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The power of this study can be criticized, with exposures as rare as they were. Also, the inclusion of
cancer cases from the early 1960s can be questioned. These cases would not have had sufficient
latency to have been caused by an exposure in Vietnam.
In 1983, an Australian Royal Commission began investigating the effects of Agent Orange exposure to
Australian Vietnam veterans. However, their report, released in 1985, does not supply much
information on the effects of PCDDs. The executive summary concluded that "only a very limited
number of Australian servicemen were ever directly exposed," and further, that the dose received by the
majority of Australian veterans was "so minute that it may, without doubt, be ignored," (e.g., it noted
that no Australians developed chloracne). Not surprisingly, the Commission found no evidence of any
cancer excess among the "exposed" servicemen (Royal Commission, 1985).
Abate et al. (1982) summarized the series of studies following the 1976 accidental release of TCDD
from a TCP-producing plant in Seveso, Italy. The investigators looked at mortality rates for 11
municipalities for four years after the accident and reported no increase in cancer mortality. These
studies served mainly to provide baseline rates for future studies, because clearly not enough time had
elapsed to provide the minimum 10 to 20 years required for an increased cancer risk to become
manifest (Bruzzi, 1983).
Animal Studies
Van Miller et al. (1977 a,b) reported the results of a study in which rats were fed diets containing from
1 ppt to 1 ppm of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) for 78 weeks. Surviving rats were
killed after 95 weeks. Laparotomies were performed on all surviving rats at 65 weeks and all tumors
were biopsied. Rats in the three highest dose groups, receiving 50 ppb or more, died early. A variety
of tumors were found in rats receiving 5 ppt to 5 ppb while no-neoplasms were found in the control or
low-dose groups. The absence of tumors in these two groups is unusual in this strain of rats. In
addition, because of the small number of animals in each group (10) the study was inadequate to
determine the carcinogenic potential of TCDD.
Toth et al. (1979) administered TCDD to male Swiss/H/Riop strain mice by gavage once a week for a
year, then followed them for their lifetime. The weekly doses were 0.007, 0.7, and 7.0 µg/kg. Analysis
of the results from this study focused on the incidence of liver tumors. A significant increase in the
incidence of liver tumors was observed in the intermediate-dose group compared to the four separate
control groups. The high-dose group, however, had an incidence of liver tumors that was similar to the
control group. This finding may be explained by the early mortality in the high-dose group. The average
life span was 424 days for this group, compared to average life spans of between 577 and 651 days for
the control groups. If the treated animals had lived it is possible that more tumors may have formed.
Kociba et al. (1978) conducted a two-year feeding study in male and female Sprague-Dawley rats
given diets containing 2200, 210, or 22 parts per trillion (w/w) TCDD for two years. Consumption of
these diets resulted in daily doses of 0.1, 0.01, and 0.001 µg/kg body weight, respectively. There were
50 male and 50 female rats in each treatment group and 86 animals of each sex in the control group.
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