21St International Neurotoxicology Conference
NTX XXI: Twenty-First International Neurotoxicology Conference
Tuesday Morning - 10 Feb 2004
Session I: Opening Ceremonies, Overview, Goals and Welcome Keynote
Opening of the conference, Overview & Goals: why hawaii?
Conference Chair: Joan M. Cranmer, PhD
Professor, University of Arkansas for Medical Sciences
Conference Co-Chairs:
Lynn R. Goldman, MD, MPH – Professor, Johns Hopkins University
Donald R. Mattison, MD– Senior Advisor to the Directors of NICHD and CRMC, National Institutes of Health
Deborah C. Rice, PhD
Senior Scientist, Maine Department of Environmental Protection
aloha!
(Hawaii Official: The Governor’s Office, Mayor of Oahu, Health Commissioner, or Dean of the Medical School)
Greetings on Behalf of All Sponsors: Sponsors Expectations
Kenneth Olden, PhD- Director, NIEHS/NIH
Recognition of federal leaders by the governer of hawaii
The Honorable Linda Lingle
Governor, State of Hawaii (invited)
Recognition of the leaders of Federal Agencies for their contributions to Children, Environmental Health, and the special needs of oceanic people!
Duane Alexander, MD
Director, National Institute of Child Health and Human Development/NIH
Jose Cordero, MD
Director, National Center for Birth Defects and Developmental Disabilities/CDC
Henry Falk, MD, MPH
Director, National Center for Environmental Health/CDC and Assist. Administrator, Agency for Toxic Substances and Disease Registry
Paul Gilman, PhD
Assistant Administrator for Research and Development, and Science Advisor to the EPA Administrator
Richard Jackson, MD, MPH
Senior Advisor to the Director, CDC
Kenneth Olden, PhD
Director, National Institute of Environmental Health Sciences/NIH
Introduction of Keynote Speaker
Robert Amler, MD, MPH
Regional Health Administrator, USDHHS/PHS
Welcoming Keynote:
“Children’s Environmental Health:
An International Perspective”
Henry Falk, MD, MPH
Director, NCEH/CDC and Assistant Administrator, ATSDR
Session II: Cross-Cutting Issues
Chair: Donald Mattison
Neurodevelopmental Effects of Persistent Pollutants: Data Gaps and Policy Implications
Lynn Goldman - Johns Hopkins University
Biomonitoring: An Integral Part of Exposure Analysis
Larry L. Needham
Chief, Organic Analytical Toxicology Branch, NCEH/CDC
Open Discussion
Tuesday afternoon - 10 Feb 2004
Session III: Hot New Results from the NIEHS/EPA Children’s Centers
Co-Chairs: Gwen Collman, NIEHS & Chris Saint, EPA
This session will feature the hottest and most exciting new findings from the NIEHS/EPA-funded Children’s Centers that address the issues in this conference including: Pesticides, PCBs, Methylmercury, Mixtures, Autism, Neurodevelopment, Growth and Development, Intervention, Outreach
Centers and Principal Investigators
Friend's Children's Environmental Health Center
Susan L. Schantz - University of Illinois, Urbana-Champaign
Center for Child Environmental Health Risks Research
Elaine Faustman
Univ. of Washington School of Public Health & Community Medicine
Exposures and Health of Farm Worker Children in California
Brenda Eskenazi
University of California at Berkeley, School of Public Health
Center for Childhood Neurotoxicology and Assessment
George H. Lambert
University of Medicine & Dentistry, NJ
The Center for the Study of Environmental Factors in the Etiology of Autism
Isaac N. Pessah
University of California, Davis
Columbia Center for Children's Environmental Health
Frederica Perera
Columbia University School of Public Health
Low-Level Environmental Lead Exposure and Intellectual Impairment in Children
Bruce Lanphear - Children’s Hospital Research Fdn, Cincinnati
Inner City Toxicants and Neurodevelopmental Impairment
Mary Wolff - Mount. Sinai School of Medicine
6:00 –8:00 PM
Welcoming Reception
Hosted Buffet Dinner
Ginger Terrace Poolside
Wednesday Morning - 11 Feb 2004
Session IV: Infant and Child Longitudinal Neurotoxicity Studies – Part I
(Methylmercury, PCBs, Pesticides, Lead, Combinations)
Co-Chairs: Deborah Rice and Sherry Selevan
Persistent Bioaccumulative Toxicants (PBTs) are chemicals that are persistent in the environment, bioaccumulate and bioconcentrate in living organisms, and are toxic to ecosystems and human health. Epidemiological studies in the 1970s and 1980s largely studied the effects of single toxicants on the neuropsychological development of children. However, there is increasing concern regarding the fact that children and exposed simultaneously to multiple chemicals, particularly PBTs, and that studying only a single chemical may result in misleading interpretations. Several cohort studies begun in the 1990s are studying the effects of multiple PBTs, allowing exploration of the pattern of effects of individual chemicals in the same group of children, as well as chemical-chemical interactions. This symposium will present new data from ongoing studies.
