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EC number: 270-471-7 | CAS number: 68441-67-8
- 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
Genetic toxicity in vitro - Ames Assay
Hatcol 3178 is not mutagenic in the Salmonella typhimurium strains TA97a, TA98, TA100, TA102 and TA1535 in the absence and presence of metabolic activation.
Chromosome aberration: Negative with and without metabolic activation
RA-S, CAS 68424-31-7, Key, Croda, Griffiths, 1992, CTL/P/3792, Micronuc., RL2 - not genotoxic
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Genetic toxicity in vivo
Endpoint conclusion
- Endpoint conclusion:
- no study available
Additional information
Genetic toxicity in vitro - Ames Assay
Three valid experiments were performed.
The test item Hatcol 3178 was tested in the Salmonella typhimurium reverse mutation assay with five strains of Salmonella typhimurium (TA97a, TA98, TA100, TA102 and TA1535). The test was performed in three experiments in the presence and absence of S9-mix (rat liver S9-mix induced by Aroclor 1254).
In experiment 1a, Hatcol 3178 (dissolved in ethanol) was tested up to concentrations of 5000 μg/plate in the absence and presence of S9-mix in the strains TA97a, TA98, TA100, TA102 and TA1535 using the plate incorporation method.
Hatcol 3178 showed no precipitates on the plates at any of the concentrations. The bacterial background lawn was not reduced at any of the concentrations and no relevant decrease in the number of revertants was observed in all bacteria strains. The test item Hatcol 3178 showed no signs of toxicity towards the bacteria strains in both the absence and presence of metabolic activation.
The results of this experiment showed that none of the tested concentrations showed a significant increase in the number of revertants in all tested strains, in the presence and the absence of metabolic activation.
Due to an experimental error, no evaluation of the bacteria strains TA97a and TA98 was possible.
In experiment 1b, Hatcol 3178 was tested up to concentrations of 5000 μg/plate in the absence and presence of S9-mix in the strains TA97a and TA98 using the plate incorporation method.
Hatcol 3178 showed no precipitates on the plates at any of the concentrations. The bacterial background lawn was not reduced at any of the concentrations and no relevant decrease in the number of revertants was observed in all bacteria strains. The test item Hatcol 3178 showed no signs of toxicity towards the bacteria strains in both the absence and presence of metabolic activation.
The results of this experiment showed that none of the tested concentrations showed a significant increase in the number of revertants in all tested strains, in the presence and the absence of metabolic activation.
On the base of the experiments 1a and 1b, Hatcol 3178 was tested up to concentrations of 5000 μg/plate in the absence and presence of S9-mix in all bacteria strains using the pre-incubation method.
Hatcol 3178 showed no precipitates on the plates at any of the concentrations.
The bacterial background lawn was not reduced at any of the concentrations and no relevant decrease in the number of revertants was observed in all bacteria strains. The test item Hatcol 3178 showed no signs of toxicity towards the bacteria strains in both the absence and presence of metabolic activation.
The results of this experiments showed that the test item Hatcol 3178 caused no increase in the number of revertants in all bacteria strains compared to the solvent control, in both the absence and presence of metabolic activation. The test item Hatcol 3178 did not induce a dose-related increase in the number of revertants colonies in all strains, in the presence and absence of metabolic activation.
Based on the results of this study it is concluded that Hatcol 3178 is not mutagenic in the Salmonella typhimurium strains TA97a, TA98, TA100, TA102 and TA1535 in the absence and presence of metabolic activation under the experimental conditions in this study.
Evaluation of the ability of Hatcol 5236 to induce chromosome aberrations in cultured peripheral human
lymphocytes.
This report describes the effect of Hatcol 5236 on the number of chromosome aberrations in cultured peripheral human lymphocytes in the presence and absence of a metabolic activation system (Aroclor-1254 induced rat liver S9-mix). The possible clastogenicity of Hatcol 5236 was tested in two independent experiments.
Batch H20139 of Hatcol 5236 was a clear pale yellow liquid with a purity of 97.6%. The test substance was soluble in ethanol.
In the first cytogenetic assay, Hatcol 5236 was tested up to 100 μg/ml for a 3 h exposure time with a 24 h fixation time in the absence and presence of S9-mix. Hatcol 5236 precipitated in the culture medium at this dose level.
In the second cytogenetic assay, Hatcol 5236 was tested up to 100 μg/ml for a 24 hand 48 h continuous exposure time with a 24 hand 48 h fixation time in the absence of S9-mix. In the presence of 1.8% (v/v) S9 -frction Hatcol 5236 was also tested up to 100 μg/ml for a 3 h exposure time with a 48 h fixation time. Positive control chemicals, mitomycin C and cyclophosphamide, both produced a statistically significant increase in the incidence of cells with chromosome aberrations, indicating that the test conditions were adequate and that the metabolic activation system (S9-mix) functioned properly.
First cytogenetic assay
In the absence of S9-mix, Hatcol 5236 did not induce a statistically significant or biologically relevant increase in the number of cells with chromosome aberrations.
In the presence of S9-mix, Hatcol 5236 induced a statistically significant increase in the number of cells with chromosome aberrations at the intermediate concentration of 33 μg/ml, only when gaps were included. Since the type of aberrations observed were only breaks and gaps, the increase was not dose related, only observed at the intermediate concentration of 33 μg/ml, only when gaps were included and the number of cells with chromosome aberrations was well within our historical control data range, the increase was considered not to be biologically relevant.
Second cytogenetic assay
Hatcol 5236 did not induce a statistically significant or biologically relevant increase in the number of cells with chromosome aberrations in the absence and in the presence of S9-mix.
Finally, it is concluded that this test is valid and that Hatcol 5236 is not clastogenic in human lymphocytes under the experimental conditions described in this report.
An in vitro mammalian chromosome aberration test was performed in chinese hamster ovary (CHO) cells (Key, Exxon, Gudi, 1996, CA, RL1). The occurrence of chromosome aberrations was investigated in the presence and absence of metabolic activation (rat liver S9-mix) with test substance concentrations of 0 (Vehicle control), 157, 313, 625, 1250, 2500, 5000 μg/mL diluted with ethanol. Cytotoxicity of 48% was observed in the highest dose for treatment of 4 h without metabolic activation, 33% with metabolic activation and 3% for 20 h exposure without metabolic activation. The test substance did not induce an increase in the number of metaphases with aberrations at any preparation time and dose level.
Positive control substances significantly increased the rate of chromosome aberrations indicating the sensitivity of the assay. In conclusion, the test substance did not induce chromosome aberrations in CHO cells, neither in the presence nor in the absence of a metabolic activation system, under experimental conditions.
An in vitro Mammalian Cell Gene Mutation Test was conducted with the structural analogue substance with CAS No. 85186-89-6 (Fatty acids, C8-18 and C18-unsatd., esters with trimethylolpropane) according to OECD Guideline 476. Mouse lymphoma L5178Y cells were dosed with 0.3, 1, 3, 10, 33, 100, 333 and 750 μg/ml with and without metabolic activation. No signs of toxicity were observed, DMSO was used as vehicle, precipitation was observed at and above 100 μg/ml. There was no significant increase in the number of forward mutations at the thymidine kinase locus of L5178Y mouse lymphoma
cells treated with the test material, indicated by the total number of colonies per plate (RA-S, CAS 85186-89-6, Key, Croda, Verspeek-Rip, 2010, gene mut in mamm cells, RL2).
Justification for classification or non-classification
Based on the available information the substance is not classified as mutagenic, in accordance with Regulation (EC) 1272/2008.
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