Carbon Monoxide and Human Lethality: Fire and Non-Fire Studies

CARBON MONOXIDE AND HUMAN LETHALITY: FIRE AND NON-FIRE STUDIES

CARBON MONOXIDE AND HUMAN LETHALITY: FIRE AND NON-FIRE STUDIES Editor in Chief:

Marcelo M.Hirschler Safety Engineering Laboratories Rocky River, Ohio, USA Associate Editors:

Sara M.Debanne1, James B.Larsen2 and Gordon L.Nelson3 1

Case Western Reserve University, Cleveland, Ohio, USA University Southern Mississippi, Hattiesburg, Mississippi, USA 3 Florida Institute of Technology, Melbourne, Florida, USA

2

Project Sponsor: Society of the Plastics Industry, Inc., Washington D.C., USA

ELSEVIER APPLIED SCIENCE LONDON and NEW YORK

ELSEVIER SCIENCE PUBLISHERS LTD Crown House, Linton Road, Barking, Essex IG11 8JU, England This edition published in the Taylor & Francis e-Library, 2006. To purchase your own copy of this or any of Taylor & Francis or Routledge’s collection of thousands of eBooks please go to http://www.ebookstore.tandf.co.uk/. WITH 213 TABLES AND 59 ILLUSTRATIONS © 1993 ELSEVIER SCIENCE PUBLISHERS LTD British Library Cataloguing in Publication Data Carbon Monoxide and Human Lethality: Fire and Non-Fire Studies I.Hirschler, M.W. 615.9 ISBN 1-85861-015-X Library of Congress CIP Data applied for No responsibility is assumed by the Publisher for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions or ideas contained in the material herein. Special regulations for readers in the USA This publication has been registered with the Copyright Clearance Center Inc. (CCC), Salem, Massachusetts. Information can be obtained from the CCC about conditions under which photocopies of parts of this publication may be made in the USA. All other copyright questions, including photocopying outside the USA, should be referred to the publisher. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the publisher. ISBN 0-203-98681-4 Master e-book ISBN

ISBN - (OEB Format) ISBN 1-85861-015-X (Print Edition)

CONTENTS Chapter 1: Introduction MARCELO M.HIRSCHLER (Safety Engineering Laboratories) Chapter 2: Effects of Carbon Monoxide in Man: Exposure Fatality Studies GORDON L.NELSON (Florida Institute of Technology) Chapter 3: Effects of Carbon Monoxide in Man: Low Levels of Carbon Monoxide and their Effects GORDON L.NELSON (Florida Institute of Technology) Chapter 4: Physiological Effects of Carbon Monoxide JAMES B.LARSEN (University of Southern Mississippi) Chapter 5: Carbon Monoxide Determination in Human Blood GORDON L.NELSON (Florida Institute of Technology) Chapter 6: Carbon Monoxide and Fatalities: A Case Study of Toxicity in Man GORDON L.NELSON (Florida Institute of Technology) DENNIS V.CANFIELD (University of Southern Mississippi) JAMES B.LARSEN (University of Southern Mississippi) Chapter 7: Carbon Monoxide and Fatalities: Secular Trends SARA M.DEBANNE (Case Western Reserve University) DOUGLAS Y.ROWLAND (D.Y.Rowland Assoc.) Chapter 8: Lethal Carboxyhemoglobin Level: The Epidemiological Approach SARA M.DEBANNE (Case Western Reserve University) DOUGLAS Y.ROWLAND (D.Y.Rowland Assoc.) Chapter 9: Carbon Monoxide and the Toxicity of Fire Smoke MARCELO M.HIRSCHLER (Safety Engineering Laboratories)

1 3 63 117 175 181

200 215 232

Appendix Tables for the Data base in Chapter 6 A:

257

Appendix Tables for the Data base in Chapter 7 B:

338

Appendix Tables for the Data base in Chapter 8 C:

432

Appendix Carbon Monoxide Bibliography D:

452

Chapter 1 INTRODUCTION MARCELO M.HIRSCHLER Safety Engineering Laboratories, Inc., 38 Oak Road, Rocky River, OH, 44116, USA It has been known since about 1930 that one of the major causes of deaths in fires has been smoke toxicity. It was also known that carbon monoxide (CO), a highly toxic combustion product, was one of the major components of smoke derived from fires. Thus, it became likely that carbon monoxide was one of the primary causes of the lethality of smoke in fires. The way in which carbon monoxide caused poisoning was by combining with blood hemoglobin and generating carboxyhemoglobin. The levels of carboxyhemoglobin (COHb) found in the blood of a fatality were used by medical examiners to decide whether the victim had died of CO poisoning. It was soon decided that a 50% COHb level was the threshold to cause human lethality due to CO. In the period between the mid 1970s and the late 1980s, the issue of smoke toxicity took on a large importance in the public domain. This reflected two emerging trends. Firstly, small scale studies were being conducted, using tests of very dubious validity and animals (usually rodents) as models (and surrogates for man), to determine the toxicity of the smoke from burning materials. Great publicity was generated from the fact that one or two materials gave off smoke which appeared to be much more toxic than that of other materials. Secondly, as carboxyhemoglobin measurements became more widespread, some fire victims were found to have COHb levels of less than 50%. This created a fear of the presence of some “new” toxicants in fire atmospheres. It was feared that if such new toxicants existed they made fire atmospheres more toxic than traditional fire atmospheres. In 1984 the Society of the Plastics Industry, Inc. (SPI), in the United States, felt that the issue of the importance of carbon monoxide in the toxicity of fire atmospheres needed to be studied in greater detail. Moreover, the focus had to be human studies, especially lethality. Therefore, SPI commissioned a team headed by Professor Gordon L.Nelson, University of Southern Mississippi (USM), to carry out a study including the following tasks: 1. Analysis of the literature on carbon monoxide and toxicity, to include: (a) Effects of CO on man at low exposure levels (b) Studies of human fatality and exposure to CO. (c) Means of analyzing human blood COHb. (d) Physiological effects of CO to humans.

Carbon monoxide and human lethality

2

2. A case study, involving over 2,000 victims, of human fatalities associated with fires or with other exposures to CO. In 1986, the USM team presented a report to SPI where all the tasks were completed. On analysis of the results it was found that neither the population of fire victims nor that of victims of other exposures to CO were fully representative of the average human population. It was thus decided that a statistical analysis of the data needed to be carried out using epidemiological techniques. A team headed by Professor Sara M.Debanne, Case Western Reserve University (CWRU) was commissioned to carry out this investigation, using multivariate statistical techniques. They prepared a report which was presented to SPI in 1987. The victims included in the USM data base covered a large geographical area in the United States: data were collected in places as far apart as West Palm Beach, FL (Southeast), Seattle, WA (Northwest), Farmington, CT (Northeast) and Tucson, AZ (Southwest). Most of the victims analyzed for the USM data base, however, had died in fires which took place in the late 1970s and early 1980s. It was thus felt that it would be important to investigate whether the conclusions reached would change if data was collected for victims who had died earlier. Cuyahoga County (surrounding the city of Cleveland, OH) was not one of the contributors to the USM study. It was a very interesting location, however, because a very respected scientist, Dr. Samuel R.Gerber, was the county coroner during the period 1938–1979. This period started at a time when synthetic materials (e.g. plastics) were a rarity and concluded when plastics have become, as they are now, a fundamental part of life in the developed world. The total number of fatalities related to CO in that period exceeded 2,000 cases, which gave it good statistical validity. The CWRU team was thus commissioned by SPI to investigate all those fatalities and apply the same statistical analysis techniques they had used for the earlier studies. Their report was presented to SPI in 1990. Between 1990 and 1991 all of the various aspects that form the basis of this investigation were updated. Thus, chapters 2, 3 and 4 were written by Gordon L.Nelson and covered aspects 1(a), 1(b) and 1(c) of the original USM charter. Chapter 5 was written by James B.Larsen and covered aspect 1(d) of the USM charter. Chapter 6, written by Sara M.Debanne and Douglas Y.Rowland, covered the study of Cuyahoga County (OH) which became the CWRU data base. Chapter 7, written by Gordon L.Nelson, Dennis V.Canfield and James B. Larsen, presents the USM data base. Chapter 8, written by Sara M.Debanne and Douglas Y.Rowland, presents the multivariate statistical analysis of both the USM and CWRU data bases. The final piece needed to complete this puzzle was provided by Marcelo M. Hirschler. He analyzed data on smoke toxicity and on CO concentration from a variety of large scale and small scale fire tests, carried out by a variety of organizations. Using all of this information and the conclusions from the CO studies sponsored by SPI, he put together an overall analysis of the importance of CO in the toxicity (or lethality) of fire atmospheres as regards humans. Thus, Chapter 8 summarizes the implications of this entire study and puts into perspective the various smoke toxicity studies that are being made using animals as surrogates for humans.

Chapter 2 EFFECTS OF CARBON MONOXIDE IN MAN: EXPOSURE FATALITY STUDIES GORDON L.NELSON Florida Institute of Technology, College of Science and Liberal Arts, 150 West University Boulevard, Melbourne, FL, 32901–6988, USA ABSTRACT This report examines the various factors affecting carbon monoxide fatalities. Sources of carbon monoxide are examined. Effects of low oxygen, heat, carbon dioxide, hydrogen cyanide, alcohol, drugs, and disease are each discussed, as are time of exposure and level of activity. Human fatality data show that a significant percentage of exposed individuals die from carbon monoxide poisoning (automobile exhaust) at blood COHb levels thought by some to be less than “normal”, i.e, less than 50 percent COHb. Nearly 20% of individuals may die at such “low” levels. In the case of fire exposures, twice the number of victims are in the less than 50 percent category than for automobile exhaust victims, the two largest categories of CO exposure. Fire victims, however, have a very different age distribution and level of infirmity than do automotive exhaust victims. Carbon monoxide is the prime source of fire fatalities as well as automotive exhaust victims. In human carbon monoxide fatality cases the victims are predominantly male and alcohol is frequently present, regardless of the source of carbon monoxide. Individuals suffering from systemic hypoxemia (eg. anemia or cardiopulmonary (disease) or increased oxygen demand are at greater risk. In order to ensure meaningfulness of results special care is required in the determination of COHb in the blood victims, particularly from fire victims and for aged blood samples. Carbon monoxide is an ever present hazard which manifests itself in ways far more diverse than previously recognized. Many examples are provided.

Carbon monoxide and human lethality

4

2.1 GENERAL COMMENTS Carbon monoxide (CO) is a highly toxic, nonirritating gas. One of the products of combustion, it is invisible, odorless, tasteless, and slightly lighter than air. Carbon monoxide poisoning is not new. Man’s difficulties with CO date back to the time prehistoric man first used fire. Instances of CO poisoning have been found in early Greek and Roman literature. The increased use of coal for domestic purposes in the 1400s brought with it an increase in CO poisoning. The *

Note: In every case, if no further details are given, the venue for the study is the United States.

hazard was intensified by the introduction of illuminating gas, and later by natural gas, for heat, power, and light.1 The first understanding of the pathophysiology of CO dates from the work of Claude Bernard in 1857 when he ascribed the toxic effects to tissue hypoxia. In 1895 Haldane described the underlying mechanism for CO toxicity when he demonstrated that CO reversibly interacts with hemoglobin in the blood, blocking the binding of oxygen to hemoglobin, thus causing tissue hypoxia. He also demonstrated that rats poisoned with potentially lethal concentrations of CO survived if treated with hyperbaric (high pressure) oxygen, a treatment still used extensively for severely exposed CO victims today.2,3,4 Until recent years, concern over CO poisoning has been directed mainly toward the rather high concentrations sometimes found in closed spaces, such as homes, offices, factories, and mines. But with the increased use of motor vehicles, with their high CO emission rate, attention has also been focused on the more subtle effects of relatively low concentrations of CO that can often be found in outdoor environments, particularly in urban areas. In Stewart’s review of the effects of carbon monoxide in humans,4 he notes that humans have always been exposed continuously to small quantities of CO produced internally from the normal destruction of hemoglobin, with a minor fraction contributed by the breakdown of nonhemoglobin heme. In healthy male subjects at rest, the average rate of endogenous CO production is approximately 0.4 ml/h. During the progesterone phase of the menstrual cycle, endogenous CO production is approximately double that of the estrogen phase. The presence of these small quantities of CO in the blood results in a COHb saturation of 0.4–0.7 percent and is considered neither beneficial nor harmful. In patients with hemolytic anemia, COHb saturation may rise to 4–6 percent. Most environmental CO is produced from incomplete oxidation of carbon containing materials. Because complete combustion is seldom attained, varying concentrations of CO can be expected to be produced in most combustion processes. Tobacco smokers are the nonindustrial segment of the population most heavily exposed to carbon monoxide. The majority of cigarette smokers consuming one pack per day have blood COHb levels of 5–6 percent during their waking hours. Two- to three-pack-a-day smokers average 7.9 percent saturation, while heavy cigar smokers may reach peak saturations of 20 percent. The COHb saturation resulting from tobacco smoking is additive to that resulting from other CO sources in the environment. For example, a one-pack-a-day cigarette consumer

Effects of carbon monoxide in man

5

in one city would have a COHb saturation of 5.5 percent when nonsmokers in the same area had 1.2 percent, compared with a COHb of 6.5 percent in a second city when nonsmokers had 2.2 percent.4 The major environmental source of CO is the exhaust of motor vehicles, which accounts for approximately 67 percent of the total CO emissions per year. Exhaust tailpipe CO concentrations range from 0.5–7 percent, depending upon the year the automobile was manufactured, the state of engine tuning, and operation of pollution controls. A lethal CO concentration can be reached in a closed one-car garage in ten minutes. Concentrations of 25 ppm can be encoun-tered on expressways in major metropolitan areas during peak traffic periods.4 Fuel combustion in stationary sources, industrial processes, and solid waste disposal account for about 23 percent of total CO emissions. In the home environment improperly vented hot water heaters, furnaces, space heaters, and fire-places are the usual sources of CO exposure.4 Of course exposure to fire gases can provide very high levels of carbon monoxide in addition to other gases. CO concentrations up to 7 percent have been found in combustion gases during forest fires for example1. An unexpected indoor source of excessive CO exposure occurs following the use of a paint stripper whose basic ingredient is methylene chloride. Methylene chloride is metabolized in the body to CO, and a 3-hr exposure to paint stripper vapors in a well-ventilated room can result in COHb saturations of 8–16 percent.4 One frequently finds comments such as the following in texts and surveys: “Carbon monoxide is present in significant amounts in virtually all fires. It is highly toxic when inhaled, and acts by combining with hemoglobin in the blood to form carboxyhemoglobin (COHb). Hemoglobin’s function is to carry oxygen throughout the body, and it cannot do this if it is tied up, as COHb and, therefore, unavailable for oxygen transport. The level of carboxyhemoglobin in the blood of fire victims can be determined fairly easily. In the absence of other contributing factors a COHb concentration of 50 percent or greater is generally considered lethal.”5 Most medical discussions of carbon monoxide poisoning deal with “normal, healthy” individuals. However, the population is composed of a spectrum of individuals in a variety of environments. Conclusions for a small set of fatalities without reference to their detailed health can therefore be misleading. A number of studies have been reported which discuss carbon monoxide fatalities from specific sources. In this chapter focus will be on human exposure studies, largely analysis of exposure fatality cases. First carbon monoxide victims will be discussed in general and then fire victims in particular. Finally, the factors which affect carbon monoxide fatalities will be discussed.

Carbon monoxide and human lethality

6

2.2 CARBON MONOXIDE EXPOSURE STUDIES In 1977 CPSC presented a discussion of unvented space heater related deaths. Age and percent COHb are presented in Table 1.6 For 15 victims COHb levels were measured: 11 were males and 4 were females. Twelve (80 percent) of the victims were in their 20’s, 30’s or 40’s with an equal distribution of victims over the 3 age groups. Of the remaining 3 victims, one was age 52 and two were in their late 60’s. Twelve of the victims had blood COHb levels of 40 percent or more (10 of these victims were in the 40–59 percent range, and two were in the 70–79 percent range.) Three of the 15 victims had existing physical disorders; i.e., cardiovascular disease. Two of these victims exhibited blood COHb levels in the 30–39 percent range (a 23 year old male and a 69 year old male). The third victim’s

Table 1 Deaths from CO Poisoning from Unvented Gas Heaters6 Record of Death

Age of Victim

%COHb

x=CPSC file o=Dr. Davis

75%

x (76%)

37

70%

x (73%)

21

o (72%)

19 Fetus had 84%

65%

o (68%)

81 Coronary History

60%

o (60%)

21

55%

x (57%)

36

o (56%)

43

x (55%)

36

x (54%)

35

x (52%)

45

x (47%)

46

o (45%)

77

x (45%)

21

x (43%)

40

x (42%)

48

x (41%)

67-Hypertensive

x (40%)

22

50%

45%

40%

Comments

Heart Disease

Effects of carbon monoxide in man

35%

30%

25%

7

x (36%)

52

x (35%)

69-Arteriosclerotic Disease

o (33%)

49

x (33%)

23-Cardio. Resp. failure

o (26%)

54-Blood Alcohol 0.12%

20% 15% 10% 5% 0%

blood COHb level was 41 percent (a 67 year old male). Victims of carbon monoxide poisoning can exhibit a wide range of COHb levels.6 Additional cases were reported by CPSC based upon testimony given by Dr. Joseph H.Davis during unvented gas space heater hearings in Miami, March 29, 1978. Dr. Davis presented four incidents of CO poisoning associated with unvented gas space heaters that resulted in seven deaths. All of these deaths occurred in Dade County, Florida. Five of these victims were male, and two were female (one female was 41/2 months pregnant). Four of the seven victims ranged in age from 19–54 years; the remaining three were in their 70’s and 80’s. The blood COHb levels ranged from 26 percent (a 54 year old male whose blood alcohol level was 0.12 percent) to 72 percent (for the pregnant woman whose fetus’s blood COHb level was 84 percent). The COHb levels for the remaining 5 victims fell between 33.60 percent, and the ages ranged from 21 to 81. A pre-existing physical disorder was noted for one of these five victims (the 81 year old male was reported as having a coronary history). None of these victims had alcohol in their blood. Two married couples were represented in these four incidents. Within each couple, the spouses were close in age. In both incidents, the wife exhibited a higher tolerance for COHb than did her husband. (First couple, 21 year old male-60 percent COHb and 19 year old female-72 percent COHb; second couple, 79 year old male-33 percent COHb and 77 year old female-45 percent COHb).6 From this small sample of victims who died from CO exposure, it appears that tolerances to COHb levels can vary greatly, and may depend on age, sex, and pre-existing physical condition. Of 22 victims, 17 died with COHb levels less than 60 percent and 12 with less than 50 percent, the value frequently reported to be as “normal” for healthy adults. Other studies support the CPSC findings. Early work in New York reported a study of 68 cases exposed to carbon monoxide. Nearly one-quarter of the fatalities in this 1942 study had COHb levels less than 60 percent. Example data for the New York study are as follows7:

Carbon monoxide and human lethality

8

New York CO Fatality Study CASE %COHb 68

31.3 Each one of the 68 cases was found dead in a gas filled room or in a garage containing high concentrations of exhaust gases. 33.6

19

42.2

17

43.6

50

49.3

4

50.4

37

52.9

5

53.6

2

58.9

52

65.1

67

81.1

1

3% of the 68 cases died with 30–40% saturation 3% of the 68 cases died with 40–50% saturation 10% of the 68 cases died with 50–60% saturation 19% of the 68 cases died with 60–70% saturation 35% of the 68 cases died with 70–88% saturation

Effects of carbon monoxide in man

9

FIGURE 1. The Distribution of COHb Values Among Survivors and Fatalities8

Carbon monoxide and human lethality

10

FIGURE 2. The Age of Survivors and Fatalities in 1975–76 Study8 More recently, workers in Poland have reported data on carbon monoxide poisonings. While the source of CO was not discussed, 321 cases from 1975–76 were analyzed with 101 fatalities and 220 survivors. The distribution of COHb values for both sets of victims is shown in Figure 1. Some fatalities are in the 30–50 percent range, yet some survivors are in the 50–60 percent range.8 The ages of victims are shown in Figure 2. Older persons are more predominant in the fatalities than in the survivors. Differences by sex were also noted. Males predominated in fatalities, while females predominated in survivors (60 versus 41 for decedents and 66 versus 92 for survivors). The effects of blood alcohol showed no significant difference between those with 0.1 plus percent blood alcohol (26 victims, COHb mean 65 percent), and those without (75 victims, COHb mean 62 percent). Circulatory system problems were noted in 17 fatalities (COHb mean 59 percent). The mean COHb value was somewhat lower for those victims, than for those not showing circulatory system problems (COHb mean 63 percent). For fatalities, advanced age and severe arteriosclerosis led to lower COHb values.8 Another study of 304 fatalities due to carbon monoxide, largely exhaust fumes (287 cases), was performed by the Center of Forensic Sciences in Ontario, Canada. This study covered the years 1965–1968. The population was studied as the whole group, then divided into suicides, accidents, presence of alcohol and other drugs, and the presence of diseases. Data are shown as follows:9

Effects of carbon monoxide in man

11

%COHb

Category

Number of Cases Mean

Standard Deviation (±)

Minimum Maximum

Highest Single Frequency Range %

Majority Range

Whole group

304

51

12

23–89

45–59

(18)

40–59

Suicides

162

53

12

24–83

50–54

(19)

45–64

Accidents

135

49

12

23–89

45–49

(24)

40–59

Presence of Alcohol and Drugs

135

52

13

24–89

45–49

(16)

40–59

Presence of Pathological Conditions

25

46

17

23–89

35–39

(36)

30–44

The mean lethal percent saturation of carbon monoxide was found to be 51± 12 percent. COHb levels of 23 and 24 percent were found in two individuals in the survey. For a majority (approximately 68 percent) of the fatalities studied, the blood saturation of carbon monoxide ranged between 39 and 64 percent. The suicide group showed a somewhat higher mean lethal saturation than the accident group, 53.3 percent versus 49.4 percent,9 perhaps resulting from shorter exposure times for the suicide group. The category of fatalities in which alcohol or other drugs were found in addition to carbon monoxide, is of particular interest. The drugs involved were mostly alcohol and barbiturates, with blood concentrations ranging from traces to possibly lethal values. It is to be noted that the presence of drugs had no effect on the mean or the frequency distribution pattern of the lethal carbon monoxide saturations of this group. No evidence was found for enhancement of the toxicity of carbon monoxide by central nervous system depressants such as alcohol or barbiturates.9 The last category studied included carbon monoxide fatalities in which autopsy findings revealed cardiovascular, respiratory, or severe anemic disorders. The lowered mean lethal saturation and the generally lower distribution pattern in this category would appear to indicate that individuals with such diseases can succumb with somewhat lower saturations of carbon monoxide as compared with the whole group. It is to be noted, however, that individuals with low COHb levels are found in all groups, and not all individuals with pathological conditions have low COHb values.9 Carbon monoxide exposure in man must focus particularly on motor vehicle exposures. Over 1000 people die in the US annually from exhaust fumes. One study of unintentional CO poisoning is particularly revealing. Reports of victims in the state of Maryland during 1966–1971 were reviewed. The ages of the 68 victims were as follows10:

Carbon monoxide and human lethality

12

Ages of Persons Who Died AGE

PERCENT

14–19

13

20–29

35

30–39

24

40–49

25

50–59

6

60–69

4

70+

3

The percent carboxyhemoglobin measured in the blood of the victims was as follows7:

COHb of Victims COHb%

Number of Victims (%)

30–39

2

40–49

8

50–59

15

60–69

66

70–79

9

Severe arteriosclerotic coronary artery disease was noted in the person who died with a COHb saturation of 30 percent and in the one who died at 40 percent. Alcohol intoxication of four of the five persons with COHb in the 40–49 percent range was thought to have contributed to death at COHb saturations which the author of the study did not consider usually lethal. As shown below, alcohol over 0.1 percent was present in over one-quarter of the victims. Motor vehicles involved were statistically older than the population of registered vehicles.10

CIRCUMSTANCES OF EVENT AND BLOOD ALCOHOL CONCENTRATION Alcohol (% by wt.) Circumstances Sleeping

.00

.01–.09 0.10+ Unk. Total 6

3

11

0

20

17

8

3

2

30

Driving

3

0

0

0

3

Stuck in snow or mud

0

2

1

0

3

Couple Parking

Effects of carbon monoxide in man

13

Working on car

1

1

1

0

3

Warming car or changing battery

2

0

0

0

2

Other

4

1

2

0

7

33

15

18

2

68

TOTAL

A rusted body or exhaust pipes jammed against the body by a past accident so as to allow exhaust fumes to seep into the trunk are frequent automotive scenarios. A detailed report on several other cases in Maryland reveals the seriousness of these scenarios.11 Such accidents are common in late fall and winter in northern states, in rural regions, and in low income areas. Data follow:

Vehicular Carbon Monoxide Fatalities Age

COHb

CO Test of Vehicle Passenger Compartment

63 male

60 (heart patient)

0.045% at 10 min.

23 male

60 (0% alcohol)

0.02% at 30 min.

30 male

60 (0.14% alcohol)

0.02% at 30 min.

50 male

40 (0.11% alcohol)

0.045% at 30 min.

44 male

60 (0.12% alcohol)

0.02% at 25 min.

54 male

20±(0.17% alcohol)

0.005% at 45 min.

±vehicular crash

A review of 87 vehicular exhaust deaths for 1978–84 in West Virginia showed the typical victim to be male (78%), aged 15–34 years (64%), in a stationary passenger car, testing positive for blood alcohol (68%). Vehicles tended to be older, 10 years versus a state average of 6 years, with defective exhaust systems. Episodes generally occurred between midnight and 6 a.m. (76%). Of 14 episodes in garages, six had the main garage door open and 3 others occurred with an access door or window open, showing the ineffectiveness of passive ventilation to insure against carbon monoxide poisoning.12 In fact, three deaths have been reported by San Antonio, Texas, authorities involving incidents in a field or parking lot, with COHb results of victims, 58–81%.13 Two studies of mass carbon monoxide poisoning have been reported. In the first, carbon monoxide fumes began to enter the forced air heating system of a high school at 7:30 a.m., when the furnace was turned on, because a door to the exhaust chamber had been inadvertently left ajar. Soon both teachers and pupils throughout the school began to feel ill, complaining of headache, nausea, and weakness. Exposure ended at approximately 10:00 a.m., when a science teacher correctly associated the symptoms with carbon monoxide (CO) poisoning, the fire alarm was rung, and the school evacuated. Maximum time of exposure was two and a half hours. One hundred eighty-four persons were exposed; 160 (87 percent) became ill; 96 (60 percent) were transported to four hospitals for treatment. Carbon monoxide poisoning was confirmed by carboxyhemoglobin (COHb) levels measured on 66 persons that ranged from 4 percent to

Carbon monoxide and human lethality

14

28 percent saturation, with almost half falling between 21 and 25 percent. The mean COHb concentration was 18 percent. Atmospheric CO levels were assessed to have been fairly uniform throughout the school.14 The same week as the event, a questionnaire was prepared and circulated to all occupants of the school. A second questionnaire was circulated to physicians and administrators at the four hospitals where victims were treated, along with release forms for medical information. Symptoms reported are shown as follows14:

Symptoms reported by 159 persons who became ill from exposure to CO Symptom

Frequency (%)

Headache

90

Dizziness

82

Weakness

53

Nausea

46

Trouble Thinking

46

Shortness of Breath

40

Trouble with Vision

26

Loss of Consciousness

6

One hundred sixty of the 184 persons exposed (87 percent) reported becoming ill. One hundred (54 percent) first felt sick before the alarm was rung; 37 (20 percent), within one hour after the alarm; and 17 (9 percent), more than one after the alarm.14 Since victims arrived at school at irregular intervals throughout the morning, the duration of exposure varied from less than 30 minutes to 150 minutes. Those who reported they did not become ill had a mean duration of exposure of 71± 44 minutes; those who became ill but did not receive hospital care, 87±42 minutes; and those who were treated at hospitals, 107±34 minutes.14

Effects of carbon monoxide in man

15

FIGURE 3. Plot of percent COHb in blood versus duration of exposure for victims of a high school exposure incident.14 There were no significant differences between sexes or among age groups with regard to the kind or severity of symptoms, except that muscle weakness was more prominent among nonsmokers. There was no difference in the frequency of symptoms between smokers and nonsmokers. There was a strong correlation between most (but not all) symptoms and the duration of the exposure. A graphical representation of the association between duration of exposure and COHb concentration in the blood of 66 victims is shown in Figure 3. In order to estimate more accurately the actual COHb levels of victims at the time the alarm was rung, correction was made for the delay between exposure and the drawing of blood samples. The corrected mean COHb level was 20.7±7.0 percent. The points cluster very closely about the 500 parts per million isobar, suggesting that the concentration of carbon monoxide to which persons in the school were exposed was approximately 500 ppm.14 Of most significance for this work was the fact that, despite what were thought to be fairly uniform CO levels throughout the school, the results showed both significant variation among symptoms reported by victims with similar exposure times as well as different COHb levels in the blood, the latter of course complicated by differing activity levels of victims14. In a second case of mass exposure, 171 persons were involved when an exhaust pipe of a natural gas engine split apart in a sports arena in Anchorage, Alaska. CO was dispersed into the circulatory air. Of 316 exposed persons, 171 developed symptoms as shown below15:

Carbon monoxide and human lethality

16

Distribution of Illness Among Broomball Players, Hockey Players, and Adults Number Present Broomball Players

Number ill

Attack Rate Percent

247

131

53

Hockey Players

39

30

77

Coaches and teachers

30

10

33

316

171

54

TOTAL

Symptoms and Signs of Carbon Monoxide Poisoning Reported by 51 Ill Persons Present in the Sports Arena on March 20, 1969 Symptom

35 Broomball Players 7 Hockey Players Percent Percent

9 Adults Percent

51 Total Percent

Headache

91

57

100

88

Dizziness

77

43

11

61

Nausea

49

43

44

47

Tinnitus

43

14

0

31

Disorientation

31

14

0

24

Numbness of feet

26

29

11

24

Blurred vision

20

–

–

14

Numbness of hands

9

–

–

6

Vomiting

3

–

–

2

Loss of Consciousness

3

–

–

2

In this case 6 victims lost consciousness. It is estimated that the CO concentration was 900 to 1000 ppm. Exposure was varied both in time and circumstance. The hockey players were exposed earlier and for a longer period of time. Players were involved in more vigorous of action. COHb determinations were unfortunately not made. Again persons of seemingly similar exposure reported differing symptoms. Specific carbon monoxide exposure cases have been reported in the forensics literature. Several are worthy of mention. In one such case a 42-year-old intoxicated male arrived at his residence in the early morning. The male victim activated an automatic garage door opener and drove his fullsize automobile into the garage; he then placed the automobile in “park” and closed the garage door by once again using the remote control device. Sometime after this point,

Effects of carbon monoxide in man

17

while remaining in the vehicle, he became unconscious. The automobile’s engine was still running, all the windows were rolled up, and the headlights were left on.16 The two-car garage was located directly beneath the three bedrooms of the family dwelling, each of which was occupied. A 32-year-old female, wife by second marriage to the adult male victim, was sleeping in the north bedroom. An 18-year-old female, daughter by first marriage to the adult male victim, was sleeping in the southeast bedroom. A five-year-old male, son to the adult male by second marriage, was sleeping in the south central bedroom.16 Death occurred to the husband, wife, and daughter, with the five-year-old son surviving. Cause of death was confirmed as carbon monoxide asphyxiation in all three victims, who were otherwise in apparent good health. Carboxyhemoglobin data and blood alcohol data are shown below:16

Blood-alcohol analysis Victim

Age, years

Carboxy-hemoglobin, %

Blood Alcohol, %

Male (deceased)

42

69

0.240

Female (deceased)

32

59

0.000

Female (deceased)

18

57

0.000

5

–

–

Male (survivor)

The author of the study concluded that the male died earlier due to exposure to higher levels of CO. The reasons for the child’s survival were not altogether clear. Such cases of the survival of younger children are not unique.16 One case from New Zealand is also interesting. The bodies of a young married couple were found inside an unventilated caravan. It was established that they died from carbon monoxide poisoning. Field tests showed that fatal atmospheric levels of carbon monoxide were produced in the caravan by a poorly designed propane heater. The couple’s onemonth-old child survived even though he was exposed to the same carbon monoxide levels as the parents. COHb levels for the husband and wife were 75 percent and 65 percent, respectively.17 It was originally thought that the child must have been exposed to a lower CO concentration than his parents. However, the possibility of interference by a third party was ruled out and the caravan tests showed that very similar CO levels were established at three well-spaced sampling points. The child was therefore exposed to a CO level exceeding 800 ppm for ten hours. When found he as very hot and sleepy, but otherwise in no apparent distress. He had not been fed for more than twelve hours and was still on four-hourly feedings; this suggests he had an appreciable COHb level. He recovered quickly and had no apparent ill effects.17 In another case the body of a man was found near a defective gas stove. His wife’s body was found in an adjoining room, but their baby, lying beside his father, showed no signs of CO poisoning.17 Clearly, persons undergoing similar exposures can exhibit different outcomes. In a 1986 case in a Tennessee motel a 60 year old executive missed an early morning meeting. At 11 a.m., motel security opened his door and found the victim dead in the

Carbon monoxide and human lethality

18

floor (90% COHb) and his wife lying across the bed, comatose (35% COHb). That evening a 65 year old woman in a room directly below phoned a local relative and reported that she and her husband were ill. A search of other guest rooms found a fifth victim, comatose in a room adjacent to the room where the first patient had died. Subsequent investigation revealed that the source of carbon monoxide was the swimming pool heater. Exhaust fans above the building atrium maintained the building under negative pressure. There was thus potential for back draft from pool heater vents and subsequent carrying of CO into adjacent guest rooms.18,19 Indeed, a report from Denmark shows gas water heaters to be a frequent scenario.20 A Maryland study of heating victims showed COHb values ranging from 77 to 37%, with 2 of the 14 victims below 50% COHb.21 In a 1988 report a 27 month-old girl was brought to Johns Hopkins hospital after being the middle passenger in the backseat of a car that had been traveling from Washington, DC, to Baltimore. Two other children were in the backseat. The patient had repeatedly crawled down to the floor and back up to the seat in the 50 minute trip. She had fallen asleep 15 minutes before arrival. She was unresponsive with a COHb of 35%. Her 7 yearold sister who had been sitting to her right had a COHb of 34.7% but was largely asymptomatic. A 28 month old infant sitting to the left was totally asymptomatic despite a COHb of 33.6%. The front passengers (25 years and 72 years) showed COHb values of 18.4% (headache) and 16.1% (lightheadedness) respectively. The male driver of the car had dropped the passengers at the emergency room and had driven to work and felt fine. The driver’s window had been ajar during the trip. Again, persons with similar COHb values do not have identical symptoms.22 Sources of carbon monoxide in our environment are legion. The Utah Medical Examiners Office has reported several cases of carbon monoxide poisoning from the misuse of charcoal grills. Unrecognized by most individuals, charcoal produces substantial concentrations of carbon monoxide. Two of those cases follow.23 Case 1.—After cooking steaks outside their trailer on a cool evening, a husband and wife took their hibachi inside “to warm up the trailer.” The trailer was “closed up tight” because of the cool night. While asleep that evening the wife became nauseated, went into the bathroom in the trailer where she vomited and collapsed. When she awakened she found her husband dead in bed. The wife was hospitalized briefly and then released, without apparent effect. She reported that they had never before used the hibachi to heat the trailer. Autopsy of the husband revealed healed rheumatic heart disease. His heart blood contained 71 percent carbon monoxide. Case 2.—One day in late winter a father filed a missing persons report on his son. The following morning the father noticed the altered appearance of a stairway leading down to an old potato cellar near his property. Located at the bottom of the stairway was the only door and it was covered tightly with a plastic sheet. Inside the cellar on a foldaway type bed were his son and the son’s 18-year-old girlfriend, both covered to just below the shoulders by a sheet and a bedspread. The boy was unconscious. The girl was dead. The cellar measured approximately 10×8×6 feet. A nonusable oil stove stood on the floor. On top of it was a hub cap containing charcoal briquette ashes. Along-side the stove was a nearly empty bag of charcoal briquettes. Aside from the door covered by a plastic sheet, there was one small vent in the center of the ceiling. Autopsy revealed a

Effects of carbon monoxide in man

19

healthy girl whose heart blood contained 65 percent carbon monoxide and 0.054 percent ethanol. The boy survived without apparent effect. In a more recent report two hibachi cases were reported. In one, a 53 year old black male was found dead at his residence. He had moderate, generalized artereosclerosis. His blood COHb level was 41%. In the second case a 12-year old white male was found dead in his sleeping bag by his father who had been sleeping in the same tent. His blood COHb level was 30%.24 These cases demonstrate that a small volume of a seemingly harmless combustible can be fatal. Individuals exposed to the same atmosphere do not experience the same effects. And, victims of carbon monoxide poisoning can die at less than 50% COHb. 2.3 VARIATION BY SOURCE OF EXPOSURE It has been noted in the literature that the source of carbon monoxide makes a difference in the mean COHb at death. Data from Japan are as follows:25 Cause of Death Number of Cases Age Range COHb Range Mean City gas

15

4–50

64.3–83.1

74.8

Fire

12

1–87

40.1–68.5

54.9

Exhaust

10

19–46

50.3–81.6

64.6

It was speculated that oxides of nitrogen in exhaust gases led to a lower mean for these cases. For fire victims the four fatalities with the lowest COHb values were aged 67, 87, 78, and 1 respectively. Victim age plays a role. In another Japanese study the following data were presented.26 Cause of Death Number of Cases COHb Range City gas

4

64.2–79.5%

Fire

4

40.0–67.5%

Exhaust fumes

4

54.1–72.4%

City gas

3

71.9–78.7%

Fire

3

13.4–92.4%

Exhaust fumes

3

53.2–78.7%

From such data one might indeed conclude that fire is different and that perhaps even exhaust fume victims are different. In this latter study no data were presented on the age or health of victims. It is not surprising that exposure to fire gases might, on balance, lead to death at lower average COHb values. Fire gases, exhaust gases, and city gas are not pure carbon monoxide, although the concentrations of carbon monoxide are high in all three. For fire gases, elevated temperature and oxygen depletion are generally unassessable variables in addition to the presence of other gases such as hydrogen cyanide, aldehydes, CO2, etc.

Carbon monoxide and human lethality

20

Exhaust gases include oxides of nitrogen, and hydrocarbons. City gas includes hydrogen, methane, ethane, propane and carbon dioxide. However, city gas lacks the irritants such as aldehydes and oxides of nitrogen present in the other two. Wistar rats have been exposed to CO, and automotive exhaust gases from unleaded gasoline and 96% ethanol. The exhaust fumes were generated by two new identical Fiat engines. The LC50 values for 3 hour exposures were as follows: LC50 (ppm) Confidence Limits Gasoline

1968

1940–1992

Ethanol

2076

2042–2102

CO

2093

2068–2121

It was noted that high levels of aldehydes exist in ethanol exhaust which are absent in gasoline, while high levels of sulphur oxides exist in gasoline exhaust but are absent in ethanol. The LC50 value for ethanol exhaust was identical to CO while that of gasoline was somewhat less.27 The Institute of Forensic Medicine in Oslo has reported a study contrasting carboxyhemoglobin concentrations in fire victims (87 cases) with that from automobile exhaust victims (54 cases), mostly suicides. Their data are depicted visually in Figures 4 and 5. For the exhaust victims the mean fatal COHb was 70 percent. Little blood alcohol was found. The relationship between COHb and victim age is shown as follows:28

The Relationship Between Age and Post Mortem COHb Concentrations in Cases of Fatal Carbon Monoxide Poisoning (non-fire) Age

Number of Persons

Mean COHb concentration in % (Standard Deviation)

Less than 40 years

11

74 (5)

Between 40 and 50 years

12

74 (7)

Between 50 and 60 years

18

70 (11)

More than 60 years

13

65 (12)

The older group showed large variations in COHb concentrations and a lower mean. For fire victims 32% died with COHb concentrations below 45 percent. 54 percent of the victims were alcohol intoxicated. Figure 6 presents blood alcohol data for these victims. The distribution of victims with alcohol was the same as those without alcohol. Alcohol did not appear to alter the toxicity of carbon monoxide.

Effects of carbon monoxide in man

21

FIGURE 4. Post mortem carboxyhemoglobin concentrations in 54 cases of fatal carbon monoxide poisoning (non-fire).28

FIGURE 5. Post mortem carboxyhemoglobin concentrations in 87 fire victims.28

Carbon monoxide and human lethality

22

FIGURE 6. Post mortem carboxyhemoglobin concentrations in 54 alcohol intoxicated fire victims. The values within the columns indicate the post mortem blood alcohol con centration (percent×10).28

FIGURE 7. Post mortem carboxyhemoglobin concentrations in 72 fire victims with burns.28

FIGURE 8. Post mortem carboxyhemoglobin concentrations in 15 fire victims without burns.28 In Figures 7 and 8 carboxyhemoglobin data are given for fire victims who had burns and those who did not. A similar pattern is seen. Of the latter victims, five died with COHb values below 50 percent. In three of these cases heart disease was detected, in one case severe bronchopneumonia, and in the fifth case heavy alcohol intoxication. The authors of the Oslo study concluded that burns rather than carbon monoxide poisoning were the main cause of death in at least thirty percent of fire victims, that alcohol intoxication does not seem to influence the fatal COHb concentration, and that a low post mortem carboxyhemoglobin concentration is often found in victims suffering from disease.

Effects of carbon monoxide in man

23

Japanese workers have contrasted the COHb profiles of victims from carbon monoxide poisoning, mainly inhalation of city gas, with that of fire victims. Data from this study from the early 1960s are shown on facing page:29 COHb in Deaths from CO Poisoning (non-Fire) COHb Deaths in Fire COHb (%)

CO Fatalities Number

COHb %

Fire Fatalities

(%)

Number

%

10

–

–

10

12

7.2

20

3

1.3

20

15

9.0

30

–

–

30

12

7.2

40

7

3.0

40

17

10.2

50

11

4.7

50

22

13.2

60

26

11.2

60

30

18.0

70

52

22.3

70

22

13.2

90

115

49.4

90

34

20.4

90.1

19

8.1

90.1

3

1.8

Total

233

100.0

Total

167

100.2

Some nine percent of city gas victims have COHb values below 50 percent with another 11 percent in the 50 to 60 percent range. Fire victims show a substantially higher percentage at low COHb values, with 47 percent showing less than 50 percent COHb and another 18 percent in the 50 to 60 percent range. COHb values for fire victims in the Japanese work are lower than that reported in the foregoing studies. While fire victims clearly die with COHb levels less than exhaust or city gas victims, those exposed to carbon monoxide in these latter circumstances show a broad range of COHb values with upwards of 20 percent of the victims showing less than 60 percent COHb blood saturation. 2.4 FIRE GAS EXPOSURE STUDIES Having contrasted non-fire and fire carbon monoxide fatality studies, it is appropriate to discuss fire gas exposure studies in more detail. Data for two aircraft fires in the early 1960’s have been reported. The mean COHb value was 59 percent with a range of 25 to 85 percent for 85 victims.30 CO Values Found in Victims of Aircraft Fires Percent Carboxyhemoglobin

Number of Fatalities 0–20

0

21–30

4

Carbon monoxide and human lethality

24

31–40

9

41–50

16

51–60

18

61–70

19

71–80

16

81–85

3

TOTAL

85

A report on 15 persons from the 1940’s showed a range of 18 to 78 percent COHb with a mean of 48 percent.31 A study by the University Institute of Forensic Medicine of Copenhagen, Denmark is particularly interesting. Data were collected on 169 consecutive cases involving fire victims. Some 56 percent were men and 44 percent women, all autopsied at the Medicolegal Institute of Copenhagen. The data originated from two periods, 63 cases were from the years 1966 to 1971 and 106 cases 10 years later (1976–1981). The reason for this subdivision was to attempt to elucidate the possible role, if any, which might be played by the increasing amount of synthetic products, which are replacing natural products in the built environment. However, no difference occurred between the distribution of the carboxyhemoglobin levels in the two data sets, and they are consequently combined and dealt with as one.32 At autopsy, special attention was paid to the possible presence of soot particles in the respiratory tract, and blood was collected for the determination of carbon monoxide and of alcohol. The distribution of victims according to age proved to correspond to the age distribution of the entire population of Copenhagen with the exception of the 15–35 year group, where only half the number of fire victims expected according to the age distribution of the population was found. The explanation offered is the greater agility of young persons, enabling them to move more easily to escape a life threatening situation.32 More than half of the fire victims had a significant blood alcohol level (over 0.05 percent), and in well over 20 percent of the cases the blood alcohol level surpassed 0.2 percent. In these cases the ability to react adequately may have been reduced to such an extent that alcohol may be considered to have contributed substantially to the victim’s presence in the incident.32 The distribution of the fire victims according to the percent of carbon monoxide in their blood is shown in Figure 9. The Figure also shows the number of victims with soot in the respiratory tract. It is immediately apparent that the two findings are closely related so that there are very few cases with significant amounts of carbon monoxide in the blood and without soot in the airways. Half of the victims showed blood with more than 50 percent of carboxyhemoglobin.32 Of interest is the group showing no significant carbon monoxide in the blood (less than 10 percent saturation) and no soot in the airways, consisting of 12 cases. The autopsies indicated that death had occurred before the onset of fire in five of the cases (the dotted top of the column). There remain seven cases, where the authors felt that

Effects of carbon monoxide in man

25

causes of death may have been heat (neurogenic shock) or carbon dioxide poisoning/oxygen deficiency.32 Concerning the groups showing low or negligible carboxyhemoglobin levels, the Danish authors speculated that carbon monoxide was not evolved at the onset of the fire, but instead carbon dioxide, which accentuates the lack of oxygen. This is said to be the case in flash fires, where a sudden, large consumption of oxygen takes place. In flash fires the intense heat alone may also be considered the cause of death.32

FIGURE 9. Victim distribution according to carbon monoxide in the blood. The dark part of the columns indicates cases with soot in the respiratory tract The white top (- -) of the zero column signifies the number of deaths before the fire.32 The Danish workers plotted their COHb profiles versus those from two other studies (Figure 10). The profiles are quite similar but not identical, showing perhaps differences in the studied populations as well as differences in techniques of COHb determination.32

FIGURE 10. The distribution according to carboxyhemoglobin

Carbon monoxide and human lethality

26

levels of victims in three fire fatality studies: Anderson et al. (—–),33 Birky and Clarke (. . . .),34 and the Danish work (- - - -). 32 In the Danish study half of the victims died as a consequence of smoking in bed. Characteristic for this type of fire is initial smoldering with comparatively low heat at the beginning of the fire. The distribution of carboxyhemoglobin of the victims of smoking in bed proved to be the same as that for the other half of the victims. In a detailed British report some 58 fire fatalities were investigated and categorized as to their presence in the room of fire origin or remote from the room of origin. COHb data were available on 12 and 34 victims respectively. That data is plotted in Figure 11,35 which shows that 74% of victims were found away from the room of origin.

FIGURE 11. Plot of COHb percent versus fire victims age.35 For the 34 victims remote from the room of origin 19 had COHb levels over 65 percent, six between 50 and 65 percent and four between 40 and 49 percent. The remaining five, who all died in the same fire, had levels between 14 and 28 percent—the causes of death

Effects of carbon monoxide in man

27

being recorded as carbon monoxide and cyanide poisoning together with superficial burns.35 Thirty-six of the victims had lung or respiratory tract damage recorded in the postmortem reports. This typically comprised black soot and ash in, and severe inflammation of, the air passages, with lungs oedmatous or congested. Such information was not available for the remaining seven victims but there was no reason to suppose that similar damage did not occur. Most victims had burns ranging from superficial to severe although burns may have occurred after collapse or death.35Cyanide tests were carried out on the blood of 15 victims. Thirteen gave results ranging between 26 and 180 µg CN/100 ml of blood, and none was detected in the other two.35 Alcohol was present in the blood of victims of two of the fires (124, 47, and 43 mg alcohol/100 ml blood); in another fire blood alcohol determinations were performed on four victims but none was found. Children, only, died in three other fires. In the remaining six fires in which adults died no alcohol tests were performed.35 Overall the British author’s conclusions in this study were as follows: a) In nearly all fires investigated some firespread occurred beyond the item first ignited. Almost all the fatalities, both in and remote from the room of fire origin were overcome by, and died from, the effects of smoke and toxic gases. Of these, only about one quarter had burns considered a contributory cause of death. Despite this, most of them had external burns but these may have occurred after collapse or death. b) More than half the fatalities had COHb levels which alone were clearly high enough to account for death in healthy individuals. c) Nearly all the fatalities had lung and respiratory tract damage due to the effect of smoke and hot gases. d) Cyanide was found in measurable amounts in victims. Although these amounts were all below the minimum lethal level, cyanide may have been a contributory cause of death at higher levels. e) People who died at night in fires starting on the floor below were generally not overcome in their beds. In most cases they got up and moved around before collapsing. f) It was not possible to say whether alcohol played a part in the death of most of the victims. g) Once out of the house people were unable to re-enter to rescue others due to their injuries or to the rapid development of the fire. As the foregoing studies indicate, the fire environment is a complex environment. Indeed, hydrogen cyanide has been found in fire victims over the years. While it is beyond the scope of this report to focus on the causes of fire deaths in detail, it is perhaps useful to cite some of the more relevant human exposure studies on the interaction of hydrogen cyanide with carbon monoxide.

Carbon monoxide and human lethality

28

2.5 WITH HYDROGEN CYANIDE In 1966 the Wayne County Michigan Medical Examiner’s Office reported a study of 53 fire victims (38 adults and 15 children) taken over a 16 month period in 1964–1965. Forty-eight victims were either dead at the fire scene or dead on arrival at the hospital. Five victims lived for two hours or less. All victims had significant levels of carbon monoxide (17 to 90 percent COHb) in their blood. In addition, blood cyanide was found in 39 victims at levels of 17 µg/100 ml to 220 µg/100 ml (six above 100 µg/1100 ml). (A background level of up to 25 µg/100 ml blood cyanide is found in smokers and .5 µg/100 ml for non-smokers.) All values were less than the 300–500 µg/100 ml (3–5 µg/ml) lethal level. Of victims with blood cyanide, 27 also had COHb levels in excess of 50 percent. Sixty percent of the adult victims were intoxicated to a greater or lesser degree. It was noted that while the primary cause of death was likely to be carbon monoxide, the action of cyanide to cause respiratory stimulation and inhibition of the cytochrome system may have been a contributing factor to fire death in some cases.36 Three survivable, relatively low crash-force, air carrier accidents in the first half of the 1960’s were investigated. These accidents were the 11 July 1961 United Airlines DC-8 at Denver, the 23 November 1964 Trans World Airlines 707 at Rome, and the 11 November 1965 United Airlines 727 at Salt Lake City.37 Medical investigators conducted blood tests on the victims and found that carbon monoxide was present in amounts sufficient to have caused toxic incapacitation during the brief period available for emergency evacuation prior to the progressive destruction of the aircraft passenger cabin by fire. In connection with the accident investigations, investigators found that the acrid smoke caused laryngospasms and that this caused breathing difficulties. Carbon monoxide data are shown as follows:37 Passengers Passengers

Deceased Passengers

Tested for Carbon Monoxide

Carbon Monoxide (as blood COHb)

Denver DC 8

114

17

17

30–85% range (mean=62%)

Rome 707

62

45

24

3–49% range (mean=23%)

Salt Lake City 727

85

43

35

13–82% range (mean=37%)

105

76

Four accidents were reported which included cyanide analysis. These accidents were the 27 November 1970 Capitol International Airways DC-8 at Anchorage, the 7 June 1971 Allegheny Convair 580 at New Haven, the 8 December 1972 United Airlines 737 at Midway and the 20 December 1972 North Central DC-9 at O’Hare. These accidents also involved relatively low crash forces. During the emergency escape period fire and toxic smoke occurred.25

Effects of carbon monoxide in man

29

It was determined through blood analysis of the victims that cyanide was present in some cases in amounts which could be incapacitating, in combination with the carbon monoxide that was present. A summary of the accident investigation findings of these four accidents with respect to cyanide and carbon monoxide ranges is given below:37 Carbon Monoxide (as blood Cyanide in blood sample carboxyhemoglobin) in fatal victims Anchorage DC-8

19 positive (5–69% range)

18 positive (0.1 µg/ml to 2.26 µg/ml range)

New Haven 580

23 positive (9–49% range)

23 positive (0.007 µg/ml to 3.38 µg/ml range)

Chicago 737

Pilot 40%

Pilot 3.9 µg/ml

Chicago DC-9 9 positive (26–64% range)

9 positive (1.10 µg/ml to 2.65 µg/ml range)

It was noted in the FAA report, that incapacitation should occur at lower levels than death, and it was speculated that it may occur at half the fatal concentration. For example, the 30 percent blood carboxyhemoglobin range (coma and death begin to occur at the 60– 70 percent blood level range in “normal” healthy adults) was thought to produce severe headache, weakness, dizziness, dimness of vision, nausea, vomiting, and collapse. Cyanide alone causes death at about the 3–5 µg/ml blood level in mammals but incapacitation at about half that level might be anticipated. Thus together, assuming additivity, lethal effects could perhaps be anticipated with a blood carbon monoxide of 30 percent plus a blood cyanide of about 2 µg/ml (200 µg/100 ml).37 Despite such speculations as above, in fire fatality studies, victims with high COHb levels characteristically show high blood cyanide. Low COHb levels are seldom associated with high cyanide levels. Data for 10 victims of the Tennessee jail fire 34,38 are shown below:34

Correlation of Blood COHb with HCN Victim Age

Cyanide (µg/ml)

COHb%

45

0.05

59

37

0.30

61

18

0.35

76

25

0.42

64

20

0.43

58

22

0.59

60

26

0.93

45

19

1.06

58

59

1.64

58

18

1.83

77

Carbon monoxide and human lethality

30

Cyanide approaching 2 µg/ml in fact showed little effect on COHb values in these victims. Cyanide and other toxicants may play an intermediate role leading to incapacitation, preventing escape but the role of cyanide in conjunction with CO is unclear. In the 1983 Ramada Inn Central Fire, Fort Worth, Texas data for the five victims were as follows:39 Sex Female Male Male Male Male Age

27

25

54

46

26

Location within room

side of bed near bath wall

corner near window

bathroom

corner near window

Side of bed 5 ft from window

Burns (degree/% body surface)

2nd, 3rd/ 30%

2nd, 3rd/ 75– 2nd, 3rd/ 80% 15–20%

2nd, 3rd/ 60%

2nd, 3rd/ 10– 15%

Blood CO a) (Carboxyhemoglobin b) Normal: less than 1.5%)

79% Saturation 82%

77% Saturation 74%

62% Saturation 60%

75% Saturation 70%

28% Saturation 25%

Blood Ethanol

0.08%

0.02%

None Detected

None Detected

None Detected

Blood Cyanide

None Detected None Detected

3.0 µg/ml

4.5 µg/ml

2.5 µg/ml

a) (Normal: less than b) 0.2 µg/ml)

0.6

6.3

2.4

5.7

1.8

Two sets of COHb and blood cyanide data are shown. Four of five victims have COHb values greater than 60%, which is consistent with carbon monoxide poisoning being the primary cause of all fatalities. Blood cyanide is a factor of two different between the two sets of results provided, showing the difficulty of blood cyanide determination.39 The lethal cyanide level in man is higher than that in rodents. Esposito and Alarie have found a lethal blood cyanide level of 1 µg/ml at an LC50 concentration of 177 ppm and an LT50 of 29 minutes in mice,40 but a value of 2 µg/ml was found in rats41 by Levin and coworkers for a 30 minute exposure. Several reports note that the acute lethal blood cyanide level in man is 5 µg/ml.42,45,46 While Rieders notes that blood cyanide in fatal cases may be below 1 µg/ml on inhalation of hydrogen cyanide gas,43 yet fire data seem to show high cyanide levels only in conjunction with high blood CO levels. A study by Symington of 52 fire victims for example showed cyanide levels up to 3.5 µg/ml.44 In a study by Memon and Alarie of 177 fire cases, of 29 cases with blood cyanide over 1.5 µg/ml, all but five cases had COHb over 50%.47,48 In pure exposures, recovery has been noted in victims whose cyanide level in the blood reached 7.5 µg/ml.49 The estimated LC50 in humans for HCN alone on inhalation is 3400 ppm for 1-minute; HCN is listed as fatal at 270 ppm in 6–8 minutes, 181 ppm in 10 minutes, and 135 ppm in 130 minutes.50 The LCLo, the lowest concentration in air reported to cause death, is 166 ppm at 10 minutes and 100 ppm at one hour. In cats the LCLo for 30 seconds is 2075 ppm and in rabbits 1660 ppm.51 However, survival in man

Effects of carbon monoxide in man

31

has been reported for an individual exposed to 415 ppm HCN for approximately 6 minutes.52 While the concentrations of HCN in controlled human exposures have not exceeded 450–520 ppm, men employed in fumigation with HCN have been tested while at rest in 250 ppm for two minutes and 350 ppm for 1½ minutes but felt no dizziness. Other tests have exposed individuals to 500 ppm for about a minute without injury. A ten minute LC50 value of 539 ppm has therefore also been suggested for humans. Clearly humans are able to tolerate exposure to a given concentration longer than other mammals, including monkeys.53 The most comprehensive studies on rats would suggest that the effects of HCN and CO are additive36,54–59 rather than synergistic.60 However, in papers by Davis and coworkers using five minute rat exposures, the author examined HCN singly and in combination with CO, either during the exposure or within 20 minutes CO post exposure.61–62 No alteration in the time-to-death pattern of HCN was seen in the presence of CO (25% COHb). The five minute LC50 value was 503 ppm for HCN, while the HCN-CO combination produced an LC50 value of 467 ppm, a value within confidence limits of the HCN value. For mice an LC50 of 323 ppm was seen for HCN for 5 minutes alone and 289 ppm in combination with CO (25% COHb level). Their results were clearly less than additive. Pitt, et al., examined individual and combined effects of cyanide and CO on cerebral blood flow and on cerebral oxygen consumption. They found that cerebral blood flow increases with CO-hypoxia and with cyanide hypoxia and in combination. Cerebral oxygen consumption declines at 50% COHb and in combination with HCN. Test animals had 30 or 50% COHb with or without 1.0 µg/ml HCN or 1.5 µg/ml HCN. Their results were additive.63 Studies in monkeys by Purser have looked at the relationship between atmospheric HCN concentrations and time to incapacitation. HCN levels of 100–200 ppm can be extremely hazardous. Incapacitation occurred at blood cyanide levels of approximately 2.7 µg/ml (2.2–5.3 µg/ml). Unfortunately, no direct relationship was found between venous blood cyanide levels and atmospheric HCN concentrations over a 30 minute exposure period, nor a clear relationship between venous blood cyanide and time to, or degree of, incapacitation. There was a loose linear relationship between HCN concentration and time to incapacitation. It may be that blood cyanide measurements are poor predictors of the degree of incapacitation caused by cyanide and that the rate of uptake during the hyperventilatory stage is more closely related to incapacitation and subsequent death than is the actual blood level after a period of exposure.64,65 Instudiesexposing cynomolgus monkeys to fumes from polyurethane foam (HCN 115 ppm and CO 1016 ppm) and polyacrylonitrile (HCN 115 ppm and CO Oppm) times to incapacitation were 20 minutes and 22.5 minutes respectively. These experiments suggest only weak additivity between HCN and CO.66 Before proceeding further, two complications should be noted. While 67 percent carboxyhemoglobin generally results in death for “normal individuals” if untreated, levels of 16–20 percent may be lethal for victims with cardiovascular disease, anemia, lung disease, and increased metabolic rate. Such victims show far greater susceptibility to the toxic effects of carbon monoxide. As shown by the blood COHb values in CO victims as cited in Section 1.2, the identification of the role of carbon monoxide based upon a specific COHb loading is not straightforward. This will be discussed further in subsequent sections. Likewise, the role of hydrogen cyanide is not only complicated by

Carbon monoxide and human lethality

32

factors similar to those above, but also by recognized difficulties in obtaining valid blood cyanide measurements (increase or decrease in cyanide is observed on sample aging).67–71 2.6 LARGE FIRE FATALITY STUDIES In 1972, Zikria, et al., of Columbia University, reported on an extensive analysis of autopsy records of 311 New York City fire victims during 1966 and 1967. One hundred eighty-five survived less than 13 hours, and 72 over 12 hours with 54 not having survival time indicated. Smoke poisoning or asphyxia was the most common primary diagnosis in fire deaths under 12 hours.72–75 Carbon monoxide poisoning occurred in 79 percent of all victims with a primary diagnosis of smoke poisoning or asphyxia. Of the 185 victims surviving less than 12 hours, 59 percent of the 70 percent tested clearly had lethal or significant levels of carbon monoxide.72–75 Among the 105 victims with less than 40 percent body burns—who would not have been expected to die from surface burns alone—three-fourths also had respiratory involvement. In the total group, half clearly had carbon monoxide poisoning, almost as many had smoke poisoning or asphyxia, and over one-quarter had respiratory damage. In deaths under 12 hours, carbon monoxide poisoning was found almost equally in the presence or absence of body surface burns, in 50 percent of those with body burns and in 30 percent of those without body burns.72–75 Of particular interest in the Zikira work is that respiratory tract involvement was found in 70 percent of deaths under 12 hours and in 46 percent of victims who survived over 12 hours. Zikira noted that it is likely that the agents causing the tracheobronchial and pulmonary parenchymal damage of smoke poisoning in man are also the aldehydes such as acrolein, which are found in large quantities in smoke and combustion of wood, cotton, furniture, and nonsynthetic structural materials.72–75 However, from the data given in the preceeding sections carbon monoxide alone was the likely cause of deaths in more cases than Zikria recognized. The reason for the discrepancy is the excessively conservative lethal COHb level (50%) that the author used. One of the most detailed fatality studies reported to date is from Maryland. Research conducted from 1972 to 1977 by the Applied Physics Laboratory of Johns Hopkins University and the Maryland State Medical Examiner’s Office focused on 530 fatalities.21,76–79 The causes offires were as follows:76 Causes Fires Fatalities Percentage Smoking

135

184

44.4

Electrical

20

29

7.0

Heating Equipment

19

33

8.0

Stove

11

14

3.4

Matches

18

27

6.5

Candle

4

5

1.2

Flammable Substance

9

9

2.2

Cooking

10

16

3.9

Suicide

14

14

3.4

Effects of carbon monoxide in man

Arson/Suspicious

33

16

31

7.4

Other

3

4

1.0

Explosions

8

13

3.1

Set Fire

5

5

1.2

Automobile

11

14

3.4

Unknown

12

16

3.9

295

414

100.0

TOTAL

Fires caused by smoking were predominant in the list of causes. Also, the study indicated that smoking and alcohol were a bad pairing. A blood alcohol content of 0.1 percent (the intoxication limit in some states) was involved in 50 percent of all fire fatalities above age 20. Data show that about 25 percent of the fires in this study involved both alcohol use and smoking. This comprehensive study found a number of interesting differences in different populations.76 Location: Fire fatality data were available for three areas (Baltimore City, 4 large counties, 19 small counties) that represent, on the average, differing styles of living conditions (urban, suburban, rural). See Figure 12.69 A value of 1 in actual/ census indicates fatalities identical to population group proportion in census. In all three locations (and consequently in the state of Maryland as a whole), the distribution of actual versus census-predicted occurrences of fire deaths as a function of age of fire victims indicates a similar trend. The age group 50–60+ shows a substantial predisposition to being fire victims (approximately two times census expectation i.e., 2.0), whereas the age group 10–39 is well below the casualty rate predicted from census data alone (i.e., approximately 0.6). For the state of Maryland, on average, the age group 0–9 fatality rate agrees with the census prediction (observed casualties, 21.6 percent of the total; predicted casualties from census, 19.0 percent). However, the actual/census value for Baltimore City (1.39) is sufficiently different from the 19 small counties (0.74) that a location-specific cause may be indicated for the 0–9 age group.76

Carbon monoxide and human lethality

34

FIGURE 12. Fire fatalities as function of location and age. The ratios of observed fire fatalities compared to random occurrence based on population census are given for the state of Maryland and three subdivisions. Values greater than 1 indicated a greater than random chance of becoming a fire fatality in a given age group.76 Sex: The male-female distribution among fire fatalities as a function of age showed trends similar to the previously discussed overall distribution except for a pronounced minimum of female fatalities in the age group 30–39 (0.32 compared to 0.775 for men in the state of Maryland and observed in all three locations) and a noticeable increase in female fatalities (1.34) in the age group 0–9, compared to males (1.00).76 At all ages, the absolute number of male fire deaths exceeded that of females (on the average, by a factor of 1.5/1 and is particularly pronounced in the age group 30–60). Considerable fluctuations in the male-female ratios were observed in the various locations within the state. High consumption of alcohol by men, which has a profound effect on the probability of becoming a fire victim, is a key factor in the male/female ratio being substantially in excess of 1 beyond the age of 20.76 Race: The distribution of fire fatalities as a function of race and age shows a very substantial contribution to black fatalities in the age group 0–9 (1.66) which is well above

Effects of carbon monoxide in man

35

the census prediction, as compared to low values for white fatalities in the same age group (0.65). As a consequence, the age distribution curves for the black population have two age group peaks (0–9 and 60+), while the corresponding curve for whites has only one peak (50–60+). This pattern is particularly pronounced in Baltimore City and the four large counties.76

FIGURE 13. The involvement of alcohol on the absolute number of fire fatalities as a function of age and blood alcohol level. Alcohol of 0.1% represents the legal definition of drunkenness. For each age group, the fraction of fatalities with alcohol in excess of 0.1% and the male/female ratios are given. In the age group 30– 59, more than half of the fatalities have greater than 0.1%. Male deaths exceed female deaths in all instances where alcohol exceeds 0.1%.76 On an absolute basis, fatalities among the black population, averaged for the state of Maryland, always exceed the census-predicted values, with a particularly low value to predicted white/black ratio (0.13) in the age group 0–9. In some locations, however, such as in Baltimore City, this ratio is near or above 1 for the age group 30–65+, as are the ratios in most age categories of the 19 small counties. Indeed, the probability of being involved in fire is very situation dependent.76 Alcohol: The involvement of alcohol with fire fatalities is shown in Figure 13. With increasing age (up to 60), the fraction of casualties with blood alcohol levels in excess of 0.1 percent (the legal limit for drunkenness) raised rapidly to approximately 70 percent of

Carbon monoxide and human lethality

36

all fatalities in the age group 30–59, with a decline to 39 percent in the age group 60+. This pattern of very substantial consumption of alcohol prior to becoming a fire fatality parallels the substantially higher alcoholism rate of men in these age groups. Men account for more than two-thirds of the heavily intoxicated cases. Fifty percent of all fire fatalities above the age of 20 show an alcohol level above 0.1 percent. Drugs other than alcohol were rarely found in these fire victims.76 The fraction of fire victims in the Maryland study with carboxyhemoglobin (COHb) levels in excess of 50 percent was 60 percent This distribution is shown below:34

Distribution of Fire Victims According to Blood CO Saturation Levels COHb (%)

No. of Victims

%

0–9

48

9

10–19

42

8

20–29

37

7

30–39

38

7

40–49

43

8

50–59

58

11

60–69

79

15

70–79

111

21

>−80

74

14

TOTAL

530

100

Measurements of hydrogen cyanide showed that a substantial number of fire victims with high carbon monoxide intake had also been exposed to substantial amounts of hydrogen cyanide. Whether the cyanide intake makes a significant contribution to the final outcome was difficult to assess, since the time sequence of inhalation of the two gases was not known. However, concentrations that were considered possibly toxic by the authors (1–2 µg/ml) were found in 24% of the cases where determinations were made, and probably toxic concentrations (>2.0 µg/ml) were found in 10% of the cases.34 In the Maryland study, a number of the fire victims with COHb levels below 50 percent (and therefore thought not to have died from that cause alone) were found to have ingested substantial, but also subfatal, doses of hydrogen cyanide.76 A second cause of death cited from seemingly sublethal carbon monoxide uptakes was that the condition of the cardiovascular system of fire victims, expressed in terms of blood flow obstruction in the main heart blood vessels, which was substantially inferior to that of the comparable population at large.59 One of the surprising findings of the Maryland study was the amount of heart disease, expressed in terms of coronary artery stenosis, found in the fire victims and, in particular, in the youngest age group. The maximum narrowing found in the coronary arteries of the victims subdivided into age groups is as follows:34

Effects of carbon monoxide in man

37

CORONARY ARTERIAL NARROWING IN FIRE VICTIMS* Age

0–24%

25–49%

50–74%

75–89%

90–100%

Total

20–39

16

5

6

6

8

41

40–49

6

1

3

2

9

21

50–59

4

1

5

5

11

26

60–69

2

1

3

3

11

20

70+

1

0

2

0

8

11

29

8

19

16

47

119

TOTAL

(24.2%)

(6.7%)

(16.0%)

(13.4%)

(39.4%)

(100%)

*

Maximum observed in any one coronary branch.

Of the victims in the youngest age group (20 to 39 years), eight had more than 90 percent narrowing in at least one segment of their major coronary arteries. In addition to the unexpected amount of heart disease in the young, of the 119 victims, 40 percent had at least one location of 90 percent or more narrowing and more than half had greater than 75 percent narrowing.34 When the relationship between blood carbon monoxide levels and coronary artery stenosis was examined, however, no constant relationship between the two factors was found. More victims with significant heart disease achieved a higher than 50 percent carbon monoxide saturation than died with lower levels. Further to explore the relationship between blood carbon monoxide content and coronary artery narrowing, men and women were studied separately because of the reported different pattern of atherosclerosis in the sexes. Of the 85 men studied, 44 had significant heart disease and of these victims 13 succumbed to lower than 50 percent carbon monoxide levels. However, 31 of those with significant heart disease achieved greater than 50 percent carboxyhemoglobin levels before death, suggesting that those with cardiovascular disease do not necessarily succumb at a lower carboxyhemoglobin level.34 The authors suggested that preexisting heart disease contributes to inability to escape from the fire but does not necessarily contribute to early death. This incapacitated group would then continue to inhale and to increase their amount of carbon monoxide. This cardiac-based incapacitation would also explain the high incidence of heart disease because heart disease would “select” them to be fatalities.34 The contribution of inhaled soots and adsorbed materials or of irritating gases, such as a aldehydes or hydrochloric acid, was not known. Heavy concentrations of inorganic metals (lead, antimony, and others) and adsorbed pulmonary irritants were observed in the soots that were deposited throughout the trachea and lung tissues. Acetaldehyde was also recovered from lung specimens

Carbon monoxide and human lethality

38

FIGURE 14. Medical causes leading to fire fatalities. Shaded boxes indicate fatal out comes.76 of fire victims. The contributions of the soots and adsorbed materials to breathing difficulties (such as lung edema) are likely to be considerable, but their specific contributions to fatalities were not clear. They are probably a minor factor in the “rapid” fatality cases, but may be significant in “delayed” fatalities from pulmonary causes where the soot deposits may play a contributory role.76 A summary of the Maryland findings is shown in Figure 14. The available quantitative information concerning the numbers and nature of fire deaths that occur more than six hours after the fire exposure was labelled as approximate. However, the involvement of toxic gases is the primary cause of fire deaths, i.e., 75 percent of all fatalities are due to toxic gas ingestion.76 As seen from the above studies, fire fatalities are due largely to carbon monoxide, compounded by hydrogen cyanide, aldehydes, such as acrolein, other irritants, alcohol and heart disease. Run nearly parallel to the Maryland study was a study in the UK. This study contrasted data from Scotland with data from other parts of the UK. The project started in 1976, was carried out by the Department of Forensic Medicine and Science at the University of Glasgow. For the first five years the study was confined to the Strathclyde area of Scotland (surrounding the city of Glasgow, and hereafter called Glasgow); a total of 227 fire deaths were investigated, including both pathological and toxicological aspects. In 1981 it was extended to include a further 71 cases from other parts of the United Kingdom to validate the conclusions of the Glasgow study nationally.33,80–83

Effects of carbon monoxide in man

39

FIGURE 15. Frequency distribution of percent COHb in fire fatalities.80 Most of the deaths were in single fatality fires in dwellings, in which the fire was restricted to the room of origin. The fires occurred particularly during the winter and early spring, and often over the weekend. Old people were especially vulnerable.80 Severe burns had been sustained in about 80 percent of cases, although it was not possible in general to establish to what extent they had occurred after death or whether they were a cause of death. The respiratory tract was injured in more than 70 percent of the victims, and most had inhaled smoke and fire gases, leading to soot deposition in the airways and an increase in the level of carboxyhemoglobin (COHb) in the blood.80 The investigators concluded that carbon monoxide was the cause of death in 51 percent of cases in the UK study (with the assumption that lethal levels are those where COHb>50%) (54 percent in Glasgow), and was implicated in the death of 37 percent of the other UK cases (31 percent in Glasgow).80 COHb distribution for the Glasgow study is shown in Figure 15.80 The incidence of heart disease and surface burns versus COHb is shown in Figure 16. This figure indicates that 37% of the victims died with less than 35% surface burns.

Carbon monoxide and human lethality

40

FIGURE 16. Diagram showing the incidence of burn injuries versus percent COHb in fire fatalities. Fatalities with heart disease are indicated by open circles. The vertical line is set at 35% surface burns, considered the fatal threshold. The horizontal line is set at 50 percent COHb above which CO is considered probably fatal in normal healthy adults. The predominance of heart disease in less than 50 percent COHb cases was considered noteworthy.80 In the Glasgow study younger and older persons were more likely to be victims, while those aged 10–39 were much less likely to be victims of fire as shown as follows:80 Age No. No. % of % distribution of Scottish Group Males Females Fatalities population 0–9

11

8

20.4

15.8

10–19

4

1

5.4

17.8

20–29

0

2

2.2

13.8

Effects of carbon monoxide in man

41

30–39

3

1

4.3

11.6

40–49

6

3

9.7

11.5

50–59

7

4

11.8

11.5

60–69

14

5

20.4

10.2

70–79

6

6

12.9

6.0

80–

3

9

12.9

1.9

This shows once again the additional vulnerability of the very young and old in fires and is in agreement with other studies. Cyanide gas, produced in the course of most fires, was estimated to be a factor in 33 percent of the deaths in the UK study (24 percent in Glasgow). Although there were few cases in which cyanide might have caused death.80 One of the most important contributing factors in the deaths examined in Glasgow was alcohol: 50 percent of all fatalities had alcohol in their blood, and in 38 percent of the cases the level was above 150 mg/100 ml blood. This would have been enough to cause marked symptoms of intoxication and would have severely impaired the ability of those involved, either to fight the fire or to escape from it.81 In the UK segment of the study the percentage of victims who had alcohol in their blood was similar but the quantity of alcohol which had been consumed was much lower: only 14 percent had blood alcohol concentrations above 150 mg/100ml. It is probable that the Glasgow region is not typical of the UK as a whole and that the figures reflect the social pattern of that area. Data are given as follows:81

Blood alcohol concentrations in fire deaths Incidence Concentration mg/100 ml blood

UK Study No.

Glasgow Study

%

No.

%

Negative

38

54

113

50

50

15

21

10

4

50–100

5

7

10

4

100–150

3

4

8

4

150–200

5

7

14

6

200–300

4

6

42

19

300 and above*

1

1

29

13

71

101

227

100

Total * Highest concentrations observed:

UK study 376 mg/100 ml. Glasgow study 585 mg/100ml.

Carbon monoxide and human lethality

42

2.7 EFFECTS OF HEAT AND OTHER FACTORS The fire environment includes more than just carbon monoxide. It includes heat, oxygen depletion, carbon dioxide and other toxic gases. In this section these other factors are discussed in additional detail. Let us first examine heat. Indeed, many fire victims sustain burns. Unfortunately one can seldom determine whether death occurred before or after the victims sustained the observed burns or other effects of severe heat exposure. Heat over 50°C is life threatening. Heat enters the body mainly through the skin and usually increases the peripheral blood flow. This effect causes an increased heat conductivity of the periphery and, therefore, an increase of temperature of the body core. Profuse sweating, which usually commences a few minutes after heat exposure, may, through evaporation cooling, counteract the overheating with air temperatures up to 60°C. In moist air this limit will be reached at lower temperatures. The more heat enters the body, the greater the imbalance of physiological factors, such as the temperatures of different parts of the body or of the circulatory system. Signs of breakdown occur. The rise of the average body temperature is a valuable indicator of this stress.84 Concerning rescue from distress caused by heat, the “survival time” is a less decisive factor than the span of time in which man is still able to act, i.e., “escape time.” Figure 17 provides an estimation of escape time.84 The chart holds for dry, motionless air, with equality of air and radiation temperature. According to the authors, one must anticipate the possibility of incapacitation when the average body temperature rises by as little as one degree (C). Acclimation is possible since firemen frequently experience a 1–2°C body temperature rise in fires.85 The line of Figure 17 is calculated on the assumption of a subject with a heat capacity of 50 calories per degree (C), a projection surface of 1.2 sq. M., an evaporation from skin and lungs of 250 calories per hour, a metabolic heat production of 250 calories per hour and heat permeability of clothes (worn, above 80°C) of 5 calories per square meter per hour per degree (C). Figure 17 demonstrates the safe periods in which man is still able to act. This diagram is only approximate and restricted to passive overheating, including only moderate exercise, like standing or walking. Persons with fever or doing hard work may withstand a much higher increase of temperature, because the consequences of active and passive hyperthermia differ. With extremely high temperatures and correspondingly short period of heat tolerance, the heat capacity of thick clothing may lengthen periods by one minute or more.84 If a person is exposed to a hot environment, especially if the humidity is high and the person active, there is a danger of incapacitation and death due to hyperthermia. Incapacitation can occur for some people by breathing air as low as 65°C.86 Moritz and coworkers87–88 studied the effects on pigs of exposure to air temperatures ranging from 70°C to 550°C for varying lengths of time. In the extremes, exposures on the order of 15 minutes to an air temperature of 80°C or on the order of 30 seconds to air temperatures greater than 500°C were capable of causing acute hyperthermic death. During exposure the animals breathed air

Effects of carbon monoxide in man

43

FIGURE 17. Average “escape time” for lightly clad man in surroundings of high temperatures. Wall and air temperatures are equal: no wind except the natural uplift. The straight line is calculated on the assumption that a rise of one degree (C) of total body temperature is critical in determining the limit of escape time.84 at room temperature. At temperature extremes the mechanisms of death were different. In the long exposures at lower temperatures there was little or no cutaneous burning and death appeared to result from peripheral vascular collapse. In the case of brief exposure to high air temperature, there was severe general cutaneous burning with circulatory failure of central rather than peripheral origin. The cause of the central circulatory failure was traced to the rapid liberation of potassium from erythrocytes in the heated cutaneous and subcutaneous tissues, with consequent damaging effects on the heart of the liberated potassium. Figure 18 shows results of 71 individual pig exposures. For 49 pigs, 90% of

Carbon monoxide and human lethality

44

their cutaneous surface was exposed to heat. For 22 pigs, hot air was breathed as well, or larger animals were used, or animals were anesthetized after rather than before exposure. No significant differences were observed so all data were included on one chart.

FIGURE 18. Effect of Time Elevated Temperature on Injury to Pigs.86 The upper limits of exposures in which pigs survived without either cutaneous burning or total systemic hyperthermia are indicated by the first line (I). Exposures lying below this line failed to cause lasting effects. Exposures lying between the first and second lines resulted in mild or localized burning. The second line (II) represents the approximate threshold at which generalized hyperemic burning occurred. The third line III represents the threshold at which the burned skin and subcutaneous tissue underwent coagulation. The skin of most pigs that received exposures above this threshold was pale and the loss

Effects of carbon monoxide in man

45

of elasticity of the coagulated superficial tissues resulted in the formation of deep fissures when the extremities were flexed. The uppermost curve (IV) represents the approximate threshold at which rapidly fatal systemic hyperthermia occurred. Most pigs receiving exposures in excess of this threshold died within a few minutes after the oven had been lifted from their exposure platform, usually within 15 minutes.87 The most constant postmortem finding in animals that died of hyperthermic shock within thirty minutes of the exposure was the presence of hemorrhages throughout the internal viscera. These were seen most frequently and prominently beneath the endocardium of the right and left ventricle.87 It is interesting to note that pigs showed little pulmonary edema even on exposure to very hot gases. Dogs and goats, however, on similar exposure showed moderate to severe pulmonary edema which was a result of circulatory failure.87 In the tests with pigs, all pigs that died during the early post exposure period had rectal or heart’s blood temperatures of 42.5°C or higher. No pig whose rectal temperature rose above 44°C survived more than a few minutes. Eleven of fifteen animals with rectal temperatures 43–44°C died and four of thirteen animals with rectal temperatures 42– 43°C died.89–90 Cardiac dysfunction and edema have been noted in heat stroke patients whose body temperatures have reached 40°C.91 Work with monkeys has noted damage to intestine walls when core temperatures reach 40°C releasing a bacterial lipopolysaccharide (LPS) into the portal vein. That LPS not removed in the liver enters the systemic circulation causing vascular collapse, shock, and death.92–93 Morris, et al., have demonstrated bacterial translocation in studies of sheep exposed to smoke from cotton toweling and to thermal injury or to thermal injury alone. This was observed not only in the mesenteric lymph nodes but in liver and lung for thermal injury and liver, spleen, kidney, and lung for thermal injury plus smoke. This lends support to the theory that systemic infections may arise from the translocation of organisms across the wall of the intestine. Animals were sacrificed at 48 hours. Bacteremia combined with damage that occurs to the immune system in the shocked, traumatized patient would set the stage for multi-organ failure.94–95 Pain from the application of heat to the skin occurs when the skin temperature at the depth of 0.1 mm reaches 44.8°C. Human exposures at temperatures between 160° and 200°C result rapidly in intolerable pain. Figure 19 summarizes physiological effects of elevated temperatures. Exposures to fire gases at temperatures of 300 to 400°C would cause unbearable pain in less than 7 seconds, with collapse after taking a few steps.89 Heat can interact in combination with carbon monoxide. The combined effects of heat and carbon monoxide have been assessed in mice and rats.96 In mice the 1 hr LC50 was 2524 mg/m3 at 25°C and 836 mg/m3 at 36°C. Survival times at 25°C and 36°C were as follows:

Carbon monoxide and human lethality

46

FIGURE 19. Physiological Effects of Elevated Temperatures.88 CO Concentration (ppm)

Survival Time 25°C

(min) at 36°C

634

–

94

1005

–

40

1595

120

25

Effects of carbon monoxide in man

47

2525

51

8

4000

24

6

For rats, purebred males, weighing 170–220 g were subjected in groups of 16 animals to 600 ppm CO for 1 hr each day for 23 consecutive days. Data were as follows:

Blood COHb Concentration (X±SE) in Subacute Toxicity Experiment (%) Time Before Experiment

Group A (35°C+CO)

Group C (25°C+CO)

0.52±0.06

3.00±1.60

6.50±1.10 8.50±3.20 25.00±5.80 39.00±4.85 46.5±3.20

6.60±1.22 14.50±3.40 25.50±5.00 27.00±3.60 31.50±4.00

5 min 10 min 20 min 40 min 60 min

40.00±1.80 29.50±2.80 27.50±4.00 11.00+2.50 5.50±0.80

21.00±3.65 23.00±1.92 11.50±4.05 5.50±3.00 2.00±0.75

Before Experiment

0.27±0.06

0.72±0.08

42.67+2.10 31.58±2.16 23.31±2.56 22.75±1.38

30.92±1.99 26.92±2.92 22.42±1.85 22.32±2.10

During Experiment 5 min 10 min 20 min 40 min 60 min After Experiment

After Experiment Day 1 Day 7 Day 17 Day 23

Control animals were kept at each temperature. The animals exposed to CO at 36°C built CO to a higher level initially, but by the 23rd day both groups were equivalent. Hemoglobin increased significantly in rats exposed to heat and CO over the 23 day period, as animals built tolerance to the exposure conditions. The animals initially exposed to 36°C and CO showed a 2.5°C higher rectal temperature than controls at 36°C. By day 23 this had declined to 0.8°C. It is known though that rodents are particularly sensitive to temperature.96 Carboxyhemoglobin is not elevated in all fire victims. Flash fire victims die from thermal trauma, without elevation of blood carboxyhemoglobin or with COHb values at a low level if some smoke has been inhaled prior to a victim’s being engulfed in the flash fire.68,97–99 Fires can produce atmospheres low in oxygen and high in carbon dioxide. Approximate tolerance times for man for each are shown below:

Carbon monoxide and human lethality

48

Tolerance Times for Exposure to Reduced Oxygen Atmospheres Length of Exposure

Oxygen Limit %

5 min

9

30 min

11

2 hr

14

4–8 hr

15

24–72 hr

16

14 days

17

Tolerance Times for Exposure to Carbon Dioxide Length of Exposure

Carbon Dioxide Limit (In Air) %

5 min

5.0

30 min

4.0

2 hr

3.5

4–8 hr

3.2

24–72 hr

2.0

14 days

1.5

With low oxygen the respiration rate increases, then becomes irregular and compulsive, followed by collapse (Figure 20). Carbon dioxide induces asphyxia through exclusion of oxygen. In initial stages the respiration rate increases. CO2 at 3% doubles lung ventilation. The limit of CO2 tolerance is 10%, with unconsciousness in 10 minutes.89 Studies with rats show that low oxygen (14%) and elevated CO2 (to 5.4%) decrease the mean survival time but do not change the final COHb at death.59,100 In a crucial series of experiments goats were chosen for study because their body surface area to body weight ratio is nearly identical to man. Goats were exposed to inhalation of 3 percent oxygen, 2.7 percent carbon monoxide, and 3.0 percent oxygen plus 2.7 percent carbon monoxide plus 7.0 percent carbon dioxide. In some experiments body temperatures of subjects were raised to between 42.5 and 43.6°C (rectal). Carbon monoxide in conjunction with low oxygen showed a shortened time to death. The addition of CO2 slightly accelerated time to death. Increased temperature markedly increased the susceptibility of goats to anoxia and hastened the time of death from exposure to all gas mixtures studied. Most importantly, death of animals at elevated temperatures occurred at markedly decreased COHb levels, a result not seen with low oxygen plus carbon monoxide alone. Data are shown below:101 Number of Respiration Ceased Last Gasp %COHb at 5 Animals (@ min) (@ min) min. 2.7% CO/in air

5

3.0

7.2

86

Effects of carbon monoxide in man

49

2.7% CO/3.0% O2/in N2

9

1.9

4.8

90

3% 02

3

4.6

6.9

–

2.7% CO/3.0 % O2/7.0% CO2 in N2

5

1.3

4.1

91

4.2% O2/in N2/heat

4

2.1

3.7

–

2.7% CO/in air/heat

3

2.5

4.4

79

2.7% CO/3.0% O2/in N2/heat

8

1.3

2.9

38

2.7% CO3.0% 02/7.0% CO2 in N2/heat

2

1.1

2.8

49

A variety of factors can complicate human response to carbon monoxide poisoning. Physical activity of the victim, while hard to assess, also plays a role. It is known that in a healthy individual, severe toxic signs including collapse can occur at COHb levels of 30– 40 percent. An active individual would be severely affected at 25–30 percent, and with light physical activity, incapacitation at 27–37 percent. This is in addition to more rapid uptake of CO for an active individual. Also in fire, once victim knockdown occurs, high CO2 levels or oxygen depletion can play a role in time to death.64 Indeed, studies in monkeys show that the slow, insidious onset of CO intoxication may result in a victim being unaware of the predicament until he suddenly reaches the catastrophic stage where normal body functions can no longer be maintained, and the victim passes rapidly into a state of severe incapacitation and semiconsciousness. Whether or not such severe incapacitation occurs will depend upon the amount of CO inhaled and upon how active the victim is. Thus with animals sitting in chairs, it was noticed that when they were very quiet and relaxed they tended to reach the end of the exposure (30 minutes) with only minor signs of incapacitation, while if they were active, especially towards the end of an exposure, they were likely to pass into a state of semiconsciousness. In work where monkeys were placed in a chamber where they were active and free to move about, and trained to perform a behavioral task involving a certain amount of exercise and the application of psychomotor skills, the animals were found to be severely intoxicated after a 30 minute exposure to 1000 ppm CO with COHb levels of approximately 30 percent, while 40 percent COHb levels were normally necessary to produce severe intoxication in the chairbound animals.102

Carbon monoxide and human lethality

50

FIGURE 20. Effects of Reduced Oxygen Atmospheres. 89 2.8 EFFECTS OF DISEASE OR DRUGS As has been shown in earlier sections, diseases are clearly a factor in susceptibility to carbon monoxide. It is logical that individuals suffering from systemic hypoxemia (e.g., as in anemia, cardiopulmonary disease, congestive failure) or increased oxygen demand (e.g., thyrotoxicosis, fever) might suffer acceleration or aggravation of these pathologic processes under circumstances where carboxyhemoglobin might decrease their blood oxygen content or availability.103

Effects of carbon monoxide in man

51

Indeed groups at special risk include pregnant women, fetuses and young infants, the elderly, individuals with obstructed coronary arteries, individuals with congestive heart disease, individuals with peripheral vascular or cerebrovascular disease, individuals with anemia, individuals with genetically unusual forms of hemoglobin, individuals with chronic obstructive lung disease, individuals using CNS depressant drugs, and individuals newly at high altitude. Effects of cardiovascular disease on carbon monoxide poisoning have been discussed by Stewart.104 The acute effects of CO on myocardial function in healthy adults, in patients with coronary artery heart disease and in patients with non-coronary heart disease have been examined. A rapidly increasing COHb saturation to around 9 percent over 30–120 seconds in patients with no evidence of coronary heart disease results in increased coronary blood flow, increased oxygen extraction ratio by the myocardium and an insignificant decrease in coronary sinus oxygen tension. In patients with coronary heart disease the rapid increase in COHb did not result in a significant increase in coronary blood flow; but the oxygen extraction ratio by the myocardium was increased, the coronary sinus tension decreased significantly, and a significant decrease in the lactate extraction ratio and the pyruvate extraction ratio were observed. Thus a potentially serious state could result from the inhalation of CO by the patient with advanced coronary heart disease incapable of responding to the anoxic stress by increasing coronary blood flow.104 Investigators have demonstrated that in patients with advanced coronary artery disease, angina pectoris exercise tolerance is significantly decreased following exposure to low concentrations of CO sufficient to increase their COHb to 5 percent.104 Stewart carried the interpretation of these data one step further than did the original investigators by suggesting that there is no level of COHb which does not exert a significant effect upon a diseased cardiovascular system. Individuals with coronary heart disease will be stressed to some degree by any exposure sufficient to cause an increase in the COHb level. It is not possible therefore to set a “no effect” level of CO for such individuals.104 Stewart has provided a norm for healthy human response to various concentrations of COHb as follows.104

Human response to various concentrations of COHb Blood saturation % COHb

Response of healthy adult

0.3–0.7

Normal range due to endogenous CO production

1–5

Increase in blood flow to vital organs to compensate for the reduction in oxygen of the blood.

Blood saturation Response of healthy adult % COHb 2–9

Response of patient with severe heart disease

Heart patient may lack sufficient cardiac reserve to compensate for loss of the oxygen carrying capacity of the blood.

Response of patient with severe heart disease

Exercise tolerance reduced: Visual Less exertion required to induce chest

Carbon monoxide and human lethality

light threshold increased

52

pain in patients with angina pectoris

16–20

Headache; visual evoked response May be lethal for patients with severely abnormal compromised cardiac function

20–30

Throbbing headache, nausea; fine manual dexterity abnormal

30–40

Severe headache; nausea and vomiting; cyncope

–50–

Coma, convulsions

67–70

Lethal if not treated

Discussions in this report have already shown the approximate nature of such norms. A particularly interesting study is that of a survey of all deaths that were certified by the Cuyahoga County Ohio Coroner’s Office from the years 1958 through 1980, wherein asphyxia by carbon monoxide was the primary cause of death and a natural disease was the “other” diagnosis or vice versa. For the purposes of the study, the primary cause of death was defined as the disease or injury responsible for initiating the train of events, brief or prolonged, which produced the fatal end result. The “other” condition was that condition or conditions contributing to death but not related to the primary cause of death. The Cuyahoga County Coroner’s Office serves Cleveland, OH and its suburbs.105 During this 23-year period the Cuyahoga County Coroner’s Office certified 38 such deaths. These were divided into two groups. Group 1 consisted of 28 cases where all diagnosis including the levels of carboxyhemoglobin were documented by complete postmortem examination. All major coronary arteries were studied in detail to determine the severity (mild, moderate, and severe) and extent (focal or diffuse) of the atherosclerotic process, by cross-sectioning these arteries at about 2- to 5-mm intervals. A gross examination estimate of percentage occlusion was thus made. The myocardium was sliced at about 1-cm intervals to look for areas of acute or chronic myocardial infarction. Microscopic sections of the coronary arteries and myocardium were examined in all of these cases. The left coronary artery with its anterior descending and circumflex branches and the right coronary artery with its posterior descending branch were considered major coronary arteries for the purposed of this study. Group 2 consisted of ten cases where the diagnosis of the “other” condition was based on review of medical records, including results of coronary angiogram, serum enzymes, and clinical history. Autopsy was not performed on these ten cases. In all cases, hospital charts, office records of private physicians, and eyewitness accounts were reviewed.105 In cases where death occurred immediately following exposure, chemical tests were performed to determine the level of carboxyhemoglobin. In instances where death occurred several days following exposure to carbon monoxide, such tests were not carried out. Blood levels of ethyl alcohol were measured in all cases. Blood levels of drugs were measured in twelve cases belonging to Group 1 and in five cases belonging to Group 2.105 For a control group all deaths that were reported to the Cuyahoga County Coroner’s Office during the years 1958 through 1980 in individuals 35 to 86 years of age in whom the carboxyhemoglobin was 60 percent and more were reviewed. A complete autopsy had been performed in each of these cases. The coronary arteries and the hearts were

Effects of carbon monoxide in man

53

examined adhering to the techniques that are outlined for the examination of cases in Group 1. There was a total of 100 cases in the control group.105 The following is a summary of results:105

Summary of Victim Data Age

Carboxy hemoglobin %

Ethyl Alcohol Drugs 30 41 51 61 71 81 Sex Race 10 40 60 De Not Not to to to to to to M F W B to to and layed Pre Ab Tes Pre Ab Tes Total 40 50 60 70 80 90 30 50 More Death sent sent ted sent sent ted Group 1 1 28 Group 2 0 10 Control 22 100

7 10 5 4 17 11 24 4 14

4

0

10

2 4 2 2 9 1 7 3 5

3

0

2

28 10 6 3 59 41 68 32 0

0

100

0

5 23

0

2 10

16

2

8

0

0

5

5

48 52

0

9 72

19

Findings related to heart Number of Cases Heart Weight, g Coronary Atherosclerosis

Myocardial Infarct

Mild Moderate Severe

Recent

415 415 and Old More

History of Exertion Less Yes No Total

Group 1

2

2

24

1

4

20

8

2

26

28

Group 2

–

–

5

0

1

–

–

–

10

10

Control

89

5

6

0

2

13

87

0 100

100

*

Note: Diseased hearts tend to increase in weight.

These data show clearly that severe atherosclerosis is often present in fire victims with low COHb values.105 It should be noted from the Maryland study, however, that findings of coronary atherosclerosis do not necessarily reflect a low COHb case. The role of alcohol is interesting. Two studies, one on rats and one of humans, suggest that alcohol may be an antagonist to CO poisoning. In studies of rats, Hume concluded that if alcohol is present in sufficient quantity to produce a central nervous system depression, the survival time is longer. The depressant effect of alcohol decreases animal activity and thus the rate of CO uptake.106 In a study of records in the UK for 1976–81, carbon monoxide deaths were studied. Deaths were classified by zero blood alcohol, less than .150% and greater than .150 %.

