cobalt(II) sulfate | 10124-43-3

• 物质功能分类: 无机化工 - 无机盐 - 金属硫化物及硫酸盐
• 分子结构分类: 无机化合物 - 混合金属/非金属化合物 - 过渡金属氧阴离子化合物
• 英文名称: cobalt(II) sulfate
• 英文别名: cobalt sulfate；cobalt(II) sulphate；cobaltous sulfate；cobalt sulphate；cobalt(2+);sulfate
• CAS: 10124-43-3
• 化学式: Co*O₄S
• 分子量: 155.057
• InChiKey: KTVIXTQDYHMGHF-UHFFFAOYSA-L

物化性质

• 熔点：
  decomposes at 1140℃ [JAN85]
• 密度：
  d425 3.71
• 溶解度：
  可溶于水中
• LogP：
  -1.031 (est)
• 物理描述：
  Cobalt sulfate is an odorless rose-pink solid. Sinks and mixes with water. (USCG, 1999)
• 颜色/状态：
  Red to lavender dimorphic, othorhombic crystals
• 气味：
  Odorless
• 稳定性/保质期：

  Stable to 708 °C.

• 分解：
  735 °C. This produces toxic fumes of sulfur oxides. The dust reacts with strong oxidants. This generates fire and explosion hazard.
• 相对蒸发率：
  Evaporation at 20 °C is negligible

计算性质

• 辛醇/水分配系数(LogP)：
  -1.34
• 重原子数：
  6
• 可旋转键数：
  0
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  88.6
• 氢给体数：
  0
• 氢受体数：
  4

ADMET

代谢

钴通过肺部、胃肠系统和皮肤被吸收。由于它是维生素B12（氰钴胺）的一个组成部分，因此它被分布到身体的大多数组织中。它在血液中运输，通常与白蛋白结合，肝脏和肾脏中的含量最高。钴主要通过尿液和粪便排出。

Cobalt is absorbed though the lungs, gastrointestinal tract, and skin. Since it is a component of the vitamin B12 (cyanocobalamin), it is distributed to most tissues of the body. It is transported in the blood, often bound to albumin, with the highest levels being found in the liver and kidney. Cobalt is excreted mainly in the urine and faeces. (L29)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 毒性总结

识别：硫酸钴是一种红色粉末。它用于蓄电池；在钴电镀浴中；作为平版印刷油墨和清漆的干燥剂；在陶瓷、搪瓷和釉料中防止变色；用于装饰瓷器的钴颜料。人类暴露和毒性：在饮用大量添加了硫酸钴作为泡沫稳定剂的啤酒的个体中观察到了心肌病。反复或长期接触可能会导致皮肤敏感。反复或长期吸入暴露可能会导致哮喘。该物质可能对心脏、甲状腺和骨髓产生影响，导致心肌病、甲状腺肿大和红细胞增多症。动物研究：短期通过吸入暴露于硫酸钴的大鼠和小鼠表现出呼吸道上皮细胞的坏死和炎症。大鼠出现胸腺坏死和睾丸萎缩。大鼠在2-3个月内通过饮食暴露于硫酸钴24周，心脏酶活性水平显著降低。大鼠和小鼠每天6小时，每周5天，共13周通过吸入硫酸钴七水合物暴露，整个呼吸系统出现不良反应。在较高浓度下，大鼠和小鼠均出现喉部鳞状上皮化生。在大剂量下，大鼠出现慢性喉炎，以及更严重的鼻、喉和肺的影响。小鼠表现出急性鼻、喉和肺的炎症。小鼠还表现出纵隔淋巴结的增生和睾丸萎缩，以及雌性增加的动情周期。大鼠和小鼠在类似的暴露水平下表现出肺的嗜酸性细胞浸润。小鼠的精子活力降低，接受高剂量的小鼠出现异常精子增加和睾丸及附睾重量降低。在大鼠饮食中暴露于硫酸铜2-3个月的大鼠心脏重量增加和心脏变性病变。在大鼠饮食中暴露于硫酸钴24周的大鼠心脏酶活性水平显著降低，如锰超氧化物歧化酶、细胞色素c氧化酶、NADH、细胞色素还原酶，以及线粒体ATP生成的降低。每组50只雄性和50只雌性大鼠每天6小时，每周5天，共105周通过吸入硫酸铜七水合物暴露。平均体重和存活率未受到处理的影响。大鼠表现出雄性和雌性大鼠肺泡/支气管肿瘤的良性及恶性肿瘤发生率增加，以及雌性大鼠良性及恶性嗜铬细胞瘤。研究了硫酸钴七水合物通过吸入的小鼠致癌性。还评估了肺肿瘤中K-ras突变频率和光谱。与腔室对照组相比，在K-ras的12号密码子中检测到更高的G-T转位。

