Some of these, the heavy metals, already have 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 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 (e.g., dichlorodiphenyltrichloroethane [DDT]) or chlorinated polycyclic compounds (Kepone), used as insecticides; diethylene dioxide (Dioxane); carbon disulfide; 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 disulfide, carbon tetrachloride and tetrachloroethane, acrylamide, n-hexane, and diethylene glycol [Sterno; see Rollins et al]) may cause polyneuropathy, which becomes evident with recovery from acute toxicity.
Extrapyramidal symptoms may result from chronic exposure to carbon disulfide. 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 nonspecific, 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 (see editorial on this subject in references). 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 on imaging studies (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 (see Chap. 43). 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. 43). Impure trichloroethylene, through its breakdown product dichloroacetylene, has a predilection for the trigeminal nerve, which can be damaged selectively.