Cobalt chloride (cocl2)

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

3.36 at 25 °C/4 °C

Mol wt: 165.87; violet-blue, monoclinic or triclinic crystals; density: 2.477 at 25 °C/26 °C; slightly soluble in ether /Cobaltous chloride dihydrate/

3.348 @25 °C

Pale-blue hygroscopic leaflets; colorless in very thin layers

Blue hexagonal leaflets

Soluble in water

53.420 lb/100 lb water at 70 °F

In water, 1.16 kg/L at 0 °C

Soluble in alcohols, acetone, ether, glycerol, and pyridine

For more Solubility (Complete) data for Cobaltous chloride (6 total), please visit the HSDB record page.

1049 °C

1049 °C @760 [mm Hg]

Dec 400 °C on long heating in air.

When heated to decomp it emits toxic fumes of /hydrogen chloride/

187 °F (USCG, 1999)

735 °C

737 °C

VP: 10 kPa (75 mm Hg) at 818 °C; 100 kPa (750 mm Hg) at 1048 °C

75 [mm Hg] @818 °C

Danger

H302: Harmful if swallowed [Warning Acute toxicity, oral]

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

Danger

H302 (98.4%): Harmful if swallowed [Warning Acute toxicity, oral]

P203, 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, P391, P403, P405, and P501 (click each P-code to see the statement)

Chemical: Cobalt chloride (CoCl2)

Hazard Traits - Carcinogenicity; Reproductive Toxicity; Respiratory Toxicity

Cobalt chloride (CoCl2) is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Cobalt chloride (CoCl2) 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: 11-11-2021 https://echa.europa.eu/registration-dossier/-/registered-dossier/14346

Substance: Cobalt dichloride

Cobalt chloride: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.

An eye irritant; May cause skin sensitization and asthma after prolonged contact; [ICSC] The anhydrous form is very hygroscopic and converts into the hexahydrate form in moist air, changing color from blue to red. [Ullmann] Cobalt chloride is a potent allergen; [Kanerva, p. 506] See Cobalt.

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.

A 0.2 molar aqueous solution has a pH of 4.6. COBALT CHLORIDE acts as a weakly acidic inorganic salt, which is soluble in water. The resulting solutions contain moderate concentrations of hydrogen ions and have pH's of less than 7.0. They react as acids to neutralize bases. These neutralizations generate heat, but less or far less than is generated by neutralization of inorganic acids, inorganic oxoacids, and carboxylic acid. They usually do not react as either oxidizing agents or reducing agents but such behavior is not impossible. Many of these compounds catalyze organic reactions. Potassium or sodium metals act to reduce metal halides, producing exothermic reactions, even explosions [Bretherick, 5th Ed., 1995].

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.

Cobalt, in the form of cobaltous sulfate or cobaltous chloride, was used as a foam stabilizer in beer during the mid-1960's in various countries, including the United States. Between 1964 and 1966, American breweries reportedly added 1-1.5 ppm of cobaltous chloride to 20-25% of all beer sold in the United States. At the same time, several epidemics of a peculiar form of cardiomyopathy occurred among heavy beer drinkers in Quebec, Belgium, Omaha, Minneapolis, and New York. All patients were heavy beer drinkers. For example, the Quebec group consumed daily from 2 to more than 6 L of beer containing 0.8 to more than 1.6 ppm cobalt/L. The signs and symptoms of illness in beer drinking patients included gastrointestinal problems labored breathing, abdominal pain, cyanosis, lowered blood pressure, heart enlargement, pericardial effusion, rapid heart rate, and electrocardiographic (ECG) abnormalities. In one group, azotemia or oliguria, or both, were frequently noted, especially in fatal cases.

Unfair athletes seek ways to stimulate erythropoiesis, because the mass of hemoglobin is a critical factor in aerobic sports. Here, the potential misuse of cobalt deserves special attention. Cobalt ions (Co(2+) ) stabilize the hypoxia-inducible transcription factors (HIFs) that increase the expression of the erythropoietin (Epo) gene. Co(2+) is orally active, easy to obtain, and inexpensive. However, its intake can bear risks to health. To elaborate this issue, a review of the pertinent literature was retrieved by a search with the keywords 'anemia', 'cobalt', 'cobalt chloride', 'erythropoiesis', 'erythropoietin', 'Epo', 'side-effects' and 'treatment', amongst others. In earlier years, cobalt chloride was administered at daily doses of 25 to 300 mg for use as an anti-anemic agent. Co(2+) therapy proved effective in stimulating erythropoiesis in both non-renal and renal anemia, yet there were also serious medical adverse effects. The intake of inorganic cobalt can cause severe organ damage, concerning primarily the gastrointestinal tract, the thyroid, the heart and the sensory systems. These insights should keep athletes off taking Co(2+) to stimulate erythropoiesis.

A case of cobalt poisoning is reported in a 6-yr-old boy who ingested two-thirds of a glass of a drink with half a teaspoon of about 2.5 g of cobalt chloride crystals from a toy crystal growing set. During the morning the patient complained of abdominal pain and vomiting. The mother suspected that the boy might have swallowed some crystals, and the boy was taken to the local emergency department where the patient was given an emetic. Physical examination was normal and cardiac monitoring revealed no abnormalities. The serum contained cobalt at 7230 nmol/L (normal range is 2-17 nmol/L). Examination of the blood film confirmed neutropenia. Blood urea and electrolytes were normal.

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.

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)

/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.

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.

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.

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/

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

... 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.

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