Pulmonary Arterial Hypertension Exacerbated by Traffic-Related Air Pollution

car traffic on a highway
Traffic-related air pollution exposure has been linked to baseline disease severity in idiopathic/heritable pulmonary arterial hypertension.

Traffic-related air pollution exposure has been linked to baseline disease severity in idiopathic/heritable pulmonary arterial hypertension (PAH), according to a study published in the European Respiratory Journal. In addition, shorter transplant-free survival rates may be associated with higher exposure to particulate matter ≤2.5 μm3 (PM2.5).

This study included 301 individuals with idiopathic/heritable PAH, all of whom had lived at the same address since being diagnosed. Participants were recruited from the National Cohort Study of Idiopathic and Heritable PAH in the United Kingdom. Data collected included household income, socioeconomic status, education level, and epidemiological information. Participants’ addresses were linked to exposure of nitrogen dioxide (NO2), PM2.5, and air pollution caused by traffic (estimated by distance to main road and nearby road lengths). Correlations between exposures and baseline pulmonary hemodynamic severity and transplant-free survival were assessed. Transplant-free survival after diagnosis constituted the primary outcome. Cox proportional hazards regression models were used to estimate associations between exposure and risk for mortality or lung transplant.

During a follow-up of 3.5 to 4.5 years, there was a 13% mortality rate and 2% transplantation rate among participants, yielding a 97% 1-year transplant-free survival rate, 85% 3-year transplant-free survival rate, and 67% 5-year transplant-free survival rate among incident patients. Increased exposure to PM2.5 correlated with an unadjusted hazard ratio of 2.68 (95% CI, 1.11-6.47 per 3 μg/m3; P =.028) for mortality or lung transplant.

Adjustments for possible confounders yielded a higher result of 4.38 (95% CI, 1.44-13.36 per 3 μg/m3; P =.009). NO2 and other indicators of traffic pollution showed no associations with transplant-free survival. Greater lengths of main roads in participants’ buffer zones (within 500 m) showed associations with greater baseline PAH risk scores, which in turn, increased the chance of a European Society of Cardiology/European Respiratory Society high-risk diagnosis.

Limitations to this study included the use of 2010 annual average air pollution maps, the potential for false positive findings, and a lack of detail on factors such as prevailing winds, how much time participants spent indoors, and the sources and types of PM2.5 particles.

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Researchers concluded that “traffic-related air pollution and PM2.5 exposure may be associated with disease severity and outcomes in PAH.  However, our findings require validation and replication in a larger cohort to increase confidence in the reliability of these estimates. The present study thus encourages further investigations on air pollution exposure as a potentially removable risk factor influencing PAH incidence, severity and outcomes.”


Sofianopoulou E, Kaptoge S, Gräf S, et al. Traffic exposures, air pollution and outcomes in pulmonary arterial hypertension: a United Kingdom cohort study analysis [published online March 28, 2019]. Eur Respir J. doi:10.1183/13993003.01429-2018