COBALT

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.

MOLECULAR FORMULA

ERG GUIDE NUMBER

135-SUBSTANCES - SPONTANEOUSLY COMBUSTIBLE

SYNONYM REFERENCE

(HSDB , 2000; Lewis, 1996; RTECS , 2000)

USES/FORMS/SOURCES

USES

Cobalt is used in the manufacture of extremely hard steel and cutting tools (Lewis, 1998). It is also used in cemented carbide cutting tools, jet engines, as a coordination and complexing agent (Ashford, 1994; Lewis, 1997) ITI, 1994; (Lewis, 1998). Together with nickel, aluminum, copper, beryllium, chromium and molybdenum, cobalt is utilized in the electrical, automobile, aircraft and other industries (Sittig, 1991).
Cobalt is used in the manufacture of chemicals (cobalt salts); in alloys; cobalt steels for permanent magnets (in telephones, magnetic tape, microphones, speakers, computers, and motors) and for soft magnets and high-speed tool steels; in nuclear technology; and as oxidizing agent (ACGIH, 1996; (Budavari, 1996; ITI, 1995; Lewis, 1997). This metal is a constituent of stellite alloys (used for extrusion dies, turbine blades, and valve seats), of super alloys, and of magnetic cobalt-rare earth alloys (Ashford, 1994).
Cobalt is primarily used in alloys (nickel-aluminum-cobalt alloys), heat resistant alloys (gas turbines, electrical heating elements, and aircraft engines), and high-strength alloys (specialized axles, space equipment, cobalt steels (contain 40% to 65% cobalt)) (ACGIH, 1996; (Lewis, 1997; Sittig, 1991).
Cobalt has long been used for cementing tungsten (and other) carbides (ACGIH, 1996).

In these processes, cobalt is the preferred metal because it can be milled to an extremely fine powder (0.01 mcm), it supplies a liquid phase at low temperatures and can dissolve carbides, and in the liquid state, it can wet solid particles (ACGIH, 1996).

Cobalt is found in lamp filaments, as a trace element in fertilizers, and as drying agent in printer inks, paints, and varnishes (Lewis, 1997), as a binder in tungsten carbide tool manufacturing, and as a catalyst in afterburners (Sittig, 1991), and in the metal hip prosthesis used in hip arthroplasty (Steens et al, 2006).
Cobalt compounds are contained in enamels, glazes, glass, pottery and paints. They are also used in glass pottery, photography and electroplating processes (ACGIH, 1996; (Sittig, 1991).
Cobalt bombs contain cobalt-59. During the nuclear explosion, cobalt-60 is formed from cobalt-59 by neutron capture, emitting intense beta and gamma radiation (Budavari, 1996).
Cobalt chloride may be present in chemistry sets (Everson et al, 1988) and in crystal-growing sets sold in supermarkets and toy-stores (Mucklow et al, 1990).
Cobalt has been added to beer to promote the formation of foam. However, in combination with alcohol, cobalt produces severe cardiac effects, even at low concentrations (1.2 to 1.5 mg/L of beer)(Sittig, 1991).
Cobalt-60 can be encapsulated compactly. This property allowed cobalt-60 to replace radium in experimental medicine and cancer research (Budavari, 1996).
Cobalt is a trace mineral. The artificial radioactive isotope cobalt-60 is used as an antineoplastic radiation source (Budavari, 1996).
A component of vitamin B-12 (cyanocobalamin), cobalt plays an important role in animal nutrition. Vitamin B-12 is necessary for proper development of red blood cells; its absence causes pernicious anemia (ACGIH, 1996; (Budavari, 1996; Lewis, 1998). The recommended daily allowance of cobalt in the form of Vitamin B-12 is 0.13 mcg/day (Sittig, 1991).

FORMS

Cobalt is a transition metal. It exists as a hard, steel-gray to silvery-blue, magnetic, lustrous, ductile, somewhat malleable metal (Lewis, 1996; Lewis, 1997).
Cobalt is available in rondels (1 x 3/4 inch), shot, anodes, 150 and finer mesh powder (up to 99.6% purity), ductile strips (95% cobalt, 5% iron), high-purity strips (99.9% purity), and single crystals (Lewis, 1997).
Cobalt-59 is the only naturally occurring, widely distributed, isotope of cobalt. The following artificial radioactive isotopes have been described (Lewis, 1998):

Cobalt-57 (half-life of 272 days); emits medium-energy gamma rays
Cobalt-58 (half-life of 72 days); emits positrons
Cobalt-60 (half-life of 5.26 years); emits beta particles and high-energy gamma rays; used in radiation therapy and diagnosis
HSDB (2000) reports the half-lives of radioactive isotopes as:

Cobalt-56 (half-life of 78.8 days)
Cobalt-57 (half-life of 271 days)
Cobalt-58 (half-life of 70.8 days)
Cobalt-60 (half-life of 5.27 years)

At ordinary temperatures, cobalt is stable in air and toward water.
Hydrated salts of cobalt are of red color. Dissolving the soluble salts results in formation of red solutions, which turn blue when concentrated hydrochloric acid is added (Lewis, 1996).
Cobalt has exceptional magnetic properties in alloys (Lewis, 1997).

SOURCES

Cobalt is an important trace element in soil (Lewis, 1997).
Cobalt is widely distributed in nature and is found in the earth's crust in amounts of 0.001-0.002% (Budavari, 1996). Typical soil concentrations range from 1.0 ppm to 40 ppm (Dragun, 1988). In the US the average cobalt concentration in soil is 7.2 mg CO/kg (Barceloux, 1999).
In nature, cobalt is typically found in association with other metals, such as manganese, copper, nickel, and arsenic. It exists in 0, 1, 2, 3, 4, and 5 valence states (ATSDR, 1992).

Cobalt has unusual coordinating properties, especially the trivalent ion (Lewis, 1997).
Principle cobalt ores are: smaltite (CoAs2), cobaltite (CoS2.CoAs2), chloanthite, erythrite (3CoO.As2O5.8H2), and linnaeite (Co3S4) (Budavari, 1996; Lewis, 1997).

