U.S. Department

of Transpor tation

Federal Aviation

Administration

Arvind K. Chaturvedi

Dudley R. Smith

Dennis V. Canfield

Civil Aeromedical Institute

Federal Aviation Administration

Oklahoma City, Oklahoma 73125

February 2000

Final Report

This document is available to the public

through the National Technical Information

Service, Springfield, Virginia 22161.

Office of Aviation Medicine

Washington, D.C. 20591

Blood Carbon Monoxide and

Hydrogen Cyanide Concentrations

In the Fatalities of Fire and

Non-Fire Associated Civil Aviation

Accidents, 1991-1998

DOT/FAA/AM-00/9
NOTICE

This document is disseminated under the sponsorship of

the U.S. Department of Transportation in the interest of

information exchange. The United States Government

assumes no liability for the contents thereof.
i

Technical Report Documentation Page

1. Report No. 2. Government Accession No. 3. Recipient's Catalog No.

DOT/FAA/AM-00/9

4. Title and Subtitle 5. Report Date

February 2000

6. Performing Organization Code

Blood Carbon Monoxide and Hydrogen Cyanide Concentrations in the

Fatalities of Fire and Non-Fire Associated Civil Aviation Accidents,

1991-1998

7. Author(s) 8. Performing Organization Report No.

Chaturvedi, A.K., Smith, D.R., and Canfield, D.V.

9. Performing Organization Name and Address 10. Work Unit No. (TRAIS)

FAA Civil Aeromedical Institute

P.O. Box 25082 11. Contract or Grant No.

Oklahoma City, Oklahoma 73125

12. Sponsoring Agency name and Address 13. Type of Report and Period Covered

Office of Aviation Medicine

Federal Aviation Administration

800 Independence Ave., S.W.

Washington, D.C. 20591 14. Sponsoring Agency Code

15. Supplemental Notes

This work was accomplished under the approved tasks AM-B-91-TOX-65, AM-A-92-TOX-71, AM-A-93-

TOX-71, AM-B-94-TOX-71, AM-B-95-TOX-201, AM-B-96-TOX-202, AM-B-97-TOX-202, AM-B-98-

TOX-202, and AM-B-99-TOX-202.

16. Abstract

Postmortem blood samples submitted to the Federal Aviation Administration's Civil Aeromedical Institute (CAMI) from

fatal civil aviation accident victims are analyzed for the primary toxic combustion gases carbon monoxide (CO), as

carboxyhemoglobin (COHb), and hydrogen cyanide, as cyanide (CN-

). These analyses are performed to establish possible

exposure of victims to smoke produced during in-flight/post-crash fires or to CO leaked into cabin/cockpit from faulty

exhaust/heating systems. The presence of both gases in blood would suggest that the victim was alive and inhaled smoke

from a fire. If only COHb is elevated, then the accident (or death) could be the result of CO contamination of the interior.

Information pertaining to blood levels of the 2 gases in aviation fatalities, in relation to the associated accidents, is scattered

or not available, particularly with regard to toxicity. Therefore, considering that COHb ≥ 10% and CN-

≥ 0.25 μg/mL are

sufficient to produce some degree of undesired physiological effects, the necessary information was extracted from the

CAMI's toxicology database. Biological samples from 3857 fatalities of 2837 civil aviation accidents, occurring during 1991-

1998, were received at CAMI. Out of these, 1012 accidents, encompassing 1571 (41%) fatalities, were fire associated,

whereas 1820 accidents were non-fire related. The remaining 5 accidents were of unkown fire status. There were fewer firerelated fatalities and associated accidents in the category wherein COHb ≥ 10% and CN-

≥ 0.25 μg/mL than that in the

category wherein COHb < 10% and CN-

 < 0.25 μg/mL. No in-flight fire was documented in the former category, but inflight fires were reported in 14 accidents (18 fatalities) in the latter category. No fatality under non-fire accidents was found

in which the levels of both gases were determined to be at or above the stated levels. There were 15 non-fire accidents with

17 fatalities in which only COHb (10-69%) was elevated, indicating that these accidents were associated with the inhalation

of CO of non-fire origin. The present study suggests that the aviation fire accidents/fatalities were fewer than the aviation

non-fire accidents/fatalities, with the fact that the fire-associated fatalities had COHb and CN-

 at levels high enough to

produce some degree of impairment/toxicity. Furthermore, the study confirms that aviation accidents related to in-flight

fires and to CO-contaminated interiors are rare.

