Environmental Toxicants and Polycystic Ovary Syndrome: Implications for a Metabolic-Ovarian Framework (PMOS) - A...

Polycystic ovary syndrome (PCOS) is increasingly recognized as a systemic condition characterized by intricate endocrine and metabolic dysregulation. Emerging evidence suggests that environmental contaminants may drive its pathogenesis, supporting an expanded conceptualization of the disorder as polycystic metabolic-ovarian syndrome (PMOS). This systematic review aimed to evaluate the association between exposure to potentially toxic elements (PTEs) and endocrine disruptors and the reproductive, hormonal, and metabolic clinical features of PCOS.

Following PRISMA guidelines, a systematic search was conducted across PubMed, Embase, Scopus, and Web of Science for human observational studies published up to 31 December 2025. Methodological quality was appraised using the Newcastle-Ottawa Scale (NOS). Due to heterogeneity in biological matrices and toxicant classes, a narrative synthesis was performed.

Fourteen high-quality studies (NOS scores 8-9) from seven countries met the inclusion criteria. The evidence consistently linked exposure to endocrine disrupting chemicals specifically bisphenol A (BPA) and phthalates-with hyperandrogenism, altered luteinizing hormone/follicle-stimulating hormone ratios, and impaired ovarian reserve. Furthermore, heavy metals (cadmium, lead, mercury, arsenic) and emerging rare earth elements were significantly elevated in women with PCOS across multiple matrices (serum, urine, and follicular fluid). These exposures were strongly associated with metabolic disturbances, including insulin resistance, obesity indices, and lipid abnormalities, mediated predominantly by oxidative stress pathways and impaired antioxidant defences.

Current observational evidence suggests associations between exposure to selected environmental toxicants and endocrine‑metabolic features of PCOS. However, heterogeneity in exposure assessment, biological matrices, PCOS diagnostic criteria, and confounder adjustment limits causal interpretation. Future prospective studies with repeated biomonitoring are needed.