Carbonic acid, cobalt(2+) salt (1:1): Human health tier II assessment
27 November 2014
CAS Number: 513-79-1
- Chemical Identity
- Import, Manufacture and Use
- Existing Work Health and Safety Controls
- Health Hazard Information
- Risk Characterisation
- NICNAS Recommendation
This assessment was carried out by staff of the National Industrial Chemicals Notification and Assessment Scheme (NICNAS) using the Inventory Multi-tiered Assessment and Prioritisation (IMAP) framework.
The IMAP framework addresses the human health and environmental impacts of previously unassessed industrial chemicals listed on the Australian Inventory of Chemical Substances (the Inventory).
The framework was developed with significant input from stakeholders and provides a more rapid, flexible and transparent approach for the assessment of chemicals listed on the Inventory.
Stage One of the implementation of this framework, which lasted four years from 1 July 2012, examined 3000 chemicals meeting characteristics identified by stakeholders as needing priority assessment. This included chemicals for which NICNAS already held exposure information, chemicals identified as a concern or for which regulatory action had been taken overseas, and chemicals detected in international studies analysing chemicals present in babies’ umbilical cord blood.
Stage Two of IMAP began in July 2016. We are continuing to assess chemicals on the Inventory, including chemicals identified as a concern for which action has been taken overseas and chemicals that can be rapidly identified and assessed by using Stage One information. We are also continuing to publish information for chemicals on the Inventory that pose a low risk to human health or the environment or both. This work provides efficiencies and enables us to identify higher risk chemicals requiring assessment.
The IMAP framework is a science and risk-based model designed to align the assessment effort with the human health and environmental impacts of chemicals. It has three tiers of assessment, with the assessment effort increasing with each tier. The Tier I assessment is a high throughput approach using tabulated electronic data. The Tier II assessment is an evaluation of risk on a substance-by-substance or chemical category-by-category basis. Tier III assessments are conducted to address specific concerns that could not be resolved during the Tier II assessment.
These assessments are carried out by staff employed by the Australian Government Department of Health and the Australian Government Department of the Environment and Energy. The human health and environment risk assessments are conducted and published separately, using information available at the time, and may be undertaken at different tiers.This chemical or group of chemicals are being assessed at Tier II because the Tier I assessment indicated that it needed further investigation.
For more detail on this program please visit:www.nicnas.gov.au
NICNAS has made every effort to assure the quality of information available in this report. However, before relying on it for a specific purpose, users should obtain advice relevant to their particular circumstances. This report has been prepared by NICNAS using a range of sources, including information from databases maintained by third parties, which include data supplied by industry. NICNAS has not verified and cannot guarantee the correctness of all information obtained from those databases. Reproduction or further distribution of this information may be subject to copyright protection. Use of this information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner. NICNAS does not take any responsibility whatsoever for any copyright or other infringements that may be caused by using this information.
|Synonyms|| Cobalt carbonate|
Cobalt (2+) carbonate
|Molecular Weight (g/mol)||118.9|
|Appearance and Odour (where available)||Solid red crystalline substance.|
Import, Manufacture and Use
Safety data sheets identify the use of the chemical in hobbyist and commercial pigments used in pottery glazes.
The following international uses have been identified through European Union Registration, Evaluation, Authorisation and Restriction of Chemicals (EU REACH) dossiers; Galleria Chemica; Substances and Preparations in the Nordic countries (SPIN) database and the US National Library of Medicine's Hazardous Substances Data Bank (HSDB).
The chemical has reported domestic use including as a pigment in glazes for pottery and ceramics by hobbyists.
The chemical has reported commercial use including as:
- a pigment in glazes for pottery and ceramics; and
- an electroplating agent.
The chemical has reported site-limited use including:
- as a process regulator;
- in the manufacture of other cobalt compounds; and
- as a constituent of water treatment chemicals.
Cobalt and its compounds are listed in Schedule 10 (prohibited carcinogens, restricted carcinogens and restricted hazardous chemicals) of the Work Health and Safety Regulations for restricted use in abrasive blasting at a concentration of greater than 0.1 % of cobalt (WHS, 2014).