World-wide, cobalt and its oxide are mainly produced in Zaire (58% of world's supply), Belgium-Luxembourg, Norway, and Finland (Clayton & Clayton, 1994).
Cobalt can be derived through concentrating copper-cobalt sulphide ores by roasting, followed by thermal reduction using aluminum, or by electrolysis (Ashford, 1994; Lewis, 1997).
Cobalt can also be obtained by leaching with either ammonia or an acid in an autoclave under elevated temperatures and pressures, with subsequent reduction by hydrogen (Lewis, 1997).
It can also be produced via pressure leaching or reduction using nickel-copper matte or nickel matte and hydrogen (Ashford, 1994).
Cobalt is found naturally in foods, especially in fish, cocoa, bran and molasses (greater than 1 ppm), and green leafy vegetables, such as lettuce, cabbage and spinach (greater than 0.6 ppm) (Menne & Maibach, 1987; Domingo, 1989). The average daily intake of cobalt from diet ranges from 5 to 45 mcg Co/day (Barceloux, 1999).
Chronic or sub-acute cobalt toxicity may occur in children exhibiting pica behavior (repetitive ingestion of non-nutritive objects), particularly following ingestion of cobalt-containing magnets from electronic parts (Henretig & Shannon, 1998).
Cobalt is usually not detected in drinking water. When present, it is usually in the range of 0.1 to 5 mcg Co/L (Barceloux, 1999).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

USES: Cobalt is a natural element and is produced as a by-product or co-product of other metals. It is used in the manufacture of extremely hard steel and cutting tools. It is also used in the manufacture of cobalt salts and alloys, and is a component of vitamin B-12 (cyanocobalamin). Refer to the IONIZING RADIATION management for information specific to the radioactive isotopes of cobalt.

TOXICOLOGY: Cobalt depresses oxygen uptake by myocardial mitochondria and interferes with energy metabolism in a manner similarly to thiamine deficiency. Cobalt toxicity may work synergistically with excessive alcohol consumption and malnutrition.

EPIDEMIOLOGY: Cobalt exposures causing significant medical symptoms are rarely reported, but manifestations can be quite severe with the development of cardiomyopathy, blindness, and deafness.

WITH POISONING/EXPOSURE

The classic toxidrome of chronic soluble cobalt poisoning is the tetrad of goiter, polycythemia, cardiomyopathy, and metabolic acidosis. Reports of cobalt toxicity associated with the breakdown of metal hip implants have been reported. Symptoms associated from this include cardiomyopathy, pericardial effusion, optic atrophy, retinopathy, deafness, and polyneuropathy.
ORAL EXPOSURE: Side effects reported in patients taking cobalt chloride for anemia included nausea, vomiting, and diarrhea. "Beer drinker's cardiomyopathy" with frequent pericardial effusions has been described. Ingestion of cobalt can cause stimulation of the bone marrow and blood-forming components, resulting polycythemia.
INHALATIONAL EXPOSURE: Occupational inhalation exposure to metallic cobalt or cobalt alloys usually produce cough, dyspnea, wheezing, asthma, or interstitial fibrosis ('hard metal disease"). Fume exposures can cause conjunctivitis and rhinitis.
DERMAL EXPOSURE: "Cobalt itch" or "carboloy-itch", an allergic erythematous papular eruption, can occur after dermal exposures.

POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)

Fire will produce irritating, corrosive and/or toxic gases.
Inhalation of decomposition products may cause severe injury or death.
Contact with substance may cause severe burns to skin and eyes.
Runoff from fire control may cause pollution.

ACUTE CLINICAL EFFECTS

SUMMARY

TOXICOLOGY: Cobalt depresses oxygen uptake by myocardial mitochondria and interferes with energy metabolism in a manner similarly to thiamine deficiency. Cobalt toxicity may work synergistically with excessive alcohol consumption and malnutrition.
EPIDEMIOLOGY: Cobalt exposures causing significant medical symptoms are rarely reported, but manifestations can be quite severe with the development of cardiomyopathy, blindness, and deafness.
TOXICITY: The classic toxidrome of chronic soluble cobalt poisoning is the tetrad of goiter, polycythemia, cardiomyopathy, and metabolic acidosis. Reports of cobalt toxicity associated with the breakdown of metal hip implants have been reported. Symptoms associated from this include cardiomyopathy, pericardial effusion, optic atrophy, retinopathy, deafness, and polyneuropathy.
ORAL EXPOSURE: Side effects reported in patients taking cobalt chloride for anemia included nausea, vomiting, and diarrhea. "Beer drinker's cardiomyopathy" with frequent pericardial effusions has been described. Ingestion of cobalt can cause stimulation of the bone marrow and blood-forming components, resulting polycythemia.
INHALATIONAL EXPOSURE: Occupational inhalation exposure to metallic cobalt or cobalt alloys usually produce cough, dyspnea, wheezing, asthma, or interstitial fibrosis ('hard metal disease"). Fume exposures can cause conjunctivitis and rhinitis.
DERMAL EXPOSURE: "Cobalt itch" or "carboloy-itch", an allergic erythematous papular eruption, can occur after dermal exposures.

Inhalation of the metallic dust can irritate the lungs. Metallic cobalt is retained in and slowly absorbed from the lungs with an estimated half-life of 5 to 15 years (HSDB , 2001). Cobalt is not particularly toxic in acute exposure, and was formerly used as a defoaming agent in beer (causing cardiomyopathy following chronic intake -- see below under EFFECTS OF CHRONIC EXPOSURE).

In a controlled study in human volunteers, soluble COBALT CHLORIDE was absorbed to a greater extent than insoluble COBALT OXIDE (Christensen et al, 1993).

Ultrafine cobalt particles administered to rats by the inhalation route for 1 or 4 days accumulated in the lungs; the cobalt was rapidly transferred to the blood (Kyono et al, 1992). Intratracheal administration of cobalt dust to rats caused alterations in reactions to unconditioned stimuli and conditioned reflexes, suggesting a possible neurological effect (Sozieva, 1964).

The biological role of cobalt is as a cofactor for enzymes and vitamins (Clayton & Clayton, 1994).

CHRONIC CLINICAL EFFECTS

Because its half-life in the lungs is several years (HSDB , 2001), chronic inhalation exposure to metallic cobalt could produce CUMULATIVE TOXICITY.

