THE RELATIONSHIP BETWEEN AMBIENT CARBON MONOXIDE LEVELS,
POSTMORTEM CARBOXYHEMOGLOBIN, SUDDEN DEATH AND
MYOCARDIAL INFARCTION
Lewis H. Kuller, M.D., Dr. P.H.
Edward P. Radford, M.D.
David Swift, Ph.D.
Joshua A. Perper, M.D.
Russell Fisher, M.D.
Department of Epidemiology & Environmental Medicine
Johns Hopkins School of Hygiene & Public Health
Office of the Chief Medical Examiner, State of Maryland,
Department of Epidemiology, Graduate School of Public Health,
The University of Pittsburgh
Supported by: Contract No. 68-0082 from the Environmental Protection Agency,
Coordinating Research Council, Inc., APRAC Project CAPM-13-69,
Contract N. I. H. 70-2071, Myocardial Infarction Branch of the
National Heart and Lung Institute.
Part of the work was completed while Dr. Kuller was Established
Investigator of the American Heart Association.
September 20, 1974
-------
ABSTRACT
The relationship between carbon monoxide exposure and heart attacks was studied
in Baltimore, Maryland.
Four hypotheses were tested: (1) Is there a relationship between sudden death
and myocardial infarction and ambient carbon monoxide levels, (2) Are post-
mortem carboxyhemoglobin levels higher for ASHD sudden deaths as compared to
sudden deaths from other causes, (3) Are there differences in postmortem carboxy-
hemoglobin levels between ASHD sudden deaths and living controls, and (4) Is
there any difference in the pathologic characteristics of ASHD sudden death with
high or low carboxyhemoglobin levels.
There was no evidence of clustering of either myocardial infarction or sudden
ASHD on a specific day, nor between the number of cases per day and ambient
carbon monoxide levels.
Postmortem carboxyhemoglobin levels were slightly higher for ASHD sudden deaths
than for sudden deaths due to other causes. Any differences were probably pri-
marily due to cigarette smoking.
Cigarette smokers who died suddenly due to ASHD had substantially higher post-
mortem carboxyhemoglobin levels than nonsmokers. Practically all of the elevated
carboxyhemoglobin levels could be related to cigarette smoking or specific environ-
mental exposure. There were no differences in carboxyhemoglobin levels between
ASHD sudden deaths and living controls. There was also no relationship between
cardiac pathology and postmortem carboxyhemoglobin levels among ASHD sudden
deaths.
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THE RELATIONSHIP BETWEEN AMBIENT CARBON MONOXIDE LEVELS,
POSTMORTEM CARBOXYHEMOGLOBIN, SUDDEN DEATH AND
MYOCARDIAL INFARCTION
Clinical, experimental and epidemiological studies have shown a relationship be-
tween carbon monoxide exposure and various aspects of clinical coronary artery
disease.'')
Major sources of carbon monoxide can be subdivided into three categories:^ '
(1) tobacco smoking, (2) occupational, and (3) community air pollution.
Clinical and experimental studies of the relationship between carbon monoxide
and clinical coronary artery disease have noted an increase in symptoms of angina
among men exposed to heavy freeway traffic in Los Angeles,^ ' or after breathing
50 or 100 ppm of carbon monoxide for up to four hours.''*' Acute exposure to
high levels of carbon monoxide resulted in increased coronary blood flow in pa-
tients without coronary disease, but not in those with coronary disease.'**)
Experimental studies have also shown a possible relationship between carbon
monoxide exposure and the development of atherosclerotic-like disease. Rabbits
exposed to moderate doses of carbon monoxide (carboxyhemoglobin 11%) were
noted to develop focal degenerative and reparative vascular changes which were
possibly precursors of atherosclerotic plaque formation.' ' Similarly, exposure of
rabbits to carbon monoxide and a high cholesterol diet enhanced the development
of atherosclerosis when compared to feedings of cholesterol alone.' '
Epidemiological studies have clearly shown an increased risk of coronary artery
disease among cigarette smokers. ("/') The increased risk has been noted pri-
marily for sudden death and myocardial infarction, and much less so for angina
pectoris.' ' The risk is directly correlated with the number of cigarettes smoked.
Furthermore, the risk of coronary disease was substantially decreased following
cessation of cigarette smoking.
