질산,코발트염

1.54 at 68 °F (USCG, 1999) - Denser than water; will sink

2.49 g/cu cm

2.49 g/cm³

2.49 @25 °C

Pale red powder

Red crystals

Solubility: 97.929 lb/100 lb water at 70 °F /Cobaltous nitrate hexahydrate/

Water solubility: >669.6 g/L at 20 °C /Cobaltous nitrate hexahydrate/

Soluble in water

Solubility in water: soluble

Decomposes at 75 °C.

When heated to decomposition it emits toxic fumes of /nitric oxide/.

Decomposes at 100-105 °C.

100-105 °C

131 °F (USCG, 1999)

Decomposes at 100-105 °C

MP: 55-56 °C (loses three H2O at 55 °C); liquid becomes green and decomposes to the oxide above 74 °C; soluble in water 1338 g/L at 0 °C, 2170 g/L at 80 °C); soluble in acetone and most organic solvents; slightly soluble in ammonium hydroxide /Cobaltous nitrate hexahydrate/

Cobalt nitrate is an odorless red solid. Sinks and mixes with water. (USCG, 1999)

Dry Powder; Liquid; Liquid; Other Solid

Pale red solid; [Merck Index] Red crystals, soluble in water; [MSDSonline]

PALE RED POWDER.

Standard enthalpy of formation: -420.5 kJ/mol

Red deliquescent monoclinic crystals; melting point: approximately 55 °C; red liquid becomes green and decomposes to oxide above 74 °C; density 1.88 g/cu cm; very soluble in water, alcohol, and most organic solvents /Cobalt (II) nitrate hexahydrate/

Mol wt: 291.03; red, monoclinic crystals; density: 1.88 at 25 deg C; MP: 55 °C (loses 3H2O); solubility: 103.8 g/100 cc water at 25 °C; soluble in acetone and ethanol; slightly soluble in ammonia /Cobaltous nitrate hexahydrate/

Oxidizing agent; deliquescent in moist air; soluble in most organic solvents /Cobaltous nitrate hexahydrate/

155 parts by wt (of the formula wt)/100 parts by wt of water at 30 °C /Cobaltous nitrate hexahydrate/

Odorless /Cobaltous nitrate hexahydrate/

Danger

H317: May cause an allergic skin reaction [Warning Sensitization, Skin]

P203, P233, P260, P261, P271, P272, P273, P280, P284, P302+P352, P304+P340, P318, P321, P333+P317, P342+P316, P362+P364, P391, P403, P405, and P501 (click each P-code to see the statement)

Danger

H272 (54%): May intensify fire; oxidizer [Danger Oxidizing liquids; Oxidizing solids]

P203, P210, P220, P233, P260, P261, P264, P264+P265, P270, P271, P272, P273, P280, P284, P301+P317, P302+P352, P304+P340, P305+P354+P338, P317, P318, P321, P330, P333+P317, P342+P316, P362+P364, P370+P378, P391, P403, P405, and P501 (click each P-code to see the statement)

Chemical: Nitric acid, cobalt(2+) salt

Hazard Traits - Carcinogenicity; Reproductive Toxicity; Respiratory Toxicity

Nitric acid, cobalt(2+) salt (2:1) is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Nitric acid, cobalt(2+) salt (2:1) are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 23-03-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/14964

Substance: Cobalt(II) dinitrate

Nitric acid, cobalt(2+) salt: HSNO Approval: HSR001322 Approved with controls

Special Hazards of Combustion Products: Toxic oxides of nitrogen may form in fire.

Not combustible but enhances combustion of other substances. Gives off irritating or toxic fumes (or gases) in a fire. Risk of fire and explosion on contact with combustible substances.

Mixtures of metal/nonmetal nitrates with alkyl esters may explode, owing to the formation of alkyl nitrates; mixtures of a nitrate with phosphorus, tin (II) chloride or other reducing agents may react explosively [Bretherick, 1979 p. 108-109].

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Cobaltous nitrate is included on this list.

Excerpt from ERG Guide 140 [Oxidizers]:

In case of fire in the surroundings, use appropriate extinguishing media.

Fresh air, rest. Refer for medical attention.

First rinse with plenty of water for at least 15 minutes, then remove contaminated clothes and rinse again.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Give one or two glasses of water to drink. Refer for medical attention .

Not combustible but enhances combustion of other substances. Gives off irritating or toxic fumes (or gases) in a fire.

Will increase the intensity of a fire. Poisonous gases may be produced in fire.

Isolation and Evacuation: ... If tank, rail car or tank truck is involved in a fire, isolate for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.

Small fire: Use water. Do not use dry chemicals or foams. /Carbon dioxide/ or Halon may provide limited control.

Large fire: Flood fire area with water from a distance. Do not move cargo or vehicle if cargo has been exposed to heat. Move containers from fire area if you can do it without risk.

Fire involving tanks or car/trailer loads: Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. Always stay away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.

Use water spray. ...Wear goggles and self-contained breathing apparatus. Flood discharge area with water.

Isolation and Evacuation: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. Large spill: Consider initial downwind evacuation for at least 100 meters (330 feet). Fire: If tank, rail car or tank truck is involved in a fire, isolate for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.

Keep combustibles (wood, paper, oil, etc.) away from spilled material. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Do not get water inside containers.

Small dry spill: With clean shovel, place material into clean, dry container and cover loosely; move containers from spill area.

Small liquid spill: Use a non-combustible material like vermiculite or sand to soak up the product and place into a container for later disposal.

For more Cleanup Methods (Complete) data for Cobaltous nitrate (7 total), please visit the HSDB record page.

