Gong H, Shamoo D A, Anderson K R, Linn W S
Environmental Health Service, Los Amigos Research, Education Institute, Inc., Downey, California 90242, USA.
Arch Environ Health. 1997 Jan-Feb;52(1):18-25. doi: 10.1080/00039899709603795.
We tested responses to ozone (O3) under simulated "worst-case" ambient exposure conditions. Subjects included 9 men who had severe chronic obstructive pulmonary disease (COPD) with subnormal carbon monoxide diffusing capacity (i.e., an emphysemic component) and 10 age-matched healthy men. Each subject was exposed to 0.24 ppm O3 and to clean air (control) in an environmentally controlled chamber at 24 degrees C and 40% relative humidity. Exposures were randomized, they occurred 1 wk apart, and they lasted 4 h. During each half-hour interval, light exercise occurred (i.e., average ventilation 20 l/min) for 15 min. During both control and O3 exposures, group mean symptom intensity and specific airway resistance (SRaw) increased, whereas forced expiratory performance decreased. The healthy subgroup's mean arterial oxygen saturation (SaO2) rose slightly, and the COPD subgroup's mean SaO2 declined slightly, during exercise. Group mean forced expiratory volume in 1 s (FEV1.0) declined significantly in O3 exposures, compared with controls (p approximately .01). Mean excess FEV1.0 loss after 4 h in O3 (relative to control) was 8% of the preexposure value in the COPD subgroup, compared with 3% in the healthy subgroup (p > .05 [nonsignificant]). Overall FEV1.0 loss during O3 exposures, including exercise effects, averaged 19% in the COPD subgroup, compared with 2% in the healthy subgroup (p < .001). Symptoms, SRaw, and SaO2 responses, as well as healthy subjects' postexposure bronchial reactivity, differed little between O3-exposed and control subjects. We therefore concluded that in older men with or without severe COPD, O3 causes lung dysfunction under "worst-case" ambient exposure conditions, despite older subjects' comparative unresponsiveness to O3. The combined effect of O3 and exercise on lung dysfunction is markedly greater with COPD. It is still unclear whether COPD causes an increased response to O3 per se.
我们在模拟的“最坏情况”环境暴露条件下测试了对臭氧（O₃）的反应。受试者包括9名患有严重慢性阻塞性肺疾病（COPD）且一氧化碳弥散能力低于正常水平（即存在肺气肿成分）的男性和10名年龄匹配的健康男性。每位受试者在温度为24℃、相对湿度为40%的环境控制舱内暴露于0.24 ppm的O₃和清洁空气（对照）中。暴露是随机的，间隔1周进行，每次持续4小时。在每个半小时的时间段内，进行15分钟的轻度运动（即平均通气量为20升/分钟）。在对照和O₃暴露期间，组平均症状强度和比气道阻力（SRaw）增加，而用力呼气性能下降。在运动期间，健康亚组的平均动脉血氧饱和度（SaO₂）略有上升，COPD亚组的平均SaO₂略有下降。与对照相比，O₃暴露组的组平均第1秒用力呼气量（FEV₁.₀）显著下降（p约为0.01）。在O₃暴露4小时后，COPD亚组相对于暴露前值的平均FEV₁.₀额外损失为8%，而健康亚组为3%（p＞0.05[无显著性差异]）。在O₃暴露期间，包括运动影响在内，COPD亚组的总体FEV₁.₀损失平均为19%，而健康亚组为2%（p＜0.001）。O₃暴露组和对照组之间的症状、SRaw和SaO₂反应，以及健康受试者暴露后的支气管反应性差异不大。因此，我们得出结论，在有或没有严重COPD的老年男性中，尽管老年受试者对O₃的反应相对不敏感，但在“最坏情况”环境暴露条件下，O₃会导致肺功能障碍。O₃和运动对肺功能障碍的联合作用在COPD患者中明显更大。目前尚不清楚COPD本身是否会导致对O₃的反应增加。
