In utero bisphenol a exposure and epigenetic programming of neurobehavioral outcomes

Abstract

Bisphenol A (BPA) is a ubiquitous environmental toxicant widely used for the production of plastics. There is substantial evidence that low-dose in utero BPA exposure can disrupt neurodevelopment, sexual dimorphism, behavior, and learning in animals, and the consequences may extend to future generations. While studies in humans are far more limited and more difficult to interpret, increasing evidence suggests that high maternal BPA exposure during pregnancy may contribute to later behavioral problems in children. BPA has been shown to disrupt the brain epigenome in rodents, and it is likely that DNA methylation-dependent mechanisms contribute to lasting BPA effects on brain function and behavior. Early studies in humans show that prenatal BPA exposure may leave DNA methylation signatures in peripheral blood that could possibly be used to predict behavioral vulnerability. More detailed studies in both animals and humans are needed to understand BPA effects on the epigenome and its consequences for brain function and behavior of multiple generations. Epigenetic findings could be used to shape the regulatory policies on BPA use and may open new opportunities for the early detection and interventions for the environmentally contributed behavioral disorders.