No international restrictions have been identified.
Existing Work Health and Safety Controls
The chemical is classified as hazardous, with the following risk phrases for human health in the Hazardous Substances Information System (HSIS) (Safe Work Australia):
Carc. Cat. 2; R49 (Carcinogen);
Muta Cat. 3; R68 (Mutagen);
Repr Cat. 2; R60 (Reproductive toxicity);
R42; (Respiratory sensitisation); and
R43; (Skin sensitisation).
No specific exposure standards are available.
The following exposure standards are identified (Galleria Chemica):
An exposure limit—time weighted average (TWA) of 0.05–0.1 mg/m3 in different countries such as Ireland (0.1 mg/m3 inhalable fraction), Japan (0.05 mg/m3, cobalt and compounds), and Switzerland (0.05 mg/m3, cobalt and cobalt compounds as respirable dusts/aerosols).
Health Hazard Information
Limited data are available for cobalt carbonate (CAS No. 513-79-1). The available bioaccessibility data indicate that cobalt carbonate is likely to have a hazard profile similar to soluble cobalt compounds (NICNASa) and cobalt oxide (NICNASb) for oral and inhalation exposure, respectively. It must be noted that the bioavailability of cobalt oxide has been shown to be highly dependent on its preparation (sintered, calcined or precipitated), and the bioavailability of cobalt carbonate is expected to be similar to the more bioavailable forms of cobalt oxide.
No toxicokinetic data are available for this chemical. Bioaccessibility studies conducted by Stopford et al. (2003) indicate that this chemical releases Co2+ ions into artificial gastric fluid at the same rate as soluble cobalt compounds (cobalt sulfate heptahydrate and cobalt chloride). In artificial alveolar fluid the release of Co2+ ions from cobalt carbonate is substantially lower at 2.9 % compared with 100 % for both cobalt sulfate heptahydrate and cobalt chloride (Stopford et al., 2003). Therefore, cobalt oxide, which was reported to release Co2+ ions up to 2.4 % in artificial alveolar fluid is a better analogue for inhalation toxicokinetics (Stopford et al., 2003). Based on this information, the chemical is likely to have a toxicokinetic profile similar to soluble cobalt compounds (NICNASa) and cobalt oxide (NICNASb) for oral and inhalation exposure, respectively.
The chemical had moderate acute toxicity in animal tests following oral exposure. The median lethal dose (LD50) in rats is 697 mg/kg bw. Observed sub-lethal effects included diarrhoea, decreased activity and ataxia (REACH). Based on these data, a classification is recommended for this chemical (refer to Recommendation section).
In a study carried out similarly to OECD Test Guideline (TG) 401, cobalt (II) carbonate hydrate (300, 480, 770, 1240 or 2000 mg/kg bw) was administered via single oral gavage to five female and five male Sprague Dawley (SD) rats which were then observed for 15 days. Mortality was reported at ³480 mg/kg bw (480 mg/kg bw- 1 male, 770 mg/kg bw- 3 males and 3 females, 1240 mg/kg bw- all animals and 2000 mg/kg bw- all animals). Based on these data, the LD50 was calculated as 697 mg/kg bw (REACH).
No data are available. Considering that the absorption of soluble cobalt chloride was less than 1 % through intact guinea pig skin, acute toxicity by the dermal route is not expected for this chemical (NICNASc).
The chemical had low acute toxicity in animal tests following inhalation exposure. The median lethal concentration (LC50) in rats is >5.08 mg/L. Observed sub-lethal effects included ataxia and dyspnoea immediately after exposure (REACH).
In a study carried out similarly to OECD TG 436, male and female CRJ: CD(SD) rats were exposed to cobalt carbonate—1.05 mg/L (five males and five females) or 5.08 mg/L (three males and three females) (mass median aerodynamic diameter of 2.9 mm) once via inhalation for four hours and observed for 14 days. A satellite study at the same exposure concentrations was also conducted in three male and three female rats, although the observation period was only 24 hours. In the main study group, mortality occurred in 2/3 males (observation days three and six, respectively) and 1/3 females (observation day three) at 5.08 mg/L. No mortality was reported at the low dose group in the main study (1.05 mg/L), and at either dose in the satellite group.
