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EC number: 237-358-4 | CAS number: 13762-14-6
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Carcinogenicity
Administrative data
Description of key information
Read-across data:
LOAEC (rat): 0.114 mg Co2+/m³
LOAEC (mouse): 0.114 mg Co2+/m³
Key value for chemical safety assessment
Carcinogenicity: via oral route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Carcinogenicity: via inhalation route
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- LOAEC
- 0.114 mg/m³
- Study duration:
- chronic
- Species:
- other: rats and mice
Carcinogenicity: via dermal route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Justification for classification or non-classification
The cobalt sulphate heptahydrate was found to be carcinogenic in mice and rats when administered by inhalation. There was clear evidence of carcinogenicity in male and female mice and female rats, based on increased incidences of lung tumors. In addition, female rats had an increased incidence of pheochromocytoma of the adrenal medulla.
Available studies on the carcinogenicity of cobalt compounds in humans are based on occupational exposure to cobalt, often in the presence of carbides such as tungsten carbide. Due to co-exposure with other substances, the data are insufficient to conclude on the carcinogenic potential of elemental cobalt solely. Based on inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals, soluble cobalt(II)salts are classified as a carcinogen Category 1B according to Regulation (EC) 1272/2008.
The surrogate substance molybdenum trioxide induced alveolar/bronchiolar carcinoma in rats and mice when administered by inhalation. Both in rats and mice (male and female), there was no evidence of systemic carcinogenicity. The marginal evidence for carcinogenicity in the lung of male rats and male and female mice due to observed localized carcinoma is considered to be an effect which is specific to molybdenum trioxide. The observed localized carcinoma are secondary to local lung tissue inflammation, considered to be a result of the acidic reaction of MoO3in the lung fluids.
Based on the observed effects, which are restricted to local effects in the respiratory tract, molybdenum trioxide is classified as a carcinogen Category 2 according to Regulation (EC) 1272/2008.
Taking into account all available data on carcinogenicity using the analogue approach, it is expected that the cobalt ion is the critical ion for human health effects. Therefore, the classification of cobalt molybdenum oxide is based on the classification of other soluble cobalt compounds: Category 1B accordingto Regulation (EC) 1272/2008 and R49 (Category 2) according to Directive 67/548/EEC.
Based on an analogue approach, the available data on carcinogenicity meet the criteria for classification as Category 1B (H350) according to Regulation (EC) 1272/2008 and as R49 (Category 2) according to Directive 67/548/EEC.
Additional information
There are no data available on carcinogenicity for cobalt molybdenum oxide. However, there are reliable data for soluble cobalt and molybdenum substances considered suitable for read-across using the analogue approach. For identifying hazardous properties of cobalt molybdenum oxide, the existing forms of cobalt molybdenum oxide at very acidic and physiological pH conditions are relevant for risk assessment of human health effects. Cobalt molybdenum oxide is a metal-organic salt, which is highly water soluble (~ 508 mg/L) and nearly completely dissociates in aqueous solutions. As it is expected that cobalt molybdenum oxide is capable of forming ions at very acidic and physiological pH conditions, cobalt cations and molybdate anions will be present and completely bioavailable, same as for other soluble cobalt and molybdenum compounds.Due to the existing cobalt and molybdate ions, data from other soluble cobalt and molybdenum substances are used in the derivation of toxicological endpoints for cobalt molybdenum oxide. For further details refer to the analogue justification.
Cobalt substances
In a 2 year inhalation study, groups of mice and rats were exposed to cobalt(II)sulfate heptahydrate aerosols at concentrations of 0.3, 1, and 3 mg/m³ (calculated as anhydrous salt and equivalent to 0.114, 0.38 and 1.14 mg Co2+/m³) for 6 hours/day and 5 days/week (NTP, 1998).
In mice, mean body weights were increased in all treated females and decreased only in the high-exposed males. Survival was not adversely affected by treatment. The incidences of benign and malignant alveolar/bronchiolar neoplasms were increased in a concentration-dependent manner in male and female mice (significant at high-concentration for males; significant at mid- and high- concentration for females).
Males: 11/50, 14/50, 19/50, and 28/50 for 0, 0.114, 0.38, and 1.14 mg Co2+/m³, respectively
Females: 4/50, 7/50, 13/50, and 18/50 for 0, 0.114, 0.38, and 1.14 mg Co2+/m³, respectively.
In rats, mean body weights and survival were unaffected by treatment. Female rats exhibited a concentration-related increase in the incidence of benign and malignant alveolar/bronchiolar neoplasms (significant at mid- and high-concentration) and of benign and malignant pheochromocytomas of the adrenal medulla (significant at high-concentration). The incidences of benign and malignant alveolar/bronchiolar neoplasms were 0/50, 3/49, 15/50, and 15/50 and of benign and malignant pheochromocytomas 2/48, 1/49, 4/50, and 10/48 for 0, 0.114, 0.38, and 1.14 mg Co2 +/m³, respectively.
