Journal of Analytical Toxicology, Vol. 29, October 2005
[CaseReport
ApparentSuicidalCarbonMonoxidePoisoningswith ConcomitantPrescriptionDrug Overdoses Avneesh Gupta, Melissa A. Pasquale-Styles, Bradford R. Hepler, Daniel S. Isenschmid*, and Carl J. Schmidt
Wayne CountyMedical Examiner'sOffice, 1300 EastWarrenAvenue, Detroit, Michigan 48207
Abstract]
Methods
We report four separate suicides by apparent motor vehicle-related carbon monoxide (CO) poisoning in which complete toxicological analysis showed the absence of, or lower than expected, percent carboxyhemoglobin saturation and high concentrations of concomitant prescription drugs. These cases, within a population of 71 apparent CO suicides from the Wayne County Medical Examiner's Office over 1998-2004, represent cases where additional factors are in play. Multiple rnodalities (CO poisoning and drug overdose) and/or undetectable carbon dioxide poisoning from the vehicle exhaust of cars manufactured after laws regulating vehicle emissions were enacted are examples of additional factors that require consideration in these selected cases. All four cases demonstrated some degree of decomposition, so the possible loss of CO could not be ruled out. The need for full toxicological analysis in apparent suicidal CO poisoning is emphasized.
Introduction
The Wayne County Medical Examiner's Office (WCMEO) serves a population base of 2 million people in the Detroit, Michigan metropolitan area and routinely handles on average 12,000 case inquiries on an annual basis. Over the past 7 years (1998-2004), 2900-3400 cases annually have been ordered into its facilities for comprehensive death investigation. During that period suicides accounted for approximately5-6% of the annual caseload, of which 5-6% were determined to be due to carbon monoxide (CO) poisoning for a total of 68 cases during the study period (Table I). In addition to these 68 cases, 3 cases initially thought to be CO poisonings that were negative for carboxyhemoglobin (COHb) but found to have high prescription drug concentrations had their death certificates amended to reflect the toxicological findings. These three cases plus one (of the 68) whose cause of death remains a CO intoxication because of the evidence at the scene, lack of overwhelming toxicological findings, and a detectable, albeit low, percent COHb saturation (%COHb) are presented in this report.
Medical examiner cases in which CO intoxication is suspected as a result of investigation and/or measurement of %COHb in blood are usually signed out on inspection at the WCMEO. However, specimens are collected for toxicologic evaluation. Typically, blood (subclavian on inspected cases, heart and femoral on autopsied cases), urine, and vitreous humor are collected. In the event of a severely burned or decomposed body, spleen is collected in lieu of blood. Spleen and blood have been shown to be comparable %COHbat low and high amounts (1). Routine testing in these cases consists of the determination of %COHb using an Instrumentation Laboratories 682 CO-Oximeter (Lexington, MA) with confirmation by Conway microdiffusion (2). In addition, testing for alcohol and drugs of abuse is performed. From 1998 through September 2002 drugs-of-abuse testing consisted of barbiturates, benzodiazepines, cocaine metabolites, opiates, phencyclidine, and sympathomimetic amines by enzyme immunoassay when urine was available or benzodiazepines, cocaine metabolites, and opiates by radioimmunoassay when only blood was collected. Beginning in October 2002, radioimmunoassays were discontinued and all six enzyme immunoassays were Table I. Total Cases, Suicides, and Carbon Monoxide Suicides at the Wayne County Medical Examiner's Office (1998-2004) Year 1998 1999 2000 2001 2002 2003 2004
Total
Total Cases* 2926 3308 3336 3242 3295 3138 2977 22,222
Total Suicides(%)
Carbon Monoxide Suicides(%)+
177 (6.0) 199 (6.0) 175 (5.2) 188 (5.7) 178 (5.4) 188 (6.0) 176 (5.9) 1281 (5.8)
9 (5.1) 10 (5.0) 9 (5.1) 11 (5.8) 10 (5.6) 8 (4.2) 11 (6.3) 68 (5.3)
* Total casesordered into office. Percent of total suicides.
