Traffic exposures, air pollution and outcomes in pulmonary arterial hypertension: a UK cohort study analysis

Abstract

While traffic and air pollution exposure is associated with increased mortality in numerous diseases, its association with disease severity and outcomes in pulmonary arterial hypertension (PAH) remains unknown. Exposure to particulate matter ≤2.5 μm³ (PM_2.5), nitrogen dioxide (NO₂) and indirect measures of traffic-related air pollution (distance to main road and length of roads within buffer zones surrounding residential addresses) were estimated for 301 patients with idiopathic/heritable PAH recruited in the UK PAH national Cohort study. Associations with transplant-free survival and pulmonary hemodynamic severity at baseline were assessed, adjusting for confounding variables defined a priori. Higher estimated exposure to PM_2.5 was associated with higher risk of death or lung transplant (Unadjusted hazard ratio (HR) 2.68; 95% CI 1.11–6.47 per 3 μg·m⁻³, p=0.028). This association remained similar when adjusted for potential confounding variables (HR 4.38; 95% CI 1.44–13.36 per 3 μg·m⁻³, p=0.009). No associations were found between NO₂ exposure or other traffic pollution indicators and transplant-free survival. Conversely, indirect measures of exposure to traffic-related air pollution within the 500–1000 m buffer zones correlated with the ERS/ESC risk categories as well as pulmonary hemodynamics at baseline. This association was strongest for pulmonary vascular resistance. In idiopathic/heritable PAH, indirect measures of exposure to traffic-related air pollution were associated with disease severity at baseline, whereas higher PM_2.5 exposure may independently predict shorter transplant-free survival.