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eported. Cause-specific expected deaths were calculated based on both U.S. age and calendar
specific white male mortality and mortality rates for other rubber workers from the same city; however,
most results reported in this study used expected deaths calculated using U.S. white male mortality
rates. An excess risk of lung cancer mortality was observed when either U.S. mortality rates (9
observed, 5.9 expected) or Akron rubber industry mortality rates (9 observed, 4.7 expected) were
used to calculate expected lung cancer deaths. Workers employed for 5-15 years and followed for at
least 15 years demonstrated a significantly increased risk of lung cancer (4 observed, 0.8 expected, p <
0.01). Cohort members could potentially have been exposed to other chemicals used in the same area
(butadiene, styrene, vinyl pyridine). Also, smoking controls were not included. However, US EPA
(1983) commented that the possibility that the excess risk of lung cancer demonstrated in this study was
due to acrylonitrile exposure could not be dismissed.
Chen et al. (1987) examined cancer incidence and mortality in a cohort of 1083 male employees at a
E.I. du Pont de Nemours and Co., Inc. textile plant in Waynesboro, VA who were potentially exposed
to acrylonitrile in the period 1944-1970. Worker exposure levels were assessed by an Exposure
Classification Committee consisting of seven DuPont employees with long-term experience in the
acrylonitrile exposure area; plant environmental monitoring data was not available for the 1944-1970
period. High, moderate and low exposure categories were established. Expected numbers of deaths
were calculated from both U.S. and DuPont mortality rates; however, the authors only listed the results
of cancer incidence and mortality calculations using the DuPont “control” data set as the source of the
expected numbers of cancer cases and mortality. No significant increase in incidence was noted for
either all types of cancer (37 observed, 36.5 expected) or lung cancer (5 observed, 6.9 expected).
However, a significant increase in the incidence of prostate cancer (5 observed, 1.9 expected) was
noted; of these, 4 occurred in the 1975-1983 period (0.9 expected).
US EPA (1983) also reviewed several unpublished studies of cancer mortality and/or morbidity
potentially caused by acrylonitrile (Kiesselbach et al., 1980; Zack, 1980; Gaffey and Strauss, 1981;
Herman, 1981; Stallard, 1982). These studies indicated no cancer increase in workers potentially
exposed to acrylonitrile. However, US EPA concluded that due to design and methodological
deficiencies including short followup, small cohort size and young cohort age, “none of these studies can
be cited as adequate evidence that acrylonitrile is not carcinogenic”.
Animal Studies
Maltoni et al. (1977) (reviewed by US EPA, 1983) exposed male and female Sprague-Dawley rats
(30/sex/exposure group) to 0, 5, 10, 20 or 40 ppm acrylonitrile by inhalation for 4 hours/day, 5
days/week for 12 months. The animals were then maintained for the remainder of their lifetime. Slight
increases in the incidence of the following tumor types were noted: mammary gland tumors in males and
females, nonglandular forestomach tumors in males and skin tumors in females. Tumor incidence data
are listed in Table 1.
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