TY - JOUR
T1 - Controlled exposure to diesel exhaust causes increased nitrite in exhaled breath condensate among subjects with asthma
AU - Hussain, Sabiha
AU - Laumbach, Robert
AU - Coleman, Jakemia
AU - Youssef, Hatim
AU - Kelly-Mcneil, Kathie
AU - Ohman-Strickland, Pamela
AU - Zhang, Junfeng
AU - Kipen, Howard
PY - 2012/10
Y1 - 2012/10
N2 - 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.
AB - 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.
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U2 - 10.1097/JOM.0b013e31826bb64c
DO - 10.1097/JOM.0b013e31826bb64c
M3 - Article
C2 - 23001278
AN - SCOPUS:84867580697
SN - 1076-2752
VL - 54
SP - 1186
EP - 1191
JO - Journal of occupational and environmental medicine
JF - Journal of occupational and environmental medicine
IS - 10
ER -