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EC number: 278-503-1 | CAS number: 76622-74-7
- 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
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- Solubility in organic solvents / fat solubility
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- Flash point
- Auto flammability
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- 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
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- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
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- Endpoint summary
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- Environmental data
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- 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
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- 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
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- Additional toxicological data
Endpoint summary
Administrative data
Key value for chemical safety assessment
Genetic toxicity in vitro
Description of key information
Bacterial Mutagenicity (WoE, OECD 471, Ames): negative with and without metabolic activation
RA from source substances (Z)-N-methyl-N-(1-oxo-9-octadecenyl)glycine (CAS 110-25-8), N-(1-oxooctadecyl)sarcosine (CAS 142-48-3), and Sodium N-methyl-N-(1-oxo-9-octadecenyl)aminoacetate (CAS 3624-77-9)
Mammalian Cytogenicity (WoE, OECD 473, Chromosome Aberration): negative with and without metabolic activation
RA from source substances Sodium N-lauroylsarcosinate (CAS 137-16-6), Sodium N-methyl-N-(1-oxotetradecyl)aminoacetate (CAS 30364-51-3) and (Z)-N-methyl-N-(1-oxo-9-octadecenyl)glycine (CAS 110-25-8)
Mammalian Mutagenicity (WoE, OECD 476): negative with and without metabolic activation
RA from source substances Sodium N-lauroylsarcosinate (CAS 137-16-6), Sodium N-methyl-N-(1-oxotetradecyl)aminoacetate (CAS 30364-51-3) and (Z)-N-methyl-N-(1-oxo-9-octadecenyl)glycine (CAS 110-25-8)
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Genetic toxicity in vivo
Endpoint conclusion
- Endpoint conclusion:
- no study available
Additional information
No data on genetic toxicity are available for the target substance Potassium (Z)-N-methyl-N-(1-oxo-9-octadecenyl)aminoacetate (CAS 76622-74-7). Therefore, read across from the source substances Sodium N-lauroylsarcosinate (CAS 137-16-6), Sodium N-methyl-N-(1-oxotetradecyl)aminoacetate (CAS 30364-51-3), (Z)-N-methyl-N-(1-oxo-9-octadecenyl)glycine (CAS 110-25-8), N-(1-oxooctadecyl)sarcosine (CAS 142-48-3) and Sodium N-methyl-N-(1-oxo-9-octadecenyl)aminoacetate (CAS 3624-77-9) was applied.
Genetic toxicity (mutagenicity) in bacteria in vitro
A bacterial gene mutation assay (Ames test) was performed with (Z)-N-methyl-N-(1-oxo-9-octadecenyl)glycine (CAS 110-25-8) according to OECD TG 471 and in compliance with GLP (LAUS, 2007). The strains Salmonella typhimurium TA 97a, TA 98, TA 100, TA 102 and TA 1535 were tested in two independent experiments according to the plate incorporation and pre-incubation procedure in the absence and presence of a metabolic activation system (Aroclor 1254-induced rat liver S9-mix). The experiments were conducted each in 4 replications at concentrations from 50 to 5004 µg/plate (vehicle: DMSO). No increase in the number of revertant colonies was noted in any of the bacterial strains, with and without metabolic activation system. No cytotoxicity was recorded in any tester strain up to and including the highest dose tested. Appropriate positive and negative controls were included in the study and gave the expected results. Under the conditions of the study, the test substance did not induce mutations in the bacterial mutation assay in the absence and presence of a metabolic activation system in any of the strains tested.
A bacterial gene mutation assays (Ames test) was performed with N-(1-oxooctadecyl)sarcosine (CAS 142-48-3) according to OECD TG 471 and in compliance with GLP (LAUS, 2012a). The strains Salmonella typhimurium TA 97a, TA 98, TA 100, TA 102 and TA 1535 were tested in two independent experiments according to the plate incorporation and pre-incubation procedure in the absence and presence of a metabolic activation system (Aroclor 1254-induced rat liver S9-mix). The experiments were conducted each in 4 replications at concentrations from 53 to 5005 µg/plate in the first experiment and 323 to 4792 µg/plate in the second experiment (vehicle: water). No increase in the number of revertant colonies was noted in any of the bacterial strains, with and without metabolic activation system. No cytotoxicity was observed up to the highest dose tested. The included positive and negative controls showed the expected results. Under the conditions of the study, the test substance did not induce mutations in the bacterial mutation assay in the absence and presence of a metabolic activation system in any of the strains tested.
A bacterial gene mutation assays (Ames test) was performed with Sodium N-methyl-N-(1-oxo-9-octadecenyl)aminoacetate (CAS 3624-77-9) following OECD TG 471 and in compliance with GLP (LAUS, 2012b). The strains Salmonella typhimurium TA 97a, TA 98, TA 100, TA 102 and TA 1535 were tested in two independent experiments according to the plate incorporation and pre-incubation procedure in the absence and presence of a metabolic activation system (Aroclor 1254-induced rat liver S9-mix). The experiments were conducted each in 4 replications at concentrations from 50 to 5004 µg/plate (vehicle: water). No increase in the number of revertant colonies was noted in any of the bacterial strains, with and without metabolic activation system. No cytotoxicity was observed up to the highest dose tested. The included positive and negative controls showed the expected results. Under the conditions of the study, the test substance did not induce mutations in the bacterial mutation assay in the absence and presence of a metabolic activation system in any of the strains tested.
