Several studies in rodents have shown that exposure to bisphenol A (BPA) during pregnancy is associated with adverse effects in the offspring; however, there are few studies on the mechanism by which these effects might occur. Of particular concern is the possible route by which BPA is transferred from the mother to the fetus. Numerous studies in adult animals have shown that BPA is highly glucuronidated in the liver, and the resultant inactive metabolite BPA-glucuronide (BPA-GA) is excreted primarily into bile. Nishikawa et al. (p. 1196) hypothesized that BPA-GA produced by the mother can pass to the fetus through the placenta, where it may be reactivated to BPA in the fetus. Using uterine perfusion with BPA-GA in pregnant rats, these investigators studied the expression and localization of the placental transporters for drug metabolites and the deconjugation of BPA-GA in the fetus. They observed BPA-GA and deconjugated BPA in the fetus and amniotic fluid after perfusion, thus providing a potential mechanism to explain long-term adverse effects in animals whose mothers were exposed to BPA during pregnancy.