Carbon monoxide and human lethality

54

The overall mean was .148%. The effect of alcohol was found to be an increase in the COHb percentage at which a given proportion of deaths occurred. For example, 50% of deaths occurred with a COHb concentration of 68% or less without alcohol, but with alcohol less than .150%, only 30% of deaths occurred with 68% COHb or less. Alcohol between .05 and .2% appeared to increase survival. The author speculates that other depressant drugs should have a similar effect.107 These data contrast with time to incapacitation results in rats exposed to 1947 ppm CO at levels of 1.2g/kg, 0.6g/kg and nil alcohol. The presence of alcohol shortened times to incapacitation.108 These latter observations perhaps correlate with those of Barillo and coworkers on a group of 39 fire victims in which victims found in bed had a mean blood alcohol level of .268% compared with a mean level of .88% for those victims found near an exit.109 A study of alcohol-CO interactions on driving performance has shown that alcohol and CO effects are additive and at 12% COHb the combined effects were greater than the sum of the effects of CO and alcohol alone.110 Animal studies also show that behavior can be affected by alcohol plus CO exposures.111–112 The direct role of other drugs in carbon monoxide poisoning in man remains unclear. In one animal study mice were pretreated with phenobarbital, chlorpromazine, or alcohol prior to exposure to 1900 ppm carbon monoxide (CO) or 7.5 percent oxygen O2 environments. Pretreatment for one hour with chlorpromazine or ethanol increased the lethality of mice exposed to both CO and 7.5 percent O2, while one-hour phenobarbital pretreatment had no effect on CO lethality but increased 7.5 percent O2 lethality. Slightly lowered carboxyhemoglobin concentrations (55 percent versus 63 percent) were observed only with chlorpromazine. Unfortunately time to effect was not reported. Studies of red blood cell 2.3-diphosphoglycerate concentrations and rate of carboxyhemoglobin formation in vitro showed that the apparent affinity of hemoglobin for oxygen and CO remained unchanged following drug or alcohol pretreatments. The different effects of the pretreatments on CO and 7.5 percent O2 lethality and the lack of correlation of CO lethality withs carboxyhemoglobin concentrations suggests that there are other factors besides extracellular events directly associated with oxygenation of tissues which are critical determinants of the lethal potential of CO or 7.5 percent O2. Data for one hour pretreatment exposures are shown as follows:113

Effect of 1 hr. Pretreatments on Lethality Associated with Carbon Monoxide (CO) or 7.5% O2 Environments CO lethalitya Dead/Total

%COHb

7.5% O2 lethalityb Dead/Total

Saline

17/30

63±2.0

5/12

Phenobarbital 80 mg/kg, ip

19/32

67±2.1

11/12

Chlorpromazine 20 mg/kg, ip

29/32

55±0.2

11/11

Water

18/30

64±1.9

3/10

Ethanol

25/30

66±4.0

10/10

Pretreatment

Effects of carbon monoxide in man

55

7.5 g/kg, po Saline

22/30

61±1.8

–

Phenobarbital 160 mg/kg, ip

20/30

69±0.9

–

a

Exposed for 4 hr to 1900 ppm CO. Exposed for 4 hr to 7.5% O2

b

Interestingly, longer pretreatments (24 hr and 3 day) with phenobarbital, chlorpromazine, or ethanol showed no increased toxic effect. 2.9 TIME OF EXPOSURE The time of exposure to carbon monoxide is known to be important. That relationship is difficult to ascertain in after-the-fact studies of human victims. The relationship between conditions of exposure to carbon monoxide and biochemical effects has, however, been investigated in experiments on rats. The magnitude and the time of biochemical disturbances in the tissues resulting from two different exposures consisting of 1 Volume percent CO for 4 minutes and 0.4 Volume percent for 40 min. respectively were compared. In both cases, at the end of exposure the same level of blood carboxyhemoglobin (about 50%) was reached. The biochemical determinations in the blood (pH, glucose, lactate, pyruvate) and brain tissue (lactate, pyruvate) were carried out immediately after termination of the exposure and after periods of recovery. CO exposure resulted in a decreased blood pH, increased level of blood glucose, as well as that of lactate and pyruvate both in blood and brain tissue. These changes were much more pronounced following the “longer-lesser” exposure than after the “shorter-intense” one, although blood concentrations of COHb were the same. The observed phenomenon puts some light on the lack of the correlation between COHb level in blood and field severity of CO intoxication.114 Of course, that different individuals have different behavior to a toxic agent is hardly surprising. Japanese work is particularly interesting. A toxicological study of carbon monoxide was carried out with special consideration to eliminate the effect of carbon dioxide expired by animals in the atmosphere. When 0.6 percent carbon monoxide in air was inhaled, mice did not manifest any toxic symptoms. When a one percent carbon monoxide-air mixture was inhaled, about 30 percent of the exposed mice died from respiratory failure following a violent convulsion within the first 30 minutes. Another 30 percent were alive at the end of 3 hours’ observation, while the remainder died with an almost even death rate in the course of the observation time. At a concentration of 1.5 percent carbon monoxide all the mice were killed within 30 minutes. Thus, the minimum lethal concentration was around 1.0 percent, but a normal distribution curve was not obtained for the death rate of mice by the inhalation of this concentration of carbon monoxide. With over 1.5 percent carbon monoxide, nearly 75 percent of mice died within ten minutes as shown in Figure 21, but others were alive two or three times longer. There were very susceptible, comparatively tolerant and very tolerant mice relative to the development of respiratory failure. Attempts were made to test whether the variance in the susceptibility was due to an intrinsic nature of the

Carbon monoxide and human lethality

56

FIGURE 21. Distribution of the death rate of mice in 1.0% (A) and 1.5% (B) carbon monoxide poisoning. Each column represents each death rate at ten minute intervals within three hours of exposure. The number of mice used is given in parenthesis.115 individuals or not. Surviving mice were exposed again to 1.0 percent carbon monoxide four weeks after the first exposure. The same susceptibility could not be reproduced in each animal. Furthermore, when the same trials were repeated with the animals having tolerated over three hours in 1.0% carbon monoxide, the distribution of death rate was similar to that at the first exposure. Therefore, the variance in the tolerance does not appear to be due to differences in the intrinsic nature of animals but to more subtle factors.115 2.10 CONCLUSIONS Several statements can be made in conclusion. While carbon monoxide exposure is seldom in its ultra-pure state, human exposure to city gas and exhaust gas, however, shows that a significant percentage of exposed individuals die from carbon monoxide

Effects of carbon monoxide in man

57

poisoning at COHb levels thought by some to be less than “normal,” i.e., less than 50 percent COHb. Nearly 20 percent of individuals may die at such levels. While persons with cardiovascular and other diseases are included in that group, it also includes other individuals who do not exhibit identifiable pathology. Persons with identifiable pathology do not necessarily die below 50 percent COHb. The length of time of exposure to CO is important, as are the level of victim activity and the age and the physical condition of the victims. Why do very young children occasionally survive although they had been exposed to the same atmosphere as their dead parents? Clearly carbon monoxide poisoning is much more complex than the simple percentage of COHb in the blood of the victim. Therefore, without additional information, a COHb value of X percent (below 50 percent) does not allow a ready conclusion for a given victim. For identical exposures different individuals exhibit different symptoms and outcomes. In the case of fire exposures, twice the number of victims are in the less than 50 percent COHb category than for automobile exhaust victims. Fire victims, however, have very different age distribution and level of infirmity than do automobile exhaust victims. Yet despite the presence of different materials in the environment the fire fatality/COHb profiles in Japan in the early 1960s, in Denmark in the late 1960s and 1970s, in the United States in the late 1970s, and in the UK in the late 1970s are all very similar. Despite population and environmental differences, the role of carbon monoxide in fire deaths is the same. Carbon monoxide is the prime source of fire fatalities. In fire victims males predominate and alcohol is a key factor. Most victims have burns. Clearly exposure to heat and hot fire gases plays a role, difficult to evaluate, yet known to markedly lower COHb levels essential for death. Finally, the determination of COHb in the blood of victims has a variety of opportunities for error. Care must be exercised in COHb determinations as well as in interpretation of results.

ACKNOWLEDGEMENT The tables on pages 10 (9), 19 (16) and 72 (105) are Copyright ASTM and are reprinted by permission. Figure 11 is British Crown Copyright 1978 and is reprinted by permission. The permission of publishers for tables and graphs is acknowledged with appreciation.

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53. B.P.McNamara, “Estimate of the Toxicity of Hydrocyanic Acid Vapors in Man,” Edgewood Arsenal Technical Report, EB-TR 76023, August 1976, 25 pp. 54. G.E.Hartzell, W.G.Switzer and D.N.Priest, “Modeling of Toxicological Effects of Fire Gases: V. Mathematical Modeling of Intoxication of Rats by Combined Carbon Monoxide and Hydrogen Cyanide Atmospheres,” J. Fire Sciences, 3, 330–342 (1985). 55. T.Sakurai, “Toxic Gas Tests with Several Pure and Mixed Gases Using Mice,” J. Fire Sciences, 7, 22–77 (1985). 56. P.M.Smith, C.R.Crane, D.C.Sanders, J.K.Abbott and B.Endecott “Effects of Exposure to Carbon Monoxide and Hydrogen Cyanide,” Physiological and Toxico-logical Aspects of Combustion Products—International Symposium, National Academy of Sciences, Washington, D.C, 1976, pp. 75–88. 57. R.D.Lynch, “On the Non-Existence of Synergism Between Inhaled Hydrogen Cyanide and Carbon Monoxide,” Fire Research Station, Fire Research Note No. 1035 (May 1975). 58. Y.Tsuchiya, “On the Unproved Synergism of the Inhalation Toxicity of Fire Gases,” J. Fire Sciences, 4, 346–354 (1986). 59. B.C.Levin, M.Paabo, J.L.Gurman, and S.E.Harris, “Effects of Exposure to Single or Multiple Combinations of the Predominant Toxic Gases and Low Oxygen Atmospheres Produced in Fires,” Funaamental and Applied Toxicology, 9, 236–250 (1987); Toxicol., 47, 135–164 (1987). 60. J.C.Norris, S.J.Moore, and A.S.Hume, “Synergistic Lethality Induced by the Combination of Carbon Monoxide and Cyanide,” Toxicology, 40, 121–129 (1986). 61. L.C.DiPasquale and H.V.Davis, “The Acute Toxicity of Brief Exposures to Hydrogen Fluoride, Hydrogen Chloride, Nitrogen Dioxide, and Hydrogen Cyanide Singly and in Combination with Carbon Monoxide, Aerospace Medical Research Laboratory, Wright-Patterson Air Force Base, Ohio, December, 1971, AD-751 442, 13 pp. 62. E.A.Higgins, V.Fiorca, A.A.Thomas, and H.V.Davis, “Acute Toxicity of Brief Exposures to HF, HCl, NO2 and HCN with and without CO,” Fire Technology, 8, 120–130 (1972). FAA Report FAA-AM-71–41, July 1971. 63. B.R.Pitt, E.P.Radford, G.H.Gurtner, and R.J.Traystman, “Interaction of Carbon Monoxide and Cyanide on Cerebral Circulation and Metabolism,” Arch. Environ. Health, 34, 354–359 (1979). 64. D.A.Purser and W.D.Woolley, “Biological Studies of Combustion Atmospheres, J. Fire Sciences, 1, 118–144 (1983). 65. D.A.Purser, P.Grimshaw and K.R.Berrill, “Intoxication by Cyanide in Fires: A Study in Monkeys Using Acrylonitrile,” Archives of Environmental Health, 39, 394–399 (1984). 66. D.A.Purser and P.Grimshaw, “The Incapacitative Effects of Exposure to the Thermal Decomposition Products of Polyurethane Foams,” Fire and Materials, 8, 10–16, (1984). 67. R.J.Lokan, R.A.James and R.B.Dymock, “Apparent Post-Mortem Production of High Levels of Cyanide in Blood,” J. Forensic Science Soc., 27, 257–59 (1987). 68. B.C.Levin, P.R.Rechani, J.L.Gurman, F.Landron, H.M.Clark, M.F. Yoklavich, J.R.Rodriguez, L.Droz, F.M.de Cabrera, and S.Kaye, “Analysis of Carboxyhemoglobin and Cyanide in Blood from Victims of the Dupont Plaza Hotel Fire in Puerto Rico,” J. Forensic Sci., 35(1), 151–168 (1990). 69. B.Ballantyne, “The Forensic Diagnosis of Acute Cyanide Poisoning” in Forensic Toxicology, B.Ballantyne, Ed., John Wright and Sons, Ltd., Bristol, 1974, pp. 99–112. 70. B.Ballantyne, J.E.Bright, and P.Williams, “The Post-Mortem Rate of Transformation of Cyanide,” Forensic Sci., 3, 71–76 (1974). 71. B.Ballantyne, “In Vitro Production of Cyanide in Normal Human Blood and the Influence of Thiocyanate and Storage Temperature,” Clinical Tox., 11(2), 173–193 (1977). 72. B.A.Zikria, D.C.Budd, F.Floch, and J.M.Ferrer, “What is Clinical Smoke Poisoning?,” Ann. Sur., 1975, 151–156. 73. B.A.Zikria, J.M.Ferrer, and H.F.Floch, “The Chemical Factors Contributing to ‘Smoke Poisoning’,” Surgery, 71(5), 704–709, (1972). 74. B.A.Zikria, G.C.Weston, M.Chodoff, and J.M.Ferrer, “Smoke and Carbon Monoxide Poisoning in Fire Victims,” The Journal of Trauma, 12(8), 641–645 (1972).

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75. B.A.Zikria, et al., “A Clinical View of Smoke Poisoning,” Physicological and Toxicological Aspects of Combustion Products-International Symposium, National Academy of Sciences, (Washington, D.C., 1976) pp. 36–46. 76. W.G.Berl and B.M.Halpin, “Human Fatalities from Unwanted Fires,” Fire Journal, 1979, (Sept.) 105–123. 77. B.M.Halpin, E.P.Radford, R.Fisher, and Y.Caplan, “A Fire Fatality Study,” Fire Journal, 1975, (May) 11–13, 98–99. 78. E.P.Radford, B.Pitt, and B.Halpin, “Study of Fire Deaths in Maryland,” Physicological and Toxicological Aspects of Combustion Products-International Symposium, National Academy of Sciences, (Washington, D.C., 1976) pp. 26–35. 79. W.G.Berl, and B.M.Halpin, “Fire-Related Fatalities: An Analysis of Their Demography, Physical Origins, and Medical Courses,” Fire Standards and Safety, ASTM STP 614, A.F.Robertson, Ed., American Society for Testing and Materials, 1977, 26–54. 80. W.A.Harland and W.D.Wooley, Fire Fatality Study—University of Glasgow, Building Research Establishment Information Paper, 1P, 18/79, August 1979, 3 pp. 81. Cause of Death in Fire Victims, BRE News, 58, 8–9 (Winter, 1982). 82. R.A.Anderson, A.A.Watson, and W.A.Harland, “Fire Deaths in the Glasgow Area: 1 General Considerations and Pathology,” Med. Sci. Law, 21, 175–183 (1981). 83. R.A.Anderson, and W.A.Harland, “Fire Deaths in the Glasgow Area: 3 The Role of Hydrogen Cyanide,”Med. Sci. Law, 22, 35–40 (1982). 84. K.Buettner, “Effects of Extreme Heat on Man. Protection of Man Against Conflagration Heat,” J. Am. Med. Assn., 144(9), 732–738 (1952). 85. B.Dupont, “How Much Heat Can Firemen Endure?” Fire Engineering, Feb. 1960, pp 122–24, 173. 86. J.A.Zapp, “Fires, Toxicity, and Plastics,” Physiological and Toxicological Aspects of Combustion Products, International Symposium, National Academy of Sciences, Washington, D.C., 1976, pp. 58–74. 87. A.R.Moritz, F.C.Henriques, F.R.Dutra, and J.R.Weisiger, “Studies of Thermal Injury IV, Archives of Pathology, 43, 466–488 (1947). 88. The Committee on Fire Safety Aspects of Polymeric Materials, Vol. 3, Smoke and Toxicity, Publication NMAB 318–3, National Academy of Sciences, Washington, D.C., 1978, pp. 13–16. 89. A.J.Pryor and C.H.Yuill, “Mass Fire Life Hazard,” Report for the Office of Civil Defense, NTIS AD 642790, pp. 39–53 and 62–69. 90. P.J.Berenson and W.G.Robertson, “Temperature,” Chapter 3 in Bioastronautics Data Book, 2nd Ed., J.F.Parker, Jr. and V.R.West, Eds., NASA, Washington, D.C., 1973, pp. 65–148. 91. D.Zahger, A.Moses, and A.T.Weiss, “Evidence of Prolonged Myocardial Dysfunction in Heat Stroke”, Chest, 95, 1089–91 (1989). 92. P.Gathiram, M.Wells, D.Raidoo, J.Brock-Utne, and S.L.Gaffin, “Portal and Sytemic Arterial Plasma Lypopolysaccharide Concentrations in Heat-Stressed Primates.” Circ. Shock, 25, 223– 230 (1988). 93. S.L.Gaffin, “Heat Stroke, Cardiac Dysfunction, and Edema,” Chest, 97, 1503 (1990). 94. S.E.Morris, N.Navartnam, and D.N.Herndon, “A Comparison of Effects of Thermal Injury and Smoke Inhalation on Bacterial Translocation,” J. Trauma, 30, 639–645 (1990). 95. B.F.Rush, A.J.Sori, T.F.Murphy, S.Smith, J.J.Flanagan, and G.W. Machiedo, “Endotoxemia and Bactermia During Hemorrhagic Shock—A Link Between Trauma and Sepis,” Ann. Surg., 549–554, 1988. 96. L.Yang, W.Zhang, H-Z He, and G-G Zhang, “Experimental Studies on Combined Effects of High Temperature and Carbon Monoxide,” J. of Tongli Medical Univ., 8, 60–65 (1988). 97. 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(3), 317–320 (1977). 98. C.S.Hirsch and L.Adelson, “Absence of Carboxyhemoglobin in Flash Fire Victims,” J. Am. Med. Assn., 210(12), 2279–2280 (1969).

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99. W.G.Eckart, “The Medical, Legal and Forensic Aspect of Fires,” Am J. Forensic Med. Pathol, 2, 347–357 (1981). 100. F.L.Rodkey and H.A.Collison, “Effects of Oxygen and Carbon Dioxide on Carbon Monoxide Toxicity, J. Combustion Toxicology, 6, 208–212 (1979). 101. J.A.Zapp, The Toxicology of Fire, Medical Division Special Report No. 4, Chemical Corps, Army Chemical Center, Maryland, April 1951, 106 pp. 102. D.A.Purser and K.R.Berrill, “Effects of Carbon Monoxide on Behavior in Monkeys in Relation to Human Fire Hazard,” Arch. Environ. Health, 38(5), 308–315 (1983). 103. B.D.Dinman, “Pathophysiologic Determinants of Community Air Quality Standards for Carbon Monoxide,” J. Occupational Medicine, 10, 446–463 (1968). 104. R.D.Stewart, The Effects of Low Concentrations of Carbon Monoxide on Man, Scand. J. Respir. Dis., 91, 56–62 (1974). 105. E.K.Balraj, “Atherosclerotic Coronary Artery Disease and ‘Low’ Levels of Carboxyhemoglobin; Report of Fatalities and Discussion of Pathophysiologic Mechanisms of Death,” J. Forensic Sciences, 29(4), 1150–1159 (1984). 106. A.S.Hume, B.H.Douglas, and K.Harden, “Effect of Ethanol on Carbon Monoxide Poisoning,” IRCS Med. Sci., 4, 300 (1976). 107. L.S.King, “Effect of Ethanol in Fatal Carbon Monoxide Poisonings,” Human Toxicol., 2, 155– 157 (1983). 108. W.E.Fitzgerald, D.S.Mitchell, and S.C.Packham, “Effects of Ethanol on Two Measures of Behavioral Incapacitation of Rats Exposed to Carbon Monoxide,” J. Combustion Toxicology, 5, 64–74 (1978). 109. D.J.Barillo, B.F.Rush, Jr., R.Goode, R.L.Lin, A.Freda, E.J.Anderson, Jr., “Is Ethanol the Unknown Toxin in Smoke Inhalation Injury,” Am. Surg., 52, 641–645 (1986). 110. T.J.Rockwell and F.W.Weir, “The Interactive Effects of Carbon Monoxide and Alcohol on Driving Skills,” Ohio State University Research Foundation, Columbus, Ohio, 1975, NTIS PB242266. 111. D.S.Mitchell, S.C.Packham, and W.E.Fitzgerald, “Effects of Ethanol and Carbon Monoxide on Two Measures of Behavioral Incapacitation of Rats,” Proc. West. Pharmacol. Soc., 21, 427– 431 (1978). 112. J.S.Kinsely, D.C.Rees, R.L.Balster, “Effects of Carbon Monoxide in Combination with Behaviorally Active Drugs on Fixed Ratio Performance in the Mouse,” Neurotoxicol. Teratol., 11, 447–452 (1989). 113. J.W.Winston, J.M.Creighton, and R.J.Roberts, “Alteration of Carbon Monoxide and Hypoxic Hypoxia-Induced Lethality Following Phenobarbital, Chlorpromazine, or Alcohol Pretreatment,” Toxicology and Applied Pharmacology, 30, 458–465 (1977). 114. J.A.Sokal, “Lack of the Correlation Between Biochemical Effects on Rats and Blood Carboxyhemoglobin Concentrations in Various Conditions of Single Acute Exposure to Carbon Monoxide,” Archives of Toxicology, 34, 331–336 (1975). 115. M.Hirata, M.Hioki, and K.Hashimoto, “Distribution of Death Rate in Acute Carbon Monoxide Intoxication in Mice,” Tohoku J. Exp. Medicine, 97, 67–73 (1969).

Chapter 3 EFFECTS OF CARBON MONOXIDE IN MAN: LOW LEVELS OF CARBON MONOXIDE AND THEIR EFFECTS GORDON L.NELSON Florida Institute of Technology, College of Science and Liberal Arts, 150 West University Boulevard, Melbourne, FL, 32901–6988, USA ABSTRACT This report discusses the effects of carbon monoxide on health, and human mental and physical performance from both acute and chronic exposures. Smoking and environmental exposures are discussed, with specific examples given. Carbon monoxide is commonly present in our environment. Build-up and downloading from the body depend upon a variety of factors including gender, activity, and physical health. Worker exposures leading to upwards of 32% COHb have been reported. The level at which carbon monoxide exposures lead to reduced performance in human subjects remains a matter of controversy. Examples from representative literature are presented. COHb levels of 30% are escapable for healthy subjects, with 40% required for incapacitation, depending upon exercise level, but levels as low as 20% can lead to fatalities in impaired subjects. While performance degradation at as low as 4–5% COHb has been reported in man, on the whole, data suggest that healthy individuals can tolerate 10% COHb with heavy physical work with minimal decrement in physical or mental performance and perhaps up to 20% COHb at rest. However, infants, the elderly and individuals with cardiovascular disease, anemia, lung disease, and an increased metabolic rate are at greater risk from CO than the healthy subjects normally addressed. It is also important to note that CO poisoning is not always recognized, given vague, non-specific but persistent symptoms. Diagnosis of carbon monoxide poisoning may require astute examination. Misdiagnosis can return the victims and others to a contaminated evnironment.

3.1 GENERAL COMMENTS In the previous chapter discussion was given of the factors involved in carbon monoxide fatalities, both fire and non-fire exposures. Given that carbon monoxide is ubiquitous, a large body of work has been done to elucidate the effects on health and human mental

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64

and physical performance when man is subjected to non-fatal carbon monoxide exposures, both acute and chronic. At interest are *

Note: In every case, if no further details are given, the venue for the study is the United States. questions such as (a) does low CO exposure cause persons exposed in fire incidents to make decisions leading them to become victims, (b) does CO exposure in heavy traffic lead to accidents, (c) at what level does CO exposure cause serious performance deterioration, (d) is that performance deterioration assessable by COHb determination? The discussion is begun with an assessment of environmental exposure. 3.2 SMOKING AND CARBON MONOXIDE Sources of carbon monoxide are numerous, both natural and man-made.1–2 Carbon monoxide is always with us. Endogenous CO production in humans leads to COHb levels of 0.45 percent in adults and 0.30 to 0.35 percent in children under 10 years.3–4 In a study of blood donors from across the country average COHb values ranged from 3.2 to 6.2 percent for smokers and 1.2 to 2.0 percent for non-smokers. Data are provided below, showing effects of carbon monoxide from our urban environment:1

Median Carboxyhemoglobin (COHb) Saturation and 90% Range for Smokers and Nonsmokers

Location

Cigarette Smokers

No. of Nonsmokers

% of Nonsmokers With COHB Nonsmokers

>1.5%

Anchorage

4.7 (0.9–9.5)

1.5 (0.6–3.2)

152

56

Chicago

5.8 (2.0–9.9)

1.7 (1.0–3.2)

401

74

Denver

5.5 (2.0–9.8)

2.0 (0.9–3.7)

744

76

Detroit

5.6 (1.6–10.4)

1.6 (0.7–2.7)

1,172

42

Honolulu

4.9 (1.6–9.0)

1.4 (0.7–2.5)

503

39

Houston

3.2 (1.0–7.8)

1.2 (0.6–3.5)

240

30

Los Angeles

6.2 (2.0–10.3)

1.8 (1.0–3.0)

2,886

76

Miami

5.0 (1.2–9.7)

1.2 (0.4–3.0)

398

33

Milwaukee

4.2 (1.0–8.9)

1.2 (0.5–2.5)

2,720

26

New Orleans

5.5 (2.0–9.6)

1.6 (1.0–3.0)

159

59

New York

4.8 (1.2–9.1)

1.2 (0.6–2.5)

2,291

35

Phoenix

4.1 (0.9–8.7)

1.2 (0.5–2.5)

147

24

St. Louis

5.1 (1.7–9.2)

1.4 (0.9–2.1)

671

35

Low levels of carbon monoxide and their effects

65

Salt Lake City

5.1 (1.5–9.5)

1.2 (0.6–2.5)

544

27

San Francisco

5.4 (1.6–9.8)

1.5 (0.8–2.7)

660

61

Seattle

5.7 (1.7–9.6)

1.5 (0.8–2.7)

585

55

Vermont, New Hampshire

4.8 (1.4–9.0)

1.2 (0.8–2.1)

959

18

Washington, DC

4.9 (1.2–8.4)

1.2 (0.6–2.5)

850

35

It is found that CO exposed individuals show a larger hemoglobin mass than those lesser exposed, to compensate for the body’s anoxic stress.3 A comparison of smokers versus never smokers shows an increase in mean hemoglobin levels for smokers of 137+0.4g/1 versus 133±0.5g/1 for females and 156±0.4 to 152±0.5g/1 for men.5 Some non-smokers in urban situations can show COHb levels of 5 to 8 percent depending upon pollution and work environments. Tobacco smoke reaching the alveoli is approximately 200 ppm. Cigarette smoke contains high levels of CO, ca. 14mg per cigarette.6 Thus, rapid smoking can lead to COHb values of 10 percent. Coupled with occupational exposure, cigarette smoking cab drivers in New York City have shown up to 13 percent COHb.3 In a study of over 16,000 blood donors in Missouri/Illinois, smokers had a mean COHb saturation of 4.6 percent and non-smokers 0.9 percent. Smokers were 39 percent of the population; 43 percent of these had COHb values greater than 5 percent. There were 191 samples in excess of 10 percent with the highest being 18.2 percent. Thirty of the >10 percent samples came from the same site, people without apparent problem.7 A study was conducted in Finland of 21 smokers and 28 non-smokers. The smokers averaged 15 cigarettes per day. Seven tests were done in an unventilated room of 37.5m3. In each experiment three smokers and four non-smokers sat around a table for 90 minutes. Each smoker smoked a new cigarette every 15 minutes for a total of six during the test. The atmosphere in the room was approximately 30 ppm carbon monoxide at the end of the test. The room at the end of the test was very smokey with most subjects experiencing eye irritation. Smokers experienced an increase in COHb from 5.3 percent to 9.1 percent while the non-smokers showed an increase in COHb from 1.6 percent to 2.2 percent. While experimental conditions were identical for individuals, a great variation was seen individual by individual for CO uptake. One smoker showed an increase from 1.6 to 8.5 percent COHb over the 90 minutes while another showed 7.1 to 9.5 percent. Clearly smoking influences our indoor carbon monoxide environment and individual by individual experience is different.8 In another study of 19 smokers, this time in Britain, it was found that their initial COHb level in the mornings was 3.2 percent. Each cigarette caused a mean rise of 1.3 percent COHb. Levels fell between cigarettes with each subject establishing a mean COHb level which was then maintained. The half-life of CO unloading from the blood was 6.9 hours during sleeping and 3.1 hours during the day with normal activity. The half-life for women was 59 percent that of men. Nine subjects retired in the evening with mean COHb levels of 8 percent. One individual (male) had 11.8 percent, another 10 percent.9 The half-life of downloading of carbon monoxide is of some uncertainty, affected of course by a variety of factors. In one study of 39 separate experiments, the half-life of

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66

COHb in the blood was found to range from 128 to 409 minutes, with an average of 320 minutes. Variations in the half-life of COHb in blood did not appear to be related to the amount of COHb in the blood, to the duration of exposure, to the number of exposures, or to the concentration inhaled. Other workers have reported half-lives of 2 to 2½ hours.10–11 Activity of smokers as well as amount of tobacco used is important in determining the COHb levels found in smokers. One study of a group of 63 smokers was carried out to examine those who exercise versus those who do not. Subjects were aged 24–27 and of apparent good health. Backgrounds were similar. Thirty were joggers and thirty-three seldom exercised. All smoked nearly three packs of cigarettes per day. Sedentary persons averaged 8.5 percent COHb with 10.1 percent maximum and 7.5 percent minimum from blood taken at 9 am and 3 and 8 pm. Joggers showed an average value of 4.7 percent with a maximum and minimum of 5.8 percent and 3.9 percent respectively. Effects of exercise were explained by more rapid gas exchange, increased capillary movement and adaptive carboxyhemoglobin transport to and from muscular tissue.12 In a study of 50 subjects, the effects of inhaling or not inhaling cigars or cigarettes were studied. The group consisted of 16 current non-smokers, 24 cigarette inhalers and 10 cigar inhalers. Data are presented below:

Carboxyhemoglobin (COHb), Oxygen Saturation (SaO2), and Hemoglobin (Hb) Determinations COHb (%)

SaO2 (%)

Hb (%)

Non-smoking control Subjects (n=16)

1.0

96.7

11.4

Cigarette inhalers (n=24)

4.6

93.0

13.5

Cigar inhalers (n=10)

8.4

88.4

14.2

Cigar inhalers showed COHb levels of 8.4 percent and measured oxygen saturation of 88.4 percent, less than the minimum 90 percent considered by some as healthful. Cigar inhalers had considerably higher carbon monoxide exposure than cigarette smokers.13 In a follow-on study of 130 subjects, cigarette, cigar, and pipe smokers were examined. Secondary smokers are those who originally smoked cigarettes. It is interesting that primary cigar smokers (i.e., always cigar smokers) here showed COHb levels of 13.8 percent with oxygen saturation levels of 85.7 percent. Data are shown as follows:14

Carboxyhemoglobin Level and SaO2 in 130 Subjects Grouped by Smoking Habit Group

No. of Subjects

COHb Level (%)

SaO2 (%)

Nonsmokers

16

1.0

96.7

Cigarette inhalers

41

5.6

91.8

3

13.8

85.7

Primary cigar inhalers

Low levels of carbon monoxide and their effects

67

Secondary cigar inhalers

34

11.8

85.7

Primary cigar noninhalers

8

2.1

95.6

Secondary cigar noninhalers

4

1.9

96.4

Primary pipe inhalers

1

5.0

94.6

Secondary pipe inhalers

12

5.4

92.4

Primary pipe noninhalers

5

1.3

96.3

Secondary pipe noninhalers

6

2.5

96.3

Other studies of cigar and pipe smokers have shown similar results.15–16

FIGURE 1. Half-life of COHb in relation to alveolar ventilation rate. Adjustment has been made for the increase in transfer factor for CO with activity, taking a value from 30 ml min−1 mg−1 at rest to 50 ml min−1 mg−1 with strenuous exercise such as football. The energy expenditure for each activity is converted into alveolar ventilation rates using a 3.45 ml oxygen per calorie, a respiratory quotient of 0.8, and a mean alveolar CO2 concentration of 5.6%. It has been assumed that the inspired air contains no CO.17

Carbon monoxide and human lethality

68

A study of 9 cigarette smokers showed substantial variation in CO uptake depending upon number of cigarettes smoked, uptake per cigarette, and activity level. This is not unlike subjects exposed to CO in other circumstances. CO downloading is very dependent upon activity as shown in Figure 1.17 The equilibrium between CO in the atmosphere and in the bloodstream is heavily dependent on the time of exposure, activity level, level of smoking, and physical health of the individual. 3.3 ENVIRONMENTAL CARBON MONOXIDE The EPA standard is 9 ppm for 8 hours and 35 ppm for 1 hour. That standard is exceeded, however, in a variety of circumstances. A study was made of 38 parking garage attendants in 1967 in Dayton, Ohio. Air samples showed a range of 7 to 240 ppm with a mean of 59 ppm in 6 garages. Attendants were all male aged 18 to 50. Twenty of the 38 were smokers. Data are shown below:18

COHb and Hb of Exposed and Control Groups % of COHb Group No. Exposed

Range

Mean

Hb gm/100 cc Mean

38

15.8

8 am

0.4–6.9

2.4

5 pm

2.9–15.8

8.4

Controls

27

0.5–7.6

2.8

FIGURE 2A. Relationship of carboxyhemoglobin (COHb) level before and after shiftdue to methylene chloride (MeCl2) exposure of smokers and nonsmokers. (TWA=time-

15.0

Low levels of carbon monoxide and their effects

69

weighted average,—=before-shift values,——=after-shift values.25

FIGURE 2B. Relationship of alveolar carbon monoxide (COA) level before and after shift due to methylene chloride (MeCl2) exposure of smokers and nonsmokers. (TWA= timeweighted average,—=before-shift values,——=after-shift values).25 From a mean of 2.4 percent COHb on entering work the subjects, on leaving at 5 pm, had a mean of 8.4 percent COHb, with a high of 15.8 percent. Garage workers who had been employed 6 months to 16 years had 0.8 percent more hemoglobin than the control group. Unexpected exposures are possible. A study of one office building showed eight hour averages of 26 ppm carbon monoxide in basement offices with up to 50 ppm late in the afternoon. The adjacent parking garage showed 100–200 ppm in the late afternoon. Activation of inoperative ventilation fans in the garage was found to reduce exposure in the offices by better than 50 percent.19 A study in London showed that sidewalk exposure can range as high as 360 ppm for short periods. Average concentrations were about 25 ppm. Between the hours of 9 am and 8 pm concentrations measured exceeded 50 ppm with a peak of 100 ppm at 6 pm. The UK workers also studied firemen and those in confined spaces, 295 subjects. Of most interest was the 31.9 percent COHb shown by a rotary cultivator operator working in a closed greenhouse, apparently without effect.20 A study of the urban atmosphere in Toronto revealed street levels of 10–50 ppm carbon monoxide with excursions to 170 ppm. A check of underground garages found children playing in excess of 100 ppm. A reading 13 feet from a car which was being adjusted showed 700 ppm. Those who habitually work on busy city streets were viewed as likely to be exposed periodically to 100+ ppm.21 It should be noted that in the U.S. Federal emission control standards have resulted in a reduction in the carbon monoxide content of automobile exhaust, from 8.5% in 1968 to 0.05% in 1980. This has resulted in about a 45% reduction of carbon monoxide in the

Carbon monoxide and human lethality

70

environment due to automobile exhaust (given older cars still on the road and more automobiles overall).22 One interesting source of carbon monoxide exposure is methylene chloride (23–26). Methylene chloride is converted in the body to carbon monoxide. Occupational employee exposures of 500 ppm methylene chloride are possible. In smokers that concentration would yield a COHb of 13 percent and about 8 percent in non-smokers as shown in Figure 2. In a 1974 study 100 men in the blast furnace department of an integrated steel works were studied in the UK. Blast furnace workers showed an increase of 2.6 percent COHb versus 0.2 percent for office workers. Four blast furnace individuals of the 100 showed increases of 10 percent COHb or greater. 20 men showed increases of 5 percent or more at the end of the shift. No subject complained of symptoms.27 A study in Finland was made of foundry workers. Air sampling in iron foundries was done in problem areas, with 76 percent of the samples near cupolas, 72 percent of the samples near casing areas and 67% in breathing zones of casters in excess of the 50 ppm TLV. Mean values were 240 and 110 ppm respectively. Blood COHb samples were taken from 145 workers at six foundries. Data are shown in Figure 3.28 In Japan factory workers were studied. COHb values were assessed versus observed CO concentrations in the workplace as shown as follows:29 Group 1

2

3

4

No. Examined

47

39

45

23

No. of Persons COHb% 0–1

0

0

12

9

1–5

5

2

27

12

5–10

7

4

5

2

10–15

12

5

1

0

15–20

10

8

0

0

20–25

8

11

8

8

25–30

5

7

0

0

15.5

19.5

3.0

2.3

Over 30 Average COHb (%)

CO p.p.m. by vol. in air Work place of group 1 50–250 Work place of group 2 60–1370 Work place of group 3 10–20 The office of the factory 4 below 20 Out-of-doors 4 below 10

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71

FIGURE 3. Carboxyhemoglobin levels of carbon monoxide exposed iron foundry workers at the end of a work shift.28 While the investigator found a higher frequency of subjective symptoms in subjects exposed to carbon monoxide than in the controls, none of them felt ill. Despite COHb values to 30 percent, he reported that no grave cases of poisoning occurred. He observed that repeated and long term exposures to carbon monoxide had not caused disorders of the human health which might be diagnosed as “chronic poisoning of carbon monoxide” or even as “ill condition” by clinicians, and the workers thought themselves to be healthy without paying attention to complaints such as headache or forgetfulness.29

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An extensive Swedish study has been performed on workers in ironworks, mines, gasworks, and motor repair shops. Carbon monoxide levels were measured and medical history and data obtained. Ironworks and mines produced the highest values, with a few subjects showing 20+ percent COHb. There were no significant differences between the groups of exposed and unexposed workers who had, in pairs, the same type of shift work. This was true of the group with the greatest degree of exposure and of that with the least, and of the two groups taken together. There were no significant differences in performance tests between exposed workers on shift work and unexposed workers on the day shift.29 The Swedish workers held the view that the absence of significant differences in the results of the performance tests in the exposed and unexposed groups of workers was evidence that exposure to carbon monoxide to the degree and duration present in the study did not have a detrimental effect on the variables measured by the tests used, or that such effects are at least insignificant. In the Swedish studies median COHb at work was approximately five to six percent. A scrutiny of Swedish National Health Insurance records for a period of ten years revealed no differences in the frequency of illness between the groups.29 In a study of fatal motor vehicle accidents, of 44 accidents studied, 13 had COHb values in excess of 10 percent with six showing blood alcohol in excess of 0.15 percent.30 In other work COHb concentrations of 10 to 28 percent in 23 percent of drivers who died in accidents in Dade County, Florida were reported. Twenty-seven victims (15.7 percent) had COHb concentrations of 10 to 20 percent, and 13 (7.6 percent) had concentrations of 20 to 28 percent. However, only nine of 423 victims in a California study had COHb concentrations of 10 to 15 percent. The pattern of alcohol plus carbon monoxide is interesting in its similarity to fire victims.30 Commuters are one group of the population who face daily carbon monoxide exposure. One study looked at commuters in the metropolitan Washington, D.C., area in the winter of 1983. Fifteen routes were chosen involving automobile, bus and rail. Sampling involved a total of 266 trips. Automobile travelers were exposed to means of 9–14 ppm with one evening route to 22 ppm. Trips took 40–70 minutes. Bus commuters were exposed to 4–8 ppm with one morning route at 10 ppm. Trips took 80–115 minutes. Rail commuters were exposed to means of only 2–5 ppm on trips of 27–48 minutes. These values contrast with ambient fixed site readings during the commuting hours of 1.8–3.1 ppm in the Washington area.31 Monitoring at city sites in El Paso, Texas, showed similar values to the Washington, D.C., study. Based on hourly averages for each month, high concentrations were at 7 am and 5 pm, with the highest hourly average being 13 ppm.32 The most comprehensive report of exposure to carbon monoxide is a study of disease mortality among bridge and tunnel officers in metropolitan New York City.33 The study population consisted of all male bridge and tunnel officers employed between January 1, 1952 and February 10, 1981, at one of nine major water crossings (two tunnels and seven bridges) operated by the Triborough Bridge and Tunnel Authority of New York City. Data available from personnel records contained name, Social Security number, sex, date of birth, date of hire, date of separation, and specific work history information identifying the bridge(s) or tunnel(s) at which the officers had worked. Information on race was obtained from the Social Security Administration. The primary duties of the bridge and tunnel officers included toll collections from booths, traffic observation within and outside the tunnels, and direction of traffic within the

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tunnels and on the bridges when necessary (i.e., during rush hours or motor vehicle accidents).33 Continuous monitoring of carbon monoxide levels within the tunnels began in 1940 at the Queens Midtown Tunnel and in 1950 at the Brooklyn-Battery Tunnel. Measurements showed peak concentrations exceeding 400 ppm. In 1961, an investigation demonstrated 24-hour average carbon monoxide levels inside the tunnels of 53 ppm in the summer (with peaks of 200–300 ppm) and 49 ppm in the winter (with peaks of 100–200 ppm). In 1968, 24-hour average carbon monoxide concentrations measured inside the tunnels were 35–40 ppm. Carbon monoxide exposures measured during rush hour traffic were found to range from 120–165 ppm in the morning and 65–145 in the evening in the tunnel toll booths, and 15–45 ppm in the morning and 12–22 ppm in the evening in the bridge toll booths. During the same year, fresh-air ventilation systems were installed in all toll booths. In 1971, an increase in electrical service to the ventilation fans in the tunnels yielded an increase of approximately 15 per cent in tunnel ventilation capacity. Starting in 1971, officers were allowed one half-hour “air-break” for each day’s work, which consisted of two two-hour tours inside the tunnel. In 1977, ventilation equipment for the tunnels was linked electrically to continuously reading carbon monoxide monitors. In 1981, sampling found mean area levels of carbon monoxide of 38.3 ppm inside the tunnels and 23.0 ppm outside the bridge toll booths. Peak carbon monoxide levels measured in the traffic lanes of both the tunnels and the bridges and on the tunnel catwalks were frequently greater than 100 ppm and occasionally greater than 400 ppm. Exposure to contaminants for tunnel and bridge officers were 0.3 and 0.1 ppm for nitrogen dioxide, 0.07 and 0.02 mg/m3 for polycyclic aromatic hydrocarbons, 0.005 and 0.004 mg/m3 for lead, and 0.06 and 0.02 fibers/cm3 for asbestos.33 Carboxyhemoglobin levels measured in 1970 (before ventilation systems were installed in the toll booths) averaged 2.12 and 3.90% in nonsmokers and smokers, respectively, for bridge officers and 2.93 and 5.01% in nonsmokers and smokers, respectively, for tunnel officers. Post-shift carboxyhemoglobin levels measured in 1981 were not found to be significantly different between bridge (4.9% carboxyhemoglobin) and tunnel officers (4.5% carboxyhemoglobin), with pre- vs post-shift carboxyhemoglobin levels rising about 20 percent in nonsmokers and 10 percent in smokers.33 The status of each officer was ascertained as of December 31, 1982. For deceased officers, death certificates were obtained from the appropriate state vital statistics offices. Death rates for New York City were obtained for the years 1950–1984. The mortality experience of those officers employed only in tunnels and of those employed only on bridges was examined separately, because previous environmental sampling had indicated that carbon monoxide levels had been substantially higher within and around the tunnels than on the bridges. Because environmental sampling results for carbon monoxide were only available for a few years of the study, duration of employment was used for cumulative exposures. Two categories, less than 10 years and greater than or equal to 10 years employment, were used to ascertain effects from cumulative long-term vehicular exhaust exposures. For cancers only, an additional analysis by latency was performed.33 There were 4,317 bridge officers and 1,212 tunnel officers employed between January 1, 1952 and February 10, 1981, by the Triborough Bridge and Tunnel Authority. There were a total of 103,900 person-years at risk. As of December 31, 1982, 88 percent of the officers were alive, 9 percent were deceased, and 3 percent were lost to follow-up. Death

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certificates were obtained for 97 percent (460 out of 474) of all known deaths. The percentage of tunnel officers who died (13 percent) was almost twice that of bridge officers (7 percent). On average, the bridge officers and tunnel officers were very similar in racial composition and calendar year of birth. On average, the tunnel officers had worked for five years at the Triborough Bridge and Tunnel Authority, while the bridge officers had worked there for only three years. Mortality data are shown in Table 1.

Table 1 Mortality (1952–1982), by duration of employment, among male bridge and tunnel officers, Triborough Bridge and Tunnel Authority, New York City133 Duration (years) of Employment Cause of Death

<10 Obs

Exp

>10 SMR

Obs

Exp

Total SMR

Obs

Exp

SMR

Bridge Officers All heart disease

78

96

0.82

30

33

0.91

108

129

0.84

ASHD

66

76

0.87

23

28

0.81

89

104

0.85

Lung Cancer

13

16

0.83

5

6

0.91

18

21

0.85

All other causes

154

223

0.69

34

37

0.93

188

259

0.73

All causes

245

334

0.73

69

75

0.92

314

409

0.76

Tunnel Officers All heart disease

35

36

0.98

32

19

1.722

67

54

1.243

ASHD

31

29

1.07

30

16

1.882

61

45

1.353

5

6

0.83

4

3

1.29

9

9

0.97

69

63

1.01

15

21

0.72

84

89

0.94

109

110

0.99

51

43

1.20

160

153

1.04

Lung cancer All other causes All causes

1 ASHD, arteriosclerotic heart disease; Obs, observed number of deaths; Exp, expected number of deaths; SMR, standardized mortality ratio (Obs\Exp). Expected number of deaths are based on the death rates for New York City rounded to the nearest whole number. 2 Significantly different from 1.00 (p<0.01). 3 Significantly different from 1.00 (p<0.05).

In the 31-year period between January 1, 1952, and December 31, 1982, the overall mortality among bridge officers was less than expected—314 deaths observed versus 409 expected (standardized mortality ratio (SMR)=0.76)—when compared with the mortality experience of the New York City population. The overall mortality among tunnel officers was approximately equal to that expected—160 deaths observed compared with 153 expected (SMR=1.04). Heart disease mortality among tunnel officers was the only cause

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of death that was statistically significantly elevated among bridge and tunnel officers. There were 67 deaths among tunnel officers from heart disease compared with 54 expected, an excess of 24 percent. This excess was more pronounced among tunnel officers for deaths due to arteriosclerotic heart disease—61 deaths observed compared with 45 expected, a 35 percent increase. The mortality from arteriosclerotic heart disease increased to 88 percent over that expected among tunnel officers employed for more than 10 years by the Triborough Bridge and Tunnel Authority (30 deaths observed compared with 16 expected).33 To investigate the effect of lowering of carbon monoxide exposure which began after 1970 with the addition of fresh air ventilation in all tunnel booths along with an increase in tunnel ventilation, trends in arteriosclerotic heart disease mortality after that time were modeled. A significant decrease in relative risk of arteriosclerotic heart disease mortality was found. The risk of arteriosclerotic heart disease in tunnel officers was modeled as an exponential decline of 6.4 percent per year after 1970 when compared with the lessexposed bridge officers.33 The results suggest that exposure to carbon monoxide may be an important factor in arteriosclerotic heart disease mortality. Analysis of the data suggests that two factors contribute to produce the elevated risk of heart disease: the high levels of exposure to carbon monoxide experienced by the tunnel officers, and movement into a critical higher age group.33 The authors noted that the absence of any significant relation between duration of employment and arteriosclerotic heart disease mortality tends to discredit the contribution of long term exposure. Age is an essential contributing factor in the excess risk of arteriosclerotic heart disease. The adverse effects of carbon monoxide poisoning on the risk of arteriosclerotic heart disease mortality seem to be reversible upon cessation of exposure.33 A Swedish study of bus garage workers in a much smaller study showed similar results.34 Cynomolgus monkeys have been exposed to 200 to 400 ppm CO for 10 alternate half hours daily for approximately 12 months. Histological and biochemical studies (aortic cholesterol content, arterial cholesterol influx, aortic oxygen consumption, as well as plasma triglyceride concentrations and HDL cholesterol to total-cholesterol ratios) did not suggest any association between periodic carbon monoxide exposure and the development of atherosclerosis (35). Advanced age as well as CO exposures were required. A Finnish study followed 1711 men aged 40–59 in 1959 for 15 years, and found that COHb levels (or smoking history) were similarly associated with a prevalence of atherosclerotic disease as well as with coronary heart disease or myocardial infarction.36 3.4 THOSE EXPOSED TO FIRE GASES Occupational exposures can lead to exposures resulting in COHb values of 25 plus percent, apparently without significant overt symptoms but with potential for long term effects. Fire, both for victims as well as fire fighters, is a less controlled environment, taking individuals to full endurance. Fire exposure is thus worth examining separately. A Yale study has reported data on 16 fire fighters before and after building fire exposure, with and without the use of self-contained breathing apparatus. Their results are as follows:37

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Blood carboxyhemoglobin levels in 16 fire fighters before and after building fires with and without the self-contained air breathing apparatus.37 Without Breathing Apparatus Fire Fighter NonSmokers [6]

Baseline COHb%

With Breathing Apparatus

After the fire Fire COHb% Fighter

Baseline COHb%

After the Fire COHb%

(1)

1.93

3.40

(9)

2.63

3.70

(2)

1.40

3.0

(10)

2.68

3.63

(3)

2.0

13.20

(11)

2.0

4.80

(4)

4.23

8.27

(12)

5.0

5.87

(5)

6.0

8.40

(13)

4.80

7.20a

(6)

4.47

7.83

(14)

6.13

7.93a

(7)

5.10

9.27a

(15)

2.25

2.53

(8)

2.20

5.80

(16)

2.57

6.33a

Mean

3.42

7.40

Mean

3.51

5.25

Smokers [10]

a

Smokes cigarettes after the fire before COHb was determined

The duration of fire fighting was 15 to 150 minutes. In another study of 16 firemen, blood COHb samples were taken before and after fire fighting operations.38 A peak of 23% COHb was found after fire fighting operations. A mean increase of 4.4 percent COHb was shown for non-smokers and 8.7 percent for smokers. Data are shown in Table 1. The mean baseline COHb level in non-smoking firemen was 2.5 versus 1.4 in the population at large. This would suggest that firefighters have higher background COHb levels than the general population. However, the mean COHb level of 5.5 in smoking firemen was comparable to the 5.2 observed in civilians. In contrast to COHb levels, no significant difference was found in the study between the mean hemoglobin of non-smoking and smoking firemen.38 It was found at most fire scenes, that atmospheric samples had normal oxygen levels (approximately 20 percent). In some circumstances, however, oxygen levels were as low as 14 percent, especially in fires associated with high heat. Low oxygen levels were accompanied by high carbon monoxide and high carbon dioxide levels.33 Carbon monoxide levels over 3,000 ppm were observed.39

Table 1. Summary of Percent COHb in Firemen Before and After Exposure to Smoke38 Subject

Before Exposure

After Exposure

Comments

Non-Smokers 1

3.6 Blood taken at end of tour; light exposure to smoke

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approximately 1 hour before blood sample. 2

1.0

8.1 Subjects 2 and 3: Blood taken at end of tour; exposure to basement fire 0.5 hour before blood sample.

3

1.5

5.2

4

2.6

5

1.1

6.6 Worked on nozzle at 2nd alarm where smoke was heavy; blood taken 0.5 hour after exposure.

6

2.9

3.8 This man had active duty the previous day with heavy exposure to smoke; last exposure 7 hours before sample.

7

3.2

4.4 This man worked an average tour with blood sample taken about 3 hours after exposure.

11.5 Worked nozzle at structural fire about 1 hour before sample.

Smokers 1

12.4

2

8.0

3

6.4

15.5 Subjects 3 and 4: Worked on nozzle at 2nd alarm where smoke was heavy; blood taken 0.5 to 1 hour after exposure.

4

1.8

11.4

5

13.9 Blood taken at end of tour; light exposure to smoke approximately 1 hour before blood sample. 8.3 Chauffeur on truck exposed to smoke while overhauling mattress job about 1 hour before blood sample taken.

9.7 This man had active duty the previous day with heavy smoke exposure; last exposure 7 hours before sample.

6

12.4

16.2 This man worked an average tour with blood sample taken about 1 and 1/2 hour after exposure.

7

6.3

18.1 Subjects 7, 8, 9 and 10: Worked above the fire floor doing search and ventilation at hospital residence fire. Firemen had no recent smoke exposure and did not get sick. Blood samples taken about 0.5 hours after exposure.

8

3.5

23.4

9

5.9

19.3

10

7.0

18.5

11

4.2

20.1 Worked at a structural fire and was exposed to various degrees of smoke; blood taken about 1 hour after exposure.

Two studies have been done where fire fighters have entered houses which were onfire with combustion product monitors. They measured the concentrations of major toxic products including carbon monoxide, carbon dioxide, hydrogen cyanide, acrolein, and oxygen, and found concentrations of carbon monoxide ranging up to 7500 ppm.40–41 Stewart has provided a chart for estimation of COHb levels on exposure to high CO concentrations during heavy exertion. That data follow:42

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Increase in Blood Carboxyhemoglobin (COHb) Level During Heavy Exertion* Increase in COHb Saturation After Brief Carbon Monoxide Exposure,% Carbon Monoxide Concentration

10 sec

30 sec

60 sec

120 sec

1,000 ppm (0.1%)

0.2

0.6

1.3

2.5

10,000 ppm (1%)

2.5

7.5

15

30

20,000 ppm (2%)

5

15

30

60

50,000 ppm (5%)

12.5

38

75

–

25

75

–

–

100,000 ppm(10%) *

“Heavy exertion”: Labor demanding alveolar ventilation rate of 30 liters/min.

He also developed a technique for estimation of COHb values from measuring CO concentration of alveolar air. Using that technique on firefighters, 55 nonsmoking firefighters showed COHb levels of 5 percent (range 1.4 to 9.1) and smoking firefighters showed 7.0 (range 2.9 to 13.0) after the first fire fighting episode of a 24-hour tour of duty. An extensive study of Baltimore firefighters showed lesser elevation of carbon monoxide for both smokers and nonsmokers.43 One particularly interesting report for comparison is a study of controlled exposure to high concentrations of carbon monoxide. Six healthy male human volunteers were exposed to seven high carbon monoxide (CO) concentrations ranging from 1,000 ppm for ten minutes to 35,600 ppm for 45 seconds. Carbon monoxide was rapidly absorbed and the increase in percent carboxyhemoglobin (COHb) saturation in venous blood per liter of CO mixture inhaled could be accurately predicted. The abrupt increase in carboxyhemoglobin concentration of 11.6% and 9.1% saturation in two subjects produced the immediate onset of mild frontal headaches.44 Thirteen fire survivors were studied in Chicago. These patients, ranging in age from 16 to 64 years, were seen in the emergency rooms of the University of Chicago Hospitals and Clinics 15 to 60 minutes after exposure to fire or smoke. All patients except one were awake but confused when first seen in the emergency room. Arterial blood was drawn and analyzed for percent carbon monoxide hemoglobin, arterial oxygen saturation (percent SaO2), hemoglobin (gm/100 ml), pH, and partial pressure of carbon dioxide (PCO2) and oxygen (PO2). In five patients, determinations of carbon monoxide hemoglobin levels were made over a period of 2½ hours during which oxygen by mask was continuously administered.45 Twelve patients survived without apparent after effects. One patient arrived in the emergency room comatose with second- and third-degree burns over 30 percent of her body surface. During her hospitalization, she exhibited symptoms of cerebral anoxia and required artificial ventilation for the entire period. The patient never regained consciousness and died after three days of hospitalization. All of the other victims reported headache, dizziness, and confusion at the time of the fire or smoke exposure and for varying periods up to several hours after admission. Seven of the 12 surviving

Low levels of carbon monoxide and their effects

79

patients coughed up soot and had localized or generalized wheezing for a period of three to five days after hospitalization. The percent of carbon monoxide ranged from 8 percent to 40 percent in the 13 patients studied with a median value of 28 percent, six were in the range of 33–40 percent:45

Fire Survivors—Emergency Room Data Patient No.

Age, yr.

Sex

%COHb*

%SaO2

Hgb, gm/100ml

pH

Smoke 1

64

F

21

81.0

14.0

7.46

2

34

F

40

65.0

11.4

7.34

3

16

M

33

71.0

14.0

7.45

4

28

M

34

70.0

14.4

7.37

5

24

F

24

79.0

12.4

7.43

6

35

M

14

–

–

7.37

7

63

F

8

94.0

9.7

7.56

8

–

F

9

–

–

4.49

9

38

M

36

–

–

7.49

10

32

M

33

–

–

7.40

11

39

M

28

60.6

16.4

7.40

12

16

M

15

–

–

7.48

13

–

F

35

74.0

15.0

7.43

Fire and Smoke

COHb data are similar to that reported by Polish workers and shown in Figure 2 of Chapter 2.46 One Scottish study looked at the levels of carbon monoxide and hydrogen cyanide in fire survivors. The mean carboxyhemoglobin concentration of the 36 patients who had inhaled smoke was 14.5 percent (range 0.3–45). The 12 patients with clinical evidence of considerable smoke inhalation had raised carboxyhemoglobin concentrations. Of the remaining 24 patients with minor smoke inhalation only two showed marginal elevation of carboxyhemoglobin above the upper limit of normal for their respective smoking categories. Data are shown as follows:47

Blood Cyanide and Carboxyhemoglobin Concentrations in 53 House-Fire Survivors Cyanide (umol/1)

Carboxyhemoglobin (%)

No Smoke Inhalation (n=17)

5.0 (0.5–13)

3.8 (0.8–9.6)

Smokers (n=11)

6.6 (2.2–13)

4.7(2.9–9.6)

Nonsmokers (n=6)

2.1 (0.5–3.9)

2.1 (0.8–3.2)

Carbon monoxide and human lethality

Smoke Inhalation (n=36)

25.8 (2.0–126)

80

14.5 (0.3–45)

Results are given as mean and range. The upper ranges of normal cyanide in smokers and non-smokers are 20 µmol/1 and 10 µmol/1, respectively. Those for carboxyhemoglobin are 10% and 5%, respectively.

To allow interpretation of carboxyhemoglobin levels obtained on admission, the authors prepared a nomogram from which likely carboxyhemoglobin levels at exposure can be calculated from COHb levels on admission and the interval between exposure and sampling. The nomogram (Figure 4) assumes a half-life of

FIGURE 4. Nomogram for calculating carboxyhemoglobin concentration at time of exposure. The time since exposure is given on two scales in order to allow for the effects of previous oxygen administration on the half-life of carboxyhemoglobin (left

Low levels of carbon monoxide and their effects

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hand scale assumes a half-life of three hours).47 four hours for COHb in a subject breathing room air. The scale on the left hand side of the time column in the nomogram makes an allowance for prior oxygen supplements by assuming a shorter half-life of three hours.47 The reader is reminded, however, of the large uncertainties in reported carbon monoxide downloading half-lives as discussed earlier in this chapter. Several patients had near-lethal cyanide levels, a high of 3.4 µg/ml versus approximate lethal level of 5 µg/ml. Since the half-life for cyanide elimination is short (approximately one hour) the initial exposure levels in survivors were probably considerably higher than the levels measured on admission.47 Clearly fire survivors can have quite elevated carboxyhemoglobin values, values approaching lethality. 3.5 CARBON MONOXIDE AND HUMAN PERFORMANCE At what level carbon monoxide exposures lead to reduced performance of human subjects is a matter of some controversy. Whether carbon monoxide levels significantly below incapacitation can lead to inability to think rationally or to escape is of course a key question in fire exposures. Laties and Merigan have performed a comprehensive review of carbon monoxide’s behavioral effects on both animals and humans. Literature through 1978 was discussed.48 Readers are referred to that review and to a National Research Council monograph for additional narrative.49 The purpose of the following pages will be to focus on a more detailed discussion of a select number of papers to give a flavor of the experiments made and conclusions given. Experimental observations on the behavioral effects of carbon monoxide date back to J.S.Haldane in 1895. In order to ascertain the relationship between the carboxyhemoglobin level and symptoms, he exposed himself to CO and recorded his own behavior. He described deficiences in vision, audition, balance, reading and writing at COHb levels ranging from 25 percent to 50 percent.50 We would not be as daring today. In work by Forbes, et al., in 1937, eight test subjects were exposed to carbon monoxide or to exhaust gases to assess degradation of skills needed in automobile driving. Two sets of experiments were performed. In the first, about 900 ml of pure carbon monoxide was put into 1,000 liters of air in a large bag from which the subject breathed for an hour through a mouthpiece. Subjects were tested several times before starting the experiment, learning the task to be performed using an apparatus for measuring various skills needed in driving. They were retested every ten minutes during experimental exposure to the carbon monoxide mixture. Blood samples were taken before the exposure to carbon monoxide, after 30 minutes of exposure, and at the end of the experiment. The inspired and expired air were analyzed and the volume of respiration was followed, together with the respiration rate, pulse, and blood sugar.51 The second set of experiments was substantially the same as the first except that automobile exhaust gases were used instead of pure carbon monoxide and the subject sat in a small room into which the exhaust gases were pumped, instead of breathing the

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mixture through a mouthpiece. The concentration of carbon monoxide in the test room fluctuated considerably but was on the whole higher than in the first series.51 In the first set of experiments the first test consisted of measuring the time taken to remove the foot from an accelerator and the time to push down a brake pedal after a red light was flashed on; the second test was for perception of depth; the third for ability to see dim objects at the side of a bright light; the fourth for ability to perceive the approach or recession of objects; and the fifth for accuracy of steering.51 In the second set of exposures the steering test and the one with the bright light were abandoned and a device for testing coordination was tried. This consisted of a phonograph with an insulating disk with one metal button set into it near the rim. The subject tried to keep a metal pointer on the button as the disk revolved.51 In the first set (5 subjects) none of the three subjects whose blood was 25 percent saturated was affected sufficiently so that his performance in these tests was degraded. The two subjects who reached 30 percent saturation were very slightly slower in the braking test but the change was too small to be significant. Not only was there no perceptible effect upon the performance of the tests but also their pulse, volume and frequency of respiration, and blood sugar remained substantially unchanged. The subjects themselves noticed no clear change in their feelings or abilities, but three of them had headaches which came on an hour or so after the experiment and lasted three or four hours.51 In the second set of experiments, involving 6 subjects the poisoning was more severe. Two subjects (47 and 50 percent COHb) were well aware that they were unable to drive a car and were not far from collapse, but they were able to concentrate on a test long enough to do reasonably well. Their pulse was rapid and they looked groggy. One of them felt nauseated and became unconscious for a few seconds after walking up a few steps during the tests. In short, both the subjects and the observers felt that the impairment of the ability to drive was much greater at high concentrations than the tests indicated, but they also felt that there was little or no effect until the saturation was 30 percent or more.51 In both sets of experiments the length of time during which the blood was at or near its maximum saturation for the experiment was short, roughly 10–20 minutes. It is possible that were saturations maintained at 25 to 30 percent for longer periods there would have been clearly noticeable effects both subjective and objective.43 Half of the subjects developed headaches. The impression was that an hour of 30 percent saturation was more likely to cause one than 15 minutes of 45 percent saturation. In those cases in which the saturation of the blood was 45 percent or over, a mixture of 95 percent oxygen and 5 percent carbon dioxide was given for 5 minutes immediately after the test and repeated at intervals for 30 or 40 minutes.51 Overall, in eleven experiments with eight normal men it was found that their performances in the simple tests of reaction time, binocular vision, coordination of the hand and eye, etc., were unaffected by breathing carbon monoxide until their blood COHb was 30 percent. Subjectively, they felt normal at 30 percent saturation or less but at 45 percent they appeared and felt unequal to driving a car; they were unable to think of many things at once and would collapse if sub jected to exercise.51 These results are very similar to recent results on cynomolgus monkeys. Animals were exposed to CO concentrations of 1000 to 2000 ppm for 20 to 30 minutes. The onset of incapacitation was insidious, occurring near the end of the exposure period when animals had blood COHb levels approaching 40 percent.52–53 Whether incapacitation occurred

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depended upon CO concentration, respiratory activity, and the activity of the animal. For 12 exposures to 1000 ppm CO, where blood levels of approximately 30% COHb were achieved at the end of the exposure, signs of intoxication were seen on only two occasions. When exposure levels of 1500–2000 ppm CO were used and COHb levels near 40 percent were obtained, incapacitation occurred, and tended to occur more readily in animals that were active. In some tests, animals which remained particularly quiet and relaxed came through the exposure without showing signs of intoxication.52–53 In additional experiments, animals which were free moving and trained to perform a behavioral task designed to simulate escape (exercise, coordinated body movements, and psychomotor skills) were exposed to 900 ppm CO for 30 minutes. At 20–25 minutes into the exposure a rapid decline of performance occurred, with poor coordination, a state resembling severe alcohol intoxication. Animals showed COHb values of approximately 33 percent, with initial signs of intoxication occurring at 25 percent COHb. Exposures to higher concentrations showed that animals passed rapidly from the stage of intoxication to one of a deep coma, where they were incapable of any action.52–53 These experiments deduce little decrement of performance prior to severe intoxication, but intoxication was followed rapidly by severe incapacitation. Sedentary animals were unaffected at COHb levels up to 40 percent while light activity resulted in effects at 25– 30 percent COHb. These results suggest that CO exposure can seem innocuous yet when the victim attempts light exercise, collapse and unconsciousness can occur.52–53 At Wright-Patterson Air Force Base a study was made of the effects of low levels of CO exposure on human performance. In the main study, 10 male university students between the ages of 19 and 22, in good health and non-smokers, were exposed for three hours to 0, 50 and 125 ppm CO in closed chambers. The subjects spent a three-hour session at each of these levels, and the order of exposures was counterbalanced to avoid sequence effects. A double-blind procedure designed to include not only the subjects and experimenters, but also all technicians that worked in the general area, was employed throughout the study.54 Following the main study, five subjects were exposed to 200 ppm CO, and three to 250 ppm. The program was essentially the same except that the subjects were told they would be receiving higher levels of CO. Because of the small number of subjects, no statistical analysis was performed on the additional data.54 Performance was assessed using three tasks: (1) a highly cognitive task-time estimation; (2) a psychomotor tracking task; and (3) the Pensacola Ataxia Battery. In the Ataxia Battery a number of balancing tasks were performed either on narrow rails or on the floor. A session consisted of a three-hour exposure starting from the time the subject entered the chamber. The CO levels were established prior to entry. The subjects performed 15 minutes out of every 30 during which they had five trials on the tracking trials, three minutes of time estimation, and then five more tracking trials. Following 90 minutes of exposure, they were permitted to walk and stretch within the chamber to reduce fatigue and boredom. The subjects were always in constant communication with the experimenters via headphones. It was considered extremely important that the subjects be able to see outside the chamber to preclude sensory restriction effects which could mimic or confound CO effects. Following the three-hour exposure, venous blood was drawn for COHb, Hb and hematocrit. The Pensacola Ataxia Battery was performed immediately thereafter.54 The blood COHb levels from the 10 subjects measured at the end of each session were as follows:54

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Carboxyhemoglobin Levels for all Subjects Following Three Hour CO Exposures Subject No.

0 ppm

50 ppm

125 ppm

200 ppm

250 ppm

1

0.7

2.8

6.5

2

1.2

2.4

6.6

3

0.8

2.7

6.5

4

1.0

3.1

7.4

5

1.0

3.0

6.8

10.1

6

1.3

3.6

6.8

10.1

7

1.1

3.3

6.4

10.0

8

0.9

3.0

6.6

10.0

9

0.6

2.9

6.2

10.9

12.1

0.96

2.98

6.64

10.35

12.37

Mean

9.8 13.1

11.9

This study attempted to determine whether short-term low level CO exposures affected human performance by using a broad range of performance measures. On an ordered scale, these tasks ranged from the cognitive task of estimating time, during which the subject supplied his own counting stimuli, and the tracking task which required the coordination of visual input with rapid motor responses, to the psychomotor task involving vestibular and gross motor controls for dynamic equilibrium. The results indicated that three hours of exposure to CO levels up to 125 ppm, and probably as high as 250 ppm, produced no performance decrement in any of these parameters.54 In very early work (1922) three subjects were studied. In this work, exposure was made to concentrations of from 200 to 400 ppm CO for several hours. The conditions and results of these tests are given in Charts 1–3.

CHART 155 Test for low concentrations of CO without exercise (sitting) Subject

Time in Parts Percent Respi Tempe Pulse Symptoms Minutes CO in blood ration rature Rate During 10,000 saturation (°F) test (time with CO in minutes)

After test

Test No. 1 Sayers

Start

2.1

14

60 120

98.9

76 Before— Feels O.K. 100-No symptoms

8

12

72 200-Slight

No symp toms

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85

tightness across forehead 180 240

McConnell

Start

210Yawning 1.9

11

13

300

16

14

2.1

13

99.4

80 300-All symptoms gone 96.7

60 9

14

320-Eyes hurt, tightness across forehead 1.8

300

Start

11

15

20

14

2.1

14

99.2

74 340Drowsy, 90 slight headache, increasing exertion

98.3

78 Before— Feels good

60

240Yawning

120

5

18

14

21

17

18

84 310Tightness across forehead, sleepy, yawning

180

240 300

No symptoms

90 300Yawning

180

Meriweather

86 Before— Feels good 240-No symptoms

120

240

78 250-Slight tightness across forehead

1.5

Test No. 2

99.0

92 300Sleepy, no 92 headache, feels lazy

No symptoms

Carbon monoxide and human lethality

Sayers

Start

2.1

60

2.7

16

120

99.2

86

74 Before— Feels good

9

45Yawning

14

65Yawning and sleepy 105Yawning

180

2.8

17

240

2.7

23

16

99.9

72 185Tightness across forehead

No ill effects on running up 40 stair steps. Slow in acting dull nerves. Did not sleep well. Feels good next morning.

215-Slight headache, shortness of breath, fingers cold Meriweather

Start

2.1

14

98.3

60

120

5

18

14

21

84 155Yawning and slight frontal headache

180

240

1.5

78 Before— Slight pain in right frontal sinus

99.0

92 185-Slight nausea on exertion 215-Dizzy

Subject

Time in Minutes

Parts Percent Respi Tempe Pulse Symptoms CO in blood ration rature Rate During 10,000 satu (°F) test (time ration in with minutes) CO

No ill effects on running up 40 stair steps. Headache increased after walking 11 blocks; of a throbbing basal type; continued until 1 am. Dull and irritable the following day.

After test

Test No. 3 Sayers

Start

2.9

120

3.1

16 17

99.0

74 Before— Feels good 68 167-Stops

Slight dizziness on running t i

Low levels of carbon monoxide and their effects

240

300

2.6

24

16

98.0

27

20

98.6

87

upstairs. Increasing headache during night, with 84 209chilly Headache sensations, followed by 234-After sweating. eating lunch slight Did not sleep well. temple, headache 80 reading, eyes hurt, forehead feels tight

250Headache basal incharacter, continuing until end of test Meriweather

Start

2.9

120

3.1

240 300

2.6

16

98.4

23

17

98.0

20

18

98.2

16

88 Before— Slight pain 74 in right frontal sinus

Headache exaggerated on exertion such as running up stairs. 88 72-Slight Severe dizziness headache 88 87-Slept 13 all night. Went to minutes hospital for 102-Severe sinus temple operation headache, next day. slight dizziness 234-Ate lunch in gas chamber, headache increased 274Occipital headache and very dizzy on rising

Test No. 4 Sayers

Start

4.2

17

99.4

84 Before— Feels good

Did not sleep well.

Carbon monoxide and human lethality

88

30

8

18

78 40Tightness across

60

15

19

78 60Constant desire to yawn

90

18

18

21

18

80 80Tightness 80 across forehead, increasing to headache on walking, feels very dull, slightly dizzy

120

3.5

99.2

Dull headache during night. O.K. next morning.

130Slightly dizzy, on climbing stairs palpitation and puffing. Frontal headache and dizziness. McConnell

Start

4.2

14

90.4

84 Before— Feels O.K.

30

10

15

88 60-Slight headache

60

19

18

88 85-Dull headache on walking

19

88 120Headache, 88 after going to bed, puffing, palpitation, and dizziness,

90 120

3.5

Meriweather Start

4.2

28

19

99.4

15

99.0

86 Before— Feels O.K.

Throbbing headache lasting until 10:30. Irritable and dull. Didn’t feel like working.

Aftersymptoms

Low levels of carbon monoxide and their effects

30

6

17

90

15

19

90

19

21

23

21

120

33

89

84 60Tightness 90 across forehead 90 90-Slight temple 92 headache on walking or shaking head

99.8

lasting until 2 or 3 o’clock am. Dull and irritable next day.

106-Slight dizziness 120-All symptoms exaggerated on going upstairs. Palpitation and puffing quite noticeable.

CHART 255 Test on low concentrations of CO with exercise Subject

Time in Parts Percent Respi Tempe Pulse Work Symptoms Minutes CO in blood ration rature (°F) done During After test 10,000 saturaion Rate in ft test (time with CO lbs in minutes) Test No. 1

Sayers

Start

2.5

16

15

2.6

3

30

130

30

2.6

8

26

144

24

135

15-Slight headache, little dizzy, feels effects of exercise; sweating

82

30Headache gone, dizzy on moving.

45

60 After

99.4

74 67,272 Before— Feels good

14 20

101.0

Pain in eyes, dull headache, head heavy.

Carbon monoxide and human lethality

90

60-No other symptoms during test. Meriweather

Start

2.5

17

15

2.6

4

30

134

30

2.6

7

28

126

28

120

45 60

99.4

16

After

20

99.8

Breathed oxygen for 30 minutes; 15all Yawning, symptoms dizzy, gone nauseated except lassitude 30-Very and dizzy, nauseated dullness. on moving, weak, air hunger, sweating profusely

96 33,835 Before— Feels good

90

45-Dizzy, nauseated, weak, cold hands, feels faint 60-No additional symptoms

Test No. 2 Sayers

Start

2.6

17

15 30

2.3

11

45 60

2.3

After Meriweather

Start 15

2.6

98.8

76 67,195 Before— Feels good

21

124

21

95

24

106

17

105 19

99.6

18

99.8

31

On running upstairs headache 30-Slight becomes headache, basic. Just perceptible dizziness; did not sleep well

96 90 32,700 Before— Frontal 135 headache due to sinus

Severe headache lasting until going to sleep

Low levels of carbon monoxide and their effects

30

2.3

13

45

60

2.3

17

After

20

90

32

144

36

126

22

91

30-Slight 1:00 am. headache, Feels good dizziness next morning. 60Slightly nauseated

99.6

90

17

99.4

72 62,292 Before— Feels good

24

99.2

108

16

30

99.4

110

22

30

99.0

130

Test No. 3 Sayers

Start

4.4

15 30 45

3.7

30-Tight feeling across forehead

Basal headache of moderate severity. moving

40Sleepy, drowsy, and yawning 42Slightly dizzy on quick moving 50Puffing, shortness of breath, palpitation of heart. 60-Slight basal headache.

In test No. 1 the subjects were exposed to approximately 200 ppm for 6 hours. This caused a saturation of 16 to 20 percent of hemoglobin with CO. One subject had a slight headache, but the subjective symptoms were extremely mild, and there were no symptoms of CO poisoning in any of the subjects after the test. COHb levels were built to between 20 and 28 percent in subsequent tests. Tests were then done with exercise; symptoms built much more rapidly, with headaches a common symptom after test.55 Data are given in Chart 2. For the data in Chart 2, strenuous exercise was taken at intervals during exposure to concentrations ranging from 250 to 400 ppm CO. Exercise was taken on a bicycle ergometer, and the amount of work done was calculated in foot-pounds. While there was

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92

a great difference in the amount of work done by the subjects, the amount represents strenuous exercise for the individuals working. Both men worked at the same rate—about 4,500 foot-pounds per minute—but one was able to continue the work for a full five minutes, whereas the other could work only about half as long. After each working period the subjects rested for about 15 minutes. In test No. 1 (Chart 2), the subjects were exposed to 250 ppm CO which caused 14 to 16 percent COHb at the end of one hour. The symptoms during the first half of the test were probably due chiefly to the severe exercise; during the latter half they were probably due to oxygen deficiency in the tissues caused by both the exercise and CO. The subject doing the lesser amount of work in this test had more severe symptoms. This may have been caused by the fact that it was his first test of this nature, and the psychological effects emphasized the symptoms, and to the fact that he was less physically fit than the other subjects. Effects of temperature and humidity were studied. Increases in symptoms were observed as shown on Chart 3.55

CHART 355 Test on low concentrations of CO with heat and humidity Subject Time in Parts Percent Respiration Temperature Pulse Minutes CO in blood (°F) Rate 10,000 saturation with CO

Symptoms During test (time in minutes)

After test

Test No. 1 Sayers

Start

3.1

98.8

10

30

101.4

110 21-Sweating profusely

16

30

102.8

120 27-Room very uncomfortable, dizzy on rising

10 30 60

3.2

72 Before—Feels Basal headache, good moderate 5-Sweating severity freely

17

34-Room very uncomfortable 40-Sweating profusely, weak, dizzy, head feels full, slight headache 50-Shortness of breath 52-Dull frontal headache 60-Slight basal headache

Low levels of carbon monoxide and their effects

93

Temperature and Humidity Time in Minutes

Wet Bulb

Dry Bulb

Relative Humidity

Start

93.0

113

52

15

97.5

113

30

99.0

111

65

43

99.0

108

72

48

97.5

107

60

97.0

102

83

Overall the following observations were reported in this early work:55 With the subject at rest 1. Exposure for 6 hours to 200 ppm of CO caused a. Saturation of 16 to 20 percent of the hemoglobin of the blood with CO. b. Very mild subjective symptoms of CO poisoning at the end of the test. c. No noticeable effects after the test. 2. The exposure to 300 ppm of CO caused a. Saturation of 22 to 24 percent of the hemoglobin with CO after 4 hours, and 26 to 27 percent after 5 hours. b. Symptoms at the end of 2 hours were absent; after 4 hours, mild effects attributed to CO poisoning; and after 5 hours, moderate effects c. After effects of 4 hours’ exposure, mild; of 5 hours’ exposure, moderate. 3. The exposure of 400 ppm of CO caused a. Saturation of 15 to 19 percent of the hemoglobin with CO at the end of 1 hour, and 21 to 28 percent at the end of 2 hours. b. After effects, moderate to marked. With subject exercising strenuously 1. The exposure for 1 hour to 250 ppm CO caused a. Saturation of 14 to 16 percent of the hemoglobin with CO. b. Moderate symptoms of CO poisoning at the end of the test. c. After effects mild to moderate. 2. The exposure for 1 hour to 330 ppm of CO caused a. Saturation of 17 percent of the hemoglobin with CO. b. Moderate symptoms of CO poisoning. c. Moderate after effects.

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With the subject at rest but with temperature and high humidity 1. The exposure for 1 hour to 310 ppm caused a. Saturation of 16 percent of the hemoglobin with CO. b. Mild symptoms of CO poisoning. c. Mild to moderate after effects. Overall conclusions reached by the workers were as follows:44 1. The combination of CO with hemoglobin takes place slowly when the subject is exposed to low concentrations and remains at rest, many hours being required before equilibrium is reached. 2. The rate of combination of CO with hemoglobin takes place much more rapidly during the first hour of exposure than during any succeeding hour, with the subject remaining at rest. 3. Strenuous exercise causes much more rapid combination of CO with hemoglobin than when the subject remains at rest. The symptoms of CO poisoning are increased by exercise. 4. High temperature and humidity, with a given concentration of CO, cause more rapid combination of CO with hemoglobin than do normal conditions of temperature and humidity. The above work attempted to deduce gross physiological effects of COHb levels to 30%, work unlikely to be repeated due to recognized hazards today. In much more recent work, eighteen subjects were studied by Beard and Wertheim for time discrimination when exposed to lesser levels of carbon monoxide. All subjects were university students. The 1,000 hz tone signals used were generated electronically. The signals were free of onset and offset clicks. The volume was adjusted to a comfortable level, well above the auditory threshold. The stimuli were presented by the psychophysiological method of constant stimuli. On each trial, there were two presentations of the tone separated by a one-half-second interval. The first or “standard” signal was always one second in duration; the second or “variable” signal was varied in 18 steps between 0.675 seconds and 1.325 seconds. The subject was asked to judge whether the duration of the second signal was shorter, the same, or longer than the first, and to indicate this by pressing one of three levers. The subject received no indication of the correctness of response.56 The comparison stimuli were presented in blocks of 25 trials with approximately 7.5 seconds between trials. In each block of 25 trials, eight of the comparison stimuli were identical to the standard, eight were longer, and nine were shorter; these were arranged in a nonsystematic sequence.53 Each subject received a total of 600 trials in each four-hour session. After each set of 50 trials, a six- to seven-minute work period, there was a pause of about 13 minutes during which the subject would read, sleep, or watch television. He stayed in the chamber throughout the session. A warning light and tone signalled the onset of each set of 50 trials.56 The eighteen subjects were observed in at least 15 sessions each. CO was administered in concentrations of 0, 50, 100, 175, and 250 parts per million in the different sessions. None of the subjects experienced any discomfort attributed to CO during the experiments, and none felt that he could reliably tell when CO was present. No changes

Low levels of carbon monoxide and their effects

95

in overt motor behavior were seen. However, a dose-related reduction of correct judgements of time intervals was observed. Significant decrements of response for two and one-half hours of exposure to all concentrations, from 50 parts per million upward, were observed.56 The rapidity of the onset of deterioration of time discrimination under the influence of small concentrations of CO was of particular interest. Using as a criterion a reduction in correct responses equal to two standard deviations from the mean performance in an uncontaminated atmosphere, 90 minutes were sufficient to produce a significant decrement in an atmosphere of 50 ppm, and much shorter times were needed for higher concentrations. These data are displayed in Figure 5.56 The data for individual subjects show that not only did the proportion of correct responses diminish in association with inhalation of CO, but that the perceptual behavior of the subjects became erratic. Unfortunately, COHb levels or

FIGURE 5. Time after initial exposure to each CO dose that the mean percent correct responses fell below 2 s.d. of mean performance without CO during auditory-duration discrimination.56

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96

other physiological parameters were not measured. COHb values of 4–5 percent can be anticipated at onset of performance degradation.56 Horvath, et al., have presented results which suggest that a critical level of COHb must be present before significant physiological alterations can be demonstrated. They noted that the absolute level of CO may be more important than the mode of exposure at least at low levels of COHb and in nonsmokers. Deteriorated performance as indicated by decreased maximal aerobic power and depression of certain central nervous system functions when COHb levels are about 4–5 percent was indicated in these studies.57 Small decreases in work capacity have been seen at COHb levels as low as 2.3%.58 Results indicating performance loss in the 5 percent range have, however, been challenged. Many authors have found no significant effect of carbon monoxide on cerebral performance, even with exposures producing fairly high blood carboxyhemoglobin (COHb) levels. Beard and Wertheim thus attracted considerable interest with their report suggesting that impairment of discrimination of the duration of a pure tone (auditory duration discrimination) had resulted from exposure to CO concentrations that as a threshold could not have increased the level of COHb much beyond three to five percent. Other experiments from the same laboratory supported this position. Rats were found to develop impaired discrimination of time, while human subjects had impaired discrimination of visual intensity and increased difficulty in estimation of time. Attempt to replicate the auditory discrimination results with a light discrimination task were unsuccessful, however.59 Subsequent investigators have failed to confirm an effect of CO on either visual or auditory discrimination. Weir and Rockwell60 found no deterioration in the skill of brightness matching with CO exposures sufficient to increase levels of COHb to seven percent and 14 percent. O’Donnell, et al.,61 noted no loss of auditory discrimination with COHb levels of 5.9 percent or 12.7 percent; and Guest, et al.,62 reported an increase rather than a decrease of auditory temporal discrimination after exposure to CO. In work by Davies, et al., six different groups of non-smoking young male subjects were studied separately for 18 consecutive days each in a closed controlled environment exposure chamber. It was concluded that CO exposure yielding up to 7 percent COHb was without significant effect on auditory vigilance.63 It has been suggested that the experimental findings of Beard and Wertheim might reflect sensory isolation rather than CO exposure. To test this hypothesis, Stewart, et al.,64 had their subjects carry out various time estimation tasks in three settings—while alone in an audiometric booth; while isolated in an environmental chamber; and in a group setting in an environmental chamber. Whereas time estimation in the group setting was improved after CO exposure, isolation in the audiometric booth led to an increase of errors, with seven of the nine subjects performing less effectively at their final COHb level of 9.4%. In a 1978 study by Wright and Shephard two young adults performed an auditory duration discrimination task while sitting in an open office. The percentage of errors rose when carboxyhemoglobin readings of 3.2 percent or 4.7 percent were produced by a rebreathing method; there was a parallel but insignificant trend at 2.0 percent COHb. Statistical analysis of the data, however, showed no significant changes of difference threshold, criterion value, or point of subjective equality, the psychological testing parameters used.59 After the test audio tape was rearranged to meet criteria of a constant interval, a balanced order of presentation, and psychological rather than physical equality of tone length, eight young adults performed the task better in an isolation booth than in an open

Low levels of carbon monoxide and their effects

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office, scores in both situations being unaffected by increases of COHb to >8 percent. Further trials with five young adults compared responses before and after administration of 80 ml of CO (COHb 4.92 percent); again, no effect of carbon monoxide was seen relative to control experiments.39 Studies of carbon monoxide performance degradation have used braking response as a parameter. The braking response is an important component of performance in the automobile driver. At a speed of 120 km/hr, a delay of 0.01 second increases the distance traveled before braking by 33 cm. In one study, fifty adults who received sufficient carbon monoxide to increase blood carboxyhemoglobin levels by an average of 3.4 percent showed suggestive but statistically insignificant deterioration in each of a number of simple measures of driving skill, including the braking response time.65 In a second study by the same group, simulated braking responses were tested in relation to blood carboxyhemoglobin levels. The main determinants of percentage of COHb in 352 subjects attending a fall fair were daily cigarette consumption and minutes since the last cigarette. In the women tested the brake response time deteriorated from age 16 years and upward, but in the men tested there was an improvement from age 16 to the early 20’s. Times at all ages were better for men than for women. Average response times and the rate of aging of the braking response were very similar in smokers and in non-smokers. In the non-smokers, however, response times were inversely correlated with the square of the percentage of COHb. Laboratory studies showed no change of total response time with step function CO increments of as much as seven percent COHb. There was a suggestion of a small increase of reaction time, with an opposing decrease of leg movement time, during the first few minutes after CO exposure; nevertheless, these trends were statistically insignificant.66 Given the foregoing discussion, one of the more interesting studies on human performance was reported by Schulte. Forty-nine healthy adult males were used as subjects in this study. The mean age for the group was 37.5 years with a median age of 39 years.67 The variation in the time and amount of exposure to mixtures of carbon monoxide and air resulted in levels of carboxyhemoglobin in subjects ranging from 0 to 20.4 percent. One subject reported that he had developed a headache during the test. His headache began when the level of COHb in his blood reached 20 percent. The remaining 48 subjects denied the existence of this or any other subjective symptoms which could be attributed to carbon monoxide. There was no change in the spinal or cranial nerve reflexes in any of the subjects throughout the study. There was no impairment in static steadiness. 16 other physiological and psychological activities were recorded.67 Schulte stated that these results show that there is no correlation between the level of carboxyhemoglobin in the blood and any of the physiological activities which were evaluated. Furthermore, there was no correlation between the level of carboxyhemoglobin in the blood and the reaction time in a simple choice response test. There was, however, a definite, appreciable, and statistically significant relationship between the level of COHb in the blood and all other psychological activities with the exception of errors in plural noun underlining. The data for psychological tests are shown in Figure 6.67 The relatively simple cognitive abilities required to perform choice discrimination, arithmetic, plural noun underlining, and t crossing tests were impaired by levels of 10 percent COHb. It is thus possible that more complex psychological functions involving judgements, and situational decisions and responses, would be affected by exposure to

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levels of carbon monoxide which are sufficient to produce similar concentrations. The Schulte work shows that an impairment of function due to exposure to carbon monoxide occurs earliest in cognitive and psychomotor abilities. While impairment is perhaps detectable at levels of COHb of five percent, and the degree of impairment increases with increasing concentration of the carboxyhemoglobin in the blood beyond 10 percent.67 In their review of the literature through 1977, Laties and Merigan make a number of important conclusions.48 They note that some behavioral changes seem to be associated with COHb as low as 5 to 8%, but that the scattered reports of impairment at lower levels of COHb are not very compelling. The strongest evidence for such effects comes from work on vigilance, driving, tracking, and vision, but the findings are not buttressed by independent confirmation.48 Recent work to replicate a compensatory tracking and monitoring study in healthy young men did not find a statistically significant effect even at 9% COHb versus 5% of the original study.68 The most common impairment is a depression or slowing of responding, with the magnitude depending upon the precise way performance was tested. For example, compensatory tracking was degraded only when the vertical oscillations to be matched by subjects occurred at the higher of two rates used. In driving studies, slowed reactions were often found only to less salient stimuli: Reactions to gradual increases in the speed of a lead automobile were slowed by CO whereas reactions to a dashboard warning light were not. Subjects also reacted more slowly when they detected signals on a vigilance task that was part of a dual procedure that included compensatory tracking. The only measure of coordination on which performance was impaired was the timed Purdue Pegboard test of the rate of assembly of pegs, bushing, and rings.48 A general depression of responding may also partially account for decrements in vigilance performance: fewer observed responses by subjects could lead to fewer detected signals. There may, however, also be direct effects on other aspects of vigilance performance, such as changes in sensory thresholds. Changes in visual threshold, even though small, may have important consequences for other types of performance. For instance, if visual function during CO exposure is impaired primarily at low luminance levels, then already marginal night vision might be critically degraded.48 In recent work, while dark adaptation time was longer and light sensitivity of the dark adapted eye was reduced in smokers versus non-smokers, effects of CO at 17–19% COHb were marginal.69

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99

FIGURE 6. Psychological test data.67 Laties and Merigan note that the differential sensitivity of various types of behavior to disruption by CO has not been systematically explored in comparative studies that could point to those behaviors most at risk (e.g. high vs low response rate, learned vs unlearned, or performance under strong vs weak stimulus control). A second unresolved issue is the relative importance of various parameters of CO exposure (concentration, duration, COHb level) in determining the extent of behavioral impairment.48 Most CO effects appear to be truly marginal CO probably does not have large and consistent effects upon behavior when given for short periods at low levels. Therefore, the ease with which effects can be established is heavily dependent on such factors as the reliability of tests used, amount of practice, the number of subjects, their physical condition, and the adequacy of the data treatment.48 This lack of effect is perhaps

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reasonable given that vasodilation occurs in the brain in response to COHb buildup. The vasodilation is sufficient to keep cerebral O2 consumption from being reduced, up to 20% COHb. The presence of COHb also causes a shift of the O2Hb dissociation curve to the left. If compensatory mechanisms are operative and oxygen consumption is not reduced, then behavioral effects should not be seen in healthy individuals up to 20% COHb, but of course not all individuals are healthy.70 In a recent study small effects at 10 percent COHb on two aspects of cognitive performance were observed, the decrements being on the order of 10 percent. On the whole, data suggested that man can tolerate COHb levels as high as 10 percent with accompanying heavy physical work while displaying little increase in physical or psychological discomfort and only mild performance decrements confined to specific aspects of cognitive tasks and no effect on other tasks.71–72 The dose-effect and time-effect relationships for CO may not be monotonic. Several investigators have reported CO effects that appeared only transiently, diminishing in magnitude or disappearing completely as exposure continued. Others have reported reversals, with higher exposure levels apparently producing less effect than lower ones. The possibility of physiological compensatory mechanisms exists, triggered when certain levels are reached. Behavior compensatory adjustments might also be occurring. There are, for example, reports of noise and vibration actually improving performance. Since the behavioral effects of CO are usually studied in healthy young subjects, judicious extrapolation is needed in using results for the establishment of exposure levels for the general public. For instance, effects may be exaggerated in utero, in the elderly, or in persons with cardiovascular or respiratory diseases.48 One final recent report is perhaps worthy of mention in this section, the effects of alcohol and CO.73 A test of the combined effects of 7% COHb and 80 mg/100 ml of alcohol in 7 subjects, 6 male and 1 female, showed a significantly lower sensitivity to the individual effects of odor detection versus CO or alcohol alone. Odor detection is certainly a skill needed in the early stages of a fire.74 In a study of driving skills on the combined effects of alcohol and CO, synergistic effects were observed in curve negotiation at 12% COHb. At 0.04% blood alcohol marginally antagonistic effects were observed for visual information processing skills, however, with CO exposure. Thus both synergistic and antagonistic effects have been observed.75 3.6 CARBON MONOXIDE AND ALTITUDE Altitude makes a difference in uptake of carbon monoxide. When persons at high altitude are exposed to low concentrations of CO, symptoms are experienced at much lower blood concentrations and the effects are more severe. In aviation the assumption has been that, for practical purposes, the effect of a given blood level of COHb is the same as that of an equivalent degree of arterial O2 unsaturation due to reduced barometric pressure. On this basis, an altitude of 10,000 ft. (3,050 m.), which reduces the arterial O2 saturation to about 85 percent, is equivalent to a COHb saturation of 12 percent; and 12 percent COHb at 10,000 ft. (3,050 m.) is equivalent to a height corresponding to an arterial O2 saturation of 73 percent, or 16,000 ft. (4,875 m.). Altitude has no significant effect on the rate of CO absorption in man, but it does influence the final concentration reached in the blood after many hours of exposure, because of the change in the partition of Hb between CO and O2

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at low O2 tension as shown below. Such changes are of interest for in flight aircraft accidents as well as for fires at higher elevation.76

COHb content of blood as percent of Hb saturation, in the presence of various partial pressures of CO at sea-level and at 10,000 ft. (3,050 m.), calculated from a standard O2, dissociation curve assuming the arterial pO2, at 10,000 ft. to be 63 mm. Hg and the relative affinity of CO for Hb to be 238 times that of O2. CO%

COHb

(Dry Gas at Sea Level)

pCO mm. Hg.

Percentage Saturation Sea-Level

1,000 ft. (3,050 m.)

0.005

0.04

8.5

11.6

0.010

0.25

15.6

20.7

0.020

1.50

27.0

35.2

0.030

2.25

36.1

46.2

0.040

3.00

44.8

52..4

Long term exposure studies on animals have been conducted at low pressure to simulate 27,000 ft. altitude. In studies of Rhesus monkeys using dual continuous avoidance techniques, animals were worked 15 minutes every hour for eight hours a day, five days per week. Each 15-minute session included three tasks: a right and left lever had to be pressed once every 15 seconds continuously, and 12 visual and 12 auditory cues were randomly presented.54 Each study consisted of two weeks of baseline data collected prior to CO exposure under conditions similar to the exposure, except for the presence of CO. The animals were then exposed continuously to CO, and the performance data collected during the exposure were compared to the baseline data for each animal. Studies over a two year period are summarized below:54 Study I

CO conc. (mg/m3)

Blood COHb Mean Rise (% Sat.) Hb Conc. Above Atmosphere Duration Mean Range Total Control (Days)* Animals

Performance Animals with Decrement

55

Ambient

100

3.7 (2.0– 5.0)

+0.6 gm%

12

0

55

5 psi, amixed gasb

105

4.7 (4.0– 6.0)

+1.4 gm%

12

0

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110

5 psi, mixed gas

7

8.3 (7.0– 10.0)

12

0

220

5 psi, mixed gas

7

19.5 (17– 21)

12

2

440

5 psi, mixed gas

7

30.1 (27– 34)

12

2

Study II 220

5 psi, mixed gas

100

440

5 psi, mixed gas

99

21.6 (20– 24)

+3.3 gm%

12

0

31.2 (28.5– 34)

+3.5 gm%

12

0

*

Days=days of continuous exposure 5 psi equivalent to 27,000 feet altitude b Mixed gas=68% O2, 32% N2 a

Except for the first exposure, all others were done at altitude (5 psi., 68 percent O2, 32 percent N2). Included above are the exposure concentrations of CO, the duration of exposure, the respective COHb levels, the mean rise in hemoglobin concentration, and the over-all performance. During Study 1, following exposure for 105 days to 55 mg/m3 of CO at altitude, the CO concentrations were doubled over three successive weeks, causing the mean COHb levels to rise from 4.7 to 30.1 percent. During this step-up phase, 6 to 12 animals appeared outwardly “ill,” which was associated with a marked reduction in food consumption at the 440 mg/m3 level. Despite this, only two monkeys showed performance changes. The mean COHb levels were 19.5 and 30.1 percent, respectively. In Study II, using 12 newly trained unexposed monkeys, no performance decrements were noted during exposure to 220 and 440 mg/m3 of CO for 100 days and 99 days, respectively.54 In general, carbon monoxide up to 440 mg/m3 did not appear to impair operant behavior in monkeys at altitude. A criticism of this performance program is that it is not sensitive enough to indicate subtle changes, and the animals must be virtually overwhelmed before they cease to perform well. However, it is also apparent that at COHb levels of 30 percent the animals certainly were capable of performing learned tasks.54 Studies of the effects of carbon monoxide at high ambient pressures are rare. Diving accidents involving carbon monoxide poisoning are not infrequent. Studies in Sprague Dawley rats show a linear relationship between COHb and pressure for 500 (3 min) and 1000 (1 min) ppm CO. This was not so at 100 and 250 ppm (130 min).77 3.7 CARBON MONOXIDE AND DISEASE For diseased patients effects can be observed at lower levels than otherwise expected. Infants, the elderly and patients with cardiovascular disease, anemia, lung disease, and an increased metabolic rate are at greater risk. Fozycki, et al., studied electrocardiographic changes in 880 patients treated for acute poisonings. Effects were observed in 279 cases, with the most marked changes observed

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in CO cases. The most common change was a T-wave abnormality and in 6 cases a pattern of acute myocardial infarction was present. Conduction disturbances were common but arrhythmias less so.78 Aronow has noted that carbon monoxide exposure from heavy smoking or heavy atmospheric carbon monoxide pollution depresses myocardial function in patients with coronary heart disease, aggravates intermittent dauducation of the calf or thigh, increases myocardial ischemia in patients with clincal and subclinical coronary heart disease, and contributes to an increased, incidence of nonfatal and fatal myocardial infarction and sudden death from coronary heart disease.79 Aronow, et al., exposed 10 patients to heavy freeway automobile traffic by driving them in a station wagon for 90 minutes. Mean COHb concentration rose from 1.12 to 5.08 percent saturation and then decreased to 2.91 percent two hours later. Four of the subjects exhibited electrocardiographic changes during the exposure period; they did not experience changes during a subsequent drive when provided with a source of uncontaminated air. Immediately following the exposure period, the subjects were exercised on a bicycle until they developed angina pectoris. The time necessary to develop angina was 249.4 seconds prior to exposure. The time fell to 174.3 seconds after exposure and rose to 210.8 seconds two hours later. In addition, angina developed at lower heart rates and systemic blood pressures following exposure to freeway air.80 In another study of 15 patients exposed to 50 ppm of CO for 1 hour (2% COHb), mean exercise times until the onset of angina pectoris dropped from 322 to 289 seconds.81 Effects have been shown by other workers as well (82). Such effects are complicated by smoking and other factors.83 Yet a study of patients with ischemic heart disease showed no clinically significant effect of 3.8 percent COHb (representing a 2.2 percent increase from resting values) on parameters examined during exercise and rest;84 but at a level of 6 percent COHb early onset of angina on exercise was observed.35 The investigators attribute these deleterious effects of carbon monoxide to a worsening of myocardial ischemia due to impaired oxygen delivery to the working myocardium. A 1989 multicenter study of 63 men indeed shows small reductions of time to angina on exercise and in the product of heart rate and blood pressure at 2 and 4 percent COHb in patients with myocardial ischemia.86,87 Despite differences in methodology and results, there is a consistent relationship in percent decrease in time of onset of angina with CO across multiple studies. For a general review readers are referred to Turino’s work.88–89 A study of aversive or rapid smoking has been reported on 10 subjects. Analysis revealed an average increase in COHb of 3.1 percent from an average value of 4.2 percent before rapid smoking to 7.3 percent after smoking. Of most interest, oxygen saturation decreased on the average 5.6 percent (from 95.5 percent to 89.9 percent) and oxygen tension decreased 7.6 mm Hb (from 89.7 mm Hg to 82.1 mm Hg).90 It is to be noted that tissue oxygenation is dependent on several functions in addition to arterial oxygenation; including hemoglobin concentration, cardiac output, and blood flow distribution in tissues. Tolerance to oxygen desaturation may thus be dependent upon age and general physical health. An oxygen saturation value less than 90 percent, which is distinctly abnormal, is considered clinically significant, with potential danger to a patient, particularly one with coronary heart disease.90 A regression analysis of daily mortality in Los Angeles County shows that there is a significant association between community carbon monoxide concentrations and mortality. Data are shown in Figure 7.

