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EC number: 235-008-5 | CAS number: 12054-48-7
- 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
Three reliable in vitro gene mutation studies in mammalian cells were available while no proper mutagenicity study was available in vivo to characterize the potential genetic toxicity associated with nickel dihydroxide. 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 nickel 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, nickel 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 nickel hydroxide 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.
The single in vivo study evaluating the potential for genetic toxicity (Ono et al., 1979) 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 alters the ability of nucleic acids synthesis in the nuclei.
Collectively, the limited in vitro mutagenicity andin vivogenotoxicity data indicate that nickel dihydroxide has the potential to induce genetic toxicity under laboratory conditions.
The following information is taken into account for any hazard / risk assessment:
Collectively, available 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. Recently, nickel compounds have been recognized as genotoxic carcinogens with threshold mode of action in the ECHA RAC opinion on nickel and nickel compounds OEL (see ECHA 2018 report discussion in Appendix C2).
Value used for CSA:Genetic toxicity: positive
Justification for classification or non-classification
Nickel dihydroxide has a harmonized CLP classification of Muta. 2: H341. Supporting information can be found in the discussion section for this endpoint.
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