Corrosion / Irritation
The chemical is not a skin irritant.
In an in vitro study conducted according to OECD TG 439, 10 mg of cobalt carbonate was applied to artificial human skin (EpiSkin kit) for 15 minutes. Based on a cell viability assay, the chemical was concluded not to be a skin irritant under the conditions of the assay (REACH).
The chemical is reported to be a slight eye irritant in animal studies. Effects were not sufficient to warrant a hazard classification.
In a study conducted similarly to OECD TG 405, 0.1 g of the chemical was instilled into one eye of six New Zealand White rabbits. The eyes of three animals were rinsed 30 seconds after exposure. Animals were then observed at 24, 48 and 72 hours. At 24-48 hours following exposure, all animals were reported to have slight to moderate conjunctivitis which persisted until 72 hours after administration. No further data are available (REACH).
The chemical is classified as hazardous with the risk phrase ‘May cause sensitisation by inhalation’ (R42) in HSIS (Safe Work Australia). Refer to Observations in Humans.
The chemical is classified as hazardous with the risk phrase ‘May cause sensitisation by skin contact’ (R43) in HSIS (Safe Work Australia). No data are available to evaluate this classification. However, compared with cobalt oxide, this chemical has a two fold greater release of Co2+ into artificial sweat (CDI, 2014). Therefore, skin sensitisation is a concern based on cobalt oxide data, confirming this classification.
In a LLNA assay conducted according to OECD TG 429, 25 mL of a suspension of cobalt oxide (CAS No. 1307-96-6) (12.5, 25 or 50 %) in acetone/olive oil was applied to the dorsal area of each ear of CBA female mice once daily for three consecutive days. Based on the LLNA study results, stimulation indexes of 1.8, 2.6 and 3.4 were reported for 12.5, 25 and 50 % suspensions of the chemical. After linear interpolation of the results, an EC3 (estimated concentration needed to produce a stimulation index of three) value of 37.5 % was reported. Based on the results of this study, cobalt oxide is classified as a skin sensitiser (REACH).
Observation in humans
Based on the available epidemiological evidence, the exisiting classification for sensitisation via the inhalation route of exposure is supported.
Several epidemiological studies conducted in cobalt-producing facilities support the findings that occupational exposure to inorganic cobalt compounds is associated with occupational asthma (ATSDR, 2004; WHO, 2006; CoRC 2014). Specifically, studies have shown that there was a significant correlation between decreasing lung function tests (FEV1/FVC ratio) and increasing concentrations of cobalt in the air and urine of occupationally exposed workers (CoRC, 2014).
Repeated Dose Toxicity
No data are available for this chemical. As data for this chemical show similar bioaccessibility and bioavailability in artificial gastric fluid to soluble cobalt compounds (Stopford et al., 2003), data from the NICNAS assessment of soluble cobalt compounds is read-across to the chemical (NICNASa; OECD, 2014). Data available from the NICNAS assessment of soluble cobalt compounds (NICNASa), particularly data available for cobalt sulfate heptahydrate (CAS No. 10026-24-1) and cobalt chloride hexahydrate (CAS No. 7791-13-1) show that the main effect after repeated oral exposure to soluble compounds is polycythaemia (increased erythrocytes). However, this effect is reversible after cessation of exposure (NICNASa). The severity and/or reversibility of effects seen in these studies do not meet the criteria for hazard classification.
No data are available.
Given that low dermal absorption is anticipated based on soluble cobalt chemicals (NICNASa; NICNASc), repeated dose toxicity through the dermal route is not expected.
No data are available for the chemical. Considering that the chemical has similar bioaccessiblity to cobalt oxide in artificial alveolar fluid and released at similar rates to soluble cobalt compounds (cobalt sulfate heptahydrate, CAS No. 10026-24-1) in artificial lysosomal fluid (Stopford et al., 2003), systemic toxicity may be read across from soluble cobalt compounds after the chemical is phagocytosed. In addition, local toxicity can be read across from cobalt oxide, for repeated dose toxicity via the inhalation route. Human data from occupational studies suggest the chemical causes serious damage to health by prolonged exposure through inhalation. Refer to section Observations in Humans.
