Thallium Toxicity

Updated: Dec 12, 2021
  • Author: David Vearrier, MD, MPH; Chief Editor: Sage W Wiener, MD  more...
  • Print

Practice Essentials

Thallium is a heavy metal used in the manufacture of electronic components, optical lenses, semiconductor materials, alloys, gamma radiation detection equipment, imitation jewelry, artist's paints, low temperature thermometers, and green fireworks. [1, 2, 3] Trace amounts of thallium are used as a contrast agent in the visualization of cardiac function and tumors. Thallium exposure may occur at smelters in the maintenance and cleaning of ducts and flues and through contamination of cocaine, heroin, and herbal products. Criminal and unintentional thallium poisonings are still reported, some leading to death. [4, 5]

Acute thallium poisoning is primarily characterized by gastrointestinal, neurologic, and dermatologic symptoms, while neurologic findings predominate with chronic exposure and tend to progress, even despite decreasing blood thallium levels. [6, 7] (See Presentation.)

Treatment of thallium toxicity consists of initial stabilization, prevention of absorption, enhanced elimination, and antidotal therapy. [8] (See Treatment and Medication.)

For patient education resources, see Poisoning.

See Clues on the Skin: Acute Poisonings, a Critical Images slideshow, to help diagnose patients based on their dermatologic presentations.





Thallium is a heavy metal that was serendipitously discovered by Sir William Crookes in 1861 while trying to extract selenium from the by-products of sulfuric acid production. Crookes named the new element "thallium" from the Greek thallos, meaning "green shoot or twig" after the bright green spectral emission lines that identified the element. In 1862, Claude-Auguste Lamy independently isolated thallium, studying both its chemical and physical properties. [9]

In the past, thallium was used as a therapeutic agent to treat syphilis, gonorrhea, tuberculosis, and ringworm, and it was also used as a depilatory for excess hair. In the early part of the last century, a product known as Koremlu (thallium acetate) was marketed in the United States for the treatment of ringworm as well as a depilatory agent. By 1934, 692 cases of thallium poisoning were reported with at least 31 deaths. [4, 5] Thallium was also widely used as a rodenticide. Its use as a household rodenticide was banned in the United States in 1965 after multiple unintentional poisonings. [10] Commercial use was banned a decade later. Unfortunately, unintentional poisonings are still reported in other countries where thallium is used as a rodenticide and ant killer.

Thallium is a soft and pliable metal. It melts at 303.5°C and boils at 1482°C. It is colorless, odorless, and tasteless. Thallium has a similar ionic radii to potassium (Tl 0.147 nm vs K 0.133 nm), which is one principle behind its toxicity. [9]





The biochemical research on the cellular effects of thallium is extensive, but few data exist in humans. The structural similarity of thallium to potassium results in the body treating it as such—an action that is key in poisoning. [11] Thallium demonstrates at least the following 5 major toxicologic effects [12] :

  • Disruption of potassium-dependent processes
  • Riboflavin sequestration
  • Interference with cysteine residues
  • Ribosomal inhibition
  • Myelin sheath injury

Thallium accumulates in tissues with high potassium concentrations such as muscle, heart, and central and peripheral nerve tissue. Thallium’s similar size to potassium results in early stimulation then inhibition of potassium-dependent processes. Key enzymes involved in thallium toxicity include pyruvate kinase and succinate dehydrogenase. Their inhibition leads to impaired glucose metabolism and disrupts the Krebs cycle, leading to decreased ATP production. In addition, sodium-potassium ATPase is affected, resulting in cell membrane injury. This enzymatic injury results in swelling and vacuolization of mitochondrial and cell death. Within the mitochondria, thallium also causes sequestration of riboflavin resulting in the inhibition of flavin coenzyme flavin adenine dinucleotide (FAD), impairing the electron transport chain, and further reduction of ATP.

