Cobalt chloride (CoCl2)

129.83900

128.87100

231-589-4

0783

51149

Pale-blue hygroscopic leaflets; colorless in very thin layers|Blue hexagonal leaflets

2827393000

0

1.37900

Cobalt chloride is a pink to red solid with a slight sharp odor. Sinks and mixes with water. Pale blue leaflets, turns pink upon exposure to moist air.

3.36 g/cm³ @ Temp: 25 °C

735 °C

1049 °C

500ºC

Solubility in water, g/100ml at 20°C: 53 (good)

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/

33900mmHg at 25°C

LD50 in mice, rats (mg/kg): 360.0, 171.0 orally; 92.6, 36.9 i.p.; 23.3, 4.3 i.v. (Singh, Junnarkar)

Slight sharp odor

A 0.2 molar aqueous solution has a pH of 4.6

Decomposes at 400 °C on long heating in air; sublimes at 500 °C in HCl gas forming iridescent, fluffy, colorless crystals; turns pink on exposure to moist air|Cobaltous chloride hydrolyzes in aqueous solution to extent of 0.11% at 0.062 molar and 0.17% at 0.031 molar.|Mol wt: 237.93; red monoclinic crystals; density: 1.924 at 25 °C/25 °C; MP: 86 °C (loses 6H2O); soluble in alcohol (blue color); solubl in acetone /Cobaltous chloride hexahydrate/|Monoclinic crystals; pink to red, slightly deliquescent, monoclinic, prismatic crystals; melting point 87 °C; density: 1.924 at 20 °C; soluble in water, alcohols, acetone, ether, glycerol; pH of 0.2 molar aqueous solution: 4.6; the aqueous solution is pink to red, but turns blue when heated or when HCl or H2SO4 is added /Cobalt(II) chloride hexahydrate/|On heating loses 4H2O at 52-56 °Forming the dihydrate, violet or blue crystals, specific gravity at 25 °C referred to water at 25 °C: 2.477; stable unless exposed directly to moisture; loses another water by 100 °C giving the monohydrate; violet, hygroscopic, amorphous solid or needles; remaining water lost at 120-140 °C /Cobalt(II) chloride hexahydrate/|Ruby red crystals /Cobaltous cloride hexahydrate/|Heat of solution: 22 BTU/lb = 12 cal/g = 0.50X10+5 J/kg|Heat of fusion: 56.9 cal/g|For more Other Experimental Properties (Complete) data for Cobaltous chloride (8 total), please visit the HSDB record page.

III

UN 2923 8/PG 3

2

R22; R42/43; R49; R50/53

S22-S45-S53-S60-S61

GF9800000

T; N

Dry. Separated from oxidants and food and feedstuffs. Store in an area without drain or sewer access. Provision to contain effluent from fire extinguishing.

hygroscopic

P201-P261-P273-P280-P284

H302-H317-H318-H334-H341-H350i-H360F-H410

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).

Incompatible materials: Oxidizing agents, alkali metals.|Mixtures of potassium with metal halides are sensitive to mechanical shock, and the ensuing explosions have been graded. Very violent explosions occurred with ... cobalt(II) chloride ... .|Sodium dispersions will reduce many metal halides exothermically. ... Cobalt chloride ... /requires/ higher temp to initiate the reaction, the exotherm with cobalt chloride incr the temp from 325 to 375 °C and causing evaporation of most of the dispersing oil. ... Very violent explosions occurred with ... cobalt(II) chloride ... .|A very violent explosion results when a mixture of sodium and ... /cobaltous chloride/ is struck with a hammer ... .

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.

