Background: Air pollutants can activate low-grade subclinical inflammation which further impairs respiratory health. We aimed to investigate the role of polygenic susceptibility to chronic air pollution-induced subclinical airway inflammation.
Methods: We used data from 296 women (69-79 years) enrolled in the population-based SALIA cohort (Study on the influence of Air pollution on Lung function, Inflammation and Aging). Biomarkers of airway inflammation were measured in induced-sputum samples at follow-up investigation in 2007-2010. Chronic air pollution exposures at residential addresses within 15 years prior to the biomarker assessments were used to estimate main environmental effects on subclinical airway inflammation. Furthermore, we calculated internally weighted polygenic risk scores based on genome-wide derived single nucleotide polymorphisms. Polygenic main and gene-environment interaction (GxE) effects were investigated by adjusted linear regression models.
Results: Higher exposures to nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter with aerodynamic diameters of ≤ 2.5 μm, ≤ 10 μm, and 2.5-10 µm significantly increased the levels of leukotriene (LT)B4 by 19.7% (p-value = 0.005), 20.9% (p = 0.002), 22.1% (p = 0.004), 17.4% (p = 0.004), and 23.4% (p = 0.001), respectively. We found significant effects of NO2 (25.9%, p = 0.008) and NOx (25.9%, p-value = 0.004) on the total number of cells. No significant GxE effects were observed. The trends were mostly robust in sensitivity analyses.
Conclusions: While this study confirms that higher chronic exposures to air pollution increase the risk of subclinical airway inflammation in elderly women, we could not demonstrate a significant role of polygenic susceptibility on this pathway. Further studies are required to investigate the role of polygenic susceptibility.
Keywords: Aged; Air pollution; Biomarkers; Gene-environment interaction; Leukotriene B4; Lung; Tumor necrosis factor-alpha.
© 2022. The Author(s).