Thallium has again become a toxicity concern. Discovered in the 1800s by Sir William Crookes, it was used in medical treatments, for venereal diseases, gout, and tuberculosis. Its toxicity, however, caused it to fall into disuse, though thallium acetate continued to be employed for fungal skin infections for some time.
Industrial use of thallium has increased in recent years. It can form useful alloys with silver or lead and may be a byproduct of zinc and lead production. In electronics, thallium is used in power systems, such as batteries or semiconductors. It is also employed in optical lenses, photo film, jewelry, dyes and pigments, and fireworks. A bigger concern was its uses in pesticides and rodentocides, which were banned in 1975. Thallium sulfate was used with starch and glycerin to treat grains for poisoning squirrels and rodents. This led to some fatalities when humans mistakenly consumed some of that grain.
Thallium is in low concentration in the earth’s crust. Humans cannot tolerate much thallium in their bodies. This mineral and its salts can enter our body through our skin, respiratory tract, or gastrointestinal route. It can be toxic in several ways. First, it can substitute for potassium in certain functions within the red blood cells, such as in the sodium/potassium ATPase. Thallium also has a strong attraction to sulfhydryl groups and thus may interact with these active enzyme sites. Thallium can pass the placenta into the fetus. There is some suggestion that thallium has teratogenic effects.
Thallium has significant toxicity effects both with large acute exposure and lower-level, chronic intake. Acute ingestion can lead to nausea, vomiting, abdominal pain, bloody diarrhea, fatigue, and fever. This can be fatal through its secondary agitation state which can cause seizures and then coma and respiratory failure. If people survive this exposure, further problems can affect the kidneys, heart, and nervous system. Sensory and motor changes, peripheral neuropathy, loss of reflexes, hair loss, arrhythmias, and renal disease may result. This may progress over several weeks. Most ingested thallium goes to and is excreted by the kidneys; the remainder is stored in many other tissues.
Chronic poisoning may cause polyneuritis with an inability to walk, fatigue, weight loss, and possibly reduced immunity. Thallium acetate has been used as a purposeful poison on several known occasions. Since it has no color or taste, it is well concealed in food and drinks; and it is not commonly looked for.
Thallium can be measured in the blood or urine. A 24-hour urine collection may reveal increased levels of this toxic mineral. A treatment with potassium chloride or EDTA may show increased levels of thallium in the urine.
Treatment for thallium poisoning is somewhat complex. Agents such as EDTA, dimercaprol, penicillamine, sodium iodide, and thiouracil have all been used with some benefit. Diuresis and potassium chloride are used more standardly to reduce thallium toxicity by increasing excretion levels. Prussian Blue (potassium ferric cyanoferrate) dye has been used to trap thallium in the gut after initial ingestion. Hemoperfusion or dialysis is used to reduce blood concentrations of thallium. Overall, we would be wise to avoid exposure to thallium.