Blazka M E, Dixon D, Haskins E, Rosenthal G J
Environmental Immunology and Neurobiology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.
Fundam Appl Toxicol. 1994 Feb;22(2):231-9. doi: 10.1006/faat.1994.1027.
The use of indium by the semiconductor industry has risen sharply in recent years with the discovery that the electrical properties of compounds such as indium phosphide and indium arsenide are better than those of silicon. However, relatively little is known about its potential to induce lung damage. These studies examined the effect of indium trichloride (InCl3) on the lung. To examine the disposition and removal of InCl3 from the lung, groups of female Fischer 344 rats received a single intratracheal dose of 1.3 mg In/kg as InCl3 and were euthanized after 1, 2, 4, 7, 14, 28, and 56 days at which time lung samples were analyzed for metal content. Furthermore, the histology, hydroxyproline levels, and bronchoalveolar lavage (BAL) fluid cellularity of the lung were studied. In addition, the effect of 0.00016, 0.00325, 0.065, and 1.3 mg In/kg on inflammatory response and BAL fluid cellularity was compared. While a dose as low as 0.00325 mg In/kg was capable of initiating an influx of inflammatory cells, instillation of 1.3 mg In/kg resulted in an inflammatory response that was still evident 56 days later. After 28 days, the lung weight of the InCl3-treated animals was 2.5 times greater than that of the controls. The total cell number in the BAL fluid of the treated animals after 28 days was 32 times higher than that in the control rats. Sixty-seven percent of these cells were granulocytes. Compared to the controls, the hydroxyproline content of the lungs from the InCl3-treated animals were two-fold greater after 28 and 56 days. Furthermore, the levels of fibronectin and TNF alpha present in the BAL fluid of InCl3-treated rats increased sharply during the first 24 hr and remained elevated 56 days later. These data and the histological examination of the lung following InCl3 treatment suggest that InCl3 is capable of causing severe lung damage and the development of fibrosis.
近年来，随着磷化铟和砷化铟等化合物的电学性能被发现优于硅，半导体行业对铟的使用急剧增加。然而，关于其诱发肺损伤的潜力却知之甚少。这些研究考察了三氯化铟（InCl3）对肺的影响。为了研究InCl3在肺中的分布和清除情况，将雌性Fischer 344大鼠分组，经气管内给予1.3 mg铟/千克体重的InCl3单次剂量，并在1、2、4、7、14、28和56天后实施安乐死，此时对肺组织样本进行金属含量分析。此外，还研究了肺的组织学、羟脯氨酸水平以及支气管肺泡灌洗（BAL）液细胞成分。另外，比较了0.00016、0.00325、0.065和1.3 mg铟/千克体重对炎症反应和BAL液细胞成分的影响。虽然低至0.00325 mg铟/千克体重的剂量就能引发炎症细胞的流入，但给予1.3 mg铟/千克体重后，炎症反应在56天后仍然明显。28天后，InCl3处理组动物的肺重量比对照组大2.5倍。28天后，处理组动物BAL液中的总细胞数比对照大鼠高32倍。这些细胞中有67%是粒细胞。与对照组相比，InCl3处理组动物的肺组织在28天和56天后的羟脯氨酸含量增加了一倍。此外，InCl3处理大鼠的BAL液中纤连蛋白和肿瘤坏死因子α（TNFα）水平在最初24小时内急剧上升，并在56天后仍保持升高。这些数据以及InCl3处理后肺组织的组织学检查表明，InCl3能够导致严重的肺损伤并引发纤维化。
