Genetic susceptibility in air pollution-induced lung function decline

Abstract

Background Air pollution exposure is linked to reduced lung function. The interaction between genetic susceptibility and air pollution exposures on lung function in elderly women with and without current airflow obstruction was assessed. Methods Cross-sectional data from the German SALIA study (Study on the Influence of air pollution on lung function, inflammation and aging) was used to assess 458 women aged 54 years in 1985-94, and 358 women in 2007-10. Weighted genetic risk scores (GRS) (continuous and dichotomized by median) were calculated using 119 lung-related single nucleotide polymorphisms. Air pollution exposures (nitrogen dioxide (NO2/x), particulate matter with diameters <2.5, <10 and 2.5-10 µm (PM2.5/10/coarse), and PM2.5 absorbance) were modeled and assigned to residential address. Gene-environment interactions (GxE) were estimated on z-scores of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), and the ratio of FEV1 to FVC using adjusted linear regression models. Stratified analysis was performed for women with and without airflow obstruction (FEV1/FVC< lower limit of normal, presences of asthma, COPD or bronchitis). Results The analysis on all women showed significant interactions between GRS and NOx on FVC at follow-up (p= 0.042). Baseline analysis showed no interaction effects. 18.5% of women had a current airflow obstruction at baseline. For women with airflow obstruction, we found significant interactions between GRS and NO2 on FEV1/FVC (p= 0.010), GRS and PM2.5 on FEV1/FVC (p= 0.033), and GRS and PM2.5 absorbance on FEV1 (p= 0.017). No other interaction effects were found. Conclusion Genetic susceptibility might play a role in air pollution-related obstructive lung disease.