17. Key Words 18. Distribution Statement

Forensic Sciences, Toxicology, Carbon Monoxide,

Hydrogen Cyanide, Smoke Toxicity, Fire/Non-Fire Civil

Aviation Accidents, Aircraft Accident Investigation

Document is available to the public through the

National Technical Information Service

Springfield, Virginia 22161

19. Security Classif. (of this report) 20. Security Classif. (of this page) 21. No. of Pages 22. Price

Unclassified Unclassified 13

Form DOT F 1700.7 (8-72) Reproduction of completed page authorized

1

BLOOD CARBON MONOXIDE AND HYDROGEN CYANIDE CONCENTRATIONS

IN THE FATALITIES OF FIRE AND NON-FIRE ASSOCIATED

CIVIL AVIATION ACCIDENTS, 1991-1998

INTRODUCTION

Postmortem biological samples collected at autopsy from the victims of fatal civil aircraft (air carrier

and general aviation) accidents are submitted to the

Federal Aviation Administration’s (FAA’s) Civil Aeromedical Institute (CAMI) for toxicological evaluation (Public Law, 1988). The sample submission is

coordinated through the FAA’s Office of Accident

Investigation by the National Transportation Safety

Board (NTSB), which is responsible for investigating

all U.S. civilian aircraft accidents. For such evaluation, biological samples are analyzed for drugs,

alcohols, and the 2 primary toxic combustion gases,

carbon monoxide and hydrogen cyanide. The former

gas is measured in blood as carboxyhemoglobin

(COHb), while the latter in blood as cyanide (CN-

).

The blood gas analyses are performed to establish

possible exposure of victims to smoke produced during in-flight/post-crash fires or to carbon monoxide

leaked into the cabin/cockpit air from a faulty exhaust or heating system (Aviation Monthly, 1991;

Chaturvedi, 1995). In the majority of cases, the

submitted postmortem samples are from pilots and

co-pilots. However, depending upon the nature of an

accident—for example, an accident involving fire—

samples from other crewmembers and passengers are

sometimes submitted.

It is well established that carbon-containing materials (such as cotton and polyethylene) generate carbon monoxide and carbon dioxide upon burning,

whereas nitrogen-containing materials (such as Nylons, silk, and wool) also generate hydrogen cyanide

(Gad, 1990; Sanders et al., 1992; Chaturvedi, 1995;

Chaturvedi & Sanders, 1996; Hartzell, 1996). Since

the aircraft structure is composed of a variety of

carbon- and nitrogen-containing polymeric materials, there is a strong potential for the generated smoke

to be rich in carbon monoxide and hydrogen cyanide.

In the absence of fire, the presence of carbon monoxide in the aircraft’s interior would be indicative of the

malfunctioning of heating/exhaust systems: Engine

exhaust would contain a negligible amount of hydrogen cyanide, since aviation fuel is primarily a mixture

of non-nitrogen-containing hydrocarbons.

In-flight smoke and fire are rare occurrences in

modern aviation, but if that happens, then the consequences are generally deadly (McKenna, 1996;

Proctor, 1996; ABC News, 1998; CNN, 1998).

