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EC number: 941-652-4 | 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
Link to relevant study record(s)
Description of key information
Key value for chemical safety assessment
Additional information
Limited data were identified characterizing the toxicokinetics, metabolism, and distribution of nickel hydroxycarbonate. Data on the bioaccessibility of Ni hydroxycarbonate in six biological fluids as a surrogate for bioavailability are reported within Section 7.1.1 of this IUCLID file (KMHC, 2010).
Due to the structural similarities of Pentanickel Octahydroxide Carbonate and Nickel Hydroxycarbonate, all information in this section is relevant for Pentanickel Octahydroxide Carbonate (see section 13 for full discussion of read-across strategy)
Absorption - Inhalation:
The summary information below is taken from the 2008/2009 EU Risk Assessment for Ni Carbonate:
No data regarding the absorbed fraction of nickel in humans or experimental animals following inhalation of nickel carbonate have been located. The deposition of particles in the respiratory tract depends on the particle sizes (MMADs) as well as on other characteristics of the particles, and the absorption of nickel from the respiratory tract into the blood stream depends on the solubility of the nickel compound inhaled. Soluble nickel compounds are absorbed from the respiratory tract, while slightly soluble nickel compounds are expected only to be absorbed from the respiratory tract following inhalation exposure to a very limited extent. For the slightly soluble compounds the particles are expected to be retained in the airways and/or to be removed by the mucociliary action and translocated into the gastrointestinal tract, depending on the particle size.
In the 2008/2009 EU Risk Assessment of Ni carbonate, there was an industry statement (Laine, 2003, reference not reported here) indicating that in the absence of relevant data derogation to either soluble or insoluble nickel compounds, whichever is worst-case, is appropriate. The report states that derogation to soluble nickel compounds would represent the worst-case. Therefore, for the purpose of risk characterisation, a value of 100% was taken forward to the risk characterisation for the absorbed fraction of nickel from the respiratory tract following exposure by inhalation of nickel hydroxycarbonate for particulates with an aerodynamic diameter below 5 μm (respirable fraction). For nickel particulates with aerodynamic diameters above 5 μm (non-respirable fraction), the absorption of nickel from the respiratory tract is considered to be negligible as these particles predominantly will be cleared from the respiratory tract by mucociliary action and translocated into the gastrointestinal tract and absorbed. The bioaccessibility of nickel from nickel hydroxycarbonate in synthetic lung fluids, together with the results of a recently conducted acute inhalation toxicity study, allows us to refine the read-across for inhalation toxicity and absorption. Based on a comparison of these data to the Source Substances (Ni subsulfide, Ni oxide and Ni sulphate) it was determined that the most appropriate read across fro the inhalation endpoints is from nickel subsulfide. See CSR Appendix B2 for a complete summary of this read-across program.
The inhalation absorption of nickel subsulfide is conservatively estimated to be 50% for respirable size particles (assumes 100% deposition).
Absorption - Oral:
The summary information below is taken from the 2008/2009 European Union Risk Assessment for Nickel Carbonate:
No studies providing specific information about the absorbed fraction of nickel in humans or experimental animals following oral administration of nickel carbonate have been located. Slightly soluble nickel compounds, such as nickel carbonate, are expected to be absorbed from the gastrointestinal tract following oral exposure to a limited extent. However, some nickel compounds such as nickel carbonate may be more soluble in the acidic gastric fluid than in water thus facilitating absorption from the gastrointestinal tract. This is supported by one study in rats (Phatak & Padwardhan 1950 - quoted from IPCS 1991), which demonstrated that appreciable quantities of nickel from diets containing nickel carbonate were retained and tissue accumulation was significant; according to the authors, this was attributed to ready solubility of the compound in the stomach and the easier absorption from the intestine. For the purpose of risk characterisation, the same value of 30% as is used for the three soluble nickel compounds will be taken forward to the risk characterisation for the absorbed fraction of nickel from the gastrointestinal tract following oral exposure to nickel carbonate in the exposure scenarios where fasting individuals might be exposed to nickel carbonate. In all the other exposure scenarios, a value of 5% will be used for the absorbed fraction of nickel from the gastrointestinal tract. For further details, the reader is referred to the Background document in support of the individual Risk Assessment Reports.
The bioaccessibility of nickel from nickel hydroxycarbonate in synthetic gastric and intestinal fluids, together with the results of a recently conducted acute oral study, allows us to refine the read-across for oral toxicity (Henderson et al., 2012a)and absorption of nickel hydroxycarbonate. Based on a comparison of these data to the Source Substances (Ni subsulphide, Ni oxide and Ni sulphate) it was confirmed that the most appropriate read-across for the oral endpoints is still from nickel sulphate (based on Ishimimatsu et al., 1995 and Nielsen et al., 1999). However, contrary to the conclusions of the 2008/2009 European Union Risk Assessment, the absorption of Ni hydroxycarbonate is expected to be lower (possibly up to 10-fold lower) than that of Ni sulphate based on the relative LD50values after oral exposure (2000 mg/kg for Ni hydroxycarbonate and 361.9 mg/kg for nickel sulphate). See CSRAppendix B1for a complete summary of this read-across program.
