Hanania N A, Tarlo S M, Silverman F, Urch B, Senathirajah N, Zamel N, Corey P
Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
Chest. 1998 Sep;114(3):752-6. doi: 10.1378/chest.114.3.752.
In a previous study published by our group, six out of nine subjects with mild allergic asthma were shown to have an enhanced response to allergen challenge following a 1-h exposure in an 0.8-m3 exposure chamber (modified from a body plethysmograph) to an average of 120 parts per billion (ppb) ozone at rest. Other studies failed to confirm this effect. In the present study, using a similar design, we reexamined this effect using a larger group of asthmatics and a larger chamber allowing minimal fluctuations in ozone levels during exposures.
Prospective, randomized single-blinded crossover study.
Pulmonary function laboratory equipped with an exposure chamber.
Fifteen subjects had mild allergic asthma; 9 men and 6 women; the mean (SD) age was 32.5 (10) years; FEV1 was 3.4 (0.8) L; baseline methacholine provocation concentration causing a 20% fall in FEV1 was (PC20) 3.28 (4.1) mg/mL.
Each participant was exposed, at rest, on 1 day to filtered air and on another day to ozone (mean level=120 ppb) in a larger exposure chamber than the one used in our first study with less variability in ozone level (110 to 130 vs 85 to 175 ppb) using a random, single-blinded design. After each exposure, the subject was challenged with allergen (nine with grass pollen extract and six with ragweed extract) and allergen PC15 was measured.
Ozone preexposure did not affect allergen PC15 when compared with clean air preexposure (allergen PC15 dilution 1/114 vs 1/119, respectively). Ozone vs air preexposure resulted in an allergen PC15 that was lower in five subjects, higher in six, and unchanged (within one doubling dose) in four.
At this low level with less variability and lower peaks than our previous study, ozone had no significant effect on airway allergen responsiveness.
在我们小组之前发表的一项研究中,9名轻度过敏性哮喘患者中有6名在0.8立方米的暴露舱(由人体体积描记器改装)中静息暴露于平均浓度为十亿分之120(ppb)的臭氧1小时后,对过敏原激发的反应增强。其他研究未能证实这一效应。在本研究中,我们采用类似的设计,使用更大规模的哮喘患者群体和更大的暴露舱,使暴露期间臭氧水平的波动最小,重新检验了这一效应。
前瞻性、随机单盲交叉研究。
配备暴露舱的肺功能实验室。
15名轻度过敏性哮喘患者,9名男性和6名女性,平均(标准差)年龄为32.5(10)岁,第一秒用力呼气容积(FEV1)为3.4(0.8)升,使FEV1下降20%的乙酰甲胆碱激发浓度(PC20)为3.28(4.1)毫克/毫升。
采用随机、单盲设计,让每位参与者在一个比我们第一项研究中使用的更大的暴露舱中静息暴露,一天暴露于过滤空气中,另一天暴露于臭氧中(平均水平 = 120 ppb),该暴露舱中臭氧水平的变异性较小(110至130 ppb,而之前为85至175 ppb)。每次暴露后,用过敏原(9人用草花粉提取物,6人用豚草提取物)对受试者进行激发,并测量过敏原PC15。
与清洁空气预暴露相比,臭氧预暴露对过敏原PC15没有影响(过敏原PC15稀释倍数分别为1/114和1/119)。臭氧预暴露与空气预暴露相比,5名受试者的过敏原PC15降低,6名受试者升高,4名受试者不变(在一个加倍剂量范围内)。
与我们之前的研究相比,在这种低水平、变异性较小且峰值较低的情况下,臭氧对气道过敏原反应性没有显著影响。