Cobalt and its salts are potent sensitizers and can produce FATAL ANAPHYLACTIC REACTIONS WITH EXPOSURE TO AIRBORNE CONCENTRATIONS AS LOW AS 1 MG/M(3) (ACGIH, 1986). Contact dermatitis is common among persons chronically exposed to cobalt (Fischer & Rystedtd, 1983).

While this contact dermatitis is somewhat similar to that caused by nickel, the immunological profiles are slightly different (Bencko, 1986; Bencko, 1983). Skin lesions, such as eczema and erythema, occurred more frequently in persons occupationally exposed to cobalt metal dust, oxides, and salts than in a control group (Swennen et al, 1993).

Elevated levels of IgE specific for cobalt were seen in 7 cobalt workers with asthma. Atopy, positive IgE antibody against cobalt, age of 40 or older, and previous exposure to cobalt at low concentrations (=/< 50 mcg/m(3)) were all risk factors for asthma (Kasaka et al, 1996).

The major target organs for chronic cobalt inhalation exposure are the LUNGS. It can cause interstitial pneumonitis and fibrosis, and pulmonary sensitization (Hathaway et al, 1996). The following three major effects have been noted: an asthma-like condition with wheezing, cough, and shortness of breath; progressive fibrosis with deteriorating pulmonary function, which may continue to evolve even after cessation of exposure; and an obstructive airway syndrome (HSDB , 2001; Hartmann, 1982; Hathaway et al, 1996). While most cases of cobalt pneumoconiosis (HARD METAL DISEASE) have involved mixed exposures, notably to tungsten carbide as well as cobalt (Friberg et al, 1986; Ott & Mikuz, 1982), cobalt may be the responsible agent (Hartung & Valentin, 1983; ACGIH, 1996a). Hard Metal Disease has been seen in diamond polishers not exposed to tungsten carbide (Demedts, 1984).

Whether or not pure cobalt can cause Hard Metal Disease remains controversial. In one study, 82 refinery workers exposed to pure cobalt metal dust, oxides, or salts at a mean airborne concentration of 125 mcg/m(3) for an average of 8.0 years did not have signs of pulmonary fibrosis. This study suggests that exposure to both cobalt and other air pollutants is necessary for development of Hard Metal Disease (Swennen et al, 1993). Initial signs and symptoms of hard metal disease may be misleadingly mild. In one case, irreversible pulmonary failure developed in a 22-year-old tool grinder when the initial symptoms were only dry cough and exertional dyspnea (Ruokonen et al, 1996).

A Swedish study reported development of obstructive lung symptoms at average airborne cobalt exposures of 0.06 mg/m(3) (Alexandersson, 1979). Another study reported no lung disease with occupational exposure to airborne cobalt levels of 0.5 mg/m(3) (Morgan, 1983).

Parenchymal reactions induced by cobalt-containing dust usually involve the co-inhalation of other compounds, such as tungsten carbide in the case of hard metal disease. The interaction results in the generation of active oxygen species, which is responsible for the lung damage (Lison, 1996).

Cobaltous chloride was formerly used as a defoaming agent in beers. Many cases of fatal cardiomyopathy occurred in beer drinkers imbibing these products. At least one fatal case of cardiomyopathy has been reported from industrial exposure to cobalt (Kennedy et al, 1981).

Cobalt is GOITEROGENIC, as shown in persons receiving cobalt therapy for anemia (Friberg et al, 1986). The cobaltous ion interferes with iodine uptake (Clayton & Clayton, 1994).

Polycythemia, and the subsequent development of thyroid hyperplasia, has been reported following ingestion of cobalt salts (HSDB , 2001). Polycythemia is not likely to occur with occupational exposures to cobalt, unless occupational exposure standards are greatly exceeded (ACGIH, 1996a).

Rats administered cobalt by inhalation over four months developed higher levels of serum cholesterol and prolonged blood clotting times than controls (pp 31-33).

Guinea pigs can be sensitized to COBALT CHLORIDE by repeated skin application. The lungs of sensitized animals reacted to inhaled cobalt chloride differently; more lavage liquid was retained, and a higher percentage of neutrophils and eosinophils were recovered (Camner et al, 1993).

-FIRST AID

FIRST AID AND PREHOSPITAL TREATMENT

No prehospital gastrointestinal decontamination is recommended. Skin or eye exposures should be treated with initial decontamination and irrigation with water or normal saline.

-MEDICAL TREATMENT

LIFE SUPPORT

Support respiratory and cardiovascular function.

SUMMARY

FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)

Move victim to fresh air.
Call 911 or emergency medical service.
Give artificial respiration if victim is not breathing.
Administer oxygen if breathing is difficult.
Remove and isolate contaminated clothing and shoes.
In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes.
Keep victim warm and quiet.
Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.

FIRST AID

FIRST AID

EYE EXPOSURE: Immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Contact lenses should not be worn when working with this chemical.
DERMAL EXPOSURE: Wash contaminated skin with soap and water.
INHALATION EXPOSURE: Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible.
ORAL EXPOSURE: If this chemical has been swallowed, get medical attention immediately.
TARGET ORGANS: Skin and respiratory system (National Institute for Occupational Safety and Health, 2007).

GENERAL

Removal of patients with interstitial fibrotic lung disease, occupational reactive airway disease, and hypersensitivity dermatitis from further exposure is the most important action. Inhaled sympathomimetic agents may be required in the treatment of reactive airway disease.

SCOPE

This document does not cover potential clinical effects or treatment of radiation injury from radioactive cobalt isotopes. If exposure to radioactive isotopes of cobalt has occurred, refer to the IONIZING RADIATION medical document for further information.

INHALATION EXPOSURE

INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
Systemic corticosteroid or cytotoxic drug therapy has been used in patients with cobalt-induced interstitial lung disease.
BRONCHOSPASM SUMMARY

Administer beta2 adrenergic agonists. Consider use of inhaled ipratropium and systemic corticosteroids. Monitor peak expiratory flow rate, monitor for hypoxia and respiratory failure, and administer oxygen as necessary.

ALBUTEROL/ADULT DOSE

2.5 to 5 milligrams diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response, administer 2.5 to 10 milligrams every 1 to 4 hours as needed OR administer 10 to 15 milligrams every hour by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.5 milligram by nebulizer every 30 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).