IDENTIFICATION: Cobalt sulfate is a red powder. It is used in storage batteries; in cobalt-electroplating baths; as drier for lithographic inks, and varnishes; in ceramics, enamels, and glazes to prevent discoloring; in cobalt pigments for decorating porcelain. HUMAN EXPOSURE AND TOXICITY: Cardiomyopathy has been observed in individuals who consume large quantities of beer where cobalt sulfate was added as a foam stabilizer. Repeated or prolonged contact may cause skin sensitization. Repeated or prolonged inhalation exposure may cause asthma. The substance may have effects on the heart, thyroid and bone marrow, resulting in cardiomyopathy, goiter and polycythemia. ANIMAL STUDIES: Rats and mice exposed short term to cobalt sulfate by inhalation exhibited necrosis and inflammation of the respiratory tract epithelium. Rats developed thymus necrosis and testicular atrophy. Rats exposed for 2-3 months to cobalt sulfate in the diet for 24 weeks had significant reductions in heart enzyme activity levels. Rats and mice were exposed to cobalt sulfate heptahydrate by inhalation 6 hr/day, 5 days/week for 13 weeks developed adverse effects throughout the respiratory system. At higher concentrations both rats and mice developed squamous metaplasia of the larynx. At high doses, rats developed chronic inflammation of the larynx along with more severe effects in the nose, larynx and lung. Mice exhibited acute inflammation of the nose, larynx and lungs. Mice also exhibited hyperplasia of the mediastinal lymph nodes and testicular atrophy and increased esterous cycle in females. Both rats and mice exhibited histiocytic infiltrates of the lung at similar exposure levels. Sperm motility was decreased in mice and mice that received high dosages developed increased abnormal sperm and decreased testis and epididymal weights. Rats exposed for 2-3 months of copper sulfate in the diet exhibited increased heart weight and degenerative heart lesions. Rats exposed to cobalt sulfate in their diet for 24 weeks experienced significant reductions in cardiac enzyme activity levels, such as manganese superoxide dismutase, cytochrome c oxidase, NADH, cytochrome reductase and a reduction in mitochondrial ATP production. Groups of 50 male and 50 female rats exposed to copper sulfate heptahydrate by inhalation for 6 hr/day, 5 days/week for 105 weeks. Mean body weights and survival were unaffected by treatment. Rats exhibited a concentration increase in the incidence of benign and malignant alveolar/bronchiolar neoplasms in male and female rats and benign and malignant pheochromocytomas in female rats. The carcinogenicity of cobalt sulfate heptahydrate by inhalation was studied in mice. Also evaluated was the K-ras mutation frequency and spectra in lung tumors. A higher G-T transversions was detected in codon 12 of K-ras compared to chamber controls.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 毒性总结

钴被认为通过氧化剂和自由基过程表现出其毒性。它产生氧自由基，并可能被氧化成离子态的钴，导致脂质过氧化增加、DNA损伤，并诱导某些酶，导致细胞凋亡。钴还被证明可以阻断无机钙通道，可能损害神经传递。钴还可以与硫辛酸螯合，损害丙酮酸或脂肪酸的氧化。此外，钴可能通过与锌指DNA修复蛋白相互作用来抑制DNA修复，并且已被证明可以抑制血红素合成和葡萄糖代谢。钴可能激活特定的辅助性T淋巴细胞，并直接与免疫蛋白（如抗体IgA和IgE或Fc受体）相互作用，导致免疫致敏。

