Cobalt oxide (CoO)

74.93

74.928

215-154-6

1551

3288

DTXSID6051649

Powder or cubic or hexagonal crystals; color varies from olive green to red depending on particle size, but the commercial material is usually dark gray|Gray cubic crystals|Grayish powder under most conditiond; can form green brown crystals.|Black to green crystals or powder

28220000

17.1

-0.11880

Green-brown Powder

6.45

1935 °C (approx)

3800ºC

insoluble

Keep container tightly closed in a dry and well-ventilated place. Keep in a dry place. Storage class (TRGS 510): Non-combustible, acute toxic Cat. 1 and 2 / very toxic hazardous materials.

Oral-Rat LD 202 mg/kg; subcutaneous-mouse LD50: 125 mg/m3/4 hours

Non-combustible; produces toxic cobalt-containing fumes in the fire

When cobalt oxide is reduced with ammonia so that it contains 14-16% /molecular oxygen O2/, it glows when exposed to air. [|Standard enthalpy of formation: -237.9 kJ/mol; heat capacity: 55.2 J/mol K|The commercial cobalt oxides are not usually definite chemical compounds, but are mixtures of two or more cobalt oxides.|Dissolution in water varied from 0.602 mg/L to 32.825 mg/L at about 21-22 °C depending upon concentration loading (1-100 mg/L), time-period (7-28 days) and pH (between 5 and 7)

III

6.1(b)

UN 3288 6.1/PG 3

3

22-43-50/53-42/43-26

24-37-60-61-45-36/37-28

GG2800000

Xn,N,T+

Warehouse low temperature, ventilated, dry

Stability Stable, but may be moisture sensitive.

P201, P202, P260, P261, P264, P270, P271, P272, P280, P281, P284, P285, P301+P310, P302+P352, P304+P340, P304+P341, P308+P313, P310, P314, P320, P321, P330, P333+P313, P342+P311, P363, P403+P233, P405, P501

H301

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.

Incompatible materials: Strong oxidizing agents.|Violent reaction with hydrogen peroxide

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 oxide is included on this list.

HHS/ATSDR; Toxicological Profile for Cobalt 486 pp PB2004-10733 (April 2004)[Available from, as of March 28, 2017: http://www.atsdr.cdc.gov/toxprofiles/index.asp]

Not combustible.

|Warning|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P261, P264, P270, P272, P273, P280, P301+P312, P302+P352, P321, P330, P333+P313, P363, P391, and P501|Danger|H301 (57.47%): Toxic if swallowed [Danger Acute toxicity, oral]|P201, P202, P260, P261, P264, P270, P271, P272, P273, P280, P281, P284, P285, P301+P310, P301+P312, P302+P352, P304+P340, P304+P341, P308+P313, P310, P320, P321, P330, P333+P313, P342+P311, P363, P391, P403+P233, P405, and P501|Aggregated GHS information provided by 395 companies from 23 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H301: Toxic if swallowed [Danger Acute toxicity, oral]|P201, P202, P260, P261, P264, P270, P271, P272, P273, P280, P281, P284, P285, P301+P310, P302+P352, P304+P340, P304+P341, P308+P313, P310, P314, P320, P321, P330, P333+P313, P342+P311, P363, P391, P403+P233, P405, and P501|P201, P202, P260, P261, P264, P270, P271, P272, P273, P280, P281, P284, P285, P301+P310, P302+P352, P304+P340, P304+P341, P308+P313, P310, P320, P321, P330, P333+P313, P342+P311, P363, P391, P403+P233, P405, and P501|P201, P202, P260, P261, P264, P270, P272, P280, P281, P285, P301+P310, P302+P352, P304+P341, P307+P311, P308+P313, P309+P311, P314, P321, P330, P333+P313, P342+P311, P363, P405, and P501|P201, P202, P260, P261, P264, P270, P272, P280, P281, P285, P301+P310, P302+P352, P304+P341, P307+P311, P308+P313, P309+P311, P321, P330, P333+P313, P342+P311, P363, P405, and P501|Not Classified

Wear appropriate personal protective clothing to prevent skin contact. /Cobalt metal dust and fume (as Co)/|Respirator Recommendations: Up to 0.25 mg/cu m: /Cobalt metal dust and fume (as Co)/[Table#918]|Respirator Recommendations: Up to 0.5 mg/cu m: /Cobalt metal dust and fume (as Co)/[Table#919]|Respirator Recommendations: Up to 1.25 mg/cu m: /Cobalt metal dust and fume (as Co)/[Table#920]|For more Personal Protective Equipment (PPE) (Complete) data for Cobaltous oxide (12 total), please visit the HSDB record page.