Introduction of Keynote Speaker
Lynn Goldman
Johns Hopkins University
Opening Keynote
“Children, Obesity
and Environmental Health”
Richard Jackson, MD, MPH
Director, National Center for Environmental Health/CDC
Interaction of Environmental Risk Factors and Modulation of Developmental Neurotoxicity
Deborah Cory-Slechta
Rutgers, The State University of New Jersey and EOSHI
Strategies for Assessing the Effects of Environmental Toxicant Exposure in Developmental Epidemiological Studies
Deborah Rice
Maine Dept Environmental Protection
New Data from Ongoing Children’s Environmental Health Studies
Effects of Methylmercury and PCBs on Behavior of Children at 14 years: The Faroe Islands Study
Roberta White
Boston University, Boston, MA
Interactions of PCBs, Pesticides, and Nutritional Factors on Early Development in an Inuit Community
Gina Muckle
University of Laval, Montreal, Quebec, Canada
Specificity of the Neuropsychological Effects of Prenatal Exposure to PCBs, Methylmercury, and Lead on Infant Cognitive Development (Effects of PBTs on neuropsychological function in children in circumpolar regions)
Sandra W. Jacobson
Wayne State University, Detroit, Michigan
Effects of Exposure to Chemicals from Industrial Contamination in New Bedford, Mass
Susan Korrick
Harvard University, Boston, MA
Wednesday Afternoon - 11 Feb 2004
Session V: Infant and Child Longitudinal Neurotoxicity Studies – Part II
Co-Chairs: David Bellinger and TBA
This session is a continuation of Session IV, involving presentation of four additional studies of the neuro-developmental effects from prenatal and early postnatal exposures to environmental contaminants
What is an Adverse Effect? Resolution of Clinical and Epidemiological Perspectives on Neurobehavioral Toxicity
David Bellinger
Harvard Medical School, Boston, MA
New Data from Ongoing Long-term Children’s Environmental Health Studies:
Neurodevelopmental Outcomes at Age 9 in the Seychelles Child Development Study
Philip W. Davidson
Univ of Rochester School of Medicine & Dentistry, Rochester, NY
Cognitive Development in Children Exposed Prenatally to PCBs and MeHg: The Oswego Newborn and Infant Study
Paul W. Stewart
State University of New York at Oswego, NY
Organochlorines, Lead and Mercury in Akwesasne Mohawk Youth
Lawrence M. Schell and/or Joan Newman
State University of New York at Albany, NY
Prenatal Exposure to PCBs and Infant Development: The Collaborative Perinatal Project
Matthew P. Longnecker
National Institute of Environmental Health Science, RTP, NC
Methylmercury/PCB Studies with First Nation Populations in Canada: Maximizing Nutritional Value from Traditional Foods and Minimizing Toxic Risks
Donna Mergler - University of Montreal, Quebec
Children Exposed to PCBs in Taiwan: Long-Term Follow-up Studies
Leon Guo, Taiwan and George Lambert, UMDNJ
Panel and Open Discussion:
Interpretation of Child Epidemiological Studies of Subtle Effects“
Moderator: David Bellinger
Panelists: Speakers in Sessions III, IV & V-A
Wednesday Evening - 11 Feb 2004
Session VI:General Poster Session
No Host Bar & Refreshments
The poster session is a highlight of this conference series. It has proven to be an effective venue for informal in-depth discussion and collaboration building as well as an important networking opportunity for all participants. Judging and selection of Pre – and Post-Doctoral Student Awardees will be made during this session. Papers on any aspect of neuroscience, toxicology or children’s environmental health are invited and welcome!
