Controlled exposure to diesel exhaust causes increased nitrite in exhaled breath condensate among subjects with asthma.

Abstract

To determine whether oxidative/nitrosative stress plays a role in the acute effects of diesel exhaust (DE) on subjects with asthma. In this crossover study, 16 subjects with mild to moderate asthma were exposed to clean filtered air or diluted DE (300 μg/m as PM2.5) for 1 hour with intermittent exercise. Airway hyperreactivity increased 24 hours after exposure to DE compared with clean filtered air (PC20, 14.9 mg/mL vs 19.7 mg/mL; P = 0.012). Nitrite in exhaled breath condensate was elevated immediately after diesel exposure (P = 0.052) and remained elevated 4 and 24 hours after exposure. After exposure to DE, subjects with asthma demonstrated increased airway hyperreactivity and obstruction. Increased nitrite in exhaled breath condensate, in the absence of increased exhaled nitric oxide, suggests a noninflammatory oxidative stress mechanism by which DE affects the lung.