The role of hydrogen cyanide and carbon monoxide in fire casualties: a prospective study

Determinations of blood cyanide and carboxyhemoglobin concentrations were performed in 18 victims found dead in buildings after fires during a 2-year period. The results indicated that 50% of the victims had been exposed to toxic levels of hydrogen cyanide and 90% to toxic levels of carbon monoxide. Lethal concentrations of carbon monoxide were found in 83% of the victims. In one case a lethal blood cyanide but a non-toxic blood carboxyhemoglobin value was found. It is concluded that carbon monoxide appears to be more important than hydrogen cyanide as a toxic agent in the fire atmosphere, but cyanide poisoning without carbon monoxide poisoning may, under certain circumstances, be the cause of death in fire victims.     

A study on house fire victims: age, carboxyhemoglobin, hydrogen cyanide and hemolysis.

Correlation among age, concentrations of carboxyhemoglobin and hydrogen cyanide, oxygen density and hemolysis were studied in 120 house fire victims. Victims aged over 60 years comprised approximately 50% of the pooled subjects. Blood samples were mainly collected from the left ventricle, but sometimes from both the right and left ventricles. The concentration of carboxyhemoglobin ranged from 1-95%, of which 71 persons (59.7%) died with carboxyhemoglobin concentrations below 60%. Carboxyhemoglobin concentrations below 10% were found in 9 persons (7.5%). Most of these cases involved the elderly persons. In this paper, we report on the death of elderly victims as a result of low carboxyhemoglobin concentrations. A significant correlation of blood carboxyhemoglobin concentrations existed between the right and left ventricles. The concentration of carboxyhemoglobin in the left ventricle was significantly higher than that in the right. Two out of 31 victims whose hydrogen cyanide concentrations were determined, succumbed to hydrogen cyanide poisoning, having a high concentration of hydrogen cyanide and a low concentration of carboxyhemoglobin. On analysis, oxygen density was found to be low in 13 persons. A negative correlation was shown between carboxyhemoglobin concentration and hemolysis. Inasmuch as hemolysis may indicate the extent of heat dissociation, hemolysis should provide an index of carbon monoxide dissociation from carboxyhemoglobin. In the present study of victims, possible causes of death i.e., carbon monoxide gas poisoning, hydrogen cyanide poisoning, oxygen deprivation, burning, shock due to burns and others were estimated. The survival time for elderly victims was considered to be short.     

Fetal death due to nonlethal maternal carbon monoxide poisoning

Fetal death due to acute carbon monoxide poisoning is rarely reported in the medical literature. Of the eight cases found in literature review, only one documented the fetal carboxyhemoglobin concentration. This paper reports a fetal death due to accidental nonlethal maternal carbon monoxide intoxication in which both maternal and fetal carboxyhemoglobin concentrations were obtained. The corrected carboxyhemoglobin concentration was 61% at the time of death in utero, while the maternal carboxyhemoglobin was measured at 7% after one hour of supplemental oxygen. The authors review the mechanisms of fetal death and emphasize the different carbon monoxide kinetics in the fetal circulation.     

The toxicological examination of the victims of the British Air Tours Boeing 737 accident at Manchester in 1985

The results of toxicological analyses of the body fluids of the victims from the accident involving the British Air Tours Boeing 737 in August 1985 are presented for carboxyhemoglobin, cyanide, and volatiles. All the victims except one had raised concentrations of carbon monoxide. All the victims had raised concentrations of cyanide. All the victims showed the presence of volatile substances in the blood. Autopsies revealed that all the victims had carbon particles in the trachea and bronchi. Thus, all the victims must have inhaled fire products in the burning aircraft cabin. Six victims had concentrations of carbon monoxide or cyanide in the blood that were neither fatal nor incapacitating; therefore, it is reasonable to suggest that these six victims survived for a comparatively short time and that there may have been other causes, in addition to toxic fumes, for their deaths. The other 48 victims must have survived long enough in the fire to accumulate incapacitating or fatal concentrations of carbon monoxide or cyanide or both. The effects of these substances found in the blood of each of the 48 victims must have combined to produce an insurmountable impediment to escape from the aircraft.     

