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

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 with a 50% cut-off aerodynamic diameter ≤2.5 μm (PM _2.5 ), nitrogen dioxide (NO ₂ ) 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 National Cohort Study of Idiopathic and Heritable PAH. Associations with transplant-free survival and pulmonary haemodynamic 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 NO ₂ 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 European Society of Cardiology/European Respiratory Society risk categories as well as pulmonary haemodynamics 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.
Competing Interests: Conflict of interest: E. Sofianopoulou has nothing to disclose. Conflict of interest: S. Kaptoge reports grants from UK Medical Research Council and British Heart Foundation, during the conduct of the study. Conflict of interest: S. Gräf has nothing to disclose. Conflict of interest: C. Hadinnapola has nothing to disclose. Conflict of interest: C.M. Treacy has nothing to disclose. Conflict of interest: C. Church has nothing to disclose. Conflict of interest: G. Coghlan has nothing to disclose. Conflict of interest: J.S.R. Gibbs reports grants and personal fees from Actelion, Bayer, GSK and MSD, personal fees from Arena, Bellerophon, Complexa and Pfizer, grants from Amco and United Therapeutics, outside the submitted work. Conflict of interest: M. Haimel has nothing to disclose. Conflict of interest: L.S. Howard has nothing to disclose. Conflict of interest: M. Johnson reports grants and personal fees for attendance at meeting and lectures from Actelion, Bayer, GSK and MSD, outside the submitted work. Conflict of interest: D.G. Kiely reports grants, personal fees and nonfinancial support from Actelion, Bayer and GSK, personal fees and nonfinancial support from MSD, outside the submitted work. Conflict of interest: A. Lawrie reports grants and personal fees from Actelion and GSK, grants from British Heart Foundation and UK Medical Research Council, outside the submitted work. Conflict of interest: J. Lordan has nothing to disclose. Conflict of interest: R.V. MacKenzie Ross has nothing to disclose. Conflict of interest: J.M. Martin has nothing to disclose. Conflict of interest: S. Moledina has nothing to disclose. Conflict of interest: M. Newnham reports education support (travel, registration and accommodation) to attend conferences from MSD and GSK, outside the submitted work. Conflict of interest: A.J. Peacock reports grants and personal fees from Actelion and Bayer, personal fees from GSK, grants from Gilead, outside the submitted work. Conflict of interest: L.C. Price has nothing to disclose. Conflict of interest: C.J. Rhodes has nothing to disclose. Conflict of interest: J. Suntharalingam has nothing to disclose. Conflict of interest: E.M. Swietlik has nothing to disclose. Conflict of interest: M.R. Toshner has nothing to disclose. Conflict of interest: J. Wharton reports personal fees for advisory board work from Actelion, outside the submitted work. Conflict of interest: M.R. Wilkins has nothing to disclose. Conflict of interest: S.J. Wort reports grants and personal fees from Actelion and Bayer, personal fees from GSK and MSD, outside the submitted work. Conflict of interest: J. Pepke-Zaba (or her institution) received research, education grants from Actelion, Merck and Bayer; and has served on advisory boards for Actelion, Merck, Bayer and GSK. Conflict of interest: R. Condliffe reports personal fees for advisory board work from Actelion, Bayer and MSD, during the conduct of the study. Conflict of interest: P.A. Corris reports grants and personal fees from Actelion and Bayer, personal fees from MSD, outside the submitted work. Conflict of interest: E. Di Angelantonio reports grants from European Commission Framework 7, European Research Council, British Heart Foundation, UK Medical Research Council and National Institute for Health Research, during the conduct of the study; grants from NHS Blood and Transplant, outside the submitted work. Conflict of interest: S. Provencher has nothing to disclose. Conflict of interest: N.W. Morrell reports personal fees from GSK and Johnson & Johnson/Actelion, outside the submitted work.
(Copyright ©ERS 2019.)