摘要：Background Traffic-related air pollution is related with asthma, and this association may be modified by genetic factors. Objectives We investigated the role of genetic polymorphisms potentially modifying the association between home outdoor levels of modeled nitrogen dioxide and asthma. Methods Adults from 13 cities of the second European Community Respiratory Health Survey (ECRHS II) were included ( n = 2,920), for whom both DNA and outdoor NO2 estimates were available. Home addresses were geocoded and linked to modeled outdoor NO2 estimates, as a marker of local traffic-related pollution. We examined asthma prevalence and evaluated polymorphisms in genes involved in oxidative stress pathways [gluthatione S -transferases M1 ( GSTM1 ), T1 ( GSTT1 ), and P1 ( GSTP1 ) and NAD(P)H:quinine oxidoreductase ( NQO1 )], inflammatory response [tumor necrosis factor α ( TNFA )], immunologic response [Toll-like receptor 4 ( TLR4 )], and airway reactivity [adrenergic receptor β2 ( ADRB2 )]. Results The association between modeled NO2 and asthma prevalence was significant for carriers of the most common genotypes of NQO1 rs2917666 [odds ratio (OR) = 1.54; 95% confidence interval (CI), 1.10–2.24], TNFA rs2844484 (OR = 2.02; 95% CI, 1.30–3.27). For new-onset asthma, the effect of NO2 was significant for the most common genotype of NQO1 rs2917666 (OR = 1.52; 95% CI, 1.09–2.16). A significant interaction was found between NQO1 rs2917666 and NO2 for asthma prevalence ( p = 0.02) and new-onset asthma ( p = 0.04). Conclusions Genetic polymorphisms in the NQO1 gene are related to asthma susceptibility among persons exposed to local traffic-related air pollution. This points to the importance of antioxidant pathways in the protection against the effects of air pollution on asthma.
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