Genetic toxicity (cytogenicity) in mammalian cells in vitro
An in vitro mammalian chromosome aberration test was conducted with Sodium N-lauroylsarcosinate (CAS 137-16-6) in accordance with OECD TG 473 under GLP conditions (Harlan, 2010a). The induction of structural chromosome aberrations was evaluated in vitro in lymphocytes of fresh heparinised human whole blood cultures, incubated for 4 and 24 h with and without a metabolic activation system (S9-mix from rats treated with phenobarbitone and beta-naphthoflavone). Concentrations of 22 - 360 µg/mL (4 h incubation) and 22.5 - 270 µg/mL (24 h incubation) of the test substance in Minimal Essential Media (MEM) were applied. The negative as well as the positive controls showed the expected results and were within the historical control data. In the preliminary toxicity test, haemolysis of the cultures was observed at 732.5 µg/mL and above in the 4 and 24 h exposure groups. In the main experiment, haemolysis was seen at the end of exposure at and above 270 µg/mL in the exposure groups. The test material did not induce a statistically significant increase in the numbers of polyploid cells at any dose level in any of the exposure groups. No statistically or biologically significant increase in the incidence of chromosome aberrations was observed. Therefore, under the conditions of the study, the test substance did not show clastogenic activity in this chromosomal aberration test with and without metabolic activation performed in peripheral human lymphocytes in vitro.
An in vitro mammalian chromosome aberration test was conducted with sodium N-methyl-N-(1-oxotetradecyl)aminoacetate (CAS 30364-51-3) in accordance with OECD TG 473 under GLP conditions (Harlan, 2013a). The induction of structural chromosome aberrations was evaluated in vitro in lymphocytes of freshly heparinised human whole blood cultures, incubated for 4 and 24 h with and without a metabolic activation system (S9-mix from rats treated with phenobarbitone and beta-naphthoflavone). Concentrations of 12 - 200 µg/mL (4 h and 24 h incubation) of the test substance in Minimal Essential Media (MEM) with and without metabolic activation were applied. The negative as well as the positive controls showed the expected results and were within the historical control data. Haemolysis was also observed at and above 100.4 µg/mL in the two 4(20) h exposure groups and at above 200.9 µg/mL in the 24 h continuous exposure group. In the first experiment, haemolysis was seen at and above 100 µg/mL in the exposure groups in absence of metabolic activation, and at 200 µg/mL in presence of metabolic activation. The mitotic index data show that 19% mitotic inhibition and 34% mitotic inhibition was achieved at 100 µg/mL in the absence and presence of metabolic activation, respectively. In the second experiment haemolysis and reduced cell pellets were observed at the end of the exposure period at 200 µg/mL in the absence of metabolic activation, and at 100 µg/mL in the presence of metabolic activation. The mitotic index data show that 63% mitotic inhibition was achieved at 75 µg/mL in the absence of metabolic activation. In the presence of metabolic activation the response was not marked with a modest 16% mitotic inhibition being observed. The test material did not induce a statistically significant increase in the numbers of polyploid cells at any dose level in any of the exposure groups. No statistically or biologically significant increase in the incidence of chromosome aberrations was observed. Therefore, under the conditions of the study, the test substance did not show clastogenic activity in this chromosomal aberration test with and without metabolic activation performed in peripheral human lymphocytes in vitro.
An in vitro mammalian chromosome aberration test was conducted with (Z)-N-methyl-N-(1-oxo-9-octadecenyl)glycine (CAS 110-25-8) in accordance with OECD TG 473 under GLP conditions (LAUS, 2010). The induction of structural chromosome aberrations was evaluated in vitro in lymphocytes of fresh heparinised human whole blood cultures, incubated for 4 h with and without and for 22 h without a metabolic activation system (S9-mix from rats treated with Aroclor 1245). Concentrations of 10 - 40 µg/mL (4 h incubation) and 0.5 - 50 µg/mL (22 h incubation) of the test substance in the vehicle DMSO were applied. The negative as well as the positive controls showed the expected results. In the pre-experiment cytotoxicity was observed from 55.3 µg/mL with and without metabolic activation. In the main experiments a reduction in the mitotic index was observed from 30 µg/mL without and from 40 µg/mL with metabolic activation. No statistically or biologically significant increase in the incidence of chromosome aberrations was observed. Therefore, under the conditions of the study, the test substance did not show clastogenic activity in this chromosomal aberration test with and without metabolic activation performed in peripheral human lymphocytes in vitro.
