In smoke inhalation

Kirk M, Kulig K, Rumack BH. 1989. Methemoglobin and cyanide kinetics in smoke inhalation [Abstract]. Vet Hum Toxicol 31 353. 

Houeto P, Borron SW, Sandouk P et al. (1996). Pharmacokinetics of hydroxocobalamin in smoke inhalation victims. Clin Toxicol, 34, 397-404. 

Kirk MA, Gerace R and Kulig KW (1993). Cyanide and methemoglobin kinetics in smoke inhalation victims treated with the cyanide antidote kit. Ann Emerg Med, 22, 1413-1418. 

Hjalmarson A, Nilsson F, Sjostrom L, et al The nicotine inhaler in smoking cessation. 

Hazardous smoke. The potential for smoke inhalation damage is judged to be most severe in the descending order gasoline, methane, and hydrogen fires. 

Baron-Marano, F.L. and M.C. Izard. 1968. Observation d anomalies ultrastructurales dans la descendance d algues traitees par l acroleine. Compt. Rend. Hebdom. Sean. Acad. Sci. D, Sci. Natur. 267 2137-2139. Barrow, R.E., C-Z. Wang, R.A. Cox, and M.J. Evans. 1992. Cellular sequence of tracheal repair in sheep after smoke inhalation injury. Lung 170 331-338. 

A common metabolite found in the urine and plasma of patients treated with gold drugs is [Au(CN)2], an ion which readily enters cells and can inhibit the oxidative burst of white blood cells. It may therefore be an active metabolite of gold drugs. It also exhibits anticancer and anti-HIV activity. The high Au contents of red blood cells of smokers receiving gold therapy has been attributed to the inhalation of HCN in smoke (420). 

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). 

In addition, other chemicals such as a-adrenergic blocking agents like chlorpromazine (O Flaherty and Thomas 1982 Way and Burrows 1976) or oxygen (Burrows et al. 1973 Sheehy and Way 1968) may be used to enhance the protective action of other antidotes. However, the mechanism of their action is not well understood. Further research for a potent and safe antidote, particularly among smoke inhalation victims who have carbon monoxide poisoning, to mitigate cyanide toxicity is desirable. 

Reported levels of cyanide in tobacco smoke are quite variable. Cyanide levels in mainstream (inhaled) smoke from U.S. commercial cigarettes have been reported to range from 10 to 400 pg per cigarette, with the ratio of cyanide concentration in sidestream smoke to mainstream smoke ranging from 0.006 to 0.27... 

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