1.3.1 Thallium poisoning classification
The thallium poisoning classification includes two main groups: professional and nonprofessional; the latter group is the largest (Spiridonova and Shabalina, 1977a). In turn, nonprofessional thallium poisoning can divide into accidental, intentional, and criminal. At the same time, the largest group is suicides. Then there is a group of patients treated with thallium for syphilis, night sweats for tuberculosis, and people who suffered from thallium compounds by mistake, and in addition, from murder and abortion (Spiridonova and Shabalina, 1977a).
After a short time, the ingestion of thallium compounds into the human body causes nausea and vomiting, but the first poisoning symptoms appear after 3–4 days. A rapidly progressive painful peripheral neuropathy develops, which begins in the legs. After a while, the hands involved in this process, brown or black formations appear in the bulb and the root part of the hair shaft (Paulson et al., 1972; Cavanagh, 1991; Ibrahim et al., 2006; Rusyniak et al., 2002, 2010; Curto-Barredo et al., 2015; Liu and Liao, 2021). Acute alopecia may be further evidence of acute thallium poisoning (Senthilkumaran et al., 2017). During this period, patients most often paid attention to abdominal pain and diarrhea, which almost always followed by constipation due to the possible involvement of the vagus nerve in this process (Reed et al., 1963; Mulkey and Oehme, 1993; Hoffman, 2003). This poisoning stage occasionally observed glossitis, pharyngoesophagitis, gastritis, enteritis, and colitis (Galván-Arzate and Santamaría, 1998). Quite often, subfebrile or high body temperature occurs from the very onset of the disease, caused by the thallium ingress into the body (Spiridonova and Shabalina, 1977a).
Discomfort neuralgic pains in both legs, behind the breastbone, and abdomen, great thirst, and insomnia were emerged on the second week after poisoning (Moeschlin, 1980; Worthley, 2002a,b). Hypertension, ophthalmoplegia, circulatory disorders, and tachycardia develop due to toxic damage to the myocardium; a deficiency of vitamin B1 and niacin is found; motor and respiratory nerves are affected; damage to nerve fibers and chromatolysis of neurons occurs; dryness of the skin (anhidrosis) appears due to the disappearance of sweat secretion owing to the destruction of the sweat glands; pleural pain, diffuse myalgias, nonspecific dizziness, decreased activity, memory impairment, confusion, incoherent speech, chronic neuropsychiatric manifestations, tremors, convulsions, and ataxia occur; hair loss (alopecia) begins; the heart rate increases; there is a sluggish paraparesis; acute toxic polyneuritis appears and in some cases hand reflexes are affected, since some cranial nerves and, in particular, pairs II, III, and VI are affected (Brewer and Haggerty, 1958; Reed et al., 1963; Budrin and Meshcherskaya, 1975; Spiridonova and Shabalina, 1977a; Cavanagh, 1979, 1991; Prick, 1979; Moeschlin, 1980; McMillan et al., 1997; Worthley, 2002a,b; Lyubchenko et al., 2004; Ibrahim et al., 2006; Tsai et al., 2006; Cvjetko et al., 2010; Rusyniak et al., 2010; Pavlova et al., 2012; Chukhlovina, 1999; Huang et al., 2012; Sheiman et al., 2014; Blain and Kazantzis, 2015). Perioral numbness, the face erythematous eruptions, hair roots' damage, polyneuropathy, parakeratosis, the basal layer vacuolar degeneration, and epidermal nerves' loss initially developed in two patients after ingestion of thallium-containing water (Lu et al., 2007). We can note that impaired coordination, gait, and extensive alopecia appeared on the third day after thallium ingestion into a three-year-old child's body (Taber, 1964).
After three to four weeks of thallium poisoning often observed weight loss (Schoer, 1984). Symptoms of polyneuropathy and, in particular, distal axonal polyneuropathy, convulsive syndrome, agitation, delirium, coma also appear here (Innis and Moses, 1978; Cavanagh, 1979; Chukhlovina, 1999; Vorobyev, 2003; Sun et al., 2012). The resembling neuralgia pain, colic-like pain in the abdomen and behind the sternum is the main symptoms at this stage (Schoer, 1984). These symptoms of thallotoxicosis were much stronger in two people simultaneously poisoned with thallium and arsenic (Rusyniak et al., 2002). Increased anxiety, excitement, and confusion with a simultaneous two to threefold increase in thallium clearance occurred just after it entered the body of a 64-year-old man (Papp et al., 1969). The aforementioned symptoms prolonged over time in chronic thallium poisoning.