9Authorto whom co,'respondenceshould be addressed.E-mail:
[email protected]. 744
Reproduction (photocopying) of editorial content of this journal is prohibited without publisher's permission.
Journal of Analytical Toxicology, Vol. 29, October 2005
replaced with enzyme-linked immunosorbant assays and performed in blood (or another matrix if blood was not available). Additionaltoxicologicaltesting (organic bases, acidic and neutral drugs, and other specific assays) would be performed based on presumptive positive immunoassay results but were not routinely performed otherwise. However,in the four cases presented, comprehensive toxicology was performed because of the negative or low %COHb. This included Conwaymicrodiffusion [confirmationby headspace gas chromatography (GC)] for alcohol screening, immunoassay [confirmationusing either GC with mass spectrometry (MS) in the select ion monitoring mode, GCwith nitrogen-phosphorus detection (NPD)or highperformance liquid chromatography with diode-array detection] for drugs-of-abuse screening, color tests for acetaminophen and salicylates (confirmation by fluorescence polarization immunoassay), and GC-MS with quantitation by GC-NPD for organic bases.
Case Histories Case 1
A 42-year-old white female was found in the driver seat of a Dodge Shadow (estimated to be a late 1980s model based on examination of scene photographs) with its engine running, parked insidea closedgarage. The bodywas in rigor mortis, and there was a red-tinged purge emanating from her mouth. No suicide note was found, but she had a history of previous suicide attempts by prescription drug overdose requiring hospitalization. She was known to abuse both illicit and prescription drugs, namely heroin, diazepam, and carisoprodol. Scars consistent with previous suicide attempts were on the right forearm. Early changes of decomposition were noted with no mention of cherry-red lividity.Although circumstantial evidence pointed strongly towards COtoxicity, the blood was negative for COHb,
prompting a full autopsy and pending of the case by the medical examiner. Internal examination revealed mild softening and discoloration of the viscera and no injuries or diseaseprocesses. Toxicology results were positive for acetaminophen, caffeine, carisoprodol, codeine, diazepam, diphenhydramine, doxepin, meprobamate, morphine, nicotine, norchlorcyclizine, and propoxyphene (Table II). The codeine concentration in heart blood was very high (11.7 rag/L) and supported by a femoral blood codeine concentration of 4.2 mg/L. The striking nature of this finding in collaboration with the circumstances resulted in the assignment of codeine toxicity as the cause of death. The manner was suicide. Case 2
A 37-year-oldwhite male was found in the driver seat of his vehicle, which was parked in the backyard of his home with a hose duct-taped around the exhaust pipe and extending to the inside of the vehicle. The engine was still running in a neutral gear. The make and model of the car are unknown. No suicide note was found, but he had two suicide attempts one and two weeks prior to his death via overdose on prescription drugs. The body had early changes of decomposition and a cherry-colored lividity.Again, circumstantial evidencepointed strongly toward CO toxicity. Although the %COHb in blood ranged between 9 and 15% on several sampling attempts, it was reported as unsuitable because of turbidity errors. Additional testing of the blood, decomposition fluid, and spleen fluid by Conwaymicrodiffusion and analysis of spleen fluid by a referral laboratory using visible spectrophotometry all failed to provide a suitable result. As a result of the initially inconclusive CO tests, an autopsy was performed. The internal examination revealed no injuries or diseaseprocesses and the case was originallysigned out as a CO poisoning. Toxicologyresults were positive for bupropion, citalopram, diphenhydramine, norpropoxyphene, propoxyphene, and quetiapine (TableII). The diphenhydramine concentration in the liver and spleen were determined to be 30
Table II. Tabulation of Cases Involving Low or Negative Carboxyhemoglobin Saturations Case
Causeof Death
Manner
Carboxyhemoglobin (% saturation)
Other Drugs* all concentralionsare in mg/L(blood)or mg/kg(tissue)
I
Codeine toxicity
Suicide
Negative (B2)~
Codeine (BI, B2: 11.7, 4.2), Acetaminophen (BI, B2: 130, 88), Meprobamate (BI, B2: 18.9, 43.7), Carisoprodol (BI, B2: 39.8, 23.6), Morphine (BI: 0.I 7), Diazepam (BI, B2:0.18, 0.13), Doxepin (BI, B2: 0.33, 0.I0), Propoxyphene (BI, B2: 0.06, 0.02), Diphenhydramine*, Doxylamine*, Norchlorcyclizine*
