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BACKGROUND: Particulate matter (PM) air pollution has been associated with decreased pulmonary function, but the exposure-response relationship in chronic obstructive pulmonary disease (COPD) patients is uncertain, and most studies have only focused on exposures to ambient pollution.

OBJECTIVES: We aimed to assess associations between pulmonary function and indoor and ambient PM <= 2.5 mu m (PM2.5) and black carbon (BC).

METHODS: Between November 2012 and December 2014, 125 patients with COPD (mean age, 73.4 y) who were not currently smoking and without known indoor BC sources were recruited. Indoor BC and PM2.5 were measured in each home for a week in each season, up to four times a year, followed by in-person spirometry pre- and post-bronchodilator. Ambient exposures were available from a central site monitor. Multivariable adjusted mixed effects regression models were used to assess associations scaled per interquartile range (IQR) of exposure.

RESULTS: There were 367 study visits; the median (IQR) indoor BC and PM2.5 were 0.19 (0.22) mu g/m(3) and 6.67 (5.80) mu g/m(3), respectively. Increasing indoor exposures to BC were associated with decreases in pre-bronchodilator forced expiratory volume in 1 s (FEV1) and forced vital capacity (INC), and FEV1/FVC. For example, in multivariable adjusted models, each IQR increase in indoor BC from the weekly integrated filter was associated with a 17.87 mL [95% confidence interval (CI): -33.76, -1.98] decrease in pre-bronchodilator FEV1. Increases in indoor PM2.5 were associated with decreases in FEV1 and FVC of smaller magnitude than those for indoor BC; however, the results were less precise. Ambient BC was not associated with pre-bronchodilator pulmonary function, ambient PM2.5 was only associated with decreases in FVC and increases in FEV1/FVC, and neither indoor nor ambient BC or PM2.5 were associated with post-bronchodilator pulmonary function.

CONCLUSIONS: Low-level exposures to indoor BC and PM2.5, but not ambient exposures, were consistently associated with decreases in pre-bronchodilator pulmonary function. There was no association between exposures and post-bronchodilator pulmonary function.