· Cadmium is a bluish, lustrous, and light metal which is a common contaminant of several metal ores such as lead, copper, and zinc. Cadmium is highly resistant to corrosion and is widely used in industry. An important derivative is cadmium acetate which is a white metallic salt.
· Daily cadmium intake from food averages 10 to 25 mcg/ day. Shellfish such as mussels, scallops, and oysters may be a major source of dietary cadmium, and may contain 100 to 1,000 mcg/kg. Smokers usually have twice the body burden of cadmium as non-smokers due to cadmium in cigarettes (up to 30 mcg/pack) producing inhalation of 2 to 4 mcg cadmium/ pack smoked.
· Electroplating: of automobile engine parts, aircraft parts, radio and TV parts, and nuts and bolts.
· Alloys: in jewellery making.
· Batteries (nickel-cadmium).
· Shampoo: as a 1% solution for the treatment of seborrheic dermatitis and dandruff.
· Cadmium’s toxic effects may be due to the displacement or substitution of cadmium for zinc in critical metabolic processes. Cadmium interferes with the uptake, distribution and action of zinc.
· Cadmium may also cause apoptosis (programmed cell death), based on a study involving cultured human T cells.
· Oral or inhaled cadmium is transported to the liver where it induces metallothionein, which binds and detoxi-fies cadmium. A slow release of this complex produces cadmium-metallothionein complex in all organs, particu-larly the kidney. Half of a non-smoker’s body burden of 15 to 30 mg cadmium is in the liver and kidneys. Cadmium bound to metallothionein is filtered through the renal glomeruli, reabsorbed and released in the tubules. Unbound cadmium stimulates synthesis of new metallothionein which then binds cadmium in the renal tubular cells. If this step does not occur, toxic effects can result.
· The kidney accumulates cadmium over a lifetime. Renal damage is believed to occur once the cadmium concentration in the kidney cortex reaches or exceeds about 200 micrograms per gram of kidney weight. Low levels of metallothionein, excessive accumulation of cadmium in the renal cortex, high concentrations of cadmium-metallothionein complexes which may directly affect the brush border membranes, interference with zinc-containing enzymes, and autoimmunological processes have been proposed as mechanisms involved in nephrotoxicity.
Acute Poisoning: a. Ingestion—
· Nausea, metallic taste, salivation, vomiting, abdom-inal pain, diarrhoea, and myalgia. Sudden muscle cramps can cause the victim to cry out in pain peri-odically (Itai-Itai* disease, or Ouch-Ouch disease).
· There is also bone demineralisation with osteoma-lacia and pathological fractures.
· Vertigo, shock, unconsciousness and convulsions have been reported.
· Death can occur due to dehydration or renal failure.
The symptoms of acute poisoning after inhalation exposure may be delayed 12 to 36 hours. These include chest pain, cough (with bloody sputum), difficulty breathing, sore throat, ‘metal fume fever’ (shivering, sweating, body pains, headache) dizziness, irritability, weakness, nausea, vomiting, diarrhoea, tracheobronchitis, pneumonitis and pulmonary oedema.
· Yellow staining of teeth (yellow teeth line).
· Anorexia, fatigue.
· Rhinitis and anosmia (due to damage to olfactory nerve).
· Musculoskeletal pain (due to osteopenia-osteomalacia).
· Dyspnoea, emphysema.
· Hypochromic or normochromic normocytic anaemia.
· Renal damage producing microhaematuria, proteinuria, leukocyturia, urinary calculi).
· Cadmium is said to be carcinogenic, and increased inci-dence of lung, prostate, pancreas and bladder cancers in humans have been reported.
· Normal blood cadmium level in non-smokers is 0.4 to 1 mcg/L, and in smokers 1.4 to 4 mcg/L.
· Urinary cadmium excretion of more than 2 mcg/24 hrs or 10 mcg/L is potentially nephrotoxic.
· Chest X-ray findings after acute inhalation exposures may indicate diffuse pulmonary oedema. Later they are those of bronchopneumonia (proliferative interstitial pneumonitis).
· In chronic poisoning, x-ray findings are characteristic of osteomalacia and may show multiple fractures.
· Chelation with CaNa2 EDTA or DMSA for acute poisoning. BAL is contraindicated since it can aggravate nephrotox-icity.
o Dosage of CaNa2 EDTA is as follows: 75 mg/kg/24 hrs deep intramuscular or slow IV infusion, given in 3 to 6 divided doses for up to 5 days. May be repeated for a second course after a minimum of 2 days drug holiday; each course should not exceed a total of 500 mg/kg body weight.
o For DMSA, the initial dose is 10 mg/kg orally every 8 hours for 5 days. The dosing interval then is increased to every 12 hours for the next 14 days. Repeat course may be given if indicated by elevated blood levels. A minimum of 2 weeks between courses is recom-mended.
· Chronic poisoning may not require chelation. Removal from exposure and supportive treatment usually will suffice.
· Most cases of poisoning result from occupational or indus-trial exposure.
· Cadmium contamination of the environment can occur through soil, water, and food. The outbreak of Itai-Itai disease in Japan occurred in 1945 and was the result of consumption of rice grown in paddy fields which were irrigated by the local Jintzu river containing cadmium contaminated water (as a result of effluents from a nearby mine). The drinking water was also found to be contami- nated.
· Certain types of soil have high cadmium content, and consumption of vegetables grown in such soil can result in elevated blood cadmium levels. This may be a factor in the aetiology of some cases of hypertension and renal failure. Tobacco smoke contains cadmium, and significant concen- trations may be inhaled by chronic smoking, especially unfiltered cigarettes. Accumulation occurs mainly in the lung and kidney with resultant inflammatory and degenera- tive changes.
· Some types of industrial and laboratory fires can release significant quantities of cadmium fumes and produce serious consequences in firemen. It is imperative that such fires should be tackled only after wearing self-contained breathing apparatus.
· Consumption of acid fruit juices stored in cadmium- plated metal ware can cause poisoning in families. Other sources of food contamination include pots and pans with cadmium-containing glazing, and vending machines for hot/cold drinks in which cadmium soldering has been done.