Amblyopia, tobacco

Much of the toxicological interest in cyanide relating to mammals has focused on its rapid lethal action. However, its most widely distributed toxicologic problems are due to its toxicity from dietary, industrial, and environmental factors (Way 1981, 1984 Gee 1987 Marrs and Ballantyne 1987 Eisler 1991). Chronic exposure to cyanide is correlated with specific human diseases Nigerian nutritional neuropathy, Leber s optical atrophy, retrobulbar neuritis, pernicious anemia, tobacco amblyopia, cretinism, and ataxic tropical neuropathy (Towill etal. 1978 Way 1981 Sprine etal. 1982 Beminger et al. 1989 Ukhun and Dibie 1989). The effects of chronic cyanide intoxication are confounded by various nutritional factors, such as dietary deficiencies of sulfur-containing amino acids, proteins, and water-soluble vitamins (Way 1981). 

The nervous system is the most sensitive target for cyanide toxicity, partly because of its high metabolic demands. High doses of cyanide can result in death via central nervous system effects, which can cause respiratory arrest. In humans, chronic low-level cyanide exposure through cassava consumption (and possibly through tobacco smoke inhalation) has been associated with tropical neuropathy, tobacco amblyopia, and Leber s hereditary optic atrophy. It has been suggested that defects in the metabolic conversion of cyanide to thiocyanate, as well as nutritional deficiencies of protein and vitamin B12 and other vitamins and minerals may play a role in the development of these disorders (Wilson 1965). 

Persons with a metabolic disturbance in the conversion of cyanide to thiocyanate may be at greater risk. A defect in the rhodanese system and vitamin B12 deficiency have been associated with tobacco amblyopia and Leber s hereditary optic atrophy in persons exposed to cyanide in tobacco smoke (Wilson 1983). 

Contraindications Compensatory hypertension (atrioventricular AV shunt or coarctation of aorta), congenital (Leber s) optic atrophy, inadequate cerebral circulation, moribund patients, tobacco amblyopia... 

Tobacco amblyopia has been attributed to cyanide intoxication from strong tobacco which interferes with the coenzyme fimction of vitamin hydroxocobalamin (not cyanocobalamin) may be given. 

Abnormalities suggestive of deranged cyanide emd vitamin Bi2 metabolism have been demonstrated in Leber s disease (hereditary optic atrophy) and in dominantly inherited optic atrophy, and consist of significant elevations of pleisma cyanocobalamin [56]. Similar changes have been reported in sporadic cases of bilateral optic atrophy occurring in Europeans, and in cases of so-called tobacco amblyopia. 

Inadequacy of the enzyme system may play a role the available amount of endogenous thiosulphate is certainly a factor. Patients with Leber s optic atrophy or tobacco amblyopia have already relatively high cya-nide/thiocyanate levels and the use of nitroprusside in such patients is contraindicated, as it is in patients with deranged liver function and with vitamin BI2 deficiency. 

The patient with tobacco or alcohol amblyopia usually has either low serum levels of vitamin B12 or cannot absorb this vitamin in sufficient amoimts. Thus the treatment for this condition involves supplemental vitamin therapy. 

After documenting a serum vitamin B12 deficiency, the patient should receive 300 mg oral thiamine each week and 1,000 g intramuscular hydroxocobalamin each week for 10 weeks.The sooner this therapy begins, the better the prognosis. The hydroxocobalamin fc>rm of vitamin B12 appears to be more effective than cyanocobalamin. In terms of recovery from the amblyopia, cessation of smoking or drinking does not appear to produce remission unless the patient concurrently improves their diet.Thus it is unnecessary and, in practice, difficult to persuade patients who are habitual abusers of tobacco and alcohol to stop the use of such agents. Improvement of dietary status seems to be the most important factor in recovery. 

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