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Pathophysiology: The toxic effects of thallium are related, in part, to its similarity with potassium; both elements have the same charge and similar ionic radii, therefore allowing thallium to alter a number of potassium-mediated processes. Possible toxic mechanisms of thallium include ligand formation with protein sulfhydryl groups, inhibition of cellular respiration, interaction with riboflavin cofactors, and disruption of calcium homeostasis. Most cases of thallium toxicity occur after oral ingestion, but toxicity also may occur after inhalation of contaminated dust from pyrite burners, cadmium manufacturing, lead and zinc smelting, and even snorting what is believed to be cocaine.
The lethal dose for humans is approximately 15-20 mg/kg; however, fatality and significant toxicity may occur with a smaller amount. Following absorption, thallium uptake into the circulatory system is rapid. Thallium is quickly distributed from the blood to the tissues with an apparent blood half-life of less than 5 minutes. Thallium is readily distributed into tissues, including the brain and through the placenta. Penetration into tissue compartments is reflected by the large volume of distribution of approximately 4-20 L/kg. The high concentrations of thallium found in the kidney (>5.5 times more than other tissues) result from renal filtration and intracellular thallium accumulation. The primary elimination pathway for thallium is through excretion into the feces, but renal elimination may be substantial (approximately 35%). The elimination half-life of thallium is 3-30 days, but it varies with the dose and chronicity of the exposure. Because of this prolonged elimination phase, thallium may act as a cumulative poison.
Time after thallium intake
12-48 h Nausea, vomiting, diarrhoea, gastritis, duodenitis, pancreatic and parotid damage.
damage 2-5 days Paraesthesiae, hyperaesthesia, headaches, respiratory depression, nystagmus (scanning movement of the eyes when they should be still), optic neuropathy (damage to optic nerves) and atrophy, myalgia (muscle pain), myopathy (muscle wasting), severe pain, loss of reflexes, convulsions, coma, delirium, acute motor neuropathy , dementia and psychosis.
2-3 weeks Characteristic changes at the bases of hair shafts, followed by loss of hair.
> 3 weeks Cardiac arrhythmias may occur for up to 2 months (due to damage to the controlling autonomic nerves or direct toxicity. However, if there is sinus tachycardia, this is probably due to increased catecholamine production.) Skin rash as in riboflavin deficiency.
Thallium poisoning by ingestion may be diagnosed by x-ray as thallium is radio-opaque. Severe poisoning occurs if more than 1g or 8 mg per kg of body weight has been ingested 8.
Chronic exposure to thallium causes effects on the nervous system, and patients experience numbness of fingers and toes 13. After around 2-3 weeks, they also will loose their hair, and this is a characteristic feature of thallium poisoning 1.
Include documentation of a skin and scalp examination.
A characteristic bandlike dark pigmentation pattern frequently is noted in the scalp within 4 days. Scalp alopecia, probably the most described symptom of chronic thallium toxicity, usually occurs 10-21 days postexposure and primarily is caused by atrophy of the hair follicles. The appearance of the hair mount, showing tapered or bayonet anagen hair with black pigmentation at the base, may be highly diagnostic even before the onset of alopecia.
In the skin, acneiform eruptions, pellagralike rashes, crusting and dry scaling of distal parts of the extremities, and development of nail dystrophy (Mees lines) may be observed.
Neurologic findings are dose related and may appear in 2-5 days. Signs of a peripheral neuropathy occur with marked leg and foot tenderness and paresthesias. Actual weakness may be difficult to assess because of pain, but weakness is mild.
In the setting of severe neurologic symptoms, respiratory paralysis and fatality occur in 7 days.
If the patient is seen within 6 hours of ingestion of the thallium, gastric lavage and induced emesis may be useful to try to stop the absorption of thallium into the body 8. Thallium can be succesfully treated as a specific antidote exists and this is known as potassium ferrihexacyanoferrate, or Prussian blue or Berlin blue. This works by sequestering the ions in the intestine, preventing their absorbtion 1, 8. Unlike other forms of metal poisoning, activated charcoal is useful, and can help reduce the severity of the poisoning by disrupting the enterohepatic circualtion. Other treatments that may be tried include forced diuresis, treatment with potassium chloride (this promotes the renal excretion of thallium), and peritoneal dialysis 8.
Toxicol Clin Toxicol 1994;32(6):723-30
Thallium poisoning from maliciously contaminated food.
Meggs WJ, Hoffman RS, Shih RD, Weisman RS, Goldfrank LR
New York City Poison Center, New York 10016.
