BPA Alternative May Not Be Any Safer Than BPA for Embryonic Brain
Working with zebrafish, researchers show that prenatal exposure to bisphenol A (BPA)—as well as a related chemical used in “BPA-free” products—may affect embryonic brain development and behavior later on in life. The work, published in Proceedings of the National Academy of Sciences this week, suggests that BPA-free products, unfortunately, aren’t necessarily safer.
Found in all sorts of household products ranging from water bottles to DVDs to receipts, BPA has recently been shown to be an endocrine disruptor linked to behavioral problems in children who were exposed while in the womb. Now, to clarify the mechanism that underlies this link, a University of Calgary team led by Deborah Kurrasch exposed zebrafish embryos to BPA at a point in time that’s analogous to the second trimester in people. Zebrafish (Danio rerio) are animal models commonly used for understanding embryonic brain development in humans.
Specifically, the team exposed embryonic zebrafish to a low dose of BPA that’s about 1,000-fold lower than the accepted human daily exposure. “I was actually very surprised at our results. This was a very, very, very low dose, so I didn’t think using a dose this low could have any effect,” Kurrasch says in a news release. They used the same levels as that found in the Bow and Old Man rivers of Alberta, Canada.
Embryonic zebrafish immersed in a low-dose BPA treatment showed a 180 percent increase in neuronal birth (or neurogenesis) within the hypothalamus—a brain region that’s previously been implicated in aggression and hyperactivity. Furthermore, exposure to bisphenol S (BPS), a common compound used in products considered BPA-free, led to a 240 percent increase in neurogenesis in the hypothalamus.
Both BPA and BPS appeared to change the timing of when neurons formed in the brain. “In the second trimester, brain cells become the specialized neurons that make up our brain,” Kurrasch explains. “What we show is that the zebrafish exposed to BPA or BPS were getting twice as many neurons born too soon and about half as many neurons born later, so that will lead to problems in how the neurons connect and form circuits.” The treated fish demonstrated greater hyperactivity later in life.
This BPA-mediated neurogenesis, they were surprised to find, relies on the activation of an androgen receptor—and were not dependent on estrogen receptors as they had predicted. Further work is needed to explore that link.
Images: shutterstock.com (top), Deborah Kurrasch by Riley Brandt, University of Calgary (bottom)