TOXICITY OF PURE
EXACHLOROBENZENE AND HCB-CONTAMINATED PORK TO CATS
Eighteen domestic short-hair queens were obtained from a commercial source and conditioned for up to four months. Four did not respond well and were eliminated from the study early while a fifth incurred a severe infection one week after dosing began and was also
eliminated. The queens weie housed in 1.1 X 0.8 X 0.8 m stainless steel
cages equipped with wooden shelves for comfort. Food (Wayne’s Complete, Allied Mills, Chicago, IL) and water were provided ad lib, except
that the food was removed overnight prior to dosing.
For all dosing, 97% pure HCB was further purified by repeated recrystallization from hot benzene to greater than 99.5% purity. To generate
the pilot contaminated pork, a weanling gilt was fed a standard swine
ration containing 110 ppm purified HCB for 3 weeks and then feed was
restricted for 7 days to cause an increased concentration of stored HCB
residues (Villeneuve 1975). The carcass was trimmed, ground and subdivided in 50 g spheres which were covered and baked at 130°C for 1.5
hr. The liver from this gilt was processed in a similar manner, except
that the spheres weighed 46 g. The cooked pork spheres were frozen,
thawed individually and fed to the queens each morning following an
overnight fast.
After confirming that the cats would readily accept the cooked pork,
a second gilt was fed for 6 weeks and fasted for 10 days in order to
achieve a higher HCB concentration. A control gilt was treated similarly. The cooked pork contained 43 ? 6% water, 12 * 5% fat, 1.04 f 0.37
ppm Cu and 0.38 f 0.10 ppm Zn as determined from replicate analysis
of 2 batches. Fresh weight HCB concentration (mean ? S.D. for 2
replicate analysis of 2 batches) in the pork were: pilot gilt pork = 18.2
f 2.0 ppm; pilot gilt liver = 41.6 f 3.6 ppm; 2nd gilt = 40.0 * 3.5 ppm;
control gilt < 0.05 ppm. Weight loss on cooking was 25-35% and
cooked pork from gilt 2 contained 98.1 f 15.6 ppm HCB (mean ? S.D.
for n = 8). Some increase in HCB concentration was anticipated due to
weight loss during cooking, but part of the apparent 2%-fold increase
was probably due to migration of fat (and HCB) toward the periphery
of the sphere from where the samples were taken.
RESULTS AND DISCUSSION
Although the concentration of HCB in the pork was quite high compared to chronic swine feeding studies (Hansen et al. 1977). The relative
daily and total doses for cats (Table 1) were not as high as doses
previously administered to other animals to elicit toxic effects (Gralla
et al. 1977; Hansen et al. 1977; Kuiper-Goodman et al. 1977). Up to 2
mg/day were administered to the cats for 24 days with no notable signs
of toxicity. Weight loss and hepatomegally were observed at the higher
doses administered in gelatin capsules (Table 2).
Serum chemistries were well within normal ranges and did not vary
with treatment. There were no adverse changes in the hematology of
queens fed HCB contaminated pork (Table 3). Group I1 cats, receiving
the liver, apparently responded to the additional Fe, Cu and some B,