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EC number: 204-411-8 | CAS number: 120-61-6
- 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
Genetic toxicity in vitro
Assays for DNA damage
No evidence of DNA damage is provided by the results of three studies.
The potential of DMT to cause DNA strand breaks was investigated in primary cultures of rat hepatocytes and in CHO cells in the absence of exogenous metabolic activation. Concentrations of 3.75, 7.5 and 15 µmole/tube did not produce any evidence of strand breaks in either cell type (Monarca et al, 1991). No evidence of DNA damage (as assessed by UDS) was seen in two studies using cultured HeLa cells (Lerda, 1996; Monarca et al, 1991).
Bacterial assays
No evidence of mutagenicity is reported in a number of Ames tests performed with DMT.
The potential mutagenicity of DMT was investigated in Salmonella typhimurium strains TA98, TA100, TA1535 and TA1537 using a pre-incubation modification of the Ames test. Five concentrations of up to 6666 ug/plate were used in the absence and presence of an exogenous metabolic activation system (rat liver S9 fraction). Exposure to DMT did not increase the number of revertant colonies; appropriate positive control compounds confirmed the sensitivity of the assay (Zeiger et al, 1982). Monarca et al (1991) evaluated the mutagenic potential of dimethyl terephthalate in a standard Ames test, with six Salmonella typhimurium strains in the presence and absence of metabolic activation. All the dose levels assayed (from 0.5 to 5000 µg/plate) were negative in the Ames test, with all the strains, with or without metabolic activation. Evidence of toxicity was observed at the highest dose levels in TA98 (-S9) and TA1537 (+S9).
Lerda (1996) also studied dimethyl terephthalate bacterial mutagenicity with five Salmonella typhimurium strains by means of the Maron & Ames (1983) standard plate method. Dimethyl terephthalate was not mutagenic in either the presence or absence of metabolic activation, when tested up to a concentration of 5000 µg/plate.
Dimethyl terephthalate was tested for mutagenic potential according to the Ames method, in Salmonella typhimurium strains TA1535, TA1537, TA 98 and TA10 at concentrations of 500, 1000, 2500, 5000, 10000 µg/plate (Du Pont, 1979). Dimethyl terephthalate was not toxic at the concentrations tested and was found to be non mutagenic, in the presence or absence of a metabolic activation system
An Ames test conducted (Anonymous, 1993d), was carried out according to GLP and EU method B.14. The test organisms were five Salmonella typhimurium strains (TA98, TA100, TA1535, TA1537 and TA1538). The substance was found to be insoluble in any of the prescribed Ames test solvents; therefore a Spot-Test was conducted. A sterile micro-spatula was used to apply the test substance to the top agar. There was no evidence of mutagenic activity in any of the strains tested, with and without metabolic activation.
Chromosomal aberration assays
No evidence of chromosomal effects is reported in a number of studies investigating different endpoints.
Loveday et al (1990) tested dimethyl terephthalate for its ability to induce chromosome aberrations and sister chromatid exchanges in cultured Chinese hamster ovary (CHO) cells, with and without exogenous metabolic activation (S9 mix). No induction of chromosomal aberrations, sister chromatid exchanges, or cytotoxicity was observed. The highest concentration of DMT tested in this study was 101 µg/ml. Lerda (1996) also found that dimethyl terephthalate was negative in an in vitro mammalian cell micronucleus test with human blood peripheral lymphocytes. There was no increase in the frequency of micronuclei in lymphocytes treated with test substance concentrations of 0.5, 5, 50 and 500 µg/ml, compared to the solvent control.
Dimethyl terephthalate was also evaluated in a chromosome aberration assay with human peripheral blood lymphocytes (Monarca et al,1991). Blood was obtained from two healthy volunteers. Cells were incubated with the test substance at concentrations of 0, 50, 100, 250 and 500 µg/ml, and mitotic activity was arrested with Colcemid. The frequency of chromatid and chromosomal gaps (achromatic lesions) and breaks was not significantly different from the controls. Only in the positive control (bleomycin) were rings, dicentrics, acentric fragments and double minutes present in addition to gaps and breaks. The mean number of aberrations per cell was 1 for all the cell sample; it was >1 only in the positive control. It can therefore be concluded that DMT was negative in the chromosome aberration assay in human peripheral lymphocytes, under the conditions of this study. The same authors also investigated micronucleus formation in human peripheral blood lymphocytes exposed to 0, 50, 100, 250 and 500 µg/ml DMT. The difference in frequency of micronuclei between the treated samples and controls was not significantly different and it was concluded that DMT did not induce micronuceli in human peripheral lymphocytes, under the conditions of this study.
