Adding important new findings to extensive scientific evidence that Bisphenol A (BPA) is a harmful substance, Dr. Catherine VandeVoort, staff scientist in Reproductive Sciences and Regenerative Medicine at the CNPRC, has been part of a team effort investigating the effects of BPA on the fetal development in nonhuman primates and the first paper, focusing on the fetal mammary gland, is now being published. (Tharp AP, et al. Bisphenol A alters the development of the rhesus monkey mammary gland. Proceedings of the National Academy of Sciences, 2012).
BPA, used in the manufacturing of various plastics and resins for food packaging, consumer products, some cash register receipts, and medical devices, is controversial because it exerts weak, but detectable, hormone-like properties which can mimic estrogen and may lead to far-ranging negative health effects including increased cardiovascular disease and diabetes in adults, increased cancer rates, including breast cancer, neurological difficulties, and hormonal and reproductive issues in both sexes and at all stages of life. A 2011 study demonstrated just how pervasive the chemical is – analyzing the number of chemicals pregnant women are exposed to in the U.S. found BPA in 96% of women.
The aim of the overall study, conducted at the CNPRC, was to determine whether maternal circulating levels of unconjugated BPA, similar to those found in human serum, affected the development of female rhesus monkey offspring. Rhesus monkeys pregnant with female fetuses were daily fed a small piece of fruit containing BPA during the late third trimester that resulted in serum levels of unconjugated BPA similar to those observed in humans, making the results of this study relevant to human exposure and health issues. Many tissues from the fetuses were sent to experts around the country – in the case of the mammary gland, to Dr. Ana Soto at Tufts University.
A quantitative analysis that compared the morphology of exposed and unexposed female neonatal mammary glands was conducted, and demonstrated that gestational exposure to BPA affected the nonhuman primate mammary gland development in ways similar to rodent results. Previous rodent studies had shown significant alterations in the gland’s morphology that varied from subtle ones observed during the exposure period to precancerous and cancerous lesions manifested in adulthood.
From what is known about the role of endogenous hormones in the development of the mammary gland it was also concluded that BPA affects several developmental parameters of the mammary gland of rhesus monkeys, including some that are relevant to breast cancer risk in humans.
“We think that our results suggest that it is very likely that fetal exposure to BPA would also increase the propensity to develop mammary cancer in monkeys,” Soto said.
The sum of all the findings “strongly suggest that BPA is a breast carcinogen in humans and human exposure to BPA should be curtailed,” she said.
This study took advantage of an ongoing research project by Dr. VandeVoort that was designed to assess the effect of BPA on ovarian morphogenesis and to determine the circulating levels of unconjugated BPA in orally exposed female rhesus monkeys. Other tissues are also being analyzed for possible affects of BPA, including lung development.