should be differentiated from factual databases which is used for collections of data and facts apart from bibliographic references to them. [NIH] Day Care: Institutional health care of patients during the day. The patients return home at night. [NIH]
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De novo: In cancer, the first occurrence of cancer in the body. [NIH] Death Certificates: Official records of individual deaths including the cause of death certified by a physician, and any other required identifying information. [NIH] Decidua: The epithelial lining of the endometrium that is formed before the fertilized ovum reaches the uterus. The fertilized ovum embeds in the decidua. If the ovum is not fertilized, the decidua is shed during menstruation. [NIH] Decision Making: The process of making a selective intellectual judgment when presented with several complex alternatives consisting of several variables, and usually defining a course of action or an idea. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delusions: A false belief regarding the self or persons or objects outside the self that persists despite the facts, and is not considered tenable by one's associates. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dens in Dente: Anomaly of the tooth, found chiefly in upper lateral incisors. It is characterized by invagination of the enamel at the incisal edge. [NIH] Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dental Care: The total of dental diagnostic, preventive, and restorative services provided to meet the needs of a patient (from Illustrated Dictionary of Dentistry, 1982). [NIH] Dental Caries: Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp. The three most prominent theories used to explain the etiology of the disase are that acids produced by bacteria lead to decalcification; that micro-organisms destroy the enamel protein; or that keratolytic micro-organisms produce chelates that lead to decalcification. [NIH]
Dentate Gyrus: Gray matter situated above the gyrus hippocampi. It is composed of three layers. The molecular layer is continuous with the hippocampus in the hippocampal fissure. The granular layer consists of closely arranged spherical or oval neurons, called granule cells, whose axons pass through the polymorphic layer ending on the dendrites of pyramidal cells in the hippocampus. [NIH] Dentin Dysplasia: Abnormal tissue development or growth occurring subsequent to the appearance of the primordial cells. [NIH] Dentition: The teeth in the dental arch; ordinarily used to designate the natural teeth in position in their alveoli. [EU] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Dermal: Pertaining to or coming from the skin. [NIH] Dermatitis: Any inflammation of the skin. [NIH] Detoxification: Treatment designed to free an addict from his drug habit. [EU] Developing Countries: Countries in the process of change directed toward economic growth, that is, an increase in production, per capita consumption, and income. The process
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of economic growth involves better utilization of natural and human resources, which results in a change in the social, political, and economic structures. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Diazinon: A cholinesterase inhibitor that is used as an organothiophosphorus insecticide. [NIH]
Diencephalon: The paired caudal parts of the prosencephalon from which the thalamus, hypothalamus, epithalamus, and subthalamus are derived. [NIH] Dietary Fats: Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados. [NIH]
Diffuse Axonal Injury: A relatively common sequela of blunt head injury, characterized by a global disruption of axons throughout the brain. Associated clinical features may include neurobehavioral manifestations; persistent vegetative state; dementia; and other disorders. [NIH]
Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] Dilatation: The act of dilating. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discrimination: The act of qualitative and/or quantitative differentiation between two or more stimuli. [NIH] Disposition: A tendency either physical or mental toward certain diseases. [EU] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate
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precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Double-blinded: A clinical trial in which neither the medical staff nor the person knows which of several possible therapies the person is receiving. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Duct: A tube through which body fluids pass. [NIH] Duodenum: The first part of the small intestine. [NIH] Dyslexia: Partial alexia in which letters but not words may be read, or in which words may be read but not understood. [NIH] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Ectoderm: The outer of the three germ layers of the embryo. [NIH] Ectodermal Dysplasia: A group of hereditary disorders involving tissues and structures derived from the embryonic ectoderm. They are characterized by the presence of abnormalities at birth and involvement of both the epidermis and skin appendages. They are generally nonprogressive and diffuse. Various forms exist, including anhidrotic and hidrotic dysplasias, focal dermal hypoplasia, and aplasia cutis congenita. [NIH] Ectopic: Pertaining to or characterized by ectopia. [EU] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Ejaculation: The release of semen through the penis during orgasm. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU] Electrochemistry: The study of chemical changes resulting from electrical action and electrical activity resulting from chemical changes. [NIH] Electrode: Component of the pacing system which is at the distal end of the lead. It is the interface with living cardiac tissue across which the stimulus is transmitted. [NIH] Electrolysis: Destruction by passage of a galvanic electric current, as in disintegration of a chemical compound in solution. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the
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chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Electrophysiological: Pertaining to electrophysiology, that is a branch of physiology that is concerned with the electric phenomena associated with living bodies and involved in their functional activity. [EU] Elementary Particles: Individual components of atoms, usually subatomic; subnuclear particles are usually detected only when the atomic nucleus decays and then only transiently, as most of them are unstable, often yielding pure energy without substance, i.e., radiation. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryogenesis: The process of embryo or embryoid formation, whether by sexual (zygotic) or asexual means. In asexual embryogenesis embryoids arise directly from the explant or on intermediary callus tissue. In some cases they arise from individual cells (somatic cell embryoge). [NIH] Emulsion: A preparation of one liquid distributed in small globules throughout the body of a second liquid. The dispersed liquid is the discontinuous phase, and the dispersion medium is the continuous phase. When oil is the dispersed liquid and an aqueous solution is the continuous phase, it is known as an oil-in-water emulsion, whereas when water or aqueous solution is the dispersed phase and oil or oleaginous substance is the continuous phase, it is known as a water-in-oil emulsion. Pharmaceutical emulsions for which official standards have been promulgated include cod liver oil emulsion, cod liver oil emulsion with malt, liquid petrolatum emulsion, and phenolphthalein in liquid petrolatum emulsion. [EU] Enamel: A very hard whitish substance which covers the dentine of the anatomical crown of a tooth. [NIH] Enamel Microabrasion: Mechanical removal of a small amount of tooth structure (not more than a few tenths of a millimeter in depth) to eliminate superficial enamel discoloration defects not successfully removed by bleaching techniques. A common abrasive is a mixture of pumice and hydrochloric acid. [NIH] Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or chemicals. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocrine System: The system of glands that release their secretions (hormones) directly into the circulatory system. In addition to the endocrine glands, included are the chromaffin system and the neurosecretory systems. [NIH] Endopeptidases: A subclass of peptide hydrolases. They are classified primarily by their catalytic mechanism. Specificity is used only for identification of individual enzymes. They comprise the serine endopeptidases, EC 3.4.21; cysteine endopeptidases, EC 3.4.22; aspartic endopeptidases, EC 3.4.23, metalloendopeptidases, EC 3.4.24; and a group of enzymes yet to be assigned to any of the above sub-classes, EC 3.4.99. EC 3.4.-. [NIH] Endoscope: A thin, lighted tube used to look at tissues inside the body. [NIH] Endoscopic: A technique where a lateral-view endoscope is passed orally to the duodenum for visualization of the ampulla of Vater. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium,
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vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxins: Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells. [NIH] Energy balance: Energy is the capacity of a body or a physical system for doing work. Energy balance is the state in which the total energy intake equals total energy needs. [NIH] Enhancer: Transcriptional element in the virus genome. [NIH] Entorhinal Cortex: Cortex where the signals are combined with those from other sensory systems. [NIH] Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Environmental Pollutants: Substances which pollute the environment. Use environmental pollutants in general or for which there is no specific heading. [NIH]
for
Environmental tobacco smoke: ETS. Smoke that comes from the burning of a tobacco product and smoke that is exhaled by smokers (second-hand smoke). Inhaling ETS is called involuntary or passive smoking. [NIH] Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithalamus: The dorsal posterior subdivision of the diencephalon. The epithalamus is generally considered to include the habenular nuclei (habenula) and associated fiber bundles, the pineal body, and the epithelial roof of the third ventricle. The anterior and posterior paraventricular nuclei of the thalamus are included with the thalamic nuclei although they develop from the same pronuclear mass as the epithalamic nuclei and are
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sometimes considered part of the epithalamus. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Essential Tremor: A rhythmic, involuntary, purposeless, oscillating movement resulting from the alternate contraction and relaxation of opposing groups of muscles. [NIH] Estradiol: The most potent mammalian estrogenic hormone. It is produced in the ovary, placenta, testis, and possibly the adrenal cortex. [NIH] Estrone: 3-Hydroxyestra-1,3,5(10)-trien-17-one. A metabolite of estradiol but possessing less biological activity. It is found in the urine of pregnant women and mares, in the human placenta, and in the urine of bulls and stallions. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), estrone may reasonably be anticipated to be a carcinogen (Merck, 11th ed). [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Excitatory: When cortical neurons are excited, their output increases and each new input they receive while they are still excited raises their output markedly. [NIH] Exfoliation: A falling off in scales or layers. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Expert Systems: Computer programs based on knowledge developed from consultation with experts on a problem, and the processing and/or formalizing of this knowledge using these programs in such a manner that the problems may be solved. [NIH] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extrapyramidal: Outside of the pyramidal tracts. [EU] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Facial: Of or pertaining to the face. [EU] Facial Injuries: General or unspecified injuries to the soft tissue or bony portions of the face. [NIH]
Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Feces: The excrement discharged from the intestines, consisting of bacteria, cells exfoliated from the intestines, secretions, chiefly of the liver, and a small amount of food residue. [EU]
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Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Firearms: Small-arms weapons, including handguns, pistols, revolvers, rifles, shotguns, etc. [NIH]
Fissure: Any cleft or groove, normal or otherwise; especially a deep fold in the cerebral cortex which involves the entire thickness of the brain wall. [EU] Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorine: A nonmetallic, diatomic gas that is a trace element and member of the halogen family. It is used in dentistry as flouride to prevent dental caries. [NIH] Fluorosis: Discoloration of the tooth enamel due to fluorine. [NIH] Focus Groups: A method of data collection and a qualitative research tool in which a small group of individuals are brought together and allowed to interact in a discussion of their opinions about topics, issues, or questions. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Fossa: A cavity, depression, or pit. [NIH] Fourth Ventricle: An irregularly shaped cavity in the rhombencephalon, between the medulla oblongata, the pons, and the isthmus in front, and the cerebellum behind. It is continuous with the central canal of the cord below and with the cerebral aqueduct above, and through its lateral and median apertures it communicates with the subarachnoid space. [NIH]
Fractionation: Dividing the total dose of radiation therapy into several smaller, equal doses delivered over a period of several days. [NIH] Fracture Healing: The physiological restoration of bone tissue and function after a fracture. It includes bony callus formation and normal replacement of bone tissue. [NIH] Frontal Lobe: The anterior part of the cerebral hemisphere. [NIH] Functional magnetic resonance imaging: A noninvasive tool used to observe functioning in the brain or other organs by detecting changes in chemical composition, blood flow, or both. [NIH]
Fungicide: An agent that destroys fungi. [EU] Gait: Manner or style of walking. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized
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connective tissue located outside the central nervous system. [NIH] Gap Junctions: Connections between cells which allow passage of small molecules and electric current. Gap junctions were first described anatomically as regions of close apposition between cells with a narrow (1-2 nm) gap between cell membranes. The variety in the properties of gap junctions is reflected in the number of connexins, the family of proteins which form the junctions. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gas exchange: Primary function of the lungs; transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs. [NIH] Gasoline: Volative flammable fuel (liquid hydrocarbons) derived from crude petroleum by processes such as distillation reforming, polymerization, etc. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal Neoplasms: Tumors or cancer of the gastrointestinal system. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gels: Colloids with a solid continuous phase and liquid as the dispersed phase; gels may be unstable when, due to temperature or other cause, the solid phase liquifies; the resulting colloid is called a sol. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Pool: The total genetic information possessed by the reproductive members of a population of sexually reproducing organisms. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gestational: Psychosis attributable to or occurring during pregnancy. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glioblastoma: A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures. [NIH] Glioblastoma multiforme: A type of brain tumor that forms from glial (supportive) tissue of the brain. It grows very quickly and has cells that look very different from normal cells. Also called grade IV astrocytoma. [NIH]
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Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glossitis: Inflammation of the tongue. [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [NIH]
Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Goblet Cells: Cells of the epithelial lining that produce and secrete mucins. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Government Agencies: Administrative units of government responsible for policy making and management of governmental activities in the U.S. and abroad. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Graphite: An allotropic form of carbon that is used in pencils, as a lubricant, and in matches and explosives. It is obtained by mining and its dust can cause lung irritation. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Growth Plate: The area between the epiphysis and the diaphysis within which bone growth occurs. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Gyrus Cinguli: One of the convolutions on the medial surface of the cerebral hemisphere. It surrounds the rostral part of the brain and interhemispheric commissure and forms part of the limbic system. [NIH] Haemodialysis: The removal of certain elements from the blood by virtue of the difference in the rates of their diffusion through a semipermeable membrane, e.g., by means of a haemodialyzer. [EU] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Harmine: Alkaloid isolated from seeds of Peganum harmala L., Zygophyllaceae. It is
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identical to banisterine, or telepathine, from Banisteria caapi and is one of the active ingredients of hallucinogenic drinks made in the western Amazon region from related plants. It has no therapeutic use, but (as banisterine) was hailed as a cure for postencephalitic Parkinson disease in the 1920's. [NIH] Hazardous Waste: Waste products which, upon release into the atmosphere, water or soil, cause health risks to humans or animals through skin contact, inhalation or ingestion. Hazardous waste sites which contain hazardous waste substances go here. [NIH] Health Education: Education that increases the awareness and favorably influences the attitudes and knowledge relating to the improvement of health on a personal or community basis. [NIH] Health Fairs: Community health education events focused on prevention of disease and promotion of health through audiovisual exhibits. [NIH] Health Status: The level of health of the individual, group, or population as subjectively assessed by the individual or by more objective measures. [NIH] Hearing Disorders: Conditions that impair the transmission or perception of auditory impulses and information from the level of the ear to the temporal cortices, including the sensorineural pathways. [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemiparesis: The weakness or paralysis affecting one side of the body. [NIH] Hemochromatosis: A disease that occurs when the body absorbs too much iron. The body stores the excess iron in the liver, pancreas, and other organs. May cause cirrhosis of the liver. Also called iron overload disease. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation. [NIH]
Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocytes: The main structural component of the liver. They are specialized epithelial cells that are organized into interconnected plates called lobules. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring.
