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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Genetic toxicity in vitro

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

Genetic toxicity in vivo

Endpoint conclusion
Endpoint conclusion:
no study available

Additional information

There are no data available on genetic toxicity of 2 -amino-1,3-propanediol (APD). However, there are reliable data for another member of the chemical category APD belongs to. Therefore, read-across was performed based on a category approach. Within this chemical category, the members are 2-amino -1,3-propanediol (APD), 2-amino-2-methyl-1,3-propanediol (AMPD) and AEPD, collectively called aminopropanediols. All the members contain a propane backbone carrying the same functional groups, one primary amine group and two hydroxyl groups, at the same position. The three category members differ only in the length of the alkyl side chain, which contains 0, 1 or 2 carbon atoms for APD, AMPD and AEPD, respectively. The modelling of potential metabolites via the OECD QSAR toolbox v.2.0 (2010) did not predict relevant metabolites of the category members. Based on the chemical structure of the parental compounds, no metabolism is expected. Therefore, it can be assumed that aminopropandiols will not show reactive properties under in-vitro and in-vivo test conditions.

All the category members are of low concern with regard to systemic toxicity. Available studies via the oral, dermal and intraperitoneal route indicate low acute and repeated dose toxicity. Inhalation is of no concern, because the low vapour pressure means that exposure is unlikely to occur.The results of the acute studies, as well as the repeated dose studies, demonstrate that the main cause of toxicity was the intrinsic alkalinity of the category members at the site of contact.The Cramer classification (related mainly to the oral route) also indicates a low toxicological concern for all the category members. No metabolism by cytochrome P450 enzymes in-vivo is expected; this is supported by predictions from QSAR modelling. With respect to molecular structures, no mutagenic potency is predicted using QSAR modelling and no structural alerts were detected. “H-acceptor-path3-H-acceptor” is alerted in a large number of molecules and thus of practically no prediction value. Due to the structural similarity between the members of the category and the similar toxicological properties, APD, AMPD and AEPD form a robust chemical category and read-across within this category is justified. In conclusion, it is considered appropriate to read-across from AEPD (CAS 115-70-8) to APD within the category approach.

The in vitro genetic toxicity of 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 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 conformatory gene mutation assay. At the highest tested concentration, AEPD caused cell growth inhibition, evaluated by relative cloning efficiency.

Taking into account all available data, AEPD showed no evidence of a clastogenic and mutagenic potential with and without metabolic activation in in-vitro test systems. Therefore, it can be assumed that APD possesses no genotoxic potential. Based on read-across within the chemical category, APD is considered to be not genotoxic.

Justification for classification or non-classification

Based on read-across within the chemical category, the available data on genetic toxicity 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.