Analysis of carboxyhemoglobin and cyanide in blood from victims of the Dupont Plaza Hotel fire in Puerto Rico

Ninety-seven people died from a fire that occurred in the Dupont Plaza Hotel in Puerto Rico on 31 Dec. 1986. All, except four who died later in the hospital, were found dead at the scene. All of the fatalities at the hotel (except for eight) were burned beyond recognition. Blood from seventy-eight of the victims was screened for carboxyhemoglobin at the Institute for Forensic Sciences in Puerto Rico and was then sent to the National Institute of Standards and Technology, Gaithersburg, Maryland, for analysis of carboxyhemoglobin and cyanide concentrations. The blood data indicated that carbon monoxide and hydrogen cyanide, singly or combined, were probably not responsible for the majority of the deaths that occurred in the badly burned victims. On the other hand, the significantly higher carboxyhemoglobin in the nonburned victims indicated that carbon monoxide alone or combined with hydrogen cyanide probably played a major role in the cause of their deaths.     

甲醛对一氧化碳中毒血检验干扰的研究

目的探讨甲醛对一氧化碳中毒血的检测是否产生干扰,提高一氧化碳中毒鉴定的可靠性。方法采用常用的血中一氧化碳或碳氧血红蛋白饱和度的检测方法对未加甲醛和加甲醛的血样分别进行实验研究。结果甲醛对加热法、氢氧化钠法、氯化钯法、分光光度法等检测方法均可产生不同程度的干扰。结论经福尔马林灌注或固定的检材不宜用于一氧化碳中毒血检测,否则可能导致错误的鉴定结论。     

The causes of death in fire victims

In 169 consecutive cases of autopsied fire victims about 50% had lethal levels of carboxyhemoglobin. Soot in the respiratory tract was found in about 90% of the cases. The age distribution of the fire victims showed significantly less persons in the 15-35-year group than should be expected according to the age distribution of the population, presumably due to greater agility of younger people. More than half of the fire victims had alcohol in the blood exceeding 0.05%, and alcohol intoxication should be considered accessary to many deaths in fire. The characteristic biphasic distribution of carboxyhemoglobin in fire victims together with other observations suggest that the principal causes of death are carbon monoxide followed by carbon dioxide poisoning and/or oxygen deficiency, while the influence of heat is considered to be of minor importance.     

Suicide by inhalation of carbon monoxide in a residential fire

Fire deaths are usually accidental, but atypical cases of homicide or suicide have been described. In suicide by fire, the only method reported by several authors consists of self-immolation. We present here the unusual case of an adult female who committed suicide by waiting in the living room after setting fire to her bedroom. The autopsy revealed smoke inhalation and the toxicological analysis revealed carboxyhemoglobin levels of 67%. Very few cases of suicide by fire not of the self-immolation type have been reported, and all have been anecdotal. A review of the literature is presented and a new term, "suicide by inhalation of carbon monoxide in a fire," is proposed for such cases.     

Cyanide, carboxyhemoglobin and blood acid-base state in animals exposed to combustion products of various combinations of acrylic fiber and gauze

In order to examine the usefulness of blood cyanide concentrations as an indicator of whether or not a victim was alive at the start of a fire, blood cyanide concentrations were measured in the bodies that we autopsied in our institute between January 1986 and March, 1987. In the present study, bodies with advanced decomposition were excluded. Thirty-six bodies were included: cyanide as well as carboxyhemoglobin (COHb) were detected in four charred bodies found at the scene of a fire. On the other hand, cyanide was not detected in any of the remaining 30 bodies except in two cases suspected of having ingested a cyanide compound. Rats and rabbits were made to inhale the combustion products of various combinations of acrylic fiber (hydrogen cyanide generating material when heated) and gauze (carbon monoxide generating material when heated). The exposure to the combustion products was continued until death in the rat and until apnea in the rabbit. The concentration of hydrogen cyanide in the exposure chamber and that of blood cyanide, at the time the animal died, correlated with the amount of acrylic fiber heated. In addition to differences in blood COHb and cyanide concentrations, there were also differences in blood gas concentrations between the acrylic fiber and the gauze groups. When the rabbits were switched to room air after the occurrence of apnea, the blood gas value began to normalize.     

Never say never. Negligible carboxyhemoglobin in the victim of a smoldering mattress fire

For many years, a high blood carboxyhemoglobin concentration has been used as a criterion for determining that a victim of conflagration was alive in the fire. We report a case in which a man died from the combined effects of burns and hypertensive cardiovascular disease. He had a negligible blood carboxyhemoglobin concentration, but the environmental evidence and autopsy findings are indicative of life in the fire, which arose in a smoldering mattress. We conclude that uncritical, rigid adherence to the requirement that fire victims have high carboxyhemoglobin concentrations can be misleading.     

