- Email: [email protected]
Carbon monoxide-related fatalities: A 60-year single institution experience
Journal of Forensic and Legal Medicine 48 (2017) 23e29
Contents lists available at ScienceDirect
Journal of Forensic and Legal Medicine j o u r n a l h o m e p a g e : w w w . e l s e v i e r . c o m / l o c a t e / j fl m
Carbon monoxide-related fatalities: A 60-year single institution experience , M.D. b, 1, Step nka Ku , M.D. b, Martin Janík, M.D., PhD a, *, 1, Michaela Ublova a cerova Petr Hejna, M.D., PhD, MBA b a
Department of Forensic Medicine and Medicolegal Expertises, Jessenius Faculty of Medicine, Comenius University, University Hospital, Martin, Slovak Republic Department of Forensic Medicine, Faculty of Medicine, Charles University, University Hospital, Hradec Kralove, Czech Republic
b
a r t i c l e i n f o
a b s t r a c t
Article history: Received 20 January 2017 Accepted 12 April 2017 Available online 13 April 2017
Objective: Though carbon monoxide (CO) poisonings account currently for a relatively small percentage of total non-natural deaths in Europe, they represent a serious public health burden and significant component of avoidable mortality in many countries. Our aim was to investigate long-term trends and to determine epidemiologic characteristics of the CO-related deaths in the Czech Republic, recorded at the . Department of Forensic Medicine in Hradec Kr alove Methods: This was an autopsy-based single-centre retrospective cohort study of all fatalities caused by CO poisoning over six decades (1947e2006). All data were numerically evaluated and processed using NCSS 10 Statistical Software. Statistical significance was defined as a p-value less than 0.05. Results: A total of 1233 CO-related deaths were identified for inclusion in the study. The manner of death was ranked in order as follows: 45% accidental poisoning, 40% suicidal poisoning, 1% homicidal poisoning, 14% remained undetermined. There were slightly more male victims (59%) than female, and the mean age overall was 48 years. The majority of CO-related fatalities were attributed to coal gas inhalation, with the remainder being from inhaled motor vehicle exhaust fumes, inhaled fire smoke, and other combustion sources such as charcoal, gas and wood-burning appliances. The mean blood carboxyhemoglobin (COHb) level was 66%. A positive blood ethanol concentration was measured in 455 (37%) cases examined. Non-intentional poisonings were highly correlated with the winter months. Conclusion: This study shows that the prevalence of CO-related deaths has decreased significantly in the Czech Republic following the widespread detoxification of the domestic gas in the 1990e1995. Our findings suggest that acute ethanol use, poorer socioeconomic position, and inadequate education status about the danger of CO are associated with an increased risk of fatal CO poisoning. Finally, our results demonstrate the continued value of the autopsy in monitoring global public health security issues and socioeconomic situation. Further similar large-scale studies in different populations are needed to improve the targeting of interventions to the groups with the highest level of risk, and to understand the sources of variation in CO-related mortality. © 2017 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.
Keywords: Carbon monoxide Poisoning Fatality Autopsy Coal gas Carboxyhemoglobin
1. Introduction Carbon monoxide (CO) is a colorless, odorless and tasteless gas
* Corresponding author. Institute of Forensic Medicine and Medicolegal Expertises, Jessenius Faculty of Medicine, Comenius University, University Hospital, 036 59 Martin, Slovak Republic, EU. E-mail address: [email protected] (M. Janík). 1 ) contributed equally to The first two authors (Martin Janík and Michaela Ublova this study.
that is less dense than air and non-irritating. It is produced from the incomplete combustion of carbon-containing compounds. Although the global replacement of coal gas with non-toxic natural gas have contributed substantially towards a decline in the number of CO-related deaths, accidental CO poisoning remains in the cause of over half of all fatal poisonings annually all over the world.1,2 Though CO poisoning account for a high percentage of total poisoning, almost all cases of accidental CO poisoning can be prevented with appropriate public education, and prevention programs on CO-emitting devices.3
http://dx.doi.org/10.1016/j.jflm.2017.04.002 1752-928X/© 2017 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.
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M. Janík et al. / Journal of Forensic and Legal Medicine 48 (2017) 23e29
Forensically relevant sources of exogenous CO include predominantly inferior or faulty heating devices and gas-powered engines, motor vehicle exhaust fumes, fire-related inhaled smoke and burning charcoal. Rarely, CO poisoning may also result from methylene chloride (a common component of paint remover and other solvents). CO poisoning is infrequent, but potential lifethreatening jeopardy of scuba diving.4 Additionally, tobacco smoke is an important source of CO. The mechanism of CO toxicity is tissue hypoxia and inhibition of cellular respiration, because the affinity of hemoglobin for CO is 210 times as great as its affinity for oxygen, and COHb liberates CO very slowly.5 Recent investigations also suggest other mechanisms of CO-mediated toxicity. One hypothesis is that CO-induced tissue hypoxia may be followed by re-oxygenation injury to the central nervous system.6,7 CO also causes inflammation by increasing levels of cytosolic heme and the heme oxygenase-1 protein, resulting in intracellular oxidative stress.8 In addition to fairy pathognomonic autopsy signs attributable to CO poisoning (cherry-red lividity, bright red coloration of the fingernail bed, blood, and the skeletal musculature), novel markers such as pulmonary macrophage activity, or expression of CIRBP, RBM3, and SIRT1 antigens in the myocardium or in the cerebellum could provide useful diagnostic information for revealing COinduced hypoxic damage.9e11 According to a recent study, bilateral globus pallidus necrosis, formerly described as a characteristic lesion for delayed CO poisoning, is now deemed non-specific and rarely associated with CO poisoning.12 The clinical signs of CO poisoning are said to be non-specific and vary with CO saturation levels, duration of exposure, pre-existing medical conditions and individual predisposition. Blood COHb concentrations of 5-10% may aggravate pre-existing cardiovascular diseases, while concentrations of 15-25% often cause dizziness and nausea. The levels of COHb exceeding 50% saturation are generally considered to be life-threatening. In the presence of alcohol or chronic cardiovascular disorder, however, fatal CO saturations may be significantly lower. Delayed neurotoxicity, which could occur 2e3 weeks after an acute CO exposure, may consist of bradykinesia, seizures, Parkinson's disease-like symptoms, and other cognitive impairments. In one study, patients who were 36 years of age or older or who had been exposed to CO for at least 24 h, or who had cerebellar abnormalities on presentation had an increased risk of cognitive sequelae at 6 weeks as compared with those without these characteristics.13 Moreover, CO exposure has an especially deleterious effect on pregnant women, because of the greater sensitivity of the fetus to the harmful effects of the gas.14 The aim of this retrospective study was to assess long-term
trends, demographic data, high-risk groups, the relationship between COHb concentrations and blood ethanol levels/age, the correlation between gender and time of poisoning, and sources of CO resulting in CO-related deaths, as recorded at the Department of love (HK), Czech Republic, between Forensic Medicine in Hradec Kra 1947 and 2006. 2. Methods The region of HK encompasses an area of 4758 square kilometers in northeastern Bohemia, with a population of more than half a million in 2016. The region of HK includes the city of HK, which consist of 93,000 residents. The Department of Forensic Medicine in HK investigates all sudden, unexpected, and non-natural deaths that occur within the region. This study was purely retrospective and relied on observational data recorded at the time of death. We included all cases of CO poisoning over a period of 60 years (1947e2006), which were autopsied at the Department of Forensic Medicine, HK. In each fatality, the autopsy report, warrant for postmortem examination, police report, emergency report and hospital records (if any) were reviewed. The following details were evaluated: age, sex, time of year the death occurred, manner of death, concentration of COHb and blood ethanol level. The records were also reviewed for sources of CO and categorized as follows: coal gas leakage, fire-related smoke, motor vehicle exhaust fumes, inadequately ventilated gas heating sources and faulty wood furnaces. Descriptive analysis was presented with frequency (percentage) and mean (SD, standard deviation). The relationship between elevated COHb concentration and blood ethanol level was analyzed using Spearman's rank correlation coefficient. We also performed a chi-squared test to evaluate the relationship between gender and seasonality of CO poisoning. All data were numerically evaluated and processed using NCSS 10 Statistical Software. Statistical significance was defined as a p-value less than 0.05. 3. Results 3.1. Demographic profile From the 36 189 autopsy records retrieved from January 1947 to December 2006, 1233 (3.4%) cases met inclusion criteria for the fatal CO poisoning. As shown in Fig. 1 the highest number COrelated fatalities were recorded in the 1970s and 1980s. In the following years, the overall trend indicated an obvious decrease in both accidental and suicidal CO poisoning. Male victims were slightly more common (731 cases, 59%), while 502 cases (41%) were
35 30 25 20 15 10 5 0
Suicide
Non-intentional
Undetermined
Fig. 1. Distribution of CO-related deaths (1947e2006).