More recent experimental and epidemiological studies have strengthened the
association between atherosclerotic cardiovascular disease, smoking and carbon
monoxide. Individuals who smoked nonnicotine cigarettes had increased carboxy-
hemoglobin levels. Following the smoking of cigarettes, there was a decrease in
time that patients with angina could exercise before developing chest pain.'' ' '
Few studies have attempted to correlate ambient carbon monoxide exposure and
coronary disease in a community. In Los Angeles, postmortem blood carboxy-
hemoglobin levels were measured in a sample of deaths certified at the coroner's
office.{'"*' The carboxyhemoglobin levels were higher for cigarette smokers than
non-smokers. The postmortem carboxyhemoglobin levels were weakly but posi-
tively correlated with the ambient carbon monoxide exposures just prior to death.
A further analysis of the same data failed to note any significant difference in
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the postmortem carboxyhemoglobin levels between individuals dying of myocardial
infarction or other cardiovascular disease.O^)
In the Los Angeles region, the case-fatality percentage for hospitalized myo-
cardial infarction patients was greater in the areas with high ambient carbon
monoxide (8 to 14 ppm) than in the lower areas.' '' The differences were
apparent during the weeks of increased pollution (weekly mean CO of 7.7 to
14.0). In the higher polluted areas there were also positive correlations between
the ambient carbon monoxide levels and the daily myocardial infarction case-
fatality percentage in the hospital. There was/ however, no association between
ambient carbon monoxide levels and the number of admissions for myocardial in-
farction each day.
No other study has attempted to relate the ambient carbon monoxide levels to
either the incidence, case-fatality or deaths due to ASHD. An ongoing study
of sudden death and myocardial infarction in Baltimore City made it possible to
relate the incidences of myocardial infarction and sudden death to ambient car-
bon monoxide levels and blood carboxyhemoglobin. Since approximately 70% of
all ASHD deaths occur outside of a hospital and approximately two-thirds of the
ASHD deaths were sudden, the Baltimore study included both hospital and non-
hospital ASHD deaths, with a particular emphasis on ASHD sudden deaths since
their time of onset could be more clearly identified.
Four specific hypotheses were tested:
1. Is there a temporal relationship between the incidence of sudden cardiac
death, transmural myocardial infarction or total ASHD deaths in a com-
munity and the ambient carbon monoxide level?
2. Are the postmortem carboxyhemoglobin levels higher for ASHD sudden deaths
as compared to sudden deaths from other causes?
3. Are there differences in the postmortem carboxyhemoglobin levels between
ASHD sudden deaths and normal living controls after adjustment for differ-
ences in cigarette smoking?
4. Are there differences in the pathology of sudden cardiac death in relation
to carboxyhemoglobin levels or cigarette smoking?
METHODS AND RESULTS
1 . Relationship Between Events Per Day and Ambient Carbon Monoxide Levels:
The first hypothesis of a relationship between events per day and ambient carbon
monoxide levels was tested in the following ways. All sudden, non-traumatic
deaths, patients hospitalized with a transmural myocardial infarction and non-sudden
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deaths due to arteriosclerotic heart disease, between the ages of 25-64, were
identified during a two-year period, June 1970-June 1972, in a defined geo-
graphic area of Baltimore City. This area had a population of about 500,000.
The detailed surveillance methods have been previously described. (''/ During
the two year period, 522 ASHD sudden deaths, 336 ASHD non-sudden deaths
and 539 transmural myocardial infarctions were ascertained.
The methods of case ascertainment have been described previously. (''' Sudden
death was defined as occurring within 24 hours of onset to individuals able to
function without assistance outside of their home. The deaths were further sub-
classified by length of survival, history of heart disease and by whether witnessed
or not. Cause of death was based on a review of history, clinical records and
postmortem examinations. Approximately 50% of the ASHD sudden deaths were
certified by the medical examiner. For the sudden deaths certified by the medi-
cal examiner, a detailed study of the pathology of sudden nontraumatic deaths
was conducted. About 95% of the sudden deaths certified by the medical ex-
aminer had a postmortem examination, including a special examination of the
heart to assay the degree of coronary stenosis, presence of acute lesions, and
types of myocardial pathology.
