Cobalt sulfate

154.99600

154.88500

233-334-2

H7965X29HX

1127

DTXSID1031042

C44360

Red to lavender dimorphic, othorhombic crystals|Red orthorhombic crystals|Red powder|Rose-pink solid

2833299010

88.64000

-0.25720

Cobalt sulfate is an odorless rose-pink solid. Sinks and mixes with water. (USCG, 1999)

3.71 g/cm³ @ Temp: 25 °C

735 °C

330ºC at 760mmHg

Solubility in water, g/100ml at 20°C: 36.2 (good)

Cool, dry location. Tightly sealed container.

3.35E-05mmHg at 25°C

Odorless

Acidic salts, such as cobalt sulfate ... resulting aqueous solutions contain moderate concentrations of hydrogen ions and have pH's of less than 7.0. They react as acids to neutralize bases.

Stable to 708 °C|Mol wt: 281.10; red-pink, monoclinic crystals; index of refraction: 1.477, 1.483, 1.489; density: 1.948 at 25 °C/25 °C; MP: 96.8 °C; BP: 420 °C (loses 7H2O); solubility: 60.4 g/100 cc water at 3 °C, 67 g/100 cc water at 70 °C, 2.5 g/100 cc alcohol at 3 °C, 54.5 g/100 cc methanol at 18 °C /Cobaltous sulfate heptahydrate/|Mol wt: 263.08; red monoclinic crystals; index of refraction: 1.531, 1.549, 1.552; density: 2.019 at 15 °C/15 °C; MP: 95 °C (loses 2H2O) /Hexahydrate/|Mol wt: 173.011; red monoclinic crystals; density: 3.08 g/cu cm; water solubility 38.3 g/100 g water at 25 °C /Cobaltous sulfate monohydrate/|Pink to red monoclinic, prismatic crystals; on heating dehydrates to the hexahydrate (monoclinic prismatic crystala) at 41.5 °C, and to the monohydrate at 71 °C. /Cobaltous sulfate heptahydrate/|Structure reported to be Co(H2SO5) /Cobaltous sultate monohydrate/|Rose color monoclinic crystals; specific gravity: 3.08; dissolves slowly in boiling water /Cobalt(II) sulfate monohydrate/|Standard enthalpy of formation: -888.3 kJ/mol|Effloresces in dry air to form the hexahydrate /Cobalt(II) sulfate heptahydrate/

Water soluble.

Salts, Acidic

Acidic salts, such as COBALT SULFATE, are generally soluble in water. The resulting solutions contain moderate concentrations of hydrogen ions and have pH's of less than 7.0. They react as acids to neutralize bases. These neutralizations generate heat, but less or far less than is generated by neutralization of inorganic acids, inorganic oxoacids, and carboxylic acid. They usually do not react as either oxidizing agents or reducing agents but such behavior is not impossible. Many of these compounds catalyze organic reactions.

UN 3082

2

R49; R42/43; R51/53

53-23-36/37-45-61-60-22

GG3100000

T; N

Separated from strong oxidants. Store in an area without drain or sewer access. Provision to contain effluent from fire extinguishing.

Stable to 708 deg C.

P201-P261-P280-P284-P304 + P340-P308 + P313

H290-H317-H319-H334-H341-H350i-H360F-H410

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.|Sweep spilled substance into containers; if appropriate, moisten first to prevent dusting. Carefully collect remainder, then remove to safe place. Do NOT let this chemical enter the environment.

Reacts as a dust with strong oxidants causing fire and explosion hazard.

Trace minerals added to animal feeds. These substances added to animal feeds as nutritional dietary supplements are generally recognized as safe when added at levels consistent with good feeding practice. All substances listed may be in anhydrous or hydrated form. Cobalt sulfate is included on this list.