M. Janík et al. / Journal of Forensic and Legal Medicine 48 (2017) 23e29
female victims. The victims' ages ranged from 0 to 95 years, with the average age being 48 ± 24.15 years [mean ± standard deviation]. The age of suicidal CO poisoning victims was 45.15 ± 18.32 years. In cases of accidental CO intoxication, the age of victims was 49.91 ± 25.02 years. The age of homicidal CO poisoning victims was 16.43 ± 21.25 years. There were 69 child victims between the ages of 0 and 15 years. The highest incidence of CO-related deaths was recorded in the month of January, followed by December and March. We found that as one might expect, non-intentional poisonings were highly correlated with the need for heating during the winter months, while suicides remained steady across the year. There was no statistically significant relationship between the month and the victim gender (p ¼ 0.869).
3.2. Manner of death Accidental CO poisoning was found to be cause of death in 548 cases, 45% (Table 1, and Fig. 2). In most accidents, direct coal gas leakage (239 cases) was the most common source of CO, followed by inhaled smoke from fires (116 cases), poorly functioning gas heating systems (87 cases), motor vehicle exhaust fumes (47 cases), and faulty wood furnaces (21 cases). The number of individuals who committed suicide through CO inhalation was 495, 40%. Of all the CO poisoning suicides, 326 cases were found to use inhalation of coal gas as the delivery method, followed by intentionally inhaled motor vehicle exhaust fumes (94 cases), fumes from gas
25
devices and wood furnaces (37 cases), and inhaled fire-related smoke (6 cases). We found 14 cases of homicidal CO poisoning (13 of them were filicides). The manner of death in coal-gas related CO inhalation is shown in Fig. 3. Finally, the manner of death remained undetermined in 176 cases. 3.3. Source of carbon monoxide The most common source of CO was found to be coal gas, accounting for more than half of the CO-related deaths (Fig. 4). After coal gas leaks, the second most common source of CO was motor vehicle exhaust fumes, causing fatal CO inhalation in 174 cases. Fire-related CO poisoning was the reported cause of death in 133 cases. Fatal CO poisonings involving defective gas appliances, with an inadequate supply of oxygen, occurred in 121 cases. Incomplete combustion of solid fuels such as wood or charcoal briquettes resulted in 41 CO-related fatalities. 3.4. Coal gas use vs. natural gas use In addition to the aforementioned goals of this study, we collected data on all CO-related deaths during 1970-1979 and compared them with a later period (1990e1999) when coal gas had been entirely replaced by non-toxic CO-free natural gas. Most of the poisoning in the 1970s occurred after coal gas leaks. Unsurprisingly, the number of coal gas CO-associated deaths decreased
Table 1 Manners of death and sources of CO. Source of CO
Male/female Mean age Fire-related smoke Vehicle Exhaust fumes Coal gas Faulty gas devices Faulty wood furnaces
Manner of death Suicide (495 victims)
Accident (548 victims)
Homicide (14 victims)
Undetermined (176 victims)
305/190 45.1 6 94 326 21 16
301/247 49.9 116 47 239 87 21
10/4 16.4 1 0 13 0 0
133/43 41.4 10 33 83 13 4
Fig. 2. Manner of death in CO-related fatalities (1947e2006).
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M. Janík et al. / Journal of Forensic and Legal Medicine 48 (2017) 23e29
Fig. 3. Manner of death in coal gas-related CO inhalation.
Fig. 4. Sources of CO.
significantly during the period 1997e2006. The number of fatal CO poisoning from malfunctioning wood-burning heaters decreased slightly. The number of CO-related fatalities from fire-related smoke and motor vehicle emissions was similar in both these decades, as was the total number of cases autopsied. While the overall incidence of suicide and the incidence of suicide by CO inhalation over a decade 1970e1979 remained relatively constant, a trend was seen over the period 1990e1999 toward a decrease of both total suicides and suicides by CO intoxication (Fig. 5).
the cases examined. The overall average concentration of blood ethanol was 0.41 ± 0.69 g/kg. The average ethanol concentration in accidental CO poisoning was 0.35 ± 0.65 g/kg. The median blood ethanol concentration for suicidal poisoning was 0.5 ± 0.75 g/kg. Statistical analysis of these concentrations showed that there was no significant relationship between blood alcohol concentration and COHb levels (p ¼ 0.159) and between age and alcohol/COHb levels (p ¼ 0.153/p ¼ 0.125). 4. Discussion
3.5. Carboxyhemoglobin and ethanol levels in blood Carboxyhemoglobin (COHb) levels were measured in all reviewed cases. The average blood level of COHb was 66% ± 16.74 (max. 98%, min. 3%). The COHb level was zero in 13 cases (delayed deaths). The blood ethanol level was measured in 1017 cases. A positive blood ethanol concentration was detected in 455 (45%) of
We studied fatal CO poisoning cases from 1947 to 2006 to investigate their characteristics. The results of this study give an indication of the status and trends of CO-related fatalities, as well as their heterogeneous circumstances, during the six past decades in the Czech Republic. It also enables further discussion concerning the target population for future preventive measures.
M. Janík et al. / Journal of Forensic and Legal Medicine 48 (2017) 23e29
27
160 140 120 100 80 60 40 20 0
Total suicides
CO suicides
Fig. 5. Overall and CO-specific suicide rate, 1970e1979; 1990-1999.
