Kuschner W G, Wong H, D'Alessandro A, Quinlan P, Blanc P D
Division of Occupational and Environmental Medicine, Department of Medicine, University of California, San Francisco, California 94117, USA.
Environ Health Perspect. 1997 Nov;105(11):1234-7. doi: 10.1289/ehp.971051234.
Exposure to air polluted with particles less than 2.5 micron in size is associated epidemiologically with adverse cardiopulmonary health consequences in humans. The goal of this study was to characterize human pulmonary responses to controlled experimental high-dose exposure to fine and ultrafine magnesium oxide particles. We quantified bronchoalveolar lavage (BAL) cell and cytokine concentrations, pulmonary function, and peripheral blood neutrophil concentrations in six healthy volunteers 18 to 20 hr after inhalation of fine and ultrafine magnesium oxide particles produced from a furnace system model. We compared postexposure studies with control studies from the same six subjects. Mean +/- standard deviation (SD) cumulative magnesium dose was 4,138 +/- 2,163 min x mg/m3. By weight, 28% of fume particles were ultrafine (<0.1 micron in diameter) and over 98% of fume particles were fine (<2.5 micron in diameter). There were no significant differences in BAL inflammatory cell concentrations, BAL interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor, pulmonary function, or peripheral blood neutrophil concentrations postexposure compared with control. Our findings suggest that high-dose fine and ultrafine magnesium oxide particle exposure does not produce a measurable pulmonary inflammatory response. These findings are in marked contrast with the well-described pulmonary inflammatory response following zinc oxide particle inhalation. We conclude that fine and ultrafine particle inhalation does not result in toxicity in a generic manner independent of particle composition. Our findings support the concept that particle chemical composition, in addition to particle size, is an important determinant of respiratory effects.
暴露于粒径小于2.5微米的空气污染中,在流行病学上与人类心肺健康不良后果相关。本研究的目的是描述人类肺部对受控实验性高剂量暴露于细颗粒和超细氧化镁颗粒的反应。我们在6名健康志愿者吸入由炉系统模型产生的细颗粒和超细氧化镁颗粒18至20小时后,对支气管肺泡灌洗(BAL)细胞和细胞因子浓度、肺功能以及外周血中性粒细胞浓度进行了量化。我们将暴露后研究与来自相同6名受试者的对照研究进行了比较。平均±标准差(SD)累积镁剂量为4138±2163分钟×毫克/立方米。按重量计算,28%的烟尘颗粒为超细颗粒(直径<0.1微米),超过98%的烟尘颗粒为细颗粒(直径<2.5微米)。与对照相比,暴露后BAL炎性细胞浓度、BAL白细胞介素(IL)-1、IL-6、IL-8、肿瘤坏死因子、肺功能或外周血中性粒细胞浓度均无显著差异。我们的研究结果表明,高剂量暴露于细颗粒和超细氧化镁颗粒不会产生可测量的肺部炎症反应。这些发现与吸入氧化锌颗粒后所描述的肺部炎症反应形成鲜明对比。我们得出结论,吸入细颗粒和超细颗粒不会以与颗粒成分无关的一般方式导致毒性。我们的研究结果支持这样一种观点,即除了粒径外,颗粒化学成分也是呼吸效应的重要决定因素。