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GlutathioneS-transferases detoxify polycyclic aromatic hydrocarbons found in tobacco smoke by glutathione conjugation. Polymorphisms within theGSTM1,GSTT1andGSTP1genes, coding for enzymes with deficient or reduced activity, have been studied as potential modifiers of lung cancer risk. It is hypothesized that risk associated with potential susceptibility gene polymorphisms might be most evident at low levels of exposure. Never smokers developing lung cancer represent a highly susceptible subset of the population, exposed to tobacco carcinogens only through environmental tobacco smoke. This population-based case-control study examines the association betweenGSTM1,GSTT1andGSTP1genotypes and lung cancer in one of the largest samples of never smokers to date. Cases (n= 166) were identified through the metropolitan Detroit Surveillance, Epidemiology and End Results (SEER) program and age- and race-matched population-based controls (n= 181) were identified using random digit dialing. Overall, there was no significant association between single or combinations of genotypes atGSTM1,GSTT1orGSTP1and lung cancer risk after adjustment for age, race, sex and household ETS exposure in years. However, in never smokers exposed to 20 or more years of household ETS, carrying theGSTM1null genotype was associated with a 2.3-fold increase in risk [95% confidence interval (CI) 1.05–5.13]. Individuals in this high ETS exposure category carrying theGSTM1null and theGSTP1Val allele were at over 4-fold increased risk of developing lung cancer (OR = 4.56, 95% CI: 1.21–17.21). These findings suggest that in the presence of ETS, theGSTM1genotype both alone and in combination with theGSTP1genotype alters the risk of developing lung cancer among never smokers.

carcinogenesis

GSTM1              ,               GSTT1               and               GSTP1               polymorphisms, environmental tobacco smoke exposure and risk of lung cancer among never smokers: a population-based study