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EC number: 231-152-8 | CAS number: 7440-43-9
- Significant associations were found between the cumulative air cadmium levels and all the parameters used to indicate tubular proteinuria.
- Significant associations were found with current U-Cd or current B-Cd when used as dose estimates.
All the tables and figures are attached in an MS word document in background material.
An investigation was carried out to follow up the tubular function of 46 workers (initially examined in 1984 and heavily exposed to cadmium from 1955 to 1978) and the occurrence of renal stones among these workers. Three different markers of tubular dysfunction were also studied and blood cadmium was evaluated as an estimate of dose after the cessation of cadmium exposure.
Cadmium in blood (B-Cd) and urine (U-Cd) and the urinary excretion of β2-microglobulin (U-β2- microglobulin), protein HC (α1-microglobulin) and N-Acetyl-β-D-glucosaminidase (N AG) were determined.
Although cadmium exposure ceased in 1978, 40% of the workers showed signs of tubular dysfunction both in 1984 and in 1993. The current B-Cd was the best dose indicator of cadmium. Dose-response relationships were found for Cd-B and various tubular markers (U-β2-microglobulin, protein HC and NAG). Elevated dose response curve (adjusted to age, i.e., 55 years) was observed for HC (α1-microglobulin) than that of β2-microglobulin. The levels of Cd-U had an average decrease of 48% for persons with a normal tubular function, 56% for those with slight tubular dysfunction, and 62% for workers with severe tubular damage. A history of renal stones was significantly more common for workers with high B-Cd levels.
Hence, cadmium induced tubular dysfunction is irreversible and best assessed by an analysis of protein HC (α1,-microglobulin) in urine. B-Cd is the best dose estimate several years after the cessation of exposure, whereas U-Cd is less suitable for dose assessment in follow-up studies of persons with persistent tubular damage.
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