DHHS/NTP; NTP Report on the Toxicity Studies of Cobalt Sulfate Heptahydrate in F344/N Rats and B6C3F1 Mice (Inhalation Studies) NTP TOX 5 (1991) NIH Pub No. 91-3124|National Toxicology Program. Eleventh Report on Carcinogens (2005). The Report on Carcinogens is an informational scientific and public health document that identifies and discusses substances (including agents, mixtures, or exposure circumstances) that may pose a carcinogenic hazard to human health. Cobaltous Sulfate (10124-43-3) is listed as reasonably anticipated to be a human carcinogen.[Available from, as of July 31, 2009: http://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s048zcob.pdf]

Special Hazards of Combustion Products: Toxic cobalt oxide fumes may form in fire. (USCG, 1999)|Not combustible. Gives off irritating or toxic fumes (or gases) in a fire.

|Danger|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P261, P264, P270, P272, P273, P280, P281, P285, P301+P312, P302+P352, P304+P341, P308+P313, P321, P330, P333+P313, P342+P311, P363, P391, P405, and P501|H302 (99.81%): Harmful if swallowed [Warning Acute toxicity, oral]|Aggregated GHS information provided by 2598 companies from 30 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|P201, P202, P260, P261, P264, P270, P272, P273, P280, P281, P285, P301+P312, P302+P352, P304+P341, P305+P351+P338, P308+P313, P314, P321, P330, P333+P313, P337+P313, P342+P311, P363, P391, P405, and P501|P201, P202, P260, P261, P264, P270, P272, P280, P281, P285, P301+P312, P302+P352, P304+P341, P308+P313, P314, P321, P330, P333+P313, P342+P311, P363, P405, and P501

Bu. Mines approved respirator; goggles; protective gloves (USCG, 1999)|Respiratory protection equipment: Use NIOSH approved respiratory protection where airborne level exceeds appropriate occupational exposure limit.|Protective gloves: Gloves, rubber or impervious coating.|Eye and face protection: Wear safety glasses or face shield in operations that do scatter fine particles in the air.|To prevent repeated or prolonged skin contact, wear impervious clothing and boots.|AVOID ALL CONTACT! Protective gloves. Protective clothing. Safety goggles, or eye protection in combination with breathing protection if powder.

Special firefighting procedures: None required; however, when fighting chemical fires, self-contained breathing apparatus and protective clothing is recommended.

High concentrations of dust may present a dust explosion hazard.

The spill should first be contained and the area should be cleaned by wet-sweeping or vacuum cleaning (HEPA filter). Minimize the creation of dust. Approved NIOSH respirator for dust should be worn.|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/

Handling: Keep from freezing. Avoid contact with skin and eyes. Avoid breathing dust. Use only with adequate ventilation. Always use gloves and safety glasses when opening/emptying containers or processing this material. Do not eat or drink in work area. Wash in soap and water after exposure to any dust.|Use local exhaust ventilation directed towards the source of dust and which is adequate to limit personal exposure to levels which do not exceed the PEL or TLV. If such equipment is not available use respirators ... .|SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.|Employers should institute programs that emphasize good personal hygiene to prevent skin and respiratory irritation caused by cobalt containing dusts. After working with cobalt products, workers should thoroughly wash their hands and face before drinking, eating, or smoking. If skin contact with cobalt solutions occurs, the worker should wash the affected skin promptly. The employer should provide showers if workers have substantial contact with cobalt. These workers should be encouraged to wash or shower after each workshift. Employers should prohibit smoking or carrying of tobacco products, and should prohibit eating, food handling, or food storage within the work area. /Cobalt and cobalt salts/|For more Preventive Measures (Complete) data for Cobaltous sulfate (6 total), please visit the HSDB record page.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

Separated from strong oxidants. Store in an area without drain or sewer access. Provision to contain effluent from fire extinguishing.

A harmful concentration of airborne particles can be reached quickly when dispersed, especially if powdered.

The substance is severely irritating to the respiratory tract. The substance is irritating to the eyes.

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

PREVENT DISPERSION OF DUST! AVOID ALL CONTACT!

Use local exhaust or breathing protection.

Protective gloves. Protective clothing.

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

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 sulfate is included on this list.

