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Respiratory exposure to polymethyl methacrylate nanoplastics impairs female fertility via ovarian accumulation and oocyte quality deterioration in mice.
Summary
Breathing in tiny plastic particles (from things like spray paints, coatings, or dust) may do more than affect your lungs — in mice, these nanoplastics traveled through the body and built up in the ovaries, throwing off key reproductive hormones and damaging egg-producing follicles. This led to fewer healthy eggs and lower pregnancy success when exposure continued into early pregnancy. While this study was done in mice, not humans, it raises real concerns about how everyday plastic pollution in the air we breathe could affect fertility.
Respiratory exposure to airborne polymethyl methacrylate (PMMA) nanoplastics (NPs) represents a critical, yet poorly mechanistically defined, hazard to female reproductive physiology. Here, we investigated the reproductive toxicity of PMMA NPs (average diameter ~55nm; negative surface charge) following intratracheal instillation in mice (0.2-100μg/day for 7 days). Fluorescently labeled PMMA NPs translocated systemically and accumulated in ovarian tissue. Exposure disrupted the estrous cycle and suppressed the pituitary-ovarian endocrine axis, characterized by marked reductions in circulating follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol, and progesterone. Histological analysis revealed selective depletion of secondary follicles accompanied by increased follicular atresia. Transcriptomic and protein-level analyses identified widespread downregulation of genes essential for ovarian function, including Esr1, Angpt1, Cftr, and Cd36. Specifically, we confirmed the suppression of the local CYP19A1-estradiol-ESR1-AKT survival signaling axis, accompanied by reduced expression of CFTR and CD36, which are associated with follicular growth and maturation. In vitro maturation assays further indicated impaired oocyte developmental competence following exposure to PMMA NPs. In reproductive outcome assessments, pre-pregnancy exposure alone did not significantly affect initial pregnancy rates, whereas continuous exposure extending into early gestation resulted in reduced pregnancy success. Collectively, these findings demonstrate that respiratory exposure to PMMA NPs compromises female fertility by disrupting both systemic gonadotropin support and localized intraovarian networks.