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EC number: 208-584-0
CAS number: 534-03-2
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
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
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
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