Environmental Pollution, Endocrine Disruptors, and Metabolic Status: Impact on Female Fertility—A Narrative Review

Cristina Popescu, Romina‐Marina Sima, Mircea-Octavian Poenaru, Ancuta-Alina Constantin, Gabriel-Petre Gorecki, Andrei-Sebastian Diaconescu, Mara Mădălina Mihai, Cristian Toma, Liana Pleș
In: Reproductive Medicine · 2025 · vol. 6(4) , pp. 37 · doi:10.3390/reprodmed6040037 · W4416393312
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⚙ AI-generated summary by claude@2026-06, 2026-06-10 ⓘ

Environmental pollutants like PM2.5, NO2, and PFAS, along with microplastics, negatively impact female fertility by affecting ovarian competence and implantation, with metabolic changes potentially exacerbating these effects.

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Abstract

Objectives: Female fertility is increasingly threatened by environmental pollutants such as fine particulate matter (PM2.5 and NO2), endocrine-disrupting chemicals (BPA, phthalates, PFAS, and PCBs), and microplastics. These exposures are associated with impaired ovarian reserve, reduced implantation rates, and lower assisted reproductive technology (ART) success. Given the rising prevalence of obesity and weight-loss interventions, particularly bariatric surgery, understanding the combined influence of metabolic and environmental factors on reproductive outcomes is of critical importance. This review aimed to synthesize recent evidence on how these exposures interact to affect female fertility. Methods: A narrative review was conducted of studies published between 2019 and 2025 using PubMed, Google Scholar, Web of Science, and Wiley Online Library. The PubMed Boolean search string was “female fertility”, “ovarian function”, “IVF” and “pollution”, “endocrine disruptors”, “air pollutants”, and “microplastics”. Searches were limited to English language publications, with the last search performed on 30 March 2025. Human, animal, and in vitro data were screened separately. Human evidence was prioritized, and confounding factors (age, BMI, and smoking) were considered during interpretation. Results: Environmental pollutants were consistently associated with diminished ovarian reserve, poor oocyte quality, and reduced live birth rates in ART. PFAS exposure correlated with lower fecundability, while PM2.5 and NO2 were linked to decreased AMH and AFC levels. Mechanistic animal and in vitro studies support these findings through pathways involving oxidative stress, endocrine disruption, and epigenetic alterations. Rapid metabolic changes, particularly post-bariatric surgery, may transiently increase circulating lipophilic toxicants and reduce antioxidant defenses, amplifying reproductive vulnerability. Conclusions: Environmental exposures, especially PM2.5, NO2, PFAS, and microplastics, adversely influence ovarian and embryonic competence. Rapid metabolic transitions may further modulate this susceptibility through pollutant mobilization and micronutrient imbalances. Future interdisciplinary prospective studies integrating exposure monitoring, metabolic profiling, and reproductive endpoints are essential to guide clinical recommendations and precision fertility counseling.

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