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Thallium Toxicity Clinical Presentation

  • Author: Chip Gresham, MD, FACEM; Chief Editor: Asim Tarabar, MD  more...
Updated: Apr 23, 2014


The clinical presentation of thallium toxicity can vary depending on the type, severity, and timeframe of the exposure. Acute thallium poisoning is primarily characterized by gastrointestinal, neurological, and dermatological symptoms, while neurologic findings predominate with chronic exposure and tend to progress, even despite decreasing blood thallium levels.[13]

  • Gastrointestinal symptoms: These symptoms predominate early, usually within the first 3-4 hours, with the most common being abdominal pain with nausea/vomiting and diarrhea or constipation.[14, 15] It is important to remember that, unlike most other metal salts exposures, gastrointestinal findings in thallium toxicity may be mild or nonexistent, especially in chronic poisoning. Rarely, the vomitus and stools are bloody.
  • Neurologic symptoms: These symptoms usually appear 2-5 days (though some reports are for < 24 h) postexposure and include severely painful, rapidly progressive, ascending peripheral neuropathies.[14, 15] This is generally the reason patients seek medical care. Pain and paresthesias of the hands and the lower extremities, especially the soles of the feet, are also common. Distal motor weakness occurs, with the lower limbs more affected than the upper limbs. Ataxia, tremor, athetosis, cranial nerve palsies, headache, seizures, insomnia, coma, and death may also occur.
  • Neuropsychological manifestations may include anxiety, confusion, delirium, hallucinations, and psychosis. Acute agitation and aggression, personality changes, depression, apathy, and confabulation have been observed in both adults and children. Psychosis and associated symptoms can occur with or without a psychiatric history.[16]
  • Ocular symptoms: Diplopia, abnormal color vision, and impairment of visual acuity may develop.[17] Other manifestations may include loss of the lateral half of the eyebrows, skin lesions on the lids, ptosis, seventh nerve palsy, internal and external ophthalmoplegia, and nystagmus. Noninflammatory keratitis, lens opacities, and optic atrophy due to toxic optic neuropathy also may occur.
  • Dermatologic symptoms: The first cutaneous signs are not specific and include scaling of the palms and soles and acneiform or pustular eruptions of the face.[18] During weeks 2-3, a sudden onset of hair loss quickly progresses to diffuse alopecia. The hair loss primarily affects the scalp, temporal parts of the eyebrows, the eyelashes, and the limbs. Less often, the axillary regions are affected. Hair discoloration may also occur. One month after the poisoning, Mees lines (transverse white lines on the nails) appear in the nail plate.[19] Other dermatologic findings include crusted eczematous lesions, hypohidrosis, anhidrosis, palmar erythema, stomatitis, and painful glossitis with redness of the tip of the tongue.[20]
  • Cardiovascular symptoms: Include tachycardia and hypertension. Significant ongoing tachycardia may be associated with a poor prognosis.[1]
  • Pulmonary symptoms: Some patients can experience pleuritic chest pain or tightness upon exposure. The mechanism for this particular symptom is unclear.


Focus the physical examination primarily on the organ systems most commonly affected.