Not combustible. Gives off irritating or toxic fumes (or gases) in a fire.

|Danger|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P261, P264, P270, P272, P273, P280, P281, P285, P301+P312, P302+P352, P304+P341, P308+P313, P321, P330, P333+P313, P342+P311, P363, P391, P405, and P501|H302 (98.26%): Harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P260, P261, P264, P270, P272, P273, P280, P281, P285, P301+P312, P302+P352, P304+P341, P305+P351+P338, P308+P313, P310, P314, P321, P330, P333+P313, P342+P311, P363, P391, P405, and P501|Aggregated GHS information provided by 230 companies from 25 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|P201, P202, P261, P264, P270, P272, P273, P280, P281, P285, P301+P312, P302+P352, P304+P341, P305+P351+P338, P308+P313, P310, P321, P330, P333+P313, P342+P311, P363, P391, P405, and P501|H301: Toxic if swallowed [Danger Acute toxicity, oral]|P201, P202, P260, P261, P264, P270, P271, P272, P273, P280, P281, P285, P301+P310, P302+P352, P304+P340, P304+P341, P305+P351+P338, P307+P311, P308+P313, P312, P314, P321, P330, P332+P313, P333+P313, P337+P313, P342+P311, P362, P363, P391, P403+P233, P405, and P501|P201, P202, P260, P261, P264, P270, P272, P280, P281, P285, P301+P312, P302+P352, P304+P341, P307+P311, P308+P313, P314, P321, P330, P333+P313, P342+P311, P363, P405, and P501|Warning|H401: Toxic to aquatic life [Hazardous to the aquatic environment, acute hazard]|P273, P391, and P501

Eye/face protection: Face shield and safety glasses. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).|Skin protection: Handle with gloves.|Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.|Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Reacts violently with alkali metals such as potassium or sodium causing fire and explosion hazard.

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.

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: 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.

The substance irritates the eyes, the skin and the respiratory tract. Inhalation of aerosol may cause asthmatic reactions.

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.

Dry. Separated from oxidants and food and feedstuffs. Store in an area without drain or sewer access. Provision to contain effluent from fire extinguishing.

A harmful concentration of airborne particles can be reached quickly when dispersed.

The substance is irritating to the eyes.

Repeated or prolonged contact may cause skin sensitization. Repeated or prolonged inhalation may cause asthma. Ingestion may cause effects on the heart, bone marrow and thyroid. This substance is possibly carcinogenic to humans. Animal tests show that this substance possibly causes toxic effects upon human reproduction.

PREVENT DISPERSION OF DUST! AVOID ALL CONTACT!

Use local exhaust or breathing protection.

Protective gloves. Protective clothing.

Wear safety goggles or eye protection in combination with breathing protection.

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.

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.

... 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.

LD50 Guinea pig oral 55 mg/kg|LD50 Mouse ip 49 mg/kg|LD50 Mouse oral 80 mg/kg|LD50 Rat iv 20 mg/kg|For more Non-Human Toxicity Values (Complete) data for Cobaltous chloride (6 total), please visit the HSDB record page.

/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.|/PLANTS/ Phytotoxicity tests were performed to set ecological soil screening levels for cobalt (Co) and nickel (Ni) following the American Society for Testing and Materials international E1963-98 Standard Guide for Conducting Terrestrial Plant Toxicity Tests. Two soils (a modified artificial soil mixed with 5% organic matter, pH 5.01, and a native riverine sandy soil with 0.1% organic matter, pH 6.3) were treated with cobalt(II) chloride or nickel chloride and allowed to age for four weeks before initiating tests. Alfalfa, barley, radish, perennial rye, and brassica were used to determine the appropriate range of concentrations and to select the most sensitive plant species for definitive tests. The tests were designed to have one to three test concentrations below the 20% effects concentration (EC20), and five to six test concentrations above the EC20. Definitive tests for each chemical used two soil matrices, three plant species, and replicates at 10 nominal concentrations, including negative control. Soil chemical concentrations were determined before planting and on completion of the phytotoxicity tests. Threshold responses interpreted as the EC20 for each species endpoint were calculated from regression analyses. The geometric mean of the EC20 values (excluding emergence, mortality, and nodule numbers) for each species resulted in values of 30.6 mg/kg for Co and 27.9 mg/kg for Ni.|/PLANTS/ We used the anaphase-telophase chromosome aberration and comet (Single Cell Gel Electrophoresis, SCGE) assays to evaluate the genotoxic effects of copper sulfate (CS) and cobalt chloride (CC) chemicals prepared in two concentrations (EC(50), 2xEC(50)), using methyl methanesulfonate (MMS) as a positive control and untreated cells as a negative control. In Allium root growth inhibition test, EC(50) values for CS and CC are 1.5 and 5.5 ppm, respectively. Mitotic index (MI) decreased in all concentrations tested of CS and CC compared to the control at each exposure time. The bridge, stickiness, vagrant chromosomes, fragments, c-anaphase and multipolarity chromosome aberrations were observed in anaphase-telophase cells. The total chromosome aberrations were more frequent with an increasing in the exposure time and the concentrations of both chemicals. The genotoxicity of CS and CC in Allium cepa root cells was analyzed using a mild alkaline comet assay at pH 12.3, which allows the detection of single strand breaks. In all the concentrations, CS and CC induced a significant increase (P<0.05) in DNA damage. No significant difference was found between positive control (300+/-5.81) and 3 ppm CS (280+/-4.61). The methods used are applicable for biological monitoring of environmental pollutants.

