Fire smoke cyanide exposure

Smoking cigarettes and breathing smoke filled air during fires are major sources of cyanide exposure. 

Retrospective identification of cyanide poisoning in a CW context would be complicated by exposure from other sources, which include cigarette smoke, smoke from fires and some foods, e.g. cyanogenic glycosides in bitter almonds, fruit seeds and a number of plants. Quoted blood concentrations in non-smokers vary from a few ng/ml to >100 ng/ml. In nine fire victims, the concentrations determined were 687 597 ng/ml (Ishii et al., 1998). In smokers, cyanide levels in blood may rise to 500 ng/ml. 2-Aminothiazoline-4-carboxylic acid was detected in the urine of moderate cigarette smokers at concentrations between < 44-162 ng/ml (Lundquist et al., 1995). 

Cyanide binds to the in the heme of the cytochrome aaj component of cytochrome c oxidase and prevents electron transport to Oj. Mitochondrial respiration and energy production cease, and cell death rapidly occurs. The central nervous system is the primary target for cyanide toxicity. Acute inhalation of high concentrations of cyanide (e.g., smoke inhalation during a fire) provokes a brief central nervous system stimulation rapidly followed by convulsion, coma, and death. Acute exposure to lower amounts can cause lightheadedness, breathlessness, dizziness, numbness, and headaches. 

The symptoms of cyanide poisoning are well known from industrial exposure or exposure to cyanide in smoke from residential or industrial fires. Early signs and symptoms of acute cyanide poisoning include attempts of the... 

Cyanide is an instant killer at a certain dose level. However, deaths by pulmonary edema after a lag period (Paintal, 1986) and other toxicities observed in Bhopal victims (Varma, 1987) are not known to be caused by cyanide. Some cyanide is present in most individuals, and more so if there is smoke and fire. Any beneficial effect of sodium thiosulfate could be explained by environmental exposure to cyanide, especially because a... 

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