2
Diphenhydramine toxicity
Suicide
Unsuitable (S)
Diphenhydramine (S, L: 3.9, 30), Propoxyphene (S: 0.09), Quetiapine (S, L: 5.2, 2.8), Citalopram (S, L: 0.11,0.47), Bupropion*
3
Carbon monoxide poisoning
Suicide
10.6% (A)
Alcohol (A: 0.03), Desipramine (A: 0.65), Imipramine (A: 0.16), Quetiapine (A: 0.09)
4
Nortriptyline toxicity
Suicide
Negative (S)
Nortriptyline (S: 22)
* Excluding nicotine and caffeine. ~"Abbreviations: A, cavity blood; BI, subclavian blood; B2, heart blood (2% sodium fluoride); L, liver; and S, spleen. * Drug was confirmed but not quantitated.
745
Journal of Analytical ToxicoJogy,Vol. 29, October 2005
and 3.9 mg/kg, respectively. The high concentration of diphenhydramine in the liver and the lack of evidence supporting CO poisoning resulted in the cause of death being amended to acute diphenhydramine intoxication. The manner was suicide. Case 3
A 20-year-old white male was found in the driver seat of his 1995 Acura Integra, which was parked in closed garage with a hose extending from the exhaust pipe through the rear window and into the car. The ignition was in the "on" position, and the gas tank was empty. The subject was in an early stage of decomposition and had a bright cherry-red lividity. The decedent had a history of grinding prescription drug tablets and sniffing the powder. He was also known to use illicit drugs. No suicide note was found, and he had no history of previous suicide attempts. Based on the scene investigation and external examination, the case was signed out as CO monoxide poisoning on inspection. The manner was suicide. This case presented at the WCMEO on a Sunday when stat COHb determinations are not performed. Subsequent analysis of the sample labeled as cavity blood ranged from 10 to 13%COHb but was not reported because of interferences by turbidity, sulfhemoglobin, and methemoglobin. Attempts to reduce methemoglobin were unsuccessful. Analysis by Conway microdiffusion was positive for COHb resulting in the specimen being sent to a referral laboratory for quantitation using visible spectrophotometry. The COHb saturation reported was only 10.6%. Additional toxicology results were positive for alcohol, caffeine, desipramine, imipramine, nicotine, and quetiapine (Table II). The only potentially significant toxicology findings were for imipramine and desipramine, whose concentrations in cavity blood (the only specimen provided) were 0.16 and 0.65 rag/L, respectively. However, given that the concentrations were skewed toward the metabolite of imipramine (at least suggesting chronic use), and the lack of additional more appropriate samples to lend context to the drug findings, the toxicology findings were not considered sufficient to override the scene investigation and external examination. In this case, the cause of death remains attributed to CO poisoning, despite the low %COHb. The manner was suicide. Case 4 A 39-year-old white male was found in his 1989 Mercury Marquis, parked in a closed garage with the ignition in the "on" position and the gas tank empty. A suicide note was found in his home. The body was moderately decomposed with green discoloration, marbling and slipping of the skin, and bloating. The cause and manner of death were reported as CO poisoning and suicide, respectively, on inspection prior to performing a COHb determination. Because blood could not be obtained, the body was opened only to obtain a spleen sample for toxicology. This was the only specimen submitted to the toxicology laboratory for testing in this case. Analysis of spleen fluid for COHb using the CO-Oximeter yielded negative results that were not reported because of interference by turbidity and a high methemoglobin. However, subsequent analysis by Conway microdiffusion was also negative and supported the COOximeter results. Analysis by visible spectrophotometry at a 746
referral laboratory was reported as unsuitable. Additional toxicological testing revealed the presence of nortriptyline and caffeine (Table II). The nortriptyline concentration in the spleen was 22 mg/kg. Although no other specimens were collected to provide additional context to the apparently very high nortriptyline concentration, it was determined that because there was no evidence of COHb in the spleen and evidence of large amounts of nortriptyline that the cause of death should be amended to nortriptyline intoxication. The manner remained suicide.
