Cobalt chloride (cocl2)

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

In case of fire in the surroundings: all extinguishing agents allowed.

Keep container tightly closed in a dry and well-ventilated place. ... Moisture sensitive. Handle and store under inert gas. Hygroscopic. ... Storage class (TRGS 510): Non-combustible, acute toxic Cat.3 / toxic hazardous materials or hazardous materials causing chronic effects.

Dry.

Store in airtight containers. /Hexahydrate/

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

Liquid material spills can be copiously flushed with water and channeled to a treatment system or holding tank for reclamation or proper disposal. Spills of dry material can be removed by vacuuming or wet mopping. Some spills can be removed by hosing, first with a mist of water to dampen the spilled material and then with a more forceful stream that flushes it into a holding tank or other facility for handling contaminated water. Work surfaces or contaminated clothing should never be cleaned by dry sweeping or blowing with pressurized hoses. Recovery systems used to reclaim waste metals should comply with federal, state, and local regulations. All waste materials generated in the handling of cobalt-containing substances should be disposed of in compliance with federal, state, and local regulations. /Cobalt and cobalt salts/

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.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber; Contaminated packaging: Dispose of as unused product.

Sweep spilled substance into containers; if appropriate, moisten first to prevent dusting. Carefully collect remainder, then remove to safe place. Do NOT let this chemical enter the environment. (extra personal protection: P3 filter respirator for toxic particles).

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.

Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

For more Preventive Measures (Complete) data for Cobaltous chloride (10 total), please visit the HSDB record page.

0.02 [mg/m3], as Co

8 hr Time Weighted Avg (TWA): 0.02 mg/cu m. /Cobalt and inorganic compounds, as Co/

Peak Exposure Recommendation: Transient increases in workers' exposure levels may exceed 3 times the value of the TLV-TWA level for no more than 15 minutes at a time, on no more than 4 occasions spaced 1 hour apart during a workday, and under no circumstances should they exceed 5 times the value of the TLV-TWA level. In addition, the 8-hour TWA is not to be exceeded for an 8-hour work period. /Cobalt and inorganic compounds, as Co/

A3: Confirmed animal carcinogen with unknown relevance to humans. /Cobalt and inorganic compounds, as Co/

Biological Exposure Index (BEI): Determinant: cobalt in urine; Sampling Time: end of shift at end of workweek; BEI: 15 ug/L. Notation: The determinant is nonspecific, since it is also observed after after exposure to other chemicals. /Cobalt and inorganic compounds, including cobalt oxides but not combined with tungsten carbide/

Biological Exposure Index (BEI): Determinant: cobalt in urine; Sampling Time: end of shift at end of workweek; BEI: None. Notation: The determinant is nonspecific, since it is also observed after exposure to other chemicals. Biological monitoring should be considered for this compound based on the review; however, a specific BEI could not be determined due to insufficient data. /Cobalt with tungsten carbide/

... Immortalized alveolar epithelial type II cells were incubated for 4 hr with various concentrations of either NiCl2, CoCl2, or NiCl2 and CoCl2 together, and cell viability assessed 24 hr later. The LD50 for NiCl2 was 5.7 mM. CoCl2, with an LD50 of 1.1 mM, was about five times more potent than NiCl2. Mixtures of NiCl2 and CoCl2 decreased cell viability synergistically.

Rats ... /were administered/ ... (60)Co by gavage as inorganic (60)CoCl2 or in a form incorporated into freshwater fish. Orizias latipes were placed in vessels containing 2 L of tap water with radioactive cobalt. Periodically thereafter the fish were sacrificed, homogenized, and administered to rats via a stomach tube... Rats gavaged with (60)Co incorporated into the fish retained much more (60)Co than control rats. This trend was notable in rats given fish kept in radioactive solution for longer periods. Marked differences in tissue distribution of (60)Co were also observed between rats given (60)Co incorporated into fish and control rats.