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. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.|Liquid material spills can be copiously flushed with water and channeled to a treatment system or holding tank for reclamation or proper disposal. Spills of dry material can be removed by vacuuming or wet mopping. Some spills can be removed by hosing, first with a mist of water to dampen the spilled material and then with a more forceful stream that flushes it into a holding tank or other facility for handling contaminated water. Work surfaces or contaminated clothing should never be cleaned by dry sweeping or blowing with pressurized hoses. Recovery systems used to reclaim waste metals should comply with federal, state, and local regulations. All waste materials generated in the handling of cobalt-containing substances should be disposed of in compliance with federal, state, and local regulations. /Cobalt and cobalt salts/

The worker should immediately wash the skin when it becomes contaminated. /Cobalt metal dust and fume (as Co)/|Work clothing that becomes wet or significantly contaminated should be removed and replaced. /Cobalt metal dust and fume (as Co)/|Workers whose clothing may have become contaminated should change into uncontaminated clothing before leaving the work premises. /Cobalt metal dust and fume (as Co)/|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. Discharge into the environment must be avoided.|For more Preventive Measures (Complete) data for Cobaltous oxide (13 total), please visit the HSDB record page.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. 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 hydrogen peroxide.

A harmful concentration of airborne particles can be reached quickly when dispersed.

May cause mechanical irritation. Inhalation may cause asthma-like reactions.

Repeated or prolonged contact may cause skin sensitization. Repeated or prolonged inhalation may cause asthma. This substance is possibly carcinogenic to humans.

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.

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 oxide is included on this list.

highly toxic

IDENTIFICATION AND USE: Cobalt oxide is found in two forms, CoO and Co2O3. The commercial oxides are usually not definite chemical compounds but mixtures of the cobalt oxides. It could be found in the form of powder or cubic or hexagonal crystals; color varies from olive green to red depending on particle size, but the commercial material is usually dark gray. Cobalt oxide is used in pigments for ceramics, in glass coloring and decolorization, as oxidation catalyst for drying oils, and fast-drying paints and varnishes, in preparation of cobalt-metal catalysts, and cobalt powder for binder in sintered tungsten carbide; in semiconductors. HUMAN EXPOSURE AND TOXICITY: Three cases of pneumoconiosis in the tungsten carbide tool industry were reported, where exposure to cobalt powder, oxide or salt led to disease in three out of 1500 exposed workers. Particulate cobalt oxide was cytotoxic and genotoxic to human lung epithelial cells. ANIMAL STUDIES: Hamsters exposed by inhalation to cobalt oxide for a lifetime developed emphysema, but the incidence of pulmonary tumors was not different from controls. Cobalt oxide and cobalt sulfide were administered by single intramuscular injection in rats and mice and the sulfide was found to be more carcinogenic than the oxide. The carcinogenic response on injection in mice was much lower. In a later study, intramuscular injection of CoO resulted in a 50% incidence of rhabdomyosarcomas in rats but was completely negative in mice. Prolonged exposure (3-4 months) of rats and rabbits to mixed cobalt oxides (0.4-9 mg cobalt/mg) resulted in lesions in the alveolar region of the respiratory tract characterized histologically by nodular accumulation of Type II epithelial cells, accumulations of enlarged highly vacuolated macrophages, interstitial inflammation, and fibrosis. ECOTOXICITY STUDIES: Exposure to cobalt oxide (CoO <100 nm) nanoparticles was toxic to zooplankton, which is an important source of food in aquatic food chain.

Prolonged exposure (3-4 months) of rats and rabbits to mixed cobalt oxides (0.4-9 mg cobalt/mg) resulted in lesions in the alveolar region of the respiratory tract characterized histologically by nodular accumulation of Type II epithelial cells, accumulations of enlarged highly vacuolated macrophages, interstitial inflammation, and fibrosis.|... Fibrosarcomas were induced in mice 6 months after the parenteral injection of an industrial refining dust containing cobalt oxide and cobalt sulfide. /Dust containing cobalt oxide and cobalt sulfide/