Discussion
CO is a byproduct of the incomplete combustion of hydrocarbons. It is also a product of heme catabolism and is found in low amounts (0.55 to 0.77 %COHb) in normal, nonsmoking individuals who have not been exposed to CO (3), while COHb saturations of < 10% are considered normal in smokers (4). CO exerts its toxic effect by binding to hemoglobin (Hb) with an affinity that is estimated to be over 200 times that of oxygen (5). This inhibits red blood ceils from carrying oxygen to the tissues from the lungs as well as carrying carbon dioxide back to lungs from the tissues. In addition, the presence of CO on Hb causes a shift toward the left of the oxyhemoglobin dissociation curve, as it prevents the dissociation of any oxyhemoglobin still available. Both of these effects result in what is referred to as either anoxic anoxia or anemic hypoxia. Most accidental and non-accidental deaths attributed to CO poisoning are associated with COHb saturations of 50% or greater with most values falling between 50 and 70% (4). In one review of CO poisoning deaths by car exhaust fumes, the average COHb saturation was 76% (6). In our population, 64 out of 67 cases (96%) tested positive for the presence of COHb with an average saturation of 71% (+ 17% SD, median 77%). (There were two cases that were negative because of hospital survival time and one additional case that had insufficient sample for testing). All of these cases were signed out as CO poisoning. Deaths attributed to CO poisoning with low or absent COHb as seen in the four cases presented are not unheard of. Children and adults with co-morbid conditions such as coronary artery disease will asphyxiate at a lower %COHb than healthy adults. A low %COHb may also be observed in delayed deaths such as sublethal hypoxic injury when prolonged respiration occurred after the source of CO had been removed (7). In addition, flashfires may incinerate a victim so quickly that death due to thermal burns occurs prior to significant CO inhalation (8). Cyanide may also play a significant role in fire deaths (9). Changes in vehicle emissions standards have affected the interpretation of vehicle-exhaust-related deaths, and it is possible that carbon dioxide poisoning may have contributed to or accounted for one or all of the four deaths described. The Clean Air Act of 1970 required that CO emissions be no more than 15 g/mile starting with vehicles manufactured in 1975, which brought about the use of catalytic converters. Since the limit on vehicle CO emissions was further reduced to 3.4 g/mile for automobiles manufactured starting in 1981, the newest auto-
Journal of Analytical Toxicology, Vol. 29, October 2005
mobiles produce less than 5% of the CO emissions of vehicles manufactured before 1975 (10). With the decline in CO content of emissions, some recent deaths have simply been attributed to "inhalation of vehicle exhaust" with the major hypoxic effect caused by the high carbon dioxide content of emissions. Schmunk and Kaplan (11) reported two separate suicides by inhalation of automobile exhaust in which the primary causes of Table III. Incidence and Frequency of Drug and Ethanol Findings in CO Suicide Case Population (Excluding Nicotine and Caffeine)* No. of Times Tested Fort
Analyte Carbon monoxidew Ethanol Benzoylecgonine Cocaine Hydrocodone Morphine Ethyl cocaine Diazepam Desmethyldiazepam Doxylamine Fluoxetine Noffluoxetine Codeine Bupropion
No. of Times Detected % Incidence*
67 66 67 67 66 66 67 65 65 20 20 20 66 20
64 19 11 9 8 5 4 3 3 3 3 3 2 2
95.5 28.8 16.4 13.4 12.1 7.6 6.0 4.6 4.6 15.0 15.0 15.0 3.0 10.0
* Analytes found only once (number of times tested for in parentheses): 6-acetylmorphine (67), alprazolam (66), acetaminophen (5), chlorpheniramine (20), doxylamine (20), diltiazem (20), diphenhydramine (20), ephedrine/ pseudoephedrine (20), fentanyl (20), hydromorphone (67), imipramine (20), methamphetamine (42), MDMA (42), methadone (20), noffentanyl (20), norpropoxyphene (20), nortriptyline (20), propoxyphene (20), quetiapine (20), trazodone (20), temazepam (66), trimethobenzamide (20), and zolpidem (20). t Frequency and incidence studies based upon a total of 69 cases. * % Incidence calculated as a function of number of times detected when tested for. wTwo negative cases from hospital, and one case had insufficient sample to test.
