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EC number: 203-818-8 | CAS number: 110-95-2
- 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
Gene mutation assay
The potential of N, N, N', N'-tetramethyltrimethylenediamine (TMPDA) to induce reverse mutation in Salmonella typhimurium strains TA98, TA100, TA1535, TA1537 and TA1538 and Escherichia coli WP2 uvrA was evaluated in accordance with the OECD guidelines no. 471 and 472 (Bichet, 1988; BASF, 1999). TMPDA did not induce any noteworthy increase in the number of revertants, both with and without S9 mix, in any strains. Under these experimental conditions, TMPDA did not show any mutagenic activity in the bacterial reverse mutation test with Salmonella typhimurium and Escherichia coli.
N, N, N', N'-tetramethyltrimethylenediamine (TMPDA) was assayed for the ability to induce mutation at the hypoxanthine-guanine phosphoribosyl transferase (hprt) locus (6‑thioguanine [6TG] resistance) in mouse lymphoma cells using a fluctuation protocol (Lloyd, 2013). 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). The test article was formulated in purified water. A 3 hour treatment incubation period was used for all experiments. The study was conducted in compliance with the Good Laboratory Practice Regulations and with OECD Guideline 476. In the cytotoxicity Range-Finder Experiment, six concentrations were tested in the absence and presence of S-9, ranging from 40.63 to 1300 µg/mL (equivalent to 10 mM at the highest concentration tested). The highest concentrations to provide >10% relative survival (RS) were 325 mg/mL in the absence of S-9 and 650 mg/mL in the presence of S-9, which gave 45% and 27% RS, respectively. In Experiment 1 twelve concentrations, ranging from 50 to 700 µg/mL, were tested in the absence of S-9 and eleven concentrations, ranging from 100 to 1300 mg/mL, were tested in the presence of S-9. Seven days after treatment the highest concentrations analysed to determine viability and 6TG resistance were 650mg/mL in the absence of S-9 and 800 mg/mL in the presence of S-9, which gave 19% and 14% RS, respectively. In Experiment 2 eleven concentrations, ranging from 50 to 750 µg/mL, were tested in the absence of S-9 and ten concentrations, ranging from 150 to 1100 mg/mL, were tested in the presence of S-9. Seven days after treatment the highest concentration analysed to determine viability and 6TG resistance was 750mg/mL, which gave 10% and 15% RS in the absence and presence of S-9, respectively. Negative (vehicle) and positive control treatments were included in each Mutation Experiment in the absence and presence of S-9. Mutant frequencies in negative control cultures fell within acceptable ranges and clear increases in mutation were induced by the positive control chemicals 4-nitroquinoline 1-oxide (without S-9) and benzo(a) pyrene (with S-9). The study was accepted as valid. In Experiments 1 and 2, no significant increases in mutant frequency(MF), compared to the vehicle controls, were observed following treatment with TMPDA at any concentration analysed in the absence and presence of S-9 and there were no significant linear trends. It is concluded that TMPDA 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 toxic concentrations in two independent experiments in the absence and presence of a rat liver metabolic activation system (S-9).
Chromosomal aberration assay
The potential of N, N, N', N'-tetramethyltrimethylenediamine (TMPDA) to induce structural chromosome aberrations in human lymphocytes was evaluated according to OECD 473 and EC 92/69/EEC B.10 guidelines in compliance with the Principles of Good Laboratory Practice (Marzin, 2000). The test item was tested in two independent experiments, with and without a metabolic activation system. In the first assay, lymphocytes cultures were exposed with or without activation for 4 hours to positive and negative controls or test item at concentrations of 2.5, 5 and 10 mM and sampled 20h after the start of treatment. In the second assay, lymphocyte cultures were continuously exposed without metabolic activation to 0.313, 0.625, and 1.25 mM for 20h and 1.25, 2.5 and 5 mM for 44 h and for 4h with metabolic activation at 2.5, 5 and 10 mM. TMPDA did not induce any noteworthy increase in the number of cells with structural chromosome aberration, both with and without S9 mix, in either experiment or at either harvest time.
Justification for selection of genetic toxicity endpoint
None selected, all in vitro assays were negative
Short description of key information:
N, N, N', N'-tetramethyltrimethylenediamine (TMPDA) produced no genetic changes in standard in vitro tests using bacterial and mammalian cells and performed according to OECD guidelines and GLP. No gene mutations were induced in Salmonella typhimurium strain TA98, TA100, TA1535, TA1537 and TA1538 and in Escherichia coli WP2 uvr A and at the hprt locus of mouse lymphoma L5178Y cells (MLA) and no chromosomal aberrations was induced in human lymphocytes.
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
According to REGULATION (EC) No 1272-2008 and Annex VI of Commission Directive 2001/59/EC:
Not classified, based on the battery of negative genetic toxicology studies that have been conducted with N, N, N', N'-tetramethyltrimethylenediamine.
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