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Review
. 2016 Jan:59:167-82.
doi: 10.1016/j.reprotox.2015.09.006. Epub 2015 Oct 19.

A review of the carcinogenic potential of bisphenol A

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Review

A review of the carcinogenic potential of bisphenol A

Darcie D Seachrist et al. Reprod Toxicol. 2016 Jan.

Abstract

The estrogenic properties of bisphenol A (BPA), a ubiquitous synthetic monomer that can leach into the food and water supply, have prompted considerable research into exposure-associated health risks in humans. Endocrine-disrupting properties of BPA suggest it may impact developmental plasticity during early life, predisposing individuals to disease at doses below the oral reference dose (RfD) established by the Environmental Protection Agency in 1982. Herein, we review the current in vivo literature evaluating the carcinogenic properties of BPA. We conclude that there is substantial evidence from rodent studies indicating that early-life BPA exposures below the RfD lead to increased susceptibility to mammary and prostate cancer. Based on the definitions of "carcinogen" put forth by the International Agency for Research on Cancer and the National Toxicology Program, we propose that BPA may be reasonably anticipated to be a human carcinogen in the breast and prostate due to its tumor promoting properties.

Keywords: Bisphenol A; Cancer; Estrogen receptor; Mammary; Ovary; Prostate; Testes; Uterus.

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Figures

Figure 1
Figure 1
While the mechanism of action of BPA in humans is largely unknown, in vitro BPA effects are primarily mediated through its binding to classical nuclear ERs or through membrane-initiated non-genomic signaling by GRP30. In vivo, early life exposure to BPA rewrites the epigenetic code to stably alter gene expression in the breast, uterus and prostate. M=methylation.

References

    1. De Coster S, van Larebeke N. Endocrine-disrupting chemicals: associated disorders and mechanisms of action. J Environ Public Health. 2012;2012:713696. - PMC - PubMed
    1. Howlander N, Noone AM, Krapcho M, Garshell J, Miller D, Altekruse SF, et al. SEER Cancer Statistics Review, 1975-2012. National Cancer Institute; p based on November 2014 SEER data submission.
    1. Maffini MV, Rubin BS, Sonnenschein C, Soto AM. Endocrine disruptors and reproductive health: the case of bisphenol-A. Mol Cell Endocrinol. 2006:254–255. 179–86. - PubMed
    1. Brody JG, Rudel RA. Environmental pollutants and breast cancer. Environ Health Perspect. 2003;111:1007–19. - PMC - PubMed
    1. Burridge E. Bisphenol A: product profile. European Chemical News. 2003:14–20.

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