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EC number: 218-871-2 | CAS number: 2269-22-9
- 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
Genetic toxicity in vitro
Description of key information
Upon contact with water or moisture (e.g. within mucous membranes) aluminium tri-sec-butanolate hydrolyses immediately to butan-2-ol and aluminium 3+ cations (as hydroxide and oxyhydroxide). Hence, toxicity is determined by the toxicity of these two species.
2-Butanol was tested negative for mutagenicity in two Ames tests, a test investigating reverse mutations in yeast, and in-vitro chromosome aberration study using mammalian cells.
In a test according to OECD 471 Salmonella typhimurium strains TA 100, TA1535, TA98, TA97a and TA102 were exposed to aluminium oxide with and without metabolic activations. No increase in the number of revertants was observed in any of the strains tested. Therefore it is concluded that the substance is not mutagenic (Balasubramanyam 2010).
No forward mutations at the thymidine kinase (tk) locus in the L5178Y mouse lymphoma assay with the use of AlCl3 at concentrations from 2.36-2.59 mM were observed. The lowest relative survival observed in the study was 38% at 600 µg/mL, which is considered insufficient to allow a valid definitive conclusion (Oberly 1982).
DNA damage in human (Jurkat) T-cells at concentrations of 50, 100, 500, 1000 and 5000 µM-Al (AlCl3) using the neutral Comet Assay. Aluminium did not result in significant increases in DNA double strand breaks. The pH used for lysing and unwinding was not clear from the report in the article (Caicedo 2008).
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Genetic toxicity in vivo
Description of key information
Upon contact with water or moisture (e.g. within mucous membranes) aluminium tri-sec-butanolate hydrolyses immediately to butan-2-ol and aluminium 3+ cations (as hydroxide and oxyhydroxide). Hence, toxicity is determined by the toxicity of these two species
The direct metabolite of secondary butanol being methyl ethyl ketone was tested negative in an in-vivo micronucleus test and consequently 2-butanol is considered negative for mutagenicity.
In a study according to OECD 475 female rats (5/group) received aluminium
oxide by oral at of 500, 1000 and 2000 mg Al2O3/kg bw in 1% Tween
80/doubly-distilled water (265, 529 and 1058 mg Al/kg bw)
(Balasubramanyam 2009). A negative control group was treated orally with
the vehicle. A positive control group received a
single intraperitoneal dose of 40 mg/kg bw of cyclophosphamide. 500
well-spread metaphases (100 per animal) were analysed for each treatment
18 and 24 hours after the last dosing. Organ tissue was analyzed for
aluminium content by ICP-MS.
There was no indication of an effect of treatment on the mitotic
index. Eighteen hours after the final dosing, the mean±sd total
aberrations for the control, 265, 529 and 1058 mg Al/kg bw/day were
0.6±0.3, 0.6±0.3, 2.2±0.8, and 4.3±1.0, respectively. Statistical
testing reported in the article indicated no significant differences for
any treatment level of this group compared with the control group. The
levels of aluminium in tissues show an increase with dose that does not
reach statistical significance. A significant (p<0.01) increase in the
Al2O3 content in faeces relative to the control was observed at 1058 mg
Al/kg bw.
In a test according to OECD 474 (Balasubramanyam 2009) the frequency of micronuclei in polychromatic (immature) erythrocytes (MN-PCEs) in bone marrow was not significantly different from the vehicle control (1% Tween 80 in DDW) in any treated group indicating that cell death was not occurring as a result of treatment. At both 30 and 48 hours after administration of the last dose Al2O3 did not increase the number of MN-PCEs. The levels of Al in the Al2O3-bulk treated groups showed an increase but were not reported as significantly different from the controls, but showed consistent increases in levels of Al in tissues and organs with increasing dose.
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Additional information
Upon contact with water or moisture (e.g. within mucous membranes) aluminium tri-sec-butanolate hydrolyses immediately to butan-2-ol and aluminium 3+ cations (as hydroxide and oxyhydroxide). Hence, toxicity is determined by the toxicity of these two species
Justification for classification or non-classification
Based on the outcome of the tests with both hydrolysis products it can be concluded that aluminium tributanolate is not mutagenic and does not needs to be classified according to CLP (Regulation EC No 1282/2008)
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