Fetal Exposure to Toxin in Plastics Can Lead to Endometriosis and Other Estrogen-related Diseases

Fetal Exposure to Toxin in Plastics Can Lead to Endometriosis and Other Estrogen-related Diseases

People exposed as fetuses to bisphenol-A (BPA) in plastics may be at risk for a range of diseases as they mature into adults, including endometriosis, endometrial cancer, prostate cancer, osteoporosis, breast cancer, neurodegenerative diseases, and obesity, according a recent study published in The FASEB Journal.

The study, developed by researchers at the Yale University School of Medicine, “Preferential epigenetic programming of estrogen response after in utero xenoestrogen (bisphenol-A) exposure,” suggests that the plastic compound is associated with epigenetic alterations that result in the modified expression of genes regulated by estrogen.

“Our study demonstrates that fetal exposure to BPA leads to a detrimental change in the adult uterine response to estrogens,” said Dr. Hugh S. Taylor, a senior researcher and chief of Obstetrics and Gynecology at Yale-New Haven Children’s Hospital, in a news release. “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.”

BPA, an industrial chemical, is found in consumer plastics such as water bottles or food preparation containers, and in industrial items such as medical devices, food can liners, and thermal receipt paper. Approximately 93 percent of Americans have detectable levels of BPA in their urine.

The compound is known as a xenoestrogen because it can mimic estrogen and activate its signaling pathways. Exposure to the molecules during fetal development affects the development of the female reproductive tract, and can affect gene expression long after exposure has ended. Given the universal exposure of women and their fetuses to BPA, it is crucial to understand its long-term effects.

Taylor and colleagues exposed fetal mice to human ranges of BPA, followed by an analysis of the uterine epigenetic profile of the female offspring and modifications in gene expression in response to estrogen.

The researchers observed that no changes were found at birth or in early post-natal life. But when mice reached sexual maturity, more than 1,000 genes had distinct expression profiles upon estrogen exposure, compared to fetal mice that had not been exposed to BPA

“This study reaches into the antecedent fetal exposure axis and reveals a striking, delayed onset of uterine gene expression effects in the offspring,” said Thoru Pederson, editor-in-chief of The FASEB Journal. “To the extent that these findings could be envisioned to translate to the human, we have in this study a very important body of information.”

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