Chen Lisa L, Tager Ira B, Peden David B, Christian Dorothy L, Ferrando Ronald E, Welch Barbara S, Balmes John R
Lung Biology Center, Center for Occupational and Environmental Health, Cardiovascular Research Institute, and Medical Service, San Francisco General Hospital, University of California, San Francisco, CA, USA.
Chest. 2004 Jun;125(6):2328-35. doi: 10.1378/chest.125.6.2328.
Controlled human exposure studies have produced conflicting results regarding the effect of ozone on the early bronchoconstrictor response to inhaled allergen in specifically sensitized asthmatic subjects. Spirometric parameters do not necessarily reflect the airway inflammatory effects of inhaled ozone or allergen.
This study was designed to investigate whether exposure to ozone enhances the late airway inflammatory response, as well as the early bronchoconstrictor response, to inhaled house dust mite allergen in sensitized asthmatic subjects.
Randomized, counter-balanced, cross-over study.
Human exposure laboratory.
Fourteen subjects were exposed to 0.2 ppm O(3) or filtered air, on separate days, for 1 h during exercise. After each exposure, the subjects were challenged with doubling doses of Dermatophagoides farinae (DF) allergen (provocative concentration of DF causing a 15% decrease in FEV(1) [PC(15)]). At 6 h after allergen challenge, bronchoscopy with BAL, proximal airway lavage (PAL), and endobronchial biopsy were performed. The second exposure/allergen challenge/bronchoscopy sequence was performed at least 4 weeks after the first sequence.
No significant difference in cellular or biochemical markers of the late inflammatory response after allergen was found between the ozone and air exposures (although a trend toward increased neutrophils was noted after ozone exposure in the PAL fluid, p = 0.06). For the group as a whole, no significant difference in PC(15) was demonstrated after ozone exposure compared to air exposure. However, subjects with the greatest ozone-induced decrements in FEV(1) tended to have lower PC(15) values after ozone exposure.
Exposure to a relatively low-level concentration of ozone does not enhance the late inflammatory or early bronchoconstrictor response to inhaled antigen in most allergic asthmatic subjects. Our results do suggest, however, that a subgroup of asthmatics may acquire increased sensitivity to aeroallergens after exposure to ozone.
关于臭氧对特异性致敏哮喘患者吸入变应原后早期支气管收缩反应的影响，人体对照暴露研究得出了相互矛盾的结果。肺量计参数不一定能反映吸入臭氧或变应原对气道的炎症作用。
本研究旨在调查臭氧暴露是否会增强致敏哮喘患者对吸入屋尘螨变应原的晚期气道炎症反应以及早期支气管收缩反应。
随机、平衡、交叉研究。
人体暴露实验室。
14名受试者在不同日期分别于运动期间暴露于0.2 ppm的臭氧或过滤空气中1小时。每次暴露后，受试者接受双倍剂量的粉尘螨变应原激发（使第1秒用力呼气量[FEV₁]降低15%的粉尘螨变应原激发浓度[PC₁₅]）。在变应原激发后6小时，进行支气管镜检查及支气管肺泡灌洗（BAL）、近端气道灌洗（PAL）和支气管内活检。第二次暴露/变应原激发/支气管镜检查序列在第一次序列至少4周后进行。
臭氧暴露组和空气暴露组在变应原激发后晚期炎症反应的细胞或生化标志物方面无显著差异（尽管在PAL液中臭氧暴露后中性粒细胞有增加趋势，p = 0.06）。对于整个组而言，与空气暴露相比，臭氧暴露后PC₁₅无显著差异。然而，臭氧诱导FEV₁下降幅度最大的受试者在臭氧暴露后PC₁₅值往往较低。
在大多数过敏性哮喘患者中，暴露于相对低浓度的臭氧不会增强对吸入抗原的晚期炎症反应或早期支气管收缩反应。然而，我们的结果确实表明，一部分哮喘患者在暴露于臭氧后可能会对气传变应原的敏感性增加。
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