Transmural myocardial infarction was defined as admission for a heart attack in
which there were evolving "Q" and "ST-T" wave changes on the electrocardio-
gram with or without serum enzyme changes. All cases were reviewed indepen-
dent of the ambient carbon monoxide levels.
During approximately a concurrent nine-month period of the surveillance study
described above (November 1, 1971 -August 31, 1972), a special air pollution
monitoring station was operated at the Johns Hopkins School of Hygiene and
Public Health. Ambient carbon monoxide levels and other pollutants were
measured continuously. The number of new sudden, non-sudden ASHD deaths
and living myocardial infarction patients occurring on each day was determined
and compared with the expected number of cases per day, assuming a random
poisson distribution.
There was no evidence of any clustering of sudden deaths, myocardial infarctions
or non-sudden deaths on any specific day within the geographic area of the
surveillance study (Figure 1). The absence of any clustering of events over time
would be evidence against a major effect of an environmental factor, presuming
the level of the environmental factors varied over time.
The distribution of cases in the defined area was then compared with the 24 hour
mean ambient carbon monoxide levels measured at the Hopkins station (Table 1).
There was no evidence of any association between the ambient carbon monoxide
levels and the number of cases of any type per day. Because of the relatively
- 5 -
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small number of days with high ambient carbon monoxide levels/ the analysis was
continued throughout the summer of 1972.
There was still no evidence of any association between the carbon monoxide levels
and number of cases. The only time there was any evidence of a relationship be-
tween an environmental factor and clustering of events occurred in July 1972 when
during a brief "heatwave" on July 24-25, there were six deaths on July 24 and
six on July 25 in the surveillance area. The ambient carbon monoxide level re-
mained low during this period. Therefore, the surveillance mechanisms were able
to identify a possible environmental precipitent such as excessive temperatures.
However, the first hypothesis that ambient carbon monoxide was correlated with
the distribution of heart attacks was unsupported as we found no evidence of
clustering of cases in time or relationship between number of cases per day and
the ambient carbon monoxide level.
As previously noted, the Los Angeles Study included both a spatial and temporal
distribution in relation to ambient carbon monoxide levels. The spatial distribu-
tion of events in relation to ambient carbon monoxide in Baltimore could not be
analyzed for two reasons;
a. Approximately 70% of the ASHD deaths were sudden and occurred
outside of a hospital. It would be necessary to pinpoint the area
of onset for each event and relate it to a "carbon monoxide level."
Unfortunately, there would have been no way of obtaining a de-
nominator, the number of individuals at risk in that specific area at
the time of the event.
b. In order to compare events in each area, we needed to have measure-
ments of ambient carbon monoxide levels within specific subareas.
Unfortunately, the number and quality of the sampling stations pre-
cluded any detailed subarea analysis.
2. Relationship between Postmortem Carboxyhemoglobin and Cause of Death
In order to determine the relationship between postmortem carboxyhemoglobin
levels and causes of sudden death, postmortem blood specimens were collected
from 2,366 deaths certified by the medical examiner of the State of Maryland.
This sample included deaths in the Baltimore City surveillance area and also from
the rest of the City and State of Maryland. All age groups and both traumatic
and non-traumatic sudden deaths were included.
The Carboxyhemoglobin levels were measured in duplicate by a spectophotometric
technique that determined both carboxyhemoglobin and methemoglobin at the same
time.('°) The technique was carefully validated for postmortem blood specimens of
- 6 -
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carboxyhemoglobin by comparison with gas chromatography. Carboxyhemoglobln
levels remained stable after death.0°) This observation has also been reaffirmed
in the present study.
The cause of death for these 2,366 people and circumstances associated with the
deaths were ascertained from the death certificates and medical examiner's re-
ports, including an autopsy examination in a high percentage of the deaths.
The carboxyhemoglobin levels were slightly higher for the ASHD sudden deaths
than for sudden deaths from other natural causes and lower than for deaths due
to homicides (Table 2, Appendix Table 1). The differences were small and can
probably be explained by variations in smoking habits. Unfortunately, data on
smoking habits were obtained for too few of the sudden deaths from other causes
than ASHD, so this hypothesis could not be critically tested.
In a recent attempt to study the association between carboxyhemoglobin, smoking
and causes of death, blood thiocyanate and carboxyhemoglobin levels were
measured. Thyocyanate levels are a measure of long-term smoking experiences.
