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Assays / Trace
Metals/ Cadmium
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.
Toxicity
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.
References:
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
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