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FIGURE 7. Mortality, temperature, and carbon monoxide concentrations in Los Angeles, 1962–1965. Points plotted are the medians of 15-day intervals. The dashed line is the mortality predicted by the model with trend and cyclic variation terms.91 The estimated contribution to excess mortality for Los Angeles County for an average carbon monoxide concentration of 20.2 ppm (the highest concentration observed during the 4-year period), as compared with an average carbon monoxide concentration of 7.3 ppm (the lowest concentration observed), is 11 deaths for that day, all other factors being equal. Similar regression models were formulated with oxidant as an environmental variable. The association of oxidant with excess mortality was substantially less than that for carbon monoxide.91 A study of 8556 encounters with patients at Colorado General Hospital in the winter of 1976 showed a relationship of ambient carbon monoxide and frequency of cardiorespiratory complaints.92 That adaptations occur due to COHb induced hypoxia over long term carbon monoxide exposures has been long known.93 Mammalian cardiopulmonary systems exhibit one or more of the following responses, which minimize cellular hypoxia when

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exposed to carboxyhemoglobin-induced hypoxia: (1) decrease in oxygen requirements; (2) increase in blood flow; (3) polycythemia, that is an overall increase in blood cells; (4) rightward shift of the oxyhemoglobin dissociation curve mediated through increases in 2,3 diphosphoglycerate and (5) increased oxygen extraction. The response appears to depend upon species, status of the vascular bed and intensity and duration of the hypoxic stress.94 Studies of resting human subjects indicate that an increase in coronary blood flow was an almost universal response to either high or low concentrations of carbon monoxide. In contrast, systemic blood flow increased only when the subjects were exposed to higher concentrations. With a lower CO concentration for longer periods of time investigators observed that exercise produced higher than control cardiac outputs and lower maximal oxygen consumptions, suggesting that both increased blood flow and a reduction in oxygen requirements were important responses to carboxyhemoglobin-induced hypoxia during exercise.94 Studies of resting monkeys, intermittently exposed to low CO concentrations, minimized hypoxia by decreasing oxygen requirements while monkeys continuously exposed to somewhat lower CO concentrations developed polycythemia. The inability of this polycythemic response to protect the monkeys against myocardial hypoxia is revealed by uniformly observed electrocardiographic abnormalities.94 Calverley, et al., looked at the effects of CO on exercise performance in older subjects with chronic lung disease. Fifteen patients with severe reversible airway obstruction due to chronic bronchitis and emphysema were studied. A significant decrease in walking distance was reported when the mean blood COHb value reached 12.3%.95 The foregoing discussion describes existing data. The full effects of carbon monoxide at low levels remain unclear despite extensive study.96,97 The reader should note that air quality standards are based upon the assumption that there is probable health deterioration when COHb concentrations reach the 5 to 10 percent range.98 It is also to be noted that high CO exposure can yield myocardial infarction in patients with normal coronary arteries.99 3.8 CO POISONING-IDENTIFICATION, MITIGATION AND POTENTIAL FOR CONTINUING PROBLEMS Carbon Monoxide poisoning may not only affect performance at work and at school but the symptoms may be mistaken for those of other illnesses. Symptoms of repeated exposure to low concentrations of CO include headache, fatigue, difficulties in thinking, dizziness, chest pain, palpitations, visual disturbance, nausea, diarrhea, and abdominal pain. Symptoms can be vague and non-specific but persistent. Confirmation may be difficult analytically because of the time lapse between exposure and presentation to a physician.100–101 Several studies have examined the carboxyhemoglobin levels in patients with flu-like symptoms. In one study in Chicago investigators developed an algorithm for patients who presented themselves to an emergency department with headache or dizziness. Questions asked included use of gas stoves for heating and cohabitants similarly affected. The algorithm correctly identified patients with COHb levels greater than 10 percent and excluded patients with lower levels in some 65 cases.102

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A study in Louisville, Kentucky, of 55 patients, self selected from 637 eligible patients, with headache, dizziness, nausea, vomiting, diarrhea, weakness, general malaise, or shortness of breath found 13 or 24 percent with COHb greater than 10 percent, with the highest having 21 percent.103 Criticism of the Louisville work rests in the high number of patients found with COHb levels greater than 10 percent.104 While noting the issues of bias resulting from selfselection, the incidence of CO poisoning varies greatly from one jurisdiction to another. In another Chicago study screening of emergency department patients regardless of complaint and of all patients who underwent arterial blood gas analysis found 29 of 1038 (3 percent) who had abnormal CO breath readings on COHb levels.105 Children are a group where diagnosis of flu-like symptoms is perhaps more difficult. In Philadelphia some 46 patients and 10 control patients were studied. The 46 were selected by at least one exposure and one symptom criterion. Twenty-two patients had COHb less than 2 percent while 11 had 2–5 percent, 7 had 5–10 percent, and 6 had greater than 10 percent COHb. Thirteen of 24 patients with COHb levels greater than 2 percent would not have been suspected of having elevated COHb levels on the basis of routine history or physical findings alone.106 In a Texas study of 28 confirmed pediatric carbon monoxide exposures, 89 percent were a result of faulty venting or faulty combustion of gas furnaces.107 In a study in Grenoble, France, misdiagnosis of carbon monoxide poisoning from 1975 to 1980 showed a reduction from 30 to 5 percent on hightened awareness of CO symptoms. Cerebral diseases, cerebral hemorrhage, cerebral tumor, migraine, psychiatric diseases, acute alcohol intoxication, acute solvent intoxication, heart disease, and food poisoning were all original diagnosis later found to be actual cases of carbon monoxide poisoning, with food poisoning being the most common.108 A study of 26 patients in Seattle noted that bizarre pet behavior and death can be an important clue to carbon monoxide poisoning.109 The diagnosis of carbon monoxide poisoning may depend upon an exact clinical history, an astute physical examination, and a high degree of suspicion. Misdiagnosis may return the patient and others to a contaminated environment.110–111 It is noted that cherry color of skin and mucous membranes is in fact an uncommon finding in subacute carbon monoxide poisoning.112 One danger of carbon monoxide poisoning is the potential for delayed neurological sequelae. Sequelae may develop during a prolonged acute phase of poisoning or after a period ranging from days to weeks without overt symptoms. Transitory cortical blindness and memory defects are common. Other characteristics may include disorientation, headaches, personality changes, hallucinations, muscular rigidity, nausea, incontinence of urine and feces, dementia, amnesia, parkinsonism, depression, hysteria, schizophrenia, or simply poorer work or school performance.113 In a Korean study of 2360 carbon monoxide patients 65 or 3 percent showed delayed neurological deterioration. Virtually all showed mental deterioration and the majority were incontinent, had gait disturbances, and mutism.114 The median age of those exhibiting delayed deterioration was older, 56 years, than the group as a whole, 43 years. Coma, followed by a 2–4 week lucid interval, commonly preceded the onset of neurological sequelae. Even mild cases may at times go on to delayed sequelae.115 Children may be particularly vulnerable due to circumstances of poisoning and vagueness of initial symptoms.116–119

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In another Korean study, 3% of nearly 3,000 patients developed neuropsychiatric sequelae. In a study of 86 patients with sequelae, increased age, the presence of previous physical illness, and a long duration of unconsciousness following CO poisoning related positively to sequelae. Longer, lower exposure is more toxic than higher, shorter exposure.120 Electroencephalographic studies and ophthalmoscopy have proved useful in carbon monoxide studies. Retinal hemorrhages are an indication of carbon monoxide poisoning.121–122 Computed tomography and MR imaging have also proved of some value in evaluation of patients with CO exposure.123–131 Treatment may be important in the development of sequelae. A Maryland study notes that for 213 patients seen in 1980–1983, 131 received hyperbaric oxygen and had no sequelae, while of 82 patients who received normobaric oxygen, 10 developed sequelae. The recurring symptoms were resolved with hyperbaric oxygen therapy.132 Hyperbaric oxygen has been suggested for victims who are or have been unconscious, patients who on thorough testing show neurological or psychiatric symptoms or signs more than headache, patients with cardiac complications, patients with COHb levels above 20 to 40 percent, and pregnant women, although hyperbaric oxygen cannot totally prevent sequelae.125–146 Assistance for patients even after long delay has been discussed.147 It has been reported that hyperbaric oxygen antagonizes CO-mediated brain lipid peroxidation, although a mechanism is unclear.148). Carbon monoxide appears to have teratogenic and embryotoxic potential when exposures are sufficient to cause significant increase in maternal COHb levels and/or moderate to severe maternal toxicity.149 Finally, inhalation of carbon monoxide does not normally result in lung injury.150–154 However, experimental results with rats have shown that inhalation of moderately heated (110–130°C) dry air in the presence of high blood COHb can produce pulmonary injury due to hyperventilation.155 3.9 CONCLUSIONS Human carbon monoxide exposure is ubiquitous. Some degradation of performance occurs at COHb levels above 10 percent, yet the nature and extent of that degradation is unclear. Normal healthy subjects can handle 20–25 percent for short periods of time without gross effect. And 30–40 percent is clearly survivable for a majority of healthy subjects. Persons with disease, however, can be affected at very low COHb levels. Except for diseased or infirm individuals, the desire for survival ought to provide the stimulus necessary for escape in life threatening situations such as fire. Such drives and the chemistry of poisoning producing the psychological effects are, however, much more subtle than measured by COHb; thus it is not surprising that difficulties are encountered when correlation with COHb is attempted. To date no work has been done on how CO affects judgement, or on how people react under life-threatening conditions, or on how other agents such as alcohol affect judgement when present together with carbon monoxide. This is a fruitful area of technical investigation.

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ACKNOWLEDGEMENT The permission of publishers for tables and graphs is acknowledged with appreciation. REFERENCES 1. C.F.Cullis and M.M.Hirschler, “Man’s Emissions of Carbon Monoxide and Hydrocarbons into the Atmosphere”, Atmos, Environ., 23, 1195–1203 (1989). 2. C.F.Cullis and M.M.Hirschler, “A Simple Model for Estimating Emissions of Carbon Monoxide and Hydrocarbons from the Combustion of Coal”, Atmos. Environ., 24A, 1153–60 (1990). 3. R.R.Stewart, E.D.Baretta, L.R.Platee, A.B.Stewart, D.Kalbfleisch, W.Van Yserloo, and A.A.Rimm, “Carboxyhemoglobin Levels in American Blood Donors,” J. Am. Med. Assoc., 229, 1187–1195 (1974). 4. L.O.Hanson, N.M.Kjellman, J.Ludvigsson, and B.Lundh, “Blood Carboxyhemoglobin Percentage Saturation in Children”, Scand. J. Clin. Lab. Invest., 43, 363–365 (1983). 5. D.Nordenberg, R.Yip, and N.J.Binkin, “The Effect of Cigarette Smoking on Hemoglobin Levels and Anemia Screening”, J. Am. Med. Assoc., 264(12), 1556–9 (1990). 6. C.F.Cullis and M.M.Hirschler, “Smoking and Air Pollution,” Proc. 7th Int. Clean Air Conf., Clean Air Society of Australia and New Zealand, Adelaide, Australia, 24–28 August, 1981, p.115–129. 7. G.L.Davis and G.E.Gartner, “Carboxyhemoglobin in Volunteer Blood Donors,” J. Am. Med. Assoc., 230, 996–7 (1974). 8. A.Seppanen, “Smoking in Closed Space and Its Effect on Carboxyhemoglobin Saturation of Smoking and Non-smoking Subjects,” Ann. Clin. Res., 9, 281–283 (1977). 9. C.M.Castleden and P.B.Cole, “Variations in Carboxyhemoglobin Levels in Smokers,” Brit. Med. J., 4, 736–738 (1974). 10. J.E.Peterson and R.D.Stewart, “Absorption and Elimination of Carbon Monoxide by Inactive Young Men,” Arch. Environ. Health, 21, 165–171 (1970). 11. H.Ashton and R.Telford, “Blood Carboxyhemoglobin Levels in Smokers,” Brit. Med. J., 1973, 740. 12. J.K.Kam, “Carboxyhemoglobin Levels Between Jogging and Non-Jogging Smokers,” Experientria, 36(12), 1397–1398 (1980). 13. A.L.Goldman, “Cigar Inhaling,” Am. Review of Respiratory Disease, 113, 87–89 (1976). 14. A.L.Goldman, “Carboxyhemoglobin Levels in Primary and Secondary Cigar and Pipe SMokers,” Chest., 72, 33–35 (1977). 15. C.M.Castleden and P.B.Cole, “Inhalation of Tobacco Smoke by Pipe and Cigar Smokers,” Lancet, 2, 21–22 (1973). 16. J.Cowie, R.W.Sillett and K.Ball, “Carbon-Monoxide Absorption by Cigarette Smokers Who Change to Smoking Cigars,” Lancet., 1, 1033–1035 (1973). 17. N.Wald, S.Howard, F.G.Smith, and A.Bailey, “Use of Carboxyhemoglobin Levels to Predict the Development of Diseases Associated With Cigarette Smoking,” Thorax, 3C, 133–140 (1974). 18. R.M.Ramsey, “Carboxyhemoglobinemia in Parking Garage Employees,” Arch. En viron. Health, 15, 580–583 (1967). 19. L.A.Wallace, “Carbon Monoxide in Air and Breath of Employees in an Underground Office,” Journal of the Air Pollution Control Association, 33(7), 682 (1983). 20. P.J.Lawther and B.T.Commins, “Cigarette Smoking and Exposure to Carbon Monoxide,” Annals of the New York Academy of Sciences, 174, 135–147 (1970).

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21. G.R.Wright, S.Jewczky, J.Onrot, P.Tomlinson and R.J.Shepard, “Carbon Monoxide in the Urban Atmosphere. Hazards to the Pedestrian and Street-Worker,” Arch. Environ. Health, 30, 123–129 (1975). 22. D.Lester, “Changing Rates of Suicide by Car Exhaust in Men and Women in the United States after car Exhaust was Detoxified,” Crisis, 10, 164–168 (1989). 23. M.E.Stevenson, M.B.Chenoweth, and G.L.Cooper, “Effect of Carboxy-hemoglobin on Exposure to Aerosol Spray Paints with Methylene Chloride,” Clin. Toxicol., 12, 551–561 (1978). 24. R.D.Stewart and C.L.Hake, “Paint-Remover Hazard,” J. Am. Med. Assn., 235(4), 390–392 (1976). 25. N.G.Ott, L.K.Skory, B.B.Holder, J.M.Bronson, and F.R.Williams, “Health Evaluations of Employers Occupationally Exposed to Methylene Chloride,” Scand. J. Work. Environ. Health, 1983, 1–38. 26. H.P.Cuichta, G.M.Savell, and R.C.Spiker, “The Effect of Alcohols and Toluene upon Methylene Chloride-Induced Carboxyhemoglobin in the Rat and Monkey,” Toxicology and Applied Pharmacology, 49, 347–354 (1979). 27. J.Butt, G.M.Davies, J.G.Jones, and A.Sinclair, “Carboxyhemoglobin Levels in Blast Furnace Workers,” Annals of Occupational Hygiene, 17, 57–63 (1974). 28. M.Virtamo and A.Tossavainen, “Carbon Monoxide in Foundry Air,” Scand. J. Work. Environ. and Health 2 (1976); Suppl. 1, 37–41. 29. S.A.Lindgren, “A Study of the Effect of Protracted Occupational Exposure to Carbon Monoxide,” Acta Medica Scandinaviaca, 167, Suppl. 356, 135 pp. 30. I.Sunshine, N.Hodnett, C.R.Hall, and F.Rieders, “Drugs and Carbon Monoxide in Fatal Accidents,” Postgraduate Medicine, 1968, 152–155. 31. P.G.Flachsbart, G.A.Mack, J.E.Howes, and C.E.Rodes, “Carbon Monoxide Exposures of Washington Commuters,” J. Air Pollution Control Assn., 37, 135–142 (1987). 32. H.G.Applegate, “Carbon Monoxide Concentrations in El Paso for 1977,” in Air Quality Issues in the El Paso/CD. Jauarez Border Region; Occasional Papers #5, Center for Inter-American Studies, University of Texas at El Paso, El Paso, Texas, 23 pp, 1980. 33. F.B.Stern, W.E.Halperin, R.W.Hornung, V.L.Ringeburg, and C.S.McCammon, “Heart Disease Mortality Among Bridge and Tunnel Officers Exposed to Carbon Monoxide,” Am. J. of Epidemiology, 128, 1276–1288 (1988). 34. C.Edling and O.Axelson, “Risk Factors of Coronary Heart Disease Among Personnel in a Bus Company,” Int. Arch. Occup. Environ. Health, 54, 181–183 (1984). 35. R.J.Bing, J.S.M.Sarma, R.Weishaar, A.Rackel, and G.Pawlik, “Biochemical and Histological Effects of Intermittent Carbon Monoxide Exposure in Cynomolgus Monkeys in Relation to Atherosclerosis,” J. Clinical Pharmacology, 20, 487–499 (1980). 36. M.Helliovaara, M.J.Karvonene, R.Vilhunen and S.Punsar, “Smoking, carbon monoxide and atherosclerotic diseases,” Brit. Med. J., i, 268–70 (1978). 37. J.Loke, W.Farmer, R.A.Matthay, J.A.Virgulto, and A.Bouhlys, “Carboxy-hemoglobin Levels in Fire Fighters,” Lung, 154, 35–39 (1976). 38. A.L.Levy, G.Lum and F.J.Abeles, “Carbon Monoxide in Firemen Before and After Exposure to Smoke,” Annals of Clinical and Laboratory Science, 6(5), 455–458 (1976). 39. R.J.Barnard, “Carbon Monoxide: A Hazard to Fire Fighters,” Arch. Environmental Health, (July-Aug.) 255–257 (1979). 40. W.A.Burgess, A.Gold and R.D.Treitman, “Fireground survey of Air Contaminants”, for the National Fire Prevention and Control Administration (NFPCA) and the Society of the Plastics Industry, Inc. (SPI), Final Report, Harvard School Public Health, 53 pp, 1978. and W.A.Burgess, R.D.Treitman and A.Gold, “Air Contaminants in Structural Firefighting”, N.F.P.C.A. Project 7X008, Harvard School Public Health, 1979. 41. A.F.Grand, H.L.Kaplan and G.H.Lee, II, “Investigation of Combustion Atmospheres in Real Building Fires”, U.S. Fire Administration (USFA) and Society of the Plastics Industry, Inc. (SPI) Project 80027, Southwest Research Institute, 1981, 105 pp.

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87. E.N.Allred, E.R.Bleecker, B.R.Chaitman, T.E.Dahms, S.O.Gottlieb, J.D. Hackney, D.Hayes, M.Pagano, R.H.Selvester, S.M.Walden, and J.Warrren, “Acute Effects of Carbon Monoxide Exposure on Individuals with Coronary Artery Disease,” Health Effects Institute, Research Report No. 25 (Cambridge, MA, 1988) 98 pp. 88. G.M.Turino, “Effect of Carbon Monoxide on the Cardiovascular System,” Circulation, 63, 253A–258A (1981); and E.M.Dauyer and G.M.Turino, “Carbon Monoxide and Cardiovascular Disease,” The New England J. Med., 321, 147405 (1989). 89. E.M.Dwyer and G.M.Turino, “Carbon monoxide and cardiovascular disease”, New England J. Med., 321, 1474–75 (1989). 90. H.H.Dawley, E.B.Ellinthorpe, and R.Tretola, “Aversive Smoking: Carboxyhemoglobin Levels Before and After Rapid Smoking,” J. Behavioral Therapy and Experimental Psychiatry, 7, 13– 15 (1976). 91. A.C.Hexter and J.R.Goldsmith, “Carbon Monoxide: Association of Community Air Pollution with Mortality, Science, 172, 265–267 (1971). 92. T.L.Kurt, R.P.Mogielnicki, and J.E.Chandler, “Association of the Frequency of Acute Cardiorespiratory Complaints with Ambient Levels of Carbon Monoxide,” Chest, 74, 10–14 (1978). 93. E.M.Killick, “The Acclimatization of Mice to Atmospheres Containing Low Concentrations of Carbon Monoxide,” J. Physiol., 91, 279–292 (1937). 94. S.M.Ayres, S.Giannelli, Jr., H.Mueller, and A.Criscitiello, “Myocardial and Systemic Vascular Responses to Low Concentrations of Carboxyhemoglobin,” Annals. of Clinical Laboratory Science, 3(6), 440–447 (1973). 95. P.M.A.Calverley, R.J.E.Leggett, D.C.Flenley, “Carbon Monoxide and Exercise Tolerance in Chronic Bronchitis and Emphysema,” Br. Med. J., 283, 878–880 (1981). 96. R.D.Stewart, “The Effect of Carbon Monoxide on Humans,” Annual Review of Pharmacology, 15, 409–423 (1975). 97. R.D.Stewart, “The Effects of Low Concentrations of Carbon Monoxide on Man.” Scand. J. Respir. Dis., 91, 56 (1974). 98. Carbon Monoxide, Community Air Quality Guides, American Industrial Hygiene Association, 1969. 99. A.L.Marius-Nunez, “Myocardial Infarction with Normal Coronary Arteries after Acute Exposure to Carbon Monoxide”, Chest 97(2), 491–94 (1990). 100. R.Rylander and J.Veterlund, “Carbon Monoxide Criteria-With Reference to Effects on the Heart, Central Nervous System and Fetus,” Scand. J. Work Environ. Health, 7, Suppl. 1, 1981, 39 pp. 101. T.Meridith and A.Vale, “Carbon Monoxide Poisoning,” Brit. Med. J., 296, 77–79 (1988). 102. P.S.Heckerling, J.B.Leikin, and A.Matusen, “Occult Carbon Monoxide Poisoning: Validation of a Prediction Model,” Am. J. Med., 84, 251–256 (1988). 103. M.C.Dolan, T.L.Haltom, G.H.Barrows, C.S.Short, and K.M.Ferriell, “Carboxyhemoglobin Levels in Patients with Flu-Like Symptoms,” Annals of Emergency Med., 16, 782–786 (1987). 104. J.B.Leikin, A.Maturen, J.T.Perkins, and D.O.Hryhorczuk, “Carboxyhemoglobin Levels in Patients with Flu-Like Symptoms,” Annals of Emergency Medicine, 17, 383–4 (1988). 105. T.L.Turnbull, R.G.Start, G.R.Strange, M.A.Cooper, R.Linblad, J.M. Watkins, and C.M.Ferraro, “Emergency Department Screening for Unexpected Carbon Monoxide Exposure,” Annals of Emergency Medicine, 17, 478–483 (1988). 106. M.D.Baker, F.M.Henretig, S.Ludwig, “Carboxyhemoglobin Levels in Children with Nonspecific Flu-Like Symptoms,” The J. of Pediatrics, 113, 501–504 (1988). 107. P.J.Crocker and J.S.Walker, “Pediatric Carbon Monoxide Toxicity,” The J. of Emergency Med., 3, 443–448 (1985). 108. L.Barret, V.Danil, and J.Faure, “Carbon Monoxide Poisoning, A Diagnosis Frequently Overlooked,” Chemical Toxicology, 23, 309–313 (1985). 109. J.N.Kirkpatrick, “Occult Carbon Monoxide Poisoning,” Western J. of Med., 146(1), 52–56 (1987).

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110. T.W.Grace and F.W.Platt, “Subactive Carbon Monoxide Poisoning—Another Heat Imitator,” JAMA, 246, 1698–1700 (1981). 111. R.Crawford, D.G.D.Campbell and J.Ross, “Carbon Monoxide Poisoning in the Home: Recognition and Treatment”, Brit. J. Med., 301, 977–79 (1990). 112. T.Krantz, B.Thisted, J.Strom, and M.B.Sorensen, “Acute Carbon Monoxide Poisoning,” Acta Anaesthesiol Scand., 32, 278–282 (1988). 113. B.Werner, W.Back, H.Akerblom, and P.O.Barr, “Two Cases of Acute Carbon Monoxide Poisoning with Delayed Neurological Sequelae After a Free Interval,” Clinical Toxicology, 23, 249–265 (1985). 114. H.S.Choi, “Delayed Neurologic Sequelae in Carbon Monoxide Intoxication,” Arch Neurol., 40, 433–435 (1983). 115. M.D.Ginsberg, “Carbon Monoxide Intoxication: Clinical Features, Neurophathology and Mechanisms of Injury,” Clinical Toxicology, 23, 281–288 (1985). 116. J.W.Binder and R.J.Roberts, “Carbon Monoxide Intoxication in Children,” Clinical Toxicology, 16, 287–295 (1980). 117. S.S.Zimmerman and B.Truxal, “Carbon Monoxide Poisoning,” Pediatrics, 68, 215–224 (1981). 118. D.J.Lacey, “Neurologic Sequelae of Acute Carbon Monoxide Intoxication,” Am. J. Dis. Child, 135, 145–47 (1981). 119. M.Kless, M.Heremans, and S.Dougan, “The Science of the Total Environment,” 44, 165–176 (1985). 120. S.K.Min, “A Brain Syndrome Associated with Delayed Neuropyschiatric Sequelae Following Acute Carbon Monoxide Intoxication,” Acta Psychiatr. Scand., 73, 80–86 (1986). 121. J.S.Kelly and G.J.Sophocleus, “Renal Hemorrhages in Subacute Carbon Monoxide Poisoning,” JAMA, 239, 1515–1517 (1978). 122. L.S.Ferguson, M.J.Burke, and E.A.Choromokos, “Carbon Monoxide Retinopathy,” Arch. Ophthalmol., 101, 66–67 (1985). 123. T.Miura, M.Mitomo, R.Kawai, and K.Harada, “CT of the Brain in Acute Carbon Monoxide Intoxication: Characteristic Features and Prognosis,” Am. J. Neuro-radiology, 6, 739–42 (1985). 124. A.L.Horowitz, R.Kaplan, and G.Sarpel, “Carbon Monoxide Toxicity: MR Imaging in the Brain,” Radiology, 787–88 (1987). 125. Y.Sawada, N.Ohaski, K.Maemusa, T.Yoshioka, M.Takahashi, H.Fusamoto, H. Kobayashi, and T.Sugimoto, “Computerized Tomography as an Indication of Long-Term Outcomes After Acute Carbon Monoxide Poisoning,” The Lancet, 8172, 783–784 (1980). 126. Y.Sawada, T.Sakamoto, K.Nishide, D.Sadamitsu, H.Fusamoto, T.Yoshioka, and T.Sugimoto, “Correlation of Pathological Findings with Computed Tomo-graphic Findings after Acute Carbon Monoxide Poisoning,” The New England Journal of Med., 1983, 1296. 127. J.Pach, A.Mitka, O.Billewicz, and B.Czeczotko, “Usefulness of Brain Computed Tomography, Electroencephalographic, Psychological and Psychiatric Tests in Evaluating the CNS State in Severe Poisoning by Carbon Monoxide,” J. Toxicol. Clin. Toxicol., 23, 430–431 (1985). 128. H.L.Klawans, R.W.Stein, C.M.Tanner, C.G.Goetz, “A Pure Parkinsonian Syndrome Following Acute Carbon Monoxide Intoxication,” Arch. Neurol., 39, 302–3–3 (1982). 129. S.M.Pulst, T.M.Walshe, J.A.Romero, “Carbon Monoxide Poisoning with Features of Gilles de la Tourette’s Syndrome,” Arch. Neurol., 40, 443–444 (1983). 130. I.K.Hart, P.G.E.Kennedy, J.H.Adams, and N.E.Cunningham, “Neurological Manifestation of Carbon Monoxide Poisoning,” Postgraduate Med. J., 64, 213–216 (1988). 131. P.Vieregge, W.Klostermann, R.G.Blumm, and K.J.Borgis, “Carbon Monoxide Poisoning: Clinical, Neurophysiological, and Brain Imaging Obervations in Acute Disease and Follow-up,” J. Neurology, 236, 478–481 (1989). 132. R.A.M.Myers, S.K.Snyder and T.A.Emhoff, “Subacute Sequelae of Carbon Monoxide Poisoning,” Annals of Emergency Medicine, 14, 1163–1167 (1985).

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133. “Treatment of Carbon Monoxide Poisoning,” Drug and Therapeutics Bulletin, 26, 77–78 (1988). 134. D.M.Norkoll, and J.N.Kirkpatrick, “Treatment of Acute Carbon Monoxide Poisoning with Hyperbaric Oxygen: A Review of 115 Cases,” Annals of Emergency Med., 14, 1168–71 (1985). 135. D.Mathieu, M.Nolf, A.Durocher, F.Saulnier, P.Primat, D.Furon and F.Wattel, “Acute Carbon Monoxide Poisoning-Risk of Late Sequelae and Treatment by Hyperbaric Oxygen,” Clinical Toxicology, 23, 315–24 (1985). 136. W.Patrick, A.Miele, C., J.Hannigan, and R.M.Hurley, “Accidental Carbon Monoxide Poisoning,” Clinical Pediatrics, 23, 694–95 (1984). 137. A Registry for Carbon Monoxide Poisoning in New York City, Clinical Toxicology, 26, 419– 41 (1988). 138. D.Gozal, A.Ziser, A.Shupak, and Y.M.Melamed, “Accidental Carbon Monoxide Poisoning— Emphasis on Hyperbaric Oxygen Treatment,” Clinical Pediatrics, 24, 132–35 (1985). 139. L.Marzella and R.A.M.Myers, “Carbon Monoxide Poisoning,” Am. Family Physician, 34, 186–94 (1986). 140. E.P.Slvan, D.G.Murphy, R.Hart, M.A.Cooper, T.Turnbull, R.S.Barreca, and B.Ellerson, “Complications and Protocol Considerations in Carbon Monoxide—Poisoned Patients who Require Hyperbaric Oxygen Therapy: Report from a Ten Year Experience,” Annals of Emergency Medicine, 18, 629–634 (1989). 141. A.Ziser, A.Shupak, P.Halpern, D.Gozal, and Y.Melamed, “Delayed Hyperbaric Oxygen Treatment for Acute Carbon Monoxide Poisoning,” British Medical J., 289, 960 (1984). 142. J.S.Bretten and R.A.M.Myers, “Effects of Hyperbaric Treatment on Carbon Monoxide Elimination in Humans,” Undersea Biomedical Research, 12, 431–438 (1985). 143. K.B.Van Hoesen, E.M.Camporesi, R.E.Moon, M.L.Hage, C.A.Piantadosi,” Should Hyperbaric Oxygen be Used to Treat the Pregnant Patient for Acute Carbon Monoxide Poisoning? A Case Report and Literature Review,” J. Am. Med. Assoc. 261, 1039–1043 (1989). 144. E.M.Caravati, C.J.Adams, S.M.Joyce, and N.C.Schafer, “Fetal Toxicity Associated with Maternal Carbon Monoxide Poisoning,” Annals of Emergency Medicine, 17, 714–717 (1988). 145. G.D.Herman, A.B.Shapiro and J.Leikin, “Myonecrosis in Carbon Monoxide Poisoning,” Vet. Hum. Toxicol., 30, 28–30 (1988). 146. S.R.Thom and L.W.Keim, “Carbon Monoxide Poisoning: A Review-Epidemiology, Pathophysiology, Clinical Findings, and Treatment Options Including Hyperbaric Oxygen Therapy,” Clinical Toxicology, 27, 141–156 (1989). 147. R.A.Thompson, “Carbon Monoxide Poisoning: Treatment with Hyperbaric Oxygen,” Arizona Medicine, 4(1), 21–22 (1984). 148. S.R.Thom, “Antagonism of Carbon Monoxide—Mediated Brain Lipid Peroxidation by Hyperbaric Oxygen”, Toxicology and Applied Pharmacology, 105, 340–44 (1990). 149. C.A.Norman and D.M.Halton, “Is Carbon Monoxide a Workplace Teratogen? A Review and Evaluation of Literature”, Ann. Occup. Hyg. 34(4), 335–49 (1990). 150. K.Sugi, J.L.Teissen, L.D.Traber, D.N.Herndon and D.L.Traber, “Impact of Carbon Monoxide on Cardiopulmonary Dysfiunction After Smoke Inhalation Injury”, Circulation Research, 66(1), 69–75 (1990). 151. T.Shimazu, H.Ikeuchi, G.B.Hubbard, P.C.Langlinais, A.D.Mason and B.A. Pruitt, “Smoke Inhalation Injury and the Effect of Carbon Monoxide in the Sheep Model”, J. Trauma, 30(2), 170–75 (1990). 152. C.-Z.Wang, A.(N.) Li and Z.-C.Yang, “The Pathophysiology of Carbon Monoxide Poisoning and Acute Respiratory Failure in a Sheep Model with Inhalation Injury”, Chest, 97(3), 736–42 (1990). 153. R.R.R.Rowland, K.T.Yamaguchi, A.B.Santibanez, K.T.Kodama, V.T.Ness and D.E.Grubbs, “Smoke inhalation Model for Lung Permeability Studies”, J. Trauma, 26(2), 153–56 (1986). 154. S.R.Sharar, D.M.Heimbach, M.Howard, J.Hildebrandt and R.K.Winn, “Cardiopulmonary Respknses after Spotaneous Inhalation of Douglas Fir Smoke in Goats”, J. Trauma 28(2), 164– 70 (1988).

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155. K.Watanabe and K.Makino, “The Role of Carbon Monoxide Poisoning in the Production of Inhalation Burns”, Ann. Plast. Surg., 14, 284–95 (1985).

Chapter 4 PHYSIOLOGICAL EFFECTS OF CARBON MONOXIDE JAMES B.LARSEN Department of Biological Sciences, University of Southern Mississippi ABSTRACT In this chapter the action of CO is investigated in the following sequence: hematologic activity, actions on the respiratory system, effects on the circulatory system, neuromuscular effects, cytotoxic effects, effects of chronic exposure and relationships to other toxic gases. The toxicity of CO results from interruption of energy metabolism in cells. This can be produced by interference with the oxygen delivery through blood (COHb formation) or by direct inhibition of the metabolic intermediates. While the former mechanism is, probably the dominant one, the latter one also occurs. Although CO does not materially inhibit oxygen uptake in the lungs, it “uses up” the hemoglobin, preventing it from transporting oxygen and it is the focus of a series of compensatory mechanisms by which the cardiovascular system tries to continue functioning. These mechanisms are capable of protecting tissues at different levels of circulating COHb, depending on the individual affected. Thus, the presence of cardiovascular impairment tends to increase the danger of CO toxicity. It has also been found that inhaled CO is more lethal than injected CO, indicating that the rate of diffusion of CO into the blood plasma from the alveoli is much faster than the inverse, so that when CO gas is injected, the equilibrium tends be directed towards the expulsion of the toxicant. It is not possible to establish universal lethal COHb threshold levels.

4.1 INTRODUCTION Carbon monoxide (CO) is a ubiquitous and dangerous gas encountered in various environments. Intoxication is characterized by symptoms commonly related to the atmospheric concentration of CO, the duration of exposure, and the concentration of carboxyhemoglobin (COHb), which is formed when CO combines with hemoglobin (Hb) in the blood (Table 1). The toxicity of this gas has been known since the mid-nineteenth century.112,372 John Haldane is generally considered to have conducted the first scientific analysis of physiological effects resulting from exposure to CO; he performed a series of experiments on himself and published the results in 1895.165 A vast body of information dealing with the chemical and biological aspects of exposure currently exists. A landmark conference on the biological effects of

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*

Note: In every case, if no further details are given, the venue for the study is the United States.

CO in Atmosphere, %

COHb in Blood, %

Physiological and Subjective Symptoms

0.007

10

No appreciable effect, except shortness of breath on vigorous exertion; possible tightness across the forehead; dilation of cutaneous blood vessels

0.012

20

Shortness of breath on moderate exertion; occasional headache with throbbing in temples

0.022

30

Distinct headache; irritability; reduced stamina; impaired judgement and vision; dizziness

0.035–0.052

40–50

Headache; confusion; collapse, especially on exertion

0.080–0.122

60–70

Unconsciousness; intermittent convulsions; respiratory failure; death if exposure is prolonged

0.195

80

Rapid death

TABLE 1 Typical symptoms developing in humans as a result of exposure to atmospheres containing CO. The values for COHb saturation represent nominal equilibrium levels under normal conditions. (From Winter, P.M. & Miller, J.N., J. Amer. Med. Assoc., Vol. 236 (13), 1503; Sept. 27, 1976. Copyright 1976, American Medical Association. Adapted with permission). CO was convened by The New York Academy of Sciences during 1970. In the proceedings of those meetings91 is compiled most of the information available at that time, and the biological literature has been reviewed periodically since then by several authors. Among the recent comprehensive reviews is that by Tusl, Vyskocil, and Obrsal, which was published in 1987.453 Other reviews include those by Rylander and Vesterlund, on nervous, cardiovascular, and developmental effects;375 by Piantadosi, on extravascular and cytotoxic effects;343 by Laites and Merigan, on behavioral effects;241 and by Longo, on maternal, fetal, and neonatal effects.256 Among poison-related fatalities, CO intoxication ranks first in the United States. The use of catalytic converters in automobile exhaust systems, and greater concern with exhaust and emission standards, may be helping to reduce accidental CO poisoning from automobile exhaust. However, concern about the cost of home heating, which is leading to increased use of insulation, greater dependence on space heaters which use combustion fuels, and homes which are more air tight, require an increased awareness of this problem by physicians and emergency personnel. During winter months in northern climates, inner-city populations are at particular risk in this respect, due to the common practice of sealing windows with plastic film and the common use of improperly-vented heaters.110,111,113,217,291 In the suite of inhalation injuries resulting from exposure to fires, CO poisoning is clearly the major component, as the work in this book shows. This has already been

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discussed by several authors (e.g. 182). Reviews which treat the medical aspects of smoke inhalation, including the contribution of CO to this problem, have been provided by Coleman,95 and Hill.185 Exposure to CO may produce a wide variety of general symptoms (Table 1) which are difficult for a physician to differentiate from those associated with nonspecific viral infections (e.g. “the flu”), or various neurological conditions. Victims frequently complain of cardiovascular or pulmonary problems, dizziness, visual disturbances, fatigue, headache, nausea (“food-poisoning”), and/or abnormal cutaneous sensations.37,42,47,111,217 Intoxication with barbiturates, cyanide, or hydrogen sulfide may be mimicked, and seizures, contact dermatitis involving cutaneous edema and blisters, muscle necrosis, myoglobinuria, acute renal failure, and hemolytic anemia are also reported.51,181,289,307,490 Symptoms of CO intoxication may persist in humans for several days after the initial exposure, and medical treatment is complicated by the wide variety of psychological and neurological disturbances which develop in a significant number of victims (see Section 4.5). These conditions may seem at first unrelated to the original intoxication, because the onset may be delayed for several days or weeks, during which period the patient may appear completely normal.81,101,148,171,213,228,233,313,352,471 From a diagnostic standpoint, it is axiomatic that equivalent concentrations of circulating COHb will not always produce equivalent symptoms, since saturation of Hb with CO is a function of exposure duration as well as concentration in the atmosphere, and protracted exposures may be more damaging than brief exposures to high concentrations. Thus one individual may be completely asymptomatic at a COHb concentration which incapacitates a similar individual, and the reasons for differing symptoms are often not immediately apparent upon initial examination.275,380 (See also chapter 2 in this book). The presence of COHb imparts a distinctive scarlet color to the blood, which can usually be distinguished from the bright red color of arterial, or oxygenated blood. As a consequence of this, victims of CO intoxication can sometimes be recognized by a “cherry-red” color which develops in areas of the skin, such as the lips. However, skin color is extremely unreliable as a diagnostic sign because victims of CO poisoning may exhibit skin of various shades, depending on the circumstances involved during the exposure. Moreover, the original skin color of an individual will also affect the color the skin adopts after CO poisoning. The “cherry-red” color will be seen only if blood accumulates in the superficial vascular plexus of the skin, but congestion in the deeper dermal veins, even though COHb is present, will produce skin of the grey-blue color associated with cyanosis.132 Ophthalmological disorders, such as “flame-shaped” hemorrhages in the retina, retinal edema, or tortuous retinal vessels, are often a more reliable indicator of subacute intoxication with CO than skin color. Accordingly, an eye examination can be of great value in differentiating CO poisoning from other conditions, when various nonspecific symptoms are present.131,212,448,490 Experimental, contrasted with clinical, studies of physiological effects produced by CO typically involve animals. A wide variety of animals have been employed to investigate CO, ranging from squirrels to monkeys. Information about the effects of CO obtained from experiments involving animals has been reviewed by Penney,330 and early methods employing animals to assess the incapacitating effects of CO have been reviewed by Kaplan and Hartzell.207 While animal studies are absolutely essential as a means of understanding CO toxicity, and the mechanisms by which CO exerts its effects, care must be taken in extrapolating from animals to humans. It is evident that organisms vary in their sensitivity to CO, that within a species, variation may exist between

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genetically inbred strains, and that within a strain, resistance may differ between sexes.104,105,300,428,430 Inaddition, experimental stress alters the sensitivity of animals to CO: Unrestrained rats can survive in test atmospheres containing higher concentrations of CO than animals subjected to stress imposed by restraint114 (see Sections 4.5.B, 4.7.A). This chapter will present a comprehensive review of the literature on effects exerted by CO which alter the function of physiological systems. Special attention will be devoted to general principles, which integrate data from various studies and thus help to provide a general understanding of the mechanisms by which CO acts on man. 4.2 HEMATOLOGIC EFFECTS A. General Effects on the Blood All investigators agree that chronic exposure to CO results in polycythemia (increased red cell count) which develops over a period of several days.33,76,98,273,317,327,328,332,333,336,339,372,389,404,425,439 This leads to an increase in blood viscosity33,273,274,322,470 and blood volume.333 Under these conditions the Hb concentration is also increased, and there is some indication that CO elevates this more rapidly than equivalent hypoxia.76,98,322,323,324,327,332,333,404,439,470 The elevated Hb concentration appears to reflect a true increase in the rate of red cell production, under the influence of erythropoietin, and not merely a mobilization of erythrocyte reserves in the spleen.322 The amount of 2,3-diphosphoglycerate (DPG), another normal constituent of red blood cells, may be affected by the formation of COHb (see Section 4.2.B). Although high levels of COHb (above 40–50%) do not seem to affect DPG concentration,327,439 lowlevels of COHb (20% or less) have beenreported to both increase108,389 and decrease25 DPG levels in the red cells. Chronic exposure to CO thus produces a degree of tolerance to the gas, as well as to conditions of environmental hypoxia such as might be encountered at high altitudes. This results not only from the polycythemia, but also from an increased affinity for oxygen (O2) which develops in the presence of COHb 327,372 (see Section 4.2.B). Effects of chronic exposure to CO are reversible, and blood parameters will return to normal within about 30 days after exposure is terminated.332 Where acclimatization to CO or hypoxia has not occurred, individuals exposed to CO at high altitudes are at a much greater risk due to the decreased amount of O2 in the atmosphere.140,450 A postmortem study of Air Force pilots killed in crashes not involving fire revealed that one-third of the victims had more than 30% saturation of CO-binding compounds in blood and tissue.372 Experiments with rats reveal that reducing the O2 level in test atmospheres containing GO decreases the mean survival time and increases the final concentration of COHb. Pulmonary hypoxia facilitates the formation of COHb, and accelerates this process by increasing the rate of pulmonary ventilation.368 Indeed, reduction in the atmospheric O2 content may be a factor of great importance in many cases where deaths occur from fire or other causes at low COHb levels, and analyses of blood for its COHb concentration provides no information about the role of O2 deprivation.124,158,368,378 Hypoxia may also lead to life-threatening metabolic and/or respiratory acidosis,123,228,249,358,417,418,437,479 but the COHb concentration usually fails to correlate with the degree of acidosis.243

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Equivocal effects of COHb on clotting time have been reported,470 largely because of conflicting results from experiments designed to determine the effect of CO on platelet aggregation. Exposure to CO has been reported to promote platelet aggregation, and thus increase the probability of thrombus formation,15,273,296 but there is also evidence which suggests that platelet aggregation is inhibited by CO: the activity of guanylate cyclase is promoted, which inhibits aggregation by accelerating cyclic guanosine monophosphate (GMP) synthesis;63 the production of cardiac prostacyclin, which inhibits aggregation, is increased;119 the release of serotonin and adenosine diphosphate (ADP), which increase platelet “stickiness” and adhesion, is inhibited;269 increased aggregation induced by arachidonic acid and epinephrine is inhibited.268 In addition, thrombus formation would be expected to decrease as a consequence of decreased platelet count. This has been observed in rabbits exposed chronically to sub-lethal levels of CO, and may reflect the diversion of hemopoietic stem cells to support increased erythrocyte production.204 B. Reaction Kinetics of Hemoglobin with Oxygen and Carbon Monoxide Respiratory pigments, such as Hb, transport gases, but do not “react irreversibly” with them. The combination of Hb with gas molecules is thus reversible; gas is normally loaded by the pigment in the lungs, and unloaded where it is used within the tissues. Saturation of the pigment at any point depends on the partial pressure (Pg) or “tension” of the gas in question. Partial pressures are the individual pressures exerted by each gas component of a mixture, and are calculated by multiplying the total gas pressure by the fraction which represents the contribution of a given gas to the mixture; Pg values are usually expressed in millimeters of mercury (mm Hg) or “torr”. The relationship between Pg and saturation of a pigment can be represented graphically as a “dissociation curve” which is produced by plotting saturation of the pigment as a function of Pg. The shape of a dissociation curve depends on the nature of the pigment; it is affected by the number of sites for binding gas molecules and the interrelationships between these sites.426 The position of the curve along the partial pressure axis depends on the affinity of the pigment for the gas. Where the affinity is high, pigments will be saturated with gas at low Pg. Where the affinity for the gas is low, a high Pg will be required to saturate the pigment. Thus dissociation curves resulting from high-affinity relationships will be located to the left on the partial pressure scale (toward the low end), and dissociation curves resulting from low-affinity relationships will be located to the right (toward the high end). The partial pressure of a gas that will give 50% saturation of the pigment (P50), as revealed by the dissociation curve, is frequently used to characterize the affinity of that gas for the pigment. A low P50 reflects high affinity for the gas, whereas a high P50 reflects a low affinity (Fig. 1). Detailed treatments of these principles can be found in standard physiology texts.78,118,164,254,351,391,473

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FIGURE 1. Representative O2 dissociation curves for transport pigments. Hyperbolic curves (A) are typical of single-heme pigments, such as myoglobin (Mb); sigmoid curves (B, C) are typical of multi-heme pigments, such as Hb. When comparing the O2 affinity of pigments, note that curves positioned to the left reveal higher affinity, and lower P50 values, than curves positioned to the right, regardless of their shape. Thus the hyperbolic curve here (A) represents a pigment with higher O2 affinity than either of the sigmoid curves, among which B represents a pigment with higher affinity than C. Hemoglobins are tetrameric proteins having an iron-containing porphyrin (heme) associated with each of their four subunits. The iron atoms provide four binding sites for O2 or CO, which are loaded by the Hb tetramers in a complex process involving subunit

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interactions which make binding of gas molecules progressively easier as the hemes become occupied. This results in an O2 dissociation curve with a sigmoid shape.13,426 The P50 value for O2 combining with adult human Hb in whole blood falls between 25–35 torr,257,327,426 and the pigment is almost fully saturated at the normal partial pressure of oxygen (PO2) available in the lungs, which is about 100 torr138,164 (Fig. 2). The CO dissociation curve has essentially the same shape as the curve for O2,13,315,370 although it lies far to the left of the O2 dissociation curve. The CO affinity of adult Hb is about 220 times greater than the O2 affinity, this factor or “affinity constant” being normally designated “M”. Values for M as low as 185 and as high as 300 have been reported.26,44,107,116,200,203,241,369,373,374,425,450,474 The sick letrait, a red blood cell disorder, does not affect M, although CO does react more slowly with sickled red blood cells.240,371 The value of M for fetal Hb is about 20% less than for adult Hb, or between 170 and 180.107,369 The P50 value for CO when it combines with Hb in whole blood is about 0.1 torr.201,257,370 Very low levels of CO can produce high saturations of COHb, because CO binds to Hb with extreme tenacity. Oxygen binds to Hb more rapidly than CO, but also dissociates more rapidly.55,189,231,480 Since both gases compete for the same binding sites on Hb, and each can displace the other,44 the COHb concentration will depend on the PO2. Since O2 competes more effectively at elevated partial pressures, the concentration of COHb at a given partial pressure of CO (Pco) will be higher at a low PO2 and lower if the PO2 is high156,180,368,474,479 (see Section 4.2.C). Carbon monoxide has two major effects on the transport of O2 by Hb: 1) Hemoglobin occupied by CO is not available for the transport of O2; this reduces the O2 transport capability of blood. 2) Any Hb sites not occupied by CO have a greater affinity for O2. As a result, the O2 dissociation curve is shifted to the left,25,26,44,58,116,156,167,200,201,241,374,425,450,456,491 and the P50 for O2 of the remaining Hb is lowered. The value falls about 1.3 torr for each 5% increase in COHb, and will be about 12 torr below normal at 50% COHb187,327,376 (Fig. 3). This effect of CO has very important physiological implications152,373,439 (see Section 4.2.D).

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FIGURE 2. Oxygen dissociation curve for human hemoglobin. Whole blood can transport about 20 ml of O2 per deciliter. Arterial blood is almost completely saturated, at a PO2 which is typically near 100 Torr in the lungs, when it enters the systemic circulation. Mixed venous blood is about 75% saturated, at a PO2 near 40 Torr, when it is returned to the lungs; each deciliter thus delivers approximately 5 ml of O2 as it circulates through the tissues. The P50 for Hb in whole blood lies near 30 Torr. The CO dissociation curve has a similar configuration, although it cannot be resolved at this scale because the P50 for CO is so low (near 0.1 Torr). Various factors affect the binding of both O2 and CO to Hb: The affinity of Hb for O2 is decreased by DPG. This is normally found associated with Hb inside red blood cells, and

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accounts for the fact that the P50 value for purified Hb is much lower than that obtained when Hb contained in whole blood is analyzed.12,391,445,480 Some difference of opinion regarding the relationship between DPG and CO exists. Astrup argues that the increased O2 affinity associated with partial COHb saturation results from a decrease in DPG concentration in the red cells.25,29 Other studies provide results that do not link COHbinduced changes in O2 affinity to DPG, although it is clear that hypoxia increases the DPG concentration.58,315,439,456 Inanycase, CO does not alter the effect of DPG on O2 affinity, provided that the COHb concentration is below 20%.483 The O2 affinity of hemoglobin is also reduced by carbon dioxide (CO2) and

FIGURE 3. Effect of CO on the transport and delivery of O2. The required delivery of O2 (5 ml/100 ml blood) can typically be maintained by normal blood at a venous PO2 of 40 Torr. Anemic blood with only half the normal concentration of Hb can deliver the same amount of O2 if the venous PO2 falls to 27 Torr, which is generally acceptable. However, an equivalent reduction in O2 capacity resulting from

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the formation of 50% COHb requires a much lower venous PO2 (14 Torr) for constant delivery of O2, due to the increased O2 affinity of the remaining Hb; this is frequently not acceptable. (From Nunn, J.F., Applied respiratory physiology, p. 353. Copyright, Butterworths (Butterworth-Heinemann Ltd). Used with permission. acidity. This is normally revealed by a shift in the O2 dissociation curve to the right, and has been named the “Bohr Shift” or “Bohr Effect”, after its discoverer.391 The studies conducted by Rodkey et al. suggest that the pH and partial pressure of CO2 (Pco2) do not alter the relative affinity of Hb for CO and O2,369,370 although an earlier study indicated that the Bohr effect is greater for CO than O2.372 In either case, the absolute magnitude of the effect is much smaller in the case of CO, because the P50 value for CO is so low.201 There is also disagreement as to whether partial COHb saturation effects the magnitude of the Bohr shift demonstrated by the remaining oxyhemoglobin (O2Hb). Okada and his collaborators report that no change in the Bohr effect for oxygen could be detected at any COHb concentrations up to 55%,315 while Hlastala and his group have reported that the Bohr effect may be four times greater in the presence of COHb, particularly at low O2 saturations.187 Yamaguchi et al.483 also report that CO augments the Bohr effect, but only at COHb concentrations above 40%; no effect of CO was detected at COHb concentrations below 20%. C. Uptake and Clearance of Carbon Monoxide All CO is taken into the body through the lungs; uptake by other routes, such as the skin, has never been demonstrated.369, 425, 474 From the lungs CO passes immediately into a portion of the blood termed the “fast vascular pool”, which is about 30% of the total blood volume, or about 1.5 L. Blood in this pool passes through the lungs at about 5 L/min, and is mixed into the remaining circulatory volume, or “slow vascular pool”, at about 1 L/min.149 The slow vascular pool includes blood in such reservoirs as the spleen, abdominal veins, and skin vessels. During initial uptake CO dissolves in the plasma before combining with Hb.152 Considerable effort, theoretical as well as experimental, has been expended to develop mathematical formulae which can be used to predict rates of CO uptake and equilibrium levels of COHb. These formulae have been refined enough so that some may provide results which are both accurate and precise. Moreover, they allow consideration of numerous physiological and environmental factors. Derivation of such formulae are beyond the scope of this review, but detailed information may be obtained from the important contributions to this effort by Forbes, Sargent, and Roughton (136); Coburn, Forster, and Kane;82,86,441,442 Beard;44 Forbes;135 Peterson and Stewart;341,342,425 Cagliostro;66 Joumard et al.;203 and Hauck.178 The rate of uptake increases with increasing PCO, and at the onset of exposure 50–80% of the CO inspired in each breath will be absorbed.136, 372 The initial rate of uptake is

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rapid and logarithmic, or initially linear and then logarithmic.44,86,136,342 Asa consequence of this, brief exposuresathigh Pco can result in high COHb concentrations,425 and the time required for incapacitation thus decreases as the PCO increases.267 Reduced barometric pressures, down to 140 torr, have no effect on the rate of CO uptake provided that the intrapulmonic PCO remains constant.136 The uptake of CO at elevated barometric pressures depends upon the relative concentrations of CO and O2. At CO concentrations of above 0.05% or more in air the formation of COHb increases rapidly with increasing barometric pressure. However, in atmospheres having lower concentrations of CO in air, the elevated PO2 resulting from increased barometric pressure may actually cause the percentage of COHb in the blood to decrease as the total pressure increases.367 The duration of exposure to CO is as important to COHb concentration as the PCO, because the high CO affinity of Hb allows CO to continually displace O2.479 The logarithmic rate of uptake becomes obvious during extended exposures, as the COHb concentration rises at progressively slower rates. This occurs because the CO gradient between alveolar gas and blood is reduced, due to elevated back-pressure of CO, which rises as the COHb concentration increases, and elevated alveolar PCO, which in turn rises because less CO is being absorbed from each breath.136,372 One study has indicated that the severity of human intoxication with CO correlates more strongly with the duration of exposure than with the final COHb concentration.418 A study on rats appears to confirm this, the median lethal concentration (LC50) for CO was found to be about 0.88% when the exposure time is 10 min. This value decreases to about 0.61% at 20 min of exposure, to about 0.55% at 30 min, and to about 0.47% at 60 min.184 More recent studies found CO lethality exposure values in rats of 0.76% at 10 min, 0.56% at 20 min, 0.46% at 30 min and 0.335% at 60 min.246 The overall rate of uptake increases with increasing ventilation rate, particular at high PCO values. However this relationship is not directly proportional, because a smaller percentage of CO is extracted from the inspired air at higher rates of ventilation.86,116,136,372,408 Uptake of CO also increases with the diffusion capacity of the lungs,86,170 and this may involve carrier-mediated (or facilitated) diffusion in which the carrier may be cytochrome P450, which is an intracellular, heme-containing coenzyme.290 An increase in the rate of blood flow through the lungs, resulting from increased cardiac output, increases the rate of CO uptake,479 and thus uptake increases with exercise, because this stimulates both the cardiovascular and respiratory systems.203,271 The effect of ambient temperature on CO uptake appears to be similar to the effect of exercise. The COHb concentration in rats exposed to CO at 36°C is significantly higher than in rats exposed at 25°C, apparently due to the hyperventilation and increased cardiovascular activity involved in thermoregulation. Increased uptake apparently increases the lethality of CO at high temperatures, the LC50 for mice at 36°C being about one-third of the value obtained at 25°C.485 The uptake of CO will be reduced at high PO2 values due to competition for binding sites on heme, as already described.86,136,372 This relationship also depends upon the type of Hb involved, since the affinity for oxygen varies somewhat between Hb types: for a given exposure to CO, Hb types having a higher O2 affinity will develop a lower COHb concentration.429 The cell membrane does not appear to limit CO uptake by red blood cells, although movement of CO from the plasma into the erythrocytes may be slowed by an unstirred layer which surrounds each cell.14,231,403 Analysis of blood samples has revealed that all erythrocytes do not take up CO, and that CO binds preferentially to Hb

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near the periphery of those cells in which CO uptake can be demonstrated. Once combined as COHb, redistribution of CO does not occur among erythrocytes during the circulation.55 It is important to note that factors related to the uptake of CO can act synergistically. Thus the expected COHb saturation resulting from an individual exposure to CO may differ from reported “mean” values for that exposure by 10–15% (e.g. COHB values between 30 and 45%) if all the operating variables are not known or considered in the calculation.136 However, empirical data from numerous papers permits the rate of uptake in mammals to be estimated,1,79,136,160,311,340,369,383,416 and certain general conclusions can be drawn: Under “normal” circumstances the COHb concentration will increase at about 1 %/min when the inspired CO concentration is a few tenths of a percent. The increase in COHb will be closer to 0.5 %/min with exposures at lower concentrations (near 0.1% CO), and nearer 1.5–2 %/min with exposures near 0.5% CO. Rates of uptake will increase about ten-fold once the level of exposure reaches about 1% CO. At exposures to greater than 1% CO, uptake will be very rapid due to the logarithmic relationship between CO concentration and uptake,342 and high levels of activity can double whatever rate of uptake is produced by other factors.136,372 Studies with mice reveal that physical collapse can occur as soon as about 1 min in an atmosphere containing 1.3% CO and in about 15 s if the CO concentration is 5%.143 Physiological uptake (in the lungs) is much faster than physical uptake re-sulting from agitation of whole blood in an atmosphere containing CO: in vitro experiments have revealed an increase in COHb concentrations of only 4.5 %/min during exposure to an atmosphere of 100% CO.153 Similar empirical data is available on the concentrations of COHb reached at equilibrium, and the time required for this, given a particular exposure level 69,156,157,340,341,385 At low CO concentrations (less than 0.01%) equilibrium will develop at about 5% COHb in approximately 24 h; when the concentration of CO is a few hundredths of a percent, equilibrium will require about 15 h and will develop at 15–20% COHb; at concentrations of about 0.1% CO the equilibrium concentration of COHb will be about 60%, which will develop in 6–8 h; when CO concentrations exceed 0.1–0.2%, equilibrium is reached in less than an hour, if death does not occur sooner. Once a given quantity of CO is taken into the blood, COHb equilibrium within the fast and slow vascular pools occurs within 15 min.149,464,481 Carbon monoxide is cleared principally by diffusion across the alveolar membranes of the lungs, this process being the exact reverse of uptake.450,470 Since CO is not a cumulative poison, given time it will be completely cleared from the body, provided a CO-free atmosphere is available.369,474 Some CO is oxidized to CO2,260,487,488 but the rate of oxidation is very slow and the amount of CO involvedis insignificant, being less than 1% of that cleared by the lungs 425,470 (see Section 4.6.B). Rates of CO clearance are expressed as “half-times”, or the time required to reduce an existing COHb concentration to half of its original value. This is a common means of describing processes related logarithmically to time. There is close agreement among most studies which have assessed clearance of CO:9,149,294,372,383,425,474 the half-time for clearance of CO is about 4 h for individuals breathing room air at atmospheric pressure; this half-time is reduced to 1 h or less if pure O2 is supplied at atmospheric pressure, and the time can be reduced even further by supplying O2 at elevated pressures (in a hyperbaric chamber). Clearance times are extended in individuals with chronic lung disease; thus COHb levels will remain high for a longer period.271,343,425 Clearance times

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are shorter in children, but do not change significantly after about 20 years of age.203 When a pulse of CO is administered to anesthetized dogs, the post-administration concentration of COHb in arterial blood decreases exponentially for about 15 min as the CO is distributed from the fast vascular pool into the slow vascular pool. Subsequently, the arterial concentration of COHb decreases in linear fashion for about 90 min. The halftime for clearance in such dogs is about 2 h for initial COHb concentrations of 20– 43%.464 Short exposures, even to high CO concentrations, may produce few symptoms because the CO may be cleared from the fast vascular pool before much mixing into the “slow pool” can occur.136,276,343 D. Distribution of Carbon Monoxide and its Relationship to Oxygen Delivery At equilibrium the amount of CO physically dissolved in the plasma and other body fluids is very small compared to the amount bound as COHb, although dissolved CO is extremely important to the extravascular activity of CO153,470 (see Section 4.6). Distribution will be uneven in the blood for the first several minutes because of movement into the slow vascular pool, which at rest includes the muscle capillaries,149 and because CO is not redistributed among erythrocytes once it is bound as COHb.55 A given quantity of blood will lose about 2% of its CO to the tissues during transit through the capillaries,408 and equilibrium between blood and tissue will require 30 min to 1 h.44,86,88,137 The extravascular compartment is commonly reported to contain about 25% of the total body CO (although estimates vary from 10 to 40%), most of which is apparently bound to myoglobin (Mb), which is a heme-containing pigment found in skeletal and cardiac muscle.44,149,372,470 Such a distribution of CO produces a carboxymyoglobin (COMb) saturation which is about equal to the COHb saturation, under normal (resting) conditions. That is, the COMb/COHb ratio normally falls between 0.75 and 1.0087,321 (see Section 4.6.C). Under certain conditions the COMb/COHb ratio can rise to values as high as 3.0, reflecting COMb saturations which are three times greater than COHb saturations. Such changes in this ratio indicate shifts of CO from the blood into the tissues, perhaps involving as much as 50% of the vascular CO, where it binds to Mb. Redistribution of CO into the extravascular compartment results from reduction in tissue PO2, which follows reduction of arterial PO2 and/or blood pressure, or increased activity (which depletes O2 stores in the tissues and reduces the venous PO2). Shifts of CO into the tissues will also occur if the circulating COHb saturation rises above 55%, provided the victim survives, of course.83,87,88,193,260,421 Effects on O2 delivery are hard to assess, because of the numerous variables involved, the complex relationships between these, and the wide range of “normal” values. However, it is clear that O2 delivery is reduced by CO for three reasons: 1) Carbon monoxide reduces the oxygen transport capability of blood.138,187,315,369,425 2) Carbonmonoxide inhibits facilitated diffusion of O2. The diffusion of O2 is normally accelerated by Hb and Mb, which increase the rate of O2 transfer into cells. This effect may triple the intracellular delivery of O2, but COHb and COMb do not facilitate O2 diffusion and do not affect diffusion of CO.59,232,480 3) The left-shift of the O2 dissociation curve (increased O2 affinity) in the presence of COHb results in a higher O2 saturation of remaining Hb at a given PO2; thus less O2 will be unloaded for delivery to the tissues at that PO2 (Fig. 3). This effect of CO reduces O2 delivery much more than equivalent

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hypoxia or anemia (at COHb saturations greater than 10%), and thus is more important than the reduction in O2 capacity by COHb.24,44,57,96,97,98,137,138,152,187,216,315,369 A saturation of 5% COHb will reduce O2 delivery by 20–25% at normal PO2,58 and this reduction is increased to 50% with an increase in COHb saturation to only 25%.315,343 Maintenance of O2 delivery in the presence of COHb involves levels of physiological compensation that may be neither possible nor acceptable, depending on the circumstances. In cases of chronic exposure to sublethal levels of CO, compensation involves increases in erythrocyte production (which elevates Hb concentration), red cell mass, hematocrit, and blood viscosity,57,76,321,376,377,404 and reduction in the metabolic rate.106 The compensatory response to acute exposures involves two major physiological processes, as follows: 1) Blood flow through the tissues is increased.57,58,121,137,156,166,336,343,456 2) Cellular processes operate at reduced PO2 so that an equivalent amount of O2 can be extracted from Hb having an increased O2 affinity.24,33,34,35,146,215,361,425,456,465,474 Cells normally operate at a venous or capillary PO2 of about 40 torr. At constant flow, this value will be reduced to about 27 torr if the normal amount of O2 is extracted from anemic blood having only 50% of the normal O2 capacity. However, in blood with an O2 capacity reduced to 50% of normal by CO (COHb=50%), a reduction in tissue PO2 to 14 torr will be required to permit extraction of the normal quantity of O2 if the flow is not increased (Fig. 3); only 10–20% COHb will reduce the PO2 to 30 torr or less in the absence of increased flow. Such reductions are particularly important in the case of muscle, which generally requires a capillary PO2 of at least 35 torr for proper activity.33,137,215,479 Working muscle can function normally, and maintain the normal rate of O2 uptake, in the presence of considerable hypoxic hypoxia. However, equivalent hypoxia resulting from elevated concentrations of COHb reduces O2 uptake, O2 extraction ratios, and twitch tension in working muscle, because of the increased O2 affinity and the formation of COMb.216 It has been reported that the effects of CO2 on O2Hb (the Bohr Effect) are sufficient to counteract the effects of COHb on O2 affinity, and thus maintain O2 delivery,166,187 but this effect could not be confirmed by other investigators.222,315 Venous blood returning to the heart with an abnormally low PO2 will reduce the arterial PO2 if vascular shunts exist in the pulmonary circulation to by-pass functional alveoli. Some shunting of this sort occurs even in healthy lungs, and can become a serious problem in chronic lung disease.78,254,405 Effects on arterial PO2 can be observed if only 2% of the cardiac output flows through shunts, given COHb saturations as low as 10%.33,34,35,60,137 4.3 EFFECTS ON THE RESPIRATORY SYSTEM A. Pulmonary Effects Conflicting results have been reported from studies assessing the effects of CO on the lungs. Fisher et al.,133 Brody and Coburn,61 Loke et al.,255 and Hugod194 could detect no direct effect of CO on pulmonary function or the structure of lung tissue. However, there seems to be implicit agreement that lung tissues would be among those affected by levels of CO sufficiently high to produce generalized toxic effects. Humans and experimental animals exposed to CO often develop symptoms of pulmonary distress, and postmortem examinations following CO intoxication frequently

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reveal pathological evidence of pulmonary congestion and edema,130,228,305,362,411 which may result from increased permeability of alveolar-capillary barriers.444,490 In rabbits, acute exposure to highlevelsofCO (COHb= 63%) has been associated with increased alveolar-epithelial permeability, interstitial edema, and ultrastructural alterations of endothelial and epithelial cells.130It has also been suggested that pulmonary edema has a neurogenic basis, involving sympathetically-mediated vasoconstriction, secondary to cerebral hypoxia caused by CO.305 Pathological changes in the lungs may also result from pulmonary emboli, formed in response to effects of CO on blood clotting159 (see Section 4.2.A). Pulmonary hypertrophy develops in rats exposed chronically to CO, but this does not result from edema or fibrosis.333 At the cellular level, exposure to CO inhibits protein synthesis in rat lungs,142 and reduces the total content of lipid, carbohydrate, and protein in the lungs of squirrels.362 Chronic exposure to CO may involve inflammatory and immune responses which depend on the circumstances of exposure: the number of pulmonary alveolar macrophages and polymorphonuclear leukocytes increased in the lungs of guinea pigs exposed to regular pulses of 1% CO for 4 weeks, but fewer immunologically-competent B-lymphocytes could be isolated from the lungs.413 In rats, continuous exposure to 0.01% CO appears to reduce the number of alveolar macrophages, impair macrophage adhesion, and reduce the pulmonary level of histamine.452,453 Unfortunately, several results of these studies failed to achieve statistical significance, due to the large variation in cell counts within the control and experimental groups. In some cases the use of pulmonary function tests has revealed effects of CO inhalation. Performance was decreased among bridge and tunnel officers exposed regularly to CO from automobile exhaust. Such individuals also had elevated COHb levels, and a high incidence of symptoms associated with pulmonary disease.126 Direct inhalation of 0.5% CO in air by human subjects reduced the pulmonary diffusing capacity, inspiratory capacity, and total lung capacity, but increased the maximum breathing capacity. Differences between control and experimental subjects were consistent and statistically significant, but experimental values remained within the normal range for each parameter.79 Dynamic lung compliance was reduced and airway resistance was increased in rabbits breathing 0.8% CO.130 Irregular changes in total respiratory resistance (increases alternating with decreases) were recorded from rats and guinea pigs exposed to 3% CO in air, but similar changes were also produced by hypoxic atmospheres without CO, at about 10% O2.300 Taken together, the available evidence suggests that lung tissue does not have a special sensitivity to CO.330 Certain effects, such as increased capillary perme-ability, appear to reflect general actions of CO,28 and would thus be expected in tissues which cannot avoid direct contact with the gas when it is present in the atmosphere. Furthermore, in experiments with intact organisms it is difficult to distinguish direct effects on the lungs from other effects which produce a pulmonary response, because of the complex mechanisms which regulate respiratory activity.118,164 Finally, doubt is cast on the case for direct pulmonary effects by the failure of data to satisfy statistical requirements for significance, and by the well-conceived and carefully executed studies which reveal no effects.

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B. Effects on Respiratory Control Although exposure to CO increases the ventilation rate,33,35,44,71,75,284,400,408,410,439 this response develops only after 5–10 min of exposure, even at high levels, which are often lethal. Respiratory stimulation depends upon the concentration of COHb, 40–50% COHb being required at rest,311,381,474 although the same effect is observed at 15% COHb during maximum exercise.347 Because of the delayed response, and high concentrations of COHb required, the results of several studies reveal no effect on ventilation rate.80,121,340,372,479 At higher COHb concentrations (55–65%) the ventilation rate decreases, and breathing ceases at 70–75% COHb. Respiratory depression at these extreme COHb concentrations results from medullary anoxia which inhibits the respiratory center.80,284,474 Although some data suggests that CO affects respiratory control directly,276 a direct effect on the neural mechanisms which control respiration has not been consistently identified. Most studies have concluded that CO exerts its effects via hypoxia and metabolic acidosis, or occasionally respiratory alkalosis,410 which affect respiratory control functions in the brain. Such hypoxia acts on respiratory neurons associated with the pons, and also inhibits cortical control of these neurons, thus producing the characteristic hyperventilation.75,305,311,368,381 Sensory chemoreceptors in the medulla and carotid bodies, which normally play an important role in respiratory regulation are not affected by CO. Carotid bodies respond to reduced PO2 in the blood, which will frequently remain above the threshold for these receptors even in the presence of significant COHb concentrations. Effective CO concentrations are so low that the percent composition of blood gases is changed very little, even though the formation of COHb will reduce the O2 content of blood and increase the affinity of remaining Hb for O264,75,169,234,235,311,372,381 (see Section 4.2.B). Chemoreceptors in the aortic bodies are activated in the presence of COHb, even at normal PO2, because these respond to reductions in O2 delivery. However, these sensory receptors are principally involved in initiating the cardiovascular response to CO (see Section 4.4.A), and have a very small role in stimulating ventilation.234,235 SinceO2sensingchemoreceptors have only minimal involvement with the respiratory response to CO, severing the vagus nerves (which link the carotid and aortic bodies with the brain) has very little effect on CO-induced hyperventilation.75,381 4.4 EFFECTS ON THE CIRCULATORY SYSTEM A. General Cardiovascular Effects The basic response of this system to CO derives from the reduced O2 capacity of blood and increased O2 affinity of Hb caused by the formation of COHb, which have already been described (see Sections 4.2.B, 4.2.D). The delivery of sufficient O2 to the tissues at an acceptable PO2, depends on an increased flow of blood through the cardiovascular system.39,137,205,224,425 Under normal conditions such demands for increased flow can be met, even at considerably elevated COHb concentrations. Tissues (other than the heart and brain, which will be considered in Sections 4.4.B and 4.4.C) require only 25–30% of the O2 delivered to them in the absence of COHb,33,39,254 and even though a COHb

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concentration of 8–10% would require a 40–60% increase in blood flow to maintain O2 delivery at constant PO2 (57), some reduction in both O2 delivery and PO2 can be tolerated.479 The hemodynamic changes observed in the presence of COHb, which produce the required increase in blood flow are: 1) Increased cardiac output.21,44,74,80,98,120,166,205,214,215,225,278,328,336,372 This frequently results from increased heart rate,1,28,71,74,98,120,205,328,334,337,340,381,411,454 althoughthe heart rate does not always increase.19,284,300,311,336,338,400,411,431,435,454,479 The heart rate decreases in isolated rat hearts, possibly due to a direct effect on the pacemaker and/or cardiac conduction system.280 Since cardiac output may increase at a constant heart rate, as a result of increased venous return and increased stroke volume,74,98,164,456 there is convincing evidence that CO does not accelerate the heart directly in vivo, but that it acts as a stressor via the sympathetic division of the autonomic nervous system, once COHb reaches some critical concentration. Tachycardia induced by CO can be blocked with propranolol, a non-specific beta-adrenergic blocker, and ICI 118,551, a selective beta-2 blocker.74 In addition, the myocardial content of norepinephrine (NE) decreases,310 the arterial concentration of catecholamines is elevated,433 and the rate of catecholamine excretion increases.1,33,35,205,320,330,381,400,435 2) Reduced resistance to flow through the blood vessels.74,98,205,214,215,216, 257,328,336,408,433 This is generally accomplished by vasodilation,164,250,252,330 which appears to result from a direct action of CO on vascular smooth muscle. At constant PO2, segments of isolated rat aorta contracted with NE or potassium relax in the presence of CO; removing the vascular endothelium does not abolish the CO-response.250 In such preparations, CO decreases the intracellular concentration of calcium in the smooth muscle,252 and inhibits calcium uptake;285 in cells cultured from vascular smooth muscle, CO increases the level of cyclic GMP.360 Thus, CO may act by interfering with calcium exchange at the cellular level,250,251 or through a second messenger system involving guanylate cyclase,360 although pulmonary vasodilation may involve the binding of CO to cytochrome P450.432 Vasodilation of appropriate cutaneous vessels is responsible for the “cherry-red” color which often develops as a symptom of CO poisoning132,257 (see Section 4.1). The decrease in vascular resistance is frequently greater than required to ac-commodate the increased flow, and thus the blood pressure usually decreases,28,71,74,98,205,214,215,216,227,228,284,300,328,330,338,340,404,407,408,411,431,433,435 which may beresponsible for the renal dysfunction sometimes observed clinically in cases of CO intoxication.228 If a decrease in resistance is prevented, as in hypertensive Dahl rats, the blood pressure will increase.404 The elevated red cell count, and consequent increase in blood viscosity and volume, which results from chronic exposure to sub-lethal levels of CO (see Section 4.2.A), compromises the effectiveness of vasodilation in reducing vascular resistance, and imposes additional strain on the heart.44,57,227,333,470 The overall response of the cardiovascular system results from local regulation of blood flow within individual tissues,118,164 and the activity of chemo- and baroreceptors in the carotid433 and/or aortic bodies. Chemoreceptors in the aortic bodies are sensitive to O2 delivery, even in the presence of normal PO2 in arterial blood.235 The chemoreceptor response is mediated by the sympathetic division of the autonomic nervous system which acts via adrenergic synapses. Specific blockade of receptors in such synapses has revealed that beta-2 receptors are required for the response to CO.74,214 Exercise places the same demands on the cardiovascular system as COHb, since increased O2 utilization demands increased O2 delivery. Thus exercise studies conducted during exposure to CO reveal two characteristic results: 1) The cardiovascular response

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to CO is intensified at moderate activity levels,454 reflecting summation of the exercise and CO effects. 2) Maximum effort, which is limited by the availability of O2, can be sustained for periods of shorter duration when CO is present.79,121,192,347,450,456 Cardiovascular and pulmonary disease impede blood flow and reduce the O2 content of blood. Thus, these conditions compromise cardiovascular efficiency, interfere with O2 delivery, and increase the risk from CO. Conditions important in this regard include occlusive arterial disease, both coronary and peripheral,15,22 chronic lung disease, such as emphysema,21 and anemia.157,425 B. Myocardial Effects Many parts of the body may extract more O2 from the blood if the rate of delivery is reduced. However, O2 extraction by the heart is so great that it is particularly vulnerable to any factor which reduces O2 delivery,39 and acute exposure to high levels of CO usually result in death from cardiac arrest.411,425,429 The heart normally extracts about three times more O2 from the blood (75%) than most other tissues, and the PO2 in venous blood leaving the coronary circulation (20 torr) is about half that typically found in venous blood from the systemic circulation.33,34,44,137,156 Since increased extraction of O2 would quickly reduce the PO2 to an unacceptable level, the heart responds to increased O2 demand, reduced O2 content of the blood, or elevated COHb levels, by increasing the coronary flow rate;32,414 O2extraction by the myocardium does not increase,33,156,389 and may actually decrease.32 In general, the myocardial effects of CO reflect the hypoxia which develops because COHb reduces the O2 content of blood and increases the O2 affinity of Hb to which CO is not bound.19,23,33,34,35,39,44,46,96,137,156,203,257,425,470,474,479 Specifically, exposure to CO affects the heart as follows: 1) Flow is increased through the coronary vessels as a result of vasodilation.26,35,44,46,200,252,253,278,280,287,349,388,425 This compensatory response is usually sufficient to maintain competent myocardial activity even at moderate COHb concentrations, provided that the heart is healthy and other demands on it are not excessive,35,46,151,152,153,296,414,470 even though coronary blood flow may be distributed to produce subendocardial underperfusion and hypoxia, resulting in cardiac damage.120 However, hearts with coronary artery disease may not be able to increase blood flow by the required amount. Insufficient blood flow (ischemia) will thus reduce the PO2,15,17,30,32,33,34,35,39,44,46,64,116,120,203,296,376,414,421,425,440,450,479 and cause cardiac failure due to death of myocardial cells (infarctions).64,157,272,421,450 Small infarcts may even be produced by isolated vascularlesions, due to localized reduction in coronary flow which affects the average PO2 very little;33 15–20% COHb may be lethal if coronary artery disease is severe.425 A study involving post-mortem examinations conducted on COrelated casualties who succumbed at low COHb concentrations (COHb=10–50%), discovered moderate or severe coronary atherosclerosis in 93% of the cases.39 A similar study, which identified victims of CO intoxication with minimal coronary disease, revealed that 85% died at COHb concentrations in excess of 50%.134 In patients with diagnosed angina pectoris, CO reduces the exercise time (or the level of exertion), required for the onset of pain or the development of electrocardio-graphic changes which indicate myocardial ischemia. These effects have been reported at COHb levels as low as 2%, although the actual threshold remains controversial.2,7,16,17,64,116,155,156,179,200,203,241,389,402,425,450,470,479,489 Coronary vasodilation

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produced by CO does not involve the sympathetic division of the autonomic nervous system, since blocking agents do not affect the response.46,227,250,278,360,388 Experiments with isolated rat hearts reveal that vasodilation, which develops at constant pulse pressure and heart rate, does not result from decreased PO2 or the formation of COHb, and that neither adenosine nor prostaglandins mediate the effect.250,253,278,279,287 Accordingly, the direct action of CO on vascular smooth muscle, which has already been described (see Section 4.4.A), appears to be responsible for increasing the rate of coronary flow. 2) Cardiac muscle is damaged, which reduces the pumping effectiveness of the heart. Such injury has been identified by elevated serum levels of the creatine phosphokinase isoenzyme, and other enzymes, associated with the myocardium.145,440 Damage to hearts from squirrels exposed to CO has been reported, based on analyses which demonstrate that cardiac tissue from exposed animals contains less protein, lipid, and carbohydrate than similar tissue from control animals.362 Exposure to CO reduces myocardial contractility, especially in the left ventricle,77 and this may be accompanied by prolapse of the mitral valve.19,23,44,156,199,227,296,470 Contractile activity is also disrupted by CO in isolated preparations of right ventricles from rats. The effects are similar to those produced during hypoxia created with nitrogen (N2), but the mechanism of action appears to be different, because preparations exposed to CO recover more completely when O2 is resupplied.286 Cardiac hypertrophy, usually involving the right ventricle, may develop from chronic exposure to CO44,76,92,98,157,282,323,328,333,334,336,337,339,404 as a result of increased blood viscosity and volume (see Section 4.4.A). Cardiomegaly induced by CO can be detected in prenatal rats as a result of maternal exposure, but heart weight will return to normal if CO is not encountered during postnatal development. However, cardiac hypertrophy produced as a result of postnatal exposure to CO persists in adults.331 Increased DNA content in hypertrophied hearts suggests that cardiomegaly is caused by proliferation of myocytes.334 Histological and ultrastructural examination of hearts from chronically exposed subjects has revealed a variety of degenerative changes in the muscle fibers.9,26,27,44,92,157,218,241,350,372,421,440,450,469 3) Electrical activity of the heart is altered, as a consequence of ischemia and physical damage to the myocardium.9,15,17,18,46,116,228,411,470,489 Electrocardiographic analysis reveals various arrhythmias, including premature ventricular contractions and both atrial and ventricular fibrillation, as well as patterns of normal configuration but reduced amplitude.9,15,16,156,157,228,238,262,264,288,296,330,401,411,421,425,440,450,470,479 Human subjects chronically exposed to 0.05% CO (COHb=7%) developed consistent electrocardiographic abnormalities in the P wave, which suggests that CO exerts a specific toxic effect on the atrial pacemaker and/or the cardiac conduction system.100 Data from experiments with isolated, perfused rat hearts supports a similar conclusion, since exposure to CO produces bradycardia more quickly in unstimulated preparations than N2anoxia.77 Both myocardial infarction and exposure to CO reduce the voltage threshold for ventricular fibrillation. When these conditions coexist, the effects are additive,102 but hearts with healed infarcts do not demonstrate any additional sensitivity to CO.454 In animals with known infarcts, the voltage required to produce fibrillation is reduced at COHb concentrations as low as 6%,17,23,156,421,470 and a significant increase in the occurrence of ventricular arrhythmias can also be detected among humans with known coronary artery disease at 6% COHb.401

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C. Cerebral Effects The brain, like the heart, requires a consistently high rate of O2 delivery to support a high metabolic rate, and thus is particularly susceptible to CO intoxication.257,289,479 Accordingly, the effects of CO on the brain are similar to those described for the heart (see Section 4.4.B): Vasodilation greatly increases the cerebral flow of blood in the presence of cOHb.64,102,109,169,223,225,228,325,329,330,348,372 The resulting edema52,113,338 and elevated pressure of cerebrospinal fluid initiates the intense headaches commonly reported as early symptoms of CO intoxication,28,64,200,228,372 and may cause subsequent irreversible damage to the brain.113 Cerebral blood flow increases more than required to compensate for the reduced O2 content of blood resulting from COHb formation. The hyperperfusion is thus thought to reflect metabolic autoregulation in response to reduced O2 delivery caused by increased O2 affinity of free Hb, rather than a direct effect of CO on brain tissue.109,223,225,325,343,446 Although direct effects of CO on the cerebral vasculature have not been specifically identified,225 CO-induced flow rates about twice that resulting from equivalent anemia have been measured experimentally,325,400 and output from chemo- or baroreceptors in the carotid bodies is not required for the increased cerebral flow associated with CO.446 Given a competent vascular system, the increased blood flow can maintain cerebral O2 at normal levels if the COHb concentration does not exceed about 30%, but flow cannot be increased sufficiently to prevent a decrease in O2 consumption once the COHb concentration reaches 40–50%.343,348 If cerebral circulation is impaired, or if blood flow does not increase uniformly throughout the brain, increased risk from CO will develop at much lower concentrations.203,343 Hypoxia may cause swelling of neuroglial cells which form the blood-brain barrier, and thus cause persistent disruption of cerebral functions by reducing blood flow through specific regions of the brain.115,146 Non-uniformity of cerebral perfusion apparently contributes to the development of lesions in the basal ganglia, which often characterize CO intoxication (see Section 4.5.A). Due to its location, this region is vulnerable to CO hypoxia because it receives end-arterial blood, and is somewhat poorly vascularized relative to other parts of the brain.52,148,289 D. Vascular Effects Since CO is transported by the blood, uptake and clearance expose the blood vessels to dissolved CO, as well as COHb. Considerable effort has been expended to determine if damage to vascular tissues result from this exposure, with special attention being given to the role of CO in atherogenesis. It is frequently asserted that exposure to CO promotes the formation of atherosclerotic lesions. This view is supported by data which falls into two broad categories: 1) Hypoxia, usually attributed to the left-shifted O2 dissociation curve resulting from the formation of COHb, is thought to damage arterial walls and increase their permeability. Increased vascular permeability causes subendothelial edema and intramural accumulation of lipids (particularly cholesterol) and protein, which appear to accelerate the development of atherosclerotic plaques.26,241,382,450,451,469 A computer simulationof O2 transport through arterial walls in the presence of COHb has predicted maximum hypoxia in the middle layers, where histological examination has most often demonstrated damage.392 It has also been suggested that exposure to CO causes vascular

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damage in certain individuals by creating a pyridoxine (vitamin B6) deficiency which elevates serum levels of homocystine.67 2) Evidence exists that CO promotes adhesion of platelets and mononuclear leukocytes to the arterial lining, and initiates the formation of thrombi at the sites of adhesion. Electron microscopy (scanning and transmission) reveals that these sites may be areas of incipient or early endothelial damage.273,274 Increased platelet adhesion has been invoked to explain the decrease in circulating platelet count which follows acute exposure of rabbits to CO.54 However, it is also argued that CO lacks atherogenic activity. Findings which do not indicate a role for CO in atherogenesis can also be organized into two categories: 1) Several studies fail to show any CO-induced accumulation of lipid or protein in arterial walls, even in the presence of increased vascular permeability. The vascular accumulation of cholesterol often appears to be determined by the serum cholesterol level, and not by the presence of CO.422 In monkeys maintained on a normal diet, intermittent chronic exposure to CO (COHb=20%) had no effect on the formation of atherosclerotic lesions. Such exposure was also without effect on the influx or arterial content of cholesterol, although an increase in the plasma and tissue levels of free fatty acids was noted.53 A similar lack of effect on cholesterol accumulation has been reported from experiments with pigeons maintained at normal cholesterol levels.451 In dogs, CO increases arterial permeability to fibrinogen, but does not cause fibrinogen to accumulate in the vascular walls. The increased permeability is not associated with endothelial damage, even though fibrinogen is typically involved in atherogenesis.6 2) Platelet responses consistent with atherogenic activity are not always produced by CO. The extent of aggregation caused by ADP is not modified by 100% CO in plateletrich plasma from human blood,172 and CO does not reduce the inhibition of platelet aggregation mediated by prostacyclin. The production of prostacyclin by isolated preparations of rat aorta was not decreased in the presence of CO;172 heart muscle from rabbits exposed to CO increased prostacyclin production.119 Other results which reveal an inhibition of platelet aggregation have already been presented (see Section 4.2.A). Thorough histological examination of pulmonary capillaries from CO-exposed rabbits revealed no platelet aggregations or thrombi, and no histological or ultrastructural changes in the morphology of pulmonary or aortic vasculature could be detected in such rabbits.194,450 While data which relates atherogenesis to CO-exposure appears to predominate, the controversy regarding vascular effects cannot be completely resolved with available information, and great care must be exercised to avoid any interspecific extrapolation of results which has not been confirmed. Experiments with cultured cells from the aortic endothelium of pigs and cows reveal that the effects of CO depend on the animal from which the cells were obtained. In both species the effects of hypoxia differ from the effects produced by exposure to CO.244 4.5 NEUROMUSCULAR EFFECTS A. Neurological Effects Acute, severe intoxication with CO often produces characteristic lesions in the brain, normally detected by computed tomographic scanning,52,148,171,195,220,298,318,385,386,387,438,490

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or magnetic resonance imaging.191 The lesions usually occur among the basal ganglia of the cerebrum, most frequently in the globus pallidus,123,148,191,195,289,385,386,387,395,490 but may also appear in the hippocampus117,191,406 and the cerebral white-matter.52,171,298,349,438 They may develop over a period of several days post-exposure,52,171,406 and are typically bilateral,52, 171,191,195,220,289,298,385,386,387,395 although unilateral lesions have been reported.52,438 The validity of computed tomographic findings has been confirmed with subsequent post-mortem examinations,which have revealed necrosis as well as neuronal de-myelination and degeneration in the indicated locations.123,148,171,349,385,387,479 The basal ganglia are involved with the control of movement,164 thus injury to this region of the brain may produce neurological sequelae such as parkinsonism,220,372 Gillesde la Tourette’s syndrome,352 dysarthria, and other motor malfunctions.349,372,395,399 Recovery may ber emarkable,385,395or protracted and 52,115,195,200,220,221,289,298,349,372,386,438,490 incomplete, the overall prognosis following in toxication apparently depending on the extent of white-matter involvement.298 Damage to the globus pallidus, also associated with poor recovery or death if the insult is extensive and persistent,386 may cause latent symptoms which do not develop for days, weeks, or months after initial recovery.123,191,200,228,298,349,385,395 The lesions themselves may disappear,385 or become calcified and remain indefinitely.195 Other effects of CO on the central nervous system have been reported, involving the hypothalamus. Thermoregulatory activity is often disrupted, producing the progressive hypothermia which is a typical symptom of CO poisoning.338,431,485 intoxication with CO appears to damage neurosecretory neurons within the hypothalamic-hypophyseal axis. Diabetes insipidus may develop if antidiuretic hormone secretion is affected,167,411 and activity of the thyroid and adrenal glands can be modified if releasing factors which control secretion of trophic hormones by the adenohypophysis are involved.358,463 A definitive mechanism to account for the effects of CO on brain tissue has yet to be developed. However considerable progress toward this end can be made using available data, which presents a consistent view on several points: 1) It seems evident that these effects derive from cerebral hypoxia,117,190,195,330,349,372,385,411,425,479,490 complicated by regional ischemia and hypoperfusion52,70,115,148,167,200,298,340,395,406,438 secondary to systemic hypotension289,330,350 (see Section 4.4.C). Clinically-induced hypertension has been of some value in treating the neurological aspects of CO poisoning,115 but without intervention the situation apparently causes vascular damage,122,200 disrupts the blood-brain barrier,52,115,148 and culminates in edema,52,122,184,228,238,338,350,386,490 compounded by acidosis330 resulting from increased production and accumulation of lactate. Hypoxic conditions favor the formation of lactate, and glycolysis is accelerated by the stress-induced hyperglycemia which generally accompanies CO exposure.329,338 Edema leads to softening of the tissue, necrosis, and the demyelination which is commonly observed.122,171,190,385,386,387,420,490 2) At the cellular level, damage has also been attributed to direct, cytotoxic effects of CO,123,137,171,276,277,309,340,343,386,395,438,458 although the supporting data remains somewhat controversial (see Sections 4.6.A, 4.6.B). Biochemical and metabolic studies have demonstrated that exposure to CO decreases the rate of protein and myelin synthesis,122,438 alters the metabolism of bioamines265 as well as their levels throughout the brain,399 decreases the stability of lysosomes,122,384 and disrupts the nuclear processing of RNA,5 but in these cases the effects of CO have not been shown to exceed those produced by equivalent hypoxic hypoxia.

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3) Cerebral lesions caused by CO may reflect an altered distribution of dopamine, the neurotransmitter specifically identified with the basal ganglia.164,265 In synaptosome preparations from this region of the rat brain, CO hypoxia stimulates the release and inhibits the uptake of dopamine, which would thus be expected to accumulate outside the cells. Extracellular accumulations of this neurotransmitter are associated with neuronal damage.70 4) The peroxidation of membrane lipids may disrupt intracellular functions during recovery from CO intoxication. Exposure of rats to CO reduces the cerebral concentration of glutathione, which normally helps protect cells from oxidizing reactions potentially destructive to lipids. Altered metabolic and enzymatic activity can only be detected after the exposure period, indicating that mitochondrial and lysosomal membranes are damaged during reoxygenation, in neurons vulnerable to O2-related injury.70,330,384,406 Exposure to CO decreases the velocity of impulse conduction in peripheral nerves and the brain of rats,319,340,353 and alters electrical activity recorded in the electroencephalogram (EEG) of humans as well as rats, even at low concentrations.44,71,115,117,167,308,340,395,411,425,490 The amplitude of action potentials recorded from rat muscle is also reduced by CO, and at high COHb concentrations (65–70%) electrical activity is completely inhibited in nerve and muscle.319,340 The effect on conduction velocity becomes apparent at 20% COHb,319 but develops slowly, requiring 1 h even at 60% COHb.340 Impaired conduction persists for several weeks following exposure, and episodes of recovered function may alternate with deterioration during this period.228,319,330,340,406 Effects on the EEG and impulse conduction may be secondary to hypoxia and/or ischemia induced by CO,117,340,395,490 but similar effects on conduction in the rat sciatic nerve disappear after 48 h when caused by the formation of equivalent methemoglobin, suggesting that CO affects peripheral neurons directly.319 B. Psychomotor and Sensory Effects Many studies of perception, behavior, and performance, have been conducted by various investigators to establish the actions of CO in these areas. These evaluations have involved analysis of: light threshold and brightness discrimination,26,44,45,115,116,137,277,361,372,394,425,457 visualacuity and dark adaptation,45,277 flicker-fusion rate,20,44,48,277,361,372,397,450 visualfield,372 depth perception,361 visualization performance,20,68 evokedcortical potentials,170 visual and auditory vigilance,20,31,48,50,99 perceptual speed,292,397 two-tone and sound intensity discrimination,129,137,357,486,490 time interval discrimination,20,26,31,44,45,48,144,157,293,364,425 reaction time,20,170,292,361,364 coordination and manual dexterity,20,48,49,292,293,397,425 balance,293 reflex activity,293,372 psychomotor performance,44,139,157,354,393 driving skills, 44,168,364,474 judgment,425 and task performance related to stress.206,292,354,357 Stewart424,425 has thoroughly reviewed the literature on human behavior and cognitive functions, and a similar review by Laites and Merigan has been published,239 which includes information from animal studies. Data considered by these authors, as modified by subsequent work, supports the following conclusions: 1) Results obtained at very low COHb concentrations (less than 5%), are frequently controversial, equivocal, and contradictory.170,241,261 However, this rule appears to be violated where light is involved, since the ability to distinguish differences in intensity becomes impaired at 3–5% COHb. Although hypoxia has been invoked as the cause of

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this effect,44,372 the low COHb concentrations and persistence of the impairment suggest that CO may act directly.26,137,198,221,277 2) At about 10% COHb, the ability to discriminate between time intervals of differing duration begins to fail, and additional effects on vision are revealed at low light intensities. The time required for dark adaptation is increased, light sensitivity in the dark-adapted state is reduced, and alterations in the dark-adapted electroretinogram can be detected.197,457 At this level some cognitive functions and response times are also slightly impaired, and emotional states may be altered. Victims of chronic exposure at low concentrations often fail to recognize that such symptoms may indicate the presence of CO in their environment.62 3) General mental acuity, motor coordination, the ability to perform complex tasks involving judgment, and overall behavioral responsiveness, begins to deteriorate once COHb concentrations reach 15–20%. Moreover, the ability to perform such tasks may degrade at lower concentrations of COHb under stressful or demanding circumstances, particularly if the duration of exposure to CO is extended. Individuals thus affected could have much greater difficulty escaping from a fire situation.10,31,65,99,292,338,354,357,393,450 The performance of rats trained to traverse a complex maze decays rapidly when trials are conducted in an atmosphere containing 0.2–0.4% CO. Animals remaining active become uncharacteristically confused and either require much longer to reach the goal, or fail to reach it, due to poorly directed movements involving excess travel and frequent backtracking.10 4) Exposure to atmospheres of CO which will produce 20–25% COHb is generally required to initiate the headache, disorientation, lassitude, nausea, and retinal hemorrhage commonly associated with CO toxicity (see Section 4.1), although there is considerable variation in susceptibility, among different animal species and also within humans or within a particular animal species.10,28,47,131,200,212,303,372,411,425 At about 50% COHb these symptoms typically become very severe, with loss of consciousness, and often death, although coma may develop asymptomatically if CO concentrations in the atmosphere are very high (1% or greater). It should be emphasized, however, that lethality due to CO toxicity can be found at COHb levels much lower than 50% COHb. Stress appears to impede survival as well as performance. At 1 h the LC50 for unrestrained rats is 0.4% CO in air, but greater lethality is demonstrated (LC50= 0.19% CO) when stress is increased by the restraint necessary for nose-only exposure under conditions otherwise equivalent. The effect of restraint can still be detected in rats conditioned in exposure tubes for 3 months.114 Similar effects of stress have also been found with mice exposed to smoke.237 Persistent psychological damage involving personality and memory, develops regularly in survivors of critical intoxication,43,115,157,159,190,200,221,228,233,241,266,275,295,303,304,313,352,411,455,479,490 along with neurological disturbances typically revealed by seizures195 and other characteristic motor dysfunctions,81,101,123 as well as visual disorders.122,148,471 Such symptoms often do not appear for several weeks,148,471 and may become permanent,81 although complete recovery has also been reported.81,148,385 A favorable prognosis is likely to depend on the repair of cerebral demyelinization, which can only occur if synthetic pathways for lipids can rebound from the hypoxic insult produced by CO122 (see Section 4.5.A).