Note: The General Poster Session traditionally is scheduled as an evening session because it is conducive to discussion and getting acquainted in a less formal atmosphere without time constraints. This year it has the added advantage of allowing more Hawaiians to participate without work or school conflicts.
Thursday Early Morning -12 Feb 2004
SESSION VII-A:
Methylmercury Risks vs. Fish Benefits
Co-Chairs: Linda Rosen, Hawaii State Health Dept and TBA
Background/Justification: to be supplied
Introduction and Session Overview
Linda Rosen
Hawaii State Health Department
Volcanic Sources of Mercury in Hawaii, Levels of Mercury in Hawaii Fish, and Hawaiian/Pacific Islander Cultural and Social Issues
Bruce Anderson
University of Hawaii School of Medicine (former health commissioner)
Proposition 65 and Methylmercury in Fish
Mark Miller
Environmental Protection Agency, California
Perspectives of the US Food and Drug Administration
Mike Bolger or TBA
Methylmercury in Hawaii Fish: Risk/Benefit issues
Lynn Goldman - Johns Hopkins University
Panel and Open Discussion
SESSION VII–B: Parkinson’s Disease, Environment and Genes
Cellular Mechanisms Involved in Environmental Neurotoxin-Induced Selective Neuronal Damage and Its Relevance to Parkinson’s Disease
Co-Chairs: Anumantha G. Kanthasamy, Cindy Lawler and Syed F. Ali
Environmental neurotoxic chemical exposures are increasingly recognized as dominant risk factors in the etiology of Parkinson’s disease. Exposure to pesticides, PCBs and metals promote selective neuronal damage that is often superimposed with the pathological hallmarks of Parkinson’s disease. However, cellular mechanisms underlying selective neuronal degenerations remain to be established. In recent years, cell death signaling has been investigated extensively. Despite this growing amount of information regarding the cell death process, little effort has been made to integrate this body of knowledge with the field of selective neuronal injury and establish its relevance to neurodegenerative diseases. This symposium is designed to fill this gap by entertaining discussion of key cell death signaling molecules and other cellular targets that may impact the disease process of Parkinson’s disease. Specifically, novel findings obtained from neurotoxicity models using state-of-the-art approaches including toxicogenomics, transgenics, knockouts, and RNA interference (RNAi) will be presented. The symposium presentations are expected to uncover unifying concepts and set the groundwork for translation of key analogies between neurotoxicity research and neurodegenerative disorders. Furthermore, this symposium is likely to accelerate understanding of the role of environmental chemicals in the etiopathogenesis of Parkinson’s disease as well as to foster the development of novel therapeutic strategies.
Introduction to Chemicals-induced Selective Neuronal Injury
Syed Ali
FDA -National Center for Toxicological Research, Jefferson, AR
Role of Oxidative Stress-Sensitive Kinase in Dieldrin-induced Dopaminergic Cell Death: Relevance to Parkinson’s disease
Anumantha Kanthasamy - Iowa State University, Ames, IA
Dopamine Transporters as Mediators of Environmentally-Induced Dopamine Damage
Gary Miller
Center for Neurodegenerative Diseases, Atlanta, GA
Do PCBs Alter Dopamine Mediated Function in Aging Workers?
