Cobalt chloride (cocl2)

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

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

H334: May cause allergy or asthma symptoms or breathing difficulties if inhaled [Danger Sensitization, respiratory]

H341: Suspected of causing genetic defects [Warning Germ cell mutagenicity]

H350i: May cause cancer by inhalation [Danger Carcinogenicity]

H360F ***: May damage fertility [Danger Reproductive toxicity]

H400: Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410: Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

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)

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

H317 (100%): May cause an allergic skin reaction [Warning Sensitization, Skin]

H318 (60.9%): Causes serious eye damage [Danger Serious eye damage/eye irritation]

H334 (100%): May cause allergy or asthma symptoms or breathing difficulties if inhaled [Danger Sensitization, respiratory]

H341 (99.5%): Suspected of causing genetic defects [Warning Germ cell mutagenicity]

H350 (48.4%): May cause cancer [Danger Carcinogenicity]

H350i (51.3%): May cause cancer by inhalation [Danger Carcinogenicity]

H360 (54.3%): May damage fertility or the unborn child [Danger Reproductive toxicity]

H360Fd (41%): May damage fertility; Suspected of damaging the unborn child [Danger Reproductive toxicity]

H400 (99.2%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410 (91.5%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

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)

Aggregated GHS information provided per 376 reports by companies from 31 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

H350: May cause cancer [Danger Carcinogenicity]

P203, P280, P318, P405, and P501 (click each P-code to see the statement)

H351: Suspected of causing cancer [Warning Carcinogenicity]

H361: Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

H370: Causes damage to organs [Danger Specific target organ toxicity, single exposure]

H372: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

H373: May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]

P203, P233, P260, P261, P264, P270, P271, P272, P280, P284, P301+P317, P302+P352, P304+P340, P308+P316, P318, P319, P321, P330, P333+P317, P342+P316, P362+P364, P403, P405, and P501 (click each P-code to see the statement)

H318: Causes serious eye damage [Danger Serious eye damage/eye irritation]

H360F: May damage fertility [Danger Reproductive toxicity]

P203, P233, P260, P261, P264, P264+P265, P270, P271, P272, P273, P280, P284, P301+P317, P302+P352, P304+P340, P305+P354+P338, P317, P318, P319, P321, P330, P333+P317, P342+P316, P362+P364, P391, P403, P405, and P501 (click each P-code to see the statement)

H360: May damage fertility or the unborn child [Danger Reproductive toxicity]

INHALATION: move victim to fresh air; if breathing has stopped, begin artificial respiration and call a doctor.

INGESTION: give large amount of water; induce vomiting.

EYES: flush with water at least 15 min.; consult physician if irritation persists.

SKIN: flush with water. (USCG, 1999)

Excerpt from ERG Guide 151 [Substances - Toxic (Non-Combustible)]:

SMALL FIRE: Dry chemical, CO2 or water spray.

LARGE FIRE: Water spray, fog or regular foam. If it can be done safely, move undamaged containers away from the area around the fire. Dike runoff from fire control for later disposal. Avoid aiming straight or solid streams directly onto the product.

FIRE INVOLVING TANKS, RAIL TANK CARS OR HIGHWAY TANKS: Fight fire from maximum distance or use unmanned master stream devices or monitor nozzles. Do not get water inside containers. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks in direct contact with flames. For massive fire, use unmanned master stream devices or monitor nozzles; if this is impossible, withdraw from area and let fire burn. (ERG, 2024)

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.

Excerpt from ERG Guide 151 [Substances - Toxic (Non-Combustible)]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.

SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary.

FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2024)

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.

Excerpt from ERG Guide 151 [Substances - Toxic (Non-Combustible)]:

Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Cover with plastic sheet to prevent spreading. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS. For solids, prevent dust cloud and avoid inhalation of dust. (ERG, 2024)

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.

Store in airtight containers. /Hexahydrate/

Biological Exposure Indices (BEI) [ACGIH] - Cobalt in urine = 15 ug/L; sample at end of shift at end of workweek;

0.060 [mg/m3]

2.6 [mg/m3]

16 [mg/m3]

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/

Chronic Inhalation: 0.0001 mg/m3 (L134)

Intermediate Oral: 0.01 mg/kg/day (L134)

Rubber gloves; side-shield goggles; Bu. of Mines respirator; protective clothing (USCG, 1999)

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).

