Occupational Exposure to Chemical Solvents and Heavy Metals and Oxidative Stress‐Related Sperm Dysfunction in Textile Workers

ABSTRACT Occupational exposure to chemical solvents and heavy metals among workers in textile‐related industries has emerged as a significant risk factor for male reproductive dysfunction; however, the underlying biological mechanisms remain incompletely understood. Oxidative stress has been proposed as a key mediator linking occupational exposure to impaired sperm morphology and function. This study aimed to evaluate the association between occupational exposure to chemical solvents and toxic metals and alterations in sperm function, with particular emphasis on oxidative stress‐mediated pathways. In this case–control study, semen samples were collected from teratozoospermic men occupationally exposed to chemical solvents and heavy metals ( n = 60) and from age‐matched normozoospermic controls without known occupational exposure ( n = 30). Standard seminal parameters were assessed according to WHO guidelines. Oxidative stress status was evaluated by measuring reactive oxygen species (ROS) and malondialdehyde (MDA) levels, along with antioxidant defense markers, including superoxide dismutase (SOD), catalase, and reduced glutathione (GSH). Sperm functional integrity was assessed through acrosome integrity assays and sperm DNA fragmentation (SDF), evaluated using the comet assay and flow cytometry. Levels of toxic metals (cadmium, lead, and chromium) were quantified using atomic absorption spectrophotometry. Occupationally exposed teratozoospermic men exhibited significantly elevated oxidative stress markers, with increased ROS levels (32.0 ± 9.0 vs. 15.0 ± 5.0) and MDA concentrations (4.8 ± 1.1 vs. 2.1 ± 0.6 nmol/mL), accompanied by a marked reduction in antioxidant defense markers (SOD, catalase, and GSH; p < 0.05) compared with controls. The proportion of acrosome‐intact spermatozoa was significantly lower in exposed men (38.3% ± 9.2% vs. 62.4% ± 10.1%). Both comet assay and flow cytometric analyses demonstrated significantly higher levels of sperm DNA fragmentation in the exposed group. Furthermore, quantitative analysis revealed significantly elevated body burdens of cadmium, lead, and chromium among occupationally exposed individuals. These findings indicate that oxidative stress represents a central pathophysiological mechanism linking occupational exposure to chemical solvents and heavy metals with sperm functional impairment and teratozoospermia. The results underscore the importance of routine reproductive health surveillance and oxidative stress monitoring among workers in high‐risk occupational settings.