Bisphenol A exposure causes high levels of meiotic failure in mice The potential effect of low doses of chemicals with hormone-like activity (‘endocrine disruptors’) on animal reproduction is an area of growing concern. In an important new study, published in the peer-reviewed, open-access journal PLoS Genetics, Susiarjo and colleagues report high levels of meiotic failure caused by exposure of female mice to bisphenol A (BPA). The authors observed an increase in chromosomally-abnormal eggs and embryos in adult females that were exposed to BPA while in the womb. Their data demonstrate that there is a multi-generational effect: exposing pregnant females alters the early events of egg development in the female fetus. Because female mice (like human females) develop all of their eggs while in the womb, exposure to chemicals in utero can have lifetime effects on these eggs and future embryos. Since these eggs will give rise to the next generation, exposure during this critical window of fetal development has consequences for succeeding generations. Importantly, these findings raise the possibility that chemicals that mimic the actions of estrogen have the ability to influence the prenatal events of egg development. These results are noteworthy given the widespread use of BPA in a number of consumer products, including polycarbonate plastics. Indeed, in an editorial published in the same issue of PLoS Genetics, Hawley and Warburton provide an analysis of the implications of these research findings, and believe it is important to ask the question: ‘Are chemicals such as BPA aneugenic in humans?’