The objective of this study was to assess whether arsenic exposure is a risk factor for diabetes mellitus as indicated in a few earlier studies. Arsenic in drinking water is known to occur in western Bangladesh, and in 1996, two of the authors conducted a survey of the prevalence of diabetes mellitus among 163 subjects with keratosis taken as exposed to arsenic and 854 unexposed individuals. Diabetes mellitus was determined by history of symptoms, previously diagnosed diabetes, glucosuria, and blood sugar level after glucose intake. The crude prevalence ratio for diabetes mellitus among keratotic subjects exposed to arsenic was 4.4 (95% confidence interval 2.5-7.7) and increased to 5.2 (95% confidence interval 2.5-10.5) after adjustment for age, sex, and body mass index. On the basis of a few earlier measurements of arsenic concentrations in drinking water by the authorities in Bangladesh and another 20 new ad hoc analyses, approximate time-weighted exposure levels to arsenic in drinking water could be estimated for each subject. Three time-weighted average exposure categories were created, i.e., less than 0.5, 0.5-1.0, and more than 1.0 mg/liter. For the unexposed subjects, the corresponding prevalence ratios were 1.0, 2.6, 3.9, and 8.8, representing a significant trend in risk (p < 0.001). The result corroborates earlier studies and suggests that arsenic exposure is a risk factor for diabetes mellitus.

Abstract-A prevalence comparison of hypertension among subjects with and those without arsenic exposure through drinking water was conducted in Bangladesh to confirm or refute an earlier observation of a relation in this respect. Wells with and without present arsenic contamination were identified, and we interviewed and examined 1595 subjects who were depending on drinking water from these wells for living, all Ն30 years of age. The interview was based on a questionnaire, and arsenic exposure was estimated from the history of well-water consumption and current arsenic levels. Of the 1595 subjects studied, 1481 had a history of arsenic-contaminated drinking water, whereas 114 had not. Time-weighted mean arsenic levels (in milligrams per liter) and milligram-years per liter of arsenic exposure were estimated for each subject. Exposure categories were assessed as Ͻ0.5 mg/L, 0.5 to 1.0 mg/L, and Ͼ1.0 mg/L and alternatively as Ͻ1.0 mg-y/L, 1.0 to 5.0 mg-y/L, Ͼ5.0 but Յ10.0 mg-y/L, and Ͼ10.0 mg-y/L, respectively. Hypertension was defined as a systolic blood pressure of Ն140 mm Hg in combination with a diastolic blood pressure of Ն90 mm Hg. Corresponding to the exposure categories, and using "unexposed" as the reference, the prevalence ratios for hypertension adjusted for age, sex, and body mass index were 1.2, 2.2, 2.5 and 0.8, 1.

Residential exposure to radon is an important cause of lung cancer in the general population. The risks appear consistent with earlier estimates based on data in miners.

For various reasons, data on smoking are frequently missing, or only partially available, in retrospective epidemiologic studies of occupational risk factors. In such situations, indirect methods may be used to evaluate the magnitude and direction of the potentially confounding effects of smoking. Such an evaluation can be made quantitatively or qualitatively. Here we describe both approaches. A specific problem relates to case-referent studies, where sampling variation in referent selection may limit the possibility of controlling for confounding by smoking, even when smoking data are available. We present data showing that estimates of risk from occupational exposures which are not controlled for smoking may be as accurate as estimates derived after controlling for smoking, when the number of referents is relatively small. The problem of interaction is also discussed. In the absence of smoking data, the investigator has no indication of how smoking and occupation jointly affect disease risk (eg, additively or multiplicatively). The multiplicative model is usually assumed. However, if exposure and smoking act independently (additively), rate ratios are diminished. In such situations, in the presence of negative confounding by smoking, rate ratios may actually even be less than one--also when exposure and disease are strongly related.

PURPOSE AND METHODS: To investigate the possible impact of nutritional and environmental risk factors for idiopathic Parkinson's disease (IP), a case-control study was performed in the county of O ¨stergo ¨tland in southeastern Sweden. The study involved 113 cases of IP and 263 control subjects. Dietary, drinking, and smoking habits, as well as previous occupation, were requested in a structured questionnaire.RESULTS: No increased risk was found for any of the nutritional items in which information was requested. A reduced risk was found for coffee, wine, and liquor at various consumption levels but also for fried or broiled meat, smoked ham or meat, eggs, French loaf or white bread, and tomatoes. All these food and drink items contain niacin. As in many studies, the frequency of preceding and present smoking was reduced in IP patients.Various occupational groups and exposures were analyzed and increased risks of IP in men were found for agricultural work along with pesticide exposure; this was also the case for male carpenters and female cleaners.CONCLUSIONS: The findings indicate that nutritional factors and occupational exposures, especially to pesticides, could be of etiologic importance in IP.