2,3,7,8-Tetrachlorodibenzodioxin (TCDD) was formed in an uncontrolled decomposition reaction at BASF Aktiengesellschaft on 17 November 1953. This report presents the findings of a 34-year mortality follow-up study of 247 workers who were partly heavily exposed; 78 thereof had died. We divided these employees into three cohorts based on the amount and reliability of the exposure information. The mortality was compared with the national mortality rates in the Federal Republic of Germany (FRG) and is presented in terms of standardized mortality ratios (SMRs) together with 90% confidence intervals (CI) for different periods of time since the first exposure. In general, the overall mortality of these workers was similar to the rates of the national population. The SMR for all malignant neoplasms based on 23 deaths was 117 (90% CI: 80, 166), suggesting no overall increase in cancer among those employees. When workers with chloracne were examined separately, the SMR for all malignant neoplasms was not significantly elevated overall (SMR 139; 87, 211), but it was for the time period 20 or more years after the first exposure (SMR 201; 122, 315). Results for 22 causes of death as well as additional information on the type of exposure and skin findings are presented and discussed in relation to the current literature. In general, our results do not appear to support a strong association between cancer mortality and TCDD, but they do suggest that some hazard may have been produced.
Although gastrointestinal (GI) illnesses account for considerable sick absenteeism, there have been few workplace studies of GI disorders. We determined the prevalence of Helicobacter pylori infection by serology and assessed its relation to upper GI tract complaints, personal ulcer history, and family history of stomach cancer in 6,143 employees (mean age, 40.4 years) at BASF's main chemical production facilities in Ludwigshafen, Germany. Employees were recruited during occupational health clinic visits (n = 4,488) and through broad communications efforts (n = 1,655). Participation among clinic attendees was 66%, and this recruitment method was particularly effective in reaching shift employees. Positive immunoglobulin G (IgG) serology (38.2%), ulcers (4.9%), nonulcer dyspepsia (20.4%), and a family history of stomach cancer (6.1%) were common occurrences in this work setting. Further diagnostic evaluation and eradication therapy was recommended for 795 employees (12.9%), based on a combination of positive serology and either upper GI tract complaints or family stomach cancer history, and has been completed for 541 employees. A weak but consistent association was seen between positive serology and cigarette smoking, and shift work was found to be associated with positive serology, but not with ulcer or nonulcer dyspepsia occurrence.
Current 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) concentrations were determined in blood samples for 138 persons who had been involved in assessment, clean-up and demolition activities after the 1953 BASF trichlorophenol reactor accident. From these data and detailed descriptions of the circumstances and duration of individual exposure, a regression model was developed for describing the relationships between various exposure situations and TCDD concentration. The model explained 65% of the variability in log (TCDD) concentration. Using half-life assumptions and the regression model parameters we estimated cumulative TCDD concentrations back-calculated to the time of exposure for all 254 members of the accident cohort. The geometric mean cumulative TCDD concentration for all cohort members averaged 137.7 ppt. Estimated cumulative TCDD concentrations correlated well with chloracne severity. The mean TCDD concentrations were 38.4 ppt for the no chloracne subgroup (n = 139), 420.8 ppt for the moderate chloracne subgroup (n = 59) and 1008 ppt for the severe chloracne subgroup (n = 56). The estimation procedure should be helpful in assessing the relationships between various health outcomes and TCDD exposure in this cohort.
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