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EC number: 200-875-0 | CAS number: 75-50-3
- 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
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- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
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- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
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- Specific investigations
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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
Covance, 8218065, Mutation at the hprt locus
of mouse lymphoma L5178Y cells (MLA) using the MicrotitreR fluctuation
technique - negative
Covance, 8218071, Induction of chromosome aberrations in cultured human
peripheral blood lymphocytes - negative
Nakajima et al., 2001. Trimethylamine (CAS No. 75-30-3), Reverse
Mutation Test and Mammalian Chromosome Aberration Test - negative
Mortelmanns et al in 1986, Trimethylamine,
Reverse Mutation Test and Mammalian Chromosome Aberration Test (OECD
guideline 471, not GLP) Salmonella typhimurium strains TA98, TA100,
TA1535, and TA1537 and Salmonella typhimurium strain TA97 - negative
Nakajima et al. 2001. Trimethylamine (CAS No. 75-30-3), In Vitro
Chromosomal Aberration Test - positive result for clastogenicity
(possibly the pH value had an influence on this result). As no detailed
information was available on this study result ( only a summary was
available in English) and the results are not consistent with the other
results, this study is disregarded
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Genetic toxicity in vivo
Endpoint conclusion
- Endpoint conclusion:
- no study available
Additional information
Trimethylamine (TMA-opl in water) was assayed by Mn Lloyd BSc for Covance in 2010 for its potential to induce mutation at the hypoxanthine‑guanine phosphoribosyl transferase (hprt) locus (6-thioguanine [6TG] resistance) in mouse lymphoma cells (according to OECD guideline 476, under GLP conditions). The study consisted of a cytotoxicity Range-Finder Experiment followed by two independent experiments, each conducted in the absence and presence of metabolic activation by an Aroclor 1254 induced rat liver post‑mitochondrial fraction (S‑9). In the cytotoxicity Range-Finder Experiment, six concentrations were tested in the absence and presence of S‑9, ranging from 18.47 to 591.0 mg/mL (equivalent to approximately 10 mM at the highest concentration tested). The highest concentration to provide >10% relative survival (RS) was 295.5 mg/mL, which gave 67% and 54% RS in the absence and presence of S‑9, respectively. Accordingly, for Experiment 1 ten concentrations, ranging from 100 to 591.1 µg/mL, were tested in the absence and presence of S‑9. Seven days after treatment, the highest concentrations selected to determine viability and 6TG resistance were 400 µg/mL in the absence of S‑9 and 450 mg/mL in the presence of S-9, which gave 25% and 5% RS, respectively. In the absence and presence of S-9, no concentration gave 10‑20% RS (in the absence of S‑9, cultures treated at 350 and 400 µg/mL, gave 50% and 25% RS, respectively and in the presence of S-9, cultures treated at 400 and 450 µg/mL, gave 38% and 5% RS, respectively). Both concentrations were therefore analyzed under each treatment condition. In Experiment 2 ten concentrations, ranging from 100 to 500 µg/mL, were tested in the absence and presence of S‑9. Seven days after treatment, the highest concentration selected to determine viability and 6TG resistance was 500 µg/mL, which gave 20% and 33% RS in the absence and presence of S‑9, respectively. Cultures treated at 475 µg/mL in the presence of S-9 gave 23% RS, which was sufficiently close to 10‑20% RS to be considered acceptable. In Experiments 1 and 2, no statistically significant increases in mutant frequency were observed following treatment with Trimethylamine at any concentration tested in the absence and presence of S‑9 and there were no significant linear trends. It is concluded that Trimethylamine did not induce mutation at thehprtlocus of L5178Y mouse lymphoma cells when tested under the conditions employed in this study. These conditions included treatments up to highly toxic concentrations in two independent experiments in the absence and presence of a rat liver metabolic activation system (S‑9).
Trimethylamine (TMA-opl in water) was tested by Mn Lloyd BSc for Covance in 2010 in an in vitro cytogenetics assay using duplicate human lymphocyte cultures prepared from the pooled blood of three male donors in two independent experiments (according to OECD 473 under GLP conditions). Treatments covering a broad range of concentrations were performed both in the absence and presence of metabolic activation (S-9) from Aroclor 1254 induced animals. The highest concentration used in the Main Experiments, 591.1 mg/mL(equivalent to 10 mM) was determined following a preliminary cytotoxicity Range-Finder Experiment. The test article concentrations for chromosome analysis were selected by evaluating the effect of Trimethylamine on mitotic index. Treatment of cultures with Trimethylamine in the absence and presence of S-9 resulted in frequencies of cells with structural aberrations that were similar to those observed in concurrent negative controls. Numbers of aberrant cells (excluding gaps) in all treated cultures fell within normal ranges. No increases in the frequency of cells with numerical aberrations, which exceeded the concurrent controls and the normal ranges, were generally observed in cultures treated with Trimethylamine in the absence and presence of S-9. The only exception to this was observed in Experiment 2 in the absence of S-9 at one intermediate concentration (320.0 µg/mL), where the frequency of cells with numerical aberrations marginally exceeded the 95thpercentile of the normal range (but fell within the observed normal range) in both cultures. The increases were almost entirely attributable to hyperdiploid cells but they were small and there was no evidence of a concentration-related response, therefore they were not considered biologically relevant.
It is concluded that Trimethylamine did not induce chromosome aberrations in cultured human peripheral blood lymphocytes when tested to the limit of cytotoxicity for 20+0 hours in the absence of S-9 and up to a maximum of 10 mM for 3+17 hours in the absence and presence of S-9.
The gene mutation properties of trimethylamine were also investigated in a bacterial reverse mutation assay (Ames test) conducted by Nakajima et al. in 2001. This test was performed according to the OECD guideline 471 with Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537 as well as with Escherichia coli strain WP2 uvr A. The concentrations of the test substance ranged from 0 to 5000 µg and the test result was negative according to all strains, with and without metablic activation.
Another bacterial reverse mutation assay (Ames test) was performed by Mortelmanns et al in 1986, in accordance to OECD guideline 471 not under GLP conditions. Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537 were investigated with and without metabolic activation, whereas Salmonella typhimurium strain TA97 was tested only with metabolic activation system, which was rat / hamster S9 - mix (Aroclor 1254 included). A preincubation assay was done and the test concentration were 10, 33, 100, 333, and 1000 µg/plate, as vehicle water was used. The genotoxicity test showed for all strains under all circumstances a negative result.
Nakajima et al. reported in 2001 an in vitro mammalian chromosome aberration test, which was performed under GLP conditions according to OECD guideline 473. Chinese Hamster Lung (CHL/IU) cells were used with and without metabolic activation system. The test concentration of trimethylamine was up to 591 µg/mL with a positive result for clastogenicity. Possibly the pH value had an influence on this result.
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
- GHS: no classification
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