CYP1A1 gene polymorphisms modify the association between PM 10 exposure and lung function.

Genetic epidemiological studies have provided evidence that several genes modify the link between air pollution and lung function. We assessed whether the adverse impacts of particulate matter with an aerodynamic diameter ≤10 μm (PM10 ) on lung function are modified by CYP1A1 gene polymorphisms in Korean adults. We used health check-up data from 1817 men, and the annual mean concentrations of ambient PM10 estimated from the ambient data. Three single nucleotide polymorphisms (SNPs) of CYP1A1 were selected for our study. We identified significant CYP1A1 SNPs-by-PM10 interactions for forced expiratory volume 1 s (FEV1 ) and forced vital capacity (FVC) (all pint  < 0.05). Minor allele carriers of the SNPs were more susceptible to PM10 -induced FEV1 and FVC reduction. The subgroup analysis of SNP genotypes showed that no significant association between PM10 and FEV1 or FVC was observed in homozygous reference genotype groups of all SNPs (all passoc  > 0.05), whereas in heterozygous or homozygous alternate genotype groups, PM10 was significantly associated with decreased FEV1 (all passoc for FEV1  < 0.05). The association between persistent exposure to PM10 and lung function decline in Korean men may be determined in part by several functional variants of the CYP1A1 gene.