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Environmental pollutants and testicular toxicity in male reproductive health: Basic evidence and translational prospects — A narrative review
Summary
Sperm counts have dropped by more than half over the past 50 years, and this review pulls together lab evidence showing everyday pollutants, microplastics, BPA-related chemicals in plastics, and air pollution, may be damaging the testicles directly, including microplastics that have actually been found in human testicular tissue. The research even identifies a specific window (70-90 days before sperm is made) when air pollution exposure seems most harmful, though most of this evidence comes from animal studies and cells in labs, so human trials are still needed to confirm these effects and guide prevention strategies.
Global sperm concentration has declined by over 50% in the past five decades, with environmental pollutants identified as a critical driving factor. This review focuses on testicular-level evidence regarding the effects of microplastics, bisphenol compounds, and air pollution on male reproductive health, with an emphasis on spermatogenic and testicular somatic cell mechanisms. Microplastics have been detected in human testicular tissue, with a causal pathway established linking gut microbiota dysbiosis, immune activation, and blood-testis barrier disruption. Bisphenol A substitutes show comparable or greater reproductive toxicity than BPA, with BCAT1-mediated ferroptosis identified as a novel testicular injury mechanism. For air pollution, spermatogenesis stage I (70-90 days prior to semen collection) has been pinpointed as the critical PM2.5 exposure vulnerability window, with metal constituents of traffic-derived PM2.5 as the primary toxicity drivers. Future research should prioritize prospective cohort studies and clinical intervention trials targeting these emerging mechanistic pathways.