Fucosterol is a phytosterol commonly extracted from algae. It has been proved that fucosterol possesses antioxidant activity that is capable of scavenging the free radicals causing skin damages. In this study, we investigated the protective mechanisms of fucosterol on cobalt chloride (CoCl2) induced hypoxia damages to keratinocytes (HaCaT). We found that fucosterol inhibited CoCl2 induced cytotoxicity and inflammation in a dose-dependent manner. Furthermore, fucosterol attenuated CoCl2 induced excess expression of IL-6, IL-1beta and TNF-a in HaCaT cells. In addition, fucosterol surpressed the phosphorylation of PI3K and Akt and accumulation of HIF1-a simulated by CoCl2. Taken together, these results suggested that fucosterol executed its protective effects against CoCl2 induced cytotoxicity and inflammation by the inhibition of hypoxia inducible factor through PI3K/Akt pathway.

Epithelial-mesenchymal transition (EMT) occurs during adult tissue remodeling responses including carcinogenesis and fibrosis. Existing evidence reveals that hepatocytes can undergo EMT in adult liver, which is critically involved in chronic liver injury. We herein established a hypoxia-induced EMT model in human LO2 hepatocytes treated with cobalt chloride (CoCl2) in vitro, and evaluated the effects of curcumin, a natural antifibrotic compound, on hepatocyte EMT and explored the underlying molecular mechanisms. We found that CoCl2 at non-toxic doses induced a mesenchymal cell phenotype in hepatocytes and upregulated several mesenchymal markers including a-smooth muscle actin, vimentin, N-cadherin, fibronectin and Snail (an EMT-related transcription factor), but downregulated the epithelial marker E-cadherin in hepatocytes. However, curcumin reversed the morphological changes, abrogated the increased expression of mesenchymal markers, and rescued E-cadherin expression in CoCl2-treated hepatocytes, suggesting the inhibition of hepatocyte EMT in vitro. We further found that curcumin interfered with the transforming growth factor-beta (TGF-beta) signaling by reducing the expression of TGF-beta receptor I and inhibiting the expression and phosphorylation of Smad2 and Smad3. Use of SB431542, a specific inhibitor of TGF-beta receptor I, demonstrated that interference with the TGF-beta/Smad pathway was associated with curcumin suppression of hepatocyte EMT. Our in vivo data showed that curcumin affected hepatic EMT in rat fibrotic liver caused by carbon tetrachloride, which was associated with the inhibition of TGF-beta/Smad signaling.

For more Interactions (Complete) data for Cobaltous chloride (12 total), please visit the HSDB record page.

EC50; Species: Chlorella pyrenoidosa (Green Algae); Conditions: freshwater, static, 24 °C, pH 6.8; Concentration: 520 ug/L for 24 hr; Effect: population, decreased population growth rate /total Co ion/

EC50; Species: Chlorella pyrenoidosa (Green Algae); Conditions: freshwater, flow through, 24 °C, pH 6.3-6.5; Concentration: 98 ug/L for 24 hr; Effect: population, decreased population growth rate /total Co ion/

EC50; Species: Artemia salina (Brine Shrimp) 2-3 instar Nauplii; Conditions: saltwater, static, 25 °C, pH 7.8, dissolved oxygen 8.5 mg/L; Concentration: 2815000 ug/L for 24 hr (95% confidence interval: 2450000-3180000 ug/L); Effect: intoxication, immobilization /total Co ion/

LC50; Species: Daphnia pulex (water flea) adult; Conditions: freshwater, static, 25 °C, pH 8.2, hardness 142 mg/L CaCO3, dissolved oxygen 8.5-8.9 mg/L; Concentration: 9720 ug/L for 48 hr (95% confidence interval: 7940-11890 ug/L) />99% purity/

For more Ecotoxicity Values (Complete) data for Cobaltous chloride (11 total), please visit the HSDB record page.

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).

Cobaltous chloride is prohibited from direct use in food in the US(1), however, it is allowed for use in animal feeds as a supplement(2). Cobaltous chloride was formerly used (1960s) as a foam stabilizer in some beers(3), but this is no longer permitted(1). Cobaltous chloride was added to beer to stabilize the foam which otherwise might disappear if the glass contained traces of synthetic detergent(4). Cobalt levels of 1.1 to 1.2 mg/L were found in beer in Omaha, NE and 0.5 to 5.5 mg/L in Belgian beer(4).