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4.6 CYTOTOXIC EFFECTS A. General Extravascular Activity There is abundant evidence that CO acts on the cells of the body, exerting effects in addition to those resulting from the formation of COHb in the blood. As already noted, a significant amount of the CO contained in the body is located outside the blood (onefourth to one-third, or more), under normal conditions260,372,470 (see Section 4.2.D), and low PO2 in the blood or tissues will cause a shift of much more CO into the tissues.3,4,83,88,180,260,415,421 The results of experiments with dogs, conducted by Goldbaum and others,150,151,152,153,316,359 are often invoked as evidence for cytotoxic activity. In these experiments it was demonstrated that equivalent anemia, CO administered by transfusion with COHb-erythrocytes, or intraperitoneal injection of CO gas, lacked the toxicity associated with inhaled CO. Concentrations of COHb commonly thought to be uniformly lethal, the highest being about 80%, were tolerated by these dogs if the CO was not inhaled, which demonstrated that the presence of COHb alone could not account for CO toxicity. In similar experiments, rats maintained at about 60% COHb for 21 weeks with daily injections of CO gas did not die,321 and asymptomatic inhalation of methylene chloride vapor, which is metabolized to CO230 (see Section 4.7.B), has been reported in humans to COHb concentrations of 30–40%.43,236 Several other studies, involving animals or isolated organs exposed to CO in the absence of Hb, have also confirmed that COHb is not required for toxic activity: muscle tension is decreased by CO in isolated preparations of aorta perfused with physiological saline solution (PSS) and treated with cyanide (CN) to eliminate O2 uptake.85 Cultures of smooth muscle cells from the rat aorta are relaxed by CO. This effect is associated with increased concentrations of cyclic guanosine monophosphate, which suggests direct action of CO involving a second messenger system.360 The uptake of O2 by primary cultures of chick heart cells decreases in perfusion solutions containing dissolved CO. This effect is not due to reduced PO2 in the perfusion solution, since O2 uptake is not affected by an equivalent reduction produced with N2.468 The contractile activity of isolated rat and rabbit hearts perfused with PSS is impaired by CO,199,283 and subsequent examination of the rat hearts has revealed ultrastructural deterioration.420 The production of prostacyclin is increased by CO in isolated preparations of myocardial tissue maintained in PSS.119 Blood pressure decreases in rabbits exposed to CO after the blood is completely replaced with a perfluorochemical substitute; equivalent N2-hypoxia did not have this effect.435 Extravascular activity has been investigated as a potential basis for most of the toxic effects exerted by CO. Additional data which reveals the cytotoxicity of CO includes the following: 1) Although COHb-induced increases in O2 affinity creates a reduction in O2 delivery for which cardiovascular compensation is required (see Section 4.4.A), effects of CO are observed in addition to this, since the lethality of CO is not increased in animals having Hb with increased O2 affinity resulting from treatment with potassium cyanate (KOCN).477 Effects on the heart in addition to those resulting from sympathetic activity

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induced by hypoxia, such as altered pyruvate and lactate metabolism, have also been observed in the presence of CO.205,213,241,388 2) Hepatic metabolism is altered by CO, apparently as a result of mitochondrial damage.209,210 This effect may contribute to the changes in serum glucose levels often observed in victims of CO intoxication, although the exact mechanism by which CO affects glucose metabolism is not known. An increase in serum glucose is usually detected in humans if the COHb concentration exceeds 25%.154,243 In rats exposed to high levels of CO the hyperglycemic response is typically followed by hypoglycemia, which is particularly evident in those animals which ultimately fail to survive. Among survivors a second hyperglycemic surge occurs during recovery.330,335 Exposure to CO, even at low levels, reduces glucose tolerance in diabetic mice.390 Uptake of ethanol by the liver is reduced and its detoxification pathway is altered.335,443 After treating mice with alcohol, phenobarbital, or chlorpromazine (Thorazine), the lethality of CO depends upon the pretreatment and not upon the COHb concentration.475 Exposure to CO reduces the rate of protein synthesis in pulmonary tissue142 (see Section 4.3.A). 3) Data which suggests a direct effect of CO on the nervous system is commonly encountered, such as that which reveals the effects on impulse conduction speed319 and discrimination of light intensity137,198,277 already described (see Section 4.5). In addition, direct effects of CO on the brain are reported to include inhibition of energy and lipid metabolism, reduction in the DNA content and turnover of the neurotransmitter dopamine,85,122,220,265,309,310,329,330,344 and elevation of the phosphocreatine concentration.343 In cultures of cells from rat brain, CO disrupts the electrical activity of neurons365 and reduces O2 uptake by glia.468 Exposure to CO affects both functions to a greater extent than equivalent N2-hypoxia. 4) Pretreatment with a variety of amino acids increases the survival time of mice exposed to an atmosphere containing a lethal concentration of CO. Protection can be demonstrated for at least 24 h without further treatment.226 Acute exposure to a non-lethal level of CO produces a transient decrease in the lethality associated with subsequent exposure. This effect is observed at equivalent COHb concentrations, and in the absence of any change in blood or other parameters associated with the tolerance that develops from chronic exposure to CO. Analysis of lactate/pyruvate ratios suggests that preexposure to CO induces a shift in cellular metabolism which decreases the level of anaerobic activity. Acute hypoxia also reduces the lethality from subsequent exposure to CO, but preexposure to potassium cyanide (KCN) does not modify CO lethality.476 5) In platelets, CO may interfere with aggregation by disrupting the intracellular pathway responsible for synthesis of thromboxane (see Sections 4.2.A, 4.4.D). This pathway employs a cyclooxygenase containing a heme to which CO could bind.269 B. Activity Involving Cellular Coenzymes Although CO binds to several intracellular enzymes and coenzymes, such as tryptophan dioxygenase, catalase and peroxidase,85,116,137,241,343,372,398,425,458 the effects of such binding has been poorly studied, and evidence for direct inhibition of cellular metabolism usually involves the combination of CO with cytochrome oxidase and cytochrome P450,26,141,200,330,365,420,434,489 although some evidence suggests that CO binds to other cytochromes in mitochondria, such as cytochrome b.343,345,346 Cytochrome oxidase catalyzes the terminal step in aerobic metabolism, and is also the site of CN activity.472 Indeed, the synergistic relationship reported to exist between CO and CN has been

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attributed to combined interference with cytochrome oxidase312 (see Section 4.8.A). In both skeletal and cardiac muscle cytochrome oxidase can oxidize CO to CO2, but the reaction occurs slowly and it is thus unlikely that this mechanism provides any protection from CO intoxication.260,487,488 The oxidation of CO does prevent ATP production by the respiratory chains thus involved, but interactions between blocked and unblocked chains appear to compensate for this effect at the mitochondrial level.73,487 Cytochrome P450 is important in detoxification pathways, especially for drugs such as barbiturates and antipsychotics,97,125,303,330,447 and participates in the metabolic conversion of methylene chloride to CO434 (see Section 4.7.B). The binding of CO to cytochrome P450 may produce pulmonary vasodilation,432 and contribute to the transfer of CO across alveolar membranes290 (see Section 4.2.C). Considerable data indicates that dependence on anaerobic metabolism is increased by CO, which would be the expected result of cytochrome oxidase inactivation: oxygen uptake is reduced;1,109,192,225,470 oxygen debt following exercise is increased;44,79 intracellular levels of adenosine triphosphate (ATP) are reduced, as production is decreased and stores are depleted;177,199,485 reduced mitochondrial coenzymes are accumulated;72,177,343,414 serum levels of lactate and pyruvate are increased.19,35,44,56,64,121,208,243,284,311,329,344,389,416,417,418,424,443,450,489 Metabolic activity in the brain appears to reflect increased efficiency of oxidative phosphorylation in those respiratory chains not blocked by the binding of CO to cytochrome oxidase.344 These effects are prolonged because CO dissociates from cytochromes very slowly.73,116,147,148,303,343,384 In heart tissue, the inhibition of cytochrome oxidase reaches a maximum about 3 h after subcutaneous injection of CO.323 Recovery from ischemia is thus compromised, which could have serious consequences if the coronary circulation is impaired414 (see Section 4.4.B). Inactivation of cytochrome P450 and cytochrome oxidase has also been implicated in the vascular manifestations of CO toxicity (see Section 4.4.D), including increased permeability, accumulation of cholesterol, inhibition of platelet aggregation, and acceleration of atherosclerotic processes,29,156,269,382,444,450 as well as the reduced rate of drug metabolism by the liver which is associated with CO.324,436 However, some results show that CO decreases O2 uptake only slightly,85,468 and that equivalent hypoxia produces an equal or greater shift to anaerobic metabolism.265,283,381,456 In mice, preexposure to CO or hypoxic hypoxia increases the tolerance to a subsequent challenge with CO, and anaerobic metabolism is less prominent during the second exposure478 (see Section 4.6.A). The CO-induced inhibition of cytochrome P450 activity in rat liver is not observed after repeated exposures.324 Reduced cytochrome oxidase activity can be demonstrated in brain tissue from rats exposed to 0.1% CO for 3 h (COHb=56%), but only after a delay following the end of exposure, as the COHb level decreases. This inhibition has been attributed to mitochondrial damage caused by lipid peroxidation as O2 levels increase during recovery, rather than a direct effect of CO on cytochrome oxidase384 (see Section 4.5.A). Taken as a body, the available evidence is insufficient to support an explanation of CO toxicity based primarily on direct, CN-like inhibition of cellular metabolism.107,148,162,166,200,225,265,345,346,384,447,456 Support for this conclusion is derived from considerations related to the affinity of intracellular cytochromes for O2 and CO, and the partial pressures of these gases which develop within cells. The affinity of cytochrome oxidase and cytochrome P450 for both gases has been determined repeatedly: it seems clear that cytochrome P450 has an affinity for O2 which is about equal to its affinity for CO.44,97,125,425,447 A similar value has been obtained for cytochrome oxidase,85 but most

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analyses reveal that this compound has an affinity for O2 which is 2–20 times greater than its affinity for CO, values approximating 10 being most consistently reported.11,21,38,97,133,148,213,351,388,466 This means that an intracellular PCO about 10 times greater than the PO2 will be required to reduce the rate of mitochondrial (aerobic) respiration by half; CO/O2 ratios less than 5 will have very little effect.188 Thus factors which decrease the intracellular PO2 or increase the intracellular PCO will affect CO toxicity,9,73,137,343 but most exposures to CO will be unlikely to generate the conditions required for lethality by direct inhibition of cellular respiration: The intracellular PO2 is normally maintained at 1–5 torr, although reported values range from 0.1 to 40 torr.72,83,85,87,133 The intracellular PCO tensions at COHb concentrations of 10–60% are usually much lower, reported values falling between 0.1 and 0.4 torr.85,137 If an acceptable intracellular PO2 can be preserved, animals will survive exposure to concentrations of CO which are normally lethal. Thus replacement of blood with a perfluorochemical substitute eliminates mortality among rats maintained for long periods in an atmosphere containing 10% CO,213 because O2 delivery to the tissues does not depend on Hb. Even complete conversion of Hb to COHb may not be lethal: certain insects and fish are known to survive in environments containing CO sufficient to completely saturate their Hb. In experiments with goldfish it was estimated than only 29% of their cytochrome oxidase was inactivated at 100% COHb.11,127 Muscle cells from embryonic rat hearts can be cultured in atmospheres which contain large amounts of CO, provided that the CO concentration remains less than 95%. Experimental cultures grown in the presence of both O2 and CO do not differ from controls maintained in CO free atmospheres, but the growth and differentiation of such cells is reduced as a function of increasing CO concentration if O2 is completely absent from test atmospheres.306 Although it is difficult to invoke interference with cellular respiration as the primary cause of CO toxicity, the possibility always exists that such activity could become significant under extreme or unusual circumstances, given the wide range of biological variability and the great variation in exposure conditions. It must be recognized that the intracellular Pco will increase with exposure time, because CO is not metabolized, while the intracellular O2 content may be abruptly decreased to extremely low levels, as a result of increased utilization to support intense exercise, or decreased delivery as a result of environmental anoxia.29,73,83,87,148,343 Extended exposures to CO are known to be more serious than short exposures, even though the same COHb concentration may develop,416 and maximal exercise can reduce even the venous PO2 by a factor of three.83,121,421 Given the proper combination of such situations, particularly if values for affinity and partial pressures at appropriate extremes of the reported ranges are involved, the development of CO/O2 ratios favoring metabolic inhibition can certainly be imagined.343,344 Indeed, extremely high levels of CO have been reported to completely eliminate the cytochrome oxidase activity normally detected with histochemical tests.343,420 C. Activity Involving Myoglobin Myoglobin is a respiratory pigment concentrated in the cells of red muscle which facilitates the transfer of O2 from circulating Hb to the mitochondrial sites of cellular respiration.94 Cardiac muscle cells are particularly rich in Mb,472 the myocardial concentration of which is increased by chronic or repeated exposure to sublethal concentrations of CO.323,324 Facilitated diffusion of O2 is extremely important to tissues

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which operate at a high level of activity, such as heart and skeletal muscle, and a large proportion of the O2 utilized by these tissues is handled by Mb.35,148,391,419 It is very likely that the combination of CO with Mb to form COMb is extremely important to CO toxicity in most situations.26,73,148,216,303 The same factors which affect the binding of CO to cytochromes also regulate the partition of CO between Hb and Mb (see Section 4.2.D). Affinity constants (M) which give the affinity for CO relative to O2, are useful in describing these relationships. A much greater CO affinity is exhibited by Mb (M=20–40) than by the cyto-chromes (M=0.05–1.0), and most of the extravascular CO thus exists as COMb,12,35,38,39,83,85,87,133,147,196,216,260,330,344,351,388,421 which is formed simultaneously with COHb by loading dissolved CO from the plasma. Although some variation exists among muscle tissues,419 the COMb and COHb saturations will be about equal at any CO level,83,85,87,321 even though the CO affinity of Hb is much greater (M=about 220) than the CO affinity of Mb. Because the oxygen affinity of Mb is 30–40 times greater than the oxygen affinity of Hb (Fig. 1), O2 can usually compete with CO for binding sites on Mb as effectively at a low intracellular PO2 as it can for sites on Hb at a higher arterial PO2.12,196,421,480 The relative distribution of CO changes very little over a wide range of COHb concentrations, but is altered drastically if the arterial PO2 drops below 40 torr, or the COHb concentration exceeds 55% in the blood. Thus, exercise or hypoxia insufficient to significantly modify the saturation of intracellular cytochromes may triple the saturation of intracellular Mb.3,4,9,46,73,83,85,87,137,216,260,415,421 Accordingly, the formation of COMb can impair performance and disrupt energy production in such tissues indirectly, by interfering with uptake, extraction, and transfer of O2, well in advance of any direct effects of CO on cellular respiration.3,39,59,83,85,216,419,421,450,470 4.7 EFFECTS OF CHRONIC EXPOSURE A. Results from Long-Term Experiments Considerable data has been accumulated on the effects of extended exposure to sublethal concentrations of CO, derived from laboratory studies involving experimental animals as well as epidemiological studies involving human populations occupationally or environmentally exposed. Laboratory studies have revealed effects on various physiological systems and processes. The first response of rats to CO during chronic exposures is a transient increase in the number of circulating reticulocytes (immature erythrocytes). The characteristic polycythemia (see Section 4.2.A) does not develop until the reticulocyte count has returned to normal. The reticulocyte response probably results from renal hypoxia which stimulates the production of erythropoietin.76 Chronic experiments with rabbits reveal that exposure to low levels of CO produces a persistent reduction in the platelet count which develops after one week.204 Exposure of guinea pigs to short bursts of CO at high levels for several weeks reduces the number of plaque-forming cells which can be isolated from the lungs and spleen, suggesting a reduction in the immune capacity.413 Chronic exposure of neonatal rats to CO results in cardiac hypertrophy and tachycardia. These conditions persist as the animals mature into adults, even in the absence of any exposure to CO beyond the first post-natal month. During development, CO appears to act by increasing the number of cardiocytes, since the myocardial content of DNA rises as hearts increase in size, even though the concentration of cytochrome c

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decreases.334,337,339 Similar exposures produce cardiomegaly in mature rats, although less effectively, which may be more pronounced on one side of the heart.282,328,333,339 This develops largely as a consequence of increased ventricular dimensions secondary to elevated blood viscosity, although some hypertrophy of the ventricular walls is seen.328,333 Mature animals maintain the pretreatment concentration of cytochrome c in the additional heart muscle,339 but the concentration of myoglobin increases.323,321 Cardiac damage at the ultrastructural level, involving myocytes as well as vascular tissue, can be detected in chronically exposed rabbits218,241,469 (see Sections 4.4.B, 4.4.D). Pulmonary and renal hypertrophy have also been reported as effects of chronic CO exposure.282,333 While the cardiovascular system plays a major role in the response to acute intoxication with CO (see Section 4.4.A), metabolic adaptation is more important during chronic exposure.166 The response of monkeys to chronic CO poisoning involves reduced O2 consumption, which indicates a reduction in the metabolic rate.106 Chronic exposure of rats to CO reduces the serum level of thyroxine and increases the catecholamine content of the adrenal glands.320,453,462 Such reduced mobilization of both hormones also signals a decrease the metabolic rate. Less O2 demand by the tissues allows the PO2 of capillary blood to be maintained, even though the O2 affinity of free Hb is increased in the presence of COHb106 (see Sections 4.2.B., 4.2.D). At the same time, evidence of a non-specific stress response to CO often becomes apparent through altered levels of adrenal corticosteroids, serotonin, histamine, and pituitary hormones,453,460,463 which may increase the apparent toxicity. In rats, increased lethality of CO associated with the stress imposed by restraint is not eliminated by 3 months of conditioning to the restraining devices114 (see Section 4.5.B). The minimum atmospheric concentration of CO required to elicit a stress response in long-term exposures appears to lie between 0.005 and 0.01%.460,463 Indeed, extensive investigation of rats and mice exposed to CO at 0.005% for periods extending to 2 years, reveals no significant changes in a wide variety of physiological and bio-chemical parameters.427 Epidemiologic studies involving human populations generally, but not uniformly, reveal an association between cardiovascular disease and CO exposure. Such data supports an wide variety of experimental evidence which suggests that exposure to CO either promotes cardiovascular disease or increases mortality when such disease already exists. In New York City, continuous records are maintained of CO levels at automobile toll booths on bridges and in tunnels. Using this data, an extensive study was conducted on more than 5,000 bridge and tunnel workers thus chronically exposed to CO during three decades prior to 1981. An increased incidence of atherosclerotic heart disease and mortality was revealed among tunnel officers, who were typically exposed to higher levels of CO.423 A study conducted in Los Angeles considered fatalities among more than 30,000 patients admitted to hospitals with myocardial infarctions during 1958. There were significantly more deaths among such patients admitted from high-pollution areas during periods of elevated atmospheric CO, than among patients admitted from areas considered to be relatively free of pollution.93 Conversely, a similar study conducted in Baltimore on 14,000 heart attack victims failed to reveal a statistical relationship between the incidence of myocardial infarctions, or sudden death from atherosclerotic heart disease, and ambient levels of CO.229 Chronic studies with human volunteers monitored in an exposure chamber suggest that CO, present continuously even at 0.005%, has a specific effect on the heart which alters the activities of the atrial pacemaker and/or the cardiac conduction system.100 Thus the abnormally high incidence of heart disease noted among fire fighters may result from chronic or repeated exposures to high levels of CO

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encountered in building fires. Myocardial ischemia resulting from atherosclerotic damage to coronary arteries, as well as direct damage to the myocardium itself, may be involved.41 B. Effects Related to Endogenous Production The body produces CO continuously as metabolic product resulting from the normal degradation of Hb-derived heme to bilirubin. Heme-containing enzymes from hepatic microsomes are also apparently degraded to bilirubin, with the production of CO. This catabolic activity maintains a typical COHb concentration of about 0.5%, which is without physiological effect.84,89,90,156,157,200,241,260,263,369,459 High rates of heme catabolism secondary to hemolytic or pernicious anemia can elevate this level to 4–6%, or more.44,96,203,271,372,425 The small percentage of endogenous CO converted to CO2 by cytochrome oxidase (see Section 4.6.B) has little effect on the equilibrium level of COHb resulting from metabolic production.260,470 Methylene chloride, a volatile solvent commonly employed in paint removers, is readily absorbed via the respiratory system when the vapor is present in atmospheric air. In the body this compound is rapidly metabolized to CO, which is subsequently loaded by Hb to produce COHb concentrations which may reach 30–40%. Dangerously high levels of COHb may persist for an extended period after exposure to the methylene chloride has ceased.43,128,236 C. Effects Related to Tobacco and/or Marijuana Smoke The smoking of tobacco represents a common, important source of CO for many humans, and has been extensively studied in this regard. However, tobacco smoke is extremely complex and it is frequently difficult to attribute effects of smoking to a particular component of the smoke. Many investigations of tobacco smoke toxicology have given special consideration to the roles of nicotine as well as CO, and their interactions, but the results are not always consistent. Tobacco smoke contains 4–6% CO,26,79,474 thus smoking will elevate COHb concentrations above endogenous levels. Habitual smokers who inhale can easily maintain COHb saturations of 10–15%,28,29,138,163,270,279,425,479,481 and among heavy smokers the COHb level may approximate 20%.363 Such persons may develop symptoms of chronic CO poisoning,321,327,376,377,397 including chest pain, dyspnea, fatigue, headache, and reduced exercise capacity (see Section 4.1), which typically disappear as CO is cleared from the body.219,363 Elevated concentrations of COHb in the blood of smokers reflect not only the CO concentration in tobacco smoke, but also the frequency with which cigarettes are smoked. In general, frequent smokers can minimize the formation of COHb by smoking less of each cigarette.366 The levels of COHb produced by smoking marijuana may be 4–5 times that resulting from an equivalent quantity of tobacco. This probably reflects a difference in smoking technique rather than a difference in CO content of the smoke.482 The contributions of CO and nicotine to the increased coronary heart disease observed among smokers have been widely discussed. Cardiovascular conditions such as “smoker’s polycythemia”271 and “tobacco angina”33 have been traditionally related to the CO inhaled with tobacco smoke, and a study of pipe smokers has indicated that CO is more important than nicotine: Among pipe smokers, who do not demonstrate an

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increased risk of heart disease as a population, serum cotinine (a metabolite of nicotine) is significantly higher than among cigarette smokers, but COHb saturations are lower.467 However, reducing the level of CO in cigarette smoke does not reduce the risk of myocardial infarctions from smoking.211 In fact, both nicotine and CO can reduce the threshold for fibrillation and may act synergistically to interfere with cardiac function, especially in the presence of angina. Nicotine increases the myocardial O2 demand and mobilizes catecholamines, while elevated levels of COHb reduce O2 delivery to the heart and prolong the effects of nicotine by inhibiting hepatic detoxification pathways.8,19,379 In isolated rat hearts the rate of coronary flow is increased by CO and decreased by nicotine. Individually these effects are reversible, but when both compounds are supplied simultaneously in the perfusion solution an irreversible decrease in coronary flow occurs.281 Tobacco smoking has been clearly demonstrated to promote atherosclerosis.172,274,326 However, agreement regarding the role of CO in this process is lacking, due essentially to results which reveal conflicting effects of CO on platelets, which are involved in the early stages of atherogenesis (see Sections 4.2.A, 4.4.D). Data from minipigs exposed to cigarette smoke or CO suggests that CO plays a central role in the increased incidence of atherosclerosis among smokers,274 but the component of tobacco smoke which exacerbates the development of atherosclerotic lesions in the chicken aorta does not appear to be CO.326 Although the smoking of cigarettes increases platelet aggregation, it is not clear that CO is the component of tobacco smoke responsible for this effect, since data derived from smoker’s blood and platelets exposed to cigarette smoke are inconsistent.269,366 Experiments with platelet-rich plasma and preparations of isolated rat aorta failed to demonstrate that CO promotes atherogenic processes, such as increased platelet stickiness and decreased production of prostacyclin.172 The increased incidence of emphysema and other pulmonary disorders in smokers may be partially attributed to the inhibitory effects of CO on protein synthesis in lung tissue. This effect may prevent lungs exposed to CO from repairing structural damage resulting from atmospheric pollutants or other components of tobacco smoke.142 Among tobacco smokers a correlation between the level of COHb and the permeability of alveolar-capillary barriers in the lungs has been observed, but available data suggests that the COHb concentration increases as a result of permeability changes produced by other components of the smoke.297 Smokers with obstructive lung disease, which produces hypoxic hypoxia and prevents the normal clearance of CO, may accumulate COHb to saturations approaching 40%, although this is very rare.180 The role of CO in visual disorders associated with tobacco smoking has been investigated. In cat electroretinograms the b-wave amplitude is depressed by CO and cigarette smoke, but not by nicotine, which suggests that CO is important in the development of “tobacco amblyopia”.197 The inhibition of dark adaptation and decreased light sensitivity exhibited by dark-adapted eyes, which characterizes low-level CO intoxication, are more pronounced in smokers than non-smokers, even at equivalent COHb concentrations. It has been suggested that the enhancement reflects a subtle effect of chronic exposure to CO as experienced by smokers457 (see Section 4.5.B).

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4.8 RELATIONSHIPS TO OTHER TOXIC GASES A. Hydrogen Cyanide Both CO and hydrogen cyanide (HCN) are produced as combustion products of many materials, and considerable effort has been expended to investigate the toxic interactions between these gases. Unfortunately, the vast majority of the work involves animal models only, the experimental data is equivocal in certain respects and the relationship remains somewhat poorly defined. In general, CO appears to be much more important as a cause of fire-related fatalities than HCN,259 although one evaluation of fire victims has revealed that HCN can clearly contribute to lethality.409 In rats and monkeys, the toxic effects of HCN cause rapid incapacitation, which follows a period of hyperventilation, once a threshold concentration is reached in the atmosphere. Thus, victims exposed to fire atmospheres containing HCN may be rapidly incapacitated at relatively low concentrations, and then accumulate a lethal burden of CO.202,300,355,356 The situation will become more complex if the fire atmosphere is also deficient in O2, under which conditions the toxicity of HCN with respect to mice is increased124 and CO is loaded more rapidly by Hb (see Sections 4.2.B, 4.2.C). The consequences of exposure may also be affected by the order in which toxic gases are encountered. Animal tests involving CO and HCN supplied serially reveal that mice survive longer in atmospheres containing HCN to which CO is added than in atmospheres containing CO to which HCN is added.124 Intoxication with any cyanide toxicant is generally treated using an agent such amyl nitrate. This forms methemoglobin in the blood, which is rapidly converted to cyanmethemoglobin by cyanide. As a consequence, less cyanide remains available to block electron transport chains. The use of methemoglobin-formers where CO is also an intoxicant leads to increased mortality from the CO, because such compounds, like CO, reduce the O2 capacity of the blood and shift the O2 dissociation curve to the left299 (Fig. 3). The controversy associated with CO and cyanide toxicity has developed because the results of animal exposure studies involving these compounds have been interpreted in various ways. Although a synergistic effect on lethality and brain metabolism is suggested by some data, especially that obtained from experiments which have employed injections of KCN to provide the cyanide exposure,202,301,312,348 most investigations provide support for the view that CO and cyanide act in an additive manner on experimental animals. The additive relationship has been demonstrated for incapacitation and lethality using rats, mice, and cats;124,248,378,412,449 it also holds for the combined effects of CO and HCN on cerebral blood flow in dogs.348 The times required for incapacitation and death in atmospheres containing both CO and HCN can be predicted from a mathematical model based on the fractional effective doses calculated for each gas. When an additive relationship is modeled, predictions have been confirmed experimentally using rats.174,176 The data obtained from analyses of COHb and HCN in fire victims (again mostly animals) is far from conclusive. Frequently no information is available regarding other conditions which might have affected the toxicity of either gas, or about the identity of some other toxic components which may have been present in the inhaled

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smoke.40,248,258,302,356 Indeed, some analyses reveal neither a synergistic nor an additive relationship between CO and HCN,484 and either suggest that exposure to one does not affect the toxicity of the other,183 or that any interactive effect on toxicity disappears rapidly,104,476 but the most recent work suggests additivity, both in small scale and in full scale fires.36,245,247 Synergism at the cellular level, suggested by effects on the cerebral uptake of O2,348 could not be identified using hepatic mitochondria: the decrease in ATP production observed at elevated COHb concentrations is not affected by low levels of cyanide.177 However, a consensus regarding the additivity of interactions of CO and cyanide may be forming. B. Carbon Dioxide Ventilation is intensely stimulated by CO2, and acidosis results from an elevated PCO2 in the blood.164 In addition, environments high in CO2 are often deficient in O2, as a consequence of combustion. The combined effects of these factors can produce very dangerous situations158,368 (see Sections 4.2.A, 4.2.B, 4.2.C). In rats, CO is lethal at lower concentrations when administered with CO2 than when it is administered alone. Combined exposures reduce the mean survival time but do not alter the equilibrium COHb level, even though the rate of COHb formation is accelerated because of increased pulmonary activity. The increase in lethality is most evident in atmospheres containing 5% CO2 and 0.25% CO; at CO concentrations above approximately 0.4% the CO2 effect is not observed. Animals breathing combinations of CO and CO2 become more severely acidotic, and recover more slowly from the acidosis, than those breathing the individual gases. All effects of CO and CO2 in combination are more pronounced at reduced PO2. Mathematical modeling of rat data reveals synergism between the two gases at CO2 concentrations greater than 1.5%, in which relationship the increased rate of COHb formation and excessive, protracted acidosis appear to be important. Experiments with human subjects also suggest a synergistic interaction between CO and CO2, developing at 3–5% CO2.248,249,368,396 Given the increased lethality of CO-CO2 mixtures, unusual results have been obtained from incapacitation and “time of useful function” studies: Mice can exercise significantly longer in atmospheres containing both CO and CO2, than in atmospheres containing equivalent CO but no CO2, provided that the PO2 remains constant. These results are based entirely on observations of gross motor activity, and the experiments provided no data to suggest a physiological explanation for the phenomenon.143,378 C. Hydrogen Chloride Because it is a sensory irritant, hydrogen chloride (HCl) inhibits respiratory activity in rats, thereby decreasing gas flow through the lungs. Thus, the formation of COHb and the toxic effects of CO may be delayed in rodents, due to reduced pulmonary ventilation (see Section 4.2.C), when HCl and CO are present simultaneously in an exposure mixture.173,175 This action apparently extends the time to incapacitation for CO in tests with mice exposed to atmospheres which also contain HCl.378 For these two gases the delay is significant only if mixtures have more than 0.4% CO and 0.04–0.10% HCl. Lower concentrations of HCl have little effect on the respiratory minute volume, and inhibition of ventilation is not substantially increased at higher concentrations. At very high concentrations of CO the uptake is so rapid that a change in ventilation rate has little

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effect.175 Primates exposed to HCl behave differently from rodents: they have a short (10–20 s) period when they hold their breath, followed by an increase in respiratory frequency.186 Thus, effects of HCl on CO toxicity may be different in rats than in primates, although the lethal levels found in primates and rats for both pure gas mixtures and smoke containing CO and HCl suggest that the rat is an adequate model for primate smoke lethality. A small scale study using rats showed that the acute lethality of HCl at high concentrations was not statistically increased by adding small levels of CO.183 In general, the lethal effects of CO and HCl appear to be additive in rodents under experimental conditions.173 Although it has not yet been fully proven whether this relationship holds in an actual fire environment, recent full scale fire toxicity studies suggest that it does.36 D. Oxides of Nitrogen Nitric oxide (NO) reacts with Hb to produce nitrosylhemoglobin (NOHb) and methemoglobin (met-Hb). Following simultaneous exposure to both CO and NO, mice develop levels of COHb and NOHb which do not differ from the levels produced by equivalent exposure to the gases supplied separately at the same concentration.314 However, more met-Hb is produced by NO in rats when CO is present. Behavioral experiments involving the exposure of rats to CO and NO indicate that learned responses are decreased by both gases, and that they appear to act synergistically when supplied simultaneously at high levels. In the same study, analysis of electrical activity recorded from the brain following auditory stimulation (auditory evoked potentials) revealed a similar relationship.161 Nitrogen dioxide (NO2) is a pulmonary irritant, mortality from exposure to which is often the result of delayed pulmonary edema and hemorrhage; terminal symptoms may not become apparent for several hours or days. Experimental animals differ widely in their sensitivity to NO2, but among rats and mice the presence of CO in test atmospheres does not appear to alter the lethality of NO2.183,184 Chronic exposure of rats to CO and NO2 combined at low concentrations produces physiological changes associated with stress, involving increased levels of pituitary and adrenal catecholamines. In this setting the gases appear to interact, the effective concentrations being below those required to produce a stress response when each gas was tested alone.453,461 4.9 CONCLUSIONS In the final analysis, poisoning by CO results from interruption of ATP production by cells. Energy metabolism may be impaired either by direct inhibition of the metabolic intermediates involved, or by interference with O2 delivery to the mitochondria. In either case, the structural and functional integrity of tissues will be disrupted. While the literature suggests that the principal effects of CO derive from reduced O2 delivery, direct actions on cellular metabolism cannot be ignored: The cytochromes are known to bind CO, and although favorable conditions for this may not be commonly encountered, significant inhibition may occur under certain circumstances. Cytochrome oxidase activity is essential to ATP production, and inhibition of cytochrome P450 will certainly interfere with drug metabolism, increasing the risk from combined exposures.

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When considering effects on O2 delivery, a persistent controversy is revealed regarding the site of action, since several steps are involved in conveying molecules of atmospheric O2 to the intracellular sites at which they are utilized: following transfer across the alveolar walls, O2 is transported by the blood to the tissues, where it must be transferred out of the capillaries and into the cells. Although it seems clear that CO does not materially inhibit O2 uptake in the lungs, it seems almost certain that CO is involved with the other two processes. Many mechanisms proposed to explain the effects of CO have been developed from analysis of activity in only one of these domains, and have thus failed to account for all the data. Hemoglobin occupied by CO cannot transport O2, and in the presence of COHb any remaining Hb will bind O2 more tightly. Accordingly, if sufficient CO enters the blood, the delivery of O2 will be critically impaired. However, the quantity of COHb required to reach this point depends not only upon the amount of CO absorbed, but also on the ability of the cardiovascular system to compensate for the reduced availability of O2. Compensatory activity can take two forms, and some combination of both is usually involved. That is, the supply of O2 to the tissues can remain constant, or at least acceptable if the rate of blood flow can be sufficiently increased, or the tissues can extract more O2 from the blood which is supplied. Many tissues escape CO poisoning by increasing the extraction of O2, since only about 25% of the available O2 is extracted under normal conditions. However, certain organs, such as the heart and brain, depend for survival on increased blood flow, because they operate at high metabolic rates and thus normally extract much more of the available O2.414 These mechanisms are capable of protecting tissues at very high levels of circulating COHb, as indicated by the lack of mortality in transfusion and CO-injection experiments at COHb levels reaching 80%,150,151,152,153,316,359 and by the high but asymptomatic COHb concentrations generated metabolically from methylene chloride in a CO-free environment.236 The initial results from non-atmospheric exposures to CO consisted of survival data only, but experiments conducted more recently162,205,284 confirm that CO-injections induce the same cardiovascular responses known from numerous inhalation studies. The implications of this are that it is not possible to establish universal lethal COHb threshold levels. Conditions which impair cardiac efficiency or vascular function have a potential for compromising the cardiovascular response to CO, and thus increase the risk from exposure,30,116,134,241,414,450,489 although it must not be concluded that cardiovascular disease will increase the lethality of CO in every case, given the wide variety of cardiovascular malfunctions which may exist. Clearly disease involving the coronary and/or cerebral circulation will be most critical, since increased flow is essential in these areas. The greater lethality of inhaled CO, as compared to CO administered by injecting the gas or transfusing erythrocytes previously loaded with COHb, results from interference with O2 transfer from the capillaries into the cells. Blood is a conduit for respiratory gases (O2 and CO2) and CO, which operates in two directions. Normally O2 is transported to the cells and CO2 is returned to the lungs; all gases must dissolve physically in the plasma upon entering the blood regardless of their ultimate mode of transport through the vascular system. The diffusion gradient for CO is directed into the blood across the alveolar membranes of the lungs when it is present in the atmosphere, and it moves into the body as dissolved CO. The dissolved gas is loaded simultaneously by respiratory pigments in the blood (Hb) and in the muscles (Mb), the relationship between these two pigments being such that they develop about equal saturations with CO. Myoglobin is

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extremely important, particularly in the heart, because it transfers much of the O2 to the mitochondria.435 Thus as inactivation of Mb with CO proceeds, the cardiovascular response to CO becomes progressively less effective, not because insufficient O2 is being delivered to the tissues but because the O2, once delivered, cannot reach the oxidative sites in the cells rapidly enough. Of course the situation will be further aggravated under appropriate conditions by the binding of CO to intracellular cytochromes. When CO is administered intraperitoneally or by transfusion (or created internally from methylene chloride), the diffusion gradient is directed out of the body into the alveolar gas, and CO is efficiently removed from blood in the pulmonary capillaries.43,150,152,162,166 As a consequence, arterial blood subsequently distributed to the body will contain very little dissolved CO, Mb will be prevented from loading CO, and any other extravascular stores will be continually depleted. Thus uncomplicated by interference with intracellular transfer of O2, the cardiovascular mechanisms of compensation will maintain O2 delivery at much higher concentrations of COHb. REFERENCES 1. Adams, J.D., Erickson, H.H., and Stone, H.L. Myocardial metabolism during exposure to carbon monoxide in the conscious dog. J. Appl. Physiol., 34, 1973, 238–242. 2. Adams, K.F., Koch, G., Chatterjee, B., Goldstein, G.M., O’Neil, J.J., Bromberg, P.A., and Sheps, D.S. Acute elevation of blood carboxyhemoglobin to 6% impairs exercise performance and aggravates symptoms in patients with ischemic heart disease. J. Am. Coll. Cardiol., 12, 1988, 900–909. 3. Agostoni, A., Perrella, M., Sabbioneda, L., and Zoni, U. CO binding to hemoglobin and myoglobin in equilibrium with a gas phase of low PO2 value. J. Appl. Physiol., 65, 1988, 2513– 2517. 4. Agostoni, A., Stabilini, R., Viggiano, G., Luzzana, M., and Samaja, M. Influence of capillary and tissue PO2 on carbon monoxide binding to myoglobin: A theoretical evaluation. Microvasc. Res., 20, 1980, 81–87. 5. Albrecht, J. Effect of carbon monoxide intoxication on the Poly(A) polymerase activity in the rat brain nuclei. Bull. Acad. Pol. Sci. Ser. Sci. Biol., 25, 1977, 269–273. 6. Allen, D.R., Browse, N.L., and Rutt, D.L. Effects of cigarette smoke, carbon monoxide and nicotine on the uptake of fibrinogen by the canine arterial wall. Atherosclerosis, 77, 1989, 83– 88. 7. Allred, E.N., Bleecker, E.F., Chaitman, B.R., Dahms, T.E., Gottlier, S.O., Hackney, J.D., Pagano, M., Selvester, R.H., Walden, S.M., and Warren, J. Short-term effects of carbon monoxide exposure on the exercise performance of subjects with coronary artery disease. N. Engl. J. Med., 321, 1989, 1426–1432. 8. Altland, P.D. and Rattner, B.A. Effects of nicotine and carbon monoxide on tissue and systematic changes in rats. Environ. Res., 19, 1979, 202–212. 9. Anderson, R.F., Allensworth, D.C., and deGroot, W.J. Myocardial toxicity from carbon monoxide poisoning. Ann. Intern. Med., 67, 1967, 1172–1182. 10. Annau, Z. Complex maze performance during carbon monoxide exposure in rats. Neurotoxicol. Teratol., 9, 1987, 151–155. 11. Anthony, E.H. Survival of goldfish in presence of carbon monoxide. J. Exp. Biol., 38, 1961, 109–129. 12. Antonini, E. Interrelationship between structure and function in hemoglobin and myoglobin. Physiol. Rev., 45, 1965, 123–170 13. Antonini, E. Hemoglobin and its reaction with ligands. Science, 158, 1967, 1417–1425.

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389. Schievelbein, H. Evaluation of the role of carbon monoxide and nicotine in the pathogenesis of arteriosclerosis and cardiovascular disease. Prev. Med., 8, 1979, 379–389. 390. Schlipkoter, H.W., Klitzke, M., and Unnewehr, J. Effect of lead and carbon monoxide under the condition of diabetic metabolism. Zentralbl. Bakteriol. Parasitenkd. Infektionskr. Hyg., 168, 1979, 395–402. 391. Schmidt-Nielsen, K. Animal Physiology: Adaptation and environment. Fourth edition. Cambridge: Cambridge University Press; 1990:602 pp. 392. Schneiderman, G. and Goldstick, T.K. Carbon monoxide-induced arterial wall hypoxia and atherosclerosis. Atherosclerosis, 30, 1978, 1–15. 393. Schrot, J., Thomas, J.R., and Robertson, R.F. Temporal changes in repeated acquisition behavior after carbon monoxide exposure. Neurobehav. Toxicol. Teratol., 6, 1984, 23–28. 394. Schutz, V.A. and Waurabenstein, K. Influence of low carbon monoxide content in outside air on mental and central nervous parameters in humans and animals—an aspect of the MIC-COvalue. Arbeitsmed. Sozialmed. Praeventivmed, 15(3), 1980, 53–57. 395. Schwartz, A., Hennerici, M., and Wegener, O.H. Delayed choreoathetosis following acute carbon monoxide poisoning. Neuroradiology, 35, 1985, 98–99. 396. Sedov, A.V., Surotsev, N.A., Bychkov, S.Y., and Mazneva, G.Y. Combined effect of carbon monoxide and dioxide on subjects working in sealed chambers. Gig. Sanit., 12, 1985, 17–19. 397. Seppanen, A., Hakkinen, B., and Tenkku, M. Effect of gradually increasing carboxyhemoglobin saturation on visual perception and psychomotor performance of smoking and nonsmoking subjects. Ann. Clin. Res., 9, 1977, 314–319. 398. Sharma, V.S., Ranney, H.M., Geibel, J.G., and Traylor, T.G. A new method for the determination of ligand dissociation rate constant of carboxyhemoglobin. Biochem. Biophys. Res. Commun., 66, 1975, 1301–1306. 399. Shellenberger, M.K. Persistent alteration of rat brain monoamine levels by carbon monoxide exposure: Sex differences and behavioral correlation. Neurotoxicology, 2, 1981, 431–444. 400. Shephard, R.J. The influence of small doses of carbon monoxide upon heart rate. Respiration, 29, 1972, 516–521. 401. Sheps, D.S., Herbst, M.C., Hinderliter, A.L., Adams, K.F., Ekelund, L.G., O’Neil, J.J., Goldstein, G.M., Bromberg, P.A, Dalton, J.L., Ballenger, M.N., Davis, S.M., and Koch, G.G. Production of arrhythmias by elevated carboxyhemoglobin in patients with coronary artery disease. Ann. Intern. Med., 113, 1990, 343–351. 402. Sheps, D.S., Kirkwood, F.A., Bromberg, P.A., Goldstein, G.M., O’Neil, J.J., Horstman, D., and Koch, G. Lack of effect of low levels of carboxyhemoglobin on cardiovascular function in patients with ischemic heart disease. Arch. Environ. Health, 47, 1987, 108–116. 403. Shibuya, I., Niizeki, K., and Kagawa, T. Estimation of the transfer coefficients of oxygen and carbon monoxide in the boundary of human and chicken red blood cells by a microphotometric method. Adv. Exp. Med. Biol., 222, 1988, 219–229. 404. Shiotsuka, R.N., Drew, R.T., and Wehner, R.W. Carbon monoxide enhances development of hypertension in Dahl rats. Toxicol. Appl. Pharmacol., 76, 1984, 225–233. 405. Siebens, A.A. Pulmonary gas exchange. In: Broebeck, J.R., ed. Best and Taylor’s Physiological basis of medical practice, Section 6: Respiration. Ninth edition. Baltimore: The Williams & Wilkins Co.; 1973: pp. 20–27. 406. Siesjo, B.K. Carbon monoxide poisoning: Mechanism of damage, late sequelae and therapy. Clin. Toxicol., 23, 1985, 247–248. 407. Silbaugh, S.A. and Horvath, S.M. Effect of acute carbon monoxide exposure on cardiopulmonary function of the awake rat. Toxicol. Appl. Pharmacol., 66, 1982, 376–382. 408. Silbaugh, S.A. and Horvath, S.M. Effect of carbon monoxide exposure on cardiopulmonary function in the awake rat. Toxicol. Appl. Pharmacol., 66, 1982, 376–382. 409. Silverman, S.H., Purdue, G.F., Hunt, J.L., and Bost, R.O. Cyanide toxicity in burned patients. J. Trauma, 28, 1988, 171–176. 410. Skorodin, M.S., King, F., and Sharp, J.T. Carbon monoxide poisoning presenting as hyperventilation syndrome. Ann. Intern. Med., 105, 1986, 632.

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Chapter 5 CARBON MONOXIDE DETERMINATION IN HUMAN BLOOD GORDON L.NELSON Florida Institute of Technology, College of Science and Liberal Arts, 150 West University Boulevard, Melbourne, FL, 32901–6988, USA ABSTRACT A large variety of techniques have been used to measure the concentration of carboxyhemoglobin in blood. However, in practice, spectrophotometric techniques account for the vast majority of the work carried out. These are not the most accurate techniques but they are less difficult for most laboratories to be able to deal with. There are a large number of experimental variables which need to be controlled very carefully to avoid serious errors in the final result. This work presents a variety of common problems encountered. Therefore, it should be concluded that the determination of COHb, which has such a multitude of opportunities for error, is often inaccurate.

DETERMINATION The conclusions in the foregoing sections depend upon accurate COHb determinations. Laboratory technique and aged specimens can hinder the accuracy of measurements in fatalities, and delay in sampling can underestimate COHb in survivors. Many procedures have been proposed for the analysis of carboxyhemoglobin in blood including spectrophotometry,1–2 gas chromatography (G.C.),3–5 colorimetric,6–7 gasometric,8–9 infrared,10electrochemical,11microdiffusion with silver nitrate12–13 and differential protein precipitation methods. Spectrophotometry and gas chromatography are in most common use. Canfield, in a recent literature study, noted that 80% of references dealt with spectrophotometric techniques, 13% with gas chromatographic techniques, and 7% dealt with other analytical methods.14 Most forensic laboratories are not equipped to conduct the complex specialized gas chromatographic procedures described in the literature for the G.C. analysis of carbon monoxide in blood. Although, G.C. is considered the most accurate method for measuring carbon monoxide in blood, it is too demanding for routine or emergency use in clinical laboratories.15,16 The proper collection and preservation of toxicological samples is critical to obtaining accurate results. Each blood specimen should contain an appropriate anticoagulant and be refrigerated to retard composition. In many instances the *

Note: In every case, if no further details are given, the venue for the study is the United States.

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specimen is almost entirely clotted, while in others, a person performing the autopsy may submit a specimen consisting of about 5 percent or less of cells suspended in “serum’ in an effort to avoid submitting clots.17 “When the specimen is not taken from the heart or major blood vessels it is not unusual to have an admixture of the blood with globules of fats or oils floating on the surface of the specimen; and, sometimes, even pieces of fatty tissue”.17 Instrumentation and procedures must use standards. Obtaining a 100% COHb standard is not a simple matter of bubbling CO through a blood specimen. It requires the deoxygenation of blood using sodium dithionite with subsequent saturation by bubbling a mixture of 90% N2 to 10% CO for a minimum of 45 minutes. This procedure yields a 100% standard, oxygen free, and with minimal residual CO in solution. Residual CO should not be a major factor in spectrophotometric methods but can prove detrimental to G.C. methods where total CO content is measured. Spectrophotometric methods of analysis are based on the simultaneous solution of the concentration of N different chromophores in a mixture, assuming the total absorbance at any wavelength is the sum of the contributions of each absorbing chromophore:

where a is the absorbance at the wavelength λ, l is the path length, Xi is the molar absorption coefficient at the wave length for component Xi, and [Xi] is the substance concentration of component Xi.18 While the most common method of analysis is spectrophotometric, it has a significant potential for error. Any procedure utilizing wavelengths between 400 and 800 nm presents a problem when analyzing complex natural mixtures such as those found in COHb analysis because of the many substances which absorb in that region. Errors can be minimized by selecting multiple wavelengths for analysis such as those used in the CO-Oximeter. However, this does not necessarily eliminate the problem. One paper states, “The use of spectrophotometric analysis as a means of determining the carboxyhaemoglobin content of post mortem blood is not recommended and is unreliable”.19 Clots and blood turbidity are a particular source of error. One worker notes, “In attempting the use of postmortem blood, even when no gross evidence of clot was present, we found that even a small amount of debris would contaminate the extremely short path-length cuvette thus making the instrument unusable”.14,17 The CO-Oximeter is a simple and expeditious spectrophotometric method, based on the simultaneous solution of hemoglobin, oxyhemoglobin, and carboxyhemoglobin concentrations, which can be used to quantitate COHb. For clinical blood samples, where the samples are well preserved, one can be fairly confident that only hemoglobin, oxyhemoglobin, and carboxyhemoglobin are present in significant quantities and the results will be accurate. “A large portion of the interfering pigments arising from hemoglobin breakdown in postmortem blood is eliminated by discarding the plasma portion of postmortem blood specimens whenever possible. Particular care must be exercised while analyzing postmortem specimens in verifying the post analysis zero settings to assure absence of blood clots from the cuvette, since their presence can cause significant errors in the analysis”.14,20 When using a spectrophotometer “significant errors in the procedure can arise from improper collection and preservation of blood. Precautions should be taken to minimize hemolysis during the collection of the sample, during mixing with anticoagulant and during its subsequent storage”.20

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All spectrophotometric methods suffer a systematic error which occurs, “because of dissociation of the carboxyhaemoglobin caused by physical dissolution of the carbon monoxide in the solution. This error can be serious, particularly at high carboxyhaemoglobin concentrations”.6 On occasion the use of spectrophotometric analysis has proven to be grossly in error when testing for COHb. A patient with diabetic ketoacidosis showed a 44.8% COHb level when tested by spectrophotometric techniques. However, the patient had not been exposed to carbon monoxide and G.C. analysis showed no carbon monoxide. It was determined that the high lipid content in the blood was interfering with the spectrophotometric analysis of COHb.21 A number of researchers have studied the use of gas chromatography for the analysis of carbon monoxide released from blood.22–24,5 There are two primary methods of gas chromatographic analysis used in laboratories doing COHb testing. All techniques involve the release of CO from the sample. In some methods the CO is chromatographed directly and detected with a thermal conductivity detector.3,5 Inother methods CO is converted to methane with a Ni catalyst in the presence of H2 at elevated temperatures (300°C) and detected with a flame ionization detector.7,22–24 COHb determinations in blood are not as easy as some perceive. Blood is a complex substance, subject to degradation. Those performing COHb determinations and those utilizing COHb data need to recognize the potential for error.25 In a careful study of two CO-Oximeters and a gas chromatography method one recent paper has shown good agreement. G.C. showed somewhat higher results from post-mortem blood for >45% COHb, however.26 Numerous factors affecting the loss of carbon monoxide from stored blood samples were identified in another recent study. Effects of temperature, surface area versus volume, initial COHb saturation, storage temperature versus volume of air, initial hemoglobin concentration, non-physiological versus post-mortem samples, and air versus oxygen versus nitrogen storage were all investigated. The exposure of CO-containing blood to an oxygen atmosphere will result in a decrease in COHb saturation. The rate is highest when the exposed surface area to volume of blood is large, when the temperature is not kept low, and when the initial saturation is high. In a sealed container with air, loss of CO to air will occur until equilibrium is reached between the air and the specimen. Use of a syringe technique to provide for total exclusion of air was recommended by the authors of the study. Storage at −20°C was not effective as the sole preservative condition. Very rapid loss of COHb was observed at 23°C.27 In studies of post-mortem blood Levin and coworkers have shown a drop of nearly 20% from initial values of 71.5% and 24.6% with 4 month storage at −20°C. On the day of analysis, the thawed blood was stored in an ice bath. The samples were in screw-top vials sealed with rubber septa and containing the anticoagulant sodium fluoride.13 Aged blood samples and blood samples from fire victims may contain sulphemoglobin (SHb) which will interfere with the determination of COHb by spectrophotometry and yield results approximately 10 percent low.28 One final concern is the effect caused by heat in victims with burns. Turbidity in blood samples, when samples are heated above 50°C, affects results. Above 70°C coagulation and hemoglobin degeneration results in accelerating errors in determined values. Methods can overcome these issues, but are not commonly in use.29 Indeed, determination of COHb is not without a multitude of opportunities for error.

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REFERENCES 1. A.H.J.Maas, M.L.Hamelink, and R.J.M.Leeuw, “An Evaluation of the Spectrophotometric Determinations of HbO2, HbCO, and Hb in Blood with the COOximeter IL 182,” Clin. Chem. Acta, 29, 303–309 (1970). 2. K.A.Small, E.P.Radford, J.M.Frazier, F.L.Rodkey and H.A.Collison, “A Rapid Method for Simultaneous Measurement of Carboxy- and Methemoglobin in Blood,” J. Appl. Physiol., 31(1), 154–160 (1971). 3. C.A.Ainsworth, E.L.Schloegel, T.J.Domanski, and L.R.Goldbaum, “A Gas Chromatographic Procedure for the Determination of Carboxyhemoglobin in Post-Mortem Samples,” J. Forensic. Sci., 12, 529–537 (1967). 4. S.M.Ayers, A.Criscitello and S.Gianelli, “Determination of Blood Carbon Monoxide Content by Gas Chromatography,” Upsala J. Med. Sci., 77, 22–24 (1972). 5. A.M.Dominguez, H.E.Chrostensen, L.R.Goldbaum, and V.A.Stembridge, “A Sensitive Procedure for Determining Carbon Monoxide in Blood and Tissue Utilizing Gas-Solid Chromatography,” Toxicol. Appl. Pharmacol., 1, 135–143 (1959). 6. T.H.Allen, and W.S.Root, “An Improved Palladium Chloride Method for the Determination of Carbon Monoxide in Blood,” J. Biol. Chem., 216, 319–323 (1955). 7. K.G.Paul, and H.Theorell, “A Colorimetrical Carbonmonoxide-Hemoglobin Method of Determination for Clinical USe,” Acta. Physiol. Scand., 4, 285–292 (1942). 8. S.M.Horvath, and F.J.Roughton, “Improvements in the Gasometric Estimation of Carbon Monoxide in Blood,” Clin. Chem., 144, 747 (1942). 9. F.J.W.Roughton, and W.S.Root, “The Estimation of Small Amounts of Carbon Monoxide in Blood,” J. Biol. Chem. 147, 123 (1945). 10. R.F.Coburn, W.S.Danielson, W.S.Blakemore and R.E.Forster, “Carbon Monoxide in Blood. Analytical Method and Sources of Error,” J. Appl. Physiol., 19, 510–515 (1964). 11. H.W.Bay, K.F.Blurton, J.M.Sedlak, and A.M.Valentine, “Electrochemical Technique for the Measurement of Carbon Monoxide,” Anal. Chem. 46, 1837–39 (1974). 12. S.Kays, Handbook of Emergency Toxicology, 4th ed., Charles C.Thomas, Springfield, IL, 1980, 255–256, 287. 13. B.C.Levin, P.R.Rechani, J.L.Gurman, F.Landron, H.M.Clark, M.F. Yoklavich, J.R.Rodriguez, L.Droz, F.M.de Cabrera, and S.Kaye, “Analysis of Carboxyhemoglobin and Cyanide in Blood from Victims of the Dupont Plaza Hotel Fire in Puerto Rico,” J. Forensic Sci., 35(1), 151–168 (1990). 14. D.V.Canfield, private communication (1986). 15. Y.M.Katsumata, M.Aoki, M.Oya, O.Suzuki, and S.Yada, “Simultaneous Determination of Carboxyhemoglobin and Methemoglobin in Victims of Carbon Monoxide Poisoning,” J. Forensic Sciences, 25(3), 546–549 (1980). 16. Y.M.Katsumata, M.Aoki, K.Sato, M.Oya, S.Yada, and O.Suzuki, “A Simple Spectrophotometric Method for the Determination of Carboxyhemoglobin in Blood,” Forensic Sci. Int., 18, 175–9 (1981). 17. A.W.Freidrich, and D.Lanau, “Carbon Monoxide Determination in Post-Mortem Clotted Blood,” J. Forensic Sci., 16, 112–119 (1971). 18. O.Siggaard-Andersen, B.Norgaard-Pedersen, and J.Rem, “Hemoglobin Pigments, Spectrophotometric Determination of Oxy-, Carboxy-, Met-, and Sulfhemoglobin in Capillary Blood,” Clin. Chem. Acta, 42, 85–100 (1972). 19. D.J.Blackmore, “The Determination of Carbon Monoxide in Blood and Tissue,” Analyst, 95, 439–458 (1970). 20. K.M.Dubowski, and J.L.Luke, “Measurement of Carboxyhemoglobin and Carbon Monoxide in Blood,” Ann. Cln. Lab. Sci., 3, 53–65, (1973). 21. J.E.Hodgkin, and D.M.Chan, “Diabetic Ketoacidosis Appearing as Carbon Monoxide Poisoning,” JAMA, 231, 1164–1165 (1975).

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22. J.G.Guillot, J.P.Weber, J.Y.Savoie, “Quantitative Determination and Carbon Monoxide in Blood by Head-Space Gas Chromatography,” J. Anal. Toxicol., Nov–Dec, 264–266 (1981). 23. L.D.Hobbs, J.A.Jachimezyk, and E.L.Schloegel, “A Gas Chromatographic Integrator Procedure for the Determination of Carboxyhemoglobin Percent Saturation in Post-Mortem Samples,” J. Anal. Toxic., 4 181–184 (1980). 24. F.L.Rodkey, “Carbon Monoxide Estimation in Gases and Blood by Gas Chromatography,” Ann. N.Y. Acad. Sci., 174, 261–267 (1970). 25. B.J.Perrigo and B.P.Joynt, “Evaluation of Current Derivative Spectrophotometric Methodology for the Determination of Percent Carboxyhemoglobin Saturation in Postmortem Blood Samples,” J. Anal. Tox., 13, 37–46 (1989). 26. A.G.Costantino, J.Pack, and Y.H.Caplan, “Carbon Monoxide Analyses: A Comparison of Two CO-Oximeters and Headspace Gas Chromatography,” J. Anal. Tox, 10, 190–193 (1986). 27. D.H.Chace, L.R.Goldbaum, N.T.Lappas, “Factors Affecting the Loss of Carbon Monoxide form Stored Blood Samples,” J. Anal. Tox., 10, 181–189 (1986). 28. V.S.Rai and P.S.B.Minty, “The Determination of Carboxyhemoglobin in the Presence of Sulphemoglobin,” Forensic Sci. Int., 33, 1–6 (1987). 29. Y.Fukui, M.Matsubara, A.Akane, K.Hama, K.Matsubara, and S.Takahashi, “Determination of Carboxyhemoglobin in Heated Blood—Sources of Error and Utility of Derivative Spectrophotometry,” J. Anal. Tox., 9, 81–84 (1985).

Chapter 6 CARBON MONOXIDE AND FATALITIES: A CASE STUDY OF TOXICITY IN MAN GORDON L.NELSON Florida Institute of Technology, College of Science and Liberal Arts, 150 West University Boulevard, Melbourne, Fl, 32901–6988, USA & DENNIS V.CANFIELD AND JAMES B.LARSEN University of Southern Mississippi, Department of Biological Studies, Southern Station, Box 5018 Hattiesburg, MS, 39406–6018, USA ABSTRACT Carbon Monoxide exposure is common. Questions of interest are: What are the lethal levels of CO in man? How are these levels related to blood COHb? What are the roles of age, disease, drugs, alcohol, and gender? What is the relationship to the fatal event (fire, city gas, or exhaust fumes)? The present study involved data collection on 2241 fatalities and software manipulation to allow analysis of key parameters. Data were from the United States and Canada, and 98% of cases were from between 1976 and 1985. Cases with COHb greater than 20% were evaluated. Information was gathered on age, gender, method of COHb analysis, blood % COHb, blood% ethanol, presence of drugs, disease, source of CO, and physical condition, yielding 128 cross-tabulated contingency tables. For fire victims increased age and the presence of impairment were associated with low COHb levels. For non-fire victims the presence of ethanol was associated with decreased percentage of low COHb. The distribution of COHb levels for fire victims has a (2x) greater fraction below 60% COHb than does that of non-fire victims; however non-fire victims succumb at low COHb levels as well. Different segments of the exposed population exhibit different outcomes. A victim with 30% COHb can clearly be a case of carbon monoxide poisoning without other agents required, a fact of considerable importance in the analysis of carbon monoxide exposure cases.

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INTRODUCTION Carbon monoxide (CO) is a toxic, nonirritating gas. One of the products of combustion, it is invisible, odorless, tasteless, and slightly lighter than air. Carbon monoxide poisoning is not new. Man’s difficulties with CO date back *

Note: In every case, if no further details are given, the venue for the study is the United States.

to the time prehistoric man first used fire. Instances of CO poisoning are found in early Greek and Roman literature. The increased use of coal for domestic purposes in the 1400s brought with it an increase in CO poisoning. The hazard was intensified by the introduction of illuminating gas, and later natural gas, for heat, power, and light. One frequently finds comments such as the following in texts and surveys: “Carbon monoxide is present in significant amounts in virtually all fires. It is highly toxic when inhaled, and acts by combining with hemoglobin in the blood to form carboxyhemoglobin (COHb). Hemoglobin’s function is to carry oxygen throughout the body, and it cannot do this if it is tied up, as COHb and, therefore, unavailable for oxygen transport. The level of carboxyhemoglobin in the blood of fire victims can be determined fairly easily. In the absence of other contributing factors a COHb concentration of 50 percent or greater is generally considered lethal.”1 Most medical discussions of carbon monoxide poisoning deal with “normal healthy” individuals. But the population is composed of a spectrum of individuals in a variety of environments. While one frequently sees conclusions given about a small set of victims without regard to other factors, conclusions which implicate particular combustible materials for example, such conclusions may not be justified given the full spectrum of expected human response to carbon monoxide exposure. Because of the general uncertainties about the detailed factors involved in carbon monoxide poisoning. A major descriptive forensic study of carbon monoxide poisoning in man has been undertaken. A summary of results are provided in this report. Data are from the United States and Canada. The vast majority of the cases studied are recent fatalities, 98% occurred between 1976 and 1985. This study involved data collection on over 2000 fatalities and software manipulation to allow analysis of some key parameters. The issues to be addressed include the following: What are the lethal levels of CO in man? How are these levels related to COHb? What are the roles of age, disease, drugs, alcohol, and gender? What are the mechanisms of CO toxicity? What is the relationship to the fatal event (fire, city gas, exhaust fumes)? Have fires changed over the years? Background Literature Survey More than 1300 papers were reviewed,2 from which several summary statements can be made. Whereas CO exposure seldom occurs with CO in its ultrapure state, studies of

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human exposure to city gas and exhaust gas show that nearly 20% of exposed individuals die from CO poisoning at blood COHb levels less than the concentration thought by some to be required for lethality i.e. <50% COHb). While persons with cardiovascular and other diseases were included in that group, other individuals did not exhibit identifiable pathology, and persons with identifiable pathology did not necessarily die with concentrations of <50% of COHb. The length of time of CO exposure, level of victim activity, and the age of the victim are all important variables. Clearly, lethality from CO poisoning is more complex than the attainment of a fixed percentage of COHb in the blood of the victim and involves more than reduction in the oxygen-carrying capacity of the blood. Therefore, without additional information, a blood COHb value <50% does not provide conclusive evidence regarding a given victim’s response. Indeed, for identical exposures, different individuals would be expected to exhibit different symptoms and outcomes. In the case of fire exposures, more victims are in the <50% COHb category than for automotive exhaust victims. However, despite the presence of different materials in the environment, and different populations, the fire fatality/COHb profiles in Japan in the early 1960s, in Denmark in the late 1960’s and 1970s, in the United States (Maryland) in the late 1970s, in the United Kingdom in the late 1970s, and in other studies over the period 1940 to 1980 are very similar. In CO-related deaths, male victims predominate; alcohol use is also a key factor. Many fire victims have burns. Clearly, exposure to heat and hot fire gases plays a role that is difficult to evaluate, yet it is known to markedly alter COHb levels required for death from fire. A number of conclusions about the physiology of carbon monoxide can be drawn from an analysis of the published literature. These include the following: ● Under most circumstances the acute lethality of CO depends upon interruption of energy production (ATP) by cells. ● CO has the capacity to inhibit cellular metabolism directly and to affect other cellular activities, but the high CO: oxygen ratios required for this suggest that such actions are not the primary cause of acute toxicity, except under extreme or unusual circumstances. ● It is most likely that CO interrupts cellular production of energy through interference with oxygen delivery to the intracellular sites of oxidative metabolism. ● CO impairs oxygen delivery by decreasing the oxygen carrying capacity of blood and by increasing the oxygen affinity of hemoglobin, to which CO is not bound. ● CO also impairs oxygen delivery by inhibiting the facilitated diffusion of oxygen, which is essential to the heart and other active tissues. This inhibition of facilitated diffusion is most likely to result from the binding of CO to intracellular myoglobin. ● The physiological response to CO is largely cardiovascular, since the rate of blood flow must be increased to compensate for the reduced oxygen content and increased oxygen affinity of hemoglobin. ● Cardiovascular disease, particularly that involving the coronary and/or cerebral circulation, increases the risk posed by CO exposure.

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Forensic Study Although, several prior case studies of carbon monoxide poisoning have been reported, it was decided that this study would need a larger data base and additional information not available in the literature to answer some of the more difficult questions. Method: Forensic laboratories were contacted to determine what information would be readily available to them and how they would prefer to submit the data. The final data submission sheet (Figure 1) is an example of the survey sheet developed from these meetings and sent to 400 members of the American Academy of Forensic Science. Figures 2 and 3 are the instruction sheet and an example submission sheet included in the data request package.

FIGURE 1 A total of 2241 cases were received, as reported by 37 forensic laboratories (list of contributors is attached). These cases included 1867 cases with COHb greater than 20%, 186 cases with COHb less than 20% and 194 cases with unknown COHb levels. Those cases where the reported COHb levels were less than 20% saturation were excluded. This is an important distinction, since values below 20% are complicated by a variety of factors, including tobacco smoking and flash fires. Nine hundred cases were obtained by visiting laboratories and examining case records. The remainder were received by mail from submitting laboratories. Of all the cases received, 1203 represented fire cases (54%), 660 represented non-fire cases (29%), and 378 were unknown as to origin (17%). Information was gathered on age, gender, method of COHb analysis, %COHb, %Ethanol, presence of drugs, diseases, Source of CO, and Physical Condition of the victim and entered into a computer data base. Not all of the Instruction Form for Levels of Carboxyhemoglobin Submission Sheet Item: 1. Laboratory—Enter submitting laboratory name and address 2. Method—Procedure used in analysis 3. Date Submitted—Date submission sheet was completed and mailed 4. Date of Occurrence—Date of carbon monoxide exposure

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5. Place of Occurrence—Address of victim 6. L—Enter a check mark under L if victim survived exposure to carbon monoxide D—Enter a check mark under D if victim died from exposure to carbon monoxide 7. Age—Age of victim 8. Sex—Sex of victim 9. %COHb—Level of carboxyhemoglobin found 10. %ETHOL—Level of ethanol found 11. Other drugs—Type and amount of other drugs found in the body 12. Source of CO—Enter the source of carbon monoxide exposure. Example would be car, Wre, gas stove, charcoal stove, etc. 13. Diseases—Enter any diseases which were present at the time of exposure 14. Physical condition—Enter the physical condition of the victim. Excellent—muscular and athletic. Good—at the proper weight. Fair— people slightly out of shape. Poor—obese and out of shape. See examples attached

FIGURE 2 information requested could be provided in every case and the data base reflects that fact. A Fortran program was written to analyze the data. One hundred and twenty eight cross tabulated contingency tables, which illustrate the factors affecting lethal levels of carboxyhemoglobin, were generated by the program for initial evaluation.

FIGURE 3 A summary of the data collected is presented in Table 1. In Table 2 are presented the number and percent of fire and non-fire victims by reporting laboratory. Most of the data (82%) came from seven laboratories, each chosen for their geographic diversity. The

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186

mean COHb levels, standard deviations, and mode for the different groups studied are given in Table 3, which allows identification of those segments of the data base representing victims who die at very high or very low COHb values and those which have broad or narrow distributions, ie, have larger or smaller standard deviations. The data obtained correlate well with previous studies but also provide several new observations. Data showing the percentage of victims with <60% COHb on

TABLE 1 Reported Carbon Monoxide deaths Group

Fire #

Non-Fire

%

#

Unknown

%

a

Total

#

%

#

a

All

1203

54

(65)

660

29

(35)

378

17

2241

All >20% COHb

959

52

(62)

598

32

(38)

310

16

1867

Males

588

47

(58)

439

35

(42)

219

18

1246

Females

344

61

(71)

142

25

(29)

80

14

566

All

345

58

(64)

196

33

(36)

55

9

596

Males

266

57

(63)

155

45

(37)

45

10

466

Females

76

60

(65)

41

33

(35)

9

7

126

>0.5% Ethanol

Note (a): percent fire versus non fire excluding unknown cases

TABLE 2 Number and Percent of Fire and NonFire Victims by Laboratory Lab#

#

Fire Percent

#

Non Fire Percent

#

Total Percent of Grand Total

1

8

53.3

7

46.7

15

0.84

2

3

75.0

1

25.0

4

0.22

3

3

33.3

6

66.7

9

0.51

4

0

0.0

14

100.0

14

0.78

5

0

0.0

0

0.0

0

0.00

6

8

61.5

5

38.5

13

0.73

7

4

23.5

13

76.5

17

0.95

8

0

0.0

0

0.0

0

0.00

9

56

60.2

37

39.8

93

5.21

10

66

70.2

28

29.8

94

5.27

11

7

100.0

0

0.0

7

0.39

Carbon monoxide and fatalities

187

12

9

25.7

26

74.3

35

1.96

13

0

0.0

0

0.0

0

0.00

14

3

75.0

1

25.0

4

0.22

15

191

68.5

88

31.5

279

15.64

16

9

29.0

22

71.0

31

1.74

17

2

20.0

8

80.0

10

0.56

18

12

66.7

6

33.3

18

1.01

19

28

73.7

10

26.3

38

2.13

20

6

42.9

8

57.1

14

0.78

21

8

47.1

9

52.9

17

0.95

22

131

62.1

80

37.9

211

11.83

23

14

41.2

20

58.8

34

1.91

24

4

100.0

0

0.0

4

0.22

25

0

0.0

1

100.0

1

0.06

26

0

0.0

1

100.0

1

0.06

27

0

0.0

4

100.0

4

0.22

28

0

0.0

1

100.0

1

0.06

29

0

0.0

1

100.0

1

0.06

30

0

0.0

1

100.0

1

0.06

31

0

0.0

4

100.0

4

0.22

32

0

0.0

1

100.0

1

0.06

33

0

0.0

1

100.0

1

0.06

34

7

33.3

14

66.7

21

1.18

35

130

70.3

55

29.7

185

10.37

36

235

68.9 106

31.1

341

19.11

37

188

72.0

28.0

261

14.63

1784

100.0

Total

1132

73 652

TABLE 3 Mean and Mode for Subcategories in Carbon Monoxide Data Base Group

Mean Standard Deviation

Mode %

ALL

64.20

17.47

70

FIRE

61.97

18.27

70

NON-FIRE

68.68

15.00

70

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188

ETHANOL >0.05%

65.76

17.61

70

ETHANOL <=0.05%

63.82

17.39

70

ALL ETHANOL =>0.30%

61.21

19.40

50 (60. & 70.)

ALL ETHANOL 0.30–0.34%

59.70

18.80

50 (60.)

ALL ETHANOL 0.35-UP

62.42

19.79

50 (70.)

FIRE ETHANOL >0.05%

61.77

18.54

80

FIRE ETHANOL <=0.05%

62.08

18.11

70

NON-FIRE ETHANOL <=0.05%

67.65

15.37

70

NON-FIRE ETHANOL >=0.05%

70.80

13.98

80

MALES

64.49

17.28

70

FEMALES

64.25

17.58

70

MALES FIRE

61.34

18.22

70

FEMALES FIRE

63.31

18.25

70

MALES NON-FIRE

69.34

18.22

70 (80.)

FEMALES NON-FIRE

67.13

15.53

70

MALES ETHANOL >0.05%

64.41

17.74

80

FEMALES ETHANOL >0.05%

67.51

16.61

70

MALE FIRE >0.05% ETHANOL

60.61

18.50

70

FEMALE FIRE >0.05% ETHANOL

65.59

18.27

70

MALE NON-FIRE >0.05% ETHANOL

70.53

14.54

80

FEMALE NON-FIRE >0.05% ETHANOL

71.81

11.59

70

MALES ETHANOL <0.05%

64.55

17.00

70

FEMALES ETHANOL <0.05%

63.32

17.74

70

MALE FIRE <0.05% ETHANOL

61.92

17.98

70

FEMALE FIRE <0.05% ETHANOL

62.67

18.19

70

MALE NON-FIRE <0.05% ETHANOL

68.46

15.14

80

FEMALE NON-FIRE <0.05% ETHANOL

65.25

16.48

70 (80.)

AGE 1–10 YRS

64.91

19.10

70

AGE 11–20 YRS

67.13

15.84

70

AGE 21–30 YRS

64.83

17.38

70

AGE 31–40 YRS

66.71

16.80

70

AGE 41–50 YRS

65.80

15.65

70

AGE 51–60 YRS

62.16

17.67

60

AGE 61–70 YRS

60.94

17.75

50 (70. & 80.)

Carbon monoxide and fatalities

189

AGE 71–80 YRS

60.14

17.59

50 (70.)

AGE 81–90 YRS

56.78

14.66

50 (70.)

AGE 91 & UP

58.10

12.87

50 (70.)

blood analysis for each category are also key indicators. Data representative of the entire data base are presented in Table 4 below:

TABLE 4 Representative Carboxyhemoglobin levels in Forensic Data Base. Percentage of Victims with <60% COHb Given for Each Subcategory Total Data Base (1,626 cases, with age reported): Overall:

34%

Male:

32%

Female:

36%

Age:

11 to 50 years:

29%

61 to 80 years:

47%

Blood Alcohol >0.05% (596 cases, 33% of population: 38% for males, 23% for females): Overall:

31%

Male:

33%

Female:

27%

>0.05% to 0.20% alcohol

28%

>0.30% alcohol:

46%

Alcoholics:

12% Disease:

Cardiovascular:

44%

Male:

46%

Female:

41%

Liver, pulmonary, kidney

43%

The total data base comprises 68% males and 32% females. Overall, 34% of the CO victims died with COHb values <60%. Age was a factor; 29% of victims aged 11 to 50 years had COHb values <60% versus 47% of victims aged 61 to 80. Alcohol use is a pervasive factor in all CO fatality studies. Approximately 33% of the population showed blood alcohol levels >0.05% (38% for males and 23% for females). For victims with blood alcohol >0.05% to 0.29%, 28% had blood COHb values <60%. By contrast, of victims with blood alcohol >0.30%, 46% had COHb values <60%. Only 12% of alcoholic victims had COHb values <60%. The significant variations for victims with >0.30% blood alcohol and for alcoholics were not observed in previous studies. Disease

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190

was also a factor; victims with cardiovascular disease and with other reported physical disorders showed elevated percentages of the population with COHb values <60%. Given the diversity of the data base there is some utility in an examination of segments of the data base, separately. Fire victims constitute 61% of the data base (63% male). Data for the fire segment are shown in Table 5.

TABLE 5 Characteristics of Fire Cases in Forensic Data Base. Percentage of Victims with <60% COHb are given for Each Subcategory. Fire Cases [61% of data base (877), blood alcohol >0.05% (37% of population, 46A% for Males, 23% for Females), Data Base 63% Male]: All Fire Cases:

41% Male:

41%

Female:

39%

11 to 50 years:

37%

61 to 80 years:

51%

1 to 10 years:

34%

(1 to 10 years:

9%>90% COHb)

Age:

Alcohol >0.05% segment (78% male) Overall:

39%

Male:

42%

Female:

30%

Alcohol >0.05% to 0.29%:

35%

Alcohol 0.30 to 0.35+%:

47%

Alcoholics:

29%

Cardiovascular:

55%

Liver, Pulmonary, Kidney

57%

Disease:

Hydrogen Cyanide:

51%

Of fire victims, 41% had COHb values <60%. Age differences were observed, with a substantially higher proportion of the over-60 age groups in the <60% COHb category. Hydrogen cyanide was measured in 142 victims. With 51% of the population in the <60% COHb category, CO and HCN appear to exert a combined effect to some degree. For the non-fire segment of the data base (Table 6), 85% were automobile exhaust gas victims and 75% were male. Despite the higher male population, the percentage of victims with >0.05% alcohol was similar to that on the fire segment.

Carbon monoxide and fatalities

191

Overall, 22% of the non-fire population had COHb values <60%. Females showed a higher value which originated in the portion of the population with <0.05% blood alcohol. To examine the extent to which age and ethanol explain differences in COHb levels, a multivariate analysis is required, which separates variables. Such an analysis is separately reported.

TABLE 6 Characteristics of Non-fire Cases in Forensic Data Base. Percentage of Victims with <60% COHb are given for Each Subcategory Non-fire Cases [39% of Data Base (558), blood alcohol>0.05% (34% of population, 36% of Males, 29% of Females), 85% Exhaust Victims, Data Segment 75% Male]. All Non-Fire Cases: Male:

20%

Female:

28%

Exhaust Source:

19%

Natural Gas Source:

26%

Gas Heater Source:

76%

Age: 11 to 50 years:

30%

61 to 80 years:

31%

>0.05% Alcohol Segment Overall:

17%

Male:

18%

Female:

14%

Alcohol>0.05% to 0.29%:

15%

Alcohol 0.30% to 0.35=+%:

57%

Alcoholics:

6%

Disease: Cardiovascular:

34%

Liver, Pulmonary, Kidney:

27%

Figure 4 shows the victim profiles for both fire and non-fire victims. Fire victims include a larger number of <60% victims, about twice as many as non-fire victims (41 versus 22%), a value consistent with previous studies. The source of CO is important because most CO exposures do not occur with the gas in its pure state. Natural gas and gas heater exposures show larger populations with <60% COHb than does exhaust gas. Other constituents must have been present from these atmospheres. Overall, for non-fire victims other observations were similar to those for fire victims.

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192

The foregoing observations are based upon the percentage of the population with COHb values <60%. The reader is directed back to Table 3. Table 3 shows mean values, standard deviations, and highest peaks (modes) for a variety of data segments. The mean of all COHb values is 64.2%. For fire victims the mean is 61.97 versus 68.2% for nonfire victims. A smaller mean value and a larger standard deviation signify a broader population distribution (a higher <60% COHb population) in the fire segment. The lowest COHb mean values are observed for ages 81–90 (56.8%), ages 91 and up (58.1%) and for victims with ethanol 0.30−0.34% (59.7%). The highest mean values are observed for non-fire victims with >0.05% blood alcohol (all 70.8%, males 70.5%, and females 71.8%).

FIGURE 4 Victim COHb profile for fire (n=887) and non-fire (n=558) segments of the data base. Fire victims include a larger number of <60% COHb victims than non-fire victims (41% vs 22%). The interaction of CO with alcohol is worth further comment. One observation made from the data in Table 3 is that death occurs for non-fire victims at a higher mean COHb value with some blood alcohol (0.05% to 0.30%). There appears to be a possibility that some blood alcohol increases the amount of CO needed to cause death, this is, alcohol acts as an incapacitating agent preventing escape from a life threatening situation. The mechanism of CO toxicity is not simple and is not understood in great detail. Yet the differences in different populations exposed to CO are to be expected, because it is known that more factors than hemoglobin’s oxygen-carrying capacity are involved. Different segments of the exposed population respond differently. Therefore, conclusions for given victims can be made only after thorough analysis of all factors actually present.

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193

Indeed, a victim with 30% COHb can clearly be a case of CO poisoning without other agents required. There have been comments made about the number of low COHb deaths encountered with fire victims. Some have suggested this increased number of low COHb deaths is caused by toxic fire gases from burning specific materials. Yet, many fire victims exposed to the modern fire environment die at the “normal level” of 60–80% COHb (Table 3) and people exposed to a non-fire environment die at low COHb levels (Table 7). Table 8 shows the fraction of fire and non-fire victims with alcohol by reporting laboratory. Table 9 shows data for alcohol by gender and percent of victims with COHb less than 60%. Given the importance of alcohol, age, and source of CO on CO toxicity, data tables are provided as an appendix to this report. A statistical investigation of the data base is provided by other workers as a separate chapter (Chapter 8).

TABLE 7 Factors affecting letahl levels of carboxyhemoglobin Cases of Particular Interest Case %COHb Age No. 1

Remarks

24

19

Full autopsy of male victim of a faulty gas heater showed cherry red color of tissue and no signs of heart disease or other contributing factors.

2

27

Man was stopped by police for driving in a drunken manner. Victim signed form to have blood taken when he arrived at the hospital.

3

45

38

Man committed suicide by sealing all windows of his truck and running a hose to a window and sealing with towels. Complete autopsy showed no heart or other condition to cause low COHb. No re-suscitation attempts were attempted.

4

21

22

Man committed suicide by taping all windows of his car and running a metal tube to the interior of the car from the exhaust. Complete autopsy showed no evidence of heart disease or other contributing factors.

5

48

19

Three people were exposed to carbon monoxide from a faulty gas heater. All three were treated at the hospital. Only one of the victims died from the exposure. When the victim was admitted to the hospital he had a 48% COHb reading. Postmortem tests of his blood gave a reading of 24%. A complete autopsy revealed a cherry red coloration of the tissue and no evidence of heart disease or other contributing factors.

6

38

26

Male victim exposed to carbon monoxide from faulty gas heater was given a complete autopsy. No heart disease or other contributing factors were found.

7

65

21

Female victim of car exhaust died but her male companion in the car survived the same carbon monoxide exposure. Complete autopsy showed no evidence of other contributing factors.

8

60

22

Female victim of car exhaust died but her male companion in the car survived the same carbon monoxide exposure. Complete autopsy showed no signs of other contributing factors.

9

64

84

Female victim of car exhaust died at 64% COHb level but her 40 year old

Carbon monoxide and human lethality

194

female companion died at 75% COHb even though they were both exposed to the same concentration of carbon monoxide. Complete autopsy showed no evidence of other contributing factors. 10

60

17

Female victim of exposure to car exhaust died whereas her male companion survived. Complete autopsy showed no signs of other contributing factors.

11

65

23

Female victim died of exposure to car exhaust and her male friend, exposed to the same levels of carbon monoxide, survived. Complete autopsy showed no signs of other contributing factors.

12

75

17

Female victim died at 75% COHb and her 17 year old male companion died of the same exposure at 80% COHb. Complete autopsy showed no evidence of other contributing factors.

13

65

37

Female victim died at 65% COHb and her 38 year old male companion died at 85% COHb when exposed to the same levels of carbon monoxide from a fire in another part of the building. The fire did not reach the room in which the victims were found. Complete autopsy showed no evidence of other contributing factors.

14

60

16

Male victim of faulty natural gas heater died but his brother in the same bed survived. No other contributing factors were found in a complete autopsy.

15

55

42

Female victim died from car exhaust at 55% COHb whereas male friend died of same exposure at 60% COHb. No other contributing factors could be found in complete autopsy.

16

45

19

Male victim of car exhaust with .08% ethanol died at 45% COHb whereas female friend in the same car survived the exposure. No evidence of other contributing factors were found in a complete autopsy.

17

70

34

Female suicide victim connected oxygen mask hose to car exhaust and put on mask. Complete autopsy showed no signs of other contributing factors.

18

60

28

Female victim of a car fire where report indicates that plastics were burning did not show a low COHb level.

19

42

53

Female victim suffering from heart disease died at 42% COHb a much lower level than her male companions 75% COHb in the same room. The room was not involved in the fire.

20

27

45

Male with 0.36% ethanol died from burning paper. Full autopsy showed no evidence of other contributing factors.

*

Note: A cherry red color of the blood is noted in many CO fatalities, but is not present in all cases or with CO at lower concentrations.

Table 8 Fraction of Fire and Non-Fire Victims with Ethanol By Laboratory Lab #

#

Fire Fraction With Ethanol

#

Non Fire Fraction With Ethanol Total

1

8

12.5

7

0.0

15

2

3

33.3

1

0.0

4

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195

3

3

100.0

6

50.0

9

4

0

0.0

14

64.3

14

5

0

0.0

0

0.0

0

6

8

37.5

5

20.0

13

7

4

0.0

13

23.1

17

8

0

0.0

0

0.0

0

9

56

35.7

37

51.4

93

10

66

36.4

28

42.9

94

11

7

42.9

0

0.0

7

12

9

0.0

26

0.0

35

13

0

0.0

0

0.0

0

14

3

0.0

1

100.0

4

15

191

42.4

88

60.2

279

16

9

33.3

22

40.9

31

17

2

100.0

8

12.5

10

18

12

33.3

6

100.0

18

19

28

32.1

10

50.0

38

20

6

50.0

8

62.5

14

21

8

37.5

9

44.4

17

22

131

34.4

80

38.8

211

23

14

42.9

20

40.0

34

24

4

0.0

0

0.0

4

25

0

0.0

1

0.0

1

26

0

0.0

1

0.0

1

27

0

0.0

4

0.0

4

28

0

0.0

1

0.0

1

29

0

0.0

1

0.0

1

30

0

0.0

1

0.0

1

31

0

0.0

4

0.0

4

32

0

0.0

1

0.0

1

33

0

0.0

1

0.0

1

34

7

0.0

14

0.0

21

35

130

50.8

55

61.8

185

36

235

54.9 106

42.5

341

Carbon monoxide and human lethality

37

188

3.7

Total 1132

196

73

19.2

652

261 1784

TABLE 9 Relationship of Ethanol to People Dying Below 60% COHb Cases with Ethanol Greater than 0.05%

Cases with Ethanol Less than or Equal to 0.05%

Ethanol >0.05%

COHb <60%

Ethanol ≤0.05%

COHb <60%

%

%

%

%

38

32

62

32

572 Females

22

25

78

39

440 Males

35

18

65

20

142 Females

29

14

71

32

598 Males

44

42

56

41

22

30

78

41

1252 Males ALL

Non-Fire

Fire 344 Females

CONCLUSIONS Source of CO, age, and a composite variable indicating some mental or physical impairment were found to be the strongest determinants of low COHb levels in the whole data base. For fire victims alone increased age and the presence of impairment were strongly associated with low COHb levels. Finally, for non-fire victims alone, the presence of ethanol was strongly associated with decreased percentages of low COHb. The mechanism(s) of carbon monoxide toxicity is not simple and not understood in detail. The differences that are observed in different populations exposed to carbon monoxide are to be expected since more than hemoglobin’s oxygen carrying capacity is known to be involved. The distribution of COHb levels of fire victims has a greater fraction below 60% COHb than does that of non-fire victims; however, non-fire victims succumb at low COHb levels as well. Different segments of the exposed population exhibit different outcomes. Therefore, conclusions for given victims can be made only after thorough analysis. A victim with 30% COHb can clearly be a case of carbon monoxide poisoning without other agents required.

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ACKNOWLEDGEMENT This work was performed under grants from The Society of the Plastics Industry. Their support of this work is gratefully acknowledged. REFERENCES 1. I.Benjamin and F.Clarke, “Fire Deaths—Causes and Strategies for Control,” Technomic Publishing Co., Lancaster, PA, 1984, p. 15. 2. Other chapters in this volume.

CONTRIBUTORS OF FATALITY CASES 1. Palm Beach County Medical Examiners Office 3126 Gun Club Road West Palm Beach, Florida 33406 2. Blodgett Memorial Medical Center Laboratory Grand Rapids, Michigan 3. James G.Bridgens, MD 1025 Huntington Road Kansas City, Missouri 64113 4. Larimer County Coroner’s Office Roche Biomedical Laboratories Fort Collins, Colorado 5. Claude B.Hazen 123 Redbug Way Leesburg, Florida 32748 6. Alabama Department of Forensic Sciences 1001 South 13th Street Birmingham, Alabama 35205–3498 7. Macomb County Medical Examiner Division Wayne County Medical Examiner Division Laboratory Wayne County, Michigan 8. Walla Walla County Coroner’s Office Touchet, Washington 9. Washington State Toxicology Laboratory Seattle, Washington 10. Medical Examiners Office Jacksonville, Florida 11. Medical Examiners Office 14th Judicial Circuit, Florida 12. Bellevue Hospital New York City, New York

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Taken from Gettler, Alexander O., et al “The Carbon Monoxide Content Under Various Conditons”, 1940 13. Bellaire Clinic 14. Coroners Office Lake County, Illinois 15. Office of The Chief Medical Examiner Calgary, Alberta, Canada 16. Oakland County Medical Examiner 1200 North Telegraph Road Pontiac, Michigan 48053 17. Munson Medical Center Laboratories Grand Traverse County Medical Examiner c/o Munson Medical Center Laboratories 6th and Madison Street Traverse City, Michigan 49684 18. Arkansas State Crime Lab #3 Natural Resources Drive P.O. Box 5274 Little Rock, Arkansas 72215 19. Forensic Pathologists Inc. 1529 Doctors Drive Bossier City, Louisiana 71111 20. San Mateo County Coroners Laboratory 905 Marshall Street Redwood City, California 94063 21. Onondaga County Medical Examiner 300 West Onondaga Street Syracuse, New York 13202 22. New York State Police Scientific Laboratory State Campus, Building #22 Albany, New York 12226 23. Montana Division of Forensic Science and Criminalistics Laboratory 275 West Front Street Missoula, Montana 59802 24. Office of the Medical Examiner of Harris County 1700 Holcombe, Suite 100 Houston, Texas 77030 25. Jefferson County Coroner Louisville, Kentucky 26. Ventura County Medical Examiner and Coroner Ventura, Colorado 27. Fulton County Chief Medical Examiner Atlanta, Georgia 28. Pulaski County Coroner

Carbon monoxide and fatalities

Little Rock, Arkansas 29. Ohio County Medical Examiner Wheeling, West Virginia 30. Pima County Medical Examiner Tucson, Arizona 31. Hamilton County Coroner Cincinnati, Ohio 32. San Diego County Coroner San Diego, California 33. Napa County Sheriff-Coroner Napa, California 34. Forensic Science International Vol 18, 1981, pp. 175–179 35. Georgia Bureau of Investigation Division of Forensic Science P.O. Box 370808 Decatur, Georgia 30037–0808 36. Office of the Chief Medical Examiner Chapel Hill, North Carolina 27514–1506 37. Office of the Chief Medical Examiner State of Connecticut P.O. Box 427 Farmington, Connecticut 06032–0427

199

Chapter 7 CARBON MONOXIDE AND FATALITIES: SECULAR TRENDS SARA M.DEBANNE Case Western Reserve University Department of Epidemiology and Biostatistics 2109 Adelbert Road, Cleveland, OH 44106 USA & DOUGLAS Y.ROWLAND D.Y. Rowland Associates 3189 Scarborough Road Cleveland Heights, OH 44118 USA ABSTRACT There is a great deal of variability in blood levels of %COHb in deaths related to carbon monoxide. In order to examine the relationship between %COHb and the characteristics of victims and their environment, a total of 2,637 cases of deaths involving CO during the years 1938–79 were examined from the records of the Cuyahoga County Coroner. This data base constituted all such deaths for which complete (i.e., multivariate) data was available and the entire period fit within the term of a single coroner. In this chapter, the variations over time in lethal level of COHb are examined for diverse groups, defined by demographic and other characteristics. It was found that the changes in COHb correspond to changes in population demographics, types of deaths, emergency medical interventions and the involvement of alcohol in the victim. Specifically, the ages of fire victims varied more widely over time than those of nonfire victims, which remained relatively constant as a group. On average, fire victims were younger; however, many of the fire victims were elderly (more than the non-fire victims). Racially, the proportion of black victims increased as the years went by, in both fire and non-fire deaths, while being at all times proportionally higher in the fire group. The proportion of males was seen to decrease over time in the non-fire group while no consistent pattern was discerned in the fire victims; at all points, however, there are more males among non-fire victims. Through the years, burns became less and less the cause of death reported by the coroner. The variation observed in sources of CO was due, primarily, to the decrease in cases involving natural gas.

Carbon monoxide and fatalities: Secular trends

201

*

Note: In every case, if no further details are given, the venue for the study is the United States.

The involvement of alcohol changed little over time, being found in a slightly higher fraction of non-fire victims, but being present at much higher levels among fire victims, where present. Short-term survival was greater among fire victims, with the fraction of such cases being much higher in more recent times. Most important, it is seen that the overall lethal %COHb levels have at all times (viz., even before the advent of plastics in the built environment) been lower for fire victims than for non-fire victims. However, the differences found have been relatively constant over the years and can be accounted for by the differences in demographic and other characteristics of the victims. This, and the role of other factors, makes it unlikely that changes in %COHb levels are at all related to changes in the composition of fire atmospheres.

INTRODUCTION There is a great deal of variability in levels of %COHB in CO deaths. While some of it is undoubtedly due to random (and unknown) causes, it is also true that specific characteristics of both individuals and their environment jointly influence what level of CO exposure will prove lethal in a given situation (see for example references 1–18 and others in the bibliography, appendix D). Because these characteristics may operate interactively with each other, research toward describing the most important determinants of lethality must be based on full multivariate data.1,3 The CWRU data base fits this description. It contains records of 2,637 deaths in the Cuyahoga County Coroner’s records during the years 1938 through 1979, inclusive. All this period was within the term of the late Samuel R.Gerber, M.D., Cuyahoga County Coroner; thus, the variations in the data due to reporting practices should be minimal. Information is presented with respect to: the Coroner’s identifying case number, date of death, age (attained at latest birthday), race, gender, cause of death, source of CO, Coroner’s verdict as to nature of death (viz., suicide, homicide, accidental death, etc.), blood alcohol content, COHb level, fire or non-fire mode of CO exposure and length of survival, if any, from time of CO exposure to death. These data along with an identifying case number (given for this study) comprise the variables in the data base, presented as Table 1. Complete multivariable data is available for every case. The data may be examined in two days: (1) to provide a long term historical perspective of COHb levels by focusing on recent levels versus those during the 1940’s and 1950’s, before the widespread use of plastics in construction, and

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(2) to allow cross-sectional examinations of the interplay of the many factors which, acting singly or jointly, contribute to death from CO exposure during a given period of time.

TABLE 1 Variables in the Database Name of Variable

Possible Values in Database

. case #

cases numbered consecutively 1 to 2,637

. coroner’s id

between 47,835 and 176,240, inclusive

. date

between 1/2/38 and 12/28/79, inclusive

. age

between 1* and 97 years, inclusive

. race

white, black, oriental, American Indian or unknown

. gender

male, female or unknown

. cause of death

CO poisoning alone, CO and burns, burns and secondary CO, burns alone, CO and other (besides burns), other (than burns or CO), burns and other (than CO), or undetermined/unknown

. source of CO

auto, truck, tractor or other apparatus with internal combustion motor; natural gas; a home; clothing; coal, coal gas, coke, charcoal or smudge pot; rags or bonfire, a building; propane gas, gasoline, kerosene or other fire accelerant; or undetermined/unknown

. verdict

Suicide, accident, industrial accident, homicide, justifiable homicide or undetermined

. blood alcohol

0% to 0.68% or not determined

. 7% to 99% carboxyhemoglobin . fire/non fire

non-fire, fire, or fire and explosion

. survival

0 to 9 (or more**) hours

*

All victims who had not yet achieved their second birthday were coded, “1”. All victims who survived exposure to CO for more than nine hours were coded, “9”.

**

This chapter describes in detail the CWRU database and presents the analysis of time trends of %COHb levels; the second research issue is addressed in Chapter 8. THE CWRU DATABASE Search of Cases The years 1938–54 were all treated in a similar manner. The Coroner’s daily log was examined, first, to produce a list of all cases where CO might be implicated for further study. In particular, all fires and explosions were listed, as well as a variety of cases where “poisoning” by fumes of some sort, “asphyxiation” other than strangulation, or some other cue for CO was noticed. The full Coroner’s reports for the cases on the list for

Carbon monoxide and fatalities: Secular trends

203

further study were then examined to yield laboratory determinations of COHb and blood alcohol and a review was made of the cause and nature of death. All cases where COHb levels were recorded were deemed appropriate for inclusion in the database. Laboratory log books were available for the period 1955–79, suggesting a more efficient means of compiling the list for review; namely, to consult the lab books first to determine a list of cases with COHb measured. This method was utilized for all years, 1955–79. Fire Deaths in the Database Based on a sampling of the years 1938–79, fire deaths in the database as a fraction of total annual fire deaths in the Coroner’s records19 appear to follow two distinct patterns. From 1938 to the mid-1950’s approximately one quarter (24%) of fire deaths had laboratory determinations of COHb. In several cases, victims who today might survive the incident due to better firefighting technology and better emergency medicine for burn victims, survived for intervals of time which were short, yet lengthy enough to allow COHb levels to decrease. Also, several cases involved corpses which were burned or decomposed to such an extent that procedures then in place would not have required CO determination, and which, if performed, would have been very inaccurate due to the technology available at that time. It also must be noted that in those years there were cases of single fires which were responsible for many (viz., 10 to 30) deaths in a single incident, most of which did not have COHb determinations. In the mid-1950s due in major part to the contribution to life safety of improved technology affecting firefighting, emergency medicine and laboratory capabilities developed for military use during World War II and the Korean War, the fraction of fire deaths in the database (i.e., those with COHb determination) of all fire deaths increased to the level of about one half. Since that time the fraction has shown some variation (the late 1970s yield nearly 60%), but the period, 1960–79, has an aggregated fraction of 49%. The later period may be characterized by two stereotypes of fire victims who are not in the database. One type of victim is an individual who was exposed to a fire during a hospital stay often from careless smoking. These cases rarely have CO determinations by the Coroner’s laboratory in their records. The second type of victim survived long enough to have normal levels of COHb. In summary, there is clearly a distinction between the fraction of fire cases eligible for inclusion in the database, prior to and subsequent to the mid-1950s. About 40% of all fire victims during the study period are included in the database. It should also be noted that the laboratory method of determining CO levels was changed one time during the period 1938–79. Up until mid-1973, % COHb was measured by ultra-violet spectrophotometry at which time measurements began being made by a CO-oximeter. DESCRIPTION OF CASES The 2,637 total cases consist of 1,693 cases of non-fire deaths, 925 cases of fire deaths and 19 cases involving both fires and explosions. More specific descriptions of the cases are given by cross-tabulations in Table 2.

