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EC number: 206-761-7 | CAS number: 373-02-4
- 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
Genetic toxicity in vitro
Description of key information
Data requirements in accordance with Annex IX (100-1000 tonnage band), encompassing all previous Annex requirements:
Table: Data requirements for mutagenicity
Discussion
Information characterizing the genetic toxicity of nickel acetate in vitro is limited to four in vitro studies; no in vivo studies were identified. One in vitro gene mutation study in bacteria, one in vitro gene mutation study in mammalian cells, one in vitro chromosomal aberration test in mammalian cells, and an in vitro mammalian cell transformation study.
De Flora et al. (1984) reported that nickel acetate was negative in the S. typhimurium reversion test (Ames reversion test) in all six strains evaluated and it was also found to be non-damaging to E. coli DNA in a DNA-repair test (multiple strains included). Based on these findings, the authors concluded that nickel acetate was nongenotoxic.
Nickel acetate was also tested for mutagenicity in mammalian cells in vitro. In a study of mouse mammary carcinoma cells, nickel acetate did not increase the frequency of chromosomal aberrations when tested up to 1 mM (58.7 mg Ni/liter) (Umeda and Nishimura, 1979). In a study of gene mutations at the hprt locus of mouse mammary carcinoma cell line, nickel acetate failed to significantly induce the frequency of hprt-mutants at a concentration range that decreased survival by 30-80% (Morita et al., 1991).
Nickel acetate was positive for cell transformation of primary human foreskin fibroblasts at concentrations of 10 µM (0.6 mg Ni/liter) (Biedermann and Landolph, 1987).
When considering all the data together, the results indicate that nickel acetate does not induce gene mutations (bacterial and mammalian cells) or chromosomal aberrations in mammalian cells in vitro. Yet, it can be genotoxic in vitro, causing cell transformation. Reliable data from in vivo studies with nickel acetate were not found. However according to specific rules for standard information requirements, in vivo mutagenicity tests are not needed when in vitro mutation tests are negative.
In vivo mutation data are read across from nickel sulphate, since there are no reliable studies available with nickel acetate. The in vivo studies with nickel sulphate have produced mixed results. Two studies (a K1 and a K2) looking at micronucleus in bone marrow of rats (oral) and mice (intraperitoneal) exposed repeatedly to nickel sulphate were negative (Oller and Erexson, 2007; Morita et al., 1997); two K3 studies looking at the oral induction of micronucleus in mice indicated positive results (Sharma et al., 1987; Sobti and Gill, 1989). A study by Benson et al. (2002) showed that nickel sulphate given by inhalation seemed to induce genotoxicity in lung cells at the same or higher concentrations at which it induces inflammation after repeated exposures. Evidence from human studies is limited. There are no definitive tests of nickel compounds on the germ cells but evidence for a possible effect is limited. Whilst there is evidence that the nickel ion reaches the testes, no effect on spermatogonial cells was seen in the Mathur et al. (1978) study with nickel sulphate. The effects seen in spermatozoa in the Sobti & Gill (1989) study with several water soluble Ni compounds may reflect toxic effects on germ cells rather than chromosomal damage. Two dominant lethal tests (Deknudt & Léonard, 1982, Saichenko, 1985) with water soluble Ni compounds, were negative. Whilst some effects are seen in males (e.g. sperm abnormalities) there is little evidence for inheritable effects on the germ cells.
In April 2004, the Specialised Experts concluded that nickel sulphate, nickel chloride and nickel nitrate should be classified as Muta. Cat. 3; R68 (now Muta. 2: H341 under CLP classification). This conclusion was based on evidence ofin vivogenotoxicity in somatic cells, after systemic exposure (the 2007 negative oral MN study was not available at that time). Hence the possibility that the germ cells are affected could not be excluded (European Commission, 2004). The mutagenicity of nickel acetate was not evaluated by the Specialised Experts, but nickel acetate was later classified as Muta. 2: H341 by reading across from Ni sulphate.
The following information is taken into account for any hazard / risk assessment:
In vitro mutagenicity tests with Ni acetate have been negative while in vivo tests are lacking. For water soluble nickel compounds in general, there is evidence indicating that they are weak genotoxicants in vitro, and may exhibit clastogenic activity. Some in vivo studies with soluble Ni compounds have been positive while two recent micronucleus studies via oral and intraperitoneal injection were negative. Evidence from human studies is limited. There are no definitive studies on germ cells, and little evidence concerning hereditable effects. Nickel acetate and other water soluble nickel compounds carry a harmonized Muta. 2: H341 CLP classification. 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).
