Environmental contaminants as etiologic factors for diabetes.

For both type 1 and type 2 diabetes mellitus, the rates have been increasing in the United States and elsewhere; rates vary widely by country, and genetic factors account for less than half of new cases. These observations suggest environmental factors cause both type 1 and type 2 diabetes. Occupational exposures have been associated with increased risk of diabetes. In addition, recent data suggest that toxic substances in the environment, other than infectious agents or exposures that stimulate an immune response, are associated with the occurrence of these diseases. We reviewed the epidemiologic data that addressed whether environmental contaminants might cause type 1 or type 2 diabetes. For type 1 diabetes, higher intake of nitrates, nitrites, and N-nitroso compounds, as well as higher serum levels of polychlorinated biphenyls have been associated with increased risk. Overall, however, the data were limited or inconsistent. With respect to type 2 diabetes, data on arsenic and 2,3,7,8-tetrachlorodibenzo-p-dioxin relative to risk were suggestive of a direct association but were inconclusive. The occupational data suggested that more data on exposure to N-nitroso compounds, arsenic, dioxins, talc, and straight oil machining fluids in relation to diabetes would be useful. Although environmental factors other than contaminants may account for the majority of type 1 and type 2 diabetes, the etiologic role of several contaminants and occupational exposures deserves further study

Association of blood lead concentrations with mortality in older women: a prospective cohort study

<p>Abstract</p> <p>Background</p> <p>Blood lead concentrations have been associated with increased risk of cardiovascular, cancer, and all-cause mortality in adults in general population and occupational cohorts. We aimed to determine the association between blood lead, all cause and cause specific mortality in elderly, community residing women.</p> <p>Methods</p> <p>Prospective cohort study of 533 women aged 65–87 years enrolled in the Study of Osteoporotic Fractures at 2 US research centers (Baltimore, MD; Monongahela Valley, PA) from 1986–1988. Blood lead concentrations were determined by atomic absorption spectrometry. Using blood lead concentration categorized as < 8 μg/dL (0.384 μmol/L), and ≥ 8 μg/dL (0.384 μmol/L), we determined the relative risk of mortality from all cause, and cause-specific mortality, through Cox proportional hazards regression analysis.</p> <p>Results</p> <p>Mean blood lead concentration was 5.3 ± 2.3 μg/dL (range 1–21) [0.25 ± 0.11 μmol/L (range 0.05–1.008)]. After 12.0 ± 3 years of > 95% complete follow-up, 123 (23%) women who died had slightly higher mean (± SD) blood lead 5.56 (± 3) μg/dL [0.27(± 0.14) μmol/L] than survivors: 5.17(± 2.0) [0.25(± 0.1) μmol/L] (<it>p </it>= 0.09). Women with blood lead concentrations ≥ 8 μg/dL (0.384 μmol/L), had 59% increased risk of multivariate adjusted all cause mortality (Hazard Ratio [HR], 1.59; 95% confidence interval [CI], 1.02–2.49) (p = 0.041) especially coronary heart disease (CHD) mortality (HR = 3.08 [CI], (1.23–7.70)(p = 0.016), compared to women with blood lead concentrations < 8 μg/dL(< 0.384 μmol/L). There was no association of blood lead with stroke, cancer, or non cardiovascular deaths.</p> <p>Conclusion</p> <p>Women with blood lead concentrations of ≥ 8 μg/dL (0.384 μmol/L), experienced increased mortality, in particular from CHD as compared to those with lower blood lead concentrations.</p