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TABLE 2 Comparison of Descriptive Statistics by Setting of CO Exposure Setting of CO Exposure Characteristic Total number of cases

Non-fire

Fire

1,693

944

45.11

38.72

.41

0.86

46.00

41.00

Age Average Standard Error Median Race Number of Whites (%)

1,496 (88.4%) 592 (62.7%)

Number of Blacks (%)

196 (11.6%) 350 (37.1%)

Number of other Races (%)

1 (0.1%)

2 (0.2%)

Gender Number of Males

1,261 (74.5%) 600 (63.6%)

Cause of Death Number with CO alone (%) Number with CO and another cause (%) Number with Burns and/or other causes (%)

1,675 (98.9%) 414 (43.9%) 17 (1.0%) 369 (39.1%) 1 (0.1%) 161 (17.1%)

Source of CO Automobile exhaust Natural gas

1,392 (82.2%) 270 (15.9%)

Conflagration of auto, home/dwelling, building, clothing or rags Other

925 (98.0%) 31 (1.8%)

19 (2.0%)

Suicide

931 (55.0%)

14 (1.5%)

Accident

718 (42.4%) 859 (91.0%)

Coroner’s Verdict

Industrial Accident Homicide Justifiable Homicide Undetermined

22 (1.3%)

31 (3.3%)

6 (0.4%)

23 (2.4%)

0 (0.%)

1 (0.1%)

16 (0.9%)

16 (1.7%)

Blood Alcohol Number with positive ETOH % ETOH x 100 (drinkers only)

700 (41.3%) 354 (37.5%)

Carbon monoxide and fatalities: Secular trends

Average Standard Error

205

15.42

22.83

0.32

0.61

63.94

54.04

0.28

0.54

65.00

60.00

35 (2.7%)

61 (6.5%)

1.00

1.00

%COHb Average Standard Error Median Survival Number of (short-term) survivors of CO exposure (%) Median hours of survival

Strikingly different profiles of fire and non-fire victims emerge: (1) fire victims have been younger (by about five years or so) in the aggregate than nonfire victims. Infant deaths are much more common among fire cases than non-fires. (2) the racial composition of the fire victims consists proportionately of blacks to a greater extent than non-fire victims (a greater than three-fold difference), (3) proportionally there are slightly fewer males among fire victims than among non-fire victims, (4) the vast majority (nearly 99%) of non-fire victims have CO alone listed as cause of death; whereas, for fire victims there are, proportionally, nearly as many cases listing CO and another cause (as causes of death) and there is another one-sixth of the cases listed as having died from burns and other causes, (5) sources of CO are not comparable for fire versus non-fire victims; however, for each group the chosen categorizations of sources leave very small “other” categories containing no more than 2% of the cases, (6) more than nine-tenths of the fire victims’ deaths have Coroner’s determinations of accidental; whereas, for non-fires more than half are suicides, (7) there are, proportionately, slightly more drinkers among non-fire victims than among fire victims; however, the %ETOH levels of the latter drinkers are nearly one-third higher, (8) aggregately, the %COHb levels are lower in fire victims than non-fire victims, and (9) fire victims are much more likely (than non-fire victims) to have survived the exposure to CO for a short period of time. Thus, we see that the profiles differ in ways that relate to demographic and situational differences. Characteristics of the database that are aggregated over time must be seen as mixing representatives of the Cuyahoga County population which was, itself, undergoing great changes. It is important to see how these characteristics varied during the study period; this issue is addressed in Chapter 8.

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GENERAL TIME TRENDS Table 3 illustrates the time trends of the variables through the years, 1938–79. From a statistical point of view, there are some minor changes in demographic characteristics (i.e., age, race and gender) of victims. The fluctuations of average age for fire victims is explained to a large extent by single incidents with multiple victims: of the 119 fire cases in the 1938–49 period, 11 were victims of a single nursing home fire in 1946, with an average age of 78.45. The other multiple fire death situations involved four separate house fires in the years 1955 and 1958; these tragedies involved a total of 18 cases in the database (out of 161 fire victims during 1950–59), with an average age of 3.28. Disregarding these clusters

TABLE 3 Time Trends of Various Characteristics in the Database by Setting of CO Exposure Time period Characteristic Total Number of Cases

Average Age (in years)

Whites

Blacks

Males

Setting 1938– 49

1950– 1960– 1970– Overall 1938– 59 69 79 79

NonFire

339

338

473

543

1,693

Fire

119

161

318

346

944

NonFire

45.01

45.89

45.78

44.10

45.11(se:0.41)

Fire

46.49

31.66

38.27

39.75

38.72(se:0.86)

NonFire

96.2%

87.6%

86.5%

85.6%

88.4%

Fire

73.9%

62.7%

61.3%

60.1%

62.7%

NonFire

3.5%

12.4%

13.5%

14.4%

11.6%

Fire

26.1%

36.0%

38.7%

39.9%

37.1%

NonFire

82.6%

78.4%

72.3%

68.9%

74.5%

Fire

61.3%

69.6%

61.0%

63.9%

63.6%

NonFire

100.0%

99.7%

98.7%

98.0%

98.9%

29.4%

32.9%

41.2%

56.4%

43.9%

34.5%

42.2%

41.8%

36.7%

39.1%

36.1%

24.9%

17.0%

6.9%

17.1%

Cause of Death: CO alone CO alone CO and other Burns/other

Fire

Carbon monoxide and fatalities: Secular trends

207

Source of CO: Auto Exhaust

NonFire

72.0%

72.8%

86.0%

91.2%

82.2%

26.8%

23.7%

12.5%

7.4%

15.9%

Fire

97.5%

98.1%

98.1%

98.0%

98.0%

NonFire

54.0%

47.9%

55.6%

59.5%

55.0%

43.1%

47.9%

42.5%

38.5%

42.4%

Fire

89.9%

91.9%

91.8%

90.2%

91.0%

NonFire

36.3%

42.3%

44.0%

41.6%

41.3%

14.48

14.91

16.13

15.60

15.42(se:0.32)

37.8%

34.8%

37.7%

38.4%

37.5%

21.71

23.09

22.85

23.08

22.83(se:0.61)

NonFire

75.00

60.00

60.00

65.00

65.00

Fire

70.00

55.00

60.00

60.00

60.00

NonFire

0.9%

0.3%

1.7%

4.2%

2.7%

2.00

2.00

1.00

1.00

1.00

4.2%

1.2%

3.1%

12.7%

6.5%

1.00

5.00

1.50

1.00

1.00

Natural Gas Conflagration of structure, clothing, bedding, and/or rags Coroners’ Verdict/Determination: Suicide Accident Accident Blood Alcohol: ETOH>0 Average Concentration* ETOH>0

Fire

Average Concentration* Carboxyhemoglobin: Median Level (in per cent COHb)

Short-term Survival rate Median Survival (Survivors only) Short-term Survival Rate Median Survival (Survivors only)

Fire

* Average concentration among ethanol positives in units of per cent ETOH×100. se denotes standard error. % denotes per cent of total cases for setting during time period.

of events, age has remained fairly stable for fire and non-fire victims, the latter being consistently older, on average, than the former. The changes in racial composition of both fire and non-fire groups reflect the changing demographics of the Greater Cleveland area.20,21 The proportion of black victims has increased in both groups, while being at all times proportionately higher in the fire group. The proportion of males has decreased in the non-fire group while no consistent pattern is seen in the fire victims; at all points, however, there are proportionately more males among non-fire victims.

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Thus, in spite of changes in demographic profiles within the non-fire and fire groups, the differences between the two groups are of the same type at all times. With respect to the variables related to the setting of the incidents, the only changes in cause of death over time involve a steadily decreasing incidence of fire cases with burns and/or another (not CO) cause listed. This probably reflects advances in the treatment of burn victims. Sources of CO show little variation through the years other than the decrease in natural gas cases, attributable in great part to the decline in gaslights and safety improvements by the natural gas industry. Little or no variation is seen in coroner’s verdict. Regarding laboratory determinations, blood alcohol findings change little over time for non-fire as well as fire victims, the latter group exhibiting a consistently higher alcohol concentration. Time trends of median COHb levels for fire victims seem to track those for non-fire victims; both having major decreases followed by smaller increases. Finally, the 1970–79 period has higher rates of short-term survival following the incident of exposure. This probably reflects accomplishments in emergency medicine since the 1960’s. What arises, in balance, from this consideration of time trends, is that the changes in COHb levels for fire and non-fire victims parallel each other. Underlying this phenomenon, and in spite of certain changes in each group, is the fact that fire and nonfire victims differ with respect to behavior and demographics at all times of the study period. The time-dependent variation of COHb is examined more closely in the next section. COMPARISON OF FORCES AFFECTING TIME TRENDS OF COHB The major historical trend manifested in both fire and non-fire median COHb levels (Figure 1) is one of steady decrease followed by a period of stability and some retrenchment, the so-called “U-shaped curve.” The similar shapes of the curves suggest that there are similar main forces at work. However, it is worthwhile investigating whether there are explanations for the changes within each type of setting. The most dramatic change that has occurred among non-fire victims is the de crease in the proportion of cases where natural gas was the source of CO: from 26.8% in the first time period to 7.4% during the last one. It might be expected that this trend could be related to the down trend in COHb for non-fire victims.

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FIGURE 1 However, as Figure 2 shows, the five year medians for natural gas are generally lower than those for automobile exhaust and therefore, COHb medians for all non-fires should be increased by the drop in natural gas cases, contrary to what is observed.

FIGURE 2

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FIGURE 3 Similarly, for fire cases the most striking change has been the decrease in the proportion of cases with burns listed as cause of death: from 36.1% to 6.9%. At the same time, Figure 3 shows that for fire cases, five year COHb medians for burn victims are lower than for cases with CO (alone or in combination, themselves similar). Again, these two trends operate against, rather than explain, each other. This means that for both fire and non-fire cases, the changes over time in the relative mix of cases do not help to explain the time trends of five year median COHb levels. There is no clear indication that time trends of other factors are related to trends of COHb levels within each setting. It is more likely that other factors, such as laboratory procedures, are affecting both fires and non-fires. Investigating this gross similarity of curves, time series analysis of single year COHb medians indicates that fire and non-fire settings generate the same structural models: singly differenced one term moving average time series, with fires showing greater variability. Regardless of the shape of the curves, it is noteworthy that they parallel each other with a near constant difference between them at all times. The observation of the previous section is relevant here; namely, that fire and non-fire victims differ in a consistent way, at all times of the study period, with respect to demographics, alcohol and short-time survival. This suggests that the difference between COHb medians may be related to intrinsic differences in fire and non-fire victims. If that is the case the observed difference in median COHb levels should diminish when comparing more homogeneous subgroups of fire and non-fire victims.

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FIGURE 4 Figure 4 presents so-called “clean” time trends of COHb five year medians for: (1) Fire victims with CO alone as cause of death, no alcohol and no survival; (2) Non-fire victims with CO alone as cause of death, automobile exhaust as source of CO, no alcohol and no survival; and (3) Non-fire victims with CO alone as cause of death, natural gas as source of CO, no alcohol and no survival. There it is seen that consideration of these “clean” medians tends to wipe out the constant differential between COHb levels in fire and non-fire victims. As the variation of five year “clean” medians visually appear to track each other well, there are statistical means appropriate for addressing the issues of distinguishing if they are the same curves (or significantly different) and deciding whether the curves are adequately described by linear or non-linear models.22 Clearly, there is at most a single point of inflection in the curves, thus suggesting that quadratic is the only non-linear form that need be considered. If x represents time (years since 1900), y represents median %COHb, and y= a0+a1 x+a2 x2, the three equations estimated by least squares quadratic regression are: y=179.69−3.89 x+0.031 x2 (fires, CO alone) y=186.09−3.72 x+0.027 x2 (non-fires, auto) y=158.90−3.17 x+0.024 x2(non-fires, gas) All coefficients are highly significant (p<.001) and therefore, all terms need to be included in each equation. The quadratic term is still needed for

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FIGURE 5 regressions performed deleting the rather deviant pre-1940’s values. This finding suggests that the intuitive description of COHb time trends as “U-shaped curves” was accurate in the sense that both the decreasing of COHb levels early on in the study period and the upturn late in the period are statistically significant. See Figure 5. In summary, there has been a sequential effort to statistically describe different situations of CO exposure through the process of making more homogenous groups of victims. The latter process may be described by the increasingly multivariate specification of the groups. It has been found that as cleaner time trends of medians have been created, there has been less of a difference between fire and non-fire cases. Ultimately, for “clean” medians, there were only minor differences between fire and non-fire settings. Therefore, as the occurrence of increases or decreases in COHb levels over time appear to be independent of setting (for groups of victims that are free of the influence of some confounders), it is unlikely that the changes in COHb levels have resulted from changes in the composition of fire atmospheres. It is significant that the control of just two factors, short-term survival and presence of alcohol can do this. It is of great interest to refine even more the groups compared so that variations due to demographic characteristics may also be eliminated. Because of sample size considerations, this approach also requires disregarding calendar time. The concept of disregarding time when comparing fire and non-fire cases is, essentially, crosssectional. Chapter 8 presents cross-sectional examinations of data, where the findings of this chapter may be confirmed and expanded.

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REFERENCES 1. E.H.Sonnenblick, J.Ross, Jr. and E.Braunwald, “Oxygen consumption of the heart: Newer concepts of its multifactorial determination”, Am. J. Cardiol. 22, 328–36 (1968). 2. I.Sunshine, N.Hodnett, C.R.Hall and F.Rieders, “Drugs and carbon monoxide in fatal accidents”, Postgraduate Medicine, pp. 152–5 (1968). 3. T.J.Rockwell and F.W.Weir, “The interactive effects of carbon monoxide and alcohol on driving skills”, Ohio State University Research Fund, Columbus, OH, 1975, NTIS PB-242266. 4. A.S.Hume, B.H.Douglas and K.Harden, “Effect of Ethanol on Carbon monoxide Poisoning”, IRCS Med. Sci. 4, 300 (1976). 5. B.Teige, J.Lundevall and E.Fleischer, “Carboxyhemoglobin concentrations in fire victims and in cases of fatal carbon monoxide poisoning”, Z. Rechtsmedizin 80, 17–21 (1977). 6. E.L.Covey, “Death sequence in multiple carbon monoxide asphyxiations”, J. Forensic Sciences pp. 602–6 (1977). 7. J.W.Winston, J.M.Creighton and R.J.Roberts, “Alteration of carbon monoxide and hypoxic hypoxia-induced lethality following phenobarbital, chlorpromazine or alcohol pretreatment”, Toxicol. Appl. Pharmacol. 30, 458–65 (1977). 8. M.M.Birky. M.Paabo and J.E.Brown, “Correlation of autopsy data and materials involved in the Tennessee jail fire”, Fire Safety J. 2, 17–19 (1979). 9. M.J.Cretney, R.C.Ginger and G.M.Bullivant, “Some unusual toxicological aspects of two carbon monoxide deaths”, J. Forensic Science Society, 2, 211–18 (1979). 10. V.G.Laties and W.H.Merigan, “Behavioral effects of carbon monoxide on animals and man”, Ann. Rev. Pharmacol. Tox. 19, 357–92 (1979). 11. M.M.Birky and F.B.Clarke, “Inhalation of toxic products from fires”, Bull NY Acad. Medicine, 57, 997–1013 (1981). 12. R.A.Anderson, A.A.Watson and W.A.Harland, “Fire Deaths in the Glasgow Area: I General Considerations and Pathology”, Med. Sci. Law 21, 175–83 (1981). 13. R.A.Anderson, A.A.Watson and W.A.Harland, “Fire Deaths in the Glasgow Area: II The Role of Carbon monoxide”, Med. Sci. Law 21, 288–94 (1981). 14. R.A.Anderson, A.A.Watson and W.A.Harland, “Fire Deaths in the Glasgow Area: III The Role of Hydrogen Cyanide”, Med. Sci. Law 22, 35–40 (1982). 15. L.S.King, “The effect of ethanol in fatal carbon monoxide poisonings”, Human Toxicol. 2, 155– 7 (1983). 16. D.J.Barillo, B.F.Rush, R.Goode, R.L.Lin, A.Freda and E.J.Anderson, Jr., “Is ethanol the unknown toxin in smoke inhalation injury?”, AM Surgery 52, 641–45 (1986). 17. R.Sanchez, P.Fosarelli, B.Felt, M.Green, J.Lacovara and F.Hackett, “Carbon monoxide due to automobile exhaust: Disparity between carboxyhemoglobin levels and symptoms of victims”, Pediatrics 82, 663–66 (1988). 18. E.N.Allred, E.R.Bleecker, B.R.Chaitman et al., “Short-term effects of carbon monoxide exposure on the exercise performance of subjects with coronary heart disease”, New England J. Med. 321, 1426–32 (1989). 19. S.R.Gerber, “County of Cuyahoga, OH: Coroner’s Statistical Annual Report” (All reports for years 1938 to 1979) Cleveland, OH, Cuyahoga County Coroner’s Office (Publication dated in the year following the reporting period). 20. U.S. Bureau of the Census, Census of Population: 1970, Vol. 1, Characteristics of the Population, Part 1. U.S. Government Printing Office, Washington, DC, 1973. 21. “Where Clevelanders Live: Neighborhoods population changes 1980–1990”, The Plain Dealer, March 10, 1991, p. 19A, Cleveland, OH. 22. N.R.Draper and H.Smith, “Applied Regression Analysis”, John Wiley & Sons, New York, NY, 1981.

Chapter 8 LETHAL CARBOXYHEMOGLOBIN LEVEL: THE EPIDEMIOLOGICAL APPROACH SARA M.DEBANNE Case Western Reserve University Department of Epidemiology and Biostatistics 2109 Adelbert Road Cleveland, OH, 44106, USA & DOUGLAS Y.ROWLAND D.Y.Rowland Associates 3189 Scarborough Road Cleveland Heights, OH, 44118, USA ABSTRACT The concerns of this chapter are: “how similar are fire and non fire victims?” and “can differences between the two populations explain differences in their %COHb levels?”. Two large forensic data bases are examined cross sectionally utilizing an epidemiologic approach to address these concerns. The use of parallel statistical analyses of the two data bases avoids the common pitfall of utilizing the same data set for both the generation and the testing of hypotheses. Analysis of both data bases supports the notion that the way fire victims and non fire victims differ in COHb levels corresponds to the way they differ in several other characteristics. They differ as groups in age, race, gender, impairment, involvement of alcohol and short term survival, although not all issues were addressed independently in both data bases. A variety of statistical techniques were used to sort out the effects of the various factors, with a summary consideration involving the stratification of groups into multivariately defined subgroups, composed of relatively homogeneous “equals”. A subgroup consisting of white, female, non fire victims, in the middle age group, with no impairments, who tested negative for alcohol was created as a control. A variety of other subgroups, defined by combinations of the various factors were compared against this subgroup. The effect of each factor in being associated with lower COHb levels (viz. no more than 50%) was determined. Thus, the following factors all had an association with lower lethal COHb levels: presence of impairment, age frailty (i.e. vulnerability of being either very young or very old), absence

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*

Note: In every case, if no further details are given, the venue for the study is the United States.

of alcohol, male gender and non white race. Fire victims have much larger fractions of cases of impaired, frail and non white victims than non fire victims. There are also fewer fire victims with alcohol content in their blood. It is concluded that much of the relationship connecting lower COHb levels to fire victims is actually a consequence of the inherent differences between the populations of fire and non fire victims.

INTRODUCTION Two main concerns are addressed in this chapter. The first is whether the populations of fire and non-fire victims are similar to each other with respect to demographic and health characteristics. A negative response to this inquiry prompts the second concern of whether differences in some of those characteristics can help explain the non-uniformity of the determination of lethal levels of COHb exposure, and if so, what might be the relative contribution of each determinant of lethality. Two large forensic databases, described in previous chapters, provide the data required for the exploration. They are the University of Southern Mississippi (USM) database and the Case Western Reserve University (CWRU) database. Both are analyzed by a variety of statistical procedures whose main features are outlined in the Statistical Methods section. The purpose of the parallel statistical analyses of the two databases is to avoid the common pitfall of utilizing the same data set for both the generation and the testing of hypotheses.1 It is intuitively clear that the relationships among explanatory variables and COHb levels which are consistent across databases can be argued rather compellingly to be valid. OVERVIEW OF DATA BASES Chapter 6 provided a description of the methodology used to construct the University of Southern Mississippi (USM) database and gave some cases of unique interest which demonstrate the extreme variability of lethal COHb levels, even among individuals exposed at the same time and place. This database is ideally suited for an analysis which does not take time variation into account (i.e., a cross-sectional analysis), since 98% of the exposures to CO recorded there occurred in the years 1976 to 1985. The Case Western Reserve University (CWRU) database, described in Chapter 7, is, on the other hand, better suited for a longitudinal analysis, such as the one presented there. However, it may also be examined in a cross-sectional manner, since the difference in median lethal COHb level for fire and non-fire victims remains approximately constant for the entire period of data collection (1938 through 1979). Table 1 presents listings of variables of interest and their availability in each database, Table 2 contains their summary statistics. Clearly, the two databases

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TABLE 1 Variables of Interest and their Availability Variable

USM Database

CWRU Database

Age

Yes

Yes

Gender

Yes

Yes

Race

No

Yes

%COHb

Yes

Yes

Source of Co

Yes

Yes

Cause of Death

Yes

Yes

Verdict

No

Yes

Time survived

No

Yes

Fire/Non-fire

Yes

Yes

Date of Event

Yes

Yes

Blood Alcohol

Yes

Yes

Drugs

Yes

No

Presence of Disease

Yes

No

Physical condition

Yes

No

TABLE 2 Comparison of Descriptive Statistics for USM and CWRU Studies USM Database (N=2241)

CWRU Database (N=2263)

Non-Fire

Fire

Non-Fire

Fire

38.4%

61.6%

64.2%

35.8%

Average age (yrs)

37.9

32.6

45.1

38.7

Proportion—Males

74.7%

64.7%

74.5%

63.6%

Proportion—White

–

–

88.4%

62.7%

%COHb (at least 20%)

68.7%

62.0%

63.9%

54.0%

Median COHb (at least 20%)

70.0%

65.0%

65.0%

60.0%

Proportion with positive ETOH

40.3%

36.5%

41.3%

37.5%

Average ETOH (among positives)

.14%

.21%

.15%

.23%

Proportion of cases with drugs (other than ethanol)

6.1%

3.6%

–

–

Proportion of cases specifying presence of a disease

15.6%

7.4%

–

–

Proportion of cases specifying physical condition

17.0%

9.4%

–

–

Percent of cases by setting

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Proportion of cases with fair or poor physical condition (among cases specifying physical condition)

26.1%

26.4%

–

–

Proportion determined to be accidental deaths

–

–

42.4%

91.0%

are not fully comparable. The USM database contains, for example, information which allows the construction of an impairment index, found to be a factor affecting lethal COHb level, whereas the CWRU database does not permit such construction. On the other hand, the latter database has information on race, also found to be a contributing factor, not available in the USM database. A consequence of this disparity is that the manner in which impairment and race interplay with each other and with other variables and the role of their combined effect on lethal level of COHb cannot be assessed. Equally important, the two databases represent different populations. Roughly, 60% of cases in the USM database are from fires, whereas approximately 40% of the CWRU cases are from fires. Since the latter database contains a complete count of all CO deaths in Cuyahoga County in the years 1938 through 1979, it is quite possible that fires are over-represented in the USM database. Therefore, while a general corroboration of findings is certainly to be expected, there could not be complete agreement between the analyses of the two databases. COMPARABILITY OF FIRE AND NON FIRE VICTIMS In both databases the distribution of values of %COHb is different for fire and non-fire victims, with more fire victims dying at lower concentrations of COHb (Graphs 1 and 2). Before deciding that this difference is due to the setting alone, it seems reasonable to ask whether the victims of both groups are comparable with respect to other characteristics.

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GRAPH 1

GRAPH 2 It becomes immediately apparent that, indeed, they are not. Looking at the age distribution of both groups, one sees that, in the USM database, there are very few nonfire victims under the age of 18, whereas this age group makes up 25% of the fire victims (Graph 3). Also, the older age groups have a higher representation among fire victims. It also appears, in the USM database, that the distributions of concentration of alcohol in blood are strikingly different for

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GRAPH 3

GRAPH 4 both groups: fire victims have, as a rule, higher alcohol concentrations than non-fire victims (Graph 4). At the same time, alcohol is present in more non-fire victims. The racial composition of the two settings is also different: almost 90% of non-fire victims are white, versus slightly over 60% of fire victims.

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These facts lead one to the conclusion that the comparisons of COHb levels have to take into account the differences in other factors. STATISTICAL METHODS A variety of statistical techniques are available for exploring the data bases, each having its own requirements about the data to be used. For instance, while Analysis of Variance (ANOVA)2 requires a continuous outcome variable, logistic regression3 calls for a dichotomous one. In each case the data needs to be transformed to fit these requirements. In all analyses that follow, COHb is the outcome of interest. When performing an ANOVA, COHb is taken as a continuous (i.e., interval) variable; whereas for logistic regression, its range is split into two intervals: low (20–50%) and high (over 50%). Following are brief descriptions of the main techniques used. Stratification In studying the effect of an exposure of interest (viz., fire versus non-fire) on an outcome (viz., COHb level), the effect of potential confounders, such as alcohol and age, must be taken into account. The most intuitive way of accomplishing this is by means of the technique of stratification. This method simply divides individuals into subgroups defined by levels of important variables that may be confounding (i.e., obscuring) the issue of primary importance. Comparisons are then made within each subgroup. In the present study, one would want to compare fire and non-fire victims of, roughly, the same age and with the same alcohol concentration. A first step is to identify all (available) potential confounders and to ascertain whether they act alone or in combination with each other. Analysis of Variance ANOVA is used to sort out the effects that various factors, acting either alone or jointly, have on an outcome variable of interest.2 In real life situations of exposure to CO, one finds that fire and non-fire victims are not directly comparable in ways other than setting. Since those other factors may play an important role in determining lethal COHb level, either individually or in combinations, ANOVA is an ideal technique to get first line impressions on the identities of variables likely to be important determinants of mortality. ANOVA was originally used in agriculture to sort out the varying and potentially interacting effects on crop yield of types of seed, methods of plowing and other, uncontrolled, factors such as wind. To get maximum utilization of fertile land and growing seasons, it was necessary to gain as much information as possible from a single experimental planting. Further, if the resultant finding was ultimately that seed A grew best on type of land B when plowed by method C (a three-way interaction), it was important to learn that fact as soon as possible. Early uses of this technique occurred in the chemical industry, especially where testing was destructive of expensive compounds or where long period of time were required to conduct experiments. In the present situation, ANOVA may be used to identify those factors that have the biggest effects on COHb. It also helps in the identification of interactions among those factors, so that later comparisons of COHb levels of victims are made on an equal to

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equal basis. The basic assumptions underlying ANOVA are that the outcome variable is continuous, taking on a full range of values over an interval, and that there is an additive structure to the relation of the outcome variable to its explanatory factors. Distributional Analysis Once the factors determining lethal levels of COHb have been identified, it is possible to stratify individuals by levels of these factors so that equals are compared to equals. Distributional analysis provides a powerful, as well as intuitively appealing, way of making such comparisons. It examines the frequency distributions of COHb for different subgroups of victims in the two settings. When it is found that the bell shaped curves differ either by differences in mean (average value), variance (dispersion as indicated by thickness of tails) or skewness (deviations from symmetry), this is an indication that the stratification needs further refinement. It is possible to detect gross differences by visual inspection of the curves; however, it is also possible to compare these distributional curves by statistical tests. When two curves are compared, the statistical test that classifies them as similar or different is known as the Kolmogorov-Smirnov test. When three or more curves are compared, the test is known as the Kruskal-Wallis test.4 This leads to the task of identifying other factors which may not have been included in the initial investigations. Discriminant Analysis Discriminant analysis is a technique which is used to construct an assignment rule for group membership based on a set of explanatory variables.5 In this study, group membership is defined by “low” COHb versus “high” COHb. The explanatory variables are selected as those factors that lead to the most error free assignment rule. Some of those may have been already identified through other techniques, such as ANOVA, but others, with sparse data available, can be brought in at this time in a fine tuning of differences. Logistic Regression Having succeeded in identifying those factors which best classify individuals as being in one or the other category, it is important to then quantify the contribution of each of the factors. The equation which produces the probability of an individual belonging to the category of interest is referred to as a logistic regression equation. It is based on the logarithm of the odds of membership in that category (i.e., log(p/(1−p)), where p denotes the probability of membership). Logistic regression has the effect of ascribing in a multiplicative model the amount of excess (or decreased) risk contributed by various factors with respect to a baseline level.3 THE ROLE OF ALCOHOL There are several indications that alcohol works differently in fire and non-fire victims. Tables 3 and 4, constructed using stratification techniques, show fractions of victims in

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“low” COHb ranges in the USM and CWRU databases, respectively. It is clear that presence of alcohol, in a given age group and setting, produces a very irregular pattern of changes from the corresponding baseline group without alcohol present. This is dramatically exemplified in Graph 5 where the presence of alcohol is seen to sometimes raise and sometimes lower lethal COHb levels. Overall, alcohol tends to be associated with higher COHb levels, but its effects are different depending not only on age, but also on sex, race and the actual amount of alcohol consumed. This is not surprising. Whereas in accidental

TABLE 3 Percentage of Deaths within Low COHb Ranges for Age-Source-Alcohol Specific Groups (USM Database) % COHb Range 20–40%

Age

Alcohol

No Alcohol

Alcohol

Under 6

.150

–

–

–

6–20

.076

(.067)

.133

(.043)

21–40

.097

.142

.085

.036

41–60

.177

.119

.119

.022

61–80

.141

.151

.095

(.188)

(.148)

–

(.077)

–

All

.126

.133

.083

.041

Under 6

.256

–

–

–

6–20

.162

(.100)

.222

(.087)

21–40

.243

.271

.144

.090

41–60

.403

.228

.146

.044

61–80

.365

.283

.119

(.250)

(.185)

–

(.231)

–

All

.266

.249

.156

.083

Under 6

.444

–

–

–

6–20

.276

(.300)

.289

(.304)

21–40

.379

.439

.254

.189

41–60

.661

.376

.260

.133

61–80

.565

.453

.262

(.500)

(.481)

–

(.615)

–

.454

.419

.276

.199

Over 80

20–60%

Non-Fire

No Alcohol

Over 80

20–50%

Fire

Over 80 All

Note: Parentheses indicate that estimate is based on fewer than 40 cases.

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TABLE 4 Percentage of Deaths within Low COHb Ranges for Age-Source-Alcohol Specific Groups (CWRU Database) % COHb Range 20–40%

Age

Alcohol

No Alcohol

Alcohol

Under 6

.095

(.000)

(.077)

–

6–20

.079

(.125)

(.000)

(.000)

21–40

.173

.057

.011

.004

41–60

.181

.095

.018

.025

61–80

.128

.136

.046

.024

(.065)

(.333)

(.000)

(.000)

All

.118

.096

.021

.016

Under 6

.240

(.000)

(.538)

–

6–20

.270

(.250)

.062

(.000)

21–40

.327

.124

.071

.049

41–60

.277

.259

.083

.094

61–80

.231

.258

.154

.096

(.194)

.500

(.231)

(.000)

All

.254

.219

.099

.074

Under 6

.654

(.000)

(.692)

–

6–20

.652

(.375)

.506

(.429)

21–40

.596

.533

.392

.424

41–60

.602

.592

.396

.403

61–80

.530

.621

.482

.422

(.548)

(.833)

(.500)

(.667)

.608

.577

.428

.415

Over 80

20–60%

Non-Fire

No Alcohol

Over 80

20–50%

Fire

Over 80 All

Note: Parentheses indicate that estimate is based on fewer than 40 cases.

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225

GRAPH 5 deaths alcohol helps select the victims, in the sense that the presence of alcohol represents an impairment of their physical and mental abilities that may well contribute to their demise, the suicide victims select themselves and, in their situation, alcohol may be used merely as a help in accomplishing their objective. Thus, two different sampling techniques are acting in the selection of cases and we end up with two very different populations. As the vast majority of fire victims tend to be accidental deaths and more than half of the non-fire victims are suicides, it makes sense that the presence of alcohol is so differently related to COHb for fire versus non-fire settings. The next point is subtle, yet important. Statistical techniques, by themselves, cannot sort out differences between two groups that arise from a true “treatment” effect (alcohol, in this case) from those differences in the groups that are a consequence of the manner by which the groups came about. The first distinction concerns the measurement of an effect, which is a straightforward statistical concern. The second distinction is one of selection bias, and can actually confound results unless properly handled. For this reason, the statistical treatment of several other key variables is performed, in the main, only on the victims found to be free of alcohol. The very last analysis, when all effects are properly sorted out, puts alcohol back in the picture. THE AGE EFFECT Age is a significant determinant of lethal COHb levels. Tables 3 and 4 showed differences due to age for “low” level COHb deaths. Tables 5 and 6 give results of ANOVA’s of the two databases. They show that, for alcohol-free cases, the

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TABLE 5 Analysis of Variance of COHb Values (USM Database) Source of Variation

Degrees of Freedom

Sum of Squares

Mean Square

F-ratio

Main Effects: Setting of CO (fire or nonfire)

1

3,026.8

3,026.8 11.502***

Age

2

1,173.6

586.8

2.23

Sex

1

.1

.1

.00

Setting of CO by Age

2

2,025.0

1,012.5

3.85*

Age by Sex

2

60.5

30.2

.11

Within Cells Residual

685

180, 263.6

263.16

Total

693

186, 549.6

Interactions:

*** denotes very highly significant (p< .001) * denotes significant (p< .05)

TABLE 6 Analysis of Variance of COHb Values (CWRU Database) Source of Variation

Degrees of Freedom

Sum of Squares

Mean Square

F-ratio

Main Effects: Setting of CO (fire or nonfire)

1

31,498.1

31,498.1 163.06***

Age

2

1,010.8

505.4

2.62

Sex

1

40.1

40.1

.22

Setting of CO by Age

2

2,323.2

1,161.6

6.01**

Setting of CO by Sex

1

2,439.8

2,439.8

12.63***

Age by Sex

2

352.2

176.1

.91

Setting of CO by Age by Sex

2

2,378.0

1,189.0

6.16**

Within Cells Residual

1,211

233,926.9

193.2

Total

1,222

277, 248.5

Interactions:

*** denotes very highly significant (p<.001) ** denotes highly significant (p<.001)

Lethal carboxyhemoglobin level

227

* denotes significant (p<.05)

age effect is manifested most strongly in interaction with setting. Very importantly, age fails to appear as a main effect in the ANOVA’s. This is an indication that age acts differently in certain categories. Specifically, in fire victims lethal COHb levels tend to be lower for the middle age groups than for the other age groups, whereas the trend is reversed for non-fire victims, in whom lethal levels of COHb tend to be higher in the middle age groups and lower in the others. A distributional analysis of COHb by setting and age group is appropriate at this point. Four age strata are considered: the group of those 6–20 years old, those 21–40, those 41– 60 and those 61–80. The youngest group (0–6 years old) is not considered here because there are very few non-fire victims in this young category. There are, then, eight histograms to consider. They appear to represent two distinct shapes of COHb relative distributions. One is a thin, skewed, unimodal distribution peaking in the 70–80% COHb range, the other is flatter, possibly bimodal, peaking in the 50–60% range and then again in the 70–80% range. The thin unimodal family of distributions includes the 6–20 age group of fire victims as well as all the non-fire age groups. The flatter family of distributions includes the over 20 age groups of fire victims. These descriptive statements are corroborated by statistical testing. No significant difference is detected between the 6–20 fire group and all non-fire groups combined using the Kolmogorov-Smirnov test (p=0.77). See Graph 6. Therefore, it is legitimate to pool these two groups and compare their distribution of COHb against that of the over 20 fire group. The same test now indicates a statistically significant difference for that comparison (p<0.001). See Graph 7. It is possible to determine the ranges of COHb in which the two distributions depicted in Graph 7 differ significantly. They are the 50–65% range (p<0.05)

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GRAPH 6

GRAPH 7 and the 50–70% range (p<0.01). Since presence of alcohol, setting and age are, at this point, accounted for, it is natural to ask what other variables can help explain this difference in distribution of COHb. IS PHYSICAL CONDITION IMPORTANT? Discriminant analysis is ideally suited to address the issue brought up at the end of the previous section; that is, to flag additional variables that have an effect on COHb but have not been previously brought in, mainly, in the present situation, because of considerations related to sample size. It seems obvious that, along with setting, alcohol and age, the general state of health of individuals must play a role in the lethality of a given level of COHb. A discriminant analysis of COHb as a function of several explanatory variables indicates that the variables most helpful to distinguish individuals belonging in the range of 50% to 65% of COHb for the group composed of fire victims ages 6–20 and non-fire victims versus the group of fire victims 21 and over are, for alcohol-free individuals, the setting, age, sex and presence of certain diseases. The percent of individuals correctly classified as belonging to one or the other group through knowledge of these variables is 93.5%.

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A parallel analysis for the 50% to the 70% range of COHb flags the setting, age, presence of certain drugs and the physical condition of the victims. In this analysis, the percent of individuals that would be correctly classified with knowledge of these variables is 94.4% So it is clear that the general state of health of an individual plays an important role in the lethality of exposure to CO. Ideally, a thorough review of medical charts would be required for a definitive determination of actual condition. This level of detail was outside the scope of work of the USM and the CWRU databases. The USM database contains three variables that address the issue: (i) The variable labeled “physical condition” might more aptly be named “obesity”. Codes range from “excellent” to “very overweight”, based on the appearance of the corpse. No direct information, such as, for example, whether the victim even could walk, is available. (ii) For some individuals in the database the presence of particular diseases is recorded. In this study, the presence of cardiovascular or pulmonary problems is flagged. (iii) Another variable, “other drugs” (i.e., drugs detected other than alcohol), is used here to gain information about the health status of the victims. Similar to “diseases”, the presence of certain drugs in the system (i.e., those drugs recognized as medications used in the treatment of cardiovascular or pulmonary diseases) are taken as evidence of the presence of the diseases of interest.6 To incorporate the information on health status in the USM database, taking into account that the data is fairly sparse, an impairment index is used. Along with (i), (ii) and (iii) above, this index also contains information on the presence of psycho-active drugs detected in victims which, along with alcohol, can be taken as evidence of mental impairment. Thus, the impairment index has the effect of indicating cases where the victims can be taken as unable (for physical or mental reasons) to react to an exposure to CO in the same way as others in their age category. The creation of this index allows the inclusion of a health indicator in the all inclusive analysis that follows, where all variables that have been flagged as important contributors to lethality can interact with each other. WHERE DOES “RACE” COME IN? Just before the final analysis, we focus on the role that the important variable “race” plays. Information on race is available only in the CWRU database. It is relevant to want to know its effect vis-a-vis the other variables, including physical condition and impairment (both mental and physical) which are available only in the USM database. Ultimately, the technique of logistic regression will allow all relevant variables to be considered simultaneously. As a prelude, we once again analyze the CWRU data with ANOVA techniques, this time with race as a candidate explanatory variable. The results show that race appears as a significant main effect (p<0.001) and also as a significant factor when acting in interaction with setting (p<0.05).

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There is a very straightforward explanation for this result. Race, in and of itself, probably has no direct effect. It is known that the changing racial composition is a correlate of urban decay, where more affluent whites migrate from urban centers leaving the aging housing stock (more vulnerable to fires) to non-whites of lower socioeconomic status. Thus, it seems clear that, in this data set, race is actually a proxy for the role of poverty and aging housing stock in fire cases. In non-fire cases the role of race is even less direct. Consequently, for the purpose of the statistical analysis that follows, the effect of race may be seen as an amalgamation of basic factors. PUTTING IT ALL TOGETHER In the final step, all the information gathered so far about significant determinants of lethal levels of CO exposure is used in a comprehensive mathematical model that parcels out the relative contribution of each of the factors using logistic regression analysis. In order to use this technique, we must first dichotomize the outcome (COHb level). It seems appropriate to divide its range into a “low” (up to 50%) category and a “high” (over 50%) category. Next, a list of promising explanatory variables must be developed. The results of the previous sections indicate that setting, alcohol, age, sex, race and impairment all play a part in determining outcomes. Therefore, all are considered at this point in defining a reference group against which comparisons for each variable are made. This reference group consists of white, female, non-fire victims in the middle age group, with no impairments, who test negative for alcohol. The term “baseline”, commonly used in the context of logistic regression, is not used here, to avoid the connotation of lowest risk, which is not apt in this situation. Two models for each database are considered: one with all variables included, another with all variables except setting included. The reason for the second type of model is to see how much the role of setting is taken over by those variables whose levels are not evenly distributed across setting. Recall, for instance, that the more frail age groups (very young and very old) tend to be fire victims rather than non-fire victims and they also are more vulnerable to lower levels of COHb. Let us first focus on the analyses of the USM data. In this data set the variables considered for the first model are setting, alcohol, impairment, age and sex. Each has its own particular effect; we examine them one by one. Alcohol has what is termed a protective effect, meaning that when the influence of all other variables is controlled, the presence of alcohol makes an individual less likely to die at low levels of COHb, lowering the odds by about 25%. Being male increases the odds of low COHb by about 15% and having a physical impairment is responsible for about 23% increased odds. In this model, with setting included as a determinant of low COHB, age has a negligible effect. This is not surprising; recall that age did not appear as a main effect, but rather as having an interactive effect with setting in the ANOVA of this data set. Since age acts differently in the two settings, its overall effect tends to be cancelled out as a main effect in the two regression equations. In the second model, where setting is not included, alcohol, sex and impairment have similar effects to those seen in the first model. In contrast, age increases the odds by

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231

about 15%. Thus, it is seen that age acts as a proxy for setting in precisely the way, qualitatively, predicted by the imbalance of victims of frail ages tending toward fire settings. Quantitatively, the strength of the effect of setting is not taken over by age in this data set, however. In the analysis of the CWRU data set, the same variables are considered except for impairment (which is not considered) and race (which is considered). The results are seen to be quite similar, qualitatively. In the first model, setting has a stronger effect in the sense that a fire setting approximately doubles the odds of low COHb. Alcohol continues to have a protective effect, reducing the odds by about 10%. Sex has the same effect, quantitatively, as in the USM database. Age has a more direct effect, the frail age group increasing odds of low COHb by about 10%, which is about equal to the effect of race (non-whites being at greater risk). In the second model, with setting removed, age takes on a much stronger role, increasing odds of low COHb by 37%. Race, being unevenly distributed across settings, also plays a stronger role in this equation, non-whites having an increase in the odds of nearly 30%. The removal of setting from consideration affects sex and alcohol in a way very comparable to that seen for the USM data set. CONCLUSIONS It is concluded that much of the relationship connecting lower COHb levels to fire victims is actually a consequence of the inherent differences between the populations of fire and non-fire victims. Such differences, as was shown in this chapter, have a profound effect on COHb. REFERENCES 1. Miller, R.G Jr. Beyond ANOVA, basics of applied statistics. New York: Wiley, 1986. 2. Johnson, N.L., Leone, F.C. Statistics and experimental design. Volume II. New York: Wiley, 1964. 3. Glantz, S.A., Slinker, B.K. Primer of applied regression and analysis of variance. New York: McGraw-Hill, 1990. 4. Gibbons, J.D. Nonparametric statistical inference. 2nd ed. New York: Dekker, 1985. 5. Lachenbruch, P.A. Discriminant analysis. New York: Hafner, 1975. 6. Barnhart, E.R (pub.) Physicians’ desk reference. 45th ed. Oradell, NJ: Medical Economics, 1991.

Chapter 9 CARBON MONOXIDE AND THE TOXICITY OF FIRE SMOKE MARCELO M.HIRSCHLER Safety Engineering Laboratories 38 Oak Rd Rocky River, OH, 44116, USA ABSTRACT This paper summarizes the various aspects associated with a comprehensive study sponsored by the Society of the Plastics Industry, Inc., USA, to address the issue of determining the importance of CO in fire atmospheres. The work involves: (a) a literature study of background information on the toxicity of carbon monoxide to humans, from studies of fires and of non fire CO atmospheres, (b) a literature study of the toxicity to humans of low levels of CO, (c) a literature study of methods of carboxyhemoglobin determination in blood, (d) a literature study of the physiological effects of CO, (e) an extensive forensic study (2,241 cases) of CO deaths in fires and non fires throughout the US in the late 1970s and early 1980s, (f) an extensive forensic study (2,637 cases) on human lethality involving CO in fires and non fires in a certain locality between before the plastics era and today, (g) statistical analyses of the forensic data, to ensure full separation of variables, and (h) an analysis of the relevance of these effects to fire fatalities and of the importance (or lack of it) of small scale toxicity tests. This work has shown that: 1. The toxicity of fire atmospheres is determined almost solely by the amount of CO. There is no universal lethal CO threshold level. This depends on the age and physical condition of the victim. Any blood COHb value >20% can produce lethality on its own. 2. Fire and non fire CO victim populations are inherently very different: fire victims are both much older and much younger, and suffer from more preexisting disease. Thus fire victims are more sensitive to CO than those in non fire exposures. 3. The use of man-made materials to make household goods has made no difference to fire atmosphere toxicity. 4. CO concentrations in flashover fire atmospheres, those most likely to cause fire fatalities, are determined by oxygen availability and

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233

geometrical variables, but are virtually unaffected by chemical composition of fuels. 5. Small scale tests underpredict CO yields so that they cannot be used to predict toxic fire hazard for ventilation controlled flashover fires, unless CO yields are calculated by analogy with full scale fire test results. *

Note: In every case, if no further details are given, the venue for the study is the United States.

INTRODUCTION As long ago as 1933, the National Fire Protection Association (NFPA) Quarterly published an article stating that the main direct cause of death in fires was combustion product (i.e. smoke) toxicity.1 Smoke in fires is not a uniform material, but rather has a composition dependent on its generation mode. However, one constant aspect of smoke is that it contains two types of toxic gases: asphyxiants and irritants. One of the most important asphyxiants, and the one this work focusses on, is carbon monoxide (CO). Smoke from fires always contains carbon oxides and water, since all organic (i.e. carboncontaining) materials give off CO, carbon dioxide and water on combustion.2 All the other combustion products released from burning materials are characteristic of some particular class or classes of fuels. CO is a highly toxic, odorless and tasteless asphyxiant. Many other components of smoke are much more toxic, but they are usually present in smaller concentrations. Some smoke gases (e.g. carbon dioxide and water) are present at higher concentrations than CO, but are of lower toxicity. It is possible to define toxic hazard of an individual combustion product as the ratio of its concentration to the concentration needed to cause a serious effect, particularly lethality. With that concept in mind, thus, the toxic hazard associated with CO in fires tends to be higher than that associated with any other fire gas. Harvard University and Southwest Research Institute carried out separate studies were made, in the late 1970s and early 1980s, in which fire fighters were equipped with combustion product monitors3,4 while on the job. Both these studies confirmed the fact that by far the highest toxic hazard in fire atmospheres is associated with CO. The fire fighter studies mentioned found that the other principal toxicants in fires are acrolein (with the second highest toxic hazard, after CO, and is emitted by polyolefins and cellulosic materials), hydrogen cyanide (emitted by N-containing materials) and hydrogen chloride (emitted by Cl-containing materials).5 Carbon monoxide can also be a component of atmospheres unrelated to fire. Two typical examples are the output of malfunctioning unvented gas or charcoal heaters or of automobile exhaust. In both of these cases there is consensus that CO is virtually the only toxicant of consequence present. This is an important difference from fire atmospheres, where some other toxicants may also cause toxicological concern. The mechanism by which CO acts on mammals is by competing with oxygen for the hemoglobin in blood and tying it up as carboxyhemoglobin (COHb) rather than as the normal oxyhemoglobin. The lack of oxyhemoglobin then leads to hypoxia, which can cause cerebral damage and eventual death by asphyxiation. The hemoglobin (Hb) fraction

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234

tied up as COHb is normally expressed as %COHb (which means the percentage of the total hemoglobin present as COHb rather than as oxyhemoglobin). The reaction of CO with hemoglobin to yield COHb is reversible, so that COHb levels will decrease when the CO exposure ceases, or when a victim is given oxygen during treatment after exposure. The blood COHb levels can be measured from an analysis of the blood of a victim or suspected victim. It has, traditionally, been “accepted” that 50% COHb is the “threshold” level for human lethality.5,6 This has led to the assumption that if blood COHb levels are ≥50% COHb death is inevitable, and, more importantly, if a fatality is autopsied and its COHb level is <50%, CO poisoning could not have been the sole cause of death. These firm statements require some investigation. The reasons that this work has concentrated on carbon monoxide and human fatalities are: 1) CO is undoubtedly the single fire toxicant representing the highest toxic hazard in smoke, 2) the presence of CO is easily detectable in human victims, but 3) the relative importance of CO and of other toxicants in fire atmospheres is generally addressed by investigations using animal models rather than humans. The work described here has relevance to several areas, principally in terms of fire hazard assessment. The objectives of the work are to investigate the following eight issues. 1. The presence of toxicants other than CO is not always detectable in fire victims. Therefore, their relative importance in the toxicity of fire atmospheres, which has crucial implications for fire hazard assessment and for material development, cannot be determined directly. Thus, one of the issues that needs to be understood is the relative role of the non CO toxicants in causing fire fatalities and whether there is a critical threshold value of COHb that represents human lethality. This issue is addressed from literature data in Chapter 2.7 2. The mechanism of toxicity of CO, especially with regard to humans, has been thoroughly studied, but has not been documented in a single source, together with all the fire data. This study will address that deficiency, both in terms of low level, chronic, effects and high level, acute, effects. Chapters 38 and 49, respectively, address these issues from the data in the literature. 3. There is a dearth of understanding as to the techniques required for measuring COHb levels in human blood, since the practitioners generally feel that their work is very mundane. Thus they rarely publish their important information in the scientific literature. Chapter 510 puts together the available information on COHb analysis. 4. Fire fatalities are usually accidental victims who are overtaken by events. On the other hand, those who succumb to the intoxicating effects of automobile exhaust often do so at their own initiative. It is worth investigating, thus, whether the populations that lose their lives in fire atmospheres and in other CO-containing atmospheres are identical. Moreover, how do either of them compare with the normal population distribution in the United States. If it is found that the populations are significantly different, it remains to be seen whether the effects of CO can be separated from some other effects, which may be pre-existing problems of the population involved. Chapter 611 presents a data base which incorporates a large number of victims of fires and of other, non fire, CO exposures.

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5. In the modern world synthetic materials (mostly plastics) have substituted a large number of natural materials. When these materials burn they can generate toxicants which are different from those emitted by natural materials. This work attempts to discover whether the toxicity of modern fires is significantly different from that of fires of another era, when the use of plastics was not yet widespread. Chapter 712 analyzes the variability in COHb levels between the times when plastics were not commonly available and the present era, both for fires and non fire CO atmospheres. 6. It is essential, when carrying out a statistical analysis of a large data base, to separate the combined effects of diverse variables so as to find the individual factors affecting the results. In particular, issues such as age, degree of intoxication and degree of health/incapacitation of a victim will influence his/her capability to withstand a toxic insult. Such an investigation, by an analysis of variance, has been done in Chapter 8.13 7. In the United States, the overwhelming majority of fire fatalities are found in a room away from the room of fire origin. This can be equated to stating that they died in “big” fires: high intensity flaming fires, which have involved the entire room of origin and gone beyond it. Such fires are often described as “flashover” or “post-flashover” fires14 and are characterized by typical CO yields. This work needs to investigate whether the conclusions of smoke toxicity studies are also relevant to these postflashover fires, particularly in terms of the CO content of the corresponding atmospheres. This work assesses the literature available on CO yields and various types of fires. 8. Small scale toxicity tests using animal models (usually rodents) are the most common means of assessing smoke toxicity of materials or products. The final issue addressed in this study regards the CO yields in such tests and their relative relevance to the full scale fires that cause most human fire fatalities. Appendix D contains a very large bibliography of papers that have addressed the subject of carbon monoxide toxicity in fires, either directly or indirectly. This includes all the references of each chapter and much more besides. LITERATURE SEARCH The literature search by Dr. Gordon L.Nelson7 unearthed >100 references on human exposure to CO and fatalities. It also found several major forensic studies, both of fire victims and of victims of non fire CO exposure. The 12 most notable studies are all described in Table 1.15–29 Only 2 of these studies have been really widely publicized in the United States, viz. those in Maryland (USA)24–25 and in Glasgow (Scotland).26–27 Interestingly, all the studies were relatively small

TABLE 1 Important Carbon Monoxide Forensic Studies Site

Year(s)

Source

Cases

Authors

Ref #

1 New York City

1942

Non fire

68

Gettler

15

2 USA

1960’s

Fire—Aircraft

85

Dominguez

16

Carbon monoxide and human lethality

236

3 New York City

1966–7

Fire

311

Zikria et al.

17–8

4 Ontario

1965–68

Non fire

304

Cimbura et al.

19

5 Japan

1960’s

Fire and non fire

400

Kishitani

20

6 Oslo

1970’s

Fire and non fire

141

Teige et al.

21

7 USA

1977

Non fire—Gas Heaters

22

CPSC

22

8 Poland

1975–76

Unknown

321

Pach et al.

23

9 Maryland

1972–77

Fire

530

Berl, Halpin

24–5

10 Glasgow

1977–81

Fire

298

Anderson, Harland

26–7

11 Las Vegas

1980

Fire—Hotel

84

Birky et al.

28

12 Copenhagen

1976–81

Fire

169

Gormsen et al.

29

compared to the two case studies presented in Chapters 6 and 7:11–12 none involved 1000 cases. Thus, even if this had been attempted, a statistically valid separation of variables would have been impossible to make for most of them. Among the most interesting results of these studies is the fact that when various individuals are exposed to a particular atmosphere, their COHb levels can be very different. Furthermore, when two or more people were exposed to the same atmosphere, occasionally one of them survives and one of them, for no apparent reason, succumbs. Moreover, survivors exist who have blood COHb levels of well over 50% together with fatalities, from exposure to atmospheres where the only toxicant is CO, with COHb levels in the range of 20–40 %. In fact, around the turn of the century, John Scott Haldane injected himself with CO and measured COHb levels of over 50%, and continued doing scientific work for many more years.30–31 The age distribution of fire victims in the Maryland24 and Glasgow26 studies was bimodal, (Figure 1) while that for non fire suicide victims, from automobile exhaust in the Oslo study21, has a single peak (Figure 2). This issue of age distribution of victims is important, because it can be compared to the age distribution in the general United States population, as recently published by the NFPA (Figure 3).32 This is also a unimodal distribution, but it is different from that of suicide victims, who have a very large predominance of young and middle aged victims. Another interesting comparison that can be made is between the fire death rates in the United States and Japan, in recent times.32,33 While the populations as a whole are reasonably similar, the fire death rates are very different, since many more very young children die in fires in the USA while many more elderly die in fires in Japan (Table 2). The differences serve, however, to point out, once again that fire fatalities are skewed towards the very young and the very old.

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237

FIGURE 1. Age distributions for victims in two fire fatality studies: Glasgow (Refs 26–27) and Maryland (Refs 24–25).

FIGURE 2. Age distribution for victims in a non fire CO fatality study,

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238

associated mainly with automobile deaths: Ref. 21.

FIGURE 3. Age distribution for the population of the United States, 1984– 88, as published by NFPA: Ref. 32. TABLE 2 Age Distribution Age Group

0–5 years

6–64 years

>64 years

Ref.

9.1

43.1

47.8

33

20.7

54.8

24.5

32

9.0

78.9

12.1

32

Japan Fire Fatality Rate USA Fire Fatality Rate USA Population Group

There is, of course, a large difference in the COHb levels found in accidental victims (CPSC study of gas heaters)22 and in suicide victims (Oslo study of automobile exhaust).21 Figure 4 shows that while those who take their own lives end up with very high COHb levels, typically in the 65–85% levels, victims of accidental CO poisoning end up with much lower levels, between 26 and 81%, for a median value of 45%. This

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239

indicates that accidental victims of CO poisoning can die at very low COHb levels, without requiring any unusual other toxicant.

FIGURE 4. COHb distribution for victims in two non fire CO fatality studies, one accidental (CPSC/Gas, space heater CO emissions, Ref. 22) and one largely automobile suicides (Oslo, Ref. 21). Another interesting comparison is between the frequency distribution of COHb levels for fire fatalities and that of an accidental non fire CO exposure forensic study, the CPSC investigation22 (Figure 5). This comparison indicates that the distributions for accidental CO fatalities are very similar, irrespective of the origin (fire or non fire) of the CO. Moreover, both types of victims can die at levels well under 50% COHb. Interestingly, Zapp34 has found that the minimum lethal COHb level is much lower for animals exposed to heat stress as well as carbon monoxide, than for those exposed purely to CO. This indicates that the COHb levels found in fire victims can be lower than those found in non fire victims without there being a need to invoke the effect of any other toxicant. Similarly, a recent study has found that high temperatures decrease the CO levels needed to cause incapacitation.35 Another recent study has also found that stress can increase the lethality of fire atmospheres, since stressed test animals died at lower levels of smoke.36

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240

The study of the effects of low levels of CO8 has shown that CO can be found throughout the inhabited environment and that its inhalation is something to which all human beings are exposed. Normal healthy subjects can handle levels of 20–25% COHb for short periods without gross effects. Smokers can have chronic levels of ca. 15% COHb without it seriously affecting their capabilities.37 However, persons with infirmities, disabilities or diseases can be affected at very low levels of COHb. Moreover, CO is a narcotic and there are no significant

FIGURE 5. COHb distributions for victims in 5 studies, one of which is a non fire fatality study (CPSC, Ref. 22) while the others are fire fatality studies: MGM Grand Hotel (Ref. 28), aircraft fires (Ref. 16), Maryland (MD) (Refs 24–25) and SCOT (Glasgow, in Scotland) (Refs 22–23). studies to show how CO affects judgement of victims, particularly when they are also under the influence of alcohol or drugs. The analysis of the overall medical effects of CO on humans9 shows that CO has a variety of physiological effects. These include attacks on the respiratory system (pulmonary and respiratory control issues), the circulatory system (general cardiovascular effects, and specific effects on the heart and the brain), neuromuscular action (neurological, psychomotor and sensory effects) and cytotoxic activity (both general

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extravascular and that involving cellular coenzymes). However, the best known activity is the hematological activity whereby it reacts with hemoglobin to yield carboxyhemoglobin. The final effect of this action is the interruption of cellular production of adenosine triphosphate (ATP) so that energy metabolism is impaired. This results in damage to the central nervous system, which needs a constant supply of fresh oxygenated blood, because it operates at high metabolic rates. The fact that CO has all of these physiological effects indicates that, a victim of CO exposure will be more susceptible to fatal poisoning if he/she is already impaired by suffering from one of the various problems that can be enhanced by carbon monoxide, typically heart, or other cardiovascular, disease or respiratory problems. Another part of this investigation involved analyzing the methods for COHb determination.10 The main conclusion obtained from this was that most forensic laboratories do valiant efforts with very few resources and that they fight a losing battle against a very difficult problem. Analysis of COHb in blood can be done quite well using gas chromatography or spectrophotometry. The most common methods used (as evidenced by 80% of the literature references and by 36 of the 37 laboratories involved in the first case study) are spectrophotometric, typically the CO-oximeter. This method works well if the samples are well preserved, but they usually contain many sources of errors. Moreover, the blood is often not in the ideal state for analysis. The gas chromatograph is a better tool, but it is usually more expensive and is, therefore, used more rarely. Consequently, the COHb data can be seriously in error: a study at NBS has shown differences in over 20% COHb when samples were tested after long storage.38 Thus, the results of the literature search are that: 1. A 50% COHb level can be neither a threshold value nor an inevitable pass/fail CO lethality index. 2. The populations dying in fires are very different from the populations living in developed countries: fires preferentially kill the very old and the very young.

FORENSIC CASE STUDY OF CO VICTIMS: FIRE AND NON FIRE The Department of Polymer Science at the University of Southern Mississippi (USM) did an extensive case study, on a countrywide basis, of fatalities associated with CO.11 This investigation prepared a data base of 2,241 cases, originating in 37 laboratories across the whole USA. The vast majority of the victims died over a relatively short time frame, in the late 1970s and early 1980s. Table 3 shows the data collected and Table 4 presents some information on the overall case study. It is worth pointing out that the data base, which is at least twice as big as any one of the earlier ones, contains roughly twice as many victims of fires as of non fire CO poisoning. Appendix A contains a number of Tables of separate analyses of variables within the data base; these Tables will allow a perusal of various aspects of the overall data.

TABLE 3 Main Data Included in the USM Data base 1. Type of incident: Fire/Non fire

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2. Source of CO 3. Date and Location of Incident 4. Age of the victim 5. Gender of the victim 6. Blood COHb level 7. Blood cyanide Level 8. Blood alcohol 9. Presence of Drugs 10. Preexisting Diseases 11. Physical condition of the victim 12. Survival of the victim after the fire 13. Cause of Death, as reported in death certificate 14. Laboratory and COHb analysis method

TABLE 4 Details of USM and CWRU Data bases All Cases Fire

Non fire

Unknown

Total

USM #Cases

1203

660

378

2241

%Total

54

29

17

100

%Known Source

65

35

100

CWRU #Cases

938

1698

1

2637

%Total

36

64

0.04

100

%Known Source

36

64

100

Cases with known %COHb Levels Fire

Non fire

Unknown

Total

USM #Cases

1037

641

372

2050

%Total

51

31

18

100

%Known Source

62

38

100

1698

1

CWRU #Cases

938

2637

Carbon monoxide and the toxicity of fire smoke

%Total

36

64

243

0.04

100

Cases with COHb% Above 20% Fire

Non fire

Unknown

Total

USM #Cases

961

600

303

1864

%Cases in Source

80

91

80

83

%Known Cases in Source

93

94

81

91

CWRU #Cases %Cases in Source

865

1685

92

99

The cases that were retained for further investigation were only those where the COHb level was ≥20%, because it is very unlikely that victims with lower levels of COHb will have died exclusively of CO poisoning. Moreover, such levels are somewhat suspect, both from the point of view that there can be serious measurement errors and that smokers can exhibit COHb levels of up to 14% (e.g. reference 37). Only ca. 8% of all the cases in the data base had known COHb blood levels of <20% saturation, evenly distributed among fire and non fire cases. Of more interest is the fact that >10% of the victims in either data base (fire or non

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FIGURE 6. Age distributions for victims in the study carried out at the University of Southern Mississippi (USM) on fire and non fire CO fatalities (throughout the USA, late 1970’s and early 1980’s). fire) had a blood COHb level between 20% and 50%. This proportion becomes even bigger when one excludes those victims with alcohol in their blood. Figure 6 has the age distribution of the fire and non fire victims in this study. It is clear that, just as was seen in other fire fatality data bases, the age distribution is bimodal, with most of the victims being either very young or elderly. Moreover, there is a very large percentage of the fire fatality population with some degree of disease or adverse physical condition. On the other hand, the non fire victim data base has a unimodal age distribution, which peaks between 30 and 40. Because of this effect of population characteristics on susceptibility to CO poisoning, the COHb distributions for both sets of data are not identical, with the fire one being centered at a somewhat lower COHb level than the non fire one, as shown in Chapter 6.11 The fact that the two populations are so different indicates the necessity of carrying out a proper statistical analysis, as was done by Debanne and Rowland,13 in order to separate the effects of the toxic atmosphere from the effects of the predispositions of the populations exposed. This case study allows a few very simple conclusions to be drawn. They represent a strong reinforcement of the conclusions discussed at the end of the previous section. CO can kill at COHb saturation levels of well under 50% without requiring an additional toxicant, and this is exacerbated in fires by the presence of babies and very old people, and particularly weakened individuals, who are more susceptible to any toxic insult, including CO poisoning. STATISTICAL ANALYSIS OF FORENSIC STUDIES BY VARIABLE SEPARATION The Case Western Reserve University (CWRU) team analyzed statistically the USM data base by the ANOVA separation of variables.13 It was found that 35% of the victims had positive alcohol in their blood, which has a definite effect on their physiological capability to survive a toxicological exposure and on their capability to react to any stimulus, i.e. to be able to escape. Similarly, 6% of all victims were found to have a drug present and 9% were described as ill before the incident that caused their death. The main variables analyzed separately, apart from the source of CO (fire or non fire) were: age, alcohol level, presence of drugs and preexisting physical condition. A general impairment variable was also defined which combined disease, physical condition and drugs. It was found that COHb levels were strongly affected by the impairment index, which increased the probability of finding lower COHb levels. Similarly, higher age also increased the probability of finding lower COHb levels. The odds for age and impairment index were relatively similar.

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245

After this analysis was undertaken, two sets of populations were searched which were fairly similar in their propensities to die at low COHb levels. The results are shown in Figure 7. They indicate that the COHb frequency distributions

FIGURE 7. COHb distribution for selected victims (comparable populations) in the study carried out at the University of Southern Mississippi (USM) on fire (ethanol-free 6–20 years old) and non fire (ethanol-free>6 years old) CO fatalities.

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FIGURE 8. Joint COHb distribution for selected victims (comparable populations) in the study carried out at the University of Southern Mississippi (USM), including both fire (ethanolfree 6–20 years old) and non fire (ethanol-free>6 years old) CO fatalities. are very similar, once these other preexisting factors have been accounted for. The Figure presents COHb distributions for two very comparable populations (fire victims between the ages of 6 and 20 and non fire victims above age 6), both with alcohol-free blood levels. Therefore, this strongly suggests that CO is the principal, if not overwhelming, cause of death in fires. It is very interesting to view the joint histogram of the two sets of data together (Figure 8). As can be seen from the Figure, and from Table 5, the results are extraordinarily similar,

TABLE 5 Frequency Data for COHb Levels in Figures 7 and 8 Fire

Non Fire

Joint

Mean COHb

64.03

63.91

63.94

Median COHb

71.90

70.00

70.00

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Std Error

247

1.98

1.14

0.99

Std Deviation

20.92

20.83

20.83

Maximum

92.00

94.00

94.00

Range

91.90

92.80

93.90

Fire: Ethanol free victims between the ages of 6 and 20 years Non Fire: Ethanol free victims above the age of 6 years Joint: Combination of the above two sets of data

which indicates that similar populations die at similar COHb levels, irrespective of whether the CO comes from fire or non fire atmospheres. Therefore, the statistical analysis indicates that it is, generally, unnecessary to search for any other toxicant in the fire atmosphere when the COHb level lies between 20 and 50%. Thus, as CO alone is capable of accounting for all fire deaths, the effect of other toxicants in fire atmospheres is invariably small, if not negligible, in most cases. FORENSIC INVESTIGATION OF CO VICTIMS ACROSS TIME IN CLEVELAND (OH) The same CWRU team also created a new data base of CO victims of fires and non fires. This data base contains all the victims of carbon monoxide poisoning investigated by the Cuyahoga County (surrounding the city of Cleveland, OH) Coroner’s office for the period 1938–1979, during which the coroner was Dr. Samuel Gerber (a respected scientist). The data contains autopsies on the victims of every fire in the county as well as of every case of accidental death. The CWRU data base contains 2,637 cases, making it the largest data base ever put together on CO and fatalities. It differs from the USM data base in that there are roughly twice as many non fire victims as fire victims. Table 4 shows some of the main features of this data base, and compares it with the corresponding data of the USM data base. There were two reasons to carry out this study: the first was to discover whether the COHb levels at which fire victims died have changed over the years and the second was to compare, once again, fire and non fire data, but covering a wide time frame rather than a large geographical area. As discussed earlier, the developed world population uses many products made with synthetic materials. Such materials, first developed in the 1930s and 1940s, started to represent a large proportion of the combustible products in use in the 1960s or 1970s. Figure 9 presents each year’s median COHb level for fire and non fire cases in Cuyahoga county (OH). The data are represented in terms of the differences between each year’s value and the 1941 value. The shape of the curve is a “U”, for both sets of data. In other words, blood COHb levels decreased from the 1940s to the early 1960s and then started rising again. Moreover, the patterns for fire and non fire cases are parallel. This has two implications: 1. The change in COHb levels is not related to the content of fire atmospheres, which cannot affect COHb levels in victims not exposed to fire.

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2. The changing composition of the combustible mixture present in fires has not made recent fire atmospheres any more toxic than those that predate the plastics era. This means that, on average, the combustion products generated by the burning of synthetic materials is equally toxic as that of natural materials.

FIGURE 9. Differences in median yearly COHb values between 1941 and all subsequent years up to 1979, in the Case Western Reserve University study, for fire and non fire CO fatalities. Two important aspects of this data base are the sources of the CO in both fire and non fire cases, and the number of victims who survived the incident. Table 6 shows that 82% of all non fire victims come from automobile exhaust, which means that they are probable suicides. Table 7 shows that twice as many fire

TABLE 6 Sources of CO in CWRU Data Base Non Fire Cases Automobile exhaust City Gas Other

1393 cases (82%) 272 cases (16%) 33 cases (2%)

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Fire Cases Fire

919 cases (98%)

Explosion

19 cases (2%)

TABLE 7 Survival of Victims in CWRU data base Fire # Cases %Cases in Source

Non Fire 59

43

6

3

FIGURE 10. Age Distributions for victims in the study carried out at the Case Western Reserve University

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(CWRU) on fire and non fire CO fatalities (1938–79, in Cuyahoga County, OH). victims as non fire victims survive the incident. This has a powerful implication to their COHb levels, since victims who survive will rapidly decrease the blood COHb content, both from normal respiration of CO-free air and from the resuscitation attempts by the emergency rescue crews. This analysis is obviously much more comprehensive than a study which compares the toxicity of individual products, as determined by small scale toxicity tests. Morikawa et al. have made some research comparing the toxicity of natural and synthetic materials which bear investigating in detail. In one case39 they generated a fire fuelled by combustible products made out of natural materials, in a room, and caused lethality of exposed rabbits, in a different room. These results were then compared with those of a burn where 23% of the products were replaced by products made from synthetic materials. Unfortunately, the materials used in both tests had very different fire performance, so that the fraction of combustibles burnt was very different in both tests. Moreover, the fuel load used was very low (8.4 kg/m2), compared to the normal US residential fuel load (17.7 kg/m2).40 The results showed that the products that burnt more vigorously caused more smoke to be generated and more animal fatalities. Although the authors interpreted the results as suggesting that smoke from synthetic materials is more toxic than that from natural materials, that conclusion is clearly an unwarranted extrapolation.

FIGURE 11. COHb distributions for victims of two partial aspects of the CWRU study: the non fire CO

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251

fatalities who are also not victims of automobile exhaust and all the fire fatalities (1938–79, in Cuyahoga County, OH). Figure 10 shows the overall age distributions of the fire and non fire populations in this case study. This shows a remarkable similarity with the USM case study: the populations of fire and non fire victims are very different and fire victims contain many more very young and very old individuals, making them more susceptible to carbon monoxide poisoning. The separation of variables suggests that the difference in population characteristics is sufficient to account for the COHb differences found. In view of the large proportion of suicide victims, it was decided to separate out, from the non fire data base all the non fire victims who are not victims of automobile exhaust. Figure 11 presents the COHb levels for those victims, in histogram form, and compares them with the overall COHb levels for fire (not explosion) victims in the entire data base. The similarity of the curves is striking. Although it is not possible, at this stage, to explain satisfactorily the unusual change in population susceptibility to CO, it can be concluded that the effect of new materials on the toxicity of fire atmospheres appears to be negligible. USEFULNESS OF SMALL SCALE ANIMAL TOXICITY TESTS The Center for Fire Research at the National Institute for Standards and Technology carried out a study on behalf of the Fire Retardant Chemicals Association.41 In the study the fire properties of 5 sets of products were investigated in fire retarded (FR) and non fire retarded (non FR) versions. The products were upholstered chairs, business machines, TV cabinets, circuit boards and electrical cables. The study used small scale (cone calorimeter and NBS cup furnace smoke toxic potency), medium scale (furniture calorimeter) and full scale techniques. In the small scale tests the materials were tested as mock-up combinations. In the furniture calorimeter the products were burnt individually. The full scale test used combined all 5 products together in a single room. The results indicated a foregone conclusion: the fire retarded products are safer than the non fire retarded products. Thus, they reinforced the concept that improved fire performance leads to lower fire hazard. The main conclusions from the full scale tests were: * Mass loss: FR products non FR products (ca. one half). * Heat release: FR products non FR products (ca. one quarter). * Toxic gases: FR products non FR products (ca. one third). * Smoke obscuration: FR products ≈ non FR products. Of more interest to the analysis being done here is the issue of toxic gas yields. The NIST work indicated that the cone calorimeter was a very useful device to predict full scale ignitability, heat release and flame spread. However, its yields of carbon monoxide were too low. In fact, any bench-scale test can give adequate yields of gases other than CO, but

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will almost inevitably give excessively low yields of CO. The production of combustion gases in small scale tests is, thus, heavily influenced by the chemistry of the materials being burnt. Thus, small scale tests are, inevitably, biased in favour of non CO species: they exaggerate the relative importance of such non CO species compared to CO. The reason for this statement is that the CO production in large scale fires appears to be dominated by the availability of oxygen in the fire. The oxygen levels are, in turn, affected by variables such as geometry, ventilation, configuration, turbulence and mixing. The production of CO in large scale fires is, thus, only somewhat influenced by the chemical properties of the substance being burned.42 Thus, Babrauskas et al. conclude that the use of any less-than-room-sized tests for making CO predictions will only be possible once oxygen supply variables have been sorted out.41 Experience shows that in those full scale fires with full flaming room involvement (i.e. those fires that cause most fire fatalities) there is ventilation control and the oxygen levels get very close to zero. In small scale tests there is virtually never low oxygen and high heat flux, because flaming combustion does not occur under such conditions. Thus, instead of extrapolating CO yields from small scale tests it is possible to propose a CO yield common to all materials, with a value of ca. 0.2 g CO/g mass burnt.43 Thus, the toxicity of smoke in real fires is unlikely to be much affected by the type of materials burning. The mass of materials burning and their fire performance will determine the intensity of the fire, governed by its rate of heat release, and thus, the amount of smoke present.44 However, the CO levels are defined by the geometry and oxygen characteristics of the room. Toxic potency of smoke is a quantitative expression which relates the concentration of smoke and the exposure time to the achievement of an adverse effect, usually lethality, on a test animal, according to the ASTM definition.45 Thus, it becomes obvious that the toxic potency of smoke is heavily dependent on the conditions under which the smoke is generated, which affect both the quality and the quantity of smoke. This is particularly important when addressing real fires, since toxic potency is almost always determined using one of a variety of small scale toxic potency tests, with rodent models.5,46 These tests differ in a number of respects, including: fire model, whether they are static or dynamic, the type of animal used and the end point. Partly due to all these differences, the tests lead to large ranking variations for the smoke of various materials. This was illustrated in a study where one test ranked one material the most toxic of a set of 14 materials, while a different protocol ranked it the least toxic of the same set! The toxic potency of the smoke of most ordinary materials (whether natural or synthetic) is very similar.5 Thus, relative smoke toxic potency rankings depend on the exact composition of the smoke being tested, i.e. the small scale test protocol, and are of little interest from the viewpoint of fire hazard assessment, since those small scale smoke toxicity tests give inadequately low yields of CO and adequate yields of other toxicants. Thus these tests require post computational correction for CO before their results are relevant to fire hazard in the fires causing most fire deaths. The correction for CO yields in full scale post-flashover recognizes the toxicity of the CO inevitably present (25 mg/L) and a factor of 3, which is the best to date, level of comparison between small scale and full scale toxocity test results; this yields an inevitable toxic potency of 8 mg/L, so that any material with smoke less toxic than this value is of normal toxicity and needs no further toxicity considerations. This correction for CO yields has been validated in recent

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work,43 where it has been applied to the results of full scale and small scale tests using rats as animal models. The conclusion of this last analysis is that small scale toxicity tests are of very limited validity for the assessment of the lethality of fire atmospheres because they are dominated by toxicants other than CO. CONCLUSIONS The introduction to this paper described 8 issues to be investigated, and it is now possible to summarise all the findings. 1. The literature shows that the lethal level of carbon monoxide depends on the characteristics of the victim, and the 50% COHb threshold normally mentioned is not realistic. Both fire atmospheres and non fire atmospheres can cause lethality due exclusively to CO at COHb levels of 20%. 2. The toxicity of CO is very complex and has several facets, and there is now a single reference source summarising it. 3. The methods of determining COHb in blood suffer from many deficiencies and that may be the cause of some errors and inconsistencies found in the data reported. 4. The population of fire victims has a bimodal distribution, with an excess of very young and very old and infirm people. Victims of automobile exhaust CO exposures usually have a unimodal distribution. Thus, fire victims are more sensitive to CO poisoning than non fire victims and are prone to die at lower COHb levels, irrespective of any other insult. 5. Replacement of large proportions of natural materials by man-made materials has made no difference to the toxicity of fire atmospheres. 6. Once the different variables affecting COHb levels in the blood of fatal victims are analyzed separately, the COHb distributions of fire and non fire CO victims are virtually the same. 7. CO yields and CO concentrations in flashover fire atmospheres are determined by oxygen availability, ventilation, mass loading and other such variables, but are virtually unaffected by the chemical composition of fuels. 8. Small scale tests give excessively low CO yields and adequate yields of other combustion products. Thus, such tests cannot be used to predict toxic fire hazard for the fire scenarios causing most fire fatalities: ventilation controlled flashover fires. Such tests can be used as part of fire hazard assessment studies if CO yields have been corrected and other fire test response characteristics are taken into account.

REFERENCES 1. G.E.Ferguson, “Fire Gases”, NFPA Quarterly, 27(2), 110 (1933). 2. C.F.Cullis and M.M.Hirschler, “The Combustion of Organic Polymers”, Oxford University Press, Oxford, 1981. 3. W.A.Burgess, R.D.Treitman and A.Gold, “Air Contaminants in Structural Firefighting”, N.F.P.C.A. Project 7X008, Harvard School Public Health, 1979.

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4. A.F.Grand, H.L.Kaplan and G.H.Lee, “Investigation of Combustion Atmospheres in Real Fires”, U.S.F.A. Project 80027, Southwest Research Institute, 1981. 5. M.M. Hirschler, “Fire hazard and toxic potency of the smoke from burning materials”, J. Fire Sciences, 5, 289–307 (1987). 6. I.Benjamin and F.B.Clarke, in “Fire Deaths—Causes and Strategies for Control”, Technomic Publ., Lancaster, PA, 1984, p. 15. 7. G.L.Nelson, “Exposures of Carbon Monoxide in Man: Exposure Fatality Studies”, Chapter 2, this volume. 8. G.L.Nelson, “Effects of Carbon Monoxide in Man: Low Levels of CO and their Effects” Chapter 3, this volume. 9. J.B.Larsen, “Physiological Effects of Carbon Monoxide”, Chapter 4, this volume. 10. G.L.Nelson, “Carbon Monoxide Determination in Human Blood”, Chapter 5, this volume. 11. G.L.Nelson, D.V.Canfield and J.B.Larsen, “Carbon Monoxide and Fatalities: A Case Study of Toxicity in Man”, Chapter 6, this volume. 12. S.M.Debanne and D.Y.Rowland, “Carbon Monoxide and Fatalities: Secular Trends”, Chapter 7, this volume. 13. S.M.Debanne and D.Y.Rowland, “Lethal Carboxyhemoglobin Level: The Epidemiological Approach”, Chapter 8, this volume. 14. R.W.Bukowski, S.W.Stiefel, J.R.Hall and F.B.Clarke, Fire Risk Assessment Method: Description of Methodology—NISTIR 90–4242, National Institute of Standards and Technology, Gaithersburg, MD, 1990. 15. A.O.Gettler, “The significance of some toxicological procedures in the medico-legal autopsy”, Am. J. Clin. Pathology, 13, 169–77 (1943). 16. A.M.Dominguez, “Symposium—Fire and Incendiarism. Problems of Carbon Monoxide in Fires”, J. Forensic Sci. 7(4), 379–93 (1962). 17. B.A.Zikria, J.M.Ferrer and H.J.Floch, “The chemical factors contributing to ‘Smoke poisoning’”, Surgery, 71(5), 704–709 (1972). 18. B.A.Zikria, G.C.Weston, M.Chodoff and J.M.Ferrer, “Smoke and Carbon Monoxide Poisoning in Fire Victims”, The Journal of Trauma, 12(8), 641–45 (1972). 19. G.Cimbura, E.McGarry and J.Daigle, “Toxicological Data for Fatalities due to Carbon Monoxide and Barbiturates in Ontario—A Four Year Survey 1965–1968”, J. Forensic Sci. 640– 42 (1972). 20. K.Kishitani, “Study of Injurious properties of Combustion products of Building Materials at Initial Stage of Fire”, J. Faculty of Engineering Univ. Tokyo (B), 31, 1–35 (1971). 21. B.Teige, J.Lundevall and E.Fleischer, “Carboxyhemoglobin Concentrations in Fire Victims and in Cases of Fatal Carbon Monoxide Poisoning”, Z. Rechtsmedizin, 80, 17–21 (1977). 22. Consumer Product Safety Commission, Fed. Register, 45(182), 61880, Sept. 17, 1980. 23. J.Pach, et al., “Analysis of Predictive factors in Acute Carbon Monoxide Poisonings”, Toxicological Clinic and Institute of Forensic Medicine, Krakow, Poland, 158–59. 24. W.G.Berl and B.M.Halpin, “Human Fatalities from Unwanted Fires”, Fire Journal, 105–23, September 1979. 25. B.M.Halpin, E.P.Radford, R.Fisher and Y.Caplan, “A Fire Fatality Study”, Fire Journal, 11–1– 3, May 1975. 26. R.A.Anderson, A.A.Watson and W.A.Harland, “Fire Deaths in the Glasgow Area: 1. General Considerations and Pathology”, Med. Sci. Law, 21, 175–83 (1981). 27. R.A.Anderson, A.A.Watson and W.A.Harland, “Fire Deaths in the Glasgow Area: 1. The Role of Carbon Monoxide”, Med. Sci. Law, 21, 288–94 (1981). 28. M.M.Birky, D.Malek and M.Paabo, J. Anal. Toxicol., 7, 265 (1983). 29. H.Gormsen, N.Jeppesen and A.Lund, “The Causes of Death in Fire Victim”, Forensic Sci. Internat., 24(2), 107–11 (1984). 30. J.S.Haldane, “The action of carbonic oxide on man”, J. Physiol. (London), 45, 430–62 (1895).

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31. J.S.Haldane, “The relation of the action of carbonic oxide to oxygen tension”, J. Physiol. (London), 18, 201–17 (1895). 32. M.J.Karter and A.L.Miller, “Patterns of Fire Casualties in Home Fires by Age and Sex, 1984– 88”, National Fire Protection Association, Quincy, MA, April 1991. 33. A.Sekizawa, “Statistical Analyses on Fatalities’ Characteristics of Residential Fires”, Third Int. Symposium on Fire Safety Science, Edinburgh, Scotland, July 8–12, 1991. 34. J.A.Zapp “The Toxicology of Fire”, Medical Division Special Report No. 4, Chemical Corps, US Army Chemical Center, Maryland, PB143632, 1951. 35. D.C.Sanders and B.R.Endecott, “The effect of elevated temperature on carbon monoxideinduced incapacitation”, J. Fire Sci., 9, 296–310 (1991). 36. J.B.Larsen, G.L.Nelson, B.K.Williams, E.G.Spencer and L.M.Spencer, “The toxicity of combustion products from engineering plastics”, in Proc. Sixteenth Int. Conf. Fire Safety, San Francisco, CA, Jan. 14–18, 1991, Ed. C.J.Hilado, Product Safety Corp., p. 189–202 (1991). 37. B.C.Levin, P.R.Rechani, J.L.Gurman, F.Landro, H.M.Clark, M.F.Yoklavich, J.R.Rodriguez, L.Droz, F.M.de Cabrera and S.Kaye, “Analysis of carboxyhemoglobin and cyanide in blood from victims of the DuPont Plaza Hotel fire in Puerto Rico”, J. Forensic Sci., 35(1), 151–68 (1990). 38. N.Wald, S.Howard, P.G.Smith and A.Bailey, “Use of Carboxyhaemoglobin levels to Predict the Development of Diseases Associated with Cigarette Smoking”, Thorax, 30, 133–40 (1975). 39. T.Morikawa, E.Yanai, T.Watanabe, T.Okada and Y.Sato, “Toxic gases from house fires of natural polymers or both synthetic and natural polymers under different conditions”, in Proc. Interflam ‘90, Fifth Int. Fire Conference, Canterbury, UK, 3–6 September, 1990, p. 249–55, Interscience, London, UK, 1990. 40. B.Bush, G.Anno, R.McCoy, R.Gaj and R.D.Small, “Fuel loads in U.S. Cities”, Fire Technology 27(1), 5–32 (1991). 41. V.Babrauskas, R.H.Harris, R.G.Gann, B.C.Levin, B.T.Lee, R.D.Peacock, M. Paabo, W.Twilley, M.F.Yoklavich and H.M.Clark, “Fire Hazard Comparison of Fire-Retarded and Non-Fire-Retarded Products,” NBS Special Publ. 749, July 1988, Gaithersburg, MD. 42. W.M. Pitts, “Executive Summary for the Workshop on Developing a Predictive Capability for CO Formation in Fires”, NISTIR 89–4093, National Institute of Standards and Technology, Gaithersburg, MD, 1989. 43. V.Babrauskas, R.H.Harris, E.Braun, B.C.Levin, M.Paabo and R.G.Gann, “The Role of BenchScale Data in Assessing Real-Scale Fire Toxicity”, NIST Tech. Note # 1284, National Inst. Standards Technology, Gaithersburg, MD, 1991. 44. V.Babrauskas and R.D.Peacock, “Heat release rate: The single most important variable in fire hazard”, in “Fire Safety Developments and Testing”, Fire Retardant Chemicals Association, Fall Technical Meeting, Oct. 21–24, 1990, p. 67–80 (1990). 45. ASTM E176–91, Standard terminology of fire standards, American Society for Testing and Materials, Philadelphia, PA. 46. M.M.Hirschler, “Smoke toxicity measurements made so that the results can be used for improved fire safety”, J. Fire Sciences, 9, 330–47 (1991).

