아코발트 플루오르화

4.46 at 77 °F (USCG, 1999) - Denser than water; will sink

4.43 g/cu cm

Red orthorhobic crystals; density 2.22 g/cc; soluble in water /Cobalt(II) fluoride tetrahydrate/

Rosy-red tetragonal crystals

Red tetragonal crystals

Forming a red liquid at melting point of 1100-1200 °C

Rose-red crystals or powder

For more Color/Form (Complete) data for Cobaltous fluoride (6 total), please visit the HSDB record page.

In water, 1.4 g/100 mL at 25 °C

Readily soluble in warm mineral acids

Soluble in cold water and hydrofluoric acid

Insoluble in alcohol, ether, benzene

Volatilizes at about 2552.0 °F (USCG, 1999)

1400 °C

Hazardous decomposition products formed under fire conditions: Hydrogen fluoride, cobalt/cobalt oxides.

Decomposes in hot water.

When heated to decomposition it emits toxic fumes of Co and F-

2192 °F (USCG, 1999)

1127 °C

Violet to red solid. Sinks and mixes slowly with water. (USCG, 1999)

Rose-red solid; Soluble in cold water; Decomposed by hot water; [Hawley] Red odorless powder; Soluble in water; [MSDSonline]

Forms di, tri, and tetrahydrates; all soluble in water; these aqueous solutions decompose upon boiling forming the oxyfluoride CoF.CoO.H2O

Standard enthalpy of formation: -692.0 kJ/mol

Heat of solution: -271 BTU/lb = -150.6 cal/g = -6.3X10+5 J/kg

Enthalpy of fusion: 58.1 kJ/mol at a melting pt of 1127 °C

For more Other Experimental Properties (Complete) data for Cobaltous fluoride (6 total), please visit the HSDB record page.

Danger

H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]

P203, P260, P261, P264, P270, P272, P280, P301+P316, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P316, P318, P321, P330, P333+P317, P362+P364, P363, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 48 reports by companies from 4 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Danger

H301: Toxic if swallowed [Danger Acute toxicity, oral]

COBALT FLUORIDE is a toxic, light brown crystalline material, when exposed to water it forms highly corrosive hydrofluoric acid. When heated to decomposition it emits toxic fumes of metallic cobalt and fluorides [Lewis, 3rd ed., 1993, p. 344].

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Cobaltous fluoride is included on this list.

Biological Exposure Indices (BEI) [ACGIH] - Fluorides in urine = 2 mg/L prior to shift or 3 mg/L at end of shift; (Repeated measurements recommended.) Cobalt in urine = 15 ug/L; sample at end of shift at end of workweek;

1.0 [mg/m3], inhalable fraction, as F[German Research Foundation (DFG)]

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.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. 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. 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.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. 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.

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: Avoid contact with skin, eyes and clothing. Wash hands before breaks and immediately after handling the product.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

For more Preventive Measures (Complete) data for Cobaltous fluoride (8 total), please visit the HSDB record page.

2.5 [mg/m3], as F (0.02 mg/m3 as Co)

8 hr Time Weighted Avg (TWA): 2.5 mg/cu m. /Fluorides, as F/

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. /Fluorides, as F/

A4: Not classifiable as a human carcinogen. /Fluorides, as F/

Biological Exposure Index (BEI): Determinant: fluoride in urine; Sampling Time: prior to shift; BEI: 2 mg/L; Notation: The determinant may be present in biological specimens collected from subjects who have not been occupationally exposed, at a concentration that could affect interpretation of the result. Such background concentrations are incorporated in the BEI value.; The determinant is nonspecific, since it is also observed after exposure to other chemicals. /Fluorides/

For more Threshold Limit Values (TLV) (Complete) data for Cobaltous fluoride (10 total), please visit the HSDB record page.

ATMOSPHERIC FATE: Inorganic cobalt compounds are nonvolatile and released into the atmosphere in particulate form(1). Particulate-phase cobalt compounds are removed from the air by wet and dry deposition(SRC). Cobalt has been detected in atmospheric deposition(2) and in rain-snow precipitation(3).

IDENTIFICATION AND USE: Cobalt fluoride forms rose-red crystals or powder. It is used as a catalyst for organic reactions, and as a fluorinating agent. HUMAN EXPOSURE AND TOXICITY: Initial symptoms from ingestion include salivation, nausea, abdominal pain, vomiting, and diarrhea and are secondary to the local action of fluoride on the intestinal mucosa. Systemic symptoms are varied and severe: increased irritability of the central nervous system consistent with the Ca2+ binding effect of fluoride and the resulting hypocalcemia; hypotension, presumably owing to central vasomotor depression as well as direct cardiotoxicity; and stimulation and then depression of respiration. Death can result from respiratory paralysis or cardiac failure. ANIMAL STUDIES: The liver, heart and kidneys of rats given acute exposure to cobalt fluoride were examined microscopically. Hyperemia, hemorrhage and cytoplasmic changes were noted, while the kidney glomeruli were rich in cells and basal membranes were thickened. Cells of the proximal tubules were swollen and showed vacuolization and degeneration. In the hearts of some rats proliferative and edematous interstitial tissue and swollen muscle fibers were observed and focal degeneration, vacuolization and necrosis associated with disappearance of the cross striations were noted. Chronic manifestations of excess fluoride in cattle are dental fluorosis and osteofluorosis.

