A scientific review article published on October 19, 2015 in the peer-reviewed journal Reproductive Toxicology reports on the evaluation of carcinogenic properties of bisphenol A (BPA, CAS 80-05-7), carried out by a panel of experts assembled by the U.S. National Institutes of Health and the U.S. Environmental Protection Agency. BPA is a monomer used in the production of polycarbonate plastics, as well as in epoxy resins. It is also used as an additive in different materials for food contact, and in a multitude of other consumer products. BPA is an estrogenic substance that recently has been classified as a reproductive toxicant (FPF reported), and it has been highlighted in regard to its ability to disrupt the immune system (FPF reported).

The present study by Darcie Seachrist and colleagues from Case Western Reserve University, University of Cincinnati, University of Illinois, and Tufts University (all U.S.) is a follow-up to an earlier assessment of BPA by the same panel. In 2007, the experts concluded that BPA “[confidently] displayed estrogenic properties” and was “likely to be associated with increased malignancies of the testes and hematopoietic system and increased susceptibility to neoplastic lesions in mammary and prostate glands following early-life exposures.” As at that time the data on tumor formation in vivo in response to BPA were insufficient, the review panel emphasized the need to address the carcinogenic impact of BPA “using environmentally relevant doses,” i.e. doses below the lowest observed adverse effects level (LOAEL, 50 mg/kg/day). The present updated analysis evaluates the numerous studies carried out in response to this call since 2007.

To properly evaluate BPA-associated health effects by epidemiological methods, small-scale studies are insufficient, as they provide only “limited data regarding extent, timing and duration of BPA exposure.” Instead, “large birth cohorts documenting fetal/early life BPA exposure with lifetime follow-up are needed to fully evaluate the impact of environmental BPA exposure during early life on cancer risk,” the panel points out. However, since such studies are currently not available and “would not be available for decades,” the authors deem it “critical to focus on other data streams [i.e. animal studies] to assess the potential impact of BPA exposure on cancer risk.”

The authors performed an extensive review of the literature that investigated BPA involvement in “cancers of the female breast and reproductive tract” (including breast, ovarian and uterine cancer), “cancers of the male reproductive tract” (including prostate and testicular cancer) and “cancers in non-reproductive estrogen target tissues” (focusing on hepatic cancer). From this review it is clear that the early developmental period is the most sensitive to BPA effects which often manifest only much later in life.

Fourteen general conclusions were formulated by the authors. Most importantly, they are confident that “[p]renatal exposure to low doses of BPA […] increases risk of mammary cancer [in rodents] later in life” and “BPA may be reasonably anticipated to be a human carcinogen in the breast independent of route of exposure.” The evidence on BPA association with incidence of ovarian cysts and malignancies of the hematopoietic system, testes and prostate was judged by the panel as “likely, but requiring confirmation.” Several other areas were highlighted as requiring further investigation.

Based on the classification by the International Agency for Research on Cancer (IARC), the authors proposed to classify BPA as a chemical carcinogen in Group 2A, which includes substances that are “probably carcinogenic to humans as there is inadequate evidence of carcinogenicity in humans, yet sufficient evidence of the carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans.” Similarly, based on the guidelines by the U.S. National Toxicology Program (NTP), the authors could also conclude that “BPA may be presumed to be a human carcinogen due to its ability to enhance tumor susceptibility and promote tumorigenic properties in the breast and prostate glands.”


Seachrist, D.D. et al. (2016). “A review of the carcinogenic potential of bisphenol A.Reproductive Toxicology 59:167-182.

Keri, R.A. et al. (2007). “An evaluation of evidence for the carcinogenic activity of bisphenol A.Reproductive Toxicology 24:240-252.