Survivable crashes followed by conflagration do occur, primarily originating from fuel spills around the

crashed aircraft. Aircraft occupants may survive the

initial forces of such crashes, but they are frequently

unable to escape from the fire environment because

of physical injuries and/or performance impairment

from smoke-induced toxicity and visual obscuration,

leading to incapacitation and death. Post-crash fire

has been determined to be the most important reason

for pilot fatalities in commuter aircraft/air taxi crashes

(Li & Baker, 1993).A study by the International Cabin

Water Spray Research Management Group has concluded that there were 95 fire-related civil passenger

aircraft accidents worldwide over a 26-year period,

claiming approximately 2400 lives (ICWSRMG, 1993).

A U.S. General Accounting Office publication further

concluded that approximately 16% (32 accidents) of

all U.S. transport aircraft accidents between 1985

and 1991 involved fire, and 22% (140 fatalities) of

the fatalities in these accidents resulted from the

effects of fire and smoke (GAO, 1993).

Although previous studies report the number of

fatalities in smoke/fire-related aviation accidents,

information on blood levels of the 2 combustion

gases found in fire and in non-fire aviation accident

fatalities is scattered or not available, particularly in

relation to performance impairment, toxicity, incapacitation, and death. This type of information will

be valuable to establish whether a particular victim

succumbed to smoke before or after the plane crashed

and to determine possible interactive toxic effects of

these gases. The presence of both gases in the blood

would suggest that the victim was alive and inhaled

smoke from a fire. If both gases were not found in

blood and the victim had physical and external burn
2

injuries, then it can be deduced that the cause of

death was not the inhalation of smoke, but instead

should be attributed to severe injuries. If only COHb

is elevated, it can be inferred that the accident (or

death) was because of the contamination of the aircraft interior environment with carbon monoxide.

Therefore, the necessary information from the CAMI’s

toxicology database was extracted to determine the

number and nature of fire/non-fire involved aviation

accidents and associated fatalities wherein blood carbon monoxide and/or hydrogen cyanide reached

concentrations sufficient to produce impairment/

toxicity. Attempts were also made to obtain any

available accident/case histories and pathological findings observed during autopsy.

EXPERIMENTAL

Since 1991, a database on toxicological findings of

civil aircraft (air carrier and general aviation) accident fatalities (pilots, co-pilots, other crewmembers,

and/or passengers) has been maintained at CAMI.

This CAMI toxicology database was searched for

aviation accidents that occurred during 1991-1998.

The search was based on the criteria associated with

fire and non-fire accidents in the presence and absence of the 2 combustion gases in blood. At or above

10% COHb and 0.25 μg CN-

/mL blood, some degree of clinical manifestations of the poisonings of

carbon monoxide and hydrogen cyanide has been

reported (Gossel & Bricker, 1994; Baselt & Cravey,

1995). Accordingly, the selected criteria were: (i)

total numbers of accidents and associated fatalities

from which biosamples were submitted to CAMI for

analysis, (ii) numbers of fire-involving accidents and

related fatalities wherein COHb was 3 10% and CN-

3 0.25 μg/mL, (iii) numbers of non-fire accidents

and related fatalities wherein COHb was 3 10% and

CN- 3 0.25 μg/mL, (iv) numbers of fire-related

accidents and fatalities wherein COHb was < 10%

and CN-

 < 0.25 μg/mL, and (v) numbers of non-fire

accidents and related fatalities wherein COHb was <

10% and CN-

 < 0.25 μg/mL.

Submitted blood samples were spectrophotometrically analyzed for COHb (Blanke, 1976; Canfield et

al., 1999) and for CN-

 colorimetrically using the

chloramine-T/pyridine/barbituric acid reagent

(Blanke, 1976; Lundquist et al., 1985; Sunshine,

1987a; Chaturvedi et al., 1995). Based on the sensitivities of the respective analytical methods, the cutoff concentrations were established as 10% for COHb

and 0.25 μg/mL for CN-

. These analytical cutoffs are

above the levels reported in normal tobacco smokers;

that is, COHb levels in the range of 0.7 to 6.5%

(Trinder & Harper, 1962; Ayres et al., 1969; Sunshine, 1987b) and blood CN-

 in the range of 0.006 to

0.041 μg/mL (Baselt & Cravey, 1995). Although the

submitted biological samples were also analyzed for

drugs and alcohols by using the laboratory standard

analytical procedures, the database search was focused on the aforementioned 5 criteria (see previous

paragraph) to be within the scope of the present

study; furthermore, passenger biosamples are not

always analyzed for drugs and alcohols.