Richard Seegal
New York State Dept of Health, Albany, NY
Selective Vulnerability of Dopaminergic Neurons to Oxidative Damage: Implications to Parkinson’sDisease
Donato Di Monte - The Parkinson’s Institute, Sunnyvale, CA
Others planning to submit abstracts and present their latest related research results: Deborah Cory-Slechta, Clem Furlong, Web Ross, James O’Callaghan. Other talks to be selected from submitted abstracts
Thursday LATE MORNING - 12 Feb 2004
Session VIII-A: Role ofObesity in Children’s Environmental Health
Co-Chairs: William Slikker and TBA
The prevalence of childhood obesity has nearly doubled during the last two decades and is the most common nutritional disorder, showing an increasing prevalence. Overweight children have a higher risk for being overweight in adulthood and are therefore at risk for disease states associated with obesity, including Type 2 diabetes, cancer, and cardiovascular problems. Although family genetic factors are prime risk factors for childhood obesity, non-genetic factors also show a strong association with obesity. Some of these non-genetic factors include frequent TV viewing/video games and frequent consumption of snacks while watching TV. While a large number and variety of agents are associated with abnormal human development, efforts to identify an association between perinatal exposure to a substance and subsequent childhood obesity are just beginning. Recent studies have demonstrated an increased risk for overweight and obesity in children of mothers who smoked during pregnancy. These data and other clinical observations and animal model studies support the hypothesis that obesity in children of mothers who smoked during pregnancy is the result of long lasting behavioral teratogenic effects of nicotine exposure in utero. The search for environmental explanations of childhood obesity should be expanded because of the detrimental effect on health quality and the impact on our already-stressed health care capabilities. In addition, understanding the risk factors associated childhood obesity may lead to successful strategies for prevention.
Impact of Childhood Obesity on Children's Health
Rear Admiral Ken Moritsugu, Deputy Surgeon General, Washington, DC
or Bern Schwetz, HHS/Office of Human Research Protection Rockville, MD
The Fetal Programming Hypothesis: Possible Role in Childhood Obesity
William Slikker, Jr., NCTR/FDA, Jefferson, AR
or Julia Steinberger, University of Minnesota, Minneapolis, MN
Maternal Smoking During Pregnancy and Association with Childhood Obesity
Michael Toschke or Rüdiger von Kries
Ludwig-Maximilians-University, Munich, Germany
Animal Models of Developmental Nicotine Exposure: Possible Mechanisms of Childhood Obesity
Edward Levin or Theodore Slotkin - Duke University, Durham NC
Obesity Exacerbates Neurotoxicity
James O’Callaghan, NIOSH-CDC, Morgantown, WV
Session VIII–B: The Honolulu-Hawaii-Asia Aging Cohort Study
A Population-Based Longitudinal Study Providing Clues as to how Lifestyle & Workplace Factors Can Contribute to Neurodegenerative Disease
Co-Chairs: James O’Callaghan and Dan Sharp
The Honolulu-Asia Aging Study (HAAS) began in 1991 as a supplement to the Honolulu Heart Program, a longitudinal study of cardiovascular disease in a cohort of Japanese-American men living on Oahu at the time of the baseline examination in 1965. The original cohort consisted of 8006 men born 1900 through 1919. Some members of this cohort were occupationally exposed to persistent pesticides, including Heptachlor.Brain samples from descendentsof the HAAS cohort are being analyzed for levels ofpesticides and an attempt is being made to relate these data to occupational exposures, premortem diagnosis of neurological disease as well as postmortem evidence ofgliosis and neuropathological hallmarksof specific neurological disease states. Participation at NTX-XXI allows CDC-NIOSH scientists to present their most recent data to the neurotoxicological community as part of their visit to Honolulu.
