A new study presented at the 2011 Era of Hope breast cancer conference has reported that chronic exposure to low concentrations of bisphenol A (BPA), a known endocrine disruptor, promotes mammary tumor development of in a mouse model of breast cancer. Bisphenol A is an organic compound used to make plastics and is found in a variety of consumer goods. Recently, it has been reported that bisphenol A leaches from these products in meaningful amounts, resulting in widespread human exposure. The study used mice that spontaneously develop mammary tumors even without being administered a carcinogen. Groups of mice were given either 2.5, 25, 250, or 2,500 μg bisphenol A per liter of drinking water beginning at eight weeks of age; a control group received water without any bisphenol A. These levels of exposure can be divided into two broad dose categories: environmentally relevant (2.5 and 25 μg BPA/L), which are realistic levels given actual exposures, and "regulatory-based" (250 and 2,500 μg bisphenol A/L), exposures considered unsafe according to current regulations.

Only the environmentally relevant doses of bisphenol A were found to significantly reduce the time until mammary tumors first appeared, as well as increase the number and size of tumors and the rate of metastasis. All doses of bisphenol A resulted in significantly increased cell proliferation. This increased proliferation was accompanied by increased apoptosis (programmed cell death) in the regulatory-based bisphenol A doses, which served to offset its carcinogenic effect. However, no increases in apoptosis was observed in mice given environmentally relevant doses. This has implications for breast cancer risk due to current levels of exposure to bisphenol A in the general population. The author concludes that chronic bisphenol A exposure resulted in a non-monotonic dose response (i.e., not consistently increasing in value) for mammary tumor development in mice, with the environmentally relevant doses of bisphenol A significantly increasing tumor number and growth. Regulatory-based doses of bisphenol A did not result in higher than expected mammary tumor development, apparently because increased cell proliferation was offset by heightened cell death. Because the environmentally relevant bisphenol A doses lacked this compensatory increase in apoptosis, cell turnover was greatly increased, which translated into increased tumor development.