IDENTIFICATION AND USE: Cobalt chloride is a pale-blue solid. It is used as absorbent for ammonia, gas masks, electroplating hygrometers, manufacture of vitamin B12, solid lubricant, dye mordant, fertilizer additive. It is also used formerly, as a therapeutic agent and foam stubilizer in beer. HUMAN EXPOSURE AND TOXICITY: Humans ingesting cobalt chloride for 22 days experienced polycythemia and an increase in hemoglobin. Red blood cell numbers increased over normal values. Studies have also reported cardiomyopathy in individuals who consumed large amounts of beer. Among 853 patch-tested hard metal workers in Sweden, 39 (4.6%; 9 males and 30 females) had a conformed allergic reaction to 1% cobalt chloride. Reactions to cobalt chloride have included anorexia, nausea and vomiting, diarrea, precordial pain, cardiomyopathy, flushing of the face and extremities, skin rashes, tinnitus, tempoary nerve deafness, renal injury, diffuse thyroid enlargement, and hypothyroidism. in large doses it may reduce the production of erythrocytes. ANIMAL STUDIES: Male rats exposed orally to cobalt chloride for three weeks exhibited cardiac damage. Rats exposed to cobalt chloride in drinking water exhibited increased heart weight and degenerative heart lesions. Rats exposed to cobalt chloride in drinking water exhibited lesions of the respiratory tract. Rats exposed to cobalt chloride daily for 2-3 months and mice exposed daily for 13 weeks exhibited testicular degeneration and atrophy. Rabbits exposed to cobalt chloride by inhalation for 1-4 months exhibited lesions of the alveolar region of the respiratory tract that were identified as nodular accumulation of Type II epithelial cells and interstitial inflammation. Rats exposed to cobalt chloride for 4-5 months exhibited renal injury, such as histological alteration of proximal tubules. Male mice administered a single dose of cobalt chloride exhibited a dose response increase in the percentages of chromosomal breaks and chromosomal aberrations in bone marrow cells. A single ip injection of cobalt chloride in mice caused an increase in micronucleus formation after 30 hr. Sexually mature male mice exposed to cobalt chloride in their drinking water for 12 weeks were assessed for effects on fertility by breeding these exposed males to unexposed females. Fertility was reduced and the number implantation sites significantly reduced. In the males epididymal weights were reduced and epididymal sperm count was decreased. Males also exhibited reduced testicular sperm counts and daily sperm production. The testes displayed severe abnormalities, including hypertrophy of the interstitial Leydig cells, congested blood vessels, degeneration of the spermatogonial cells and necrosis of seminiferous tubules and interstitial tissues. Oral exposure of female rats to cobalt chloride from gestation day 14 to lactation day 21 caused newborn pups to exhibit stunted growth and decreased survival. These effects occurred at exposures that also caused maternal toxicity, such as reduced body weight, reduced food consumption and altered hematological measurement. No teratogenic effects were noted. Dermal exposures on 3 consecutive days to cobalt chloride in dimethylsulfoxide caused an increase in cellular proliferation in the lymph node assay in mice, rats and Guinea pigs. ECOTOXICITY STUDIES: LC50 values of cobalt in C. carpio were 327 and 328 mg/L in two replicates, respectively. The fish were more sensitive to Co and Ni toxicity in hard water than in very hard water.

/AQUATIC SPECIES/ In this study, we investigate the toxic effects of cobalt chloride on some hematological factors of the carp Cyprinus carpio, such as white blood cell count, red blood cell count, hemoglobin, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration. At first, LC50 of cobalt in C. carpio was measured during 96 hr after exposure. Also, physicochemical parameters of water including pH, dissolved oxygen, viscosity, temperature, and conductivity were monitored, continuously. The results showed that LC50 values of cobalt in C. carpio were 327 and 328 mg/L in two replicates, respectively. Then, the changes in some hematological factors in the five treatment groups placed under concentration of 100, 200, 300, 400, and 500 mg/L cobalt were compared with the control group. Based on hematological tests conducted in this research, exposure of carp to 500- and 300-mg/L concentrations of cobalt in 48 h showed significant difference (p<0.05) in white blood cell count. The concentration of 500 mg/L cobalt in 24 hr showed a significant difference in the amount of hemoglobin, number of red blood cells, and hematocrit level as compared with the control group. The concentration of 100 mg/L cobalt in 48 hr did not show a significant difference in comparison with the control group (p>0.05). Also, the concentration of 500 mg/L cobalt in 24 hr showed a significant difference in the amount of mean corpuscular volume and mean corpuscular hemoglobin as compared with the control group and other treatments. Also, the percentage of mean corpuscular hemoglobin concentration in a concentration of 200 mg/L cobalt in 24 hr showed a significant difference as compared with the control group and other treatments.

