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EC number: 204-697-4 | CAS number: 124-40-3
- 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
![](https://echa.europa.eu/o/diss-blank-theme/images/factsheets/A-REACH/factsheet/print_toxicological-information.png)
Endpoint summary
Administrative data
Key value for chemical safety assessment
Genetic toxicity in vitro
Description of key information
Zeiger E. et al, 1987, test in Salmonella typhimurium species: no cytotoxicity, no genotoxicity
Hsie et. al., Multiple-endpoint mutagenesis with Chinese Hamster Ovary (CHO) cells: Evaluation with eight carcinogenic and non-carcinogenic compounds, Hemisphere Publishing Corporation) and (Ihidate, and Odashima, 1977) no cytotoxicity, no genotoxicity
Link to relevant study records
- Endpoint:
- in vitro gene mutation study in bacteria
- Remarks:
- Type of genotoxicity: gene mutation
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: similar to guideline study; no data regarding GLP
- Qualifier:
- according to guideline
- Guideline:
- other: Haworth, S. et al.: Environ. Mutagen. 5, Suppl. 1, 3-142
- Principles of method if other than guideline:
- Use of S. typhymurium strain TA98, TA100, TA1535, TA1537 and/or TA97, but no E.coli strain.
not toxic chemicals tested up to a maximum dose of 10 mg/plate, poorly soluble chemicals were tested up to the dose defined by solubility, A maximum of 0.05 ml solvent was added to each plate, only 2-Aminoanthracene was used as the indicator of the efficacy of the S9-Mix, not every individual plate count is displayed, no justification that no confirmation of the negative result has been made - GLP compliance:
- no
- Type of assay:
- bacterial reverse mutation assay
- Target gene:
- his-
- Species / strain / cell type:
- S. typhimurium, other: Salmonella Typhimurium TA98, TA100, TA1535, TA1537, TA97
- Metabolic activation:
- with and without
- Metabolic activation system:
- rat and hamster S9 (10% Aroclor 1254-induced)
- Test concentrations with justification for top dose:
- 0.000, 33.000, 100.000, 333.000, 1000.000, 3333.000, 4500.000 µg/plate
- Vehicle / solvent:
- H2O
- Untreated negative controls:
- not specified
- Negative solvent / vehicle controls:
- yes
- Remarks:
- run with each trial
- Positive controls:
- yes
- Remarks:
- without S9: Sodium azide (TA1535, TA100), 9-aminoacridine (TA1537), 4-nitro-o-phenylenediamine (TA98) with S9: 2-aminoanthracene
- Evaluation criteria:
- An individual trial was judged mutagenic (+) if a dose-related increase over the corresponding solvent control was seen, and it was judged weakly mutagenic C+W) if a low-level dose response was seen. A trial was considered questionable (?) if a dose related
increase was judged insufficiently high to justify a call of " + W," if only a single dose was elevated over the control, or if a non-dose-related increase was seen.
The distinctions between a weak mutagenic response and a mutagenic response, or between a weak mutagenic response and a questionable mutagenic response are highly subjective.
A chemical was judged to be mutagenic (+), or weakly mutagenic (+W), if it produced a reproducible, dose-related increase in his+ revertants over the corresponding solvent controls in replicate trials. A chemical was considered to be questionable (?) if a reproducible increase of hist revertants did not meet the criteria for either a " + " or " + W," or if only single doses produced an increase in his+ revertants in repeat trials - Statistics:
- no data
- Species / strain:
- S. typhimurium TA 98
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- other: > 1000 µg/plate
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- not specified
- Positive controls validity:
- valid
- Species / strain:
- S. typhimurium TA 100
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- other: > 1000 µg/plate
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- not specified
- Positive controls validity:
- valid
- Species / strain:
- S. typhimurium TA 1535
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- other: > 1000 µg/plate
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- not specified
- Positive controls validity:
- valid
- Species / strain:
- S. typhimurium TA 1537
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- other: > 1000 µg/plate
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- not specified
- Positive controls validity:
- valid
- Species / strain:
- S. typhimurium TA 97
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- other: > 1000 µg/plate
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- not specified
- Positive controls validity:
- valid
- Conclusions:
- Interpretation of results: negative
Dimethylamine was considered not mutagenic in the tests performed. - Executive summary:
This test was performed according to Haworth, S. et al.: Environ. Mutagen. 5, Suppl. 1, 3-142 with Salmonella typhimurium TA1535, TA1537, TA98, TA100, and TA 97. The concentrations of the test substance ranged from 0.000, 33.000, 100.000, 333.000, 1000.000, 3333.000 and 4000.000 or 4500.000 µg/plate using the pre-incubation method in either the presence or absence of 10% rat or hamster liver metabolic activation. The highest in some strains nontoxic dose tested was 1000.000 mg/plate and the test result was negative according to all strains, with and without metabolic activation. (Zeiger et al., 1987).
