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Diss Factsheets
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EC number: 231-765-0 | CAS number: 7722-84-1
- 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
Additional information
In vitro data
The following text is copied from the EU risk assessment report (2003), pg. 123: "Hydrogen peroxide is a mutagen and genotoxicant in a variety of in vitro test systems (…). In bacterial tests, most gene mutation assays (in the Ames test especially the strains sensitive to oxygen radicals), and DNA damage and repair assays have yielded positive results. With mammalian cells, positive results were mostly observed in gene mutation assays, DNA damage and repair assays, UDS assays, SCE assays, and cytogenetic assays for chromosomal aberrations. The responses were often, but not invariably (Abu-Shakra and Zeiger, 1990) modified by the amount of catalase present, which varies in bacteria and mammalian cells: bacterial strains lacking catalase activity seem to be especially sensitive (Abril and Pueyo, 1990), the hydrogen peroxide resistant Chinese hamster cell line R-8 had 10-fold higher catalase activity in comparison to the parental cells (Sawada et al., 1988). Although few tests have employed metabolic activation, it can be inferred from the results that the microsomal mix (like added catalase) markedly reduced or abolished the genotoxic response indicating that S9 contains hydrogen peroxide degrading enzymes (Mehnert et al., 1984a; 1984b; Speit et al., 1982; Procter & Gamble, 1985). Apart from protecting enzymes, other recognised variables of the cells determining their sensitivity to mutation were the extent of Fenton reaction (formation of hydroxyl radical) and the cells’ repair abilities (Kruszewski and Szumiel, 1993)."
In vivo data
In vivo studies with high reliability are available: micronucleus assays in mice (Molinier 1995, Sarver 1995) or an Unscheduled DNA Synthesis (UDS) Test with mammalian liver cells in rats (Clare 1997) demonstrated that hydrogen peroxide does not have genotoxic effects in vivo when administered by intraperitoneal or intravenous injection or ad libitum via drinking water.
Short description of key information:
The following text is copied from the EU Risk Assessment Report (2003), pg. 123: "Hydrogen peroxide is a mutagen and genotoxicant in a variety of in vitro test systems (…). In bacterial tests, most gene mutation assays (in the Ames test especially the strains sensitive to oxygen radicals), and DNA damage and repair assays have yielded positive results. With mammalian cells, positive results were mostly observed in gene mutation assays, DNA damage and repair assays, UDS assays, SCE assays, and cytogenetic assays for chromosomal aberrations. The responses were often, but not invariably (Abu-Shakra and Zeiger, 1990) modified by the amount of catalase present, which varies in bacteria and mammalian cells: bacterial strains lacking catalase activity seem to be especially sensitive (Abril and Pueyo, 1990), the hydrogen peroxide resistant Chinese hamster cell line R-8 had 10-fold higher catalase activity in comparison to the parental cells (Sawada et al., 1988). Although few tests have employed metabolic activation, it can be inferred from the results that the microsomal mix (like added catalase) markedly reduced or abolished the genotoxic response indicating that S9 contains hydrogen peroxide degrading enzymes (Mehnert et al., 1984a; 1984b; Speit et al., 1982; Procter & Gamble, 1985). Apart from protecting enzymes, other recognised variables of the cells determining their sensitivity to mutation were the extent of Fenton reaction (formation of hydroxyl radical) and the cells’ repair abilities (Kruszewski and Szumiel, 1993)."
In contrast, the available in vivo studies with high reliability performing micronucleus assays in mice (Molinier 1995, Sarver 1995) or an Unscheduled DNA Synthesis (UDS) Test with Mammalian Liver Cells in rats (Clare 1997) demonstrated that hydrogen peroxide does not have genotoxic effects in vivo when administered by intraperitoneal or intravenous injection or ad libitum via drinking water.
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
The following discussion of mutagenicity is copied from the EU risk assessment report for hydrogen peroxide (European Commission 2003, page 126-127):
“Hydrogen peroxide is a mutagen and genotoxicant in a variety of in vitro test systems. The responses observed were modified by the presence of degrading enzymes (catalase), the extent of formation of hydroxyl radicals by Fenton reaction, and the cells repair abilities. Regarding in vivo genotoxicity, studies employing modern methodologies have explored DNA repair in liver cells of rats administered hydrogen peroxide by intravenous infusion for 30 minutes(…) (Clare 1997), as well as micronucleus formation in mice in the context of a 2-week drinking water exposure (…) (Sarver 1995), or after a single intraperitoneal injection(…) (Molinier 1995), all with a negative outcome. Intravenous administration of hydrogen peroxide in the in vivo-in vitro unscheduled DNA synthesis study ensured that the substance had a fair chance to reach the target (liver) cells, although the duration of exposure was limited (Clare 1997). In the micronucleus study by oral drinking water exposure (…) (Sarver 1995), the systemic fate of hydrogen peroxide was uncertain, and there was no decrease in the ratio of polychromatic/normochromatic erythrocytes in the bone marrow. (…)
According to the principles followed in the EU, hydrogen peroxide is not considered for classification as a mutagen.”
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