/AQUATIC SPECIES/ /The study objective was/ to determine the effects of water hardness on the toxicities of cobalt (Co) and nickel (Ni) to a freshwater fish, Capoeta fusca. Toxicity was investigated by static bioassay. Fish were exposed to cobalt (as CoCl(2)) and nickel (as NiCl(2)) for 96 h in waters with two levels of hardness ("hard" and "very hard", nominally 130 mg/L and 350 mg/L as CaCO(3), respectively). Water hardness had a significant effect on the acute toxicity of both elements. The 96 hr LC(50) values for Co were 91.7 mg/L and 204.8 mg/L in hard and very hard waters, respectively, and for Ni the 96 hr LC(50) values were 78.0 mg/L and 127.2 mg/L, respectively. The fish were more sensitive to Co and Ni toxicity in hard water than in very hard water; very hard water protects C. fusca against the toxicity of Co and Ni.

/OTHER TERRESTRIAL SPECIES/ ... /The/ current study aimed to evaluate CoCl2 induced genotoxicity in Eisenia hortensis earthworms coelomocytes by alkaline comet assay (CA) and micronucleus (MN) test. The earthworms (n = 10 for each group) were exposed to different series of CoCl2 concentrations (100 ppm, 200 ppm, 300 ppm, 400 ppm, 500 ppm, 600 ppm) to find LD50. The LD50 for CoCl2 was found at 226 ppm. Then, doses of LD50/2, LD50 and 2XLD50 for 48 hr were used. CA and MN demonstrated the significant increase (P < 0.05) in DNA damage and chromosomal aberrations. Dose dependent relationship was found. Highest DNA damage and chromosomal aberrations were noticed at 2XLD50. The results concluded that CoCl2 induced DNA damage, cytokinesis failure and chromosomal aberrations in E. hortensis earthworms.

Trace minerals added to animal feeds. These substances added to animal feeds as nutritional dietary supplements are generally recognized as safe when added at levels consistent with good feeding practice. All substances listed may be in anhydrous or hydrated form. Cobalt chloride is included on this list.

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 chloride is included on this list.

Used in invisible inks, humidity indicators, temperature indicators, catalysts, electroplating, glass and porcelain pigments, fertilizers, feed additives, poison gas absorbents, and veterinary medication; [Merck Index] Used as a flux (magnesium refining), lubricant, and dye mordant; Also used in barometers and as a laboratory reagent; [Hawley]

Metal Preparation and Pouring [Category: Foundry]

Invisible ink; humidity and water indicator; color standard; in hygrometers; temp indicator in grinding; in electroplating; for painting on glass and porcelain; prepn of catalysts; fertilizer and feed additive; foam stabilizer in beer; as absorbent for military poison gas and ammonia; in manufacture of vitamin B12.

The fact that the anhydrous chloride is blue and the hexahydrate red is used as a humidity indicator in silica gel desiccants.

As germicide /Dihydrate & hexahydrate/

Ingredient of culture medium for vitamin B12 production with Propionibacterium freudenreichii /Hexahydrate/

2023: 947,220 lb

Non-confidential 2012 Chemical Data Reporting (CDR) information on the production and use of chemicals manufactured or imported into the United States. Chemical: Cobalt chloride. National Production Volume: Withheld.

Preparation of anhydrous from cobalt powder and Cl2. ... From the acetate and acetyl chloride ... . By dehydration of the hexahydrate with SOCl2.

By the action of hydrochloric acid on cobalt; its oxide, hydroxide, or carbonate.

ACS reagent grade /Hexahydrate/

-80 mesh, 99.9% purity grade; high purity grades; liquid, crystal grades; crystal and solution form, technical and reagent grades

Synthetic Rubber Manufacturing

Cobalt chloride (CoCl2): ACTIVE