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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Administrative data

Link to relevant study record(s)

Description of key information

Due to lack of quantitative data, absorption rates of 100% are indicated for all three routes. Available studies do not indicate a concern for bioaccumulation.

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential
Absorption rate - oral (%):
Absorption rate - dermal (%):
Absorption rate - inhalation (%):

Additional information

No specific toxicokinetic, metabolism or distribution studies were identified for Fatty acids, C18 unsat, reaction products with diethylenetriamine. (FA + DETA: Fatty acids reaction products with DETA; also AAI-DETA).


The manufacturing process basically involves the reaction under controlled conditions of a fatty acid with a primary amine of DETA, leading to the formation of an amide.Upon heating there is ring forming to imidazoline. In principle this always lead to a mixture ofAlkyl amidoamines/imidazolines (AAI).


AAI are mainly protonated under environmental conditions. The protonated fraction will behave as salt in water. AAI are surface active and have a low solubility in the form of CMC. For DETA based AAI, the observed CMC was 99 mg/L. The actual dissolved concentration in water will be extremely low as alkyl amidoamines/imidazolines will sorb strongly to sorbents. As a consequence, absorption from gastro-intestinal system is likely to be slow.


The mode of action of for AAI follows from its structure, consisting of an apolar fatty acid chain and a polar end of a primary amine from the polyethyleneamine. The structure can disrupt the cytoplasmatic membrane, leading to lyses of the cell content and consequently the death of the cell.

The AAI are all corrosive to skin, and toxicity following dermal exposure is characterised by local tissue damage, rather than the result of percutaneously absorbed material.


The likelihood of exposure via inhalation is low considering its high boiling point (> 300 °C) and very low vapour pressure (1.7 x 10-7 Pa at 25°C) and use applications that do not involve the forming of aerosols, particles or droplets of an inhalable size.


1. Physical-chemical properties

AAI-DETA is described as a clear, slightly viscous, amber liquid. No mp or bp were observed between -30 and 300 ºC; a low vapour pressure of 1.7 x 10-7Pa at 25°C.

The octanol-water partition coefficient (log Pow) is2.2.As the substance forms micelles in water the water solubility is expressed as the critical micelle concentration (CMC, a solubility limit) which is 99mg/L.


In physiological circumstances the nitrogen is positively charged (at pH 7.2 and below > 99% cationic), resulting to a cationic surfactant structure which leads to high adsorptive properties to negatively charged surfaces as cellular membranes. The apolar tails easily dissolve in the membranes, whereas the polar head causes disruption and leakage of the membranes leading to cell damage or lysis of the cell content. As a consequence, the whole molecule will not easily pass membrane structures. Cytotoxicity at the local site of contact through disruption of cell membrane is considered the most prominent mechanism of action for toxic effects.


In the table below are molecular chemical profile and estimated properties listed. The experimentally determined and calculated properties are reasonably well comparable.

The alert forprotein binding indicates that the chemical is a strong sensitizer as a result of Amide aminolysis. Animal studies for skin sensitisation confirmed this concern.

The alert for DNA binding by OECD has not been confirmed by the various genotoxicity tests performed. This can possibly explained by low bioavailability due to the combination of low solubility and difficulty of surfactants to pass cell membranes.


2. Data from toxicity studies and irritation studies

AAI- DETA is corrosive to the skin.Acute toxicity datashows low acute oral toxicity hazardsand effects observed are attributable to its corrosive properties in the GI-tract. The two available studies indicate an acute oral toxicity of > 2000 mg/kg based on two acuteAcute Toxic Class (OECD 423) studies. As the substance is corrosive, symptoms of local respiratory irritation are expected, which is expected to limit the systemic uptake of amounts needed for systemic toxicity.

Also for acute dermal toxicity, effects will be characterised by local tissue damage. Systemic uptake via skin is likely to be very limited, in view of the use of protective measure related to the handling of corrosive material.


Data from animal studies for skin sensitisation indicate that the substanceshould beclassified as Skin sensitizer Category 1A. 

For corrosive and sensitising substances, the use of protective gloves and other equipment, such as face shields, aprons and good work practices are mandatory. As a result, direct dermal contact is very unlikely.

Lack of exposures, also via inhalation, explains that although the substance can be considered a strong sensitiser based on the results from both studies, the producers are not aware of reported incidences of sensitisation among own employees or from customers.


For each endpoint, bacterial mutagenicity, mammalian mutagenicity and mammalian clastogenicity, a recent guideline and GLP compliant study is available which all indicate that there is no concern for genotoxicity.


Data from repeated dose toxicity studies also point at low systemic toxicity with a sub-chronic NOAEL from a 90-day gavage study in rats of 10 mg/kg bw/day. The first effects occurring at higher levels are mediated by local responses in the GI-tract.


Available reproduction screening (OECD 422) studies and 90-day sub-chronic studies further did not indicate specific effects on reproductive organs.There were specifically no indications of possible reproduction toxicity based on the additional parameters determined in the 90-day study: All females showed a normal (regular) estrous cycle, and histopathological examination of the male and female reproductive organs did not show treatment-related lesions. An additionally performed Prenatal developmental toxicity has furthermore shown thatAAI- DETAhad no impact on any of the fetal developmental parameters up to the highest dose level of 150 mg/kg bw/day, over 15 times the 90-day NOAEL. In view of the lack of effects in on reproductive parameters in these available studies, further testing of for fertility is of low priority.


