Exposure to Concentrated Ambient Particles Does Not Affect Vascular Function in Patients with Coronary Heart Disease

Inhalation exposure Nitrotyrosine
DOI: 10.1289/ehp.11016 Publication Date: 2008-02-22T16:30:08Z
ABSTRACT
BackgroundExposure to fine particulate air pollution is associated with increased cardiovascular morbidity and mortality. We previously demonstrated that exposure dilute diesel exhaust causes vascular dysfunction in humans.ObjectivesWe conducted a study determine whether ambient matter dysfunction.MethodsTwelve male patients stable coronary heart disease 12 age-matched volunteers were exposed concentrated ultrafine particles (CAPs) or filtered for 2 hr using randomized, double-blind cross-over design. measured peripheral vasomotor fibrinolytic function, inflammatory variables—including circulating leukocytes, serum C-reactive protein, exhaled breath 8-isoprostane nitrotyrosine—6–8 after both exposures.ResultsParticulate concentrations (mean ± SE) the chamber (190 37 μg/m3) higher than levels (31 8 (0.5 0.4 μg/m3; p < 0.001). Chemical analysis of CAPs identified low elemental carbon. Exhaled (16.9 8.5 vs. 4.9 1.2 pg/mL, 0.05), but markers systemic inflammation largely unchanged. Although there was dose-dependent increase blood flow plasma tissue plasminogen activator release (p 0.001 all), had no effect on function either group.ConclusionsDespite achieving marked increases matter, CAPs—low combustion-derived particles—did not affect middle-aged healthy disease. These findings contrast previous exposures highlight importance particle composition determining effects humans.
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