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EC number: 203-865-4
CAS number: 111-40-0
DETA; N-(2-aminoethyl-1,2-ethanediamine); diethylenetriamine; bis (2-aminoethyl) amine, 2,2-diaminodiethylamine; aminoethylethandiamine
Completely miscible (w/v) 
0.25 mm Hg at 25°C (estimated by EPI Suite version 4.0)
-2.13 (estimated by EPI Suite version 4.0)
8.8 (estimated by KOAWIN version 1.67)
11.6 (1% aqueous solution) 
DETA has moderate toxicity by the oral route. The oral LD50in the rat has been reported to be 0.82-2.6 g/kg bw [3,4]. The oral LD50of DETA in guinea pig was 0.6 g/kg bw . Reanalysis of the data of a previously reported pharmacokinetic study  conducted in rats after oral and intravenous dosing showed that orally administered DETA was rapidly absorbed reaching plasma Cmaxwithin an hour. Oral bioavailability of DETA was reported to be between 77 and 83% in the rat . Oral bioavailability of DETA in humans has been estimated to be ~ 73% (ACD/ADME Suite QSAR program, v5.0).
DETA has moderate dermal toxicity. The dermal LD50in rabbits has been reported to be 0.95-1.24 g/kg , while the LD50in guinea pig after dermal application is 0.5 g/kg . From these data it is reasonable to conclude that dermal absorption of DETA is similar to the reported oral absorption of >70%. The reported relatively high dermal toxicity in rabbit and guinea pig is most likely due to dermal corrosion from the high pH of the dosing solutions causing severe burns  leading to higher penetration than that would be expected from intact skin. In contrast, the dermal penetration rate (Kp) of an aqueous solution of DETA through human skin is low, estimated to be 1.58 x 10-5cm/h (EPA DERMWIN QSAR version 2.00).
Due to very low vapour pressure (0.25 mm Hg at 25oC) and high octanol:air partitioning (Koa= 8.8; EPI Suite version 4.0) of DETA inhalation of vapor is not a significant route of exposure under normal conditions. Aerosolize DETA if inhaled will be absorbed through lungs as reported in rats , and would damage the lungs due to corrosion. DETA is an intermediate in closed systems where aerosolization is not expected to occur.
Due to its non-lipophilicity (log Kow= -2.13) and low predicted plasma protein binding (~19%), a low volume of distribution (1.1 L/kg) is estimated for DETA in humans by the ACD/ADME Suite application. A similar low volume of distribution of DETA (1.3-1.9 ml/kg) has been reported in rats after oral or intravenous exposure . The absorbed dose was distributed to almost all rat tissues ; however, only about 2% of the administered dose remained in carcass after 48 hours with over 96% recovered in excreta .
Although DETA has high oral bioavailability (77-83%) in rat, due to its low plasma protein binding, low volume of distribution and rapid elimination, DETA is expected to have very low bioaccumulation potential.
In Fischer rat, metabolism of DETA appeared to play a small role in its elimination from the body after oral, endotracheal or intravenous dosing as the major urinary metabolite was identified as unchanged DETA . Three minor metabolites (three fractions from cation exchange chromatography) were also detected but not identified in this previous study .
Based on the structural similarity of DETA and ethylenediamine (EDA), DETA would be expected to metabolize to N-acetylDETA formed from acetylation of the primary amino group of DETA as described in a report on EDA metabolism . DETA also has the potential to be metabolized to the aldehyde metabolite[(2-aminoethyl)amino acetaldehyde], formed by deamination with liver monoamine oxidase . The formed aldehyde metabolites would be further metabolized to the corresponding acids.
As described above, the potential metabolites of DETA are expected to be excreted in urine. Based on the previous data , DETA was almost equally eliminated urine and feces . The rats given oral or endotracheal14C-DETA excreted at least 96% of the radioactivity within 48 hours, 40-46% in feces and 31-43% in urine.The absorbed DETA was eliminated biphasically with most of the elimination occurring rapidly during the initial phase . The terminal plasma elimination half-life after intravenous injection was 10 hours and after oral administration was 17 hours (re-evaluation of Tyler et al.  data) This longer half-life after oral dosing was probably due to the influence of continuous low absorption from the GI tract for some time before the secession of absorption/depletion of the dose in the GI tract. Since, no difference was seen in the toxicity of DETA after dermal or oral dosing [3,4,6], it is logical to expect that the dermally absorbed DETA will be rapidly eliminated, similar to that observed after oral dosing in rats .
1. Riddick JA, Bunger WB and Sakano TK (1986).Organic Solvents: Physical Properties and Methods of Purification. 4thEdition,,.
2. Dow online product information – Diethylenetriamine (DETA) CAS #000111-40-0, N-(2-aminoethyl-1,2-ethanediamine). The Dow Chemical Company,,,http://www.dow.com/amines/prod/ethyl-deta.htm
3. Smyth HF, Jr. (1942). Range finding tests on diethylene triamine. Mellon Institute of Industrial Research,offor Carbide and Carbon Chemicals Corporation, Industrial Fellowship No. 274-5, Archived at The Dow Chemical Company,,.
4. IUCLID Dataset (2007). 201-16635A, Substance ID: 111-40-0. available at the website: http://www.epa.gov/HPV/pubs/summaries/ditribis/c14300rt2.pdf.
5.TR, Lento JW, McKelvey JA and Tallant MJ (1981). Pharmacokinetics and metabolism of diethylenetriamine in the rat. Union Carbide Corporation, Bushy, Export,.
6. Carpenter CP (1948). The acute toxicity of diethylene triamine. Mellon Institute of Industrial Research,offor Carbide and Carbon Chemicals Corporation, Industrial Fellowship No. 274-11, Archived at The Dow Chemical Company,,.
7. Yang RS and Tallant MJ (1982) Metabolism and pharmacokinetics of ethylenediamine in the rat following oral, endotracheal or intravenous administration. Fundam Appl Toxicol 2, 252-260.
8. Yu PH (1989) Deamination of aliphatic amines of different chain lengths by rat liver monoamine oxidase A and B. The Journal of pharmacy and pharmacology 41, 205-208.
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