A study conducted in Syrian Golden hamsters evaluated the effect of lifetime exposure to cobalt oxide (CAS No. 1307-96-6) at10 mg/L (seven hours a day, five days a week). Compared with controls, lifetime exposure to cobalt oxide did not affect survival, but induced pneumoconiosis (emphysema) (WHO, 2006).
Cobalt sulfate heptahydrate
The National Toxicology Program (NTP) conducted 13-week (NTP, 1991) and two-year studies (NTP, 1998) in male and female Fischer 344/N (F344/N) rats and B6C3F1 mice. In the 13-week study, rats and mice (10 animals/sex/species) were exposed to aerosols containing 0, 0.3, 1.0, 3.0, 10 or 30 mg/m3 cobalt sulfate heptahydrate (CAS No. 10026-24-1) for six hours a day, five days a week for the duration of the study. Male rats exposed to any concentration of the chemical showed a significant increase in relative kidney weights. Histopathological examination of the kidneys did not indicate any increase in kidney lesions in rats or mice in the 13-week study, although in male rats there was a concentration-related increase in epithelial cells and granular casts observed in the urine, suggesting slight renal toxicity. There was also a significant increase in the relative lung weights of rats exposed to 0.3 mg/m3 and higher for males, and 1 mg/m3 and higher for females. In mice, this was observed in both sexes from 10 mg/m3 and higher. Absolute and relative testicular and epididymal weights were significantly decreased in male mice at 30 mg/m3. Polycythaemia was observed in rats at 3 mg/m3 and higher. Histopathological lesions were observed in the respiratory tract of both rats and mice at all exposure levels from the chemical. A LOAEC of 0.3 mg/m3 was determined based on squamous metaplasia in the larynx (NTP, 1991).
The chemical is classified as hazardous—Category 2 mutagenic substance—with the risk phrase ‘May cause heritable genetic damage’ (T; R46) in HSIS (Safe Work Australia). No data are available to evaluate this classification. Based on the high solubility of the chemical in artificial gastric and lysosomal fluid, genotoxicity data will be read-across from the NICNAS assessment of soluble cobalt compounds (NICNASa). It was concluded that effective protective processes exist in vivo to prevent genotoxicity in humans (OECD, 2014a; NICNASa). The available data support a removal of this classification from the current HSIS (refer to Recommendation section).
Data from the analogue chemical cobalt chloride (CAS No. 7646-79-9) are read across according to the principles of the OECD (2007) considering the similar bioaccessibility of cobalt chloride to cobalt sulfate (CAS No. 10124-43-3) in artificial fluids (Stopford et al., 2003).
Point mutation studies conducted in bacteria with cobalt chloride (CAS No. 7646-79-9) (Ames test in Salmonella typhimurium and Escherichia coli) and cobalt chloride hexahydrate (CAS No. 7791-13-1) (Ames test in Salmonella typhimurium) were predominantly negative with and without metabolic activation (IARC, 2006). However, clastogenicity studies conducted in human white blood cells, mononuclear leukocytes, lymphocytes and mammalian cell cultures (Chinese hamster ovary and mouse lymphoma) showed that cobalt chloride heptahydrate is clastogenic and induces chromosomal effects (DNA-protein cross-linkage, DNA strand breakage and sister chromatid exchange) in most studies (IARC, 2006).
For cobalt sulfate (CAS No. 10124-43-3) both positive and negative results were obtained in Ames tests in Salmonela typhimurium (strain TA100, TA98 and TA1535). Positive results were obtained for chromosomal aberrations and aneuploidy in plant cells, in producing reactive oxygen species (ROS) (by degradation of 2-deoxyribose), and malondialdehyde assay. Positive results were seen for chemical changes in DNA bases in the calf thymus DNA (IARC, 2006).
Cobalt acetate (CAS No. 71-48-7) inhibited the repair of UV-induced pyrimidine dimers in human HeLa cells and enhanced cell transformation by simian adenovirus SA7 in Syrian hamster embryo cells (IARC, 2006).
