Sun J, Chung K F
Department of Thoracic Medicine, National Heart & Lung Institute, London, United Kingdom.
J Toxicol Environ Health. 1997 May;51(1):77-87. doi: 10.1080/00984109708984012.
The effect of prior ozone (O3) exposure on airway hyperresponsiveness and inflammation induced by trimellitic anhydride (TMA) has been investigated in TMA-sensitized guinea pigs. Airway responsiveness was measured as the concentration of acetylcholine needed to increase baseline lung resistance (RL) by 300% (PC300). Ozone (3 ppm for 3 h) caused an increase in -log PC300 at 1 h after exposure, with return of -log PC300 to control levels at 8 h. Ozone also increased baseline RL at 8 h. TMA challenge increase -log PC300 in TMA-sensitized guinea pigs at 8 h after challenge from 3.85 +/- 0.09 to 4.11 +/- 0.09. Ozone exposure prior to TMA challenge prevented the induction of airway hyperresponsiveness with a mean -log PC300 of 3.51 +/- 0.20, which was not different from that of control TMA-sensitized group. Baseline RL was significantly higher in ozone-pretreated animals after TMA challenge when compared to those of either control or challenged with TMA alone. Ozone had no effect on TMA challenge-induced BAL eosinophilia and neutrophilia. We conclude that a single exposure to ozone inhibits the increase in airway responsiveness but increases the bronchoconstrictor response induced by TMA in TMA-sensitized guinea pigs; however, the inflammatory airway response to TMA is unchanged by preexposure to ozone.
在偏苯三酸酐（TMA）致敏的豚鼠中，研究了预先臭氧（O₃）暴露对TMA诱导的气道高反应性和炎症的影响。气道反应性通过使基线肺阻力（RL）增加300%所需的乙酰胆碱浓度（PC300）来衡量。臭氧（3 ppm，持续3小时）暴露后1小时导致-log PC300增加，8小时时-log PC300恢复到对照水平。臭氧在8小时时也增加了基线RL。TMA激发使TMA致敏的豚鼠在激发后8小时的-log PC300从3.85±0.09增加到4.11±0.09。TMA激发前的臭氧暴露可预防气道高反应性的诱导，平均-log PC300为3.51±0.20，与对照TMA致敏组无差异。TMA激发后，臭氧预处理动物的基线RL显著高于单独对照或单独TMA激发的动物。臭氧对TMA激发诱导的支气管肺泡灌洗嗜酸性粒细胞增多和中性粒细胞增多无影响。我们得出结论，单次臭氧暴露可抑制气道反应性增加，但会增加TMA致敏豚鼠中TMA诱导的支气管收缩反应；然而，预先暴露于臭氧不会改变对TMA的炎症气道反应。
