The overarching goal of this Superfund Research Center is a broad understanding of chemical impacts on developing organisms and approaches for reducing these impacts. Center research concentrates on a mechanistic approach: mechanisms underlying developmental perturbations, mechanisms underlying ameliorations of and adaptations to these effects, and mechanisms underlying engineered solutions for the ultimate removal of these chemicals from the environment. A major cross-cutting theme in this renewal application is that of potential biological """"""""costs"""""""" of early life exposures to humans and ecosystems, and of remediation strategies. The primary goals of this Center are: 1) To elucidate mechanisms of developmental toxicity of selected Superfund and emerging chemicals. 2) To develop efficient assays for developmental toxicants, 3) To determine later-life consequences of early life exposures to toxicants. 4) To develop effective strategies for remediating systems contaminated by developmental toxicants that combine microbial- and nanomaterials-based strategies, 5) To effectively deliver the Center's research results to critical members of the scientific, governmental, business and lay communities, 6) To enhance interdisciplinary research, and undergraduate, graduate and post-graduate training, in the biomedical and environmental sciences. The objectives will be achieved through the integrated activities of two biomedical and two non-biomedical research projects, two research support cores (Analytical Chemistry and Neural and Behavioral Toxicity Assessment), and an Administrative, Research Translation, &Training Core. Biomedical projects focus on developmental neurotoxicology and later life sensitizations caused by organophosphates using cell lines and the rat model (Project 1), and the effects of chemicals, particularly flame retardants, on thyroid hormone homeostatsis and resulting behavioral effects in cell cultures and the zebrafish model (Project 2). The ecological Project 3 explores mechanisms of adaptation to developmental toxicity and subsequent consequences for a population of killifish inhabiting a PAH-contaminated estuary. The engineering Project 4 explores the efficacy and safety of combined nanomaterial- and microbial-based remediation strategies.

Public Health Relevance

Development during early life stages (i.e, embryo, fetus, infant, larva) is a period inherently sensitive to exposures to environmental contaminants, for humans and free-living organisms in the environment. This Center is highly relevant to SRP research themes of mechanisms of toxicity;susceptibility, mixtures, remediation, and ecological/evolutionary impacts of Superfund chemical, here in the context of development.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Hazardous Substances Basic Research Grants Program (NIEHS) (P42)
Project #
3P42ES010356-13S2
Application #
8909672
Study Section
Special Emphasis Panel (ZES1-SET-V (04))
Program Officer
Henry, Heather F
Project Start
2000-06-01
Project End
2015-03-31
Budget Start
2014-08-13
Budget End
2015-03-31
Support Year
13
Fiscal Year
2014
Total Cost
$86,787
Indirect Cost
$28,459
Name
Duke University
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
044387793
City
Durham
State
NC
Country
United States
Zip Code
27705
Raftery, Tara D; Jayasundara, Nishad; Di Giulio, Richard T (2017) A bioenergetics assay for studying the effects of environmental stressors on mitochondrial function in vivo in zebrafish larvae. Comp Biochem Physiol C Toxicol Pharmacol 192:23-32
Mu, Jingli; Chernick, Melissa; Dong, Wu et al. (2017) Early life co-exposures to a real-world PAH mixture and hypoxia result in later life and next generation consequences in medaka (Oryzias latipes). Aquat Toxicol 190:162-173
Slotkin, Theodore A; Skavicus, Samantha; Card, Jennifer et al. (2017) In vitro models reveal differences in the developmental neurotoxicity of an environmental polycylic aromatic hydrocarbon mixture compared to benzo[a]pyrene: Neuronotypic PC12 Cells and embryonic neural stem cells. Toxicology 377:49-56
Luz, Anthony L; Godebo, Tewodros R; Smith, Latasha L et al. (2017) Deficiencies in mitochondrial dynamics sensitize Caenorhabditis elegans to arsenite and other mitochondrial toxicants by reducing mitochondrial adaptability. Toxicology 387:81-94
Hartman, Jessica H; Kozal, Jordan S; Di Giulio, Richard T et al. (2017) Zebrafish have an ethanol-inducible hepatic 4-nitrophenol hydroxylase that is not CYP2E1-like. Environ Toxicol Pharmacol 54:142-145
Meyer, Joel N; Chan, Sherine S L (2017) Sources, mechanisms, and consequences of chemical-induced mitochondrial toxicity. Toxicology 391:2-4
Slotkin, Theodore A; Skavicus, Samantha; Seidler, Frederic J (2017) Diazinon and parathion diverge in their effects on development of noradrenergic systems. Brain Res Bull 130:268-273
Lindberg, C D; Jayasundara, N; Kozal, J S et al. (2017) Resistance to polycyclic aromatic hydrocarbon toxicity and associated bioenergetic consequences in a population of Fundulus heteroclitus. Ecotoxicology 26:435-448
Abreu-Villa├ža, Yael; Levin, Edward D (2017) Developmental neurotoxicity of succeeding generations of insecticides. Environ Int 99:55-77
Jayasundara, Nishad; Fernando, Pani W; Osterberg, Joshua S et al. (2017) Cost of Tolerance: Physiological Consequences of Evolved Resistance to Inhabit a Polluted Environment in Teleost Fish Fundulus heteroclitus. Environ Sci Technol 51:8763-8772

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