Controlled Exposure to Diesel Exhaust Causes Increased Nitrite in Exhaled Breath Condensate Among Subjects With Asthma

This is the authors' abstract. We don't add key points for this paper.

OBJECTIVE: To determine whether oxidative/nitrosative stress plays a role in the acute effects of diesel exhaust (DE) on subjects with asthma. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.