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EC number: 201-058-1 | CAS number: 77-78-1
- 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
DMS is a directly acting mutagen, which methylates DNA especially at the N7-guanine and the N3-adenine sites (Shiner 1988, Newbold 1980).
Bacterial and fungal systems
DMS induced reverse mutations in different strains ofS. typhimuriumand in various fungi, and was found positive in a forward mutation assay. Primary DNA damage was reported in assays inE. coli,P. mirabilisandS. typhimurium. A host-mediated assay with Salmonella was positive.
Mammalian cells in vitro
DMS induced an increase in cells with chromosomal aberrations in V79-cells. An induction of HPRT gene mutations was found in CHO- and in V79-cells. Moreover, DMS induced an increase in SCE’s and UDS in mammalian cells in vitro.
Studiesin vivo
Drosophila
Assays inDrosophila melanogasterwere positive, i.e., in tests for somatic gene-mutations and recombination, for sex-linked recessive lethals, and in tests for sex chromosome loss.
Mammals
DMS administrated to male mice (23 mg/kg bw i.p.), did not induce dominant lethal mutations as appeared from pregnancy rate, number of total implants, and early and late deaths. However, only one dose-group of 5 animals was tested (Epstein, 1968). No indication was given on toxicity, therefore it is not possible to establish whether the dose was sufficiently high. The toxicological significance of this study cannot be assessed because of the limited study design.
In the mouse spot test (performed according to OECD 484), DMS was administered to pregnant mice (25 or 50 mg/kg bw i.p.). The number of somatic coat colour patches was not increased compared to controls (Braun, 1984).
A brief paper reported DMS positive in a cytogenetic assay in rat bone marrow cells, however, the results are not suitable for evaluation due to the poor reporting (Sharma, 1980). The number of DNA breaks increased significantly after alkaline elution of brain DNA of rats treated with 0.25 mmol/kg i.v. DMS (Robbiano, 1987). The methylating capacity of DMS is demonstrated in several tissuesin vivoin Wistar rats (Swann, 1968).
In a publication of Molodkina et al. it is stated that repeated inhalative exposure to 20.26±1.34, 2.64±0.43, and 0.29±0.02 mg/m3for 4 months did not induce dominant lethal mutations in germ cells of rats. Inhalative exposure to DMS at concentrations of 0, 0.29±0.02 and 2.69±0.43 mg/m3in rats, and at concentrations of 0, 0.24±0.2, 4.32±0.75, and 22.1±2.35 mg/m3in mice (8 animals per group and species) induced a dose-dependent increase in chromosomal aberrations in bone marrow cells. (Molodkina et al., 1986). The study is considered not suitable for evaluation of the genotoxicity of DMS in mammalsin vivo, because of the very limited reporting of study design and results.
Conclusion
The data submitted are in accordance with the basic requirements as specified in Annex VIIA of Directive 67/548/EC. Several tests indicate that DMS is an alkylating agentin vivoandin vitro.DMS is a potent direct acting genotoxicant in bacteria and mammalian cellsin vitro. It is positive in tests for primary DNA damage, gene mutations, and chromosome aberrationsin vitro. DMS is mutagenic in Drosophila. From the results of the tests with mammals it is concluded that DMS did not induce an increase in dominant lethals in mouse and there were no indications for induction of gene mutationsin vivo.
Short description of key information:
EU RISK ASSESSMENT – DIMETHYL SULPHATE
Endpoint Conclusion: Adverse effect observed (positive)
Justification for classification or non-classification
According to EC criteria DMS is considered a category 3 mutagen and classified as R40.
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