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EC number: 235-715-9 | CAS number: 12607-70-4
- 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
Carcinogenicity
Administrative data
Description of key information
ORAL: Data for Ni hydroxycarbonate are read-across from Ni sulphate, as this is the most bioavailable of the Ni compounds. A well-conducted OECD 451 study in rats did not show any carcinogenic potential of nickel sulphate following oral administration. A summary document on this topic can be found in the attached document entitled, "Background-Oral Carcinogenicity for all Nickel Compounds" (Section 7.7 of IUCLID) and in Appendix B1 of the CSR.
INHALATION Inhalation carcinogenicity information can be derived from epidemiological data (e.g. ICNCM, 1990). These studies demonstrated that exposures to mixtures of nickel compounds, including nickel hydroxycarbonate, are associated with carcinogenicity of the respiratory tract. Available carcinogenicity animal data from Ni sulphate (oral) and human data from epidemiological studies (inhalation) indicate that nickel hydroxycarbonate does not cause carcinogenicity after oral exposure but does have the potential to cause respiratory tract carcinogenicity after inhalation exposure.
DERMAL: Dermal absorption to Ni compounds including Ni hydroxycarbonate is very low (1-2%). As oral exposure to nickel sulphate resulting in highest systemic bioavailability does not show any carcinogenic potential, there are good reasons to assume that cancer is not a relevant end-point with respect to dermal exposure either.
Key value for chemical safety assessment
Justification for classification or non-classification
Ni hydroxycarbonate is classified Carc. 1A; H350i via inhalation route of exposure according to the 1st ATP to the CLP Regulation.Background information can be found in the discussion section.
In addition, a background document summarizing the potential of Ni compounds to cause cancer via the oral route of exposure can be found in the attached document entitled, "Background-Oral Carcinogenicity for all Nickel Compounds" (Appendix B1to CSR). In summary, absence of oral carcinogenicity of the nickel (II) ion demonstrates that the possible carcinogenic effects of nickel-containing substances in humans are limited to the inhalation route of exposure and the associated organ of entry (i.e., the respiratory tract). After inhalation, respiratory toxicity limits the systemic absorption of Ni (II) ion to levels below those that can be achieved via oral exposure.
Additional information
No specific information regarding carcinogenicity of nickel hydroxycarbonate following inhalation, oral, or dermal exposure in experimental animals have been located. Data from epidemiological studies with cohorts exposed to Ni hydroxycarbonate can be used for classification purposes, while animal and humans studies with other nickel compounds are read-across for carcinogenicity DNEL-DMEL setting to Ni hydroxycarbonate. Humans are only exposed via inhalation, oral intake or dermal contact to nickel hydroxycarbonate so data from intraperitoneal and intramuscular data are not relevant.
Data on the oral carcinogenicity of Ni hydroxycarbonate are read-across from Ni sulphate. The lack of oral carcinogenic potential for nickel sulphate hexahydrate can be extrapolated to other soluble and insoluble nickel compounds. Nickel sulphate hexahydrate represents a worst-case scenario for systemic absorption and systemic bioavailability of nickel since nickel sulphate hexahydrate is readily solubilized in gastrointestinal fluid and results in the highest systemic absorption of Ni (II) ions compared to less soluble nickel-containing substances (Ishimatsu et al., 1995). A background document summarizing the potential of Ni compounds to cause cancer via the oral route of exposure can be found in the attached document entitled, "Background-Oral Carcinogenicity for all Nickel Compounds" (Section 7.7) and in Appendix B1of this CSR.
Inhalation carcinogenicity information can be derived from epidemiological data (e.g. ICNCM, 1990). These studies demonstrated that exposures to mixtures of nickel compounds, including nickel hydroxycarbonate, are associated with carcinogenicity of the respiratory tract. Available carcinogenicity animal data from Ni sulphate (oral) and human data from epidemiological studies (inhalation) indicate that nickel hydroxycarbonate does not cause carcinogenicity afteroral exposure but does have the potential to cause respiratory tract carcinogenicity after inhalation exposure.
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