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-aged women. Symptom heterogeneity among clinical cases and in sibling studies suggests that PCOS is a multifactorial disease with environmental components. Investigators hypothesize that endocrine disruptors may contribute to the pathophysiological origins of PCOS in utero. The goal of this literature review is to present and compare the available research investigating the developmental origins of PCOS deriving from prenatal exposure to three major classes of endocrine disruptors: bisphenol A (BPA), phthalates, and androgenic endocrine disruptors. Considerable evidence has been found to suggest links between fetal exposure to endocrine disruptors and PCOS. Rodent studies reported that maternal BPA exposure dysregulates postnatal development and sexual maturation. In rats, gestational exposure to dibutyl phthalate (DBP) and di(2-ethylhexyl)phthalate (DEHP) resulted in polycystic ovaries among first and third generation offspring. Additionally, serum DBP concentrations are higher among women with PCOS. Regarding DEHP, animal studies have shown that prenatal exposure results in an endocrinological profile similar to PCOS. Nicotine and 3,4,4'-trichlorocarbanilide (TCC) are known androgenic endocrine disruptors. Inducing prenatal exposure to excess androgens in animal models has successfully recreated a PCOS-like phenotype that includes abnormal ovarian function, anovulatory cycling, impaired fertility, and increased visceral fat distribution. Based on the literature, endocrine disruptors appear to have an etiological role in PCOS development through prenatal exposure and thus may pose one of the greatest hazards to fetal health and development.