Molfino N A, Wright S C, Katz I, Tarlo S, Silverman F, McClean P A, Szalai J P, Raizenne M, Slutsky A S, Zamel N
Department of Medicine, University of Toronto, Ontario, Canada.
Lancet. 1991 Jul 27;338(8761):199-203. doi: 10.1016/0140-6736(91)90346-q.
The relation between inhalation of ambient concentrations of ozone and airway reactivity to inhaled allergens may be important in asthma, since both agents can produce inflammatory changes in the airways. Seven asthmatic patients (mean age 40 [SD 13] years), with seasonal symptoms of asthma and positive skin tests for ragweed or grass, took part in a study to investigate whether exposure to low concentrations of ozone potentiates the airway allergic response. The patients were studied during 4 separate weeks in the winter. In each week there were 3 study days: on days 1 and 3 methacholine challenges were carried out; and on day 2 the subject received one of four combined challenges in a single-blind design--air breathing followed by inhalation of allergen diluent (placebo); ozone followed by inhalation of allergen diluent; air followed by allergen; or ozone followed by allergen. The ozone concentration was 0.12 ppm during 1 h of tidal breathing at rest, and allergens were inhaled until the forced expiratory volume in 1 s (FEV1) had fallen by 15% (PC15). There were no significant differences in baseline FEV1 after exposure to ozone but PC15 was significantly reduced when allergen was preceded by ozone inhalation: the mean PC15 after air was 0.013 (SD 0.017) mg/ml compared with 0.0056 (0.0062) mg/ml after ozone (p = 0.042). Thus, low ozone concentrations, similar to those commonly occurring in urban areas, can increase the bronchial responsiveness to allergen in atopic asthmatic subjects. This effect does not seem to be the result of changes in baseline airway function.
在哮喘中,吸入环境浓度的臭氧与气道对吸入变应原的反应性之间的关系可能很重要,因为这两种因素均可在气道中产生炎症变化。七名患有季节性哮喘症状且对豚草或草的皮肤试验呈阳性的哮喘患者(平均年龄40 [标准差13]岁)参与了一项研究,以调查暴露于低浓度臭氧是否会增强气道过敏反应。这些患者在冬季的4个不同周内接受研究。每周有3个研究日:在第1天和第3天进行乙酰甲胆碱激发试验;在第2天,受试者采用单盲设计接受四种联合激发试验之一——先呼吸空气,然后吸入变应原稀释剂(安慰剂);先吸入臭氧,然后吸入变应原稀释剂;先呼吸空气,然后吸入变应原;或先吸入臭氧,然后吸入变应原。在静息潮式呼吸1小时期间,臭氧浓度为0.12 ppm,吸入变应原直至第1秒用力呼气量(FEV1)下降15%(PC15)。暴露于臭氧后,基线FEV1无显著差异,但在吸入变应原之前先吸入臭氧时,PC15显著降低:空气激发后的平均PC15为0.013(标准差0.017)mg/ml,而臭氧激发后为0.0056(0.0062)mg/ml(p = 0.042)。因此,与城市地区常见的低臭氧浓度相似,可增加特应性哮喘患者气道对变应原的反应性。这种效应似乎不是基线气道功能变化的结果。