During the past few years, CO-associated mortality rates in the Czech Republic tend to oscillate between 110-140 deaths each year.15 In addition to this, approximately 300 emergency department visits annually are attributable to CO poisoning.15 Estimates for the United States indicates approximately 50,000 emergency department attends for CO poisoning annually.16 Numbers of deaths in Britain reported by the National Health Service vary between 40 and 50 a year.17 Our results indicate that fatal CO poisoning predominantly affects the middle-aged male population. These findings are in accordance with the results of previous studies (18e21). It is wellrecognized that men are at greater risk of fatal CO intoxication because of their inclination towards risk-taking behavior and more frequent handling of fuel-burning tools and gas-powered engines. Interestingly, non-fatal CO poisoning is higher in females.22 This reaffirms the fact that the causes of CO exposure are still not well understood. In our study, the average age of the deceased after CO intoxication was 48 years. According to several other studies, accidental CO deaths occurred in individuals who were considerable older than those who committed suicide by CO inhalation.19e22 The general opinion is that older people are at higher risk of unintentional CO intoxication because of their cardiovascular disease, cognitive impairment, limited mobility and poor socioeconomic situations. Our results are also in line with the general idea that CO intoxication is more frequent during winter months. Risser et al. reported that in 417 CO-related deaths in Vienna, the majority of cases were accidents, with the higher incidence in the winter months.21 These findings are similar to those of Homer et al. in Cleveland, USA18 and Ait El Cadi et al. in Morocco.23 Additionally, because flu-like illness and CO poisoning peak in winter, there is the possibility that misdiagnosis can occur. From a medico-legal standpoint, fatal CO poisoning is often deemed accidental because CO is almost impossible to detect in an exposed person.19,25 Considering the aggregated data from our study and those previously reported, the most common source of non-intentional fatal CO poisoning is domestic fuel, either from piped gas or faulty domestic gas sources, or wood heaters and firerelated fumes. Typical accidental CO poisoning usually involves unsuspected increases in CO levels in enclosed or poorly ventilated areas, which can include sealed rooms, homes, secured motor vehicles, parking garages, car washes and camping tents. Most recently, accidental CO poisoning due to “mud bogging” has been reported.26 “Mud bogging” is an off-road motorsport in which drivers navigate vehicles over a muddy pit or track. Immobilization
of these vehicles occurs frequently and may cause exhaust pipes to become clogged with mud. Subsequent permeation of CO throughout the cabin places occupants at risk of inhaling toxic exhaust fumes. Because of its easy accessibility, rapid lethality, and painless exposure, intentional inhalation of CO is a commonly used method for committing suicide. In some Asian countries such as Japan and China, CO poisoning from charcoal burning is a leading method of suicide, and it is now the second most common suicide method in Taiwan and Hong Kong.24,27,28 An increasing number of similar charcoal burning deaths have been reported throughout Europe and the United States in recent years.29e31 In such cases, the Internet and suicide web forums may play an important role in advancing this method of suicide.20 In the past few years, inhalation of motor vehicle fumes became more common as a suicide mechanism. The results of our study show that 19% of all CO suicides used this method. However, introduction of the catalytic converter in the 1970s reduced the CO concentration of automobile exhausts. While inhalation of automobile exhaust fumes used to be fatal within minutes, the modern exhaust may be tolerated for extended periods. This is suggested in a published report of an individual who ran a car engine for 10 h, with a tube attached directly from the tailpipe to the passenger compartment of the vehicle, without developing a critically elevated COHb level.32 Most recently, Bakovic et al. reported a rare case of suicidal intoxication with CO produced after the reaction of formic and sulfuric acid.33 Our work suggests that acute ethanol use is associated with an increased risk of fatal CO poisoning. This is in line with other research linking alcohol and drug intoxication to CO fatalities.34e36 Although homicidal CO poisoning is rare, our study identified 14 murder-suicide cases where CO inhalation was the cause of death. Ruszkiewicz et al. reported one case of a victim of CO poisoning mimicking a natural death.37 Several cases of filicides utilizing CO, particularly in Asian regions, have also been reported.38e40 Formerly, the main source of the exogenous CO that caused fatal poisoning was coal gas, supplied via a piped distribution system.21,41,42 Consequently, CO was readily accessible by simply turning on a home oven, because of the widespread use of coal gas for the domestic gas supply. In the late 19th and early 20th centuries, coal gas contained a high percentage of CO and exposed a large number of people to acute and chronic CO poisoning.43 Bowen et al. reported 896 cases of CO poisoning, and 777 of them were a result of inhaling the CO produced from coal gas.44 Following the widespread detoxification of home gas supply, domestic gas no longer contains significant levels of CO. In the United Kingdom,
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M. Janík et al. / Journal of Forensic and Legal Medicine 48 (2017) 23e29
after the elimination of domestic coal gas, it was shown that the overall suicide rate decreased, suggesting that restricting access to this lethal supply could reduce the total number of suicides.41 Similarly, replacement of coal gas with natural gas in the Czech Republic, which was completed in 1992, dramatically reduced the number of both intentional and accidental CO poisoning deaths. Until the late 1990s, the vast majority of CO poisoning in the Czech Republic was caused by coal gas inhalation. In the following years, the most common sources of fatal CO intoxication were fire-related or from motor vehicle emissions and other combustion sources such as gas, coal, wood stoves and fireplaces, home water heaters, kerosene or other fossil-fuel-burning heaters and appliances. Other atypical sources of CO that have been reported include running gasoline-powered engines such as a gas-powered washer, diesel engine or lawn mower in an enclosed space.31 The COHb levels of victims who subsequently die after CO intoxication can vary greatly, depending on the circumstances, manner of death, source of CO, and the health condition of the individual. This is in line with our findings and other research linking COHb levels to heterogeneity of CO-related deaths. The COHb levels are typically higher for suicidal CO poisoning than in accidental cases.19 Analysis of a series of 41 fatalities after intentional or accidental inhalation of automobile exhaust fumes has revealed COHb levels ranging from 48 to 93%, with an average of 72%.45 In 85 victims of fire, COHb levels ranged from 25 to 85% with an average value of 59%.46 In conclusion, CO poisoning remains relatively frequent cause of death across the world. Furthermore, because both clinical symptoms and autopsy indications of CO intoxication are only indicative rather than specific, CO poisoning may be overlooked which could lead to a miscalculation of CO-associated morbidity and mortality rates for European populations. Although a variety of interventions directed at CO poisoning have been developed, their effectiveness is unclear. Reviewing 1233 cases of fatal CO poisoning covering a period of 60 years, this study was the first comprehensive retrospective study on CO poisoning conducted in the Czech Republic. Results of this study demonstrate that many features and trends of fatal CO poisoning cases that occurred in the Czech Republic are comparable with those reported in case studies conducted in Europe and the United States. The elimination of domestic coal gas and introduction of catalytic converters in the exhaust system of vehicles dramatically reduced the number of both intentional and accidental CO poisoning deaths. Nonetheless, CO fatalities can still occur in a variety of different settings, particularly in relation to malfunctioning heating systems or gas-powered engines. Finally, our analysis and the previously reported ones on trends of deaths by CO poisoning hold the key to identifying the groups with the highest level of risk and provides a rich and up-to-date resource for clinical applications and public health perspectives. Conflict of interest None declared. References 1. Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR. Carbon monoxide poisoningea public health perspective. Toxicology. 2000;145:1e14. 2. Stefanidou ME, Maravelias CP, Dona AA, Pistos CM, Spiliopoulou CA, Athanaselis SA. Carbon monoxide-related deaths in Greece: a 23-year survey. Am J Forensic Med Pathol. 2012;33:128e131. 3. Khadem-Rezaiyan M, Afshari R. Carbon monoxide poisoning in Northeast of Iran. J Forensic Leg Med. 2016;41:1e4. 4. Novomeský F. [Diving Medicine] Book in Slovak. 1th ed. Martin: Osveta; 2013. 5. Barrett KE, Barman SM, Boitano S, Brooks H. Ganong's Review of Medical Physiology. 25th ed. McGraw-Hill Education; 2015. 6. Prockop LD, Chichkova RI. Carbon monoxide intoxication: an updated review.
