On January 13, 2015 Amy Ellis Nutt, journalist of The Washington Post, reports on a new study showing that both bisphenol A (BPA) and its replacement bisphenol S (BPS) cause abnormal growth surges of neurons in embryonic zebrafish. The Canadian study published in the peer-reviewed journal Proceedings of the National Academy of Sciences (PNAS) shows that low-doses of BPA and BPS altered the timing of when neurons were formed in the brains of zebrafish resulting in hyperactive behavior. Nutt reports that the authors found surprising that the early abnormal growth of brain cells observed in embryonic zebrafish affected male hormones in particular. This finding may indicate why more boys than girls are diagnosed with certain neurodevelopmental disorders e.g. autism. The U.S. Food and Drug Administration (FDA) has just recently reaffirmed the safety of BPA in food contact applications (FPF reported). The European Food Safety Authority’s (EFSA) scientific opinion on BPA will be published in January 2015 (previously reported on by the FPF). The American Chemical Council (ACC) has already questioned the relevance of the study arguing that it examines effects of relatively high BPA concentrations, whereas humans are exposed to only trace BPA levels via diet. Further, humans metabolize BPA to a substance with no known biological activity that is quickly eliminated from the body and therefore it would not be scientifically appropriate to draw any conclusions about human health based on this limited experiment.
Read more
Amy Ellis Nutt (January 13, 2015). “BPA alternative disrupts normal brain-cell growth, is tied to hyperactivity, study says.” The Washington Post
ACC (January 13, 2015). “Study on zebrafish, BPA and hyperactivity has questionable relevance to human health.”
Reference
Kinch, C. D. et al. (2015). “Low-dose exposure to bisphenol A and replacement bisphenol S induces precocious hypothalamic neurogenesis in embryonic zebrafish.” PNAS (published online January 12, 2015; freely available online through the PNAS open access option).