ALBUTEROL/PEDIATRIC DOSE

0.15 milligram/kilogram (minimum 2.5 milligrams) diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.25 to 0.5 milligram by nebulizer every 20 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).

ALBUTEROL/CAUTIONS

The incidence of adverse effects of beta2-agonists may be increased in older patients, particularly those with pre-existing ischemic heart disease (National Asthma Education and Prevention Program, 2007). Monitor for tachycardia, tremors.

CORTICOSTEROIDS

Consider systemic corticosteroids in patients with significant bronchospasm. PREDNISONE: ADULT: 40 to 80 milligrams/day in 1 or 2 divided doses. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 or 2 divided doses (National Heart,Lung,and Blood Institute, 2007).

DERMAL EXPOSURE

DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

EYE EXPOSURE

DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.

ORAL EXPOSURE

No prehospital gastrointestinal decontamination is recommended.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

CASE REPORTS

Fatal interstitial lung disease developed in workers chronically exposed to 1 to 2 milligrams per cubic meter (ACGIH, 1986).
A 19-month-old child died after ingestion of a "mouthful" (approximately one ounce) of a cobalt chloride solution used as a weather indicator (Jacobziner & Raybin, 1961).
Workplace exposure to cobalt or arsenic may result in heart disease. This is suggested by cases of death from myocarditis, resulting from drinking beer that was contaminated with cobalt or arsenic (Clayton & Clayton, 1993).
Fatal allergic dermatitis has been observed following exposures to 1 to 2 mg (or less) of cobalt per cubic meter (HSDB , 2000).

MAXIMUM TOLERATED EXPOSURE

ROUTE OF EXPOSURE

INHALATION

Interstitial pulmonary fibrosis and wheezing have been shown in experimental animals exposed to as little as 0.1 milligram per cubic meter 6 hours daily and 5 days weekly for 3 months (ACGIH, 1986)
No new cases of cobalt-induced pulmonary disease or dermatitis have been reported in one industry that reduced air concentrations to at or below 0.1 milligram per cubic meter (ACGIH, 1986).
Life-span exposures to 10 micrograms per liter of cobalt oxide resulted in pneumonoconiosis in hamsters (Wehner et al, 1979).
Both interstitial fibrosis and reactive airway disease have been described in workers from plants where peak air cobalt concentrations exceeded 0.5 milligrams per cubic meter (Sprince et al, 1984).
Animal and human studies of oral exposure have been reviewed and compiled (ASTDR, 1992).

ORAL INGESTION

Estimated ingestion of about 2 grams of cobalt chloride crystals resulted in abdominal pain, vomiting, and neutropenia in a 6-year-old child. Plasma levels were markedly elevated at 7230 nmoL/L (normal 2 to 17 nmoL/L) (Mucklow et al, 1990).
Animal and human studies of inhalation exposure have been reviewed and compiled (ASTDR, 1992).

Carcinogenicity Ratings for CAS7440-48-4 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Cobalt

A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Cobalt and inorganic compounds, as Co

A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Cobalt
EPA (U.S. Environmental Protection Agency, 2011): Not Listed
IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 2A ; Listed as: Cobalt

2A : The agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.

IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 2B ; Listed as: Cobalt metal (without tungsten carbide)

2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.

IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 2A ; Listed as: Cobalt metal (with tungsten carbide)

2A : The agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.

NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Cobalt metal dust and fume (as Co)
MAK (DFG, 2002): Category 2 ; Listed as: Cobalt and cobalt compounds (as inhalable dusts/aerosols): Metallic cobalt

Category 2 : Substances that are considered to be carcinogenic for man because sufficient data from long-term animal studies or limited evidence from animal studies substantiated by evidence from epidemiological studies indicate that they can make a significant contribution to cancer risk. Limited data from animal studies can be supported by evidence that the substance causes cancer by a mode of action that is relevant to man and by results of in vitro tests and short-term animal studies.

MAK (DFG, 2002): Category 2 ; Listed as: Cobalt and cobalt compounds (as inhalable dusts/aerosols)

Category 2 : Substances that are considered to be carcinogenic for man because sufficient data from long-term animal studies or limited evidence from animal studies substantiated by evidence from epidemiological studies indicate that they can make a significant contribution to cancer risk. Limited data from animal studies can be supported by evidence that the substance causes cancer by a mode of action that is relevant to man and by results of in vitro tests and short-term animal studies.

NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

TOXICITY AND RISK ASSESSMENT VALUES

EPA IRIS

EPA Risk Assessment Values for CAS7440-48-4 (U.S. Environmental Protection Agency, 2011):

Not Listed

TOXICITY VALUES

References: (ACGIH, 1996; HSDB, 2000 ITI, 1995 Lewis, 1996 RTECS, 2000
- LD- (INTRAPERITONEAL)MOUSE:
- LD- (INTRAVENOUS)RABBIT:
- LD- (INTRAPERITONEAL)RAT:
- LD- (INTRAVENOUS)RAT:
- LD50- (INTRAPERITONEAL)RAT:
- LD50- (ORAL)RAT:
- LDLo- (INTRAPERITONEAL)MOUSE:
- LDLo- (INTRAVENOUS)RABBIT:
- LDLo- (ORAL)RABBIT:
- LDLo- (INTRATRACHEAL)RAT:
- LDLo- (INTRAVENOUS)RAT:
- LDLo- (ORAL)RAT:
- TCLo- (INHALATION)PIG:
- TCLo- (INHALATION)RAT:
- TD- (INTRAMUSCULAR)RAT:
- TDLo- (IMPLANT)RABBIT:
- TDLo- (INTRAMUSCULAR)RAT:

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS7440-48-4 (American Conference of Governmental Industrial Hygienists, 2010):

Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

Adopted Value

Cobalt

TLV:

TLV-TWA: 0.02 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A3
Codes: BEI
Definitions:

A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.

TLV Basis - Critical Effect(s): Asthma; pulm func; myocardial eff
Molecular Weight: 58.93

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

Adopted Value

Cobalt and inorganic compounds, as Co

TLV:

TLV-TWA: 0.02 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A3
Codes: BEI
Definitions:

A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.

