Comparison of chamber 6.6-h exposures to 0.04-0.08 PPM ozone via square-wave and triangular profiles on pulmonary responses
Comparison of chamber 6.6-h exposures to 0.04-0.08 PPM ozone via square-wave and triangular profiles on pulmonary responses
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DOI：
10.1080/08958370500306107
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发表时间：
2006-02-01
影响因子：
2.1
通讯作者：
Adams, WC
中科院分区：
文献类型：
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作者：
Adams, WC
人们越来越清楚地认识到，空气污染风险评估的实验室模拟需要采用O-3浓度分布，更准确地模拟夏季白天环境空气污染事件中遇到的情况。本研究旨在比较6.6小时方波0.08 ppm O-3室暴露与三角形O-3暴露曲线中观察到的肺功能和呼吸不适反应症状（平均值为0.08 ppm），以及0.06 ppm方波和三角波平均值0.06 ppm暴露，以及在三角平均值0.04 ppm暴露和过滤空气（FA）方波暴露期间观察到的那些。30名年轻人（男女各15名）作为受试者，每人完成所有暴露。虽然急性三角形暴露于平均O-3浓度为0.08 ppm的暴露后6.6小时的反应与方波暴露中观察到的反应没有显著差异，但1秒用力呼气量（FEV）与暴露前相比，暴露后4.6 h的总症状严重度（TSS）和总症状严重度（1.0）有显著差异（当O-3浓度为0.15ppm时），在三角波照射下，细胞死亡率最高，而在方波照射下，细胞死亡率最高，为6.6h。因此，在平均O-3浓度为0.08 ppm的三角形暴露方案中，在较长时间内观察到显著的肺功能和症状反应。这些结果支持以前的证据，O-3浓度有一个更大的单一的影响，在总吸入O-3剂量比V-E和曝光时间。减去暴露于O-3后的肺功能影响到现有的8小时平均背景水平（例如，类似于0.04 ppm，而不是在FA暴露中观察到的那些）与在较高浓度下观察到的那些（例如，类似于0.08 ppm）代表了将监管工作集中在可以控制的影响上的一种手段。0.04 ppm三角波暴露观察到的最大肺功能和症状反应与FA方波暴露几乎相同。因此，本研究的结果表明，计算暴露于0.08 ppm的净肺功能效应，并对FA反应进行“校正”，或对0.04 ppm O-3的净肺功能效应进行校正，不会导致任何统计学显著差异。
It has become increasingly well realized that laboratory simulations of air pollution risk assessment need to employ O-3 concentration profiles that more accurately mimic those encountered during summer daylight ambient air pollution episodes. The present study was designed to compare the pulmonary function and symptoms of breathing discomfort responses to a 6.6-h square-wave 0.08-ppm O-3 chamber exposure to those observed in a triangular O-3 exposure profile (mean of 0.08 ppm), as well as to both a 0.06-ppm square-wave and triangular mean 0.06-ppm exposure, and to those observed during a triangular mean 0.04-ppm exposure and to a filtered air (FA) square-wave exposure. Thirty young adults (15 of each gender) served as subjects, each completing all exposures. While the 6.6-h postexposure responses to the acute triangular exposure to a mean O-3 concentration of 0.08 ppm did not differ significantly from those observed in the square-wave exposure, forced expiratory volume in 1 s (FEV)(1.0) and total symptoms severity (TSS) were significantly different from preexposure at 4.6 h (when O-3 concentration was 0.15 ppm) in the triangular exposure, but not until 6.6 h in the square-wave exposure. Thus, significant pulmonary function and symptoms responses were observed over a longer period in the triangular exposure protocol at a mean O-3 concentration of 0.08 ppm. These results support previous evidence that O-3 concentration has a greater singular effect in the total inhaled O-3 dose than do V-E and exposure duration. Subtracting pulmonary function effects consequent to O-3 exposure to existent 8-h average background levels (e.g., similar to 0.04 ppm, rather than those observed in FA exposures) from those observed at higher concentrations (e.g., similar to 0.08 ppm) represents a means of focusing the regulatory effort on effects that can be controlled. The greatest pulmonary function and symptoms responses observed for a 0.04-ppm triangular exposure were nearly the same as those for the FA square-wave exposure. Thus, results of the present study show that calculating the net pulmonary function effect of exposure to 0.08 ppm with "correction" for FA response, or for that incurred for 0.04 ppm O-3, does not result in any statistically significant difference.