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total); an untreated control group was included in the study (Gothoskar et al., 1970). Interim sacrifices<br />

were performed at 6, 9 and 13 months. An increased incidence of liver tumors (hepatomas) was noted<br />

in both males and females. Tumor incidence data is listed in Table 1.<br />

Table 1.<br />

Thioacetamide-induced hepatoma incidence in male and female Swiss mice<br />

(Gothoskar et al., 1970)<br />

Dose group Average dose 1<br />

(mg/kg-day)<br />

Tumor incidence<br />

male control 0 0/6<br />

male treated 36 6/6<br />

female control 0 0/6<br />

female treated 39 6/7<br />

1. Doses as reported by Gold et al. (1984).<br />

2. Tumor incidences as reported by Gold et al. (1984).<br />

IV.<br />

DERIVATION OF CANCER POTENCY<br />

Basis for Cancer Potency<br />

Gold et al. (1984) list results from the study of thioacetamide by Gothoskar et al. (1970) in male and<br />

female Swiss mice. A total of 89 mice of both sexes were fed a diet containing 0.03% thioacetamide<br />

for 6, 9, 13 or 17 months. The group studied for 17 months consisted of 12 control mice (6 male and 6<br />

female) and 13 treated mice (6 male and 7 female). Hepatomas were seen in all treated male mice,<br />

precluding estimation of the upper bound on potency in these animals. Females were slightly less<br />

sensitive; six of the seven dosed female mice developed hepatomas. Because this is the only doseresponse<br />

data available in Gold et al., the data for the females are used to derive potency (see Table 1).<br />

The value presented here may be an underestimate, but is the best value currently available (Cal/EPA,<br />

1992).<br />

Methodology<br />

Expedited Proposition 65 methodology (with cross-route extrapolation) was used to derive a cancer<br />

potency factor. A unit risk factor was then calculated by <strong>OEHHA</strong>/ATES from the cancer potency<br />

factor using a reference human body weight of 70 kg and an inspiration rate of 20 m 3 /day.<br />

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