Hormonal perturbations induced by multicategory endocrine-disrupting chemicals increase the risk of polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is intricately linked to both reproductive and metabolic health, and its pathogenesis remains unclear. Previous studies suggest that exposure to endocrine disrupting chemicals (EDCs) may contribute to PCOS. However, there is still a lack of systematic researches and analyses on this topic. In this study, we investigated the association between PCOS and EDC exposure and established a mechanistic link between the two by analyzing hormone levels. The meta-analysis pointed out that the levels of EDCs in patients with PCOS were significantly higher than those in the control group (standardized mean differences: bisphenol A, 1.92; phthalates (PAEs), 0.07; per- and perfluoroalkyl substances, 0.21; polychlorinated biphenyl (PCBs), 0.80; organochlorine pesticides (OCPs), 0.71). Subgroup analyses revealed that age and body mass index were potential sources of heterogeneity. EDC levels in urine in Asian populations (36.23 ng/mL) were higher than those observed in European and American cohorts (6.91 and 20.63 ng/mL, respectively). Structural equation modeling indicated that the alterations in fasting insulin caused by PCBs (β = 0.284) and HOMA-IR levels caused by OCPs and PAEs were exactly contribute to the formation of PCOS (β = 0.231, 0.257), thereby suggesting an underlying pathogenic mechanism. Low levels of PCBs pose a relatively high risk. Additionally, EDC-induced elevations in luteinizing hormone and testosterone promote ovarian cell overactivity and enhance insulin resistance. It is imperative to cultivate a more comprehensive understanding of overall impact of EDCs on human health in the future by multifaceted monitoring and assessment strategies.