LD50 Mouse sc 125 mg/kg|LD50 Rat oral 202 mg/kg

/AQUATIC SPECIES/ In this study, the effects of exposure to engineered nickel oxide (NiO 40-60 nm) and cobalt oxide (CoO <100 nm) nanoparticles (NP) were investigated on Artemia salina. Aggregation and stability of the aqueous NP suspensions were characterized by DLS and TEM. Acute exposure was conducted on nauplii (larvae) in seawater in a concentration range from 0.2 to 50 mg/L NPs for 24 hr (short term) and 96 hr (long term). The hydrodynamic diameters of NiO and CoO NPs in exposure medium were larger than those estimated by TEM. Accumulation rate of NiO NPs were found to be four times higher than that of CoO NPs under the same experimental conditions. Examinations under phase contrast microscope showed that the nanoparticles accumulated in the intestine of artemia, which increased with increasing exposure concentration. Differences were observed in the extent of dissolution of the NPs in the seawater. The CoO NPs dissolved significantly while NiO NPs were relatively more stable. Oxidative stress induced by the NP suspensions was measured by malondialdehyde assay. Suspensions of NiO NPs caused higher oxidative stress on nauplii than those of CoO NPs. The results imply that CoO and NiO NPs exhibit toxicity on Artemia (e.g., zooplankton) that are an important source of food in aquatic food chain. /Cobalt oxide nanoparticles/

Cobaltous oxide was detected in meteorites collected from Monturaqui meteorite crater in the Andes Mountains, Chile(1); the CoO content varied from 0.2 to 0.8% wt with a mean of 0.5% wt(1).|Cobaltous oxide's production and use as a pigment in ceramics, paints and varnishes, in glass coloring and decorating and as a precursor for the production of cobalt chemicals and catalysts(1,2) may result in its release to the environment through various waste streams(SRC). Release to the environment of cobaltous oxide is likely to occur from: indoor use in long-life materials with low release rate (e.g. flooring, furniture, toys, construction materials, curtains, foot-wear, leather products, paper and cardboard products, electronic equipment) and outdoor use in long-life materials with low release rate (e.g. metal, wooden and plastic construction and building materials(3).

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).

According to the 2012 TSCA Inventory Update Reporting data, 8 reporting facilities estimate the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of cobaltous oxide in the United States may be as low as 25-49 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 3,559 workers (1,767 of these are female) are potentially exposed to cobalt(II) oxide in the US(1).|... survey made by the Pennsylvania Dept of Health showed breathing zone concentration could be controlled to about 0.07 mg/cu m /cobalt metal fume & dust/; without control, concentrations were about 0.5 mg/cu m.

/EXPL THER/ The development of smart nanoparticles that can exhibit the anti-cancer activity, introduces better efficacy and lower toxicity for treatment. The present study was aimed to evaluate the anti-cancer activity of surface functionalized CoO nanoparticles against Jurkat (T-cell lymphoma) and KB (oral carcinoma) cell lines. The nano-sized cobalt oxide nanoparticles (CoO) was prepared by thermal decomposition method followed by surface modification using phosphonomethyl iminodiacetic acid (PMIDA). The PMIDA-coated CoO nanoparticle was characterized by X-ray diffraction, dynamic light scattering, and transmission electron microscopy; and the conjugation was analyzed by Fourier transform infrared spectroscopy. The resultant nanoparticles with an average size less than 100 nm measured by dynamic light scattering and transmission electron microscopy. Cytotoxicity study, flow cytometric analysis and scanning electron micrographs have been revealed that PMIDA-coated nanoparticles significantly enhances the cellular uptake of the nanoparticle and thus facilitates apoptosis of cancer cell (Jurkat and KB). For the application of PMIDA-coated CoO nanoparticles in the medical field, doxorubicin, a potent anti-cancer drug, has been used in similar fashion in this experimental design and all these effects or patterns were observed. /Cobalt oxide nanoparticles/