RESULTS

Fire and non-fire aviation fatality accidents

Biological samples from 3857 fatalities of 2837

aviation accidents that occurred during 1991-1998

were received at CAMI for toxicological evaluation

(Fig. 1; Table 1). This aviation accident number was

77% of the total number of fatal aviation accidents

(3684) investigated by NTSB for that period, as

given in the FAA’s National Aviation Safety Data

Analysis Center (NASDAC) database, Washington,

DC. The higher number of fatalities in relation to the

number of accidents was obviously attributed to the

presence of more than one occupant3⁄4pilot, co-pilot,

other crewmembers, and passengers—in some of the

aircraft of those accidents. Out of these, 1012 accidents encompassing 1571 (41%) fatalities were fire

associated, whereas 1820 accidents (2280 fatalities)

were non-fire related. The remaining 5 accidents

totaling 6 fatalities were of unknown fire status.

As exhibited in Fig. 1, the majority of samples

(80%) received came from pilots and co-pilots.

Samples from other crewmembers and/or passengers

were considerably lower (20%). However, the number of samples from passengers of fire-involved accidents was relatively higher (28%) than that of non-fire

accidents (15%). These patterns were consistent with

the fact that biological samples from passengers of

fire-involved accidents are also frequently submitted,

but only the COHb and CN-

 analyses are performed.

Out of the total 2837 accidents (Table 1), COHb

and/or CN-

 analyses were performed on blood samples

from the fatalities of only 1974 (70%) accidents

(Table 2). Blood samples from the fatalities of the

remaining accidents were either not suitable or not
3

Table 1. Number of aviation fatality accidents (1991-1998) from which postmortem biological

samples were submitted to CAMI for toxicological evaluation.

Number of Accidents (CAMI Cases)

Year

Fatality Accidents

Investigated by

NTSB*

Total

Accidents

Accidents

With Fire

Accidents

Without Fire

Accidents With

Unknown Fire

Status

1991 498 382 126 255 1

1992 512 397 146 251 0

1993 446 344 124 219 1

1994 463 351 148 202 1

1995 467 361 127 234 0

1996 423 337 102 235 0

1997 414 326 123 202 1

1998 461 339 116 222 1

Total 3684 2837 1012 1820 5

*

Numbers obtained from the FAA National Aviation Safety Data Analysis Center (NASDAC) database,

Washington, DC. Fatalities (CAMI Cases)

1991 1993 1994 1995 1996 1997 1998

Year

600

500

400

300

200

100

1992

TOTAL WITH FIRE WITHOUT FIRE

Figure 1. Number of cases analyzed by CAMI during the 1991-1998 period.

Each bar has 2 parts. The lower part represents cases related to pilots

(pilots and co-pilots); the upper part represents other crewmember and/or

passenger cases.
4

available for the analyses. Because of these limitations, blood samples from 2374 (62%) cases out of

the total 3857 cases received were analyzed for the 2

gases (Table 2; Fig. 1). Only 43 (2%) of the total

1974 accidents had a total of 73 (3%) fatalities with

COHb and CN-

 levels high enough to produce some

degree of toxicological effects. As shown in Table 2,

the numbers of fire-related fatalities and associated

accidents were lower in the category wherein COHb

3 10% and CN- 3 0.25 mg/mL (Category A) than the

category wherein COHb < 10% and CN-

 < 0.25 mg/

mL (Category B). No in-flight fire was documented

in the former category, but in-flight fires were reported in a small number of accidents in the latter

category (detailed in a later section). No fatality with

the concentrations of the 2 gases at or above the stated

cutoff values was found in the database under nonTable 2. Number of fatalities and related fire and non-fire accidents in the presence and

absence of COHb and CNin postmortem blood (Numbers in parenthesis indicate

number of accidents).