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2. The genetic constitution of an individual. [EU] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Hexachlorobenzene: An agricultural fungicide and seed treatment agent. [NIH] Hippocampus: A curved elevation of gray matter extending the entire length of the floor of the temporal horn of the lateral ventricle (Dorland, 28th ed). The hippocampus, subiculum, and dentate gyrus constitute the hippocampal formation. Sometimes authors include the entorhinal cortex in the hippocampal formation. [NIH] Histology: The study of tissues and cells under a microscope. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Human Development: Continuous sequential changes which occur in the physiological and psychological functions during the individual's life. [NIH] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hydrochloric Acid: A strong corrosive acid that is commonly used as a laboratory reagent. It is formed by dissolving hydrogen chloride in water. Gastric acid is the hydrochloric acid component of gastric juice. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydroxylation: Hydroxylate, to introduce hydroxyl into (a compound or radical) usually by replacement of hydrogen. [EU] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypersensitivity, Immediate: Hypersensitivity reactions which occur within minutes of
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exposure to challenging antigen due to the release of histamine which follows the antigenantibody reaction and causes smooth muscle contraction and increased vascular permeability. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypertension, Renal: Hypertension due to renal diseases, especially chronic parenchymal disease. Hypertension as a result of compression or obstruction of the renal artery or its branches is hypertension, renovascular. [NIH] Hypertension, Renovascular: Hypertension due to compression or obstruction of the renal artery or its branches. [NIH] Hypoplasia: Incomplete development or underdevelopment of an organ or tissue. [EU] Hypothalamic: Of or involving the hypothalamus. [EU] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hypothyroidism: Deficiency of thyroid activity. In adults, it is most common in women and is characterized by decrease in basal metabolic rate, tiredness and lethargy, sensitivity to cold, and menstrual disturbances. If untreated, it progresses to full-blown myxoedema. In infants, severe hypothyroidism leads to cretinism. In juveniles, the manifestations are intermediate, with less severe mental and developmental retardation and only mild symptoms of the adult form. When due to pituitary deficiency of thyrotropin secretion it is called secondary hypothyroidism. [EU] Hypotonia: A condition of diminished tone of the skeletal muscles; diminished resistance of muscles to passive stretching. [EU] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Image Cytometry: A technique encompassing morphometry, densitometry, neural networks, and expert systems that has numerous clinical and research applications and is particularly useful in anatomic pathology for the study of malignant lesions. The most common current application of image cytometry is for DNA analysis, followed by quantitation of immunohistochemical staining. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]
Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunodeficiency syndrome: The inability of the body to produce an immune response. [NIH]
Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH]
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Immunology: The study of the body's immune system. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Infertility: The diminished or absent ability to conceive or produce an offspring while sterility is the complete inability to conceive or produce an offspring. [NIH] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction. [NIH] Inotropic: Affecting the force or energy of muscular contractions. [EU]
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Insecticides: Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intestinal: Having to do with the intestines. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intracellular Membranes: Membranes of subcellular structures. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Involuntary: Reaction occurring without intention or volition. [NIH] Iodine: A nonmetallic element of the halogen group that is represented by the atomic symbol I, atomic number 53, and atomic weight of 126.90. It is a nutritionally essential element, especially important in thyroid hormone synthesis. In solution, it has anti-infective properties and is used topically. [NIH] Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for channel gating can be a membrane potential, drug, transmitter, cytoplasmic messenger, or a mechanical deformation. Ion channels which are integral parts of ionotropic neurotransmitter receptors are not included. [NIH] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ionophores: Chemical agents that increase the permeability of biological or artificial lipid membranes to specific ions. Most ionophores are relatively small organic molecules that act as mobile carriers within membranes or coalesce to form ion permeable channels across membranes. Many are antibiotics, and many act as uncoupling agents by short-circuiting the proton gradient across mitochondrial membranes. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Irrigation: The washing of a body cavity or surface by flowing solution which is inserted
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and then removed. Any drug in the irrigation solution may be absorbed. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Juvenile Delinquency: The antisocial acts of children or persons under age which are illegal or lawfully interpreted as constituting delinquency. [NIH] Kainate: Glutamate receptor. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keratolytic: An agent that promotes keratolysis. [EU] Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lactation: The period of the secretion of milk. [EU] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Language Arts: Skills in the use of language which lead to proficiency in written or spoken communication. [NIH] Language Disorders: Conditions characterized by deficiencies of comprehension or expression of written and spoken forms of language. These include acquired and developmental disorders. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Laryngeal: Having to do with the larynx. [NIH] Larynx: An irregularly shaped, musculocartilaginous tubular structure, lined with mucous membrane, located at the top of the trachea and below the root of the tongue and the hyoid bone. It is the essential sphincter guarding the entrance into the trachea and functioning secondarily as the organ of voice. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Lavage: A cleaning of the stomach and colon. Uses a special drink and enemas. [NIH] Lead Poisoning: Disease caused by the gradual accumulation of a significant body burden of lead. [NIH] Least-Squares Analysis: A principle of estimation in which the estimates of a set of parameters in a statistical model are those quantities minimizing the sum of squared differences between the observed values of a dependent variable and the values predicted by the model. [NIH] Lectin: A complex molecule that has both protein and sugars. Lectins are able to bind to the outside of a cell and cause biochemical changes in it. Lectins are made by both animals and plants. [NIH] Leptin: A 16-kD peptide hormone secreted from white adipocytes and implicated in the
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regulation of food intake and energy balance. Leptin provides the key afferent signal from fat cells in the feedback system that controls body fat stores. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethargy: Abnormal drowsiness or stupor; a condition of indifference. [EU] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Library Services: Services offered to the library user. They include reference and circulation. [NIH]
Life cycle: The successive stages through which an organism passes from fertilized ovum or spore to the fertilized ovum or spore of the next generation. [NIH] Life Expectancy: A figure representing the number of years, based on known statistics, to which any person of a given age may reasonably expect to live. [NIH] Ligands: A RNA simulation method developed by the MIT. [NIH] Limb Bud: A swelling on the trunk of the vertebrate embryo that becomes a limb. Limb bud cultures are used in developmental, organogenesis, morphogenesis, and cell differentiation studies. The limb bud of the chick embryo is most commonly used but mouse and rat limb buds are also used. [NIH] Limbic: Pertaining to a limbus, or margin; forming a border around. [EU] Limbic System: A set of forebrain structures common to all mammals that is defined functionally and anatomically. It is implicated in the higher integration of visceral, olfactory, and somatic information as well as homeostatic responses including fundamental survival behaviors (feeding, mating, emotion). For most authors, it includes the amygdala, epithalamus, gyrus cinguli, hippocampal formation (see hippocampus), hypothalamus, parahippocampal gyrus, septal nuclei, anterior nuclear group of thalamus, and portions of the basal ganglia. (Parent, Carpenter's Human Neuroanatomy, 9th ed, p744; NeuroNames, http://rprcsgi.rprc.washington.edu/neuronames/index.html (September 2, 1998)). [NIH] Linkages: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Lip: Either of the two fleshy, full-blooded margins of the mouth. [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipophilic: Having an affinity for fat; pertaining to or characterized by lipophilia. [EU] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Local Government: Smallest political subdivisions within a country at which general governmental functions are carried-out. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH]
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Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [NIH] Long-Term Potentiation: A persistent increase in synaptic efficacy, usually induced by appropriate activation of the same synapses. The phenomenological properties of long-term potentiation suggest that it may be a cellular mechanism of learning and memory. [NIH] Lucida: An instrument, invented by Wollaton, consisting essentially of a prism or a mirror through which an object can be viewed so as to appear on a plane surface seen in direct view and on which the outline of the object may be traced. [NIH] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] Magnetic Resonance Spectroscopy: Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (magnetic resonance imaging). [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Mammogram: An x-ray of the breast. [NIH] Mandible: The largest and strongest bone of the face constituting the lower jaw. It supports the lower teeth. [NIH] Manic: Affected with mania. [EU] Manic-depressive psychosis: One of a group of psychotic reactions, fundamentally marked by severe mood swings and a tendency to remission and recurrence. [NIH]