The aim of this study was to verify the relationship between the cobalt oxide concentration in air and the cobalt concentration in urine. In the first study, we measured the cobalt concentration in the urine of 16 workers exposed to cobalt oxide in a Digital Video Cassette manufacturing plant at the beginning and end of their workshift during 2 working cycles. In the second study, we measured the exposure level to cobalt oxide and the cobalt concentration in urine at the end of the workshift of other 16 workers on 3 out of 5 consecutive work days (Monday, Wednesday and Friday). Four workers among the 16 participated twice. In the first study, the cobalt concentration in the urine increased about 1.5-3 fold during each workshift and then tended to decrease rapidly to the control value before the next workshift. In the second study, we examined the relationship between air and urine concentration using 22 samples after excluding data from workers with dust respirators. Comparing the air and urine concentrations for samples under 30 ug/cu m (n = 20), a significant correlation was found (r = 0.76). These results indicate that most of the inhaled cobalt oxide was excreted rapidly, and a good relationship was found between air and urine concentrations at the end of the workshift when the exposure level was under 30 ug/cu m. Therefore, the cobalt concentration in urine at the end of a workshift can be used as an indicator of one-day exposure to cobalt oxide when the exposure is low level.|The 24-hr deposition and clearence in hamsters exposed by inhalation and gavage to CoO showed that 87% was distributed throughout the body form an inhaled dose of 784 ug and 11.3%, form a 5-mg dose by gavage. The greatest amounts from both routes (60 and 11% respectively) remained in the gastrointestinal tract. The carcass retained the next largest amounts, 23% from inhalation and 0.34% by gavage; the lung, 3.3% by inhalation and less than 0.06 by gavage. The liver and kidneys had small fractional percentages of the administered dose.|Three beagle dogs were exposed to 60Co3O4 /cobaltosic oxide/ and sacrificed singly at 8, 64 and 128 days. Three beagle dogs were exposed to 60CoO /cobaltous oxide/ and sacrificed at 8, 16 and 64 days after exposure. Whole-body retention patterns showed that 60CoO left the body with a shorter effective half life than 60Co3O4. The concentration of 60Co detected in the blood was at least an order of magnitude higher in the dogs exposed to 60CoO than in the dogs exposed to 60Co3O4. Cobalt-60 translocated from the lung accumulated predominantly in the kidney, liver, skeleton and cartilagenous structures such as the trachea. Higher concentrations were reached earlier in the dogs exposed to 60CoO. After early fecal excretion of material deposited in the upper respiratory tract, excretion was greatest via the urine. The higher solubility of the 60CoO formed at 1400 °C relative to 60Co3O4 formed at 850 °C is noteworthy considering that generally aerosols formed at higher temperatures are more insoluble than aerosols formed at lower temperatures /Cobaltosic and cobaltous oxides/.|Cobalt concentration from processing cobalt oxide in urine: mean: 0.34 mg/L; range: 0.1-0.9 mg/L /From table/|For more Absorption, Distribution and Excretion (Complete) data for Cobaltous oxide (6 total), please visit the HSDB record page.

Chest counting data have been collected for about 4 yr for a case which involved inhalation of (60)Co-oxide. The measured chest burden ... decreases with successively increasing half times (about 10 months at early times to about 30 months after 3 yr)... With the exception of the long-term fraction in the lymph nodes, only one rate of elimination seems to be present, 225 days, throughout the period of observation.|The behavior of (60)Co has been studied in 5 men for periods of up to 11 yr after accidental inhalation of the irradiated metal or its oxide. It is concluded from body radioactivity measurements that long term clearance from the chest may be extremely slow, with observed biological half lives of up to 17 yr, while for the clearance of systemic burdens of (60)Co, a value in the region of 7 yr is suggested.|Intratracheally instilled cobaltous oxide (1.5 ug) was retained in the lung for a relatively long period with a half-time of about 15 days.

The aim of this study was to find out the intracellular signaling transduction pathways involved in cobalt oxide nanoparticles (CoO NPs) mediated oxidative stress in vitro and in vivo system. Cobalt oxide nanoparticles released excess Co++ ions which could activated the NADPH oxidase and helps in generating the reactive oxygen species (ROS). Our results showed that CoO NPs elicited a significant (p<0.05) amount of ROS in lymphocytes. In vitro pretreatment with N-acetylene cystine had a protective role on lymphocytes death induced by CoO NPs. In vitro and in vivo results showed the elevated level of TNF-alpha after CoO NPs treatment. This TNF-alpha phosphorylated the p38 mitogen-activated protein kinase followed by activation of caspase 8 and caspase 3 which could induce cell death. This study showed that CoO NPs induced oxidative stress and activated the signaling pathway of TNF-alpha-caspase-8-p38-caspase-3 to primary immune cells. This study suggested that bare CoO NPs are a toxic for primary human immune cells that deals directly with human health. Surface modification or surface functionalization may open the gateway for further use of CoO NPs in different industrial use or in biomedical sciences. /Cobalt oxide nanoparticles/

Fresh air, rest. Refer for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap.

