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The first aim of the study was to evaluate calculated dietary intake and concentrations measured in blood or urine of essential and toxic elements in relation to nutritional and toxicological reference values. The second aim was to identify patterns of the element concentrations in blood and urine and to identify possible dietary determinants of the concentrations of these elements. Adults with a known high consumption of environmental contaminants (n=111), and a random sample of controls (n=76) answered a validated food frequency questionnaire (FFQ). Complete data on biological measures were available for 179 individuals. Blood and urine samples were analyzed for selenium, iodine, arsenic, mercury, cadmium and lead. Principal component analysis was used to identify underlying patterns of correlated blood and urine concentrations. The calculated intakes of selenium, iodine, inorganic arsenic and mercury were within guideline levels. For cadmium 24% of the high consumer group and 8% of the control group had intakes above the tolerable weekly intake. Concentrations of lead in blood exceeded the bench-mark dose lower confidence limits for some participants. However, overall, the examined exposures did not give rise to nutritional or toxicological concerns. Game consumption was associated with lead in blood (B(ln) 0.021; 95%CI:0.010, 0.031) and wine consumption. Seafood consumption was associated with urinary cadmium in non-smokers (B(ln) 0.009; 95%CI:0.003, 0.015). A novel finding was a distinct pattern of positively associated biological markers, comprising iodine, selenium, arsenic and mercury (eigenvalue 3.8), reflecting seafood intake (B 0.007; 95%CI:0.004, 0.010). The study clearly demonstrates the significance of seafood as a source of both essential nutrients and toxic elements simultaneously and shows that exposure to various essential and toxic elements can be intertwined., (© 2013 Elsevier B.V. All rights reserved.)

Objectives: The aim of this study was to investigate renal function and immunologic markers among chloralkali workers with long-term low exposure to mercury vapor., Methods: Forty-seven currently exposed workers were compared with reference workers matched for age in a cross-sectional design., Results: The mean urinary mercury concentration was 5.9 (range 1.1-16.8) nmol/mmol creatinine (Cr) for the exposed workers and 1.3 (range 0.2-5.0) nmol/mmol Cr for the referents. The chloralkali workers had been exposed for an average of 13.3 (range 2.8-34.5) years. The activity of N-acetyl-beta-D-glucosaminidase in urine (U-NAG) was higher in the exposed workers (mean 0.18 U/mmol Cr versus 0.14 U/mmol Cr, P=0.02). Associations between current urinary mercury, cumulative urinary mercury, and cumulative urinary mercury per year (intensity) and U-NAG, autoantibodies to myeloperoxidase (anti-MPO) and proteinase 3 in serum, respectively, were observed. The activity of U-NAG and anti-MPO was increased in the workers with the highest exposure, as assessed by their mean intensity of exposure. The highest activity of U-NAG was observed in the exposed workers with the lower concentrations of selenium in whole blood., Conclusions: The study indicates an effect of exposure on the kidney proximale tubule cells, possibly modified by individual selenium status, and an effect mediated by neutrophil granulocytes.

The object of this work was to investigate possible interactions of mercury, cadmium and selenium in humans. Selenium and cadmium in blood and urine were determined in this cross-sectional study of 130 males, of whom 77 had been previously exposed to mercury vapour at a chloralkali plant. Of the participants, 61.5% were smokers and 16.2% were never-smokers. The concentration of selenium in blood (B-Se) was significantly lower in subjects currently smoking more than 50 g of tobacco per week compared to never-smokers, whereas the concentration of cadmium in blood (B-Cd) was significantly higher in all categories of current smokers. In the multiple linear regression analysis, B-Se as a dependent variable was negatively associated with B-Cd, whereas current smoking habits were not included in the model as a predictor variable. In contrast, B-Cd as a dependent variable was positively associated with current as well as previous smoking habits, and negatively with both B-Se and the 'cumulative dose' of previous mercury vapour exposure. The concentration of selenium in blood was also negatively associated with B-Cd in the group of never-smokers (Spearman's r = -0.80; P < 0.001). In conclusion, these results suggest a depressive effect of cadmium on the concentration of selenium in blood, while smoking alone did not operate as a true predictor for this effect. Furthermore, previous exposure to mercury apparently modifies the concentration of cadmium in blood.

Urinary selenium excretion was studied in 21 mercury vapour (Hgo)-exposed workers involved in the demolition of a chloralkali plant. The subjects had no known previous occupational exposure to mercury. Their mean pre-exposure urinary mercury concentration, determined on average 1.2 days prior to the exposure, was 0.8 nmol mmol-1 creatinine (range 0.3-1.9). Their last mean urinary mercury concentration, determined on average after 51.4 days (range 19-103) of exposure, was 4.8 nmol mmol-1 creatinine (range 1.2-10.0). The exposure ceased on average 4.1 days after the last determined urinary mercury concentration. The corresponding concentrations of urinary selenium decreased from an average of 39.1 nmol mmol-1 creatinine (range 13.9-89.5) to 29.0 nmol mmol-1 creatinine (range 10.1-52.9) (P = 0.002). This finding may indicate that even a low to moderate work-related exposure to Hgo may reduce the urinary selenium concentration in humans in a manner that is not yet fully known.

The concentrations of total mercury (B-Hg), inorganic mercury (B-IHg), and methyl mercury (B-MeHg) in whole blood, urinary mercury (U-Hg), and selenium in urine (U-Se) and whole blood (B-Se) were determined in 74 chloralkali workers previously exposed to Hg vapour, and compared with 51 age matched referents. Dental amalgam state, fish consumption, and exposure related indices were studied with regard to the determined elements. A significant relation between the surface of dental amalgam and U-Hg (Pearson's r = 0.63, p < 0.001) was found among the referents. Mean U-Se was significantly lower (p < 0.001) among the subjects previously exposed to Hg (34.1 nmol/mmol creatinine) compared with that for the referents (42.6 nmol/mmol creatinine). A significant negative relation between the cumulative Hg dose and U-Se was also found. The mechanisms and the clinical significance of these findings are not clear. No relation between current U-Hg and previous occupational exposure to Hg was found among subjects in whom exposure had ceased more than one year before the study.

The object of this work was to investigate possible interactions of mercury, cadmium and selenium in humans. Selenium and cadmium in blood and urine were determined in this cross-sectional study of 130 males, of whom 77 had been previously exposed to mercury vapour at a chloralkali plant. Of the participants, 61.5% were smokers and 16.2% werenever-smokers. The concentration of selenium in blood (B-Se) was significantly lower in subjects currently smoking more than 50 g of tobacco per week compared to never-smokers, whereas the concentration of cadmium in blood (B-Cd) was significantly higher in all categories ofcurrent smokers. In the multiple linear regression analysis, B-Se asa dependent variable was negatively associated with B-Cd, whereas current smoking habits were not included in the model as a predictor variable. In contrast, B-Cd as a dependent variable was positively associated with current as well as previous smoking habits, and negatively with both B-Se and the 'cumulative dose'of previous mercury vapour exposure. The concentration of selenium in blood was also negatively associated with B-Cd in the group of never-smokers (Spearman's r = -0.80; P < 0.001). In conclusion, these results suggest a depressive effect of cadmium on the concentration of selenium in blood, while smoking alone did not operate as a true predictor for this effect. Furthermore, previous exposure to mercury apparently modifies the concentration of cadmium in blood. [ABSTRACT FROM AUTHOR]