Objective-To evaluate the long term health consequences of past occupational exposure to 2,3,7,8 tetrachlorodibenzo-pdioxin (TCDD). Methods Polychlorinated dioxins and furans have been identified as unwanted byproducts of numerous chemical and thermal processes.' The toxic potency of these planar halogenated compounds is well documented and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most toxic member of the class, has been shown to cause a wide range of effects including hyperplastic changes in epithelial tissues of the skin, liver, gastric mucosa, bile duct, and urinary bladder.2 It is an animal carcinogen and promotes skin, lung, and liver tumours under appropriate experimental conditions.34 The mechanisms through which TCDD acts to alter tumour incidence are unknown, but are unlikely to include direct genetic effects. Three recent mortality studies with exposure assessments supported by TCDD measurements in blood, have been interpreted as showing an increased risk of cancer in humans after dioxin exposure.25 The present investigation updates the mortality experience of one of the three cited studies,7 reports cancer incidence for the first time, and examines cancer outcomes in relation to dose of TCDD with more extensive biomonitoring than was previously available. Materials and methods STUDY BACKGROUNDOn 17 November 1953, an uncontrolled decomposition reaction occurred in a trichlorophenol (TCP) production unit owned by BASF AG and located in Ludwigshafen, Germany. Byproducts that escaped from the damaged autoclave contaminated surfaces throughout the immediate work area of the enclosed production building. Within days, workmen who were engaged in clean up efforts developed severe acne as well as other signs and symptoms and some were taken into hospital. The agent most likely to have caused these responses was not identified until 1957 when TCDD was chemically shown to be a byproduct p of TCP production and was shown to be a potent acnegen.9 1lFurther confirmation that TCDD had been present was provided by biomonitoring data collected more than 30 years after the incident.7' 1 These data showed increases of TCDD concentrations in blood lipid that related to both the extent of involvement in clean up activities and an employee's chloracne status. A non-linear regression model relating TCDD concentrations in blood lipid to duration of exposure under various working conditions was developed in 1993

Objective-The aim was to examine the long term morbidity experience of men exposed to 2,3,7, (Occup Environ Med 1994;51:479-486)

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.

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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.