Abstract

PP-30-049 Background/Aims: Traffic-related air pollution has been associated with increased pulmonary and cardiovascular morbidity and mortality. Evidence from human, animal, and in vitro studies suggests that oxidative stress may mediate the adverse effects of traffic-related air pollutants. We hypothesized that exposure during passenger vehicle rides simulating a rush-hour commute on a highway would cause measurable acute changes in biomarkers of airway oxidative stress among healthy human volunteers. Methods: Twenty nonsmoking subjects aged 18–45 years will be passengers in a Ford Taurus sedan for two 2-hour car rides at least 1 week apart. To date, 4 subjects have each completed 1 ride with the air intake vent open and 1 ride with the vent closed (recirculation mode) in random order. The route was primarily on the New Jersey Turnpike, a major highway with heavy duty diesel truck traffic. In-vehicle exposure measurements included total particle count, particulate matter less than 2.5 microns (PM2.5), nitrogen dioxide and carbon monoxide, temperature, and humidity. We collected exhaled breath condensate (EBC) using an Ecoscreen device before and 0, 6, and 24 hours after the car rides. We measured the concentration of EBC nitrite, a marker of nitrosative stress, using chemiluminescence detection, and EBC malondialdehyde, a marker oxidative stress, with HPLC with fluorescence detection. Results: Mean particle counts were significantly higher during the vent open rides compared to recirculation mode rides (43,653 vs. 26,362 p/cc, P = 0.03). Among these 4 subjects over 8 car rides, we have observed a 22% increase in EBC MDA from pre- to 0 hour post-ride (95% CI: −24%, 68%), which did not persist at 6-hour post-ride. Conclusion: Having the vent closed substantially reduced total particle counts in the vehicle. To date, these short-term, on-road exposures in traffic were associated with increased oxidative stress in the respiratory tract of healthy humans.

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