Mammalian Cell Assays
The potential mutagenicity of dimethyl terephthalate was investigatied in a mouse lymphoma assay performed as part of the US NTP testing propgramme (Myhr & Caspary, 1991). NTP was not mutagenic to L5178Y cells and typically was not toxic with or without the addition of S9 mix. No significant increases in mutant frequency were observed. Low relative total growth values (as low as 27%) were observed randomly for individual cultures without relationship to dose. Concentrations up to 100 µg/mL were tested with and without S9, although the solubility limit in the culture medium was exceeded at 75 µg/mL.
Genetic toxicity in vivo
The mutagenic activity of dimethyl terephthalate was evaluated in a micronucleus test in groups of male C57B1/6j x CBA)F1 mice (Goncharova et al, 1987). Mice were administered single intraperitoneal injections of DMT (in DMSO) and femoral bone marrow harvested at 24, 48 or 72 hours after administration. Positive control animals were administered MNU. A number of deaths occurred in the control and test groups. A clear clastogenic effect was apparent at all concentrations of DMT studied (0.2 -1.0 mmole/kg bw), with the maximum number of micronuclei occurred 24 h after a single intraperitoneal injection. The reliability of the study is considererd to be severely compromised by the incidence of mortality apparently caused by the dosing vehicle.
Dimethyl terephthalate was tested in the mouse bone marrow micronucleus assay, for the US National Toxicology Program. The test substance was administered in three daily exposures by intraperitoneal injection, at doses of 0, 438, 875 and 1750 mg/kg bw. Bone marrow samples were obtained 24 h following the final exposure. DMT did not induce micronuclei in the bone marrow of male mice following three intraperitoneal injections at up to and including a dose of 1750 mg/kg. Administration of DMT did not result in any mortality.
The result is different to that reported in Goncharova et al (1988) which found dimethyl terephthalate to induce micronuclei in the bone marrow cells of male mice following single intraperitoneal injections of doses ranging from 0.2 to 1.0 mmol/kg (approximately 33 to 166 mg/kg bw). It is notable that DMSO was used as the solvent in that study, which may have contributed to the difference in results between these two studies. The OECD Guideline 474 specifically states that 'the solvent/vehicle should not produce toxic effects at the dose levels used'.
Short description of key information:
A number of studies of genotoxicity in vitro and in vivo are available for DMT. No evidence of DNA damage was seen in primary cultures of rat hepatocytes or CHO cells (strand breaks) or in cultured HeLa cells (UDS). Negative results are reported in a number of Ames tests in various strains of Salmonella typhimurium. Negative results were obtained in studies investigating chromosomal effects (clastogenicity, CSE, micronucleus induction) in a number of mammalian cell types. A negative mouse lymphoma assay is also reported. In vivo, high quality NTP studies report negative results for the mouse micronucleus assay and Drosophila SLRL assay. An older published mouse micronucleus assay reports a positive result at lower dose levels than those used on the NTP study; the reliability of this study is severely compromised by the choice of dosing vehicle, which caused mortalities in control and treated groups. The weight of evidence from reliable studies therefore clearly indicates that DMT is not genotoxic.
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
No evidence of genetic toxicity has been reported for DMT in a comprehensive battery of studies in vitro investigating DNA damage (strand breakage, UDS), in numerous studies of mutation in bacterial strains (Ames tests) and mammalian cells (mouse lymphoma assay). Negative results were obtained in studies investigating chromosomal effects (clastogenicity, SCE, micronucleus induction) in a number of mammalian cell types. A negative mouse lymphoma assay is also reported. In vivo, high quality NTP studies report negative results for the mouse micronucleus assay and Drosophila SLRL assay. An older published mouse micronucleus assay reports a positive result at lower dose levels than those used in the NTP study; the reliability of this study is severely compromised by the choice of dosing vehicle, which caused mortalities in control and treated groups. The weight of evidence from reliable studies therefore clearly indicates that DMT is not genotoxic.
It is concluded that DMT therefore does not require classification according to Regulation (EC) No. 1272/2008.
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