Abstract

BackgroundFor many individuals, daily commuting activities on roadways account for a substantial proportion of total exposure, as well as peak-level exposures, to traffic-related air pollutants (TRAPS) including ultrafine particles, but the health impacts of these exposures are not well-understood. We sought to determine if exposure to TRAPs particles during commuting causes acute oxidative stress in the respiratory tract or changes in heart rate variability (HRV), a measure of autonomic activity.MethodsWe conducted a randomized, cross-over trial in which twenty-one young adults took two 1.5-hr rides in a passenger vehicle in morning rush-hour traffic. The subjects wore a powered-air-purifying respirator, and were blinded to high-efficiency particulate air (HEPA) filtration during one of the rides. At time points before and after the rides, we measured HRV and markers of oxidative stress in exhaled breath condensate (EBC) including nitrite, the sum of nitrite and nitrate, malondialdehyde, and 8-isoprostane. We used mixed linear models to evaluate the effect of exposure on EBC and HRV outcomes, adjusting for pre-exposure response levels. We used linear models to examine the effects of particle concentrations on EBC outcomes at post-exposure time points.ResultsMean EBC nitrite and the sum of nitrite and nitrate were increased from baseline at immediately post-exposure comparing unfiltered to filtered rides (2.11 μM vs 1.70 μM, p = 0.02 and 19.1 μM vs 10.0 μM, p = 0.02, respectively). Mean EBC malondialdehyde (MDA) concentrations were about 10% greater following the unfiltered vs. filtered exposures, although this result was not statistically significant. We found no significant associations between exposure to traffic particles and HRV outcomes at any of the time points. At immediately post-exposure, an interquartile range increase in particle number concentration was associated with statistically significant increases in nitrite (99.4%, 95% CI 32.1% to 166.7%) and nitrite + nitrate (75.7%, 95% CI 21.5% to 130.0%).ConclusionsIncreases in markers of oxidative stress in EBC may represent early biological responses to widespread exposures to TRAPs particles that affect passengers in vehicles on heavily trafficked roadways.

Highlights

  • For many individuals, daily commuting activities on roadways account for a substantial proportion of total exposure, as well as peak-level exposures, to traffic-related air pollutants (TRAPS) including ultrafine particles, but the health impacts of these exposures are not well-understood

  • Exposure measurements With the high-efficiency particulate air (HEPA) filter in place, the mean (+/− SD) particle number concentration that subjects breathed inside the respirator hood was reduced by approximately 99.99% compared to unfiltered rides (3.5 +/− 4.1 vs. 37,999 +/− 9,545 pt/cm3) (Table 2) (Figure 1)

  • Among young adults riding as passengers for 90–110 min in heavy motor-vehicle traffic, we found increased nitrite and nitrite + nitrate in exhaled breath condensate (EBC) immediately after rides during which the subjects breathed unfiltered vehicle cabin air compared to rides during which they breathed HEPAfiltered air

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Summary

Introduction

Daily commuting activities on roadways account for a substantial proportion of total exposure, as well as peak-level exposures, to traffic-related air pollutants (TRAPS) including ultrafine particles, but the health impacts of these exposures are not well-understood. We sought to determine if exposure to TRAPs particles during commuting causes acute oxidative stress in the respiratory tract or changes in heart rate variability (HRV), a measure of autonomic activity. Exposure to traffic-related air pollutants (TRAPs) has been associated with cardiovascular and respiratory health effects [1,2,3]. Short-term exposures to TRAPs on or near roadways have been associated with increased respiratory tract inflammation, decreased lung function, and changes in heart rate variability (HRV) [13,14,15,16,17,18,19]. Oxidative stress has been implicated in inflammatory responses to diesel exhaust and diesel exhaust particles in cell systems, animal models, and the human respiratory tract [26,27]

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