Similar to other metals, thallium has a high affinity of disulfide bonds. This interferes with cysteine residue cross-linking reducing keratin formation. This results in alopecia and the formation of Mees lines. Decreased cysteine cross-linking also leads to decreased glutathione resulting in accumulation of lipid peroxides in the brain, which are most prominent in the cerebellum, often seen as dark pigmented lipofuscinlike areas. [13]

Thallium interferes with protein synthesis by damaging ribosomes, particularly the 60s ribosomal subunit, further leading to cellular injury and death. [14]

Although the exact mechanism of myelin injury by thallium is unknown, there are consistent findings of fragmentation and degeneration of myelin in both the central and peripheral nervous systems. A Wallerian degeneration pattern first develops in long peripheral axons (lower then upper extremities) with sensory then motor impairment.

Thallium follows a 3-phase toxicokinetics: first intravascular distribution, then CNS distribution, and finally elimination. In the first 4 hours following exposure, thallium is rapidly distributed to the blood and to well-perfused organs such as the kidney, liver, and muscle. Over the next 4-48 hours, thallium is distributed into the CNS. The elimination phase begins about 24 hours after ingestion.

Thallium is primarily eliminated through excretion in the feces (51.4%) and the urine (26.4%). The high concentrations of thallium found in the kidney (> 5.5 times more than other tissues) result from renal filtration with approximately 50% reabsorbed in the kidney tubules. Elimination is slow, with an elimination half-life of 3-30 days, varying with the dose and chronicity of the exposure. Because of this prolonged elimination phase, thallium may act as a cumulative poison.





Because it is odorless and tasteless, thallium has successfully been used worldwide as a rat poison and ant killer. It was restricted for household use in the United States in 1965 and banned commercially in 1975. Thallium is still commonly used as a rodenticide and insecticide in other countries, resulting in severe unintentional poisoning, despite the World Health Organization's recommendation against its use in 1973. [15]

Thallium has been used as a pesticide in other countries, such as in Africa, causing poisoning through contaminated foods. It has been discovered as a contaminant in some Chinese herbal medications.

Thallium is toxic by cumulative intake; it can be absorbed through the skin, respiratory, and GI tracts. Besides oral ingestion, inhalation of contaminated dust during manufacture, sniffing what was thought to be cocaine, and skin absorption through protective gloves have all been reported as causes of thallium toxicity. In addition, cases of thallium intoxication by intravenous injection of contaminated heroin have been reported. However, the vast majority of cases result from oral exposures.

Because chronic thallium exposure mimics other diseases, cases of industrial thallium exposure may go unnoticed. Accidental poisoning caused by direct contact with and careless handling of thallium-containing materials occurs more frequently.

Thallium is used most widely in the semiconductor and optical industries. In addition, it is used in some industries for the production of photoelectric cells, scintillation counters, chemical catalysts, green-emitting fireworks, cement plants, and imitation jewelry.

Trace amounts of thallium are used as a radioactive contrast agent (thallium-201) to visualize cardiac function. The amount of carrier thallium used for this purpose is 4000 times less than the dose at which some toxic effects develop in humans.




In 2019, 49 single exposures with no major outcome and no deaths were reported by the American Association of Poison Control Centers' National Poison Data System (AAPCC-NPDS). All but one exposure involved adults, and none of the exposures were intentional. [16]

Thallium toxicity is likely more common in developing countries where thallium rodenticides are still in use, but few data exist as to the incidence of thallium poisoning outside the United States. [17, 8]

No scientific data substantiate any differences in thallium toxicity that are attributable to race, sex, or age.





If recognized and treated early, thallium intoxication carries a favorable prognosis; however, the course of recovery may be lengthy. [18] Neurologic damage may persist if detoxification therapy is delayed. Patients have demonstrated persistent signs and symptoms of peripheral neuropathy at least 6 years after intoxication. Reports of persistent findings most commonly involve the feet and lower extremities.

Persistent psychiatric symptoms have been reported following thallium exposure, including the following:

  • Agitation
  • Aggression
  • Personality changes
  • Depression

The mortality rate for acute thallium toxicity has been reported as 6-15%; among survivors, 33-50% have neurologic or ocular sequelae.

The lethal dose for humans is 10-15 mg/kg (around 1 g for a 70-kg person). However, death can still occur at lower doses (minimal reported dose was 8 mg/kg). Some treated patients have survived exposure up to 28 mg/kg.