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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

The physical-chemical properties and toxicological findings from in vitro and animal studies provide a valid basis for determining the ADME profile for APDEA. These data indicate that absorption via the dermal route and inhalation is possible. Following oral ingestion, APDEA is expected to be rapidly eliminated via the urine due to its high water solubility and low molecular weight. Evidence for absorption following oral dosing was only seen following repeated dosing at a high dose level. APDEA is a basic molecule, and consequently evidence of irritation of the skin and stomach was observed in the dermal and oral toxicity studies, respectively.

Key value for chemical safety assessment

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

Additional information

Physico-chemical properties and the results of in vitro studies and acute and repeat dose toxicity studies with animals for N-(3-Aminopropyl) diethanolamine (APDEA) are available to determine a toxicokinetic profile. The substance APDEA is a clear, slightly yellow liquid and has the molecular formula C7H18N2O2with a molecular weight of 162.23 g/mol. It is highly water soluble (miscible with water in all proportions at 20°C) with a low log Pow of -1.74 at 25°C. APDEA contains a primary amine group and is therefore basic in nature, with a pH of 14.1.




Dermal absorption:

According to REACH Guidance R7c, although APDEA is a low molecular weight liquid, the high water solubility (above 10,000 mg/l) and the low log Pow (below 0) of APDEA suggests that it is too hydrophilicto cross the lipid rich environment of the stratum corneum to any great extent, and therefore significant dermal penetration would not be expected, in which case a value of 10% skin absorption is chosen. However, the basic nature of APDEA would be expected to cause some skin corrosion, and this was observed in the acute dermal toxicity study. If the substance is a skin irritant or corrosive, damage to the skin surface may enhance penetration. Considering the low acute toxicity observed by oral gavage, it is difficult to determine if the low acute dermal toxicity is due to a low dermal penetration and/or the low intrinsic toxicity of APDEA. Therefore, a default dermal absorption of 100% will be used for risk assessment.


Oral absorption:

The low molecular weight and high water solubility of APDEA favour oral absorption. The substance can readily diffuse across the biological membranes, but this process might be hampered because of low log Pow. It is therefore important to consider both, the water solubility of a substance and its log Pow value, when assessing the potential of that substance to be absorbed. The pKa of APDEA suggests that this substance will be predominantly in its non-ionized form at physiological pH.

There were no signs of systemic toxicity following a single oral dose of 2000 mg/kg bodyweight to male or female rats, with all animals showing an overall weight gain during the study and no abnormalities noted at necropsy. In the 28 day oral dose study, parental toxicity was observed at the top dose level of 1000 mg/kg bodyweight/day, but this was not corroborated by toxicologically relevant microscopic findings. No reproductive or developmental toxicity effects were observed at any dose level. Minimal to slight treatment related stomach findings were observed in the 28-day study and are attributed to the irritancy of APDEA. Even though APDEA is expected to be readily absorbed, systemic toxicity was only observed following high, repeated dose exposures, indicating a low order of toxicity of APDEA. In addition, the data indicated that APDEA would be cleared from the system rapidly.



APDEA has a low vapour pressure (0.0011 Pa at 25°C) and therefore inhalation of the substance is not anticipated. Furthermore, the high water solubility of APDEA means that any inhaled vapour is likely to become trapped within the fluids lining the upper respiratory tracts and will eventually be swallowed. Thus, any inhaled APDEA reaching the lungs is likely to be readily absorbed into the blood stream due to the high water solubility and low molecular weight of APDEA.



Any APDEA that is absorbed will be distributed via the blood to the liver and other organs and tissues. Due to its high water solubility and hydrophilic nature, it will tend to remain in the circulating blood and will not distribute into fatty tissues. The changes in organ weights (including those of the liver and kidneys) at the top dose level in the 28-day rat study provide evidence that the substance is distributed to several limited tissues, and changes to haematological and clinical chemistry parameters are also evidence of distribution.



Based upon the structure, low molecular weight and high water solubility of APDEA, it is anticipated that any intact APDEA reaching systemic circulation would be rapidly eliminated, either unchanged or after hydrolysis and/or glucuronide conjugation.



APDEA is of low molecular weight and is highly water soluble, therefore it is expected that any APDEA that is absorbed will be primarily eliminated unchanged via the urine. Any oxidation products or glucuronide conjugates that are formed would also be expected to be eliminated primarily in urine.