Thallium Poisoning

Authored by , Reviewed by Dr Laurence Knott | Last edited | Meets Patient’s editorial guidelines

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Thallium is a heavy metal. It has an atomic number of 81, atomic weight of 204.3833, two stable isotopes 203 Tl and 205 Tl and a specific gravity of 11.9.

It occurs naturally in elemental metallic form but is more frequently found as thallic and thallous compounds. Thallic cations are trivalent or, more commonly, univalent.

It was discovered in 1861 by Sir William Crookes who named it after its spectroscopic appearance. The name comes from the Greek thallos meaning a green young shoot.

Thallium poisoning is rare in Western societies. It has occasionally been the tool for murder.[1]

Poisoning can be acute or chronic and the presentation can be highly variable. The doctor may not be aware that the patient has been exposed to thallium and this makes the diagnosis much more difficult. Occupational history is important but the patient may not know that he or she has been exposed.

NB: alopecia is a feature that should lead to suspicion of thallium toxicity.

Thallium poisoning usually follows oral ingestion but it can be inhaled from contaminated dust from pyrite burners, cadmium manufacturing, lead and zinc smelting and in contamination of heroin or cocaine. Its toxic effect is due to its ability to inhibit a number of intracellular potassium-mediated processes. It is used in the manufacture of electronic components, optical lenses, semiconductor materials, alloys, gamma radiation detection equipment, imitation jewellery, artists' paints, low-temperature thermometers and green fireworks. In some parts of the world it is still used for killing rodents and this may lead to inadvertent ingestion by humans.

The lethal dose is around 15-20 mg per kg body weight but serious toxicity and even death can occur with rather less. It is rapidly distributed throughout all tissues of the body. Most thallium is excreted by the faecal route but up to 35% may be excreted by the kidneys. Nevertheless, prolonged exposure may lead to build-up and chronic toxicity.

It was originally used for treating skin infections but had a low therapeutic index. Thallium isotopes are now used in some cardiac investigations but the dose is too low to be toxic.

Acute poisoning tends to produce gastrointestinal (GI) effects, whilst chronic poisoning tends to produce neurological manifestations. The classical triad of acute poisoning that should suggest the diagnosis of acute thallium toxicity is:

  • Nausea and vomiting.
  • Followed by painful peripheral neuropathy.
  • Then alopecia.
  • Abdominal pain, nausea and vomiting occur within a few hours of an acute exposure. There may be blood in the stool.
  • Painful sensory neuropathy occurs, especially on the soles and palms. It may take a couple of days to develop. It may be followed by weakness of the lower leg, ataxia, confusion, hallucinations, convulsions and coma.
  • Neuropsychiatric complications include anxiety, confusion, delirium, hallucinations and psychosis. Acute agitation and aggression, personality changes, depression, apathy and confabulation have been observed both in adults and in children.[2] Psychosis can occur even without a psychiatric history.
  • Diplopia, abnormal colour vision and reduced visual acuity are reported.
  • Sometimes there is shortness of breath and pleuritic chest pain. The mechanism is unknown.

Chronic poisoning can lead to tiredness, headaches, depressions, lack of appetite, leg pains, hair loss and disturbances of vision.

In the early stages, abdominal examination shows some tenderness, hyperactive bowel sounds and possible guarding.


  • A full neurological examination is required including examination of the cranial nerves and assessment for visual field defects. Optic neuropathy and cranial nerve palsies are the most obvious features.
  • Signs take 2-4 days to develop with the severity dependent upon the level of poisoning.
  • There is peripheral neuropathy with marked leg and foot tenderness and paraesthesia. Weakness may be difficult to elicit because of pain and it tends to be mild.
  • With severe neurological involvement, respiratory paralysis can be fatal at the end of a week.
  • Examination of the eyes and face may show loss of the lateral half of the eyebrows, drooping eyelids, facial nerve palsy, ophthalmoplegia and nystagmus.
  • Specialist examination is required with slit-lamp assessment and documentation of colour vision.
  • Keratitis and corneal opacities occasionally occur.


