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cancers, were less than expected. The power of this study to detect an increase in STS was poor,
however, as only 0.1 case of STS was expected based on general population rates. Furthermore, as
deaths in the cohort were studied only after 1972, 45 deaths that occurred in this group before 1972
were not tallied. (Even for post-1971 deaths, however, the follow-up period may also have been too
short for a sufficient tumor latency period to have elapsed.)
There have been four potentially exposed occupational cohorts studied in the United States. Zack and
Suskind (1980) reported the follow-up of Monsanto employees in Nitro, West Virginia, who were
involved in a 1949 accident during the processing of trichlorophenol. A sudden violent reaction
released fumes and residues into a building interior. Apparently, the released chemical mixture was not
analyzed, but the authors assumed that it contained TCDD, as exposed workers developed chloracne.
A historical cohort of 121 white male employees was assembled from company records on the basis of
their having exhibited skin disorders "attributed to the 1949 TCP process accident." Their vital status
was traced through 1978, providing a maximum of 29 years of follow-up per person. The standardized
mortality ratio (SMR) for all causes of death in this cohort (relative to US white males) was significantly
decreased (32 observed deaths vs. 46.4 expected). One cancer site showed an excess: lung cancer (5
observed vs. 2.85 expected), although this SMR of 1.75 was not statistically significant. Interestingly,
there occurred one STS, a fibrous histiocytoma. However, the authors calculated SMRs (and expected
numbers of deaths) only for causes with five or more observed deaths.
Zack and Gaffey (1983) described another cohort from this plant, composed of 884 male workers
employed for at least one year between 1955 and 1977. It is not clear whether workers exposed in the
1949 accident were included. The same methods were used to calculate SMRs. Only 25 malignancies
occurred, compared to 30.9 expected. However, two specific sites were notably elevated: lung cancer,
with 14 observed vs. 9.9 expected (SMR 1.4; 95% CI 0.8-2.4), and bladder cancer, with 9 observed
vs. 0.9 expected (SMR 9.9; 95% CI 4.5-18.8). One STS occurred in a worker judged to have been
exposed to TCDD. One drawback to this study is that exposure histories were only constructed for the
163 decedents - and only 36% of these were judged to have had potential exposure to 2,4,5-T (and
therefore TCDD). Therefore, the true exposed cohort may only have been one-third the size of the
entire study group.
Cook et al. (1980) presented a similar historical cohort study of Dow chemical employees. In 1964,
chloracne occurred in workers in a trichlorophenol manufacturing area. Industrial hygiene investigations
concluded that TCDD was responsible and changes were made in the operations to decrease exposure.
Levels of TCDD during this period were unknown because concentrations fell below the limit of
detection at that time, 0.02 µg/ml of air (Cook 1981a); however, wipe samples were positive for
TCDD. Cook et al. (1980) assembled a cohort of 39 workers thought to have high exposure potential,
and 22 workers thought to have lower exposure. Among the high-exposure group, 87% had a history
of chloracne, compared to 68% of the low-exposure group. Their vital status was determined through
1978. There were only four deaths (vs 7.8 expected based on US white males), although three of these
deaths were due to neoplasms (vs 1.6 expected). One neoplasm was a fibrosarcoma.
Another Dow cohort was investigated by Ott et al. (1980). This cohort contained 204 white males
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