death were determined to be asphyxia due to carbon dioxide intoxication and diminished atmospheric oxygen concentrations. These findings were based on the absence of COHb, full toxicologic analyses and testing of the automobiles' exhaust gas streams for both CO and carbon dioxide content. There have been other case reports of decreased CO concentrations in exhaust of late-model automobiles equipped with catalytic converters (12), but others have suggested that the degree of ventilation in the enclosed space may also play a role (13). The postmortem loss of CO in the four cases presented cannot be ruled out. However, any loss would likely have occurred in situ, not in vitro, as the samples were analyzed shortly after collection, within 2 h in cases I and 2. By standard operating procedure, the % methemoglobin must be reducible (by sodium dithionite) to less than 10% and the total hemoglobin must be > 2% to report a %COHb by CO-oximetry. In addition, there may be no sulfhemoglobin or turbidity warning flags. Three of the four cases discussed in this communication were in early stages of decomposition (cases 1-3), and one (case 4) was moderately decomposed. All cases, except case 1, had a turbidity flag on the CO-Oximeter,and cases 3 and 4 still had high % methemoglobin saturations after dithionite reduction. In our laboratory such cases may be analyzed by Conway microdiffusion (limit of detection 10%COHb) and, if positive, sent to a referral laboratory for analysis by visible-spectrophotometry. Ideally, especially at low COHb saturations, testing of questionable specimens for CO should be accomplished using headspace GC. After releasing CO from Hb with potassium ferricyanide, quantitation of CO is possible with a flame*ionization detector and a methanizer that catalyticallyreduces CO to methane (14). However, this technique is currently not available to this office, and it is unlikely that utilizing this technique would have changed the interpretation of the cases presented. There does appear to be a relationship between diminished COHb saturation and decomposition. In the population studied (all 71 cases including the 4 cases presented in detail), there were 16 cases with a COHb saturation of less than 60%. Ten
Table IV. Tabulation of Cases Involving Toxic Drug or Ethanol Concentrations and Lethal Carboxyhemoglobin Saturations
Case 5
Other Drugs* all concentrationsare in mg/L (blood)or mg/kg (tissue)exceptethanol(g%)
Carboxyhemoglobin (% saturation)
Causeof Death
Manner
Carbon monoxide poisoning
Suicide
83% ( B 1 ) t
Methadone (BI: 1.2), Alprazolam (B1 : 0.0058), Methadone metabolite*
Carbon monoxide poisoning
Suicide
80% (B1)
Ethanol (B2: 0.53, U: 0.39, V: 0.42 )
Carbon monoxide poisoning
Suicide
54% (81)
Morphine (B2: 2.9, V: 0.23), Zolpidem (B2: 3.0), Hydrocodone (B2: 0.20; V: 0.19)
Carbon monoxide poisoning
Suicide
77% (B1)
Acetaminophen (BI: 370), Codeine (B1 : 16), Trazodone (BI: > 3.0), Fentanyl (BI: 0.011), Norfentanyl (BI: 0.010), Fluoxetine (BI: 1.5), Noffluoxetine (BI: 3.5)
* Excluding nicotine and caffeine. t Abbreviations: B1, subclavian blood; B2, heart blood (2% sodium fluoride); U, urine; and V, vitreous humor. * Drug was confirmed but not quantitated.