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.

Pale-blue hygroscopic solid; Turns pink in moist air; [Merck Index] Blue granules with a chlorine-like smell and soluble in water; [MSDSonline]

Pale-blue hygroscopic leaflets; colorless in very thin layers

Blue hexagonal leaflets

Slight sharp odor

1049 °C @760 [mm Hg]

187 °F (USCG, 1999)

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.

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

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

75 [mm Hg] @818 °C

Stable under recommended storage conditions.

Dec 400 °C on long heating in air.

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

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.

dielectric constant

crystal structure

enthalpy

electrode potential

molar conductivity

Gibbs energy

spin-spin coupling constant

positional coordinate

temperature-composition section

Hygroscopic. Soluble in water.

Salts, Acidic

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].

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 ... .

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)

... There is limited evidence for the carcinogenicity of cobalt(II) chloride in experimental animals. ... Overall Evaluation: Cobalt and cobalt compounds are possibly carcinogenic to humans (Group 2B). /Cobalt and cobalt compounds/

There is inadequate evidence for the carcinogenicity of cobalt and cobalt compounds in humans. There is sufficient evidence for the carcinogenicity of cobalt metal powder in experimental animals. There is limited evidence for the carcinogenicity of metal alloys containing cobalt, chromium and molybdenum in experimental animals. ... Overall Evaluation: Cobalt and cobalt compounds are possibly carcinogenic to humans (Group 2B). /Cobalt and cobalt compounds/

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

Cobalt and cobalt compounds that release cobalt ions in vivo are reasonably anticipated to be human carcinogens based on sufficient evidence of carcinogenicity from studies in experimental animals and supporting data from studies on mechanisms of carcinogenesis. /Cobalt and cobalt compounds/

2B, possibly carcinogenic to humans. (L135)

Exposure to high amount of cobalt can cause heart, lung, kidney, and liver damage. Skin contact is known to result in contact dermatitis. Cobalt may also have mutagenic and carcinogenic effects. (L29, L30)

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

Cobalt inhalation can cause asthma-like breathing problems. Skin contact is known to result in contact dermatitis, which is characterized by irritation and rashes. Ingesting large amounts of cobalt may cause nausea and vomiting. (L2090)

Skin Sensitizer - An agent that can induce an allergic reaction in the skin.

Asthma - Reversible bronchoconstriction (narrowing of bronchioles) initiated by the inhalation of irritating or allergenic agents.

IARC Carcinogen - Class 2: International Agency for Research on Cancer classifies chemicals as probable (2a), or possible (2b) human carcinogens.

LD50: 80 mg/kg (Oral, Rat) (T14)

LD50: 17 mg (Intraperitoneal, Rat) (T14)

LD50: 20 mg/kg (Intravenous, Rat) (T14)

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.

Treatment of cobalt poisoning is symptomatic. (L29)

... 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.

/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.

/LABORATORY ANIMALS: Acute Exposure/ Acute intravesical instillation of cobalt /chloride/ ion solution into the rat bladder initiated a hypoxia response accompanied by increased bladder angiogenesis and growth. This finding supports the idea that hypoxia is a stimulus for bladder growth subsequent to partial bladder outlet obstruction.

/LABORATORY ANIMALS: Acute Exposure/ Guinea pigs sensitized to cobalt by repeated dermal application and then exposed to 2.4 mg cobalt/cu m as cobalt chloride showed pulmonary inflammatory changes (altered BAL fluid recovery, increased neutrophils and eosinophils following BAL) that were different than those in exposed animals not sensitized to cobalt.[

/LABORATORY ANIMALS: Acute Exposure/ In Sprague-Dawley rats, death has been reported to occur at 161 mg cobalt/kg given by gavage as cobalt chloride.[

/LABORATORY ANIMALS: Acute Exposure/ Cobalt chloride is toxic... to the cornea in rabbits when brought into direct contact with the corneal stroma after removal of the epithelium, causing dense opacity and vascularization. Systemic poisoning of rats and rabbits with cobalt chloride has induced vacuoles and slight clouding in lenses, edema of retina and degenerative changes in choroid, retina, and optic nerve.

For more Non-Human Toxicity Excerpts (Complete) data for Cobaltous chloride (42 total), please visit the HSDB record page.

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.

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.

/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.

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.

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).