- Endpoint:
- in vitro gene mutation study in mammalian cells
- Remarks:
- and further multiple-endpoint mutagenesis tests
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: well-described experimental result, no guideline followed
- Principles of method if other than guideline:
- CHO cells were treated with DMA in the presence of metabolic activation (Aroclor-1254 induced rat liver microsomes) and analyzed for cytotoxicity and specific gene mutation, and collected for chromosome aberration and SCE assays.
- GLP compliance:
- no
- Type of assay:
- other: Chinese Hamster Ovary (CHO) cells
- Target gene:
- hprt locus
- Species / strain / cell type:
- Chinese hamster Ovary (CHO)
- Additional strain / cell type characteristics:
- other: subclone CHO-KrBH4 of the CHO-K-, cell line, referred to as CHO cells
- Metabolic activation:
- not specified
- Metabolic activation system:
- no data
- Test concentrations with justification for top dose:
- 0.5% (5 µL in 5 mL medium)
- Vehicle / solvent:
- details see below
- Remarks:
- details see below
- Details on test system and experimental conditions:
- details see below
- Evaluation criteria:
- details see below
- Statistics:
- details see below
- Species / strain:
- Chinese hamster Ovary (CHO)
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- other: no but tested up to a concentraton of 22 mM
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- valid
- Positive controls validity:
- valid
- Additional information on results:
- all details are given below
- Conclusions:
- Interpretation of results: negative
DMA exhibits no cytotoxic and mutagenic effects. - Executive summary:
Hsie et al. reported in 1987 an multiple-endpoint mutagenesis test was performed. Chinese Hamster Ovary (CHO) cells were used with and without metabolic activation system. The test concentration of dimethylamine was up to 22 mM. Before performing this experimental study it was known that DMA is a noncarcinogen. It was used as analogue to the cancerogen DMN (dimehylnitrosamine).
Referenceopen allclose all
Table 82.1 DIMETHYLAMINE (LAB: EGG SOLVENT: H2O) |
||||||||||||||||||||||||
DOSE |
TA100 |
TA1535 |
TA1537 |
TA98 |
||||||||||||||||||||
NA |
10% HLI |
10% RLI |
NA |
10% HLI |
10% RLI |
NA |
10% HLI |
10% RLI |
NA |
10% HLI |
10% RLI |
|||||||||||||
ug/PLATE |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
0.000 |
93 |
8.0 |
89 |
9.1 |
76 |
2.5 |
24 |
1.9 |
8 |
1.7 |
13 |
1.2 |
4 |
1.5 |
4 |
0.9 |
8 |
1.5 |
18 |
5.2 |
20 |
0.6 |
24 |
3.2 |
33.000 |
92 |
5.4 |
|
|
|
|
21 |
1.5 |
|
|
|
|
8 |
1.0 |
|
|
|
|
20 |
2.7 |
|
|
|
|
100.000 |
91 |
8.7 |
90 |
3.1 |
77 |
2.0 |
19 |
2.5 |
7 |
1.5 |
11 |
0.9 |
8 |
0.6 |
6 |
0.9 |
8 |
2.6 |
15 |
2.8 |
24 |
2.2 |
17 |
1.0 |
333.000 |
92 |
6.4 |
80 |
4.5 |
91 |
0.6 |
20 |
4.0 |
10 |
0.6 |
10 |
2.7 |
5 |
1.3 |
6 |
2.3 |
6 |
2.2 |
17 |
4.8 |
20 |
2.0 |
17 |
2.7 |
1000.000 |
88 |
6.3 |
92 |
7.0 |
88 |
5.2 |
16 |
2.3 |
7 |
1.2 |
8 |
1.7 |
5 |
1.5 |
8 |
0.3 |
5 |
1.7 |
17 |
1.2 |
20 |
3.9 |
24 |
3.0 |
3333.000 |
t |
|