Quantitative evaluation of volatile hydrocarbons in post-mortem blood in forensic autopsy cases of fire-related deaths

Volatile hydrocarbons in post-mortem blood from victims of fires were analyzed quantitatively by headspace gas chromatography mass spectrometry. The benzene and styrene concentrations in the blood were positively correlated with the carboxyhemoglobin (CO-Hb) concentration, which is evidence that the deceased inhaled the hydrocarbons and carbon monoxide simultaneously. By contrast, the concentrations of toluene and CO-Hb in the blood were not significantly correlated. This lack of correlation could be explained by two different sources of toluene, with low blood concentrations of toluene arising when the deceased inhaled smoke and high blood concentrations of toluene arising when the deceased inhaled petroleum vapor or other unknown vapors. The quantity of soot deposited in the respiratory tract was classified into four grades (-, 1+, 2+, 3+). The mean CO-Hb concentration in the 1+ soot group was significantly lower than those in the 2+ (p<0.05) and 3+ (p<0.01) soot groups. The blood CO-Hb concentrations in the 1+ soot group were all below 30%. Those indicated that the deceased aspirated smoke that contained both soot and carbon monoxide. The wide variation in CO-Hb concentrations for each soot classification could be caused by the different types of smoke produced by different materials. For example, petroleum combustion with a limited supply of oxygen, like in a compartment fire, may produce a large volume of dense black smoke that contains a large quantity of soot. Soot deposits in the airways and the blood CO-Hb concentration are basic and essential autopsy findings that are used to investigate fire-related deaths. The quantitative GC-MS analysis of blood volatile hydrocarbons can provide additional useful information on the cause of the fire and the circumstances surrounding the death. In combination, these three findings are useful for the reconstruction of cases.     

Deaths caused by carbon monoxide poisoning in an open environment (outdoors)

Three deaths as a result of inhalation of carbon monoxide from the exhaust fumes of automobiles are reported. All deaths occurred outside and not in a structure. The individuals were white males, ages 24 to 26 years. Blood carboxyhemoglobin concentrations ranged from 58 (in a decomposing body) to 81%. The three cases illustrate the fact that even in the outdoors death from carbon monoxide inhalation can occur if an individual is in close proximity to a rich source of carbon monoxide.     

Subarachnoid Hemorrhage and Carbon Monoxide Exposure: Accidental Association or Fatal Link?

This case study reports a fatal subarachnoid hemorrhage (SAH) with concomitant accidental carbon monoxide (CO) exposure in 32‐year‐old man. Autopsy results indicated an antemortem aspiration of smoke, and a massive SAH was identified as the cause of death. Intriguingly, the carboxyhemoglobin level was 30%, suggesting that CO could have played a specific role. Intracranial hemorrhages following CO exposure in brain areas and tissues such as the basal ganglia, globus pallidus, or white matter are rare, but well characterized, whereas SAH related to CO exposure has not been previously described. In this case report, the possible role of CO, either as a primary cause or as a facilitating factor, in the pathogenesis of SAH is discussed. In particular, we propose the hypothesis that the excessive vasodilating effects produced by CO on the cerebral endothelium results in consequential loss of microvascular integrity.     

Asphyxial deaths caused by automobile exhaust inhalation not attributable to carbon monoxide toxicity: study of 2 cases

The authors report two suicides that resulted from the intentional inhalation of automobile exhaust gases in which death occurred without the formation of physiologically significant amounts of carboxyhemoglobin. These circumstances are correlated with measurements of the involved vehicles' exhaust gases, which showed reduced concentrations of carbon monoxide present, reflecting improvements in automobile engine technology. In the absence of carbon monoxide toxicity, the authors attribute death in these cases to asphyxia caused by carbon dioxide intoxication and diminished atmospheric oxygen concentrations.     

Postmortem formation of carbon monoxide

Since carbon monoxide (CO) production after death was suggested in a drowned body, CO and carboxyhemoglobin (HbCO) levels in blood and body cavity fluids of cadavers which were not exposed to fire and CO have been analyzed. CO released from the tissues was determined by gas chromatography and gas chromatography-mass spectrometry, and the total concentration of hemoglobin (Hb) was measured as cyanmethemoglobin (CNmHb). The HbCO level was calculated by the ratio of CO content and CO-binding capacity. CO levels (ml/100 g at STP) of the seven cases in which blood and body cavity fluids could be collected ranged from 0.13 to 0.87 in blood and 0.02 to 0.80 in body cavity fluids. HbCO levels in blood and body cavity fluids were from 0.3 to 6.0% and from 2.3 to 44.1%, respectively. In a typical case showing postmortem formation of CO, the CO levels in body cavity fluids were higher than that in blood. It is suggested that CO in a putrefied body is due to CO in blood prior to death and the CO formed by the decomposition of Hb, myoglobin and other substances during putrefaction. The significance of HbCO levels in body cavity fluids of cases with marked postmortem decomposition seems difficult to interpret without the value of HbCO in blood.     

