Internal stress to chromium is only relevant in occupational medicine if it is due to the handling of hexavalent chromium. Cr(VI) ions, after uptake by inhalation or percutaneously are carried in the blood plasma and penetrate--depending on the concentration--into the erythrocytes. Due to the intracellular reduction to Cr(III) and the concurrent intracellular protein binding, the erythrocytes represent an easily accessible target organ for quantitative chromium determination after occupational exposure to Cr(VI) compounds. The results of an earlier experimental study indicate that human plasma too is capable of spontaneous reduction of Cr(VI) ions of up to 2 ppm to Cr(III). This plasma reduction capacity (PRC) can be increased and accelerated considerably by adding ascorbic acid (AA). These findings were supported in this investigation by proving a decreased binding of Cr(VI) inside the erythrocytes under the effect of AA. This leads to the assumption that only those Cr(VI) concentrations can penetrate the membrane of the erythrocytes and enter the cell which either come into contact with the membrane during the reduction process or exceed this limit concentration of 2 ppm. Only in these two instances can corresponding chromium findings be analyzed in isolated and washed erythrocytes. These results are compared with those obtained by conventional methods, such as Cr determination in the blood and/or urine. Our findings indicate that a single determination of chromium concentration in the erythrocytes will permit the monitoring of critical cases of Cr(VI) exposure. This is a new type of biological monitoring in the sense of a condensed longitudinal study, in order to find out whether threshold concentrations have been respected over a given period.

The most frequent outcome of the usually transdermal absorption of hexavalent chromium compounds is uraemia due to tubular necrosis. We have confirmed earlier observations that this can be prevented by the immediate application of ascorbic acid (AA) with the aim of reducing Cr(VI) to Cr(III). The spontaneous reducing capacity of samples of serum and plasma for Cr(VI) compounds was polarographically determined to be about 2 ppm. Addition of AA in doses of 50 to 1000 ppm led to a rapid and dose-dependent reduction of chromium(VI), which was studied on the concentration level of 5 ppm. For example in the presence of 1000 ppm AA, five ppm chromium(VI) fade to 0.7 ppm within 20 min and to undetectable concentrations after 40 min. These experiments demonstrate the effectiveness of AA for the treatment of Cr(VI) poisoning. Reduction is increased and accelerated by AA and the resulting Cr(III)-protein complexes are non-toxic and can be excreted with the urine. Early and repeated high i.v. doses of AA are recommended as the therapy of choice for Cr(VI) poisoning. In cases of delayed medical treatment, AA should be immediately applied orally.

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Perfluoralkansulfonylfluoride 2 werden von Hydrazin bei Temperaturen über 30°C unter Stickstoffentwicklung zu Hydrazinium‐perfluoralkansulfinaten 3 reduziert. Reaktionen und Eigenschaften der aus den Sulfinaten 3 dargestellten Perfluoralkansulfinsäuren 1 werden beschrieben.

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