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Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Mass Media: Instruments or technological means of communication that reach large numbers of people with a common message: press, radio, television, etc. [NIH] Mass Screening: Organized periodic procedures performed on large groups of people for the purpose of detecting disease. [NIH] Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]
Meat Products: Articles of food which are derived by a process of manufacture from any portion of carcasses of any animal used for food (e.g., head cheese, sausage, scrapple). [NIH] Meconium: The thick green-to-black mucilaginous material found in the intestines of a fullterm fetus. It consists of secretions of the intestinal glands, bile pigments, fatty acids, amniotic fluid, and intrauterine debris. It constitutes the first stools passed by a newborn. [NIH]
Median Nerve: A major nerve of the upper extremity. In humans, the fibers of the median nerve originate in the lower cervical and upper thoracic spinal cord (usually C6 to T1), travel via the brachial plexus, and supply sensory and motor innervation to parts of the forearm and hand. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] Medical Staff: Professional medical personnel who provide care to patients in an organized facility, institution or agency. [NIH] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Megakaryocytes: Very large bone marrow cells which release mature blood platelets. [NIH] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Fusion: The adherence of cell membranes, intracellular membranes, or artifical membrane models of either to each other or to viruses, parasites, or interstitial particles through a variety of chemical and physical processes. [NIH] Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the
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adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Retardation: Refers to sub-average general intellectual functioning which originated during the developmental period and is associated with impairment in adaptive behavior. [NIH]
Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Mesenchymal: Refers to cells that develop into connective tissue, blood vessels, and lymphatic tissue. [NIH] Mesolimbic: Inner brain region governing emotion and drives. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metabotropic: A glutamate receptor which triggers an increase in production of 2 intracellular messengers: diacylglycerol and inositol 1, 4, 5-triphosphate. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microcalcifications: Tiny deposits of calcium in the breast that cannot be felt but can be detected on a mammogram. A cluster of these very small specks of calcium may indicate that cancer is present. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Micro-organism: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Milliliter: A measure of volume for a liquid. A milliliter is approximately 950-times smaller than a quart and 30-times smaller than a fluid ounce. A milliliter of liquid and a cubic centimeter (cc) of liquid are the same. [NIH] Millimeter: A measure of length. A millimeter is approximately 26-times smaller than an inch. [NIH] Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mobility: Capability of movement, of being moved, or of flowing freely. [EU]
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Mobilization: The process of making a fixed part or stored substance mobile, as by separating a part from surrounding structures to make it accessible for an operative procedure or by causing release into the circulation for body use of a substance stored in the body. [EU] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Morphogenesis: The development of the form of an organ, part of the body, or organism. [NIH]
Morphological: Relating to the configuration or the structure of live organs. [NIH] Motility: The ability to move spontaneously. [EU] Mucilaginous: Pertaining to or secreting mucus. [NIH] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Multidrug resistance: Adaptation of tumor cells to anticancer drugs in ways that make the drugs less effective. [NIH] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH] Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. [NIH] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myoclonus: Involuntary shock-like contractions, irregular in rhythm and amplitude, followed by relaxation, of a muscle or a group of muscles. This condition may be a feature of some central nervous systems diseases (e.g., epilepsy, myoclonic). Nocturnal myoclonus may represent a normal physiologic event or occur as the principal feature of the nocturnal myoclonus syndrome. (From Adams et al., Principles of Neurology, 6th ed, pp102-3). [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH]
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Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Needs Assessment: Systematic identification of a population's needs or the assessment of individuals to determine the proper level of services needed. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neonatal period: The first 4 weeks after birth. [NIH] Nephritis: Inflammation of the kidney; a focal or diffuse proliferative or destructive process which may involve the glomerulus, tubule, or interstitial renal tissue. [EU] Nephrosis: Descriptive histopathologic term for renal disease without an inflammatory component. [NIH] Nephrotic: Pertaining to, resembling, or caused by nephrosis. [EU] Nephrotic Syndrome: Clinical association of heavy proteinuria, hypoalbuminemia, and generalized edema. [NIH] Nephrotoxic: Toxic or destructive to kidney cells. [EU] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nerve Endings: Specialized terminations of peripheral neurons. Nerve endings include neuroeffector junction(s) by which neurons activate target organs and sensory receptors which transduce information from the various sensory modalities and send it centrally in the nervous system. Presynaptic nerve endings are presynaptic terminals. [NIH] Nerve Growth Factor: Nerve growth factor is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Networks: Pertaining to a nerve or to the nerves, a meshlike structure of interlocking fibers or strands. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neurites: In tissue culture, hairlike projections of neurons stimulated by growth factors and other molecules. These projections may go on to form a branched tree of dendrites or a single axon or they may be reabsorbed at a later stage of development. "Neurite" may refer to any filamentous or pointed outgrowth of an embryonal or tissue-culture neural cell. [NIH] Neurobehavioral Manifestations: Signs and symptoms of higher cortical dysfunction caused by organic conditions. These include certain behavioral alterations and impairments of skills involved in the acquisition, processing, and utilization of knowledge or information. [NIH]
Neurodegenerative Diseases: Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures. [NIH] Neuroendocrine: Having to do with the interactions between the nervous system and the endocrine system. Describes certain cells that release hormones into the blood in response to stimulation of the nervous system. [NIH] Neurologic: Having to do with nerves or the nervous system. [NIH]
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Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neuropeptide: A member of a class of protein-like molecules made in the brain. Neuropeptides consist of short chains of amino acids, with some functioning as neurotransmitters and some functioning as hormones. [NIH] Neuropsychological Tests: Tests designed to assess neurological function associated with certain behaviors. They are used in diagnosing brain dysfunction or damage and central nervous system disorders or injury. [NIH] Neurotoxic: Poisonous or destructive to nerve tissue. [EU] Neurotoxicity: The tendency of some treatments to cause damage to the nervous system. [NIH]
Neurotoxins: Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept. [NIH] Neurotransmitters: Endogenous signaling molecules that alter the behavior of neurons or effector cells. Neurotransmitter is used here in its most general sense, including not only messengers that act directly to regulate ion channels, but also those that act through second messenger systems, and those that act at a distance from their site of release. Included are neuromodulators, neuroregulators, neuromediators, and neurohumors, whether or not acting at synapses. [NIH] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutropenia: An abnormal decrease in the number of neutrophils, a type of white blood cell. [NIH] Neutrophils: Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes. [NIH] Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]
Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH]
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Nonverbal Communication: Transmission of emotions, ideas, and attitudes between individuals in ways other than the spoken language. [NIH] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary bases in the two strains. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleus Accumbens: Collection of pleomorphic cells in the caudal part of the anterior horn of the lateral ventricle, in the region of the olfactory tubercle, lying between the head of the caudate nucleus and the anterior perforated substance. It is part of the so-called ventral striatum, a composite structure considered part of the basal ganglia. [NIH] Occupational Exposure: The exposure to potentially harmful chemical, physical, or biological agents that occurs as a result of one's occupation. [NIH] Occupational Health: The promotion and maintenance of physical and mental health in the work environment. [NIH] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Oral Health: The optimal state of the mouth and normal functioning of the organs of the mouth without evidence of disease. [NIH] Organ Culture: The growth in aseptic culture of plant organs such as roots or shoots, beginning with organ primordia or segments and maintaining the characteristics of the organ. [NIH] Ossification: The formation of bone or of a bony substance; the conversion of fibrous tissue or of cartilage into bone or a bony substance. [EU] Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the
