Genetic susceptibility, residential radon an lung cancer risk in never smokers. Results from the LCRINS Study

Abstract

Objective: Analyze the interaction between GSTM1/GSTT1 polymorphsms (wild type, hemizygous deletion, homozygous deletion) and residential radon (RR) exposure in the lung cancer risk in never smokers Material and Methods: Multicentric, case-control study. Consecutive cases of lung cancer diagnosed in never smokers in 10 Spanish hospitals were included. Controls were never smokers undergoing minor, non-oncologic surgery at the same hospitals. Participants were interviewed through a questionnaire, focusing on risk factors for lung cancer. A blood sample was obtained for genetic analysis. Radon at dwellings was measured using alpha-track detectors Results: We included 322 cases (80,4%women) and 338 controls (78% women), median age:70. The most frequent histologic type was adenocarcinoma (78.5%). RR concentration was >200 Bq/m3 in 45.3% of cases and in 30.2% of controls. GSTM1 and GSTT1 status was analyzed in 207 and 197 cases and in 299 and 302 controls, respectively. Table 1 shows that lung cancer risk increases for the same radon exposure when the gene is absent compared to non-deleted gene. This effect is more evident when only adenocarcinoma patients are analyzed Conclusions: Homozigous deletion of GSTM1 is associated with an increased risk of lung cancer in never smokers exposed to residential radon concentrations above 200 Bq/m3, suggesting that this gene could modulate the effect of residential radon