747
Journal of Analytical Toxicology,Vol. 29, October 2005
(63%) of these cases showed early to moderate decomposition. By contrast, of the 40 cases with a COHb saturation of greater than 70% only 5 cases (13%) were noted to be decomposed. A report examining the stability of CO in postmortem samples stored in Vacutainer | tubes under refrigerated conditions (with or without preservative) demonstrated no significant loss of CO in most cases over a two-year period (15). However, earlier studies under other conditions suggested factors such as increased headspace volume above the sample, higher temperature, absence of preservatives and higher initial %COHb result in greater and more rapid CO loss (16-18). In one study blood samples with 40 and 70%COHb saturations were allowed to putrify at room temperature, in vitro. These showed a 50% decrease in %COHb after 15 and 30 days, respectively (19). To our knowledge the effects of decomposition in situ on COHb have not been studied. Regardless, the high drug concentrations detected in three of the four cases presented here were sufficient to change the cause of death to reflect drug intoxication in the absence of any reportable COHb. Cases in which a high %COHb is detected are frequently not analyzed for drugs because the cause of death is known. Reports of drug findings in vehicle-related CO deaths are especially sparse. In a study of 194 suicides by inhalation of car exhaust in Sweden, 51% of the 193 cases tested were positive for ethanol, but only 7% of the 181 cases tested for drugs were positive for either antiepileptic drugs, sedatives, psychostimulants, neuroleptics, or analgesics (20). Only one case had drug concentrations that were considered toxic (drugs not specified). Our findings appear to suggest a different pattern. In our study population, 37 (54%) out of the 68 cases in which CO poisoning was determined to be the cause of death were positive for at least one drug (including alcohol but excluding nicotine and caffeine). The overall incidence and frequency of CO, drug, and ethanol findings in this population of cases is seen on Table III. Of the most frequently tested for analytes, ethanol was the most commonly detected analyte followed by cocaine and/or benzoylecgonine. Parent cocaine was present in 9 of 11 cases in which cocaine and its metabolites were detected. Cocaine is a drug associated with sudden death, however, in each of these cases a toxic or lethal %COHb was obtained. Of the 20 cases which received comprehensive toxicology testing, 15 (75%) were positive for at least one drug (excluding nicotine and caffeine) and 6 cases were positive for 5 or more drugs. It is significant that 10 of these 15 cases were positive for either an antidepressant and/or anti-anxiety agent. The presence of these types of drugs in a depressed population that ultimately committed suicide is not surprising. However, it suggests the importance of performing toxicology in cases such as these to support the history and/or intent to commit suicide. Out of the 71 cases studied, there were 7 cases in which toxic drug or ethanol concentrations were observed to be present in the specimens provided. This data set included three out of four cases presented on Table II. The distinction specific to the remaining four cases of toxic drug/ethanol concentrations was the presence of a confirmed lethal or toxic %COHb (Table IV). The high concentrations of concomitant drugs in seven cases
748
presented in this paper, including three in which COHb was undetected or unsuitable, suggests that each individual attempted to commit suicide using multiple modalities----drug overdose and inhalation of vehicle exhaust. The drugs may have been taken in large quantities as a "failsafe" mechanism in case either the drug or the CO exposure was insufficient to cause death. An alternative explanation is that they may have been taken to facilitate sleep or unconsciousness to ease the suffering of prolonged inhalation of vehicle exhaust and/or the mental anguish of impending death. These cases exemplify the need for full postmortem toxicologic analysis in vehicle-related suicides in order to identify and determine the role of prescription drugs and ethanol in these circumstances. Additionally, comprehensive toxicological investigations are also important in the effort of continuing study of reduced CO content in vehicle emissions and related fatalities. Finally, in cases of suspected vehicular CO intoxication when an immediate COHb determination is not available or negative, a full autopsy is recommended.
