Sunday, December 2, 2012

Traffic-related air pollutants and exhaled markers of airway inflammation and oxidative stress in New York City adolescents

Traffic-related air pollutants and exhaled markers of airway inflammation and oxidative stress in New York City adolescents
http://www.sciencedirect.com/science/article/pii/S001393511200312X

Patel, M. et. al. 
Available online 23 November 2012.  In Press.

Abstract

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.

Highlights
► We measured airway inflammation in urban youth with and without asthma for 4 weeks. ► We measured daily ambient air black carbon as an indicator of diesel air pollution. ► Black carbon was associated with airway inflammation and oxidative stress over time. ► Ambient air nitrogen dioxide was associated with airway oxidative stress over time. ► Traffic emissions may increase airway inflammation in youth with and without asthma.

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