[Cadmium toxicity: summary of personal studies].

Occupational and environmental exposure to cadmium leads to a progressive and almost irreversible accumulation of the metal in the body. The epidemiological and experimental studies carried out by the authors allow them to draw the following conclusions: 1) the kidney is usually the critical organ i.e. the organ exhibiting the first signs of adverse effects following long term moderate exposure to cadmium by inhalation or by ingestion. 2) Cadmium interferes not only with the tubular reabsorption process(es) for low molecular weight proteins (e.g. beta 2 . microglobulin, retinol binding protein) but also with the glomerular or tubular mechanism determining the excretion of high molecular weight proteins (e.g. albumin, transferrin). Both types of proteinuria may occur independently. 3) The renal functional disturbances induced by cadmium and compatible not only with a tubular dysfunction but also a glomerular dysfunction. 4) The early detection of renal disturbances induced by cadmium should not rely only on the determination of total proteinuria but necessitates the analysis in urine of at least one low molecular weight protein (beta 2-microglobulin or retinol binding protein) and one high molecular weight protein (albumin). 5) Before the occurrence of renal dysfunction and providing the intensity of exposure to cadmium is moderate, urinary cadmium reflects mainly the body burden whereas blood cadmium reflects mainly the last few months exposure. 6) In adult male workers occupationally exposed to cadmium, the critical concentration of cadmium in the renal cortex is in the order of 200 ppm. The corresponding critical urinary level is approximately 10 micrograms/g creatinine. The critical level of cadmium in the renal cortex is not reached if the exposure is kept at a level where cadmium in blood does no exceed 1 microgram/100 ml. 7) Comparison of literature data on current exposure of the general population to cadmium and the critical exposure level indicates that some groups of the general population absorb daily amounts of cadmium closed to the critical level. 8) The critical biological levels indicated under (6) do not necessarily prevent an exacerbation of the age-related decline in renal function. 9) A preliminary study performed in Belgium suggests that cadmium might play a role in the increased mortality by renal diseases in a population living in an area polluted by cadmium. More detailed studies are necessary to confirm this hypothesis.