In experiments on male albino rats after subcutaneous injection of a single toxic dose it was found that cobaltous nitrate (Co(NO3)2 significantly inhibited the hexobarbital-oxidizing enzyme system, Aniline hydroxylase was significantly inhibited by Co(NO3)2. In determination of ethylmorphine demethylase activity Co(NO3)2, significantly inhibited the enzyme activity, /and/ reduced also the microsomal cytochrome P-450 content.
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. Intake of some amount of nitrates and nitrites is a normal part of the nitrogen cycle in humans. In vivo conversion of nitrates to nitrites can occur in the gastrointestional tract under the right conditions, significantly enhancing nitrates' toxic potency. The major metabolic pathway for nitrate is conversion to nitrite, and then to ammonia. Nitrites, nitrates, and their metabolites are excreted in the urine. (L1137, L29)
IDENTIFICATION AND USE: Cobalt nitrate forms red crystals, or pale red powder. It is used in manufacture of cobalt pigments and invisible inks; decorating stoneware and porcelain; preparation of catalysts; production of vitamin B12 supplements. Cobalt nitrate is an important source of high-purity cobalt for use in the electronics and related industries. HUMAN EXPOSURE AND TOXICITY: Repeated or prolonged contact may cause skin sensitization. Repeated or prolonged inhalation may cause asthma. Ingestion may cause effects on the bone marrow, heart and thyroid. ANIMAL STUDIES: After four daily injections of 0.03 g cobalt nitrate, the pancreas of guinea pigs showed an increase in number of endocrine islands. The majority of alpha cells were degranulated with nuclei surrounded by a colorless cytoplasm. When animals were allowed to recover after the last injection, islands returned to normal. Cobalt nitrate given to rats sc twice over 24 hr period increased erythropoietic activity of the serum by greater than 3-fold, decreased renal blood flow by 18%, and disrupted metabolism in kidney. Rats exposed to 6.44 mg cobalt/kg/day as cobalt nitrate in the drinking water showed an increased sensitivity and decreased maximal response to a cholinergic agonist.
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) Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (A2450, L1613)
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)
毒理性
致癌性证据
A3：已确认的动物致癌物，对人类的相关性未知。/钴和钴的无机化合物/
A3: Confirmed animal carcinogen with unknown relevance to humans. /Cobalt and inorganic compounds, as Co/
Cobalt and cobalt compounds that release cobalt ions in vivo are reasonably anticipated to be human carcinogens based on sufficient evidence of carcinogenicity from studies in experimental animals and supporting data from studies on mechanisms of carcinogenesis. /Cobalt and cobalt compounds/
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
该物质可以通过吸入其气溶胶和通过吞食被吸收进人体。
The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.
The lung retention and respiratory clearance pathway of inhaled cobalt-nitrate (CN) and cobalt-oxide (CO) aerosols labelled with cobalt-57 (Co-57) were investigated in male beagle-dogs. A gamma camera was used to measure lung retention, while lung clearance was assessed by blood and excretion analysis. Physically and chemically uniform Co-57 particles were retained similarly in the lungs, although the retention of CO particles in the 0.3 to 2.7 micron range was greatly dependent on their physicochemical properties. /In dogs/ The primary clearance pathway was dissolution of the inhaled particles. The rate of dissolution was inversely proportional to the diameter of the /cobalt nitrate or oxide/ particle; depending on particle size, particle dissolution half time ranged from 6 to 80 days. After inhalation, most of the Co-57 was identified in the lungs, followed by muscles, bone, and skin. Less than 10 percent of the initial lung burden was present in the lungs of dogs long term, with a biological half life of 400 days. Dogs exposed to CN retained 90 percent of the body burden in the lung as late as 1050 and 1500 days after exposure, while the other dogs retained only 50 to 70 percent of the body burden in the lungs at 350 and 500 days after exposure. The presence of high concentrations of Co-57 in the trachea and upper respiratory tract at the time of death of the animals confirmed the long term retention of cobalt in some tissues.
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
在大鼠心内注射硝酸钴后，药物在肝脏积累（剂量的29%，肾脏10%，肠道4.6%）。
... Accumulation was found in the liver (29% of dose, 10% kidneys, and 4.6% in the intestines) were found following intracardiac injection of cobalt nitrate in rats.
Following intravenous injection of cobalt nitrate (with a 57Co tracer) in various species of animals, most of the injected dose was excreted in the urine; about 80% of the given dose was excreted in the urine within 21 days.
A process for preparing an improved cobalt oxide catalyst for ammonia oxidation comprising decomposing a cobalt compound such as basic cobalt carbonate by heating to form cobalt oxide, then saturating the cobalt oxide with cobalt nitrate solution and reheating to give an active, durable cobalt oxide catalyst. In ammonia oxidation processes, the durable catalyst of this invention has a long catalyst life and gives improved conversion of ammonia to nitric oxide. Additionally, the catalyst of this invention is capable of performing at higher operating rates than known catalysts. Optimum yields are obtained when the catalyst is prepared from compounds derived from electrolytic grade cobalt.
Selective recovery of aluminium, cobalt and platinum values from a spent catalyst composition
申请人：——
公开号：US20040219082A1
公开（公告）日：2004-11-04
The invention provides a process for the selective recovery of aluminium, cobalt and platinum, and compounds thereof, from a catalyst composition including aluminium, cobalt and platinum, said proscess including the steps of treating the catalyst composition to selectively get ions of substantially only one of the aluminium. cobalt and platinum into solution, recovering, in separate process steps, the thus treated aluminium, cobalt, or platinum in salt or metal form, and repeating the treating and recovering steps for each of the aluminium, cobalt and platinum. The treating steps may include process steps such as leaching, washing, dissolving, stripping, and the like. The recovery steps may include filtration, precipitation, separation, flocculation, and the like.
Process for preparing rare earth containing hard alloy
申请人：General Research Institute For Non-Ferrous Metals
公开号：US05248328A1
公开（公告）日：1993-09-28
This invention discloses a process for preparing rare earth containing hard alloy, comprising preparing metal carbide powder containing rare earth metals or cobalt powder containing rare earth metals by using wet coprecipitating method; according to the composition of alloy, at least one kind of the metal carbide powder containing rare earth metal and cobalt powder containing rare metals being mixed homogeneously with other raw materials, shaping and finally sintering under high temperature. The process of the invention is simple technologically. The properties of the products produced by the process of the invention are good, stable and repeatable.
Process for the production of metal carboxylates and their use for the
申请人：Bayer Aktiengesellschaft
公开号：US05220045A1
公开（公告）日：1993-06-15
Metal carboxylates which may be used for the polymerization of monomers suitable for Ziegler-Natta polymerization are prepared by reaction of the organic C.sub.2-20 carboxylic acids on which the carboxylates are based with ammonia and/or amines and/or tetraalkyl ammonium hydroxides and the corresponding metal nitrates in the presence of inert organic solvents at temperatures of 0.degree. to 150.degree. C.
Silver/transition metal catalysts are made by calcining the polysilver salt of a polycarboxylic acid and at least one transition metal salt of an organic polycarboxylic acid at temperatures from 200.degree.-500.degree. C., and oxidizing the said calcined salts with oxygen at temperatures from 20.degree.-500.degree. C.
