Synergistic Impact of Environmental Pollution and Occupational Stress on Sperm DNA Integrity Unveiling Hidden Drivers of Male Infertility

Infertility is the inability of a sexually active couple to conceive within 1 year. It affects 10-15% of couples globally, with male factors accounting for 40-50% of these cases. The decline in semen quality, often with unknown causes, emphasises the need to evaluate sperm count, motility, and morphology when assessing male reproductive health. Environmental, occupational, and lifestyle factors are increasingly recognised as important contributors to male infertility, often linked to oxidative stress and disruptions in spermatogenesis. Exposure to pesticides, such as organochlorines and organophosphates, is associated with lower sperm count, poor motility, testicular issues, and negative reproductive outcomes in offspring. Similarly, exposure to metals like lead may harm spermatogenesis and raise the chances of low birth weight and prematurity. Diets high in ultra-processed foods (UPFs) have been associated with increased oxidative stress, cause inflammation, and limit essential nutrients needed for sperm quality, contributing to infertility. Psychosocial and occupational stress, along with heat exposure and electromagnetic radiation, further hinder sperm function by disrupting hormonal balance, increasing reactive oxygen species (ROS) formation, and causing apoptosis in testicular cells. Together, these factors illustrate the complex interactions among chemical, physical, nutritional, and psychosocial influences on male reproductive health. Reducing these risks may be important for maintaining male reproductive health through safe work practices, dietary changes, stress management, and environmental awareness is vital for maintaining fertility. Understanding how these exposures impact spermatogenesis and sperm quality can guide public health initiatives, workplace safety rules, and lifestyle changes aimed at enhancing male reproductive health. While oxidative stress-mediated sperm dysfunction is supported by substantial clinical and experimental evidence, data regarding epigenetic alterations, microplastics, occupational stress interactions, and dietary influences represent emerging areas of investigation and require further validation. This manuscript is a narrative review article. We did not conduct any original observational or experimental study. No primary data collection, participant recruitment, or laboratory analysis was performed. All evidence discussed is derived from previously published peer-reviewed in vitro studies.