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)

/SIGNS AND SYMPTOMS/ Symptomatology: Liver injury, consisting of hemorrhagic necrosis which is usually reversible. Death from shock, usually in 4-5 hr. Sometimes following apparent recovery, pneumonia with fever or secondary shock may cause death 1-3 days later. Among survivors pyloric stenosis and mild hepatic cirrhosis may be encountered as persistent sequelae, but recovery is usually complete. /Fluoride/

/SIGNS AND SYMPTOMS/ Symptomatology: Ingestion of soluble fluoride salts. Salty or soapy taste, salivation, nausea. Repeated small doses (as in drinking water) may produce no other symptoms, but polyuria and polydipsia have also been reported. Large doses lead promptly to burning or crampy abdominal pain, intense vomiting and diarrhea, often with hematemesis and melena. Dehydration and thirst. Muscle weakness, tremors and rarely transient epileptiform convulsions, preceded or followed by progressive central nervous depression (lethargy, coma and respiratory arrest, even in the absence of circulatory failure). Shock characterized by pallor, weak and thready pulse (sometimes irregular), shallow unlabored respiration, weak heart sounds, wet cold skin, cyanosis, anuria, dilated pupils, followed almost invariably by death in 2 to 4 hours. Even in the absence of shock, arrhythmias may occur, especially multiple episodes of ventricular fibrillation leading eventually to cardiac arrest. If the victim survives a few hours, paralysis of the muscles of deglutition, carpopedal spasm and painful spasms of the extremities. Occasionally localized or generalized urticaria. The above signs and symptoms are related to a variety of metabolic disorders that may occur in acute fluoride poisoning, including hypocalcemia (which may be the only invariable finding), hypomagnesemia, metabolic and/or respiratory acidosis and sometimes hyperkalemia. /Fluoride/

/SIGNS AND SYMPTOMS/ Initial symptoms /from ingestion include/ salivation, nausea, abdominal pain, vomiting, and diarrhea /and/ are secondary to the local action of fluoride on the intestinal mucosa. Systemic symptoms are varied and severe: increased irritability of the central nervous system consistent with the Ca2+ binding effect of fluoride and the resulting hypocalcemia; hypotension, presumably owing to central vasomotor depression as well as direct cardiotoxicity; and stimulation and then depression of respiration. Death can result from respiratory paralysis or cardiac failure. /Fluoride salts/

Cobaltous fluoride's production and use as a catalyst for organic synthesis(1,2) and alloying of metals(3), use for optical deposition to improve optical quality(3) and potential use in dental care(3) may result in its release to the environment through various waste streams(SRC).

/LABORATORY ANIMALS: Acute Exposure/ ... If sufficient fluoride is absorbed ... fluoride ion increases capillary permeability and also produces a coagulation defect. These actions lead to hemorrhagic gastroenteritis and hemorrhages, congestion, and edema in various organs including the brain. Clinical manifestations ... include excitability, muscle tremors, weakness, urination, defecation, salivation, emesis, sudden collapse, clonic convulsions, coma, and death due to respiratory and cardiac failure. Cyanosis and early rigor mortis ... /Fluoride/

/LABORATORY ANIMALS: Acute Exposure/ Signs of acute systemic fluoride intoxication are increased salivation, lacrimation, vomiting, diarrhea, muscular fibrillation, and respiratory, cardiac, and general depression. ... /Fluorides/

/LABORATORY ANIMALS: Acute Exposure/ The liver, heart and kidneys of rats given /acute exposure to/ cobalt(II) fluoride or oxide were examined microscopically. Hyperemia, hemorrhage and cytoplasmic changes were noted, while the kidney glomeruli were rich in cells and basal membranes were thickened. Cells of the proximal tubules were swollen and showed vacuolization and degeneration. In the hearts of some rats proliferative and edematous interstitial tissue and swollen muscle fibers were observed and focal degeneration, vacuolization and necrosis associated with disappearance of the cross striations were noted.