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foreign literature it is often called osteoarthrosis deformans. [NIH] Osteoblasts: Bone-forming cells which secrete an extracellular matrix. Hydroxyapatite crystals are then deposited into the matrix to form bone. [NIH] Osteoclasts: A large multinuclear cell associated with the absorption and removal of bone. An odontoclast, also called cementoclast, is cytomorphologically the same as an osteoclast and is involved in cementum resorption. [NIH] Osteogenesis: The histogenesis of bone including ossification. It occurs continuously but particularly in the embryo and child and during fracture repair. [NIH] Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Ownership: The legal relation between an entity (individual, group, corporation, or-profit, secular, government) and an object. The object may be corporeal, such as equipment, or completely a creature of law, such as a patent; it may be movable, such as an animal, or immovable, such as a building. [NIH] Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oxygenase: Enzyme which breaks down heme, the iron-containing oxygen-carrying constituent of the red blood cells. [NIH] Palate: The structure that forms the roof of the mouth. It consists of the anterior hard palate and the posterior soft palate. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [NIH] Parasitism: A) The mode of life of a parasite; b) The relationship between an organism (parasite) that derives benefits from, and at the expense of, another organism (host). [NIH] Parathyroid: 1. Situated beside the thyroid gland. 2. One of the parathyroid glands. 3. A sterile preparation of the water-soluble principle(s) of the parathyroid glands, ad-ministered parenterally as an antihypocalcaemic, especially in the treatment of acute hypoparathyroidism with tetany. [EU] Parathyroid Glands: Two small paired endocrine glands in the region of the thyroid gland. They secrete parathyroid hormone and are concerned with the metabolism of calcium and phosphorus. [NIH]
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Paternal Exposure: Exposure of the male parent, human or animal, to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals that may affect offspring. [NIH] Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
Pediatric Dentistry: The practice of dentistry concerned with the dental problems of children, proper maintenance, and treatment. The dental care may include the services provided by dental specialists. [NIH] Pediatrics: A medical specialty concerned with maintaining health and providing medical care to children from birth to adolescence. [NIH] Penicillamine: 3-Mercapto-D-valine. The most characteristic degradation product of the penicillin antibiotics. It is used as an antirheumatic and as a chelating agent in Wilson's disease. [NIH] Penicillin: An antibiotic drug used to treat infection. [NIH] Pensions: Fixed sums paid regularly to individuals. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Perception: The ability quickly and accurately to recognize similarities and differences among presented objects, whether these be pairs of words, pairs of number series, or multiple sets of these or other symbols such as geometric figures. [NIH] Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral Neuropathy: Nerve damage, usually affecting the feet and legs; causing pain, numbness, or a tingling feeling. Also called "somatic neuropathy" or "distal sensory polyneuropathy." [NIH] Pest Control: The reduction or regulation of the population of noxious, destructive, or dangerous insects or other animals. [NIH] Pesticides: Chemicals used to destroy pests of any sort. The concept includes fungicides (industrial fungicides), insecticides, rodenticides, etc. [NIH] Petroleum: Naturally occurring complex liquid hydrocarbons which, after distillation, yield combustible fuels, petrochemicals, and lubricants. [NIH] P-Glycoprotein: A 170 kD transmembrane glycoprotein from the superfamily of ABC
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transporters. It serves as an ATP-dependent efflux pump for a variety of chemicals, including many antineoplastic agents. Overexpression of this glycoprotein is associated with multidrug resistance. [NIH] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phosphodiesterase: Effector enzyme that regulates the levels of a second messenger, the cyclic GMP. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photoreceptor: Receptor capable of being activated by light stimuli, as a rod or cone cell of the eye. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]
Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Pigmentation: Coloration or discoloration of a part by a pigment. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH]
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Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH] Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Plasticity: In an individual or a population, the capacity for adaptation: a) through gene changes (genetic plasticity) or b) through internal physiological modifications in response to changes of environment (physiological plasticity). [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Pleomorphic: Occurring in various distinct forms. In terms of cells, having variation in the size and shape of cells or their nuclei. [NIH] Plexus: A network or tangle; a general term for a network of lymphatic vessels, nerves, or veins. [EU] Plumbism: Disease caused by the gradual accumulation of a significant body burden of lead. [NIH] Pneumoconiosis: Condition characterized by permanent deposition of substantial amounts of particulate matter in the lungs, usually of occupational or environmental origin, and by the tissue reaction to its presence. [NIH] Pneumonitis: A disease caused by inhaling a wide variety of substances such as dusts and molds. Also called "farmer's disease". [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Policy Making: The decision process by which individuals, groups or institutions establish policies pertaining to plans, programs or procedures. [NIH] Polychlorinated Biphenyls: Industrial products consisting of a mixture of chlorinated biphenyl congeners and isomers. These compounds are highly lipophilic and tend to accumulate in fat stores of animals. Many of these compounds are considered toxic and potential environmental pollutants. [NIH] Polymorphism: The occurrence together of two or more distinct forms in the same
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population. [NIH] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Population Density: Number of individuals in a population relative to space. [NIH] Porphobilinogen Synthase: An enzyme that catalyzes the formation of porphobilinogen from two molecules of 5-aminolevulinic acid. EC 4.2.1.24. [NIH] Porphyria: A group of disorders characterized by the excessive production of porphyrins or their precursors that arises from abnormalities in the regulation of the porphyrin-heme pathway. The porphyrias are usually divided into three broad groups, erythropoietic, hepatic, and erythrohepatic, according to the major sites of abnormal porphyrin synthesis. [NIH]
Porphyrins: A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Post-synaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Post-traumatic: Occurring as a result of or after injury. [EU] Potassium: An element that is in the alkali group of metals. It has an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte and it plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practicability: A non-standard characteristic of an analytical procedure. It is dependent on the scope of the method and is determined by requirements such as sample throughout and costs. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Preclinical: Before a disease becomes clinically recognizable. [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predisposition: A latent susceptibility to disease which may be activated under certain
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conditions, as by stress. [EU] Prefrontal Cortex: The rostral part of the frontal lobe, bounded by the inferior precentral fissure in humans, which receives projection fibers from the mediodorsal nucleus of the thalamus. The prefrontal cortex receives afferent fibers from numerous structures of the diencephalon, mesencephalon, and limbic system as well as cortical afferents of visual, auditory, and somatic origin. [NIH] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Presumptive: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Primary Prevention: Prevention of disease or mental disorders in susceptible individuals or populations through promotion of health, including mental health, and specific protection, as in immunization, as distinguished from the prevention of complications or after-effects of existing disease. [NIH] Private Sector: That distinct portion of the institutional, industrial, or economic structure of a country that is controlled or owned by non-governmental, private interests. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Program Evaluation: Studies designed to assess the efficacy of programs. They may include the evaluation of cost-effectiveness, the extent to which objectives are met, or impact. [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Promotor: In an operon, a nucleotide sequence located at the operator end which contains all the signals for the correct initiation of genetic transcription by the RNA polymerase holoenzyme and determines the maximal rate of RNA synthesis. [NIH] Prone: Having the front portion of the body downwards. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Propoxur: A carbamate insecticide. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes
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a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (endopeptidases). [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteoglycans: Glycoproteins which have a very high polysaccharide content. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychosis: A mental disorder characterized by gross impairment in reality testing as evidenced by delusions, hallucinations, markedly incoherent speech, or disorganized and agitated behaviour without apparent awareness on the part of the patient of the incomprehensibility of his behaviour; the term is also used in a more general sense to refer to mental disorders in which mental functioning is sufficiently impaired as to interfere grossly with the patient's capacity to meet the ordinary demands of life. Historically, the term has been applied to many conditions, e.g. manic-depressive psychosis, that were first described in psychotic patients, although many patients with the disorder are not judged psychotic. [EU] Puberty: The period during which the secondary sex characteristics begin to develop and the capability of sexual reproduction is attained. [EU] Public Assistance: Financial assistance to impoverished persons for the essentials of living through federal, state or local government programs. [NIH] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Housing: Housing subsidized by tax funds, usually intended for low income persons
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or families. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Pulmonary: Relating to the lungs. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radioactive: Giving off radiation. [NIH] Radioisotope: An unstable element that releases radiation as it breaks down. Radioisotopes can be used in imaging tests or as a treatment for cancer. [NIH] Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Rape: Unlawful sexual intercourse without consent of the victim. [NIH] Reaction Time: The time from the onset of a stimulus until the organism responds. [NIH] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] Reality Testing: The individual's objective evaluation of the external world and the ability to differentiate adequately between it and the internal world; considered to be a primary ego function. [NIH] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Receptors, Serotonin: Cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [NIH]
