Registration Dossier
Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 231-111-4 | CAS number: 7440-02-0
- 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
There are no mutagenicity studies of nickel metal powder in bacteria; these studies are not informative for metals due to the limited capacity for metal uptake by bacteria. Recently, in vitro gene mutation and micronucleus (MN) studies in mammalian cells with nickel metal powder were conducted according to GLP, and OECD 476 and 487 guidelines, respectively. These K1, guideline-compliant studies used V79 Chinese Hamster cells. The gene mutation study accessed nickel metal powder mutagenicity at the HPRT locus after short-term (4 h) exposure with and without metabolic activation. No biologically relevant increase in mutants was observed after treatment with Ni metal, with and without metabolic activation. Although statistical analysis of the results showed that the mutant frequency of the experiment with metabolic activation was significantly increased at 0.25 mM test concentration over the solvent controls, this did not follow a concentration-response trend and was within the historical control data. Similarly, although some of the mutant frequencies in the experiment without metabolic activation were increased above the solvent controls, these increases were within the historical control data and did not follow a concentration-response trend. In the micronucleus study, the micronucleus frequency of nickel metal powder after 4h exposure was investigated with and without metabolic activation. There was no statistically nor biologically relevant increase in MN frequency after 4h exposure. According to the OECD 487 guideline, a 24h treatment was conducted due to the negative results after 4h treatment. The long term (24h) treatment without metabolic activation did not produce an increase in micronucleus frequency above controls nor historical control limits, thus confirming the negative micronuclei mutagenicity of nickel metal. Both studies thus demonstrate that nickel metal is non-mutagenic. In one study of chromosomal aberrations in human cells in culture, the results were negative but the study lack sufficient details for a proper evaluation (Paton and Allison, 1972). Cellular uptake and cell transformation studies with nickel metal powders have indicated very low uptake and weak transforming potential, respectively (Costa et al., 1981). The only in vivo mutagenicity study with Ni metal is inconclusive (Zhong et al.,1990).
In the European Union Risk Assessment for Nickel Metal (2008-2009), the Rapporteur recognized the lack of information about the genotoxic effects of metallic metal, both with respect to possible effects in germ cells or in somatic cells, and the implications for the risk assessment of the carcinogenicity of the substance. The target cell of interest for the evaluation of the carcinogenicity is the lung cell, and at the time there was no adequate data to predict the genotoxicity of metallic nickel on this target cell. When results from an inhalation carcinogenicity study with nickel metal powder became available (Oller et al., 2008), they indicated that inhalation of nickel metal powder for up to 2 years did not increase the frequency of lung tumors. These results, together with the negative findings in an oral MN study with the most bioavailable of the Ni compounds (Oller and Erexson, 2007) indicated that no further testing for mutagenicity of nickel metal in lungs of animals was warranted. Further, the negative results obtained from the two recently completed guideline-compliant in vitro gene mutation and micronucleus studies support this conclusion and precludes the need for in vivo mutagenicity studies with nickel metal.
The following information is taken into account for any hazard / risk assessment:
The European Union Risk Assessment for Nickel Metal (2008-2009) concluded that the current data are inadequate to support a proposal for classification for mutagenicity. This is supported by a negative inhalation carcinogenicity study with metallic nickel (Oller et al., 2008). Further support to not classify nickel metal for mutagenicity is provided by the two recently completed guideline-compliant in vitro gene mutation and micronucleus studies showing no mutagenicity of nickel metal.
Justification for classification or non-classification
Ni metal is not classified for mutagenicity in the 1st ATP to the CLP Regulation. Background information is available in the discussion section above.
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.

Route: .live1