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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Description of key information

2-Diethylaminoethanol was not carcinogenic to rats when given by feed for 2 years in a limited 1960’s study (tested up to ca. 50 – 400 mg/kg/d). While this data is limited, the lack of a carcinogenic effect of 2-diethylaminoethanol is supported by the negative data for genotoxicity.

Key value for chemical safety assessment

Carcinogenicity: via oral route

Endpoint conclusion
Dose descriptor:
50 mg/kg bw/day

Justification for classification or non-classification

2-Diethylaminoethanol (DEAE) was not found to be carcinogenic to rats in a 2 -year repeated dose feeding study conducted in the sixties, i.e., prior to the implementation of the current guidelines. Nevertheless, the data obtained from this study are acceptable for assessment and indicate lack of a carcinogenic potential for DEAE, which is further supported by negative data for genotoxicity.

Thus, there is no need for classification according to the EU Directive 67/548/EEC and to the CLP Regulation EC/1272/2008.

Additional information

The carcinogenic potential of DEAE was examined within a 2 year repeated dose feeding study (Pennsalt 1967; Val. 2). Each test group comprised 35 rats/sex whereas the control group comprised 60 rats/sex. The testes dose levels were 0, 200, 500 and 1000 ppm, corresponding to ca. 11, 25 and 50 mg/kg bw/day. It has to be noticed that the initial high dose level of 1000 ppm (i.e. 50 mg/kg bw/day) was increased step by step over the course of the study until reaching 10,000 ppm (i.e., ca. 400 mg/kg bw/day). The data referring to the systemic toxicity are entered and discussed in IUCLID chapter 7.5.1. Referring to carcinogenicity, tumours were found in both sexes in all control and treated groups. The majority (more than 90%) of the tumours appeared within the final 6 months of the study or were discovered at the time of necropsy. As evidenced by the gross necropsy and micropathological results, the onset, type, size and frequency of the tumours were similar amongst the DEAE-treated and control groups, and the development of the neoplastic structures within the test groups could not be related to ingestion of the test preparation in the diet. Thus, no carcinogenic potential could be evidenced for DEAE in the present 2 -year repeated dose feeding study.