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EC number: 700-071-4
CAS number: 932742-30-8
Hardener LI is designed to rapidly react upon contact with water, which
is reflected in its properties. The hydrolysis reaction is catalysed in
an acid environment. The molecular weight is 703.13 g/mol, the
calculated partition coefficient logPow is 16.97, the estimated water
solubility is 1.065E-13 mg/L and the experimental determined vapour
pressure is 0.00138 Pa at 25°C.
on the low vapour pressure corresponding to a low volatility potential,
inhalation of the substance as a vapour to a high extend is unlikely.
estimated partition coefficient indicates that the compound is not
likely to penetrate skin. However, even if dermally absorbed, its
toxicity is very low. An acute dermal toxicity study revealed a LD50 >
2000 mg/kg in a limit dose test. No local irritation effects were noted
in the acute dermal toxicity study, therefore testing of dermal
irritation was waived. An eye irritation test with rabbits showed no eye
irritation effects. In the local lymph node assay (LLNA), SIKA Hardener
LI revealed sensitization potential. Furthermore, the aldehyde
hydrolysis product did not cause any systemic toxicity, following dermal
application (LD50 > 2000 mg/kg bw) nor did any of the polyamines formed
(LD50 > 2000 mg/kg bw).
products might be absorbed to a small extend following oral application
as indicated by a subchronic oral repeated dose toxicity study, which
revealed a NOAEL of 300 mg/kg bw/day in female rats due to changes in
spleen weights at the highest dose tested (1000 mg/kg bw/day). Due to
its high reactivity, orally ingested SIKA Hardener LI will undergo
spontaneous hydrolysis upon reaching the stomach, especially as the
hydrolysis reaction is acid catalysed. The portion of SIKA Hardener LI
not immediately hydrolysed will, most probably, not solubilise in the
stomach, due to its low solubility. Consequently, SIKA Hardener LI is
not likely to cross GI-tract membranes.
together, absorption of SIKA Hardener LI and consequently
bioavailability is rather unlikely. However, some effects were revealed
by a subchronic oral toxicity study as mentioned above. The products of
SIKA Hardener LI decomposition are the aldehyde
2,2-dimethyl-3-lauroyloxy-propanal and respective diamine
(3-aminomethyl-3,5,5-trimethylcyclohexylamine). The aldehyde is not
stable in water-based systems and further degrades, forming carbonic
acid and several short-chain polar compounds. The polyamine formed might
also be transformed further, most likely in enzyme catalysed metabolism.
Even though the SIKA Hardener LI degradation products might be absorbed
and become bioavailable, they are of low toxicity. One of the most
important pathways of aldehyde metabolism is oxidation to carboxylic
acids by aldehyde dehydrogenases (Vasiliou et al., 2000). The enzymes
involved in these detoxification reactions most probably belong to the
category of aldehyde dehydrogenases, known to be relatively substrate
unspecific, but effective in protecting organisms from potentially
harmful xenobiotics (Sladek, 2003). Other phase I metabolic reactions
may include cytochrome P450 mediated transformations such as aldehyde
reductions or aldehyde scissions. Following phase I metabolic reactions
or chemical decomposition, the formed metabolites are rendered more
polar by phase II metabolism. Most likely the carboxylic acid
metabolites are ultimately conjugated with glycine or glutamine and
excreted in urine or bile. Any polyamine, formed by hydrolysis of SIKA
Hardener LI, that reaches the body’s systemic circulation is probably
either excreted in unchanged form or metabolised by the cytochrome P450
system or by amine oxidases. Phase I metabolism of polyamines is likely
to be followed by phase II metabolism, possibly rendering molecules even
more polar. Likely conjugation compounds are glycine and glutamine,
preceding the metabolites eventual elimination in urine or bile.
Toxicokinetic assessment of hexamethylenediamine (EC IUCLID, 2000), used
as a model compound, revealed that the amine is rapidly distributed
systemically following i.v. administration to rats, and completely
excreted within 72 hours, via urine (47 %), feces (27 %) and respiration
excretion can be assumed for all polyamine degradation products.
Excretion analysis in humans following oral administration, using the
same model compound hexamethylenediamine, revealed that more than 90 %
is eliminated in urine, during the first 10 hours post administration,
either unchanged or metabolised to 6-aminohexanoic acid. A human
inhalation study revealed that 90 % were eliminated within the first 28
hours following exposure to 25μg/m3.
In a second human inhalation study and exposure to 30μg/m3,
90 % hexamethylenediamine was eliminated via the urine within the first
three hours. For the human inhalation studies the renal half-life of
hexamethylenediamine was determined to be 1.4 hours and 1.2 hours,
respectively. A similar excretion pattern can be assumed for all
polyamine degradation products in humans. It is unlikely that metabolism
will render neither the parent compound nor its degradation products
more toxic. This assumption is supported by results obtained in an in
vitro Ames test, a chromosome aberration test and a mouse lymphoma
assay. In all three assays no significant increases in toxicity were
noted, in the presence of a rodent microsomal S9-fraction. This clearly
indicates that formation of reactive metabolites is unlikely. Based on
the reactive nature of SIKA Hardener LI and its limited stability in
water-based systems, bioaccumulation is not likely to occur. Orally
consumed hardener is most rapidly hydrolysed to aldehyde and diamine,
with the reaction being acid catalysed. Even though the degradation
products might be absorbed and become bioavailable, toxicity is low and
bioconcentration rather unlikely. Absorbed or bioavailable degradation
products are probably excreted, either in original form or further
metabolised, prior to elimination via urine or bile.
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
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