Prospective studies of blood cobalt concentrations in maintenance hemodialysis patients and normal subjects after the administration of cobaltous chloride were carried out. It was found that prolonged elevation of blood cobalt concentrations occurred in both normal and maintenance hemodialysis patients, but that the blood cobalt concentrations were much higher in the dialysis patients.|Among 853 patch tested hard metal workers in Sweden, 39 (4.6%; 9 males and 30 females) had a confirmed allergic reaction to 1% cobalt chloride.|... Some of beer drinking patients /were studied/ and reported typical signs of heart failure with shortness of breath, ankle edema, and in some cases, cyanosis and ECG changes /were observed/. ... /Cobaltous sulfate or cobaltous chloride/|The aim of the present study was to investigate the prevalence of contact sensitization in older patients (older than 65 years) referred to an allergologic clinic. All patients were patch-tested with the standard series of the Societe Italiana di Dermatologia Allergologica, Professionale e Ambientale, and 32 patients were also tested with additional series. Of 117 examined subjects, 48 (41%) developed at least one positive reaction whereas 22 of 117 (19%) showed more than one sensitization. Allergic contact dermatitis was detected in 13% of our sample. The five most frequent allergens were nickel sulfate (13.7%), potassium dichromate (11.1%), cobalt chloride (7.7%), para-phenylenediamine (5.2%), and balsam of Peru (4.3%). These findings suggest an age-dependent decline of overall positive patch-test reactions but a higher sensitization rate to some allergens.

Cobaltous chloride's production and use in inks, dyes and paints, in hygrometers and humidity indicators, in electroplating, in the preparation of catalysts and cobalt compounds and as an absorbent for military poison gas and ammonia in gas masks(1,2) may result in its release to the environment through various waste streams(SRC). Cobalt compounds, such as the chloride, are added in very small amounts to livestock feeds, salt licks, and fertilizers in many parts of the world where a cobalt deficiency exists in the soil and natural vegetation(3), and these uses may result in the direct release of cobaltous chloride to the environment(SRC). Cobaltous chloride was formerly used (1960s) as a foam stabilizer in beer(4), but this use no longer permitted(5). Cobaltous chloride has recently (post-2010) been identified as a blood doping agent in racehorses(6) that may release the compound to the environment through urine and feces.

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).

Food Chain Concentration Potential: Microorganisms concentrate the cobalt (from cobaltous chloride) in water up to 200 to 1000 times(1).

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).

According to the 2012 TSCA Inventory Update Reporting data, 3 reporting facilities estimate the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of cobaltous chloride in the United States may be as low as <10 workers and as high as 10-24 workers per plant; the data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).|NIOSH (NOES Survey 1981-1983) has statistically estimated that 9,392 workers (4,192 of these are female) are potentially exposed to cobaltous chloride in the US(1). Occupational exposure to cobaltous chloride may occur through inhalation of dust and dermal contact with this compound at workplaces where cobaltous chloride is produced or used(SRC). Use data indicate that the general population may be exposed to cobaltous chloride via dermal contact with consumer products containing cobaltous chloride(SRC). Cobaltous chloride is used in dermatologist skin patch-tests to test for allergic contact dermatitis(2).

Upon autopsy ... hearts of /beer-drinking/ victims were shown to have about 10 times the cobalt concentration of controls, 0.5 mg/kg wet wt and 0.04 mg/kg wet wt, respectively.