These genotoxic effects observed in vitro are consistent with a reactive oxygen mechanism (OECD, 2014a).
Genotoxicity studies conducted using cobalt chloride (CAS No. 7646-79-9) injected intraperitoneally into Syrian hamsters showed aneuploidy, pseudodiploidy and hyperploidy in the bone marrow and testes (IARC, 2006). Enhanced micronucleus formation in male BALB/c AnNCrj mouse bone marrow was observed 30 hours after a single intraperitoneal injection of 50 or 200 mg/kg, but not at 25 mg/kg of cobalt chloride (CAS No. 7646-79-9) (IARC, 2006). Dose-dependent chromosomal aberrations were observed in the bone marrow of male Swiss mice given a single oral dose of 0, 20, 40 or 80 mg/kg bw cobalt chloride (CAS No. 7646-79-9) (ATSDR, 2004). However in a study similar to TG 474 and 475, a single oral dose of 50, 200 or 600 mg/kg cobalt chloride hexahydrate (CAS No. 7791-13-1), did not induce a significant increase in cells with structural and numerical chromosome aberrations or micronucleated polychromatic erythrocytes using SD rats (REACH).
Cobalt acetate (CAS No. 71-48-7) caused DNA base damage (products of hydroxyl radical attack) in the liver, kidney and lung in male and female Fischer 344/NCr rats from a single intraperitoneal injection of 50 µM/kg, indicating an increased incidence of oxidative stress (IARC, 2006).
In a study similar to OECD TG 475, but with some deviations, cobalt sulfate heptahydrate (10026-24-1) had no genotoxic effect in a mammalian bone marrow chromosome aberration test, in four SD rats administered a single oral gavage dose of 80, 160 or 320 mg/kg bw (REACH).
In an occupational study in 35 workers in a cobalt refinery, there was no indication of increased DNA strand breaks or micronuclei in blood lymphocytes compared with 27 unexposed workers (Government of Canada, 2011; OECD, 2014a).
The chemical is classified as hazardous: Category 2 carcinogenic substance, with the risk phrase ‘May cause cancer by inhalation’ (T; R49) in HSIS (Safe Work Australia). Based on the chemical having similar bioaccessiblity to cobalt oxide in artificial alveolar fluid and released at similar rates to soluble cobalt compounds (cobalt sulfate heptahydrate, CAS No. 10026-24-1) in artificial lysosomal fluid (Stopford et al., 2003), systemic toxicity may be read across from soluble cobalt compounds after the chemical is phagocytosed, while local toxicity can be read-across from cobalt oxide, for toxicity via the inhalation route ((NICNASa, NICNASb). Considering that the chemical is currently classified and that there are difficulties in reading across data as discussed below, there is insufficent evidence to remove the current classification.
Cobalt oxide is not currently classified as carcinogenic and available carcinogenicity data were determined to be insufficient for classification due to non-physiologically relevant exposure routes used, absence of guideline laboratory studies and confounding in epidemiological studies arising from mixed exposure to cobalt oxide with other cobalt compounds and metals (nickel, arsenic, tungsten carbide).
Although the International Agency for Research on Cancer (IARC) has classified cobalt sulfate and other soluble cobalt (II) salts as possibly carcinogenic to humans (Group 2B) (IARC, 2006), the findings relate to local effects in the lung, for which the soluble salts are not suitable analogues for cobalt carbonate. The mechanisms for carcinogenicity have not been clearly identified, making read across for compounds of different solubility difficult.
The carcinogenic potential of cobalt compounds is also likely to be contributed to by the indirect genotoxic mechanisms previously mentioned (inhibition of DNA repair and generation of reactive oxygen species causing cellular oxidative stress) (ATSDR, 2004; IARC, 2006).
Reproductive and Developmental Toxicity
The chemical is classified as hazardous: Category 2 substance toxic to reproduction, with the risk phrase ‘May impair fertility’ (T; R60) in HSIS (Safe Work Australia). Based on the high solubility in artificial gastric fluid, and similar oral bioaccessibility to soluble cobalt compounds, reproductive and developmental toxicity data are read-across from the NICNAS assessment of soluble cobalt compounds (NICNASa). The available data on analogue chemicals, cobalt chloride (CAS No. 7646-79-9) and cobalt sulfate heptahydrate (CAS No. 10026-24-1), support this classification and the extension of this classification to the current assessment.
