Cadmium metal is used as an antirust coating on ferrous metals, and as a component of welding and brazing alloys. Cadmium compounds are used as pigments in paints and plastics, and as electrode components in rechargeable batteries. Acute toxicity may arise from the ingestion of cadmium salts or from the inhalation of fumes from the heating of cadmium-coated metal, for example, when structures are being dismantled by oxy-acetylene torch, or from brazing with cadmium-containing materials in badly ventilated spaces.
Acute ingestion of cadmium salts causes nausea, vomiting and diarrhoea, whereas inhalation of cadmium fumes gives rise to acute pulmonary oedema and to pneumonitis. Chronic exposure to lower concentrations of cadmium vapour results in respiratory impairment with increasing breathlessness on exertion. Attribution of the condition to cadmium may be difficult due to the common occurrence of chronic bronchitis and emphysema secondary to cigarette smoking. Cadmium entering the body is bound to a low molecular weight protein metallothionein, which contains a high proportion of cysteine residues. Initial concentration is in the liver, followed by translocation to the kidney, and long term absorption of cadmium causes renal tubular damage with a marked increase of cadmium excretion in the urine and a low molecular weight proteinuria. The latter has usually been assessed by measurement of the urinary excretion of ß-2 microglobulin; however this protein is rapidly degraded at low urinary pH, and an alternative measurement such as retinol binding protein (RBP) is now preferred. A variety of other tubular disorders may occur, such as aminoaciduria, glycosuria and impaired hydrogen ion excretion.
Long term absorption of cadmium has significant effects on calcium metabolism, which may result from renal damage, although the mechanism remains unclear. The effects were seen most clearly in the exposure of a Japanese population to oral ingestion of cadmium salts from contaminated crops and water, giving rise to the condition known as ‘Itai-itai’ disease. The subjects showed the renal damage mentioned above but in addition extreme bone pain, easily-caused fractures, and osteomalacia. The disease was most manifest in women who had had multiple pregnancies or who were post menopausal, and may have been exacerbated by dietary inadequacies of calcium and/or vitamin D. However, instances of cadmium toxicity elsewhere have also shown derangements of calcium metabolism, in particular, osteomalacia, hypercalciuria and nephrocalcinosis.
Laboratory Indices of Cadmium Status
Circulating cadmium is largely bound to the erythrocytes, so that measurement of blood cadmium is the determination of choice, especially for chronic exposure. It is less reliable, however, in assessing acute toxicity in previously exposed individuals as such exposure may give rise to a continuing elevation of the blood cadmium long after the exposure has ceased. It should be noted that cadmium is one of the most persistent poisons known, its biological half-life in the liver and kidney being of the order of seven and thirty years respectively. Urine cadmium concentration may remain low during significant cadmium exposure until a critical renal concentration is reached. When renal damage occurs, output then increases markedly. The degree of renal damage may be assessed by measurement of the proteinuria which is, however, frequently small in amount. A qualitative assessment by electrophoresis to distinguish the characteristic tubular pattern is useful, but quantitative estimation of retinol binding protein is more satisfactory. Creatinine clearance, glycosuria and aminoaciduria can also be assessed, although the changes are frequently mild.
Stokinger HE Chapter 29 – Metals, in Patty’s Industrial Hygiene and Toxicology, 3rd Revised Edition, Volume 2A. Eds Clayton GD and Clayton FE. Wiley Interscience, 1981.
UNEP/ILO/WHO. International Programme on Chemical Safety, Environmental Health Criteria 134 Cadmium. WHO, Geneva, 1992
Jung K, Pergande M, Graubaum H-J, Fels LM, Endl U, Stolte H. Urinary proteins and enzymes as early indicators of renal dysfunction in chronic exposure to cadmium. Clin Chem 1993; 39: 757-65