/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Cobaltous chloride is included in the database.|The following drug products were withdrawn or removed from the market because such drug products or components of such drug products were found to be unsafe or not effective. The following drug products may not be compounded under the exemptions provided by section 503A(a) of the Federal, Food, Drug, and Cosmetic: Cobalt. All drug products containing cobalt salts (except radioactive forms and its salts and cobalamin and its derivatives.|MEDICATION: Hematinic.|MEDICATION (VET): Nutritional factor. Used in cobalt deficiency in ruminants.|For more Therapeutic Uses (Complete) data for Cobaltous chloride (9 total), please visit the HSDB record page.

The goitrogenic effect has been elicited by the oral administration of 3-4 mg/kg to children in the course of treatment of sickle cell anemia. Toxicity resulting from overzealous therapeutic administration has been reported to produce vomiting, diarrhea, and a sensation of warmth. IV administration leads to flushing of the face, increased blood pressure, slowed respiration, giddiness, tinnitus, and deafness due to nerve damage.|Cardiomyopathy in 17 yr old girl on maintenance hemodialysis, who had been given cobalt chloride 25 mg twice daily for about 9 months.|... Great enlargement of thyroid with all symptoms of myxedema /occurred/ in a child of 17 mo who had received over period of 2 wk daily dose of iron-cobalt preparation representing 4 mg/kg of cobalt chloride. A marked drop in (131)-iodine uptake after a wk (approaching nil after 2 wk) of dosage of 150 mg/day of cobaltous chloride was observed ... This toxic effect is not invariable in patients receiving cobalt therapy; several observers have failed to find any adverse clinical effect on thyroid activity ... .|... Optic atrophy has been reported in a case in which a patient was treated with cobalt chloride for pancytopenia.|For more Drug Warnings (Complete) data for Cobaltous chloride (6 total), please visit the HSDB record page.

Agents that reduce the frequency or rate of spontaneous or induced mutations independently of the mechanism involved. (See all compounds classified as Antimutagenic Agents.)

... gastrointestinal absorption of cobalt chloride given to rats is estimated to be about 30%.|When radioactive (60)cobalt as cobaltous chloride was given orally to humans, the avg absorption was calculated at 5-44%, with these figures being based on the amt of unabsorbed cobalt remaining in the feces. Based on 24 hr urinary excretion figures of perorally given (60)cobalt absorption has been estimated to be on avg 18%, individual values ranging from 9% to 42%. Absorption and/or excretion is influenced by the amt of cobalt given and by nutritional factors.|Twelve to 36 hr after the admin of a small dose of radioactive cobalt chloride to pregnant mice ... the highest activity of radioactive cobalt /was found/ in liver, kidney, fetus, and placenta.|... One week after /rats/ ... had received ten daily sc injections of cobalt chloride (40 mg/kg) and ... the highest amt of cobalt /was found/ in the liver, which on avg contained 11% of the admin dose.|For more Absorption, Distribution and Excretion (Complete) data for Cobaltous chloride (22 total), please visit the HSDB record page.

Following a single oral dose /of cobalt chloride/, the blood cobalt concentration-time curve /in male fischer 344 rats/ was triphasic, peaked at 3.2 hr, and had an absorptive half-life of 0.9 hr, an elimination phase half-life of 3.9 hr, and a terminal elimination half-life of 22.9 hr. ... Following intravenous administration, 10.1% of the dose was excreted in the feces, indicating that cobalt can be secreted in the bile. Following a single intravenous injection, the concentration-time curve displayed three segments. The first segment, which occurred during the first 4 hr, had a rapid half-life of 1.3 hr. The second phase, from 4 to 12 hr, demonstrated a slower clearance rate with a half-life of 4.3 hr. The final and slowest phase, from 12 to 36 hr, had a half-life of 19 hr.|The retention of (60)CoCl2 (cobaltous chloride) given iv has been studied by total body counting for periods of up to 1000 days. Following a rapid initial clearance within days of about 90% of a given dose, 10% was eliminated with a biological half-time of about 2 yr. /(60)Cobaltous chloride/

