326
Trace Elements in Abiotic and Biotic Environments
body over time and mostly ends up in the skeleton. It is found in all tissues, except
fat, and it can even pass the placental barrier (Emsley 2006). Thallium has a short
half-life in the human body, and its intake is conveniently measured in urine, fingernails, and especially in the hair (Lansdown 2013).
Water-soluble Tl salts are readily absorbed by mucous membranes, such as
the mouth, stomach, and intestines, and they can even penetrate trough the skin.
Absorption of Tl by mucosa is almost complete (80%–100%) and very quick. After
absorption Tl is distributed from the blood to the tissue. In humans, the kidneys
display the highest concentrations, followed, in a decreasing order, by the bones,
stomach, intestines, spleen, liver, muscle, lung, and brain.
Thallium can be absorbed following inhalation of contaminated air (e.g., workplace), ingestion of contaminated food and water, or dermal contact. However, the
levels of Tl in air and water are very low. The greatest exposure occurs by food,
mainly homegrown fruits and green vegetables, may be contaminated by Tl.
The positively charged Tl ion (Tl + ) is almost of the same size as the K ion (K + ),
which is essential to living cells. Thallium mimics K so effectively that it can displace it at all sites around the body, but the most damaging is its concentration along
the central nervous system (Emsley 2006). Moreover, Tl follows K distribution pathways, and in this way alters many of K-dependent processes. For example, Tl may
substitute K in the Na + /K + -ATPase. Thallium seems to inhibit a range of enzymatic
reactions and to interfere with a variety of vital metabolic processes, disrupting cell
equilibrium, which in turn leads to generalized poisoning. At present, no data are
available about mutagenic, carcinogenic, or teratogenic effects of Tl compounds in
humans (Cvjetko et al. 2010).
Thallium is a cumulative poison, which can cause adverse health effects and
degenerative changes in many organs. The effects are the most severe in the nervous system. The exact mechanism of Tl toxicity still remains unknown, although
impaired glutathione metabolism, oxidative stress, and disruption of K-regulated
homeostasis may play a role.
Thallotoxicosis, or Tl poisoning, is usually the result of accidental or intentional
ingestion of Tl compounds. Clinical manifestations of Tl poisoning can be classified as acute, subchronic, and chronic, depending on the level of toxin, severity, and
time of exposure. The most prominent feature of Tl poisoning is the loss of hair or
alopecia.
Acute Tl poisoning is usually accompanied by gastrointestinal symptoms, although
neurological findings predominate in chronic exposure. Other symptoms include
polyneuritis; encephalopathy; tachycardia; degenerative changes of the heart, liver,
and kidney; subarachnoid hemorrhage; and bone marrow depression. Gastrointestinal
symptoms usually appear within the first few hours of acute poisoning. Severe abdominal pain goes along with vomiting, nausea, and bloody diarrhea. By contrast, these
symptoms are mild or nonexistent in chronic exposure. Thallium poisoning can also
be associated with neuropsychological symptoms and psychosis, such as depression,
apathy, anxiety, confusion, delirium, and hallucinations (Cvjetko et al. 2010).
Little information is available on levels of Tl in foods. Its normal level in most
food products is much less than 3 μg/kg fresh weight (FW) (Table 49.1). Low concentrations of Tl are detected in some brands of cigarette.