Department of Environmental and Occupational Health Sciences, Downstate Medical Center School of Public Health, State University of New York, Brooklyn, NY, USA; Columbia Center for Children's Environmental Health, Mailman School of Public Health, Columbia University, New York, NY, USA. Electronic address: [Email]
There is significant evidence of globally ubiquitous prenatal exposures to bisphenol A (BPA). Childhood obesity as an epidemic has been a global concern for over a decade. Experimental models and epidemiological evidence suggest that BPA may act as an obesogen during adipogenesis. Results from stem cell models and birth cohort studies support the developmental origins of health and disease theory. While literature reviews have presented a variety of potential mechanisms of BPA action during adipogenesis, there remains no consensus. This review is the first to explore the proliferator-activated receptor gamma (PPARγ) mechanism in detail. This review will also examine the obesogenic effect of prenatal exposure to BPA during critical windows of vulnerability. Although vast experimental literature exists, there is limited epidemiological evidence to support the hypothesis for the obesogenic effect of BPA. The primary goal of this review is to provide researchers with a roadmap of existing research and suggestions for future directions for analyzing the relationship between prenatal BPA exposures and childhood obesity.