This study investigates the interaction between exposure to environmental polycyclic aromatic hydrocarbons (PAHs) and DNA repair gene polymorphisms on bulky DNA adducts in human sperm. The research involved 465 infertile adults, with sperm PAH-DNA adducts measured using immunofluorescent assay and flow cytometry. Polymorphisms in XPA, XPD, ERCC1, XPF, and XRCC1 genes were analyzed using PCR and RFLP techniques. Urinary 1-hydroxypyrene (1-OHP) levels were used as a biomarker for PAH exposure. The study found that XRCC1 polymorphisms, specifically 5'UTR-T/C, Arg194Trp, and Arg399Gln, were associated with increased sperm adduct levels. These effects were more pronounced in individuals with high PAH exposure. The results suggest that XRCC1 gene polymorphisms may modify sperm PAH-DNA adduct levels and could serve as biomarkers for identifying individuals susceptible to DNA damage from PAH exposure. The study also found that dietary intake of PAH-rich meals significantly influenced sperm adduct levels. Subjects who consumed such meals at least three times a week had higher adduct levels compared to those who did not. However, no significant association was found between cigarette smoking and PAH-DNA adducts in sperm. The study highlights the importance of DNA repair genes in protecting against DNA damage caused by environmental pollutants. It suggests that genetic variations in these genes may influence an individual's susceptibility to PAH-induced DNA damage. The findings provide the first evidence that XRCC1 polymorphisms may modify sperm PAH-DNA adduct levels and could be useful in identifying individuals at risk of DNA damage from PAH exposure. The study also emphasizes the need for further research to explore the combined effects of genetic and environmental factors on sperm DNA damage.This study investigates the interaction between exposure to environmental polycyclic aromatic hydrocarbons (PAHs) and DNA repair gene polymorphisms on bulky DNA adducts in human sperm. The research involved 465 infertile adults, with sperm PAH-DNA adducts measured using immunofluorescent assay and flow cytometry. Polymorphisms in XPA, XPD, ERCC1, XPF, and XRCC1 genes were analyzed using PCR and RFLP techniques. Urinary 1-hydroxypyrene (1-OHP) levels were used as a biomarker for PAH exposure. The study found that XRCC1 polymorphisms, specifically 5'UTR-T/C, Arg194Trp, and Arg399Gln, were associated with increased sperm adduct levels. These effects were more pronounced in individuals with high PAH exposure. The results suggest that XRCC1 gene polymorphisms may modify sperm PAH-DNA adduct levels and could serve as biomarkers for identifying individuals susceptible to DNA damage from PAH exposure. The study also found that dietary intake of PAH-rich meals significantly influenced sperm adduct levels. Subjects who consumed such meals at least three times a week had higher adduct levels compared to those who did not. However, no significant association was found between cigarette smoking and PAH-DNA adducts in sperm. The study highlights the importance of DNA repair genes in protecting against DNA damage caused by environmental pollutants. It suggests that genetic variations in these genes may influence an individual's susceptibility to PAH-induced DNA damage. The findings provide the first evidence that XRCC1 polymorphisms may modify sperm PAH-DNA adduct levels and could be useful in identifying individuals at risk of DNA damage from PAH exposure. The study also emphasizes the need for further research to explore the combined effects of genetic and environmental factors on sperm DNA damage.