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EC number: 239-183-9 | CAS number: 15123-80-5
- 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
Aluminium molybdenum oxide was investigated in a Bacterial Reverse mutation assay following OECD 471 (Andres, 2012). The S. typhimurium strains TA 1535, TA 97a, TA 98, TA 100 and TA 102 were used as tester strains. Aluminium molybdenum oxide was applied in concentrations of 50 – 5000 µg/plate in 2 experiments (standard plate test and preincubation test). No increase in the number of revertants compared to the vehicle control (sterile aqua) was observed in any strain at any concentration. No signs of toxicity were observed. The background lawn was visible and the number of revertant colonies was not reduced. However, no complete dissolution was possible and undissolved particles were visible on the plates. In both experiments, the sterility control and the determination of the titre did not show any inconsistencies.
The genotoxic potential of aluminium molybdenum oxide was assessed in a micronucleus assay in human blood lymphocytes similar to OECD 487 (Andres, 2013). The test item (50 g/L) was suspended in RPMI 1640 medium without FCS. The suspension was shaken for 24 h (experiment I and II) or 96 h (experiment III). Afterwards, the suspension was centrifuged and the supernatant was used (= resulting test item solution). A geometric series of dilutions was prepared from the resulting test item solution, leading to final test dilutions of 1:10, 1:20, 1:40, 1:80, 1:160, 1:320, 1:640 and 1:280. No test concentrations were given, as the concentration of the supernatant is unknown. In all experiments with and without metabolic activation, no test dilution showed cytotoxicity. Therefore, the final test dilutions of 1:10, 1:20 and 1:40 were selected for micronuclei scoring in experiment I and II. For experiment III, only the final test dilution of 1:10 was tested. The exposure duration in the experiment I was 4 h with and without S9 mix. In experiment II and III, the exposure duration with S9 mix was 4 h; in the presence of S9 mix 22 h.
In all experiments neither a statistically significant nor a biologically relevant increase in the number of cells containing micronuclei with and without metabolic activation. All positive controls caused statistically significant increases in the proportion of micronucleated cells, demonstrating the sensitivity of the test system.
In conclusion, under the experimental conditions of this study, the test item did not show any evidence of genotoxicity in an in-vitro micronucleus test in human lymphocytes.
There are no data available on gene mutation in mammalian cells for aluminium molybdenum oxide. However, there are reliable data for aluminium and molybdenum compounds considered suitable for read-across using the analogue approach.
For identifying hazardous properties of aluminium molybdenum oxide concerning human health effects, the existing forms of the target substance at very acidic and physiological pH conditions are relevant for the risk assessment.As aluminium molybdenum oxide is an inorganic metallic compound, the tendency to hydrolyze is based on its solubility which is highly pH-dependent.At the physiological pH of 7.4, the availability of aluminium is decreased due to the formation of insoluble Al(OH)3; molybdenum species exist as molybdate anion (MoO42-). At acidic pH conditions (pH < 4), aluminium is predominantly present as Al3+, whereas molybdenum species are primarily available in the acidic forms HMoO4-or H2MoO4. Since the releaseof aluminium and molybdate species is affected by the biological and pH conditions, the use of data on soluble aluminium and molybdenum compounds is justified for toxicological endpoints representing a worst case scenario. For further details, please refer to the analogue justification attached in section 13 of the technical dossier.
Read-across with sodium molybdate
In an in-vitro gene mutation assay (tk locus) in mouse lymphoma cells, sodium molybdate dihydrate was tested up to 10 mM with and without metabolic activation (Lloyd, 2009). The test subtance did not induce gene mutation at the tk locus of L5178Y mouse lymphoma cells when tested in two independent experiments under the conditions employed in this study.
Read-across with aluminium chloride and aluminium hydroxide
In the study of Covance (2010) negative findings were obtained in the mouse lymphoma assay at the tk locus of L5178Y mouse lymphoma cells. They conducted two experiments with Al(OH)3, each with a 3 hour treatment duration. Two experiments were also conducted with AlCl3, one with a 3-hour and the other with a 24-hour treatment duration. Each experiment included incubations with and without metabolic activation. Concentrations of the test items were selected based on results of range-finding studies and observation of precipitation in the incubations. In the Al(OH)3 experiments, eight concentrations ranging from 6.094 µg/mL to 780 µg/mL were used for determination of mutation frequencies. For AlCl3, results from five concentrations (from 3.125 to 50 µg/mL) were used in the experiments with 3-hour treatment duration both in the presence and absence of metabolic activation. In the experiments with 24 hour duration treatments, 8 concentrations were used: from 5 to 120 µg/mL in the absence of metabolic activation and from 5 to 50 µg/mL in the presence of metabolic activation. Negative (vehicle) and positive (methyl methane sulphonate with S9 activation; benzo-[a]-pyrene without S9 activation) controls were included in each experiment. The results of the experiments with AlCl3 were negative: the mutant frequencies at all the tested concentrations were less than the sum of the mean control mutant frequency plus the global evaluation factor (GEF). A negative linear trend was also observed. In the experiments with Al(OH)3, the mutation frequencies at all the tested concentrations were less than the sum of the mean control mutant frequency plus GEF. Although a significant positive linear trend in mutation frequencies was observed in the presence of S-9 in one of the experiments with Al(OH)3, no corresponding increase in mutant frequencies approaching the GEF was observed, and the effect was not observed in the other experiment; therefore, this observation was not considered biologically relevant. Under the conditions of the study, the AlCl3 and Al(OH)3 were not considered genotoxic.
Short description of key information:
Gene mutation (bacterial reverse mutation assay / Ames test): S. typhimuriumTA 1535, TA97a, TA98, TA100, and TA102: negative with and without metabolic activation (according to OECD 471)
Chromosome aberration (in-vitro mammalian microcnucleus test): human lymphocytes: negative with and without metabolic activation (similar to OECD 487)
Read-across with sodium molybdate dihydrate:
Gene mutation in mammalian cells (mouse lymphoma assay): L5178Y mouse lymphoma cells: negative with and without metabolic activation (according to OECD 476)
Read-across with aluminium chloride and aluminium hydroxide:
Gene mutation in mammalian cells (mouse lymphoma assay): L5178Y mouse lymphoma cells: negative with and without metabolic activation (according to OECD 476)
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
Based on all available information on genetic toxicity using the target and source chemicals, the data do not meet the criteria for classification according to Regulation (EC) 1272/2008 or Directive 67/548/EEC, and are therefore conclusive but not sufficient for classification.
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