/VETERINARY CASE REPORTS/ Chronic manifestations of excess fluoride in cattle are ... dental fluorosis and osteofluorosis. Animals with moderate to severe osteofluorosis sometimes exhibit an intermittent, non-specific, a typical lameness or stiffness that may be associated with calcification of periarticular structures and tendon insertions. This lameness or stiffness is often transitory in nature; and limits feeding or grazing time, thereby impairing animal performance. Other general non-specific signs or symptoms sometimes associated with chronic fluoride toxicosis include thickened, dry unpliable skin and poor performance. /Fluoride/

/VETERINARY CASE REPORTS/ ... Lameness; painful, stiff gait or posture; decreased feed intake; anorexia; rough haircoat; emaciation; and decreased milk production. Bony exostoses ... teeth have ... mottling and patchy loss of dentine. ... Spontaneous fractures may occur. ... Lesions consist of hyperostosis, porosis, enlargement ... roughening. /Fluoride/

Patients with kidney dysfunction may be particularly susceptible to fluoride toxicity. /Fluoride/

Populations that appear to be at increased risk from the effects of fluoride are individuals that suffer from diabetes insipidus or some forms of renal impairment. These high risk populations represent a relatively small segment of the general populations. /Fluoride/

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Cobaltous fluoride is included on this list.

... Fluoride interacts with bones and teeth by replacing hydroxyl or bicarbonate ions in hydroxyapatite to form fluorohydroxyapatite. ... The presence of fluorohydroxyapatite increases the crystalline structure of the bone and reduces its solubility. ... Dental fluorosis results from toxic effects of fluoride on the epithelial enamel organ. /Fluoride/

In acute poisoning, fluoride kills by blocking normal cellular metabolism. Fluoride inhibits enzymes, in particular metalloenzymes involved in essential processes, causing vital functions such as the initiation and transmission of nerve impulses, to cease. ... /Fluoride/

Inhibition of one or more enzymes controlling cellular glycolysis (& perhaps resp) may result in a critical lesion. ... Binding or precipitation of calcium as calcium fluoride ... suggested as mechanism underlying many diverse signs & symptoms in fluoride poisoning, particularly if death is delayed. ... At least in some species fluoride interferes with both contractile power of heart and the mechanism of beat in a way that cannot be ascribed to hypocalcemia. /fluoride/

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

... Most of the absorption takes place in the intestine. The degree of fluoride absorption correlates with its water solubility ... A second route of absorption is through the lungs ... Fluoride is distributed widely in organs and tissues but is concentrated in bone and teeth, and the skeletal burden is related to intake and age. ... The kidneys are the major site of fluoride. Small amounts of fluoride also appear in sweat, milk, and intestinal secretions; in a very hot environment, sweat can account for nearly 50% of the total fluoride excretion. /Fluorides/

Bone is natural "sink" for fluoride ... 95-96% of body burden of fluoride is in bones & teeth. ... Fluoride is gradually excreted in urine. /fluoride/

...Experiments demonstrated that storage of fluoride in bones occurs as result of repeated exposures to concentrations that are but slightly, if at all, irritant. /Fluoride/

Following ingestion, soluble fluorides are rapidly absorbed from the gastrointestinal tract at least to the extent of 97%. Absorbed fluoride is distributed throughout the tissues of the body by the blood. Fluoride concentrations in soft tissues fall to pre-exposure levels within a few hours of exposure. Fluoride exchange with hydroxyl radicals of hydroxyapatite (the inorganic constituent of bone) to form fluorohydroxyapatite. Fluoride that is not retained is excreted rapidly in urine. In adults under steady state intake conditions, the urinary concentration of fluoride tends to approximate the concentration of fluoride in the drinking water. This reflects the decreasing retention of fluoride (primarily in bone) with increasing age. Under certain conditions perspiration may be an important route of fluoride excretion. The concentration of fluoride retained in bones and teeth is a function of both the concentration of fluoride intake and the duration of exposure. Periods of excessive fluoride exposure will result in increased retention in the bone. However, when the excessive exposure is eliminated, the bone fluoride concentration will decrease to a concentration that is again reflective of intake. /Fluoride/

Exposure to aqueous solution of cobaltous fluoride reduced wettability & free surface energy of org layers of tooth enamel & dentine from humans or whales in vitro. It is possible that effect on wettability may contribute to anticaries effect.

Used as catalyst for organic reactions; [Merck Index] Used as a fluorinating agent; [Ullmann]

Catalyst for organic reactions.

Cobalt difluoride, used primarily for the manufacture of cobalt trifluoride, CoF3.

Fluorinating agent.

Cobalt(II) fluoride can be used as a catalyst to alloy metals and for optical deposition. (L489)

... Manufactured commercially by the action of aqueous or anhydrous hydrogen fluoride on cobalt carbonate ... in a plastic, i.e., polyethylene/polypropylene, Teflon, Kynar, rubber, or graphite-lined container to avoid metallic impurities. ... It is dried at 150-200 °C and then pulverized to obtain the anhydrous salt.