Kerri A Johannson1, Eric Vittinghoff2, Julie Morisset3, Paul J Wolters4, Elizabeth M Noth5, John R Balmes6, Harold R Collard4. 1. Departments of Medicine and Community Health Sciences, University of Calgary, Calgary, AB, Canada. Electronic address: kerri.johannson@ahs.ca. 2. Department of Biostatistics and Epidemiology, University of California San Francisco, San Francisco, CA. 3. Département de Médecine, Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. 4. Department of Medicine, University of California San Francisco, San Francisco, CA. 5. Division of Environmental Health Sciences, School of Public Health, University of California Berkeley, Berkeley, CA. 6. Department of Medicine, University of California San Francisco, San Francisco, CA; Division of Environmental Health Sciences, School of Public Health, University of California Berkeley, Berkeley, CA.
Abstract
BACKGROUND: Air pollution exposure is associated with acute exacerbation, disease progression, and mortality in patients with idiopathic pulmonary fibrosis (IPF). The objective of this study was to describe the impact of air pollution exposures on disease severity, as well as changes in lung function, in patients with IPF. METHODS: Using home spirometers and symptom diaries, 25 patients with IPF prospectively recorded FVC weekly for up to 40 weeks. Residential addresses were geocoded to estimate weekly mean air pollution exposures for ground-level ozone (O3), nitrogen dioxide (NO2), and particulate matter < 2.5 or 10 μm in aerodynamic diameter (PM2.5 and PM10, respectively). The dependence of weekly clinical measurements on preceding levels of each pollutant was assessed with the use of linear mixed models, yielding beta-coefficients with 95% CIs, using varying lag times. RESULTS: Lower mean FVC % predicted was consistently associated with increased mean exposures to PM10 in the 2 to 5 weeks preceding clinical measurements (range, -0.46 to -0.39 [95% CI, -0.73 to -0.13]; P < .005). Lower mean FVC % predicted over the study period was inversely related to mean levels of NO2 (-0.45 [95% CI, -0.85 to -0.05]; P = .03), PM2.5 (-0.45 [95% CI, -0.84 to -0.07]; P = .02), and PM10 (-0.57 [95% CI, -0.92 to -0.21]; P = .003), averaged over the study. Weekly changes in FVC and changes over 40 weeks were independent of pollution exposures. CONCLUSIONS: Higher air pollution exposures were associated with lower lung function, but not changes in lung function, in patients with IPF. Further studies are needed to characterize the mechanisms underlying this relationship.
BACKGROUND: Air pollution exposure is associated with acute exacerbation, disease progression, and mortality in patients with idiopathic pulmonary fibrosis (IPF). The objective of this study was to describe the impact of air pollution exposures on disease severity, as well as changes in lung function, in patients with IPF. METHODS: Using home spirometers and symptom diaries, 25 patients with IPF prospectively recorded FVC weekly for up to 40 weeks. Residential addresses were geocoded to estimate weekly mean air pollution exposures for ground-level ozone (O3), nitrogen dioxide (NO2), and particulate matter < 2.5 or 10 μm in aerodynamic diameter (PM2.5 and PM10, respectively). The dependence of weekly clinical measurements on preceding levels of each pollutant was assessed with the use of linear mixed models, yielding beta-coefficients with 95% CIs, using varying lag times. RESULTS: Lower mean FVC % predicted was consistently associated with increased mean exposures to PM10 in the 2 to 5 weeks preceding clinical measurements (range, -0.46 to -0.39 [95% CI, -0.73 to -0.13]; P < .005). Lower mean FVC % predicted over the study period was inversely related to mean levels of NO2 (-0.45 [95% CI, -0.85 to -0.05]; P = .03), PM2.5 (-0.45 [95% CI, -0.84 to -0.07]; P = .02), and PM10 (-0.57 [95% CI, -0.92 to -0.21]; P = .003), averaged over the study. Weekly changes in FVC and changes over 40 weeks were independent of pollution exposures. CONCLUSIONS: Higher air pollution exposures were associated with lower lung function, but not changes in lung function, in patients with IPF. Further studies are needed to characterize the mechanisms underlying this relationship.
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