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

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.

Introduction

Asthma prevalence and morbidity are higher in New York City communities such as Harlem and South Bronx compared with other neighborhoods and surrounding suburbs (Garg et al., 2003, New York State Department of Health, 2007). These New York City communities also contain numerous diesel emissions sources including major trucking routes, bus depots, and waste transfer stations; and higher levels of diesel exhaust particles have been measured in New York City communities with higher traffic volumes (Maciejczyk et al., 2004, Patel et al., 2009).

Several epidemiologic studies have demonstrated associations between short-term increases in ambient concentrations of elemental or black carbon, widely-used indicators of diesel exhaust particles, and increases in respiratory hospital admissions or symptoms (Bell et al., 2009, Gent et al., 2009, Patel et al., 2010, Spira-Cohen et al., 2011). Specifically, daily black carbon concentrations have been associated with daily respiratory symptoms among New York City children and adolescents, including those residing in Harlem and South Bronx (Patel et al., 2010, Spira-Cohen et al., 2011). Mechanistic support has been provided by controlled human exposure studies that found diesel exhaust particle exposures to induce transient increases in inflammatory cell counts and/or cytokine concentrations in airways (Behndig et al., 2006, Kongerud et al., 2006). Epidemiologic studies increasingly are finding that short-term increases in ambient pollutants such as fine particulate matter (PM_2.5) and nitrogen dioxide (NO₂) are associated with increases in airway inflammation in children and adults (Adamkiewicz et al., 2004, Barraza-Villarreal et al., 2008, Delfino et al., 2006, Delfino et al., 2010, Koenig et al., 2003, Liu et al., 2009, McCreanor et al., 2007, Romieu et al., 2008, Zhang et al., 2009). Investigation of associations between diesel exhaust particle exposures and airway inflammation in children (Delfino et al., 2006), particularly healthy children, is limited, and investigation in adults has focused largely on road-side exposures (McCreanor et al., 2007, Zhang et al., 2009). Hence, the changes in airway inflammation associated with short-term exposure to ambient diesel particles and the potential effects in healthy individuals have not been well characterized.

Several indicators of airway inflammation and oxidative stress, including pH, 8-isoprostane, and cytokines have been measured in exhaled breath condensate. These indicators differ between asthmatics and nonasthmatics and change acutely upon asthma exacerbation or treatment with asthma medication (Antus et al., 2010, Baraldi et al., 2003, Hunt et al., 2000, Montuschi et al., 2006). As biological markers of lung responses, analysis of these biomarkers may provide insight into diesel exhaust particle mechanisms of action and serve to link findings between experimental and epidemiologic studies.

To improve understanding of the association between short-term exposure to ambient diesel exhaust particles and respiratory morbidity, we conducted a panel study involving continuous monitoring of black carbon outside two New York City high schools and measurement of pH and 8-isoprostane in exhaled breath condensate collected twice a week from students with and without asthma. Observations that ambient black carbon concentrations are associated with diesel exhaust particle concentrations and volume of diesel traffic but not car traffic support the measurement of black carbon as an indicator of diesel exhaust particles (Patel et al., 2009, Wu et al., 2007). We hypothesized that short-term increases in ambient black carbon would be associated with decreases in exhaled breath condensate pH, reflecting increases in airway inflammation, and with increases in 8-isoprostane, reflecting increases in airway oxidative stress. Further, we hypothesized that the associations between black carbon and exhaled biomarkers would differ between asthmatic and nonasthmatic adolescents.