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Table 4.<br />

Epichlorohydrin-induced forestomach tumor incidence in male and female Wistar rats<br />

(Wester et al., 1985)<br />

Sex<br />

Dose level<br />

(mg/kg body weight)<br />

Tumor type<br />

Tumor incidence<br />

male 0 papilloma 1/50<br />

2 6/49<br />

10 4/49<br />

0 squamous cell carcinoma 0/50<br />

2 6/49<br />

10 35/49<br />

female 0 papilloma 2/47<br />

2 3/44<br />

10 0/39<br />

0 squamous cell carcinoma 0/47<br />

2 2/44<br />

10 24/39<br />

IV.<br />

DERIVATION OF CANCER POTENCY<br />

Basis for Cancer Potency<br />

Cancer potency values are based on the most sensitive site, species and study demonstrating<br />

carcinogenicity of a particular chemical, unless other evidence indicates that a value derived from that<br />

data set would not be appropriate (CDHS, 1985). Several studies describe ECH-induced tumor<br />

incidence data which can be used to generate a cancer potency factor (male Wistar rat forestomach<br />

papilloma and squamous cell carcinoma data, Konishi et al. (1980); male Sprague-Dawley rat nasal<br />

tumor data, Laskin et al. (1980); male and female ICR/HA Swiss mouse forestomach squamous cell<br />

carcinoma data, Henschler et al. (1984); male and female Wistar rat papilloma and squamous cell<br />

carcinoma data, Wester et al. (1985). The data from the study by Konishi et al. (1980) was chosen<br />

by CDHS (1988) as the basis for a cancer potency factor for ECH. Data from the Laskin et al. (1980)<br />

study was considered to be less suitable for generating a cancer potency factor than data from the<br />

Konishi et al. (1980) study because of the poor survival of the study animals. The studies by Henschler<br />

et al. (1984) and Wester et al., (1985) contained potential confounding factors. The ECH-exposed<br />

animals in the Henschler et al. (1984) study were also exposed to trichloroethylene. The animals used<br />

in the Wester et al. (1985) study exhibited trichobezoar-induced intestinal obstructions early in the<br />

study due to the diet composition; CDHS (1988) noted that those obstructions could have been a<br />

contributing factor to the observed forestomach carcinogenesis.<br />

280

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