  • Perform careful abdominal and rectal examinations, including stool guaiac tests. Abdominal tenderness, hyperactive bowel sounds, mild guarding, and guaiac-positive stools can be found as early findings in thallium intoxication.
  • Perform a detailed neurologic examination, including a complete cranial nerve and visual field assessment.
    • All cranial nerves can be affected by thallium. Nystagmus (fourth and sixth CN involvement) and ptosis (third CN) may be present.
    • Decreased lower extremity strength with the lower limbs more affected than the upper limbs, hyperesthesia (especially of the soles of the feet), and decreased sensation to pinprick, touch, temperature, vibration, and proprioception in the fingers and toes may be present.
  • Perform a slit lamp examination and funduscopic examination, and carefully document visual acuity and color perception.
    • Decreased visual acuity with impairment of contrast sensitivity and tritanomaly (blue color vision defect) may be observed.[17]
    • In the early stages of thallium toxicity, funduscopic examination may reveal signs of an optic neuritis characterized by a red and poorly defined papilla. Continued thallium exposure causes atrophy of the optic nerve, which results in the development of a pale or white papilla.
    • Noninflammatory keratitis and lens opacities are also described.
  • Perform a skin and scalp examination.
    • Early skin findings include scaling of the palms and soles and acneiform lesions of the face.[18] Scalp alopecia, which is one of the most characteristic manifestations of thallium toxicity and is related to atrophy of the hair follicles, usually occurs 10-21 days postexposure.[21] In addition to the scalp, hair loss also occurs in the lateral eyebrows, the eyelashes, the limbs, and occasionally the axillary regions.
    • Hair roots may have dark brown or black pigmentation as a result of the accumulation of gaseous inclusions that diffract the light. With chronic exposure, these darker regions appear in bands, demonstrating multiple thallium exposures.
    • Approximately 1 month after thallium exposure, Mees lines (transverse white lines on the nails) appear in the nail plate.[19]
    • Other dermatologic findings include well-demarcated hyperkeratosis of the palms and soles, crusted eczematous lesions, hypohidrosis, anhidrosis, palmar erythema, crusted perioral dermatitis, painful glossitis with redness of the tip of the tongue, stomatitis, and hair discoloration.[20]


See the list below:

  • 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. This is despite the World Health Organization recommendation against its use in 1973.
  • Thallium has been used as a pesticide in other countries, such as Africa, causing poisoning through contaminated foods. It has been discovered as a contaminant in some Chinese herbal medications.
  • In review of the American Association of Poison Control Centers Annual Report for toxic exposures from 2003-2006, unintentional thallium poisoning accounts for the majority of reported cases. There is likely an overlap of reports from patients with concerns of the radioactive contrast agent (thallium-201) following noninvasive cardiac studies. However, homicide and suicide represent a significant percentage of cases in the United States.
  • Thallium is toxic by cumulative intake; it can be absorbed through the skin, respiratory, and GI tracts. Therefore, 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 disease, many cases of industrial thallium exposure most likely go unnoticed. On the other hand, accidental poisoning caused by direct contact with and careless handling of thallium-containing materials occurs more frequently.
  • Thallium is used most often 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 first appear in humans.
Contributor Information and Disclosures

Chip Gresham, MD, FACEM Emergency Medicine Physician and Medical Toxicologist, Department of Emergency Medicine, Clinical Director of Medication Safety, Middlemore Hospital; Senior Lecturer, Auckland University Medical School, New Zealand

Chip Gresham, MD, FACEM is a member of the following medical societies: American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.


Emma A Lawrey, MBChB, Dip Paeds, PG Cert ClinEd, FACEM Emergency Medicine Consultant and Clinical Toxicology Fellow, Department of Emergency Medicine, Middlemore Hospital, New Zealand

Emma A Lawrey, MBChB, Dip Paeds, PG Cert ClinEd, FACEM is a member of the following medical societies: Australasian College for Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Undersea and Hyperbaric Medical Society, Wilderness Medical Society, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center

William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


Mary L Arvanitis, DO, FACOEP Clinical Assistant Professor, Department of Emergency Medicine, Michigan State University, College of Human Medicine; Consulting Staff, Department of Emergency Medicine, Covenant Hospital; Director, Osteopathic Medical Education, Synergy Medical Education Alliance

Disclosure: Nothing to disclose.

Igor Boyarsky, DO Emergency Room Physician, Kaiser Permanente Southern California

Igor Boyarsky, DO is a member of the following medical societies: American Academy of Anti-Aging Medicine, American Academy of Emergency Medicine, American College of Emergency Physicians, and American Osteopathic Assocation

Disclosure: Nothing to disclose.

Adrian D Crisan, MD Staff Physician, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center

Disclosure: Nothing to disclose.

G Patrick Daubert, MD Assistant Professor, Assistant Medical Director, Sacramento Division, California Poison Control System; Director of Clinical and Medical Toxicology Education, Department of Emergency Medicine, University of California, Davis Medical Center

G Patrick Daubert, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Wendy R Regal, MD Clinical Instructor, Department of Emergency Medicine, Synergy Medical Education Alliance, Michigan State University

Disclosure: Nothing to disclose.

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