Fire Accidents

_______________________________

Non-Fire Accidents

_________________________________

Year

Category A

Fatalities with

COHb ≥ 10%

and CN- ≥ 0.25

μg/ml (Number

of Accidents*

)

Category B

Fatalities with

COHb < 10%

and CN- < 0.25

μg/ml (Number

of Accidents†

)

Category C

Fatalities with

COHb ≥ 10%

and CN- ≥ 0.25

μg/ml (Number

of Accidents)

Category D

Fatalities with

COHb < 10%

and CN- < 0.25

μg/ml (Number

of Accidents)

1991 17 (7) 140 (93) None (None) 230 (194)

1992 9 (7) 120 (95) None (None) 220 (192)

1993 6 (5) 107 (83) None (None) 194 (173)

1994 7 (5) 103 (81) None (None) 167 (142)

1995 11 (9) 99 (74) None (None) 172 (156)

1996 19 (6) 61 (51) None (None) 179 (161)

1997 3 (3) 102 (77) None (None) 160 (144)

1998 1 (1) 74 (59) None (None) 173 (156)

Total 73 (43) 806 (613) None (None) 1495 (1318)

*

All accidents were associated with post-crash fires: No in-flight fires are reported in this category of

accidents.

†

Numbers represent in-flight and post-crash fire-related accidents. Relevant findings of the in-flight fire

accidents are separately summarized in the Results section.

fire accidents (Category C), albeit there were a considerable number of aviation accident fatalities in

which these gases were not detected in blood (Category D).

COHb and CN-

 concentrations

Although exposure to smoke generally results in

the presence of carbon monoxide and hydrogen cyanide in blood, the distribution of fatalities with

respect to the concentrations of each of these gases

was done to evaluate the related degree of toxicity as

if individually produced by each of the 2 gases. As

exhibited in Table 3, the search of the database for the

presence of each of the gases individually disclosed

that the numbers of accidents and related fatalities

with the COHb 3 10% group (Group A) were less

than the COHb < 10% group (Group B). Similarly,
5

the numbers were less in the CN- 3 0.25 μg/mL group

(Group C) than in the CN-

 < 0.25 μg/mL group

(Group D). Only about 4% of the 1974 aircraft

accidents had victims with COHb or CN-

 concentrations high enough to produce toxicological effects.

Further categorization of the fatalities based on

the COHb concentration-associated toxic effects revealed that 77 of the 142 victims had COHb levels in

the range of 10-20% (Fig. 2A), a level considered

sufficient to produce adverse physiological effects—

tightness across the forehead, headache, dilation of

blood vessels, and exertional dyspnea (Gossel &

Bricker, 1994). The remaining victims had COHb

ranging from 21-60%, the level at which severe toxic

effects such as confusion, dimness of vision, nausea,

collapse, and incapacitation have been reported.

Likewise, the categorization of CN-

 concentrations (Fig. 2B) reflects that 61 out of the 106 victims

had this analyte in the range (0.25-1.00 μg/mL)

sufficient to cause mild adverse effects, and 29 victims had the analyte at the level (1.01-2.50 μg/mL),

which is considered enough to produce a moderate

degree of poisoning (Gossel & Bricker, 1994; Baselt

& Cravey, 1995). Sixteen victims had CN-

 at levels (>

2.50 μg/mL) that would cause severe adverse effects,

including coma and death.

In-flight fire accidents

Of the 1991-1998 accidents, 14 accidents with a

total of 18 fatalities were in-flight fire related. Blood

samples received from these fatalities were also analyzed for both gases. In the majority of the samples,

Table 3. Distribution of cases in fire-involved aviation accidents with respect to the

concentrations of COHb and of CNin blood (Numbers in parenthesis indicate number

of accidents).