TLV Basis - Critical Effect(s): Asthma; pulm func; myocardial eff
Molecular Weight: Varies

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

Under Study

Cobalt

TLV:

TLV-TWA:
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: Not Listed
Codes: Not Listed
Definitions: Not Listed

TLV Basis - Critical Effect(s):
Molecular Weight:

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

AIHA WEEL Values for CAS7440-48-4 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS7440-48-4 (National Institute for Occupational Safety and Health, 2007):

Listed as: Cobalt metal dust and fume (as Co)
REL:

TWA: 0.05 mg/m(3)
STEL:
Ceiling:
Carcinogen Listing: (Not Listed) Not Listed
Skin Designation: Not Listed
Note(s):

IDLH:

IDLH: 20 mg Co/m3 (as Co)
Note(s): Not Listed

OSHA PEL Values for CAS7440-48-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Listed as: Cobalt metal, dust, and fume (as Co)
Table Z-1 for Cobalt metal, dust, and fume (as Co):

8-hour TWA:

ppm:

Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

mg/m3: 0.1

Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

Ceiling Value:
Skin Designation: No
Notation(s): Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS7440-48-4 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS7440-48-4 (U.S. Environmental Protection Agency, 2010):

Listed as: Cobalt Compounds

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS7440-48-4 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS7440-48-4 (U.S. Environmental Protection Agency, 2010b):

Not Listed
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS7440-48-4 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS7440-48-4 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Listed as: Cobalt Compounds: Includes any unique chemical substance that contains cobalt as part of that chemical's infrastructure
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

Listed as: Cobalt
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

DOT List of Marine Pollutants for CAS7440-48-4 (49 CFR 172.101 - App. B, 2005):

Not Listed

EPA TSCA Inventory for CAS7440-48-4 (EPA, 2005):

Listed as: Cobalt

SHIPPING REGULATIONS

SURFACE

DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):

Not Listed

ICAO International Shipping Name (ICAO, 2002):

Not Listed

LABELS

NFPA

NFPA Hazard Ratings for CAS7440-48-4 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

SUMMARY

INDUSTRIAL CHEMICALS

Store cobalt away from strong oxidizers (such as chlorine, bromine, and fluorine) as violent reactions may occur. Keep in a cool place in an inert atmosphere (Sittig, 1991). When exposed to heat or flame, cobalt is flammable. Cobalt will ignite on contact with bromine pentafluoride. When mixed with acetylene or nitryl fluoride, an incandescent reaction will occur (Lewis, 1996).
Personnel should not attempt to handle broken containers without wearing protective clothing including boots, protective gloves, goggles, rubber coveralls, and either a mechanical filter respirator or a self-contained positive pressure breathing apparatus (Student, 1981; EPA, 1985; ITI, 1995; Plunkett, 1976).
Patients who develop hypersensitivity dermatitis, pulmonary interstitial fibrosis, or asthma-related disorders should be removed from further cobalt exposure (Plunkett, 1976) Harbison, 1998).

HANDLING

Cobalt dust will spontaneously ignite in air. Cobalt will ignite on contact with bromine pentafluoride. When mixed with acetylene or nitryl fluoride, an incandescent reaction will occur (Lewis, 1996).

STORAGE

INCOMPATIBILITIES

Cobalt dust will spontaneously ignite in air (Lewis, 1993).

-PERSONAL PROTECTION

SUMMARY

RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)

Wear positive pressure self-contained breathing apparatus (SCBA).
Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
Structural firefighters' protective clothing will only provide limited protection.

Where the possibility for exposure to cobalt dust exists, personnel should wear dust respirators. Appropriate protective clothing should worn clothing should be changed daily (NIOSH , 2000; Sittig, 1991). Persons should shower after each shift and change into clean clothes before leaving the work site. Contaminated clothing should be placed in sealed containers and properly stored until the cobalt dust can be properly removed (HSDB , 2000; Sittig, 1991).

Skin that is contaminated with cobalt dust must be washed immediately with soap or mild detergent (HSDB , 2000; NIOSH , 2000). To prevent dermatitis, gloves and barrier creams may be used (Sittig, 1991).

In areas in which cobalt dust or fumes are present, a local exhaust ventilation system should be used (HSDB , 2000).

Before workers enter tanks or vessels that contain cobalt catalysts, or tanks or vessels that are used to prepare cobalt salts, all cobalt-transferring sources must be blanked to prevent entry. The interior of the vessel must be washed with water and purged with air to ensure that there are no potential fire, explosion, oxygen deficiency, or dust inhalation hazards. Persons entering a tank or vessel must also have an appropriate respirator and secured lifeline or harness. Spark- or flame-generating equipment must be used only after extensive safety precautions have been taken (HSDB , 2000).

EYE/FACE PROTECTION

Persons should not wear contact lenses when working with cobalt (HSDB , 2000). In animals, cobalt will induce a variety of toxic effects in the eyes of experimental animals. Injuries to human eyes are rare (Grant, 1993).

RESPIRATORY PROTECTION

Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 7440-48-4.

Specific recommendations and test data for this chemical were not found in the available manufacturers' product literature. A complete list of consulted manufacturers and references is presented below.

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)
- Flammable/combustible material.
- May ignite on contact with air or moisture.
- May burn rapidly with flare-burning effect.
- Some react vigorously or explosively on contact with water.
- Some may decompose explosively when heated or involved in a fire.
- May re-ignite after fire is extinguished.
- Runoff may create fire or explosion hazard.
- Containers may explode when heated.
Cobalt is non-combustible in bulk form, but powdered cobalt is combustible and will burn at high temperatures (NIOSH , 2000; Sittig, 1991). Cobalt is an extreme fire hazard (Pohanish & Green, 1997). Fires involving cobalt should be extinguished based on the surrounding fire. Very fine cobalt dust is pyrophoric; at room temperature, the particles can self-ignite in air (HSDB , 2000) Pohanish & Green, 1997). HSDB (2000) reports that cobalt is a moderate fire danger, when exposed to heat or flame.

