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Aluminium is poorly absorbed orally. Toxicity typically occurs in patients with chronic renal failure or people exposed in the workplace. Patients with renal failure are exposed to aluminium in dialysate fluid and medications. Features of aluminium toxicity include dementia, memory loss, aphasia, ataxia and seizures. Chronic exposure to aluminium dust can cause dyspnoea, cough, pulmonary fibrosis, pneumothorax, pneumoconiosis, encephalopathy and seizures.
Antimony is an irritant to skin and mucous membranes. Its toxicity resembles that of arsenic; signs and symptoms of exposure include abdominal cramps, nausea, vomiting and diarrhea. Haemolytic anaemia, myoglobinuria and renal failure may occur. Exposure to the dust can cause, rhinitis, chest tightness, shortness of breath, bronchitis, pulmonary edema, headache, and dizziness. QT prolongation and T wave changes have been reported on ECG.
Bismuth toxicity varies regarding both onset and type of toxicity due to the solubility of the salt form administered. Simple inorganic salts are not well absorbed and some organic salts decompose in the gastrointestinal tract to poorly absorbed simple salts. Other organic salts, both water and lipid soluble can be absorbed to cause bismuth toxicity. Poisoning is similar to lead and mercury with the development of an encephalopathy after large or repeated doses.
All beryllium salts are potentially harmful, particularly when inhaled. Acute beryllium poisoning causes conjunctivitis, mucous membrane irritation and occasionally an acute pneumonitis. Chronically, lymphadenopathy and an infiltrative lung disease may occur.
Cadmium is a severe irritant that can be fatal by inhalation and ingestion. The symptoms following inhalation may resemble metal fume fever and include chest pain, cough, dyspnoea, sore throat, tracheobronchitis, pneumonitis and pulmonary edema. After ingestion symptoms usually appear within 30 minutes and include abdominal pain, nausea, vomiting, salivation, muscle cramps, vertigo, shock, unconsciousness and convulsions.
Copper compounds may be toxic by inhalation, ingestion, and skin or eye exposure. Exposure to fumes or dust may cause irritation of the nose and upper respiratory tract. Metal fume fever may result from exposure to fumes. Acute ingestion of copper salts can cause irritation, nausea, vomiting, abdominal pain, haemolysis, gastrointestinal bleeding, anemia, hypotension, jaundice, seizures, coma, shock and death. Hepatic and renal failure can occur several days after acute ingestion.
Acute manganese poisoning is rare. It mainly affects the respiratory and the central nervous system. Inhalation exposure to high concentrations may result in metal fume fever. Toxicity following chronic exposure involves Parkinson-like symptoms. The neurologic disorder that develops is known as ‘manganism’. ‘Manganese madness’ is a psychiatric condition that may develop with symptoms of compulsive behaviour, emotional lability and hallucinations.
Nickel toxicity may result from ingestion, skin contact or inhalation. Inhalation of nickel alloys or dust has been linked to pulmonary irritation, asthma, pneumoconiosis, pulmonary fibrosis and pulmonary edema. Exposure to nickel fumes may result in metal fume fever. Death from adult respiratory distress syndrome has occurred.
Metal fume fever results from inhaling metal oxide fumes such as aluminium, antimony, arsenic, beryllium, cadmium, chromium, cobalt, copper, iron, lead, magnesium, manganese, nickel, selenium, silver, tin and zinc. Zinc and copper are the most common agents involved. The illness consists of fever, chills, malaise, headache, myalgias, fatigue, cough, thirst and abdominal discomfort. The onset is 3 to 10 hrs after exposure. Symptoms usually do not last beyond 24 to 48 hrs. Recovery is usually complete. Tolerance may build up after repeated exposures, but is lost after a few days of non-exposure. Symptoms often reappear after a weekend away from the job, giving rise to the term ‘Monday Fever’.
Reference: Buge A,Supino-Viterbo V, Rancurel G, Pontes C. Epileptic phenomena in bismuth toxic encephalopathy. J Neurol Neurosurg Psychiatr 1981;44:62-7 Fulltext