  • Hair loss, rashes and palmar erythema take 2-4 weeks to appear.
  • There is atrophy of the hair follicles. Alopecia is so characteristic that it should prompt suspicion.[3, 4]The hair loss primarily affects the scalp, temporal parts of the eyebrows, the eyelashes, and the limbs. Less often, the axillary regions are affected.
  • Early signs are not specific and include scaling of the palms and soles and acneform lesions of the face.
  • One month after the poisoning, Mees' lines (transverse white lines on the nails) appear in the nail plate. They also occur in arsenic poisoning and renal failure.
  • Other findings may include crusted eczematous lesions, hypohidrosis, anhidrosis, palmar erythema, painful glossitis with redness of the tip of the tongue, stomatitis and hair discoloration.
  • There is a characteristic band-like dark pigmentation of the scalp that develops within four days.
  • Few laboratories can perform an assay for thallium. A 24-hour urine thallium concentration is the most accurate way to assess thallium toxicity but a spot urine level is likely to provide a more rapid and reasonably reliable answer. Acute toxicity will produce a thallium concentration many times higher than the reference range of 0-5 ng/mL.
  • The urine may appear green.
  • FBC and blood chemistry are required, in case of anaemia from GI haemorrhage and to assess renal function.
  • Shortly after ingestion, plain abdominal X-ray may show opacities due to the heavy metal.
  • Electrophysiology tests of nerves to the feet may show abnormalities.
  • Electroretinography (ERG) demonstrates delayed visual evoked response.[5] Changes may precede clinical symptoms and so it can be used to assess people with known exposure.
  • ECG, as there may be cardiac arrhythmias.
  • Remove from the source of exposure if possible. Remove contaminated clothing but be careful not to become exposed too.
  • Assess airways, breathing and circulation. With inhalation, possible respiratory failure is a great concern and intravenous (IV) access and administration of oxygen are advised.
  • If ingestion has occurred in the preceding 30 minutes, induce vomiting. In an A&E department gastric lavage can be performed if within an hour of ingestion.
  • With ingestion, activated charcoal and Prussian blue (potassium ferric hexacyanoferrate) are recommended.[6]Prussian blue is better than charcoal at keeping thallium out of the enterohepatic circulation and enhancing faecal excretion but it is not often available.
  • Prussian blue is better than chelating agents such as penicillamine; the latter may cause redistribution of thallium into the central nervous system.[7].
  • Haemoperfusion or haemodialysis, if employed, should be performed as early as possible but can be effective even after delayed diagnosis.[7, 8]
  • All patients with significant signs and symptoms of thallium poisoning require hospital admission
  • Measure thallium levels in blood and urine three times per week to confirm a decreasing trend.
  • Although not well studied, case reports suggest that Prussian blue treatment can be discontinued when spot urine thallium levels fall to less than 100 mcg/L.[5]
  • Physiotherapy may reduce or prevent muscle contractures.
  • Of those who survive poisoning, about a third to a half have residual neurological or visual disability.
  • Exposure during pregnancy can lead to fetal abnormalities.
  • Chronic cases may lead to dementia, depression and psychosis.

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Further reading and references

  1. Rusyniak DE, Furbee RB, Kirk MA; Thallium and arsenic poisoning in a small midwestern town. Ann Emerg Med. 2002 Mar39(3):307-11.

  2. Tsai YT, Huang CC, Kuo HC, et al; Central nervous system effects in acute thallium poisoning. Neurotoxicology. 2006 Mar27(2):291-5. Epub 2005 Dec 5.

  3. Pau PW; Management of thallium poisoning. Hong Kong Med J. 2000 Sep6(3):316-8.

  4. Jha S, Kumar R, Kumar R; Thallium poisoning presenting as paresthesias, paresis, psychosis and pain in abdomen. J Assoc Physicians India. 2006 Jan54:53-5.

  5. Thallium Poisoning - the official newsletter of the California Poison Control System, Autumn 2007

  6. Dart RC, Borron SW, Caravati EM, et al; Expert consensus guidelines for stocking of antidotes in hospitals that provide emergency care. Ann Emerg Med. 2009 Sep54(3):386-394.e1. doi: 10.1016/j.annemergmed.2009.01.023. Epub 2009 May 5.

  7. Zhang HT, Qiao BP, Liu BP, et al; Study on the treatment of acute thallium poisoning. Am J Med Sci. 2014 May347(5):377-81. doi: 10.1097/MAJ.0b013e318298de9c.

  8. Misra UK, Kalita J, Yadav RK, et al; Thallium poisoning: emphasis on early diagnosis and response to haemodialysis. Postgrad Med J. 2003 Feb79(928):103-5.