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Review Open access Aug 2026

Current Evidence Linking Microplastic Exposure and Reproductive Cancers

Microplastics (MPs) and nanoplastics (NPs) have emerged as pervasive environmental contaminants with increasing evidence of human exposure and biological accumulation. Recent studies have confirmed their presence in multiple human reproductive tissues and fluids, including semen, testicular tissue, ovarian follicular fluid, cervicovaginal secretions, placenta, and breast milk, raising concerns regarding their potential implications for reproductive health. Beyond their widespread distribution, MPs have been shown in experimental studies to interact with cellular and molecular processes, including oxidative stress, inflammatory responses, mitochondrial dysfunction, and DNA damage, which are pathways commonly implicated in carcinogenesis. This review provides a comprehensive and critical synthesis of current evidence linking microplastic exposure to reproductive cancers, including prostate, testicular, ovarian, endometrial, cervical, and vaginal malignancies. Available mechanistic studies suggest that MPs may influence cancer-related biological processes through dysregulation of programmed cell death, genotoxicity, endocrine disruption, and modulation of signaling pathways such as PI3K/AKT and MAPK. Experimental findings also indicate that MPs may alter the tumor microenvironment and affect cellular behaviors associated with proliferation, migration, and invasion. However, the majority of current evidence is derived from in vitro studies, animal models, and indirect mechanistic observations, while direct epidemiological evidence in humans remain limited. Furthermore, methodological heterogeneity in microplastic detection and characterization complicates comparisons across studies and hinders causal inference. Overall, current evidence supports the biological plausibility of an association between microplastic exposure and reproductive cancer-related processes, while highlighting the need for standardized methodologies and well-designed longitudinal human studies to clarify potential health risks.

B. Rais, A. Vafa, Faten F. Bin Dayel et al. · 0 citations

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