Eighteen workers in the United Kingdom who were exposed to TCDD as a result of an industrial accident on April 24, 1968, underwent a complete clinical assessment and laboratory series to determine immunological abnormalities 17 years later (Jennings et al., 1988). Workers may have been exposed in the building when the accident occurred, during cleanup after the explosion, or while washing and repainting the building. Fifteen controls were selected from the portering and estate management at the plant, and were matched for age, sex, percentage of ideal body weight, social class, alcohol consumption, and smoking habits.

Workers exposed and possibly exposed to the above accident were also examined 10 years later, and compared to a control group for differences in health outcomes, including reproductive outcomes and biochemical and hematological tests (May, 1982). Workers selected for examination included those reporting chloracne after the accident, those who worked regularly at the TCP plant (including laboratory workers and management personnel), and a control group (recruited from remaining laboratory staff and management). Of those with chloracne who were considered to be definitely exposed to dioxin, 41 participated; 54 employees with possible exposure were included, along with 31 having no dioxin exposure. Along with the medical examination, a complete work history was obtained; contact with TCP and related chemicals was confirmed from company records.

In the Netherlands, the National Institute of Public Health and Environmental Protection contributed a cohort to the IARC registry described above, with workers from two companies that produced several chlorophenoxy herbicides; this cohort was also evaluated apart from the IARC registry for cancer mortality (Bueno de Mesquita et al., 1993). Factory A produced primarily 2,4,5-T, which can result in exposure to TCDD contamination; in March 1963, an uncontrolled reaction in the factory resulted in an explosion in which polychlorinated dibenzodioxins (PCDDs) including TCDD were released. Anyone employed at this factory between 1955 and June 30, 1985, was eligible for study inclusion; workers contracted to clean up after the accident were also included in the cohort. Factory B produced primarily MCPA and MCPP [2-(4-chloro-2-methylphenoxy)propanoic acid], with 2,4-D produced in smaller amounts; all persons employed between 1965 and June 30, 1986, were included in the cohort. The total cohort included 2,310 workers, and follow-up was 97 percent complete; analysis was presented for the 2,074 male workers who were exposed and unexposed in the factories. The causes of death were provided from the Netherlands Central Bureau of Statistics. The important steps for phenoxy herbicide exposure, which might occur in a number of different departments, included synthesis of the chemical, formulation of the herbicide, and packaging. Since individual measures of exposure were not available, occupational history including working in the above departments and exposure to the accident was used to define exposure.



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