The Design of Population-Based Longitudinal Studies and Their Role in Establishing Etiology of Human Disease
Dan Sharp, Wayne Sanderson
CDC-NIOSH, Morgantown, WV
The Honolulu-Asia Aging Study - Design, Description and Data Resources
Lon White
Pacific Health Research Institute, Honolulu, HI
Neuropathology Assessment in the HAAS
Jim Nelson
Pacific Health Research Institute, Honolulu, HI
Neurodegenerative Diseases in the HAAS
Web Ross
Department of Veteran Affairs, Honolulu, HI
Work Factors and Exposure to Pesticides in the HAAS
Helen Petrovitch,Wayne Sanderson, Michael Kashon, Pacific Health Research Institute, Honolulu, HI, CDC-NIOSH
Brain Tissue Analysis in the HAAS – Persistent Pesticides in the Caudate Putamen, Characterization of the Dopamine System and Parkinson's Disease
Diane Miller, Web Ross, Jim O'Callaghan, Michael Kashon, Edo Pellizaro, CDC-NIOSH, Dept of Veteran's Affairs, Res Triangle Inst
Thursday Early Afternoon - 12 Feb 2004
Session IX-A
Workshop:Mechanisms of Methylmercury Toxicity - The Latent Phase
Co-Chairs: Michael Aschner and Kenneth Reuhl.
Invited Participants: William Atchison, David Bellinger, Philip Davidson, Thomas Clarkson, Toshio Narahashi, Deborah Rice, Linda Rosen, Tore Syversen, Bernard Weiss, Roberta White, Others TBA
Outbreaks of methylmercury (MeHg) exposure in human populations and experimental studies in non-human primates suggest that poisoning symptoms may not occur for weeks or months after exposure, a period commonly referred to as silent or latent-phase. Since most, if not all, toxicological or pharmacological agents exert their maximal effect or efficacy at the time of peak blood concentration, this phenomenon has for decades puzzled the research community. In addition, the pathophysiology of MeHg, specifically in the adult brain, is confined to distinct brain regions, such as the cerebellum and visual cortex. Given the high affinity of MeHg for sulfhydryl groups and their ubiquitous nature, this specificity, has also been a puzzle.
Workshop Goal: The workshop should provide new hypotheses on mechanisms of MeHg neurotoxicity issues.
Workgroup Questions for Discussion: (20 minutes each = 2 hrs)
A series of questions have been developed which should help focus the workshop. These questions are meant to help structure the workshop but not unduly constrain scientific discussion.
1.What potential mechanisms can be invoked for the silent phase of MeHg?
2.Can analogies be drawn from other compounds?
3. What mechanisms guide the distribution of MeHg in the brain?
4. In the absence of differences in regional MeHg concentrations, what mechanisms might be invoked to describe cellular and regional specificity?
5.Does demethylation play a role in the neurotoxicity of MeHg?
6.Is MeHg's effect potentially mediated via extracellular effects?
Session IX-B: Emerging Issues in Children’s Health: International Perspectives
Co-Chairs: William A. Suk and Kalpana Balakrishnan
Indoor Air Pollution and Children’s Health: The Situation in Developing Countries
Kalpana Balakrishnan, Sri Ramachandra Medical College & Research Institute, India
Association Between Drinking Water and Urinary Arsenic Levels and Skin Lesions in Women and Children in Bangladesh
Iftikhar Hussein, National Institute of Preventive and Social Medicine, Bangladesh and H. Ahsan, Columbia Univ, School of Public Health
Critical Periods of Susceptibility in Neurodevelopmental Processes in Infants and Children
P.K. Seth, Industrial Toxicology Research Centre, Lucknow, India
Potential Mechanisms of Causes in Developmental and Learning Disabilities: Reflections from Developing Countries
David Carpenter, School of Public Health, University at Albany