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To evaluate apoptotic neuronal damage by carbon monoxide (CO) in medico-legal autopsy cases, we investigated the immunohistochemical distribution of single-stranded DNA (ssDNA) as a marker of apoptosis and programmed cell death in the brain. Formalin-fixed paraffin-embedded brain tissue specimens, including cerebral cortex of frontal lobe, substantia nigra of the midbrain and pallidum, from medico-legal autopsy cases of fire fatality (n=63), including cases with blood carboxyhemoglobin (COHb) of a lower (<60%) and a higher (>60%) level (n = 39 and 24, respectively), and CO intoxication without burns (n = 6) were examined, in comparison with acute ischemic heart disease (IHD, n = 29) and asphyxiation due to strangulation (AS, n= 14). In the pallidum, neuronal immunopositivity for ssDNA was significantly higher in fire fatality with a higher COHb level than in IHD (p<0.0001), and CO intoxication cases showed significantly higher positivity than other groups excluding fire fatality with a higher COHb level (p< 0.05). In cases without cardiopulmonary resuscitation, ssDNA-positivity in the pallidum mildly correlated to COHb concentrations (r = 0.31, p<0.05), and the positivity was significantly higher in higher COHb (>60%) cases than in lower COHb (<30%) cases. In the cerebral cortex and substantia nigra of the midbrain, neuronal ssDNA-positivity showed no significant findings with regard to the cause of death and COHb concentration. These findings suggest that CO causes selective neuronal damage in the pallidum.

To investigate the influence of inhaling carbon monoxide (CO)-containing gases in fires, forensic autopsy cases of fire victims (n=193) were examined in comparison with control cases involving other causes of fatal CO intoxication (n=6 :COHb, 69.5-83.0%). Fire victims with blood carboxyhemoglobin (COHb) levels over 60% (n=76) showed a larger arterio-venous difference in blood COHb level compared with other fire victims and other fatal CO intoxication. However, biochemical findings for myocardial, cerebral damage or respiratory distress were milder in most cases, independent of blood cyanide levels, being similar to those in fatality due to inhalation of blast furnace gas with an extremely high concentration of CO (ca. 40%). These observations suggest that an acutely fatal factor in fires involves inhalation of gases containing high amounts of CO, which may induce peracute circulatory collapse before causing marked myocardial and cerebral damage or respiratory distress.

Five autopsy cases were examined to investigate fatal factors involved in inhalation of "asphyxiant gases": carbon monoxide (CO, n=3), fluorocarbons (n=1) and butane (n=1). In all cases, there was severe pulmonary edema and congestion in all viscera, suggesting advanced circulatory failure. The airway was filled with bloody froth in cases of fluorocarbons and butane inhalation. In CO intoxication, a marked increase in serum cardiac troponins suggested severe myocardial damage. There were also biochemical findings of respiratory distress (an evident increase in intra-alveolar pulmonary surfactant protein A), alveolar injury (an increase in serum surfactant protein A and D), rhabdomyolysis (myoglobinuria) and prolonged hypoxia (myogenic hyperuricemia) in cases of inhaling incomplete combustion gases. In a case of fluorocarbons gas inhalation, biochemical findings suggested respiratory distress, myocardial ischemia (an increase in serum CK-MB) and advanced hypoxia. Similar findings were observed in a case of butane inhalation, although cardiac troponin levels were low in the peripheral blood. These observations suggested that myocardial damage was prominent in CO intoxication, accompanied by respiratory distress in cases of inhaling incomplete combustion gases, whereas respiratory distress and hypoxia were major findings in cases of fluorocarbons and butane gas inhalation.