Review explores associations between organochlorine pesticides and endocrine disorders in women, highlighting anti-hormonal mechanisms.
Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder among women, characterized by metabolic abnormalities and infertility. Despite its high prevalence, the etiology and pathogenesis of PCOS remain poorly understood. Emerging evidence suggests that persistent organic pollutants (POPs), known for their detrimental effects on the endocrine and reproductive systems, may play a role in the development and progression of PCOS. Among POPs, organochlorine pesticides (OCPs) are particularly widespread and pose significant health risks. This review examines the potential of OCPs as an environmental factor in the development and progression of PCOS. It highlights the mechanisms through which OCPs may disrupt the hypothalamic-pituitary-ovarian (HPO) axis and impair hormonal regulation, contributing to the onset and exacerbation of PCOS. Evidence links OCPs to insulin resistance, obesity, and type 2 diabetes mellitus. These disruptions may occur via pathways involving hypothyroidism or altered adrenal androgen secretion. While current evidence supports a plausible connection between OCP exposure and PCOS, significant gaps and inconsistencies in the data warrant further investigation. Elucidating the precise mechanisms underlying these associations is crucial for developing targeted prevention and intervention strategies.
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Yin et al. (2025) studied this question.
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