In a 12-week oral fertility study, adult male Swiss mice were exposed to cobalt chloride (CAS No. 7646-79-9) in drinking water (average of 25, 47 or 93 mg/kg bw/day) and then mated with unexposed females. The number of pregnant females and implantation sites were significantly reduced in females mated with exposed males at 47 and 93 mg/kg bw/day. At all doses, the incidence of resorption was significantly higher, whereas the number of viable foetuses decreased. Decreased relative testicular weight, decreased sperm concentration, and testicular necrosis and degeneration were observed (Elbetieha et al., 2008).
In the 13-week NTP study, rats and mice (10 animals/sex/species) were exposed to aerosols containing 0, 0.3, 1.0, 3.0, 10 or 30 mg/m3 cobalt sulfate heptahydrate (CAS No. 10026-24-1) for six hours a day, five days a week for the duration of the study. Absolute and relative testicular weights and the epididymis weight were significantly decreased, together with the number of abnormal sperm in male mice administered 30 mg/m3 cobalt sulfate heptahydrate (CAS No. 10026-24-1). Data were not collected on mice exposed to lower concentrations. Sperm motility was significantly reduced in mice exposed to >3 mg/m3, but data were not collected on mice exposed at lower concentrations (NTP, 1991).
While there are several non-guideline studies on developmental toxicity, it is difficult to draw firm conclusions about the developmental toxicity of these chemicals due to various methodological deficiencies. Testing is currently underway for this endpoint.
Other Health Effects
Critical Health Effects
The critical health effects for risk characterisation include a systemic long-term effect (reproductive toxicity), local long-term effect (carcinogenicity), systemic acute effect (acute toxicity from oral exposure) and local effects (skin and respiratory sensitisation). The chemicals may also cause toxic effects following repeated exposure through inhalation.
Public Risk Characterisation
Both overseas and in Australia, the chemical is available as a component of glazes for arts and crafts. While these products are available to the public, the concentration of the chemical in these products appears to be low (<1 %). The public may also come into contact with articles/coated surfaces containing the chemical; it is expected that the chemical will be bound within the article/coated surface and hence will have low bioavailability. Therefore, in both cases, the risk to the public is not considered to be unreasonable.
Occupational Risk Characterisation
During use of the chemical, dermal, ocular and inhalation exposure of workers to the chemical could occur, particularly where manual or open processes are used. These might include transfer and blending activities, quality control analysis, and cleaning and maintaining equipment. Worker exposure to the chemical at lower concentrations could also occur while using formulated products containing the chemical. The level and route of exposure will vary depending on the method of application and work practices employed.
Given the critical systemic long-term, local long-term, acute and local health effects, the chemical could pose an unreasonable risk to workers unless adequate control measures to minimise oral, dermal and inhalation exposure to the chemical are implemented. The chemical should be appropriately classified and labelled to ensure that a person conducting a business or undertaking (PCBU) at a workplace (such as an employer) has adequate information to determine appropriate controls.
The data available support an amendment to the hazard classification in HSIS (refer to Recommendation section).
Assessment of the chemical is considered to be sufficient, provided that the recommended amendment to the classification is adopted, and labelling and all other requirements are met under workplace health and safety and poisons legislation as adopted by the relevant state or territory.
Work Health and Safety
The chemical is recommended for classification and labelling under the current approved criteria and adopted GHS as below. This assessment does not consider classification of physical hazards and environmental hazards.
