The specific aims are to evaluate whether prenatal and early-life exposures to the endocrine disruptors, bisphenol-A (BPA) and polycyclic aromatic hydrocarbons (PAH), during pregnancy and early-childhood are associated with obesity and metabolic syndrome among children during early adolescence. The research will be conducted within the ongoing longitudinal birth cohort of African American and Dominican children from inner-city communities in New York City being conducted by the Columbia Center for Children's Environmental Health. BPA and PAH exposures are widespread among cohort mothers and children. Both compounds have been linked to obesity and metabolic syndrome in experimental and preliminary human studies. The research is timely; childhood obesity is increasing rapidly within the United States, with rates highest among minority populations. By age 5 years, 43% of our cohort children exceed the 85% of weight for age. The epidemic is likely to have significant public health implications, particularly among minority populations, as obesity is linked to risk of type 2 diabetes and cardiovascular disease. We propose to follow the children in the cohort to age 8-10 years and will assess height, weight, and body composition at ages 5, 7 and 8-10 years and metabolic syndrome components at ages 8-10. Exposure dosimeters are PAH concentrations in maternal prenatal personal air samples and PAH and BPA metabolites concentrations in urine samples collected and stored from the mother during pregnancy and from the child at ages 3,5, and 7 years. We hypothesize that prenatal exposure to PAH and BPA (1) will be associated with higher weight gain trajectories from age 5 to 8-10, and at age 8-10 years with BMI z-score, fat mass and metabolic syndrome components and (2) will alter the methylation status of key genes involved in adipogenesis and hunger control measured in umbilical cord while blood cells, which will mediate the association between postnatal exposures to the endocrine disruptors and childhood obesity outcomes. The research will provide important data on whether prenatal/early-life exposures to endocrine disruptors predicts childhood obesity/metabolic syndrome and will test hypotheses regarding underlying epigenetic mechanisms. ExpandCollapse Abstract