There was also a concentration-related increase in incidence of benign and malignant adrenal tumours (pheochromocytomas) in the exposed female rats (significant at high-concentration). The incidences of benign and malignant pheochromocytomas were 2/48, 1/49, 4/50, and 10/48 for 0, 0.114, 0.38, and 1.14 mg Co2 +/m³, respectively.
In males, increased incidence of benign and malignant alveolar/bronchiolar neoplasms was observed (significant at high-concentration), but only a marginally increased incidence of pheochromocytomas of the adrenal medulla. The incidences of benign and malignant alveolar/bronchiolar neoplasms were 1/50, 4/50, 4/48, and 7/50 and of benign and malignant pheochromocytomas were 15/50, 19/50, 25/49, and 20/50 for 0, 0.114, 0.38, and 1.14 mg Co2+/m³, respectively.
Although many of the alveolar/bronchiolar lesions were morphologically similar to those that arise spontaneously, the lesions in rats, unlike those in mice, were predominantly fibrotic, squamous or mixtures of alveolar/bronchiolar epithelium and squamous or fibrous components. Squamous metaplasia of alveolar/bronchiolar epithelium, which is a common response to pulmonary injury, was observed in a number of rats.
The marginally increased incidence of pheochromocytomas in males was considered an uncertain finding because it occurred only in the mid-concentration group and was not supported by increased incidence or severity of hyperplasia. Marginal increases in adrenal medullary tumors may have been exposure related.
In summary, test substance was found to be carcinogenic in mice and rats when administered by inhalation. There was clear evidence of carcinogenicity in male mice, female mice and female rats, based on increased incidences of lung tumors. In addition, female rats had an increased incidence of pheochromocytoma of the adrenal medulla. Some evidence of carcinogenicity in male rats was observed, based on increased incidences of lung tumors at the highest exposure level. No NOAECs were identified, neither for rats nor for mice. The LOAECs for mice and females were determined to be 0.114 mg Co2+/m³. The authors of the NTP study concluded that there was clear evidence of carcinogenicity in male and female mice and female rats and some evidence of carcinogenicity in male rats.
Available studies on the carcinogenicity of cobalt in humans are based on occupational exposure to cobalt, often in the presence of carbides such as tungsten carbide. Due to co-exposure with other substances, the data were insufficient to conclude on the carcinogenic potential of elemental cobalt alone. Based on inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals (NTP, 1998), soluble cobalt(II)salts are classified as Category 1B (H350) according to Regulation (EC) 1272/2008 and as R49 (Category 2) according to Directive 67/548/EEC.
Molybdenum trioxide
A 2 year carcinogenicity study (NTP, 1997) is available, in which the substance molybdenum trioxide was administered to rats and mice via inhalation at concentrations of 10, 30 or 100 mg/m³. The incidences of alveolar/bronchiolar adenoma or carcinoma (combined) were increased in male rats with a marginally significant positive trend. No increase in the incidences of lung neoplasms occurred in female rats. Exposure of male and female rats to molybdenum trioxide by inhalation resulted in increased incidences of chronic alveolar inflammation, hyaline degeneration of the respiratory epithelium, hyaline degeneration of the olfactory epithelium (females), and squamous metaplasia of the epiglottis.
In male mice, the incidences of alveolar/bronchiolar carcinoma in all exposed groups were significantly greater than that in the control group. Incidences of alveolar/bronchiolar adenoma in female mice in the 30 and 100 mg/m³ groups were significantly greater than that in the control group. Incidences of alveolar/bronchiolar adenoma or carcinoma (combined) in 10 and 30 mg/m³ male mice and in 100 mg/m³ female mice were significantly greater than those in the control groups and exceeded the historical control ranges for 2-year NTP inhalation studies.
Exposure of male and female mice to molybdenum trioxide by inhalation resulted in increased incidences of metaplasia of the alveolar epithelium, histiocyte cellular infiltration (males), hyaline degeneration of the respiratory epithelium, hyaline degeneration of the olfactory epithelium (females), squamous metaplasia of the epiglottis, and hyperplasia of the larynx. Both in rats and mice (male and female), there was no evidence of systemic carcinogenicity. The marginal evidence for carcinogenicity in the lung due to observed localized carcinoma/adenoma (considered by NTP in male rats to be ”equivocal” and in mice designated as “some evidence of carcinogenic activity”) is considered to be an effect which is specific to molybdenum trioxide. The observed localized carcinoma/adenoma are secondary to local lung tissue inflammation, considered to be a result of the acidic reaction of MoO3 in the lung fluids: in aqueous media, MoO3 molecules react with water and release protons according to the following equation: MoO3+ H2O -> MoO4²- + 2 H+.
Based on the observed effects, which are restricted to local effects in the respiratory tract, molybdenum trioxide (MoO3) is classified as a carcinogen Category 2 according to Commission Regulation (EC) No 790/2009, amending Regulation (EC) No 1272/2008 for the purposes of its adaptation to technical and scientific progress.
Carcinogenicity: via inhalation route (target organ): respiratory: lung
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