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several benign adenomatous lesions in the liver, but no statistical comparisons were made. In these
studies, small sample sizes (10 per group), less than lifetime exposure, and excess deaths unrelated to
PCB exposure prevented definitive conclusions about the carcinogenicity of PCBs.
The NCI (1978) conducted a 2-year bioassay on male or female Fisher-344 rats (24 per group)
exposed to Aroclor 1254 in the diet. Concentrations of PCBs in the feed were 0, 25, 50, or 100 ppm.
A significant increase in the numbers of lymphomas and leukemias was observed in the male rats. The
NCI did not conclude that these hematological tumors were treatment related. The incidence of
hepatocarcinomas in the male rats was 0/24, 1/24, and 3/24 for the 0, 50, and 100 ppm groups,
respectively. In other tissues, such as the stomach, jejunum, and cecum, rare tumors were found. The
incidence of these tumors, while not statistically significant, were considered to be treatment-related due
to the low incidence of these tumors in historical controls. The NCI concluded that PCBs were capable
of inducing proliferative lesions in the liver, but were not carcinogenic to rats in this bioassay.
A reanalysis of the NCI data by Morgan et al. (1981) found that the incidence of focal metaplasia in the
stomach increased in a dose-dependent fashion with a 6, 10, 17, and 35% occurrence in the 0, 25, 50,
and 100 ppm groups, respectively. The incidence of stomach adenocarcinomas was significantly higher
than in historical controls (4% vs. 0.03%, p < 0.001). With this reanalysis, the authors concluded that
Aroclor 1254 was carcinogenic.
A chronic dietary exposure to Aroclor 1260 in rats was reported by Kimbrough et al. (1975). In this
study, 200 young rats were fed 0 or 100 ppm Aroclor 1260 for 94 weeks. Actual dosages of PCB
were estimated to be 11.6 mg/kg/day for the first week, 6.1 mg/kg/day at 3 months, and 4.3 mg/kg/day
at 20 months. The time-weighted average dose was estimated to be 4.42 mg/kg/day (U.S. EPA,
1985). Almost all treated rats developed liver nodules (170/184). In addition, the incidence of
hepatocellular carcinomas was highly significantly increased over controls (1/173 for controls vs. 26/184
for treated rats; p < 1.0E-6). Neoplastic nodules and total neoplastic lesions were also highly
significantly increased over concurrent controls.
Schaeffer et al. (1984) reported results from a 2-year bioassay in rats using 2 PCB mixtures: Clophen
A 30 (30% chlorine by weight) and Clophen A 60 (60% chlorine by weight) in the diet. Groups
consisted of approximately 140 male weanling rats exposed to 100 ppm of either Clophen A 30 or
Clophen A 60. A significant increase in the percentage of hepatocellular carcinomas was seen in the
rats treated with Clophen A 60 (62%), but not with Clophen A 30 (3%). Hepatocarcinomas were
observed in 2% of control animals. Preneoplastic lesions were not observed before 71 weeks.
The incidence of hepatocarcinoma was increased in rats exposed to Aroclor 1260 in a 2-year study by
Norback and Weltman (1985). In this study, 70 male or female rats were exposed to 100 ppm
Aroclor 1260 in the diet for 16 months, followed by 50 ppm in the diet for 8 months. The timeweighted
average doses were calculated to be 5 mg/kg/day for the male rats, and 4.2 mg/kg/day for the
females. The incidence of neoplastic lesions in control rats living 18 months or longer was 1.2% (1/81).
The treated rats had an incidence of 95% (45/47) for the females, and 15% (7/46) for the males. The
combined tumor incidences were significantly higher in treated rats compared with controls. The
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