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EC number: 202-845-2 | CAS number: 100-37-8
- 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
Link to relevant study record(s)
Description of key information
Key value for chemical safety assessment
Additional information
2-Diethylaminoethanol has been reported to be readily absorbed via the gastrointestinal tract in humans and rats (Rosenberg et al, 1949; Schulte et al., 1972; Val. 4). In a limited study with humans, the plasma concentration peaked 3 hours after an oral administration of 5.6 g of 2-diethylaminoethanol-HCl, but was almost undetectable after 8 hours. About 25 % of the 2-diethylaminoethanol was excreted unchanged in the urine within 48 hours. Similar excretion results were observed after intravenous administration. In the same publication it was reported that 2-diethylaminoethanol-HCl given to dogs by intravenous infusion (71 mg/kg bw), distributed rapidly. Three hours after infusion the level of 2-diethylaminoethanol was higher in the tissues examined (muscle, heart, brain, lung, liver and spleen) than in the plasma.
In a gavage study with rats, 14C-labeled-2-diethylaminoethanol-HCl was reported to be rapidly absorbed into the blood stream (with a dose of 68 mg/kg the maximum concentration in the blood was reached in 30 minutes and with 679 mg/kg it was reached within 1 hour). Elimination occurred primarily via the kidney. Elimination via exhalation and the faeces played only minor role. The kinetics of urinary elimination was affected by the dose. In this regard, by 6 hours after the application of a 679 mg/kg bw dose 40 % was eliminated in the urine, and by 24 hours after application 58.5 % was eliminated. When a 68 mg/kg dose was given, then after 6 and 24 hours 17.5 % and 37.4 % were excreted via the urine, respectively. In the experiment with 679 mg/kg bw of 2-diethylaminoethanol, 90 % of the test substance had been eliminated via the urine 10 days after treatment. Some radioactivity was still detectable in the urine 40 days after treatment. 2-diethylaminoethanol was predominantly (> 60 %) excreted unchanged over the first 96 hours. In the same period, the following metabolites were seen based on the recovery of radioactive compounds: 2-ethylaminoethanol (ca. 1 %), phosphoric acid-mono-(2-diethylaminoethylester) (2-8 %), diethylaminoacetic acid (ca. 10 %) and the N-oxide of 2-diethylaminoethanol (ca. 15 - 19 %). Incorporation into phospholipids was observed. In this study, autoradiography indicated that 2-diethylaminoethanol was widely distributed throughout the body after gavaging. 2-diethylaminoethanol was concentrated in the liver, reaching a maximum at 7 hours, but thereafter, it decreased. Initially, the central nervous system showed very low levels of activity, but by day 7 it had increased. For the oral dose of 679 mg/kg the biological half-life was 19 hours and for the 67.9 mg/kg dose it was 36 hours. In a separate study 14C-labeled-2-diethylaminoethanol-HCl was given to rats by intravenous injection at doses of 2.9 μmol/rat (ca. 1.94 mg/kg bw) (Michelot et al., 1981; Val. 4).
Based on the available data and as summarized in the MAK Report Vol 14 (DFG (2000) Occupational Toxicants Critical Data Evaluation for MAK Values and Classification of Carcinogens, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Vol 14, Ed. H. Greim), Diethylaminoethanol is absorbed well after oral administration, distributed in the organism., and almost excreted unchanged with the urine and faeces. Triethylamine oxide, diethylamine and ethylamine are reported as metabolites in the urine.
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