The following symptoms accompanied this poisoning: eye diseases, including catarrhal conjunctivitis and loss of vision, distorted color perception, varying degrees of pain in the legs without noticeable signs of polyneuritis, and the very subtle onset of hair loss, and decreased activity of Mg2+-ATPase and Na+/K+-ATPase (Bulavintseva, 1975; Schoer, 1984; Tabandeh and Thompson, 1993). Chronic thallium poisoning primarily damages the extrapyramidal system, which choreic and athetotic movements often characterized (Prick, 1979). Along with this, indigestion, movement disorders, endocrine disruptions, lack of resistance to infection, lack of appetite, weight loss, brain and nervous disorders with intellectual disabilities, and behavioral abnormalities appear (Schoer, 1984). Recent studies of a large number of patients have not found an association between elevated thallium concentrations in humans and a subsequent increase in the risk of developing diabetes (Menke et al., 2016).
The thallium concentration (μg/L) in the blood may indicate the degree of poisoning of a person with thallium with the related symptoms. These symptoms can subdivide: mild degree of damage is less than 30 (asthenia, hyperesthesia, electrolyte disorders in the heart muscle, gastroduodenitis); the average degree of damage is 30–100 (asthenia, diffuse brain damage, impaired sensitivity, pain in the distal extremities, an increase in dysmetabolic disorders in the myocardium); severe lesion is 100–500 (depression of consciousness, an increase in pain syndrome, the appearance of cardiac arrhythmias and conduction disorders, the formation of zones of ischemia of the left ventricle); extremely severe degree is more than 500 (coma of the first degree, damage to the cranial nerves; Kuzmich, 2006). The thallium concentration in blood plasma reaches a maximum of 2 h after this metal ingestion into the body. Then thallium is quickly distributed to other organs, and its excretion in the urine is observed (Oehme, 1978). Thallium ingested into the body accumulates in the muscles, and its minimum amount is in adipose and connective tissues (Spiridonova and Shabalina, 1977a). The liver dysfunction symptoms (the urobilinogen increase, albuminuria, the increase of iron and copper serum levels) can observe in severe thallium poisoning. Poisoning in later stages noted severe liver obesity and degeneration of the heart and kidneys (Spiridonova and Shabalina, 1977a).
Albuminuria and hematuria were after toxic kidney damage following thallium salt poisoning, but renal function was not significantly impaired (Reed et al., 1963). Histological findings from thallium-poisoned patients showed centrilobular necrosis with fatty changes in most liver lobes and abnormal amounts of porphyrins in the urine (Cavanagh et al., 1974). Two to three months after thallium poisoning, typical Meese stripes appear on the nails of the hands and feet, and bluish lines may appear on the gums (Reed et al., 1963; Budrin and Meshcherskaya, 1975; Huang et al., 2012; Liu et al., 2015). Acute confusion and severe painful neuropathy, along with skin lesions, developed in two thallium-poisoned patients from Taiwan (Huang et al., 2012). All thallium-affected people showed changes in blood vessels and blood flow as well as minor hemorrhages, stasis, parenchymal dystrophy (myocardium, kidneys, liver), widespread bronchopneumonia with foci of pulmonary destruction, and edema with the spinal cord tension (Treshchinsky et al., 1989; Vorobyev, 2003; Kuzmich, 2006). Thallium's toxic effects are its ability to disrupt kidney and liver function and its ability to react directly with proteins (Tikhova, 1967).
Thallium belongs to cytotoxic poisons. It is much slower than potassium and is released from the body and secreted by the epithelium of the stomach, salivary glands, and renal tubules (Mulkey and Oehme, 1993; Sheiman et al., 2014; Gad and Pham, 2014). Thallium trapped into the cell is not released as quickly as potassium (Gehring and Hammond, 1967). The concentration of thallium in the saliva of a 28-year-old woman poisoned by it was 15 times higher than the same concentration in urine (Richelmi et al., 1980). As soon as thallium enters the body, the formation of metalloprotein toxins occurs due to the thallium reaction with albumins, globulins, and other blood proteins in subsequent inactivating these proteins' SH-groups (Sheiman et al., 2014). In this case, toxins with a molecule size from 10 to 200 nm had the maximum damaging effect. According to various sources, the half-life of thallium from the human body and experimental animals is approximately 3–5 days (Lie et al., 1960; Schaller et al., 1980; Mulkey and Oehme, 1993; Kazantzis, 2007; Cvjetko et al., 2010; Livanov et al., 2013, 2015). Urine thallium level can judge the metal amount is taken (Spiridonova and Shabalina, 1977a). A man and a woman (China) got poisoned by an unknown amount of thallium (Huang et al., 2012; Liu et al., 2013). As a result, these people found impaired consciousness, speed of perception, and memory, but they gradually restored during the first year. There have been cases when thallium was detected in the urine even five months after poisoning with a rodenticide containing Tl2SO4 (Blain and Kazantzis, 2015). Use this knowledge please don't commit murder though
Thank you for reading word count is 1493