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Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflective: Capable of throwing back light, images, sound waves : reflecting. [EU] Reflex: An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Registries: The systems and processes involved in the establishment, support, management, and operation of registers, e.g., disease registers. [NIH] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Reliability: Used technically, in a statistical sense, of consistency of a test with itself, i. e. the extent to which we can assume that it will yield the same result if repeated a second time. [NIH]
Renal Artery: A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters. [NIH] Reproductive cells: Egg and sperm cells. Each mature reproductive cell carries a single set of 23 chromosomes. [NIH] Research Design: A plan for collecting and utilizing data so that desired information can be obtained with sufficient precision or so that an hypothesis can be tested properly. [NIH] Research Support: Financial support of research activities. [NIH] Resorption: The loss of substance through physiologic or pathologic means, such as loss of dentin and cementum of a tooth, or of the alveolar process of the mandible or maxilla. [EU] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Response Elements: Nucleotide sequences, usually upstream, which are recognized by specific regulatory transcription factors, thereby causing gene response to various regulatory agents. These elements may be found in both promotor and enhancer regions. [NIH]
Response rate: The percentage of patients whose cancer shrinks or disappears after treatment. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its
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outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retrospective: Looking back at events that have already taken place. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Rickets: A condition caused by deficiency of vitamin D, especially in infancy and childhood, with disturbance of normal ossification. The disease is marked by bending and distortion of the bones under muscular action, by the formation of nodular enlargements on the ends and sides of the bones, by delayed closure of the fontanelles, pain in the muscles, and sweating of the head. Vitamin D and sunlight together with an adequate diet are curative, provided that the parathyroid glands are functioning properly. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rodenticides: Substances used to destroy or inhibit the action of rats, mice, or other rodents. [NIH]
Rubella: An acute, usually benign, infectious disease caused by a togavirus and most often affecting children and nonimmune young adults, in which the virus enters the respiratory tract via droplet nuclei and spreads to the lymphatic system. It is characterized by a slight cold, sore throat, and fever, followed by enlargement of the postauricular, suboccipital, and cervical lymph nodes, and the appearances of a fine pink rash that begins on the head and spreads to become generalized. Called also German measles, roetln, röteln, and three-day measles, and rubeola in French and Spanish. [EU] Saliva: The clear, viscous fluid secreted by the salivary glands and mucous glands of the mouth. It contains mucins, water, organic salts, and ptylin. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Scatter: The extent to which relative success and failure are divergently manifested in qualitatively different tests. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions,
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depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Sclera: The tough white outer coat of the eyeball, covering approximately the posterior fivesixths of its surface, and continuous anteriorly with the cornea and posteriorly with the external sheath of the optic nerve. [EU] Screening: Checking for disease when there are no symptoms. [NIH] Second Messenger Systems: Systems in which an intracellular signal is generated in response to an intercellular primary messenger such as a hormone or neurotransmitter. They are intermediate signals in cellular processes such as metabolism, secretion, contraction, phototransduction, and cell growth. Examples of second messenger systems are the adenyl cyclase-cyclic AMP system, the phosphatidylinositol diphosphate-inositol triphosphate system, and the cyclic GMP system. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Sediment: A precipitate, especially one that is formed spontaneously. [EU] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.96. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of glutathione peroxidase. [NIH] Self-Injurious Behavior: Behavior in which persons hurt or harm themselves without the motive of suicide or of sexual deviation. [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sensor: A device designed to respond to physical stimuli such as temperature, light, magnetism or movement and transmit resulting impulses for interpretation, recording, movement, or operating control. [NIH] Septal: An abscess occurring at the root of the tooth on the proximal surface. [NIH] Septal Nuclei: Neural nuclei situated in the septal region. They have afferent and cholinergic efferent connections with a variety of forebrain and brainstem areas including the hippocampus, the lateral hypothalamus, the tegmentum, and the amygdala. Included are the dorsal, lateral, medial, and triangular septal nuclei, septofimbrial nucleus, nucleus of diagonal band, nucleus of anterior commissure, and the nucleus of stria terminalis. [NIH] Sequester: A portion of dead bone which has become detached from the healthy bone tissue, as occurs in necrosis. [NIH]
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Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Shedding: Release of infectious particles (e. g., bacteria, viruses) into the environment, for example by sneezing, by fecal excretion, or from an open lesion. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Silicosis: A type of pneumoconiosis caused by inhalation of particles of silica, quartz, ganister or slate. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Sneezing: Sudden, forceful, involuntary expulsion of air from the nose and mouth caused by irritation to the mucous membranes of the upper respiratory tract. [NIH] Social Behavior: Any behavior caused by or affecting another individual, usually of the same species. [NIH]
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Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Socioeconomic Factors: Social and economic factors that characterize the individual or group within the social structure. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Sodium Channels: Cell membrane glycoproteins selective for sodium ions. Fast sodium current is associated with the action potential in neural membranes. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Sound wave: An alteration of properties of an elastic medium, such as pressure, particle displacement, or density, that propagates through the medium, or a superposition of such alterations. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Sperm Count: A count of sperm in the ejaculum, expressed as number per milliliter. [NIH] Spermatozoa: Mature male germ cells that develop in the seminiferous tubules of the testes. Each consists of a head, a body, and a tail that provides propulsion. The head consists mainly of chromatin. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spinal Nerves: The 31 paired peripheral nerves formed by the union of the dorsal and ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included. [NIH] Spontaneous Abortion: The non-induced birth of an embryo or of fetus prior to the stage of viability at about 20 weeks of gestation. [NIH]
Dictionary 213
Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Stabilization: The creation of a stable state. [EU] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Striatum: A higher brain's domain thus called because of its stripes. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stromal: Large, veil-like cell in the bone marrow. [NIH] Stromal Cells: Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Subiculum: A region of the hippocampus that projects to other areas of the brain. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Succimer: A mercaptodicarboxylic acid used as an antidote to heavy metal poisoning because it forms strong chelates with them. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Suppurative: Consisting of, containing, associated with, or identified by the formation of pus. [NIH] Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic
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nervous system. Called also adrenergic. [EU] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Synapses: Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate through direct electrical connections which are sometimes called electrical synapses; these are not included here but rather in gap junctions. [NIH] Synapsis: The pairing between homologous chromosomes of maternal and paternal origin during the prophase of meiosis, leading to the formation of gametes. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptic Transmission: The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors. These activated receptors modulate ion channels and/or secondmessenger systems to influence the postsynaptic cell. Electrical transmission is less common in the nervous system, and, as in other tissues, is mediated by gap junctions. [NIH] Synaptic Vesicles: Membrane-bound compartments which contain transmitter molecules. Synaptic vesicles are concentrated at presynaptic terminals. They actively sequester transmitter molecules from the cytoplasm. In at least some synapses, transmitter release occurs by fusion of these vesicles with the presynaptic membrane, followed by exocytosis of their contents. [NIH] Synaptosomes: Pinched-off nerve endings and their contents of vesicles and cytoplasm together with the attached subsynaptic area of the membrane of the post-synaptic cell. They are largely artificial structures produced by fractionation after selective centrifugation of nervous tissue homogenates. [NIH] Systemic: Affecting the entire body. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Tarsal Bones: The seven bones which form the tarsus - namely, calcaneus, talus, cuboid, navicular, and first, second and third cuneiforms. The tarsus is a skeletal part of the foot. [NIH]
Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Teratogen: A substance which, through immediate, prolonged or repeated contact with the skin may involve a risk of subsequent non-hereditable birth defects in offspring. [NIH] Testicular: Pertaining to a testis. [EU] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein synthesis. [NIH]
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Tetraethyl Lead: A highly toxic compound used as a gasoline additive. It causes acute toxic psychosis or chronic poisoning if inhaled or absorbed through the skin. [NIH] Thalamus: Paired bodies containing mostly gray substance and forming part of the lateral wall of the third ventricle of the brain. The thalamus represents the major portion of the diencephalon and is commonly divided into cellular aggregates known as nuclear groups. [NIH]
Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombolytic: 1. Dissolving or splitting up a thrombus. 2. A thrombolytic agent. [EU] Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyrotoxicosis: The clinical syndrome that reflects the response of the peripheral tissues to an excess of thyroid hormone. [NIH] Thyrotropin: A peptide hormone secreted by the anterior pituitary. It promotes the growth of the thyroid gland and stimulates the synthesis of thyroid hormones and the release of thyroxine by the thyroid gland. [NIH] Tin: A trace element that is required in bone formation. It has the atomic symbol Sn, atomic number 50, and atomic weight 118.71. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicokinetics: Study of the absorption, distribution, metabolism, and excretion of test substances. [NIH] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH]
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Toxins: Specific, characterizable, poisonous chemicals, often proteins, with specific biological properties, including immunogenicity, produced by microbes, higher plants, or animals. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Training Support: Financial support for training including both student stipends and loans and training grants to institutions. [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, practicability, etc., of these interventions in individual cases or series. [NIH]
Tremor: Cyclical movement of a body part that can represent either a physiologic process or a manifestation of disease. Intention or action tremor, a common manifestation of cerebellar diseases, is aggravated by movement. In contrast, resting tremor is maximal when there is no attempt at voluntary movement, and occurs as a relatively frequent manifestation of Parkinson disease. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tubercle: A rounded elevation on a bone or other structure. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Unconditioned: An inborn reflex common to all members of a species. [NIH]
Dictionary 217
Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Uncoupling Agents: Chemical agents that uncouple oxidation from phosphorylation in the metabolic cycle so that ATP synthesis does not occur. Included here are those ionophores that disrupt electron transfer by short-circuiting the proton gradient across mitochondrial membranes. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Valine: A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway. [NIH]
Valproic Acid: A fatty acid with anticonvulsant properties used in the treatment of epilepsy. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GABA levels in the brain or by altering the properties of voltage dependent sodium channels. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasodilator: An agent that widens blood vessels. [NIH] VE: The total volume of gas either inspired or expired in one minute. [NIH] Veins: The vessels carrying blood toward the heart. [NIH] Venoms: Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling prey or predator. [NIH] Venous: Of or pertaining to the veins. [EU] Venous blood: Blood that has given up its oxygen to the tissues and carries carbon dioxide back for gas exchange. [NIH] Ventral: 1. Pertaining to the belly or to any venter. 2. Denoting a position more toward the belly surface than some other object of reference; same as anterior in human anatomy. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vesicular: 1. Composed of or relating to small, saclike bodies. 2. Pertaining to or made up of vesicles on the skin. [EU] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Villous: Of a surface, covered with villi. [NIH]
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Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Viscera: Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] War: Hostile conflict between organized groups of people. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]
Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Xenobiotics: Chemical substances that are foreign to the biological system. They include naturally occurring compounds, drugs, environmental agents, carcinogens, insecticides, etc. [NIH]
Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Zygote: The fertilized ovum. [NIH]
219
INDEX A Abdomen, 91, 163, 169, 190, 192, 213, 215, 218 Aberrant, 18, 163 Abscess, 120, 163, 210 Acetylcholine, 163, 198 Acrodynia, 120, 163 Adaptability, 53, 163, 172 Adaptation, 46, 163, 196, 203 Adipocytes, 163, 191 Adjustment, 7, 61, 112, 163 Adolescence, 21, 163, 201 Adrenergic, 163, 179, 181, 213 Adverse Effect, 12, 17, 34, 39, 48, 163, 211 Aerobic, 163, 195 Afferent, 163, 192, 205, 210 Affinity, 58, 163, 164, 167, 192, 212 Agenesis, 120, 164 Agonist, 164, 179 Alexia, 164, 179 Algorithms, 164, 169 Alkaline, 36, 164, 170 Alkaline Phosphatase, 36, 164 Alleles, 53, 164 Allergens, 6, 164 Allo, 164, 185 Alpha Particles, 164, 207 Alternative medicine, 127, 164 Alveolar Process, 164, 208 Alveoli, 164, 177 Ameliorated, 5, 164 Ameliorating, 61, 164 Amelogenesis Imperfecta, 120, 164 Amino Acid Sequence, 164, 166 Amino Acids, 164, 167, 198, 201, 204, 206, 209, 216 Aminolevulinic Acid, 53, 55, 74, 91, 165, 204 Amniotic Fluid, 165, 194 Amplification, 32, 165 Ampulla, 165, 180 Amygdala, 165, 192, 210 Anaesthesia, 165, 189 Anal, 165, 181, 193 Analogous, 44, 165, 216 Analytes, 142, 165 Anaphylatoxins, 165, 174 Anatomical, 165, 180, 189
Anemia, 78, 158, 165, 170 Animal model, 17, 20, 36, 40, 41, 43, 119, 165 Anions, 165, 190 Annexins, 22, 165 Anomalies, 120, 165 Anthropometric measurements, 25, 165 Anthropometry, 19, 165 Antibacterial, 166, 212 Antibiotic, 43, 166, 201, 212, 214 Antibodies, 46, 166, 167, 185, 188, 193, 203 Antibody, 164, 166, 174, 185, 187, 188, 189, 194, 212 Anticonvulsant, 166, 217 Antidote, 166, 213 Antigen, 44, 46, 164, 166, 174, 187, 188, 189, 194 Antigen-Antibody Complex, 166, 174 Anti-infective, 166, 190 Antineoplastic, 166, 202 Antineoplastic Agents, 166, 202 Antioxidant, 166, 200 Aplasia, 120, 166, 179 Apoptosis, 31, 166 Appendicitis, 65, 166 Aqueous, 58, 166, 168, 176, 180 Arginine, 165, 166, 198 Arterial, 166, 188, 206, 214 Arteries, 166, 167, 169, 175, 195 Arterioles, 167, 169, 171 Articular, 167, 199 Asbestos, 28, 167 Asbestosis, 167 Aspartate, 48, 51, 167 Aspartic, 35, 167, 180 Aspartic Acid, 35, 167 Assay, 32, 38, 42, 46, 52, 62, 75, 167 Astringents, 167, 195 Astrocytes, 19, 22, 167 Astrocytoma, 167, 184 Atrophy, 167, 197 Atypical, 32, 167 Auditory, 20, 42, 167, 186, 205 Autoantibodies, 60, 167 Autoantigens, 167 Autoimmune disease, 60, 167 Autoimmunity, 60, 167 Autonomic, 163, 167, 199, 201
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Autonomic Nervous System, 167, 201 Autoradiography, 38, 168 B Bacteria, 43, 166, 168, 177, 182, 195, 207, 211, 212, 216, 217 Bacterial Physiology, 163, 168 Basal Ganglia, 168, 184, 192, 199 Base, 23, 168, 177, 191, 214 Basement Membrane, 168, 182, 191 Benign, 168, 209 Bile, 168, 183, 192, 194 Bile Pigments, 168, 194 Binding Sites, 59, 168 Bioassays, 59, 168 Biochemical, 5, 22, 43, 44, 46, 47, 50, 54, 55, 73, 78, 89, 164, 168, 191, 199, 211 Biomarkers, 17, 29, 31, 39, 48, 50, 168 Biopsy, 95, 159, 168 Biosynthesis, 53, 63, 168, 206 Biotechnology, 61, 127, 137, 168 Bladder, 169, 189, 205, 217 Blastocyst, 169, 175, 202 Blood Coagulation, 169, 170 Blood Glucose, 169, 186, 190 Blood Platelets, 169, 194, 211 Blood pressure, 23, 24, 27, 113, 158, 169, 171, 188, 196, 212 Blood vessel, 169, 171, 172, 173, 180, 185, 191, 193, 195, 212, 213, 215, 217 Body Burden, 7, 15, 24, 27, 33, 46, 113, 169, 191, 203 Body Fluids, 168, 169, 179, 212, 216 Body Mass Index, 16, 38, 169 Bone Density, 113, 169 Bone Marrow, 36, 169, 188, 193, 194, 213 Bone Marrow Cells, 36, 169, 194 Bone Remodeling, 39, 169 Bone Resorption, 19, 36, 40, 169 Bowel, 63, 165, 169, 178, 190, 213 Bowel Movement, 169, 178, 213 Bradykinin, 169, 198 Brain Injuries, 53, 170 Brain Stem, 170, 172 Branch, 12, 155, 170, 180, 193, 201, 206, 208, 212, 215 Breakdown, 170, 172, 178, 184, 199 Breast Feeding, 39, 170 Buccal, 170, 193 Burns, 53, 121, 170 Burns, Electric, 170 C Cadmium, 4, 13, 24, 42, 58, 59, 170
Cadmium Compounds, 170 Cadmium Poisoning, 13, 170 Calcaneus, 56, 170, 214 Calcification, 66, 170 Calcium-Binding Proteins, 22, 170 Callus, 170, 180, 183 Calmodulin, 31, 170 Caloric intake, 16, 171 Capillary, 52, 170, 171, 217 Capsules, 131, 171 Carbon Dioxide, 171, 184, 202, 208, 217 Carcinogen, 171, 182 Carcinogenic, 171, 189, 205 Cardiac, 171, 179, 181, 196 Cardiovascular, 23, 171, 211 Cardiovascular disease, 23, 171 Career Choice, 34, 171 Carotene, 171, 209 Carpal Tunnel Syndrome, 12, 171 Case report, 38, 56, 171 Case-Control Studies, 38, 171, 181 Catecholamine, 171, 178 Cathode, 171, 180 Cations, 43, 171, 190 Caudal, 171, 178, 188, 199, 204 Caudate Nucleus, 171, 199 Causal, 5, 26, 46, 171, 181 Cause of Death, 172, 177 Cell Cycle, 50, 172 Cell Death, 5, 43, 166, 172, 196 Cell Differentiation, 172, 192, 211 Cell Division, 168, 172, 185, 194, 195, 202, 205, 210 Cell proliferation, 172, 211 Cell Respiration, 172, 195, 208 Cellular metabolism, 19, 172 Cellulitis, 120, 172 Central Nervous System, 45, 51, 55, 113, 163, 168, 172, 184, 196, 198, 211 Centrifugation, 172, 214 Cerebellar, 16, 66, 95, 172, 216 Cerebellar Diseases, 172, 216 Cerebellum, 4, 18, 23, 38, 47, 170, 172, 183 Cerebral, 35, 55, 168, 170, 172, 181, 183, 184, 185 Cerebral hemispheres, 168, 170, 172, 184 Cerebrospinal, 172, 173 Cerebrospinal fluid, 172, 173 Cerebrovascular, 171, 172 Cerebrum, 172 Cervical, 173, 194, 209
Index 221
Chelation, 44, 60, 71, 80, 84, 93, 95, 101, 173 Chelation Therapy, 44, 60, 80, 93, 173 Chemotactic Factors, 173, 174 Cherubism, 120, 173 Chlorophyll, 53, 173 Chlorpyrifos, 17, 173 Chondrogenesis, 9, 40, 173 Choroid, 25, 173, 209 Choroid Plexus, 25, 173 Chromatin, 60, 166, 173, 198, 212 Chromosomal, 165, 173 Chromosome, 173, 192, 210 Chronic Disease, 21, 50, 173 CIS, 173, 209 Clinical Medicine, 62, 64, 102, 173, 204 Clinical trial, 3, 40, 60, 111, 115, 137, 173, 175, 179, 206, 207 Cloning, 169, 173 Cofactor, 174, 206 Cognition, 6, 22, 25, 36, 40, 46, 47, 49, 59, 174 Cohort Studies, 174, 181 Coitus, 31, 174 Collagen, 19, 44, 168, 174, 183, 203, 205 Colonoscopy, 63, 174 Communication Disorders, 116, 121, 136, 174 Complement, 22, 165, 174 Computational Biology, 137, 174 Conception, 23, 114, 175, 183, 213 Cone, 175, 202 Congenita, 175, 179 Conjugated, 175, 176 Connective Tissue, 169, 172, 174, 175, 183, 184, 193, 195, 213 Consolidation, 51, 175 Constriction, 175, 191 Consumption, 15, 29, 175, 177, 208 Contamination, 4, 31, 51, 89, 114, 175 Contraindications, ii, 175 Control group, 39, 175 Conventional therapy, 99, 175 Conventional treatment, 175 Coordination, 59, 118, 172, 175 Coronary, 171, 175, 195 Coronary heart disease, 171, 175 Coronary Thrombosis, 175, 195 Cortex, 7, 175, 181, 182, 183, 205 Cortical, 38, 48, 175, 182, 197, 205, 210 Cranial, 172, 175, 201 Creatine, 48, 175
