Environmental Arsenic Exposure and Male Fertility: A Critical Narrative Review of Human Evidence, Mechanisms and Translational Uncertainty

Abstract

Arsenic is a widespread environmental metalloid whose inorganic forms contaminate drinking water, food chains, soil and air. Male reproductive toxicity is biologically plausible because spermatogenesis, steroidogenesis and post-testicular sperm maturation depend on tightly regulated redox, metabolic and endocrine processes. Yet the evidential basis for attributing human male subfertility to environmental arsenic remains markedly less secure than the experimental literature might suggest. This critical narrative review integrates exposure science, human epidemiology, animal and cell-model evidence, mechanistic research and methodological limitations. Literature published from 1980 to 1 June 2026 was identified through PubMed/MEDLINE, authoritative institutional websites and supplementary scholarly web searching, with backward and forward citation checking. Human studies provide signals of lower sperm concentration or motility, altered seminal biomarkers, infertility-associated urinary arsenic species and perturbation of steroid-hormone excretion. These findings are not uniform: studies are few, often clinic-based and cross-sectional, and differ in arsenic speciation, exposure range, co-exposures, semen assessment and confounder control. Experimental evidence is more coherent, linking arsenite and related compounds to oxidative injury, mitochondrial dysfunction, germ-cell loss, impaired spermatid elongation, acrosomal and flagellar defects, epididymal dysfunction, endocrine disruption, autophagy and altered sperm proteins. Developmental exposure and incomplete recovery after withdrawal raise concern about vulnerable windows, although doses and species frequently limit direct translation to human environmental exposure. The strongest current inference is that arsenic can damage male reproductive biology and may contribute to impaired semen quality in susceptible or highly exposed populations; the magnitude of risk at common low-level exposure is uncertain. Progress requires prospective preconception cohorts, repeated arsenic speciation and semen sampling, mixture-aware analysis, functional sperm and fertility outcomes, and explicit evaluation of reversibility after exposure reduction. Prevention should prioritise exposure control rather than unvalidated arsenic-specific fertility treatments.