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Diss Factsheets
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EC number: 239-707-6 | CAS number: 15630-89-4
- 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
When sodium percarbonate comes into contact with the human skin or body fluids it will dissociate into hydrogen peroxide, carbonate ions and sodium ions. Human information about the toxicokinetics of these substances is available and was discussed in the OECD SIDS dossier (OECD 2006). The following paragraphs have been copied from the OECD SIDS dossier on sodium percarbonate (OECD 2006), section 3.1.1, page 11: “The toxicokinetics, metabolism and distribution of hydrogen peroxide have been described in detail by ECETOC (1993, 1996) and European Commission (2003). Hydrogen peroxide is a normal metabolite in the aerobic cell. There are a number of different hydrogen peroxide metabolizing systems, among them the enzymes catalase and glutathione peroxidase, which control the hydrogen peroxide concentration at different levels and in different parts of the cell as well as in the blood. Hydrogen peroxide will in part be decomposed by the cells of the tissue of first contact but the remaining part could diffuse into the blood vessels. However, the European Commission (2003) concluded “In view of the high-degradation capacity for hydrogen peroxide in blood it is however unlikely that the substance is systemically distributed, and therefore the endogenous steady state levels of the substance in tissues are unlikely to be affected“. The toxicokinetics, metabolism and distribution of carbonate have been described by the OECD (2002). Carbonate could potentially increase the pH of the blood. The blood plasma of man normally has a pH of 7.4. Should the pH fall below 7.0 or rise above 7.8, irreversible damage may occur. Compensatory mechanisms for acid-base disturbances return the pH of the blood to normal. If carbonate is absorbed its concentration will be regulated and therefore elevated amounts of carbonate are not expected to be available in the body. Furthermore it should be realised that an oral uptake of sodium percarbonate results in a neutralisation of carbonate in the stomach by the gastric acid. Significant amounts of gastric acids are present in the stomach (pH about 2) which will result in a formation of bicarbonate and/or carbon dioxide. Therefore it is very unlikely that an oral uptake of sodium percarbonate will result in a pH increase of the blood. Sodium ions are readily absorbed throughout the small intestine and are subject to rapid exchange by the large majority of cells in the body. Exposure to sodium percarbonate is not expected to contribute significantly to the sodium load of the body (compared to dietary uptake) and therefore elevated amounts of sodium are not expected to be available in the body.”
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
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