IDENTIFICATION: Cobalt sulfate is a red powder. It is used in storage batteries; in cobalt-electroplating baths; as drier for lithographic inks, and varnishes; in ceramics, enamels, and glazes to prevent discoloring; in cobalt pigments for decorating porcelain. HUMAN EXPOSURE AND TOXICITY: Cardiomyopathy has been observed in individuals who consume large quantities of beer where cobalt sulfate was added as a foam stabilizer. Repeated or prolonged contact may cause skin sensitization. Repeated or prolonged inhalation exposure may cause asthma. The substance may have effects on the heart, thyroid and bone marrow, resulting in cardiomyopathy, goiter and polycythemia. ANIMAL STUDIES: Rats and mice exposed short term to cobalt sulfate by inhalation exhibited necrosis and inflammation of the respiratory tract epithelium. Rats developed thymus necrosis and testicular atrophy. Rats exposed for 2-3 months to cobalt sulfate in the diet for 24 weeks had significant reductions in heart enzyme activity levels. Rats and mice were exposed to cobalt sulfate heptahydrate by inhalation 6 hr/day, 5 days/week for 13 weeks developed adverse effects throughout the respiratory system. At higher concentrations both rats and mice developed squamous metaplasia of the larynx. At high doses, rats developed chronic inflammation of the larynx along with more severe effects in the nose, larynx and lung. Mice exhibited acute inflammation of the nose, larynx and lungs. Mice also exhibited hyperplasia of the mediastinal lymph nodes and testicular atrophy and increased esterous cycle in females. Both rats and mice exhibited histiocytic infiltrates of the lung at similar exposure levels. Sperm motility was decreased in mice and mice that received high dosages developed increased abnormal sperm and decreased testis and epididymal weights. Rats exposed for 2-3 months of copper sulfate in the diet exhibited increased heart weight and degenerative heart lesions. Rats exposed to cobalt sulfate in their diet for 24 weeks experienced significant reductions in cardiac enzyme activity levels, such as manganese superoxide dismutase, cytochrome c oxidase, NADH, cytochrome reductase and a reduction in mitochondrial ATP production. Groups of 50 male and 50 female rats exposed to copper sulfate heptahydrate by inhalation for 6 hr/day, 5 days/week for 105 weeks. Mean body weights and survival were unaffected by treatment. Rats exhibited a concentration increase in the incidence of benign and malignant alveolar/bronchiolar neoplasms in male and female rats and benign and malignant pheochromocytomas in female rats. The carcinogenicity of cobalt sulfate heptahydrate by inhalation was studied in mice. Also evaluated was the K-ras mutation frequency and spectra in lung tumors. A higher G-T transversions was detected in codon 12 of K-ras compared to chamber controls.

The present study was carried out to investigate clearance of protoporphyrin IX (PpIX) in the presence of metal ions in the cream applied on healthy skin of mice in vivo. The photosensitizer PpIX was induced in normal mouse skin by topical application of 5-aminolevulinic acid (ALA). Fluorescence spectroscopy was used to study porphyrin kinetics. Topical application of ferrous, cobalt or zinc sulfate significantly diminished the fluorescence of PpIX in mouse skin. These results show that the clearance kinetics of PpIX observed after exogenous application of ALA are determined by the conversion of PpIX into heme, and not by the clearance of PpIX from the body. Application of a vehicle containing ferrous or cobalt sulfate after photodynamic therapy might be an approach in clinical practice for the reduction of cutaneous photosensitivity and elimination of undesirable photoreactions in skin and lesions.|Near toxic concentrations of cadmium sulfate, mercuric chloride, and nickel sulfate reduced interferon action in tissue cultures, but increased intake by the intact mouse of lead acetate and mercuric chloride did not reduce interferon action. Lead and nickel given orally inhibited the protective activity of Newcastle disease virus against encephalomyocarditis virus-induced mortality, whereas cadmium, mercury, cobalt sulfate, and sodium arsenite given orally and deficiency of zinc did not influence this action. Excess lead and cobalt and deficiency of zinc, but not excess cadmium, mercury, or nickel, inhibited the protective activity of poly I/poly C against encephalomyocarditis virus-induced mortality. These results illustrate the various actions of increased concentrations of certain metals or a deficiency of zinc on interferon action or on actions of interferon inducers.|In rats a combination of a protein deficient diet and cobalt administration, resulted in severe cardiomyopathy, showing cardiac damage remarkably similar to that seen in humans. Rats were preconditioned to protein restriction for ten days (4% casein in diet), then received cobalt sulfate by oral gavage for two weeks. Cobalt sulfate, containing from 4.0 to 12.5 mg cobalt/kg bw/day was administered, severe cardiomyopathy was seen in those animals receiving 12.5 mg cobalt/kg bw/day in combination with the low protein diet.

