Mechanisms of reproductive toxicity and endocrine disruption of bisphenols and per- and polyfluoroalkyl substances (PFAS): Implications for women's reproductive health.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing experimental and epidemiologic literature without systematic methodology
PubMed 41966417 · doi:10.1016/j.reprotox.2026.109239
What was done
This review synthesized current experimental (in vitro and animal models) and epidemiologic evidence to evaluate the endocrine-disrupting mechanisms and reproductive toxicity of bisphenols (especially BPA) and per- and polyfluoroalkyl substances (PFAS) on female reproductive health.
What was found
The abstract reports no numerical data or effect sizes. BPA and PFAS exposure consistently disrupted hypothalamic-pituitary-ovarian axis signaling, ovarian steroidogenesis, folliculogenesis, oocyte quality, and uterine function through oxidative stress, mitochondrial dysfunction, and epigenetic modifications. Epidemiologic studies identified associations between exposure to these chemicals and increased risks of endometriosis, polycystic ovary syndrome, diminished ovarian reserve, premature ovarian insufficiency, infertility, and adverse pregnancy outcomes.
Why it matters
This paper links cellular and animal toxicological pathways to specific clinical reproductive disorders in women. It highlights ubiquitous environmental chemical exposures as potentially modifiable risk factors to guide future exposure assessments and regulatory interventions.
Limits
The abstract gives no quantitative values, dose-response levels, or exposure thresholds. As a narrative review rather than a systematic review or meta-analysis, study selection criteria, risk-of-bias evaluation, and total study count are not reported. Preclinical findings may not translate directly to humans, and epidemiological associations cannot establish causality.