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EC number: 700-710-7 | 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
There are no studies available characterizing the genotoxic potential of Ni oxyhydroxide. The data are read-across form studies investigating the mutagenicity of Ni dihydroxide representing a worst case scenario.
Three reliable studies characterizing the in vitro genetic toxicity of Ni dihydroxide were available while no proper in vivo mutagenicity study was available. Collectively, the studies show that nickel dihydroxide has the potential to induce genetic toxicity under laboratory conditions; however, relative to other compounds (including other nickel compounds), it is likely to be much less potent at inducing genetic toxicity. The highest-rated study based on reliability was conducted by BSL Bioscience Laboratory (BSL). This GLP, guideline-based in vitro mammalian cell gene mutation study utilized the mouse lymphoma cell line L5178Y to evaluate the potential for Ni dihydroxide to induce mutations at the thymidine kinase locus, both in the presence and absence of metabolic activation. The study report concluded that under the experimental conditions reported, Ni dihydroxide was considered to be mutagenic.
The toxicity, uptake and mutagenicity of particulate and soluble nickel compounds was evaluated by a group of investigators and reported in two separate publications. The primary article published by Fletcher et al., (1994) reported findings associated with testing of fourteen nickel compounds in AS52 cells (modified CHO cells). Results indicated that the concentrations of nickel in the nuclei, but not in the cytosol, correlated with cytotoxicity; the LC50 for Ni dihydroxide was 3.6 µg/ml. Genotoxicity was based on evaluation of mutations at the gpt locus. Though mutations were noted, the authors concluded that the results of the study would not be sufficient to deem nickel compounds mutagenic by traditional criteria. The nickel compounds tested appeared to be only weak mutagens and the mutant profile analysis suggested that induction of mutations at levels only slightly above background. An additional publication by Rossetto et al., (1994) provided a more detailed evaluation of the mutations; in this study, the authors concluded that the findings clearly demonstrated that nickel compounds were mutagenic in the AS52 cell line but noted that the exact mutagenic mechanisms associated with the compound-specific mutations could not be defined.
A single in vivo study evaluating the potential for genetic toxicity was identified (Ono et al., 1979). In this study, rats were injected subcutaneously with a single dose of Ni dihydroxide. The incorporation of 3H-dTTP and 3H-UTP by nuclei isolated from normal and regenerating liver of exposed rats was compared with those of corresponding controls in an effort to determine the mechanism of carcinogenic action by metals. Though it was not well documented, the authors reported that the synthesis of nucleic acids of normal and regenerating liver was affected after the single administration and the adverse effects continued for 10 to 13 weeks. The authors conclude that results might suggest that nickel affects directly the structure or function of the nucleoli, or indirectly through the change of binding site of nickel in the nucleoli to alter the ability of nucleic acids synthesis in the nuclei.
Collectively, available studies show that Ni dihydroxide has the potential to induce genetic toxicity under laboratory conditions; however, relative to other compounds (including other nickel compounds), it is likely to be much less potent at inducing genetic toxicity. These data are read-across to Ni oxyhydroxide which is therefore also assumed to be genotoxic. Recently, there has been some recognition that nickel compounds may be genotoxic carcinogens with a practical threshold (see SCOEL 2009 report in Appendix C3).
Short description of key information:
There are no studies available on the genetic toxicity of Ni oxyhydroxide. Studies conducted with nickel dihydroxide showed the potential to induce genetic toxicity under laboratory conditions; however, relative to other compounds (including other nickel compounds), it is likely to be much less potent at inducing genetic toxicity. Ni dihydroxide is classified as Muta. 2:H341 according to the 1st ATP to the CLP. These data are read-across to Ni oxyhydroxide as worst assumption.
Endpoint Conclusion: Adverse effect observed (positive)
Justification for classification or non-classification
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