LD50 Mouse ip 143 mg/kg|LD100 Dog iv 16.2 mg/kg /Heptahydrate/|LD50 Rat oral 424 mg/kg bw|LD50 Rat ip 31,600 ug/kg|For more Non-Human Toxicity Values (Complete) data for Cobaltous sulfate (10 total), please visit the HSDB record page.

GENETIC TOXICOLOGY: Cobalt sulfate heptahydrate was mutagenic in Salmonella typhimurium strain TA100 with and without liver S9 metabolic activation enzymes; no mutagenic activity was detected in strain TA98 or TA1535, with or without S9. /Cobalt sulfate heptahydrate/|2-YEAR STUDY IN MICE: Groups of 50 male and 50 female mice were exposed to aerosols containing 0, 0.3, 1.0, or 3.0 mg/cu m cobalt sulfate heptahydrate 6 hours per day, 5 days per week, for 105 weeks. Survival and Body Weights Survival of exposed males and females was similar to that of the chamber controls. Mean body weights of 3.0 mg/cu m male mice were less than those of the chamber controls from week 96 until the end of the study. The mean body weights of all exposed groups of female mice were generally greater than those of the chamber controls from week 20 until the end of the study. Pathology Findings The incidences of diffuse histiocytic cell infiltration in 3.0 mg/cu m males and of focal histiocytic cell infil tration in 3.0 mg/cu m females were significantly greater than those in the chamber controls. The incidences of alveolar/bronchiolar neoplasms in 3.0 mg/cu m males and females were significantly greater than those in the chamber control groups. The combined incidences of alveolar/bronchiolar adenoma or carcinoma and the incidences of alveolar/bronchiolar carcinoma in 3.0 mg/cu m males and females and the incidence of alveolar/bronchiolar adenoma in 3.0 mg/cu m females exceeded the NTP historical crical control ranges for inhalation studies. The incidences of atrophy of the olfactory epithelium in 1.0 and 3.0 mg/cu m males and females and hyper plasia of the olfactory epithelium in 3.0 mg/cu m males and females were significantly greater than in the chamber controls. Squamous metaplasia of the larynx was observed in all exposed groups of males and females. Male mice had a pattern of nonneoplastic liver lesions along with silver-staining helical organisms within the liver, characteristic of an infection with Helico bacter hepaticus. In NTP studies with H. hepaticus- associated hepatitis, increased incidences of hemangiosarcoma were seen in the liver of male mice. In this study of cobalt sulfate heptahydrate, incidences of hemangiosarcoma were increased in exposed groups of male mice. Because of the above association, interpretation of the increased incidences of hemangiosarcoma in the livers of male mice was confounded. Incidences of lesions at other sites in this study of cobalt sulfate heptahydrate were not considered to have been significantly impacted by the infection with H. hepaticus or its associated hepatitis. ... There was clear evidence of carcinogenic activity of cobalt sulfate heptahydrate in male and female B6C3F1 mice based on increased incidences of alveolar/bronchiolar neoplasms. /Cobalt sulfate heptahydrate/|2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats were exposed to aerosols containing 0, 0.3, 1.0, or 3.0 mg/cu m cobalt sulfate heptahydrate 6 hours per day, 5 days per week, for 105 weeks. Survival and Body Weights Survival of exposed males and females was similar to that of the chamber controls. Mean body weights of exposed male and female rats were similar to those of the chamber controls throughout the study. Pathology Findings The incidences and severities of proteinosis, alveolar