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EC number: 203-551-7 | CAS number: 108-11-2
- 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
In the key bacterial reverse mutation assay (equivalent to OECD guideline 471), MIBC was tested in a non-GLP study at doses of 0, 1, 5, 10, 50, 100, 500, 1,000, or 5,000 µg/plate in Salmonella typhimurium strains TA 98, TA 100, TA 1535, TA 1537, and TA 1538 and in Escherichia coli WP2 uvr A both in the presence and absence of exogenous metabolic activation (polychlorinated biphenyl-induced rat liver S9) (Shimizu et al., 1985). Incubations at each concentration were done in duplicate; however, an independent repeat experiment was not performed. Dimethyl sulfoxide (DMSO) was used as the vehicle and positive controls were included in all incubations. Growth inhibition was observed at 5,000 µg/plate; however, no increase in the reverse mutation rate were observed at any MIBC concentration in any of the tester strains either in the presence or absence of metabolic activation. Incubation with positive control substances in the absence or presence of metabolic activation resulted in anticipated increases in the reverse mutation rate.
In the supporting bacterial reverse mutation assay (equivalent to OECD guideline 471), MIBC was tested in a non-GLP study at doses of 0, 31.25, 62.5, 125, 250, 500, 1,000, 2,000, or 4,000 μg/plate in Salmonella typhimurium strains TA 98, TA 100, TA 1535, TA 1537, and TA 1538 and in Escherichia coli WP2 uvr A pKM 101 both in the presence and absence of exogenous metabolic activation (Aroclor 1254-induced rat liver S9) (Clare, 1984). Incubations at each concentration were done in triplicate and an independent repeat experiment was performed. DMSO was used as the vehicle and positive controls were included in all incubations. No cytotoxicity and no increase in the reverse mutation rate were observed at any MIBC concentration in any of the tester strains either in the presence or absence of metabolic activation. Incubation with positive control substances in the presence of metabolic activation resulted in anticipated increases in the reverse mutation rate but did not always do so in the absence of metabolic activation. This study is therefore considered reliable with restrictions.
In a non-GLP mammalian chromosome aberration test (equivalent to OECD guideline 473), MIBC was tested at doses of 0, 500, 1,000, or 2,000 µg/mL in rat liver (RL4) cells in the absence of exogenous metabolic activation (Clare, 1984). Incubations at each concentration were done in triplicate and an independent repeat experiment was performed. DMSO was used as the vehicle and positive controls were included in all incubations. No cytotoxicity was observed and no chromosome damage was observed at any MIBC concentration. Incubations with the positive control substance 7,12-dimethylbenzanthracene resulted in anticipated increases in chromatid damage.
In a non-GLP yeast gene mutation assay (equivalent to OECD guideline 480), MIBC was tested at doses of 0, 0.01, 0.1, 0.5, 1.0, or 5.0 mg/mL in Saccharomyces cerevisiae both in the presence and absence of exogenous metabolic activation (Aroclor 1254-induced rat liver S9) (Clare, 1984). Incubations at each concentration were done in triplicate and an independent repeat experiment was performed. DMSO was used as the vehicle and positive controls were included in all incubations. No cytotoxicity was observed and no increase in the rate of mitotic gene conversion was observed at any MIBC concentration in the presence or absence of metabolic activation. Incubation with positive control substances in the presence (cyclophosphamide) or absence (4-nitroquinoline-N-oxide) of metabolic activation did not always result in anticipated increases in the rate of mitotic gene conversion. Due to this, and as the post-treatment incubation period was 3 days as opposed to the recommended 4 to 7 days, this study is considered reliable with restrictions.
The potential of the test item Methyl isobutylcarbinol to induce mutations at the TK (thymidine kinase) locus in L5178Y mouse lymphoma cells was evaluated according to the international guidelines and in compliance with the Principles of Good Laboratory Practice (Sire, 2010). After a preliminary toxicity test, Methyl isobutylcarbinol was tested in two independent experiments at dose levels of 0.313, 0.625, 1.25, 2.5, 5 and 10 mM, with and without a metabolic activation system, the S9 mix, prepared from a liver microsomal fraction (S9 fraction) of rats induced with Aroclor 1254. Without S9 mix, no noteworthy decrease in the Adj. RTG was noted at any dose‑levels following the 3-hour treatment and a 42 to 67% decrease in the Adj. RTG was noted at dose‑levels ≥ 5 mM following the 24-hour treatment. No noteworthy increase in the mutation frequency was noted at any of the tested dose-levels, following either the 3- or the 20-hour treatment.With S9 mix, no noteworthy decrease in the Adj. RTG was noted at any dose-levels in the first experiment and in the second, a 31% decrease in the Adj. RTG was observed at dose-levels ≥ 5 mM. No noteworthy increase in the mutation frequency was noted at any of the tested dose-levels, in either experiment. Methyl isobutylcarbinol did not show any mutagenic activity in the mouse lymphoma assay.
Short description of key information:
MIBC was not mutagenic to bacteria (bacterial reverse mutation assay) and mammalian cells (L5178Y) in vitro with or without metabolic activation. In a mammalian cell cytogenetic assay (rat liver cells), MIBC was negative with and without metabolic activation.
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
The substance does not meet the criteria for classification and labelling for this endpoint, as set out in Regulation (EC) NO. 1272/2008.
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