4.2 Article

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

Journal

JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
Volume 54, Issue 10, Pages 1186-1191

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/JOM.0b013e31826bb64c

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Funding

  1. NIEHS
  2. UMDNJ Center for Environmental Exposures and Disease [NIEHS P30ES005022, K08 ES013520]
  3. USEPA STAR [R832144]
  4. EPA [R832144, 909014] Funding Source: Federal RePORTER

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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 mu g/m(3) 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.

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