Registration Dossier
Registration Dossier
Data platform availability banner - registered substances factsheets
Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.
The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.
Diss Factsheets
Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 201-283-5 | CAS number: 80-48-8
- 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
Genetic toxicity: in vivo
Administrative data
- Endpoint:
- in vivo insect germ cell study: gene mutation
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Study period:
- 1988
- Reliability:
- 1 (reliable without restriction)
- Rationale for reliability incl. deficiencies:
- test procedure in accordance with generally accepted scientific standards and described in sufficient detail
Data source
Reference
- Reference Type:
- publication
- Title:
- Unnamed
- Year:
- 1 988
Materials and methods
Test guideline
- Qualifier:
- equivalent or similar to guideline
- Guideline:
- OECD Guideline 477 (Genetic Toxicology: Sex-linked Recessive Lethal Test in Drosophila melanogaster)
- Deviations:
- yes
- Principles of method if other than guideline:
- Recessive lethal tests and ring-X loss tests were performed as described in the review by Wiirgler et al. (1984), using Berlin-K and Rl(2), yB; y÷ Y B s. A brooding scheme of 3-2-2 days or 3-2 days was used for all experiments. The ring-X loss
frequency was calculated on the basis of all progeny carrying a ring-X chromosome or resulting from ring-X loss. - GLP compliance:
- no
- Type of assay:
- Drosophila SLRL assay
Test material
- Reference substance name:
- Methyl toluene-4-sulphonate
- EC Number:
- 201-283-5
- EC Name:
- Methyl toluene-4-sulphonate
- Cas Number:
- 80-48-8
- Molecular formula:
- C8H10O3S
- IUPAC Name:
- methyl 4-methylbenzene-1-sulfonate
Constituent 1
Test animals
- Species:
- Drosophila melanogaster
- Strain:
- other: Various strains
- Details on species / strain selection:
- Laboratory strains used: Berlin-K and Rl(2)
- Sex:
- male/female
Administration / exposure
- Route of administration:
- other: Oral and Injection
- Vehicle:
- The mutagenic effectiveness of DMBA is dependent on the route of administration, injection being far more effective when compared with feeding. The choice of the solvent is a crucial experimental condition. DMBA, when dissolved in oil/DMF, is ineffective whereas a special fat emulsion of DMBA gives high mutation frequencies.
- Details on exposure:
- Oral (feeding) of adults and larva (3 days) anf Injection of adults (single exposure)
- Duration of treatment / exposure:
- Single exposure or 3 days feeding.
- Control animals:
- not specified
Examinations
- Evaluation criteria:
- The ring-X loss frequency was calculated on the basis of all progeny carrying a ring-X chromosome or resulting from ring-X loss.
- Statistics:
- Statistical significance was calculated according to the Fisher exact test using pooled data from all available broods. For series with enzyme inhibitors, a comparison was made with a simultaneously executed series without inhibitors. For
experiments without pretreatment with inhibitors a comparison was made with the untreated spontaneous mutation frequency.
Results and discussion
Test resultsopen allclose all
- Sex:
- male/female
- Genotoxicity:
- positive
- Remarks:
- Injection
- Toxicity:
- not specified
- Vehicle controls validity:
- not specified
- Negative controls validity:
- not specified
- Positive controls validity:
- not specified
- Sex:
- male/female
- Genotoxicity:
- positive
- Remarks:
- Feeding
- Toxicity:
- not specified
- Vehicle controls validity:
- not specified
- Negative controls validity:
- not specified
- Positive controls validity:
- not specified
Applicant's summary and conclusion
- Conclusions:
- This paper shows the dependence in Drosophila of the route of administration on the mutagenicity of relatively stable direct-acting mutagens. Noticing the chemical similarity between MMS and Me-Tos, it was anticipated that Me-Tos, like MMS, would be mutagenic.
The authors have established that application by feeding is not effective in producing genetic damage in the gonads, chemically unstable direct-acting mutagens; relatively stable direct-acting mutagens which are metabolically de-activated in the gut; and promutagens of the class of aromatic hydrocarbons.
The observations with the tosylates resemble very closely the mutagenicity of formaldehyde in Drosophila flies. This compound is not mutagenic when applied orally (Auerbach, 1952). Injection of formaldehyde does result in considerable mutagenicity but, similar to the p-toluenesulphonates, the mutagenicity increases disproportionally with the dose.
The authors have established that application by feeding is not effective in producing genetic damage in the gonads, chemically unstable direct-acting mutagens; relatively stable direct-acting mutagens which are metabolically de-activated in the gut; and promutagens of the class of aromatic hydrocarbons.
We feel this is sufficient evidence for considering as inconclusive those experiments with germ-line assays where negative results were obtained but where injection experiments had not been performed.
The near absence of mutagenicity in the feeding experiments and the considerable mutagenic effect after injection, suggested a metabolic de-activation of Me-Tos somewhere along the route between the mouth and the gonads.
Two primary metabolic deactivation processes could be responsible. The first possible candidate, glutathione S-transferase, probably was not responsible, as depletion of glutathione with a sub-toxic dose of diethylmaleate did not influence Me-Tos mutagenicity.
The second important de-activation, and activation, pathway involves cytochrome P-450-mediated oxidation. Phi is known to be a potent inhibitor of many isozymes of cytochrome P-450 in mammals and in Drosophila.
A clear increase of Me-Tos mutagenicity when the mutagen is applied in combination with this inhibitor, suggests metabolic de-activation of Me-Tos by cytochrome P-450. Inhibition of metabolic deactivation of Phi by Me-Tos is not probable as Phi is not mutagenic in both feeding and injection experiments.
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.