Cobalt is believed to exhibit its toxicity through a oxidant-based and free radical-based processes. It produces oxygen radicals and may be oxidized to ionic cobalt, causing increased lipid peroxidation, DNA damage, and inducing certain enzymes that lead to cell apoptosis. Cobalt has also been shown to block inorganic calcium channels, possibly impairing neurotransmission. Cobalt can also chelate lipoic acids, impairing oxidation of pyruvate or fatty acids. In addition, cobalt may inhibit DNA repair by interacting with zinc finger DNA repair proteins, and has also been shown to inhibit heme synthesis and glucose metabolism. Cobalt may activate specific helper T-lymphocyte cells and interact directly with immunologic proteins, such as antibodies (IgA and IgE) or Fc receptors, resulting in immunosensitization. (L29)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 致癌性证据

这项关于钴和释放钴离子的钴化合物的类别列表，取代了之前在致癌物报告中列出的硫酸钴。硫酸钴首次在2004年的第十一份致癌物报告中列出，当时基于充分的实验动物致癌性证据，预计为人类致癌物。

This listing of the class of cobalt and cobalt compounds that release cobalt ions in vivo supersedes the previous listing of cobalt sulfate in the Report on Carcinogens. The compound cobalt sulfate was first listed in the Eleventh Report on Carcinogens in 2004 as reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity in experimental animals.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 致癌性证据

硫酸钴：合理预期为人类致癌物。

Cobaltous Sulfate: reasonably anticipated to be a human carcinogen.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 致癌性证据

钴和钴化合物在人类中的致癌性证据不足。有充分证据表明钴金属粉末在实验动物中具有致癌性。有限证据显示含有钴、铬和钼的金属合金在实验动物中具有致癌性。总体评估：钴和钴化合物可能对人类具有致癌性（2B组）。/钴和钴化合物/

There is inadequate evidence for the carcinogenicity of cobalt and cobalt compounds in humans. There is sufficient evidence for the carcinogenicity of cobalt metal powder in experimental animals. There is limited evidence for the carcinogenicity of metal alloys containing cobalt, chromium and molybdenum in experimental animals. ... Overall Evaluation: Cobalt and cobalt compounds are possibly carcinogenic to humans (Group 2B). /Cobalt and cobalt compounds/

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

硫酸钴对怀孕的C57BI小鼠、OFA-SD大鼠和新西兰兔的胎儿和出生后后代的影响进行了研究。母体血液中的钴浓度随着给药剂量的增加而增加。钴穿过胎盘，出现在胎儿血液和羊水中。无论硫酸钴的给药剂量如何，血液中的钴浓度在给药后2小时达到峰值。

The effects of cobalt sulfate administered to pregnant C57BI mice, OFA-SD rats, and New Zealand rabbits was studied on fetal and postnatal offspring. Cobalt concentration in the maternal blood was increased in proportion to the administered doses. Cobalt crossed the placenta and appeared in the fetal blood and amniotic fluid. Regardless of the administered dose of cobalt sulfate, cobalt concentration in the blood peaked 2 hr after administration.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

给绵羊单次剂量的含水硫酸钴后，绵羊死亡。肝脏中含有400-1200 ppm的钴。在因大量过量含水硫酸钴死亡的牛中，肝脏含有5-300 ppm的钴，肾脏含有30-200 ppm的钴。/含水硫酸钴/

Sheep given a single dose of hydrated cobalt sulfate were killed. ...The livers contained 400-1200 ppm of cobalt. In cattle dying after a massive overdose of hydrated cobalt sulfate livers contained 5-300 ppm, kidneys 30-200 ppm. /Hydrated cobalt sulfate/

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

在饮食中长期暴露于硫酸钴（8周）后，暴露组的大鼠心肌中的钴浓度增加了30倍，比目鱼肌中的浓度增加了26倍，血清中的浓度增加了100倍，与非暴露对照组相比。大鼠长期口服氯化钴导致处理组大鼠的肝脏、肾脏、肌肉、大脑和睾丸中的钴含量显著增加。

