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EC number: 231-272-0
CAS number: 7473-98-5
The test material (164 Da) is a yellowish
liquid, well soluble in water (13.3 g/l). The material has a density of
1.08 g/cm3 and the boiling point is at 252 °C. A vapour pressure of
0.0057 hPa indicates a very low volatility. The log Pow is 1.62 (at pH
The substance is sensitive to UV-light
induced photocleavage as it was designed to serve the technical function
of a photoinitiator.
In acute oral and dermal toxicity studies,
rats were administered to the test substance. Mortality was observed in
all treatment groups after oral administration (with exception of the
lowest dose level) in a dose dependent manner. A few minutes after oral
application animals showed sedation, dyspnoe, decreased activity and
proned position. In animals which died fatty liver infiltration and
dilation of the bladder (starting at 1800 mg/kg) as well as mucous
content of the intestine (starting at 2000 mg/kg) was observed. Single
dermal application resulted in mortality from 5000 mg/kg bw onward.
Gross pathology of deceased animals revealed fatty infiltration of the
liver and dilation of the urinary bladder with hemorrhaging of the
mucosa (starting at 6400 mg/kg). Furthermore, staggered gait and
decreased activity were observed. The NOAEL in male and female rats in a
subacute oral repeated dose study is 300 mg/kg bw due to changes in
liver and kidney weight as well as centrilobular hypertrophy and
hepatocellular proliferation. Administration of the substance over a
subchronic period resulted in gait ataxia in high dose males.
Furthermore, basophillic tubules and granular cast in the kidneys were
observed. Calcium oxalate and crystals were found in the urine of the
top dose animals. The NOAEL after subchronic oral administration is
therefore considered to be 50 mg/kg bw. In regard to the results of the
acute and longterm studies and considering the low molecular weight
uptake of the substance from the gastro-intestinal system is most
likely. The test substance cannot undergo pH-dependent hydrolysis in the
stomach, thus, the unchanged (parent) substance is taken up into the
system. According to the model of Fitzpatrick , the test item is
moderately skin permeable.
The results obtained from the subchronic
toxicity study indicate the test item forms a complex with Ca2+ (2:1). A
subsequent decrease of systemic calcium may cause mobilisation of
calcium from the bones which results in turn in increased Ca-levels (as
observed in the 90d study). Additionally, the Ca-complexes are
presumably precipitated in kidney and urine.
Concerning xenobiotic metabolism, reduction
of the aliphatic ketone followed by glucuronidation of the
hydroxyl-groups seems plausible. Subsequently,
the test substance will be excreted effectively. The primary elimination
pathway of the test substance will be the urinary excretion of parent
compound and the glucuronidation product.
The low molecular weight of the test
item and its solubility in water enhance renal excretion. However,
precipitation of the Ca-bound complex and crystal formation in kidney
and urine was observed at the highest dose level when applied over a
subchronic period. It is acceptable to assume that the precipitated
material will be excreted over the time after discontinuation of
administration. Accumulation in the body is therefore not expected.
 Modelling skin permeability
in risk assessment––the future, D. Fitzpatrick et al, Chemosphere 55
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