Source-specific air pollution and risk of chronic obstructive pulmonary disease: A pooled cohort study.

The evidence linking long-term exposure to air pollution and development of chronic obstructive pulmonary disease (COPD) is still controversial. Furthermore, most studies have investigated associations with particulate matter (PM) and nitrogen dioxide (NO2), disregarding their emission source and other relevant air pollutants, such as ultrafine particles (UFP) and elemental carbon (EC). This study aimed to assess associations between long-term residential exposure to PM2.5, NO2, UFP, and EC and risk of COPD, distinguishing the effects of air pollution from local traffic and other sources. We pooled data from two large Danish cohorts - the Diet, Cancer, and Health cohort and the Danish National Health Survey. For all participants (N = 159,769), we estimated long-term air pollution exposure to total, local traffic, and other contributions, based on complete address histories. We used Cox proportional hazards models to estimate associations between 10-year time-weighted averaged air pollution and incident COPD, adjusting for demographic, socioeconomic, and lifestyle factors, including smoking.We evaluated possible modification of these associations by sex, smoking status, and previous asthma diagnosis. Long-term exposures to PM2.5, NO2, UFP, and EC were associated with higher risk of COPD. The highest hazard ratio (HR) per interquartile range of total contributions was observed for PM2.5 (HR: 1.11 [95% confidence interval: 1.05, 1.17]), followed by NO2 (1.08 [1.04, 1.13]), UFP (1.05 [0.99, 1.11]), and EC (1.02 [1.00, 1.05]), after full adjustment. PM2.5 from other sources than local traffic was more strongly associated with COPD than PM2.5 from local traffic, while for UFP and EC, the contributions from local traffic seemed most harmful. Effect modification analyses showed stronger associations among women, never smokers, and those with an asthma diagnosis. Our findings suggest that air pollution from local traffic and other sources contribute to COPD risk, with variations depending on the pollutant type. Further research is needed to validate these findings across different populations and geographical settings. https://doi.org/10.1289/EHP16554.