Genetic toxicity (mutagenicity) in mammalian cells in vitro
An in vitro mammalian cell gene mutation study of Sodium N-lauroylsarcosinate (CAS 137-16-6) was carried out according to OECD TG 476 under GLP conditions (Harlan, 2010b). Gene mutations in the thymidine kinase locus were investigated in L5178Y mouse lymphoma cells in the presence and absence of a metabolic activation system (Phenobarbital/beta-naphthoflavone-induced rat liver, S9). In the first experiment, cells were exposed for 4 h to the test substance at concentrations of 6.25 - 70 µg/mL and 12.5 - 100 µg/mL without and with metabolic activation, respectively. Concentrations of the second experiment without metabolic activation for an exposure time of 24 h ranged from 3.13 to 80 µg/mL. The vehicle and positive controls in the study showed the expected results and were within the range of historical control data of the laboratory. In the short- and long-term exposure experiments, cytotoxicity was observed from 60 and 70 µg/mL (4 h) without and with metabolic activation and from 12.5 µg/mL (24 h), respectively. There was no significant increase in the number of forward mutations at the thymidine kinase locus of L5178Y mouse lymphoma cells treated with the test material, neither in the presence nor in the absence of a metabolic activation system. Under the conditions of the study, Sodium N-lauroylsarcosinate (CAS 137-16-6) did not show gene mutation activity in this test performed in L5178Y mouse lymphoma cells in vitro.
The in vitro mammalian cell gene mutation study of Sodium N-methyl-N-(1-oxotetradecyl)aminoacetate (CAS 30364-51-3) was carried out according to OECD TG 476 under GLP conditions (Harlan, 2013b). Gene mutations in the thymidine kinase locus were investigated in L5178Y mouse lymphoma cells in the presence and absence of a metabolic activation system (Phenobarbital/beta-naphthoflavone-induced rat liver, S9). In the first experiment, cells were exposed for 4 h to the test substance at eight concentrations of 1.25 - 50 µg/mL without and with metabolic activation. Nine concentrations of the second experiment without metabolic activation for an exposure time of 24 h ranged from 5 - 60 µg/mL. Nine concentrations of the second experiment for an exposure of 4 h ranged from 10 - 50 µg/mL in the presence of metabolic activation. The vehicle and positive controls in the study showed the expected results and were within the range of historical control data of the laboratory. In the first and second experiment there was evidence of marked toxicity following exposure to the test item in both the absence and presence of metabolic activation, as indicated by the RTG and % RSG values. There was no significant increase in the number of forward mutations at the thymidine kinase locus of L5178Y mouse lymphoma cells treated with the test material, neither in the presence nor in the absence of a metabolic activation system. Under the conditions of the study, Sodium N-methyl-N-(1-oxotetradecyl)aminoacetate (CAS 30364-51-3) did not show gene mutation activity in this test performed in L5178Y mouse lymphoma cells in vitro.
The in vitro mammalian cell gene mutation study of (Z)-N-methyl-N-(1-oxo-9-octadecenyl)glycine (CAS 110-25-8) was carried out according to OECD TG 476 under GLP conditions (Harlan, 2010c). Gene mutations in the HPRT locus were investigated in Chinese hamster lung fibroblasts (V79) in the presence and absence of a metabolic activation system (Phenobarbital/beta-naphthoflavone-induced rat liver, S9). V79 cells were incubated with the test material at 0.25, 0.5, 1, 2 and 4 µg/mL for 4 h in the absence and at 4, 8, 16, 32 and 48 µg/mL in the presence of a metabolic activation system. Concentrations of the second experiment without metabolic activation for an exposure time of 24 h ranged from 4 to 96 µg/mL, and concentrations with metabolic activation for an exposure period of 4 h ranged from 4 to 56 µg/mL. The vehicle and positive controls in the study showed the expected results and were within the range of historical control data of the laboratory. Cytotoxicity was apparent at concentrations from 4 µg/mL and 48 µg/mL in experiment I without and with metabolic activation, respectively. In the second experiment, cytotoxicity was observed from 96 µg/mL and 56 µg/mL without and with metabolic activation, respectively. In the second experiment, precipitation was observed from 237.5 µg/mL after 24 h without metabolic activation. There was no significant increase in the number of forward mutations at the HPRT locus of V79 cells treated with the test material, neither in the presence nor in the absence of a metabolic activation system. Under the conditions of the study, (Z)-N-methyl-N-(1-oxo-9-octadecenyl)glycine (CAS 110-25-8) did not show gene mutation activity in this test performed in V79 cells in vitro.
Conclusion
Taken together, the available data on genetic toxicity from several relevant source substances do not indicate any mutagenic and clastogenic potential in vitro for the target substance Potassium (Z)-N-methyl-N-(1-oxo-9-octadecenyl)aminoacetate (CAS 76622-74-7).
Justification for classification or non-classification
The available data on relevant read-across source substances for genetic toxicity do not meet the criteria for classification according to Regulation (EC) No. 1272/2008. Therefore, applying the RA-A approach, the target substance potassium (Z)-N-methyl-N-(1-oxo-9-octadecenyl)aminoacetate (CAS 76622-74-7) is also considered not to meet the criteria for classification for genetic toxicity according to Regulation (EC) No 1272/2008. Data therefore are conclusive but not sufficient for classification.
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