Air pollution and subclinical inflammation in the lung: direct or indirect effect? Results from the SALIA cohort study

摘要

Background: Pulmonary inflammation is considered a first step in the induction of adverse health effects from air pollution. More than 20 years ago it could be demonstrated in women from the baseline investigation of the SALIA cohort that air pollution was associated with lung function impairment and COPD, which usually is associated with inflammatory processes. We determined markers of pulmonary inflammation in a follow-up examination of the SALIA cohort after a considerable decline in air pollution. Aims: We aimed to determine the direct effect of current exposure to particulate matter from traffic and industry on inflammatory markers in the lung. Indirect effects mediated by a long lasting deterioration of lung function should be excluded. Methods: In the baseline (1985-1994) and in the follow-up (2008) examinations of SALIA 402 women were clinically investigated. Inflammatory markers in exhaled breath condensate and in induced sputum (i.e. NO-derivatives, cell counts, leukotrienes) were measured in 2008 and lung function (FEV1) was determined at baseline and in 2008. Individually modelled air pollution exposures at baseline and follow-up were determined within the ESCAPE project. The effect of pollution on inflammatory markers was considered direct if inclusion of the lung function did not alter the linear regression results adjusted for age, smoking, BMI, height, socio-economic status and presence of indoor mould.. Results: Air pollution and lung function at baseline were highly correlated with their values at follow-up. A one litre decrease in baseline FEV1 was associated with a 19.5% (95% CI: -3.6%-37.4%) increase of NO-derivatives at follow-up. An interquartile increase in current PM2.5 was associated with a 16.2% (95% CI: 1.1%-33.5%) higher NO-derivatives in sputum. However adjustment for lung function at baseline changed this parameter estimate from 16.2% to 16.4% only. Conclusions: The effect of air pollution on inflammatory markers might be a direct effect. We did not find evidence for a mediation of effect by deteriorated lung function.