Bisphenol A and Reproductive Health: Update of Experimental and Human Evidence, 2007–2013
Open accessAbstract
Background: In 2007, an expert panel reviewed associations between bisphenol A (BPA) exposure and reproductive health outcomes. Since then, new studies have been conducted on the impact of BPA on reproduction. Objective: In this review, we summarize data obtained since 2007, focusing on a) findings from human and animal studies, b) the effects of BPA on a variety of reproductive end points, and c) mechanisms of BPA action. Methods: We reviewed the literature published from 2007 to 2013 using a PubMed search based on keywords related to BPA and male and female reproduction. Discussion: Because BPA has been reported to affect the onset of meiosis in both animal and in vitro models, interfere with germ cell nest breakdown in animal models, accelerate follicle transition in several animal species, alter steroidogenesis in multiple animal models and women, and reduce oocyte quality in animal models and women undergoing in vitro fertilization (IVF), we consider it an ovarian toxicant. In addition, strong evidence suggests that BPA is a uterine toxicant because it impaired uterine endometrial proliferation, decreased uterine receptivity, and increased implantation failure in animal models. BPA exposure may be associated with adverse birth outcomes, hyperandrogenism, sexual dysfunction, and impaired implantation in humans, but additional studies are required to confirm these associations. Studies also suggest that BPA may be a testicular toxicant in animal models, but the data in humans are equivocal. Finally, insufficient evidence exists regarding effects of BPA on the oviduct, the placenta, and pubertal development. Conclusion: Based on reports that BPA impacts female reproduction and has the potential to affect male reproductive systems in humans and animals, we conclude that BPA is a reproductive toxicant. Citation: Peretz J, Vrooman L, Ricke WA, Hunt PA, Ehrlich S, Hauser R, Padmanabhan V, Taylor HS, Swan SH, VandeVoort CA, Flaws JA. 2014. Bisphenol A and reproductive health: update of experimental and human evidence, 2007–2013. Environ Health Perspect 122:775–786; http://dx.doi.org/10.1289/ehp.1307728
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BPA is thought to be an endocrine disruptor that acts as an estrogen mimetic.
“BPA is thought to be an endocrine disruptor that acts as an estrogen mimetic [ 128–131 ], thus research has focused largely on its effects in reproductive tissues.”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [131]
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Self-citation
- Authors
- Peretz, J., Vrooman, L., Ricke, W. A., Hunt, P. A., Ehrlich, S., Hauser, R., Padmanabhan, V., Taylor, H. S., Swan, S. H., VandeVoort, C. A., & Flaws, J. A.
- Affiliations
- University of Illinois Urbana-Champaign (US)
- Washington State University (US)
- University of Wisconsin–Madison (US)
- Cincinnati Children's Hospital Medical Center (US)
- Harvard University (US)
- University of Michigan (US)
- Yale University (US)
- Icahn School of Medicine at Mount Sinai (US)
- University of California, Davis (US)
- Corresponding author
- Flaws, Jodi A.
- ORCID
- Venue
- Environmental Health Perspectives
- Publisher
- American Chemical Society (ACS)
- Published
- 2014-06-04
- Volume
- 122
- Issue
- 8
- Pages
- 775-786
- ISSN
- 0091-6765 (ISSN-L)
- 1552-9924
- PMC
- PMC4123031
- OpenAlex
- W2020338693
- Cited by
- 555
- References
- 140
- Citations by year
- 2026: 28 · 2025: 32 · 2024: 34 · 2023: 51 · 2022: 38 · 2021: 46 · 2020: 51 · 2019: 43 · 2018: 56 · 2017: 43 · 2016: 68 · 2015: 56 · 2014: 7
- FWCI
- 6.00
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- public-domain
- creativecommons.org/licenses/by/4.0/ (vor, 1304 d)
- Locations
- Environmental Health Perspectives (publishedVersion, public-domain)
- Europe PMC (PubMed Central) (publishedVersion, public-domain)
- PubMed Central (publishedVersion, public-domain)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- eScholarship (California Digital Library) (submittedVersion, public-domain)
- Funders
- National Institutes of Health (P51OD011107)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK020572)
- National Institute of Environmental Health Sciences (R01ES16541, RC2ES18764, R01ES009718, R01ES016770, R01ES9718, R01ES016541, R01ES019178, P20ES018163, R01ES16770, P01ES022844, R01ES017005, R01ES013527, R01 ES13527, P01ES022848, R01ES17005, RC2ES018764, P30ES023515, P30ES017885)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Reproductive Biology and Fertility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- bisphenol A, reproductive toxicity, endocrine disruptors, female reproduction, male reproduction, ovarian toxicity, uterine toxicity, testicular toxicity, meiosis, steroidogenesis, oocyte quality, in vitro fertilization, endometrial proliferation, endometrial receptivity, implantation failure, birth outcomes, hyperandrogenism, sexual dysfunction, mechanism of action
- MeSH terms
- Bisphenol A Compounds, Animals, Benzhydryl Compounds, Female, Humans, Male, Embryo Implantation, Phenols, Pregnancy, Reproduction
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