Horstman D H, Ball B A, Brown J, Gerrity T, Folinsbee L J
U.S. Environmental Protection Agency, National Health and Environmental Effects Research Laboratory, Research Triangle Park, NC 27711, USA.
Toxicol Ind Health. 1995 Jul-Aug;11(4):369-85. doi: 10.1177/074823379501100401.
To determine if asthmatic subjects (ASTH, n = 17) experience greater O3-induced pulmonary decrements than nonasthmatic subjects (NONA, n = 13), both groups were exposed for 7.6 h to both clean air and 0.16 ppm O3. Exposures consisted of seven 50-min periods of light exercise (VE = 14.2 and 15.3 l/min/m2 for ASTH and NONA, respectively), each followed by 10 min rest. A 35-min lunch period followed the third exercise. Following O3 exposure, decrements in forced expiratory volume in one second (FEV1) and FEV1 divided by forced vital capacity (FVC), corrected for air exposure, for ASTH (-19.4 +/- 3.1% and -6.2 +/- 2%, respectively) were significantly greater (p = 0.04 and 0.02) than for NONA (-9.8 +/- 1.9% and -1 +/- 1%, respectively). There was no difference (p = 0.33) for decrements in FVC between ASTH (-11.8 +/- 1.9%) and NONA (-8.8 +/- 2.1%). Nine of 17 ASTH experienced wheezing with O3, while only one experienced wheezing with air (p = 0.004); no NONA experienced wheezing. Six of 17 ASTH requested inhaled beta-agonist bronchodilator prior to and/or during O3 exposure and experienced some temporary alleviation of decrements. At end exposure, however, ASTH who were medicated had greater O3-induced decrements than those who were not medicated. ASTH who had the larger O3-induced decrements had lower baseline FEV1/FVC and lower baseline %predicted FEV1. These data indicate that in ASTH, unlike NONA, some portion of O3-induced pulmonary decrements experienced was related to bronchoconstriction, and that O3-responsiveness for ASTH depended upon baseline airway status.
为了确定哮喘患者(ASTH,n = 17)与非哮喘患者(NONA,n = 13)相比,是否经历更大的臭氧(O3)诱导的肺功能下降,两组均暴露于清洁空气和0.16 ppm O3中7.6小时。暴露包括七个50分钟的轻度运动时段(ASTH和NONA的每分钟每平方米分钟通气量[VE]分别为14.2和15.3升),每个时段后休息10分钟。第三次运动后有35分钟的午餐时间。O3暴露后,校正空气暴露后,哮喘患者一秒用力呼气量(FEV1)和FEV1除以用力肺活量(FVC)的下降幅度(分别为-19.4 +/- 3.1%和-6.2 +/- 2%)显著大于(p = 0.04和0.02)非哮喘患者(分别为-9.8 +/- 1.9%和-1 +/- 1%)。哮喘患者(-11.8 +/- 1.9%)和非哮喘患者(-8.8 +/- 2.1%)的FVC下降幅度无差异(p = 0.33)。17名哮喘患者中有9名在接触O3时出现喘息,而只有1名在接触空气时出现喘息(p = 0.004);非哮喘患者均未出现喘息。17名哮喘患者中有6名在O3暴露之前和/或期间要求吸入β-激动剂支气管扩张剂,并经历了下降幅度的一些暂时缓解。然而,在暴露结束时,使用药物治疗的哮喘患者比未使用药物治疗的患者有更大的O3诱导的下降幅度。O3诱导下降幅度较大的哮喘患者基线FEV1/FVC较低,基线预测FEV1百分比也较低。这些数据表明,与非哮喘患者不同,哮喘患者中经历的O3诱导的肺功能下降的一部分与支气管收缩有关,并且哮喘患者的O3反应性取决于基线气道状态。