88 |
5.2 |
89 |
11.0 |
11s |
1.5 |
8 |
1.2 |
9 |
1.3 |
6s |
0.7 |
7 |
1.5 |
10 |
0.3 |
t |
|
19 |
5.0 |
22 |
1.5 |
4500.000 |
|
|
82 |
6.7 |
86 |
2.5 |
|
|
9s |
1.8 |
8 |
2.4 |
|
|
6 |
1.3 |
6 |
3.3 |
|
|
19 |
1.2 |
20 |
1.5 |
POS |
2003 |
16.5 |
887 |
78.0 |
580 |
31.2 |
1176 |
36.1 |
80 |
1.9 |
51 |
2.7 |
573 |
199.4 |
94 |
4.2 |
58 |
8.7 |
840 |
81.5 |
1011 |
82.4 |
639 |
64.7 |
Table 82.2 DIMETHYLAMINE (LAB: EGG SOLVENT: H2O) |
||||||||||||||||||||||||
DOSE |
TA100 |
TA1535 |
TA1537 |
TA98 |
||||||||||||||||||||
NA |
10% HLI |
10% RLI |
NA |
10% HLI |
10% RLI |
NA |
10% HLI |
10% RLI |
NA |
10% HLI |
10% RLI |
|||||||||||||
ug/PLATE |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
MEAN |
SEM |
0.000 |
117 |
10.1 |
107 |
6.2 |
132 |
16.2 |
21 |
3.5 |
13 |
1.5 |
10 |
0.7 |
7 |
2.0 |
8 |
0.9 |
8 |
0.6 |
22 |
4.4 |
34 |
2.9 |
28 |
3.2 |
100.000 |
126 |
4.8 |
124 |
3.2 |
106 |
7.0 |
14 |
1.2 |
10 |
1.2 |
15 |
4.2 |
8 |
1.9 |
8 |
0.3 |
9 |
1.5 |
25 |
2.7 |
25 |
2.9 |
28 |
1.5 |
333.000 |
112 |
9.5 |
116 |
5.0 |
120 |
0.9 |
15 |
3.9 |
15 |
1.8 |
10 |
0.0 |
8 |
1.3 |
7 |
1.2 |
10 |
2.2 |
21 |
1.7 |
28 |
1.7 |
26 |
1.2 |
1000.000 |
126 |
4.4 |
136 |
4.4 |
127 |
4.3 |
18 |
3.2 |
10 |
2.0 |
10 |
1.7 |
5 |
0.3 |
5 |
0.9 |
9 |
0.6 |
22 |
0.7 |
29 |
6.2 |
31 |
1.9 |
2000.000 |
108 |
7.6 |
115 |
5.1 |
113 |
16.4 |
15s |
3.0 |
12s |
1.9 |
14 |
1.5 |
9s |
2.8 |
9 |
0.3 |
11 |
1.7 |
24s |
1.8 |
26 |
1.2 |
27 |
1.2 |
3333.000 |
97s |
11.5 |
129s |
4.7 |
117 |
14.7 |
t |
|
11s |
1.2 |
11 |
1.2 |
t |
|
7 |
0.6 |
8 |
0.6 |
20s |
1.5 |
29 |
2.4 |
27 |
1.8 |
4000.000 |
|
|
|
|
|
|
|
|
16s |
2.3 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
POS |
2012 |
55.2 |
1503 |
72.7 |
1255 |
49.0 |
1205 |
65.2 |
116 |
7.2 |
60 |
1.7 |
535 |
18.1 |
184 |
21.0 |
133 |
2.1 |
2002 |
38.4 |
1270 |
40.2 |
1022 |
55.2 |
The Mutagenicity and Toxicity of DMN and DMA
DMA did not exhibit cytotoxic and mutagenic effects up to 22 mM even with S9, and a marginal effect on SCE and chromosome aberration were seen in the presence of S9. The significance of this marginal cytogenetic activity needs to be further assesed. These results suggest that nitrosation is required for the genetic toxicity of DMN since its nonnitrosated analogue DMA is relatively inert. In addition, it shows that the carcinogenic chemical DMN causes cytotoxicity, gene mutation, chromosome aberration and SCE, while DMA, the noncarcinogenic analogue of DMN, is almost totally inert. A close examination of the SCE data indicated that DMA might exhibit a marginally weak response using the 2-fold criteria. Since DMA requires 5 times higher concentration than DMN to achieve a marginal response, it is not unreasonable to consider DMA as negative or nonpositive in the SCE assay.
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Genetic toxicity in vivo
Description of key information
Isakova et al., 1971. In vivo Mammalian Chromosome Aberration Assay; no genotoxicity
Link to relevant study records
- Endpoint:
