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Superfund Basic Research Program
Dr. Meyer's dissertation research was a component of Dr. Richard Di Giulio's SBRP-funded research project, which uses laboratory and field studies to elucidate effects of complex hydrocarbons mixtures on development in the Atlantic killifish, Fundulus heteroclitus. Dr. Meyer's studies focused upon a population of killifish that resides in an estuary in southeast Virginia adjacent to a hydrocarbon-contaminated Superfund site (Atlantic Wood) on the banks of the Elizabeth River. Over the course of many generations of exposures, this population has acquired resistance to the developmental toxicity of the hydrocarbon mixture which include cardiovascular defects. Dr. Meyer determined that fitness costs, such as increased sensitivity to hypoxia and ultraviolet (UV) light, were associated with this adaptation. Thus, this population provides a fascinating case study in "evolutionary ecotoxicology". The bulk of his work, however, focused on biochemical and molecular mechanisms underlying the adapted phenotype. Dr. Meyer's results indicated that changes in antioxidant defense systems, and genes and proteins associated with the aryl hydrocarbon pathway, were in part responsible for the resistance of these fish to hydrocarbon exposures. In collaboration with Duke Superfund investigator Dr. Jonathan Freedman, he also employed differential display to globally examine differences in gene expression between the resistant population and populations from pristine sites, and numerous differences were found in pathways previously not considered. Dr. Meyer published seven peer-reviewed papers from this work. Dr. Meyer received post-doctoral training at NIEHS in the laboratory of Dr. Bennett Van Houten. Dr. Meyer's work there was a logical progression of his Superfund-related work, and included analysis of DNA damage, repair, and gene expression changes associated with ultraviolet radiation exposure and underexpression of the frataxin protein in the model organism Caenorhabdatis elegans. Frataxin is involved in iron handling in the mitochondria. Underexpression of frataxin in humans leads to Friedrich's ataxia, a disease characterized by symptoms including high levels of iron and oxidative damage to DNA and proteins in mitochondria. The studies of ultraviolet radiation were focused on exploiting C. elegans as a model organism for the in vivo study of the effects of DNA damage, and on exploring the interactions between genotoxin exposure, genetic differences in DNA repair capacity, and age. Dr. Meyer has published six peer-reviewed papers from this and related work, with additional papers still in progress. Thus, his doctoral work was ecologically-oriented, and his post-doctoral work was human health oriented. Dr. Meyer is currently an Assistant Professor at Duke University, where he studies the effects of genotoxic agents on human and wildlife health. He focuses on understanding the mechanisms by which environmental agents cause DNA damage, the molecular processes that organisms employ to protect, prevent and repair DNA damage, and genetic differences that may lead to increased or decreased sensitivity to DNA damage. Mitochondrial DNA damage and repair are a particular focus. Dr. Meyer's interdisciplinary background enables him to work at the interface between human and environmental health, and ultimately, to help achieve needed integration between research geared to understand and protect both human and ecological health.  |
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Dr. Joel N. Meyer is an exemplary model of the contribution of SBRP-supported interdisciplinary research and education to the development of scientists with the requisite training to solve problems in environmental health in the 21st century. Dr. Meyer was a doctoral student in the Nicholas School of the Environment at Duke University and also a trainee in Duke's interdisciplinary, NIEHS-supported Integrated Toxicology Program. He received his Ph.D. in May, 2003.
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