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铟锡氧化物在大鼠和小鼠中的吸入致癌性和慢性毒性。

Inhalation carcinogenicity and chronic toxicity of indium-tin oxide in rats and mice.

机构信息

Japan Bioassay Research Center, Japan Industrial Safety and Health Association, Japan.

出版信息

J Occup Health. 2011;53(3):175-87. doi: 10.1539/joh.10-0057-oa. Epub 2011 Apr 7.

DOI:10.1539/joh.10-0057-oa
PMID:21471693
Abstract

OBJECTIVES

Carcinogenicity and chronic toxicity of indium-tin oxide (ITO) were examined by inhalation exposure of rats and mice to ITO aerosol.

METHODS

Fifty mice of both sexes were exposed to ITO at 0 (control), 0.01, 0.03 or 0.1 mg/m(3) for 6 h/day, 5 day/wk for 104 wk, and 50 rats of both sexes were exposed to 0, 0.01 or 0.03 mg/m(3) ITO for the same time period. The repeated exposure of 50 rats of both sexes to 0.1 mg/m(3) ITO was discontinued at the 26th wk, followed by clean air exposure for the remaining 78 wk.

RESULTS

In rats, incidences of bronchiolo-alveolar adenomas and carcinomas, bronchiolo-alveolar hyperplasia, alveolar wall fibrosis and thickened pleural wall, alveolar proteinosis and infiltrations of alveolar macrophages and inflammatory cells were significantly increased. Combined incidences of malignant lung tumors in male rats and total lung tumors in male and female rats were significantly increased at exposure to 0.01 mg/m(3) ITO. In mice, no carcinogenic response occurred, but thickened pleural wall, alveolar proteinosis and alveolar macrophage infiltration were induced. Mice were less susceptible to ITO than rats. The lung content of indium was the greatest, followed by the spleen, kidney and liver. Blood indium levels increased dose-dependently.

CONCLUSIONS

There was clear evidence of carcinogenicity of inhaled ITO in male and female rats but not clear evidence in mice, together with occurrence of the chronic pulmonary lesions in both rats and mice.

摘要

目的

通过对大鼠和小鼠进行 ITO 气溶胶吸入暴露,研究氧化铟锡(ITO)的致癌性和慢性毒性。

方法

将 50 只雄性和 50 只雌性小鼠分别暴露于 0(对照)、0.01、0.03 或 0.1mg/m(3)的 ITO 气溶胶中,每天 6 小时,每周 5 天,共 104 周;将 50 只雄性和 50 只雌性大鼠分别暴露于 0、0.01 或 0.03mg/m(3)的 ITO 中相同时间。将 50 只雄性大鼠重复暴露于 0.1mg/m(3)的 ITO 中 26 周后停止,随后进行清洁空气暴露 78 周。

结果

在大鼠中,细支气管肺泡腺瘤和癌、细支气管肺泡增生、肺泡壁纤维化和胸膜壁增厚、肺泡蛋白沉积、肺泡巨噬细胞和炎症细胞浸润的发生率显著增加。雄性大鼠恶性肺肿瘤的总合并发生率以及雄性和雌性大鼠的总肺肿瘤发生率在暴露于 0.01mg/m(3)的 ITO 时显著增加。在小鼠中未发生致癌反应,但出现胸膜壁增厚、肺泡蛋白沉积和肺泡巨噬细胞浸润。与大鼠相比,小鼠对 ITO 的敏感性较低。肺中铟含量最高,其次是脾脏、肾脏和肝脏。血液中铟水平呈剂量依赖性增加。

结论

吸入 ITO 对雄性和雌性大鼠有明显的致癌作用,但在小鼠中无明显证据,同时在大鼠和小鼠中均出现慢性肺部病变。

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