The classification proposed below for Repeat Dose Toxicity-Inhalation is based on read-across principles (OECD, 2014b). It should be used as a default for this chemical. If empirical data become available indicating that a lower (or higher) classification is appropriate for this chemical, these may be used to amend the default classification for the chemical.
|Hazard||Approved Criteria (HSIS)a||GHS Classification (HCIS)b|
|Acute Toxicity||Harmful if swallowed (Xn; R22)||Harmful if swallowed - Cat. 4 (H302)|
|Sensitisation||May cause sensitisation by inhalation (Xn, R42)* May cause sensitisation by skin contact (Xi; R43)*||May cause allergy or asthma symptoms or breathing difficulties if inhaled - Cat. 1 (H334) May cause an allergic skin reaction - Cat. 1 (H317)|
|Repeat Dose Toxicity||Toxic: danger of serious damage to health by prolonged exposure through inhalation (T; R48/23)||Causes damage to organs through prolonged or repeated exposure through inhalation - Cat. 1 (H372)|
|Carcinogenicity||Carc. Cat 2 - May cause cancer by inhalation (T; R49)*||May cause cancer - Cat. 1B (H350i)|
|Reproductive and Developmental Toxicity||Repro. Cat 2 - May impair fertility (T; R60)*||May damage fertility - Cat. 1B (H360F)|
a Approved Criteria for Classifying Hazardous Substances [NOHSC:1008(2004)].
b Globally Harmonized System of Classification and Labelling of Chemicals (GHS) United Nations, 2009. Third Edition.
* Existing Hazard Classification. No change recommended to this classification
Advice for industry
Control measures to minimise the risk from oral, dermal and inhalation exposure to the chemical should be implemented in accordance with the hierarchy of controls. Approaches to minimise risk include substitution, isolation and engineering controls. Measures required to eliminate or minimise risk arising from storing, handling and using a hazardous chemical depend on the physical form and the manner in which the chemical is used. Examples of control measures which may minimise the risk include, but are not limited to:
- using closed systems or isolating operations;
- using local exhaust ventilation to prevent the chemical from entering the breathing zone of any worker;
- health monitoring for any worker who is at risk of exposure to the chemical if valid techniques are available to monitor the effect on the worker’s health;
- minimising manual processes and work tasks through automating processes;
- work procedures that minimise splashes and spills;
- regularly cleaning equipment and work areas; and
- using protective equipment that is designed, constructed, and operated to ensure that the worker does not come into contact with the chemical.
Guidance on managing risks from hazardous chemicals are provided in the Managing risks of hazardous chemicals in the workplace—Code of practice available on the Safe Work Australia website.
Personal protective equipment should not solely be relied upon to control risk and should only be used when all other reasonably practicable control measures do not eliminate or sufficiently minimise risk. Guidance in selecting personal protective equipment can be obtained from Australian, Australian/New Zealand or other approved standards.
Obligations under workplace health and safety legislation
Information in this report should be taken into account to assist with meeting obligations under workplace health and safety legislation as adopted by the relevant state or territory. This includes, but is not limited to:
- ensuring that hazardous chemicals are correctly classified and labelled;
- ensuring that (material) safety data sheets ((m)SDS) containing accurate information about the hazards (relating to both health hazards and physicochemical (physical) hazards) of the chemical are prepared; and
- managing risks arising from storing, handling and using a hazardous chemical.
Your work health and safety regulator should be contacted for information on the work health and safety laws in your jurisdiction.
Information on how to prepare an (m)SDS and how to label containers of hazardous chemicals are provided in relevant codes of practice such as the Preparation of safety data sheets for hazardous chemicals— Code of practice and Labelling of workplace hazardous chemicals—Code of practice, respectively. These codes of practice are available from the Safe Work Australia website.
A review of the physical hazards of the chemicals has not been undertaken as part of this assessment.
Agency for Toxic Substances and Disease Registry (ATSDR) 2004. Toxicological Profile for Cobalt. Accessed March 2014 at http://www.atsdr.cdc.gov/toxprofiles/tp33.pdf
Cobalt Development Institute (CDI) 2014. Data on Cobalt carbonate (CAS No. 513-79-1). Unpublished report submitted to National Industrial Chemicals Notification and Assessment Scheme under the Inventory Multi-tiered Assessment and Prioritisation framework. Generated by the Cobalt Development Institute, Guildford, Surrey, United Kingdom.
Elbetieha A, Al-Thani AS, Al-Thani RK, Darmani H& Owais W 2008. Effects of Chronic Exposure to Cobalt Chloride on the Fertility of Testes in Mice. Journal of Applied Biological Sciences 2(1) pp. 1-6.
