Pesticide and Herbicide Exposure and Male Reproductive Health: A Critical Narrative Review of Semen Quality, Sperm Genomic Integrity and Mechanistic Evidence

Abstract

Pesticides are heterogeneous biological control agents, and herbicides are one functional subgroup within this broader category. Concern about their effects on male reproduction is sustained by occupational cohorts, biomonitoring studies in the general population, and experimental evidence showing that several compounds can disturb redox balance, endocrine signalling, spermatogenesis and mature sperm function. This critical narrative review evaluates the strength and limitations of evidence linking adult environmental and occupational pesticide exposure with semen quality and related male reproductive endpoints. Literature published principally from 1 January 2000 to 6 July 2026 was considered, while selected earlier studies were retained when methodologically or historically informative. Human epidemiological evidence was prioritised and interpreted alongside mechanistic in vitro and animal data. The most coherent human evidence concerns organophosphate and N-methyl carbamate insecticides, for which recent systematic synthesis supports an association with lower sperm concentration, although most contributing studies remain observational and frequently cross-sectional. Evidence for impaired motility and sperm DNA integrity is also reasonably consistent across mixed pesticide exposures, whereas morphology is less reproducible. Pyrethroid findings are heterogeneous, with adverse associations in several clinic-based and environmental studies but null results in some population-based cohorts. For herbicides, human evidence is substantially thinner: biomonitoring studies involving alachlor, atrazine and mixed current-use pesticides suggest possible adverse associations, while glyphosate evidence in men is currently stronger for seminal detection and oxidative stress biomarkers than for demonstrated impairment of conventional semen parameters. Mechanistic evidence supports oxidative, mitochondrial, endocrine, genotoxic and sperm-signalling pathways, but experimental dose relevance and formulation effects often limit translation to human exposure. The literature is constrained by short-lived exposure biomarkers, single semen samples, mixture confounding, clinic selection, inconsistent endpoint definitions and weak temporal resolution. Future work should therefore prioritise prospective repeated-measures cohorts with repeated exposure assessment, mixture-aware causal methods, harmonised semen and sperm DNA endpoints, and explicit evaluation of herbicides and formulation components. Current evidence justifies exposure reduction in high-risk settings while retaining caution about pesticide-specific causal attribution.