AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Background

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.

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 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. 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. 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.

Currently, thallium is 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. 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.

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.

Pathophysiology

The biochemical research on the cellular effects of thallium is extensive, but little data exist in humans. Thallium demonstrates at least 5 major toxicologic effects:

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

The lethal dose of thallium is approximately 15-20 mg/kg; however, significant toxicity and death may occur with smaller amounts. Severe poisoning is expected with oral exposures greater than 200 mg. Thallium poisoning more commonly occurs after oral ingestion. Thallium is rapidly distributed intracellularly throughout all body tissues. Little information is known about the volume of distribution in humans but is estimated to be 3.6-5.6 L/kg.

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 into 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.

Frequency

United States

Between 2003 and 2006, 82 cases if thallium exposures were reported to poison centers. No deaths were reported, and only one major outcome was reported. There is likely an overlap of reports from patients with concerns of the radioactive contrast agent (thallium-201) following noninvasive cardiac studies rather than true thallium poisonings. Although several deaths have been reported in the literature following suicidal or homicidal poisonings over the past few years, few data exist related to actual thallium intoxication cases in the United States.

International

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.

Mortality/Morbidity

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

Thallium is lethal to humans. The lethal dose for humans is 15-20 mg/kg (around 1 g for a 70-kg person). Nonfatal effects occur below this dose. However, it is conceivable that even smaller doses can still cause fatality (minimal reported dose was 8 mg/kg). In addition, some treated patients have survived exposure up to 28 mg/kg.

Race

No scientific data substantiate any differences in thallium toxicity that are attributable to race.

Sex

No scientific data substantiate any differences in thallium toxicity that are attributable to sex.

Age

No scientific data substantiate any differences in thallium toxicity that are attributable to age.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

History

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 symptoms, while neurologic findings predominate with chronic exposure. The neurologic manifestations tend to progress, even despite decreasing blood thallium levels. Thallium toxicity is characterized by a painful ascending peripheral neuropathy and alopecia; this clinical manifestation presents 2-3 weeks after an acute poisoning.

• Gastrointestinal symptoms: These symptoms predominate early, usually within the first 3-4 hours, and the most common symptom is severe, paroxysmal abdominal pain. 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. Nausea, vomiting, constipation, and diarrhea are reported. Somewhat characteristic for thallium exposure, patients report abdominal pain, mild diarrhea, followed by constipation. The vomitus and stools are often bloody.
• Neurologic symptoms: These symptoms usually appear 2-5 days postexposure and include severely painful, rapidly progressive, ascending peripheral neuropathies. Pain and paresthesias of the hands and the lower extremities, especially the soles of the feet, also predominate. 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.
• Ocular symptoms: Diplopia, abnormal color vision, and impairment of visual acuity may develop. 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. 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. Other dermatologic findings include crusted eczematous lesions, hypohidrosis, anhidrosis, palmar erythema, stomatitis, and painful glossitis with redness of the tip of the tongue. 
• Pulmonary symptoms: Some patients can experience pleuritic chest pain or tightness upon exposure. The mechanism for this particular symptom is unclear.

Physical

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.
  • 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. 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. 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.
  • 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.

Causes

• 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.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Other Problems to be Considered

Acute intermittent porphyria
Diabetic polyneuritis
Thiamine deficiency
Poliomyelitis
Colchicine toxicity
Vinca alkaloids
Hydralazine toxicity
Selenium toxicity
Vasculitis
Botulism

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Lab Studies

• Because laboratory studies are generally nonspecific, any unexplained peripheral neuropathy, especially accompanied by alopecia, should raise clinical suspicion for thallium toxicity. In consultation with the medical toxicologist, initiate treatment of patients with high suspicion of thallium toxicity while awaiting laboratory confirmation.
• The definitive clinical diagnosis of thallium poisoning can only be established by demonstrating elevated thallium levels. Thallium can be recovered in the hair, nails, feces, saliva, blood, and urine.
• A 24-hour urine thallium concentration is the standard toxicologic method and is assayed by atomic absorption photospectrometry. The normal level is less than 5 mcg/L.
• A urine spot test can deliver faster results. However, it often gives false-positive results, and it requires the use of 20% nitric acid, which can be dangerous and is usually not readily available.
• Because it is rapidly eliminated from the body, measurements of blood thallium reflect only recent exposures. Thus, it is not generally considered to be a reliable means of identifying or monitoring exposure to thallium.
• A CBC with differential can identify anemia, leukocytosis, eosinophilia, and thrombocytopenia, which have all been reported in cases of thallium exposure. Anemia most likely occurs secondary to GI hemorrhage.
• Electrolytes, calcium, glucose, BUN, creatinine, and liver function tests (LFTs) should be obtained. Thallium exposure can lead to electrolyte and glucose abnormalities, hypocalcemia, and impair renal and hepatic dysfunction.
• A pregnancy test should be considered for all women of childbearing age.

