Cyanide poisoning has been regarded to contribute the fatal outcome in fire victims. The toxicity of inhaled hydrogen cyanide (HCN) at the cellular level was evaluated considering the impact of methemoglobin (MetHb) produced by fire gases. Cyanide (CN) concentrations and total hemoglobin contents were measured in right heart blood (RHB) and seven organs/tissues (basal ganglia, brain stem, heart, lung, liver, kidney and psoas muscle) collected from 20 fire fatalities. MetHb and carboxyhemoglobin saturations were also measured in RHB. The amount of CN probably bound to the cytochrome c oxidase of the tissue cells (CCO-CN) was extrapolated from CN and hemoglobin contents in RHB and organs/tissues, MetHb saturation in RHB and binding capacity of MetHb for CN. CN concentrations in RHB showed a wide range with the highest concentration of 8.927 μg/mL. The lung contained the largest CN content among organs/tissues with the mean concentration of 2.219 μg/g, then the heart (0.259 μg/g) and it was lower than 0.100 μg/g in others. Exceedingly large amount of CN in the lung could be explained by high hemoglobin content, being the port of entry of HCN and postmortem diffusion of fire gases. CCO-CN was theoretically present in about 20% of organ/tissue samples, most commonly in the basal ganglia (10 samples, with the mean of 0.059 μg/g) followed by heart (eight samples, with the mean of 0.109 μg/g). No CCO-CN was found in liver and kidney. HCN might have the effect on brain and heart.
- Cytochrome c oxidase
- Fire fatality
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Issues, ethics and legal aspects