Prenatal Exposure to Endocrine Disruptors: A Developmental Etiology for Polycystic Ovary Syndrome
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Polycystic ovary syndrome (PCOS) is one of the most common and complex endocrinopathies among reproductive-age women. Polycystic ovary syndrome is characterized by symptomatology of oligomenorrhea and androgen excess, with or without presence of polycystic ovarian morphology. The etiology of PCOS is multifactorial, including genetic and environmental components. It has been previously established that prenatal androgen exposure results in a PCOS phenotype in experimental animal models and epidemiologic human studies. Investigators hypothesize that prenatal exposure to endocrine-disrupting chemicals (EDCs) may contribute to PCOS development. This review examines the emerging research investigating prenatal exposure to 3 major classes of EDCs-bisphenol A (BPA), phthalates, and androgenic EDCs-and the development of PCOS and/or PCOS-related abnormalities in humans and animal models. Highlights of this review are as follows: (1) In rodent studies, maternal BPA exposure alters postnatal development and sexual maturation;, (2) gestational exposure to dibutyl phthalate and di(2-ethylhexyl)phthalate results in polycystic ovaries and a hormonal profile similar to PCOS; and (3) androgenic EDCs, nicotine and 3,4,4'-trichlorocarbanilide, create a hyperandrogenic fetal environment and may pose a potential concern. In summary, prenatal exposure to EDCs may contribute to the altered fetal programming hypothesis and explain the significant variability in severity and presentation.
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Endocrine-disrupting chemicals may contribute to altered fetal programming and play a role in the pathogenesis of PCOS.
“In addition, emerging and concerning evidence suggests that EDC may contribute to altered fetal programming and play a role in the pathogenesis of PCOS [41,48].”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [48]
These factors include hormones, vitamins, diet-derived metabolites and environmental chemicals.
“These include hormones, vitamins, diet-derived metabolites and environmental chemicals [48,98,103,104].”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [48]
Prenatal exposure to androgenic EDC (triclosan, glyphosate, tributyltin, nicotine) is of increasing concern, given the suspected epigenetic role of in utero androgen exposure in the pathogenesis of PCOS.
“Prenatal exposure to androgenic EDC (triclosan, glyphosate, tributyltin, nicotine) is of increasing concern, given the suspected epigenetic role of in utero androgen exposure in the pathogenesis of PCOS [48,200,201].”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [48]
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- Authors
- Hewlett, M., Chow, E., Aschengrau, A., & Mahalingaiah, S.
- Affiliations
- Boston University (US)
- Corresponding author
- Mahalingaiah, Shruthi
- Venue
- Reproductive Sciences
- Published
- 2017-01
- Volume
- 24
- Issue
- 1
- Pages
- 19-27
- ISSN
- 1933-7191 (ISSN-L)
- 1933-7205
- PMC
- PMC6344820
- OpenAlex
- W2335940631
- Cited by
- 61
- References
- 16
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 4 · 2023: 10 · 2022: 9 · 2021: 6 · 2020: 8 · 2019: 7 · 2018: 5 · 2017: 1 · 2016: 2
- FWCI
- 6.65
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Reproductive Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- OpenBU (Boston University) (submittedVersion)
- Funders
- National Institutes of Health (HD000849)
- National Institute of Environmental Health Sciences (P42ES007381, L30 ES023231)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD000849, K12HD000849)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sexual Differentiation and Disorders
- Keywords
- polycystic ovary syndrome, endocrine disruptors, prenatal exposure, bisphenol A, phthalates, dibutyl phthalate, DEHP, nicotine, fetal programming, hyperandrogenism, oligomenorrhea, maternal exposure
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