J Neurol Sci. 2007;262:122e130. 7. Jaffe FA. Pathogenicity of carbon monoxide. Am J Forensic Med Pathol. 1997;18: 406e410. 8. Weaver LK. Carbon monoxide poisoning. N Engl J Med. 2009;360:1217e1225. 9. Morita S, Furukawa S, Wingelfeld L, Nishi K. Expression of antigens related to hypoxia, stress, and apoptosis in the myocardium after fatal carbon monoxide exposure. Rom J Leg Med. 2013;21:253e258. 10. Morita S, Furukawa S, Wingelfeld L, Matsuda W, Nishi K. Difference in the expression of CIRBP, RBM3 and HSP70 in the myocardium and cerebellum after death by hypothermia and carbon monoxide poisoning. Rom J Leg Med. 2013;21:219e224. 11. Pieri M, Giugliano P, Vacchiano G. Pulmonary macrophages activity in CO intoxication. J Forensic Leg Med. 2016;38:93e96. 12. Yarid NA, Harruff RC. Globus pallidus necrosis unrelated to carbon monoxide poisoning: retrospective analysis of 27 cases of Basal Ganglia Necrosis. J Forensic Sci. 2015;60:1484e1487. 13. Weaver LK, Valentine KJ, Hopkins RO. Carbon monoxide poisoning: risk factors for cognitive sequelae and the role of hyperbaric oxygen. Am J Respir Crit Care Med. 2007;176:491e497. 14. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med. 1998;339: 1603e1608. jek M. Carbon Monoxide Poisoning: Pathophysiology, Pathomorphology, 15. Ha Medico-legal Aspects, Possibilities of Hyperbaric Oxygen Therapy. Thesis in Czech. Doctoral dissertation. 2015. 16. Hampson NB, Weaver LK. Carbon monoxide poisoning: a new incidence for an old disease. Undersea Hyperb Med. 2007;34:163e168. 17. NHS Choices. Carbon Monoxide Poisoning; 2016. http://www.nhs.uk/conditions/ carbon-monoxide-poisoning/Pages/Introduction.aspx. Accessed 24 February 2016. 18. Homer CD, Engelhart DA, Lavins ES, Jenkins AJ. Carbon monoxide-related deaths in a metropolitan county in the USA: an 11-year study. Forensic Sci Int. 2005;149:159e165. 19. Ruas F, Mendonça MC, Real FC, Vieira DN, Teixeira HM. Carbon monoxide poisoning as a cause of death and differential diagnosis in the forensic practice: a retrospective study, 2000-2010. J Forensic Leg Med. 2014;24:1e6. 20. Nielsen PR, Gheorghe A, Lynnerup N. Forensic aspects of carbon monoxide poisoning by charcoal burning in Denmark, 2008-2012: an autopsy based study. Forensic Sci Med Pathol. 2014;10:390e394. 21. Risser D, Schneider B. Carbon monoxide-related deaths from 1984 to 1993 in Vienna, Austria. J Forensic Sci. 1995;40:368e371. 22. Nazari J, Dianat I, Stedmon A. Unintentional carbon monoxide poisoning in Northwest Iran: a 5-year study. J Forensic Leg Med. 2010;17:388e391. 23. Ait El Cadi M, Khabbal Y, Idrissi L. Carbon monoxide poisoning in Morocco during 1999-2007. J Forensic Leg Med. 2009;16:385e387. 24. Li F, Chan HC, Liu S, et al. Carbon monoxide poisoning as a cause of death in Wuhan, China: a retrospective six-year epidemiological study (2009-2014). Forensic Sci Int. 2015;253:112e118. 25. Wilson RC, Saunders PJ, Smith G. An epidemiological study of acute carbon monoxide poisoning in the West Midlands. Occup Environ Med. 1998;55: 723e728. 26. Menke NB, Fitzpatrick K, Lynch MJ, King AM. Carbon monoxide poisoning due to “mud bogging”. N Engl J Med. 2015;373:1082. 27. Yoshioka E, Hanley SJ, Kawanishi Y, Saijo Y. Epidemic of charcoal burning suicide in Japan. Br J Psychiatry. 2014;204:274e282. 28. Liu KY, Beautrais A, Caine E, et al. Charcoal burning suicides in Hong Kong and urban Taiwan: an illustration of the impact of a novel suicide method on overall regional rates. J Epidemiol Community Health. 2007;61:248e253. 29. Chen YY, Bennewith O, Hawton K, et al. Suicide by burning barbecue charcoal in England. J Public Health (Oxf). 2013;35:223e227. 30. Brooks-Lim EWL, Sadler DW. Suicide by burning barbeque charcoal: three case reports. Med Sci Law. 2009;49:301e306. 31. Schmitt MW, Williams TL, Woodard KR, Harruff RC. Trends in suicide by carbon monoxide inhalation in King County, Washington: 1996-2009. J Forensic Sci. 2011;56:652e655. 32. Vossberg B, Skolnick J. The role of catalytic converters in automobile carbon monoxide poisoning. Chest. 1999;115:580e581. 33. Bakovic M, Nestic M, Mayer D. Suicidal chemistry: combined intoxication with carbon monoxide and formic acid. Int J Leg Med. 2016;130:723e729. 34. Przepyszny LM, Jenkins AJ. The prevalence of drugs in carbon monoxiderelated deaths: a retrospective study, 2000-2003. Am J Forensic Med Pathol. 2007;28:242e248. 35. Straka L, Zubor P, Novomesky F, et al. Fatal alcohol intoxication in women: a forensic autopsy study from Slovakia. BMC Public Health. 2011;11:924. 36. Straka L, Stuller F, Novomeský F. The lethal alcohol intoxications and deaths due to severe drunkenness in North Slovakia regions (1994-1996, 2003-2005): a medicolegal comparative study. Article in Slovak Soud Lek. 2008;53:2e7. 37. Ruszkiewicz A, de Boer B, Robertson S. Unusual presentation of death due to carbon monoxide poisoning. A report of two cases. Am J Forensic Med Pathol. 1997;18:181e184. 38. Dawson M. Canadian trends in filicide by gender of the accused, 1961-2011. Child Abuse Negl. 2015;47:162e174. 39. McKee A, Egan V. A case series of twenty one maternal filicides in the UK. Child Abuse Negl. 2013;37:753e761. 40. Hon KL. Dying with parents: an extreme form of child abuse. World J Pediatr. 2011;7:266e268.
M. Janík et al. / Journal of Forensic and Legal Medicine 48 (2017) 23e29 41. Kreitman N. The coal gas story. United Kingdom suicide rates, 1960-71. Br J Prev Soc Med. 1976;30:86e93. 42. Kreitman N, Platt S. Suicide, unemployment, and domestic gas detoxification in Britain. J Epidemiol Community Health. 1984;38:1e6. 43. Blum D. The Poisoner's Handbook: Murder and the Birth of Forensic Medicine in Jazz Age New York. New York, NY: Penguin Books; 2010.
