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Chapter: Modern Medical Toxicology: Chemical Poisons: Heavy Metals

Manganese - Chemical Poisons

Manganese is a grey-white, silvery, hard, brittle, lustrous transition metal.


Manganese is a grey-white, silvery, hard, brittle, lustrous transition metal. It is found in several types of foods, and is essential in trace quantities for normal bone metabolism and many enzyme reactions.


·              Metallic manganese is primarily used in the manufacture of steel and as an ingredient in the production of ferrous and nonferrous alloys. It is combined with aluminium, copper, nickel, silver and titanium.

·              Manganese is also used as a bronze ingredient, in high- purity salts for various chemical processes, and as a scav- enging and purifying agent in metal production. Manganese salts are utilised in fertilisers, as driers for linseed oil, for glass and textile bleaching, and for leather tanning. Manganese chloride is used as a catalyst, in dry-cell batteries, and as an animal feed supplement.

·              Manganese and its compounds are utilised in the manu- facture of dry-cell batteries, paints, varnishes, inks, dyes, matches, and fireworks, as decolourisers and colouring agents in the glass and ceramics industry, and as a fertiliser, disinfectant, bleaching agent, and laboratory reagent.

·              An organic manganese compound (manganese ethylene bis-dithiocarbamate) is contained in the fungicide Maneb. Other pesticides are reported to contain manganese and may cause manganism in agricultural workers.

Mode of Action

·      Neurotoxicity from manganese results from selective disruption of dopamine neurons and production of the neurotoxins dopamine quinone and hydrogen peroxide.

Manganese also has an affinity for neuromelanin in addition to disrupting dopaminergic systems. Oxidation of dopa-mine by manganese ions produces cytotoxic free radicals probably via glutathione reduction, decreased glutathione peroxidase activity, or the inhibition of mitochondrial respiration.

·      Histopathological examination of brain has demonstrated loss of nerve cells in the inner globus pallidus and diffuse degeneration of cells in the cerebral cortex, palladium, caudate nucleus, putamen, basal ganglia and cerebellum. Some authors postulate that the neurologic features of manganism are mainly due to functional disturbances in striatal neurons.

Clinical Features

·              Acute manganese poisoning is extremely rare. Chronic expo-sure to manganese dust or fumes results in the following:

·      Dyspnoea, bronchitis, pneumonia.

·      Parkinson-like syndrome (manganism)—tremor, rigidity, ataxia, amnesia, and abnormal gait. In addition, there may be nystagmus, paraesthesia, “whispering speech”, lumbosa-cral pain, urinary incontinence, impotence, etc.

·      Manganese madness (“Locura manganica”)—insomnia,confusion, anxiety, hallucinations, and bizarre behaviour.

·      Some manganese miners on an Australian island (GrooteEylandt) have been reported to be afflicted with a peculiar neurological disease characterised by upper motor neuron and cerebellar signs, and oculomotor symptoms (Angurugusyndrome or Groote Eylandt syndrome).

·      “Metal fume fever” has been reported after inhalation exposure to manganese oxide fumes.

·              Manganese exposure has not been related to cancer occur-rence in humans. However, manganese deficiency has been related to cancer in humans.


·      Blood manganese level more than 3 mcg/100 ml. Usual urine reference range is 0.1 to 0.8 mcg/100 ml. However, plasma and urine manganese levels do not correlate well with severity of symptoms or the clinical course of manga-nese toxicity.

·      MRI: may reveal manganese in the basal ganglia.


·      Sodium para-aminosalicylic acid may help in ameliorating the neurological manifestations of chronic manganese toxicity. Dose: 6 gm/day in 500 ml of 10% glucose by IV drip for 4 days, followed by an interval of 3 days. The treat-ment is then repeated and continued with periodic intervals upto 4 months.

·      Other drugs have also been tried with varying degrees of success including L-dopa (3.5 gm to 12 gm/day), 5-hydroxytryptophan, scopolamine, procyclidine, and trihexyphenidyl.

·      Chelation therapy with CaNa2 EDTA may help in some cases. Dose: 1 gram in 500 ml D5W or saline, given over 5 hours twice a day for 3 days.

·              Supportive measures.

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