APPENDIX A DATA BASE USED BY THE UNIVERSITY OF SOUTHERN MISSISSIPPI (USM) Lab CO

SubmiExposure Ad- Surv Age Sex CO Ethano Drug Drug CO Dis. Phys ssion Date dress Hb Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 2 2 2 3 3 3 3 3 3 3 3 3 4 4 4

1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 1 1 1

11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 9 9 9 9 16 16 16 16 16 16 16 16 16 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

0 3 3 3 3 4 4 5 5 7 8 10 11 11 11 1 10 12 12 1 1 1 3 5 7 9 11 11 1 2 2

0 7 8 21 24 3 3 13 26 2 15 19 20 20 20 7 30 20 30 12 21 28 15 14 6 20 25 25 27 10 20

0 84 84 84 84 84 84 84 84 84 84 84 84 84 84 85 82 82 82 82 82 83 82 84 84 82 84 84 82 84 84

4 1 2 1 3 4 4 5 6 4 5 7 8 8 8 12 9 10 11 17 16 16 16 15 14 18 13 13 19 21 19

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

38 47 81 74 69 71 72 22 51 73 53 3 1 1 3 41 35 30 2 51 49 43 48 44 32 81 19 23 30 70 48

1 77 1 69.5 1 66 2 65 2 82 1 52 2 74 1 58 2 24 1 87 2 68.05 1 32 1 90 1 90 1 90 2 26 1 38.2 1 48 1 41.2 1 60.3 2 43.3 2 49 2 60.6 2 53 2 70 2 38 2 62 1 66 1 37.5 2 85 2 70

0 0 0 0 0 0 0 0 0.237 0 0 0 0 0 0 0 0.322 0 0 0.24 0 0 0.2 0 0.09 0.06 0.073 0.154 0.38 0 0

4 0 201 0 0 0 201 14 1 0 201 15 0 0 201 1 0 0 201 2 0 0 102 3 0 0 102 1 0 0 102 0 2 0 102 14 3 0 201 3 5 0 201 0 0 0 102 0 0 0 102 0 0 0 102 0 0 0 102 0 0 0 105 0 0 0 102 4 0 0 203 0 0 0 104 0 0 0 201 6 0 0 201 0 0 0 206 5 0 0 201 0 6 1.12 201 0 0 0 201 0 46 1.32 104 0 0 0 104 0 0 0 104 0 0 0 201 7 0 0 201 0 0 0 201 12

2 2 4 4 4 4 4 1 4 4 3 2 2 2 2 2 2 2 2 2 2 2 2 2 2 3 2 2 4 4 4

Appendix A: Tables for the data base in chapter 6 4 4 4 4 4 4 4 4 4 4 4 6 6 6 6 6 6 6 6 6 6 6 6 6 7

1 1 1 1 1 1 1 1 1 1 1 8 8 8 8 8 8 8 8 8 8 8 8 8 1

1 1 1 1 1 1 1 1 1 1 1 3 3 3 3 3 3 3 3 3 3 3 3 3 3

25 25 25 25 25 25 25 25 25 25 25 18 18 18 18 18 18 18 18 18 18 18 18 18 14

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

3 4 4 5 5 8 9 9 9 10 11 0 1 1 1 1 1 1 1 2 12 12 12 12 1

22 11 24 8 22 10 8 19 19 21 23 0 5 6 16 17 22 24 30 12 8 11 14 15 5

82 82 82 83 84 82 82 84 84 84 83 0 85 85 85 85 85 85 85 85 84 84 84 84 84

19 19 20 21 21 19 19 21 21 21 19 399 395 396 397 396 398 395 395 393 391 392 393 394 31

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

39 61 37 51 28 66 35 41 45 16 31 29 91 77 18 79 84 44 89 99 15 45 26 21 39

1 1 2 1 1 2 1 2 1 1 2 1 2 1 2 2 1 1 2 1 2 1 1 1 1

64 81.9 79.9 57.1 78.9 77.6 83.9 86.2 85.1 90.6 85.5 79 48 39 79 52 58 58 71 39 68 47 61 64 86

0 0.215 0.19 0.19 0.143 0.24 0.217 0.106 0.153 0 0 0.27 0 0 0 0 0 0 0 0 0 0.25 0.05 0.15 0

258 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0.004 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

201 8 201 9 201 8 201 0 201 8 201 10 201 0 201 0 201 0 201 0 201 11 102 0 217 0 102 0 201 0 102 0 102 0 201 0 102 0 102 0 201 0 102 0 201 0 102 0 201 0

2 4 3 2 2 4 2 2 2 1 3 0 0 0 0 3 0 0 2 2 0 0 0 0 2

Appendix A: Tables for the data base in chapter 6

259

Lab CO Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9

1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 2 2 2 2 2 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

14 14 14 14 14 14 14 14 14 14 14 14 14 14 14 14 25 25 25 25 25 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

2 3 3 3 4 4 5 6 6 10 10 10 11 11 11 12 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 2 2 2 2 2 2 2

25 9 11 29 14 25 7 2 20 28 29 29 2 21 21 21 8 26 26 26 26 3 4 13 13 16 16 16 21 21 23 23 23 23 31 3 4 4 4 4 4 4 4

84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 85 85 85 85 85 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84

31 31 32 31 33 34 34 33 36 37 36 36 31 39 39 38 40 41 41 41 41 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

21 76 64 72 33 46 49 17 37 40 2 25 5 2 5 47 61 4 8 11 32 43 55 38 69 25 33 41 34 70 20 46 78 86 53 30 1 1 1 2 3 4 5

1 1 1 1 1 1 2 1 2 1 2 2 1 1 1 2 1 2 1 1 2 0 1 1 0 1 2 1 2 1 1 1 2 1 1 1 1 2 2 2 1 1 1

47 0 0 15.8 81 75 0 56 0 0 0 0 0 0 0 79 32 83 85 78 86 74 5 80 46 66 83 54 63 68 82 5 0 0 66 65 87 71 84 70 87 71 85

0.18 0 0 0 0 0 0 0.06 0 0 0 0 0 0 0 0.24 0.23 0 0 0 0.16 0.15 0.19 0 0 0.02 0.08 0 0.19 0.01 0 0 0 0 0.27 0.06 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 41 0 0 0 0 0 0 10 0 0 0 42 0 0 25 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

201 201 201 201 201 102 201 201 201 201 201 201 102 102 102 201 102 102 102 102 102 102 201 201 102 201 201 201 104 201 201 201 138 138 201 201 104 104 104 104 104 104 104

0 22 16 9 0 0 0 0 0 22 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 41 0 0 0 0 0 0 0 0 0 0 0

2 2 2 2 2 2 2 2 2 2 2 2 2 3 3 2 3 2 2 2 2 0 0 0 0 0 0 0 0 0 0 3 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 9 9 9 9 9 9 9 9 9 9 9 9 9

6 6 6 6 6 6 6 6 6 6 6 6 6

5 5 5 5 5 5 5 5 5 5 5 5 5

23 23 23 23 23 23 23 23 23 23 23 23 23

85 85 85 85 85 85 85 85 85 85 85 85 85

2 2 2 2 2 2 2 2 2 3 3 3 3

4 4 12 12 15 17 18 19 22 3 6 19 23

84 84 84 84 84 84 84 84 84 84 84 84 84

400 400 400 400 400 400 400 400 400 400 400 400 400

2 2 2 2 2 2 2 2 2 2 2 2 2

6 8 2 24 28 84 28 42 36 36 36 32 47

2 1 2 2 1 2 1 1 1 1 1 1 1

73 78 86 85 86 70 62 42 95 47 81 88 87

260 0 0 0 0 0.29 0 0.31 0.45 0.2 0 0.2 0.16 0.18

0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0

104 104 104 104 0 104 201 104 105 201 201 201 201

0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

261

Llab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

3 3 4 4 4 4 4 4 4 4 4 5 5 5 5 5 5 5 5 6 6 6 6 6 6 6 6 7 7 7 7 7 7 7 8 8 8 8 8 8 9 9

27 31 1 1 2 8 10 14 16 20 21 4 4 8 10 15 23 23 27 2 2 4 5 9 14 16 17 2 3 3 16 20 23 30 1 5 7 7 7 28 7 8

84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84

400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

58 29 62 71 76 67 62 22 71 40 23 34 37 35 48 18 37 58 25 2 42 56 25 53 19 47 20 76 3 5 25 28 49 30 56 32 13 25 32 0 47 41

1 2 2 1 2 1 1 1 1 1 1 1 2 1 1 1 1 1 2 2 2 1 1 1 1 1 1 1 0 0 1 1 1 1 2 1 1 2 1 1 1 1

53 78 40 36 0 9 57 70 5 80 72 62 74 77 70 43 0 5 81 77 28 10 77 80 88 66 25 6 48 27 76 81 87 81 40 86 76 55 73 10 79 90

0 0 0 0 0.19 0.2 0.36 0.09 0.16 0.06 0 0.26 0 0.02 0.02 0 0.64 0 0 0 0.28 0 0 0.24 0 0.12 0 0 0 0 0 0.24 0 0 0.29 0 0.02 0.14 0.22 0.17 0.17 0.39

43 0 0 0 0 0 0 0 0 0 0 0 0 0 42 0 0 42 0 0 0 0 0 0 0 0 25 0 0 0 25 0 0 25 37 0 0 0 0 0 0 25

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

201 131 0 0 104 102 104 104 0 201 201 201 0 0 201 105 0 0 0 104 0 201 0 201 201 102 201 201 104 104 0 201 201 201 0 0 102 102 102 201 102 105

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 9 9 9 9 9 9 9 9 9 9 9 9 9

6 6 6 6 6 6 6 6 6 6 6 6 6

5 5 5 5 5 5 5 5 5 5 5 5 5

23 23 23 23 23 23 23 23 23 23 23 23 23

85 85 85 85 85 85 85 85 85 85 85 85 85

9 9 10 10 10 10 10 10 10 10 10 11 11

20 22 1 2 3 10 13 24 29 29 31 6 7

84 84 84 84 84 84 84 84 84 84 84 84 84

400 400 400 400 400 400 400 400 400 400 400 400 400

2 2 2 2 2 2 2 2 2 2 2 2 2

54 64 52 76 83 54 20 17 34 41 40 45 63

1 1 1 1 2 1 1 1 1 2 1 1 1

85 88 72 2 54 58 5 71 5 76 71 81 61

262 0 0.34 0.01 0 0 0 0.2 0 0 0 0.18 0 0

43 0 0 0 0 05 0 0 201 45 0 237 0 0 102 0 0 201 0 0 0 0 0 201 44 0.09 0 0 0 201 0 0 0 0 0 0 0 0 104

0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

263

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

11 11 11 11 11 11 11 12 12 12 12 12 12 12 12 12 12 12 12 12 12 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 2 2 2 2

11 13 15 16 20 27 29 1 4 6 10 12 15 17 21 21 21 21 21 21 31 1 4 8 11 11 13 13 15 17 19 20 20 20 23 24 25 3 5 7 7 7

84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 81 80 80 85 85 83 85 80 83 83 85 85 85 81 85 81 82 81 84 85 85

400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 400 42 42 42 42 42 42 42 42 42 42 42 42 42 42 42 42 44 42 42 42 42

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

31 75 2 20 30 47 74 65 29 32 31 57 22 0 1 3 4 25 37 65 53 1 45 62 42 60 61 26 0 61 25 55 93 94 100 61 75 59 26 39 81 84

1 0 0 2 0 1 2 2 2 1 1 1 1 1 1 1 1 2 2 2 1 2 1 1 1 1 1 1 1 1 1 1 2 1 2 2 2 1 1 2 2 1

60 10 35 90 74 62 58 69 81 63 82 76 10 10 59 5 70 12 86 10 76 71 48 25 87 71 65 64 72 80 65 54 78 70 56 48 58 64 64 80 74 74

0.1 0 0 0 0 0.1 0 0.18 0 0 0 0.19 0.29 0.2 0 0 0 0 0 0 0.23 0 0.3 0 0 0.07 0.3 0 0.2 0 0.34 0 0 0 0 0 0 0.37 0 0 0 0

0 0 0 0 0 0 0 0 42 0 0 0 0 0 46 46 46 46 42 46 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0.38 0.06 0.38 0.03 0 0.04 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 104 0 104 0 104 0 201 0 201 0 104 0 102 0 0 0 0 0 104 0 138 0 120 0 0 0 102 0 102 0 102 0 102 0 0 0 102 0 201 0 0 0 102 0 102 0 201 0 102 0 102 22 213 0 102 0 201 0 102 0 102 0 102 0 102 0 102 0 102 0 102 0 102 0 212 0 102 0 102 0 201 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 10 10 10 10 10 10 10 10 10 10 10 10 10 10

1 1 1 1 1 1 1 1 1 1 1 1 1 1

3 3 3 3 3 3 3 3 3 3 3 3 3 3

11 11 11 11 11 11 11 11 11 11 11 11 11 11

85 85 85 85 85 85 85 85 85 85 85 85 85 85

2 2 2 2 2 2 2 2 2 2 2 2 2 2

8 9 9 12 12 12 14 16 17 18 22 22 22 25

81 85 85 80 82 82 85 85 85 81 82 82 82 82

42 47 47 42 42 42 42 42 42 42 42 42 42 42

2 2 2 2 2 2 2 2 2 2 2 2 2 2

45 22 23 0 0 50 49 39 9 60 0 2 3 3

1 1 1 1 1 1 1 1 2 1 2 2 1 1

86 80 79 37 83 70 82 78 75 66 92 93 90 84

264 0.15 0.06 0.17 0.33 0.05 0.18 0 0 0 0.32 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

201 201 201 102 102 102 201 201 102 102 102 102 102 102

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

265

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10

1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

2 2 2 2 2 2 3 3 3 3 3 3 3 3 3 3 3 3 3 4 4 4 4 4 4 5 5 5 5 6 6 7 7 7 8 8 9 9 9 9 10 10

25 25 25 25 25 26 3 8 15 19 20 24 24 24 24 24 24 24 27 6 6 13 13 16 23 3 16 23 29 6 17 18 24 27 12 22 2 3 5 13 9 11

82 82 82 82 82 83 83 84 82 82 82 83 83 83 83 83 83 83 82 80 82 80 80 80 83 84 82 83 83 84 80 84 84 80 84 81 81 83 81 80 81 83

42 42 42 42 42 42 42 42 45 42 45 42 42 42 42 42 42 42 44 42 42 42 42 42 42 42 42 42 46 42 42 42 42 43 42 42 42 42 42 42 42 42

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

7 9 9 10 12 21 64 59 58 19 19 17 33 34 36 45 50 65 56 33 68 7 51 68 8 45 50 18 5 63 57 60 41 41 25 41 2 19 78 27 41 18

1 1 2 1 1 1 1 1 2 1 1 2 1 1 1 1 1 1 2 1 1 2 2 1 1 1 2 1 2 1 2 2 1 1 1 1 1 1 2 2 1 1

88 71 83 78 83 66 59 79 63 84 75 64 40 80 82 74 77 79 29 90 76 58 72 35 77 76 52 80 61 74 68 67 81 66 65 56 61 58 75 86 87 66

0 0 0 0 0 0 0.24 0.28 0.21 0.16 0 0 0 0 0 0.24 0 0 0.16 0.1 0 0 0 0 0 0.19 0 0 0 0 0 0 0 0.1 0.11 0.14 0 0.04 0 0 0.18 0.12

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 0 102 0 102 0 102 0 0 0 102 0 102 0 102 0 102 22 201 0 201 0 102 0 102 0 102 0 102 0 102 0 102 0 102 0 102 22 102 0 201 0 102 0 102 0 102 0 102 0 102 0 201 0 0 0 102 0 0 0 102 0 201 0 201 0 201 0 201 0 201 0 102 0 102 0 213 0 201 0 201 0 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 10 10 10 10 10 10 10 10 10 10 10 10 10 10

1 1 1 1 1 1 1 1 1 1 1 1 1 1

3 3 3 3 3 3 3 3 3 3 3 3 3 3

11 11 11 11 11 11 11 11 11 11 11 11 11 11

85 85 85 85 85 85 85 85 85 85 85 85 85 85

10 10 10 10 10 10 11 11 11 11 11 11 11 11

12 20 21 23 23 25 1 2 2 8 13 26 28 29

81 84 81 81 83 84 83 83 84 80 83 83 82 80

42 42 42 42 42 42 42 45 45 42 45 42 42 42

2 2 2 2 2 2 2 2 2 2 2 2 2 2

71 23 26 23 45 1 30 41 16 25 41 73 19 56

2 1 1 1 1 1 1 1 1 1 1 2 1 1

85 85 81 82 77 77 85 80 84 80 56 62 80 79

266 0.04 0.2 0.03 0.2 0.01 0 0 0 0 0.03 0.16 0.06 0 0.29

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 102 201 0 201 102 201 102 102 201 0 102 201 102

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

267

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

10 10 10 10 10 10 10 10 10 10 10 10 10 10 11 11 11 11 11 11 11 12 12 12 12 12 12 12 12 12 12 12 12 12 12 12 12 12 12 12 12 12

1 1 1 1 1 1 1 1 1 1 1 1 1 1 3 3 3 3 3 3 3 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

11 11 11 11 11 11 11 11 11 11 11 11 11 11 5 5 5 5 5 5 5 28 28 28 28 28 28 28 28 28 28 28 28 28 28 28 28 28 28 28 28 28

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

11 12 12 12 12 12 12 12 12 12 12 12 12 12 2 2 7 8 8 10 12 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

29 1 1 3 7 8 9 9 12 13 13 13 16 25 19 26 16 7 7 23 8 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

83 84 84 82 84 80 82 82 82 81 81 81 83 83 84 84 84 83 83 84 84 40 40 40 40 40 40 40 40 40 40 40 40 40 40 40 40 40 40 40 40 40

42 42 42 42 42 42 42 42 42 42 42 42 47 42 51 51 51 48 48 52 51 30 30 30 30 30 30 30 30 30 30 30 30 30 30 30 30 30 30 30 30 30

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

3 35 82 2 38 84 8 10 33 20 33 41 65 56 63 47 79 4 27 23 32 3 8 15 20 22 27 30 34 34 35 35 35 37 37 38 38 40 40 41 42 43

1 1 2 2 1 1 2 1 2 1 1 2 1 2 2 1 1 1 1 2 1 1 2 2 1 2 1 1 1 1 1 1 2 1 1 1 1 1 2 1 2 1

77 47 61 70 42 51 33 38 84 76 57 60 89 57 45 81 69 90 67 81 41 78 74.8 64.8 49.3 81.1 69 33.6 63.5 77 75 76.1 78.6 30.4 75.3 53.6 59.1 64.2 51.9 65.1 83.1 70.9

0 0 0 0 0.23 0 0 0 0.17 0.24 0.12 0.12 0.23 0 0 0.22 0 0 0.18 0 0.25 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 0 0 0 102 0 102 0 102 0 102 0 102 0 102 0 201 0 0 0 0 0 0 0 102 0 102 0 102 17 102 0 102 0 102 0 102 0 102 0 102 0 102 0 102 0 209 0 201 0 208 0 102 0 208 0 208 0 201 0 208 0 201 0 201 0 102 0 201 0 208 0 102 0 102 0 102 0 201 0 208 0 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 4 2 3 2 2 1 2 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 12 12 12 12 12 12 12 12 12 12 12 12 12 12

4 4 4 4 4 4 4 4 4 4 4 4 4 4

3 3 3 3 3 3 3 3 3 3 3 3 3 3

28 28 28 28 28 28 28 28 28 28 28 28 28 28

85 85 85 85 85 85 85 85 85 85 85 85 85 85

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

40 40 40 40 40 40 40 40 40 40 40 40 40 40

30 30 30 30 30 30 30 30 30 30 30 30 30 30

2 2 2 2 2 2 2 2 2 2 2 2 2 2

43 44 45 45 46 47 50 50 51 52 55 55 55 76

2 1 1 1 1 1 1 1 1 1 1 1 1 1

68.5 60.8 59.6 67.3 62.4 86.8 42.2 56.2 71 70.3 43.6 69 82.8 61.9

268 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

208 201 102 208 201 201 208 208 208 201 208 209 201 209

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

269

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

13 13 13 14 14 14 14 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15

0 0 0 1 1 1 1 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

3 3 3 3 3 3 3 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

5 5 5 1 1 1 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

85 85 85 85 85 85 85 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 85 85 85 85 85 85 85 85 85 85 85 85

10 11 11 1 2 11 12 1 1 1 2 2 3 4 4 5 6 7 8 8 8 9 9 11 11 11 12 12 12 12 1 1 1 2 2 2 2 3 5 5 6 6

18 23 23 19 23 29 25 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

83 81 81 85 85 84 84 78 78 78 78 78 78 78 79 78 83 78 78 78 83 78 78 77 78 78 77 77 78 78 79 79 80 79 80 80 80 79 79 80 79 80

54 53 53 56 55 57 57 58 58 85 58 58 58 98 85 85 78 96 58 95 68 58 85 85 93 97 93 94 58 85 85 105 85 104 58 58 109 68 64 108 103 85

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

71 57 62 82 21 74 70 56 61 53 18 30 54 46 38 20 44 49 58 60 34 56 31 46 43 21 45 36 51 55 18 77 39 20 19 42 59 56 64 36 49 45

1 2 1 2 1 2 1 1 1 1 1 1 2 1 1 1 1 1 1 1 1 2 1 1 1 1 1 1 1 1 1 1 2 2 1 1 1 1 1 1 1 1

0 0 0 25 67 20 44 67 80 66 78 83 73 58 71 80 90 78 74 89 0 83 67 64 65 56 67 60 82 76 65 57 72 71 94 68 84 67 53 71 68 61

0 0 0 0 0.096 0 0 0 0 0 0.132 0.168 0.078 0.1 0 0 0 0.23 0.211 0.21 0 0 0.28 0.11 0.1 0.1 0.18 0.15 0.082 0.18 0 0 0.13 0.08 0.096 0.143 0.12 0 0.1 0.25 0.26 0

0 0 0 2 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 102 201 102 102 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201

4 7 7 0 0 18 0 20 0 37 22 22 21 22 0 0 0 22 37 22 22 0 22 22 19 0 0 0 0 22 0 19 22 0 22 22 19 19 0 22 22 0

0 2 2 4 2 4 3 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 15 15 15 15 15 15 15 15 15 15 15 15 15 15

5 5 5 5 5 5 5 5 5 5 5 5 5 5

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

85 85 85 85 85 85 85 85 85 85 85 85 85 85

7 7 7 7 11 11 11 12 12 12 12 12 12 12

0 0 0 0 0 0 0 0 0 0 0 0 0 0

80 82 82 82 79 79 80 79 79 79 79 80 80 80

85 106 110 111 64 99 85 85 100 101 102 58 85 85

2 2 2 2 2 2 2 2 2 2 2 2 2 2

59 50 19 28 31 37 32 50 16 19 77 24 19 46

1 1 1 1 1 1 1 1 1 1 1 1 1 1

93 89 36 0 92 92 87 92 78 83 0 93 68 73

270 0 0.26 0 0 0.17 0.31 0 0 0 0 0 0 0.08 0.09

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

201 201 201 201 201 201 201 201 201 201 201 201 201 201

19 22 20 0 0 0 22 22 0 0 19 0 0 22

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

271

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15

5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

0 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

0 0 0 0 0 0 0 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

12 3 3 5 6 10 12 0 1 1 2 2 2 2 3 4 4 5 5 5 6 6 6 8 8 9 9 10 10 10 10 11 11 11 12 12 12 12 12 12 0 1

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

82 77 77 77 77 77 77 79 79 79 79 79 83 83 79 79 79 79 79 83 79 79 79 79 83 83 83 83 83 83 83 83 83 83 79 79 83 83 83 83 79 79

58 58 58 85 58 92 85 85 58 58 58 58 25 26 85 58 85 27 107 27 85 85 85 85 27 67 71 66 68 69 70 28 29 65 58 106 58 58 58 64 85 78

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

19 44 54 52 45 34 20 32 37 41 44 49 32 60 30 40 41 56 43 44 3 34 60 56 72 20 39 18 51 30 30 27 69 42 22 31 20 42 52 58 68 39

1 1 1 1 1 1 1 1 1 1 2 1 1 2 1 1 1 1 1 1 1 1 2 1 1 1 2 1 1 1 1 1 1 1 2 1 2 1 1 1 1 1

91 62 70 68 55 79 74 65 0 76 62 86 91 66 81 73 76 61 78 71 0 70 70 69 77 73 71 58 63 80 74 80 94 67 74 86 83 79 80 0 0 53

0.105 0.18 0.251 0.22 0.192 0.08 0.16 0.27 0 0.262 0.24 0.086 0.023 0 0.19 0.212 0.22 0.24 0.172 0.27 0 0.18 0.24 0 0.01 0 0 0.01 0 0.12 0.01 0.21 0 0 0 0 0.24 0 0 0 0 0.23

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

201 201 201 104 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 201 104 104

0 22 22 37 0 0 0 22 0 22 0 22 0 0 19 0 22 22 22 22 0 0 22 0 19 22 0 0 22 0 0 0 0 0 0 22 22 0 22 22 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 15 15 15 15 15 15 15 15 15 15 15 15 15 15

5 5 5 5 5 5 5 5 5 5 5 5 5 5

2 2 2 2 2 2 2 2 2 2 2 2 2 2

25 25 25 25 25 25 25 25 25 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85

1 1 1 1 1 1 1 1 1 1 2 2 2 2

0 0 0 0 0 0 0 0 0 0 0 0 0 0

79 79 79 79 81 81 81 81 81 81 79 79 79 79

78 181 182 182 58 58 64 86 122 171 28 58 85 85

2 2 2 2 2 2 2 2 2 2 2 2 2 2

49 34 1 3 52 58 73 1 25 32 81 75 18 19

1 1 1 1 2 1 1 1 2 1 1 2 2 1

58 0 0 0 0 76 35 0 0 80 0 80 0 42

272

0 0.138 0 0 0.204 0.329 0.24 0 0 0.31 0 0.218 0 0.12

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 104 102 102 104 104 104 104 104 104 104 104 104 104

0 8 0 0 0 8 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

273

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15

5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

2 2 2 2 2 2 3 3 3 3 3 3 3 3 3 4 4 4 4 4 4 4 4 4 4 5 5 5 5 5 5 5 6 7 7 7 8 8 8 8 8 8

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

79 81 81 81 81 81 79 79 79 79 81 81 81 81 81 79 79 79 81 81 81 81 81 81 81 79 79 79 81 81 81 81 79 79 79 79 79 79 79 79 81 81

85 111 114 114 114 123 58 75 85 85 85 115 115 115 125 68 85 85 85 86 112 113 113 117 172 58 174 177 67 85 113 124 85 85 148 175 0 85 85 178 58 119

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

37 51 2 4 20 4 21 23 40 68 20 18 20 35 49 39 51 73 7 29 20 1 23 53 2 43 23 63 59 28 30 24 71 39 47 64 43 11 70 64 28 49

1 1 2 1 1 2 1 1 2 1 1 2 1 1 2 2 1 1 1 1 2 1 1 1 1 2 2 1 1 2 1 2 2 1 1 2 1 1 1 1 1 1

58 59 67 60 67 0 63 61 0 64 77 61 38 53 0 63 0 0 23 0 61 0 90 65 0 15 79 0 62 0 0 0 83 0 0 0 58 0 0 0 0 0

0 0.4 0 0 0.26 0 0.141 0.16 0 0 0.13 0.03 0 0.235 0 0.38 0 0.26 0 0 0 0 0.4 0.22 0 0 0.21 0 0.32 0 0 0 0.2 0 0.361 0 0.35 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 11 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 21 0.006 0 0 0 0 0 0 0 0 0 0 0 0 0 0 15 3 0 0

104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 114 104 104 104 104 104 114 104 104 104 104 102 102 102 104 104 104 102 104

0 0 0 0 0 0 0 22 0 0 0 0 0 0 0 19 0 0 0 0 0 0 0 0 0 0 8 0 0 0 0 0 0 22 0 0 0 0 0 0 36 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 15 15 15 15 15 15 15 15 15 15 15 15 15 15

5 5 5 5 5 5 5 5 5 5 5 5 5 5

2 2 2 2 2 2 2 2 2 2 2 2 2 2

25 25 25 25 25 25 25 25 25 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85

9 9 9 10 10 10 10 10 10 11 11 11 11 11

0 0 0 0 0 0 0 0 0 0 0 0 0 0

79 79 79 79 79 81 81 81 81 79 79 79 81 81

85 85 85 58 178 118 120 120 126 77 176 179 64 64

2 2 2 2 2 2 2 2 2 2 2 2 2 2

33 37 83 50 27 74 38 44 3 56 8 1 13 16

1 1 1 1 1 1 1 2 2 1 2 1 1 2

88 82 0 50 78 0 90 83 24 50 78 0 70 67

274

0.28 0 0 0 0.18 0 0.445 0.467 0 0.3 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

104 22 104 0 104 0 104 0 104 0 104 8 104 0 104 8 104 0 102 0 102 0 104 0 104 0 104 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

275

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15

5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

25 25 25 25 25 25 25 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26 26

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

11 11 12 12 12 12 12 1 1 1 1 1 1 2 2 2 3 3 5 5 5 5 5 5 6 6 8 8 8 8 8 8 9 9 9 9 9 9 10 10 10 10

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

81 81 79 79 79 79 79 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80 80

64 121 58 65 116 180 180 58 85 85 113 160 165 85 162 162 68 80 58 85 85 92 167 169 58 85 58 85 85 159 170 171 58 58 85 158 166 167 78 137 150 163

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

44 62 32 34 4 19 78 60 39 46 29 2 19 54 38 39 44 57 59 30 62 36 39 18 23 24 69 22 57 59 75 54 56 60 29 3 6 29 22 49 4 3

2 1 1 1 1 1 1 1 1 2 2 2 2 1 2 2 1 1 1 1 2 1 1 1 1 1 1 1 1 2 1 1 1 1 1 2 2 1 1 2 2 2

70 74 51 78 83 0 0 60 0 62 0 90 78 58 63 70 0 67 0 58 76 0 0 0 0 57 0 0 0 0 0 97 0 0 93 0 0 0 60 0 79 0

0.184 0.11 0.17 0.03 0 0 0 0 0 0.14 0 0 0 0.03 0.47 0.35 0 0 0 0.26 0 0.36 0 0 0 0.47 0 0 0 0 0 0.29 0.298 0 0.06 0 0 0 0.24 0 0 0

0 0 0 0 0 0 6 0.068 0 0 0 0 0 0 21 33 0 0 10 0.42 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 11 0.25 0 0 0 0 12 0.008 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 13 0.015 0 0 0 0 0 0 0 0 0 0 0 0 0 0

104 104 102 110 102 102 102 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 110 104 104 104 104 104 104 104 102 104 104 104 104 104 104 104

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 8 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 15 15 15 15 15 15 15 15 15 15 15 15 15 15

5 5 5 5 5 5 5 5 5 5 5 5 5 5

2 2 2 2 2 2 2 2 2 2 2 2 2 2

26 26 26 26 26 26 26 26 26 27 27 27 27 27

85 85 85 85 85 85 85 85 85 85 85 85 85 85

11 12 12 12 12 12 12 12 12 1 1 1 1 1

0 0 0 0 0 0 0 0 0 0 0 0 0 0

80 80 80 80 80 80 80 80 80 78 78 78 78 78

58 58 58 113 164 164 168 172 173 86 87 87 87 87

2 2 2 2 2 2 2 2 2 2 2 2 2 2

1 36 47 68 3 20 54 46 59 3 28 32 46 47

1 2 1 1 1 2 1 1 1 2 1 1 2 1

1 86 93 46 0 0 0 63 0 0 0 0 0 0

276

0 0 0.394 0.23 0 0 0 0.29 0 0 0 0 0 0

11 11 0 0 0 0 0 0 0 0 0 0 0 0

0.6 0.2 0 0 0 0 0 0 0 0 0 0 0 0

104 0 104 0 104 0 102 0 104 0 104 0 110 14 102 0 104 0 104 0 102 0 102 0 102 0 104 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

277

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15 15

5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27 27

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

1 1 1 1 1 1 1 2 2 2 2 3 3 3 3 3 4 4 4 4 4 4 4 4 4 4 4 4 4 5 5 5 5 6 6 7 7 7 7 8 8 8

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

78 78 78 78 78 78 78 78 78 78 82 78 78 78 78 82 78 78 78 78 78 78 78 78 78 78 78 78 78 78 78 78 78 78 78 78 78 78 78 78 78 78

88 88 96 96 127 128 130 58 85 130 58 85 85 131 132 58 73 73 79 79 80 80 85 85 85 115 133 133 134 58 89 134 134 85 91 58 81 85 135 82 85 136

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

10 14 7 65 3 24 75 52 71 28 28 46 50 24 26 36 24 33 34 36 26 56 17 38 60 2 17 18 32 85 90 17 17 14 64 22 22 56 15 55 45 65

1 2 1 1 1 1 1 1 1 1 1 1 2 1 1 1 1 1 1 2 1 1 2 1 1 1 1 1 1 1 2 1 1 1 2 1 1 2 1 1 1 1

0 0 0 65 0 0 69 0 0 0 0 46 55 0 75 0 63 63 55 0 0 0 74 51 58 0 66 67 0 0 0 67 96 15 57 0 60 32 0 75 0 67

0 0 0 0.01 0 0.19 0.13 0.392 0 0.25 0.023 0.32 0 0.02 0.1 0 0.23 0 0.35 0 0.22 0 0.11 0 0.15 0 0.03 0.18 0.23 0 0 0.14 0.08 0 0 0.167 0.17 0 0 0.3 0.29 0.25

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 21 0.001 0 0 0 0 0 0 0 0

104 104 104 104 104 104 104 104 104 104 104 102 104 102 104 104 104 104 104 104 102 104 104 102 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 8 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 8 0 8

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 15 15 15 15 15 15 15 15 15 15 15 15 15 15

5 5 5 5 5 5 5 5 5 5 5 5 5 5

2 2 2 2 2 2 2 2 2 2 2 2 2 2

27 27 27 27 27 27 27 27 27 27 27 27 27 27

85 85 85 85 85 85 85 85 85 85 85 85 85 85

8 9 9 10 10 10 10 10 11 11 12 12 12 12

0 0 0 0 0 0 0 0 0 0 0 0 0 0

82 78 82 78 78 78 78 78 78 78 78 78 78 78

58 85 58 58 83 84 84 161 90 90 73 74 75 75

2 2 2 2 2 2 2 2 2 2 2 2 2 2

3 2 18 14 74 9 22 44 11 13 47 36 19 25

1 1 1 2 1 1 1 1 2 2 1 1 1 1

0 0 80 65 0 0 69 18 0 0 63 48 71 0

278

0 0 0.13 0.166 0.04 0 0.147 0 0 0 0.25 0.22 0.17 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

104 0 104 0 104 0 104 0 104 0 104 0 104 0 102 20 104 0 104 0 104 0 104 0 102 0 104 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

279

CO Lab

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

15 15 15 15 15 15 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 17 17 17 17 17

5 5 5 5 5 5 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 0 0 0 0 0

2 2 2 2 2 2 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 3 3 3 3 3

27 27 27 27 27 27 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 19 19 19 19 19

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

12 12 12 12 12 12 1 1 3 3 3 3 4 4 4 4 4 4 5 5 7 7 7 7 7 7 8 8 9 9 10 11 11 11 12 12 12 1 1 3 5 7

0 0 0 0 0 0 2 15 3 4 5 12 1 5 12 22 24 30 22 26 1 4 6 6 9 17 2 28 6 28 6 15 25 25 9 11 13 7 31 1 5 5

78 78 82 82 82 82 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 84 82 83 84 83 81

77 86 58 58 64 64 183 184 184 185 186 187 188 187 183 189 190 183 189 191 183 188 192 193 192 194 195 186 183 196 183 197 198 199 200 190 201 0 0 0 0 0

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

47 25 43 43 4 8 47 21 25 45 33 19 27 81 20 52 20 75 25 28 9 53 87 45 22 24 37 29 67 38 56 48 20 53 35 48 66 29 58 75 22 48

1 1 1 1 1 1 1 2 1 1 1 1 2 1 2 2 1 2 1 1 1 1 1 1 1 1 1 1 2 1 2 2 1 1 1 2 2 2 2 1 1 1

0 0 68 82 50 75 73.6 27.9 29.2 77.6 79.2 84.3 87.4 62.4 81.1 51 82.9 9.6 86 85.3 89.1 88.5 69.2 72.4 64.7 82.4 66.3 74 82.9 84.5 62.5 84.5 15.2 19.7 75 86.2 57.1 0 80 29.6 86 62

0 0 0.04 0.047 0 0 0 0 0.24 0.26 0 0 0 0 0 0.04 0.02 0 0 0 0 0.05 0 0.13 0 0 0.11 0 0 0.2 0.2 0 0 0.14 0.24 0.25 0 0 0 0 0.07 0.23

0 0 0 0 0 0 0 5 0 0 22 0 0 0 4 0 0 0 0 17 0 0 23 0 0 0 0 0 0 0 0 16 17 17 0 16 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

104 104 104 104 104 104 102 201 102 201 201 201 201 102 201 102 201 102 201 201 102 201 201 201 201 201 201 201 201 201 201 201 102 102 201 201 102 201 201 201 201 102

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 23 0 24 26 0 22

0 0 0 0 0 0 4 2 2 2 2 3 2 2 2 2 2 4 2 2 2 2 3 2 3 2 2 2 4 2 2 2 2 2 2 2 2 2 0 0 0 4

Appendix A: Tables for the data base in chapter 6 17 17 17 17 17 18 18 18 18 18 18 18 18 18

0 0 0 0 0 7 7 7 7 7 7 7 7 7

3 3 3 3 3 4 4 4 4 4 4 4 4 4

19 19 19 19 19 4 4 4 4 4 4 4 4 4

85 85 85 85 85 85 85 85 85 85 85 85 85 85

8 10 10 11 11 1 1 1 1 2 2 2 2 3

19 20 29 28 30 4 12 12 12 4 4 9 25 5

81 84 81 84 82 84 84 84 84 85 85 84 85 84

0 0 0 0 0 203 204 204 204 202 202 205 202 206

2 2 2 2 2 2 2 2 2 2 2 2 2 2

22 40 17 47 0 38 9 12 13 11 37 58 37 29

1 1 1 1 1 1 2 2 2 1 1 1 2 1

0 62 80 58 0 68.4 47.1 57 56.2 59 57.5 60.2 66.7 48.2

280 0 0 0 0.24 0 0.24 0 0 0 0 0 0.24 0.34 0.3

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

201 0 201 0 201 0 104 0 201 25 201 0 104 0 104 0 104 0 115 0 115 0 104 0 116 27 217 0

2 0 2 0 0 2 2 2 2 2 2 2 3 2

Appendix A: Tables for the data base in chapter 6

281

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

18 18 18 18 18 18 18 18 18 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19

7 7 7 7 7 7 7 7 7 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8

4 4 4 4 4 4 4 4 4 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

4 4 4 4 4 4 4 4 4 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20 20

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

3 3 3 6 6 6 7 7 12 1 2 2 2 2 2 3 3 3 3 3 3 3 3 3 3 4 5 5 5 5 6 6 7 8 9 10 10 10 10 10 11 11

15 17 25 14 14 25 2 2 5 13 9 9 9 9 23 12 12 12 12 12 12 12 16 16 22 6 20 20 21 30 13 13 25 14 14 5 5 7 9 23 12 21

84 84 84 84 84 84 84 84 84 83 84 84 84 84 83 83 83 83 83 83 83 83 84 84 83 84 84 84 84 83 83 83 83 85 84 83 84 84 84 84 84 84

207 208 202 209 209 210 211 211 212 213 220 220 220 220 214 215 215 215 215 215 215 215 221 221 214 222 223 223 223 216 217 217 218 223 213 219 224 225 226 214 227 228

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

37 49 1 3 4 27 27 28 75 2 1 3 4 16 63 1 5 23 25 28 28 28 3 4 16 26 1 26 2 12 19 23 76 34 34 43 65 25 41 53 12 21

1 1 2 1 1 1 1 1 1 2 1 1 2 2 1 1 1 2 1 1 2 2 2 2 1 1 1 2 1 1 2 1 1 2 1 2 1 1 1 1 1 1

67 66 38.6 46 24.4 63.6 28.6 68.6 54.6 50 58 48 66 28 50 50 50 50 50 50 50 50 30 49 25 47 54 42 60 7 3 64 73 44 36 40 24 51 27 41 30 33

0.22 0.12 0 0 0 0.21 0.26 0.23 0.33 0 0 0 0 0 0.33 0 0 0.22 0.28 0 0 0.04 0 0 0 0.196 0 0.22 0 0 0 0.04 0 0 0.15 0.05 0.15 0.05 0.34 0 0 0.02

0 0 0 0 0 0 0 0 0 0 0 0 0 0 2 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 24 0 0 25 0 0 25

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

201 201 104 118 118 201 104 104 219 104 104 104 104 104 104 104 104 104 104 104 104 104 104 104 120 104 105 105 105 104 201 201 104 104 104 203 203 104 201 222 213 223

23 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 28 0 0 0 0 0 29 0 0 0 0 0 0 30 0 0

3 2 2 2 2 2 2 2 3 2 2 2 2 3 2 2 2 2 2 2 2 2 4 2 2 2 2 2 2 2 2 2 4 2 2 2 3 2 2 2 2 2

Appendix A: Tables for the data base in chapter 6 19 19 19 19 19 20 20 20 20 20 20 20 20 20

8 8 8 8 8 9 9 9 9 9 9 9 9 9

3 3 3 3 3 3 3 3 3 3 3 3 3 3

20 20 20 20 20 26 26 26 26 26 26 26 26 26

85 85 85 85 85 85 85 85 85 85 85 85 85 85

11 11 11 12 12 1 1 2 2 2 2 3 4 5

22 28 30 20 20 4 8 8 9 21 22 16 2 9

84 84 84 83 83 84 84 84 84 84 84 84 84 84

229 230 214 215 215 231 231 232 232 234 235 236 238 237

2 2 2 2 2 2 2 2 2 2 2 2 2 2

30 27 68 19 19 58 78 52 81 79 39 40 40 76

2 1 1 1 2 1 1 1 2 1 1 1 1 1

44 34 47 47 55 58.3 44.4 8.7 0 4.6 52 35.4 62.4 59.1

282 0 0.21 0 0 0 0.03 0 0.29 0 0.02 0.19 0 0.17 0

25 0 7 0 0 0 0 0 0 0 26 0.001 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

104 124 104 201 201 201 102 102 102 225 201 201 201 201

30 0 32 0 0 19 33 0 0 19 0 35 0 19

2 2 4 2 2 4 4 0 4 4 3 2 2 2

Appendix A: Tables for the data base in chapter 6

283

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

20 20 20 20 20 21 21 21 21 21 21 21 21 21 21 21 21 21 21 21 21 21 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22

9 9 9 9 9 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 10 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

3 3 3 3 3 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 5 5 5 5 5 5 5 7 7 7 7 7 7 7 7 7 7 7 7 7

26 26 26 26 26 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 0 0 0 0 0 0 0 19 19 19 19 19 19 19 19 19 19 19 19 19

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

7 9 11 11 11 1 1 1 1 2 3 3 4 5 5 5 6 6 6 10 10 10 3 3 3 3 12 12 12 1 2 3 3 3 4 4 4 4 4 4 5 5

9 29 19 20 21 14 17 30 30 3 4 18 15 4 28 28 2 2 12 17 17 27 7 7 7 7 5 17 21 31 17 25 26 27 4 7 7 19 19 23 1 4

84 84 84 84 84 85 85 85 85 85 85 85 85 84 84 84 84 84 84 84 84 84 85 85 85 85 84 84 84 85 85 85 85 85 85 85 85 85 85 84 85 85

239 237 240 232 241 247 248 249 249 243 250 248 251 242 243 243 244 244 245 244 246 244 372 372 372 372 368 247 330 460 260 457 284 266 361 452 458 457 459 263 331 324

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

49 70 30 63 61 66 36 2 3 67 28 24 73 45 6 18 62 62 19 39 19 37 1 1 2 27 0 30 35 0 19 0 63 90 0 31 0 63 73 0 64 14

1 39.6 2 20 1 87 1 74 1 94 2 0 2 82 2 50.3 2 22.3 1 81.3 1 73.9 2 78.4 1 0 1 63 1 63 2 26 2 57 2 58 2 74 2 74 1 9 1 83 1 99.99 2 88.4 1 87.4 2 72.1 1 82 1 78.3 2 77.1 1 0 1 74.3 1 48.5 1 79 1 0 1 57.4 1 47.7 1 66.3 2 0 1 0 1 0 1 23.8 1 0

0.2 0 0.09 0 0.02 0 0.02 0 0 0.17 0 0 0 0.05 0 0.2 0 0 0.16 0.2 0.2 0 0 0 0 0 0 0.19 0.36 0.16 0 0 0 0 0.12 0 0.16 0 0 0 0.22 0

0 0 0 0 6 0.001 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 28 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 102 102 201 201 126 201 102 102 102 102 201 227 201 102 102 225 225 201 201 102 201 102 102 102 102 201 201 201 201 102 102 230 102 0 102 0 102 0 102 213 0

19 19 34 19 19 38 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 31 0 0 0

4 3 2 3 4 3 2 1 1 3 1 1 3 2 1 1 3 2 1 2 4 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 22 22 22 22 22 22 22 22 22 22 22 22 22 22

1 1 11 11 11 11 11 11 11 11 11 11 11 11

7 7 5 5 5 5 5 5 5 5 5 5 5 5

19 19 0 0 0 0 0 0 0 0 0 0 0 0

85 85 82 82 85 85 85 85 85 85 85 85 85 85

7 12 7 11 1 1 1 1 1 1 1 1 1 1

9 18 3 17 4 5 5 9 12 14 15 20 22 22

85 84 83 82 84 84 84 84 82 82 82 83 82 84

335 72 271 255 363 259 259 311 349 350 284 284 263 365

2 2 2 2 2 2 2 2 2 2 2 2 2 2

31 54 0 73 0 26 72 73 0 54 66 80 0 51

1 1 2 2 1 1 1 1 1 2 1 1 1 1

84.4 2.6 80 48 60.5 42.8 29.4 84.1 0.7 2 43.2 36.3 67.8 67.6

284 0.31 0 0 0 0 0.29 0 0 0.1 0 0 0 0 0.14

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

120 102 0 102 0 104 104 104 0 201 104 104 201 201

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

285

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22

11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11

5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

1 22 85 1 23 83 1 23 83 1 24 82 1 24 82 1 24 83 1 24 83 1 24 83 1 24 83 1 26 82 1 27 85 1 27 85 1 28 83 1 28 84 1 28 84 1 28 84 1 28 84 1 28 84 1 31 85 2 1 84 2 1 84 2 1 84 2 1 84 2 2 83 2 3 84 2 4 82 2 9 83 2 10 83 2 12 84 2 12 84 2 138 42 2 13 842 2 13 84 2 14 82 2 16 84 2 18 82 2 19 83 2 19 85 2 19 85 2 21 84 2 22 85 2 25 85

370 267 292 259 259 291 291 291 291 243 369 369 362 293 293 293 293 293 311 295 295 295 295 259 259 321 261 284 286 286 94 96 296 320 243 259 350 263 342 279 259 263

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

0 38 22 36 42 1 2 19 27 73 24 73 40 2 2 13 15 22 0 0 2 2 19 81 65 80 33 36 19 22 0 0 73 41 0 32 0 0 3 0 21 0

0 2 1 2 1 2 1 2 1 2 2 2 1 1 2 2 1 2 1 1 2 2 2 1 2 1 1 2 1 1 1 2 1 1 1 2 1 1 1 1 1 2

50.4 74.8 66.1 72 68.8 59.9 45 43.6 62.2 62.3 50.3 29.3 52.1 89.5 91.8 85 83.6 83.9 77 88 61.1 90.7 82.7 80.4 3.4 59.9 86.9 14.5 81 82 72.1 92.8 48.2 38.7 1.9 77.6 69.1 34.2 6.9 70.8 44.6 9.4

0 0 0.18 0 0 0 0 0 0 0 0 0.17 0.1 0 0 0 0.07 0 0.25 0 0 0 0.13 0 0 0 0 0.26 0 0.15 0 0 0 0.03 0 0 0.08 0.24 0 0 0.09 0.24

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 11 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 19 201 0 201 0 201 0 104 0 104 0 104 0 104 0 102 0 104 0 104 0 104 0 104 0 104 0 104 0 104 0 104 0 102 0 104 0 104 0 104 0 104 0 201 0 105 23 102 0 201 0 104 22 201 0 201 0 0 0 104 0 104 0 0 0 0 0 201 0 0 0 104 0 104 0 201 0 0 0 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 22 22 22 22 22 22 22 22 22 22 22 22 22 22

11 11 11 11 11 11 11 11 11 11 11 11 11 11

5 5 5 5 5 5 5 5 5 5 5 5 5 5

0 0 0 0 0 0 0 0 0 0 0 0 0 0

85 85 85 85 85 85 85 85 85 85 85 85 85 85

2 3 3 3 3 3 3 3 3 3 3 3 3 3

26 1 1 1 1 5 5 7 8 8 8 8 8 8

82 82 82 82 82 82 85 85 83 84 84 84 85 85

275 276 276 276 276 277 269 352 333 344 345 346 263 297

2 2 2 2 2 2 2 2 2 2 2 2 2 2

0 10 12 17 18 65 62 64 0 74 36 67 0 0

2 2 2 1 1 2 1 1 1 1 2 1 2 1

2 76.5 81.7 78.6 69.7 57.7 1.7 71.1 68.6 0.6 2.5 66.4 20.1 62.4

286 0 0 0 0 0 0 0 0 0 0.21 0 0.33 0 0.04

0 0 0 0 0 0 0 0 0 0 32 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

201 0 102 0 102 0 104 0 102 0 102 0 201 19 234 0 104 0 104 0 0 0 120 0 104 0 0 0

0 0 0 0 0 0 2 0 0 0 2 0 0 0

Appendix A: Tables for the data base in chapter 6

287

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22

11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11

5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

3 3 3 3 3 3 3 3 3 3 3 3 3 4 4 4 4 4 4 4 4 4 4 4 4 4 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

9 9 9 11 14 14 15 18 20 24 26 28 28 7 7 8 8 8 10 11 12 16 18 18 27 28 4 5 5 7 8 9 10 13 13 14 14 16 17 18 19 20

82 82 83 84 84 84 85 82 83 82 85 83 83 83 85 83 83 83 84 84 84 83 82 82 82 83 82 82 83 82 84 84 84 82 83 82 84 83 83 83 84 84

259 263 267 347 259 276 259 284 329 285 266 331 332 286 362 286 286 286 348 269 269 263 261 266 287 259 286 263 334 352 354 355 260 263 335 351 356 263 264 336 307 306

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

34 0 25 0 66 38 34 59 6 0 63 0 0 0 31 0 25 62 55 38 62 46 33 0 0 57 52 52 29 27 32 0 0 0 0 49 67 0 0 0 1 0

1 2 1 2 1 2 2 2 2 1 1 1 1 2 1 1 1 1 2 1 2 2 1 1 1 1 2 1 1 1 1 1 1 1 1 2 1 1 1 1 2 2

5.2 29.7 6.2 72.1 2 51.7 34.3 1.8 90.2 77 79 61.2 14.3 85.5 47.7 78.8 80.3 81.9 80.6 83.6 73 2 66.8 59.9 69.5 34.2 44.9 79.9 63.2 68.7 86 71 63 3.7 53.1 2 56.4 68.4 73.8 83.1 0 73

0.11 0 0.01 0.18 0 0.04 0 0.19 0 0 0 0.22 0.39 0 0 0 0 0 0 0 0 0 0 0.39 0 0 0 0.01 0 0.15 0 0.24 0.01 0 0.23 0 0 0.02 0.24 0 0 0

0 0 0 0 34 0 8 0.307 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 33 0.01 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 230 230 201 201 201 104 0 201 104 104 0 104 104 104 104 230 230 230 0 201 0 0 104 104 0 201 104 230 0 0 0 201 0 0 201 0 0 104 104

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 2 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 22 22 22 22 22 22 22 22 22 22 22 22 22 22

11 11 11 11 11 11 11 11 11 11 11 11 11 11

5 5 5 5 5 5 5 5 5 5 5 5 5 5

0 0 0 0 0 0 0 0 0 0 0 0 0 0

85 85 85 85 85 85 85 85 85 85 85 85 85 85

5 5 5 5 5 5 5 5 6 6 6 6 6 6

20 20 23 24 28 29 30 31 5 13 13 17 20 23

84 84 82 83 84 83 84 83 82 83 83 82 84 83

306 306 326 265 308 267 304 266 353 268 268 327 309 269

2 2 2 2 2 2 2 2 2 2 2 2 2 2

31 31 30 88 0 21 47 29 0 0 46 0 0 76

2 2 1 1 1 1 1 2 1 1 2 1 1 1

59 85 8.3 39 19 79 60.5 80 82.9 50.5 87 4 87.4 75.1

288 0.02 0.02 0.24 0 0 0 0.02 0.19 0.12 0.19 0.14 0.12 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 102 201 104 105 230 201 230 201 104 104 204 0 230

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

289

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22

11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11

5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

6 6 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 8 8 8 8 8 8 8 8 8 8 8 9 9 9 9 9 9 9 9 9 9 9

23 25 1 3 3 5 6 6 7 10 11 13 21 23 23 25 26 27 30 31 6 10 12 16 17 18 22 23 23 24 24 5 8 8 8 11 12 12 12 16 17 17

83 84 83 83 83 83 82 84 83 83 82 83 82 83 83 82 83 83 84 82 82 83 84 83 84 83 82 82 82 82 83 83 84 84 84 83 83 83 83 84 82 84

270 304 272 266 271 273 259 310 274 259 288 340 289 259 260 290 256 257 314 288 274 258 274 259 315 261 281 280 280 269 262 337 316 316 316 338 259 339 339 319 252 314

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

0 25 15 64 0 0 34 25 19 0 0 28 0 64 0 29 29 0 43 19 20 63 66 52 0 0 19 0 0 85 0 0 0 0 0 0 57 0 3 0 0 48

1 1 1 1 1 1 1 1 1 1 1 1 2 1 1 1 1 2 1 1 1 1 1 1 2 1 1 1 2 2 1 1 1 2 2 1 1 1 0 2 1 1

70 89.4 11 80 75 40 12.6 68.1 81 85.8 83.3 87 40.9 68.5 67.1 2.6 29.6 20 83.2 53.7 79.4 50.1 0 65 83 84.5 70.4 72.3 82 71.9 54 86 54.5 34.5 84.7 69 60.5 72.6 38.6 74.1 75.9 81.9

0 0.08 0.08 0 0 0.15 0.27 0.04 0.09 0 0 0.25 0 0.06 0.03 0.19 0.27 0 0.26 0.1 0 0.27 0 0 0 0.15 0 0 0 0 0 0.05 0 0 0 0.11 0 0 0 0.23 0.22 0.41

0 0 0 0 0 0 0 0 0 0 0 0 0 0 30 0.02 0 0 31 0.483 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 29 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

105 0 0 0 201 0 230 0 0 0 102 0 104 0 131 0 230 0 0 0 0 0 230 0 0 0 230 0 228 0 201 0 120 0 104 0 102 0 201 0 228 0 102 0 102 19 201 0 228 0 228 0 201 0 102 0 102 0 201 0 228 0 0 0 0 0 0 0 0 0 0 0 228 0 104 0 104 0 102 0 228 0 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 22 22 22 22 22 22 22 22 22 22 22 22 22 22

11 11 11 11 11 11 11 11 11 11 11 11 11 11

5 5 5 5 5 5 5 5 5 5 5 5 5 5

0 0 0 0 0 0 0 0 0 0 0 0 0 0

85 85 85 85 85 85 85 85 85 85 85 85 85 85

9 9 9 9 9 9 9 9 9 9 9 9 9 10

20 22 22 23 24 24 25 25 25 25 25 27 29 4

82 83 84 82 83 83 82 82 82 82 82 84 83 84

324 263 318 286 263 305 325 325 325 325 325 317 305 291

2 2 2 2 2 2 2 2 2 2 2 2 2 2

22 50 0 41 19 0 23 31 31 31 36 0 0 0

1 1 2 2 2 1 1 1 1 1 1 1 2 1

70.3 80.1 81.1 83 46.8 72.1 0.7 0.5 10.5 16.2 7.3 17.2 70.9 57.4

290 0 0.05 0.09 0.23 0 0 0.06 0 0.26 0.25 0.21 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 0 0 201 201 104 120 120 120 120 120 0 104 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

Lab

22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22 22

291

Co

Submission Exposure Date Addres Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11

5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

10 10 10 10 10 10 10 10 10 10 10 10 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 12 12 12 12 12 12 12 12 12

5 9 9 14 17 19 20 24 25 28 29 30 1 1 1 4 5 5 9 9 13 13 14 14 17 18 18 21 24 25 25 26 27 2 4 4 7 8 11 11 12 12

82 82 82 84 83 84 84 83 84 84 84 83 83 84 84 83 82 84 82 84 83 83 84 84 82 82 83 84 83 82 84 84 84 82 82 82 83 83 83 84 82 82

323 322 322 308 343 303 243 299 357 358 284 341 298 345 359 324 279 266 278 366 276 276 257 367 255 254 300 311 301 253 312 312 311 328 263 263 302 303 304 313 329 330

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

0 0 0 21 0 0 0 0 39 80 0 59 31 49 55 0 0 13 0 23 0 0 0 0 53 28 0 0 36 0 78 78 0 0 23 58 0 36 41 0 0 0

1 1 1 1 1 1 1 2 1 2 1 2 1 2 2 2 2 2 1 1 1 1 1 2 2 1 1 1 1 1 2 2 1 1 2 1 2 1 2 2 1 1

60.5 46.2 69 73.3 9 3.3 4.9 33.1 76.5 59.8 3.1 5 73.5 78.5 68.3 48.2 9.9 71.8 13.4 88.2 4 13 55 3.5 48 70 40.1 74.4 77.9 81 7.7 7.7 74.4 73.9 6.9 4.8 58.7 66.5 4.3 45.4 80.8 67

0 0.15 0.23 0 0 0.1 0.13 0 0 0 0 0 0 0.34 0 0.05 0 0 0 0.16 0 0 0 0.1 0 0.14 0.01 0 0.2 0 0 0 0 0 0 0 0 0 0.27 0.01 0 0

0 0 0 35 0 0 0 0 0 21 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 25 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 102 102 201 0 120 0 102 230 0 104 102 228 102 230 102 201 102 118 133 120 120 230 120 102 201 228 0 201 0 120 201 0 203 229 229 0 0 201 104 201 201

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 2 0 0 0 0 0 2 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 22 22 22 22 22 22 22 22 22 22 22 22 22 22

11 11 11 11 11 11 11 11 11 11 11 11 11 11

5 5 5 5 5 5 5 5 5 5 5 5 5 5

0 0 0 0 0 0 0 0 0 0 0 0 0 0

85 85 85 85 85 85 85 85 85 85 85 85 85 85

12 12 12 12 12 12 12 12 12 12 12 12 12 12

12 12 12 13 13 14 18 18 18 18 18 21 21 21

84 84 84 84 84 83 82 82 82 82 83 82 84 84

291 291 313 263 371 298 263 266 266 266 274 282 245 360

2 0 2 0 2 0 2 0 2 0 2 20 2 0 2 0 2 0 2 0 2 0 2 29 2 0 2 0

2 2 2 1 1 2 2 1 1 2 1 1 2 1

45.4 71.7 71.7 82.8 22.6 88 66.9 80 86.8 85.6 14.5 69 80.2 80.2

292 0.01 0.07 0.07 0 0 0.2 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

104 104 104 0 104 120 104 104 104 104 102 230 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

293

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

22 22 22 22 22 22 22 22 22 22 22 22 22 22 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23 23

11 11 11 11 11 11 11 11 11 11 11 11 11 11 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

0 0 0 0 0 0 0 0 0 0 0 0 0 0 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

12 12 12 12 12 12 12 12 12 12 12 12 12 12 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 2 2 2 2 3 3 3 3 3 4 4 4 5

22 22 23 24 24 25 25 27 27 27 28 28 28 28 5 9 9 9 9 9 17 19 21 23 23 23 23 23 14 14 20 23 25 5 5 6 18 25 1 2 9 7

84 84 84 82 83 84 84 82 82 82 83 84 84 84 84 84 84 84 84 85 84 85 84 84 84 84 84 84 84 85 84 85 84 84 85 85 85 84 85 84 84 84

361 361 314 259 364 264 264 283 283 283 259 263 359 359 374 373 373 373 373 388 376 378 377 375 375 375 375 377 373 383 378 389 379 380 373 390 373 381 383 380 382 383

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

0 35 0 51 0 0 0 40 57 59 7 0 0 0 74 1 4 23 25 38 56 60 25 16 16 16 33 42 0 34 72 17 53 58 56 93 34 29 54 0 80 51

2 2 1 1 2 1 1 1 1 1 1 1 1 1 2 2 1 2 1 1 1 1 1 1 2 2 1 2 1 1 1 1 1 2 1 1 2 1 1 1 1 1

12.8 12.8 79.2 57.6 81 75.1 75.1 80.5 77.8 80.7 90.3 24 79.7 79.7 82 78.6 75.6 76.3 73.7 1.9 84.5 43.2 84 5 7 13.2 5 77.1 2.6 66.4 33.8 0.1 15 83.8 1.6 1.2 76 0.5 1.4 0.1 77.7 81.2

0 0 0.26 0 0 0 0 0 0 0 0 0.33 0.37 0.37 0 0 0 0.2 0.24 0.39 0.16 0.33 0.14 0 0 0 0 0.03 0 0.16 0.23 0 0 0 0.01 0 0.11 0.02 0.16 0 0 0.21

0 0 201 0 0 0 102 0 0 0 102 0 0 0 228 0 0 0 104 0 0 0 102 0 0 0 104 0 0 0 120 0 0 0 120 0 0 0 120 0 0 0 102 0 0 0 102 0 0 0 0 0 0 0 0 0 36 0 201 0 0 0 104 0 0 0 104 0 0 0 104 0 0 0 104 0 0 0 0 22 0 0 201 0 46 0.79 104 22 0 0 201 0 0 0 201 0 0 0 201 0 0 0 201 0 0 0 201 0 0 0 201 0 0 0 0 3 0 0 104 0 0 0 104 22 0 0 104 40 0 0 201 0 37 0 201 0 39 0 0 19 0 0 201 19 40 0 201 0 0 0 0 0 0 0 104 0 0 0 201 0 0 0 104 0 0 0 201 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 3 2 2 2 2 0 0 0 2 2 2 2 2 3 0 0 0 0 0 0 0 0 0 2 0 0 0 0

Appendix A: Tables for the data base in chapter 6 23 23 23 23 23 23 23 23 23 23 23 24 24 24

6 6 6 6 6 6 6 6 6 6 6 0 0 0

5 5 5 5 5 5 5 5 5 5 5 6 6 6

8 8 8 8 8 8 8 8 8 8 8 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85

5 6 6 7 11 12 12 12 12 12 12 3 3 3

31 13 25 3 26 3 7 14 15 15 18 6 6 6

84 84 84 84 84 84 84 84 84 84 84 82 82 82

384 385 383 373 373 381 373 386 387 387 385 401 401 401

2 2 2 2 2 2 2 2 2 2 2 2 2 2

55 59 45 29 56 0 59 21 3 5 20 2 4 30

1 2 1 1 1 1 1 1 2 2 1 1 1 2

68 2 72.6 81.3 83.7 5.5 82.4 9.5 56.2 39.6 2.5 45 30 58

294 0 0.13 0 0 0.15 0 0.03 0 0 0 0.01 0 0 0

0 0 0 46 38 0 0 0 46 46 0 46 46 46

0 0 0 0.71 0 0 0 0 0.71 0.65 0 10 8 0.75

213 0 201 0 201 0 104 0 201 0 207 19 201 0 135 0 104 0 104 0 0 0 102 0 102 0 102 0

2 0 0 0 0 0 0 0 2 2 0 0 0 0

Appendix A: Tables for the data base in chapter 6

295

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

24 25 26 27 27 27 27 28 29 30 31 31 31 31 32 33 34 34 34 34 34 34 34 34 34 34 34 34 34 34 34 34 34 34 34 34 34 35 35 35 35 35

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 1 1 1 1 1 1 1 1 12 12 12 12 12 12 12 12 12 12 12 12 6 6 6 6 6

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

3 12 1 2 3 3 12 3 12 1 1 1 1 12 3 12 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 1 1 1 1

6 21 11 5 7 7 9 8 25 3 19 22 22 30 20 13 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 2 2 4 5 5

82 73 74 74 75 75 73 75 76 77 76 75 75 73 76 76 81 81 81 81 81 81 81 81 81 81 81 81 81 81 81 81 81 81 81 81 81 83 83 85 84 84

401 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 434 434 427 431 431

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

36 37 21 19 40 48 52 22 36 21 67 45 46 36 23 35 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 65 152 0 19 26

1 1 1 1 1 2 1 2 1 1 1 1 2 1 1 2 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 2 1 1 2 1

52 76 73 35 42 42 40 40 55 45 41 52 47 57 33 54 13.4 53.2 58.5 59.1 64.8 71.9 77.4 78.4 92.4 40 50.3 54.1 55.8 60.6 64.2 67.5 69 71.1 72.4 77.6 79.5 70 63 39 76 74

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

46 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 47 47 47 47 47 47 47 47 47 47 47 47 47 47 47 47 47 47 47 47 47 0 0 0 0 0

0.75 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 9.8 14.3 12.3 19.7 10.7 0.2 0 0 3 11.4 12.5 20.2 20.5 20.8 0.9 8.5 13.7 0.7 4.9 1.5 0.8 0 0 0 0 0

102 0 225 0 225 0 225 0 225 0 225 0 225 0 225 0 225 0 225 0 225 19 225 0 225 0 225 0 225 33 225 0 102 0 201 0 201 0 201 0 102 0 208 0 208 0 208 0 102 0 102 0 102 0 201 0 201 0 102 0 208 0 102 0 201 0 208 0 201 0 208 0 208 0 0 0 0 0 0 0 201 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 35 35 35 35 35 35 35 35 35 35 35 35 35 35

6 6 6 6 6 6 6 6 6 6 6 6 6 6

6 6 6 6 6 6 6 6 6 6 6 6 6 6

25 25 25 25 25 25 25 25 25 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85

1 1 1 1 1 1 1 1 1 1 1 1 1 1

8 8 9 9 10 11 12 12 12 12 16 17 17 17

83 83 84 84 85 83 83 83 83 84 82 83 84 84

404 418 418 435 439 404 450 450 453 418 455 418 423 423

2 2 2 2 2 2 2 2 2 2 2 2 2 2

89 39 47 0 0 35 0 0 47 71 22 59 0 0

1 2 1 2 1 1 1 2 1 1 1 1 1 1

59 25 63 42 24 76 81 79 70 71 80 83 43 66

296 0.2 0.15 0.03 0 0.43 0 0.06 0 0.18 0 0.02 0.21 0 0.29

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 102 102 102 0 201 225 225 201 102 102 201 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

297

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

17 19 19 19 19 20 20 20 21 22 24 24 24 25 25 26 26 26 26 26 27 1 1 1 1 1 1 3 4 5 5 7 8 8 11 12 12 14 15 16 20 20

84 83 83 83 83 84 84 84 85 84 84 84 84 83 83 84 84 85 85 85 85 84 85 85 85 85 85 84 84 84 84 83 85 85 85 84 85 83 85 84 84 85

433 418 418 418 453 421 421 421 420 427 416 416 434 435 435 418 432 421 421 421 442 428 422 440 445 445 445 421 404 418 418 418 418 436 421 404 418 418 430 430 424 422

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

0 0 70 76 0 6 9 11 63 7 0 0 75 0 0 2 0 9 13 28 35 26 0 0 0 0 0 37 56 45 64 26 40 32 38 33 63 0 0 0 45 0

2 2 1 1 1 1 2 2 1 2 0 1 1 0 1 2 1 1 1 2 1 1 1 1 1 2 2 1 1 2 1 1 1 1 1 1 1 1 1 1 1 1

82 87 67 79 74 67 42 49 51 58 45 67 70 80 91 44 71 78 80 72 73 76 38 72 60 47 51 84 20 75 65 38 39 83 45 60 76 72 79 72 27 33

0.03 0.17 0 0 0 0 0 0 0 0 0 0 0 0 0.14 0 0 0.02 0.05 0.05 0 0.11 0.12 0 0 0 0 0 0.33 0.17 0.29 0.03 0.4 0.19 0.1 0 0.09 0.14 0.18 0.23 0.36 0

49 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 102 0 102 0 102 0 0 0 102 0 102 0 102 0 0 0 120 0 0 0 0 0 201 0 0 0 0 0 102 0 0 0 102 0 102 0 102 0 0 0 102 0 0 0 0 0 0 0 0 0 0 0 201 0 102 1 102 0 102 48 225 0 102 0 201 0 201 0 201 49 102 0 0 0 0 0 0 0 102 0 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 35 35 35 35 35 35 35 35 35 35 35 35 35 35

6 6 6 6 6 6 6 6 6 6 6 6 6 6

6 6 6 6 6 6 6 6 6 6 6 6 6 6

25 25 25 25 25 25 25 25 25 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85

2 2 2 2 2 2 2 2 2 2 2 2 3 3

21 22 24 24 24 24 25 25 26 26 27 27 1 3

83 84 85 85 85 85 84 85 84 85 84 84 84 83

421 426 404 404 404 422 418 418 404 412 413 425 416 418

2 2 2 2 2 2 2 2 2 2 2 2 2 2

50 50 5 36 38 0 45 22 56 0 0 0 0 33

2 2 2 2 1 1 1 1 2 1 1 2 0 1

83 64 70 63 58 68 84 21 84 65 78 86 80 47

298 0.27 0 0 0 0 0.2 0.35 0 0 0 0 0 0.28 0.23

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 42 207 0 102 0 102 0 102 0 0 0 102 0 201 0 201 0 0 0 0 0 0 0 102 0 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

299

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 4 4 4 4 4 4 4 4 4 4 4 4 4

3 4 5 5 8 9 10 10 10 10 13 14 14 18 19 19 20 21 22 22 25 25 26 26 28 29 29 30 31 1 2 4 4 7 7 7 7 9 9 9 12 17

85 85 84 84 84 84 83 84 85 85 84 83 85 85 84 84 83 83 84 84 83 85 83 83 83 84 85 84 85 85 83 83 85 85 85 85 85 84 84 85 84 83

444 412 412 412 418 418 448 418 448 448 416 421 421 422 415 421 427 454 422 422 411 421 426 433 404 418 447 411 404 447 422 438 418 421 421 421 421 423 423 404 404 421

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

7 0 0 0 1 87 0 44 6 27 0 1 3 0 27 44 13 0 0 0 58 69 1 23 0 75 33 19 0 0 62 3 0 4 17 27 39 50 53 30 18 52

2 1 1 2 2 2 2 1 2 2 0 1 1 0 1 2 2 0 0 1 1 1 2 1 1 2 1 1 1 1 1 2 1 1 2 1 2 1 2 2 1 2

58 17 21 69 34 42 85 61 92 71 47 24 80 35.2 32 76 42 21 64 23 63 47 91 22 74 71 67 73 40 68 78 52 65 85 75 19 84 78 77 74 70 21

0 0.2 0 0 0 0 0 0.26 0 0.26 0.27 0 0 0 0.14 0 0 0.36 0 0 0 0 0 0.07 0 0 0.18 0 0.17 0 0 0 0.23 0 0 0 0 0.23 0.32 0.03 0 0.03

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 50 0.055 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 0 0 0 102 102 0 102 102 102 102 102 102 0 102 201 102 0 0 0 102 102 102 102 0 102 102 102 0 0 102 102 0 102 102 102 102 0 0 201 201 102

42 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 42 0 0 0 0 0 0 0 0 0 0 0 0 42 42 42 0 0 45 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 35 35 35 35 35 35 35 35 35 35 35 35 35 35

6 6 6 6 6 6 6 6 6 6 6 6 6 6

6 6 6 6 6 6 6 6 6 6 6 6 6 6

25 25 25 25 25 25 25 25 25 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85

4 4 4 4 4 4 5 5 5 5 5 5 5 5

19 22 28 29 30 30 1 2 2 2 5 10 11 11

83 85 84 84 85 85 84 83 84 84 84 85 83 83

440 418 410 411 420 420 418 451 418 418 418 435 404 418

2 2 2 2 2 2 2 2 2 2 2 2 2 2

0 30 0 66 36 37 61 0 1 2 25 0 36 57

1 1 1 2 2 2 1 1 2 1 1 1 1 1

54 80 21 42 94 93 80 77 68 45 75 72 80 93

300 0 0.02 0.3 0 0.38 0.38 0 0.27 0 0 0.11 0 0 0

0 0 0 0 0 0 0 0 0 0 49 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 213 0 0 0 102 0 102 0 102 0 201 0 0 0 102 0 102 0 102 0 0 0 201 42 201 42

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

301

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

5 5 5 5 5 5 5 5 5 5 5 6 6 6 6 6 6 6 6 6 7 7 7 7 7 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 9

12 13 13 13 13 14 14 18 19 23 31 2 2 7 7 14 16 19 19 19 7 16 23 27 29 3 5 13 13 13 13 14 18 20 21 31 31 31 31 31 31 2

83 84 84 84 84 84 84 85 84 84 84 83 84 83 84 84 83 83 83 83 83 84 84 84 83 84 82 83 83 83 83 84 83 82 83 83 83 83 83 83 83 84

404 420 420 420 420 419 419 421 403 406 406 421 405 404 404 402 418 418 418 418 442 407 402 404 447 412 448 418 418 418 427 0 418 418 447 427 427 427 427 427 427 421

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

56 6 10 32 36 61 65 28 19 33 31 16 1 0 70 86 74 0 27 51 20 51 28 19 47 0 0 3 28 34 39 0 35 0 60 25 27 31 37 44 53 20

1 1 1 2 1 2 1 1 1 2 1 1 2 1 2 2 2 1 1 2 1 2 1 2 2 1 0 2 2 1 1 1 1 1 2 1 2 2 1 2 1 1

62 91 80 84 80 53 45 51 79 70 80 79 21 20 66 59 65 47 42 45.6 68 73 68 59 73 74 80 77 80 79 50 59 83 84 40 79 95 85 52 60 47 52

0.02 0 0 0 0.09 0.18 0.05 0.2 0.04 0.12 0.07 0 0 0 0 0 0 0 0 0 0.08 0.03 0 0.07 0.14 0.29 0.02 0 0.05 0.36 0 0.03 0.09 0.31 0 0 0 0 0.07 0 0 0.17

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

201 45 102 0 102 0 102 0 102 0 201 0 201 0 201 0 201 0 201 0 201 0 201 0 102 0 0 0 102 0 201 19 102 0 102 0 102 0 102 0 201 0 201 0 201 0 201 0 102 0 0 0 0 0 102 0 102 0 102 0 102 0 0 0 201 0 0 0 102 0 102 0 102 0 102 0 102 0 102 0 102 0 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 35 35 35 35 35 35 35 35 35 35 35 35 35 35

6 6 6 6 6 6 6 6 6 6 6 6 6 6

6 6 6 6 6 6 6 6 6 6 6 6 6 6

25 25 25 25 25 25 25 25 25 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85

9 9 9 9 9 10 10 10 10 10 10 10 10 10

2 8 18 27 30 1 2 2 2 2 3 4 4 13

84 83 84 83 83 83 83 83 84 84 84 83 84 83

421 409 402 441 418 418 418 418 0 0 402 404 402 408

2 2 2 2 2 2 2 2 2 2 2 2 2 2

39 61 37 0 68 56 33 51 0 0 50 40 37 32

1 1 2 1 2 1 2 1 1 2 1 1 2 1

33 57 72 84 65 42 35 56 57 65 71 83 52 55

302 0.07 0.32 0.12 0.16 0.38 0 0.44 0.47 0.33 0 0.29 0.04 0.19 0.12

0 0 48 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 105 201 201 102 102 102 102 0 0 201 201 201 201

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

303

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 35

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

10 10 10 10 10 10 10 10 10 10 10 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 12 12 12 12

15 16 20 20 23 24 25 25 25 29 29 6 7 8 9 9 11 12 12 12 14 16 18 19 19 20 21 21 22 22 22 23 23 26 26 26 26 29 1 1 4 5

82 84 83 83 83 83 83 83 83 83 83 84 82 82 82 82 84 82 82 83 84 82 82 83 84 84 83 84 82 84 84 82 84 82 83 84 84 83 82 84 83 2

418 421 418 418 423 439 0 421 421 439 439 449 451 456 421 427 440 421 421 423 418 440 450 418 0 418 417 404 448 447 447 418 446 418 414 0 0 440 404 418 418 418

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

0 19 1 22 0 39 4 1 5 13 19 0 0 0 33 63 36 2 26 0 23 0 0 18 0 30 0 26 0 34 44 0 8 53 0 0 0 0 44 36 53 50

1 1 2 2 1 1 1 2 2 2 2 1 1 1 1 1 1 2 2 1 2 1 1 1 1 1 1 1 1 1 2 2 1 1 1 1 2 2 2 1 1 2

62 24 86 48 70 68 51 60 57 52 84 61 66 79 73 46 79 21 23 58 42 66 91 85 41 47 84 72 85 70 73 79 75 70 62 63 76 63 84 60 40 77

0.05 0 0 0 0.19 0.27 0.07 0.02 0 0.22 0.04 0.15 0.14 0 0.03 0.03 0.22 0 0 0.3 0.06 0.23 0 0.1 0.35 0.04 0 0.21 0.1 0.23 0.1 0.31 0 0.27 0.1 0.32 0.42 0 0.15 0.06 0.18 0.24

0 0 0 0 0 0 206 0 0 0 102 0 0 0 102 0 0 0 102 0 0 0 102 0 0 0 102 0 0 0 102 0 0 0 102 42 0 0 102 0 0 0 102 0 0 0 0 0 0 0 102 0 0 0 0 0 0 0 201 0 0 0 102 0 0 0 0 0 0 0 102 0 8 0.5 102 0 0 0 102 0 0 0 102 0 0 0 0 0 0 0 0 0 0 0 201 0 0 0 0 0 0 0 201 44 0 0 0 0 0 0 102 0 0 0 0 0 0 0 201 0 0 0 201 0 0 0 0 0 0 0 102 0 0 0 201 23 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 201 0 0 0 217 0 8 0.83 102 0 0 0 140 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 35 35 35 35 35 35 35 35 35 35 35 35 35 35

6 6 6 6 6 6 6 6 6 6 6 6 6 6

6 6 6 6 6 6 6 6 6 6 6 6 6 6

25 25 25 25 25 25 25 25 25 25 25 25 25 25

85 85 85 85 85 85 85 85 85 85 85 85 85 85

12 12 12 12 12 12 12 12 12 12 12 12 12 12

5 6 7 7 7 9 9 13 13 13 15 15 18 19

84 83 84 84 84 83 83 82 82 83 84 84 84 82

402 436 0 0 427 404 418 418 418 435 404 421 420 433

2 2 2 2 2 2 2 2 2 2 2 2 2 2

70 52 0 0 0 37 44 0 0 0 39 32 37 18

1 1 1 1 1 1 1 1 2 1 1 1 1 2

54 37 33 53 66 46 87 46 50 80 21 26 80 29

304 0.18 0.29 0 0 0 0.49 0 0.18 0 0 0.16 0 0 0.1

0 0 0 0 0 0 0 0 0 0 0 0 1 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

120 0 102 48 0 0 0 0 0 0 102 0 201 0 102 0 0 0 0 0 120 0 120 45 201 0 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

305

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

35 35 35 35 35 35 35 35 35 35 35 35 35 35 35 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

25 25 25 25 25 25 25 25 25 25 25 25 25 25 25 6 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

12 12 12 12 12 12 12 12 12 12 12 12 12 12 12 10 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

20 20 20 22 24 26 26 27 27 27 27 28 29 29 30 7 1 1 1 1 2 2 2 3 5 5 8 8 8 9 10 13 15 15 16 21 21 21 22 22 25 26

82 82 84 83 84 83 84 83 84 84 84 83 82 82 85 83 84 84 84 84 83 84 84 84 84 84 83 83 83 83 83 83 83 83 84 83 83 84 83 84 83 83

421 421 447 408 404 426 443 438 418 418 418 437 420 421 404 498 470 470 470 470 480 470 483 464 471 485 479 507 507 479 467 462 476 481 476 477 479 491 478 501 485 485

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

66 66 29 70 19 53 28 35 35 52 53 0 25 0 60 47 5 9 9 27 2 33 24 64 81 52 1 3 16 31 47 43 68 50 55 40 42 69 23 58 31 43

1 2 2 2 1 2 2 1 1 1 2 1 1 2 2 1 1 1 1 2 2 1 1 1 1 1 1 1 1 1 1 1 2 1 1 1 1 2 1 1 1 1

69 86 75 63 86 86 76 56 80 75 42 76 87 68 88 50 80 60 75 85 65 70 55 65 50 65 30 75 60 75 75 75 85 80 80 45 20 70 55 75 40 20

0.15 0 0 0.09 0.11 0 0 0.17 0.08 0.22 0.29 0.49 0 0.16 0.21 0 0 0 0 0 0 0.04 0 0 0.14 0.03 0 0 0 0.35 0.25 0.27 0.23 0.25 0.17 0.38 0.36 0 0.15 0 0.07 0.23

49 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 102 102 102 102 102 120 102 201 102 102 0 201 0 102 104 102 102 102 102 102 201 230 230 102 201 102 105 207 102 105 201 104 102 120 120 120 102 102 201 102 102

0 0 0 23 42 0 0 0 0 0 47 0 0 0 46 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 56 48 0 0 0 2 0 48 23 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 36 36 36 36 36 36 36 36 36 36 36 36 36 36

1 1 1 1 1 1 1 1 1 1 1 1 1 1

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

1 1 1 1 1 1 2 2 2 2 2 2 2 2

26 26 26 28 29 30 2 3 4 5 6 6 6 6

84 84 84 84 83 84 84 84 83 83 83 83 83 83

459 476 482 481 475 475 476 489 464 476 472 473 474 474

2 2 2 2 2 2 2 2 2 2 2 2 2 2

16 67 29 62 62 33 41 1 41 28 22 34 3 38

1 2 1 1 1 2 2 1 1 1 2 1 1 1

60 30 80 40 30 70 30 65 70 70 60 85 60 80

306 0.12 0 0 0.35 0.31 0 0 0 0.26 0.2 0.03 0.21 0 0.14

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 0 102 4 230 0 102 33 102 0 201 0 230 0 102 0 102 0 102 42 201 0 230 22 102 0 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

307

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36

1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 3 3 3 3 3 3 3 3

6 7 8 9 9 10 10 13 15 15 15 16 17 19 19 21 22 23 23 24 25 25 25 26 26 28 28 28 28 28 29 29 29 29 2 4 4 5 5 6 6 6

84 84 83 83 83 83 84 83 83 83 84 83 84 83 83 83 83 83 84 83 84 84 84 84 84 83 83 83 84 84 84 84 84 84 84 83 84 83 84 83 83 84

509 510 485 476 480 485 489 464 471 471 488 469 477 487 491 530 523 500 480 533 485 486 487 477 477 471 498 498 469 469 484 484 484 484 462 471 476 480 512 487 507 500

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

13 76 59 58 40 54 32 38 49 71 88 50 28 30 61 64 76 40 17 23 77 60 36 20 73 55 70 75 23 41 1 3 4 6 31 65 25 53 19 31 66 81

1 1 2 1 1 1 1 1 2 2 1 1 2 2 1 0 2 1 1 1 1 1 2 1 2 1 2 1 2 1 2 2 2 1 1 1 1 1 1 1 1 2

80 80 55 80 75 20 45 65 75 50 60 70 70 95 80 60 35 70 80 60 65 35 70 55 70 30 60 55 60 50 65 70 60 75 70 50 80 80 70 85 50 70

0 0 0 0.11 0.09 0.104 0.08 0 0.3 0 0 0 0.35 0 0 0 0 0.12 0 0.42 0 0.34 0.23 0.3 0.12 0.19 0 0 0 0 0 0 0 0 0 0 0.17 0.26 0 0.09 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 0 102 0 102 0 102 57 201 0 102 0 230 0 230 0 102 0 102 0 230 0 225 57 120 0 104 0 228 0 102 0 102 0 201 0 230 0 102 0 102 0 102 0 230 0 102 0 102 0 102 0 102 0 102 0 102 0 102 0 102 0 102 0 102 0 102 0 230 0 102 0 230 0 230 0 201 55 230 0 102 0 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 36 36 36 36 36 36 36 36 36 36 36 36 36 36

1 1 1 1 1 1 1 1 1 1 1 1 1 1

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

3 3 3 3 3 3 3 3 3 3 3 3 3 3

9 10 10 12 13 15 17 18 19 20 21 22 22 22

84 83 83 83 84 84 83 84 83 83 84 84 84 84

476 494 529 463 539 466 528 500 515 532 487 512 513 513

2 2 2 2 2 2 2 2 2 2 2 2 2 2

58 27 44 49 41 64 22 40 36 82 68 32 81 91

2 1 1 1 1 1 1 2 2 2 1 1 1 2

45 65 72 70 70 50 80 65 55 70 70 90 55 55

308 0.31 0 0.16 0 0 0 0.07 0 0.24 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 52 102 0 201 0 230 0 230 0 105 0 105 0 230 0 102 0 102 0 102 0 102 0 102 0 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

309

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36

1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

3 3 3 3 3 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5

24 29 30 31 31 1 1 1 5 10 11 12 16 16 17 17 19 19 19 20 20 21 23 24 25 25 25 1 1 1 1 5 5 6 6 14 14 14 21 25 26 27

83 84 83 84 84 83 83 83 83 83 84 83 83 84 83 84 83 83 84 83 84 83 83 83 83 83 84 83 84 84 84 84 84 84 84 83 83 84 84 84 83 84

521 495 466 494 511 476 476 527 501 465 515 481 500 466 535 490 522 522 514 469 472 524 531 491 521 521 506 517 465 465 468 509 509 477 477 525 525 465 496 483 462 505

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

58 38 86 24 33 37 38 59 70 52 57 22 78 59 47 62 3 4 41 26 24 3 19 21 36 42 33 29 5 8 49 29 50 1 2 27 28 40 48 44 22 17

1 1 2 1 1 2 1 1 2 1 1 2 1 1 1 2 2 1 1 1 1 2 1 1 1 2 1 2 2 2 2 1 1 1 1 1 2 1 1 1 2 2

50 80 75 70 55 65 85 60 70 60 75 85 75 70 60 70 85 90 70 65 75 90 45 50 60 55 30 50 75 75 75 70 65 85 25 40 85 75 80 80 70 85

0 0.31 0 0.24 0.07 0.09 0.38 0.25 0 0.44 0.35 0 0 0.28 0 0.39 0 0 0.23 0.1 0 0 0.08 0.1 0.08 0.09 0.17 0 0 0 0 0.07 0.09 0 0 0.21 0.07 0.04 0.05 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 8 0.006 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 31 0.009 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 102 105 102 230 102 102 140 102 102 104 102 230 102 201 102 102 102 230 102 230 102 201 201 201 201 104 201 102 102 230 104 104 102 102 102 102 230 230 230 102 102

0 0 0 0 54 2 22 0 0 22 0 0 1 48 0 0 0 0 0 0 0 0 0 0 0 0 2 0 0 0 0 0 0 0 0 0 48 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 36 36 36 36 36 36 36 36 36 36 36 36 36 36

1 1 1 1 1 1 1 1 1 1 1 1 1 1

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

5 5 5 5 5 6 6 6 6 6 6 6 6 6

27 28 30 30 31 2 3 5 8 11 13 19 19 24

84 83 83 83 83 83 84 83 84 83 83 83 84 84

505 481 468 520 468 491 471 498 493 496 518 516 471 468

2 2 2 2 2 2 2 2 2 2 2 2 2 2

20 25 60 63 34 67 37 50 44 17 75 23 58 45

1 1 1 1 2 2 1 1 1 1 1 2 2 2

80 60 50 75 70 55 80 50 75 60 50 45 75 65

310 0 0.21 0 0 0.06 0 0.08 0 0.08 0.13 0.3 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 0 102 0 230 0 230 0 201 0 102 23 230 0 230 0 230 0 102 0 102 0 102 0 102 23 230 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

311

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36

1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

6 6 6 6 6 6 7 7 7 7 7 7 7 7 7 7 7 7 7 8 8 8 8 8 8 8 8 8 8 8 8 8 8 9 9 9 9 9 9 9 9 9

24 26 27 29 29 30 2 6 8 12 13 13 17 21 25 27 27 27 31 6 6 7 12 13 17 20 22 23 23 23 24 25 28 1 2 3 4 8 8 15 16 16

84 83 84 84 84 84 84 84 84 83 83 84 84 83 83 84 84 84 83 84 84 84 83 83 84 83 83 83 83 84 84 84 83 84 83 83 84 83 83 84 84 84

492 484 491 481 507 504 498 508 503 538 534 490 470 519 524 469 469 469 519 499 499 466 518 504 469 462 474 479 479 498 469 461 517 472 476 466 507 473 482 501 469 469

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

47 49 85 25 35 25 34 80 27 58 29 63 74 51 21 2 3 21 40 1 1 52 17 3 57 33 28 40 84 35 3 57 29 1 59 66 57 51 74 42 23 24

2 1 1 1 1 1 1 2 1 1 2 1 2 1 2 2 1 2 1 1 1 2 2 1 1 1 1 2 2 1 1 1 1 1 1 2 1 1 1 1 1 1

50 80 50 30 65 25 2 55 75 25 50 75 75 55 35 90 75 70 70 60 60 45 60 65 85 50 70 75 60 65 55 80 80 80 30 40 80 75 45 75 40 45

0.28 0.27 0 0.18 0 0.16 0 0.29 0.15 0 0 0.31 0 0.06 0.15 0 0 0 0 0 0 0.14 0.03 0 0.27 0.23 0.25 0 0 0.04 0 0 0.14 0 0 0.03 0.34 0.05 0 0.25 0.25 0.18

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 104 201 120 230 120 102 102 105 102 102 104 201 201 201 102 102 102 201 102 102 230 230 102 102 102 102 230 230 230 102 230 102 102 230 201 102 102 102 230 102 102

0 0 0 0 0 0 0 48 0 22 0 0 0 0 0 0 0 0 0 0 0 0 42 0 0 0 0 0 0 0 0 22 0 0 22 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 36 36 36 36 36 36 36 36 36 36 36 36 36 36

1 1 1 1 1 1 1 1 1 1 1 1 1 1

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

9 9 9 9 10 10 10 10 10 10 10 10 10 10

23 23 26 27 2 4 5 6 7 7 9 16 17 20

84 84 84 83 83 83 84 84 83 84 83 83 83 84

467 467 476 517 473 485 489 487 468 497 484 485 535 485

2 2 2 2 2 2 2 2 2 2 2 2 2 2

34 76 69 78 57 16 70 36 55 32 53 28 55 18

1 1 1 2 1 1 1 2 1 1 1 1 1 1

90 80 45 55 55 50 65 80 60 75 75 55 80 85

312 0.08 0 0 0 0.33 0 0.32 0.21 0.38 0.22 0.26 0.19 0.09 0.05

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

104 0 104 0 104 0 201 0 102 0 201 0 104 22 102 23 102 22 102 0 102 0 102 0 201 0 230 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

313

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36

1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

10 10 10 10 10 10 10 10 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 11 12 12 12 12 12 12 12 12 12 12 12 12

27 27 27 28 28 29 30 30 4 6 7 7 9 9 10 12 14 14 15 17 18 22 23 24 24 26 26 26 27 30 1 1 2 3 4 4 4 4 5 5 5 8

83 83 83 84 84 83 83 84 84 84 84 84 83 83 83 83 83 84 83 83 83 84 84 83 84 83 83 83 83 83 83 84 83 83 83 83 83 83 83 83 84 84

476 490 490 482 482 521 515 478 496 518 479 479 474 486 504 487 523 471 468 473 500 480 517 483 482 472 536 536 471 485 495 478 470 469 468 485 517 517 467 522 516 502

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

31 4 6 6 8 23 57 56 40 44 73 98 2 74 42 76 2 44 57 35 81 47 47 24 37 56 32 33 21 40 36 70 19 32 17 34 17 17 28 39 33 24

1 1 1 1 1 2 1 1 1 1 2 2 2 1 1 1 2 1 1 1 1 1 1 1 1 1 2 1 2 1 1 2 1 1 2 2 1 2 2 1 2 1

65 65 70 75 75 65 70 80 25 70 95 40 75 50 55 55 80 50 60 85 40 55 65 85 95 75 55 60 65 75 90 80 75 60 65 80 80 75 50 65 90 80

0 0 0 0 0 0 0.26 0.07 0.19 0.11 0.2 0 0 0.23 0.24 0 0 0.38 0 0 0 0.4 0 0.03 0.23 0 0.26 0.23 0 0 0.15 0.27 0 0.18 0 0.14 0.05 0 0.08 0.19 0.28 0.14

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 9 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

230 0 102 0 102 0 104 0 104 0 201 0 104 0 105 0 120 0 230 22 104 0 102 0 102 0 102 0 120 0 104 0 104 0 102 0 102 0 102 0 201 0 102 0 201 42 201 0 102 0 201 0 102 0 102 0 201 0 232 0 104 22 104 0 201 0 102 0 102 0 230 0 201 0 201 0 102 0 104 0 104 0 104 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 36 36 36 36 36 36 36 36 36 36 36 36 36 36

1 1 1 1 1 1 1 1 1 1 1 1 1 1

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

12 12 12 12 12 12 12 12 12 12 12 12 12 12

10 10 10 11 11 11 19 21 22 23 23 23 24 25

83 83 83 83 84 84 83 83 84 83 83 84 83 83

463 472 472 526 473 496 466 465 498 461 464 481 463 462

2 2 2 2 2 2 2 2 2 2 2 2 2 2

44 40 57 34 79 70 84 31 28 48 65 38 30 28

1 2 1 1 1 2 1 1 1 1 1 2 1 1

70 80 40 80 55 30 25 70 90 75 80 75 35 75

314 0 0.25 0.23 0 0 0 0.07 0.25 0.11 0.27 0 0 0.22 0.22

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

230 0 102 0 102 56 230 0 104 0 219 0 102 0 102 0 104 0 105 0 102 0 104 0 102 51 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

315

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36

1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

7 7 7 7 7 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8

16 16 16 16 16 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

12 12 12 12 12 0 2 3 5 7 7 10 13 16 17 17 18 18 19 19 20 20 22 22 23 26 27 28 28 29 29 32 32 34 34 39 40 42 42 45 47 48

25 25 25 28 31 23 70 82 34 4 71 38 80 35 41 49 22 82 5 82 37 81 0 7 32 7 5 26 80 26 45 17 79 1 46 83 16 32 60 8 6 5

83 83 83 83 83 84 84 84 84 83 84 84 83 84 84 83 81 84 83 83 83 83 83 84 83 83 83 83 84 83 83 83 83 83 83 83 84 84 84 83 83 84

479 479 479 462 487 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

2 5 62 32 71 21 71 68 29 25 65 66 70 27 32 70 3 21 69 53 38 5 63 70 39 1 62 72 25 66 36 71 36 2 21 40 44 3 32 64 30 56

2 1 1 1 1 1 2 2 1 1 1 1 1 1 1 2 2 1 1 1 1 1 2 1 1 1 1 2 1 1 2 1 1 1 1 1 1 1 1 2 2 1

30 40 70 60 70 70 20 30 45 20 55 50 70 55 90 40 75 80 20 25 40 25 80 35 75 65 80 40 75 50 55 35 20 50 85 75 70 55 80 75 70 70

0 0 0 0.25 0.33 0.13 0 0 0.16 0.17 0.25 0.31 0.27 0.15 0.02 0.26 0 0.22 0.05 0 0 0 0.06 0 0 0 0.3 0 0.25 0 0 0.32 0.2 0 0.11 0 0.05 0 0.13 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 102 102 105 104 102 0 201 102 102 102 102 102 102 102 102 102 102 0 0 201 102 201 102 201 201 102 102 102 102 201 102 102 102 201 201 201 102 201 102 201 201

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 36 36 36 36 36 36 36 36 36 36 36 36 36 36

1 1 1 1 1 1 1 1 1 1 1 1 1 1

8 8 8 8 8 8 8 8 8 8 8 8 8 8

18 18 18 18 18 18 18 18 18 18 18 18 18 18

85 85 85 85 85 85 85 85 85 85 85 85 85 85

49 50 50 51 52 53 54 56 57 59 62 65 65 66

6 1 28 23 1 84 80 5 84 0 6 28 63 2

84 83 84 83 84 83 84 84 83 84 83 84 84 84

999 999 999 999 999 999 999 999 999 999 999 999 999 999

2 2 2 2 2 2 2 2 2 2 2 2 2 2

24 11 74 39 79 40 30 63 66 7 52 24 57 4

1 2 2 1 1 1 1 2 2 2 1 1 2 2

65 75 35 55 50 50 70 60 55 75 25 45 55 20

316 0.27 0 0 0.26 0.19 0.35 0.24 0.18 0.02 0 0.21 0.18 0.25 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 102 102 102 102 102 102 102 201 102 102 102 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

317

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 36 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37

1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 18 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

69 70 71 71 72 74 75 76 78 79 82 82 83 83 83 83 86 86 87 88 92 97 97 98 98 99 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 2 36 74 6 79 3 38 85 81 24 76 1 24 25 29 0 83 36 34 80 1 7 0 83 85 2 2 3 3 4 6 9 9 10 14 14 15 17 18 19 19

83 84 83 73 83 83 84 83 84 83 83 83 83 83 84 84 83 83 83 84 84 83 84 83 84 84 77 85 79 81 84 85 82 84 85 80 84 78 82 77 76 79

999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 999 545 543 540 540 540 545 548 543 543 545 540 542 543 541 542 540

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

30 47 48 3 60 47 30 55 21 32 59 76 82 54 26 36 10 66 38 48 44 58 53 85 39 13 55 2 64 32 4 79 28 38 47 11 39 0 3 5 76 28

2 1 1 1 1 1 2 1 1 1 2 2 2 1 1 1 2 2 1 1 1 1 2 2 1 1 2 2 1 2 2 2 2 2 1 1 1 0 1 2 2 2

85 80 45 60 25 70 70 50 30 75 55 60 70 20 65 45 70 85 70 25 70 50 30 40 20 70 56 79 60 53 80 62 79 36 47 79 80 80 44 75 82 47

0.29 0.23 0.18 0 0.24 0.26 0 0 0 0 0 0.13 0 0.14 0.14 0.12 0 0 0.19 0 0.08 0 0 0 0.16 0 0.21 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 102 0 0 102 0 0 102 0 0 102 0 0 102 0 0 102 0 0 102 0 0 102 0 0 201 0 0 201 0 0 102 0 0 102 0 0 102 0 0 201 0 0 201 0 0 102 0 0 102 0 0 201 0 0 102 0 0 201 0 0 201 0 0 102 0 0 102 0 0 0 0 0 0 0 0 102 0 0 104 46 0.18 102 0 0 201 0 0 0 46 0 102 46 0 102 46 0 102 46 0 102 46 0.08 102 46 0 104 995 0 0 18 0 201 46 0 102 998 0 102 0 0 104 54 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

0 0 0 0 0 0 0 0 0 0 0 0 0 0

19 20 21 23 24 25 26 26 27 27 28 28 30 33

85 78 82 81 85 80 76 81 76 79 77 80 77 77

540 546 545 540 540 545 540 543 544 540 542 540 540 545

2 2 2 2 2 2 2 2 2 2 2 2 2 2

80 20 0 56 17 39 30 10 35 0 91 27 62 11

2 1 1 1 1 1 1 1 1 2 2 1 1 1

59 73 74 48 67 54 60 73 78 14 57 39 73 36

318 0 0 0 0 0 0 0 0 0 0 0 0 0.05 0

46 0.87 102 0 0 201 0 0 0 0 0 0 0 0 0 46 0 102 0 0 230 46 0 104 0 0 201 0 0 120 0 0 201 0 0 0 51 0 201 0 0 219

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

319

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

35 44 48 48 53 54 60 71 72 75 76 79 84 92 93 99 0 2 3 3 5 6 6 6 7 8 8 9 11 12 12 13 13 14 15 17 18 19 21 23 26 26

79 79 78 82 82 81 79 83 82 82 84 84 82 84 84 83 76 78 77 84 82 76 78 81 83 79 84 81 77 79 85 78 80 80 79 82 77 76 79 81 81 81

545 541 540 545 542 545 540 545 548 543 540 548 540 545 548 542 540 540 545 543 540 540 540 546 543 545 542 540 540 540 540 541 540 545 547 545 541 542 541 540 543 543

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

10 16 65 0 16 25 35 64 63 30 37 33 51 85 40 37 42 78 18 46 51 43 0 57 56 37 19 56 15 22 28 25 48 38 19 67 4 78 25 24 12 12

2 2 1 0 1 2 1 1 2 1 1 1 1 1 1 2 2 1 2 1 1 1 1 1 2 1 2 1 2 1 1 1 1 1 1 1 2 1 1 1 0 2

72 0.8 22 60 74 38 5 51 80 44 72 30 65 40 61 56 74 81 75 62 84 84 67 23 43 74 72 65 75 72 0.17 69 75 74 28 48 80 78 50 52 62 62

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0.22 0 0 0 0 0 0 0 0 0 0 0 0.05 0 0 0 0 0 0.22 0 0 0 0 0 0 0

0 0 46 0 46 46 55 46 0 46 62 0 0 21 46 0 0 0 0 0 0 0 0 46 46 0 46 1 0 46 0 0 0 46 0 58 998 0 0 0 0 0

0 0 0.3 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 104 0 102 102 0 102 0 102 0 0 0 0 102 0 230 230 120 0 0 230 201 102 102 230 102 0 104 102 0 230 0 104 230 0 102 104 0 0 0 104

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

1 1 1 1 1 1 1 1 1 1 1 1 1 1

27 27 29 30 33 41 44 47 48 51 51 53 60 61

78 79 78 81 77 80 81 78 82 82 82 82 79 81

547 540 540 545 545 545 542 547 545 545 545 542 540 545

2 2 2 2 2 2 2 2 2 2 2 2 2 2

19 0 87 51 9 63 56 0 0 1 1 50 49 86

1 1 1 0 2 1 2 1 2 2 2 1 1 2

75 24 53 64 14 17 6 23 50 60 60 39 5.7 53

320 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 56 21 46 0 46 46 46 0 46

0 0 0 0 0 0 0 0 0 0 0 0 0 0

201 120 230 0 219 0 0 104 0 102 102 102 0 102

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

321

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

1 1 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

67 76 79 0 0 3 4 4 6 7 7 8 8 10 10 11 14 14 15 15 17 19 20 20 21 23 24 26 27 29 34 34 35 42 45 48 51 51 53 54 58 61

82 83 84 76 77 77 77 85 85 78 79 78 79 84 85 81 80 81 77 79 79 81 81 81 76 77 79 78 78 76 82 84 81 80 78 82 82 82 82 79 81 81

545 540 548 540 540 545 541 544 543 546 545 540 540 545 543 545 545 545 543 540 545 545 542 542 540 540 543 543 541 540 543 548 545 540 540 545 545 545 542 545 545 542

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

40 47 25 31 34 19 33 71 60 40 51 34 61 43 26 50 2 20 0 28 14 60 23 23 47 28 25 0 31 57 20 56 51 20 0 0 4 4 18 81 44 33

2 1 2 1 1 1 1 2 1 2 1 1 1 1 1 1 2 1 1 1 1 2 0 1 1 2 1 1 2 1 1 1 1 1 1 0 1 1 1 2 1 1

10 74 65 49 57 78 75 80 35 44 64 26 60 58 80 5 55 56 33 61 38 62 8 8 64 81 47 60 24 85 72 80 14 81 3 40 60 60 71 61 40 72

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0.12 0 0 0 0 0 0 0 0.06 0 0 0 0 0 0 0 0

46 0 102 0 46 0 102 0 0 0 0 0 0 0 230 0 0 0 201 0 0 0 120 0 0 0 201 0 0 0 0 0 46 0 102 0 0 0 104 0 0 0 0 0 46 0 104 0 0 0 0 19 0 0 0 0 46 0.85 102 0 0 0 0 0 46 0 104 0 0 0 0 0 46 0 114 0 53 0 0 0 46 0 104 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 230 0 0 0 213 0 0 0 104 0 0 0 120 0 0 0 201 0 0 0 201 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 241 0 0 0 0 0 46 0 102 0 46 0 102 0 46 0 102 0 0 0 104 0 0 0 0 0 997 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

2 2 2 2 2 2 2 2 2 2 3 3 3 3

69 73 74 76 79 82 84 86 87 98 0 0 3 4

82 81 84 83 83 83 84 84 82 82 76 84 77 78

543 547 543 540 545 543 543 545 543 540 540 543 540 540

2 2 2 2 2 2 2 2 2 2 2 2 2 2

34 28 31 26 12 73 0 6 63 36 57 21 21 0

1 2 2 2 1 2 1 1 2 2 1 1 1 1

64 23 25 80 18 41 28 80 37 68 48 78 23 74

322 0 0 0 0 0 0 0 0 0 0 0.06 0 0.09 0

0 55 46 46 46 46 46 46 0 46 0 46 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 102 102 102 102 102 102 0 102 230 102 104 104

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

323

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 4

6 8 8 9 10 11 11 11 15 16 17 19 20 21 21 27 27 29 30 33 33 34 35 35 37 43 44 47 48 53 54 55 57 64 67 69 73 74 79 85 86 0

82 78 82 84 80 78 80 84 79 76 79 85 81 78 78 78 82 76 77 77 84 82 78 81 83 83 80 82 82 82 79 81 80 81 81 83 81 82 83 84 84 81

540 540 545 546 540 546 547 543 545 540 545 540 542 540 540 540 545 540 540 542 548 543 545 545 546 542 547 545 545 542 544 547 545 545 542 542 545 543 545 542 545 540

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

49 9 22 41 60 10 34 24 17 49 8 46 18 42 51 0 0 0 70 21 42 0 72 49 36 72 28 0 0 81 26 0 56 22 34 60 42 29 4 24 9 39

1 2 2 1 2 2 1 2 1 2 1 1 1 1 1 1 2 2 2 1 2 2 1 2 1 2 1 0 0 1 1 1 1 1 1 1 1 1 1 1 1 1

77 53 72 55 41 64 39 53 52 66 6 75 5 20 13 9 77 63 90 90 60 70 77 9 35 70 10 20 10 32 86 40 12 85 52 65 86 6 15 80 80 42

0 0 0 0 0 0 0 0 0 0.13 0 0 0 0 0 0 0 0 0.09 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

996 46 0 46 46 0 0 46 46 0 46 0 0 46 46 46 0 0 0 0 46 46 0 46 0 46 0 0 0 46 0 46 0 0 0 46 0 59 46 46 46 0

0 0 0 0 0 0 0 0 0 0 0 0 0 4.7 0.6 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 104 0 102 102 104 0 102 114 230 104 0 0 104 104 102 0 201 104 104 102 102 228 102 0 102 0 0 0 102 230 102 0 0 0 102 0 0 102 102 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

4 4 4 4 4 4 4 4 4 4 4 4 4 4

1 3 4 5 5 8 8 8 10 10 11 13 15 15

77 77 78 77 85 78 81 83 78 85 78 84 77 79

540 542 540 548 543 540 540 545 540 543 546 545 543 545

2 2 2 2 2 2 2 2 2 2 2 2 2 2

42 21 0 30 60 7 39 74 39 42 9 0 0 18

1 1 2 1 1 2 2 1 2 1 1 2 1 1

22 63 77 76 5 54 80 55 83 74 67 63 57 72

324 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 201 0 0 201 0 0 104 0 0 201 46 0 102 46 0 104 0 0 0 0 0 0 0 0 230 46 0.68 102 0 0 104 46 0 102 46 0 114 46 0 114

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

325

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 5 5 5 5 5 5 5 5 5 5

16 17 17 17 19 21 22 23 33 34 34 38 40 41 41 47 47 48 48 49 53 57 60 63 65 65 66 71 79 86 95 98 0 2 2 3 3 4 4 5 7 8

85 77 79 82 83 83 84 81 84 80 82 82 78 82 82 78 84 82 84 84 82 81 84 80 80 81 82 82 83 84 82 83 84 78 82 77 78 78 84 84 79 84

540 541 540 540 542 548 543 540 548 540 543 545 544 540 540 547 543 545 543 540 542 545 545 548 548 546 542 548 545 545 540 542 544 540 540 542 543 540 545 540 545 540

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

38 18 36 72 39 4 30 35 11 32 7 40 1 55 55 25 0 0 61 40 15 43 31 30 26 0 6 74 32 34 20 26 45 0 0 39 0 0 4 83 3 17

2 1 1 1 2 2 1 2 1 1 1 1 2 2 2 2 1 0 1 2 1 2 1 2 1 1 2 1 2 1 2 2 1 1 1 2 1 2 1 2 2 2

42 82 61 16 53 13 4 81 66 70 79 84 53 0.01 0.01 59 4 60 4 74 78 62 55 80 22 22 58 17 58 80 56 15 80 69 61 56 18 70 78 0 78 65

0 0 0 0 0 0 0 0 0 0.18 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

46 0.03 102 998 0 102 0 0 230 0 0 0 0 0 0 46 0 102 0 0 0 0 0 0 46 0 102 0 0 0 46 0 102 0 0 0 46 3.3 104 0 0 0 0 0 0 46 0 104 0 0 0 0 0 0 0 0 0 0 0 0 46 0 102 46 0 102 0 0 0 0 0 0 0 0 0 0 0 0 46 0 102 0 0 0 46 0 102 46 0 102 0 0 0 0 0 0 56 0 0 0 0 201 46 0 102 0 0 201 46 0 241 0 0 104 46 0 102 46 0 102 0 0 104 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

