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

被引:38
作者
Hussain, Sabiha [1 ]
Laumbach, Robert [3 ]
Coleman, Jakemia [1 ]
Youssef, Hatim [2 ]
Kelly-McNeil, Kathie [3 ]
Ohman-Strickland, Pamela [4 ]
Zhang, Junfeng [5 ]
Kipen, Howard [3 ]
机构
[1] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pulm & Crit Care Med, New Brunswick, NJ 08901 USA
[2] Univ Med Ctr Princeton, Dept Pulm & Crit Care Med, Princeton, NJ USA
[3] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Environm & Occupat Hlth Sci Inst, Piscataway, NJ USA
[4] Univ Med & Dent New Jersey, Sch Publ Hlth, Dept Biostat, Piscataway, NJ USA
[5] Univ So Calif, Keck Sch Med, Dept Prevent Hlth, Los Angeles, CA 90033 USA
关键词
AIRWAY INFLAMMATION; ALLERGIC RESPONSES; OXIDE; HYPERRESPONSIVENESS; ENHANCEMENT; PARTICLES; POLLUTION; STRESS; TRPA1; M1;
D O I
10.1097/JOM.0b013e31826bb64c
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
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.
引用
收藏
页码:1186 / 1191
页数:6
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