Japan Bioassay Research Center, Japan Industrial Safety and Health Association, Japan.
J Occup Health. 2011;53(3):234-9. doi: 10.1539/joh.10-0053-br. Epub 2011 Mar 16.
Inhalation toxicities of indium-tin oxide (ITO) and indium oxide (IO) in mice were characterized in comparison with those previously reported in rats.
B6C3F(1) mice of both sexes were exposed by inhalation to ITO or IO aerosol for 6 h/day, 5 day/wk for 2 wk at 0, 0.1, 1, 10 or 100 mg/m(3) or 13 wk at 0, 0.1or 1 mg/m(3).
ITO and IO particles were deposited in the lung, mediastinal lymph node (MLN) and nasal-associated lymphoid tissue. Alveolar proteinosis, infiltrations of alveolar macrophages and inflammatory cells and increased lung weight were induced by 2- and 13-week exposures to ITO and IO, while alveolar epithelial hyperplasia occurred only in the 2-week exposures. Thickened pleural wall, hyperplastic MLN, extramedullary hematopoiesis in the spleen and increased levels of erythrocyte parameters were induced by 13-week exposure to ITO. The ITO- and IO-induced pulmonary lesions were milder in mice than those previously reported in rats, and the fibrotic lesions were different between these two species. Indium levels in the lung and pooled blood were analyzed in the mice exposed to ITO and IO for 13 wk. In the 13-week inhalation exposure of mice to ITO, alveolar proteinosis and significantly increased lung weight were induced at the same exposure concentration as the current threshold limit value for indium and its compounds.
与之前在大鼠中报告的结果相比，比较了铟锡氧化物（ITO）和氧化铟（IO）在小鼠中的吸入毒性。
B6C3F(1) 雌雄小鼠分别经呼吸道暴露于 ITO 或 IO 气溶胶，每天 6 小时，每周 5 天，浓度分别为 0、0.1、1、10 或 100mg/m(3)，或 13 周，浓度分别为 0、0.1 或 1mg/m(3)。
ITO 和 IO 颗粒沉积在肺部、纵隔淋巴结（MLN）和鼻相关淋巴组织中。2 周和 13 周暴露于 ITO 和 IO 可诱导肺泡蛋白沉积症、肺泡巨噬细胞和炎症细胞浸润以及肺重量增加，而仅在 2 周暴露时发生肺泡上皮细胞增生。13 周暴露于 ITO 可导致胸膜壁增厚、MLN 增生、脾脏髓外造血和红细胞参数水平升高。与之前在大鼠中报告的结果相比，ITO 和 IO 引起的肺部病变在小鼠中较轻，并且这两种物种的纤维化病变不同。在 ITO 和 IO 暴露 13 周的小鼠中分析了肺和 pooled 血液中的铟含量。在 ITO 对小鼠的 13 周吸入暴露中，肺泡蛋白沉积症和显著增加的肺重量在与铟及其化合物的当前阈限值相同的暴露浓度下诱导。
