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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Key value for chemical safety assessment

Additional information

Assessment of the toxicokinetic behaviour



The absorption has not been quantified; however, using the Danish QSAR database, the gastrointestinal absorption of a closely related substance (CAS No. 68155-05-5) was predicted to be 100% (1 mg dose). As Atmer 163 is a corrosive substance, no acute dermal or inhalation toxicity studies were performed. The bioavailability via the dermal route has thus not been examined experimentally. Considering the corrosive nature of the substance, it is reasonable to assume that exposure may cause damage to the skin, subsequently facilitating dermal uptake. Using the Danish QSAR database, the dermal absorption of a similar substance (CAS No. 68155-05-5) was estimated to be 0.00400 mg/cm²/event, which is relatively low. It is likely that the corrosive effect increases bioavailability due to a loss of skin barrier integrity. For risk assessment purposes, the bioavailability via the inhalation route is considered to be similar to that of the oral route, i.e. quantitative.  



No information is available regarding the metabolism of Atmer 163 specifically. The potential metabolites of a closely related substance (CAS No. 68155-05-5) in liver, skin and gastrointestinal tract were simulated using the QSAR OECD Toolbox 1.1.02. 23 hepatic metabolites were predicted. These metabolites arise from hydroxylation, N-dealkylation, and oxidation, especially beta-oxidation of intermediary fatty acids. The main reaction is most likely a dealkylation, to diethanolamine and a primary alcohol. The alcohol is typically further metabolized to a fatty acid that enters into fatty acid catabolism, and is ultimately metabolized to carbon dioxide and water. Diethanolamine is readily metabolized to monoethanolamine, which is known to be a part of the phospholipid synthesis pathway (see the KEGG database, In repeated dose studies on rats, exposure to diethanol­amine bioaccumulated in (among other) liver and kidney tissue lead to increasing levels of aberrant phospholipids and histopathological lesions (Knaak JB et al, 1997; Mathews JM et al, 1995). As the subchronic rat and dog studies did not reveal any significant histopathological changes in liver or kidneys, the bioaccumulation of diethanolamine as a metabolite of Atmer 163 is not expected to occur under experimental dosing conditions. In the skin, two metabolites were predicted, with one or two carboxy groups. These are expected to be metabolized via the same pathways as described for the liver metabolism.



Atmer 163 has a molecular weight lower than 500 u and is relatively water soluble. The QSAR simulation furthermore predicts that Atmer 163 will primarily be metabolised to molecules that are utilized in well-known human metabolic pathways. Therefore, Atmer 163 is likely to be excreted as breakdown products of these metabolic pathways. The secondary route of excretion is expected to be via the urine, including any minor hepatic metabolites.


Reference list


Knaak JB et al. Toxicology of mono-, di- and triethanolamine. Rev Environ Cont Toxicol 1997; 149:1-86. Abstract.


Mathews JM et al. Metabolism, bioaccumulation and incorporation of diethanolamine into phospholipids. Chem Res Toxicol 1995; 8(5): 625-633. Abstract.


Mathews JM et al. Diethanolamine absorption, metabolism and disposition in rat and mouse following oral, intravenous and dermal administration.Xenobiotica 1997; 27(7): 733-746. Abstract.