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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Key value for chemical safety assessment

Additional information

In vitro studies

DEA was tested for mutagenicity in the Ames test with and without metabolic activation. No mutagenic effect was observed in the Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537 tested in the concentration range from 33 - 3333 µg/plate (Haworth et al, 1993; NTP, 1992, 1999). No mutagenic effect was reported in other investigations using Salmonella typhimurium or Escherichia coli strains and concentrations from 125 – 4000 µg/plate (Dean et al., 1985).

No clastogenic potential of DEA was noted in a cytogenetic study comparable to OECD TG 473 in Chinese Hamster Ovary (CHO) cells in the absence (101, 505, 2010 µg/ml) and presence (303, 1010, 3010 µg/ml) of metabolic activation (Loveday et al., 1989). A chromosome damaging potential was also not noted in cultured rat liver epithelium-like RL1and RL4 cells at concentrations ranging from 0.125 - 0.5 of GI50 (50% growth inhibition) without metabolic activation (Dean et al., 1985).

DEA induced no sister chromatid exchanges in Chinese hamster ovary cells (similar to OECD TG 479) at concentrations from 150 – 1500 µg/ml with and without metabolic activation (Loveday et al., 1989).

A mouse lymphoma test comparable to OECD TG 476 carried out in the L5178 Y cell line with concentrations of 0, 25, 50, 100, 200, 300, 400, 600 µg/ml without and with S-9 mix showed no genotoxic potential up to the highest/cytotoxic concentration (Myhr et al., 1986; NTP, 1992, 1999).

In vivo studies

DEA was investigated for its clastogenic/genotoxic potential in vivo in a mouse micronucleus test in the peripheral blood. Male and female B6C3F1 mice were administered DEA in 95% ethanol once per working day to the uncovered skin at concentrations of 0, 37.5, 75, 150, 300, and 600 mg/ml (corresponding to 0, 80, 160, 320, 630, or 1250 mg/kg bw/day) for 13 weeks (65 applications) using a protocol equivalent or similar to OECD guideline 474. DEA treatment led to local and systemic signs of toxicity down to the lowest dose level. No induction of micronuclei was noted at any dose level (NTP, 1992; Witt et al., 2000).

Short description of key information:
DEA did not induce reverse mutations in Salmonella typhimurium or Escherichia coli.
In mammalian in vitro systems, DEA did not induce chromosomal aberrations in rat hepatocytes, sister chromatid exchange or chromosomal aberrations in Chinese hamster ovary cells and gene mutation in mouse lymphoma cells.
DEA formulated in ethanol did not induce micronuclei in vivo in peripheral blood erythrocytes of mice after repeated unoccluded dermal application for 13 weeks at doses clearly showing systemic availability.

Endpoint Conclusion: No adverse effect observed (negative)

Justification for classification or non-classification

Based on the available data, DEA does not need to be classified for genotoxicity according to Annex I of Directive 67/548/EEC and according to the EU Classification, Labelling and Packaging of Substances and Mixtures (CLP) Regulation (EC) No. 1272/2008.