Exposures to ambient
diesel exhaust particles have been associated with respiratory symptoms and
asthma exacerbations in children; however, epidemiologic evidence linking short-term exposure to ambient
diesel exhaust particles with airway
inflammation is limited. We conducted a panel study with asthmatic and nonasthmatic adolescents to characterize associations between ambient
diesel exhaust particle exposures and exhaled
biological markers of airway
inflammation and oxidative stress. Over four weeks, exhaled breath condensate was collected twice a week from 18 asthmatics and 18 nonasthmatics (ages 14-19 years) attending two New York City schools and analyzed for pH and
8-isoprostane as indicators of airway
inflammation and oxidative stress, respectively. Air concentrations of
black carbon, a
diesel exhaust particle
indicator, were measured outside schools. Air measurements of
nitrogen dioxide,
ozone, and fine
particulate matter were obtained for the closest central monitoring sites. Relationships between ambient
pollutants and exhaled
biomarkers were characterized using mixed effects models. Among all subjects, increases in 1- to 5-day averages of
black carbon were associated with decreases in exhaled breath condensate pH, indicating increased airway
inflammation, and increases in
8-isoprostane, indicating increased oxidative stress. Increases in 1- to 5-day averages of
nitrogen dioxide were associated with increases in
8-isoprostane.
Ozone and fine
particulate matter were inconsistently associated with exhaled
biomarkers. Associations did not differ between asthmatics and nonasthmatics. The findings indicate that short-term exposure to traffic-related
air pollutants may increase airway
inflammation and/or oxidative stress in urban youth and provide mechanistic support for associations documented between traffic-related
pollutant exposures and respiratory morbidity.