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EC number: 268-952-1 | CAS number: 68155-26-0
- 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
Genetic toxicity in vitro
Description of key information
In Vitro test
Strains TA97, TA98, TA100, and TA1535 were incubated in triplicate with five doses of CASRN 68603-42-9 (0.0-333.0 μg/plate) in the presence or absence of metabolic activation. The selection of the high dose of 333.0 μg/plate was based on cytotoxicity. Negative and positive controls responded as expected. The mean number of revertants/plate for all strains, with and without metabolic activation, was comparable to the control value. Amides, coco, N,N-bis(hydroxyethyl) was not mutagenic in this assay.
Strains TA97, TA98, TA100, and TA1535 were incubated in triplicate with fived oses of CASRN 93-83-4 (0.0-200.0 μg/plate) in the presence or absence of metabolic activation. The selection of the high dose of 200.0 μg/plate was based on cytotoxicity. Negativeand positive controls responded as expected. The mean number of revertants/plate for all strains,with and without metabolic activation, was comparable to the control value.Oleamide N,N-bis(2-hydroxyethyl)- was not mutagenic in this
assay.
L5178Y mouse lymphomacells were incubated with CASRN 68603-42-9 for four hours, with and without metabolicactivation. Each trial used different concentrations of CASRN 68603-42-9. Trials withmetabolic activation used concentrations that ranged from 0 - 20 μg/ml, and those withoutmetabolic activation used concentrations that ranged from 0 to 15 μg/ml. After incubation withtest substance, cells were resuspended in fresh medium and incubated for 2 additional days toexpress the mutant phenotype (i.e., a genetic change at the thymidine kinase locus). There wasno increase in the frequency of mutant colonies of L5178Y mouse lymphoma cells afterexposure to CASRN 68603-42-9.Amides, coco, N,N-bis(hydroxyethyl) was not mutagenic in this assay.
L5178Y mouse lymphomacells were incubated with CASRN 93-83-4 at 0-20 μg/ml for four hours, with and withoutmetabolic activation. After incubation with test substance, cells were resuspended in freshmedium and incubated for 2 additional days to express the mutant phenotype (i.e., a geneticchange at the thymidine kinase locus). Average mutant fractions and other test parameterssatisfied the finding of CASRN 93-83-4 as not causing point mutations.Oleamide N,N-bis(2-hydroxyethyl)- was not mutagenic in this assay.
Chinese hamster ovary cells(CHO) were incubated with CASRN 68603-52-9 at 0, 16, 30 and 50 μg/ml with and withoutmetabolic activation. After incubation and subsequent removal of treatment medium, Colcemidwas added, and the cells were harvested. Cells were scored for chromosomal aberrations. Aberrations in treated cells were comparable to those of the solvent control. Amides, coco, N,N-bis(hydroxyethyl) did not cause an elevation in chromosomal aberrations in this assay.
In Vivo test
Male and female mice were administered CASRN 93-83-4 via the dermal route at doses ≤ 800mg/kg/day . Peripheral blood samples in each of 5 animals per dose group were assessed for micronucleated normochromatic erythrocytes after 14 weeks of treatment. The frequency of micronucleated normochromatic erythrocytes in blood samples from the treatedgroups was equivalent to that of controls.Oleamide N,N-bis(2-hydroxyethyl)- did not cause chromosomal effects (increases in micronuclei) in this study.
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Genetic toxicity in vivo
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Additional information
Justification for classification or non-classification
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