Chapter 10: Hydrogen Cyanide—Physiological Effects of Acute Exposure during Fires
Published:16 Oct 2015
D. A. Purser, in Toxicology, Survival and Health Hazards of Combustion Products, ed. D. A. Purser, R. L. Maynard, and J. C. Wakefield, The Royal Society of Chemistry, 2015, ch. 10, pp. 310-360.
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Several materials commonly involved in fires contain both nitrogen and carbon. A proportion of this fuel nitrogen is released as hydrogen cyanide and a proportion of the fuel carbon is released as carbon monoxide. Both are asphyxiant gases and show additive toxicity, but the effects on exposed subjects and the time courses of their development are somewhat different. Over the short exposure periods of from a few minutes up to around an hour typical of fires, the effects of CO approximately follow Haber's rule, with incapacitation occurring after exposure to a Ct product dose capable of causing loss of consciousness at a blood carboxyhaemoglobin concentration of around 30–40%. This contrasts with the effects of HCN, which show large deviations from Haber's rule, so that exposure to high concentrations above approximately 150 ppm causes rapid incapacitation within a few minutes at a low Ct product dose. Exposure to concentrations below approximately 80 ppm causes minimal toxic effects over relatively long time scales. Also, while the blood carboxyhaemoglobin concentration in fire survivors at rescue and in post-mortem blood samples provides a reasonably good indication of the extent of CO exposure and the severity of toxic effects, the relationships are much more complex for blood cyanide concentrations. This chapter describes the physiological effects of acute HCN exposure and the relationship between exposure concentration and time to incapacitation (loss of consciousness). Expressions are derived for calculation of time to incapacitation in non-human primates and for humans for use in fire hazard calculations. The uptake and distribution dynamics of cyanide into and from the blood are then examined, including the relationship between cyanide concentrations in different body fluid compartments (erythrocytes, blood plasma, interstitial and intracellular fluids), signs of toxicity, and the possible role of hypocapnia as a contributory cause of incapacitation during HCN inhalation. Recovery after HCN exposure is considered, including rates of decrease in blood cyanide after exposure by metabolism and excretion, and effects of impaired oxidative metabolism due to cyanide poisoning on rates of cyanide metabolism. The implications for forensic interpretation of cyanide poisoning of uptake, distribution and metabolism dynamics, post-mortem losses in stored tissues, and changes in stored blood samples are then described.