Therefore, the absorption values of 30% (fasting) and 5% (with food) read across from nickel sulphate are likely to represent a very conservative estimate for nickel hydroxycarbonate.
Absorption - Dermal:
The summary information below is taken from the 2008/2009 EU Risk Assessment for Ni Carbonate:
When considering dermal absorption, a distinction should be made between penetration of nickel into skin and percutaneous transport, where nickel is transported through the skin and into the blood stream. For further details, the reader is referred to the Background document in support of the individual Risk Assessment Reports. No in vivo or in vitro studies providing information about the absorbed fraction of nickel in humans or experimental animals following dermal contact to nickel carbonate have been located. Recent human in vivo studies of nickel sulphate and nickel metal (Hostýnek et al. 2001a, 2001b) has shown that a large part of the administered dose remained on the surface of the skin after 24 hours or had penetrated into the stratum corneum. For further details, the reader is referred to the Risk Assessment Reports on nickel sulphate and nickel metal. In vitro studies using human skin support the findings in the human in vivo studies as most of the dose remained in the donor solution and only minor amounts were found in the receptor fluid; the in vitro studies also indicate that absorption following dermal contact may have a significant lag time. For further details, the reader is referred to the Background document in support of the individual Risk Assessment Reports.
In conclusion, the available data indicate that absorption of nickel following dermal contact to various nickel compounds can take place, but to a limited extent with a large part of the applied dose remaining on the skin surface or in the stratum corneum. The data are too limited for an evaluation of the absorbed fraction of nickel following dermal contact to nickel carbonate. An in vitro study of soluble nickel compounds (nickel sulphate, nickel chloride, nickel nitrate, and nickel acetate) using human skin (Tanojo et al. 2001, for details are referred to the respective reports) showed about 98% of the dose remained in the donor solution, whereas 1% or less was found in the receptor fluid and less than 1% was retained in the stratum corneum. According to the revised TGD, the amount absorbed into the skin, but not passed into the receptor fluid, should also be included in the estimate of dermal absorption. For the purpose of risk characterisation, a value of 2% will be taken forward to the risk characterisation for the absorbed fraction of nickel following dermal contact to nickel carbonate. For further details, the reader is referred to the Background document in support of the individual Risk Assessment Reports.
Again, recent results from bioaccessibility studies in synthetic sweat indicate that Ni release from Ni hydroxycarbonate is 14-fold lower than from nickel sulphate and more comparable to that of Ni subsulfide. A value of 2% for dermal absorption from Ni hydoxycarbonate can be considered as very conservative. The outcome of this read-across program is summarized in CSR Appendix B3.
Distribution and Elimination:
The information on distribution and elimination of nickel following exposure to nickel carbonate is very limited.The summary information below is taken from the 2008/2009 EU Risk Assessment for Ni Carbonate:
The information on distribution and elimination of nickel following exposure to nickel carbonate is very limited. Nickel from diets containing nickel carbonate has been reported to accumulate in tissues of rats (Phatak & Padwardhan 1950 - quoted from IPCS 1991) and of calves (O’Dell et al. 1971 – quoted from IPCS 1991). One study in mice (Furst & Al-Mahrouq 1981 - quoted from IPCS 1991) indicates that most of the nickel was eliminated 12 days after intratracheal instillation of nickel carbonate. Generally, nickel tends to deposit in the lungs of workers occupationally exposed to nickel compounds and in experimental animals following inhalation or intratracheal instillation of nickel compounds. The tissue distribution of nickel in experimental animals does not appear to depend significantly on the route of exposure (inhalation/intratracheal instillation or oral administration) although some differences have been observed. Low levels of accumulation in tissues are observed (generally below 1 ppm). A primary site of elevated tissue levels is the kidney. In addition, elevated concentrations of nickel are often found in the lung, also after oral dosing, and in the liver. Elevated nickel levels are less often found in other tissues. Limited information exists on tissue distribution in humans. Absorbed nickel is excreted in the urine, regardless of the route of exposure. Most ingested nickel is excreted via faeces due to the relatively low gastrointestinal absorption. In humans, nickel excreted in the urine following oral intake of nickel sulphate accounts for 20-30% of the dose administered in drinking water to fasting subjects or to fasting subjects compared with 1-5% when administered together with food or in close proximity to a meal. From biological monitoring in small groups of electroplaters exposed to nickel sulphate and nickel chloride, the half-life for urinary elimination of nickel has been estimated to range from 17 to 39 hours. Inhaled nickel particles can be eliminated from the respiratory tract by absorption, by removal via the mucociliary action and subsequently swallowed into the gastrointestinal tract, and by exhalation. For further details, the reader is referred to the Background document in support of the individual Risk Assessment Reports.
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