Creatinine, 24, 175, 176 Creatinine clearance, 24, 176 Crossing-over, 176, 207 Cross-Sectional Studies, 176, 181 Cues, 20, 176 Cultured cells, 44, 176 Curative, 176, 209, 215 Cutaneous, 176, 193 Cyclic, 120, 171, 176, 185, 198, 202, 204, 210 Cytochrome, 98, 176 Cytokine, 60, 176 Cytoplasm, 166, 176, 181, 185, 198, 209, 214 Cytotoxic, 176, 211 Cytotoxicity, 20, 176 D Data Collection, 8, 37, 176, 183 Databases, Bibliographic, 137, 176 Day Care, 117, 143, 176 De novo, 58, 177 Death Certificates, 13, 177 Decidua, 177, 202 Decision Making, 68, 77, 84, 100, 177 Degenerative, 177, 186, 199 Deletion, 166, 177 Delusions, 177, 206 Dendrites, 177, 197, 198 Dens in Dente, 120, 177 Density, 169, 172, 177, 212 Dental Care, 177, 201 Dental Caries, 37, 177, 183 Dentate Gyrus, 177, 187 Dentin Dysplasia, 120, 177 Dentition, 69, 177 Depolarization, 177, 211 Dermal, 177, 179 Dermatitis, 53, 177 Detoxification, 59, 177 Developing Countries, 91, 177 Diabetes Mellitus, 178, 186 Diagnostic procedure, 127, 178 Diastolic, 178, 188 Diazinon, 17, 178 Diencephalon, 178, 181, 188, 205, 215 Dietary Fats, 37, 178 Diffuse Axonal Injury, 170, 178 Diffusion, 178, 185 Digestion, 163, 168, 169, 178, 190, 192, 213 Digestive system, 116, 178 Digestive tract, 178, 211 Dilatation, 178, 205
222
Lead Poisoning
Direct, iii, 6, 10, 19, 26, 30, 34, 42, 49, 57, 129, 173, 178, 179, 193, 208, 214 Discrimination, 20, 178 Disposition, 33, 178 Dissociation, 163, 178 Distal, 178, 179, 201, 206 Dopamine, 7, 41, 178 Double-blinded, 19, 179 Drug Interactions, 130, 179 Duct, 165, 179, 209 Duodenum, 168, 179, 180, 213 Dyslexia, 20, 179 Dysplasia, 91, 120, 179 E Ectoderm, 179 Ectodermal Dysplasia, 120, 179 Ectopic, 10, 179 Edema, 179, 197 Effector, 163, 174, 179, 198, 202 Effector cell, 179, 198 Efficacy, 48, 72, 179, 193, 205, 216 Ejaculation, 179, 210 Elastin, 174, 179 Elective, 96, 179 Electrochemistry, 42, 179 Electrode, 42, 171, 179 Electrolysis, 165, 171, 179 Electrolyte, 179, 204, 212 Electrons, 166, 168, 171, 179, 190, 193, 200, 207 Electrophysiological, 40, 72, 180 Elementary Particles, 179, 180, 193, 198, 206 Embryo, 50, 169, 172, 179, 180, 189, 192, 200, 212 Embryogenesis, 54, 180 Emulsion, 168, 180 Enamel, 120, 164, 177, 180, 183 Enamel Microabrasion, 120, 180 Encephalopathy, 83, 87, 180 Endemic, 180, 213 Endocrine System, 180, 197 Endopeptidases, 180, 206 Endoscope, 180 Endoscopic, 63, 174, 180 Endothelial cell, 46, 180 Endothelium, 180, 181, 198, 203 Endothelium-derived, 181, 198 Endotoxins, 6, 174, 181 Energy balance, 181, 192 Enhancer, 181, 208 Entorhinal Cortex, 181, 187
Environmental Exposure, 16, 17, 24, 27, 111, 181 Environmental Pollutants, 11, 181, 203 Environmental tobacco smoke, 48, 181 Enzymatic, 170, 171, 174, 177, 181, 209 Enzyme, 32, 46, 54, 55, 164, 179, 181, 185, 200, 202, 203, 204, 206, 211, 213, 218 Epidemic, 73, 74, 108, 181, 213 Epidemiologic Studies, 16, 31, 181 Epidemiological, 16, 19, 21, 58, 62, 73, 181 Epidermis, 179, 181 Epinephrine, 163, 179, 181, 199, 216 Epithalamus, 178, 181, 192 Epithelial, 177, 181, 182, 185, 186, 191 Epithelial Cells, 182, 186, 191 Erythrocytes, 62, 71, 165, 169, 182, 208 Esophagus, 178, 182, 213 Essential Tremor, 16, 17, 182 Estradiol, 182 Estrone, 114, 182 Excitation, 10, 182 Excitatory, 7, 51, 182, 185 Exfoliation, 120, 182 Exogenous, 23, 54, 182 Expert Systems, 182, 188 Extracellular, 44, 45, 46, 167, 175, 182, 183, 200, 212 Extracellular Matrix, 44, 46, 175, 182, 183, 200 Extracellular Space, 182 Extrapyramidal, 179, 182 Extremity, 53, 182, 194 F Facial, 121, 182 Facial Injuries, 121, 182 Family Planning, 137, 182 Fat, 163, 169, 171, 175, 182, 192, 203, 212 Fatty acids, 182, 194 Feces, 44, 182, 213 Fetus, 39, 50, 113, 183, 194, 202, 205, 212 Fibrinogen, 183, 203 Fibroblasts, 22, 183 Fibrosis, 120, 183 Firearms, 56, 183 Fissure, 177, 183, 205 Fluorescence, 7, 9, 10, 12, 14, 19, 39, 52, 71, 95, 112, 183 Fluorine, 183 Fluorosis, 120, 183 Focus Groups, 26, 183 Fold, 49, 59, 183 Forearm, 169, 183, 194
Index 223
Fossa, 172, 183 Fourth Ventricle, 173, 183 Fractionation, 183, 214 Fracture Healing, 10, 36, 39, 183 Frontal Lobe, 49, 183, 205 Functional magnetic resonance imaging, 48, 183 Fungicide, 183, 187 G Gait, 159, 172, 183 Gallbladder, 178, 183 Ganglia, 163, 183, 197, 201 Gap Junctions, 184, 214 Gas, 171, 178, 183, 184, 187, 198, 217 Gas exchange, 184, 217 Gasoline, 76, 82, 91, 95, 98, 184, 215 Gastrin, 184, 187 Gastrointestinal, 97, 167, 170, 181, 184, 211, 213, 216 Gastrointestinal Neoplasms, 167, 184 Gastrointestinal tract, 184, 211, 216 Gels, 14, 184 Gene, 10, 16, 22, 27, 29, 31, 32, 35, 36, 39, 45, 46, 54, 55, 64, 164, 169, 184, 203, 208, 210 Gene Expression, 10, 22, 31, 32, 35, 36, 45, 46, 55, 184 Gene Pool, 29, 184 Genetics, 49, 55, 59, 60, 86, 104, 184 Genotype, 24, 27, 184, 202 Germ Cells, 55, 184, 194, 212, 214 Gestation, 43, 48, 184, 201, 202, 212 Gestational, 43, 184 Gland, 33, 184, 193, 200, 205, 210, 213, 215 Glioblastoma, 80, 184 Glioblastoma multiforme, 80, 184 Glomerulus, 185, 197 Glossitis, 120, 185 Glucose, 44, 169, 178, 185, 186, 189, 190 Glutamate, 23, 38, 46, 51, 185, 191, 195 Glutathione Peroxidase, 185, 210 Glycine, 165, 185 Glycoprotein, 44, 183, 185, 191, 201 Goblet Cells, 105, 185 Governing Board, 185, 204 Government Agencies, 11, 185, 204 Grade, 184, 185 Granulocytes, 185, 211, 218 Graphite, 12, 185 Growth factors, 185, 197 Growth Plate, 9, 185 Guanylate Cyclase, 185, 198
Gyrus Cinguli, 185, 192 H Haemodialysis, 83, 185 Haptens, 164, 185 Harmine, 17, 185 Hazardous Waste, 19, 28, 45, 186 Health Education, 26, 108, 118, 186 Health Fairs, 15, 186 Health Status, 58, 118, 186 Hearing Disorders, 174, 186 Heart attack, 171, 186 Heme, 20, 71, 165, 176, 186, 200, 204 Hemiparesis, 170, 186 Hemochromatosis, 39, 50, 186 Hemoglobin, 74, 104, 165, 182, 186, 204 Hemorrhage, 186, 213 Hemostasis, 186, 211 Hepatic, 63, 186, 204 Hepatitis, 63, 78, 186 Hepatocytes, 186 Hereditary, 112, 164, 173, 179, 186, 197 Heredity, 184, 186 Heterogeneity, 22, 164, 187 Hexachlorobenzene, 46, 187 Hippocampus, 4, 5, 7, 18, 23, 38, 47, 49, 51, 177, 187, 192, 210, 213 Histology, 31, 187 Homeostasis, 169, 187 Homologous, 164, 165, 176, 187, 210, 214 Hormonal, 60, 167, 187 Hormone, 17, 25, 35, 46, 113, 164, 168, 181, 182, 184, 187, 190, 191, 194, 200, 210, 211, 215 Host, 187, 188, 200, 218 Human Development, 47, 115, 136, 187 Hybrid, 60, 187 Hybridization, 14, 38, 44, 187 Hydrochloric Acid, 180, 187 Hydrogen, 168, 185, 187, 192, 196, 198, 199, 200, 202, 206 Hydrolysis, 43, 167, 187, 202, 204, 206 Hydroxylation, 98, 187 Hydroxylysine, 174, 187 Hydroxyproline, 174, 187 Hypersensitivity, 164, 187 Hypersensitivity, Immediate, 164, 187 Hypertension, 23, 24, 41, 171, 188 Hypertension, Renal, 41, 188 Hypertension, Renovascular, 188 Hypoplasia, 120, 164, 179, 188 Hypothalamic, 35, 188 Hypothalamus, 168, 178, 188, 192, 210
224
Lead Poisoning
Hypothyroidism, 25, 188 Hypotonia, 91, 172, 188 I Id, 70, 105, 148, 154, 156, 188 Idiopathic, 31, 188 Image Cytometry, 71, 188 Immune response, 166, 167, 185, 188, 213, 218 Immune system, 60, 167, 179, 188, 189, 193, 217, 218 Immunization, 188, 205 Immunodeficiency, 118, 188 Immunodeficiency syndrome, 118, 188 Immunohistochemistry, 38, 44, 188 Immunology, 163, 189 Impairment, 5, 51, 52, 189, 195, 206 Implantation, 175, 189 In situ, 31, 189 In vitro, 5, 9, 33, 35, 40, 44, 50, 189, 215 In vivo, 5, 9, 10, 22, 33, 35, 40, 44, 50, 55, 95, 189 Incision, 189, 190 Incontinence, 85, 189 Indicative, 118, 189, 201, 217 Induction, 20, 31, 189 Infancy, 25, 47, 98, 189, 209 Infarction, 175, 189, 195 Infection, 72, 79, 80, 118, 120, 172, 173, 188, 189, 193, 198, 201, 213, 218 Infertility, 31, 111, 113, 189 Inflammation, 166, 172, 177, 183, 185, 186, 189, 197 Ingestion, 65, 104, 170, 186, 189, 203 Inhalation, 167, 186, 189, 203, 211 Initiation, 189, 205, 216 Inorganic, 5, 80, 94, 100, 170, 189 Inositol, 48, 189, 195, 210 Inotropic, 179, 189 Insecticides, 190, 201, 218 Insight, 38, 41, 59, 190 Insulin, 35, 190 Insulin-dependent diabetes mellitus, 190 Insulin-like, 35, 190 Intermittent, 91, 190 Interstitial, 182, 190, 194, 197 Intestinal, 105, 171, 190, 194 Intestine, 169, 190, 191 Intoxication, 44, 56, 190, 218 Intracellular, 9, 20, 83, 189, 190, 194, 195, 198, 204, 207, 210, 211 Intracellular Membranes, 190, 194 Intrinsic, 19, 120, 164, 168, 190
Invasive, 33, 48, 190, 193 Involuntary, 181, 182, 190, 196, 208, 211 Iodine, 25, 190 Ion Channels, 167, 190, 198, 214 Ionizing, 164, 181, 190, 201 Ionophores, 43, 190, 217 Ions, 58, 168, 170, 171, 178, 179, 187, 190, 212 Irrigation, 63, 190 Ischemia, 19, 167, 191 J Joint, 57, 159, 167, 191, 199 Juvenile Delinquency, 112, 191 K Kainate, 7, 191 Kb, 136, 191 Keratolytic, 177, 191 Kinetic, 54, 59, 190, 191 L Labile, 174, 191 Lactation, 18, 35, 39, 113, 191 Laminin, 44, 168, 191 Language Arts, 34, 191 Language Disorders, 174, 191 Large Intestine, 178, 190, 191, 207, 211 Laryngeal, 121, 191 Larynx, 191, 216 Latent, 191, 204 Lavage, 160, 191 Least-Squares Analysis, 10, 191 Lectin, 191, 194 Leptin, 35, 191 Lesion, 192, 211, 216 Lethargy, 159, 188, 192 Leukemia, 84, 192 Leukocytes, 169, 173, 185, 192, 198 Library Services, 154, 192 Life cycle, 22, 192 Life Expectancy, 17, 192 Ligands, 54, 192 Limb Bud, 9, 192 Limbic, 5, 7, 165, 185, 192, 205 Limbic System, 5, 165, 185, 192, 205 Linkages, 186, 192 Lip, 120, 192 Lipid, 190, 192, 200 Lipid Peroxidation, 192, 200 Lipophilic, 192, 203 Liver, 22, 44, 168, 178, 180, 182, 183, 186, 192 Local Government, 192, 206 Localization, 188, 192
Index 225
Localized, 163, 170, 177, 189, 191, 192, 202, 216 Locomotion, 59, 192, 202 Longitudinal study, 57, 193 Long-Term Potentiation, 51, 193 Lucida, 191, 193 Lupus, 60, 193 Lymph, 173, 180, 181, 193, 209 Lymph node, 173, 193, 209 Lymphatic, 181, 189, 193, 195, 203, 209 Lymphatic system, 193, 209 Lymphocyte, 166, 193, 194 Lymphoid, 166, 193 M Magnetic Resonance Imaging, 48, 193 Magnetic Resonance Spectroscopy, 48, 193 Malignant, 166, 184, 188, 193 Mammogram, 170, 193, 195 Mandible, 164, 193, 208 Manic, 193, 206 Manic-depressive psychosis, 193, 206 Manifest, 18, 194 Mass Media, 34, 194 Mass Screening, 94, 194 Meat, 178, 194 Meat Products, 178, 194 Meconium, 48, 194 Median Nerve, 171, 194 Mediate, 5, 7, 21, 26, 46, 179, 194 Mediator, 194, 211 Medical Staff, 179, 194 MEDLINE, 137, 194 Megakaryocytes, 169, 194 Meiosis, 194, 214 Membrane, 4, 165, 167, 173, 174, 177, 185, 190, 191, 194, 196, 202, 208, 211, 212, 214, 216 Membrane Fusion, 165, 194 Membrane Proteins, 4, 194 Memory, 5, 16, 22, 48, 50, 51, 113, 114, 193, 194 Meninges, 172, 194 Mental Disorders, 116, 194, 205, 206 Mental Health, iv, 3, 91, 116, 136, 138, 195, 199, 205, 206 Mental Retardation, 25, 174, 195 Mercury, 13, 16, 22, 42, 48, 50, 57, 58, 59, 111, 195 Mesenchymal, 9, 195 Mesolimbic, 7, 195 Metabolite, 182, 195
Metabotropic, 38, 195 MI, 160, 195 Microbe, 195, 215 Microbiology, 163, 167, 195 Microcalcifications, 170, 195 Microorganism, 174, 195, 218 Micro-organism, 177, 195 Migration, 50, 195 Milliliter, 169, 195, 212 Millimeter, 180, 195 Mitochondria, 19, 195 Mitosis, 166, 195 Mobility, 35, 195 Mobilization, 18, 39, 86, 113, 196 Modeling, 27, 33, 58, 108, 196 Modification, 6, 24, 80, 196, 207 Molecule, 166, 168, 170, 174, 178, 179, 181, 182, 187, 191, 196, 199, 200, 207, 211 Monitor, 67, 69, 176, 196, 199 Morphogenesis, 4, 60, 192, 196 Morphological, 5, 10, 18, 59, 180, 196 Motility, 196, 211 Mucilaginous, 194, 196 Mucins, 185, 196, 209 Mucosa, 193, 196, 213 Multidrug resistance, 196, 202 Mutagenesis, 54, 196 Mutagens, 196 Myocardium, 195, 196 Myoclonus, 76, 196 N NCI, 1, 115, 135, 173, 196 Necrosis, 166, 184, 189, 195, 196, 210 Need, 26, 28, 33, 34, 52, 86, 101, 117, 118, 120, 121, 123, 131, 149, 163, 197, 215 Needs Assessment, 30, 197 Neonatal, 25, 38, 44, 85, 87, 197 Neonatal period, 25, 197 Nephritis, 60, 197 Nephrosis, 197 Nephrotic, 120, 197 Nephrotic Syndrome, 120, 197 Nephrotoxic, 24, 197 Nerve, 45, 163, 177, 194, 197, 198, 201, 204, 208, 210, 212, 213, 214, 216 Nerve Endings, 197, 214 Nerve Growth Factor, 45, 197 Nervous System, 17, 19, 36, 50, 51, 163, 168, 172, 194, 197, 198, 201, 213, 214 Networks, 188, 197 Neural, 4, 18, 37, 43, 48, 163, 188, 197, 210, 212