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations. Do NOT absorb in saw-dust or other combustible absorbents.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations. Do NOT absorb in saw-dust or other combustible absorbents.

Treatment of cobalt poisoning is symptomatic. Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (L1613, L29)

The median lethal dose (LD50) for subcutaneous administration of cobalt as cobalt-nitrate /to white mice/ was determined to be 34.6 mg/kg. After intraperitoneal injection of 40 mg/kg /dimercaprol/ (BAL), the LD50 of cobalt was 36.7 mg/kg. This difference was statistically significant. In cats and rabbits, the effects of cobalt on blood pressure and respiration rate are eliminated by intramuscular injection of BAL.

Exposure to high amount of cobalt can cause heart, lung, kidney, and liver damage. Skin contact is known to result in contact dermatitus. Cobalt may also have mutagenic and carcinogenic effects. Nitrate and nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (L1137, L29, L30)

ATMOSPHERIC FATE: Inorganic cobalt compounds are nonvolatile and released into the atmosphere in particulate form(1). Particulate-phase cobalt compounds are removed from the air by wet and dry deposition(SRC). Cobalt has been detected in atmospheric deposition(2) and in rain-snow precipitation(3).

The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.

Inhalation (L29) ; oral (L29) ; dermal (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)

Sore throat. Cough. Shortness of breath.

Redness.

Redness. Pain.

Abdominal pain. Nausea. Vomiting.

Cobalt inhalation can cause asthma-like breathing problems. Skin contact is known to result in contact dermatitis, which is characterized by irritation and rashes. Ingesting large amounts of cobalt may cause nausea and vomiting. Nitrate and nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (L2090, L1137, L29)

Cobaltous nitrate's production and use in the manufacture of pigments, inks, catalysts and vitamin supplements, in decorating porcelain and ceramics(1,2) and as a source for high-purity cobalt in electronics(3) may result in its release to the environment through various waste streams(SRC).[

/SIGNS AND SYMPTOMS/ 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. This substance is possibly carcinogenic to humans. ...

/SIGNS AND SYMPTOMS/ In one plant where calcination of cobalt nitrate was carried out the cobalt content of total dust in atmosphere ... was 79 mg/cu m ... no special ill effects /were found/ except for conjunctivitis & upper resp irritation ... .

/ALTERNATIVE and IN VITRO TESTS/ The authors tested the effects of known allergens, namely nickel sulfate, potassium dichromate, cobalt nitrate and cytotoxic cadmium sulfate on the proteins of cellular contacts (vinculin, talin, E-cadherin, desmoplaktin) and actin cytoskeleton (actin filaments) of cultivated human keratinocytes. The localization of proteins of cellular contacts was detected by means of direct immunofluorescence. The authors have detected a decrease in, and destruction of cellular contact proteins and actin cytoskeleton after testing the effect of all allergens, while the most significant changes were detected in E-cadherin, vunkulin and actin filaments. Desmoplaktin and talin were less damaged. Potassium dichromate caused damage already in concentration of 1 ug/mL. A similar effect of the other two tested haptanes was brought about in concentration being 100-fold higher. The gained results indicate that the investigation of cellular contact proteins and actin cytoskeleton of cultivated human keratinocytes can possibly become a part of the testing of allergy-triggering potential of chemical substances.

/ALTERNATIVE and IN VITRO TESTS/ Peripheral blood lymphocytes from 45 patients with a positive patch test to cobalt chloride (CoCl2) and 37 controls were stimulated with various concentrations of CoCl2 and/or cobalt sulfate (CoSO4) or cobalt nitrate (Co(NO3)2) or cobalt acetate [CH3COO)2Co) for various days in culture. Lymphocytes from 35 of these patients showed a significantly greater response than that of the controls. The response occurred in the T enriched population and was monocyte dependent. The strength of the in vivo serial dilution test results did not correlate well with the height of in vitro responses. Lymphocytes from 3 nickel and/or chromium sensitive patients failed to respond to stimulation with cobalt compounds thus confirming the specificity of the reaction. The DNA synthesis test seems to be a reliable in vitro method to aid in the diagnosis of cobalt sensitivity.

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Cobaltous nitrate is included on this list.

The primary clearance pathway was dissolution of the inhaled particles. The rate of dissolution was inversely proportional to the diameter of the particle; depending on particle size, particle dissolution half time ranged from 6 to 80 days. ... 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.

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)

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.

... 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.

Used in pigments, invisible inks, ceramics, catalysts; supplements, fertilizers, animal feeds, and hair dyes; [HSDB]

Farming (Feed Additives) [Category: Industry]

Ceramics making [Category: Hobbies]

Manufacture of cobalt pigments and invisible inks; decorating stoneware and porcelain; preparation of catalysts; production of vitamin B12 supplements.

Additive to soils and animal feeds, vitamin preparations, hair dyes.

Cobalt nitrate is an important source of high-purity cobalt for use in the electronics and related industries.

2023: 1,000,000 - <2,500,000 lb

Non-confidential 2012 Chemical Data Reporting (CDR) information on the production and use of chemicals manufactured or imported into the United States. Chemical: Nitric acid, cobalt(2+) salt (2:1). National Production Volume: 1,000,000 - 10,000,000 lb/yr.

ACS reagent grade

Liquid, flake grades; crystal grade; crystal and soln form, technical & reagent

Cobalt Manganese Pink: A pigment obtained by mixing a thin paste of magnesium carbonate with cobalt nitrate soln, drying, and heating.

All Other Chemical Product and Preparation Manufacturing

Nitric acid, cobalt(2+) salt (2:1): ACTIVE