Four young adults presented two days after one of them had received marzipan balls packaged in a box from an expensive candy manufacturer. Two ate one candy ball, while two others shared a third. The next day, variable gastrointestinal symptoms developed. On the third day, two patients developed painful paresthesiae of the hands and feet, an early but nonspecific clinical marker of thallium poisoning. A tentative diagnosis of thallium poisoning was made based on symptoms, and treatment was initiated. The remaining candies were radiographed. Metallic densities in the candies supported the diagnosis, and atomic absorption spectroscopy was used to quantitate thallium content. Each candy contained a potentially fatal dose. Five to seven days later, hypertension and tachycardia developed in the two patients who had ingested an entire candy. All patients developed alopecia but recovered without overt neurologic or other sequelae. While the diagnosis of thallium poisoning is often delayed until alopecia develops, an early diagnosis favors an effective treatment strategy.
Dokl Biochem Biophys. 2003 Sep-Oct;392:247-52.
Thallium induces opening of the mitochondrial permeability transition pore in the inner membrane of rat liver mitochondria.
Korotkov SM, Lapin AV.
Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, pr. Morisa Toreza 44, St. Petersburg, 194223 Russia.
Dokl Biochem Biophys. 2003 Sep-Oct;392:244-6.
Involvement of K+-ATP-dependent channel in transport of monovalent thallium (Tl+) across the inner membrane of rat liver mitochondria.
Nikitina ER, Glazunov VV.
Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, pr. Morisa Toreza 44, St. Petersburg, 194223 Russia
Ecotoxicol Environ Saf. 2004 Sep;59(1):84-8. Related Articles, Links
Highly toxic thallium in plants from the vicinity of Olkusz (Poland).
Wierzbicka M, Szarek-Lukaszewska G, Grodzinska K.
Environmental Plant Pollution Laboratory, Department of Morphogenesis, Institute of Plant Experimental Biology, University of Warsaw, Miecznikowa 1, 02-096 Warsaw, Poland. firstname.lastname@example.org
Thallium is a highly toxic metal that plays no role in the metabolism of plants or animals. Recent studies using small mammals and bird feathers as bioindicators demonstrated for the first time that animals from the vicinity of the Bolesl?aw metal works near Olkusz (southern Poland) had large amounts of thallium in their tissues. Because of concern over these reports, four plant species (Plantago lanceolata, Biscutella laevigata, Dianthus carthusianorum, Silene vulgaris) growing wildly in the same area on a 100-year-old calamine waste heap, as well as the waste heap soil, were examined....
J Eur Acad Dermatol Venereol. 2004 May;18(3):321-3. Related Articles, Links
Acute generalized exanthematous pustulosis due to thallium.
Aziz Jalali MH, Mirzazadeh Javaheri S, Salehian P.
Department of Dermatology, Iran University of Medicine, Hazrat Rasoul Hospital, Niyaeh st, Satarkhan Ave, Tehran, Iran. email@example.com
Acute generalized exanthematous pustulosis (AGEP) is characterized clinically by fever, pruritus and acute pustular eruption. Usually a drug is found to be the responsible agent. We present a patient who experienced an acute generalized exanthematous pustulosis due to radioactive thallium. The eruption cleared rapidly after discontinuation of the drug and systemic corticosteroid therapy.
Int J Legal Med. 2004 Jul 9 [Epub ahead of print] Related Articles, Links
Reconstruction of a case of thallium poisoning using LA-ICP-SFMS.
Hann S, Latkoczy C, Bereuter TL, Prohaska T, Stingeder G, Reiter C.
Department of Chemistry, University of Natural Resources and Applied Life Sciences, Muthgasse 18, 1190, Vienna, Austria.
The unique capabilities of laser ablation in combination with inductively coupled plasma sector field mass spectrometry (LA-ICP-SFMS) were employed to reconstruct details of a homicide by thallium poisoning, which took place 38 years ago in Austria. Thallium was determined in several human bone samples after acid digestion in a microwave oven. The ICP-SFMS results showed that the thallium concentration in the victim's bones was in the range 1.07-2.63 micro g g(-1), which is up to 170 times higher compared to concentrations found in bones of persons who have died due to natural causes. The results were in accordance with the values obtained by graphite furnace atomic absorption spectrometry (GF-AAS). Laser ablation ICP-SFMS was applied to assess the time interval between the victim's poisoning and death. Several line scans with a laser spot size of 50 microm were performed on a thumbnail of the poisoned person and on a reference thumbnail by laser ablation ICP-SFMS. Thallium peaks were detected on the nail of the victim at a distance of 2.5 mm from the younger edge of the nail.