Imaging Studies

• Thallium is radiopaque; therefore, an abdominal radiograph should be obtained. This may reveal thallium metal after an acute ingestion. Radiographs of suspected exposure sources may be useful for confirming the presence of a heavy metal.

Other Tests

• Nerve conduction studies (NCS) may reveal findings consistent with an axonal sensorimotor peripheral neuropathy, with nerves innervating the feet most significantly involved. NCS may be useful in both diagnosing and monitoring patients with thallium exposure. The severity of abnormalities on NCS has been shown to correlate with the severity of other symptoms and findings.
• An EEG may show nonspecific slow-wave activity in severe cases.
• Microscopic inspection of scalp hair reveals dark black and brown pigment in the hair roots in approximately 95% of poisoned patients. However, this may be difficult to visualize by the untrained observer. Darkening of the hair root can occur as early as 4 days postexposure. These dark regions are an optical phenomenon caused by the accumulation of gaseous inclusions that diffract the light, resulting in the appearance of a black band.
• Electroretinographic (ERG) examination reveals a delayed visual evoked response. These ERG changes tend to occur before development of clinical symptoms in thallium intoxication. ERG may be useful when persons with known thallium exposure receive follow-up examinations.
• An ECG should be obtained to identify tachycardia and cardiac arrhythmias.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Prehospital Care

The prehospital treatment should focus on 4 areas: (1) stabilizing acute life-threatening conditions, (2) initiating supportive therapy, (3) identifying the time and route of exposure, and (4) beginning the decontamination process.

• Establish ABCs.
• Administer oxygen as needed.
• Obtain intravenous access.
• Remove contaminated clothing as soon as possible. Avoid self-exposure and wear protective clothing that is appropriate to the type and degree of contamination. Wear air-purifying or supplied-air respiratory equipment as necessary.
• Activated charcoal should be considered in patients presenting within 1 hour of ingestion and have an intact or protected airway.

Emergency Department Care

The goals of treating a patient with thallium toxicity are initial stabilization, prevention of absorption, enhanced elimination, and antidotal therapy. 

• Following the initial assessment and stabilization of the patient, aggressive gastrointestinal decontamination should be instituted. If not performed in the prehospital setting, remove contaminated clothing while avoiding self-exposure. With dermal exposure, thoroughly wash exposed skin with soap and water. For eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Be sure to wear protective clothing appropriate to the type and degree of contamination, and wear air-purifying or supplied-air respiratory equipment as necessary.
• Gastrointestinal decontamination, activated charcoal, and Prussian blue (potassium ferric hexacyanoferrate) are recommended in thallium ingestions.
• Consider orogastric lavage in patients presenting within 1 hour postingestion if they have not vomited or if thallium is observed in the stomach on radiographs in patients who have vomited. In addition, whole-bowel irrigation with polyethylene glycol electrolyte lavage solution may be useful, especially when radiopaque material is visualized on an abdominal radiograph.
• Although both Prussian blue and activated charcoal absorb thallium, it appears that Prussian blue has absorptive superiority. In addition, because it has a far better safety profile than other proposed therapies, Prussian blue should be considered the drug of choice in acute thallium poisoning.
• Prussian blue is a crystal blue lattice of potassium ferric ferrocyanide. It acts as an ion exchanger for univalent cations, with its affinity increasing as the ionic radius of the cation increases. Prussian blue exchanges potassium ions from its lattice with thallium ions in the gut lumen. Removal of thallium from the gut creates a concentration gradient causing an increase in thallium exchange into the gut lumen. This interrupts its enterohepatic recirculation and increases its elimination. Prussian blue releases a negligible amount of cyanide (<1.6 mg, minimal lethal dose of cyanide in humans is approximately 50 mg) and does not present a safety concern following its use. 
• Prussian blue (Radiogardase) was approved by the Food and Drug Administration (FDA) in 2003 but is still difficult to obtain for pharmaceutical use in the United States. However, it has been obtained from The Oak Ridge Institute for Science and Education and the Radiation Emergency Assistance Center (REAC) in Oak Ridge, Tennessee. In addition, successful therapy using the laboratory reagent of Prussian blue has been documented in the United States.
• In patients in whom Prussian blue cannot be obtained and thallium poisoning is suspected, multidose activated charcoal may be effective. Because thallium undergoes enterohepatic and enteroenteric recirculation, repeated charcoal administration (0.25-0.5 g/kg q2-4h) may enhance fecal elimination.
• Forced diuresis with potassium loading was previously recommended to increase the renal clearance of thallium, but this may exacerbate the neurologic and cardiovascular symptoms and is no longer advised.
• Chelating agents such as EDTA, dimercaprol, and D-penicillamine have not been shown to be effective and should be avoided.
• The usefulness of hemodialysis and hemoperfusion is controversial, but they may be useful during early thallium poisoning before extensive distribution within the body tissues has occurred.
• N-acetylcysteine and l-cysteine have not been shown to be effective in reducing mortality in animal models.