Preliminary results showed that the differences in carboxyhemoglobin levels among
the cause of death groups were primarily a reflection of the recency of cigarette
smoking prior to death.'^^^
Since we had previously noted that cigarette smokers had carboxyhemoglobin levels
as high as 10% or more, the characteristics of death with high carboxyhemoglobin
levels greater than 10% were studied. We presumed that at least some of these
higher levels were not due to cigarette smoking alone. Note in Table 3 that
many of these deaths were related to fires or suicide by carbon monoxide. Only
1% of the ASHD deaths had carboxyhemoglobin levels that were greater than 10.
The circumstances associated with these ASHD deaths will be discussed later in
this report.
Among the ASHD sudden deaths, carboxyhemoglobin levels were higher in the
younger as compared to the older age groups (Table 4). Seven percent of the
846 ASHD sudden deaths had a postmortem carboxyhemoglobin level greater than
4% (Table 4). Above the age of 65 when it is believed that individuals are
most susceptible to air pollution effects, only 6 of 341 deaths had levels greater
than 4% and over 75% were below 1%.
The relationship between the postmortem carboxyhemoglobin levels for ASHD sudden
deaths and living controls was determined as follows:
For the ASHD sudden deaths within the special surveillance study area in Baltimore
City, a detailed follow-back interview was completed with the next of kin. Infor-
mation about place of death, activity at onset, length of survival, smoking history
and prior history of disease was collected. Interview information could be collected
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for about 90% of the ASHD sudden deaths. The data were collected independent
of the carboxyhemoglobin levels and the results of the postmortem examination.
Smoking histories and postmortem carboxyhemoglobin levels were reported in 243
ASHD sudden deaths. This included 120 deaths in which there was a special de-
tailed postmortem examination. Postmortem carboxyhemoglobin levels were sub-
stantially higher for the cigarette smokers than the nonsmokers (Table 5). Note
that 86% of the nonsmokers had carboxyhemoglobin levels less than 2%.
An attempt was then made to evaluate the circumstances at the time of death for
cases with high levels of carboxyhemoglobin. Of the eight deaths among non-
smokers with carboxyhemoglobin levels greater than 3, seven were former smokers
and three also had possible specific environmental exposures (Table 6). It is
certainly possible that some of the current nonsmokers were still smoking prior to
death since the smoking histories were obtained from the next of kin and other
relatives rather than from the deceased. Of the seven who were current smokers
and had levels greater than 10% carboxyhemoglobin, four had a definite environ-
mental exposure beside heavy cigarette smoking and one was a heavy smoker with
chronic emphysema.
3. Comparison of Carboxyhemoglobin between ASHD Sudden Deaths and Living
Controls:
The distribution of carboxyhemoglobin levels among the ASHD sudden deaths and
living controls after adjustment for the history of cigarette smoking is shown in
Table 7. Living controls who were cigarette smokers had higher carboxyhemo-
globin levels than ASHD sudden deaths who had smoked cigarettes prior to death.
The sudden deaths with a history of not smoking cigarettes prior to death had
higher carboxyhemoglobin levels than the nonsmoking living controls. The non-
smokers included both those who had never smoked cigarettes and ex-smokers.
The most likely explanation for these results was/ for the nonsmokers probably at
least a few were actually still smoking prior to death/ even though their spouse
or other relatives thought they were nonsmokers. In order to test this hypothesis
we compared the distribution of carboxyhemoglobin levels among individuals who
had never smoked cigarettes. As noted in Table 7/ there were no differences
between the sudden deaths and living controls, and all but two were below 2%
carboxyhemoglobin levels. Some of the current cigarette smokers among the
sudden ASHD deaths were probably "sick" prior to death and had stopped smoking;
hence their lower carboxyhemoglobin levels.
Other characteristics of the ASHD sudden deaths in relation to carboxyhemoglobin
levels were also reviewed. There was no substantial difference in postmortem
carboxyhemoglobin levels among the ASHD sudden deaths in relation to activity
- 8 -
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or place of onset of the heart attack. There was also no difference in postmortem
carboxyhemoglobin levels by length of survival or whether the death was witnessed
or not.
