Panel discussion: mechanisms and health effects of chromium.

The Panel was asked questions that had been prepared prior to the conference as well as queries from the audience, as follows. In response to a question from R. Bartlett as to how Crvl can get past the digestive tract without being reduced, M. Costa (New York University Medical Center) stated that it is, in fact, likely reduced. He emphasized that the pharmacokinetics of chromium have not been sufficiently studied. R. Wedeen (Veterans Administration Medical Center, East Orange, New Jersey) was then asked whether exposure to chromium causes increased renal excretion of chromium and of other compounds, a finding which seemed to be alluded to in Mutti's work (1), and if a) this is similar to low molecular weight proteinuria and b) whether the chromium excretion can be correlated with the air level of chromium. Wedeen replied that he was quoting in his talk from the work of Mutti's group (1) that showed both low molecular weight proteinuria and retinol-binding protein in the urine which is not reabsorbed and metabolized. The important point is that when the urinary chromium levels were greater than 15 ,ug/g urinary creatinine, low molecular weight proteinuria was observed. Whether the air exposure was related with the chromium excretion he did not know. He stated that the problem with the studies of this group (2) was that they did not really determine clearance because they did not take into account the protein binding of chromium in the serum. Another question put to Wedeen was whether data from long-term high-level exposure (4 years) of rats and dogs to chromium in drinking water (which did not result in kidney damage) could be extrapolated to humans. Wedeen replied that the answer is no, especially if you only look at histological damage to the kidney, which is a crude approach. He stated that such data