epithelial metaplasia, granulomatous alveolar inflammation, and interstitial fibrosis were markedly greater in all exposed groups of male and female rats than in the chamber controls. The incidences of alveolar epithelial hyperplasia in all groups of exposed males and in females exposed to 3.0 mg/cu m were significantly greater than those in the chamber control groups, as were the incidences of squamous metaplasia in 1.0 mg/cu m females and atypical alveolar epithelial hyperplasia in 3.0 mg/cu m females. In 3.0 mg/cu m males, the combined incidence of alveolar/ bronchiolar neoplasms (adenoma and/or carcinoma) was significantly greater than in the chamber controls. In female rats exposed to 1.0 or 3.0 mg/cu m, the incidences of alveolar/bronchiolar neoplasms were significantly greater than those in the chamber control group and exceeded the NTP historical control ranges. A squamous cell carcinoma was observed in one 1.0 mg/cu m and one 3.0 mg/cu m female. The incidences of benign, complex, or malignant pheochromocytoma (combined) in 1.0 mg/cu m males and in 3.0 mg/cu m females were significantly greater than those in the chamber controls and exceeded the historical control ranges. Hyperplasia of the lateral wall of the nose, atrophy of the olfactory epithelium, and squamous metaplasia of the epiglottis were observed in all exposed groups of males and females, and the severities of these lesions increased with increasing exposure concentration. The incidences of squamous metaplasia of the lateral wall of the nose and metaplasia of the olfactory epithelium were increased in 3.0 mg/cu m males and females. ... There was some evidence of carcinogenic activity of cobalt sulfate heptahydrate in male F344/N rats based on increased incidences of alveolar/bronchiolar neoplasms. Marginal increase of pheochromocytomas of the adrenal medulla may have been related to exposure to cobalt sulfate heptahydrate. There was clear evidence of the carcinogenic activity in female F344/N rats based on increased incidences of alveolar/bronchiolar neoplasms and pheochromocytomas of the adrenal medulla in groups exposed to cobalt sulfate heptahydrate. /Cobalt sulfate heptahydrate/|... Male and female F344/N rats and B6C3F1 mice were exposed to cobalt sulfate heptahydrate (approximately 99% pure) by inhalation for 2 yr. ... Groups of 50 male and 50 female F344/N rats were exposed to aerosols containing 0, 0.3, 1.0 or 3.0 mg/cu m cobalt sulfate heptahydrate 6 hr/day, 5 days/wk for 105 wk. ... Groups of 50 male and 50 female B6C3F1 mice were exposed to aerosols containing 0, 0.3, 1.0 or 3.0 mg/cu m cobalt sulfate heptahydrate 6 hr/day, 5 days/wk for 105 wk. Conclusions: Under the conditions of these 2 yr inhalation studies, there was some evidence of carcinogenic activity of cobalt sulfate heptahydrate in male F344/N rats based on incr incidences of alveolar/bronchiolar neoplasms. Marginal incr of pheochromocytomas of the adrenal medulla may have been related to exposure to cobalt sulfate heptahydrate. There was clear evidence of the carcinogenic activity in female F344/N rats based on incr incidences of alveolar/bronchiolar neoplasms and pheochromocytomas of the adrenal medulla in groups exposed to cobalt sulfate heptahydrate. There was clear evidence of carcinogenic activity of cobalt sulfate heptahydrate in male and female B6C3F1 mice based on incr incidences of alveolar/bronchiolar neoplasms. /Cobalt sulfate heptahydrate/|For more National Toxicology Program Studies (Complete) data for Cobaltous sulfate (6 total), please visit the HSDB record page.