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS7440-48-4 (NFPA, 2002):

Not Listed

INITIATING OR CONTRIBUTING PROPERTIES

Cobalt dust ignites spontaneously in air. When exposed to heat or flame, cobalt is flammable. Cobalt will ignite on contact with bromine pentafluoride. When mixed with acetylene or nitryl fluoride, an incandescent reaction will occur (Lewis, 1996). "Cobalt is attacked by dilute hydrochloric and sulfuric acids" (Lewis, 1997).

FIRE CONTROL/EXTINGUISHING AGENTS

FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)

DO NOT USE WATER, CO2 OR FOAM ON MATERIAL ITSELF.
Some of these materials may react violently with water.
EXCEPTION: For Xanthates, UN3342 and for Dithionite (Hydrosulfite/Hydrosulphite) UN1384, UN1923 and UN1929, USE FLOODING AMOUNTS OF WATER for SMALL AND LARGE fires to stop the reaction. Smothering will not work for these materials, they do not need air to burn.

SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)

Dry chemical, soda ash, lime or DRY sand, EXCEPT for UN1384, UN1923 and UN1929.

LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)

DRY sand, dry chemical, soda ash or lime EXCEPT for UN1384, UN1923 and UN1929, or withdraw from area and let fire burn.
Move containers from fire area if you can do it without risk.

TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)

Fight fire from maximum distance or use unmanned hose holders or monitor nozzles.
Do not get water inside containers or in contact with substance.
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 engulfed in fire.

NFPA Extinguishing Methods for CAS7440-48-4 (NFPA, 2002):

Not Listed

Fires involving cobalt should be extinguished based on the surrounding fire. Cobalt is an extreme fire hazard (Pohanish & Green, 1997).

COMBUSTION TOXICITY

Cobalt dust ignites spontaneously in air. When exposed to heat or flame, cobalt is flammable. Cobalt will ignite on contact with bromine pentafluoride. When mixed with acetylene or nitryl fluoride, an incandescent reaction will occur (Lewis, 1996).
No information on the combustion toxicity of cobalt was found in available references at the time of this review.

EXPLOSION HAZARD

Powdered cobalt will spontaneously ignite in air. Cobalt will explode when combined with hydrazinium nitrate, ammonium nitrate and heat (above 200 degrees C), or 1,3,4,7-tetramethylisoindole (when large volumes of both compounds are heated to 390 degrees C) (Lewis, 1996) Urben, 1996). Cobalt will ignite on contact with bromine pentafluoride. Cobalt will decompose acetylene on contact and will become incandescent (Urben, 1996).

When mixed with nitryl fluoride and slightly warmed, an incandescent reaction will occur (Lewis, 1996) Urben, 1996). Cobalt, on contact with bromine pentafluoride, will ignite (Urben, 1996). Commercial cobalt, in the presence of hydrazinium nitrate, will explode (HSDB , 2000).

Cobalt reacts with acetylene, resulting in violent polymerization (HSDB , 2000; ITI, 1995). Carbon dioxide will react with a variety of acids to form salts. However, the cobaltic form (Co3) does not (ACGIH, 1996).

"The scale of the procedure described for preparing (octamethyltetrabenzoporphinato(2-)cobalt (II)) by heating the reagents in an evacuated Carius tube at 390 degrees C must not be increased or the tube will explode" (Urben, 1996).

DUST/VAPOR HAZARD

Cobalt dust will spontaneously ignite in air (Lewis, 1996).

REACTIVITY HAZARD

Powdered cobalt will spontaneously ignite in air. Cobalt will explode when combined with hydrazinium nitrate, ammonium nitrate and heat (above 200 degrees C), or 1,3,4,7-tetramethylisoindole (when large volumes of both compounds are heated to 390 degrees C)(Lewis, 1996) Urben, 1996). Cobalt will ignite on contact with bromine pentafluoride, and it will decompose acetylene on contact and will become incandescent (Urben, 1996).

When mixed with nitryl fluoride and slightly warmed, an incandescent reaction will occur (Lewis, 1996) Urben, 1996). Cobalt, on contact with bromine pentafluoride, will ignite (Urben, 1996). Commercial cobalt, in the presence of hydrazinium nitrate, will explode (HSDB , 2000).

At temperatures above 900 degrees C, cobalt will form an oxide coating consisting of cobaltosic oxide (Co3O4)(outside) and cobaltous oxide (CoO) (inside) (ACGIH, 1996).

Divalent cobalt (cobaltous form) will react with a various acids to form salts. However, trivalent cobalt (cobaltic form) will not undergo these reactions (ACGIH, 1996).

"The scale of the procedure described for preparing (octamethyltetrabenzoporphyrinato(2-)cobalt (II)) by heating the reagents in an evacuated Carius tube at 390 degrees C must not be increased or the tube will explode" (HSDB , 2000).

EVACUATION PROCEDURES

SUMMARY

Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.

SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)

Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) in all directions for liquids and at least 25 meters (75 feet) in all directions for solids.

FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)

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

PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135(ERG, 2004)

CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number:

MEXICO:

SETIQ:

01-800-00-214-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5559-1588;
For calls originating elsewhere, call: 011-52-555-559-1588.

CENACOM:

01-800-00-413-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885;
For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.

ARGENTINA:

CIQUIME:

0-800-222-2933 in the Republic of Argentina;
For calls originating elsewhere, call: +54-11-4613-1100.

BRAZIL:

PRÓ-QUÍMICA:

0-800-118270 (Toll-free in Brazil);
For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).

COLUMBIA:

CISPROQUIM:

01-800-091-6012 in Colombia;
For calls originating in Bogotá, Colombia, call: 288-6012;
For calls originating elsewhere, call: 011-57-1-288-6012.

CANADA:

CANUTEC:

613-996-6666 (Collect calls are accepted);
*666 cellular (in Canada only).

UNITED STATES:

CHEMTREC®:

1-800-424-9300 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
703-527-3887 for calls originating elsewhere (Collect calls are accepted).

CHEM-TEL, INC.:

1-800-255-3924 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
813-248-0585 for calls originating elsewhere (Collect calls are accepted).

INFOTRAC:

1-800-535-5053 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
352-323-3500 for calls originating elsewhere (Collect calls are accepted).

3E COMPANY:

1-800-451-8346 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
760-602-8703 for calls originating elsewhere (Collect calls are accepted).