- in vivo mammalian germ cell study: cytogenicity / chromosome aberration
- Remarks:
- Type of genotoxicity: chromosome aberration
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Study period:
- 1971
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Acceptable, well-documented publication which meets basic scientific principles.
- Qualifier:
- no guideline followed
- Principles of method if other than guideline:
- DMA was investigated on male Wistar rats weighing 150-200 g. These were subjected to long-term poisning by inhalation in 100-liter chambers, predetermined vapor concentrations being maintained around the clock for 3 month.
- GLP compliance:
- no
- Remarks:
- The study was conducted prior to the adoption of the OECD guidelines
- Type of assay:
- chromosome aberration assay
- Species:
- rat
- Strain:
- Wistar
- Sex:
- male
- Route of administration:
- inhalation
- Vehicle:
- not applicable
- Details on exposure:
- Rats were exposed by inhalation in 100-L chambers
- Duration of treatment / exposure:
- 15 and 90 days
- Frequency of treatment:
- daily
- Post exposure period:
- no
- Dose / conc.:
- 0 mg/m³ air (nominal)
- Dose / conc.:
- 0.5 mg/m³ air (nominal)
- Dose / conc.:
- 1 mg/m³ air (nominal)
- No. of animals per sex per dose:
- no data
- Control animals:
- yes, sham-exposed
- Tissues and cell types examined:
- bone marrow cells
- Details of tissue and slide preparation:
- The preparation for cytological investigation were prepared by the method of Ford and Woolam (Ford C.E. and Woolam D.H. Stain technology, Vol.38, p.271, 1963).
- Evaluation criteria:
- The incidence of structural chromosome breakages and aneuploidy, recorded in metaphases of marrow cells, was used as the criterion of a mutagenic effect. The control was provided by the incidence of similar breakages in the marrow of intact rats of the same age and sex, maintained under identical conditions.
- Statistics:
- Student's test.
- Sex:
- male
- Genotoxicity:
- negative
- Toxicity:
- not specified
- Vehicle controls validity:
- not applicable
- Negative controls validity:
- valid
- Positive controls validity:
- not examined
- Additional information on results:
- The incidence of cells with structural chromosome breakages was similar to that in the control preparations (0-2%), and was independent of the duration of poisoning or the concentration of DMA. Analysis of the chromosome count in the same cells revealed that the incidence of aneuploid cells in the experimental animals was somewhat higher than in the controls, for both DMA concentrations and at various times after the beginning of exposure. Statistically significant differences from the controls (p < 0.01) were detected only after 3 month' poisoning, for both DMA concentartions. The incidence of aneuploid cells in the marrow after 90 days poisoning was nearly double that after 15 days poisoning. The significant increase in the incidence of aneuploidy with both DMA concentrations and after different poisoning periods was due to both hypoploid and hyperploid cells.