A detailed study of the thyroid pathology in 14 heavy beer drinkers who died from severe myocardiopathy in Quebec found 11 thyroids with follicular distortion, colloid depletion, and numerous cellular changes. /Beer with cobalt sulfate/

Cobaltous sulfate (hexahydrate/heptahydrate) occurs in nature as the mineral bieberite(1,2). Bieberite is an uncommon oxidation product of cobalt-bearing sulfide-arsenides minerals(3).

Cobaltous sulfate's production and use in storage batteries, electroplating baths, driers for lithographic inks, paints and varnishes, use in ceramics, pigments and glazes(1,2) and im feed supplemnets(3) may result in its release to the environment through various waste streams(SRC).

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

Food Chain Concentration Potential of Cobaltous Sulfate (heptahydrate): Bioconcentration of 200-1000 fold only under constant exposure. Not significant in spill conditions(1).

Evaporation of cobaltous sulfate heptahydrate at 20 °C is negligible(1).

According to the 2012 TSCA Inventory Update Reporting data, 6 reporting facilities estimate the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of cobaltous sulfate in the United States may be as low as <10 workers and as high as 100-499 workers per plant; the data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).|NIOSH (NOES Survey 1981-1983) has statistically estimated that 44,607 workers (11,292 of these are female) are potentially exposed to cobaltous sulfate in the US(1). Occupational exposure to cobaltous sulfate may occur through inhalation of aerosol dusts and dermal contact with this compound at workplaces where cobaltous sulfate is produced or used(SRC).

The effects of cobalt sulfate administered to pregnant C57BI mice, OFA-SD rats, and New Zealand rabbits was studied on fetal and postnatal offspring. Cobalt concentration in the maternal blood was increased in proportion to the administered doses. Cobalt crossed the placenta and appeared in the fetal blood and amniotic fluid. Regardless of the administered dose of cobalt sulfate, cobalt concentration in the blood peaked 2 hr after administration.|Sheep given a single dose of hydrated cobalt sulfate were killed. ...The livers contained 400-1200 ppm of cobalt. In cattle dying after a massive overdose of hydrated cobalt sulfate livers contained 5-300 ppm, kidneys 30-200 ppm. /Hydrated cobalt sulfate/|Following longer-term exposure (8 weeks) to cobalt sulfate in the diet, exposed rats showed a 30-fold increase in the cobalt concentration in the myocardium, a 26-fold increase in the concentration in the soleus muscle, and a 100-fold increase in the concentration in serum compared with nonexposed controls. Long-term oral exposure of rats to cobalt chloride resulted in significantly increased levels of cobalt in the liver, kidney, muscle, brain, and testes of treated rats.|Cobalt metabolism and toxicology are summarized. The biological functions of cobalt are updated in the light of recent understanding of cobalt interference with the sensing in almost all animal cells of oxygen deficiency (hypoxia). Cobalt (Co(2+)) stabilizes the transcriptional activator hypoxia-inducible factor (HIF) and thus mimics hypoxia and stimulates erythropoietin (Epo) production, but probably also by the same mechanism induces a coordinated up-regulation of a number of adaptive responses to hypoxia, many with potential carcinogenic effects. This means on the other hand that cobalt (Co(2+)) also may have beneficial effects under conditions of tissue hypoxia, and possibly can represent an alternative to hypoxic preconditioning. Cobalt is acutely toxic in larger doses, and in mammalian in vitro test systems cobalt ions and cobalt metal are cytotoxic and induce apoptosis and at higher concentrations necrosis with inflammatory response. Cobalt metal and salts are also genotoxic, mainly caused by oxidative DNA damage by reactive oxygen species, perhaps combined with inhibition of DNA repair. Of note, the evidence for carcinogenicity of cobalt metal and cobalt sulfate is considered sufficient in experimental animals, but is as yet considered inadequate in humans. Interestingly, some of the toxic effects of cobalt (Co(2+)) have recently been proposed to be due to putative inhibition of Ca(2+) entry and Ca(2+)-signaling and competition with Ca(2+) for intracellular Ca(2+)-binding proteins. The tissue partitioning of cobalt (Co(2+)) and its time-dependence after administration of a single dose have been studied in man, but mainly in laboratory animals. Cobalt is accumulated primarily in liver, kidney, pancreas, and heart, with the relative content in skeleton and skeletal muscle increasing with time after cobalt administration. In man the renal excretion is initially rapid but decreasing over the first days, followed by a second, slow phase lasting several weeks, and with a significant long-term retention in tissues for several years. In serum cobalt (Co(2+)) binds to albumin, and the concentration of free, ionized Co(2+) is estimated at 5-12% of the total cobalt concentration. In human red cells the membrane transport pathway for cobalt (Co(2+)) uptake appears to be shared with calcium (Ca(2+)), but with the uptake being essentially irreversible as cobalt is effectively bound in the cytosol and is not itself extruded by the Ca-pump. It is tempting to speculate that this could perhaps also be the case in other animal cells. If this were actually the case, the tissue partitioning and biokinetics of cobalt in cells and tissues would be closely related to the uptake of calcium, with cobalt partitioning primarily into tissues with a high calcium turn-over, and with cobalt accumulation and retention in tissues with a slow turn-over of the cells. The occupational cobalt exposure, e.g. in cobalt processing plants and hard-metal industry is well known and has probably been somewhat reduced in more recent years due to improved work place hygiene. Of note, however, adverse reactions to heart and lung have recently been demonstrated following cobalt exposure near or slightly under the current occupational exposure limit. Over the last decades the use of cobalt-chromium hard-metal alloys in orthopedic joint replacements, in particular in metal-on-metal bearings in hip joint arthroplasty, has created an entirely new source of internal cobalt exposure. Corrosion and wear produce soluble metal ions and metal debris in the form of huge numbers of wear particles in nanometric size, with systemic dissemination through lymph and systemic vascular system. This may cause adverse local reactions in peri-prosthetic soft-tissues, and in addition systemic toxicity. Of note, the metal nanoparticles have been demonstrated to be clearly more toxic than larger, micrometer-sized particles, and this has made the concept of nanotoxicology a crucial, new discipline. As another new potential source of cobalt exposure, suspicion has been raised that cobalt salts may be misused by athletes as an attractive alternative to Epo doping for enhancing aerobic performance. The cobalt toxicity in vitro seems to reside mainly with ionized cobalt. It is tempting to speculate that ionized cobalt is also the primary toxic form for systemic toxicity in vivo. Under this assumption, the relevant parameter for risk assessment would be the time-averaged value for systemic cobalt ion exposure that from a theoretical point of view might be obtained by measuring the cobalt content in red cells, since their cobalt uptake reflects uptake only of free ionized cobalt (Co(2+)), and since the uptake during their 120 days life span is practically irreversible. This clearly calls for future clinical studies in exposed individuals with a systematic comparison of concurrent measurements of cobalt concentration in red cells and in serum.