4. Relationship between Postmortem Carboxy hemoglobin and Pathology of Sudden
Deaths;
tr
An attempt was made to include a detailed postmortem examination for every ASHD
sudden death certified by the medical examiner within the special geographic sur-
veillance area in Baltimore City. Of the 522 ASHD sudden deaths, 258 were
certified by the medical examiner and 231 of the 258 had a postmortem examina-
tion. Approximately 85% (171) of the 231 had a special detailed examination of
the heart in order to ascertain the extent of coronary artery stenosis, prevalence
of acute lesions in the arteries and myocardial pathology. The special postmortem
examination study began prior to the analysis of the carboxyhemoglobin levels so,
only 120 of the 171 had both a detailed postmortem examination and carboxyhemo-
globin determination. The distribution of postmortem carboxyhemoglobin levels was
similar among the deaths with an acute pathological lesion such as recent coronary
thrombosis or hemorrhage in a plaque, and those without acute lesions. There was
also no difference in postmortem carboxyhemoglobin levels in relation to the maxi-
mum degree of coronary stenosis or the number of arteries with greater than 50%
stenosis.
Practically all of the ASHD sudden deaths had severe coronary artery stenosis,
102 of the 120 had three or four coronary arteries (left main, anterior descending,
circumflex or right coronary artery) with 50% or greater stenosis. The ASHD sud-
den deaths therefore represent very severe coronary artery diesease and probably
should be most responsive to change in ambient carbon monoxide levels.
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DISCUSSION
Exposure to carbon monoxide can have major physiological effects on the coronary
circulation. ('/ Moderately higher levels of carbon monoxide may precipitate
symptoms of angina pectoris among susceptible individuals. This study, however/
does not support the hypothesis that ambient carbon monoxide levels in an urban
area such as Baltimore were major factors in the onset of sudden death and myo-
cardial infarction.
There are several possible reasons that may explain the failure to note such a re-
lationship. First, the levels of ambient carbon monoxide were too low in Balti-
more to have any effect. The levels are obviously lower than in areas of Los
Angeles or New York, but were probably comparable to other major metropolitan
regions. Certainly, a replication of this type of study should be done in an area
with presumably much higher ambient carbon monoxide levels. It should be noted,
however, that a pilot study of postmortem carboxyhemoblobin levels in Los Angeles
reported results very similar to the current Baltimore study.'''/
Second, the major sources of carbon monoxide are occupational, environmental or
personal exposure from cigarette smoking rather than general ambient carbon mon-
oxide exposures. The risk of sudden death is much higher among smokers than
nonsmokers. Thus, the highest risk group may not be substantially adversely af-
fected by usual community ambient carbon monoxide levels. Cigarette smokers
in areas with high ambient carbon monxide levels do, however, have higher car-
boxy hemoglobin than smokers from less polluted areas.
Finally, there may be a fairly long time period between carbon monoxide exposure
and the sudden death or onset of a myocardial infarction. Thus, carboxyhemo-
globin levels measured at the time of death or onset of a myocardial infarction
may not reflect the carbon monoxide level that precipitated the sudden death or
myocardial infarction. There was, however, no relationship between carboxyhemo-
globin levels and length of survival. Many sudden deaths did have previous
symptomatology and perhaps the premonitory phase was related to carbon monoxide
exposures. Prospective type studies of the relationship between symptoms and
carbon monoxide levels might be useful. For example, it would be interesting
to determine whether patients who have angina pectoris and are nonsmokers have
a greater frequency and intensity of symptoms during days in which the ambient
carbon monoxide levels are elevated. Although cigarette smokers in areas with
high ambient carbon monoxide levels tend to have higher carboxyhemoglobin levels
than those living in less polluted areas, the differences are small in comparison to
the variations between smokers and nonsmokers. Since most ASHD deaths are
sudden and usually associated with an arrhythmia, it might be possible to determine
whether patients with angina pectoris or survivors of a myocardial infarction have
- 10 -
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a higher frequency of ventricular arrhythmias when the ambient carbon monoxide
levels are high.
If the elevation of carboxyhemoglobin levels following cigarette smoking is a major
factor in the higher risks of heart attacks among cigarette smokers, then the po-
tential for the development of a "safe cigarette" is extremely remote and possibly
the only type of safe cigarette would be a noncombustible variety.
