Seagrave JeanClare, Campen Matthew J, McDonald Jacob D, Mauderly Joe L, Rohr Annette C
Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA.
J Toxicol Environ Health A. 2008;71(20):1352-62. doi: 10.1080/15287390802271566.
Oxidative stress may mediate adverse health effects of many inhaled pollutants. Cardiopulmonary responses of Sprague-Dawley rats to inhalation of whole or filtered gasoline engine exhaust (GEE, FGEE); simulated downwind coal emission atmospheres (SDCAs) from two types of coal, each tested at two concentrations; and two concentrations of re-aerosolized paved road dust (RD) were evaluated. In situ chemiluminescence and thiobarbituric acid-reactive substances (TBARS) were used to evaluate oxidative reactions in the lungs, heart, and liver immediately following exposures. Pulmonary inflammatory responses were measured by bronchoalveolar lavage (BAL) cell counts. Respiratory function parameters during exposure were measured by plethysmography. Only GEE significantly enhanced in situ chemiluminescence (all three organs), but only exposure to the high RD concentration increased TBARS (hearts only). There was a weak trend toward increased macrophages recovered in lavage fluid from both SDCAs, and macrophages were significantly elevated by both FGEE and the lower concentration of RD. Respiratory function effects were small, though the effects of the Central Appalachian low-sulfur SDCA on enhanced pause and the effects of the Powder River Basin SCDA on tidal volume were significant. The discordance between the oxidative stress indicators may relate to the use of a single time point in the context of dynamic changes in compensatory mechanisms. These results further suggest that inflammatory responses measured by BAL cellularity may not always correlate with oxidative stress. Overall, the toxicological effects from exposure to these pollutant mixtures were subtle, but the results show differences in the effects of atmospheres having different physical/chemical characteristics.
氧化应激可能介导许多吸入性污染物对健康的不良影响。评估了斯普拉格-道利大鼠对吸入全部或经过过滤的汽油发动机尾气（GEE、FGEE）；两种类型煤炭产生的模拟下风向煤排放大气（SDCA），每种在两种浓度下进行测试；以及两种浓度的再气溶胶化铺路灰尘（RD）的心肺反应。在暴露后立即使用原位化学发光和硫代巴比妥酸反应性物质（TBARS）来评估肺、心脏和肝脏中的氧化反应。通过支气管肺泡灌洗（BAL）细胞计数来测量肺部炎症反应。在暴露期间通过体积描记法测量呼吸功能参数。只有GEE显著增强了原位化学发光（在所有三个器官中），但只有暴露于高浓度的RD才会增加TBARS（仅在心脏中）。来自两种SDCA的灌洗液中回收的巨噬细胞有微弱的增加趋势，并且FGEE和较低浓度的RD都使巨噬细胞显著升高。呼吸功能影响较小，尽管阿巴拉契亚中部低硫SDCA对增强暂停的影响以及粉河盆地SDCA对潮气量的影响是显著的。氧化应激指标之间的不一致可能与在补偿机制动态变化的背景下使用单个时间点有关。这些结果进一步表明，通过BAL细胞计数测量的炎症反应可能并不总是与氧化应激相关。总体而言，接触这些污染物混合物的毒理学影响很细微，但结果显示了具有不同物理/化学特性的大气影响的差异。
