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Table 3 (continued).
Acrylamide-induced tumor incidences in male and female Fischer 344 rats
(Johnson et al., 1986)
1, 2. As calculated by US EPA (1988).
3. Benign and malignant.
4. Tumors of glial origin or glial proliferation suggestive of early tumor.
5. Squamous cell papillomas and carcinomas.
6. Adenomas and adenocarcinomas.
7. Males: follicular adenomas; females: follicular adenomas and adenocarcinomas.
NA not available
IV.
DERIVATION OF CANCER POTENCY
Basis for Cancer Potency
The studies by Bull et al. (1984a, 1984b), Robinson et al. (1986) and Johnson et al. (1986) indicate
that acrylamide is capable of acting as both an initiator and a complete carcinogen in animals. However,
only the Johnson et al. (1986) study contained a data set suitable for generating a cancer potency
factor. Female Sencar mice developing tumors after exposure to acrylamide in the study by Bull et al.
(1984a) were also additionally exposed to TPA; animals not exposed to TPA did not develop skin
tumors. Female A/J mice exposed in that study to acrylamide by either gavage or intraperitoneal
injection developed an increased incidence of lung adenomas without requiring TPA exposure.
However, the animals were not evaluated for tumor types other than lung adenomas, and numerical
tumor incidence data for animals exposed to acrylamide by gavage was not listed. Also, the exposure
and observation durations for animals exposed by gavage (8 weeks and 7 months, respectively) and by
intraperitoneal injection (8 weeks and 6 months, respectively) were short. Female ICR-Swiss mice
exposed to acrylamide by gavage in the study by Bull et al. (1984b) were generally also exposed to
TPA; only one exposure group was included which received acrylamide (300 mg/kg) but not TPA.
Additionally, the exposure duration was only 2 weeks and the exposure duration was less than lifetime
(52 weeks). In the study by Robinson et al. (1986), all animals for which tumor incidence data was
reported were exposed to TPA as well as acrylamide. Animals in the Johnson et al. (1986) study were
exposed to acrylamide alone for the lifetime of the animals, and were comprehensively examined for
tumors. For these reasons, tumor incidence data from the Johnson et al. (1986) study was used to
derive a cancer potency factor for acrylamide.
Methodology
As recommended in the US EPA Guidelines for Carcinogen Risk Assessment (1986), US EPA (1988)
pooled tumor incidence data from different tumor sites, under the consideration that risk numbers
derived from site-specific tumor incidence data potentially may not be predictive of, and may in fact
underestimate, “whole-body” risks that are determined using the pooled individual animal data. The
dose-response curves for each sex based on the pooled tumor incidence (benign and malignant)
constituted the data sets of choice for risk assessment. Tumors at a particular site were added into the
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