Comparison of Different Analytical Methods for the Determination of Carbon Monoxide in Postmortem Blood

The determination of carbon monoxide (CO) and carboxyhemoglobin (COHb) is of utmost importance in forensic toxicology to determine the cause of death in cases of CO poisoning, fire, and explosions. To this end, reliable and updated analytical methods are required. In this paper, four different methods for the determination of carbon monoxide in postmortem blood samples were compared: (i) the spectrophotometric determination of COHb applying the method proposed by Rodkey and modified by Beutler–West, (ii) the spectrophotometric determination of CO using a micro-diffusion-based method, (iii) the determination of CO by gas chromatography coupled to a TCD detector, and (iv) the determination of COHb by blood gas analysis. Three postmortem blood samples were analyzed with all methods, and the results were comparable. The applied methodologies showed different features depending on the sensitivity, sample preparation, and volume. The HS-GC/TCD method in our hand was the most appropriate, on postmortem samples, and versatile to apply. Unfortunately, only a limited number of postmortem blood samples were available for this study due to the rarity of that kind of intoxication in our jurisdiction.     

Interaction between carbon monoxide and ethanol in fire fatalities.

Impairment due to ethanol is clearly a risk factor in deaths due to fire. However, it is less clear whether there is a physiological interaction between ethanol and carbon monoxide (CO) that would alter the carboxyhemoglobin saturation level (COHb sat.) that accounts for death. In an attempt to explore this issue further, 196 fire fatalities investigated by the Office of the Chief Medical Examiner, State of Maryland over a 3-year period were examined. COHb sat. and blood ethanol concentrations (BAC) were tabulated. Twelve cases positive for therapeutic or abused drugs other than lidocaine or atropine were excluded; 184 cases were included. The data indicate that ethanol does not affect the COHb sat. that accounts for death, since the percentage of cases positive for ethanol at a given COHb range shows no trends. Therefore, we conclude that although ethanol remains a risk factor in fire fatalities, the risk appears to be related to the impairment that it produces as opposed to a direct interaction with CO.     

An unusual case of suicidal carbon monoxide poisoning

A 35 years old student with prior suicidal tendencies was found dead laying enclosed in a plastic-bag together with four plastic-bags of minor capacity. Three bags were opened by cuts and empty, one bag contained 73 1 of 83.2 Vol.% carbon monoxide. Postmortem carboxyhemoglobin concentrations in blood of five different regions of the corpse ranged from 80.3% to 93.4%. From the circumstances--chemicals and apparatus--it could be reconstructed that carbon monoxide was produced by the reactions of formic acid and sulfuric acid.     

Hepatotoxicity of dichloromethane

We studied hepatotoxicity of dichloromethane using primary cultures of parenchymal cells (hepatocyte) from adult rat livers. The production of carbon monoxide from dichloromethane increased with time, the increased cell number, and the concentration of dichloromethane. However, the carbon monoxide production per hepatocyte decreased with increasing cell density. When dichloromethane was in a high concentration, the metabolism of dichloromethane to carbon monoxide was extensively depressed, total glutamic-oxaloacetic transaminase (GOT) and mitochondrial GOT (m-GOT) levels in the cultured medium were extensively elevated, and the cultured hepatocytes were destroyed by dichloromethane. A case of accidental exposure to dichloromethane which occurred in Japan was also considered, and it is suspected that the inhalation of dichloromethane vapors in a high concentration for many hours may cause hepatotoxicity.     

Experimental study on postmortem formation of carbon monoxide

Rats were drowned and kept immersed for 1 month in either boiled city water, or boiled or unboiled fresh water collected from a river. A small amount of carbon monoxide (CO) formed after death and a low carboxyhemoglobin (HbCO) saturation was found in blood and thoracic cavity fluid of the animals immersed in boiled city water and in boiled fresh water. A considerable amount of CO and a high HbCO saturation was observed in blood and thoracic cavity fluid in two out of three rats immersed in unboiled fresh water at 4-6 degrees C, and in one out of three at 6-16 degrees C. It is suggested that microorganisms in the water, in which the rats were drowned and kept immersed, and low temperatures of around 5 degrees C during storage, played an important role in the postmortem formation of carbon monoxide.