DNA repair capacity (DRC) was studied in 49 patients affected by basal cell carcinoma (BCC) and 68 cancer-free controls belonging to a larger case-control population enrolled for studying BCC risk factors. DRC was measured in the subjects' peripheral blood lymphocytes by using a host-cell reactivation assay that measures cellular activation of a reporter gene irradiated with UV light. A statistically significant age-related decline in DRC was observed in the controls from 20 to 70 years of age but not in the BCC cases. When the DRC values of the BCC patients and controls were compared by age, young BCC cases (age, < or =40 year) repaired less than the controls, although the difference was not statistically significant. Conversely, older BCC patients (age, >40 years) presented an enhanced repair capacity (P < 0.001) as compared with their controls. The search for possible factors associated with the high repair rate of elderly BCC cases revealed that both target cell physiology and life-style habits may affect host DNA repair. Smoking was the variable that explained most of the increase in DRC among older patients. The understanding of how these factors affect host DRC will be relevant for a correct use of this biomarker.