Certainly, much more emphasis should be given to carbon monoxide as a precipi-
tant of heart attack. Much more emphasis, however, should be aimed primarily
at cigarette smoking and occupational and unusual environmental exposures than
to general ambient carbon monoxide levels, except in unusual environmental cir-
cumstances such as the Los Angeles area.
- 11 -
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DISTRIBUTION OF NUMBER OF CASES PER DAY DURING 2-YEARS,
COMPARISON OF OBSERVED WITH EXPECTED CASES:
SUDDEN DEATH DUE TO ARTERIOSCLEROTIC HEART DISEASE — AGES 25-64
No. of Days
OBS
330
320
310
300
290
280
270
260
250
240
230
220
210
200
190
180
170
160
150
140
130
120
110
100
90
80
70
60
50
40
30
20
10
0
EXP
/""i n f
OBS
OBS
EXP
EXP
OBS
OBS EXP
1 1
4+
Number of Cases per Day
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TABLE 1
DISTRIBUTION OF CASES PER DAY IN RELATION TO MEAN CARBON MONOXIDE LEVELS AT HOPKINS STATION
CO
AVERAGE
24 Mrs.
PPM
0-4
5-9
9+
TOTAL
DAYS
145
31
20
TOTAL CASES* PER DAY
IN PERCENT
01234+
16 33 24 15 12
13 39 16 22 10
20 15 50 10 05
SUDDEN ASHD DEATHS
PER DAY IN PERCENTS
01234+
55 30 13 02
48 32 20 -
50 40 10
'Sudden and Not-Sudden ASHD Deaths and Living M. I. Patients
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TABLE 2
COMPARISON OF POSTMORTEM CARBOXYHEMOGLOBIN LEVELS BY CAUSE OF DEATH & AGE
AGE
Cause of Death
Total
Carboxyhemog lobin
Level
0 - .9
1-1.9
2 - 2.9
3 - 3.9
4+
ASHD
209
No.
75
33
27
30
44
_%.'
36
56
65
79
100
45-54
Other
Natural
169
Auto
Accidents
21
Homicides
41
CUMULATIVE PERCENTS
No.
99
37
9
11
13
%
59
81
86
93
100
No.
11
4
1
2
3
%
52
71
76
85
100
No.
17
1
3
4
16
%
41
43
50
60
100
55-64
ASHD
225
Other
Natural
122
Auto
Accidents
13
Homicides
27
CUMULATIVE PERCENTS
No.
124
34
22
24
21
%
55
70
80
91
100
No.
89
15
7
9
2
%
73
85
90
97
100
No.
6
1
3
1
2
%
47
55
78
86
100
No.
12
5
3
2
5
%
44
63
74
81
100
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TABLE 3
Distribution of Postmortem Carboxyhemoglobin Levels by Cause
of Death. Levels >10% Carboxyhemoglobin
Cause of Death
ASHD
Other Non-Traumatic
Auto Accident
Other Accidents
Homicide
Suicide
CO Suicide
Fire
TOTAL:
No. Deaths
852
599
162
190
357
52
24
34
2,366
Greater than 10%
Carboxyhemoglobin
No.
9
-
2
9
9
3
21
25
78
Percent
01
-
01
05
03
06
88
74
03
Percent (Down)
(of All Cases > 10%
Carboxyhemoglobin)
11
-
02
12
12
04
27
32
100
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TABLE 4
Cumulative Percent Distribution of Postmortem Carboxyhemoglobin Levels by Age: ASHD Deaths
Age
Number
Carboxyhemoglobin Levels
0 - .9
1-1.9
2-2.9
3 - 3.9
4 - 4.9
5 - 5.9
6 - 6.9
7 +
25-34
17
35-44
55
45-54
209
55-64
224
65-74
202
75+
139
Total
846
CUMULATIVE PERCENTS
No.
6
6
1
1
-
2
1
-
%
35
70
76
82
-
94
100
-
No.
19
10
4
10
6
2
1
3
%
35
53
60
78
89
93
95
100
No.
75
33
27
30
19
8
9
8
%
36
56
65
79
88
92
96
100
No.
124
34
22
23
5
5
4
7
%
55
70
80
91
93
95
97
100
No.
147
32
11
6
3
1
-
2
%
73
89
94
97
98
98
-
100
No.
