Figure 1.

Bisphenol A metabolism. In adults, bisphenol A is mainly metabolized to BPA-glucuronide (BPA-G) in the liver, and a smaller proportion in the intestines, via UDP-glucuronyltransferase. Hepatic sulfation is another pathway (BPA sulfate via sulfotransferase). The metabolites are excreted in urine. They are inactive, but they can be deconjugated and return to the active form via β-glucuronidase (GUSB) and steroid sulfatase (STS). Skin contact seems to lead to longer exposure to free BPA. During pregnancy, BPA can pass through the placenta. The fetus is theoretically more vulnerable because of absent or reduced UDP-glucuronyltransferase, especially during the first two trimesters. It has also been proposed that it is capable of deconjugation, and the placenta can contribute to this procedure, thereby increasing the active form. Bisphenol A concentrations are the same (a) in the blood vessels in the placenta that carry fetal blood, (b) in the umbilical cord, and (c) in the blood circulation in the fetus.