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.     

Cyanide ingestion. Case studies of four suicides.

Deliberate ingestion of cyanides is relatively rare, as reflected in the Registrar General's figures. There are no pathognomonic specific autopsy findings and even the distinctive smell may be missed by some individuals. We present four cases of cyanide ingestion, one of which appears to be the first reported case of magnesium cyanide poisoning in humans. The problems involved in investigating deaths from cyanide ingestion are discussed.     

Cyanide poisoning: forensic toxicology observations in the study of 54 cases of fatal poisoning

The present study describes various observations made during the examination of 54 cases of lethal cyanide intoxication at the Institute of Forensic Medicine of the University of Zürich during a period of more than 40 years. Data pertain to the scene of death, the medicolegal inspection, the autopsy, the histological examinations, the chemical analyses, the various types of poisoning observed and the diagnostic criteria used. The intoxicated victims were mostly adults who had professional access to various cyanogenic compounds and had ingested them with the intention of committing suicide. Cases of accidental and criminal poisoning were rare. In spite of this fact, and although its frequency has not increased in the last few decades, cyanide poisoning has maintained undiminished importance.     

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.     

Pseudolaminar necrosis in cyanide intoxication: a neuropathology case report

We describe the gross and microscopic neuropathological changes in the brain of a 17-year-old male who died 4 days after being poisoned with cyanide. Previous reports indicate that following cyanide intoxication, the brain develops diffuse hypoxic/ischemic changes, predominantly of the basal ganglia. The case we describe here had similar features but in addition showed striking laminar necrosis of the cerebral cortex. This finding in cyanide poisoning has been previously demonstrated by neuroimaging, but not pathologically.     

Simple and simultaneous quantification of cyanide,ethanol, and 1-propanol in blood by headspace GC–MS/NPD with Deans switch dual detector system

Cyanide is a powerful and rapidly acting poison. In Japan, cyanide poisoning is rare, and regular cyanide testing can be costly and time consuming. In contrast, alcohol analysis is routinely performed in most forensic laboratories. In this study, we attempted to develop a method for the simultaneous quantification of cyanide and alcohols in blood using headspace gas chromatography (HS–GC). As nitrogen-phosphorus detection (NPD) is more sensitive to hydrogen cyanide than mass spectrometry (MS), a Deans switch was used to switch the detectors during a single run. The separation provided by three analytical columns, PoraBOND Q, CP-Sil 5 CB, and HP-INNOWax, was investigated, and PoraBOND Q was selected. The use of HS–GC–MS/NPD with a Deans switch enabled the simple and simultaneous quantification of cyanide, ethanol, and 1-propanol. Eighteen other volatile compounds were detected in the SIM/scan mode of the MS.     

The biohazard potential of cyanide poisoning during postmortem examination

A case of suicide by ingestion of cyanide salts provided an opportunity to determine whether personnel involved in postmortem examination of such cases are exposed to any significant degree of biohazard from cyanide remaining in body cavities or tissues of the decedent or both. It was found that potentially toxic concentrations of cyanide can develop in personnel so exposed. These findings have implications not only for the safety of pathologists and pathology assistants, but also for first responders (for example, police, firemen, emergency medical technicians [EMTs], paramedics, R.N.s) and emergency room personnel who may be involved in resuscitation efforts or removal of gastric contents or both in cyanide poisoning victims. Symptoms of cyanide toxicity and recommendations for reducing the potential for clinically significant cyanide exposure in medical settings are briefly reviewed.     

A case of suicide by ingestion of sodium nitroprusside.

The study reports a case of suicide by ingestion of sodium nitroprusside which resulted in acute cyanide poisoning. Analyses carried out on body fluid yielded the quantitation of total (5.00 mg/L) and free (3.30 mg/L) cyanide in blood and of methemoglobin (blood = 10.5%). At the scene, some solid reddish-brown material was found in a glass, which on toxicological analysis was found to contain sodium nitroprusside; about 9 g of the same substance was identified in stomach contents. The detection and quantification of cyanide and methemoglobin in biological samples from the case indicated that the lethal effect was due to both metabolic products (cyanide and methemoglobin).     