References 1. S.C. Wu, B. Levine, J.C. Goodin, Y.H. Caplan, and M.L. Smith. Analysis of spleen specimens for carbon monoxide. J. Anal. Toxicol. 16" 4247 (1992). 2. L.A. Williams. Carbon monoxide type A procedure. In Methodology for Analytical Toxicology, I. Sunshine, Ed. CRC Press,Cleveland, OH, 1975, pp 64-66. 3. R.D. Stewart, E.D. Baretta, L.R. Platte, J.H. Kalbfleisch, B. Van Yserloo, and A.A. Rimm. Carboxyhemoglobin levels in American blood donors. J. Am. Med. Assoc. 229:1187-1195 (1974). 4. G.W. Kunsman and B. Levine. Carbon monoxide/cyanide. In Principles of Forensic ToxicoloGy, 2nd ed., B. Levine, Ed. AACC Press, Washington, DC, 2003, pp 327-340. 5. F.L. Rodkey, J.D. O'Neal, H.A. Collison, and D.E. Uddin. Relative affinity of hemoglobin S and hemoglobin A for carbon monoxide and oxygen. Clin. Chem. 20:83-84 (1974). 6. P. Theilade. Carbon monoxide poisoning. Am. J. Forensic Med. Pathol. 11 : 219-225 (1990). 7. A. Ruszkiewicz, B. De Boer, and S. Robertson. Unusual presentation of death due to carbon monoxide poisoning. Am. J. Forensic Med. Pathol. 12:181-184 (1997). 8. C.S. Hirsch, R.O. Bost, S.R. Gerber, M.E. Cowan, L. Adelson, and I. Sunshine. Carboxyhemoglobin concentrations in flash fire victims: report of six simultaneous fire fatalities without elevated carboxyhemoglobin. Am. J. Clin. Pathol. 68:317-320 (1977). 9. M.M. Birky, B.M. Halpin, Y.H. Caplan, R.S. Fisher, J.M. McAIlister, and A.M. Dixon. Fire fatality study. Fire Materials 3' 211 (1979). 10. J.A. Mott, M.I. Wolfe, C.}. Alverson, C.R. Bailey, L.B. Ball, J.E. Moorman, J.H. Somers, D.M. Mannino, and S.C. Redd. National vehicle emissions policies and practices and declining U.S. carbon monoxide-related mortality. J. Am. Med. Assoc. 288: 988-995 (2002). 11. G.A. Schmunk and J.A. Kaplan. Asphyxial deaths caused by automobile exhaust inhalation not attributable to carbon monoxide toxicity: study of 2 cases. Am. J. Forensic Med. Pathol. 23:123-126 (2002). 12. B. Vossbergand J. Skolnick. The role of catalytic converters in automobile carbon monoxide poisoning. Chest115" 580-581 (1999). 13. N. Hampton. Letter: Intentional carbon monoxide poisoning. Chest 116" 586-587 (1999). 14. B. Levine, J. D'Nicuola, G. Kunsman, M. Smith, and C. Stahl.
Journal of Analytical Toxicology, Vol. 29, October 2005 Methodologic considerations in the interpretation of postmortem carboxyhemoglobin concentrations. Toxicology 115:129-134 (1996). 15. G.W. Kunsman, C.L. Presses,and P. Rodriguez. Carbon monoxide stability in stored postmortem blood samples. J. Anal. Toxicol. 24: 572-578 (2000). 16. G.G.P. Fechner and D.J. Gee. Study on the effects of heat on blood and on the post-mortem estimation of carboxyhemoglobin and methemoglobin. Forensic Sci. Int. 40:63-67 (1989). 17. D.H. Chace, L.R.Goldbaum, and N.T. Lappas. Factors affecting the
loss of carbon monoxide from stored blood samples. J. Anal. Toxicol. 10:181-189 (1986). 18. A. Ocak, J.C. Valentour, and R.V. Blanke. The effects of storage conditions on the stability of carbon monoxide in postmortem blood. J. Anal. Toxicol. 9:202-206 (1985). 19. A. Kloppel and G. Weiler. Putrefaction-induced changes in the concentration and temporal detectability of carbon monoxide in cadaveric blood samples. Z. Rechtsmed. 97" 105-109 (1986). 20. M. Ostrom, J. Thorson, and A. Eriksson. A carbon monoxide suicide from car exhausts. Soc. Sci. Med. 42:447-451 (1996).
749
