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EC number: 224-699-9 | CAS number: 4454-16-4
- 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
Link to relevant study record(s)
Description of key information
Key value for chemical safety assessment
Additional information
Concerning Nickel compounds, three well-conducted toxicokinetic studies were selected, i.e. oral or intra-peritoneal dosing in mice (Nielsen et al., 1993), in rats (Ishimatsu et al., 1995) and via drinking water for 6 months in rats (Severa et al., 1995).
Absorption: After oral administration of NiCl2, the Whole Body Retention (WBRs) of nickel decreased within 45-75 hr to 0.02-0.36% of the dose administered in mice. After intra-peritoneal administration, the WBR decreased within 20-50 hr to 1-6% of the dose administered. The estimated intestinal absorption ranged from 1.7 to 10% of the dose administered. In rats, the Ni compound absorbed fraction was between 0.09 and 34%.
Distribution: All studies indicate that Ni compounds were concentrated mainly in the liver, kidney and testicles, and additionally in lungs when the test item was administered by intra-peritoneal route.
Excretion: 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. Observation of these studies showed that the excretion of Ni levels occurs rapidly via the liver and kidneys after oral administration and via kidneys after intra-peritoneal administration. The longest retention was found in the testes for males, and ovaries for females. Furthermore, retention time of Ni in lung was also relatively longer than in other organs after intra-peritoneal administration.
Concerning 2 -ethylhexanoic acid, one well-documented study was selected.
English et al., 2007 tested 2-ethylhexanoic acid by three routes: oral, dermal and intravenous. 2 -ethylhexanoic acid is mainly excreted in the urine (rats: 60-80%) and is readily absorbed as on the average 10% is excreted in the faeces. The major urinary metabolites of 2-ethylhexanoic acid were the glucuronic acid conjugate of EHA, 2-ethylhexanedioic acid, isomers of hydroxy-2-ethylhexanoic acid and 2 isomeric metabolites of MW 142, proposed to be lactones. The parent compound was present in the urine at approximately 1.5 to 6.7% of the dose, depending upon the dose level, indicating rapid metabolism of the substance absorbed. After dermal administration between 40 and 50 % of the absorbed substance is excreted in the urine and approximately 7 in the faeces. A relatively long terminal half-life of elimination from the blood recorded in this study suggests that the skin may have served as a depot for 2-ethylhexanoic acid.
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