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44. Bowen DA, Duffy P, Callear A, Fitton J. Carbon monoxide poisoning. Forensic Sci Int. 1989;41:163e168. 45. Baselt RC. Disposition of Toxic Drugs and Chemicals in Man. tenth ed. California, Seal Beach: Biomedical Publications; 2014. 46. Dominguez AM. Problems of carbon monoxide in fires. J Forensic Sci. 1962;7: 379e392.
Contents lists available at ScienceDirect
Journal of Forensic and Legal Medicine j o u r n a l h o m e p a g e : w w w . e l s e v i e r . c o m / l o c a t e / j fl m
Carbon monoxide-related fatalities: A 60-year single institution experience , M.D. b, 1, Step nka Ku , M.D. b, Martin Janík, M.D., PhD a, *, 1, Michaela Ublova a cerova Petr Hejna, M.D., PhD, MBA b a
Department of Forensic Medicine and Medicolegal Expertises, Jessenius Faculty of Medicine, Comenius University, University Hospital, Martin, Slovak Republic Department of Forensic Medicine, Faculty of Medicine, Charles University, University Hospital, Hradec Kralove, Czech Republic
b
a r t i c l e i n f o
a b s t r a c t
Article history: Received 20 January 2017 Accepted 12 April 2017 Available online 13 April 2017
Objective: Though carbon monoxide (CO) poisonings account currently for a relatively small percentage of total non-natural deaths in Europe, they represent a serious public health burden and significant component of avoidable mortality in many countries. Our aim was to investigate long-term trends and to determine epidemiologic characteristics of the CO-related deaths in the Czech Republic, recorded at the . Department of Forensic Medicine in Hradec Kr alove Methods: This was an autopsy-based single-centre retrospective cohort study of all fatalities caused by CO poisoning over six decades (1947e2006). All data were numerically evaluated and processed using NCSS 10 Statistical Software. Statistical significance was defined as a p-value less than 0.05. Results: A total of 1233 CO-related deaths were identified for inclusion in the study. The manner of death was ranked in order as follows: 45% accidental poisoning, 40% suicidal poisoning, 1% homicidal poisoning, 14% remained undetermined. There were slightly more male victims (59%) than female, and the mean age overall was 48 years. The majority of CO-related fatalities were attributed to coal gas inhalation, with the remainder being from inhaled motor vehicle exhaust fumes, inhaled fire smoke, and other combustion sources such as charcoal, gas and wood-burning appliances. The mean blood carboxyhemoglobin (COHb) level was 66%. A positive blood ethanol concentration was measured in 455 (37%) cases examined. Non-intentional poisonings were highly correlated with the winter months. Conclusion: This study shows that the prevalence of CO-related deaths has decreased significantly in the Czech Republic following the widespread detoxification of the domestic gas in the 1990e1995. Our findings suggest that acute ethanol use, poorer socioeconomic position, and inadequate education status about the danger of CO are associated with an increased risk of fatal CO poisoning. Finally, our results demonstrate the continued value of the autopsy in monitoring global public health security issues and socioeconomic situation. Further similar large-scale studies in different populations are needed to improve the targeting of interventions to the groups with the highest level of risk, and to understand the sources of variation in CO-related mortality. © 2017 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.
Keywords: Carbon monoxide Poisoning Fatality Autopsy Coal gas Carboxyhemoglobin
1. Introduction Carbon monoxide (CO) is a colorless, odorless and tasteless gas
* Corresponding author. Institute of Forensic Medicine and Medicolegal Expertises, Jessenius Faculty of Medicine, Comenius University, University Hospital, 036 59 Martin, Slovak Republic, EU. E-mail address: [email protected] (M. Janík). 1 ) contributed equally to The first two authors (Martin Janík and Michaela Ublova this study.
that is less dense than air and non-irritating. It is produced from the incomplete combustion of carbon-containing compounds. Although the global replacement of coal gas with non-toxic natural gas have contributed substantially towards a decline in the number of CO-related deaths, accidental CO poisoning remains in the cause of over half of all fatal poisonings annually all over the world.1,2 Though CO poisoning account for a high percentage of total poisoning, almost all cases of accidental CO poisoning can be prevented with appropriate public education, and prevention programs on CO-emitting devices.3
http://dx.doi.org/10.1016/j.jflm.2017.04.002 1752-928X/© 2017 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.
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Forensically relevant sources of exogenous CO include predominantly inferior or faulty heating devices and gas-powered engines, motor vehicle exhaust fumes, fire-related inhaled smoke and burning charcoal. Rarely, CO poisoning may also result from methylene chloride (a common component of paint remover and other solvents). CO poisoning is infrequent, but potential lifethreatening jeopardy of scuba diving.4 Additionally, tobacco smoke is an important source of CO. The mechanism of CO toxicity is tissue hypoxia and inhibition of cellular respiration, because the affinity of hemoglobin for CO is 210 times as great as its affinity for oxygen, and COHb liberates CO very slowly.5 Recent investigations also suggest other mechanisms of CO-mediated toxicity. One hypothesis is that CO-induced tissue hypoxia may be followed by re-oxygenation injury to the central nervous system.6,7 CO also causes inflammation by increasing levels of cytosolic heme and the heme oxygenase-1 protein, resulting in intracellular oxidative stress.8 In addition to fairy pathognomonic autopsy signs attributable to CO poisoning (cherry-red lividity, bright red coloration of the fingernail bed, blood, and the skeletal musculature), novel markers such as pulmonary macrophage activity, or expression of CIRBP, RBM3, and SIRT1 antigens in the myocardium or in the cerebellum could provide useful diagnostic information for revealing COinduced hypoxic damage.9e11 According to a recent study, bilateral globus pallidus necrosis, formerly described as a characteristic lesion for delayed CO poisoning, is now deemed non-specific and rarely associated with CO poisoning.12 The clinical signs of CO poisoning are said to be non-specific and vary with CO saturation levels, duration of exposure, pre-existing medical conditions and individual predisposition. Blood COHb concentrations of 5-10% may aggravate pre-existing cardiovascular diseases, while concentrations of 15-25% often cause dizziness and nausea. The levels of COHb exceeding 50% saturation are generally considered to be life-threatening. In the presence of alcohol or chronic cardiovascular disorder, however, fatal CO saturations may be significantly lower. Delayed neurotoxicity, which could occur 2e3 weeks after an acute CO exposure, may consist of bradykinesia, seizures, Parkinson's disease-like symptoms, and other cognitive impairments. In one study, patients who were 36 years of age or older or who had been exposed to CO for at least 24 h, or who had cerebellar abnormalities on presentation had an increased risk of cognitive sequelae at 6 weeks as compared with those without these characteristics.13 Moreover, CO exposure has an especially deleterious effect on pregnant women, because of the greater sensitivity of the fetus to the harmful effects of the gas.14 The aim of this retrospective study was to assess long-term
trends, demographic data, high-risk groups, the relationship between COHb concentrations and blood ethanol levels/age, the correlation between gender and time of poisoning, and sources of CO resulting in CO-related deaths, as recorded at the Department of love (HK), Czech Republic, between Forensic Medicine in Hradec Kra 1947 and 2006. 2. Methods The region of HK encompasses an area of 4758 square kilometers in northeastern Bohemia, with a population of more than half a million in 2016. The region of HK includes the city of HK, which consist of 93,000 residents. The Department of Forensic Medicine in HK investigates all sudden, unexpected, and non-natural deaths that occur within the region. This study was purely retrospective and relied on observational data recorded at the time of death. We included all cases of CO poisoning over a period of 60 years (1947e2006), which were autopsied at the Department of Forensic Medicine, HK. In each fatality, the autopsy report, warrant for postmortem examination, police report, emergency report and hospital records (if any) were reviewed. The following details were evaluated: age, sex, time of year the death occurred, manner of death, concentration of COHb and blood ethanol level. The records were also reviewed for sources of CO and categorized as follows: coal gas leakage, fire-related smoke, motor vehicle exhaust fumes, inadequately ventilated gas heating sources and faulty wood furnaces. Descriptive analysis was presented with frequency (percentage) and mean (SD, standard deviation). The relationship between elevated COHb concentration and blood ethanol level was analyzed using Spearman's rank correlation coefficient. We also performed a chi-squared test to evaluate the relationship between gender and seasonality of CO poisoning. All data were numerically evaluated and processed using NCSS 10 Statistical Software. Statistical significance was defined as a p-value less than 0.05. 3. Results 3.1. Demographic profile From the 36 189 autopsy records retrieved from January 1947 to December 2006, 1233 (3.4%) cases met inclusion criteria for the fatal CO poisoning. As shown in Fig. 1 the highest number COrelated fatalities were recorded in the 1970s and 1980s. In the following years, the overall trend indicated an obvious decrease in both accidental and suicidal CO poisoning. Male victims were slightly more common (731 cases, 59%), while 502 cases (41%) were
35 30 25 20 15 10 5 0
Suicide
Non-intentional
Undetermined
Fig. 1. Distribution of CO-related deaths (1947e2006).
