Bisphenol A and Adiposity in an Inner-City Birth Cohort.

BACKGROUND: Early-life exposure to the endocrine disruptor bisphenol A (BPA) may contribute to the development of obesity. Prospective evidence in humans on this topic is limited. OBJECTIVES: We examined prenatal and early-childhood BPA exposures in relation to childhood measures of adiposity in the Columbia Center for Children's Environmental Health (CCCEH) New York City birth cohort. METHODS: BPA concentrations were measured in prenatal (n = 375) and child ages 3 (n = 408) and 5 years (n = 518) spot urine samples. Childhood anthropometric and bioelectrical impedance outcomes included body mass index z-scores (BMIZ) at 5 and 7 years, and fat mass index (FMI), percent body fat (% BF), and waist circumference (WC) at 7 years. Associations were evaluated using multiple linear regression with continuous and tertile BPA concentrations. RESULTS: Prenatal urinary BPA concentrations were positively associated with child age 7 FMI (beta = 0.31kg/m(2); 95% CI: 0.01, 0.60, p = 0.04), % BF (beta = 0.79; 95% CI: 0.03, 1.55, p = 0.04), and WC (beta = 1.29 cm; 95% CI: 0.29, 2.30, p = 0.01), but not BMIZ, or change in BMIZ between ages 5 and 7 years (all p-values > 0.1). FMI results were sex-specific. Child urinary BPA concentrations were not associated with child anthropometric outcomes (all p-values > 0.05). CONCLUSIONS: Analyses of the CCCEH longitudinal birth cohort found associations between prenatal urinary BPA concentrations and FMI, % BF, and WC. Our results suggest that prenatal BPA exposure may contribute to developmental origins of adiposity. These findings are consistent with several prior studies, raising concern about the pervasiveness of BPA.