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Inhalation Toxicology
International Forum for Respiratory Research
Volume 20, 2008 - Issue 4
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Research Article

Changes in Lung Function and Airway Inflammation Among Asthmatic Children Residing in a Woodsmoke-Impacted Urban Area

, , , , , & show all
Pages 423-433 | Received 16 Jul 2007, Accepted 17 Dec 2007, Published online: 06 Oct 2008
 

Abstract

Fine particulate matter (PM2.5) is associated with respiratory effects, and asthmatic children are especially sensitive. Preliminary evidence suggests that combustion-derived particles play an important role. Our objective was to evaluate effect estimates from different PM2.5 exposure metrics in relation to airway inflammation and lung function among children residing in woodsmoke-impacted areas of Seattle. Nineteen children (ages 6–13 yr) with asthma were monitored during the heating season. We measured 24-h outdoor and personal concentrations of PM2.5 and light-absorbing carbon (LAC). Levoglucosan (LG), a marker of woodsmoke, was also measured outdoors. We partitioned PM2.5 exposure into its ambient-generated (Eag) and nonambient (Ena) components. These exposure metrics were evaluated in relation to daily changes in exhaled nitric oxide (FENO), a marker of airway inflammation, and four lung function measures: midexpiratory flow (MEF), peak expiratory flow (PEF), forced expiratory volume in the first second (FEV1), and forced vital capacity (FVC). Eag, but not Ena, was correlated with combustion markers. Significant associations with respiratory health were seen only among participants not using inhaled corticosteroids. Increases in FENO were associated with personal PM2.5, personal LAC, and Eag but not with ambient PM2.5 or its combustion markers. In contrast, MEF and PEF decrements were associated with ambient PM2.5, its combustion markers, and Eag, but not with personal PM2.5 or personal LAC. FEV1 was associated only with ambient LG. Our results suggest that lung function may be especially sensitive to the combustion-generated component of ambient PM2.5, whereas airway inflammation may be more closely related to some other constituent of the ambient PM2.5 mixture.

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