Researchers from Duke Medical School published a study last week (February 25, 2013) in the Proceedings of the National Academy of Sciences, concluding that bisphenol A (BPA), a chemical commonly used in plastics and resins, may suppress a gene critical to the development of the central nervous system.
According to lead author Wolfgang Liedtke, M.D., PhD, “our study found that BPA may impair the development of the central nervous system, and raises the question as to whether exposure could predispose animals and humans to neurodevelopmental disorders.”
BPA is used to make polycarbonate plastics, which are then used to produce a wide range of plastic products, like baby bottles, food can liners, CDs, and dental fillings. It can be released from containers into the food they carry when heated to high temperatures. Infant formula in baby bottles is a prime example.
Animal research has raised concerns that BPA exposure may cause obesity, cancer, behavioral issues, endocrine and reproductive disorders, and immune system disorders. The Duke study is one of the first to suggest that BPA may also impair brain and central nervous system development.
The earlier studies of BPA’s health effects led the European Union to ban BPA in baby bottles effective June 1, 2011. The U.S. Food and Drug Administration originally hesitated, but followed suit a year later, in July 2012, saying that it was responding to industry’s request for a ban, despite the American Chemistry Council’s position that BPA is safe.
The Duke research team, funded in part by NIEHS, did experiments in rodent and human nerve cells to learn how BPA disrupts gene regulation. They observed that chloride, which is normally high in neurons early on but drops as they mature, can damage neural circuits and compromise brain development if it remains elevated. Even small amounts of BPA delay the reduction of chloride in neurons. (For more specific results, see here.)
“Our findings improve our understanding of how environmental exposure to BPA can affect the regulation of the Kcc2 gene. However, we expect future studies to focus on what targets aside from Kcc2 are affected by BPA,” Liedtke said. “This is a chapter in an ongoing story.”