Consultations

• Consultation with a regional poison control center or medical toxicologist may be of benefit.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Institute treatment of thallium intoxication as soon as the diagnosis is suspected because tissue-bound thallium may cause prolonged neurologic damage if detoxification therapy is not commenced within 72 h of onset of acute poisoning.

Drug Category: GI decontaminants

These agents bind thallium in the GI tract and prevent enterohepatic recirculation.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Further Inpatient Care

• Admit all patients with significant signs and symptoms of thallium toxicity.
• Initially measure thallium concentrations in the urine 3 times per week to confirm a decreasing trend. Prussian blue treatment should be continued until the 24-hour urine thallium concentration returns to the reference range (0-5 mcg/d).
• Thallotoxicosis also is associated with a severe form of stomatitis; thus, monitor mouth hygiene closely. Shaving the patient's head may reduce the stress induced by hair loss and improve the patient's morale.
• Physical therapy may be instituted to prevent development of muscle contractures.

Further Outpatient Care

• Patients with unintentional intoxication who are asymptomatic with a minimal increase in urine thallium level may be discharged with close follow-up care.
• Patients with intentional ingestions should have a psychiatric evaluation before discharge from the hospital.

Transfer

• Consider transferring patients with severe symptomatology if a medical toxicologist is not readily available.

Deterrence/Prevention

• Regular follow-up care is recommended for persons with known thallium exposure.

Complications

• Prolonged 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 or persistent findings most commonly involve the feet and lower extremities.
• Cases of persistent agitation, aggression, personality changes, depression, and other psychiatric symptoms have been reported following thallium exposure.

Prognosis

• If recognized and treated early, thallium intoxication carries a favorable prognosis; however, the course of recovery may be lengthy.

Patient Education

• For excellent patient education resources, visit eMedicine's Poisoning Center and Poisoning - First Aid and Emergency Center. Also, see eMedicine's patient education articles Poisoning and Activated Charcoal.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical/Legal Pitfalls

• Failure to diagnose thallium toxicity in a patient with relevant signs and symptoms and a pertinent history of exposure
• Failure to initiate treatment before confirmatory testing (laboratory assays may take several days to become available)
• Failure to consult a medical toxicologist or regional poison control center for updated information regarding this unusual toxic exposure

Special Concerns

• Few human reports of acute thallium poisoning during pregnancy exist. However, in animal models, thallium is teratogenic with trends toward low birth weight and prematurity. Thallium crosses the placenta and is excreted in breast milk. Because of insufficient data to predict the outcome of pregnancy complicated by maternal thallium exposure, all patients should be evaluated on a case-by-case basis.

ACKNOWLEDGMENTS

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Wendy R Regal, MD, Mary L Arvanitis, DO, Igor Boyarsky, DO, and Adrian D Crisan, MD, to the development and writing of this article.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

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Article Last Updated: Aug 6, 2008