Following longer-term exposure (8 weeks) to cobalt sulfate in the diet, exposed rats showed a 30-fold increase in the cobalt concentration in the myocardium, a 26-fold increase in the concentration in the soleus muscle, and a 100-fold increase in the concentration in serum compared with nonexposed controls. Long-term oral exposure of rats to cobalt chloride resulted in significantly increased levels of cobalt in the liver, kidney, muscle, brain, and testes of treated rats.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

钴的代谢和毒理学概述。根据最近对钴干扰几乎所有动物细胞感知缺氧（低氧）的研究，更新了钴的生物功能。钴（Co(2+)）稳定了转录激活因子低氧诱导因子（HIF），从而模拟低氧并刺激促红细胞生成素（Epo）的产生，但可能也是通过相同的机制诱导了一系列对低氧适应性反应的协调上调，其中许多具有潜在的致癌效应。另一方面，这意味着钴（Co(2+)）在组织低氧条件下可能具有有益效果，并且可能代表低氧预处理的一种替代方法。钴在大剂量时具有急性毒性，在哺乳动物体外测试系统中，钴离子和钴金属具有细胞毒性，可诱导凋亡，在高浓度时引起坏死和炎症反应。钴金属和盐也具有基因毒性，主要由活性氧种类引起的氧化DNA损伤引起，可能还与DNA修复抑制有关。值得注意的是，钴金属和硫酸钴对实验动物具有足够证据的致癌性，但对人类尚不足够。有趣的是，钴（Co(2+)）的一些毒性效应最近被认为可能是由于假定的钙（Ca(2+)）进入和Ca(2+)-信号传导的抑制作用以及与Ca(2+)竞争细胞内Ca(2+)-结合蛋白所致。钴（Co(2+)）的组织分配及其在单次给药后随时间的变化已在人类中进行了研究，但主要是在实验动物中。钴主要积累在肝脏、肾脏、胰腺和心脏中，给药后随着时间的推移，骨骼和骨骼肌的相对含量增加。在人类中，肾排泄最初是迅速的，但在最初几天内逐渐减少，随后是持续数周的第二个缓慢阶段，并且在数年内显著长期保留在组织中。在血清中，钴（Co(2+)）与白蛋白结合，自由离子Co(2+)的浓度估计为总钴浓度的5-12%。在人红细胞中，钴（Co(2+)）的膜传输途径似乎与钙（Ca(2+)）共享，但由于钴在细胞质中有效结合并且不被Ca泵排出，因此钴的摄入本质上是不可逆的。诱人推测这也许在其他动物细胞中也可能发生。如果是这种情况，钴在细胞和组织中的组织分配和生物动力学将与钙的摄入密切相关，钴主要分配到钙转换率高的组织中，并在细胞转换率慢的组织中积累和保留。职业钴暴露，例如在钴加工厂和硬质金属工业中，是众所周知的，并且在最近几年由于工作场所卫生条件的改善而有所减少。然而，值得注意的是，最近在接近或略低于当前职业暴露限值以下的钴暴露后，已经证明了对心脏和肺的不良反应。在过去的几十年中，钴-铬硬质金属合金在骨科关节置换术中的应用，特别是在髋关节置换术中的金属对金属轴承，创造了一个全新的内部钴暴露源。腐蚀和磨损产生可溶性金属离子和以数十亿纳米尺寸磨损颗粒形式存在的金属碎片，通过淋巴和系统血管系统全身传播。这可能导致假体周围软组织的局部不良反应，并引起全身毒性。值得注意的是，金属纳米颗粒已被证明比更大的微米尺寸颗粒更具毒性，这使得纳米毒理学成为一个关键的新学科。作为钴暴露的另一个潜在来源，有人怀疑运动员可能滥用钴盐作为增加有氧性能的Epo兴奋剂的诱人替代品。体外钴的毒性主要存在于离子化钴中。诱人推测离子化钴也是体内全身毒性的主要形式。根据这一假设，风险评估的相关参数是全身钴离子暴露的时间平均价值，从理论角度来看，可以通过测量红细胞中的钴含量来获得，因为它们的钴摄入仅反映自由离子化钴（Co(2+)）的摄入，并且在它们120天的寿命期间摄入实际上是不可逆的。这显然需要未来在暴露个体中进行临床研究，系统地比较红细胞和血清中钴浓度的同时测量。

