Thallium in Microsoft Office

Printing QR-Code in Microsoft Office Thallium

In the late nineteenth century, thallium was used medicinally in the treatment of venereal disease, ringworm, and tuberculosis and later in rodenticides and insecticides Poisoning was fairly common Sporadic instances of poisoning still occur, usually as a result of accidental or suicidal ingestion of thallium-containing rodenticides and rarely from overuse of thallium-containing depilatory agents Patients who survive the effects of acute poisoning develop a rapidly progressive and painful sensory polyneuropathy, optic atrophy, and occasionally ophthalmoplegia followed, 15 to 30 days after ingestion, by diffuse alopecia (see page 1130) The latter feature should always suggest the diagnosis of thallium poisoning, which can be con rmed by nding this metallic element in the urine Two of our patients had a severe sensory and mild motor polyneuropathy and alopecia, from which they were recovering months later It is not uncommon for the neuropathy to have a painful component involving acral regions The condition can end fatally The use of potassium chloride by mouth may hasten thallium excretion

Some of these, the heavy metals, have already been considered In addition, a large number of synthetic organic compounds are widely used in industry and are frequent sources of toxicity, and the list is constantly being expanded The reader is referred to the references at the end of the chapter, particularly to the most current text, edited by Spencer and Schaumburg, for details concerning these compounds Here we can do little more than enumerate the most important ones: chlorinated diphenyls (eg, DDT) or chlorinated polycyclic compounds (Kepone), used as insecticides; diethylene dioxide (Dioxane); carbon disul de; the halogenated hydrocarbons (methyl chloride, tetrachloroethane, carbon tetrachloride, trichloroethylene, and methyl bromide); naphthalene (used in moth repellants); benzine (gasoline); benzene and its derivatives [toluene, xylene, nitrobenzene, phenol, and amyl acetate (banana oil)] and the hexacarbon solvents (n-hexane and methyl n-butyl ketone) With a few exceptions, the acute toxic effects of these substances are much the same from one compound to another In general, the primary effect is on nonneurologic structures Neural symptoms consist of varying combinations of headache, restlessness, drowsiness, confusion, delirium, coma, and convulsions, which, as a rule, occur late in the illness or preterminally Some of these industrial toxins [carbon disul de, carbon tetrachloride and tetrachloroethane, acrylamide, n-hexane, and diethylene glycol (Sterno; see Rollins)] may cause polyneuropathy, which becomes evident with recovery from acute toxicity Extrapyramidal symptoms may result from chronic exposure to carbon disul de A syndrome of persistent fatigue, lack of stamina, inability to concentrate, poor memory, and irritability has also been attributed to chronic exposure to solvents, but these symptoms are quite nonspeci c, and evidence for such a syndrome is unsupported by convincing experimental or epidemiologic studies Of the aforementioned industrial toxins, the ones most likely to cause neurologic disease are toluene (methyl benzene) and the hexacarbons The chronic inhalation of fumes containing toluene (usually in glue, contact cement, or certain brands of spray paint) may lead to severe and irreversible tremor and cerebellar ataxia, affecting movements of the eyes (opsoclonus, ocular dysmetria) and limbs, as well as stance and gait Cognitive impairment is usually associated; corticospinal tract signs, progressive optic neuropathy, sensorineural hearing loss, and hyposmia occur in some patients Generalized cerebral atrophy and particularly cerebellar atrophy are evident in CT scans (Fornazzari et al, Hormes et al) Also, it has become apparent that acute toluene intoxication is an important cause of seizures, hallucinations, and coma in children (King et al) The prolonged exposure to high concentrations of n-hexane or methyl-n-butyl ketone may cause a sensorimotor neuropathy, so-called glue-sniffer s neuropathy (page 1132) These solvents are metabolized to 2,5-hexanedione, which is the agent that damages the peripheral nerves The neuropathy may result from exposure in certain industrial settings (mainly the manufacture of vinyl products) or, more often, from the deliberate inhalation of vapors from solvents, lacquers, glue, or glue thinners containing n-hexane (see also Chap 46) Impure trichloroethylene, through its breakdown product dichloroacetylene, has a predilection for the trigeminal nerve, which can be damaged selectively Hydrogen peroxide poisoning, usually by accidental ingestion, causes multiple small cerebral infarcts through a mechanism

of gas embolus (Ijichi et al) Most cases have been reversible According to Humberson et al (cited by Ijichi and colleagues) 120 mL of 35% hydrogen peroxide releases 14 L of oxygen on contact with organic tissue The lung is involved, and the unmistakable brain lesions consist of tiny gas bubbles concentrated in parasagittal watershed areas