NATIONAL RESPONSE CENTER (NRC):

1-800-424-8802 - (24 hours) (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
202-267-2675 for calls in the District of Columbia.

MILITARY SHIPMENTS:

703-697-0218 - Explosives/ammunition incidents (Collect calls are accepted);
1-800-851-8061 - All other dangerous goods incidents.

NATIONWIDE POISON CONTROL CENTER (United States only):

1-800-222-1222 (Toll-free in the U.S.).

For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions.
As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.
Stay upwind.
Keep unauthorized personnel away.
Keep out of low areas.

AIHA ERPG Values for CAS7440-48-4 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS7440-48-4 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Cobalt
TEEL-0 (units = mg/m3): 0.02
TEEL-1 (units = mg/m3): 0.3
TEEL-2 (units = mg/m3): 2
TEEL-3 (units = mg/m3): 20
Definitions:

TEEL-0: The threshold concentration below which most people will experience no adverse health effects.
TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure.
TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape.
TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.

AEGL Values for CAS7440-48-4 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):

Not Listed

NIOSH IDLH Values for CAS7440-48-4 (National Institute for Occupational Safety and Health, 2007):

IDLH: 20 mg Co/m3 (as Co)
Note(s): Not Listed

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)
- Fully encapsulating, vapor protective clothing should be worn for spills and leak with no fire.
- ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area).
- Do not touch or walk through spilled material.
- Stop leak if you can do it without risk.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)
- Wear positive pressure self-contained breathing apparatus (SCBA).
- Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
- Structural firefighters' protective clothing will only provide limited protection.
Persons involved in the clean-up of cobalt should wear self-contained breathing apparatus and appropriate chemical protective clothing (Sittig, 1991).
Liquid spills involving cobalt may be flushed with water and directed to a treatment system or holding tank for reclamation or disposal (HSDB , 2000).
Dry spills may be removed by vacuum or wet mop (HSDB , 2000).
Other spills may be cleaned-up using a hose (after first being dampened by a light mist of water) and deposited in proper containers until proper disposal is possible. Contaminated surfaces must never be cleaned by blowing with pressurized hoses or dry sweeping (HSDB , 2000).
Cobalt waste should be sorted, classified, and put in a properly labeled box. Material can then be salvaged for reuse by a local shop or sold as scrap metal (ITI, 1995; Sittig, 1991).
Prior to disposal in lad fills, cobalt wastes must be properly mixed with soil to prevent excessive accumulation of cobalt in plants (HSDB , 2000).

SMALL LEAK/SPILL

SMALL SPILL PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 135 (ERG, 2004)
- EXCEPTION: For spills of Xanthates, UN3342 and for Dithionite (Hydrosulfite/Hydrosulphite), UN1384, UN1923 and UN1929, dissolve in 5 parts water and collect for proper disposal.
- Cover with DRY earth, DRY sand, or other non-combustible material followed with plastic sheet to minimize spreading or contact with rain.
- Use clean non-sparking tools to collect material and place it into loosely covered plastic containers for later disposal.
- Prevent entry into waterways, sewers, basements or confined areas.

WASTE TREATMENT OPTIONS

CHEMICAL TREATMENT

Sodium borohydride (NaBH4) was used to quantitatively remove cobalt ions (Co(+2)) from water. The process was effective in alkaline solutions and removed cobalt as a cobalt boride compound (Co2B) (Gomezlahoz et al, 1993).
Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.

BIOREMEDIATION

The plants Azolla pinnata R Br and Lemna minor L, were used to adsorb various metals (including cobalt) from water. Plants with the absorbed metals were used in an anaerobic digester to produce biogas (methane). Investigation of toxic effects of these metals on the biogas anaerobic fermentation process showed significant toxicity only for cobalt (Jain et al, 1992).
A fluidized bed electrolytic cell reactor was designed to remove cobalt from wastewater at dilute concentrations. Under optimized conditions, this process removed cobalt to a residual level of 0.2 ppm (Chaudhary & Grimes, 1993).
As an alternative to disposal, cobalt may be recovered from scrap (HSDB , 2000).

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

Natural sources of cobalt include soil, seawater spray, natural dust, forest fires, volcanic eruptions, and various other sources. Cobalt can also enter the environment through fossil fuel burning, automobile and aircraft exhausts, through the processing of cobalt and cobalt alloys, copper and nickel smelting, and from a variety of other processing and manufacturing processes (ATSDR, 1992).

Typical soil concentrations range from 1.0 ppm to 40 ppm. Natural concentrations in ground water are typically less than 10 ppm (Dragun, 1988).

Accumulation of cobalt above 100 ppm causes severe phytotoxicity. Only a few plant species accumulate cobalt above this level, but concentrations of over 1% cobalt have been described in dry leaves of hyperaccumulators (HSDB , 2000).

ENVIRONMENTAL FATE AND KINETICS

Cobalt, in air, is most likely dependent on the particulate size, nature, and density. In air, cobalt is subject to dry and wet deposition. At the time of this revision, no other information on the atmospheric fate of cobalt was available (ATSDR, 1992).

WATER

SURFACE WATER
- In water, cobalt is adsorbed by hydrolysate or oxidate sediments. Bacterial activity may bring cobalt into solution (HSDB , 2000).
- Mobilization of cobalt from sediment is possible in acidic water, and when excess chloride ions, or organic and inorganic chelating agents are present. In seawater, soluble cobalt has an estimated residence time ranging from less than 1 year to 52 years (ATSDR, 1992). Cobalt is not expected to significantly bioaccumulate in benthic bottom feeders (ATSDR, 1992).
- In laboratory tests using synthetic river water, it was determined that concentrations of dissolved cobalt in postoxic suspensions were limited by the precipitation of cobalt sulfide minerals (Wallmann, 1992).

SOIL

TERRESTRIAL
- Metal oxides, crystalline minerals, and natural organics in soils can all retain cobalt. Chelating/complexing agents, pH, and Eh (redox potential) each can increase the mobility of cobalt in soil (ATSDR, 1992).
- In soil, the amount of cobalt is regulated by the pH of the soil. Cobalt usually exists in the divalent state. At a low pH, cobalt will be oxidized to trivalent cobalt and it is typically associated with iron. At pH of 6 and 7, adsorption of divalent cobalt on soil colloids is rapid. At lower pH levels (pH 3.3), leaching and plant uptake of cobalt is great (ATSDR, 1992; HSDB , 2000).

