Sumitomo M, Nishikawa M, Fukuda T, Kaneko T, Ikeda H, Suzuki S, Okubo T
First Department of Internal Medicine, Yokohama City University School of Medicine, Japan.
Int Arch Allergy Appl Immunol. 1990;93(2-3):139-47. doi: 10.1159/000235293.
As ozone (O3) is known to cause airway inflammation and hyperresponsiveness, we examined the effects of O3 exposure (1, 3, or 5 ppm, 2 h) on sensitization and provocation in guinea pigs sensitized with ovalbumin (OA) through the airway. In groups exposed to O3 before sensitization, 5 ppm increased the production of IgG1 antibodies and decreased the OA sensitization threshold from 0.01 to 0.002%. In those exposed before provocation, 1, 3, or 5 ppm of O3 decreased the OA provocation threshold from 0.5 to 0.02%, and this enhancement appeared to depend on airway hyperresponsiveness. We conclude that O3 exposure may play an important role in causing asthmatic attacks rather than enhancing allergic sensitization.
由于已知臭氧（O3）会引发气道炎症和高反应性，我们研究了臭氧暴露（1、3或5 ppm，2小时）对通过气道用卵清蛋白（OA）致敏的豚鼠致敏和激发的影响。在致敏前暴露于臭氧的组中，5 ppm增加了IgG1抗体的产生，并将OA致敏阈值从0.01%降低到0.002%。在激发前暴露于臭氧的组中，1、3或5 ppm的臭氧将OA激发阈值从0.5%降低到0.02%，这种增强似乎取决于气道高反应性。我们得出结论，臭氧暴露可能在引发哮喘发作而非增强过敏致敏方面起重要作用。
