About Author
Patil D1,Nandedkar D2,Patel D3,
1 Professor & HOD, Dept Department of Agadtantra, Ahinsa Institute of Ayurveda Dondaicha, Dhule
2 Professor & HOD , Department of Agadtantra YMT Ayurved Medical College Kharghar Navi Mumbai
3 M.S. Scholar, University of Delaware U.S.
Correspondence Address
Dondaicha, Tap Shindkheda Dist Dhule
Contact No. : 09404102118, Email : drvaishaliwasade@gmail.com
Date of Acceptance : 30 Mar 2026
Date of Publication : 31 Mar 2026
Article ID : SD-IJAY_161
How to cite this article : http://doi.org/10.55552/SDNJAY.2026.4101
Abstract
Abstract
Background
Male infertility affects approximately 15% of couples globally, with male factors contributing to nearly half of all cases. Growing evidence implicates endocrine-disrupting chemicals (EDCs)—including bisphenol A (BPA), phthalates, pesticides, and polychlorinated biphenyls (PCBs)—in declining semen quality and hormonal imbalances. These chemiscals interfere with endocrine signaling and may impair spermatogenesis through oxidative, hormonal, and epigenetic mechanisms.
Objective
To systematically synthesize available epidemiological, experimental, and mechanistic evidence evaluating the association between EDC exposure and male reproductive dysfunction, including sperm parameters, hormonal profiles, and fertility outcomes.
Methods
A structured literature search was conducted in PubMed using the search term “male infertility and endocrine disruptor” covering publications from 2005 to 2025. High-quality human cohort studies, case-control studies, experimental animal research, and mechanistic investigations were included. Outcomes assessed included sperm concentration, motility, morphology, DNA fragmentation, testosterone levels, gonadotropin levels, infertility risk, and assisted reproductive technology (ART) outcomes. Due to methodological heterogeneity, qualitative synthesis was performed, and quantitative pooling was conducted where effect sizes (odds ratios, correlations) were available. Risk of bias was evaluated based on study design, exposure assessment reliability, confounder adjustment, and reproducibility.
Results
High EDC exposure was consistently associated with reduced testosterone levels (12–15% decrease in highest exposure quartiles), impaired sperm motility (average decline 12–15%), increased DNA fragmentation, and morphological abnormalities. Occupational exposure cohorts demonstrated dose-response relationships. BPA and phthalates showed strong evidence of endocrine disruption in human studies, while pesticides and PCBs demonstrated moderate evidence based on mixed human and animal data. Although one meta-analysis reported no statistically significant association, the overall pooled evidence across more than 20 studies indicated consistent adverse effects on male reproductive parameters.
Conclusion
Cumulative evidence supports a significant association between EDC exposure and impaired male reproductive health. Mechanisms include receptor-mediated hormonal disruption, oxidative stress, altered steroidogenesis, and potential transgenerational epigenetic effects. Public health strategies aimed at reducing environmental exposure to endocrine disruptors are warranted to safeguard reproductive outcomes.
Keywords
Male infertility; endocrine-disrupting chemicals; bisphenol A; phthalates; pesticides; spermatogenesis; testosterone; oxidative stress; environmental toxicology; reproductive health