Vagaggini B, Carnevali S, Macchioni P, Taccola M, Fornai E, Bacci E, Bartoli M L, Cianchetti S, Dente F L, Di Franco A, Giannini D, Paggiaro P L
Cardio-Thoracic Dept, Respiratory Pathophysiology, University of Pisa, Italy.
Eur Respir J. 1999 Feb;13(2):274-80. doi: 10.1034/j.1399-3003.1999.13b09.x.
The aim of this study was to evaluate whether ozone exposure induces a similar airway inflammatory response in subjects with different degrees of asthma severity. Two groups of asthmatic subjects were studied: seven with intermittent mild asthma not requiring regular treatment (group A); and seven with persistent mild asthma requiring regular treatment with inhaled corticosteroids and long-acting beta2-agonists (group B). All subjects were exposed, in a randomized cross-over design, to air or O3 (0.26 parts per million (ppm) for 2 h with intermittent exercise); subjects in group B withdrew from regular treatment 72 h before each exposure. Before the exposure, and 1 and 2 h after the beginning of the exposure they performed a pulmonary function test, and a questionnaire was completed to obtain a total symptom score (TSS). Six hours after the end of the exposure, hypertonic saline (HS) sputum induction was conducted. Sputum cell percentages, eosinophil cationic protein (ECP) and interleukin (IL)-8 concentrations in the sputum supernatant were measured. TSS significantly increased and forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) significantly decreased after O3 exposure in comparison with air exposure in group A, whereas no changes were observed in group B except for a significant decrement of FEV1 2 h after the beginning of O3 exposure. Sputum neutrophil percentage was significantly higher after O3 exposure than after air exposure in both groups (Group A: 70.2% (28-87) versus 26.6% (8.6-73.2); Group B: 62.1% (25-82.4) versus 27.9% (14.4-54)). IL-8 was higher in sputum supernatant collected 6 h after O3 exposure than after air, only in group A. No change due to O3 has been found in sputum eosinophil percentage and ECP concentration in both groups. In conclusion, the degree of airway response to a short-term exposure to ozone is different in subjects with asthma of different severity. The available data do not allow elucidation of whether this difference depends on the severity of the disease or on the regular anti-inflammatory treatment.
本研究的目的是评估臭氧暴露是否会在不同哮喘严重程度的受试者中引发类似的气道炎症反应。对两组哮喘受试者进行了研究:七名患有间歇性轻度哮喘且无需常规治疗的受试者(A组);以及七名患有持续性轻度哮喘且需要吸入糖皮质激素和长效β2受体激动剂进行常规治疗的受试者(B组)。所有受试者均采用随机交叉设计,暴露于空气或臭氧(百万分之0.26(ppm),间歇运动2小时);B组受试者在每次暴露前72小时停止常规治疗。在暴露前、暴露开始后1小时和2小时,他们进行了肺功能测试,并完成了一份问卷以获得总症状评分(TSS)。暴露结束后6小时,进行高渗盐水(HS)痰液诱导。测量痰液细胞百分比、痰液上清液中的嗜酸性粒细胞阳离子蛋白(ECP)和白细胞介素(IL)-8浓度。与空气暴露相比,A组臭氧暴露后TSS显著增加,用力肺活量(FVC)和一秒用力呼气量(FEV1)显著降低,而B组除臭氧暴露开始后2小时FEV1显著下降外,未观察到变化。两组臭氧暴露后痰液中性粒细胞百分比均显著高于空气暴露后(A组:70.2%(28 - 87)对26.6%(8.6 - 73.2);B组:62.1%(25 - 82.4)对27.9%(14.4 - 54))。仅在A组中,臭氧暴露后6小时收集的痰液上清液中的IL-8高于空气暴露后。两组痰液嗜酸性粒细胞百分比和ECP浓度均未发现因臭氧而发生变化。总之,不同严重程度哮喘受试者对短期臭氧暴露的气道反应程度不同。现有数据无法阐明这种差异是取决于疾病的严重程度还是取决于常规抗炎治疗。