5 5 5 5 5 5 5 5 5 5 5 5 5 5

9 10 11 11 12 13 13 13 13 17 20 21 21 22

76 81 78 83 81 77 80 82 83 77 81 77 83 78

540 540 540 546 540 546 540 545 540 541 540 540 548 541

2 2 2 2 2 2 2 2 2 2 2 2 2 2

18 56 42 11 1 48 20 0 31 6 17 65 5 17

2 2 1 2 0 2 1 1 2 1 1 2 2 1

81 49 88 62 13 0 2 41 55 82 82 82 28 72

326 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 46 0 0 46 0 998 0 0 46 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

230 0 230 0 102 228 0 102 0 102 0 201 102 201

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

327

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6 6

23 28 31 31 33 35 40 43 43 45 46 48 57 57 58 61 63 64 65 72 73 76 83 86 89 94 0 1 1 4 4 5 7 9 9 9 11 12 13 13 16 17

77 81 83 84 84 83 78 82 82 84 80 78 81 84 80 81 80 80 84 82 83 84 83 84 83 82 79 84 85 77 84 76 78 76 80 85 82 82 83 84 82 77

540 542 540 548 548 543 544 547 547 542 544 540 545 545 543 540 548 540 540 540 540 542 540 545 540 548 548 540 540 545 545 540 540 540 540 545 540 548 545 540 542 541

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

27 33 25 2 40 1 21 20 20 50 0 19 9 58 43 37 30 57 54 54 64 27 43 61 70 39 17 29 33 0 2 35 26 36 2 27 82 39 50 15 2 6

1 1 2 2 1 2 1 1 1 2 1 2 1 1 1 1 1 1 1 1 1 1 1 2 2 1 1 1 2 1 1 2 1 1 1 1 1 2 2 2 1 2

70 63 62 33 57 29 53 73 77 77 58 56 74 10 5 1.2 80 80 10 63 81 80 56 48 80 84 52 56 0.01 40 63 55 60 93 81 9.5 68 81 46 80 64 76

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0.08 0 0 0 0 0 0 0 0

0 57 60 46 46 46 46 0 0 0 0 0 46 0 0 0 0 46 0 0 0 46 46 46 46 0 46 61 46 0 46 0 0 0 46 0 46 46 0 30 46 998

0 0 0 0 0 0 4.7 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

201 0 0 102 102 102 104 0 0 0 0 201 102 0 0 0 0 102 0 0 0 102 102 102 102 0 104 0 102 104 102 219 230 230 102 0 102 102 0 0 102 102

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

6 6 6 6 6 6 6 6 6 6 6 6 6 6

24 24 24 25 28 29 29 31 33 34 35 42 48 48

77 83 84 81 78 76 84 83 78 79 78 80 78 82

541 547 540 543 547 540 548 540 540 547 547 541 540 545

2 2 2 2 2 2 2 2 2 2 2 2 2 2

47 55 54 16 65 58 21 7 40 50 35 0 19 0

2 1 1 1 2 2 1 1 2 1 1 1 1 0

6 78 68 60 51 67 64 64 47 61 75 55 67 50

328 0.3 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 46 0 0 0 0 60 50 0 0 0 0 46

0 0 0 0 0 0 0 0 0 0 0 0 0 0

104 0 102 0 104 201 0 0 201 0 0 0 201 102

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

329

Lab CO

Submission Exposure Date Adress Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

6 6 6 6 6 6 6 6 6 6 6 6 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

51 52 55 57 61 63 68 71 73 82 84 94 0 0 1 2 2 3 7 8 10 11 11 12 17 19 20 20 21 22 22 23 23 25 25 25 27 27 27 30 33 37

82 79 84 81 82 80 81 83 81 82 83 82 77 80 80 77 85 82 78 81 76 84 85 81 77 82 77 77 76 78 81 78 82 76 81 82 77 81 83 77 79 83

545 547 545 540 547 548 544 545 540 542 545 548 540 540 540 540 547 540 541 540 540 540 540 545 541 545 540 540 540 540 540 540 548 540 543 540 540 547 543 542 541 545

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

0 51 20 60 23 10 22 20 29 28 1 24 27 77 34 61 48 0 22 38 35 33 82 10 10 0 31 31 60 0 1 22 0 27 30 5 64 58 49 23 29 52

0 2 1 2 1 2 1 1 1 1 1 2 1 2 1 2 2 2 1 1 1 1 1 1 2 1 1 1 1 1 2 1 1 1 2 1 1 1 1 1 1 1

10 63 67 50 70 80 72 3 72 65 19 85 57 68 55 35 78 66 38 54 86 64 54 36 77 58 88 88 63 72 57 67 70 78 70 65 54 15 48 82 77 58

0 0.25 0 0 0 0 0 0 0 0 0 0 0 0.32 0 0 0 0 0 0 0.07 0 0 0 0 0 0.05 0.05 0 0 0 0 0 0 0 0 0 0 0 0.05 0 0

0 0 0 46 1.9 102 0 0 0 0 0 0 46 0 102 0 0 0 0 0 0 46 0 102 0 0 0 0 0 0 46 0 102 0 0 0 0 0 201 0 0 0 0 0 0 0 0 201 46 0 102 0 0 0 46 0 104 0 0 0 0 0 230 0 0 0 46 0.12 102 46 0 102 998 0 102 0 0 0 0 0 201 49 0 201 0 0 230 0 0 228 46 0 102 46 0 102 46 0 102 0 0 201 46 0 104 0 0 0 0 0 104 0 0 0 46 0 102 0 0 201 0 0 0 46 0 102

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

7 7 7 7 7 7 7 7 7 7 7 7 7 7

40 47 48 49 50 54 55 58 60 60 63 68 73 85

84 82 82 79 80 83 81 80 80 80 80 82 81 82

548 545 545 545 548 543 540 540 540 540 548 545 545 540

2 2 2 2 2 2 2 2 2 2 2 2 2 2

28 0 0 22 27 0 5 22 67 67 12 41 37 59

1 0 0 1 2 1 2 1 0 1 2 2 2 0

79 20 40 41 12 46 51 53 42 42 80 55 66 51

330 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 46 46 46 0 0 0 52 21 0

0 0 0 0 0 0 0 0 0 0 0 102 0 102 0 102 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

331

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

7 7 7 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8 8

86 88 93 0 0 1 1 1 4 7 9 10 10 11 12 14 16 17 18 20 20 21 22 22 24 24 25 25 25 25 28 28 35 35 40 46 47 47 49 53 54 64

84 84 83 76 85 76 79 80 77 82 80 78 80 84 83 79 85 77 81 77 82 78 80 84 80 81 79 81 82 83 78 84 82 84 78 82 82 84 79 81 83 81

545 546 543 541 545 541 540 540 545 548 540 546 540 540 543 544 545 541 545 540 540 540 544 543 540 543 540 543 540 540 547 547 544 540 540 545 545 542 545 545 543 545

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

5 21 25 14 79 10 24 45 0 25 54 66 56 30 17 42 45 9 27 48 0 31 66 86 42 42 29 12 22 44 50 29 32 59 44 49 0 16 20 43 0 41

2 2 1 1 1 1 2 1 1 1 1 1 1 2 1 1 1 2 1 2 1 1 1 1 1 0 1 2 1 1 1 1 1 1 2 1 0 1 2 1 2 1

80 16 57 47 55 42 64 59 15 66 3.5 75 40 58 47 52 57 81 6 91 66 68 81 73 63 65 26 68 49 52 65 71 79 80 61 61 20 69 45 24 59 63

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

46 0 0 0 0 0 46 0 0 46 0 0 0 0 0 0 0 998 0 0 46 6 49 46 0 0 21 0 0 46 0 21 0 0 0 0 0 0 0 46 46 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 0 0 104 0 104 104 0 104 102 0 114 0 0 0 201 0 102 0 201 102 201 0 102 0 0 0 104 0 102 201 0 0 0 201 0 0 0 0 102 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85

8 8 8 8 8 8 8 9 9 9 9 9 9 9

65 68 74 86 92 93 94 0 2 4 5 5 7 7

80 82 83 84 83 84 84 85 85 77 77 84 82 83

540 540 545 545 540 540 545 545 545 545 540 542 548 547

2 2 2 2 2 2 2 2 2 2 2 2 2 2

50 46 35 76 38 42 83 64 74 0 56 68 73 53

1 2 1 2 2 1 1 2 2 1 1 1 2 1

72 67 70 80 86 14 31 40 67 32 51 59 80 6

332 0 0 0 0 0 0 0 0 0 0 0.28 0 0 0

46 0 0 46 46 0 53 0 46 0 0 2 46 8

0 0 0 0 0 0 0 0 0 0 0 0 0 0

102 0 0 102 102 0 0 0 102 104 201 0 102 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

333

Lab CO

Submission Exposure Date Address Surv Age Sex COHb Ethano Drug Drug CO Dis. Phys Date Method Mnth Day Year Mnth Day Year Code Type Amnt Srce Cond

37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37 37

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7 7

16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16 16

85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85 85

9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9 9

10 11 11 11 12 12 12 12 17 18 22 23 25 25 25 25 25 31 31 32 47 47 48 49 53 62 63 65 66 86 87 95 98

76 80 81 82 77 81 84 85 76 76 83 76 78 79 81 82 82 80 81 77 82 84 78 82 81 82 81 80 82 84 82 83 83

540 545 541 548 541 545 540 542 540 541 545 543 545 545 543 540 545 545 545 545 545 542 547 545 545 547 540 540 545 545 547 540 542

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

29 33 16 0 25 55 53 60 3 58 3 64 52 35 8 54 0 23 27 33 0 19 50 0 7 26 87 38 46 57 40 37 42

1 1 1 1 1 1 1 2 1 2 1 2 2 1 1 2 0 1 0 2 0 1 1 0 1 1 2 1 1 1 1 1 1

56 68 47 72 70 44 80 80 82 89 15 81 4 13 66 39 39 23 86 80 88 61 72 20 45 51 73 80 17 58 32 70 50

0.33 0 0 0 0 0 0 0 0.04 0.21 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 46 0 0 0 0 0 0 46 999 10 0 46 0 0 46 0 0 46 0 0 0 46 46 0 46 46 46 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

140 0 0 102 201 0 0 0 230 230 102 201 0 104 102 0 0 102 0 219 102 0 201 0 102 102 0 102 102 102 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Appendix A: Tables for the data base in chapter 6

334

EXPLANATION OF ABBREVIATIONS Lab: Laboratory submitting data (see chapter 6) CO Method: Method of analysis of carbon monoxide Submission Date: Day data was obtained (Month/Day/Year) Exposure Date: Day victim inhaled CO (Month/Day/Year) Addres Code: code for city, county and state for CO exposure Surv: Survival status after fire (2 dead, 1 alive, 0, unknown) Age: Age of victim in years (<2 is coded 1) Sex: Sex of victim (1 male, 2 female, 3 unknown) COHb: %COHb measured Ethanol: % Ethanol determined Drug Type: drugs measured in blood analysis HCN: code 46, in mg/L; cocaine: in mg/100 cm3; MetHb: 47 O2, CO2: 45; Lidocaine: 5, 39, 54; codes 5, 39, 45, 47 and 54 were not used Drug Amnt: Amount of drug in previous column measured in blood CO Srce: Source of CO (100–199 fire, 200–299 non fire, 0 unknown) Dis.: Preexisting disease Phys Cond: Physical condition, i.e. appearance (4 poor, obese, 3 fair, a little overweight, 2 good, normal appearance, 1 excellent, peak athletic condition, no weight problem, 0 unknown) CO METHOD CODES 1 Ultraviolet spetrophotometer 3 Gas-chromatograph 4 Van Slyke manometer 5 Case file abstracts 6 CO oxymeter IL-282 7 Ultraviolet spectrophotometer and gas chromatograph 8 Microdiffusion 9 Blood analysis 10 CO oxymeter and gas chromatograph 11 CO oxymeter/ultraviolet spectrophotometer 12 Cyanmethemoglobin

Most of the labs measured CO by means of spectrophotometry, but one lab used exclusively gas chromatography

Appendix A: Tables for the data base in chapter 6

335

SOURCE OF CARBON MONOXIDE CODES 102: Fire

201: Auto exhaust

104: House fire

206: Water heater vent

105: House trailer fire

208: Natural gas

115: Electric house fire

209: Coal stove

118: Arson fire

212: Kerosene stove

120: Automobile fire

213: Charcoal

124: House bar fire

217: Wood stove

131: Shed fire

219: Gas stove

133: Barn fire

225: Gas heater

140: Mattress fire

228: Suicide

DISEASE CODES 1. Emphysema

22. Alcoholism

2. Cardiomegaly

23. Arteriosclerotic cardiovascular disease

3. Arteriosclerotic heart disease

24. Lung cancer

4. Micronodular cirrhosis of the liver

25. Diabetes, alcoholism

5. PID pulmonary disease

26. Ischemic peripheral vascular disease & depression

6. Alcoholism, sexual deviate 7. Severe cirrhosis 8. Depression 9. Prostate cancer 10. Asthma, hypertension 11. Invalid, mental health patient

27. Fatty liver, intense vascular congestion 28. Bronchitis 29. Arteriosclerotic cardiovascular disease

12. Chronic depression

30. Chronic gastritis

13. Cardiovascular

31. Stroke

14. Arteriosclerotic cardiovascular disease, recent myocardial infarction

32. Arteriosclerosis and gastritis 33. Heart and lung disease 34. Liver disease

15. Recent myocardial infarction

35. Kidney disease

16. Colon cancer

36. Alcoholism & depression

Appendix A: Tables for the data base in chapter 6

17. Morbid obesity

336

37. Alcoholism & heart disease

18. Leukemia, arteriosclerotic cardiovascular disease, 38. Biliary cirrhosis blood disorder 39. Arteriosclerotic coronary artery disease 19. Heart disease

40. Seizures, hypoglycemia, chest pain

20. Diabetes

41. Mechanical asphyxiation

21. Cancer

42. Pulmonary edema

45. Cerebral edema

52. Arteriosclerosis, vascular disease and alcoholism

47. Adhesion, left lung

54. Ulcer

48. Arteriosclerosis

55. Myocardia hypertrophy

49. Meningitis

56. Cardiomegaly, emphysema

51. Hepatitis

57. Alcoholism & emphysema

CODES FOR DRUGS OTHER THAN ALCOHOL 1. Acetaminophen

31. Butalbital

2. Caffeine

32. Chlorpheniramine

3. Propoxyphene

33. Isopropanol

4. Benzodiazepines

34. Methadone

5. Lidocaine

35. Codeine and nicotine

6. Diazepam

36. Mezlocillin

7. Salicylates and nicotine

37. Nortriptylene and amitriptyline

8. Phenobarbital

38. Quinine and nortriptyline

9. Acetone & isopropanol

39. Lidocaine, codeine and doxepin/nordox

10. Amitriptyline

40. Drug for treatment of mood disorders

11. Diphenyl hydantoin

41. Acetaminophen and nicotine

12. Diphenhydramin

42. Caffeine and nicotine

13. Metoprolol

43. Amoxapine

14. Codeine

44. Methadone and nicotine

15. Morphine

45. Oxygen and carbon dioxide

16. Opiates (sleeping pills)

46. Hydrogen cyanide (HCN)

17. Cannabinoids

47. Methemoglobin (Met-Hb)

18. Chloridiazepoxide (tranquilizers)

48. Cocaine and chlorpheniramine

Appendix A: Tables for the data base in chapter 6

337

19. N - DES methyldiazepam

49. Diazepam and nordiazepam

20. Chlorpromazine

50. Nordiazepam

21. Salicylate (aspirin-like drug)

51. Amitriptyline and perphenazine

22. Salicylate (aspirin-like drug)

52. Chlordiazepoxide & flurazepam (sedative)

23. Chlorpromazine, amitryptyline

53. Secobarbital

24. Methanol

54. Lidocaine, thiothixene and acetaminophen

25. Nicotine

55. Glutethimide

26. Phenytoin

56. Cyanide and phenobarbital

28. Zyloprim, lopressor, atramid

57. Caffeine and amphetamines

29. Doxylamine

58. Cyanide and phenytoin

30. Cocaine

59. Quinine, morphine, codeine & cocaine

APPENDIX B DATA BASE USED BY THE CASE WESTERN RESERVE UNIVERSITY (CWRU) CWRU Data Base—All Cases between 1938 and 1949 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1938–1949 1

1

1

2

1

1

4

99

99

0

0

2

39

3

1

1

1

1

19

99

0

0

3

24

1

1

1

1

1

12

99

0

0

4

38

2

1

1

2

2

3

99

0

0

5

53

1

1

1

1

1

0

99

0

0

6

26

1

1

1

1

1

0

99

0

0

7

49

1

2

1

1

1

0

99

0

0

8

58

1

1

1

2

2

0

99

0

0

9

53

1

1

1

1

1

0

99

0

0

10

45

1

2

1

1

1

27

95

0

0

11

27

1

1

1

1

1

24

95

0

0

12

31

1

1

1

1

1

20

95

0

0

13

30

1

1

1

1

1

20

95

0

0

14

34

1

1

1

1

1

20

95

0

0

15

26

1

1

1

1

1

18

95

0

0

16

53

1

1

1

1

2

17

95

0

1

17

48

1

1

1

1

1

17

95

0

0

18

51

1

1

1

1

1

16

95

0

0

19

32

1

1

1

2

2

14

95

0

0

20

43

1

1

1

1

1

14

95

0

0

21

33

1

2

1

1

1

9

95

0

0

Appendix B: Tables for the data base in chapter 7

339

22

34

1

1

1

1

2

8

95

0

0

23

62

1

1

1

1

1

6

95

0

0

24

53

1

1

1

1

1

0

95

0

0

25

41

1

1

1

1

2

0

95

0

0

26

28

1

1

1

1

1

0

95

0

0

27

54

1

1

1

1

2

0

95

0

0

28

56

1

2

1

1

1

0

95

0

0

29

54

1

1

1

1

1

0

95

0

0

30

38

1

1

1

1

1

0

95

0

0

31

50

1

1

1

1

1

0

95

0

0

32

54

1

1

1

2

2

0

95

0

0

33

47

1

1

1

1

1

0

95

0

0

34

58

1

1

1

1

1

0

95

0

0

35

49

1

1

1

1

1

0

95

0

0

36

70

1

1

1

1

1

0

95

0

0

37

50

1

1

1

1

1

0

95

0

0

38

53

1

1

1

1

1

0

95

0

0

39

45

1

1

1

1

1

0

95

0

0

40

39

1

1

1

1

1

0

95

0

0

41

33

1

1

1

1

2

0

95

0

0

42

19

1

1

1

1

2

0

95

0

0

43

34

1

1

1

1

1

0

95

0

0

44

40

1

1

1

1

1

0

95

0

0

45

51

1

1

1

1

1

0

95

0

0

46

43

1

1

1

1

1

0

95

0

0

47

41

1

1

1

1

1

99

90

0

0

48

57

1

2

1

2

2

99

90

0

0

49

58

1

1

1

2

2

99

90

0

0

50

1

1

1

1

2

2

99

90

0

0

Appendix B: Tables for the data base in chapter 7

340

CWRU Data Base—All Cases between 1938 and 1949 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1938–1949 51

46

1

1

1

1

1

99

90

0

0

52

36

1

1

1

1

1

33

90

0

0

53

46

1

1

1

1

2

24

90

0

0

54

44

1

1

1

1

1

22

90

0

0

55

57

1

1

1

1

2

19

90

0

0

56

30

1

2

1

1

1

19

90

0

0

57

20

1

1

1

1

2

17

90

0

0

58

31

1

1

1

1

1

15

90

0

0

59

39

1

1

1

1

1

13

90

0

0

60

48

1

2

1

1

1

12

90

0

0

61

55

1

1

1

2

2

8

90

0

0

62

25

1

1

1

2

2

6

90

0

0

63

56

1

2

1

2

2

0

90

0

0

64

52

1

1

1

1

1

0

90

0

0

65

19

1

2

1

1

2

0

90

0

0

66

41

1

1

1

1

2

0

90

0

0

67

68

1

1

1

1

1

0

90

0

0

68

25

1

1

1

2

2

0

90

0

0

69

55

1

1

1

1

1

0

90

0

0

70

66

1

1

1

1

1

0

90

0

0

71

53

1

1

1

1

1

0

90

0

0

72

66

1

1

1

1

1

0

90

0

0

73

33

1

2

1

1

2

0

90

0

0

74

39

1

1

1

1

1

0

90

0

0

75

47

1

1

1

1

2

0

90

0

0

76

59

1

1

1

1

2

0

90

0

0

77

59

1

1

1

1

1

0

90

0

0

78

54

1

1

1

1

2

0

90

0

0

Appendix B: Tables for the data base in chapter 7

341

79

47

1

1

1

1

1

0

90

0

0

80

52

1

1

1

1

1

0

90

0

0

81

69

1

1

1

2

2

0

90

0

0

82

36

1

1

1

1

1

0

90

0

0

83

51

1

2

1

1

1

0

90

0

0

84

52

1

1

1

1

1

0

90

0

0

85

57

1

1

1

1

1

0

90

0

0

86

53

1

1

1

1

1

0

90

0

0

87

68

1

1

1

1

1

0

90

0

0

88

57

1

1

1

1

1

0

90

0

0

89

59

1

1

1

1

1

99

85

0

0

90

30

1

1

1

1

1

99

85

0

0

91

44

1

1

1

1

1

99

85

0

0

92

25

1

1

1

1

1

99

85

0

0

93

45

1

1

1

1

2

24

85

0

0

94

62

1

1

1

1

2

23

85

0

0

95

38

1

1

1

1

1

23

85

0

0

96

53

1

1

1

1

1

22

85

0

0

97

46

1

1

1

1

2

19

85

0

0

98

41

1

1

1

1

1

19

85

0

0

99

43

1

1

1

1

2

18

85

0

0

100

27

1

2

1

1

2

17

85

0

0

CWRU Data Base—All Cases between 1938 and 1949 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1938–1949 101

54

1

1

1

1

2

16

85

0

0

102

30

1

1

1

1

1

16

85

0

0

103

39

1

1

1

1

1

13

85

0

0

104

25

1

1

1

1

1

13

85

0

0

105

25

1

1

1

1

2

12

85

0

0

106

22

1

2

1

2

2

11

85

0

0

Appendix B: Tables for the data base in chapter 7

342

107

48

1

1

1

1

1

10

85

0

0

108

44

1

1

1

1

2

8

85

0

0

109

22

1

1

1

2

2

5

85

0

0

110

42

1

1

1

1

1

5

85

0

0

111

29

1

1

1

1

2

5

85

0

0

112

20

1

1

1

1

3

5

85

0

0

113

38

1

1

1

1

1

4

85

0

0

114

35

1

1

1

1

1

2

85

0

0

115

65

1

1

1

1

1

0

85

0

0

116

47

1

2

1

2

2

0

85

0

0

117

37

1

1

1

2

2

0

85

0

0

118

49

1

1

1

1

2

0

85

0

0

119

31

1

1

1

1

3

0

85

0

0

120

47

1

1

1

1

1

0

85

0

0

121

50

1

2

1

1

1

0

85

0

0

122

25

1

1

1

2

2

0

85

0

0

123

54

1

1

1

1

2

0

85

0

0

124

41

1

1

1

2

2

0

85

0

0

125

63

1

1

1

1

2

0

85

0

0

126

45

1

2

1

1

1

0

85

0

0

127

24

1

1

1

1

1

0

85

0

0

128

45

1

1

1

1

2

0

85

0

0

129

44

1

1

1

2

2

0

85

0

0

130

19

1

1

1

1

3

0

85

0

0

131

48

1

1

1

1

1

0

85

0

0

132

40

1

1

1

1

1

0

85

0

0

133

69

1

1

1

1

1

0

85

0

0

134

63

1

1

1

1

1

0

85

0

0

135

55

1

2

1

1

1

0

85

0

0

136

19

1

2

1

2

2

99

80

0

0

137

52

1

1

1

1

2

99

80

0

0

138

45

1

1

1

1

1

40

80

0

0

139

33

1

2

1

1

1

24

80

0

0

Appendix B: Tables for the data base in chapter 7

343

140

45

1

1

1

1

1

18

80

0

0

141

57

1

1

1

1

1

15

80

0

0

142

62

1

1

1

1

1

14

80

0

0

143

33

1

1

1

1

1

13

80

0

0

144

43

1

1

1

1

1

8

80

0

0

145

49

1

1

1

1

1

0

80

0

0

146

52

1

1

1

1

1

0

80

0

0

147

67

1

1

1

1

1

0

80

0

0

148

52

1

1

1

1

1

0

80

0

0

149

31

1

1

1

1

1

0

80

0

0

150

47

1

2

1

1

1

0

80

0

0

CWRU Data Base—All Cases between 1938 and 1949 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1938–1949 151

67

1

1

1

1

1

0

80

0

0

152

37

1

1

1

1

1

0

80

0

0

153

46

1

1

1

1

2

0

80

0

0

154

54

1

1

1

2

2

0

80

0

0

155

60

1

1

1

1

1

0

80

0

0

156

22

1

1

1

1

2

0

80

0

0

157

39

1

1

1

1

1

0

80

0

0

158

58

1

1

1

1

3

0

80

0

0

159

21

1

2

1

1

2

0

80

0

0

160

0

1

1

1

2

2

99

75

0

0

161

55

1

1

1

1

1

99

75

0

0

162

45

1

1

1

1

2

99

75

0

0

163

46

1

1

1

2

2

29

75

0

0

164

20

1

1

1

1

2

20

75

0

0

165

38

1

1

1

1

1

19

75

0

0

166

42

1

1

1

1

2

19

75

0

0

167

47

1

1

1

1

2

19

75

0

0

Appendix B: Tables for the data base in chapter 7

344

168

33

1

1

1

1

1

18

75

0

0

169

27

1

1

1

2

2

14

75

0

0

170

53

1

1

1

2

2

14

75

0

0

171

47

1

1

1

1

2

14

75

0

0

172

63

1

1

1

1

1

11

75

0

0

173

51

1

1

1

1

1

10

75

0

0

174

25

1

1

1

1

1

10

75

0

0

175

30

1

1

1

1

1

10

75

0

0

176

30

1

1

1

1

3

7

75

0

0

177

63

1

1

1

2

2

6

75

0

0

178

41

1

1

1

2

2

5

75

0

0

179

35

1

1

1

1

1

3

75

0

0

180

44

1

1

1

1

2

0

75

0

0

181

49

1

1

1

2

2

0

75

0

0

182

71

1

1

1

2

2

0

75

0

0

183

37

1

2

1

2

2

0

75

0

0

184

23

1

1

1

1

1

0

75

0

0

185

45

1

1

1

1

1

0

75

0

0

186

44

1

1

1

1

1

0

75

0

0

187

50

1

2

1

1

1

0

75

0

0

188

64

1

1

1

1

1

0

75

0

0

189

37

1

2

1

1

1

0

75

0

0

190

14

2

2

1

2

2

0

75

0

0

191

54

1

2

1

2

2

0

75

0

0

192

38

1

1

1

1

2

0

75

0

0

193

30

1

1

1

1

1

0

75

0

0

194

66

1

1

1

1

1

0

75

0

0

195

28

1

1

1

1

1

0

75

0

0

196

50

1

1

1

1

2

0

75

0

0

197

59

1

1

1

1

2

0

75

0

0

198

53

1

1

1

2

2

0

75

0

0

199

80

1

1

1

1

2

0

75

0

0

200

11

1

2

1

2

2

99

70

0

0

Appendix B: Tables for the data base in chapter 7

345

CWRU Data Base—All Cases between 1938 and 1949 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1938–1949 201

64

1

2

1

2

2

99

70

0

0

202

32

1

1

1

2

2

99

70

0

0

203

52

1

1

1

1

1

20

70

0

0

204

44

1

1

1

2

2

20

70

0

0

205

34

1

1

1

1

1

17

70

0

0

206

53

1

1

1

1

1

16

70

0

0

207

73

1

1

1

1

1

15

70

0

0

208

47

1

1

1

1

1

15

70

0

0

209

38

1

1

1

1

2

12

70

0

0

210

32

2

1

1

1

1

11

70

0

0

211

31

1

1

1

1

1

6

70

0

0

212

65

1

2

1

2

2

0

70

0

0

213

62

1

1

1

1

1

0

70

0

0

214

70

1

1

1

2

2

0

70

0

0

215

73

1

1

1

1

1

0

70

0

0

216

40

1

1

1

1

2

0

70

0

0

217

48

1

2

1

1

1

0

70

0

0

218

24

1

2

1

2

2

0

70

0

0

219

31

2

2

1

2

2

0

70

0

0

220

32

2

2

1

2

2

0

70

0

0

221

44

1

1

1

1

2

0

70

0

0

222

43

1

1

2

1

1

0

70

0

0

223

52

1

1

1

1

1

0

70

0

0

224

48

1

1

1

1

1

0

70

0

0

225

45

1

2

1

2

2

0

70

0

0

226

48

2

1

1

2

2

0

70

0

0

227

19

1

1

1

1

2

0

70

0

0

228

57

1

1

1

2

2

0

70

0

0

Appendix B: Tables for the data base in chapter 7

346

229

31

1

1

1

1

1

0

70

0

0

230

27

1

1

1

1

1

0

70

0

0

231

17

1

2

1

1

1

0

70

0

0

232

64

1

1

1

2

2

0

70

0

0

233

49

1

2

1

1

1

0

70

0

0

234

75

1

1

1

1

1

0

70

0

0

235

70

1

2

1

2

2

99

65

0

0

236

36

1

1

1

1

2

99

65

0

0

237

52

1

1

1

2

2

99

65

0

0

238

50

1

1

1

4

2

64

65

0

0

239

39

1

1

1

2

2

29

65

0

0

240

62

1

1

1

2

2

26

65

0

0

241

35

1

1

1

1

1

19

65

0

0

242

35

1

2

1

1

2

14

65

0

0

243

39

1

1

1

1

1

14

65

0

0

244

47

1

1

1

1

1

12

65

0

0

245

42

1

1

1

2

2

12

65

0

0

246

35

2

1

1

2

1

12

65

0

0

247

48

1

1

1

1

1

11

65

0

0

248

53

1

1

1

1

1

11

65

0

0

249

44

2

1

1

2

2

10

65

0

0

250

55

1

1

1

1

1

10

65

0

0

CWRU Data Base—All Cases between 1938 and 1949 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1938–1949 251

57

1

1

1

1

1

8

65

0

0

252

29

1

2

1

5

2

0

65

0

0

253

44

1

1

1

2

2

0

65

0

0

254

66

1

1

1

2

2

0

65

0

0

255

27

1

2

1

2

2

0

65

0

0

256

45

1

1

1

1

2

0

65

0

0

Appendix B: Tables for the data base in chapter 7

347

257

38

1

2

1

1

1

0

65

0

0

258

37

1

1

1

1

1

0

65

0

0

259

54

1

2

1

1

1

0

65

0

0

260

54

1

1

1

1

1

0

65

0

0

261

22

1

1

1

1

1

0

65

0

0

262

66

1

2

1

2

2

0

65

0

0

263

50

1

1

1

2

2

0

65

0

0

264

49

1

1

1

1

1

0

65

0

0

265

54

1

1

1

2

1

0

65

0

0

266

51

1

1

1

1

1

0

65

0

0

267

32

1

1

1

1

2

0

65

0

0

268

48

1

1

1

1

2

0

65

0

0

269

59

1

2

1

2

2

0

65

0

0

270

45

1

1

1

1

1

0

65

0

0

271

32

1

1

1

2

2

0

65

0

0

272

84

1

1

1

2

2

0

65

0

0

273

23

1

1

1

1

1

0

65

0

0

274

37

1

1

1

1

1

0

65

0

0

275

54

1

2

1

2

2

99

60

0

0

276

38

1

1

1

2

2

99

60

0

0

277

26

1

1

1

5

2

99

60

0

0

278

47

1

1

1

1

2

28

60

0

2

279

48

1

1

1

1

1

19

60

0

0

280

45

1

1

1

2

2

17

60

0

0

281

59

1

1

1

2

2

12

60

0

0

282

37

1

1

1

1

1

10

60

0

0

283

67

1

1

1

1

1

6

60

0

0

284

43

1

1

1

1

1

6

60

0

0

285

35

1

1

1

1

1

0

60

0

0

286

65

1

1

1

1

1

0

60

0

0

287

36

1

1

1

1

1

0

60

0

0

288

58

1

2

1

1

1

0

60

0

0

289

61

1

1

1

2

2

0

60

0

0

Appendix B: Tables for the data base in chapter 7

348

290

17

1

2

1

2

2

0

60

0

0

291

30

1

1

1

1

1

0

60

0

0

292

22

1

1

1

1

2

0

60

0

0

293

75

1

1

1

2

2

99

55

0

0

294

59

1

1

1

2

2

99

55

0

0

295

65

1

1

1

1

1

19

55

0

0

296

55

1

1

1

1

1

16

55

0

0

297

30

1

2

1

2

2

14

55

0

0

298

47

1

2

1

2

2

10

55

0

0

299

47

1

1

1

1

1

10

55

0

0

300

28

1

2

1

2

2

8

55

0

0

CWRU Data Base—All Cases between 1938 and 1949 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1938–1949 301

37

1

1

1

1

1

6

55

0

0

302

50

1

1

1

2

2

5

55

0

0

303

28

2

1

1

2

2

5

55

0

0

304

66

1

1

1

1

1

3

55

0

0

305

34

1

1

1

2

2

0

55

0

0

306

51

1

1

1

2

2

0

55

0

0

307

48

1

1

1

1

2

0

55

0

0

308

31

1

2

1

1

1

0

55

0

0

309

27

2

2

1

2

2

0

55

0

0

310

58

1

1

1

1

1

0

55

0

0

311

65

1

1

1

1

1

0

55

0

0

312

51

1

1

1

1

1

0

55

0

0

313

59

1

1

1

1

1

0

55

0

0

314

33

1

1

1

1

1

0

55

0

0

315

18

1

2

1

2

2

0

55

0

0

316

66

1

1

1

2

2

0

55

0

0

317

31

1

2

1

1

3

7

50

0

0

Appendix B: Tables for the data base in chapter 7

349

318

57

1

1

1

1

1

4

50

0

0

319

51

1

1

1

1

1

0

50

0

0

320

55

1

1

1

1

1

0

50

0

0

321

54

1

1

1

2

2

99

45

0

0

322

46

1

1

1

2

2

28

45

0

0

323

50

1

1

1

1

3

15

45

0

0

324

49

1

1

1

1

2

4

45

0

0

325

70

1

1

1

2

2

0

45

0

0

326

35

2

2

1

2

2

0

45

0

0

327

59

1

1

1

1

1

24

40

0

0

328

67

1

1

1

2

2

19

40

0

0

329

67

1

1

1

2

2

14

40

0

0

330

58

1

2

1

1

1

0

40

0

0

331

62

1

1

1

1

1

0

40

0

0

332

67

1

1

1

1

3

0

40

0

0

333

31

2

2

1

2

2

0

40

0

0

334

55

1

1

1

5

2

0

35

0

3

335

56

1

1

1

1

2

0

35

0

0

336

48

1

1

1

2

2

37

30

0

0

337

58

1

1

1

7

5

0

30

0

0

338

63

1

1

1

2

2

0

30

0

0

339

49

1

1

1

2

1

13

15

0

0

340

54

1

2

1

2

1

0

15

0

0

CWRU Data Base—All Cases between 1938 and 1949 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1938–1949 1

12

2

1

4

3

2

99

95

1

0

2

74

1

1

2

3

2

99

95

1

0

3

41

1

1

2

3

2

18

95

1

0

Appendix B: Tables for the data base in chapter 7

350

CWRU Data Base—All Cases between 1938 and 1949 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1938–1949 4

32

1

1

3

3

2

16

95

1

0

5

62

1

1

4

7

5

5

95

1

0

6

45

1

2

1

3

2

4

95

1

0

7

56

1

2

4

4

1

0

95

1

0

8

58

1

1

2

7

5

0

95

1

0

9

1

2

1

4

3

2

99

90

1

0

10

2

2

2

2

3

2

99

90

1

0

11

71

2

1

1

3

2

99

90

1

0

12

48

2

1

2

3

2

26

90

1

0

13

49

1

1

2

7

5

24

90

1

0

14

24

1

2

2

3

2

18

90

1

0

15

52

1

1

2

7

2

10

90

1

0

16

44

1

1

1

3

2

0

90

1

0

17

39

1

2

2

3

2

0

90

1

0

18

83

1

2

2

3

2

99

85

1

0

19

60

2

1

4

3

2

18

85

1

0

20

32

1

2

2

3

2

0

85

1

0

21

85

1

2

2

3

2

99

80

1

0

22

28

1

1

4

1

2

19

80

1

0

23

59

1

1

1

3

2

19

80

1

0

24

40

2

1

4

3

2

18

80

1

0

25

24

1

1

2

3

2

15

80

1

1

26

52

2

1

1

3

2

0

80

1

0

27

40

1

1

4

3

2

0

80

1

0

28

20

2

2

2

3

2

0

80

1

0

29

4

2

2

1

3

2

99

75

1

0

30

74

1

2

2

3

2

99

75

1

0

31

8

1

1

4

3

2

99

75

1

0

Appendix B: Tables for the data base in chapter 7

351

32

76

1

2

2

3

2

99

75

1

0

33

76

1

2

2

3

2

99

75

1

0

34

74

1

2

2

3

2

99

75

1

0

35

42

1

1

4

3

2

33

75

1

0

36

46

2

2

4

4

2

19

75

1

0

37

66

1

2

4

3

2

10

75

1

0

38

42

2

2

4

3

2

7

75

1

0

39

78

1

1

1

3

2

0

75

1

0

40

69

1

1

1

3

2

0

75

1

0

41

77

1

1

1

3

2

0

75

1

0

42

68

2

1

4

2

2

0

75

1

0

43

19

1

1

4

3

2

0

75

1

0

44

4

1

1

1

3

2

99

70

1

0

45

4

1

2

1

3

2

99

70

1

1

46

4

2

2

1

3

2

99

70

1

0

47

2

2

2

2

3

2

99

70

1

0

48

5

2

2

2

3

2

99

70

1

0

49

84

1

2

2

3

2

99

70

1

0

50

39

1

2

1

3

2

32

70

1

0

51

26

1

1

1

3

2

24

70

1

0

52

65

1

1

4

3

2

18

70

1

0

53

33

1

1

1

3

2

15

70

1

0

Fire st

Surv

CWRU Data Base—All Cases between 1938 and 1949 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire Cases 1938–1949 54

82

1

1

2

3

2

0

70

1

0

55

18

2

1

1

4

2

0

70

1

0

56

70

1

2

1

3

2

0

70

1

0

57

50

1

2

4

3

2

0

70

1

0

58

44

1

1

4

3

2

0

70

1

0

59

70

1

1

1

3

2

0

70

1

0

Appendix B: Tables for the data base in chapter 7

352

60

1

2

1

4

3

2

99

65

1

0

61

80

1

2

2

3

2

99

65

1

0

62

74

1

2

2

3

2

99

65

1

0

63

43

1

2

2

3

2

30

65

1

0

64

42

1

1

4

3

2

26

65

1

0

65

33

1

1

1

3

2

24

65

1

0

66

52

1

1

1

3

2

20

65

1

0

67

67

1

1

4

3

2

19

65

1

0

68

24

1

2

2

3

2

0

65

1

0

69

46

2

1

1

6

5

0

65

1

0

70

69

1

1

1

3

2

0

65

1

0

71

67

1

1

1

3

2

0

65

1

0

72

76

1

1

2

3

2

0

65

1

0

73

50

1

1

4

4

2

0

65

1

0

74

83

1

2

1

3

2

99

60

1

0

75

11

1

2

1

3

4

99

60

1

0

76

7

1

2

1

3

2

99

60

1

0

77

3

2

1

1

3

2

99

60

1

0

78

7

2

2

2

3

2

99

60

1

0

79

39

2

2

1

4

2

28

60

1

0

80

37

1

1

4

3

2

27

60

1

0

81

36

1

1

4

3

3

16

60

1

0

82

39

2

1

4

3

2

10

60

1

0

83

67

1

1

4

3

2

0

60

1

0

84

66

2

1

4

3

2

0

60

1

0

85

49

1

1

1

3

2

0

60

1

0

86

2

2

2

5

3

2

99

55

1

0

87

42

1

2

2

3

2

40

55

1

0

88

26

1

1

0

1

2

29

55

1

0

89

27

1

1

4

3

2

24

55

1

0

90

60

2

2

4

3

2

0

55

1

0

91

56

1

1

2

7

5

0

55

1

0

92

78

1

1

4

3

2

0

55

1

1

Appendix B: Tables for the data base in chapter 7

353

93

67

1

1

2

7

5

0

55

1

0

94

59

1

2

2

7

5

0

55

1

0

95

65

1

1

1

3

2

20

50

1

0

96

56

2

2

4

3

2

0

50

1

0

97

19

2

1

4

7

2

99

45

1

0

98

47

1

1

2

3

2

24

45

1

0

99

60

1

1

2

3

2

99

40

1

0

100

51

2

1

4

3

2

32

40

1

0

101

66

1

1

1

7

2

3

40

1

0

102

32

1

1

1

1

2

0

40

1

0

103

78

1

2

2

3

2

0

40

1

0

CWRU Data Base—All Cases between 1938 and 1949 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1938–1949 104

78

1

1

2

3

2

0

40

1

0

105

57

1

2

1

3

2

0

40

1

9

106

53

1

1

4

3

3

28

35

1

0

107

53

1

1

2

3

2

19

35

1

0

108

24

1

2

4

1

2

0

35

1

0

109

33

1

2

4

3

2

36

30

1

0

110

71

1

1

1

3

2

28

30

1

0

111

72

1

1

4

3

2

28

30

1

0

112

26

2

1

4

4

2

10

30

1

1

113

65

1

2

4

4

2

0

30

1

0

114

40

1

1

4

1

5

0

30

1

0

115

77

1

2

4

3

2

0

25

1

0

Appendix B: Tables for the data base in chapter 7

354

CWRU Data Base—All Cases between 1938 and 1949 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Other Cases 1938–1949 1

26

1

2

4

7

2

0

80

2

0

2

19

1

1

2

2

2

0

65

2

0

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1950–1959 1

26

1

1

1

1

1

9

95

0

0

2

53

1

1

1

1

1

0

95

0

0

3

46

1

1

1

5

5

0

95

0

0

4

45

1

1

1

1

2

0

95

0

0

5

41

1

1

1

1

2

24

90

0

0

6

51

1

1

1

1

1

16

90

0

0

7

39

1

1

1

1

1

15

90

0

0

8

34

1

1

1

1

2

11

90

0

0

9

52

1

1

1

1

1

11

90

0

0

10

58

1

1

1

5

5

0

90

0

0

11

57

1

1

1

1

1

0

90

0

0

12

65

1

1

1

1

1

0

90

0

0

13

48

1

1

1

1

1

0

90

0

0

14

62

1

1

1

1

1

0

85

0

0

15

21

1

2

1

1

1

0

85

0

0

16

35

2

1

1

1

2

0

85

0

0

17

21

1

1

1

1

1

0

85

0

0

18

43

1

1

1

1

3

32

80

0

0

19

41

1

1

1

1

1

21

80

0

0

20

43

1

1

1

1

1

14

80

0

0

21

61

1

1

1

2

2

13

80

0

0

22

73

1

2

1

5

2

0

80

0

0

Appendix B: Tables for the data base in chapter 7

355

23

69

1

1

1

1

2

0

80

0

0

24

52

1

1

1

1

1

0

80

0

0

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1950–1959 25

57

1

1

1

1

1

0

80

0

0

26

48

1

2

1

1

2

0

80

0

0

27

12

1

1

1

1

4

99

75

0

0

28

40

1

1

1

1

1

27

75

0

0

29

43

1

1

1

1

1

24

75

0

0

30

68

1

1

1

1

1

18

75

0

0

31

37

1

1

1

2

2

17

75

0

0

32

46

1

1

1

1

2

16

75

0

0

33

50

1

1

1

1

1

14

75

0

0

34

35

2

1

1

2

2

12

75

0

0

35

63

1

1

1

1

2

8

75

0

0

36

35

1

1

1

1

2

6

75

0

0

37

66

1

1

1

1

1

6

75

0

0

38

36

1

2

1

1

1

0

75

0

0

39

74

1

1

1

2

2

0

75

0

0

40

47

1

1

1

1

1

0

75

0

0

41

52

1

1

1

1

1

0

75

0

0

42

58

1

2

1

1

1

0

75

0

0

43

54

1

2

1

1

1

0

75

0

0

44

58

1

1

1

1

1

0

75

0

0

45

44

2

1

1

1

2

13

73

0

0

46

64

1

1

1

1

1

33

70

0

0

47

66

1

1

1

1

1

30

70

0

0

48

43

1

1

1

1

2

26

70

0

0

49

41

1

1

1

1

1

22

70

0

0

50

44

1

1

1

1

2

20

70

0

0

Appendix B: Tables for the data base in chapter 7

356

51

54

1

1

1

2

2

20

70

0

0

52

83

1

1

1

1

2

20

70

0

0

53

30

1

1

1

1

1

16

70

0

0

54

30

1

1

1

1

2

15

70

0

0

55

33

1

1

1

1

1

10

70

0

0

56

19

1

1

1

1

1

10

70

0

0

57

48

1

2

1

1

1

9

70

0

0

58

35

1

1

1

1

2

7

70

0

0

59

54

1

1

1

1

1

7

70

0

0

60

56

1

1

1

2

2

0

70

0

0

61

41

1

1

1

1

1

0

70

0

0

62

43

1

1

1

1

1

0

70

0

0

63

51

1

1

1

1

1

0

70

0

0

64

25

1

1

1

1

1

0

70

0

0

65

50

1

1

1

1

1

0

70

0

0

66

58

1

1

1

2

2

0

70

0

0

67

69

1

2

1

1

1

0

70

0

0

68

25

1

1

1

1

1

0

70

0

0

69

37

1

2

1

1

1

0

70

0

0

70

48

1

1

1

1

2

0

70

0

0

71

70

1

2

1

1

1

0

70

0

0

72

47

1

1

1

1

1

0

70

0

0

73

54

2

2

1

2

2

0

70

0

0

74

31

1

2

1

1

1

0

70

0

0

Fire st

Surv

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Non Fire Cases 1950–1959 75

62

1

2

1

1

1

0

70

0

0

76

68

1

1

1

1

1

0

70

0

0

77

59

1

1

1

5

5

0

70

0

0

78

43

1

1

1

1

2

28

68

0

0

Appendix B: Tables for the data base in chapter 7

357

79

31

1

1

1

1

1

0

67

0

0

80

46

1

1

1

1

2

17

66

0

0

81

2

2

2

1

2

2

99

65

0

0

82

49

1

2

1

1

1

39

65

0

0

83

53

1

1

1

1

1

33

65

0

0

84

63

1

1

1

1

1

28

65

0

0

85

32

2

1

1

2

2

26

65

0

0

86

38

1

1

1

1

2

26

65

0

0

87

66

1

1

1

1

1

26

65

0

0

88

42

1

1

1

1

2

26

65

0

0

89

39

1

1

1

1

2

24

65

0

0

90

40

1

1

1

2

2

24

65

0

0

91

37

1

1

1

1

2

23

65

0

0

92

24

1

1

1

1

2

22

65

0

0

93

61

1

1

1

1

1

22

65

0

0

94

63

1

1

1

1

2

21

65

0

0

95

53

1

1

1

1

2

19

65

0

0

96

50

1

1

1

1

2

16

65

0

0

97

57

2

2

1

2

2

15

65

0

0

98

45

1

1

]

1

1

14

65

0

0

99

27

1

1

]

1

1

14

65

0

0

100

43

1

1

1

1

1

13

65

0

0

101

33

1

2

1

1

2

13

65

0

0

102

29

1

1

1

1

2

13

65

0

0

103

48

1

1

1

1

2

13

65

0

0

104

58

1

1

1

2

2

12

65

0

0

105

41

1

1

1

1

1

12

65

0

0

106

43

1

2

1

1

1

10

65

0

0

107

29

1

1

1

1

2

8

65

0

0

108

48

1

1

1

1

1

7

65

0

0

109

49

1

1

1

1

2

7

65

0

0

110

43

1

2

1

1

2

6

65

0

0

111

38

1

1

1

1

2

6

65

0

0

Appendix B: Tables for the data base in chapter 7

358

112

62

1

2

1

1

1

6

65

0

0

113

41

1

1

1

1

2

5

65

0

0

114

33

1

1

1

1

1

5

65

0

0

115

63

1

1

1

1

2

5

65

0

0

116

40

1

1

1

1

1

5

65

0

0

117

41

1

1

1

1

2

3

65

0

0

118

49

1

1

1

5

5

0

65

0

0

119

34

1

1

1

1

1

0

65

0

0

120

64

1

2

1

1

1

0

65

0

0

121

41

2

2

1

2

2

0

65

0

0

122

47

1

1

1

1

1

0

65

0

0

123

52

1

1

1

1

2

0

65

0

0

124

29

1

1

1

1

1

0

65

0

0

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1950–1959 125

25

2

2

1

2

2

0

65

0

0

126

32

1

1

1

2

2

0

65

0

0

127

69

1

1

1

1

1

0

65

0

0

128

41

1

1

1

1

1

0

65

0

0

129

69

1

1

1

1

1

0

65

0

0

130

41

1

1

1

1

1

0

65

0

0

131

47

1

2

1

1

1

0

65

0

0

132

21

1

1

1

2

2

0

65

0

0

133

49

1

1

1

5

5

0

65

0

0

134

30

1

1

1

1

2

0

65

0

0

135

79

1

1

1

2

2

0

65

0

0

136

48

1

1

1

1

2

0

65

0

0

137

22

1

1

1

1

1

0

65

0

0

138

55

1

2

1

1

2

0

65

0

0

139

71

1

2

1

2

2

0

65

0

0

Appendix B: Tables for the data base in chapter 7

359

140

54

1

1

1

1

2

0

65

0

0

141

58

1

1

1

1

1

0

65

0

0

142

53

1

1

1

1

1

0

65

0

0

143

68

1

1

1

1

1

0

65

0

0

144

30

1

2

1

1

1

0

65

0

0

145

44

2

1

1

1

2

0

65

0

0

146

28

1

1

1

5

5

0

65

0

0

147

51

2

2

1

2

2

0

65

0

0

148

74

1

1

1

1

1

0

65

0

0

149

33

2

1

1

2

2

0

65

0

0

150

16

1

2

1

1

2

0

65

0

0

151

55

1

2

1

1

1

0

65

0

0

152

46

2

1

1

2

2

0

65

0

0

153

42

1

1

1

1

1

0

65

0

0

154

66

1

1

1

1

1

0

65

0

0

155

33

1

1

1

1

1

0

65

0

0

156

25

1

2

1

2

2

0

65

0

0

157

56

1

1

1

1

1

0

65

0

0

158

21

1

2

1

1

1

0

65

0

0

159

44

1

2

1

1

1

0

65

0

0

160

57

1

2

1

1

1

0

65

0

0

161

78

1

1

1

1

1

0

65

0

0

162

20

1

1

1

1

1

0

65

0

0

163

60

1

1

1

1

1

0

65

0

0

164

43

1

1

1

1

2

11

63

0

0

165

56

1

2

1

2

2

0

61

0

0

166

2

2

1

2

2

2

99

60

0

0

167

6

2

1

1

2

2

99

60

0

0

168

61

1

1

1

1

2

24

60

0

0

169

27

1

2

1

1

1

22

60

0

0

170

36

2

2

1

2

2

22

60

0

0

171

45

2

1

1

2

2

22

60

0

0

172

52

1

1

1

1

1

22

60

0

0

Appendix B: Tables for the data base in chapter 7

360

173

45

1

1

1

1

2

21

60

0

0

174

46

1

1

1

1

1

21

60

0

0

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1950–1959 175

44

2

1

1

2

2

21

60

0

0

176

70

1

1

1

1

2

18

60

0

0

177

31

1

1

1

1

1

16

60

0

0

178

38

1

1

1

1

1

16

60

0

0

179

42

1

1

1

1

1

15

60

0

0

180

55

1

1

1

2

2

15

60

0

0

181

42

1

1

1

1

2

13

60

0

0

182

51

1

1

1

1

2

13

60

0

0

183

33

1

1

1

1

1

12

60

0

0

184

23

1

1

1

1

2

12

60

0

0

185

48

1

1

1

1

1

12

60

0

0

186

63

1

1

1

1

2

12

60

0

0

187

55

1

1

1

1

1

11

60

0

0

188

29

1

1

1

1

1

10

60

0

0

189

50

1

1

1

1

1

9

60

0

0

190

33

1

1

1

1

1

7

60

0

0

191

22

1

1

1

1

2

6

60

0

0

192

62

1

1

1

1

1

5

60

0

0

193

55

1

1

1

1

1

5

60

0

0

194

40

1

1

1

1

1

4

60

0

0

195

73

1

1

1

1

1

0

60

0

0

196

40

2

1

1

1

2

0

60

0

0

197

32

1

1

1

1

1

0

60

0

0

198

72

1

2

1

1

1

0

60

0

0

199

14

2

2

1

2

2

0

60

0

0

200

38

1

1

1

1

1

0

60

0

0

Appendix B: Tables for the data base in chapter 7

361

201

41

1

1

1

2

2

0

60

0

0

202

45

1

1

1

1

1

0

60

0

0

203

65

1

2

1

2

2

0

60

0

0

204

38

2

1

1

2

2

0

60

0

0

205

24

1

1

1

1

1

0

60

0

0

206

25

2

2

2

2

2

0

60

0

0

207

45

1

1

1

5

5

0

60

0

0

208

40

1

1

1

1

2

0

60

0

0

209

25

1

1

1

1

2

0

60

0

0

210

67

1

1

1

1

1

0

60

0

0

211

67

1

1

1

1

1

0

60

0

0

212

66

1

1

1

1

1

0

60

0

0

213

52

1

2

1

1

1

0

60

0

0

214

31

1

1

1

1

1

0

60

0

0

215

41

1

2

1

1

1

0

60

0

0

216

24

1

1

1

1

1

0

60

0

0

217

68

1

1

1

1

2

0

60

0

0

218

28

1

1

1

1

1

0

60

0

0

219

23

1

1

1

1

2

0

60

0

0

220

53

1

2

1

1

1

0

60

0

0

221

55

1

1

1

1

1

0

60

0

0

222

18

2

1

1

2

2

0

60

0

0

223

72

1

1

1

1

1

0

60

0

0

224

57

1

1

1

1

1

0

60

0

0

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1950–1959 225

47

1

1

1

1

1

0

60

0

0

226

28

1

1

1

1

1

0

60

0

0

227

59

1

1

1

1

1

0

60

0

0

228

54

1

2

1

1

1

0

60

0

0

Appendix B: Tables for the data base in chapter 7

362

229

27

2

2

1

2

2

0

60

0

0

230

24

1

1

1

1

2

0

60

0

0

231

44

1

2

1

2

2

0

60

0

0

232

37

1

1

1

1

2

15

58

0

0

233

50

1

1

1

1

2

12

58

0

0

234

85

1

2

1

2

2

0

57

0

0

235

2

2

1

1

2

2

99

55

0

0

236

27

1

1

1

1

1

38

55

0

0

237

57

1

1

1

1

1

27

55

0

0

238

54

1

2

1

1

1

26

55

0

0

239

46

1

1

1

1

2

21

55

0

0

240

31

2

2

1

2

2

19

55

0

0

241

51

1

1

1

1

2

16

55

0

0

242

33

2

2

1

1

2

16

55

0

0

243

60

1

1

1

1

2

15

55

0

0

244

28

2

1

1

2

2

14

55

0

0

245

63

1

1

1

1

2

14

55

0

0

246

22

1

1

1

1

1

13

55

0

0

247

35

1

2

1

1

2

12

55

0

0

248

28

1

1

1

1

2

12

55

0

0

249

35

2

2

1

2

2

8

55

0

0

250

24

1

2

1

3

2

7

55

0

0

251

35

1

1

1

1

2

7

55

0

0

252

28

1

1

1

1

2

6

55

0

0

253

61

1

1

1

2

2

6

55

0

0

254

59

2

1

1

2

2

4

55

0

0

255

73

1

1

1

1

1

2

55

0

0

256

53

1

1

1

1

1

0

55

0

0

257

37

1

1

1

5

5

0

55

0

0

258

48

1

1

1

1

1

0

55

0

0

259

71

1

1

1

1

1

0

55

0

0

260

45

2

2

1

1

1

0

55

0

0

261

59

1

1

1

1

1

0

55

0

0

Appendix B: Tables for the data base in chapter 7

363

262

72

1

2

1

2

2

0

55

0

0

263

46

1

2

1

1

1

0

55

0

0

264

22

2

2

1

1

2

0

55

0

0

265

50

2

1

1

2

2

0

55

0

0

266

33

1

1

5

5

5

0

55

0

0

267

18

1

1

1

1

1

0

55

0

0

268

26

2

1

1

1

2

0

55

0

0

269

29

2

1

1

2

2

0

55

0

0

270

69

1

1

1

1

1

0

55

0

0

271

46

1

1

1

2

2

0

55

0

0

272

55

2

1

1

2

2

0

55

0

0

273

24

1

1

1

1

1

0

55

0

0

274

34

2

1

1

2

2

0

55

0

0

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1950–1959 275

17

2

2

1

2

2

0

55

0

0

276

23

1

1

1

1

1

0

55

0

0

277

50

1

1

1

2

2

0

55

0

0

278

70

1

1

1

2

2

0

55

0

0

279

55

1

1

1

1

1

0

55

0

0

280

74

1

1

1

1

1

0

55

0

0

281

66

1

0

1

1

2

0

55

0

0

282

71

1

1

1

2

2

99

50

0

0

283

24

1

2

1

2

2

99

50

0

0

284

24

1

1

1

2

2

31

50

0

0

285

28

1

1

1

1

2

20

50

0

0

286

43

1

1

1

1

1

17

50

0

0

287

39

1

1

1

2

2

16

50

0

0

288

41

1

2

1

1

1

12

50

0

0

289

66

1

1

1

1

1

10

50

0

0

Appendix B: Tables for the data base in chapter 7

364

290

43

1

1

1

1

2

10

50

0

0

291

41

1

1

1

1

1

9

50

0

0

292

56

1

1

1

1

1

6

50

0

0

293

60

2

1

1

2

2

6

50

0

0

294

28

2

1

1

2

2

6

50

0

0

295

50

1

1

1

1

1

5

50

0

0

296

61

1

1

1

2

2

5

50

0

0

297

51

1

1

1

2

2

5

50

0

0

298

27

1

1

1

1

2

4

50

0

0

299

69

1

1

1

1

1

3

50

0

0

300

71

1

2

1

2

2

0

50

0

0

301

68

1

1

1

1

1

0

50

0

0

302

44

1

1

1

5

5

0

50

0

0

303

33

1

2

1

1

1

0

50

0

0

304

58

1

1

1

2

2

0

50

0

0

305

31

1

1

1

1

1

0

50

0

0

306

64

1

1

1

1

2

0

50

0

0

307

51

1

2

1

1

2

0

50

0

0

308

66

1

1

1

2

2

0

50

0

0

309

41

1

2

1

1

1

0

50

0

0

310

80

1

1

1

2

2

0

50

0

0

311

77

1

1

1

2

2

0

50

0

0

312

53

1

1

1

1

1

0

50

0

0

313

65

1

1

1

2

2

0

50

0

0

314

75

1

1

1

1

2

0

50

0

0

315

49

1

1

1

1

5

0

50

0

0

316

21

1

1

1

1

2

0

50

0

0

317

69

1

1

1

2

2

0

50

0

0

318

36

1

2

1

1

1

0

50

0

0

319

57

1

1

1

1

1

0

50

0

0

320

68

1

1

1

1

2

0

50

0

0

321

49

1

2

1

1

1

0

50

0

0

322

70

1

1

1

2

2

0

50

0

0

Appendix B: Tables for the data base in chapter 7

365

323

25

1

2

1

1

1

99

47

0

0

324

50

1

1

1

1

1

21

47

0

0

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non Fire Cases 1950–1959 325

14

1

2

1

2

2

0

47

0

0

326

7

2

2

1

2

2

99

45

0

0

327

30

2

1

1

2

2

99

45

0

0

328

3

1

1

1

2

2

99

45

0

0

329

47

1

1

1

1

2

32

45

0

0

330

90

1

1

1

1

1

0

45

0

0

331

25

1

2

1

2

2

0

45

0

0

332

69

1

2

1

2

2

0

45

0

0

333

49

1

1

1

1

1

7

40

0

0

334

42

1

1

1

1

3

0

40

0

0

335

74

1

1

1

2

2

0

40

0

2

336

29

1

1

1

2

2

0

40

0

0

337

71

1

2

1

2

2

0

30

0

0

338

58

1

1

1

2

1

16

15

0

0

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1950–1959 1

2

1

1

2

3

2

99

90

1

0

2

1

2

2

4

3

2

99

75

1

0

3

5

2

2

2

3

2

99

75

1

0

4

4

2

2

1

3

2

99

75

1

0

5

30

1

1

4

3

2

21

75

1

0

6

72

1

1

1

3

2

0

75

1

0

7

26

1

1

2

7

2

0

75

1

0

Appendix B: Tables for the data base in chapter 7

366

8

2

2

2

1

3

2

99

71

1

0

9

74

1

2

1

3

2

22

70

1

0

10

61

1

1

2

3

2

20

70

1

0

11

65

1

1

2

3

2

20

70

1

0

12

64

1

1

4

7

2

0

70

1

0

13

56

1

2

2

3

2

0

70

1

0

14

58

1

1

1

7

2

0

70

1

0

15

52

1

1

1

7

2

0

70

1

0

16

1

2

2

2

3

2

99

69

1

0

17

32

2

1

1

3

4

23

68

1

0

18

2

1

2

2

3

2

99

65

1

0

19

2

2

2

4

3

2

99

65

1

0

20

1

2

1

2

3

2

99

65

1

0

21

4

2

1

1

3

2

99

65

1

0

22

7

1

2

2

3

2

99

65

1

0

23

36

1

1

4

3

2

41

65

1

0

24

53

1

1

1

7

2

40

65

1

0

25

65

1

1

1

3

2

35

65

1

0

26

38

2

1

4

3

2

32

65

1

0

27

53

2

1

1

3

2

30

65

1

0

28

68

1

1

2

3

2

30

65

1

1

29

37

1

1

2

3

2

26

65

1

0

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1950–1959 30

39

1

2

2

3

2

22

65

1

0

31

63

1

1

1

3

2

19

65

1

0

32

42

1

2

2

3

2

18

65

1

0

33

25

1

1

2

7

2

17

65

1

0

34

45

1

2

2

3

2

16

65

1

0

35

25

2

1

1

7

2

9

65

1

0

Appendix B: Tables for the data base in chapter 7

367

36

31

2

1

1

6

2

0

65

1

0

37

65

1

2

2

3

2

0

65

1

0

38

6

2

2

2

3

2

99

60

1

0

39

1

2

2

2

3

2

99

60

1

0

40

2

1

1

1

3

2

99

60

1

0

41

1

2

2

4

3

2

99

60

1

0

42

3

1

1

1

3

2

99

60

1

0

43

6

1

2

2

3

2

99

60

1

0

44

1

2

2

4

3

2

99

60

1

0

45

4

2

1

2

3

2

99

60

1

0

46

4

1

1

4

3

2

99

60

1

0

47

1

1

2

2

1

2

99

60

1

0

48

5

1

2

1

3

2

99

60

1

0

49

41

1

1

1

1

2

39

60

1

0

50

50

2

3

4

3

2

34

60

1

0

51

35

2

1

2

7

2

27

60

1

0

52

41

1

2

1

3

2

26

60

1

0

53

31

1

1

1

3

2

23

60

1

0

54

60

1

1

1

7

2

22

60

1

0

55

75

1

1

4

4

2

21

60

1

0

56

65

1

1

2

3

2

20

60

1

0

57

44

1

1

1

3

2

20

60

1

0

58

54

1

2

1

3

2

17

60

1

0

59

23

2

1

1

3

2

13

60

1

0

60

48

1

1

2

3

2

10

60

1

0

61

52

1

1

4

3

2

5

60

1

0

62

33

2

1

4

7

2

1

60

1

0

63

78

1

1

1

3

2

0

60

1

0

64

38

1

1

2

7

5

0

60

1

0

65

59

1

2

1

3

2

0

60

1

0

66

61

1

2

2

3

2

0

60

1

0

67

37

1

2

4

3

2

0

60

1

0

68

16

1

1

1

7

2

0

60

1

0

Appendix B: Tables for the data base in chapter 7

368

69

36

1

1

1

3

2

0

60

1

0

70

67

1

1

2

3

4

0

60

1

0

71

82

1

1

2

3

2

0

60

1

0

72

6

2

2

2

3

2

99

57

1

0

73

2

2

1

2

3

2

99

55

1

0

74

5

1

2

2

3

2

99

55

1

0

75

4

1

2

2

3

2

99

55

1

0

76

3

2

2

1

3

2

99

55

1

0

77

1

2

1

2

3

2

99

55

1

0

78

8

2

2

1

3

2

99

55

1

0

79

7

1

1

1

3

2

99

55

1

0

Fire st

Surv

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire Cases 1950–1959 80

45

1

1

2

3

2

57

55

1

0

81

24

1

1

1

3

2

30

55

1

0

82

29

1

1

1

3

2

30

55

1

0

83

29

1

2

4

3

2

20

55

1

0

84

30

1

1

1

3

2

18

55

1

0

85

30

9

1

5

7

2

12

55

1

0

86

67

1

1

1

7

2

7

55

1

0

87

80

1

1

1

7

2

0

55

1

0

88

70

1

1

1

3

2

0

55

1

0

89

64

2

1

4

3

2

0

55

1

0

90

54

1

1

1

3

2

0

55

1

0

91

4

2

1

2

3

2

99

54

1

0

92

1

2

1

2

3

2

99

50

1

0

93

4

1

1

1

3

2

99

50

1

0

94

7

1

2

1

3

2

99

50

1

0

95

7

1

1

4

7

2

99

50

1

0

96

2

2

2

2

3

2

99

50

1

0

Appendix B: Tables for the data base in chapter 7

369

97

2

1

2

1

3

2

99

50

1

0

98

6

2

2

2

3

2

99

50

1

0

99

1

2

1

1

3

2

99

50

1

0

100

1

2

2

1

3

2

99

50

1

0

101

48

1

1

2

3

2

43

50

1

0

102

43

1

1

1

3

2

27

50

1

0

103

50

1

1

2

3

2

24

50

1

0

104

52

1

2

4

3

2

20

50

1

0

105

25

1

1

1

3

2

15

50

1

0

106

45

1

1

2

3

2

10

50

1

0

107

78

1

1

4

3

2

5

50

1

0

108

50

2

1

2

3

2

0

50

1

0

109

78

1

2

2

3

2

0

50

1

0

110

66

1

1

1

7

5

0

50

1

0

111

40

2

1

4

3

2

0

50

1

0

112

1

2

1

2

3

2

99

47

1

0

113

2

2

1

2

3

2

99

45

1

0

114

3

2

1

2

3

2

99

45

1

0

115

6

1

1

1

3

2

99

45

1

0

116

1

1

1

2

3

2

99

45

1

0

117

8

2

2

2

3

2

99

45

1

0

118

5

2

1

2

3

2

99

45

1

0

119

38

1

1

2

3

2

53

45

1

0

120

35

1

1

4

9

2

27

45

1

0

121

50

1

1

2

3

2

25

45

1

0

122

43

1

1

2

3

2

20

45

1

0

123

30

2

1

4

1

1

11

45

1

0

124

35

1

1

1

3

2

0

45

1

0

125

32

1

1

2

1

5

0

45

1

0

126

66

1

1

2

7

2

0

45

1

0

127

18

1

1

2

3

2

0

45

1

0

128

44

1

1

1

7

5

0

45

1

0

129

85

1

2

2

3

2

0

45

1

0

Appendix B: Tables for the data base in chapter 7

370

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

FireCases 1950–1959 130

6

2

1

2

3

2

99

42

1

0

131

2

2

2

2

3

2

99

42

1

0

132

5

2

2

2

3

2

99

41

1

0

133

7

1

2

1

3

2

99

40

1

0

134

4

1

2

1

3

2

99

40

1

0

135

4

2

1

4

3

2

99

40

1

0

136

3

2

2

2

3

2

99

40

1

0

137

32

2

1

2

3

2

36

40

1

0

138

36

2

1

2

7

2

19

40

1

0

139

21

1

1

5

7

5

0

40

1

0

140

65

2

1

1

3

2

0

40

1

0

141

2

2

1

2

3

2

99

37

1

0

142

47

2

1

2

3

2

26

35

1

0

143

1

1

1

2

3

2

99

33

1

0

144

16

1

1

4

1

2

5

30

1

0

145

88

1

1

4

3

2

0

30

1

0

146

15

1

2

4

1

2

0

25

1

0

147

57

3

2

4

3

2

0

20

1

0

148

44

1

1

1

7

5

0

20

1

0

149

47

2

1

4

1

2

0

20

1

0

150

1

2

1

4

3

2

99

15

1

0

151

54

2

1

4

3

2

0

15

1

0

152

25

1

1

4

3

2

0

15

1

9

153

69

1

1

4

4

1

0

15

1

0

154

1

2

1

4

3

2

99

10

1

0

155

1

1

1

4

3

2

99

10

1

0

156

64

1

1

4

3

2

34

10

1

0

157

31

1

1

4

1

2

0

10

1

0

Appendix B: Tables for the data base in chapter 7

158

81

1

2

4

9

2

0

371

10

1

0

CWRU Data Base—All Cases between 1950 and 1959 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Other Cases 1950–1959 1

57

2

1

4

8

5

0

40

2

0

2

28

2

1

4

7

5

0

15

2

0

3

47

1

1

4

7

5

0

10

2

0

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1960–1969 1

34

1

1

1

1

1

0

81

0

0

2

78

1

2

1

1

1

0

78

0

0

3

21

1

2

1

1

2

0

78

0

0

4

18

1

1

1

1

1

4

77

0

0

5

66

1

1

1

1

1

0

77

0

0

6

65

1

1

1

1

1

0

76

0

0

7

34

1

1

1

1

2

26

75

0

0

8

35

1

1

1

1

2

17

75

0

0

9

41

1

1

1

1

1

14

75

0

0

10

67

1

1

1

1

1

10

75

0

0

11

53

1

1

1

1

1

2

75

0

0

12

51

1

1

1

1

1

0

75

0

0

13

59

1

2

1

1

1

0

75

0

0

14

48

1

1

1

1

1

30

73

0

0

15

35

1

1

1

1

2

17

73

0

0

16

18

1

1

1

1

2

0

73

0

0

17

45

1

1

1

1

2

15

72

0

0

18

47

1

1

1

1

1

10

72

0

0

19

49

1

1

1

1

2

19

71

0

0

Appendix B: Tables for the data base in chapter 7

372

20

23

1

2

1

1

1

11

71

0

0

21

45

1

2

1

1

1

11

71

0

0

22

46

1

1

1

1

2

31

70

0

0

23

32

1

1

1

1

2

19

70

0

0

24

38

1

1

1

1

1

13

70

0

0

25

53

1

2

1

1

1

0

70

0

0

26

54

1

1

1

1

1

0

70

0

0

27

34

2

1

1

1

1

0

70

0

0

28

73

1

1

1

1

1

0

70

0

0

29

56

1

2

1

1

1

0

70

0

0

30

48

1

2

1

1

1

0

70

0

0

31

50

1

2

1

1

1

0

70

0

0

32

44

1

2

1

1

1

0

70

0

0

33

56

1

2

1

1

1

0

70

0

0

34

75

1

1

1

1

1

0

70

0

0

35

20

1

1

1

1

1

0

70

0

0

36

15

1

2

1

1

2

0

69

0

0

37

53

1

1

1

1

1

23

68

0

0

38

50

1

2

1

1

1

22

68

0

0

39

26

2

1

1

1

2

12

68

0

0

40

26

1

2

1

1

1

0

68

0

0

41

36

1

1

1

1

1

0

68

0

0

42

56

2

1

1

1

1

0

68

0

0

43

39

1

1

1

1

1

22

67

0

0

44

47

1

1

1

1

2

21

67

0

0

45

30

2

1

1

1

2

20

67

0

0

46

30

1

1

1

1

1

20

67

0

0

47

59

1

1

1

1

2

19

67

0

0

48

34

1

2

1

1

1

17

67

0

0

49

51

1

1

1

1

2

15

67

0

0

50

41

2

2

1

1

2

12

67

0

0

Appendix B: Tables for the data base in chapter 7

373

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1960–1969 51

33

1

1

1

1

2

11

67

0

0

52

72

1

1

1

1

2

5

67

0

0

53

24

1

1

1

1

2

5

67

0

0

54

67

1

1

1

1

2

0

67

0

0

55

51

2

1

1

2

5

0

67

0

0

56

25

1

1

1

8

2

0

67

0

0

57

46

1

2

1

1

2

33

66

0

0

58

57

1

2

1

1

1

28

66

0

0

59

54

1

1

1

1

1

25

66

0

0

60

51

1

2

1

2

2

10

66

0

0

61

20

1

1

1

1

1

9

66

0

0

62

30

2

1

1

1

1

8

66

0

0

63

51

1

2

1

1

1

7

66

0

0

64

57

1

1

1

1

1

6

66

0

0

65

43

1

2

1

1

1

0

66

0

0

66

83

1

2

1

1

1

0

66

0

0

67

44

1

2

1

1

2

0

66

0

0

68

42

1

1

1

1

2

0

66

0

0

69

25

1

1

1

1

1

0

66

0

0

70

61

1

1

1

1

1

0

66

0

0

71

28

1

2

1

1

1

0

66

0

0

72

44

1

2

1

1

1

0

66

0

0

73

80

1

1

1

2

2

0

66

0

0

74

6

2

1

1

2

2

99

65

0

0

75

64

1

1

1

1

1

40

65

0

0

76

45

1

1

1

1

1

34

65

0

0

77

42

1

2

1

1

2

32

65

0

0

78

33

1

1

1

1

2

31

65

0

0

Appendix B: Tables for the data base in chapter 7

374

79

39

1

1

1

1

1

29

65

0

0

80

39

1

1

1

1

1

28

65

0

0

81

55

1

1

1

1

2

26

65

0

0

82

56

1

1

1

1

2

26

65

0

0

83

43

1

1

1

1

2

25

65

0

0

84

35

1

1

1

1

2

23

65

0

0

85

33

1

1

1

1

1

23

65

0

0

86

31

1

1

1

1

2

23

65

0

0

87

33

2

1

1

5

5

22

65

0

0

88

51

1

1

1

1

1

22

65

0

0

89

40

1

1

1

1

2

22

65

0

0

90

48

1

1

1

1

1

21

65

0

0

91

45

1

1

1

1

1

20

65

0

0

92

44

1

1

1

1

1

20

65

0

0

93

47

1

1

1

1

2

19

65

0

0

94

44

1

1

1

1

2

18

65

0

0

95

42

1

1

1

1

1

17

65

0

0

96

56

2

1

1

1

2

16

65

0

0

97

48

1

1

1

1

1

16

65

0

0

98

49

2

1

1

1

2

16

65

0

0

99

57

1

1

1

1

1

16

65

0

0

100

39

1

1

1

1

1

16

65

0

0

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1960–1969 101

32

1

2

1

1

1

16

65

0

0

102

37

1

2

1

1

2

15

65

0

0

103

42

1

2

1

1

1

15

65

0

0

104

57

1

1

1

1

1

14

65

0

0

105

38

1

1

1

1

2

14

65

0

0

106

62

1

1

1

1

1

12

65

0

0

Appendix B: Tables for the data base in chapter 7

375

107

35

1

1

1

1

1

11

65

0

0

108

59

1

1

1

1

2

10

65

0

0

109

27

1

1

1

1

1

10

65

0

0

110

48

1

1

1

1

1

9

65

0

0

111

70

1

1

1

1

1

7

65

0

0

112

31

1

1

1

1

2

7

65

0

0

113

30

1

2

1

1

1

6

65

0

0

114

31

1

1

1

1

1

6

65

0

0

115

59

1

1

1

1

1

5

65

0

0

116

26

2

2

1

1

2

5

65

0

0

117

45

1

1

1

1

1

3

65

0

0

118

69

1

1

1

1

1

3

65

0

0

119

16

1

2

1

1

2

1

65

0

0

120

18

1

2

1

1

2

0

65

0

0

121

33

1

1

1

1

2

0

65

0

0

122

49

1

1

1

1

1

0

65

0

0

123

59

1

1

1

1

1

0

65

0

0

124

84

1

1

1

1

1

0

65

0

0

125

59

1

1

1

1

1

0

65

0

0

126

38

1

1

1

1

1

0

65

0

0

127

45

1

1

1

1

1

0

65

0

0

128

40

1

1

1

1

1

0

65

0

0

129

58

1

1

1

1

1

0

65

0

0

130

59

1

1

1

1

2

0

65

0

0

131

64

1

1

1

1

1

0

65

0

0

132

25

1

1

1

1

1

0

65

0

0

133

40

1

1

1

1

1

0

65

0

0

134

40

1

2

1

1

1

0

65

0

0

135

81

1

1

1

1

2

0

65

0

0

136

30

1

2

1

1

1

0

65

0

0

137

65

1

1

1

1

1

0

65

0

0

138

66

2

1

1

2

2

0

65

0

0

139

54

1

1

1

1

1

0

65

0

0

Appendix B: Tables for the data base in chapter 7

376

140

51

1

1

1

1

1

0

65

0

0

141

49

1

2

1

1

2

0

65

0

0

142

53

1

2

1

1

1

0

65

0

0

143

52

1

2

1

1

1

0

65

0

0

144

39

1

1

1

1

1

0

65

0

0

145

64

1

1

1

1

1

0

65

0

0

146

60

1

1

1

1

2

0

65

0

0

147

70

1

1

1

1

1

0

65

0

0

148

37

1

2

1

1

1

0

65

0

0

149

40

1

2

1

1

1

0

65

0

0

150

74

1

1

1

1

1

0

65

0

0

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1960–1969 151

20

1

1

1

1

1

0

65

0

0

152

22

]

