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EC number: 202-347-5 | CAS number: 94-60-0
- 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
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Additional information
Bacterial mutagenesis:
The test substance, Dimethyl Cyclohexane Dicarboxylate (CAS #94-60-0), was tested to evaluate its mutagenic potential by measuring its ability to induce reverse mutations at selected loci of several strains of Salmonella typhimurium and at the tryptophan locus of Escherichia coli strain WP2 uvrA in the presence and absence of an exogenous metabolic activation system. Dimethyl sulfoxide (DMSO) was used as the vehicle. In the preliminary toxicity assay, the dose levels tested were 6.67, 10.0, 33.3, 66.7, 100, 333, 667, 1000, 3333 and 5000 μg per plate. Neither precipitate nor definitive background lawn toxicity was observed. Toxicity as a reduction in revertant count was observed at 5000 μg per plate with a few conditions. Based upon these results, the maximum dose tested in the mutagenicity assay was 5000 μg per plate. In the mutagenicity assay, the dose levels tested were 15.0, 50.0, 150, 500, 1500 and 5000 μg per plate. Neither precipitate nor background lawn toxicity was observed. No positive mutagenic responses were observed with any of the tester strains in either the presence or absence of S9 activation. These results indicate Dimethyl Cyclohexane Dicarboxylate (CAS #94-60-0) was negative for the ability to induce reverse mutations at selected loci of several strains of Salmonella typhimurium and at the tryptophan locus of Escherichia coli strain WP2 uvrA in the presence and absence of an exogenous metabolic activation system.
Mammalian cell mutagenesis
The test substance, Dimethyl Cyclohexane Dicarboxylate (CAS #94-60-0), was evaluated for its ability to induce forward mutations at the thymidine kinase locus in L5178Y mouse lymphoma cells in the presence and absence of an exogenous metabolic activation system. Dimethyl sulfoxide (DMSO) was used as the vehicle. In the preliminary toxicity assay, the concentrations tested were 7.81, 15.6, 31.3, 62.5, 125, 250, 500, 1000 and 2000 μg/mL. The maximum concentration evaluated was the limit dose for this assay. Visible precipitate was observed at a concentration of 2000 μg/mL at the beginning and end of treatment. Relative suspension growth (RSG) was 31, 82 and 32% at a concentration of 1000 μg/mL for the 4-hour treatments with and without S9 and the 24-hour treatment without S9, respectively. RSG was 0% at all higher concentrations using all treatment conditions. Based upon these results, the concentrations chosen for the definitive mutagenicity assay were 5, 25, 100, 500, 1000, 1500 and 2000 μg/mL (4-hour treatment with S9), and 125, 250, 500, 1000, 1500 and 2000 μg/mL (4- and 24-hour treatments without S9). In the definitive mutagenicity assay, visible precipitate was observed at a concentration of 2000 μg/mL at the beginning of treatment, and no visible precipitate was observed at the end of treatment. Cultures treated at concentrations of 25, 100, 500 and 1000 μg/mL (4-hour treatment with S9), 250, 500, 1000, 1500 and 2000 μg/mL (4-hour treatment without S9) and 125, 250, 500, 1000 and 1500 μg/mL (24-hour treatment without S9) exhibited 35 to 99%, 20 to 102% and 12 to 112% RSG, respectively, and were cloned. Relative total growth of the cloned cultures ranged from 20 to 86% (4-hour treatment with S9), 13 to 86% (4-hour treatment without S9) and 11 to 93% (24-hour treatment without S9). No increases in induced mutant frequency ≥90 mutants/106 clonable cells were observed following 4- and 24-hour treatments without S9. However, an increase in induced mutant frequency >90 mutants/106 clonable cells was observed at concentrations ≥500 μg/mL following a 4-hour treatment with S9. These results indicate Dimethyl Cyclohexane Dicarboxylate (CAS #94-60-0) was positive for the ability to induce forward mutations at the thymidine kinase locus in L5178Y mouse lymphoma cells, in the presence of an exogenous metabolic activation system. Uniformly negative results were observed in the absence of an exogenous metabolic activation system.
Chromosome aberration studies
The test substance, Dimethyl Cyclohexane Dicarboxylate (CAS #94-60-0), was evaluated for its ability
to induce structural chromosomal aberrations using Chinese hamster ovary (CHO) cells in both the absence and presence of an of an exogenous metabolic activation system. Dimethyl sulfoxide (DMSO) was used as the vehicle. Due to error in seeding of cells, the initial preliminary toxicity assay was terminated and the assay was repeated. Cytotoxicity data from the initial preliminary toxicity assay is being maintained in the study file, but not reported. In the repeat preliminary toxicity assay, the doses tested ranged from 0.2 to 2000 μg/mL, which was the limit dose for this assay. Cytotoxicity (≥ 50% reduction in cell growth index relative to the vehicle control) was observed at 2000 μg/mL in the non-activated 4 and 20-hour exposure groups, and at doses ≥ 600 μg/mL in the S9-activated 4-hour exposure group. Based upon these results, the doses chosen for the chromosome aberration assay ranged from 200 to 2000 μg/mL for the non-activated 4 and 20-hour exposure groups, and from 50 to 600 μg/mL for the S9-activated 4-hour exposure group. In the chromosome aberration assay, cytotoxicity (55 ± 5% reduction in cell growth index relative to the vehicle control), was observed at doses ≥ 1800 μg/mL in the non-activated 4-hour exposure group, at doses ≥ 250 μg/mL in the S9-activated 4-hour exposure group; and at doses ≥ 1000 μg/mL in the non-activated 20-hour exposure group. The doses selected for evaluation of chromosome aberrations were 400, 1000, and 1800 μg/mL for the non-activated 4-hour exposure group; 100, 200, and 250 μg/mL in the S9-activated 4-hour exposure group; and 200, 600, and 1000 μg/mL in the non-activated 20-hour exposure group. No significant or dose-dependent increases in structural or numerical (polyploid or endoreduplicated cells) aberrations were observed in treatment the non-activated 4 and 20-hour exposure groups (p > 0.05; Fisher’s Exact and Cochran-Armitage tests). In the S9-activated 4-hour exposure group, statistically significant and dose-dependent increases in structural aberrations (4.3%, 9.3%, and 11.3%) were observed at doses 100, 200, and 250 μg/mL, respectively (p ≤ 0.01; Fisher’s Exact test and p ≤ 0.05; Cochran-Armitage test). No significant or dose-dependent increases in numerical aberrations were observed in the S9-activated 4-hour exposure group (p > 0.05; Fisher’s Exact and Cochran-Armitage tests). These results indicate Dimethyl Cyclohexane Dicarboxylate was negative for the induction of structural and numerical chromosome aberrations in the absence of the exogenous metabolic activation system. Dimethyl Cyclohexane Dicarboxylate was positive for the induction of structural and negative for the induction of numerical chromosome aberrations in the presence of the exogenous metabolic activation system.
Endpoint Conclusion:
Justification for classification or non-classification
Dimethyl -1,4-cyclohexanedicarboxylate (DMCD) was shown to be non-mutagenic is bacterial and mammalian cell assays without metabolic activation. DMCD was positive in mammalian chromosome aberration and mutagenicity studies with metabolic activation. Based upon these findings, DMCD does not satisfy the criteria for classification according to EU Classification, Labelling and Packaging of Substances and Mixtures (CLP) Regulation (EC) No. 1272/2008 or UN Globally Harmonized System of Classification and Labelling of Chemicals (GHS).
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