During pregnancy, women in the U.S. are exposed to more than 60 chemicals at any given time. Specifically, exposure to bisphenolic chemicals during pregnancy occurs in >90% of pregnancies and bisphenolic chemicals can cross the placental barrier reaching fetal circulation. Bisphenol A (BPA) is the leading bisphenol in exposure prevalence followed by bisphenol S (BPS). On the other hand, during pregnancy, both the fetus and the placenta are targets of chemicals that can act as endocrine disruptors (EDCs), such as bisphenols. Given the above, our laboratory is interested in understanding whether BPA and/or BPS can affect placental function and fetal growth. Studies thus far have used in vitro approaches to investigate the effects of BPA on placental invasion, transporter expression, and steroidogenesis. In our laboratory, and using a large animal model, we have first characterized internal dose exposure in the fetal compartment for both bisphenols. Additionally, our latest work has demonstrated that gestational exposure to the emerging bisphenol BPS, but not BPA, can impair placental endocrine function pointing specifically to a dysregulation in the fusogenic trophoblast signaling pathway. These findings highlight the intrinsic differences among bisphenolic chemicals and the need to evaluate the safety of BPA analogues during vulnerable windows of development.
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