Cellular metabolism depends on the availability of oxygen and the major regulator of oxygen homeostasis is hypoxia-inducible factor 1 (HIF-1), a highly conserved transcription factor that plays an essential role in cellular and systemic homeostatic responses to hypoxia. HIF-1 is a heterodimeric transcription factor composed of hypoxia-inducible HIF-1alpha and constitutively expressed HIF-1beta. Under hypoxic conditions, the two subunits dimerize, allowing translocation of the HIF-1 complex to the nucleus where it binds to hypoxia-response elements (HREs) and activates expression of target genes implicated in angiogenesis, cell growth, and survival. The HIF-1 pathway is essential to normal growth and development, and is involved in the pathophysiology of cancer, inflammation, and ischemia. Thus, there is considerable interest in identifying compounds that modulate the HIF-1 signaling pathway. To assess the ability of environmental chemicals to stimulate the HIF-1 signaling pathway, we screened a National Toxicology Program collection of 1408 compounds using a cell-based beta-lactamase HRE reporter gene assay in a quantitative high-throughput screening (qHTS) format. Twelve active compounds were identified. These compounds were tested in a confirmatory assay for induction of vascular endothelial growth factor, a known hypoxia target gene, and confirmed compounds were further tested for their ability to mimic the effect of a reduced-oxygen environment on hypoxia-regulated promoter activity. Based on this testing strategy, three compounds (o-phenanthroline, iodochlorohydroxyquinoline, cobalt sulfate heptahydrate) were confirmed as hypoxia mimetics, whereas two compounds (7-diethylamino-4-methylcoumarin and 7,12-dimethylbenz(a)anthracence) were found to interact with HIF-1 in a manner different from hypoxia. /Cobalt sulfate heptahydrate/

Inhalation causes shortness of breath and coughing; permanent disability may occur. Ingestion causes pain and vomiting. Contact with eyes or skin causes irritation. (USCG, 1999)

INHALATION: move to fresh air; if breathing has stopped, begin artificial respiration and call a doctor. INGESTION: give large amount of water; induce vomiting; call a doctor. EYES: flush with water for at least 15 min.; consult a physician if irritation persists. SKIN: flush with water. (USCG, 1999)

Fresh air, rest. Refer for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Seek medical attention if you feel unwell.

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

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

/HUMAN EXPOSURE STUDIES/ In order to investigate the causative factors of dermatitis and eczema, patch test was performed using the GB7804-87 standard allergens in 720 patients with dermatitis and eczema. There were 376 patients reacted to one or more allergens. The total positive reaction rate was 52.2%. Positive reactions were most frequently with cobalt sulfate (118 cases, 16.4%), potassium dichromate (115 cases, 16.0%), nickelchloride (108 cases, 15.0%) mercuric chloride (106 cases, 14.7%), Beihai detergent powder (63 cases, 8.8%), and p-phenylene diamine (50 cases, 6.9%). The positive rate was above 1% in 18 allergens. This study shows that the standard screening allergens are valuable in the investigation of the etiology of the dermatitis and eczema.|/HUMAN EXPOSURE STUDIES/ We patch tested 13 beauticians with hand dermatitis between 1982 and 1986. They were all young female novice beauticians or those in training. The onset of their allergic dermatitis was noticed within 1 month to 1 year of their starting this occupation. Definite positive reactions to products were seen from hair dyes (as is, open test) (6/12), cold permanent wave primary solutions (as is, open test) (7/13) and a shampoo (1% aq., closed test) (1/13). Positive reactions to allergens were seen with para-phenylenediamine (1% pet) (12/13), ammonium thioglycolate (5% aq., open test) (3/7), para-toluylenediamine (1% pet) (7/9), para-aminophenol (1% pet) (1/4), ortho-aminophenol (1% pet) (1/4), Quinoline yellow SS (0.5% pet) (1/4), nickel sulfate (2.5% pet) (1/12), cobalt sulfate (2.3% pet) (1/12), thimerosal (0.05% pet) (1/12) and procaine hydrochloride (1% pet) (1/12). Study of the prognosis showed that 5 out of 12 cases could continue their occupation, but 4 cases had persistent hand dermatitis despite protecting their hands from hair dyes with gloves, 7 cases quit their jobs, and in 5 their hands healed while 2 cases continued to have atopic hand dermatitis. A personal or family history of atopy was frequent among the cases, so we recommend that those who have such a history should not become beauticians.|/SIGNS AND SYMPTOMS/ Effects of long-term or repeated exposure: Repeated or prolonged contact may cause skin sensitization. Repeated or prolonged inhalation exposure may cause asthma. The substance may have effects on the heart, thyroid and bone marrow, resulting in cardiomyopathy, goiter and polycythemia.|/SIGNS AND SYMPTOMS/ Eight asthmatic patients who had no history of asthma before starting work in a hard-metal plant and eight control subjects (three atopic, three nonatopic asthmatic, and two normal volunteers) without a history of exposure to hard metal dust were subjected to provocation tests, skin tests, radioallergosorbent tests (RAST) and Farr test with cobalt. Four of the eight patients were atopic, and seven showed bronchial hyperresponsiveness to methacholine (BHR). Patch and intradermal skin tests with cobalt chloride (CoCl2) could not discriminate the patients from control subjects. All patients had positive reactions to CoCl2 in the provocation tests; two developed immediate asthmatic reaction (IAR), four late asthmatic reaction (LAR), and two dual asthmatic reaction (DAR), while the control subjects showed no reaction. Evidence of specific IgE antibodies to cobalt-conjugated human serum albumin (Co-HSA) was presented by four patients (RAST score greater than 2) based on comparison of serum samples from 60 asthmatic patients and 25 asymptomatic workers in the same plant. Positive serum samples selectively bound (57)Co, and the test was blocked by nonlabled cobalt sulfate (CoSO4). These findings suggest the development of hard metal-induced asthma from cobalt sensitivity.|For more Human Toxicity Excerpts (Complete) data for Cobaltous sulfate (12 total), please visit the HSDB record page.

cobalt sulfate

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

Cough. Sore throat. Shortness of breath.

Redness. Pain.

Cobalt Brown: a pigment prepared by calcining a mixture of ammonium sulfate, cobalt sulfate, and ferrous sulfate.|Cobalt Vitriol: Cobaltous sulfate, CoSO4.7H2O /Heptahydrate/|Liquid, crystal grades; crystals and soln form, feed, technical and reagent grades|Powder grades; crystal, feed grades /Monohydrate/

Agriculture, forestry, fishing and hunting|Sulfuric acid, cobalt(2+) salt (1:1): ACTIVE

In 15 commercial beers analyzed... using a colorimetric method, cobalt generally measured well below 0.1 mg/L. If cobalt sulfate had been added in processing, values of up to 1.1 mg/L were recorded.