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. 2018 May;153(5):1221-1228.
doi: 10.1016/j.chest.2017.07.034. Epub 2017 Aug 9.

Exposure to Ambient Particulate Matter Is Associated With Accelerated Functional Decline in Idiopathic Pulmonary Fibrosis

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Exposure to Ambient Particulate Matter Is Associated With Accelerated Functional Decline in Idiopathic Pulmonary Fibrosis

Christopher J Winterbottom et al. Chest. 2018 May.

Abstract

Background: Idiopathic pulmonary fibrosis (IPF), a progressive disease with an unknown pathogenesis, may be due in part to an abnormal response to injurious stimuli by alveolar epithelial cells. Air pollution and particulate inhalation of matter evoke a wide variety of pulmonary and systemic inflammatory diseases. We therefore hypothesized that increased average ambient particulate matter (PM) concentrations would be associated with an accelerated rate of decline in FVC in IPF.

Methods: We identified a cohort of subjects seen at a single university referral center from 2007 to 2013. Average concentrations of particulate matter < 10 and < 2.5 μg/m3 (PM10 and PM2.5, respectively) were assigned to each patient based on geocoded residential addresses. A linear multivariable mixed-effects model determined the association between the rate of decline in FVC and average PM concentration, controlling for baseline FVC at first measurement and other covariates.

Results: One hundred thirty-five subjects were included in the final analysis after exclusion of subjects missing repeated spirometry measurements and those for whom exposure data were not available. There was a significant association between PM10 levels and the rate of decline in FVC during the study period, with each μg/m3 increase in PM10 corresponding with an additional 46 cc/y decline in FVC (P = .008).

Conclusions: Ambient air pollution, as measured by average PM10 concentration, is associated with an increase in the rate of decline of FVC in IPF, suggesting a potential mechanistic role for air pollution in the progression of disease.

Keywords: air pollution; environmental pollution; idiopathic pulmonary fibrosis; interstitial lung disease; pulmonary fibrosis.

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Figures

Figure 1
Figure 1
Distribution of average PM exposure during the study period for all subjects included in longitudinal analysis. Median (IQR) and maximum/minimum value for the average annual concentration of PM10 and PM2.5 for each individual during the study period. EPA = Environmental Protection Agency; PM2.5 = particulate matter with diameter < 2.5 μm in diameter; PM10 = particulate matter with diameter < 10 μm in diameter.
Figure 2
Figure 2
Average FVC trajectory over time compared between subjects with PM10 concentrations greater than or less than the median exposure level. Pooled trajectory of average FVC (mean and 95% CI) over time from study entry point and split dichotomously between individuals with PM10 exposure above and below the median level of exposure. The steeper trajectory in those with above the median exposure reflects the relationship between PM10 exposure and FVC decline, although the pooled analysis does not capture the statistical power of the mixed-effects model. PM = particulate matter. See Figure 1 legend for expansion of other abbreviations.

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