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.
Keywords: endocrine disruptors; polycystic ovary syndrome; prenatal exposure.