- Conclusions:
- Interpretation of results: negative
DMA did not produce cytologically detectable chromosome breakages. - Executive summary:
Male Wistar rats were exposed to 0.5 and 1 mg/cm³ dimethylamine via continuous inhalation for 15 and 90 days. 50 to 100 bone marrow cells were scored per animal. The incidence of cells with chromosomal breakage was did not exceed controls (0 -2%) in any experimantal variant but the incidence of aneuploid cells was significantly higher at both concentrations after 90 days. No decrease in mitotic activity was observed.
Reference
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Additional information
In vitro
Gene mutation properties of dimethylamine were investigated in a bacterial reverse mutation assay (Ames test). This test was performed according to Haworth, S. et al.: Environ. Mutagen. 5, Suppl. 1, 3-142 with Salmonella typhimurium TA1535, TA1537, TA98, TA100, and TA 97. The concentrations of the test substance ranged from 0.000, 33.000, 100.000, 333.000, 1000.000, 3333.000 and 4000.000 or 4500.000 µg/plate using the pre-incubation method in either the presence or absence of 10 % rat or hamster liver metabolic activation. The highest in some strains nontoxic dose tested was 1000.000 mg/plate and the test result was negative according to all strains, with and without metabolic activation. (Zeiger et al., 1987).
Hsie et al. reported in 1987 an multiple-endpoint mutagenesis test was performed (Hsie et al., 1987). Chinese Hamster Ovary (CHO) cells were used with and without metabolic activation system. The test concentration of dimethylamine was up to 22 mM. Before performing this experimental study it was known that DMA is a noncarcinogen. It was used as analogue to the cancerogen DMN (dimehylnitrosamine).
Additionally, an in vitro mammalian chromosome aberration test with CHO cells testing among various other chemicals DMA-HCl showed no chromosomal aberrations and no mutations, therefore is stated that DMA is not genotoxic nor cytotoxic in concentrations um to 0.12 mg/mL (Ishidate et al., 1977).
In vivo
In an in Vivo Mammalian Chromosome Aberration Assay (Isakova et al., 1971), Wistar rats were exposed to vapours of DMA by inhalation at concentrations of 0.05 mg/m³ and 1 mg/m³ during 15 and 90 days. The incidence of structural chromosome breakages and aneuploidy, recorded in metaphases of marrow cells, was used as the criterion of a mutagenic effect. The control was provided by the incidence of similar breakages in the marrow of intact rats of the same age and sex, maintained under identical conditions. 50 to 100 metaphases were analyzed for each experimental and control animal.
The incidence of cells with structural chromosome breakages was similar to that in the control preparations (0 - 2 %), and was independent of the duration of poisoning or the concentration of DMA. Analysis of the chromosome count in the same cells revealed that the incidence of aneuploid cells in the experimental animals was somewhat higher than in the controls, for both DMA concentrations and at various times after the beginning of exposure. Statistically significant differences from the controls (p < 0.001) were detected only after 3 month' poisoning, for both DMA concentrations. The incidence of aneuploid cells in the marrow after 90 days poisoning was nearly double that after 15 days poisoning. The significant increase in the incidence of aneuploidy with both DMA concentrations and after different poisoning periods was due to both hypoploid and hyperploid cells.
Since only 50 to 100 metaphases from the bone marrow of each animal were evaluated, the increased aneuploidy and hyperploidy can not be evaluated.
Overall, it can be concluded that DMA is not genotoxic.
Justification for classification or non-classification
Classification is not warranted according to the criteria of EU Classification, Labelling and Packaging of Substances and Mixtures (CLP) Regulation (EC) No. 1272/2008.
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
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