Introduction Idiopathic pulmonary fibrosis (IPF) has an unpredictable course corresponding to various profiles: stability, physiological disease progression and rapid decline. A minority of patients experience acute exacerbations (AEs). A recent study suggested that ozone and nitrogen dioxide might contribute to the occurrence of AE. We hypothesised that outdoor air pollution might influence the natural history of IPF.
Methods Patients were selected from the French cohort COhorte FIbrose (COFI), a national multicentre longitudinal prospective cohort of IPF (n=192). Air pollutant levels were assigned to each patient from the air quality monitoring station closest to the patient’s geocoded residence. Cox proportional hazards model was used to evaluate the impact of air pollution on AE, disease progression and death.
Results Onset of AEs was significantly associated with an increased mean level of ozone in the six preceding weeks, with an HR of 1.47 (95% CI 1.13 to 1.92) per 10 µg/m3 (p=0.005). Cumulative levels of exposure to particulate matter PM10 and PM2.5 were above WHO recommendations in 34% and 100% of patients, respectively. Mortality was significantly associated with increased levels of exposure to PM10 (HR=2.01, 95% CI 1.07 to 3.77) per 10 µg/m3 (p=0.03), and PM2.5 (HR=7.93, 95% CI 2.93 to 21.33) per 10 µg/m3 (p<0.001).
Conclusion This study suggests that air pollution has a negative impact on IPF outcomes, corroborating the role of ozone on AEs and establishing, for the first time, the potential role of long-term exposure to PM10 and PM2.5 on overall mortality.
- air pollution
- idiopathic pulmonary fibrosis
- acute exacerbation
- particulate matter
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Contributors (1) Substantial contributions to the conception or design of the work; or the acquisition, analysis or interpretation of data for the work; (2) drafting the work or revising it critically for important intellectual content; (3) final approval of the version to be published; and (4) agreement to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All persons designated as authors meet all four ICMJE criteria for authorship (LS, HN, VC, SS, MD, ZC, DI-B, BC, JC, BW, AT, BM, GP, SM-A, SG-D, AN, SD, VG, AG, KJ, RB, MW, DV and IA-M).
Funding Chancellerie des Universités de Paris (Legs Poix, grant #637), PHRC (grant # AOR 07076) and the Medical Research Foundation.
Competing interests HN reports other from Intermune, other from Roche, other from Boehringer- Ingelheim, other from Sanofi, during the conduct of the study; other from Centocor, outside the submitted work; DV reports personal fees from Intermune, personal fees from Roche, personal fees from Boehringer Ingelheim, personal fees from Intermune, Roche, Boehringer Ingelheim, outside the submitted work. Dr AG reports grants and personal fees from Boehringer, personal fees from Roche, outside the submitted work. GP reports personal fees from Actelion, Bayer, Boehringer Ingelheim, GSK, Roche, outside the submitted work. VC reports personal fees from Actelion, Bayer, Biogen Idec, Boehringer Ingelheim, Gilead, GSK, MSD, Novartis, Pfizer, Roche/Intermune, Sanofi, grants from Actelion, Boehringer Ingelheim, GSK, Pfizer and Roche and personal fees from Boehringer Ingelheim, outside the submitted work. All other authors have no competing interests to declare.
Ethics approval Ethics Committee (Comité de Protection des Personnes Ile-de-France) and by the French data protection authority (CNIL: 908198).
Provenance and peer review Not commissioned; externally peer reviewed.
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