M. Janík et al. / Journal of Forensic and Legal Medicine 48 (2017) 23e29
female victims. The victims' ages ranged from 0 to 95 years, with the average age being 48 ± 24.15 years [mean ± standard deviation]. The age of suicidal CO poisoning victims was 45.15 ± 18.32 years. In cases of accidental CO intoxication, the age of victims was 49.91 ± 25.02 years. The age of homicidal CO poisoning victims was 16.43 ± 21.25 years. There were 69 child victims between the ages of 0 and 15 years. The highest incidence of CO-related deaths was recorded in the month of January, followed by December and March. We found that as one might expect, non-intentional poisonings were highly correlated with the need for heating during the winter months, while suicides remained steady across the year. There was no statistically significant relationship between the month and the victim gender (p ¼ 0.869).
3.2. Manner of death Accidental CO poisoning was found to be cause of death in 548 cases, 45% (Table 1, and Fig. 2). In most accidents, direct coal gas leakage (239 cases) was the most common source of CO, followed by inhaled smoke from fires (116 cases), poorly functioning gas heating systems (87 cases), motor vehicle exhaust fumes (47 cases), and faulty wood furnaces (21 cases). The number of individuals who committed suicide through CO inhalation was 495, 40%. Of all the CO poisoning suicides, 326 cases were found to use inhalation of coal gas as the delivery method, followed by intentionally inhaled motor vehicle exhaust fumes (94 cases), fumes from gas
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devices and wood furnaces (37 cases), and inhaled fire-related smoke (6 cases). We found 14 cases of homicidal CO poisoning (13 of them were filicides). The manner of death in coal-gas related CO inhalation is shown in Fig. 3. Finally, the manner of death remained undetermined in 176 cases. 3.3. Source of carbon monoxide The most common source of CO was found to be coal gas, accounting for more than half of the CO-related deaths (Fig. 4). After coal gas leaks, the second most common source of CO was motor vehicle exhaust fumes, causing fatal CO inhalation in 174 cases. Fire-related CO poisoning was the reported cause of death in 133 cases. Fatal CO poisonings involving defective gas appliances, with an inadequate supply of oxygen, occurred in 121 cases. Incomplete combustion of solid fuels such as wood or charcoal briquettes resulted in 41 CO-related fatalities. 3.4. Coal gas use vs. natural gas use In addition to the aforementioned goals of this study, we collected data on all CO-related deaths during 1970-1979 and compared them with a later period (1990e1999) when coal gas had been entirely replaced by non-toxic CO-free natural gas. Most of the poisoning in the 1970s occurred after coal gas leaks. Unsurprisingly, the number of coal gas CO-associated deaths decreased
Table 1 Manners of death and sources of CO. Source of CO
Male/female Mean age Fire-related smoke Vehicle Exhaust fumes Coal gas Faulty gas devices Faulty wood furnaces
Manner of death Suicide (495 victims)
Accident (548 victims)
Homicide (14 victims)
Undetermined (176 victims)
305/190 45.1 6 94 326 21 16
301/247 49.9 116 47 239 87 21
10/4 16.4 1 0 13 0 0
133/43 41.4 10 33 83 13 4
Fig. 2. Manner of death in CO-related fatalities (1947e2006).
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Fig. 3. Manner of death in coal gas-related CO inhalation.
Fig. 4. Sources of CO.
significantly during the period 1997e2006. The number of fatal CO poisoning from malfunctioning wood-burning heaters decreased slightly. The number of CO-related fatalities from fire-related smoke and motor vehicle emissions was similar in both these decades, as was the total number of cases autopsied. While the overall incidence of suicide and the incidence of suicide by CO inhalation over a decade 1970e1979 remained relatively constant, a trend was seen over the period 1990e1999 toward a decrease of both total suicides and suicides by CO intoxication (Fig. 5).
the cases examined. The overall average concentration of blood ethanol was 0.41 ± 0.69 g/kg. The average ethanol concentration in accidental CO poisoning was 0.35 ± 0.65 g/kg. The median blood ethanol concentration for suicidal poisoning was 0.5 ± 0.75 g/kg. Statistical analysis of these concentrations showed that there was no significant relationship between blood alcohol concentration and COHb levels (p ¼ 0.159) and between age and alcohol/COHb levels (p ¼ 0.153/p ¼ 0.125). 4. Discussion
3.5. Carboxyhemoglobin and ethanol levels in blood Carboxyhemoglobin (COHb) levels were measured in all reviewed cases. The average blood level of COHb was 66% ± 16.74 (max. 98%, min. 3%). The COHb level was zero in 13 cases (delayed deaths). The blood ethanol level was measured in 1017 cases. A positive blood ethanol concentration was detected in 455 (45%) of
We studied fatal CO poisoning cases from 1947 to 2006 to investigate their characteristics. The results of this study give an indication of the status and trends of CO-related fatalities, as well as their heterogeneous circumstances, during the six past decades in the Czech Republic. It also enables further discussion concerning the target population for future preventive measures.
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160 140 120 100 80 60 40 20 0
Total suicides
CO suicides
Fig. 5. Overall and CO-specific suicide rate, 1970e1979; 1990-1999.