Cobalt metabolism and toxicology are summarized. The biological functions of cobalt are updated in the light of recent understanding of cobalt interference with the sensing in almost all animal cells of oxygen deficiency (hypoxia). Cobalt (Co(2+)) stabilizes the transcriptional activator hypoxia-inducible factor (HIF) and thus mimics hypoxia and stimulates erythropoietin (Epo) production, but probably also by the same mechanism induces a coordinated up-regulation of a number of adaptive responses to hypoxia, many with potential carcinogenic effects. This means on the other hand that cobalt (Co(2+)) also may have beneficial effects under conditions of tissue hypoxia, and possibly can represent an alternative to hypoxic preconditioning. Cobalt is acutely toxic in larger doses, and in mammalian in vitro test systems cobalt ions and cobalt metal are cytotoxic and induce apoptosis and at higher concentrations necrosis with inflammatory response. Cobalt metal and salts are also genotoxic, mainly caused by oxidative DNA damage by reactive oxygen species, perhaps combined with inhibition of DNA repair. Of note, the evidence for carcinogenicity of cobalt metal and cobalt sulfate is considered sufficient in experimental animals, but is as yet considered inadequate in humans. Interestingly, some of the toxic effects of cobalt (Co(2+)) have recently been proposed to be due to putative inhibition of Ca(2+) entry and Ca(2+)-signaling and competition with Ca(2+) for intracellular Ca(2+)-binding proteins. The tissue partitioning of cobalt (Co(2+)) and its time-dependence after administration of a single dose have been studied in man, but mainly in laboratory animals. Cobalt is accumulated primarily in liver, kidney, pancreas, and heart, with the relative content in skeleton and skeletal muscle increasing with time after cobalt administration. In man the renal excretion is initially rapid but decreasing over the first days, followed by a second, slow phase lasting several weeks, and with a significant long-term retention in tissues for several years. In serum cobalt (Co(2+)) binds to albumin, and the concentration of free, ionized Co(2+) is estimated at 5-12% of the total cobalt concentration. In human red cells the membrane transport pathway for cobalt (Co(2+)) uptake appears to be shared with calcium (Ca(2+)), but with the uptake being essentially irreversible as cobalt is effectively bound in the cytosol and is not itself extruded by the Ca-pump. It is tempting to speculate that this could perhaps also be the case in other animal cells. If this were actually the case, the tissue partitioning and biokinetics of cobalt in cells and tissues would be closely related to the uptake of calcium, with cobalt partitioning primarily into tissues with a high calcium turn-over, and with cobalt accumulation and retention in tissues with a slow turn-over of the cells. The occupational cobalt exposure, e.g. in cobalt processing plants and hard-metal industry is well known and has probably been somewhat reduced in more recent years due to improved work place hygiene. Of note, however, adverse reactions to heart and lung have recently been demonstrated following cobalt exposure near or slightly under the current occupational exposure limit. Over the last decades the use of cobalt-chromium hard-metal alloys in orthopedic joint replacements, in particular in metal-on-metal bearings in hip joint arthroplasty, has created an entirely new source of internal cobalt exposure. Corrosion and wear produce soluble metal ions and metal debris in the form of huge numbers of wear particles in nanometric size, with systemic dissemination through lymph and systemic vascular system. This may cause adverse local reactions in peri-prosthetic soft-tissues, and in addition systemic toxicity. Of note, the metal nanoparticles have been demonstrated to be clearly more toxic than larger, micrometer-sized particles, and this has made the concept of nanotoxicology a crucial, new discipline. As another new potential source of cobalt exposure, suspicion has been raised that cobalt salts may be misused by athletes as an attractive alternative to Epo doping for enhancing aerobic performance. The cobalt toxicity in vitro seems to reside mainly with ionized cobalt. It is tempting to speculate that ionized cobalt is also the primary toxic form for systemic toxicity in vivo. Under this assumption, the relevant parameter for risk assessment would be the time-averaged value for systemic cobalt ion exposure that from a theoretical point of view might be obtained by measuring the cobalt content in red cells, since their cobalt uptake reflects uptake only of free ionized cobalt (Co(2+)), and since the uptake during their 120 days life span is practically irreversible. This clearly calls for future clinical studies in exposed individuals with a systematic comparison of concurrent measurements of cobalt concentration in red cells and in serum.