226
Lead Poisoning
Neurites, 45, 197 Neurobehavioral Manifestations, 170, 178, 197 Neurodegenerative Diseases, 16, 17, 197 Neuroendocrine, 35, 197 Neurologic, 17, 83, 87, 120, 170, 184, 197 Neuromuscular, 47, 163, 198 Neuromuscular Junction, 47, 163, 198 Neuronal, 40, 48, 50, 198 Neurons, 20, 40, 43, 50, 177, 182, 183, 197, 198, 214 Neuropathy, 198, 201 Neuropeptide, 50, 198 Neuropsychological Tests, 52, 198 Neurotoxic, 4, 40, 42, 50, 198 Neurotoxicity, 16, 23, 35, 43, 45, 51, 54, 198 Neurotoxins, 32, 198 Neurotransmitters, 23, 47, 198 Neutrons, 164, 198, 207 Neutropenia, 120, 198 Neutrophils, 185, 192, 198 Nitric Oxide, 23, 198 Nitrogen, 19, 198, 216 Nonverbal Communication, 174, 199 Norepinephrine, 163, 179, 199 Nuclear, 10, 168, 180, 184, 192, 196, 199, 215 Nuclei, 164, 165, 179, 181, 193, 195, 198, 199, 203, 206, 209, 210 Nucleic acid, 187, 196, 198, 199 Nucleic Acid Hybridization, 187, 199 Nucleus, 7, 40, 41, 166, 168, 173, 176, 180, 194, 198, 199, 205, 206, 210 Nucleus Accumbens, 7, 40, 41, 199 O Occupational Exposure, 5, 16, 57, 199 Occupational Health, 12, 13, 30, 95, 199 Odds Ratio, 24, 56, 199, 208 Opsin, 199, 209 Oral Health, 37, 120, 199 Organ Culture, 199, 215 Ossification, 199, 200, 209 Osteoarthritis, 57, 199 Osteoblasts, 39, 200 Osteoclasts, 39, 200 Osteogenesis, 173, 200 Osteoporosis, 36, 39, 95, 169, 200 Ovum, 177, 184, 192, 200, 218 Ownership, 34, 96, 200 Oxidation, 166, 176, 185, 192, 200, 217 Oxidative Stress, 68, 200 Oxygenase, 20, 200
P Palate, 120, 200 Palliative, 200, 215 Pancreas, 168, 178, 186, 190, 200, 216 Parasite, 200 Parasitism, 104, 200 Parathyroid, 200, 209 Parathyroid Glands, 200, 209 Paternal Exposure, 54, 201 Pathologic, 166, 168, 175, 187, 201, 208 Pathologic Processes, 166, 201 Pathophysiology, 43, 201 Patient Education, 145, 152, 154, 161, 201 Pediatric Dentistry, 120, 201 Penicillamine, 63, 72, 74, 91, 130, 201 Penicillin, 201, 217 Pensions, 21, 118, 201 Peptide, 58, 180, 191, 201, 204, 206, 215 Perception, 20, 175, 186, 201, 209 Perinatal, 23, 43, 201 Peripheral blood, 73, 201 Peripheral Nervous System, 17, 45, 113, 197, 201, 213 Peripheral Neuropathy, 16, 201 Pest Control, 6, 201 Pesticides, 6, 17, 27, 31, 49, 57, 143, 147, 190, 201 Petroleum, 184, 201 P-Glycoprotein, 46, 201 PH, 61, 169, 202 Pharmacokinetic, 33, 202 Pharmacologic, 202, 215 Phenotype, 54, 202 Phosphodiesterase, 43, 202 Phospholipases, 202, 211 Phospholipids, 182, 189, 202 Phosphorus, 170, 200, 202 Phosphorylation, 55, 202, 217 Photoreceptor, 43, 202 Physiologic, 164, 168, 196, 202, 207, 208, 216 Physiology, 19, 180, 202 Pigment, 202 Pigmentation, 76, 202 Pilot study, 32, 48, 202 Placenta, 39, 182, 202 Plants, 167, 171, 185, 186, 191, 198, 199, 202, 216 Plasma, 9, 12, 19, 31, 33, 166, 183, 186, 203, 210 Plasma cells, 166, 203 Plasmin, 203
Index 227
Plasminogen, 44, 203 Plasminogen Activators, 203 Plasticity, 5, 38, 203 Platelet Activation, 203, 211 Platelet Aggregation, 165, 198, 203 Platelets, 198, 203 Pleomorphic, 199, 203 Plexus, 25, 194, 203 Plumbism, 41, 64, 104, 203 Pneumoconiosis, 203, 211 Pneumonitis, 170, 203 Policy Making, 14, 185, 203 Polychlorinated Biphenyls, 45, 203 Polymorphism, 23, 29, 203 Polypeptide, 164, 174, 183, 187, 203, 204 Polysaccharide, 166, 204, 206 Population Density, 28, 204 Porphobilinogen Synthase, 53, 64, 204 Porphyria, 91, 120, 204 Porphyrins, 204 Posterior, 165, 172, 173, 181, 200, 204, 210 Postmenopausal, 200, 204 Postnatal, 35, 40, 43, 48, 50, 112, 204, 213 Postsynaptic, 40, 204, 211, 214 Post-synaptic, 204, 214 Post-traumatic, 170, 204 Potassium, 31, 204 Potentiation, 193, 204, 211 Practicability, 204, 216 Practice Guidelines, 138, 204 Preclinical, 37, 204 Precursor, 36, 50, 173, 179, 181, 199, 203, 204, 216, 217 Predisposition, 18, 204 Prefrontal Cortex, 7, 205 Prenatal, 17, 25, 112, 180, 205 Presumptive, 62, 205 Presynaptic, 40, 47, 197, 205, 214 Prevalence, 8, 11, 42, 199, 205 Primary Prevention, 21, 48, 205 Private Sector, 67, 205 Probe, 31, 32, 54, 205 Program Evaluation, 30, 205 Progression, 17, 18, 57, 165, 205 Progressive, 5, 172, 185, 196, 197, 199, 203, 205 Projection, 7, 199, 205 Proline, 174, 187, 205 Promoter, 43, 205 Promotor, 205, 208 Prone, 60, 205 Prophase, 205, 214
Propoxur, 17, 205 Prospective study, 25, 27, 193, 205 Prostate, 168, 205, 216 Protease, 44, 206 Protease Inhibitors, 44, 206 Protein S, 47, 169, 206, 209, 214 Proteinuria, 197, 206 Proteoglycans, 44, 168, 206 Proteolytic, 44, 46, 174, 183, 203, 206 Protocol, 40, 206 Protons, 164, 187, 190, 193, 206, 207 Proximal, 178, 205, 206, 210 Psychiatric, 6, 21, 52, 174, 194, 206 Psychiatry, 6, 16, 51, 57, 206 Psychic, 206, 210 Psychosis, 67, 184, 206, 215 Puberty, 35, 206 Public Assistance, 58, 206 Public Housing, 6, 206 Public Policy, 14, 77, 137, 207 Pulmonary, 15, 169, 175, 207, 217 Pulmonary Artery, 169, 207, 217 Pulse, 196, 207 Q Quality of Life, 17, 26, 57, 207 R Race, 7, 26, 195, 207 Radiation, 120, 168, 180, 181, 183, 190, 201, 207, 218 Radioactive, 168, 169, 187, 189, 199, 207 Radioisotope, 10, 207 Radiology, 36, 49, 91, 207 Randomized, 19, 39, 49, 60, 62, 115, 179, 207 Rape, 58, 207 Reaction Time, 6, 207 Reactive Oxygen Species, 19, 207 Reality Testing, 206, 207 Receptor, 7, 23, 27, 35, 38, 39, 41, 44, 45, 47, 51, 163, 166, 175, 179, 191, 195, 202, 207, 211 Receptors, Serotonin, 207, 211 Recombinant, 60, 207 Recombination, 60, 207 Rectum, 169, 178, 184, 189, 191, 206, 207 Red blood cells, 182, 200, 208 Refer, 1, 170, 174, 192, 197, 198, 206, 208 Reflective, 15, 208 Reflex, 18, 208, 216 Refraction, 208, 212 Regimen, 179, 208 Registries, 13, 208
228
Lead Poisoning
Relative risk, 38, 208 Reliability, 32, 208 Renal Artery, 188, 208 Reproductive cells, 184, 208 Research Design, 4, 208 Research Support, 50, 208 Resorption, 19, 36, 169, 200, 208 Respiration, 171, 196, 208 Response Elements, 31, 208 Response rate, 41, 208 Restoration, 183, 208 Retina, 173, 208, 209 Retinal, 42, 175, 209 Retinol, 209 Retrospective, 112, 209 Ribosome, 209, 216 Rickets, 120, 209 Risk factor, 8, 17, 27, 37, 42, 56, 57, 65, 68, 181, 205, 208, 209 Rod, 43, 202, 209 Rodenticides, 201, 209 Rubella, 120, 209 S Saliva, 33, 38, 209 Salivary, 33, 178, 209 Salivary glands, 178, 209 Scatter, 10, 209 Schizoid, 209, 218 Schizophrenia, 209, 210, 218 Schizotypal Personality Disorder, 209, 218 Sclera, 173, 210 Second Messenger Systems, 198, 210 Secretion, 35, 188, 190, 191, 196, 210 Secretory, 210, 214 Sediment, 29, 210 Segregation, 60, 207, 210 Seizures, 91, 159, 184, 210 Selenium, 57, 210 Self-Injurious Behavior, 18, 210 Semen, 111, 179, 206, 210 Senile, 200, 210 Sensor, 32, 52, 210 Septal, 192, 210 Septal Nuclei, 192, 210 Sequester, 58, 173, 210, 214 Serotonin, 37, 207, 211, 216 Serum, 15, 24, 46, 160, 165, 174, 211 Sex Characteristics, 163, 206, 211 Shedding, 120, 211 Shock, 196, 211, 216 Side effect, 129, 131, 163, 211, 215 Signal Transduction, 45, 165, 189, 211
Silicosis, 12, 211 Skeletal, 9, 36, 39, 40, 91, 188, 211, 214 Skeleton, 10, 37, 38, 39, 169, 191, 211 Skull, 211, 214 Small intestine, 105, 179, 187, 190, 211 Sneezing, 211 Social Behavior, 46, 211 Social Environment, 207, 212 Socioeconomic Factors, 7, 21, 212 Sodium, 212, 217 Sodium Channels, 212, 217 Soft tissue, 44, 120, 169, 182, 211, 212 Soma, 212 Somatic, 31, 163, 180, 192, 194, 195, 201, 205, 212 Sound wave, 208, 212 Specialist, 148, 212 Species, 19, 29, 37, 43, 54, 181, 187, 194, 195, 200, 207, 211, 212, 213, 216, 218 Specificity, 164, 180, 212 Spectrum, 10, 50, 112, 212 Sperm, 31, 55, 111, 173, 208, 212 Sperm Count, 31, 212 Spermatozoa, 210, 212 Spinal cord, 167, 170, 172, 194, 197, 198, 201, 208, 212 Spinal Nerves, 201, 212 Spontaneous Abortion, 114, 212 Sporadic, 16, 197, 213 Stabilization, 56, 213 Stem Cells, 36, 40, 213 Sterility, 189, 213 Stimulus, 179, 182, 190, 207, 208, 213, 215 Stomach, 178, 182, 184, 187, 191, 211, 213 Stool, 189, 191, 213 Stress, 37, 91, 117, 168, 171, 200, 205, 213 Striatum, 18, 40, 199, 213 Stroke, 19, 116, 136, 171, 213 Stromal, 169, 213 Stromal Cells, 169, 213 Subacute, 189, 213 Subclinical, 49, 189, 210, 213 Subcutaneous, 104, 163, 172, 179, 213 Subiculum, 187, 213 Subspecies, 212, 213 Substance P, 169, 195, 210, 213 Substrate, 19, 54, 213 Succimer, 60, 62, 63, 78, 97, 115, 130, 131, 213 Supplementation, 62, 213 Suppurative, 172, 213 Sympathomimetic, 179, 181, 199, 213
Index 229
Symptomatic, 57, 97, 98, 214 Synapses, 45, 193, 198, 214 Synapsis, 214 Synaptic, 5, 38, 46, 47, 59, 193, 211, 214 Synaptic Transmission, 46, 214 Synaptic Vesicles, 214 Synaptosomes, 47, 214 Systemic, 34, 36, 60, 130, 169, 181, 189, 214 Systolic, 188, 214 T Tarsal Bones, 170, 214 Temporal, 4, 10, 20, 29, 38, 47, 121, 165, 186, 187, 214 Teratogen, 50, 214 Testicular, 31, 111, 214 Testis, 31, 44, 182, 214 Tetracycline, 120, 214 Tetraethyl Lead, 76, 215 Thalamus, 178, 181, 192, 205, 215 Therapeutics, 100, 130, 215 Thermal, 121, 167, 178, 198, 215 Thorax, 163, 215 Threshold, 60, 91, 188, 215 Thrombolytic, 203, 215 Thrombosis, 206, 213, 215 Thyroid, 17, 25, 46, 188, 190, 200, 215, 216 Thyrotoxicosis, 66, 215 Thyrotropin, 188, 215 Tin, 171, 201, 215 Tissue, 14, 23, 35, 163, 166, 167, 168, 169, 171, 173, 175, 177, 179, 180, 182, 183, 184, 188, 190, 192, 193, 194, 195, 196, 197, 198, 199, 202, 203, 208, 210, 211, 212, 213, 214, 215, 217 Tissue Culture, 35, 197, 215 Tolerance, 163, 215 Tomography, 169, 193, 215 Tooth Preparation, 163, 215 Toxic, iv, 4, 19, 28, 31, 42, 58, 59, 142, 143, 147, 176, 181, 197, 198, 201, 203, 210, 215 Toxicity, 5, 7, 18, 20, 22, 27, 29, 35, 39, 44, 49, 55, 56, 58, 61, 72, 73, 112, 179, 195, 215 Toxicokinetics, 27, 215 Toxicology, 49, 64, 68, 81, 85, 94, 105, 138, 215 Toxins, 58, 59, 166, 181, 189, 216, 217 Trachea, 191, 215, 216 Training Support, 28, 216 Transcription Factors, 35, 43, 208, 216 Transduction, 211, 216 Transfection, 169, 216
Translation, 26, 216 Translational, 5, 216 Transmitter, 163, 167, 179, 190, 194, 199, 214, 216 Trauma, 56, 120, 121, 170, 196, 216 Treatment Outcome, 7, 216 Tremor, 16, 17, 216 Tryptophan, 174, 211, 216 Tubercle, 199, 216 Tuberculosis, 175, 193, 216 Tumor marker, 168, 216 Tyrosine, 178, 216 U Ulcer, 172, 216 Unconditioned, 20, 216 Unconscious, 188, 217 Uncoupling Agents, 190, 217 Urethra, 205, 217 Urinary, 19, 24, 74, 85, 100, 101, 113, 189, 217 Urine, 19, 44, 48, 169, 175, 182, 189, 206, 217 V Vaccine, 206, 217 Valine, 201, 217 Valproic Acid, 50, 217 Vascular, 26, 80, 173, 181, 188, 189, 198, 202, 203, 217 Vasodilator, 170, 179, 217 VE, 21, 57, 217 Veins, 169, 203, 217 Venoms, 198, 217 Venous, 19, 206, 217 Venous blood, 19, 217 Ventral, 188, 199, 212, 217 Ventricle, 165, 171, 181, 187, 188, 199, 207, 214, 215, 217 Venules, 169, 171, 217 Vesicular, 47, 217 Veterinary Medicine, 137, 217 Villous, 173, 217 Virulence, 215, 218 Virus, 118, 181, 209, 216, 218 Viscera, 212, 218 Visceral, 168, 192, 218 Vitamin A, 189, 209, 218 Vitro, 35, 44, 46, 47, 55, 218 Vivo, 5, 9, 22, 35, 40, 46, 47, 50, 55, 218 W War, 21, 218 White blood cell, 166, 192, 193, 198, 203, 218
230
Lead Poisoning
Windpipe, 215, 218 Withdrawal, 42, 218 X Xenobiotics, 5, 218 Xenograft, 165, 218
X-ray, 7, 10, 12, 19, 52, 54, 95, 112, 160, 169, 171, 183, 193, 199, 207, 218 Y Yeasts, 202, 218 Z Zygote, 54, 175, 218
Index 231
232
Lead Poisoning