During the past few years, CO-associated mortality rates in the Czech Republic tend to oscillate between 110-140 deaths each year.15 In addition to this, approximately 300 emergency department visits annually are attributable to CO poisoning.15 Estimates for the United States indicates approximately 50,000 emergency department attends for CO poisoning annually.16 Numbers of deaths in Britain reported by the National Health Service vary between 40 and 50 a year.17 Our results indicate that fatal CO poisoning predominantly affects the middle-aged male population. These findings are in accordance with the results of previous studies (18e21). It is wellrecognized that men are at greater risk of fatal CO intoxication because of their inclination towards risk-taking behavior and more frequent handling of fuel-burning tools and gas-powered engines. Interestingly, non-fatal CO poisoning is higher in females.22 This reaffirms the fact that the causes of CO exposure are still not well understood. In our study, the average age of the deceased after CO intoxication was 48 years. According to several other studies, accidental CO deaths occurred in individuals who were considerable older than those who committed suicide by CO inhalation.19e22 The general opinion is that older people are at higher risk of unintentional CO intoxication because of their cardiovascular disease, cognitive impairment, limited mobility and poor socioeconomic situations. Our results are also in line with the general idea that CO intoxication is more frequent during winter months. Risser et al. reported that in 417 CO-related deaths in Vienna, the majority of cases were accidents, with the higher incidence in the winter months.21 These findings are similar to those of Homer et al. in Cleveland, USA18 and Ait El Cadi et al. in Morocco.23 Additionally, because flu-like illness and CO poisoning peak in winter, there is the possibility that misdiagnosis can occur. From a medico-legal standpoint, fatal CO poisoning is often deemed accidental because CO is almost impossible to detect in an exposed person.19,25 Considering the aggregated data from our study and those previously reported, the most common source of non-intentional fatal CO poisoning is domestic fuel, either from piped gas or faulty domestic gas sources, or wood heaters and firerelated fumes. Typical accidental CO poisoning usually involves unsuspected increases in CO levels in enclosed or poorly ventilated areas, which can include sealed rooms, homes, secured motor vehicles, parking garages, car washes and camping tents. Most recently, accidental CO poisoning due to “mud bogging” has been reported.26 “Mud bogging” is an off-road motorsport in which drivers navigate vehicles over a muddy pit or track. Immobilization
of these vehicles occurs frequently and may cause exhaust pipes to become clogged with mud. Subsequent permeation of CO throughout the cabin places occupants at risk of inhaling toxic exhaust fumes. Because of its easy accessibility, rapid lethality, and painless exposure, intentional inhalation of CO is a commonly used method for committing suicide. In some Asian countries such as Japan and China, CO poisoning from charcoal burning is a leading method of suicide, and it is now the second most common suicide method in Taiwan and Hong Kong.24,27,28 An increasing number of similar charcoal burning deaths have been reported throughout Europe and the United States in recent years.29e31 In such cases, the Internet and suicide web forums may play an important role in advancing this method of suicide.20 In the past few years, inhalation of motor vehicle fumes became more common as a suicide mechanism. The results of our study show that 19% of all CO suicides used this method. However, introduction of the catalytic converter in the 1970s reduced the CO concentration of automobile exhausts. While inhalation of automobile exhaust fumes used to be fatal within minutes, the modern exhaust may be tolerated for extended periods. This is suggested in a published report of an individual who ran a car engine for 10 h, with a tube attached directly from the tailpipe to the passenger compartment of the vehicle, without developing a critically elevated COHb level.32 Most recently, Bakovic et al. reported a rare case of suicidal intoxication with CO produced after the reaction of formic and sulfuric acid.33 Our work suggests that acute ethanol use is associated with an increased risk of fatal CO poisoning. This is in line with other research linking alcohol and drug intoxication to CO fatalities.34e36 Although homicidal CO poisoning is rare, our study identified 14 murder-suicide cases where CO inhalation was the cause of death. Ruszkiewicz et al. reported one case of a victim of CO poisoning mimicking a natural death.37 Several cases of filicides utilizing CO, particularly in Asian regions, have also been reported.38e40 Formerly, the main source of the exogenous CO that caused fatal poisoning was coal gas, supplied via a piped distribution system.21,41,42 Consequently, CO was readily accessible by simply turning on a home oven, because of the widespread use of coal gas for the domestic gas supply. In the late 19th and early 20th centuries, coal gas contained a high percentage of CO and exposed a large number of people to acute and chronic CO poisoning.43 Bowen et al. reported 896 cases of CO poisoning, and 777 of them were a result of inhaling the CO produced from coal gas.44 Following the widespread detoxification of home gas supply, domestic gas no longer contains significant levels of CO. In the United Kingdom,
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after the elimination of domestic coal gas, it was shown that the overall suicide rate decreased, suggesting that restricting access to this lethal supply could reduce the total number of suicides.41 Similarly, replacement of coal gas with natural gas in the Czech Republic, which was completed in 1992, dramatically reduced the number of both intentional and accidental CO poisoning deaths. Until the late 1990s, the vast majority of CO poisoning in the Czech Republic was caused by coal gas inhalation. In the following years, the most common sources of fatal CO intoxication were fire-related or from motor vehicle emissions and other combustion sources such as gas, coal, wood stoves and fireplaces, home water heaters, kerosene or other fossil-fuel-burning heaters and appliances. Other atypical sources of CO that have been reported include running gasoline-powered engines such as a gas-powered washer, diesel engine or lawn mower in an enclosed space.31 The COHb levels of victims who subsequently die after CO intoxication can vary greatly, depending on the circumstances, manner of death, source of CO, and the health condition of the individual. This is in line with our findings and other research linking COHb levels to heterogeneity of CO-related deaths. The COHb levels are typically higher for suicidal CO poisoning than in accidental cases.19 Analysis of a series of 41 fatalities after intentional or accidental inhalation of automobile exhaust fumes has revealed COHb levels ranging from 48 to 93%, with an average of 72%.45 In 85 victims of fire, COHb levels ranged from 25 to 85% with an average value of 59%.46 In conclusion, CO poisoning remains relatively frequent cause of death across the world. Furthermore, because both clinical symptoms and autopsy indications of CO intoxication are only indicative rather than specific, CO poisoning may be overlooked which could lead to a miscalculation of CO-associated morbidity and mortality rates for European populations. Although a variety of interventions directed at CO poisoning have been developed, their effectiveness is unclear. Reviewing 1233 cases of fatal CO poisoning covering a period of 60 years, this study was the first comprehensive retrospective study on CO poisoning conducted in the Czech Republic. Results of this study demonstrate that many features and trends of fatal CO poisoning cases that occurred in the Czech Republic are comparable with those reported in case studies conducted in Europe and the United States. The elimination of domestic coal gas and introduction of catalytic converters in the exhaust system of vehicles dramatically reduced the number of both intentional and accidental CO poisoning deaths. Nonetheless, CO fatalities can still occur in a variety of different settings, particularly in relation to malfunctioning heating systems or gas-powered engines. Finally, our analysis and the previously reported ones on trends of deaths by CO poisoning hold the key to identifying the groups with the highest level of risk and provides a rich and up-to-date resource for clinical applications and public health perspectives. Conflict of interest None declared. References 1. Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR. Carbon monoxide poisoningea public health perspective. Toxicology. 2000;145:1e14. 2. Stefanidou ME, Maravelias CP, Dona AA, Pistos CM, Spiliopoulou CA, Athanaselis SA. Carbon monoxide-related deaths in Greece: a 23-year survey. Am J Forensic Med Pathol. 2012;33:128e131. 3. Khadem-Rezaiyan M, Afshari R. Carbon monoxide poisoning in Northeast of Iran. J Forensic Leg Med. 2016;41:1e4. 4. Novomeský F. [Diving Medicine] Book in Slovak. 1th ed. Martin: Osveta; 2013. 5. Barrett KE, Barman SM, Boitano S, Brooks H. Ganong's Review of Medical Physiology. 25th ed. McGraw-Hill Education; 2015. 6. Prockop LD, Chichkova RI. Carbon monoxide intoxication: an updated review.