来源:Hazardous Substances Data Bank (HSDB)

安全信息

• 危险品标志：
  T,N
• 安全说明：
  S22,S23,S36/37,S45,S53,S60,S61
• 危险类别码：
  R49,R51/53,R42/43
• WGK Germany：
  2
• 危险品运输编号：
  UN 3082 9/PG 3
• RTECS号：
  GG3100000
• 海关编码：
  2833299010
• 储存条件：
  库房应保持低温、通风和干燥，并将货物与食品原料分开存放。

SDS

第一部分：化学品名称

化学品中文名称：	硫酸钴；赤矾
化学品英文名称：	Cobalt sulfate；Cobaltous sulfate
中文俗名或商品名：
Synonyms：
CAS No.：	10124-43-3
分子式：	COSO 4 ·7H 2 O
分子量：	281.15

第二部分：成分/组成信息

纯化学品 混合物

化学品名称：硫酸钴；赤矾

有害物成分 含量 CAS No.

第三部分：危险性概述

危险性类别：
侵入途径：	吸入 食入
健康危害：	本品粉尘对眼、鼻、呼吸道及胃肠道粘膜有刺激作用。引起咳嗽、呕吐、腹绞痛、体温上升、小腿无力等。．皮肤接触可引起过敏性皮炎、接触性皮炎。
环境危害：
燃爆危险：

第四部分：急救措施

皮肤接触：	用肥皂水及清水彻底冲洗。就医。
眼睛接触：	拉开眼睑，用流动清水冲洗15分钟。就医。
吸入：	脱离现场至空气新鲜处。就医。
食入：	误服者，口服牛奶、豆浆或蛋清，洗胃。就医。

第五部分：消防措施

危险特性：	受高热分解，放出有毒的烟气。
有害燃烧产物：
灭火方法及灭火剂：	不燃。火场周围可用的灭火介质。
消防员的个体防护：
禁止使用的灭火剂：
闪点(℃)：
自燃温度(℃)：
爆炸下限[%(V/V)]：
爆炸上限[%(V/V)]：
最小点火能(mJ)：
爆燃点：
爆速：
最大燃爆压力(MPa)：
建规火险分级：

第六部分：泄漏应急处理

应急处理：

隔离泄漏污染区，周围设警告标志，建议应急处理人员戴好防毒面具，穿化学防护服。不要直接接触泄漏物，小心扫起，避免扬尘，倒至空旷地方深埋。用水刷洗泄漏污染区，经稀释的污水放入废水系统。如大量泄漏，收集回收或无害处理后废弃。

第七部分：操作处置与储存

操作注意事项：
储存注意事项：

第八部分：接触控制/个体防护

最高容许浓度：	中 国 MAC：未制订标准前苏联 MAC：未制订标准美国TLV—TWA：未制订标准
监测方法：
工程控制：	密闭操作，局部排风。
呼吸系统防护：	可能接触其粉尘时，佩戴防尘口罩。紧急事态抢救或逃生时，应该佩戴自给式呼吸器。
眼睛防护：	可采用安全面罩．
身体防护：	穿相应的防护服。
手防护：	戴防护手套。
其他防护：	工作现场禁止吸烟、进食和饮水。工作后，淋浴更衣。注意个人清洁卫生。

第九部分：理化特性

外观与性状：	玫瑰红色单斜晶体。
pH：
熔点(℃)：	96～98
沸点(℃)：	420(一7H20)
相对密度(水=1)：	1．948(25℃)
相对蒸气密度(空气=1)：
饱和蒸气压(kPa)：
燃烧热(kJ/mol)：
临界温度(℃)：
临界压力(MPa)：
辛醇/水分配系数的对数值：
闪点(℃)：
引燃温度(℃)：
爆炸上限%(V/V)：
爆炸下限%(V/V)：
分子式：	COSO 4 ·7H 2 O
分子量：	281.15
蒸发速率：
粘性：
溶解性：	溶于