1

1

1

2

0

65

0

0

153

72

1

1

1

1

1

0

65

0

0

154

23

1

1

1

1

1

0

65

0

0

155

72

1

1

1

1

2

0

65

0

0

156

63

1

1

1

1

2

0

65

0

0

157

60

1

1

1

1

1

0

65

0

0

158

59

1

1

1

1

2

0

65

0

0

159

23

1

1

1

1

2

0

65

0

0

160

52

1

2

1

1

1

0

65

0

0

161

52

1

1

1

1

1

0

65

0

0

162

74

1

1

1

1

1

0

65

0

0

163

19

1

1

1

1

2

0

65

0

0

164

20

1

1

1

1

1

0

65

0

0

165

71

1

1

1

1

2

0

65

0

0

166

25

1

1

1

1

1

0

65

0

0

167

58

1

2

1

1

1

0

65

0

0

Appendix B: Tables for the data base in chapter 7

377

168

54

1

2

1

1

2

0

65

0

0

169

42

1

1

1

1

1

28

64

0

0

170

62

1

1

1

1

2

24

64

0

0

171

47

2

1

1

1

2

23

64

0

0

172

52

1

1

1

1

1

19

64

0

0

173

39

1

1

1

1

2

0

64

0

0

174

38

1

1

1

1

1

0

64

0

0

175

19

1

2

1

1

1

0

64

0

0

176

54

1

1

1

1

1

27

63

0

0

177

57

1

1

1

1

2

26

63

0

0

178

46

1

1

1

1

2

22

63

0

0

179

61

1

1

1

1

2

19

63

0

0

180

26

1

1

1

1

2

15

63

0

0

181

26

1

1

1

1

1

10

63

0

0

182

51

1

1

1

1

2

7

63

0

0

183

18

1

2

1

1

2

6

63

0

0

184

36

2

1

1

1

1

0

63

0

0

185

44

2

2

1

2

2

0

63

0

0

186

37

1

2

1

1

1

0

63

0

0

187

26

1

1

1

1

2

0

63

0

0

188

22

2

1

1

1

2

0

63

0

0

189

26

1

2

1

1

1

0

63

0

0

190

57

1

1

1

1

1

0

63

0

0

191

39

1

2

1

1

2

0

63

0

0

192

55

1

2

1

1

1

21

62

0

0

193

42

1

1

1

1

2

20

62

0

0

194

41

1

1

1

1

2

18

62

0

0

195

61

1

2

1

1

1

17

62

0

0

196

25

1

1

1

1

2

14

62

0

0

197

33

2

1

1

1

1

9

62

0

0

198

80

2

2

1

9

2

0

62

0

0

199

77

1

2

1

2

2

0

62

0

0

200

30

1

1

1

1

1

0

62

0

0

Appendix B: Tables for the data base in chapter 7

378

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1960–1969 201

38

1

1

1

1

1

0

62

0

0

202

79

1

1

1

1

1

0

62

0

0

203

70

1

1

1

1

1

0

62

0

0

204

23

1

1

1

1

1

0

62

0

0

205

43

1

2

1

1

2

33

61

0

0

206

24

1

1

1

1

1

11

61

0

0

207

22

2

1

1

1

2

10

61

0

0

208

28

1

1

1

1

2

10

61

0

0

209

21

1

1

1

1

2

9

61

0

0

210

54

1

2

1

1

1

0

61

0

0

211

23

1

1

1

1

1

0

61

0

0

212

57

1

2

1

1

1

0

61

0

0

213

56

1

2

1

1

1

0

61

0

0

214

78

1

1

1

1

2

0

61

0

0

215

78

1

1

1

1

1

0

61

0

0

216

53

1

1

1

1

1

99

60

0

0

217

65

1

1

1

1

2

38

60

0

0

218

68

1

1

1

1

1

34

60

0

0

219

50

1

1

1

1

2

32

60

0

0

220

36

2

2

1

1

1

31

60

0

0

221

56

1

1

1

1

1

30

60

0

0

222

58

1

1

1

1

1

29

60

0

0

223

54

1

2

1

1

1

29

60

0

0

224

46

1

1

1

1

2

28

60

0

0

225

46

1

2

1

1

1

27

60

0

0

226

50

1

1

1

1

2

26

60

0

0

227

40

1

1

1

1

1

25

60

0

0

228

46

1

2

1

1

1

25

60

0

0

Appendix B: Tables for the data base in chapter 7

379

229

31

2

1

1

2

2

23

60

0

0

230

36

1

2

1

1

2

22

60

0

0

231

59

1

1

1

1

2

22

60

0

0

232

55

1

1

1

1

1

22

60

0

0

233

49

1

1

1

1

1

21

60

0

0

234

64

1

1

1

2

2

21

60

0

0

235

44

1

2

1

1

2

20

60

0

0

236

18

1

1

1

1

2

19

60

0

0

237

42

1

2

1

1

1

19

60

0

0

238

28

1

2

1

1

1

19

60

0

0

239

31

1

1

1

1

2

18

60

0

0

240

46

1

1

1

1

2

18

60

0

0

241

51

1

1

1

1

1

18

60

0

0

242

24

1

1

1

1

2

18

60

0

0

243

57

1

1

1

1

1

17

60

0

0

244

27

1

1

1

1

2

17

60

0

0

245

43

1

2

1

1

1

17

60

0

0

246

46

1

1

1

1

1

16

60

0

0

247

31

1

2

1

1

1

16

60

0

0

248

31

1

2

1

1

1

16

60

0

0

249

30

1

2

1

1

1

15

60

0

0

250

65

1

1

1

1

1

15

60

0

0

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1960–1969 251

18

2

2

1

2

2

15

60

0

0

252

30

2

2

1

1

2

14

60

0

0

253

63

2

1

1

2

2

14

60

0

0

254

36

2

1

1

1

2

13

60

0

0

255

54

1

1

1

1

1

13

60

0

0

256

57

1

1

1

1

2

13

60

0

0

Appendix B: Tables for the data base in chapter 7

380

257

39

1

1

1

1

1

12

60

0

0

258

51

1

1

1

1

1

12

60

0

0

259

24

1

1

1

1

1

12

60

0

0

260

46

1

2

1

1

2

12

60

0

0

261

49

2

1

1

2

2

11

60

0

0

262

47

1

2

1

1

1

11

60

0

0

263

39

1

1

1

1

2

11

60

0

0

264

50

1

1

1

1

1

10

60

0

0

265

25

1

1

1

1

2

10

60

0

0

266

73

1

1

1

2

2

10

60

0

0

267

66

1

1

1

1

1

9

60

0

0

268

29

1

1

1

1

2

9

60

0

0

269

25

2

1

1

1

2

8

60

0

0

270

25

1

1

1

1

2

8

60

0

0

271

57

1

2

1

1

1

7

60

0

0

272

29

1

1

1

1

1

7

60

0

0

273

61

1

1

1

2

2

7

60

0

0

274

23

1

1

1

1

1

6

60

0

0

275

44

1

2

1

1

1

6

60

0

0

276

57

1

2

1

1

1

6

60

0

0

277

57

1

1

1

1

1

5

60

0

0

278

29

1

1

1

1

1

4

60

0

0

279

45

2

1

1

2

2

4

60

0

0

280

41

1

1

1

1

1

3

60

0

0

281

38

1

2

1

1

1

3

60

0

0

282

28

1

1

1

1

2

2

60

0

0

283

18

1

1

1

1

2

1

60

0

0

284

57

2

1

1

2

2

0

60

0

0

285

59

1

1

1

2

2

0

60

0

0

286

52

1

1

1

1

1

0

60

0

0

287

55

1

1

1

1

1

0

60

0

0

288

65

1

1

1

1

1

0

60

0

0

289

29

1

2

1

1

1

0

60

0

0

Appendix B: Tables for the data base in chapter 7

381

290

35

2

2

1

2

2

0

60

0

0

291

38

1

2

1

1

1

0

60

0

0

292

54

1

2

1

1

2

0

60

0

0

293

33

1

1

1

1

2

0

60

0

0

294

38

1

1

1

1

1

0

60

0

0

295

48

1

1

1

1

1

0

60

0

0

296

46

1

1

1

1

1

0

60

0

0

297

50

1

1

1

1

2

0

60

0

0

298

21

1

1

1

1

1

0

60

0

0

299

51

1

2

1

1

1

0

60

0

0

300

12

1

1

1

1

2

0

60

0

0

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1960–1969 301

35

1

1

1

1

1

0

60

0

0

302

35

1

1

1

1

1

0

60

0

0

303

17

1

2

1

1

2

0

60

0

0

304

81

1

2

1

2

2

0

60

0

0

305

49

1

1

1

1

1

0

60

0

0

306

58

1

2

1

2

2

0

60

0

0

307

50

1

2

1

1

1

0

60

0

0

308

78

1

1

1

1

1

0

60

0

0

309

46

1

1

1

1

1

0

60

0

0

310

55

1

2

1

1

1

0

60

0

0

311

51

1

1

1

2

2

0

60

0

0

312

43

1

1

1

2

2

0

60

0

0

313

62

1

1

1

1

1

0

60

0

0

314

73

1

1

1

1

1

0

60

0

0

315

42

1

1

1

1

1

0

60

0

0

316

68

1

1

1

1

2

0

60

0

0

317

41

1

1

1

1

1

0

60

0

0

Appendix B: Tables for the data base in chapter 7

382

318

62

1

1

1

1

1

0

60

0

0

319

31

1

1

1

1

1

0

60

0

0

320

61

1

1

1

1

1

0

60

0

0

321

26

1

2

1

1

2

0

60

0

0

322

41

1

1

1

2

2

0

60

0

0

323

56

2

1

1

2

2

0

60

0

0

324

52

2

1

1

1

1

0

60

0

0

325

58

1

2

1

1

1

0

60

0

0

326

64

1

1

1

2

2

0

60

0

0

327

52

1

2

1

1

1

0

60

0

0

328

69

2

1

1

1

1

0

60

0

0

329

76

1

1

1

1

1

0

60

0

0

330

30

1

2

1

1

1

0

60

0

0

331

35

2

1

1

2

2

0

60

0

0

332

43

2

2

1

2

2

0

60

0

0

333

46

1

1

1

1

2

0

60

0

0

334

22

1

1

1

1

1

0

60

0

0

335

72

1

1

1

1

1

0

60

0

0

336

37

1

1

1

1

1

0

60

0

0

337

20

1

1

1

1

2

0

60

0

0

338

32

1

2

1

1

1

0

60

0

0

339

24

1

1

1

2

2

0

60

0

0

340

50

1

2

1

1

1

0

60

0

0

341

54

1

1

1

1

1

0

60

0

0

342

32

2

1

1

1

2

0

60

0

0

343

67

1

1

1

1

2

0

60

0

0

344

48

1

1

1

1

1

0

60

0

0

345

37

1

1

1

1

1

0

60

0

0

346

19

1

2

1

1

1

0

60

0

0

347

37

1

2

1

1

1

0

60

0

0

348

82

2

2

1

2

2

0

60

0

0

349

16

2

1

1

1

2

0

60

0

0

350

30

2

2

1

8

2

0

60

0

0

Appendix B: Tables for the data base in chapter 7

383

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1960–1969 351

44

2

2

1

2

2

0

60

0

0

352

60

1

1

1

1

2

0

60

0

0

353

36

1

2

1

1

1

0

60

0

0

354

43

1

2

1

1

1

0

60

0

0

355

60

1

1

1

1

1

0

60

0

0

356

43

1

1

1

1

1

0

60

0

0

357

21

1

1

1

1

2

0

60

0

0

358

61

1

1

1

1

1

0

60

0

0

359

19

1

2

1

1

2

0

60

0

0

360

19

1

1

1

1

1

0

60

0

0

361

62

1

2

1

1

1

0

60

0

0

362

46

1

1

1

1

1

0

60

0

0

363

60

2

2

1

2

2

0

60

0

0

364

73

1

1

1

1

2

0

60

0

0

365

49

1

1

1

1

1

0

60

0

0

366

56

1

1

1

1

1

0

60

0

0

367

58

1

2

1

1

3

0

60

0

0

368

45

1

1

1

1

1

0

60

0

0

369

71

1

1

1

1

1

0

60

0

0

370

25

1

1

1

1

2

15

59

0

0

371

20

1

1

1

1

2

9

59

0

0

372

19

2

2

1

1

2

3

59

0

0

373

52

1

2

1

3

2

0

59

0

0

374

73

1

1

1

1

2

0

59

0

0

375

35

1

1

1

1

2

0

59

0

0

376

32

1

1

1

1

2

0

59

0

1

377

52

1

2

1

1

1

0

59

0

0

378

30

2

1

1

2

2

9

58

0

0

Appendix B: Tables for the data base in chapter 7

384

379

81

1

1

1

2

2

8

58

0

0

380

73

1

1

1

2

2

0

58

0

0

381

47

1

1

1

1

2

0

58

0

0

382

59

1

2

1

1

1

0

58

0

0

383

34

1

1

1

1

1

0

58

0

0

384

78

1

1

1

1

2

0

58

0

0

385

71

1

1

1

2

2

0

58

0

0

386

35

1

1

1

1

1

18

57

0

0

387

48

2

1

1

2

2

4

56

0

0

388

35

1

1

1

2

2

29

55

0

0

389

61

1

1

1

1

2

25

55

0

0

390

30

1

1

1

1

2

20

55

0

0

391

69

1

1

1

1

2

19

55

0

0

392

35

2

1

1

2

2

19

55

0

0

393

42

2

1

1

1

1

17

55

0

0

394

52

2

2

1

2

2

17

55

0

0

395

43

1

2

1

1

2

16

55

0

0

396

55

2

1

1

1

2

13

55

0

1

397

51

1

1

1

1

2

13

55

0

0

398

48

1

2

1

1

1

10

55

0

0

399

31

2

1

1

2

2

7

55

0

0

400

45

1

1

1

1

1

7

55

0

0

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1960–1969 401

35

1

1

1

1

1

5

55

0

0

402

23

2

1

1

2

2

0

55

0

0

403

23

2

2

1

2

2

0

55

0

0

404

55

1

1

1

1

2

0

55

0

0

405

61

1

2

1

1

2

0

55

0

0

406

65

1

1

1

1

1

0

55

0

0

Appendix B: Tables for the data base in chapter 7

385

407

19

1

1

1

1

2

0

55

0

0

408

22

2

1

1

1

5

0

55

0

0

409

39

2

1

1

1

1

0

55

0

0

410

35

1

1

1

1

1

0

55

0

0

411

24

1

1

1

1

1

0

55

0

0

412

54

1

2

1

1

1

0

55

0

0

413

76

1

1

1

]1

1

0

55

0

0

414

85

1

1

1

2

2

0

55

0

0

415

31

1

1

1

1

1

0

55

0

0

416

70

1

1

1

1

1

0

55

0

0

417

32

1

1

1

1

1

0

55

0

0

418

48

2

1

1

2

2

0

55

0

0

419

61

1

1

1

1

1

0

55

0

0

420

50

1

2

1

1

1

0

55

0

0

421

36

1

2

1

1

1

0

53

0

0

422

63

1

1

1

1

2

0

52

0

0

423

66

1

1

1

1

1

0

52

0

0

424

3

1

2

1

1

4

99

50

0

0

425

63

1

1

1

1

2

28

50

0

0

426

70

1

1

1

1

1

26

50

0

0

427

29

1

2

1

1

1

26

50

0

0

428

54

1

1

1

1

1

25

50

0

0

429

38

1

2

1

1

2

25

50

0

0

430

45

1

1

1

2

2

22

50

0

0

431

41

2

2

1

2

2

16

50

0

0

432

46

1

1

1

1

1

16

50

0

0

433

51

1

1

1

1

1

14

50

0

0

434

51

1

1

1

1

2

8

50

0

0

435

31

1

1

5

1

1

7

50

0

0

436

46

1

1

1

1

1

6

50

0

0

437

67

2

1

1

2

2

0

50

0

0

438

20

1

1

1

1

1

0

50

0

0

439

58

1

1

1

1

1

0

50

0

0

Appendix B: Tables for the data base in chapter 7

386

440

42

2

1

1

2

1

0

50

0

0

441

46

1

1

1

1

1

0

50

0

0

442

37

1

2

1

1

1

0

50

0

0

443

52

1

1

1

1

1

0

50

0

0

444

71

1

1

1

2

2

0

50

0

0

445

54

2

2

1

2

2

0

50

0

0

446

58

1

2

1

1

1

0

50

0

0

447

62

1

1

1

1

1

0

50

0

0

448

51

2

1

1

2

2

0

50

0

0

449

43

1

1

1

5

5

0

50

0

0

450

54

1

2

1

1

1

0

50

0

0

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1960–1969 451

51

1

1

1

1

1

0

50

0

0

452

52

1

1

1

1

2

0

50

0

0

453

24

1

1

1

1

1

0

50

0

0

454

40

1

1

1

1

1

0

50

0

0

455

22

1

1

1

1

1

0

50

0

0

456

36

1

2

1

2

2

0

47

0

0

457

4

1

1

1

1

4

99

45

0

0

458

71

1

1

1

2

2

0

45

0

0

459

1

2

2

1

2

2

99

42

0

0

460

59

1

1

1

1

1

0

40

0

1

461

47

1

1

1

1

1

0

40

0

0

462

60

1

1

1

1

2

0

35

0

2

463

48

2

2

1

2

2

0

35

0

0

464

80

1

2

1

2

2

0

32

0

0

465

60

1

2

6

3

2

23

30

0

0

466

72

1

1

1

2

2

0

25

0

0

467

73

1

1

1

2

2

0

25

0

0

Appendix B: Tables for the data base in chapter 7

387

468

53

1

1

6

1

5

0

25

0

1

469

25

2

2

5

2

2

0

20

0

0

470

67

1

1

1

1

2

13

19

0

0

471

59

1

1

5

1

5

0

17

0

1

472

21

1

1

7

1

2

0

15

0

1

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1960–1969 1

5

1

2

4

3

2

99

78

1

0

2

3

1

2

4

3

2

99

77

1

0

3

43

2

2

1

3

2

50

75

1

0

4

84

1

2

1

3

2

0

72

11

0

5

52

2

1

2

3

2

40

71

1

0

6

1

2

2

1

3

2

99

70

1

0

7

34

1

1

1

3

2

44

70

1

0

8

17

1

1

2

3

2

15

70

1

0

9

34

1

1

1

3

2

0

70

1

0

10

4

2

1

1

3

2

99

68

1

0

11

45

1

1

1

3

2

27

67

1

0

12

39

2

1

1

3

2

22

67

1

0

13

36

2

1

2

3

2

8

67

1

0

14

74

1

1

2

3

2

0

67

1

0

15

62

1

2

1

2

2

32

66

1

0

16

39

2

2

2

3

2

30

66

1

0

17

40

1

2

1

3

2

16

66

1

0

18

54

1

1

1

3

2

0

66

1

0

19

46

1

2

2

3

2

0

66

1

1

20

55

1

1

1

3

2

0

66

1

0

21

14

1

1

2

3

4

0

66

1

0

Appendix B: Tables for the data base in chapter 7

388

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1960–1969 22

2

2

2

2

3

2

99

65

1

0

23

4

2

2

2

3

2

99

65

1

0

24

3

2

2

1

3

2

99

65

1

0

25

13

2

2

2

3

2

99

65

1

0

26

11

2

1

2

3

2

99

65

1

0

27

3

2

2

1

3

2

99

65

1

1

28

4

2

2

1

3

2

99

65

1

0

29

1

2

2

1

3

2

99

65

1

0

30

4

2

1

1

3

2

99

65

1

0

31

2

2

2

1

3

2

99

65

1

0

32

5

2

2

1

3

2

99

65

1

0

33

54

1

1

1

7

2

45

65

1

0

34

42

1

2

1

3

2

36

65

1

0

35

54

1

1

2

1

2

36

65

1

0

36

36

1

1

4

3

2

34

65

1

0

37

54

1

2

2

3

2

29

65

1

0

38

52

1

1

1

3

2

25

65

1

0

39

35

1

2

1

3

2

25

65

1

0

40

59

1

1

4

3

2

20

65

1

0

41

40

2

1

2

3

2

16

65

1

0

42

63

1

1

1

3

2

11

65

1

0

43

78

1

1

1

3

2

9

65

1

0

44

59

2

1

2

3

2

8

65

1

0

45

53

1

1

1

7

5

5

65

1

0

46

73

1

2

1

3

2

0

65

1

0

47

81

1

1

2

3

2

0

65

1

0

48

72

1

1

1

3

2

0

65

1

0

49

77

2

1

1

3

2

0

65

1

0

Appendix B: Tables for the data base in chapter 7

389

50

69

1

1

4

3

2

0

65

1

0

51

67

1

1

4

3

2

0

65

1

0

52

68

2

2

2

3

2

0

65

1

0

53

38

2

1

1

5

2

0

65

1

0

54

74

1

2

1

3

2

0

65

1

0

55

33

2

2

2

3

2

0

65

1

0

56

52

1

2

1

3

2

0

65

1

0

57

47

1

2

1

3

2

0

65

1

0

58

78

1

2

1

3

2

0

65

1

0

59

72

1

2

1

3

3

0

65

1

0

60

1

2

1

1

3

2

99

64

1

0

61

56

1

2

2

3

2

25

64

1

0

62

30

1

1

4

3

2

21

64

1

0

63

72

1

1

2

3

2

15

64

1

0

64

3

2

1

1

3

2

99

63

1

0

65

50

1

1

1

3

2

22

63

1

0

66

40

1

1

1

3

2

16

63

1

0

67

5

1

1

2

3

4

0

63

1

0

68

5

2

1

1

3

2

0

63

1

0

69

84

2

1

2

3

2

0

63

1

0

70

8

1

1

4

3

2

99

62

1

0

71

1

1

1

2

3

2

99

62

1

0

Fire st

Surv

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire Cases 1960–1969 72

41

2

1

2

4

2

29

62

1

0

73

63

1

2

1

7

2

26

62

1

0

74

32

1

1

1

3

2

12

62

1

0

75

60

1

1

1

3

2

9

62

1

0

76

51

1

1

2

3

2

0

62

1

0

77

8

2

1

1

3

2

0

62

1

0

Appendix B: Tables for the data base in chapter 7

390

78

67

1

2

2

3

4

0

62

1

0

79

3

2

1

2

3

2

99

61

1

0

80

29

2

1

1

3

2

32

61

1

0

81

56

1

2

1

3

2

25

61

1

0

82

20

2

1

2

3

2

17

61

1

0

83

2

2

1

2

3

2

99

60

1

0

84

3

2

1

1

3

2

99

60

1

0

85

3

2

1

2

3

2

99

60

1

0

86

7

1

1

4

3

2

99

60

1

0

87

3

2

1

1

3

2

99

60

1

0

88

3

2

1

1

3

4

99

60

1

0

89

4

1

1

1

3

2

99

60

1

0

90

4

2

1

4

3

2

99

60

1

0

91

2

1

2

1

3

2

99

60

1

0

92

1

2

1

2

7

2

99

60

1

0

93

2

1

2

2

3

2

99

60

1

0

94

1

1

2

1

3

2

99

60

1

0

95

4

2

1

2

3

2

99

60

1

0

96

1

2

1

1

3

4

99

60

1

0

97

2

2

1

2

3

2

99

60

1

0

98

2

2

1

2

3

2

99

60

1

0

99

5

1

2

1

3

2

99

60

1

0

100

5

2

1

2

3

2

99

60

1

0

101

13

2

2

2

3

2

99

60

1

0

102

2

1

2

1

3

2

99

60

1

0

103

12

2

1

2

3

2

99

60

1

0

104

2

2

2

1

3

4

99

60

1

0

105

4

2

2

4

3

2

99

60

1

0

106

1

1

1

2

3

2

99

60

1

0

107

6

2

1

1

3

2

99

60

1

0

108

55

1

1

1

3

2

45

60

1

0

109

44

1

2

2

7

3

40

60

1

0

110

37

1

1

1

3

2

36

60

1

0

Appendix B: Tables for the data base in chapter 7

391

111

50

2

1

2

3

2

34

60

1

0

112

48

1

2

2

3

3

34

60

1

0

113

63

1

1

4

3

2

29

60

1

0

114

65

2

1

2

3

2

28

60

1

0

115

42

2

1

2

3

2

28

60

1

0

116

48

1

2

2

3

2

27

60

1

0

117

35

2

1

1

3

2

27

60

1

0

118

60

1

2

1

3

2

27

60

1

0

119

43

2

1

2

3

2

25

60

1

0

120

28

1

2

1

3

2

25

60

1

0

121

77

1

1

1

7

2

23

60

1

0

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1960–1969 122

41

1

1

1

3

2

22

60

1

0

123

77

1

1

2

3

3

22

60

1

0

124

35

1

2

1

3

2

21

60

1

0

125

60

1

2

1

7

2

21

60

1

0

126

41

1

1

2

4

2

19

60

1

0

127

60

1

1

1

3

2

18

60

1

0

128

51

1

2

1

7

2

18

60

1

0

129

42

1

1

1

3

2

17

60

1

0

130

39

1

1

1

3

2

16

60

1

0

131

53

1

2

2

3

2

14

60

1

0

132

49

2

2

1

3

4

12

60

1

0

133

64

1

1

2

3

2

11

60

1

0

134

22

1

1

2

3

2

10

60

1

0

135

71

1

2

1

3

2

10

60

1

0

136

79

1

1

2

3

2

10

60

1

0

137

48

1

1

2

3

2

8

60

1

0

138

50

2

1

1

3

2

7

60

1

0

Appendix B: Tables for the data base in chapter 7

392

139

20

1

2

1

3

2

7

60

1

0

140

78

1

2

2

3

2

5

60

1

0

141

37

1

2

2

3

2

2

60

1

0

142

83

1

1

2

3

2

0

60

1

0

143

89

1

2

1

3

2

0

60

1

0

144

6

2

1

1

3

2

0

60

1

0

145

65

2

1

2

3

2

0

60

1

0

146

8

1

1

4

3

2

0

60

1

0

147

8

1

1

1

3

2

0

60

1

0

148

73

1

1

2

3

2

0

60

1

0

149

52

1

1

1

3

2

0

60

1

0

150

68

1

2

1

3

2

0

60

1

0

151

82

1

1

1

3

2

0

60

1

0

152

20

1

2

1

3

2

0

60

1

0

153

50

1

2

4

4

1

0

60

1

0

154

64

1

2

2

3

2

0

60

1

0

155

76

2

2

2

3

2

0

60

1

0

156

63

2

1

1

3

2

0

60

1

0

157

54

1

2

2

3

2

0

60

1

0

158

67

1

1

2

3

2

0

60

1

0

159

39

1

1

1

3

2

0

60

1

0

160

12

1

1

2

3

2

0

60

1

0

161

5

2

2

2

3

2

0

60

1

0

162

54

1

2

4

4

1

0

60

1

0

163

59

1

2

4

3

2

0

60

1

0

164

42

2

2

2

3

2

0

60

1

0

165

31

1

2

1

3

2

0

60

1

0

166

71

1

1

4

7

2

0

60

1

0

167

83

1

1

1

3

2

0

60

1

0

168

3

2

2

1

3

2

99

59

1

1

169

49

1

1

1

3

2

16

59

1

0

170

60

1

1

4

3

2

15

59

1

0

171

21

1

1

2

3

2

12

59

1

0

Appendix B: Tables for the data base in chapter 7

393

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1960–1969 172

70

1

1

2

3

2

2

59

1

0

173

48

1

2

1

3

2

0

59

1

0

174

25

1

2

2

3

1

0

59

1

0

175

49

1

1

2

3

2

0

59

1

0

176

3

1

1

2

3

2

99

58

1

0

177

34

2

1

2

3

2

40

58

1

0

178

62

1

1

1

3

2

34

58

1

0

179

56

1

2

2

7

3

26

58

1

0

180

84

1

1

1

3

2

14

58

1

0

181

3

2

2

1

3

2

0

58

1

0

182

49

1

2

1

3

2

0

58

1

0

183

9

2

2

1

3

2

0

57

1

0

184

49

1

2

1

3

2

0

57

1

0

185

69

1

2

2

4

2

0

57

1

4

186

4

2

1

2

3

2

99

56

1

0

187

26

1

1

4

3

2

0

56

1

0

188

6

2

2

1

3

2

99

55

1

0

189

1

2

2

2

3

2

99

55

1

0

190

2

1

1

2

3

2

99

55

1

0

191

1

1

2

1

3

2

99

55

1

0

192

2

1

2

1

3

2

99

55

1

0

193

2

1

1

1

3

2

99

55

1

0

194

1

1

1

2

3

2

99

55

1

0

195

2

1

1

1

3

2

99

55

1

0

196

3

2

1

2

3

2

99

55

1

0

197

4

2

2

2

3

2

99

55

1

0

198

1

1

1

1

3

2

99

55

1

0

199

9

2

2

1

3

4

99

55

1

0

Appendix B: Tables for the data base in chapter 7

394

200

1

2

2

1

3

2

99

55

1

0

201

30

1

1

2

1

2

37

55

1

0

202

42

2

1

4

7

2

35

55

1

0

203

50

1

2

1

3

2

28

55

1

0

204

34

1

2

1

1

2

27

55

1

0

205

39

1

1

2

3

2

25

55

1

0

206

48

1

1

2

1

2

25

55

1

0

207

62

1

2

2

3

2

23

55

1

0

208

67

1

2

2

3

4

21

55

1

0

209

77

1

1

2

3

2

19

55

1

0

210

45

1

2

1

3

2

19

55

1

0

211

27

2

1

1

3

2

14

55

1

0

212

47

1

2

2

3

2

11

55

1

0

213

31

2

2

2

3

2

1

55

1

0

214

26

1

2

1

3

2

0

55

1

0

215

73

1

1

1

3

3

0

55

1

0

216

5

2

1

1

3

2

0

55

1

0

217

4

1

2

2

3

4

0

55

1

0

218

50

2

2

2

3

2

0

55

1

0

219

11

1

1

2

3

2

0

55

1

0

220

4

2

1

1

3

2

0

55

1

0

221

6

2

2

1

3

2

0

55

1

0

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1960–1969 222

55

2

2

2

3

2

0

55

1

0

223

57

2

2

1

3

2

0

55

1

0

224

74

1

1

1

3

2

0

55

1

0

225

4

1

1

1

3

2

99

53

1

1

226

2

1

1

1

3

2

99

52

1

0

227

80

1

2

4

4

2

20

52

1

0

Appendix B: Tables for the data base in chapter 7

395

228

80

2

1

2

3

2

0

52

1

0

229

1

2

1

4

3

2

99

51

1

0

230

5

2

2

2

3

2

99

50

1

0

231

3

2

1

2

3

2

99

50

1

0

232

1

2

2

2

3

2

99

50

1

0

233

5

1

1

1

3

2

99

50

1

0

234

9

2

2

2

3

2

99

50

1

0

235

2

2

1

2

3

2

99

50

1

0

236

3

2

9

1

3

2

99

50

1

0

237

5

2

1

2

3

2

99

50

1

0

238

3

2

1

2

3

2

99

50

1

0

239

1

2

1

2

3

2

99

50

1

0

240

7

2

1

2

3

2

99

50

1

0

241

4

2

1

1

3

2

99

50

1

0

242

46

2

1

2

3

2

46

50

1

0

243

59

1

1

1

3

2

37

50

1

0

244

30

1

1

2

1

2

31

50

1

0

245

50

2

1

2

3

2

30

50

1

0

246

46

1

2

1

3

2

25

50

1

0

247

66

1

2

4

3

2

24

50

1

0

248

73

1

2

2

3

2

24

50

[

0

249

57

1

2

2

3

2

23

50

1

0

250

76

1

2

4

3

2

10

50

1

0

251

70

1

1

4

3

2

1

50

1

0

252

70

1

1

1

3

2

0

50

1

0

253

67

1

1

1

3

2

0

50

1

0

254

62

2

1

1

3

2

0

50

1

0

255

60

1

2

2

3

2

0

50

1

0

256

83

1

2

1

3

2

0

50

1

0

257

59

2

1

2

3

2

0

50

1

0

258

39

2

1

2

7

2

0

50

1

0

259

75

1

2

1

3

2

0

50

1

0

260

24

1

1

2

3

2

12

47

1

0

Appendix B: Tables for the data base in chapter 7

396

261

58

1

1

1

3

2

27

46

1

0

262

2

2

1

1

3

2

99

45

1

0

263

35

2

1

2

1

2

28

45

1

0

264

26

2

2

2

3

2

0

45

1

0

265

81

1

1

1

3

2

0

42

1

0

266

4

2

1

2

3

2

99

40

1

0

267

21

2

1

2

3

2

28

40

1

0

268

72

2

1

2

4

2

0

40

1

0

269

70

2

1

4

3

2

0

40

1

0

270

55

1

1

8

8

2

0

40

1

0

271

58

1

2

2

3

2

0

35

1

0

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1960–1969 272

4

2

2

2

3

2

99

34

1

0

273

43

1

1

4

7

5

0

30

1

0

274

4

2

1

1

3

2

0

30

1

0

275

2

1

1

4

3

2

99

27

1

0

276

47

1

1

2

3

1

0

27

1

0

277

35

1

2

1

3

2

28

25

1

2

278

70

1

1

2

3

2

27

25

1

0

279

39

2

1

2

3

2

23

25

1

0

280

52

1

1

4

7

5

0

24

1

0

281

51

1

1

4

4

2

17

22

1

0

282

65

1

1

2

3

2

0

22

1

3

283

76

1

1

4

3

2

0

22

1

3

284

1

1

1

2

3

2

99

20

1

0

285

43

2

1

4

3

2

50

20

1

0

286

64

1

2

4

4

2

0

20

1

0

287

65

1

2

4

4

2

0

20

1

0

288

89

1

1

2

3

2

0

19

1

0

Appendix B: Tables for the data base in chapter 7

397

289

48

1

1

4

3

2

38

17

1

0

290

72

1

1

4

3

2

0

17

1

0

291

61

1

1

4

3

2

41

16

1

0

292

58

2

1

4

3

2

4

16

1

0

293

27

1

1

4

4

1

0

15

1

0

294

55

1

1

6

3

2

0

15

1

0

295

61

2

2

4

4

2

0

15

1

0

296

37

1

2

2

3

2

0

15

1

0

297

73

1

1

6

3

2

0

15

1

1

298

78

1

2

5

3

2

0

13

1

0

299

43

2

1

4

4

2

28

12

1

0

300

39

1

2

4

4

2

0

12

1

5

301

67

2

1

4

4

2

0

11

1

0

302

1

2

1

4

3

2

99

10

1

0

303

86

1

1

4

3

2

99

10

1

0

304

53

1

1

4

3

2

55

10

1

0

305

51

2

1

4

4

2

9

10

1

0

306

73

2

1

4

4

2

0

10

1

0

307

57

1

1

6

7

5

0

10

1

0

308

78

1

2

1

3

2

0

10

1

0

309

41

1

2

2

4

2

0

10

1

0

310

42

1

1

2

3

2

0

9

1

0

311

66

1

2

2

3

2

0

8

1

0

312

21

1

1

8

1

2

19

7

1

0

CWRU Data Base—All Cases between 1960 and 1969 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Other Cases 1960–1969 1

1

2

2

4

8

2

99

59

2

0

2

84

2

1

2

3

2

13

55

2

0

3

25

1

1

7

7

5

8

40

2

0

4

23

1

1

2

8

2

0

34

2

0

Appendix B: Tables for the data base in chapter 7

398

5

46

2

1

4

8

2

0

23

2

0

6

43

2

2

4

3

2

42

15

2

0

1

61

1

1

1

1

1

0

38

9

0

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1970–1979 1

30

1

2

1

1

1

10

75

0

0

2

71

1

1

1

1

1

0

73

0

0

3

28

1

1

1

1

1

12

70

0

0

4

41

1

1

1

1

1

0

70

0

0

5

48

1

1

1

1

1

0

70

0

0

6

32

1

1

1

1

2

0

70

0

0

7

79

1

1

1

1

1

0

70

0

0

8

47

1

1

1

1

1

0

69

0

0

9

40

2

1

1

2

2

2

68

0

0

10

29

1

1

1

1

1

0

68

0

0

11

21

2

1

1

1

5

0

67

0

0

12

1

1

1

1

5

2

99

65

0

0

13

66

2

1

1

2

2

99

65

0

0

14

57

1

2

1

1

1

68

65

0

0

15

42

1

1

1

1

1

41

65

0

0

16

25

1

2

1

1

1

37

65

0

0

17

75

1

1

1

1

1

36

65

0

0

18

73

1

1

1

1

1

34

65

0

0

19

40

1

1

1

1

2

33

65

0

0

20

71

2

1

1

2

2

32

65

0

0

21

54

1

1

1

1

1

31

65

0

0

22

49

1

1

1

1

2

30

65

0

0

23

53

1

2

1

1

1

30

65

0

0

24

33

1

2

1

1

1

29

65

0

0

25

57

1

1

1

1

2

29

65

0

0

Appendix B: Tables for the data base in chapter 7

399

26

71

1

1

1

1

2

29

65

0

0

27

44

1

1

1

1

1

28

65

0

0

28

54

1

2

1

1

1

27

65

0

0

29

50

1

1

1

1

2

27

65

0

0

30

43

1

2

1

1

1

27

65

0

0

31

48

1

2

1

1

1

27

65

0

0

32

68

1

1

1

1

1

27

65

0

0

33

52

2

1

1

1

2

26

65

0

0

34

44

1

1

1

1

2

26

65

0

1

35

53

1

2

1

1

1

26

65

0

0

36

41

1

1

1

1

2

26

65

0

0

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1970–1979 37

26

1

1

1

1

2

25

65

0

0

38

49

1

2

1

1

2

25

65

0

0

39

50

2

1

1

2

2

25

65

0

0

40

60

1

1

1

3

2

24

65

0

0

41

47

1

1

1

1

1

24

65

0

0

42

62

1

1

1

1

2

24

65

0

0

43

48

1

2

1

1

2

22

65

0

0

44

60

1

2

1

1

1

22

65

0

0

45

30

1

1

1

1

2

22

65

0

0

46

52

1

2

1

1

1

22

65

0

0

47

48

2

1

1

1

2

22

65

0

0

48

23

2

1

1

1

2

21

65

0

0

49

58

1

1

1

1

2

21

65

0

0

50

20

1

1

1

1

1

21

65

0

0

51

29

1

1

1

1

1

21

65

0

0

52

22

1

1

1

1

2

20

65

0

0

53

39

2

1

1

1

2

20

65

0

0

Appendix B: Tables for the data base in chapter 7

400

54

49

1

1

1

1

1

20

65

0

0

55

54

1

1

1

1

1

19

65

0

0

56

30

1

1

1

1

2

19

65

0

0

57

59

1

1

1

1

1

19

65

0

0

58

41

1

1

1

1

1

18

65

0

0

59

34

1

2

1

1

2

18

65

0

0

60

26

1

2

1

1

1

17

65

0

0

61

51

1

2

1

1

1

17

65

0

0

62

46

1

1

1

1

2

17

65

0

0

63

45

1

1

1

1

2

17

65

0

0

64

31

1

1

1

1

1

17

65

0

0

65

24

1

1

1

1

1

17

65

0

0

66

50

1

2

1

1

1

17

65

0

0

67

23

1

1

1

1

2

16

65

0

0

68

66

1

1

1

1

1

16

65

0

0

69

33

1

1

1

1

2

16

65

0

0

70

30

1

1

1

1

2

16

65

0

0

71

41

1

1

1

1

2

15

65

0

0

72

60

1

2

1

1

3

14

65

0

0

73

45

2

1

1

1

2

14

65

0

0

74

22

1

1

1

1

1

13

65

0

0

75

53

1

1

1

1

1

13

65

0

0

76

50

1

2

1

1

2

13

65

0

0

77

22

1

1

1

1

2

13

65

0

0

78

42

1

1

1

1

2

13

65

0

0

79

48

1

1

1

1

1

12

65

0

0

80

31

1

1

1

1

2

12

65

0

0

81

27

1

1

1

1

2

12

65

0

0

82

69

1

2

1

1

1

12

65

0

0

83

53

1

1

1

1

2

12

65

0

0

84

60

1

1

1

1

2

12

65

0

0

85

29

1

1

1

1

2

12

65

0

0

86

73

1

1

1

1

2

11

65

0

0

Appendix B: Tables for the data base in chapter 7

401

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1970–1979 87

30

1

1

1

1

2

11

65

0

0

88

21

1

1

1

1

1

11

65

0

0

89

68

1

1

1

1

1

11

65

0

0

90

64

1

1

1

1

2

10

65

0

0

91

30

1

1

1

1

2

10

65

0

0

92

21

1

1

1

1

2

10

65

0

0

93

42

1

1

1

1

1

10

65

0

0

94

35

1

2

1

1

1

10

65

0

0

95

69

1

2

1

1

1

10

65

0

0

96

27

1

1

1

1

1

9

65

0

0

97

21

1

1

1

1

1

9

65

0

0

98

43

1

2

1

1

1

9

65

0

0

99

65

1

2

1

1

1

9

65

0

0

100

50

1

1

1

1

2

9

65

0

0

101

24

1

1

1

1

1

8

65

0

0

102

48

1

2

1

1

1

8

65

0

0

103

50

2

1

1

1

2

8

65

0

0

104

53

1

1

1

1

1

8

65

0

0

105

30

1

2

1

1

2

8

65

0

0

106

69

1

2

1

1

1

7

65

0

0

107

51

1

2

1

1

1

7

65

0

0

108

57

1

2

1

1

1

6

65

0

0

109

17

2

2

1

1

1

6

65

0

1

110

20

1

1

1

1

2

6

65

0

0

111

53

1

1

1

1

1

6

65

0

0

112

44

2

1

1

1

2

6

65

0

0

113

62

1

1

1

1

1

5

65

0

0

114

57

1

2

1

1

1

5

65

0

0

Appendix B: Tables for the data base in chapter 7

402

115

29

1

1

1

1

1

5

65

0

0

116

27

1

1

1

1

1

5

65

0

0

117

21

1

1

1

1

1

5

65

0

0

118

52

1

1

1

1

1

4

65

0

0

119

22

2

1

1

2

2

4

65

0

0

120

17

1

2

1

1

2

4

65

0

0

121

40

2

1

1

1

2

4

65

0

0

122

28

1

1

1

1

2

4

65

0

0

123

65

1

1

1

1

1

3

65

0

0

124

49

1

2

1

1

1

3

65

0

1

125

72

2

1

1

5

5

3

65

0

0

126

17

1

1

1

1

2

2

65

0

0

127

42

1

2

1

1

1

2

65

0

0

128

53

1

1

1

1

1

2

65

0

0

129

47

1

1

1

1

1

2

65

0

0

130

63

1

1

1

1

2

1

65

0

0

131

24

1

1

1

1

1

1

65

0

0

132

62

1

2

1

1

2

1

65

0

0

133

25

2

1

1

2

2

1

65

0

0

134

20

1

2

1

1

1

0

65

0

0

135

16

1

2

1

1

2

0

65

0

0

136

32

1

2

1

1

1

0

65

0

0

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1970–1979 137

52

1

2

1

1

1

0

65

0

0

138

43

1

2

1

1

1

0

65

0

0

139

47

1

1

1

2

2

0

65

0

0

140

27

1

1

1

1

2

0

65

0

0

141

22

1

1

1

1

1

0

65

0

0

142

33

1

1

1

1

1

0

65

0

0

Appendix B: Tables for the data base in chapter 7

403

143

17

1

1

1

1

1

0

65

0

0

144

37

1

2

1

1

1

0

65

0

0

145

23

1

1

1

1

1

0

65

0

1

146

33

1

1

1

1

1

0

65

0

0

147

68

1

1

1

1

1

0

65

0

0

148

27

2

1

1

1

1

0

65

0

0

149

28

1

1

1

1

1

0

65

0

0

150

57

1

1

1

1

1

0

65

0

1

151

32

1

1

1

1

2

0

65

0

0

152

63

1

2

1

1

1

0

65

0

0

153

57

1

1

1

1

1

0

65

0

0

154

16

1

1

1

1

1

0

65

0

0

155

24

1

2

1

1

1

0

65

0

0

156

34

2

2

1

2

2

0

65

0

0

157

52

1

2

1

1

1

0

65

0

0

158

87

1

2

1

1

1

0

65

0

0

159

17

1

2

1

1

1

0

65

0

0

160

55

1

2

1

1

1

0

65

0

0

161

65

1

1

1

1

1

0

65

0

0

162

70

1

1

1

1

2

0

65

0

0

163

53

1

1

1

1

1

0

65

0

0

164

12

1

1

1

1

2

0

65

0

0

165

27

1

1

1

1

1

0

65

0

0

166

76

1

2

1

1

1

0

65

0

1

167

38

1

2

1

1

1

0

65

0

0

168

12

1

1

1

1

2

0

65

0

0

169

45

1

2

1

1

1

0

65

0

0

170

58

1

1

1

1

1

0

65

0

0

171

25

1

2

1

1

2

0

65

0

0

172

59

1

1

1

1

1

0

65

0

0

173

42

1

1

1

1

1

0

65

0

0

174

22

2

1

1

1

1

0

65

0

0

175

38

1

2

1

1

1

0

65

0

0

Appendix B: Tables for the data base in chapter 7

404

176

53

1

2

1

1

1

0

65

0

0

177

47

1

1

1

1

1

0

65

0

0

178

36

1

2

1

1

1

0

65

0

0

179

17

1

1

1

2

2

0

65

0

0

180

64

1

1

1

1

1

0

65

0

0

181

68

1

2

1

1

1

0

65

0

0

182

17

1

1

1

1

1

0

65

0

1

183

55

1

1

1

1

1

0

65

0

0

184

32

1

1

1

1

1

0

65

0

0

185

25

1

1

1

1

1

0

65

0

0

186

33

1

1

1

1

1

0

65

0

0

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1970–1979 187

64

1

2

1

1

1

0

65

0

0

188

28

1

1

1

1

1

0

65

0

0

189

40

1

2

1

1

1

0

65

0

0

190

46

2

1

1

1

1

0

65

0

0

191

38

2

1

1

1

1

0

65

0

0

192

53

1

1

1

1

2

0

65

0

0

193

26

1

2

1

1

1

0

65

0

0

194

35

2

1

1

1

1

0

65

0

0

195

22

1

1

1

1

1

0

65

0

0

196

20

2

1

1

1

2

0

65

0

0

197

48

1

2

1

1

1

0

65

0

0

198

81

1

1

1

1

1

0

65

0

0

199

21

1

2

1

1

2

0

65

0

0

200

59

1

2

1

1

1

0

65

0

0

201

37

1

2

1

1

1

0

65

0

0

202

57

1

1

1

1

1

0

65

0

0

203

82

1

2

1

1

1

0

65

0

0

Appendix B: Tables for the data base in chapter 7

405

204

61

1

1

1

1

2

0

65

0

0

205

77

1

1

1

1

1

0

65

0

0

206

65

1

1

1

1

1

0

65

0

0

207

44

1

1

1

1

1

0

65

0

0

208

19

1

2

1

1

1

0

65

0

0

209

58

1

2

1

1

1

0

65

0

0

210

39

1

2

1

1

1

0

65

0

0

211

54

1

1

1

1

2

0

65

0

0

212

29

1

2

1

1

1

0

65

0

0

213

35

1

1

1

1

1

0

65

0

0

214

21

1

2

1

1

1

0

65

0

0

215

57

1

1

1

1

1

0

65

0

0

216

32

1

1

1

1

1

0

65

0

0

217

23

1

1

1

1

1

0

65

0

0

218

19

2

2

1

1

2

0

65

0

0

219

36

1

2

1

1

1

0

65

0

0

220

57

1

2

1

1

1

0

65

0

0

221

62

1

1

1

1

1

0

65

0

0

222

27

1

1

1

1

1

0

65

0

0

223

47

1

2

1

1

1

0

65

0

0

224

59

1

2

1

1

1

0

65

0

1

225

88

1

1

1

1

2

0

65

0

0

226

20

1

2

1

1

1

0

65

0

0

227

27

2

1

1

1

1

0

65

0

0

228

35

1

1

1

1

1

0

65

0

0

229

43

1

2

1

1

1

0

65

0

0

230

69

1

2

1

1

1

0

65

0

0

231

18

1

1

1

1

2

0

65

0

0

232

81

1

1

1

1

2

0

65

0

0

233

48

1

2

1

1

1

0

65

0

0

234

65

1

1

1

1

1

0

65

0

0

235

80

1

1

1

1

1

0

65

0

0

236

57

1

1

1

1

1

0

65

0

0

Appendix B: Tables for the data base in chapter 7

406

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1970–1979 237

44

1

1

1

1

2

0

65

0

0

238

77

1

1

1

1

1

0

65

0

0

239

50

1

1

1

1

2

0

65

0

0

240

50

1

2

1

1

1

0

65

0

0

241

62

1

1

1

1

1

0

65

0

0

242

20

1

1

1

1

1

0

65

0

0

243

43

1

2

1

1

1

0

65

0

0

244

64

1

2

1

1

1

0

65

0

0

245

20

1

1

1

1

1

0

65

0

0

246

46

1

2

1

1

1

0

65

0

0

247

62

1

2

1

1

1

0

65

0

0

248

49

1

2

1

1

1

0

65

0

0

249

58

1

1

1

1

1

0

65

0

0

250

21

1

1

1

1

1

0

65

0

0

251

73

1

1

1

1

1

0

65

0

0

252

22

1

1

1

1

1

0

65

0

0

253

20

1

2

1

1

1

0

65

0

0

254

37

1

1

1

1

1

0

65

0

0

255

50

1

2

1

1

1

0

65

0

0

256

58

1

2

1

1

1

0

65

0

0

257

66

1

2

1

1

1

0

65

0

0

258

66

1

1

1

1

1

0

65

0

0

259

50

1

2

1

1

1

0

65

0

0

260

84

1

1

1

2

2

0

65

0

0

261

69

1

1

1

1

1

0

65

0

0

262

47

1

1

1

1

1

0

65

0

0

263

23

1

2

1

1

1

0

65

0

0

264

58

1

1

1

1

1

0

65

0

0

Appendix B: Tables for the data base in chapter 7

407

265

38

1

1

1

1

2

0

65

0

0

266

74

1

2

1

1

1

0

65

0

0

267

58

1

2

1

1

1

0

65

0

0

268

18

1

1

1

1

2

0

65

0

0

269

81

1

2

1

1

1

0

65

0

0

270

23

1

1

1

1

1

0

65

0

0

271

53

1

1

1

1

2

0

65

0

0

272

39

1

2

1

1

1

0

65

0

0

273

27

1

1

1

1

1

0

65

0

0

274

36

1

2

1

1

1

0

65

0

0

275

31

1

2

1

1

1

0

65

0

0

276

35

1

2

1

1

1

0

65

0

0

277

53

1

2

1

1

1

0

65

0

0

278

28

2

1

1

2

2

0

65

0

0

279

51

1

2

1

1

1

0

65

0

0

280

18

1

1

1

1

1

0

65

0

0

281

28

1

1

1

1

1

0

65

0

0

282

51

1

2

1

1

1

0

65

0

0

283

35

1

1

1

1

2

0

65

0

0

284

69

1

1

1

1

1

0

65

0

0

285

18

2

1

1

1

2

0

65

0

0

286

29

1

1

1

1

1

0

65

0

0

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1970–1979 287

69

1

1

1

1

1

0

65

0

0

288

21

1

1

1

1

1

0

65

0

0

289

65

1

1

1

1

1

0

65

0

0

290

24

2

1

1

1

2

0

65

0

0

291

64

1

2

1

1

1

0

65

0

0

292

57

1

2

1

1

1

0

65

0

0

Appendix B: Tables for the data base in chapter 7

408

293

75

1

2

1

1

1

0

65

0

0

294

33

1

2

1

1

1

0

65

0

0

295

27

1

1

1

1

2

0

65

0

0

296

49

1

2

1

1

2

22

64

0

1

297

48

2

1

1

1

2

20

64

0

0

298

42

1

1

1

1

2

15

64

0

0

299

57

1

1

1

1

1

0

64

0

0

300

19

1

1

1

1

2

0

64

0

0

301

28

1

1

1

1

1

0

64

0

0

302

42

1

2

1

1

1

0

63

0

0

303

65

2

2

1

2

2

0

63

0

0

304

21

1

1

1

1

1

0

63

0

1

305

47

1

2

1

1

1

26

62

0

0

306

49

1

1

1

1

1

14

62

0

0

307

44

1

2

1

1

1

14

62

0

0

308

20

1

1

1

1

1

0

62

0

1

309

83

1

2

1

2

2

0

62

0

0

310

82

1

1

1

1

2

0

62

0

1

311

47

1

1

1

1

2

0

62

0

1

312

47

1

2

1

1

1

0

62

0

0

313

57

1

1

1

1

1

29

61

0

1

314

30

1

1

1

1

1

16

61

0

0

315

8

1

1

1

1

2

99

60

0

1

316

6

1

2

1

1

2

99

60

0

0

317

44

1

1

1

1

1

50

60

0

0

318

34

1

1

1

1

2

36

60

0

0

319

47

1

1

1

1

2

33

60

0

0

320

46

1

1

1

1

1

32

60

0

0

321

43

1

1

1

1

2

28

60

0

0

322

42

1

1

1

1

1

27

60

0

0

323

46

2

1

1

2

2

27

60

0

0

324

45

1

1

1

1

2

25

60

0

0

325

53

1

1

1

1

1

25

60

0

0

Appendix B: Tables for the data base in chapter 7

409

326

36

2

1

1

1

2

24

60

0

0

327

33

1

1

1

1

2

24

60

0

0

328

29

2

1

1

1

2

24

60

0

0

329

47

2

1

1

1

2

23

60

0

0

330

52

1

1

1

1

2

23

60

0

0

331

45

1

2

1

1

1

23

60

0

0

332

61

1

1

1

1

1

21

60

0

0

333

55

2

2

1

1

2

20

60

0

0

334

39

1

1

1

1

1

20

60

0

0

335

32

1

1

1

1

2

20

60

0

0

336

55

2

1

1

1

2

19

60

0

0

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1970–1979 337

40

1

1

1

1

2

19

60

0

0

338

31

1

1

1

1

2

18

60

0

0

339

32

2

1

1

1

2

18

60

0

0

340

52

1

1

1

1

1

18

60

0

0

341

31

1

1

1

1

2

17

60

0

0

342

46

1

1

1

1

1

17

60

0

0

343

67

1

1

1

1

1

16

60

0

0

344

29

2

2

1

1

2

16

60

0

0

345

23

1

1

1

1

2

16

60

0

0

346

37

1

2

1

1

1

16

60

0

0

347

64

1

1

1

1

2

15

60

0

0

348

51

1

1

1

1

1

15

60

0

0

349

29

1

2

1

1

1

15

60

0

0

350

67

1

1

1

1

1

14

60

0

0

351

48

1

1

1

1

1

13

60

0

0

352

30

1

2

1

1

1

12

60

0

0

353

68

1

1

1

1

1

12

60

0

0

Appendix B: Tables for the data base in chapter 7

410

354

33

1

1

1

1

1

12

60

0

0

355

21

1

1

1

1

3

11

60

0

0

356

51

1

2

1

1

1

11

60

0

0

357

35

1

2

1

1

3

11

60

0

0

358

58

1

1

1

1

1

10

60

0

0

359

19

1

1

1

1

2

10

60

0

0

360

33

1

1

1

1

2

9

60

0

0

361

38

2

1

1

1

1

9

60

0

0

362

39

1

2

1

1

1

9

60

0

0

363

47

1

1

1

1

1

9

60

0

0

364

36

1

2

1

1

1

8

60

0

0

365

30

2

2

1

1

1

8

60

0

0

366

25

1

1

1

1

1

8

60

0

0

367

21

1

1

1

1

2

7

60

0

0

368

43

1

1

1

1

2

7

60

0

0

369

38

1

1

1

1

1

6

60

0

0

370

27

1

1

1

1

1

6

60

0

0

371

36

1

1

1

1

1

6

60

0

0

372

43

1

1

1

1

1

4

60

0

0

373

75

1

2

1

1

1

4

60

0

0

374

39

1

1

1

1

1

3

60

0

0

375

20

1

1

1

1

1

2

60

0

0

376

58

1

2

1

1

1

2

60

0

0

377

50

1

2

1

1

1

0

60

0

0

378

62

2

1

1

2

2

0

60

0

0

379

85

1

2

1

2

2

0

60

0

0

380

20

1

1

1

1

1

0

60

0

0

381

27

1

1

1

1

2

0

60

0

0

382

49

1

2

1

1

1

0

60

0

0

383

32

1

2

1

1

1

0

60

0

0

384

81

1

1

1

1

1

0

60

0

0

385

62

1

2

1

1

1

0

60

0

0

386

26

1

1

1

1

1

0

60

0

0

Appendix B: Tables for the data base in chapter 7

411

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1970–1979 387

20

1

1

1

1

1

0

60

0

0

388

15

2

2

1

1

2

0

60

0

0

389

21

1

1

1

1

1

0

60

0

0

390

33

1

1

1

1

1

0

60

0

0

391

22

2

1

1

1

2

0

60

0

0

392

20

1

1

1

1

2

0

60

0

0

393

61

1

1

1

1

1

0

60

0

0

394

83

1

1

1

1

2

0

60

0

0

395

18

1

1

1

1

1

0

60

0

0

396

61

1

1

5

1

2

0

60

0

0

397

72

1

1

1

1

1

0

60

0

0

398

74

1

1

1

1

1

0

60

0

0

399

41

2

1

1

2

2

0

60

0

0

400

76

1

1

1

1

1

0

60

0

0

401

65

2

2

1

2

2

0

60

0

0

402

64

1

1

1

1

2

0

60

0

0

403

81

1

1

1

9

2

0

60

0

0

404

49

2

1

1

1

2

0

60

0

0

405

25

1

1

1

2

2

0

60

0

0

406

29

1

2

1

1

2

0

60

0

0

407

58

1

1

1

1

1

0

60

0

0

408

50

1

1

1

1

1

0

60

0

0

409

46

1

2

1

1

1

0

60

0

0

410

22

2

1

1

2

2

0

60

0

0

411

54

1

1

1

2

2

0

60

0

0

412

71

1

1

1

1

1

0

60

0

0

413

18

1

1

1

1

2

0

60

0

0

414

20

1

1

1

1

1

0

60

0

0

Appendix B: Tables for the data base in chapter 7

412

415

36

1

1

1

1

1

0

60

0

0

416

67

1

2

1

1

1

0

60

0

0

417

44

1

1

1

1

1

0

60

0

0

418

23

1

1

1

1

1

0

60

0

0

419

45

1

2

1

1

1

0

60

0

0

420

44

1

1

1

1

1

0

60

0

0

421

57

1

1

1

2

2

0

60

0

0

422

19

2

2

1

1

1

0

60

0

0

423

20

1

2

1

1

2

0

60

0

0

424

48

1

1

1

1

1

0

60

0

0

425

43

1

2

1

1

1

0

60

0

0

426

59

1

1

1

1

1

0

60

0

0

427

50

1

2

1

1

1

0

60

0

0

428

26

2

1

1

1

3

0

60

0

0

429

16

1

1

1

1

2

0

60

0

0

430

51

1

1

1

1

1

0

60

0

0

431

23

1

2

1

1

1

0

60

0

0

432

70

1

1

1

1

1

0

60

0

0

433

48

1

1

1

1

1

0

60

0

0

434

20

1

1

1

1

2

0

60

0

0

435

33

1

1

1

1

1

0

60

0

0

436

62

1

1

1

1

1

0

60

0

0

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1970–1979 437

59

1

1

1

1

1

0

60

0

0

438

41

1

2

1

1

1

0

60

0

0

439

34

2

1

1

1

1

0

60

0

0

440

55

1

2

1

1

1

0

60

0

0

441

43

1

1

1

1

1

0

60

0

0

442

57

1

1

1

1

1

0

60

0

0

Appendix B: Tables for the data base in chapter 7

413

443

29

1

1

1

1

1

0

60

0

0

444

85

1

1

1

1

1

0

60

0

0

445

18

2

1

1

1

2

0

60

0

0

446

40

1

1

1

1

2

0

60

0

0

447

61

1

1

1

1

2

19

59

0

0

448

53

1

1

1

2

2

0

59

0

0

449

86

1

2

1

2

2

0

59

0

0

450

21

1

1

1

1

1

16

58

0

0

451

48

2

1

1

2

2

7

58

0

0

452

35

1

1

1

1

1

6

58

0

0

453

43

2

1

1

2

2

0

58

0

0

454

54

1

1

1

1

1

0

58

0

0

455

71

1

2

1

1

1

0

58

0

0

456

20

1

1

1

1

2

0

58

0

0

457

79

1

1

1

1

2

0

58

0

0

458

31

1

2

1

1

2

0

58

0

0

459

44

1

2

1

1

1

15

57

0

0

460

19

1

1

1

1

2

10

57

0

0

461

57

2

1

1

2

2

0

57

0

0

462

46

2

1

1

2

2

8

56

0

0

463

54

1

1

1

1

2

0

56

0

0

464

45

1

2

1

1

1

0

56

0

1

465

53

1

1

1

1

1

0

56

0

0

466

28

2

2

1

2

2

24

55

0

0

467

49

1

1

1

1

2

24

55

0

0

468

37

1

1

1

1

2

20

55

0

0

469

57

1

1

1

1

1

20

55

0

0

470

55

1

2

1

1

2

18

55

0

0

471

21

1

1

1

1

1

18

55

0

0

472

46

2

1

1

1

2

17

55

0

0

473

36

1

1

1

1

2

16

55

0

0

474

27

1

1

1

1

2

15

55

0

0

475

20

1

1

1

2

2

15

55

0

0

Appendix B: Tables for the data base in chapter 7

414

476

57

2

1

1

1

2

12

55

0

0

477

56

1

2

1

1

1

11

55

0

0

478

24

1

1

1

1

1

10

55

0

0

479

49

2

1

1

1

2

7

55

0

0

480

34

2

1

1

1

1

6

55

0

0

481

45

1

1

1

1

1

0

55

0

0

482

57

2

2

1

2

2

0

55

0

0

483

31

1

1

1

1

1

0

55

0

0

484

17

1

2

1

1

2

0

55

0

0

485

51

1

2

1

1

2

0

55

0

0

486

18

1

1

1

1

2

0

55

0

0

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1970–1979 487

53

1

1

1

1

2

0

55

0

0

488

18

1

1

1

1

2

0

55

0

0

489

57

1

1

1

1

2

0

55

0

0

490

53

1

1

1

1

1

0

55

0

0

491

18

1

1

1

1

1

0

55

0

0

492

55

1

1

1

1

3

0

55

0

0

493

59

1

1

1

1

1

0

55

0

0

494

52

1

2

1

1

2

0

55

0

0

495

19

2

2

1

1

2

0

55

0

0

496

52

1

2

1

1

1

0

55

0

0

497

19

1

1

1

1

1

0

55

0

0

498

51

1

1

1

1

2

0

55

0

0

499

15

1

1

1

1

2

0

55

0

0

500

24

2

1

1

1

2

13

54

0

0

501

83

1

1

1

1

1

2

54

0

0

502

52

2

1

1

1

2

0

54

0

1

503

50

1

1

1

2

2

0

54

0

0

Appendix B: Tables for the data base in chapter 7

415

504

22

1

1

1

1

2

0

53

0

0

505

78

1

1

1

1

1

0

53

0

0

506

77

1

2

1

2

2

0

52

0

0

507

56

2

1

1

2

2

0

52

0

0

508

74

2

1

1

1

2

0

51

0

0

509

25

2

1

1

1

2

12

50

0

0

510

31

1

1

1

1

1

2

50

0

0

511

47

2

1

1

2

2

0

50

0

0

512

61

1

1

1

2

2

0

50

0

0

513

86

2

1

1

2

2

0

50

0

0

514

84

1

1

5

1

2

0

50

0

0

515

56

1

2

1

1

1

0

50

0

0

516

73

2

1

1

2

2

0

50

0

0

517

18

1

2

1

1

1

0

49

0

0

518

63

2

1

1

1

1

2

48

0

0

519

56

1

2

1

1

1

0

48

0

0

520

40

1

2

1

1

1

6

47

0

0

521

17

2

1

2

3

2

99

45

0

0

522

1

1

1

1

1

4

99

45

0

0

523

2

1

2

1

1

4

99

44

0

0

524

51

2

1

1

2

2

15

44

0

0

525

31

1

2

1

1

1

0

44

0

0

526

38

1

2

1

1

1

0

43

0

0

527

7

2

2

1

1

2

99

42

0

0

528

66

1

1

1

8

2

0

42

0

0

529

84

2

2

1

1

2

0

41

0

2

530

42

1

1

1

1

2

27

40

0

0

531

66

1

1

5

1

2

0

40

0

0

532

3

1

1

1

3

2

0

39

0

0

533

53

1

2

1

1

1

0

37

0

1

534

52

1

1

1

1

2

1

35

0

4

535

27

2

1

1

3

2

36

34

0

0

536

57

1

1

5

1

2

20

33

0

0

Appendix B: Tables for the data base in chapter 7

416

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Non-Fire Cases 1970–1979 537

54

1

1

5

1

1

27

28

0

0

538

26

1

1

4

5

5

0

26

0

0

539

51

2

1

5

1

2

11

25

0

0

540

56

1

1

6

2

2

0

20

0

0

541

73

1

1

6

1

2

0

20

0

0

542

27

1

1

4

1

3

29

17

0

0

543

58

2

2

6

9

2

0

17

0

0

544

58

1

1

6

1

5

0

17

0

1

545

39

1

1

4

1

5

0

16

0

0

546

77

1

1

6

1

5

0

16

0

1

547

2

2

1

4

3

2

99

15

0

0

548

33

1

1

1

1

2

0

15

0

2

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1970–1979 1

4

2

1

1

3

2

99

71

1

0

2

64

2

1

1

3

2

32

70

1

0

3

60

1

1

1

3

2

0

70

1

0

4

2

2

2

1

3

2

0

70

1

0

5

4

1

1

2

3

2

99

68

1

0

6

2

2

1

2

3

2

99

65

1

0

7

5

2

2

2

3

2

99

65

1

0

8

3

2

1

1

3

2

99

65

1

0

9

7

2

1

1

3

2

99

65

1

0

10

6

1

1

1

3

2

99

65

1

0

11

11

2

2

2

3

2

99

65

1

0

12

9

2

2

2

3

2

99

65

1

0

Appendix B: Tables for the data base in chapter 7

417

13

4

2

1

2

3

2

99

65

1

0

14

4

2

1

1

3

2

99

65

1

0

15

1

1

2

1

3

2

99

65

1

0

16

3

1

2

1

3

3

99

65

1

0

17

4

1

1

1

3

2

99

65

1

1

18

8

2

1

2

3

2

99

65

1

0

19

3

2

1

1

3

2

99

65

1

0

20

3

2

2

2

3

2

99

65

1

0

21

4

1

2

1

3

2

99

65

1

1

22

6

1

1

2

3

2

99

65

1

0

23

1

2

1

1

3

2

99

65

1

0

24

33

2

1

1

3

2

47

65

1

0

25

36

1

1

2

3

2

44

65

1

0

26

41

1

1

2

3

2

40

65

1

0

27

45

1

1

1

3

2

40

65

1

0

28

27

1

1

1

3

2

38

65

1

0

29

48

2

1

1

3

2

33

65

1

1

30

43

2

1

2

1

2

33

65

1

0

31

42

1

2

1

3

2

32

65

1

0

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1970–1979 32

61

1

1

1

3

2

32

65

1

0

33

86

1

1

2

3

2

29

65

1

0

34

21

2

1

2

4

2

29

65

1

0

35

35

1

2

2

3

2

28

65

1

0

36

44

2

1

2

3

2

27

65

1

0

37

57

1

2

1

3

2

27

65

1

0

38

39

1

1

2

3

2

24

65

1

0

39

33

1

1

2

3

2

24

65

1

0

40

65

2

1

1

3

2

24

65

1

0

Appendix B: Tables for the data base in chapter 7

418

41

51

1

2

1

3

2

24

65

1

0

42

50

1

1

1

1

2

24

65

1

0

43

39

1

2

2

3

2

22

65

1

0

44

39

2

1

1

3

2

21

65

1

0

45

51

2

1

1

3

2

21

65

1

0

46

26

2

2

2

3

2

21

65

1

0

47

40

1

1

1

3

2

19

65

1

1

48

38

2

2

1

3

2

19

65

1

1

49

57

1

1

1

3

2

19

65

1

0

50

39

2

2

2

3

2

18

65

1

0

51

29

1

1

1

3

2

18

65

1

0

52

53

1

2

2

3

2

17

65

1

0

53

51

1

2

1

1

1

17

65

1

0

54

21

1

1

1

3

2

17

65

1

0

55

48

2

1

2

3

4

17

65

1

0

56

78

1

1

1

3

2

15

65

1

0

57

42

1

2

1

1

1

14

65

1

0

58

26

1

1

1

3

2

12

65

1

1

59

23

1

1

1

3

2

11

65

1

0

60

66

1

1

1

3

2

11

65

1

1

61

48

2

1

1

3

2

9

65

1

0

62

22

2

1

1

3

2

9

65

1

0

63

2

2

2

2

3

2

9

65

1

0

64

20

1

1

1

3

4

5

65

1

0

65

18

2

2

1

3

3

5

65

1

0

66

37

2

2

1

3

2

4

65

1

0

67

36

1

2

1

3

2

4

65

1

1

68

38

1

1

1

2

1

2

65

1

0

69

2

1

1

1

3

2

0

65

1

0

70

5

2

1

1

3

2

0

65

1

0

71

77

2

1

1

3

2

0

65

1

0

72

20

2

2

1

3

2

0

65

1

0

73

52

1

1

1

3

2

0

65

1

1

Appendix B: Tables for the data base in chapter 7

419

74

67

2

1

1

3

2

0

65

1

0

75

79

2

2

1

3

2

0

65

1

0

76

16

2

2

1

3

2

0

65

1

0

77

22

1

2

1

3

2

0

65

1

0

78

76

1

2

1

3

2

0

65

1

0

79

23

2

2

1

3

3

0

65

1

0

80

76

2

1

2

3

2

0

65

1

0

81

10

2

1

2

3

2

0

65

1

0

Fire st

Surv

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire Cases 1970–1979 82

19

1

2

1

3

2

0

65

1

0

83

20

2

2

2

3

2

0

65

1

0

84

16

1

2

1

3

2

0

65

1

0

85

73

2

2

1

3

2

0

65

1

0

86

87

2

1

1

3

2

0

65

1

0

87

64

1

2

1

3

4

0

65

1

0

88

65

1

1

1

3

2

0

65

1

0

89

1

2

2

1

3

2

0

65

1

0

90

1

1

2

1

3

2

0

65

1

0

91

77

2

1

1

3

2

0

65

1

0

92

78

1

2

2

3

2

0

65

1

0

93

44

1

1

2

3

6

0

65

1

0

94

57

2

2

1

5

2

0

65

1

0

95

72

1

2

1

3

2

0

65

1

0

96

32

1

2

2

3

2

0

65

1

0

97

16

1

2

2

3

2

0

65

1

0

98

50

1

1

1

3

2

0

65

1

0

99

78

1

2

1

3

2

0

65

1

0

100

5

2

1

2

3

2

0

65

1

0

101

23

1

1

1

3

2

0

65

1

0

Appendix B: Tables for the data base in chapter 7

420

102

17

2

1

2

3

2

0

65

1

0

103

4

2

1

2

3

2

0

65

1

0

104

23

1

1

2

7

5

0

65

1

0

105

53

1

1

1

3

2

0

65

1

0

106

12

2

2

2

3

2

0

65

1

0

107

77

2

1

2

3

2

0

65

1

0

108

60

1

2

1

3

2

0

65

1

0

109

22

1

2

1

3

2

0

65

1

0

110

73

1

2

1

3

2

0

65

1

0

111

52

2

2

1

3

2

0

65

1

0

112

78

2

1

1

3

2

0

65

1

0

113

14

2

2

1

3

2

0

65

1

0

114

64

1

1

1

3

2

11

64

1

0

115

68

2

2

1

3

2

0

64

1

1

116

94

2

1

1

3

2

0

64

1

0

117

3

2

1

1

3

2

99

63

1

0

118

25

1

1

1

5

1

8

63

1

0

119

50

2

1

1

3

2

0

63

1

0

120

8

2

2

1

3

2

99

62

1

0

121

6

1

1

1

3

2

99

62

1

0

122

44

2

1

2

3

2

12

62

1

0

123

7

2

2

1

3

2

99

61

1

0

124

83

2

2

1

3

2

0

61

1

0

125

58

1

2

1

3

2

0

61

1

0

126

7

2

1

1

3

2

99

60

1

0

127

1

1

2

1

7

2

99

60

1

0

128

3

1

1

1

3

2

99

60

1

1

129

5

2

2

1

3

2

99

60

1

0

130

1

2

1

2

3

2

99

60

1

0

131

2

2

1

1

3

2

99

60

1

0

Appendix B: Tables for the data base in chapter 7

421

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1970–1979 132

4

2

1

1

3

2

99

60

1

0

133

1

1

2

4

3

2

99

60

1

0

134

36

1

2

1

3

2

46

60

1

0

135

63

1

1

1

3

2

46

60

1

0

136

66

1

1

1

3

2

38

60

1

0

137

77

1

1

1

3

2

37

60

1

0

138

40

1

1

1

3

2

34

60

1

0

139

43

1

1

1

3

2

31

60

1

0

140

38

1

1

1

3

2

28

60

1

0

141

43

2

1

2

3

2

27

60

1

0

142

46

1

1

1

3

3

27

60

1

0

143

32

1

1

1

3

2

27

60

1

0

144

38

1

2

2

3

2

26

60

1

0

145

58

2

1

1

3

2

25

60

1

0

146

26

1

1

1

3

2

25

60

1

0

147

65

1

1

1

3

2

25

60

1

0

148

56

2

1

1

3

2

24

60

1

0

149

52

2

1

1

3

2

19

60

1

0

150

28

1

1

1

3

2

19

60

1

0

151

56

1

2

1

3

2

16

60

1

0

152

61

1

1

2

3

2

8

60

1

0

153

45

1

1

1

3

4

4

60

1

1

154

39

2

1

2

3

2

3

60

1

0

155

76

1

1

1

3

2

0

60

1

0

156

46

1

2

1

3

2

0

60

1

0

157

79

1

2

1

3

2

0

60

1

0

158

8

1

2

1

3

2

0

60

1

0

159

68

1

2

1

3

2

0

60

1

0

Appendix B: Tables for the data base in chapter 7

422

160

57

1

1

1

3

2

0

60

1

0

161

65

1

1

1

3

2

0

60

1

1

162

8

1

1

1

3

2

0

60

1

0

163

84

1

2

1

3

2

0

60

1

0

164

55

1

1

1

3

2

0

60

1

0

165

17

1

2

1

3

2

0

60

1

0

166

75

1

1

1

3

2

0

60

1

0

167

87

1

2

1

3

2

0

60

1

0

168

68

2

1

1

3

2

0

60

1

0

169

52

2

2

1

3

2

0

60

1

0

170

18

1

2

1

7

2

0

60

1

0

171

70

1

1

1

3

2

0

60

1

0

172

8

1

1

1

3

2

0

60

1

1

173

73

2

1

1

3

2

0

60

1

0

174

1

2

1

2

3

2

99

58

1

0

175

4

2

1

1

3

4

99

58

1

0

176

6

2

1

1

3

2

99

58

1

0

177

61

1

1

1

3

2

40

58

1

0

178

41

1

1

1

3

2

38

58

1

0

179

78

1

1

1

3

2

0

58

1

0

180

76

1

2

2

3

2

0

58

1

0

181

73

1

2

1

3

2

0

58

1

0

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1970–1979 182

1

2

1

2

3

2

99

57

1

0

183

53

1

1

2

3

2

37

57

1

1

184

45

1

2

2

3

2

31

57

1

0

185

8

1

2

2

3

2

0

57

1

0

186

5

2

2

1

3

2

99

56

1

0

187

1

1

2

1

7

2

99

56

1

0

Appendix B: Tables for the data base in chapter 7

423

188

58

1

1

1

3

2

31

56

1

0

189

57

1

1

2

3

2

30

56

1

0

190

6

2

1

1

3

2

0

56

1

1

191

5

2

2

1

3

2

99

55

1

0

192

4

2

1

1

3

2

99

55

1

0

193

3

1

1

2

3

2

99

55

1

0

194

35

1

2

1

3

2

47

55

1

0

195

36

2

2

2

3

2

35

55

1

0

196

51

1

1

2

3

2

32

55

1

0

197

73

1

1

1

3

2

27

55

1

0

198

32

2

1

2

3

2

19

55

1

0

199

31

1

2

4

3

2

14

55

1

0

200

38

2

2

1

3

2

12

55

1

0

201

26

1

1

2

3

2

10

55

1

0

202

60

1

2

1

3

2

0

55

1

0

203

20

1

1

2

1

4

0

55

1

0

204

54

2

1

1

3

2

0

55

1

0

205

62

1

1

1

3

2

0

55

1

0

206

30

1

1

1

7

2

0

55

1

0

207

59

1

2

1

3

2

0

55

1

0

208

65

1

2

2

3

2

0

55

1

0

209

60

1

1

1

3

2

0

55

1

1

210

70

1

2

1

3

2

0

55

1

0

211

67

1

2

1

3

2

0

55

1

0

212

36

1

1

5

3

1

0

55

1

0

213

91

1

1

1

3

2

0

55

1

0

214

34

1

1

2

3

2

0

55

1

0

215

8

2

1

2

3

2

0

54

1

1

216

23

1

2

1

7

2

0

54

1

0

217

1

1

1

1

3

2

0

53

1

0

218

26

1

1

1

7

2

0

53

1

0

219

2

1

1

1

3

2

99

52

1

1

220

51

1

1

2

7

5

15

52

1

0

Appendix B: Tables for the data base in chapter 7

424

221

10

1

1

1

3

3

99

51

1

0

222

11

2

1

1

3

2

99

51

1

2

223

13

2

1

2

3

2

0

51

1

0

224

66

2

1

1

3

2

0

51

1

1

225

19

2

1

2

3

2

0

51

1

0

226

97

1

1

1

3

2

0

51

1

0

227

94

2

1

1

3

2

0

51

1

0

228

66

1

1

1

3

2

0

51

1

0

229

7

2

1

2

3

2

99

50

1

0

230

40

1

2

2

3

2

40

50

1

2

231

45

1

1

2

3

2

21

50

1

0

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1970–1979 232

79

1

1

2

3

2

0

50

1

0

233

49

2

1

2

3

2

0

50

1

0

234

47

1

2

1

3

2

0

50

1

0

235

14

1

2

2

3

2

0

50

1

0

236

38

2

1

4

3

2

0

50

1

0

237

15

2

1

1

3

2

0

50

1

0

238

47

1

1

1

3

2

37

49

1

0

239

35

1

1

1

3

2

6

49

1

1

240

58

1

1

4

3

2

0

48

1

1

241

86

1

1

1

3

2

0

48

1

0

242

3

2

1

2

3

2

99

46

1

0

243

51

1

2

1

3

2

36

46

1

0

244

44

1

2

1

1

1

5

46

1

0

245

7

2

2

1

3

2

0

46

1

0

246

7

1

1

1

3

2

0

46

1

0

247

71

1

1

1

3

3

0

46

1

0

248

40

2

1

2

3

2

99

45

1

0

Appendix B: Tables for the data base in chapter 7

425

249

50

1

1

2

1

2

41

45

1

0

250

57

2

2

1

3

2

16

45

1

1

251

62

1

1

2

3

2

9

45

1

0

252

17

1

1

2

3

2

9

45

1

0

253

7

2

2

1

3

2

0

45

1

0

254

62

1

1

2

3

2

0

45

1

0

255

59

2

1

2

3

2

29

43

1

0

256

68

1

1

1

3

2

0

43

1

0

257

68

2

1

5

3

2

0

43

1

1

258

49

2

1

2

3

2

33

42

1

0

259

90

1

1

2

3

2

3

42

1

0

260

62

1

1

1

3

2

0

42

1

2

261

23

1

1

4

1

2

0

42

1

0

262

5

2

2

2

3

2

99

41

1

0

263

42

2

2

2

3

2

46

41

1

0

264

58

1

1

2

3

2

33

41

1

0

265

53

2

2

2

3

2

18

41

1

0

266

66

2

2

1

3

2

0

41

1

0

267

59

1

1

1

7

2

0

41

1

0

268

2

2

2

2

3

2

99

40

1

0

269

64

1

1

7

1

5

5

40

1

0

270

59

1

1

1

3

2

0

40

1

1

271

1

2

1

1

3

2

99

39

1

2

272

2

2

2

1

3

2

99

38

1

0

273

13

2

2

2

3

2

99

38

1

0

274

57

1

1

1

7

2

0

38

1

0

275

3

2

2

1

3

2

0

38

1

0

276

4

2

1

2

3

2

99

37

1

0

277

84

1

1

1

3

2

0

36

1

1

278

44

1

1

2

1

2

26

35

1

0

279

78

1

2

2

3

2

0

35

1

0

280

17

1

2

1

3

2

0

35

1

0

281

33

1

1

4

1

2

0

35

1

0

Appendix B: Tables for the data base in chapter 7

426

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1970–1979 282

62

1

1

2

3

2

33

34

1

0

283

57

2

1

2

7

2

5

34

1

0

284

63

1

2

1

3

2

0

34

1

2

285

70

1

1

2

3

2

0

34

1

0

286

44

2

1

2

3

2

34

33

1

0

287

61

2

1

2

3

3

30

33

1

1

288

14

1

1

2

3

2

0

33

1

0

289

4

2

2

1

3

2

99

32

1

0

290

70

1

2

1

3

2

18

32

1

1

291

75

1

2

2

3

2

0

32

1

0

292

6

2

1

1

3

2

99

30

1

0

293

74

1

1

2

3

2

24

30

1

0

294

5

2

1

2

3

2

99

29

1

0

295

31

2

1

4

9

3

0

29

1

0

296

57

1

2

1

3

2

49

28

1

0

297

50

1

1

5

3

2

0

28

1

0

298

79

1

2

2

3

2

0

28

1

0

299

4

2

2

1

3

2

0

28

1

1

300

20

2

1

4

1

2

0

27

1

0

301

1

2

2

2

3

2

99

25

1

0

302

61

1

1

2

6

2

29

25

1

0

303

56

1

2

2

3

2

20

25

1

0

304

58

1

2

2

3

2

19

25

1

0

305

57

1

2

2

3

2

27

24

1

0

306

60

1

2

2

3

2

2

24

1

0

307

85

1

2

2

3

2

16

23

1

0

308

27

1

1

4

3

2

0

23

1

0

309

74

1

1

5

3

2

0

23

1

2

Appendix B: Tables for the data base in chapter 7

427

310

84

1

2

2

3

2

0

23

1

0

311

78

2

1

4

3

2

0

22

1

0

312

62

1

1

1

3

2

22

20

1

0

313

85

1

2

2

3

2

12

20

1

0

314

55

1

1

2

3

2

0

20

1

0

315

23

1

2

6

3

2

0

18

1

0

316

60

2

1

2

3

2

22

17

1

0

317

48

1

1

6

1

2

0

17

1

0

318

68

1

1

2

3

2

38

15

1

0

319

66

1

1

5

3

2

19

15

1

0

320

24

2

1

2

3

4

10

15

1

6

321

19

2

1

4

1

2

1

15

1

0

322

63

1

1

4

3

2

40

14

1

0

323

39

1

1

2

1

2

19

14

1

0

324

45

1

1

4

1

2

0

14

1

0

325

4

2

2

1

3

2

0

14

1

3

326

1

2

1

2

3

2

0

14

1

0

327

61

1

1

2

3

2

30

13

1

0

328

50

1

2

1

3

2

30

13

1

0

329

76

1

1

4

3

2

0

13

1

0

330

31

1

1

3

3

5

0

13

1

2

331

82

1

2

4

3

2

0

11

1

0

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Fire Cases 1970–1979 332

57

2

2

2

3

2

29

10

1

0

333

42

2

2

8

3

2

14

10

1

0

334

43

1

1

2

7

5

0

10

1

4

Appendix B: Tables for the data base in chapter 7

428

CWRU Data Base—All Cases between 1970 and 1979 Age

Race

Gend

Cause

Source

Verdct

EtOH

COHb

Fire st

Surv

Other Cases 1970–1979 1

44

1

1

2

7

4

26

65

2

1

2

42

1

2

2

8

2

0

60

2

0

3

31

2

1

2

8

5

0

60

2

0

4

37

1

1

2

7

4

34

36

2

1

5

49

1

1

8

1

4

0

33

2

0

6

14

1

1

4

1

2

5

27

2

2

7

26

2

1

4

8

5

99

23

2

0

Data from the CWRU Study: COHb Distributions COHb 0–9 10–19 20–29 30–39 40–49 50–59 60–69 70–79 80–89 90–99 Total 1938–49 Fire # %

0

0

1

9

9

11

26

31

11

17

115

0.0

0.0

0.9

7.8

7.8

9.6

22.6

27.0

9.6

0

2

0

5

13

28

58

75

71

0.0

0.6

0.0

1.5

3.8

8.2

17.1

22.1

20.9

0

9

4

5

29

40

56

14

0

0.0

5.7

2.5

3.2

18.4

25.3

35.4

8.9

0.0

0.6 100.0

0

1

0

1

14

91

154

51

13

13

0.0

0.3

0.0

0.3

4.1

26.9

45.6

15.1

3.8

3.8 100.0

3

22

13

4

11

92

158

9

0

1.0

7.1

4.2

1.3

3.5

29.5

50.6

2.9

0.0

14.8 100.0

Non Fire # %

88

340

25.9 100.0

1950–59 Fire # %

1

158

Non Fire # %

338

1960–69 Fire # %

0

312

0.0 100.0

Appendix B: Tables for the data base in chapter 7

429

Non Fire # %

0

3

4

4

6

86

334

34

1

0.0

0.6

0.8

0.8

1.3

18.2

70.8

7.2

0.2

0

20

21

23

33

64

169

4

0

0.0

6.0

6.3

6.9

9.9

19.2

50.6

1.2

0.0

0

7

5

5

15

70

439

7

0

0.0

1.3

0.9

0.9

2.7

12.8

80.1

1.3

0.0

0

472

0.0 100.0

1970–79 Fire # %

0

334

0.0 100.0

Non Fire # %

0

548

0.0 100.0

Data from the CWRU Study: Age Distributions Age 0–9 10–19 20–29 30–39 40–49 50–59 60–69 70–79 80–89 90–99 Total 1938–49 Fire #

14

5

10

12

18

15

17

18

6

% 12.2

4.3

8.7

10.4

15.7

13.0

14.8

15.7

5.2

3

10

36

73

81

88

38

9

2

0.9

2.9

10.6

21.5

23.8

25.9

11.2

2.6

0.6

59

4

10

23

16

16

18

7

5

37.3

2.5

6.3

14.6

10.1

10.1

11.4

4.4

3.2

6

8

50

50

82

67

48

23

3

1.8

2.4

14.8

14.8

24.3

19.8

14.2

6.8

0.9

92

8

16

30

38

44

35

35

14

29.5

2.6

5.1

9.6

12.2

14.1

11.2

11.2

4.5

19

62

89

95

108

51

34

10

0

115

0.0 100.0

Non Fire # %

0

340

0.0 100.0

1950–59 Fire # %

0

158

0.0 100.0

Non Fire # %

1

338

0.3 100.0

1960–69 Fire # %

0

312

0.0 100.0

Non Fire #

4

0

472

Appendix B: Tables for the data base in chapter 7

%

0.8

430

4.0

13.1

18.9

20.1

22.9

10.8

7.2

2.1

74

23

28

32

35

47

44

35

11

22.2

6.9

8.4

9.6

10.5

14.1

13.2

10.5

3.3

8

35

107

79

98

114

58

29

20

1.5

6.4

19.5

14.4

17.9

20.8

10.6

5.3

3.6

0.0 100.0

1970–79 Fire # %

5

334

1.5 100.0

Non Fire # %

0

548

0.0 100.0

Other Data, for Comparison Purposes Ages in General Population—as per NFPA 0–5

6–9

10–19

20–29

30–49

50–64

65–74

75–84

>85

%

9.0

5.7

14.7

17.5

27.3

13.7

7.2

3.8

1.2

Ages

0–5

6–9

10–19

20–29

30–49

50–64

65–74

75–84

}85

Total

#

11

3

5

10

30

19

22

14

1

115

%

9.6

2.6

4.3

8.7

26.1

16.5

19.1

12.2

0.9

100.0

3

0

10

36

154

104

27

4

2

340

0.9

0.0

2.9

10.6

45.3

30.6

7.9

1.2

0.6

100.0

1938–49 Fire

Non Fire # % 1950–59 Fire # %

46

13

4

10

39

23

14

7

2

158

29.1

8.2

2.5

6.3

24.7

14.6

8.9

4.4

1.3

100.0

4

2

8

50

132

88

46

6

2

338

1.2

0.6

2.4

14.8

39.1

26.0

13.6

1.8

0.6

100.0

79

13

8

16

68

63

37

25

3

312

25.3

4.2

2.6

5.1

21.8

20.2

11.9

8.0

1.0

100.0

Non Fire # % 1960–69 Fire # % Non Fire

Appendix B: Tables for the data base in chapter 7

# %

431

3

1

19

62

184

139

44

19

1

472

0.6

0.2

4.0

13.1

39.0

29.4

9.3

4.0

0.2

100.0

53

21

23

28

67

72

32

27

11

334

15.9

6.3

6.9

8.4

20.1

21.6

9.6

8.1

3.3

100.0

5

3

35

107

177

143

46

26

6

548

0.9

0.5

6.4

19.5

32.3

26.1

8.4

4.7

1.1

100.0

1970–79 Fire # % Non Fire # %

Explanation of Numbers and Symbols in CWRU Data Base Age:

Age:

actual age attained; if <1 =1; if >99 =99

Race:

Race:

1: white, 2: black, 3: yellow; 4: red; 9: unknown

Gend:

Gender:

1: male; 2: female; 9: unknown

Cause: Cause of Death:

1: CO poisoning; 2: CO+Burns; 3: Burns+secondary CO; 4: Burns (including incineration, charring); 5: CO+other; 6: other+secondary CO; 7: other; 8: Burns+other; 9: unknown, No death

Source: Source of CO:

1: auto, truck, tractor, or other internal combustion engine; 2: gas (natural, illuminating), 3: home; 4: clothing; 5: smudge, pot, coal, gas, coke, charcoal; 6: bonfire, rags; 7: building, 8: propane, gasoline, kerosene or other fire accelerant; 9: undetermined, unknown (It is coroner’s determination)

Verdct: Verdict:

1: suicide, 2: accident, 3: undetermined, 4: homicide, 5: industrial accident (while at work), 6: justifiable homicide

EtOH:

Actual Ethanol×100; except 99=n/a

Blood Alcohol:

COHb: COHb %: Actual COHb%, except 99 or 100=9 Fire st: Fire Status:

0: non-fire, 1: fire, 2: fire and explosion, 3: explosion only, 9: unknown

Surv:

survival time, in nearest full hours, except >9 hours=9

Survival:

APPENDIX C DATA TABLES FOR ANALYSIS OF THE DATA BASES UNIVERSITY SOUTHERN MISSISSIPPI (USM) AND CASE WESTERN RESERVE UNIVERSITY (CWRU) Distribution of Data in USM Database Data By Laboratory Lab

All Cases

Fire Cases

Data by CO Method

Non Fire Cases

Method

1

15

8

7 Missing

2

4

3

3

9

4

All Cases

Fire Cases

Non Fire Cases

34

6

23

1 1

551

342

188

3

6 2

0

0

0

14

0

14 3

467

195

73

5

2

0

0 4

35

9

26

6

13

8

5 5

348

191

88

7

17

4

13 6

443

204

134

8

0

0

0 7

18

12

6

9

117

56

37 8

51

36

15

10

105

66

28 9

14

6

8

11

12

7

0 10

17

8

9

12

35

9

26 11

251

119

74

13

3

0

0 12

12

4

8

14

4

3

1 Total

2241

1132

652

15

348

191

88

16

31

9

22

17

10

2

8

18

18

12

6

19

38

28

10 Year

Data by Exposure Year

All Cases Fire Cases Non Fire Cases

Appendix C: Tables for the data base in chapter 8

20

14

6

8

21

17

8

9

22

273

131

23

39

14

24

4

25

2

1

1

20 1940

35

9

26

4

0 1964

2

0

0

1

0

1 1973

4

1

3

26

1

0

1 1974

2

0

2

27

4

0

4 1975

5

0

5

28

1

0

1 1976

29

5

24

29

1

0

1 1977

123

22

32

30

1

0

1 1978

124

81

41

31

4

0

4 1979

105

56

35

32

1

0

1 1980

108

66

14

33

1

0

1 1981

140

68

22

34

21

7

14 1982

230

104

53

35

261

130

55 1983

465

271

133

36

347

235

106 1984

716

363

232

37

455

188

73 1985

151

85

29

2241

1132

652 Total

2241

1132

652

Total

80 Missing

433

Age Distribution Midpoint

All Cases

Fire

% COHb Distribution Non Fire Midpoint

All Cases

Fire

Non Fire

Missing

282

97

50

Missing

191

107

19

3.6

212

191

4

2.4

54

15

15

10.9

78

68

3

7.1

50

16

11

18.1

197

75

86

11.9

34

17

7

25.3

235

130

59

16.7

27

16

3

32.6

273

107

114

21.4

47

26

4

39.8

205

80

90

26.2

44

30

8

47.1

171

70

80

30.9

47

32

9

54.3

167

72

60

35.7

46

28

10

61.5

167

86

53

40.5

81

46

12

68.8

102

58

17

45.2

80

53

15

Appendix C: Tables for the data base in chapter 8

434

76.0

84

53

22

50.0

117

80

21

83.3

47

33

8

54.7

128

63

41

90.5

17

9

6

59.5

150

88

36

97.7

3

3

0

64.3

177

76

60

105.0

0

0

0

69.0

212

101

87

112.2

0

0

0

73.8

216

97

83

119.5

0

0

0

78.5

239

110

83

126.7

0

0

0

83.3

169

59

80

133.9

0

0

0

88.1

95

51

34

141.2

0

0

0

92.8

34

18

14

148.4

1

0

0

97.6

3

3

0

Total

2241

1132

652

Total

2241

1132

652

Mean

33.314

32.605

37.867

Mean

54.454

53.072

63.317

Minimum

0.000

0.000

0.000

Minimum

0.000

0.000

0.000

Median

32.000

29.000

37.000

Median

62.400

59.900

70.000

Maximum

152.000

100.000

93.000

Maximum

99.990

99.990

94.000

STD Dev

24.364

25.773

19.862

STD Dev

27.436

26.963

22.964

Ethanol Distribution Midpoint

All Cases

Fire

Source of CO Distribution Non Fire

Source

All Cases

Missing

1446

719

389

Missing

378

0.02

65

19

35

102

679

0.05

62

21

33

104

428

0.08

62

27

30

105

21

0.11

63

21

31

110

7

0.14

63

35

24

111

1

0.17

79

40

28

114

12

0.20

77

42

28

115

2

0.23

93

55

27

116

1

0.26

68

49

17

118

3

0.29

41

30

4

120

37

0.32

35

24

3

124

1

0.35

26

21

2

126

1

Appendix C: Tables for the data base in chapter 8

435

0.38

20

14

1

131

2

0.41

8

6

0

133

1

0.44

5

4

0

135

1

0.47

5

4

0

138

3

0.50

2

1

0

140

3

0.53

0

0

0

201

475

0.56

0

0

0

203

4

0.59

0

0

0

206

3

0.62

1

0

0

207

5

Total

2221

1132

652

208

19

Mean

0.064

0.077

0.055

209

3

Minimum

0.000

0.000

0.000

212

1

Median

0.000

0.000

0.000

213

7

Maximum

0.640

0.490

0.380

217

3

STD Dev

0.108

0.119

0.085

219

7

222

1

223

1

225

22

227

1

228

14

229

2

230

87

232

1

234

1

237

1

241

2

Total

2241

Survival All Cases

Fire

Non Fire

Missing

72

0

0

Alive

8

0

0

Dead

2161

1132

652

Appendix C: Tables for the data base in chapter 8

Total

2241

436

1132

652

Sex All Cases

Fire

Missing

Non Fire

63

20

16

Male

1512

720

475

Female

666

392

161

Total

2241

1132

652

Drug Distribution All Cases

Fire

Non Fire

Missing/Zero2115

10

59

601

Drug/no amount

97

23

34

Drag/amount

29

16

5

2241

1098

640

Total

Disease Distribution All Cases

Fire

Non Fire

No disease/missing

2043

1048

550

Disease

198

84

102

Total

2241

1132

652

Physical Condition Distribution All Cases

Fire

Non Fire

Missing

2012

1026

541

Excellent

12

7

4

Good

157

71

78

Fair

29

12

16

Poor

31

16

13

Total

2241

1132

652

Ethanol Distribution All Cases

Fire

Non Fire

No Ethanol/Missing

1466

719

389

Ethanol Present

775

413

263

Total

2241

1132

652

Appendix C: Tables for the data base in chapter 8

437

Number and Percentage of Fire and Non Fire Victims by Lab Lab

Fire #

%

Non Fire

%

Total #

% Total

1

8

53.3

7

46.7

15

0.84

2

3

75.0

1

25.0

4

0.22

3

3

33.3

6

66.7

9

0.50

4

0

0.0

14

100.0

14

0.78

5

0

0.0

0

0.0

0

0.00

6

8

61.5

5

38.5

13

0.73

7

4

23.5

13

76.5

17

0.95

8

0

0.0

0

0.0

0

0.00

9

56

60.2

37

39.8

93

5.21

10

66

70.2

28

29.8

94

5.27

11

7

100.0

0

0.0

7

0.39

12

9

25.7

26

74.3

35

1.96

13

0

0.0

0

0.0

0

0.00

14

3

75.0

1

25.0

4

0.22

15

191

68.5

88

31.5

279

15.64

16

9

29.0

22

71.0

31

1.74

17

2

20.0

8

80.0

10

0.56

18

12

66.7

6

33.3

18

1.01

19

28

73.7

10

26.3

38

2.13

20

6

42.9

8

57.1

14

0.78

21

8

47.1

9

52.9

17

0.95

22

131

62.1

80

37.9

211

11.83

23

14

41.2

20

58.8

34

1.91

24

4

100.0

0

0.0

4

0.22

25

0

0.0

1

100.0

1

0.06

26

0

0.0

1

100.0

1

0.06

27

0

0.0

4

100.0

4

0.22

28

0

0.0

1

100.0

1

0.06

29

0

0.0

1

100.0

1

0.06

Appendix C: Tables for the data base in chapter 8

438

30

0

0.0

1

100.0

1

0.06

31

0

0.0

4

100.0

4

0.22

32

0

0.0

1

100.0

1

0.06

33

0

0.0

1

100.0

1

0.06

34

7

33.3

14

66.7

21

1.18

35

130

70.3

55

29.7

185

10.37

36

235

68.9

106

31.1

341

19.11

37

188

72.0

73

28.0

261

14.63

1784

100.00

Total

1132

652

Fraction of Fire and Non-Fire Victims with Ethanol by Lab Lab

Fire #

%

Non Fire

%

Total #

% Total

1

1

12.5

0

0.0

15

6.67

2

1

33.3

0

0.0

4

25.00

3

3

100.0

3

50.0

9

33.33

4

0

0.0

9

64.3

14

0.00

5

0

0.0

0

0.0

0

0.00

6

3

37.5

1

20.0

13

23.08

7

0

0.0

3

23.1

17

0.00

8

0

0.0

0

0.0

0

0.00

9

20

35.7

19

51.4

93

21.51

10

24

36.4

12

42.9

94

25.53

11

3

42.9

0

0.0

7

42.86

12

0

0.0

0

0.0

35

0.00

13

0

0.0

0

0.0

0

0.00

14

0

0.0

1

100.0

4

0.00

15

81

42.4

53

60.2

279

29.03

16

3

33.3

9

40.9

31

9.68

17

2

100.0

1

12.5

10

20.00

18

4

33.3

6

100.0

18

22.22

19

9

32.1

5

50.0

38

23.68

20

3

50.0

5

62.5

14

21.43

Appendix C: Tables for the data base in chapter 8

439

21

3

37.5

4

44.4

17

17.65

22

45

34.4

31

38.8

211

21.33

23

6

42.9

8

40.0

34

17.65

24

0

0.0

0

0.0

4

0.00

25

0

0.0

0

0.0

1

0.00

26

0

0.0

0

0.0

1

0.00

27

0

0.0

0

0.0

4

0.00

28

0

0.0

0

0.0

1

0.00

29

0

0.0

0

0.0

1

0.00

30

0

0.0

0

0.0

1

0.00

31

0

0.0

0

0.0

4

0.00

32

0

0.0

0

0.0

1

0.00

33

0

0.0

0

0.0

1

0.00

34

0

0.0

0

0.0

21

0.00

35

66

50.8

34

61.8

185

35.68

36

129

54.9

45

42.5

341

37.83

37

7

3.7

14

19.2

261

2.68

1784

23.15

Total

413

263

Availability by Lab of Data having Jointly Valid Codes for Age, Sex, and Source of CO, Among Non-Surviving Cases With Greater than 20% COHb Lab

Jointly Valid

Some Missing Value

Total

9

70

26

96

10

87

18

105

15

174

2

176

22

102

111

213

35

164

90

254

36

324

11

335

37

199

189

388

Other

228

52

280

Total

1348

499

1847

Appendix C: Tables for the data base in chapter 8

440

Analysis of Variance of COHb Values Source of Variation

Degrees Freedom

Sum of Squares

Mean Square

F-Ratio

Main Effects: Source of CO

1

3,026.8

3,026.8

11.50

Age

2

1,173.6

586.8

2.23

Sex

1

0.1

0.1

0.00

Source of CO by Ag

2

2,025.0

1,012.5

3.85

Age by sex

2

60.5

30.2

0.11

Within cells residual

685

180,263.6

263.16

Total

693

186,549.6

Interactions

Distribution of Levels of COHb by Age for Ethanol Free Fire and Non-Fire Victims of Fatal Co Exposure %COHb Range Fire Victims

<6 6–10 11–20 21–40 41–60 61–80 >80 Total

20–30

14

1

2

5

5

5

1

33

30–40

6

3

2

5

6

7

3

32

40–50

14

4

5

15

14

19

1

72

50–60

25

7

5

19

16

17

8

97

60–70

18

7

10

17

6

15

9

82

70–80

26

25

18

20

13

18

5

125

80–90

25

6

6

20

2

4

0

63

>90

5

4

0

2

0

0

0

11

Total

133

57

48

103

62

85

27

515

<6

6–10

11–20

21–40

41–60

61–80

>80

Total

20–30

0

0

3

4

4

3

0

14

30–40

0

0

3

6

1

1

1

12

40–50

0

0

4

7

9

1

2

23

50–60

0

0

3

13

11

6

5

38

60–70

1

0

6

26

36

4

2

75

70–80

0

0

18

40

14

17

2

91

80–90

0

0

7

21

17

9

1

55

%COHb Range Non-Fire Victims

Appendix C: Tables for the data base in chapter 8

441

>90

0

0

1

1

4

1

0

7

Total

1

0

45

118

96

42

13

315

(summary of cases with jointly valid data for age, sex, source of CO, and COHb >20%)

Percentage of Deaths Within Low COHb Ranges For Age—Source—Ethanol Specific Groups % COHb Range 20–40%

20–50%

20–60%

Age

Fire No EthOH

Fire EthOH

Non-Fire No EthOH

Non-Fire EthOH

<6

0.150

6–20

0.076

(0.067)

0.133

(0.043)

21– 40

0.097

0.142

0.085

0.036

41– 60

0.177

0.119

0.052

0.022

61– 80

0.141

0.151

0.095

(0.188)

>80

(0.148)

All

0.126

<6

0.256

6–20

(0.077) 0.133

0.083

0.041

0.162

(0.100)

0.222

(0.087)

21– 40

0.243

0.271

0.144

0.090

41– 60

0.403

0.228

0.146

0.044

61– 80

0.365

0.283

0.119

(0.250)

>80

(0.185)

All

0.266

<6

0.444

6–20

(0.231) 0.249

0.156

0.083

0.276

(0.300)

0.289

(0.304)

21– 40

0.379

0.439

0.254

0.189

41– 60

0.661

0.376

0.260

0.133

61– 80

0.565

0.453

0.262

(0.500)

Appendix C: Tables for the data base in chapter 8

>80

(0.481)

(0.615)

All

0.454

0.419

442

0.276

0.199

(Parentheses indicate that estimate is based on fewer than 40 cases)

Midpoint

Ethanol Free Non Fire Victims

Ethanol Free Fire Victims

COHb Distribution Ages ranging

COHb Distribution Ages ranging

6–20

21–40

41–60

61–80

6–20

21–40

41–60

61–80

Missing

0

0

0

0

0

0

0

0

2.4

1

2

1

3

2

3

1

1

7.1

2

0

2

2

2

1

3

1

11.9

2

0

1

0

0

4

1

3

16.7

0

1

1

1

3

1

3

0

21.4

0

2

1

0

1

2

2

3

26.2

2

2

1

0

2

3

3

2

30.9

1

3

2

3

1

1

3

2

35.7

3

3

0

1

4

3

2

5

40.5

0

3

4

1

3

3

3

4

45.2

2

3

3

0

5

6

5

9

50.0

2

3

6

0

3

12

9

13

54.7

2

10

4

3

4

5

7

7

59.5

1

4

8

4

7

10

8

8

64.3

2

14

12

2

7

8

3

6

69.0

6

13

22

2

11

9

4

10

73.8

8

22

7

8

23

7

7

5

78.5

8

17

6

8

18

14

6

11

83.3

6

11

10

8

9

14

0

3

88.1

1

10

6

1

5

4

1

1

92.8

1

1

4

1

2

2

0

0

97.6

0

0

0

0

0

0

0

0

Total

50

124

101

48

112

112

71

94

Mean

60.778

66.980

63.925

61.560

64.029

59.563

50.154

54.510

Mode

75.000

75.000

70.000

80.000

75.000

80.000

50.000

80.000

Kurtosis

−0.001

1.889

1.576

0.271

1.156

0.039

−0.490

−0.121

Appendix C: Tables for the data base in chapter 8

443

SE Skew

0.337

0.220

1.576

0.343

0.228

0.228

0.285

0.249

Maximum

90.600

93.000

93.000

94.000

92.000

95.000

86.000

86.000

STD Err

3.444

1.568

1.983

3.790

1.977

2.152

2.506

2.034

STD Dev

24.352

17.252

19.932

26.257

20.918

22.769

21.114

19.719

SE Kurt

0.662

0.437

0.476

0.674

0.453

0.453

0.563

0.493

87.600

88.000

91.000

92.300

91.900

94.990

83.400

82.600

Range SUM

3038.900 8104.600 6456.450 2954.900 7171.200 6671.110 3560.900 5123.900

Median

70.700

72.000

67.000

74.500

71.900

63.000

54.000

55.000

Variance

593.007

297.627

397.279

689.429

437.55

518.448

445.805

388.839

Skewness

−1.076

−1.359

−1.210

−1.217

−1.290

−0.807

−0.520

−0.592

Minimum

3.000

5.000

2.000

1.700

0.100

0.010

2.600

3.400

Arc Sine Transformed Distribution Arc Sine Transformed Distribution Ethanol Free Non Fire Victims COHb Distribution Ages ranging Midpoint

6–20

21–40

41–60

61–80

Ethanol Free Fire Victims COHb Distribution Ages ranging 6–20

21–40

41–60

61–80

Missing

0

0

0

0

0

0

0

0

0.03

2

1

3

4

3

3

3

1

0.10

1

1

1

1

1

4

1

4

0.16

2

0

1

1

3

2

4

0

0.22

2

2

2

0

2

3

4

5

0.29

1

2

2

3

1

3

3

2

0.35

3

4

0

1

2

1

3

5

0.42

0

3

5

1

7

5

4

5

0.48

2

5

3

0

5

9

6

12

0.55

2

3

8

0

4

13

8

10

0.61

2

8

4

5

7

9

10

11

0.68

2

12

10

2

6

7

6

6

0.74

3

11

21

2

8

6

4

6

0.81

7

17

10

4

14

10

6

9

0.87

6

20

5

7

25

5

5

6

0.93

11

13

8

12

12

18

3

10

1.00

2

8

8

3

5

8

0

1

Appendix C: Tables for the data base in chapter 8

444

1.06

1

10

5

1

1

2

1

1

1.13

1

0

2

0

5

2

0

0

1.19

0

1

3

0

1

0

0

0

1.26

0

0

0

1

0

2

0

0

1.32

0

0

0

0

0

0

0

0

Total

50

121

101

48

112

112

71

94

Mean

0.684

0.755

0.719

0.699

0.721

0.668

0.543

0.594

Mode

0.848

0.848

0.775

0.927

0.848

0.927

0.524

0.927

Kurtosis

−0.400

0.721

0.555

−0.143

0.365

−0.396

−0.613

−0.461

SE Skew

0.337

0.220

0.240

0.343

0.228

0.228

0.285

0.249

Maximum

1.134

1.194

1.194

1.223

1.168

1.253

1.035

1.035

STD Err

0.042

0.020

0.025

0.046

0.025

0.027

0.029

0.024

STD Dev

0.296

0.222

0.255

0.318

0.261

0.285

0.247

0.238

SE Kurt

0.662

0.437

0.476

0.674

0.453

0.453

0.563

0.493

Range

1.104

1.144

1.174

1.206

1.167

1.253

1.009

1.001

SUM

34.194

91.330

72.638

33.535

80.776

74.763

38.526

55.878

Median

0.785

0.804

0.734

0.841

0.802

0.682

0.570

0.582

Variance

0.087

0.049

0.065

0.101

0.068

0.081

0.061

0.056

Skewness

−0.835

−0.905

−0.642

−0.951

−0.889

−0.401

−0.253

−0.282

Minimum

0.030

0.050

0.020

0.017

0.001

0.000

0.026

0.034

Arc Sine Transformed COHb Distribution Ethanol Free Victims Midpoint Missing

Non Fire: >5

Fire: >20

Fire: 6– 20

Fire: 6–20 Non Fire: >5 Fire+Non Fire

0

0

0

0

0.03

11

7

3

14

0.10

4

9

1

5

0.16

4

6

3

7

0.22

6

13

2

8

0.29

8

8

1

9

0.35

8

10

2

10

0.42

10

18

7

17

Appendix C: Tables for the data base in chapter 8

445

0.48

11

27

5

16

0.55

15

35

4

19

0.61

21

34

7

28

0.68

28

22

6

34

0.74

39

17

8

47

0.81

40

33

14

54

0.87

38

18

25

63

0.93

45

31

12

57

1.00

21

9

5

26

1.06

17

4

1

18

1.13

3

2

5

8

1.19

4

0

1

5

1.26

1

2

0

1

1.32

0

0

0

0

Total

334

305

112

446

Mean

0.719

0.612

0.721

0.720

Mode

0.848

0.927

0.848

0.848

Kurtosis

0.440

−0.389

0.365

0.403

SE Skew

0.133

0.140

0.228

0.116

Maximum

1.223

1.253

1.168

1.223

STD Err

0.014

0.015

0.025

0.012

STD Dev

0.260

0.257

0.261

0.260

SE Kurt

0.266

0.278

0.453

0.231

Range

1.211

1.253

1.167

1.222

240.282

186.798

80.776

321.058

Median

0.775

0.619

0.802

0.775

Variance

0.068

0.066

0.068

0.068

Skewness

−0.883

−0.259

−0.889

−0.881

Minimum

0.012

0.000

0.001

0.001

SUM

Appendix C: Tables for the data base in chapter 8

446

COHb Distribution Ethanol Feee Victims Midpoint

Non Fire: >5

Fire: >20

Fire: 6– 20

Fire: 6–20 Non Fire: >5 Fire+Non Fire

Missing

0

0

0

0

2.4

6

5

2

8

7.1

8

5

2

10

11.9

3

8

0

3

16.7

2

4

3

5

21.4

2

7

1

3

26.2

5

9

2

7

30.9

8

7

1

9

35.7

7

10

4

11

40.5

9

14

3

12

45.2

8

20

5

13

50.0

13

35

3

16

54.7

21

25

4

25

59.5

20

29

7

27

64.3

31

18

7

38

69.0

44

30

11

55

73.8

47

22

23

70

78.5

40

32

18

58

83.3

35

17

9

44

88.1

18

6

5

23

92.8

7

2

2

9

97.6

0

0

0

0

Total

334

305

112

446

Mean

63.906

55.680

64.029

63.937

Mode

75.000

80.000

75.000

75.000

Kurtosis

1.289

−0.148

1.156

1.229

SE Skew

0.133

0.140

0.228

0.116

Maximum

94.000

95.000

92.000

94.000

Appendix C: Tables for the data base in chapter 8

447

STD Err

1.140

1.204

1.977

0.986

STD Dev

20.827

21.031

20.918

20.826

SE Kurt

0.266

0.278

0.453

0.231

92.800

94.990

91.900

93.900

21344.55

16982.31

7171.200

28515.75

Median

70.000

58.000

71.900

70.000

Variance

433.759

442.288

437.55

433.733

Skewness

−1.309

−0.631

−1.290

−1.300

Minimum

1.200

0.010

0.100

0.100

Range SUM

Counts of Cases in CWRU Data Base by Coroner’s Verdict and by Setting of CO Exposure Setting of CO Exposure Verdict

Non Fire

Fire

Fire & Explosion

Unknown

Total

Suicide

930

14

0

1

945

Accident

718

850

9

0

1577

16

16

0

0

32

6

20

3

0

29

22

24

7

0

53

0

1

0

0

1

1692

925

19

1

2637

Undetermined Homicide Industrial Accident Justifiable Homicide Total

Population Characteristics in CWRU Data Base and Descriptive Statistics Setting of CO Exposure Characteristic # of Drinkers

Non Fire #

Non Fire %

Fire #

Fire %

750

44.3

587

62.2

1259

74.4

599

63.5

# of Whites

1495

88.4

592

62.7

# of Blacks

196

11.6

350

37.1

1

0.1

2

0.2

# of Males Race

# of Other Races

Appendix C: Tables for the data base in chapter 8

448

Age Average

45.10

38.72

Std Error

0.41

0.86

46.00

41.00

Average

20.99

53.06

Std Error

0.82

1.58

15.00

34.00

Average

63.96

54.04

Std Error

0.29

0.54

Median

65.00

60.00

Total

1692

944

Median Ethanol %

Median COHb %

One Year Median COHb %, over the Time Frame Year

Fire COHb

# Cases

Ratio

Non Fire COHb

# Cases

Ratio

1938

85

2

42.5

75

38

2.0

1939

37.5

2

18.8

70

34

2.1

1940

60

7

8.6

80

34

2.4

1941

75

9

8.3

85

24

3.5

1942

70

13

5.4

85

31

2.7

1943

5

9

7.2

82.5

28

2.9

1944

5

9

8.3

77.5

20

3.9

1945

70

8

8.8

75

29

2.6

1946

75

23

3.3

65

18

3.6

1947

77.5

12

6.5

80

34

2.4

1948

60

17

3.5

70

23

3.0

1949

55

7

7.9

80

27

3.0

1950

65

6

10.8

75

31

2.4

1951

55

8

6.9

75

22

3.4

1952

50

13

3.8

65

25

2.6

Appendix C: Tables for the data base in chapter 8

449

1953

50

16

3.1

65

26

2.5

1954

50

21

2.4

60

40

1.5

1955

54.5

20

2.7

65

25

2.6

1956

55

19

2.9

60

51

1.2

1957

55

16

3.4

62.5

28

2.2

1958

60

31

1.9

60

49

1.2

1959

45

11

4.1

60

41

1.5

1960

55

32

1.7

60

51

1.2

1961

55

25

2.2

60

49

1.2

1962

60

24

2.5

60

32

1.9

1963

60

28

2.1

60

38

1.6

1964

60

36

1.7

65

53

1.2

1965

53

21

2.5

65

45

1.4

1966

60

42

1.4

60

41

1.5

1967

61

32

1.9

65

59

1.1

1968

60

36

1.7

61

58

1.1

1969

58

40

1.5

60

46

1.3

1970

58

22

2.6

55

45

1.2

1971

55

42

1.3

60

62

1.0

1972

55

23

2.4

60

63

1.0

1973

60

43

1.4

60

62

1.0

1974

56

42

1.3

65

48

1.4

1975

60

31

1.9

65

47

1.4

1976

59

28

2.1

65

57

1.1

1977

65

39

1.7

65

49

1.3

1978

61

37

1.6

65

55

1.2

1979

63

39

1.6

65

55

1.2

Totals

941

1693

Time Series Analysis (of One Year Median % COHb Levels) Model: The methods of Box-Jenkins ARIMA (Autoregressive Integrated Moving Average) Time Series Analysis (see TIME SERIES ANALYSIS, Revised Edition), by G.E.P.Box and G M Jenkins Holden Day 1976) were utilized to examine the Fire and Non Fire time

Appendix C: Tables for the data base in chapter 8

450

series. In both cases the structural model chosen to describe the time series was an ARIMA (0, 1, 1), i.e. the original data singly differenced is a one term moving average series. Fires:

Let X(t) denote the median %COHb level for fire cases for years t=1938,…, 1979; then: X(t)−X(t−1)=e(t)+0.75 e(t−1) where the sequence e(t) is from a white noise process (i.e. a sequence of independednt, identically distributed, normal random variables with zero mean) with an estimated residual standard deviation of 8.09.

Non Fires:

Let Y(t) denote the median %COHb level for non fire cases for years t=1938,…, 1979; then: Y(t)−Y(t−1)=u(t)+0.40 u(t−1) where the sequence u(t) is from a white noise process with an estimated residual standard deviation of 4.75.

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