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EC number: 220-098-0 | CAS number: 2627-86-3
- 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
Read-across
No data were available for L-alpha-methylbenzylamine. Study was performed with the Racemat (DL-alpha-methylbenzylamine). Read across is done to L-alpha-methylbenzylamine, as the substance is expected to behave similar to the racemat with regard to mutagenic properties.
Ames Test:
The test substance was tested for its mutagenic potential based on the ability to induce back mutations in selected loci of several bacterial strains in the Ames test and in the Escherichia coli - reverse mutation assay. Strains: TA 1535, TA 100, TA 1537, TA 98 and E . coli WP2 uvrA Dose range: 20 µg - 5000 µg/plate Test conditions: Standard plate test and preincubation test both with and without metabolic activation (Aroclor induced rat liver S-9 mix). Solubility: No precipitation of the test substance (racemate) was found. Toxicity: A bacteriotoxic effect was observed only in the preincubation test at doses >= 2500 µg/plate (E . coli WP2 uvrA) or at 5000 µg/plate (Salmonella strains) . Mutagenicity: An increase in the number of his- or trp- revertants was not observed both in the standard plate test and in the preincubation test either without S-9 mix or after the addition of a metabolizing system. According to the results of the present study, the test substance is not mutagenic in the Ames test and in the Escherichia coli - reverse mutation assay under the experimental conditions chosen here.
HPRT test:
The study was performed to investigate the potential of the test substance (racemate) to induce gene mutations at the HPRT locus in V79 cells of the Chinese hamster. The assay was performed in two independent experiments, using two parallel cultures each. The first main experiment was performed with and without liver microsomal activation and a treatment period of 4 hours. The second experiment was performed with a treatment time of 4 hours with and 24 hours without metabolic activation. Concentration range: 37.8 to 1210 µg/mL in the 4 hour incubation period and 37.8 to 605.0 µg/mL in the 24 hour incubation period. The test item was dissolved in deionised water. No substantial and reproducible dose dependent increase of the mutation frequency was observed up to the maximum concentration 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. In conclusion it can be stated that under the experimental conditions reported the test item did not induce gene mutations at the HPRT locus in V79 cells. Therefore, the test substance is considered to be non-mutagenic in this HPRT assay.
MNT in vitro:
The test substance (racemate) was assessed for its potential to induce micronuclei in V79 cells in vitro (clastogenic or aneugenic activity). Three independent experiments were carried out with and without the addition of liver S9 mix from induced rats (exogenous metabolic activation). According to an initial range-finding cytotoxicity test for the determination of the experimental doses, the following doses were tested. The test groups printed in bold type were evaluated.
1st Experiment
4 hours exposure; 24 hours harvest time; without S9 mix (not valid due to lacking toxicity)
0; 6.25; 12.5; 25.0; 50.0; 100.0 and 200.0μg/mL
4 hours exposure, 24 hours harvest time, with S9 mix
0; 40.63; 81.25; 162.5; 325.0; 650.0 and 1 300.0μg/mL
2nd Experiment
4 hours exposure, 24 hours harvest time, without S9 mix
0; 40.63; 81.25; 162.50; 325.0; 650.0 and 1300.0 μg/mL
4 hours exposure, 24 hours harvest time, with S9 mix
0; 121.88; 243.75; 487.50; 975.0 and 1300.0 μg/mL
3rd Experiment
4 hours exposure, 24 hours harvest time, without S9 mix
0; 500.0; 600.0; 700.0; 800.0; 1 000.0 and 1300.0μg/mL
A sample of at least 1000 cells for each culture were analyzed for micronuclei, i.e. 2000 cells for each test group. The vehicle controls gave frequencies of micronucleated cells within the labs historical negative control data range for V79 cells. Both positive control substances, EMS and cyclophosphamide, led to the expected increase in the number of cells containing micronuclei.
In the absence of S9 mix, in the 1st Experiment no toxicity was observed up to the highest applied concentration. In the 2nd and 3rd Experiment cytotoxicity indicated by clearly reduced relative increase in cell count (RICC) was observed in the absence of S9 mix at the highest applied test substance concentration. Contrary, in both experiments in the presence of S9 mix no toxic effects were observed up to the highest required test substance concentration.
On the basis of the results of the present study, the test substance induced a statistically significant and biologically increase in the number of cells containing micronuclei after 4 hours exposure in the absence of S9 mix.
Thus, under the experimental conditions described, 1-Phenylethylamine is considered to have a chromosome-damaging (clastogenic) effect or to induce numerical chromosomal aberrations (aneugenic activity) under in vitro conditions in V79 cells in the absence of metabolic activation.
MNT in vivo
The study was performed to investigate the potential of 1-Phenylethylamine to induce micronuclei in polychromatic erythrocytes (PCE) in the bone marrow of the mouse. The test item was dissolved in corn oil, which was also used as vehicle control. The volume administered orally was 10 mL/kg b.w.. 24 h and 48 h after a single administration of the test item the bone marrow cells were collected for micronuclei analysis. Seven males per test group (except the vehicle and positive control groups with 5 males only) were evaluated for the occurrence of micronuclei. Per animal 2000 polychromatic erythrocytes (PCEs) were scored for micronuclei. To investigate a cytotoxic effect due to the treatment with the test item the ratio between polychromatic and normochromatic erythrocytes was determined in the same sample and reported as the number of PCEs per 2000 erythrocytes. The following dose levels of the test item were investigated, based on results of a pre-experiment: 24 h preparation interval: 62.5, 125, and 250 mg/kg b.w. 48 h preparation interval: 250 mg/kg b.w. After treatment with the test item the mean number of PCEs was not substantially decreased as compared to the mean value of PCEs of the vehicle control thus indicating that 1-Phenylethylamine did not exert a cytotoxic effect in the bone marrow. Clinical signs such as ruffled fur and reduction of spontaneous activity were observed at ≥ 125 mg/kg b.w. and in addition abdominal posture at 250 mg/kg b.w. in the main experiment. In comparison to the corresponding vehicle controls there was no biologically relevant or statistically significant enhancement in the frequency of the detected micronuclei at any preparation interval after administration of the test item and with any dose level used.Justification for selection of genetic toxicity endpoint
GLP and guideline study with mammalian cells.
Short description of key information:
The test substance is considered non-mutagenic in a reverse mutation assay in bacteria (Ames test) and in a HPRT test in mammalian cells. Induction of numerical chromosomal aberrations were observed in the in vitro mammalian cell micronucleus test in the absence of metabolic activation. No mutagenic activity was observed in an in vivo micronucleus test according to OECD 474.
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
No data were available for L-alpha-methylbenzylamine. Studies were performed with the racemat (DL-alpha-methylbenzylamine, read across, CAS 618-36-0). Based on the available data for DL-alpha-methylbenzylamine, L-alpha-methylbenzylamine has not to be classified for genetic toxicity according to Regulation (EC) No 1272/2008 and Directive 67/548/EEC.
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