Study on risk assessment of metals and metalloids used in high technology industry

本研究由两部分组成，i）半导体中使用的镓（Ga）、铟（In）和砷化合物的毒性评估，ii）超导体中使用的钇（Y）和镧。Aoki和Fowler估计了半导体材料的肾毒性。在原代培养的大鼠肾近端上皮细胞的蛋白质合成的变化进行了检查后，暴露于镓，铟和亚砷酸钠。300 μ M的GaCl_3或10 μ M的亚砷酸盐明显刺激了7种蛋白质的合成。300 μ M的InCl_3暴露对蛋白质合成无明显影响。当暴露于浓度为300 μ M的Ga和3 μ M以下的亚砷酸盐时，细胞释放的乳酸脱氢酶（LDH）并不显著增加。在没有明显细胞损伤的情况下，这些蛋白的诱导可能作为Ga暴露的早期指标。砷化氢气体是一种强有力的溶血剂。然而，在大气中砷化氢的浓度，导致母亲的脾脏大小和母亲的血液和胎儿的肝脏砷的可测量的水平的增加，并没有不利影响发育毒性的终点。平野和铃木检查了材料的超导体对肺的毒性作用。YCl_3经气管内注入大鼠。Y的肺部清除非常缓慢，半衰期估计为168天。透射电镜和X射线微区分析表明，Y定位于肺泡和间质巨噬细胞的溶酶体和基底膜。比较支气管肺泡灌洗液上清液中LDH活性的剂量-效应曲线表明，1 mol YCl_3的急性肺毒性相当于约三分之一mol镉化合物和约3 mol氧化锌。

This study consists of two Parts, which are i) toxicity assessment of gallium (Ga), Indium (In), and arsenic compounds used in semiconductor, and ii) yttrium (Y) and lanthanum used in superconductor.Aoki and Fowler estimated the renal toxicity of materials for semiconductors. Alterations in protein synthesis in primary cultures of rat kidney proximal epithelial cells were examined following exposure to Ga, In and sodium arsenite. Synthesis of seven proteins was markedly stimulated by exposure to 300 micro-M GaCl_3 or 10 micro-M arsenite. No significant changes in protein synthesis were observed with 300 micro-M InCl_3 exposure. Release of lactate dehydrogenese (LDH) from the cells was not significantly increase by exposure to concentration of 300 micro-M Ga and 3 micro-M arsenite or less. In the absence of overt cell injury, the induction of these proteins may be useful as an early indicator for exposure to Ga.Fowler at al. reported the effect of arsine exposure on pregnancy and prenatal development of mice and rats. Arsine gas was known to be a potent hemolytic agent. However, arsine at atmospheric concentrations that caused increases in maternal spleen size and measurable levels of arsenic in maternal blood and fetal livers did not adversely affect endpoints of developmental toxicity.Hirano and Suzuki examined the toxic effect of materials for superconductors on the lung. YCl_3 was instilled intratracheally into rats. Pulmonary clearance of Y was very slow and the halflife was estimated to be 168 days. Transmission electron microscopy and X-ray microanalysis suggested that Y was localized in lysosomes of alveolar and interstitial macrophages, and basement membranes. Comparative dose-effect profiles of LDH activity in bronchoalveolar lavage fluid supernatant revealed that 1 mol of YCl_3 is equivalent to about one-third mole of cadmium compounds and about 3 mol of zinc oxide in the potency for acute pulmonary toxicity.