Foster W M, Brown R H, Macri K, Mitchell C S
Department of Environmental Health Sciences, Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland 21205, USA.
J Appl Physiol (1985). 2000 Nov;89(5):1804-10. doi: 10.1152/jappl.2000.89.5.1804.
Exposure of humans to ambient levels of ozone (O(3)) causes inflammatory changes within lung tissues. These changes have been reported for the "initial" (1- to 3-h) and "late" (18- to 20-h) postexposure periods. We hypothesized that at the late period, when protein and cellular markers of inflammation at the airway surface remain abnormal and the integrity of the epithelial barrier is compromised, bronchial reactivity would be increased. To test this, we measured airway responsiveness to cumulative doses of methacholine (MCh) aerosol in healthy subjects 19+/-1 h after a single exposure to O(3) (130 min at ambient levels between 120 and 240 parts/billion and alternate periods of rest and moderate exercise) or filtered air. Exposures were conducted at two temperatures: mild (22 degrees C) and moderate (30 degrees C). At the late period, bronchial reactivity to MCh increased, i.e., interpolated dose of MCh leading to a 50% fall in specific airway conductance (PC(50)) was less after O(3) than after filtered air. PC(50) for O(3) at 22 degrees C was 27 mg/ml (20% less than the PC(50) after filtered air), and for O(3) at 30 degrees C it was 19 mg/ml (70% less than the PC(50) after filtered air). The forced expiratory volume in 1 s (FEV(1)) at the late time point after O(3) was slightly but significantly reduced (2.3%) from the preexposure level. There was no relationship found between the functional changes observed early after exposure to O(3) and subsequent changes in bronchial reactivity or FEV(1) at the late time point. These results suggest that bronchial reactivity is significantly altered approximately 1 day after O(3); this injury may contribute to the respiratory morbidity that is observed 1-2 days after an episode of ambient air pollution.
人类暴露于环境水平的臭氧（O₃）会导致肺组织内发生炎症变化。这些变化在暴露后的“初始”（1至3小时）和“晚期”（18至20小时）阶段均有报道。我们推测，在晚期，当气道表面炎症的蛋白质和细胞标志物仍异常且上皮屏障完整性受损时，支气管反应性会增加。为了验证这一点，我们在健康受试者单次暴露于O₃（在120至240 ppb的环境水平下暴露130分钟，并交替进行休息和适度运动）或过滤空气后19±1小时，测量了气道对累积剂量的乙酰甲胆碱（MCh）气雾剂的反应性。暴露在两个温度下进行：温和（22℃）和中等（30℃）。在晚期，支气管对MCh的反应性增加，即导致特定气道传导率下降50%（PC₅₀）的MCh内插剂量在O₃暴露后比过滤空气暴露后更低。22℃下O₃的PC₅₀为27 mg/ml（比过滤空气后的PC₅₀低20%），30℃下O₃的PC₅₀为19 mg/ml（比过滤空气后的PC₅₀低70%）。O₃暴露后晚期的第1秒用力呼气量（FEV₁）比暴露前水平略有但显著降低（2.3%）。在暴露于O₃后早期观察到的功能变化与晚期支气管反应性或FEV₁的后续变化之间未发现相关性。这些结果表明，O₃暴露约1天后支气管反应性会发生显著改变；这种损伤可能导致在一次环境空气污染事件后1至2天观察到的呼吸道发病率增加。
