BPA - Bisphenol A - has been besieged by so much negative public relations that it is almost indefensible. Like smoking, people are going to blame it for everything they can. 
 
But research is sometimes about inconvenient truths and so a three-year study using more than 2,800 mice that was not able to replicate a series of previous studies finding harm has to be mentioned.  The authors are quick to note they are not declaring BPA safe, rather just that they could not reproduce the developmental effects of BPA in babies in the womb - which used to be the definition of safe. The estrogenic compound found in plants, genistein, was also studied and results of other studies could not be reproduced.

Creating reliable data on the effects of the chemicals on mice is important to human health since people are frequently exposed to BPA and genistein and humans share similar biological functions with mice. BPA is used in certain plastic bottles and may be found in the lining of some canned goods and receipt paper. Genistein occurs naturally in soy beans and is sold as a dietary supplement. Research by Fredrick VomSaal, professor of biological science at University of Missouri, and others suggested the chemicals may have other adverse effects on many animals, including humans.

The original series of experiments claimed that exposure to BPA and genestein resulted in yellow coat color, or agouti, offspring that were more susceptible to obesity and type 2 diabetes compared to their brown coat color, healthy siblings. However, the new study did not obtain the same results when repeating the study over a three-year period.

After failing to repeat the original findings with similar numbers of animals, they extended the studies to include animal numbers that surpassed the prior studies to verify that their findings were not a fluke, and to provide sufficient number of animals to ensure that significant differences would be detected if they existed. 

However, even these additional numbers of animals and extended experiments failed to reproduce the earlier findings. However, the current studies demonstrate that a maternal diet enriched in estrogenic compounds leads to a greater number of offspring that express an agouti gene compared to those that do not, even though equal ratios should have been born.

"This finding suggests that certain uterine environments may favor animals with a 'thrifty genotype' meaning that the agouti gene of mice may help them survive in unfavorable uterine environments over those mice devoid of this gene, Yet, the downside of this expression of the agouti during early development is that the animals may be at risk for later metabolic disorders, such as obesity and diabetes" said Cheryl Rosenfeld, associate professor of biomedical sciences at the University of Missouri. "In this aspect, humans also have an agouti gene that encodes for the agouti signaling protein (ASIP) that is expressed in fat tissue and pancreas, and there is some correlation that obese individuals exhibit greater expression of this gene compared to leaner individuals. Therefore, the agouti gene may have evolved to permit humans the ability to survive famine, but its enhanced expression may also potentiate metabolic diseases under bountiful food conditions."

It's not all negative for the prior studies. While the research casts doubt on the other work, Rosenfeld said that by understanding the genetic profile of the mice in the first series of studies, scientists could learn more about the correlation between certain genes and obesity. This could eventually influence prevention and treatment programs for patients with diabetes and other obesity-related diseases in humans.

Citation: Cheryl S. Rosenfelda, Paizlee T. Sielia, Denise A. Warzak, Mark R. Ellersieck, Kathleen A. Pennington and R. Michael Roberts, 'Maternal exposure to bisphenol A and genistein has minimal effect on A^vy/a offspring coat color but favors birth of agouti over nonagouti mice', Published online before print December 24, 2012, doi: 10.1073/pnas.1220230110