Environmental contaminants and endocrine disrupting chemicals in female infertility: a systematic review

Infertility affects a substantial proportion of women of reproductive age worldwide. Increasing epidemiological evidence indicates that exposure to environmental contaminants (ECs) and endocrine-disrupting chemicals (EDCs) is associated with female reproductive health outcomes. However, systematic syntheses focusing specifically on human observational evidence remain limited. This systematic review therefore aimed to evaluate associations between EC and EDC exposure and female reproductive health outcomes, including infertility. This review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines. PubMed/MEDLINE, Cochrane, and Scopus databases were searched for studies published between January 2020 and May 2025. Eligible studies included observational designs involving well-characterized populations of fertile or infertile women. Randomized trials, reviews, animal studies, and studies restricted to male infertility were excluded. Primary outcomes included reproductive hormone parameters and fecundability-related measures. Study quality was assessed using the Newcastle–Ottawa Scale. Of 1,074 records identified, 38 studies met the inclusion criteria. The studies examined exposures to phthalates, bisphenols, per- and polyfluoroalkyl substances (PFAS), heavy metals, and persistent organic pollutants (POPs). Across studies, EC and EDC exposures were consistently associated with adverse reproductive indicators. Phthalates were associated with alterations in reproductive hormone profiles and oocyte-related outcomes. Bisphenol exposure was associated with hormonal changes and polycystic ovary syndrome (PCOS). POP exposure was associated with reduced oocyte yield, while heavy metal exposure was associated with PCOS risk. Evidence from recent observational studies indicates consistent associations between exposure to selected ECs and EDCs and female reproductive health outcomes. These associations may involve endocrine-related pathways, although causal inference remains limited by study design. Further longitudinal and mechanistic studies are warranted to clarify exposure–response relationships and underlying biological mechanisms.