Time- and Temperature-Dependent Changes in Cytochrome c Oxidase Activity and Cyanide Concentration in Excised Mice Organs and Mice Cadavers

Postmortem stability of cyanide biomarkers is often disputed. We assessed the time and temperature-dependent changes in cytochrome c oxidase (CCO) activity and cyanide concentration in various organs of mice succumbing to cyanide. Immediately after death, excised mice organs and mice cadavers were stored at room temperature (35°C ± 5°C) or in frozen storage (−20°C ± 2°C). At various times after death, CCO activity and cyanide concentrations were measured in excised mice organs or organs removed from mice cadavers. The study revealed that (i) measuring both the biomarkers in mice cadavers was more reliable compared to excised mice organs, (ii) measuring temporal CCO activity and cyanide concentration in vital organs from mice cadavers (room temperature) was reliable up to 24 h, and (iii) CCO activity in the brain and lungs and cyanide concentration in organs from mice cadavers (frozen) were measurable beyond 21 days. This study will be helpful in postmortem determination of cyanide poisoning.     

胃肠外途径投毒的法医学鉴定

本文报告１３例胃肠外途径投毒的法医学鉴定，其中升汞２例（Ｉ．Ｖ．），水银１例（Ｉ．Ｖ．），氰化钾２例（Ｉ．Ｍ．和乳房下注射各１）、氰化钠１例（Ｉ．Ｖ．）、一氧化碳２例（吸入）、铬酸酐１例（阴道内塞入）、敌敌畏１例（心包腔内注射）、矮壮素１例（Ｉ．Ｍ．）、氯丙嗪１例（Ｉ．Ｖ．）和溴氰菊酯１例（Ｉ．Ｖ．）。说明经胃肠外途径引起的投毒案例并不罕见，且毒物种类增多，这在法医病理和毒理工作中应引起注意和警惕。     

Gas chromatography in quantitative analysis of hydrocyanic acid and its salts in cadaveric blood

A direct gas chromatography method was designed for the quantitative determination of cyanides (prussic acid) in cadaveric blood. Its sensitivity is 0.05 mg/ml. The routine volatile products, including substances, which emerge due to putrefaction of organic matters, do not affect the accuracy and reproducibility of the method; the exception is H-propanol that was used as the internal standard. The method was used in legal chemical expertise related with acute cyanide poisoning (suicide) as well as with poisoning of products of combustion of nonmetals (foam-rubber). The absolute error does not exceed 10% with a mean quadratic deviation of 0.0029-0.0033 mg.     

家兔死后体内2-氨基噻唑啉-4-羧酸分布研究

目的 建立家兔氰化钾灌胃给药致死动物模型,研究氰化物代谢物2-氨基噻唑啉-4-羧酸(ATCA)在家兔体内的死后分布规律.方法 雄性家兔7只(体重约2.0kg～2.5kg)经口灌胃2LD50(10mg/kg)氰化钾水溶液,观察家兔反应,待家兔呼吸、心跳和反射全部消失后立即对家兔进行解剖取心、肝、脾、肺、肾、脑、睾丸、胃壁...     