Galleria Chemica. Accessed July 2014 at https://jr.chemwatch.net/galleria/
Hazardous Substances Data Bank (HSDB). National Library of Medicine. Accessed July 2014 at http://toxnet.nlm.nih.gov.
International Agency for Research on Cancer (IARC) (1991). Chlorinated Drinking-water; Chlorination By-products; Some Other Halogenated Compounds; Cobalt and Cobalt Compounds, IARC Monographs Volume 52. http://monographs.iarc.fr/ENG/Monographs/vol52/mono52-14.pdf. Accessed September 2012.
International Agency for Research on Cancer (IARC) 2006. IARC monographs on the evaluation of carcinogenic risks to humans. Volume 86. Cobalt in Hard Metals and cobalt sulfate, gallium arsenide, idium phosphide and vanadium pentoxide. Accessed in March 2014 at http://monographs.iarc.fr/ENG/Monographs/vol86/mono86.pdf
National Industrial Chemicals Notification and Assessment Scheme (NICNASa). Tier II Human health assessment for Soluble cobalt (II) and salts. Australian Government Department of Health. Accessed April 2014 at http://www.nicnas.gov.au/chemical-information/imap-assessments/imap-group-assessment-report?assessment_id=952
National Industrial Chemicals Notification and Assessment Scheme (NICNASb). Inventory Multi-Tiered and Prioritisation (IMAP): Human Health Tier II Assessment for Cobalt oxide. Available at http://www.nicnas.gov.au/chemical-information/imap-assessments/imap-group-assessment-report?assessment_id=1190
National Industrial Chemicals Notification and Assessment Scheme (NICNASc). Tier II Human health assessment for Cobalt chlorides and citrates. Australian Government Department of Health. Accessed July 2014 at http://www.nicnas.gov.au/chemical-information/imap-assessments/imap-group-assessment-report?assessment_id=1083
National Toxicology Program (NTP) 1991. Toxicity studies of cobalt sulfate heptahydrate in F344/N rats and B6C3F1 mice. NTP TOX 5. NIH Publication No. 91-3124. Accessed March 2014 at http://ntp.niehs.nih.gov/ntp/htdocs/ST_rpts/tox005.pdf
National Toxicology Program (NTP) 1998. Toxicology and carcinogenesis studies of cobalt sulfate heptahydrate (CAS No. 10026-24-1) in F344/N rats and B6C3F1 mice. NTP Technical report No. 471. Accessed March 2014 at http://ntp.niehs.nih.gov/ntp/htdocs/lt_rpts/tr471.pdf
OECD 2014b. Guidance on Grouping of Chemicals, Second Edition. Environment Directorate. Joint meeting of the Chemicals Committee and the Working party on Chemicals, Pesticides and Biotechnology. Series on Testing& Assessment No. 194. Accessed July 2014 at http://search.oecd.org/officialdocuments/displaydocumentpdf/?cote=env/jm/mono(2014)4&doclanguage=en
OECD 2014a. SIDS Initial Assessment Profile (SIAP) on soluble cobalt salts. Unpublished.
REACH Dossier. Cobalt carbonate (CAS No. 513-79-1). Accessed July 2014 at http://echa.europa.eu/web/guest/information-on-chemicals/registered-substances
Safe Work Australia (SWA). Hazardous Substances Information System (HSIS). Accessed July 2014 at http://hsis.safeworkaustralia.gov.au/HazardousSubstance
Stopford W, Turner J, Cappellini D& Brock T 2003. Bioaccessibility testing of cobalt compounds. Journal of Environmental Monitoring 5 (pp. 675-680).
Substances in Preparations in Nordic Countries (SPIN). Accessed July 2014 at http://18.104.22.168/DotNetNuke/default.aspx
Work Health and Safety (WHS) Regulations 2014. Schedule 10 - Prohibited carcinogens, restricted carcinogens and restricted hazardous chemicals. Accessed May 2014 at http://www.safeworkaustralia.gov.au/sites/swa/about/publications/pages/model-whs-regulations
Last update 27 November 2014