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Diss Factsheets
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EC number: 941-303-6 | CAS number: 1689576-55-3
- 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
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Carcinogenicity
Administrative data
Description of key information
A carcinogenicity study may be required in accordance with REACH Regulation 1907/2006, Annex X, Section 8.9.1 of Column 1, Annex X. It is proposed to waive the need to conduct this study on the basis that available information indicate no concerns for carcinogenicity.
Key value for chemical safety assessment
Carcinogenicity: via oral route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Carcinogenicity: via inhalation route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Carcinogenicity: via dermal route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Justification for classification or non-classification
A carcinogenicity study may be required in accordance with REACH Regulation 1907/2006, Annex X, Section 8.9.1 of Column 1, Annex X. It is proposed to waive the need to conduct this study on the basis that:
1) Negative findings in tests for gene mutation / mutagenicity.
2) Evaluation using Derek Nexus, an accepted (Q)SAR tool designed for the qualitative prediction of the possible toxicity of chemicals, a procedure in accordance with Annex XI of Regulation 1907/2006. In this, a structurally related trimellitate ester (containing branched C8 alcohol side chains) triggered plausible alerts (in mouse and rat only) for carcinogenicity. These alerts were fired due to the potential for the structure to induce peroxisome proliferation in rats and mice, probably by association with phthalate esters. Peroxisome proliferators have been shown to activate one or more nuclear steroid hormone-like receptors (PPARs) which induce increases in the oxidative enzyme activity associated with peroxisome proliferators. The strength of the binding with the PPAR sites is expected to be a factor in determining the potency of peroxisome proliferators. These alerts are regarded as having little relevance in human, as humans appear to be insensitive or unresponsive at doses which caused marked peroxisome proliferation in rats or mice (European Centre for Ecotoxicology and Toxicology of Chemicals (ECETOC), 1992. Hepatic peroxisome proliferation. ECETOC Monograph No. 17).
3) Molecular modelling studies performed by Kambia et al. (Kambia N, Renault N, Dilly S, Farce A, Dine T, Gressier B Luyckk M, Brunet C and Chavatte P. Molecular modelling of phthalates – PPARs interactions. Journal of Enzyme Inhibition and Medicinal Chemistry, 23(5): 611–616, 2008) indicate that TOTM is not able to fit into PPARα and PPARγ binding sites due to its larger size relative to the corresponding phthalate ester, implying that any predicted activity may not actually be able to occur.
4) A repeat-dose study to investigate the potential hepatotoxicity of TOTM (See Section 7.5.1 - Repeated dose toxicity: 28 day dietary study in rats – BIBRA) showed that TOTM produced the same spectrum of morphological and biochemical changes in the rat liver but with much less potency in its action than those produced by DEHP (the equivalent phthalate ester).
With these considerations it is concluded that there is sufficient evidence to justify the non-classification of the registered substance for carcinogenicity.
Additional information
A carcinogenicity study may be required in accordance with REACH Regulation 1907/2006, Annex X, Section 8.9.1 of Column 1, Annex X. It is proposed to waive the need to conduct this study on the basis that:
1) Negative findings in tests for gene mutation / mutagenicity.
2) Evaluation using Derek Nexus, an accepted (Q)SAR tool designed for the qualitative prediction of the possible toxicity of chemicals, a procedure in accordance with Annex XI of Regulation 1907/2006. In this, a structurally related trimellitate ester (containing branched C8 alcohol side chains) triggered plausible alerts (in mouse and rat only) for carcinogenicity. These alerts were fired due to the potential for the structure to induce peroxisome proliferation in rats and mice, probably by association with phthalate esters. Peroxisome proliferators have been shown to activate one or more nuclear steroid hormone-like receptors (PPARs) which induce increases in the oxidative enzyme activity associated with peroxisome proliferators. The strength of the binding with the PPAR sites is expected to be a factor in determining the potency of peroxisome proliferators. These alerts are regarded as having little relevance in human, as humans appear to be insensitive or unresponsive at doses which caused marked peroxisome proliferation in rats or mice (European Centre for Ecotoxicology and Toxicology of Chemicals (ECETOC), 1992. Hepatic peroxisome proliferation. ECETOC Monograph No. 17).
3) Molecular modelling studies performed by Kambia et al. (Kambia N, Renault N, Dilly S, Farce A, Dine T, Gressier B Luyckk M, Brunet C and Chavatte P. Molecular modelling of phthalates – PPARs interactions. Journal of Enzyme Inhibition and Medicinal Chemistry, 23(5): 611–616, 2008) indicate that TOTM is not able to fit into PPARα and PPARγ binding sites due to its larger size relative to the corresponding phthalate ester, implying that any predicted activity may not actually be able to occur.
4) A repeat-dose study to investigate the potential hepatotoxicity of TOTM (See Section 7.5.1 - Repeated dose toxicity: 28 day dietary study in rats – BIBRA) showed that TOTM produced the same spectrum of morphological and biochemical changes in the rat liver but with much less potency in its action than those produced by DEHP (the equivalent phthalate ester).
With these considerations it is concluded that there is sufficient evidence to justify the non-classification of the registered substance for carcinogenicity.
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.
Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
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