The induction of polyploidy is considered the reproductive end of cells, but there is evidence that polyploid giant cancer cells (PGCCs) contribute to cell repopulation during tumor relapse. However, the role of these cells in the development, progression and response to therapy in colon cancer remains undefined. Therefore, the main objective of this study was to investigate the generation of PGCCs in colon cancer cells and identify mechanisms of formation. Treatment of HCT-116 and Caco-2 colon cancer cells with the hypoxia mimic CoCl2 induced the formation of cells with larger cell and nuclear size (PGCCs), while the cells with normal morphology were selectively eliminated. Cytometric analysis showed that CoCl2 treatment induced G2 cell cycle arrest and the generation of a polyploid cell subpopulation with increased cellular DNA content. Polyploidy of hypoxia-induced PGCCs was confirmed by FISH analysis. Furthermore, CoCl2 treatment effectively induced the stabilization of HIF-1a, the differential expression of a truncated form of p53 (p47) and decreased levels of cyclin D1, indicating molecular mechanisms associated with cell cycle arrest at G2. Generation of PGCCs also contributed to expansion of a cell subpopulation with cancer stem cells (CSCs) characteristics, as indicated by colonosphere formation assays, and enhanced chemoresistance to 5-fluorouracil and oxaliplatin. In conclusion, the pharmacological induction of hypoxia in colon cancer cells causes the formation of PGCCs, the expansion of a cell subpopulation with CSC characteristics and chemoresistance. The molecular mechanisms involved, including the stabilization of HIF-1 a, the involvement of p53/p47 isoform and cell cycle arrest at G2, suggest novel targets to prevent tumor relapse and treatment failure in colon cancer.

Fresh air, rest. Refer for medical attention.

Remove contaminated clothes. Rinse skin with plenty of water or shower.

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

/SRP:/ Immediate First Aid: Ensure that adequate decontamination has been carried out as needed. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (Head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Cobalt and Related Compounds/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Cobalt and Related Compounds/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in respiratory arrest. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W TKO (to keep open). Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Cobalt and Related Compounds/

/HUMAN EXPOSURE STUDIES/ 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.|/HUMAN EXPOSURE STUDIES/ Cobalt /can/ apparently prolong the time needed for blood clot formation. Significant changes in blood clotting time (35% increase), thromboplastic activity (28% decrease), and clot retention time (20% increase) in 15 persons administered cobalt orally as a solution of cobaltous chloride at 1 mg a day for 3 days was reported.|/HUMAN EXPOSURE STUDIES/ Chronic administration of cobaltous chloride has produced a goiter, reduced thyroid activity & lowered synthesis rates and levels of cytochrome p450 in liver.|/HUMAN EXPOSURE STUDIES/ Cobalt is a strong skin sensitizer (grade 5 of 5 in the guinea-pig maximization test) that is used in various industrial and consumer applications. To prevent sensitization to cobalt and elicitation of allergic cobalt dermatitis, information about the elicitation threshold level of cobalt is important. /The study objective was/ to identify the dermatitis elicitation threshold levels in cobalt-allergic individuals. Published patch test dose-response studies were reviewed to determine the elicitation dose (ED) levels in dermatitis patients with a previous positive patch test reaction to cobalt. A logistic dose-response model was applied to data collected from the published literature to estimate ED values. The 95% confidence interval (CI) for the ratio of mean doses that can elicit a reaction in 10% (ED(10)) of a population was calculated with Fieller's method. On the basis of five included studies, the ED10 values of aqueous cobalt chloride ranged between 0.0663 and 1.95 ug cobalt/sq cm, corresponding to 30.8-259 ppm. Our analysis provides an overview of the doses of cobalt that are required to elicit allergic cobalt contactdermatitis in sensitized individuals, and thereby the basis for future prevention of cobalt allergy.|For more Human Toxicity Excerpts (Complete) data for Cobaltous chloride (30 total), please visit the HSDB record page.

cobalt chloride

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

Cough. Shortness of breath. Wheezing.

Redness. Pain.

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

Miscellaneous manufacturing|Cobalt chloride (CoCl2): ACTIVE