Fire-Involved Accidents

Year

Group A

Fatalities with

COHb ≥ 10%

(Number of

Accidents)

Group B

Fatalities with

COHb < 10%

(Number of

Accidents)

Group C

Fatalities with

CN- ≥ 0.25 μg/ml

(Number of

Accidents)

Group D

Fatalities with

CN- < 0.25 μg/ml

(Number of

Accidents)

1991 35 (13) 149 (101) 24 (14) 175 (104)

1992 22 (17) 131 (103) 14 (12) 150 (114)

1993 7 (6) 115 (87) 13 (10) 124 (91)

1994 12 (9) 117 (88) 12 (10) 123 (97)

1995 22 (20) 106 (80) 13 (11) 136 (95)

1996 27 (11) 62 (52) 20 (7) 84 (65)

1997 8 (6) 107 (81) 8(7) 135 (85)

1998 9 (9) 75 (58) 2(2) 116 (71)

Total 142 (91) 862 (650) 106 (73) 1043 (722)
6

Figure 2. COHb (A) and CN- (B) level-based distribution of fatalities

in relation to toxicological manifestations.

(A)

77

32

13

15

5

(10-20% COHb)

(21-30% COHb)

(31-40% COHb)

(41-50% COHb)

(51-60% COHb)

(B)

29 61

16

(0.25 -1.00 μg/mL CN-) (1.01-2.50 μg/mL CN-

)

(>2.50 μg/mL CN-

)
7

COHb was not detected; the highest COHb value

was found to be 5%. No CN-

 was detected in these

samples. Three samples were unsuitable for analyses.

Although detailed pathological findings with all the

casualties were not available, blunt trauma was prevalent in the victims. All involved aircraft were of the

general aviation category, as well as homemade. The

probable cause of fire with at least 3 accidents was

established to be of electrical origin. The origin of fire

in the remaining accidents could not be conclusively

determined.

COHb in non-fire aviation accident fatalities

As compiled in Table 4, there were 15 non-fire

accidents, totaling 17 fatalities (15 pilots and 2

passengers) wherein COHb was 3 10% (10-69%). In

these fatalities, CN-

 was not detected. Based on the

presence of COHb in the absence of CN-

 and fire, it

was hypothesized that these accidents were associated

with the carbon monoxide inhalation during (or

before) the flight. In the majority of the 15 accidents,

heating/exhaust system malfunctions, pilot error,

and/or carbon monoxide-induced incapacitation were

Table 4. Various investigative elements of non-fire aviation accidents that occurred during 1991-

1998, wherein blood COHb levels in the associated fatalities were determined to be ≥ 10%.

Year

Number of

Accidents

Number of

Associated

Fatalities*, †, ‡

COHb

(%) Aircraft Type Probable Cause of Accident

10 Bell 206-B In-flight structural failure

20 Aronca 7-AC Physical impairment of pilot

10 Piper 28-140 Undetermined

1991 4 4

16§ Gulfstream AA-5A Physical impairment of pilot

1992 1 1 10§ Gulfstream 690-B Severe turbulence

11§ 1993 2 2 Bell 214-B Structural failure

17 Cessna 177-RG Pilot error

1994 1 1 14§ Beech 95-B95 Fuel starvation

12§ 1995 2 2 Cessna 150-L Pilot error

11§ Cessna 150-M Pilot error

1996 1 1 41 Mankovich Sonerai Possible inadequate sealing of

engine's firewall—carbon

monoxide-induced

incapacitation

43; 69 Piper 28-236 Faulty exhaust

26§ Bell 206-B Carbon monoxide-induced

incapacitation

1997 3 4

12 Windex 1200 C Pilot error

1998 1 2 24;12 Piper 28-160 Suspected faulty exhaust

*

No fatality in the database was found in which COHb level was ≥ 10% and blood CN- was ≥ 0.25 μg/ml in non-fire

aviation accidents during the period of 1991-1998.

†

In almost all of the fatalities, pathological findings were consistent with traumatic injuries.

