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.


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,


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