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EC number: 941-652-4 | CAS number: -
- 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
Endpoint summary
Administrative data
Key value for chemical safety assessment
Additional information
Due to the structural similarities of Pentanickel Octahydroxide Carbonate and Nickel Hydroxycarbonate, all information in this section is relevant for Pentanickel Octahydroxide Carbonate (see section 13 for full discussion of read-across strategy).
Only limited information characterizing the genetic toxicity of nickel hydroxycarbonate was identified. The data on in vitro genotoxicity of nickel hydroxycarbonate is limited. In the study by Montaldi et al. (1985) nickel hydroxycarbonate is reported to increase the frequency of sister chromatid exchanges (SCE) in cultured hamster ovary cells. In the Montaldi et al. (1987) study, chromosome aberrations were also studied, with a positive result. In the Fletcher et al (1994) study, some exposure levels to nickel hydroxycarbonate are reported to increase the frequency of thio-guanine resistant mutants in mammalian CHO cells containing the bacterial gpt gene. These effects could be due to methylation of the gpt trasngene rather than true mutations. Another study characterizing the genetic toxicity of nickel hydroxycarbonate is an OECD guideline in vitro study. Bioservice Scientific Laboratories (BSL, 2008) conducted a thymidine kinase locus mutation study using mouse lymphoma L5178Y cells with and without metabolic activation over short (4 hour) and long (24 hour) exposure durations. There was no biologically significant increase in mutation frequencies under any of the experimental conditions; thus nickel hydroxycarbonate was non-mutagenic in this study.
The data on in vivo genotoxicity of nickel hydroxycarbonate is limited to studies conducted by Ciccarelli et al. (1981, 1982). Ciccarelli et al. (1982) examined lesions in nuclei from the kidney, liver, lung, and thymus gland cells in male rats following intraperitoneal (i. p.) administration. In kidney nuclei, dose-dependent DNA-protein cross-links, interstrand crosslinks, and single-strand breaks were observed. Lung nuclei showed low levels of single-strand breaks that were repaired by the end of the study period. The authors concluded that the potential for nickel hydroxycarbonate exposures to induce kidney and lung DNA damage may correlate with nuclear nickel (II) concentrations.
The available in vitro and in vivo data regarding the potential mutagenicity of Ni hydroxycarbonate are inconclusive. Collectively, the available data are conflicting given that in vitro data from a standard assay using mouse lymphoma L5178Y cells indicated that nickel hydroxycarbonate was not genotoxic. However, exposures in rats indicated that nickel hydroxycarbonate induced DNA damage in renal and pulmonary cells using non physisological routes of exposure. Therefore, in vivo data from an oral guideline compliant study with Ni sulfate is also considered here in an overall weight-of-evidence approach. A study conducted by Oller and Erexson (2007) aimed to evaluate the ability of nickel sulfate hexahydrate to induce micronuclei in polychromatic erythrocytes (PCEs) in rat bone marrow. The results of this study demonstrated that repeated exposures to nickel sulfate hexahydrate did not induce statistically significant increases in micronucleated PCEs at any dose examined, even though measured Ni levels in blood and bone marrow were elevated. Regarding inhalation effects, read across from a study conducted with nickel subsulfide is possible (Benson et al., 2002).This study found that inhalation exposuresto nickel sulphate and nickel subsulfide at toxic levels can cause genotoxicity in the respiratory tract in vivo. However, only Ni3S2 exposure (0.6 mg/m3, 0.44 mg Ni/m3) significantly increased epithelial and nonepithelial cell proliferation after 3 and 13 weeks.
During the preparation of the 2008/2009 European Union Risk Assessment for Nickel Carbonate (applicable for nickel hydroxycarbonate), the Specialised Experts (April 2004) considered the classification for mutagenicity of nickel sulphate, nickel chloride, nickel nitrate and nickel hydroxycarbonate. They concluded that nickel sulphate, nickel chloride and nickel nitrate should be classified as Muta. Cat. 3; R68 (European Commission, 2004). This conclusion was based on evidence ofin vivogenotoxicity in somatic cells, after systemic exposure and a consideration that the possibility that the germ cells are affected could not be excluded.
The Specialised Experts concluded that there was insufficient evidence for classification of nickel hydroxycarbonate and they did not consider that further testing of effects on germ cells was practicable (European Commission, 2004). Nevertheless, the Technical Classification and labeling Committee later agreed to classify nickel hydroxycarbonate as Muta. Cat. 3; R68, and this classification has been included in the 30th ATP. Despite conflicting data regarding the genetic toxicity of Ni hydroxycarbonate, this compound is currently classified as a mutagen Cat 3: R68 and Muta. 2; H341 (1st ATP to the CLP). Recently, there has been some recognition that nickel compounds may be genotoxic carcinogens with a practical threshold (see SCOEL 2009 report in Appendix C2).
Short description of key information:
The available in vitro and in vivo data regarding the potential mutagenicity of Ni hydroxycarbonate are inconclusive. Despite conflicting data regarding the genetic toxicity of Ni hydroxycarbonate, this compound is currently classified as Cat 3: R68 and Muta. 2; H341 (1st ATP to the CLP). Recently, there has been some recognition that nickel compounds may be genotoxic carcinogens with a practical threshold (see SCOEL 2009 report in Appendix C2) of the accompanying CSR.
Endpoint Conclusion: Adverse effect observed (positive)
Justification for classification or non-classification
Ni hydroxycarbonate is classified as Cat 3:R68 and Muta. 2;H341 according to the 1st ATP to the CLP Regulation. Background information can be found in the discussion section.
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