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cancer mortality. However, US EPA (1988) considers this study insufficient to assess the
carcinogenicity of acrylamide in humans because of small cohort size, multiple chemical exposures,
limited followup, and short exposure duration (167 cohort members had < 1 year of employment; 109
had 1-4 years of employment).
Animal Studies
Bull et al. (1984a) exposed female Sencar mice and male and female A/J mice to acrylamide. Female
Sencar mice (40/treatment group) were exposed to 0, 12.5, 25.0 or 50.0 mg/kg body weight
acrylamide by gavage, intraperitoneal injection or dermal application. Doses were administered 6 times
over a 2 week period; total doses were 0, 75, 150 and 300 mg/kg. Acrylamide was dissolved in
distilled water for gavage and intraperitoneal injection administration, and in ethanol for dermal
application. Two weeks after the cessation of acrylamide exposure, 1.0 µg 12-O-tetradecanoylphenol-13-acetate
(TPA) dissolved in 0.2 ml acetone was applied to the shaved back of each animal 3
times/week for 20 weeks. A promotion control group was included which received 300 mg/kg
acrylamide followed by dermal applications of 0.2 ml acetone on the same treatment schedule and
duration as the animals receiving TPA. All animals were sacrificed at 52 weeks, and were evaluated for
the presence of skin tumors. Male and female A/J mouse (40/sex/treatment group) acrylamide
exposures were conducted at laboratories of the US EPA (Cincinnati, OH) and the Medical College of
Ohio (Toledo, OH) (MCO) . Animals exposed at US EPA received acrylamide dissolved in distilled
water by gavage 3 times/week for 8 weeks at doses of 0, 6.25, 12.5 or 25 mg/kg. Animals exposed at
MCO initially received acrylamide by intraperitoneal injection 3 times/week for 8 weeks at doses of 0,
1, 3, 10, 30 or 60 mg/kg; however, peripheral neuropathy and decreased survival forced treatment
termination on the 60 mg/kg group after the 11th injection. An untreated control group was also
included. Animals were sacrificed after either 7 months (US EPA) or 6 months (MCO) and examined
for lung adenomas. Acrylamide induced skin tumors (squamous cell papillomas and carcinomas) in
TPA-promoted female Sencar mice in a dose-dependent manner when administered by gavage,
intraperitoneal injection or dermal application. Acrylamide did not induce skin tumors by any route of
administration in animals not receiving TPA. Tumor incidence data from female Sencar mice exposed to
acrylamide are listed in Table 1.
The incidence of lung adenomas in both male and female A/J mice exposed to acrylamide by either
gavage or intraperitoneal injection was significantly increased in a dose-related manner (Bull et al.,
1984a). Tumor incidence data for animals treated by intraperitoneal injection is listed in Table 2;
numerical tumor incidence data for animals exposed to acrylamide by gavage was not listed.
Acrylamide dissolved in water was administered by gavage (0, 75, 150 or 200 mg/kg body weight,
divided into 6 equal portions) to female ICR-Swiss mice (40 animals/treatment group) over a 2 week
period (Bull et al., 1984b). Two weeks after the last acrylamide exposure, the animals were exposed 3
times/week to dermal applications of 2.5 µg TPA for 20 weeks. Another group of 20 animals were
exposed to a total dose of 300 mg/kg acrylamide, but received dermal applications of acetone alone.
All animals were sacrificed after 52 weeks. Acrylamide caused a significant dose-related increase in the
incidence of skin tumors (papillomas and carcinomas combined). The incidence in animals also
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