J Neurol Sci. 2007;262:122e130. 7. Jaffe FA. Pathogenicity of carbon monoxide. Am J Forensic Med Pathol. 1997;18: 406e410. 8. Weaver LK. Carbon monoxide poisoning. N Engl J Med. 2009;360:1217e1225. 9. Morita S, Furukawa S, Wingelfeld L, Nishi K. Expression of antigens related to hypoxia, stress, and apoptosis in the myocardium after fatal carbon monoxide exposure. Rom J Leg Med. 2013;21:253e258. 10. Morita S, Furukawa S, Wingelfeld L, Matsuda W, Nishi K. Difference in the expression of CIRBP, RBM3 and HSP70 in the myocardium and cerebellum after death by hypothermia and carbon monoxide poisoning. Rom J Leg Med. 2013;21:219e224. 11. Pieri M, Giugliano P, Vacchiano G. Pulmonary macrophages activity in CO intoxication. J Forensic Leg Med. 2016;38:93e96. 12. Yarid NA, Harruff RC. Globus pallidus necrosis unrelated to carbon monoxide poisoning: retrospective analysis of 27 cases of Basal Ganglia Necrosis. J Forensic Sci. 2015;60:1484e1487. 13. Weaver LK, Valentine KJ, Hopkins RO. Carbon monoxide poisoning: risk factors for cognitive sequelae and the role of hyperbaric oxygen. Am J Respir Crit Care Med. 2007;176:491e497. 14. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med. 1998;339: 1603e1608. jek M. Carbon Monoxide Poisoning: Pathophysiology, Pathomorphology, 15. Ha Medico-legal Aspects, Possibilities of Hyperbaric Oxygen Therapy. Thesis in Czech. Doctoral dissertation. 2015. 16. Hampson NB, Weaver LK. Carbon monoxide poisoning: a new incidence for an old disease. Undersea Hyperb Med. 2007;34:163e168. 17. NHS Choices. Carbon Monoxide Poisoning; 2016. http://www.nhs.uk/conditions/ carbon-monoxide-poisoning/Pages/Introduction.aspx. Accessed 24 February 2016. 18. Homer CD, Engelhart DA, Lavins ES, Jenkins AJ. Carbon monoxide-related deaths in a metropolitan county in the USA: an 11-year study. Forensic Sci Int. 2005;149:159e165. 19. Ruas F, Mendonça MC, Real FC, Vieira DN, Teixeira HM. Carbon monoxide poisoning as a cause of death and differential diagnosis in the forensic practice: a retrospective study, 2000-2010. J Forensic Leg Med. 2014;24:1e6. 20. Nielsen PR, Gheorghe A, Lynnerup N. Forensic aspects of carbon monoxide poisoning by charcoal burning in Denmark, 2008-2012: an autopsy based study. Forensic Sci Med Pathol. 2014;10:390e394. 21. Risser D, Schneider B. Carbon monoxide-related deaths from 1984 to 1993 in Vienna, Austria. J Forensic Sci. 1995;40:368e371. 22. Nazari J, Dianat I, Stedmon A. Unintentional carbon monoxide poisoning in Northwest Iran: a 5-year study. J Forensic Leg Med. 2010;17:388e391. 23. Ait El Cadi M, Khabbal Y, Idrissi L. Carbon monoxide poisoning in Morocco during 1999-2007. J Forensic Leg Med. 2009;16:385e387. 24. Li F, Chan HC, Liu S, et al. Carbon monoxide poisoning as a cause of death in Wuhan, China: a retrospective six-year epidemiological study (2009-2014). Forensic Sci Int. 2015;253:112e118. 25. Wilson RC, Saunders PJ, Smith G. An epidemiological study of acute carbon monoxide poisoning in the West Midlands. Occup Environ Med. 1998;55: 723e728. 26. Menke NB, Fitzpatrick K, Lynch MJ, King AM. Carbon monoxide poisoning due to “mud bogging”. N Engl J Med. 2015;373:1082. 27. Yoshioka E, Hanley SJ, Kawanishi Y, Saijo Y. Epidemic of charcoal burning suicide in Japan. Br J Psychiatry. 2014;204:274e282. 28. Liu KY, Beautrais A, Caine E, et al. Charcoal burning suicides in Hong Kong and urban Taiwan: an illustration of the impact of a novel suicide method on overall regional rates. J Epidemiol Community Health. 2007;61:248e253. 29. Chen YY, Bennewith O, Hawton K, et al. Suicide by burning barbecue charcoal in England. J Public Health (Oxf). 2013;35:223e227. 30. Brooks-Lim EWL, Sadler DW. Suicide by burning barbeque charcoal: three case reports. Med Sci Law. 2009;49:301e306. 31. Schmitt MW, Williams TL, Woodard KR, Harruff RC. Trends in suicide by carbon monoxide inhalation in King County, Washington: 1996-2009. J Forensic Sci. 2011;56:652e655. 32. Vossberg B, Skolnick J. The role of catalytic converters in automobile carbon monoxide poisoning. Chest. 1999;115:580e581. 33. Bakovic M, Nestic M, Mayer D. Suicidal chemistry: combined intoxication with carbon monoxide and formic acid. Int J Leg Med. 2016;130:723e729. 34. Przepyszny LM, Jenkins AJ. The prevalence of drugs in carbon monoxiderelated deaths: a retrospective study, 2000-2003. Am J Forensic Med Pathol. 2007;28:242e248. 35. Straka L, Zubor P, Novomesky F, et al. Fatal alcohol intoxication in women: a forensic autopsy study from Slovakia. BMC Public Health. 2011;11:924. 36. Straka L, Stuller F, Novomeský F. The lethal alcohol intoxications and deaths due to severe drunkenness in North Slovakia regions (1994-1996, 2003-2005): a medicolegal comparative study. Article in Slovak Soud Lek. 2008;53:2e7. 37. Ruszkiewicz A, de Boer B, Robertson S. Unusual presentation of death due to carbon monoxide poisoning. A report of two cases. Am J Forensic Med Pathol. 1997;18:181e184. 38. Dawson M. Canadian trends in filicide by gender of the accused, 1961-2011. Child Abuse Negl. 2015;47:162e174. 39. McKee A, Egan V. A case series of twenty one maternal filicides in the UK. Child Abuse Negl. 2013;37:753e761. 40. Hon KL. Dying with parents: an extreme form of child abuse. World J Pediatr. 2011;7:266e268.
M. Janík et al. / Journal of Forensic and Legal Medicine 48 (2017) 23e29 41. Kreitman N. The coal gas story. United Kingdom suicide rates, 1960-71. Br J Prev Soc Med. 1976;30:86e93. 42. Kreitman N, Platt S. Suicide, unemployment, and domestic gas detoxification in Britain. J Epidemiol Community Health. 1984;38:1e6. 43. Blum D. The Poisoner's Handbook: Murder and the Birth of Forensic Medicine in Jazz Age New York. New York, NY: Penguin Books; 2010.
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44. Bowen DA, Duffy P, Callear A, Fitton J. Carbon monoxide poisoning. Forensic Sci Int. 1989;41:163e168. 45. Baselt RC. Disposition of Toxic Drugs and Chemicals in Man. tenth ed. California, Seal Beach: Biomedical Publications; 2014. 46. Dominguez AM. Problems of carbon monoxide in fires. J Forensic Sci. 1962;7: 379e392.