毒理性
识别和使用：钴在室温下是一种银灰色的固体。元素钴以0价态存在。钴有两种同素异形体，六方和立方。钴金属用于与铁、镍和其他金属合金化，制造具有独特磁性的铝镍钴合金；以及在司太立合金中，这种合金含有钴、铬和钨，用于高速、重载、高温切削工具。人类暴露和毒性：职业暴露于钴发生在几个行业，包括硬金属制造、焊接和研磨。吸入和皮肤接触钴可导致致敏。在各种形式钴暴露的工人中已经描述了支气管哮喘。由金属钴颗粒引起的间质性肺病是一种职业性肺病，通常被称为硬金属肺病。硬金属行业的死亡率研究表明，肺癌死亡率有所上升。吸入钴颗粒会导致上呼吸道和下呼吸道的位置。职业接触空气中的钴的工人在死亡时检查时，体内钴水平较高。铜冶炼工人的肺钴浓度显著高于非职业暴露的工人。在铜冶炼工人中，与对照组相比，肝或肾钴水平没有增加。金属工人的淋巴结、肝、脾和肾中的钴水平升高。动物研究：长期吸入钴金属在大鼠和小鼠中引起了肺癌，在大鼠中引起了全身性肿瘤。在钴金属暴露后，发现了毒性部位和致癌部位的差异。在大鼠中，血液和胰腺中观察到致癌性，在大鼠和小鼠的睾丸中观察到毒性。每组10只雄性和10只雌性长耳大鼠接受了一次钴金属粉末的肌肉注射。在122周内，雌雄大鼠在注射部位发展成了肉瘤，大多数是横纹肌肉瘤。金属钴植入两组兔子的股动脉中。在植入后三年内没有观察到肿瘤。对这些幸存者在6年后的随访研究中，在两个钴金属处理的兔子的植入部位发现了肉瘤。硬钴金属在体外系统中的遗传毒性大于钴化合物。钴金属在S. typhimurium TA98菌株中，在没有外源代谢激活（S9）的情况下具有诱变性；在S9存在时没有活性。在TA100菌株中，钴金属在没有S9的情况下使突变菌落略有增加，在S9存在时没有观察到诱变性。在E. coli WP2 uvrA/pKM101菌株中，无论是否添加S9，都没有检测到诱变性。在3个月研究中，雄性和雌性小鼠的外周血红细胞微核试验结果为阴性。
IDENTIFICATION AND USE: Cobalt is a silvery gray solid at room temperature. Elemental cobalt occurs in the 0 valence state. Cobalt has two allotropic forms, hexagonal and cubic. Cobalt metal is used in alloys with iron, nickel, and other metals to make Alnico, an alloy of unusual magnetic strength; and in Stellite alloys, which contain cobalt, chromium, and tungsten and are used for high-speed, heavy-duty, high temperature cutting tools. HUMAN EXPOSURE AND TOXICITY: Occupational exposure to cobalt occurs is several industries, including hard metal manufacturing, welding and grinding. Inhalation and dermal exposure to cobalt can result in sensitization. Bronchial asthma has been described in workers exposed to various forms of cobalt. Interstitial lung disease caused by metallic cobalt particles is an occupational lung disease generally referred as hard metal lung disease. Mortality studies of the hard metal industry suggest an increase in lung cancer mortality. Inhalation of cobalt particles results in disposition in the upper and lower respiratory tract. Workers exposed occupationally to airborne cobalt had higher tissue levels of cobalt when examined at death. Lung concentrations of cobalt are significantly higher in copper smelter workers, metal workers and coal miners who were occupationally exposed compared with non-occupationally exposed workers. In copper smelter workers, no increases in liver or kidney cobalt levels were observed with controls. Metal workers had increased cobalt levels in lymph nodes, liver, spleen and kidneys. ANIMAL STUDIES: Chronic inhalation exposure to cobalt metal has caused lung cancer in rats and mice, as well as systemic tumors in rats. There were distinct sites of toxicity and carcinogenicity noted following exposure to cobalt metal. In rats, carcinogenicity was observed in the blood and pancreas, and toxicity was observed in the testes of rats and mice. Groups of 10 male and 10 female hooded rats were treated with a single intramuscular injection of cobalt metal powder. Within 122 weeks both males and females developed sarcomas, mostly rhabdomyosarcomas at the injection site. Metallic cobalt was implanted in the femoral artery of two groups of rabbits. No tumors were observed three years post-implantation. A follow up study of these survivors at 6 years revealed sarcomas and the site of implantation in two cobalt metal treated rabbits. Hard cobalt metal is more genotoxic than cobalt compounds in in vitro systems. Cobalt metal was mutagenic in S. typhimurium strain TA98 in the absence of exogenous metabolic activation (S9); no activity was seen in the presence of S9. Cobalt metal induced a small increase in mutant colonies in strain TA100 in the absence of S9, and no mutagenic activity was seen with S9. No mutagenic activity was detected in E. coli strain WP2 uvrA/pKM101 with or without S9. Results of peripheral blood erythrocyte micronucleus tests in male and female mice in the 3 month study were negative.
来源:Hazardous Substances Data Bank (HSDB)