112
16
9
-
1
1
-
-
%
81
93
99
-
99
100
-
-
No.
483
131
74
70
34
19
15
20
%
57
72
81
89
93
95
97
100
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TABLE 5
Distribution of Postmortem Corboxyhemoglobin Levels Among ASHD Deaths
By Cigarette Smoking History: (Current Smoking Habits)*
Cumulative Percent of Carboxyhemoglobin
NUMBER OF PEOPLE
Cigarettes Only
163
Nonsmokers
58
Carboxyhemoglobin Level in Percent CUMULATIVE PERCENT
0-0.9
1 - 2.9
3 - 4.9
5 - 6.9
7 - 9.9
10 +
13
55
82
90
95
100
43
86
91
96
98
100
*Excludes pipe and cigar smokers.
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TABLE 6
Reasons for High Carboxyhemoglobin Levels Among ASHD Deaths:
By Smoking History
Eight nonsmokers, levels greater
than 3
Seven smokers* carboxyhemoglobin
level >MO
Seven were former smokers
One had severe emphysema; smoked
2 packs of cigarettes per day
Three also had environmental
exposure:
Two driving or fixing a car
One found in the basement of a
house with a possible deffective
heating system, although definite
CO exposure was not proven
Two patients smoked 2 packs per day,
one of whom was found in a car he
was repairing; with the motor running
One found dead in a car
One died in a home with a defective
heating system and definite CO ex-
posure
Two found dead at home — no defi-
nite environmental factor identified
Included one cigarette smoker who also smoked a pipe
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TABLE 7
Comparison of Carboxyhemoglobin Levels Among ASHD Sudden Deaths and Living Controls
By Current Smoking History* (Cumulative Percents)
Carboxyhemoglobin
Level in Percents
0 - 0.9
1 - 2.9
3 - 4.9
5 - 6.9
7 +
TOTAL
Cigarettes
ASHD
No.
25
71
50
16
16
178
%
14
54
82
91
100
Living
Controls
No.
7
30
31
26
13
107
%
06
35
64
88
100
Non-smokers. Inc.
Ex-smokers
ASHD
No.
28
22
3
3
2
58
%
48
86
91
96
100
Living
Controls
No.
73
31
1
-
-
105
%
70
99
100
100
-
Excluding Ex-smokers
ASHD
No.
12
8
1
-
-
21
%
57
95
100
-
-
Living
Controls
No.
34
18
1
-
-
53
%
64
98
100
-
-
''Smoking history prior to death or at time of interview
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APPENDIX TABLE 1
Median and Mean Carboxyhemoglobin Levels by Age and Cause of Death
Cause of Death
ASHD
Other Natural
Auto Accident
Other Accidents
Homicide
AGE
25-34
Median
1.5
1.2
2.0
1.0
2.4
Mean
2.0
1.6
3.2
5.4
2.9
35-44
Median
1.6
0.8
2.3
1.2
2.0
Mean
2.6
1.5
2.2
3.9
2.7
45-54
Median
1.9
0.7
0.4
1.4
2.9
Mean
2.6
1.3
1.8
7.1
3.7
55-64
Median
0.7
0.6
1.2
0.5
1.2
Mean
1.6
1.0
2.2
1.4
2.1
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REFERENCES
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Intimal-Subintimal Changes in Rabbit Aorta by a Prolonged Moderate Carbon
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('^/Aronow, W.S., Dendinger, J. and Rokaw, S.N., Heart Rate and Carbon
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* 'Curphey, T.J., Hood, L.P.L., and Perkins, N.M., Carboxyhemoglobin in
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''^'Goldsmith, J.R., and Landaw, S.A., Carbon Monoxide and Human Health,
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''°'Cohen, S.I., Deane, M., and Goldsmith, J.R., Carbon Monoxide and Sur-
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'' 'Kuller, Lo, Cooper, M., Perper, J., Epidemiology of Sudden Death: Arch. of
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(1 9)
* 'Blackmore, D.J., Interpretation of Carboxyhemoglobin Found at Postmortem
in Victims of Aircraft Accidents, Aerospace Med., 41:757-759, 1970.
' 'Radford, E., Studies of the Relationship of Thiocyanate and Carboxyhemo-
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