Genetic toxicity in vivo
Description of key information
Information characterizing the genetic toxicity of nickel acetatein vitrois limited to fourin vitrostudies; noin vivostudies were identified. Thesein vitrostudies are: one in vitro gene mutation study in bacteria, one in vitro gene mutation study in mammalian cells, one in vitro chromosomal aberration test in mammalian cells, and an in vitro mammalian cell transformation study.
De Flora et al. (1984) reported that nickel acetate was negative in the S. typhimurium reversion test (Ames reversion test) in all six strains evaluated and it was also found to be non-damaging to E. coli DNA in a DNA-repair test (multiple strains included). Based on these findings, the authors concluded that nickel acetate was nongenotoxic.
Nickel acetate was also tested for mutagenicity in mammalian cellsin vitro. In a study of mouse mammary carcinoma cells, nickel acetate did not increase the frequency of chromosomal aberrations when tested up to 1 mM (58.7 mg Ni/liter) (Umeda and Nishimura, 1979). In a study of gene mutations at thehprtlocus of mouse mammary carcinoma cell line, nickel acetate failed to significantly induce the frequency ofhprt-mutants at a concentration range that decreased survival by 30-80% (Morita et al., 1991).
Nickel acetate was positive for cell transformation of primary human foreskin fibroblasts at concentrations of 10 µM (0.6 mg Ni/liter) (Biedermann and Landolph, 1987).
When considering all the data together, the results indicate that nickel acetate does not induce gene mutations (bacterial and mammalian cells) or chromosomal aberrations in mammalian cellsin vitro. Yet, it can be genotoxicin vitro, causing cell transformation. Reliable data fromin vivostudies with nickel acetate were not found. However according to specific rules for standard information requirements,in vivomutagenicity tests are not needed whenin vitromutation tests are negative.
In vivomutation data are read across from nickel sulphate, since there are no reliable studies available with nickel acetate. Thein vivostudies with nickel sulphate have produced mixed results. Two studies (a K1 and a K2) looking at micronucleus in bone marrow of rats (oral) and mice (intraperitoneal) exposed repeatedly to nickel sulphate were negative (Oller and Erexson, 2007; Morita et al., 1997); two K3 studies looking at the oral induction of micronucleus in mice indicated positive results (Sharma et al., 1987; Sobti and Gill, 1989). A study by Benson et al. (2002) showed that nickel sulphate given by inhalation seemed to induce genotoxicity in lung cells at the same or higher concentrations at which it induces inflammation after repeated exposures. Evidence from human studies is limited. There are no definitive tests of nickel compounds on the germ cells but evidence for a possible effect is limited. Whilst there is evidence that the nickel ion reaches the testes, no effect on spermatogonial cells was seen in the Mathur et al. (1978) study with nickel sulphate. The effects seenin spermatozoa in the Sobti & Gill (1989) study with several water soluble Ni compounds may reflect toxic effects on germ cells rather than chromosomal damage. Two dominant lethal tests (Deknudt & Léonard, 1982, Saichenko, 1985) with water soluble Ni compounds, were negative. Whilst some effects are seen in males (e.g. sperm abnormalities) there is little evidence for inheritable effects on the germ cells.
In April 2004, the Specialised Experts concluded that nickel sulphate, nickel chloride and nickel nitrate should be classified as Muta. Cat. 3; R68 (now Muta. 2: H341 under CLP classification). This conclusion was based on evidence ofin vivogenotoxicity in somatic cells, after systemic exposure (the 2007 negative oral MN study was not available at that time). Hence the possibility that the germ cells are affected could not be excluded (European Commission, 2004). The mutagenicity of nickel acetate was not evaluated by the Specialised Experts, but nickel acetate was later classified as Muta. 2: H341 by reading across from Ni sulphate.
The following information is taken into account for any hazard / risk assessment:
In vitro mutagenicity tests with Ni acetate have been negative while in vivo tests are lacking. For water soluble nickel compounds in general, there is evidence indicating that they are weak genotoxicantsin vitro, and may exhibit clastogenic activity. Somein vivostudies with soluble Ni compounds have been positive while two recent micronucleus studies via oral and intraperitoneal injection were negative. Evidence from human studies is limited. There are no definitive studies on germ cells, and little evidence concerning hereditable effects. Nickel acetate and other water soluble nickel compounds carry a harmonized Muta. 2: H341 CLP classification. 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 inAppendix C2).
Additional information
Justification for classification or non-classification
Nickel acetate is classified as Muta. 2: H341 in the 1st ATP to the CLP Regulation. Background information regarding this classification is provided in the discussion section above.
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