OTHER

OTHER
- Under high chemical oxygen demand (COD) loading in an anaerobic digestion system, the COD digestion rates and the specific activity of the bacteria were increased by the addition of iron and cobalt (Shen et al, 1993).

BIOACCUMULATION

FISH

Following ingestion in fish, cobalt cobalamine accumulation was 20X higher than CoCl2 accumulation, with a half-life of 8 days. Cobalt cobalamine complex formation was used to explain the high accumulation of cobalt in marine organisms (Nolan et al, 1992).
A laboratory experiment was conducted to evaluate the bioaccumulation of the radionuclide cobalt-60 (as cobalt-chloride) in juvenile groupers. Exposure was solely through the water. Cobalt accumulated mainly in gut, liver, skin and scales. In muscle, concentration factors reached levels of 8x10(-2). Chromatographic analysis of the water after the 4-month exposure period showed that all of the radioactively labeled cobalt-chloride had been converted to non-ionic forms, presumably via microbial activity. This conversion apparently increased the bioavailability of cobalt, because a second experiment, performed with the aged water, showed a 2.5-times higher bioaccumulation of cobalt in the muscle, compared to the first experiment (Guimaraes, 1992).

PLANTS

AQUATIC
- PHYTOPLANKTON: Double radiolabelings techniques were used to show that cobalt accumulation in phytoplankton was 60X higher from the cobalt cobalamine (CCA) form compared to the cobalt chloride (CoCl2) form. Half-life of cobalt in phytoplankton was 4.4 days when accumulated from CCA, and 0.6 days when accumulated from CoCl2 (Nolan et al, 1992).
- Accumulation of cobalt above 100 ppm causes severe phytotoxicity. Only a few plant species accumulate cobalt above this level, but concentrations of over 1% cobalt have been described in dry leaves of hyperaccumulators (HSDB , 2000).
- The relationship between cobalt, copper and zinc content in soils and the vegetables grown in these soils was evaluated using atomic absorption spectroscopy. Statistically significant correlations were found between total and extractable cobalt content in soils, and the roots and bulbs of the plants (Alegria et al, 1992).

BIOCONCENTRATION FACTOR

100 to 4000 in marine fish (ATSDR, 1992)
40 to 1000 in freshwater fish (dry weight basis)(ATSDR, 1992)

ENVIRONMENTAL TOXICITY

A laboratory study was done to determine the effect of water hardness on the freshwater toxicity of cobalt. The results show a tentative criteria of 288 mcg/L and 873 mcg/L for soft and hard water, respectively. These results suggest that very hard water may significantly reduce chronic toxicity potential of cobalt (Diamond et al, 1992).

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

58.93

DESCRIPTION/PHYSICAL STATE

Cobalt exists as a steel-gray, shiny, hard, ductile, somewhat malleable metal. Its atomic number is 27 (Lewis, 1997). It has one naturally occurring isotope (cobalt-59) and several artificial isotopes (54-58; 60-64) (HSDB , 2000).

Cobalt corrodes readily in air (Lewis, 1997).

Cobalt will crystallize in hexagonal form (ITI, 1995).

It is ferromagnetic (Lewis, 1997).

It exists in two allotropic forms: the hexagonal alpha form (below 417 degrees C) and the face-centered beta form (above 417 degrees C) (ACGIH, 1996; (Budavari, 1996; Lewis, 1996). Although both forms can exist at room temperature, the hexagonal form is the more stable form (Budavari, 1996; Lewis, 1996).

VAPOR PRESSURE

0 mmHg (approximately) (NIOSH , 2000)

1 mmHg (at 1910 degrees C) (ATSDR, 1992)

SPECIFIC GRAVITY

OTHER TEMPERATURE AND/OR PRESSURE

8.92 (at 20 degrees C) (ACGIH, 1996; (HSDB , 2000)

DENSITY

OTHER TEMPERATURE AND/OR PRESSURE

8.9 kg/L (at 20 degrees C) (ATSDR, 1992; Lewis, 1997)

TEMPERATURE AND/OR PRESSURE NOT LISTED

8.92 kg/L (Budavari, 1996; Lewis, 1996)

FREEZING/MELTING POINT

FREEZING POINT

2719 degrees F (NIOSH , 2000)

MELTING POINT

MELTING POINT

1495 degrees C (Lewis, 1996)
1493 degrees C (Budavari, 1996; Lewis, 1996)
1490 degrees C (ITI, 1995)

BOILING POINT

28 degrees C (at 3100 mmHg) (Lewis, 1996)

Approximately 3100 degrees C (Budavari, 1996; Lewis, 1996)

3100 degrees C (Lewis, 1997)

2375 degrees C (ITI, 1995)

2870 degrees C (ACGIH, 1996)

5612 degrees F (NIOSH , 2000)

AUTOIGNITION TEMPERATURE

760 degrees C (for dust) (ATSDR, 1992)

EXPLOSIVE LIMITS

LOWER

Not Applicable (NIOSH , 2000)

UPPER

Not Applicable (NIOSH , 2000)

SOLUBILITY

IN WATER

Cobalt is insoluble in both hot and cold water (HSDB , 2000; Sittig, 1991).

OTHER

Cobalt is readily soluble in dilute nitric acid and other acids (Lewis, 1996; Sittig, 1991).

HSDB (2000) reports that cobaltous salts are formed when metallic cobalt is dissolved in hydrochloric acid, dilute sulfuric acid, or nitric acid.

Cobalt can be attacked slowly by hydrochloric acid, ammonium hydroxide, sodium hydroxide, or very cold sulfuric acid (HSDB , 2000; Lewis, 1996).
Cobalt is insoluble in dilute alkalis (ACGIH, 1996).
Cobalt is soluble in body fluids (such as serum) (ACIGH, 1996).

OTHER/PHYSICAL

HEAT OF FUSION

62 cal/g (Budavari, 1996; Lewis, 1996)

THERMAL CONDUCTIVITY

71.128 W/m.deg K (HSDB , 2000)

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Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents