cobalt sulfate

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

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

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

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

H350i: May cause cancer by inhalation [Danger Carcinogenicity]

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

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

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

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

H302 (99.8%): Harmful if swallowed [Warning Acute toxicity, oral]

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

H319 (15.9%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H334 (> 99.9%): May cause allergy or asthma symptoms or breathing difficulties if inhaled [Danger Sensitization, respiratory]

H341 (99.8%): Suspected of causing genetic defects [Warning Germ cell mutagenicity]

H350 (85.6%): May cause cancer [Danger Carcinogenicity]

H350i (14.4%): May cause cancer by inhalation [Danger Carcinogenicity]

H360 (84.1%): May damage fertility or the unborn child [Danger Reproductive toxicity]

H360F (10.5%): May damage fertility [Danger Reproductive toxicity]

H400 (99.9%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410 (97.3%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

P203, P233, P260, P261, P264, P264+P265, P270, P271, P272, P273, P280, P284, P301+P317, P302+P352, P304+P340, P305+P351+P338, P318, P321, P330, P333+P317, P337+P317, P342+P316, P362+P364, P391, P403, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 2654 reports by companies from 34 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

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

H350: May cause cancer [Danger Carcinogenicity]

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

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

H351: Suspected of causing cancer [Warning Carcinogenicity]

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

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

H319: Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H360F: May damage fertility [Danger Reproductive toxicity]

P203, P233, P260, P261, P264, P264+P265, P270, P271, P272, P273, P280, P284, P301+P317, P302+P352, P304+P340, P305+P351+P338, P318, P319, P321, P330, P333+P317, P337+P317, P342+P316, P362+P364, P391, P403, P405, and P501 (click each P-code to see the statement)

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.

Rinse mouth. Give one or two glasses of water to drink. Refer for medical attention .

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)

In case of fire in the surroundings, use appropriate extinguishing media.

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.

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.

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/

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.

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.

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

Separated from strong oxidants.

This material should be stored in sealed containers to avoid dampness and dust. Partly used containers should be sealed. Otherwise, no special precautions are required.

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

0.060 [mg/m3]

14 [mg/m3]

84 [mg/m3]

0.02 [mg/m3], as Co

8 hr Time Weighted Avg (TWA): 0.02 mg/cu m. /Cobalt and inorganic compounds, as Co/

Peak Exposure Recommendation: Transient increases in workers' exposure levels may exceed 3 times the value of the TLV-TWA level for no more than 15 minutes at a time, on no more than 4 occasions spaced 1 hour apart during a workday, and under no circumstances should they exceed 5 times the value of the TLV-TWA level. In addition, the 8-hour TWA is not to be exceeded for an 8-hour work period. /Cobalt and inorganic compounds, as Co/

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

Biological Exposure Index (BEI): Determinant: cobalt in urine; Sampling Time: end of shift at end of workweek; BEI: 15 ug/L. Notation: The determinant is nonspecific, since it is also observed after after exposure to other chemicals. /Cobalt and inorganic compounds, including cobalt oxides but not combined with tungsten carbide/

Biological Exposure Index (BEI): Determinant: cobalt in urine; Sampling Time: end of shift at end of workweek; BEI: None. Notation: The determinant is nonspecific, since it is also observed after exposure to other chemicals. Biological monitoring should be considered for this compound based on the review; however, a specific BEI could not be determined due to insufficient data. /Cobalt with tungsten carbide/

(as Co, inhalable fraction): 0.02 mg/m

(as Co, inhalable fraction): skin absorption (H); sensitization of respiratory tract and skin (SAH); carcinogen category: 2; germ cell mutagen group: 3A

Chronic Inhalation: 0.0001 mg/m3 (L134)

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

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.

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.

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.

Do not eat, drink, or smoke during work. Wash hands before eating.

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

Dry Powder; Large Crystals; Large Crystals; Liquid; Dry Powder; Large Crystals

Red to lavender solid; [Merck Index] Blue odorless powder; Soluble in water (362 g/L at 20 deg C); [MSDSonline]

LAVENDER-TO-DARK-BLUE CRYSTALS.

Red to lavender dimorphic, othorhombic crystals

Red orthorhombic crystals

Red powder

Rose-pink solid

Odorless

Odorless; heat of solution: 23 BTU/lb= 13 cal/g= 0.54X10+5 J/kg; solubility: 35.040 lb/100 lb water at 70 °F /Cobaltous sulfate heptahydrate/

In water, 330 g/L at 20 °C

38.3 g/100 g water at 25 °C

Dissolves slowly in boiling water

84 g/100 mL water at 100 °C

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

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

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

3.71 at 25 °C/4 °C

Light red crystalline solid; loses waters of crystallization when heated above 42 °C, producing the monohydrate at 100 °C and anhydrous salt above 250 °C; density: 2.01 kg/L at 25 °C /Cobalt(II) sulfate hexahydrate/

Density: 1.948 g/cu cm; loses heptahydrate at 420 °C /Cobalt(II) sulfate heptahydrate/

3.71 g/cm³

3.71 @25 °C

Stable to 708 °C.

When heated to decomposition it emits toxic fumes of SOx

The substance decomposes on heating to 735 /deg/ C, producing toxic fumes of sulfur oxides

When heated to decomposition it emits toxic vapors of SOx and Co. /Cobalt sulfate heptahydrate/

735 °C. This produces toxic fumes of sulfur oxides. The dust reacts with strong oxidants. This generates fire and explosion hazard.

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.

Evaporation at 20 °C is negligible

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/

Metals -> Metals, Inorganic Compounds

MALTING OR FERMENTING AID, SURFACE-ACTIVE AGENT -> FDA Substance added to food

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.

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

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.

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)

This listing of the class of cobalt and cobalt compounds that release cobalt ions in vivo supersedes the previous listing of cobalt sulfate in the Report on Carcinogens. The compound cobalt sulfate was first listed in the Eleventh Report on Carcinogens in 2004 as reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity in experimental animals.

Cobaltous Sulfate: reasonably anticipated to be a human carcinogen.

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

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

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

2B, possibly carcinogenic to humans. (L135)

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

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

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

Cough. Sore throat. Shortness of breath.

Redness. Pain.

Nausea. Vomiting. Abdominal pain.

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

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

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

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

NTP Carcinogen - Reasonably anticipated to be a human carcinogen.

LD50: 424 mg/kg (Oral, Rat) (A195)

LD50: 143 mg/kg (Intraperitoneal, Mouse) (T74)

LD50: 18 200 ug/kg (Intravenous, Rat) (T74)

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.

Treatment of cobalt poisoning is symptomatic. (L29)

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.

/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.

/LABORATORY ANIMALS: Acute Exposure/ Sheep given a single dose of hydrated cobalt sulfate were killed by quantities between 15 and 55 g, the avg lethal dose being 330 mg/kg. /Hydrated cobalt sulfate/

/LABORATORY ANIMALS: Acute Exposure/ Hemodynamic mechanisms of Co(2+)-evoked hypotension were studied in pentobarbital-anesthetized male Wistar rats. Bolus i.v. administration of cobalt sulfate (30, 90 and 270 mg/kg of Co) evoked dose-dependent hypotension followed by tachycardia and increase in left ventricular contractility index (dP/dt/P). Administration of beta-adrenoblocker propranolol (2 mg/kg) attenuated Co evoked (270 ug/kg) tachycardia and unmasked its cardiodepressive effects (dP/dt/P decreased by 11% and end-diastolic pressure increased by 55%). Cardiodepressive Co2+ effects were prevented by administration of verapamil (0.4 mg/kg). In the second group hemodynamic mechanisms of Co-evoked hypotension were studied with radioactive microspheres. Co2+ infusion (55 mg/kg) lowered blood pressure (in average by -11%) by decreasing total peripheral resistance (-25%). Cardiotoxic effects were obtained with a ++larger dose 80 mg/kg/min. It is concluded that Co decreased blood pressure by vasodilatator action and its cardiotoxic effects attenuated by sympathetic counterregulation and may be prevented by verapamil.

/LABORATORY ANIMALS: Acute Exposure/ The acute toxicities of chloride, acetate, cobalt nitrate and cobalt sulfate (II) were investigated in rats. The values obtained for the LD50 (7 days) were 133, 194, 198 and 279 mg of Co/kg respectively, when the salts were given orally. The values for intraperitoneal administration were 10.6, 8.8, 8.3 and 11.5 mg of Co/kg. The majority of deaths occurred during the first 48 hours. The physical and clinical signs appearing after the intoxication disappeared for the most part after the first 72 hours. Also, the effect produced by chloride and cobalt acetate (II) given orally and intraperitoneally, in some hematological parameters and serum parameters during the first 24 hours after intoxications, has been studied at several doses. A noteworthy increase was observed in the hemoglobin and hematocrit as well as in the plasma proteins. There was significant hyperglycemia and also significant changes in the lipid parameters such as triglycerides and cholesterol. The duration and degree of the change depended on the dose. As a general rule, no significant differences were registered between the results obtained for the two salts.

EC50; Species: Tetrahymena pyriformis (Ciliate) exponential growth phase (log), stratin GL 1000 cells/mL; Conditions: freshwater, static, 25 °C, pH 7; Concentration: 4890 ug/L for 1 hr; Effect: biochemistry, decreased fluorescence /> or =98% purity/

LC50; Species: Daphnia magna (Water Flea) age 12 hr neonate, fed; Conditions: freshwater, static, 20.4 °C, pH 8.35, hard water, alkalinity 234 mg/L CaCO3, dissolved oxygen 7.93 mg/L; Concentration: 7370 ug/L for 48 hr /Technical/

LC50; Species: Daphnia magna (Water Flea) age 12 hr neonate, not fed; Conditions: freshwater, static, 20.4 °C, pH 8.35, hard water, alkalinity 234 mg/L CaCO3, dissolved oxygen 7.93 mg/L; Concentration: 6830 ug/L for 48 hr (95% confidence interval: 5100-8990 ug/L) /Technical/

LC50; Species: Daphnia magna (Water Flea) organisms at different life stages, neonate-adult; Conditions: freshwater, renewal, 20.3 °C, pH 8.31, hard water, alkalinity 198 mg/L CaCO3, dissolved oxygen 7.44 mg/L; Concentration: 27 ug/L for 28 days /Technical/

For more Ecotoxicity Values (Complete) data for Cobaltous sulfate (9 total), please visit the HSDB record page.

The substance is toxic to aquatic organisms. The substance may cause long-term effects in the aquatic environment. It is strongly advised not to let the chemical enter into the environment.

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).

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.

Symbol: T, N; R: 49-60-22-42/43-68-50/53; S: 53-45-60-61; Note: E, 1