Experimental studies on death by fire in automobiles and exhaust gas poisoning

Studies were made on the acid-base balance, blood gases, and carbon monoxide (CO), cyanide, and sulfur dioxide concentrations in the blood of albino rabbits that died from automobile exhaust gas poisoning (group I) or fires in cars (complete combustion, group II; incomplete combustion, group III). In group I, the temperature and CO concentration increased gradually to 35 degrees C and 5.2% in 70 min. The animals died after 9 min, when the values were 20 degrees C and 5.2%, respectively. In group II the animals died after 9 min, when the values were 55 degrees C and 1.95%, respectively. In group III, the temperature was very high (870 degrees C), but the CO concentration was not (0.6-1.3%) after 4 min. The animals died after 5 min. In all experimental groups, marked acidosis and hypoxemia were seen, but the CO2 tension (PCO2) was high, in contrast to previous studies on pure CO poisoning. In group I, the level of carboxyhemoglobin (CO-Hb) was significantly higher (91.2 +/- 3.4% in arterial blood, 87.5 +/- 8.1% in venous blood; p less than 0.01) than in groups II and III. Although the O2 tensions of venous and arterial blood (PvO2, PaO2) were very low, that of arterial blood was higher, suggesting that O2 was still being utilized in the tissues at the time of death. In group II, CO-Hb was high (57.7 +/- 16.0% in arterial blood, 61.2 +/- 20.6% in venous blood) and the acid-base balance indicated marked acidosis. In group III, the CO-Hb, PCO2 and cyanide levels in the blood were very high.(ABSTRACT TRUNCATED AT 250 WORDS)     

Activation analyses of authenticated hairs of Napoleon Bonaparte confirm arsenic poisoning

In 1960, activation analyses at the Harwell Nuclear Research Laboratory of the University of Glascow, London of authenticated hairs of Napoleon Bonaparte taken immediately after his death confirmed Napoleon's chronic arsenic poisoning on the island of St. Helena. Timeline correlation of his clinical symptomatology of the preceding 4 months, as reported in the written diaries of his exiled companions, further supports the effect of fluctuating, elevated toxic levels of arsenic on his health. Independent analyses of authenticated hairs of Napoleon by the Toxicology Crime Laboratory of the United States Federal Bureau of Investigation in 1995 reveals toxic levels of arsenic. The successful assassination of Napoleon included both a cosmetic and lethal phase. The cosmetic phase consisted of arsenic poisoning over time to weaken Napoleon, making the associated debility appear to be a natural illness and thus allay any suspicions prior to instituting the lethal phase. On May 3, 1821, at 5:30 P.M., the lethal phase was carried out. Napoleon was given Calomel (HgCl), a cathartic, and a popular orange-flavored drink called orgeat, which was flavored with the oil of bitter almonds. Together they formed mercury cyanide, which is lethal. Napoleon lost consciousness and died two days later.     

Rapid and sensitive quantitation of cyanide in blood and its application to fire victims.

We developed a head-space method for the determination of blood cyanide by gas chromatography with electron-capture detection. In this technique, a reaction precolumn packed with chloramine-T was used for the conversion of hydrogen cyanide into cyanogen chloride. Since the reaction precolumn eliminated the necessity of trapping hydrogen cyanide from biological samples, blood cyanide could be analyzed quickly by acidification only. Using this method, blood cyanide levels of fire victims were determined at autopsy. The serum values of cyanide ranged from 0.11 micrograms/ml to 18.12 micrograms/ml. However, a significantly higher cyanide content was detected in the left ventricular blood than in the right. This indicates that death was caused by the fire and suggests that the collecting point of the blood sample is an important factor in the determination of inhaled cyanide. There was a positive correlation between blood cyanide and carboxyhemoglobin contents.     

Morbus Fahr--considerations on a case of sudden death

This paper presents 21 cases related to cyanide intoxication by oral ingestion. Cyanide concentrations in biological specimens are especially different from the type of postmortem specimens, and very important in interpreting the cause of death in postmortem forensic toxicology. Besides the detection of cyanide in autopsy specimens, the autopsy findings were unremarkable. Biological samples (0.2mL or equal to less than 10μg of cyanide) were analyzed colorimetrically for cyanide. In a series of 21 cyanide fatalities, the concentration ranges (mean±SD) of cyanide in heart blood, peripheral blood and gastric contents were 0.1-248.6mg/L (38.1±56.6mg/L), 0.3-212.4mg/L (17.1±45.1mg/L) and 2.0-6398.0mg/kg (859.0±1486.2mg/kg), respectively. The ranges of the heart/peripheral blood concentration ratio and gastric contents/peripheral blood concentration ratio were 0.3-10.6 (mean 3.4) and 3.4-402.4 (mean 86.0), respectively. From the difference of cyanide concentration and the concentration ratio of cyanide in different types of postmortem specimens, the possibility of the postmortem redistribution of cyanide and death by oral ingestion of cyanide could be confirmed. We reported cyanide fatal cases along with a review of literature.     

