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.
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.
|Meyer, Joel N; Hartman, Jessica H; Mello, Danielle F (2018) Mitochondrial Toxicity. Toxicol Sci 162:15-23|
|Oliveri, Anthony N; Ortiz, Erica; Levin, Edward D (2018) Developmental exposure to an organophosphate flame retardant alters later behavioral responses to dopamine antagonism in zebrafish larvae. Neurotoxicol Teratol 67:25-30|
|Slotkin, Theodore A; Skavicus, Samantha; Seidler, Frederic J (2018) Developmental neurotoxicity resulting from pharmacotherapy of preterm labor, modeled in vitro: Terbutaline and dexamethasone, separately and together. Toxicology 400-401:57-64|
|Lefèvre, Emilie; Bossa, Nathan; Gardner, Courtney M et al. (2018) Biochar and activated carbon act as promising amendments for promoting the microbial debromination of tetrabromobisphenol A. Water Res 128:102-110|
|Kollitz, Erin M; Kassotis, Christopher D; Hoffman, Kate et al. (2018) Chemical Mixtures Isolated from House Dust Disrupt Thyroid Receptor ? Signaling. Environ Sci Technol :|
|Hartman, Jessica H; Smith, Latasha L; Gordon, Kacy L et al. (2018) Swimming Exercise and Transient Food Deprivation in Caenorhabditis elegans Promote Mitochondrial Maintenance and Protect Against Chemical-Induced Mitotoxicity. Sci Rep 8:8359|
|Luz, Anthony L; Kassotis, Christopher D; Stapleton, Heather M et al. (2018) The high-production volume fungicide pyraclostrobin induces triglyceride accumulation associated with mitochondrial dysfunction, and promotes adipocyte differentiation independent of PPAR? activation, in 3T3-L1 cells. Toxicology 393:150-159|
|Day, D B; Xiang, J; Mo, J et al. (2018) Combined use of an electrostatic precipitator and a high-efficiency particulate air filter in building ventilation systems: Effects on cardiorespiratory health indicators in healthy adults. Indoor Air 28:360-372|
|Slotkin, Theodore A; Ko, Ashley; Seidler, Frederic J (2018) Does growth impairment underlie the adverse effects of dexamethasone on development of noradrenergic systems? Toxicology 408:11-21|
|Rock, Kylie D; Horman, Brian; Phillips, Allison L et al. (2018) EDC IMPACT: Molecular effects of developmental FM 550 exposure in Wistar rat placenta and fetal forebrain. Endocr Connect 7:305-324|
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