‡

Blood CNlevels were determined to be < 0.25 μg/ml. However, excluded from this table were 2 fatalities associated

with 2 different aircraft accidents in 1991. In their blood samples, only CN- was found to be present at concentrations

≥ 0.25 μg/ml (3.8 and 0.25 μg/ml): No COHb was detected. In the 3.8-μg/mL CN- fatality, this analyte was not

detected in other tissues, nor was it found in the blood sample of another occupant of the aircraft. The selective

presence of CN- in such a toxic concentration in the absence of COHb could not be logically explained. It could

possibly be associated with reason(s) other than smoke inhalation.

§

Nicotine and/or cotinine were also detected in the blood samples.
8

reported to be at least contributory factors. In relation to the total number of the fatality accidents

(2837; see Table 1), the percentage of the total carbon

monoxide associated accidents was 0.53. Out of

these, 3 accidents with 5 fatalities (12, 24, 41, 43, and

69% COHb) were determined to be attributed to the

carbon monoxide-induced incapacitation/defective

exhaust system.

In the 1997 accidents, the pilot with 26% COHb

was reported to be a heavy cigarette smoker (1 pack a

day) and postmortem examination of the body

revealed chronic pulmonary emphysema. COHb was

not detected in the other 3 occupants of the aircraft

(data not included in Table 4). The 1991 accident

pilot with 16% COHb was exposed to carbon monoxide on the ground before the flight: The pilot was

a mechanic and was exposed to carbon monoxide

from running engines in a non-ventilated workshop.

Although the pilot’s post-accident COHb level was

elevated, COHb of the other occupant of the aircraft

was not (data not given). Therefore, the pilot’s physical impairment might have been caused by the onground carbon monoxide exposure.

A further search of the database revealed that

nicotine and/or cotinine were also present in the

blood samples of 7 fatalities, including the pilots

mentioned in the previous paragraph. Pathology of

all the 17 fatalities revealed that these individuals had

traumatic body injuries.

DISCUSSION

Although fire-involved aviation accident fatalities

could be the direct result of traumatic injuries caused by

impact and/or of the inhalation of smoke generated

during in-flight or post-crash fires, blood carbon monoxide and hydrogen cyanide concentrations are indicative of respiratory exposure of victims to smoke. If an

accident victim was alive and inhaled smoke, then these

gases should be present in the victim’s system; whereas,

if an individual was dead because of injuries prior to a

post-crash fire, then the combustion gases should not be

present in blood. With these considerations, it is inferred that the 73 victims of the 43 fire-related fatal

accidents (Table 2) did not expire immediately following the impact, as both combustion gases in their blood

were present in concentrations (COHb 3 10% and CN-

3 0.25 mg/mL) sufficient to produce some degree of

adverse effects (Gossel & Bricker, 1994; Baselt & Cravey,

1995). The presence of both gases obviously suggests

that they inhaled smoke prior to death. It can be

deduced that the victims in whom COHb and CN-

 were

not detected died primarily due to the traumatic

injuries3⁄4the general pathological finding in the majority of the aviation accident casualties. Not surprisingly,

no fatality in non-fire accidents was found in which

blood COHb was 3 10% and blood CN- was 3 0.25 mg/

mL: None of the non-fire aviation accident fatalities had

both of the gases at or above these levels.

Considering fire-involved accident fatalities with

COHb 3 10% and/or CN- 3 0.25 mg/mL, about half

of them had COHb in the range of 10-20% and/or

CN-

 in the range of 0.25-1.00 mg/mL, at which

concentrations both gases cause a mild degree of

adverse effects (Gossel & Bricker, 1994; Baselt &

Cravey, 1995). In the remaining casualties, the blood

concentrations of the gases individually were high

enough to produce significant toxic effects. Since

carbon monoxide and hydrogen cyanide affect neurologic functions and have interactive effects (Gossel

& Bricker, 1994; Baselt & Cravey, 1995; Chaturvedi

et al., 1995; Hartzell, 1996), both gases, jointly, have

a potential to hasten the onset of neurotoxic effects,

including performance impairment or incapacitation, leading to death.