A test to identify cyanide origin by isotope ratio mass spectrometry for forensic investigation

Cyanide is one of the common poisons in murders. When cyanide has been used, to identify the origin of cyanide may be necessary in the forensic investigation. We have examined the possibility of distinguishing different commercial cyanide samples through the δ(13)C and δ(15)N values and developed a protocol for the isotope analysis of cyanide extracted from several matrices as food and medicine. Several cyanide precipitates were tested for the isotope analysis. The results show that cupric ferrocyanide Cu(2)[Fe(CN)(6)] is the most appropriate precipitate for the analysis. Thirteen batches of KCN and nine batches of NaCN chemicals were randomly chosen from different suppliers. The cyanides were converted to cupric ferrocyanide and then analysed by isotope ratio mass spectrometry coupled to elemental analysis (EA-IRMS). The isotopic signature of the commercial samples varied from -51.96 to -25.77 ‰ for δ(13)C and from -4.51 to +3.81 ‰ for δ(15)N, highlighting the potential of applying EA-IRMS technique to identify cyanide from different batches and sources. The influence of the cyanide extraction and isolation from spiked matrix on the isotopic analysis was also studied. Three matrices: orange juice, yogurt drink and a medicine were tested. In many cases, the isotopic analysis results obtained from the original cyanides precipitates and those isolated from the matrices showed a good accordance, especially for δ(15)N. In some matrices, the (13)C analysis was interfered by co-precipitates. With carefully elaborated working protocol, determining the isotope ratio of N and C in cyanide by EA-IRMS is a promising method for forensic investigations.     

生物检材中氰化物浓度与保存时间关系研究

通过动物试验，用荧光光度法测定生物检材中氰化物浓度，研究了氰化物浓度与保存时间关系。结果表明，染毒血液高体120h内，氰化物浓度呈平缓直线上升；120h至168h之间呈指数下降；染毒肝脏检材在168h内呈直线上升，建立了线性方程。     

铊（TI）投毒案检验

目的　通过 11例中毒者分析研究铊中毒的症状 ,达到了解和认识铊中毒的目的。方法　收集 11例铊中毒的相关资料 ,分析铊中毒的特征。结果　铊中毒的共同特征是出现症状的时候都有四肢疼痛或麻木 ,同时伴有严重脱发。结论　铊中毒依个体的年龄、性别、状态及中毒量不同 ,其发病前具有一定潜伏期。但性别、年龄与死亡的时间关系目前尚不清     

Stable carbon and nitrogen isotope ratios of sodium and potassium cyanide as a forensic signature

Sodium and potassium cyanide are highly toxic, produced in large amounts by the chemical industry, and linked to numerous high-profile crimes. The U.S. Centers for Disease Control and Prevention has identified cyanide as one of the most probable agents to be used in a chemical terrorism event. We investigated whether stable C and N isotopic content of sodium and potassium cyanide could serve as a forensic signature for sample matching, using a collection of 65 cyanide samples. Upon analysis, a few of the cyanide samples displayed nonhomogeneous isotopic content associated with degradation to a carbonate salt and loss of hydrogen cyanide. Most samples had highly reproducible isotope content. Of the 65 cyanide samples, >95% could be properly matched based on C and N isotope ratios, with a false match rate <3%. These results suggest that stable C and N isotope ratios are a useful forensic signature for matching cyanide samples.