Evidence on the negative impact of the environmentally ubiquitous chemical, bisphenol-A (BPA), continues to mount. Previous research has shown that this endocrine disruptor causes adverse health effects during development and impacts the reproductive system, mimicking estrogen and binding to nuclear estrogen receptors as well as androgen receptors. BPA has been implicated in diseases such as obesity, infertility, endometrial cancer, osteoporosis, endometriosis, diabetes, prostate cancer, neurodegenerative disease and breast cancer. In a new mouse study published in The FASEB Journal, researchers at Yale University have shown that even low levels of BPA exposure can negatively impact fetal development and that exposure to BPA during a sensitive period can lead to permanent and disruptive epigenetic alterations.
Steps have previously been taken to reduce exposure to this widespread chemical. For instance, the FDA has banned BPA from baby bottles and similar items. However, it may still be in old plastic toys or plastic products manufactured prior to the ban. In addition, this chemical can leach into food, travel through the air, be found in water, and has even been detected in soil. BPA is so prevalent that 93% of Americans have detectable levels of BPA in their urine, according to the 2003-2004 National Health and Nutrition Examination Survey. Still, the FDA claims that “BPA is safe at the current levels occurring in foods.”
“Our study demonstrates that fetal exposure to BPA leads to a detrimental change in the adult uterine response to estrogens,” said Hugh S. Taylor, M.D., who is a senior researcher and Chief of Obstetrics and Gynecology at Yale-New Haven Children’s Hospital at the Yale School of Medicine. “Our study confirms that BPA is an active compound and can negatively impact fetal development and confirms that steps should be taken to reduce maternal consumption of BPA during gestation.”
In their study, the researchers investigated two groups of pregnant mice. One group was exposed to human levels of BPA and the other group was not. The team then analyzed the genome and epigenome of the uterus – an estrogen-responsive organ – in female offspring. Although they did not find any epigenetic changes in the uterus that altered gene expression prior to sexual maturation, they did find an epigenetic impact after sexual maturity. Specifically, changes in DNA methylation adjusted gene expression once the female rats were sexually matured, at a time when the level of an estrogen known as estradiol rose. After fetal BPA exposure, the researchers detected a direct alteration in the estrogen responses of nearly 1,000 genes.
“In utero BPA exposure altered the global CpGprofile of the uterine genome and subsequent gene expression,” the group reported. Overall, they concluded that the “selective alteration of ER alpha binding genes leads to susceptibility to estrogen-induced disease.”
Thoru Pederson, Ph.D., Editor-in-Chief of The FASEB Journal said that the study has revealed a noticeable delay in the change of uterine gene expression in offspring exposed to BPA in utero and has hopes that the results can help humans.
The evidence of this study and many others suggests that gene-environment interaction influenced by exposure to bisphenol-A in early life could lead to increased risk of developing certain diseases as an adult. The important information gained from these results could translate to humans and perhaps lead to new exposure limits and regulations.
Source: Jorgensen, E.M., Alderman, M.S., Taylor, H.S. Preferential epigenetic programming of estrogen response after in utero xenoestrogen (bisphenol-A) exposure. The FASEB Journal.
Reference: Federation of American Societies for Experimental Biology. Fetal BPA exposure in mice linked to estrogen-related diseases after adolescence. EurekAlert, 17 Jun 2016. Web.
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