Carbon monoxide and hydrogen cyanide could be

also present in blood if there were in-flight fires.

However, our findings indicate that these gases were

either not detected or were below the cutoff levels,

suggesting no significant exposure of occupants to

smoke in those in-flight fire accidents. Nevertheless,

impact-associated fatal injuries were prevalent in the

victims of the in-flight smoke/fire-related accidents.

Although in-flight fire victims might not be exposed

to significant levels of combustion gases, in-flight

smoke/fire accidents have deadly consequences

(McKenna, 1996; Proctor, 1996; ABC News, 1998;

CNN, 1998). It is evident that there was little exposure to the toxic gases during in-flight fires. Death

most probably occurred from physical injuries caused

by the crash shortly after the fire started. However,

the performance of pilots (and even of other aircraft

occupants) in those situations could have been adversely affected by visual obscuration and ocular

irritation from smoke.

In accidents associated with the carbon monoxide

contamination of the cabin/cockpit, only COHb

should be elevated and CN-

 should not be present in

the blood. This criterion is consistent with the findings of the present study in that no fatality was found
9

in which both gases were present at or above the

cutoff levels in non-fire accidents. The most probable

scenario for carbon monoxide poisoning to take place

is the leakage of gases into the cockpit/cabin from

faulty heaters and/or exhaust systems.The high COHb

(3 21%) values clearly suggest the occurrence of

carbon monoxide-induced dizziness, incapacitation,

coma, or death (Gossel & Bricker, 1994). Obviously,

there would be relatively mild adverse physiological

effects at the low COHb (10-20%) levels. At higher

altitudes, there is also a probability of the coexistence

of altitude-associated hypoxic hypoxia. Therefore,

the effects of carbon monoxide would be further

exacerbated in association with hypoxia, thereby hastening a performance impairment that may contribute to an accident. The adverse effects would be more

pronounced at elevations during flight than at ground

level because of the interactive effects of altitude

hypoxia and carbon monoxide-induced anemic hypoxia (Allen & Allard, 1961; McFarland, 1970;

Nesthus et al., 1997). A typical situation could be a

pilot smoking a cigarette just before flying an aircraft

or during the flight, or working in a carbon monoxide-contaminated environment prior to flying an

airplane. In an actual situation, a pilot smoked a

cigarette while cruising at 13,500 feet over mountainous terrain in an unpressurized aircraft and quickly

lost consciousness (FAA, 1991).

The presence of nicotine and/or its metabolite

(cotinine) in blood, along with the low levels (1-7%)

of COHb (Trinder & Harper, 1962; Ayres et al.,

1969; Sunshine, 1987b) could be an indication of

tobacco smoking, but both compounds could also be

present in tobacco chewers. The presence of COHb

in the absence of nicotine and/or its metabolite

would suggest that the elevated COHb level could be

attributed to the inhalation of carbon monoxide

originating from a source other than tobacco smoking. However, elevated COHb levels in the presence

of the tobacco alkaloid and its metabolite would not

necessarily be indicative of exposure to carbon monoxide from smoking. It could result from exposure to

carbon monoxide from smoking and/or from nonsmoking sources. In spite of these perspectives, the

observed total number of non-fire, carbon monoxide-exposed fatalities was only 17 (0.44%) of the

total number of aviation fatality cases (3857) analyzed at CAMI, suggesting that non-fire carbon monoxide exposures are rare.

Overall, the present study revealed that fire-involving aviation accidents and associated fatalities

were fewer than the non-fire aviation accidents and

related fatalities. The blood levels of carbon monoxide and/or cyanide found in fire-related fatalities

were often considered sufficient to impair performance and/or to produce toxicity. The findings from

this study further suggested that aviation accidents

and fatalities associated with in-flight fires and with

the contamination of cabin environment with carbon

monoxide are rare occurrences.

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