Registration Dossier

Administrative data

Key value for chemical safety assessment

Genetic toxicity in vitro

Description of key information

AEPD was negative in the following in vitro mutagenicity asssays:
Gene mutation (bacterial reverse mutation assay / Ames test): S. typhimurium TA 1535, TA 1537, TA 98, TA 100 and E. coli WP2 uvrA: negative with and without metabolic activation (according to OECD 471)
Chromosome aberration (in vitro mammalian chromosome aberration test): negative with cultured Chinese hamster lung cells with and without metabolic activation (according to OECD 473).
Gene mutation (in vitro mammalian cell gene mutation test): negative with Chinese hamster ovary cells with and without metabolic activation (according to OECD 476).

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed (negative)

Genetic toxicity in vivo

Endpoint conclusion
Endpoint conclusion:
no study available

Additional information

The in vitro genetic toxicity of 2-amino-2-ethyl-1,3-propanediol (AEPD) was investigated in a bacterial reverse mutation assay (Ames test) according to OECD 471 (Mochizuki, 2004). The preincubation method was conducted with S. typhimurium strains TA 1535, TA 1537, TA 98, TA 100 and E. coli WP2 uvrA at concentrations up to 5000 µg/plate. AEPD did not induce reversions in any of the S. typhimurium strains or in E. coli WP2 uvrA with or without metabolic activation. No cytotoxic effects were observed and all positive controls were valid.

In a study according to OECD 473, the potential of AEPD to induce chromosomal aberrations was tested in cultured Chinese hamster lung (CHL) cells (Sono, 2004). CHL cells were exposed to AEPD at concentrations up to 1200 µg/mL. No increase in chromosomal aberrations was observed in the experiments with short-term treatment (6 h) in the presence or absence of metabolic activation. No cytotoxic effects were observed and the positive controls were valid. Because of the negative results of the short-term treatment, an additional testing without metabolic activation was performed with continuous treatment (24 and 48 h). After continuous treatment, AEPD did also not induce chromosomal aberrations in CHL cells.

AEPD was also tested for its potential to cause gene mutations in an in vitro mammalian cell mutation assay according to OECD 476 (Indrani, 2011). Chinese hamster ovary (CHO) cells were treated with AEPD at concentrations of up to 1192 µg/mL for 4 h both with and without metabolic activation. After an expression time of 9 days in growth medium, cells were incubated for 10 days with 6 -thioguanine as selection agent for forward mutation at the HPRT locus. Both with and without metabolic activation, no increases in mutant frequency were observed in the initial and in the confirmatory gene mutation assay. At the highest tested concentration, AEPD caused cell growth inhibition, evaluated by relative cloning efficiency.

AEPD showed no evidence of a clastogenic and mutagenic potential with and without metabolic activation in in-vitro test systems.


Short description of key information:
In vitro:
Gene mutation (bacterial reverse mutation assay / Ames test): S. typhimurium TA 1535, TA 1537, TA 98, TA 100 and E. coli WP2 uvrA: negative with and without metabolic activation (according to OECD 471)
Chromosome aberration (in-vitro mammalian chromosome aberration test): negative with cultured Chinese hamster lung cells with and without metabolic activation (according to OECD 473).
Gene mutation (in-vitro mammalian cell gene mutation test): negative with Chinese hamster ovary cells with and without metabolic activation (according to OECD 476).

Endpoint Conclusion: No adverse effect observed (negative)

Justification for classification or non-classification

The available data on genetic toxicity of the test substance do not meet the criteria for classification according to Regulation (EC) 1272/2008 or Directive 67/548/EEC, and are therefore conclusive but not sufficient for classification.