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EC number: 202-826-9
CAS number: 100-18-5
The test article, p-diisopropylbenzene, was evaluated in a 2-week
(subacute) oral toxicity study. Groups of five male rats were gavaged
with 1000 or 100 mg compound/ kg/day for a total of eleven treatments
over a 15 day span. A control group of five animals were gavaged with
distilled water at a dose of 1000 mg/kg/day. Weight gain and feed intake
were comparable between groups. No abnormal clinical signs were observed
with the exception of a single high-dose animal which exhibited
porphyrin nasal discharge, weight loss, and possible aspiration
pneumonia. Several slight but statistically significant differences were
noted in hematology in the high dosed group at autopsy. These included a
slight increase in platelets and an increased percentage of monocytes.
Both increases were dosage related. All other hematological parameters
(red blood cell count, hemoglobin concentration, hematocrit, red cell
indices, white blood cell counts and the remaining portions of the
differential white blood cell count) were comparable to controls. There
was a moderate decrease in serum glucose and a slight increase in
creatinine in the high dosed animals, but all other serum clinical
chemistries (alanine aminotransferase, aspartate aminotransferase,
sorbitol dehydrogenase, alkaline phosphatase, and urea nitrogen) were
unaffected by treatment. No alterations in hematology or serum clinical
chemistry were noted in blood from the low dose group.
No significant changes in absolute or relative kidney or spleen weights
were noted. There was, however, a trend which implied a dose dependent
increase in both absolute and relative liver weights. The relative liver
weights were statistically significantly increased in the high dose
group. Gross pathology examination revealed enlarged hearts in 3/5 high
dosed animals but no compound related effects were seen at
histopathology examination. The enlarged hearts were observed in animals
exhibiting extensive consolidation of the lung. The hearts in these
animals may have hypertrophied in response to general respiratory stress
resulting from compromise of the lung. The liver may be a site of toxic
action, and the no effect level (NOEL) may be in the range of 100 mg/kg.
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