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The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

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.