3. Absorption, distribution, metabolism, excretion

AAI-DETA is mainly protonated under environmental conditions. The protonated fraction will behave as salt in water. It is surface active and has a low solubility in the form of CMC. Similarly to other cationic fatty nitrile derivatives, AAI-AEP is expected to sorb strongly to sorbents. As a consequence, absorption from gastro-intestinal system is likely to be slow. The Human Intestinal absorption (HIA) is estimated to be 91% (QSAR toolbox v. 3.1). An absorption of 100% is indicated as key value here.


At this stage no data are available on dermal absorption. Itis not expected to easily pass the skin in view of its ionised form at physiological conditions.Based on the corrosive properties, dermal absorption as a consequence of facilitated penetration through damaged skin can be anticipated. Dependent on the solvent and concentration, up to 60% dermal absorption might be suggested as a worst case for assessment purposes (value taken from the existing EU risk assessment on primary alkylamines). Due to the lack of quantitative absorption data, 100% absorption is taken as a conservative approach.


Also for inhalationno data are available on absorption, and100% is proposed as worst case. With a vapour pressure of1.7 x 10-7Pa at 25°C, the potential for inhalation is limited. Relevant (in view of possible systemic absorption) exposures are therefore only possible as aerosol. If any inhalation does occur, this can only be in the form of larger droplets, as the use does not include fine spraying. Droplets will deposit mainly on upper airways, and will be subsequently swallowed following mucociliary transportation to pharynx. This results to no principal difference in absorption compared oral route. Absorption via respiratory route is therefore also set at 100%.



Considering the only limited increase of toxic effects following longer duration of dosing observed between OECD 422 (females up to 45-days) and 90-days dosing study, the potential for bioaccumulation of Tall oil reaction products with AEP is considered to be low.


The mode of action for toxicity follows from its structure, consisting of an apolar fatty acid chain and a polar end from the piperazine part. The structure can disrupt the cytoplasmic membrane, leading to lyses of the cell content and consequently the death of the cell. AAI-DETA is corrosive to skin, and toxicity following dermal exposure is characterised by local tissue damage, rather than the result of percutaneously absorbed material.



Molecular chemical profile and estimated properties AAI-DETA:



Fatty acids, C18 unsat, reaction products with diethylenetriamine



Physical state

viscous liquid


amidoamine component

imidazoline component



20565-75-7 (3528-63-0)




Chemical name


-  (Z)-2-(8-Heptadecenyl)-4,5-dihydro-1H-imidazole-1-ethylamine

(- 1H-Imidazole-1-ethanamine, 2-(8-heptadecen-1-yl)-4,5-dihydro- )

Molecular structure



Alkyl= C18:1



N - C

|     \\

C     N - CH2-CH2-NH2

\     /



Alkyl= C18:1

Molecular formula



Molecular weight



Solubility:ALogPS 3.0

          WSKOW v1.42

       WATERNT v1.01

125 mg/L

0.1068 mg/L

12.365 mg/L

8.2 mg/L

0.002416 mg/L

0.023261 mg/L

Solubility (meas)

CMC 99 mg/L (pH 7, 23°C)


926 at 20°C





2 poss. cationic amines: 6.88 / 9.60

> 99% at pH > 11.6

Max 91.91% at pH 8.2

10% at pH7.8 and >99% at pH ≤ 4.8

2 poss. cationic amines: 7.14 / 10.27

> 99% at pH > 12.4

Max 94.72% at pH 8.8

10% at pH8.1 and >99% at pH ≤ 5.0

logPow     (ALOGPS 3.0)

       (KOWWIN v1.68)





logPow (meas)

2.2 @ 25°C

logD (Chemaxon)

pH       logD

1,700   -1,232

4,600   -0,289

5,500   0,587

7,000   2,316

pH      logD

1,700   0,395

4,600   1,006

5,500   1,796

7,000   3,107


217.22 °C

174.09 °C


509.90 °C

432.56 °C

Vp (EPIWIN) 25°C

1.83E-008 Pa

1.24E-005 Pa

Mp (meas)

not in -30-300°C

bp (meas)

not in -30-300°C

Vp (meas)

1.7E-7 Pa at 25°


- DNA binding by OECD: Schiff base formers: Ethylenediamine derivatives metabolised to glyoxal.

- Protein binding by OASIS v1.3: Ester aminolysis of amide leading to acylation. (strong sensitiser)

-in vivomutagenicity (Micronucleus) alerts by ISS: H acceptor-path3-H acceptor.

- DNA binding by OECD: Iminium ion forming from aliphatic tert. amine.

-in vivomutagenicity (Micronucleus) alerts by ISS: H acceptor-path3-H acceptor.

Metabolism/ transformations

Hydrolysis (basic/acidic) predicted to oleic acid and DETA

Hydrolysis (basic/acidic) predicted to amidoamine component, and subsequent to oleic acid and DETA

Dermal penetration coefficient Kp (est)

0.057 cm/hr

1.67 cm/hr

Human Intestinal absorption (HIA)



Molecular formula, molecular weight, pKa and logD were all calculated using ChemAxon MarvinSketch (v.6.1.6).

Melting point, boiling point, vapour pressure and logPow were estimated by EPI Suite (v4.1).

Solubility and logPow are estimated using ALOGPS 3.01 (

Reactivity: QSAR Toolbox v.3.2: profiling:

Absorption properties:

- dermal: EpiSuite v. 4.1; (water:0.0005 cm/hr): log Kp = -2.80 + 0.66 log Kow - 0.0056 MW

- intestinal: HIA: QSAR toolbox (version 3.2) (Human Intestinal Absorption)

Max. dermal absorption: IH Skin Perm v1.03 from AIHA


Metabolism/transformations (QSAR Toolbox v.3.2)

Hydrolysis (basic/acidic): imidazoline component: hydrolysis to amidoamine component, and predicted hydrolysis of the amidoamine component to oleic acid and DETA.