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/ ...Three cases of pneumoconiosis in tungsten carbide tool industry where exposure to cobalt powder, oxide or salt, had varied between 0.1 and 0.2 mg Co/cu m for 2.5-7 yr /are reported/. It was stated that these 3 men were only workers with pneumoconiosis out of 1500 men with similar exposure conditions. /Cobalt powder, oxide or salt/|/CASE REPORTS/ ...Three cases of pneumoconiosis in tungsten carbide tool industry where exposure to cobalt powder, oxide or salt, had varied between 0.1 and 0.2 mg Co/cu m for 2.5-7 yr /are reported/. It was stated that these 3 men were only workers with pneumoconiosis out of 1500 men with similar exposure conditions. /Cobalt powder, oxide or salt/|/ALTERNATIVE and IN VITRO TESTS/ Fragmentary knowledge exists on cellular signaling responses underlying possible adverse health effects of CoO- and CeO2-nanoparticles (NP)s after inhalation. We aimed to perform a time kinetic study of gene expression profiles induced by these NPs in alveolar A549 and bronchial BEAS-2B epithelial cells, and investigated possible immune system modulation. The kinetics of the cell responses induced by the NPs were different between the lung epithelial models. Both CoO- and CeO2-NP exposure induced mainly downregulation of gene transcription. BEAS-2B cells were found to be more sensitive, as they showed a higher number of differentially expressed transcripts (DET) at a 10-fold lower NP-concentration than A549 cells. Hierarchical clustering of all DET indicated that the transcriptional responses were heterogeneous among the two cell types and two NPs. Between 1% and 14% DET encoding markers involved in immune processes were observed. The transcriptional impact of the metal oxide NPs appeared to be cell-dependent, both at the general and immune response level, whereas each lung epithelial cell model responded differently to the two NP types. Thus, the study provides gene expression markers and immune processes involved in CoO- and CeO2-NP-induced toxicity, and demonstrates the usefulness of comprehensive-omics studies to differentiate between NP responses. /Cobaltous oxide nanoparticles/|/ALTERNATIVE and IN VITRO TESTS/ In this study, we sought to determine the cytotoxicity and genotoxicity of particulate and soluble cobalt in normal primary human lung epithelial cells. Cobalt oxide and cobalt chloride were used as representative particulate and soluble cobalt compounds, respectively. Exposure to both particulate and soluble cobalt induced a concentration-dependent increase in cytotoxicity, genotoxicity, and intracellular cobalt ion levels. Based on intracellular cobalt ion levels, we found that soluble and particulate cobalt induced similar cytotoxicity while soluble cobalt was more genotoxic than particulate cobalt. These data indicate that cobalt compounds are cytotoxic and genotoxic to human lung epithelial cells.|/ALTERNATIVE and IN VITRO TESTS/ ... In this study, we sought to determine the cytotoxicity and genotoxicity of particulate and soluble cobalt in human lung cells. Cobalt oxide and cobalt chloride were used as representative particulate and soluble cobalt compounds, respectively. Exposure to both particulate and soluble cobalt induced a concentration-dependent increase in cytotoxicity, genotoxicity, and intracellular cobalt ion levels. Based on intracellular cobalt ion levels, we found that soluble cobalt was more cytotoxic than particulate cobalt while particulate and soluble cobalt induced similar levels of genotoxicity. However, soluble cobalt induced cell cycle arrest indicated by the lack of metaphases at much lower intracellular cobalt concentrations compared to cobalt oxide. Accordingly, we investigated the role of particle internalization in cobalt oxide-induced toxicity and found that particle-cell contact was necessary to induce cytotoxicity and genotoxicity after cobalt exposure. These data indicate that cobalt compounds are cytotoxic and genotoxic to human lung fibroblasts, and solubility plays a key role in cobalt-induced lung toxicity.

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

Cough. Sore throat. Laboured breathing. Shortness of breath.

Redness. Pain.

The commercial oxides are usually not definite chemical compounds but mixtures of the cobalt oxides.|Powder, (-324 mesh); metallurgical grade, 76% cobalt; ceramic grade, 70-71% Cobalt; -325 mesh, 99.5% purity grade; high purity powder grades; reagent grade|Grade: techincal, ceramic.|Cobalt fume and dust have the composition Co/CoO/Co2O2/Co2O4.

All other basic inorganic chemical manufacturing|Cobalt oxide (CoO): ACTIVE|... Cobalt oxide iron pellets have been placed in the reticulorumen to provide slow release of cobalt. ... A steel core pellet covered with cobalt oxide-impregnated cotton gauze has been devised as a means of cobalt supplementation. As the cotton is digested by rumen microbes, cobalt is released.