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EC number: 214-730-4 | CAS number: 1191-16-8
- 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
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Endpoint summary
Administrative data
Key value for chemical safety assessment
Additional information
In vitro test
1) Bacterial gene mutation
The mutagenicity of prenyl acetate was tested in different mutant strains of Salmonella typhimurium (TA1535, TA1537, TA98, TA100, and TA102) according to the OECD TG 471 (King & Harnasch GmbH 2000, AM04300N). The investigations were carried out using the standard plate incorporation assay with and without S9-mix prepared from liver homogenate (S9) of Aroclor 1254 pretreated male rats as metabolic activation system. Prenyl acetate was dissolved in DMSO and evaluated at concentration levels from 50 to 5000 µg/plate.
In the absence and presence of S9-mix prenyl acetate was not bacteriotoxic and precipitation in the plates was not observed. Positive controls confirmed the reversion properties and the specificity of the bacterial strains as well as the efficacy of the metabolizing system. Prenyl acetate did not induce a significant increase in the mutation frequency of the tested strains in the presence and absence of a metabolic activation system. Therefore, prenyl acetate was found to be non-mutagenic under the chosen test conditions.
2) Gene mutation in mammalian cells
The potential of prenyl acetate to induce gene mutations at the hypoxanthine-guanine phosphoribosyl transferase (HPRT) locus in Chinese hamster V79 cells was tested in a GLP conform study according to OECD guideline 476 (Key study, Harlan Cytotest Cell Research GmbH, 50M0362/10X300, 2012). Two independent experiments were carried out in DMSO as vehicle, both with and without the addition of mammalian liver microsome preparations (S9 mix).
No substantial and reproducible dose dependent increase of the mutation frequency was observed up to the maximum concentration of prenyl acetate with and without metabolic activation. Appropriate reference mutagens (EMS and DMBA), used as positive controls, induced a distinct increase in mutant colonies and thus, showed the sensitivity of the test system and the activity of the metabolic activation system.
The recommended cytotoxic range of approximately 10-20% relative cloning efficiency / or relative cell density was covered without metabolic activation.
In conclusion it can be stated that under the experimental conditions reported Prenyl acetate did not induce gene mutations at the HPRT locus in V79 cells. Therefore, prenyl acetate is considered to be non-mutagenic in this HPRT assay.
3) Cytogenicity in mammals
No data on cytogenicity are available for prenyl acetate. However, genotoxicity data on the structurally and metabolically related prenol (3-methylbut-2-en-1-ol ; CAS No. 556-82-1) are taken into account for assessment via read across. This read across is justified, based on the high likelyhood that prenyl acetate would rapidly be hydrolized to prenol and acetate in the GIT and liver, and/or show a similar GIT / liver metabolism profile as prenol.
In the chosen key study, the substance 3-methylbut-2-en-1-ol was tested for chromosomal damage (clastogenicity) and for the ability to induce spindle poison effects (aneugenic activity) in NMRI mice using the micronucleus test method in a GLP conform study according to OECD TG 474 (BASF AG, 2001; 26M0274/004055). For this purpose, prenol, dissolved in olive oil, was administered twice intraperitoneally, with a 24-hour interval between administrations, to male animals at dose levels of 125 mg/kg, 250 mg/kg and 500 mg/kg body weight in a volume of 10 ml/kg body weight.
As a negative control, olive oil was administered to male mice, by the same route, and gave frequencies of micronucleated polychromatic erythrocytes within the historical control range.
Both of the positive control chemicals, i.e. cyclophosphamide for clastogenic effects and vincristine for induction of spindle poison effects, led to the expected increase in the rate of polychromatic erythrocytes containing small or large micronuclei.
According to the results of the present study, the two intraperitoneal administrations of 3-methylbut-2-en-1-ol did not lead to any increase in the number of polychromatic erythrocytes containing either small or large micronuclei. The rate of micronuclei was nearly the range as that of the concurrent negative control in all dose groups and within the range of the historical control data. The administration of the 3-methylbut-2-en-1-ol led to evident signs of toxicity.
A slight inhibition of erythropoiesis, determined from the ratio of polychromatic to normochromatic erythrocytes, was detected at doses of 250 and 500 mg/kg body weight.
Thus, under the experimental conditions chosen here, 3-methylbut-2-en-1-ol does not have any chromosome-damaging (clastogenic) effect, and there were no indications of any impairment of chromosome distribution in the course of mitosis (aneugenic activity) in bone marrow cells in vivo.
Conclusion:
Prenyl acetate is not mutagenic in bacteria and mammalian cells. Based on the observations resulting from the metabolically and structurally related read-across substance prenol, no cytogenic effect is to be expected for prenyl acetate.
Short description of key information:
- In vitro
Bacterial gene mutation; AMES (OECD TG 471, GLP): negative (King & Harnasch 2000)
Gene Mutation in mammalian cells; HPRT (OECD TG 476, GLP): negative (Harlan 2012, 50M0362/10X300)
- In vivo
Cytogenicity in mammals; MNT (OECD TG 474, GLP): negative (BASF 2001; 26M0274/004055; read-across prenol; CAS No. 556-82-1)
Endpoint Conclusion:
Justification for classification or non-classification
The present data on genetic toxicity do not fulfill the criteria laid down in 67/548/EEC and regulation (EU) 1272/2008 and therefore, a non-classification is warranted.
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