Threshold concentration of ozone causing an increase in bronchial reactivity in humans and adaptation with repeated exposures.
Threshold concentration of ozone causing an increase in bronchial reactivity in humans and adaptation with repeated exposures.
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臭氧的阈值浓度会导致人类支气管反应性增加并适应反复接触。
DOI：
10.1164/arrd.1981.124.3.245
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Boushey,HA
中科院分区：
文献类型：
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作者：
Dimeo,MJ;Glenn,MG;Holtzman,MJ;Sheller,JR;Nadel,JA;Boushey,HA
为了确定最低浓度的臭氧，导致支气管组胺反应性的增加，并确定是否适应这种影响的臭氧开发与重复曝光，我们研究了19名健康的成年人。通过测量吸入10次组胺气雾剂（1.6%溶液）产生的比气道阻力（ΔSRaw）的升高来评估支气管反应性。在5名受试者中，连续4天在上午9：00和11：30测定不暴露于臭氧的支气管反应性（组I）。在其他7名受试者（第II组）中，连续3天在上午9：00和11：30评估支气管反应性，并在第三天上午9：30至11：30将受试者暴露于0.2 ppm臭氧。另外7名受试者（第III组）的支气管反应性以类似的方式评估2天，然后再次在连续3天的2小时暴露于0.4 ppm的臭氧。各组暴露前支气管反应性相同，重复测试但未暴露于臭氧的组支气管反应性无变化。首次暴露于0.4 ppm臭氧后，观察到组胺引起的ΔSRaw增加，但首次暴露于0.2 ppm臭氧后未观察到（p Δ 0.025）。然而，在连续3天重复暴露于0.4 ppm的2小时后，组胺产生的ΔSRaw逐渐降低，在第三次暴露后恢复到暴露前的值。我们的研究结果表明，臭氧的阈值浓度导致健康人受试者的支气管反应性增加是0.2和0.4 ppm之间，并适应这种影响的臭氧开发与反复曝光。在其他研究中确定的引起症状、肺容量或气道阻力变化的臭氧阈值浓度也在0.2和0.4 ppm之间，这些其他研究中对臭氧耐受性发展的时间过程与我们研究中观察到的相似。我们认为，症状的出现，肺功能的变化，支气管反应性的增加可能是由气道上皮传入神经末梢的活性变化引起的。
To determine the lowest concentration of ozone that causes an increase in bronchial reactivity to histamine and to determine whether adaptation to this effect of ozone develops with repeated exposures, we studied 19 healthy adult subjects. Bronchial reactivity was assessed by measuring the rise in specific airway resistance (ΔSRaw) produced by inhalation of 10 breaths of histamine aerosol (1.6% solution). In 5 subjects, bronchial reactivity was determined at 9:00 and 11:30 A.M. on 4 consecutive days without exposure to ozone (Group I). In 7 other subjects (Group II), bronchial reactivity was assessed at 9:00 and 11:30 A.M. on 3 consecutive days, and subjects were exposed to 0.2 ppm of ozone from 9:30 to 11:30 A.M. on the third day. Seven additional subjects (Group III) had bronchial reactivity assessed in a similar fashion for 2 days and then again on 3 consecutive days of 2-h exposures to 0.4 ppm of ozone. Preexposure bronchial reactivity of the groups was the same, and no change in bronchial reactivity occurred in the group tested repeatedly but not exposed to ozone. An increase in ΔSRaw provoked by histamine was noted after the first exposure to 0.4 ppm but not to 0.2 ppm of ozone (p Δ 0.025). With 3 repeated 2-h exposures to 0.4 ppm on consecutive days, however, the ΔSRaw produced by histamine progressively decreased, returning to pre-exposure values after the third exposure. Our results indicate that the threshold concentration of ozone causing an increase in bronchial reactivity in healthy human subjects is between 0.2 and 0.4 ppm, and that adaptation to this effect of ozone develops with repeated exposures. The threshold concentration of ozone identified in other studies as causing changes in symptoms, lung volumes, or airway resistance was also between 0.2 and 0.4 ppm, and the time course of the development of tolerance to ozone in these other studies was similar to that observed in our study. We propose that the appearance of symptoms, changes in pulmonary function, and the increase in bronchial reactivity may be caused by a change in the activity of afferent nerve endings in the airway epithelium.