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rent in the muffler was along the seam where the muffler had been
weld-J in manufacture. A backfire in the exhaust system probably
caused the muffler to split. The elevated carboxyhemoglobin level,
proved by the laboratory, pointed accident investigators in the
right direction, resulting ina satisfactory explanation of the
cause of the accident.

DISCUSSION.

The Occupational Safety and Health Administration (OSHA) has
succinctly summarized the toxicology of carbon monoxide as follows: (8)

“Carbon monoxide (CO) gas causes tissue hypoxia by preventing

the blood from carrying sufficient oxygen. CO combines reversibly
with the oxygen-carrying sites on the hemoglobin molecule with an
affinity ranging from 210 to 240 times greater than that of oxygen;
the carboxyhemoglobin thus formed is unavailable to carry oxygen.
In addition, carboxyhemoglobin interferes with the release of
oxygen carried by unaltered hemoglobin. With exposure to high
concentrations such as 4000 ppm and above, transient weakness
and dizziness may be the only premonitory warnings before coma
tie al the most common early aftermath of severe intoxi-
catio cerebral edema. Exposure to concentrations of ‘500 to
1000 ppm causes the development of headache, tachypnea (rapid
breathing), nausea, weakness, dizziness, mental confusion and
in some instances, hallucinations, and May result in hrain damage.

The affected person is commoniy cyanotic. Concentrations as low

as 50 ppm result in blood COhb levels up to 10% in an 8-hour day,

This greatly increases the risk of angina pectoris and coronary
infarctions by decreasing the oxygen supply in the blood and also

in the myoglobin of the heart muscle. These effects are aggravated

by heavy work, high ambient temperatures, and high altitudes. ————
Pregnant women are especially susceptible to the effects of in-
creased CO levels. Smoking also increases the risk: cigarette
smoke contains 4% CO, which results in 5.9% Colth if a pack a day
is smoked. ‘The blood of Persons not exposed to CO contains about
1% CO, probably as a result of normal heme metabolism. The diag-
nosis of CO intoxication depends primarily on the demonstration

of significantly increased carboxyhemoglobin in the blood. Levels
over 60% are usually fatal; 40% is associated with collapse and
syncope; above 25% there may be electrocardiographic evidence of

a depression of the S-T segment; between 15% and 25% there may be
headache and nausea. The reaction to a given blood level of
carboxyhemoglobin is extremely variable: some persons may be in

a coma with a carboxyhemoglobin level of 38% while others may main-
tain an apparently clear sensorium with levels as high as 55%.
The blood of cigarette smokers contains 3. to-108. carboxyhemogiobin,
and nonexposed persons have an average. level of 1%, probably as”!

a result of normal heme metabolism. Several investigators have
suggested that the results of behavioral tests such as time discrim-
ination, visual vigilance, choice response tests, visual evoked
responses, and visual discrimination thresholds may be altered at
levels of carboxyhemoglobin below 5%."

voy

4.



CARBON MONOXIDE IN-FLIGHT INCAPACITATION:
AN OCCASIONAL TOXIC PROBLEM IN AVIATION

INTRODUCTION.

Carbon monoxide is the most abundant aix pollutant in the lower
atmosphere. The compound is produced from the incomplete combustion of
organic materials. Common sources of the gas are exhaust from internal
combustion engines, cigarette smoke, and a inyriad of industrial processes.
In 1974, Stewart (1) reported that urban nonsmokers averaged 1-2
percent. carkoxyhemoglobin and smokers 5-6 percent. Seppanen (2) has
Teported that levels of carboxyhemoglobin below 12 percent saturation had no
effect on psychomotor performance but aid have a detrimental effect on
visual perception. Symptoms of carbon monoxide poisoning may vary depend-
ing on whether the exposure is to a sudden high concentration or to a
prolonged lower amount. At a blood saturation of less than 10 percent
the individual usually shows no recognizable symptoms; below 20 percent
saturation, headaches, and shortness of breath on exertion are common;:
nausea, sleepiness, severe headache, and blurred vision usually occur.
between 20-40 percent blood saturation. Crane (3) has reported that in-
capacitation occurs at a blood saturation of 46.5 percent, and a lethal
level is reached at 67.5 percent saturation. Symptoms of. carbon monoxide
poisoning, which are a result of decreased oxygen-carrying capacity, may
‘occur at lower levels of blood saturation if the subject is in an atmosphere
of decreased oxygen tension, as will occur in flying if surolemental oxygen
is not used. :

For over 14 years the Federal Aviation Administration (FAA) Civil
Aeromedical Institute (CAMI) has.operated a forensic toxicology laboratory
analyzing blood and other specimens from aix carrier and general aviation
accident victims. During that period, specimens have been received from
over 4,300 fatal accidents and 7,000 victims. Findings from a number of
cases have been previously reported. (4). In a number of accidents, no
significant traumatic injuries were demonstrated at autopsy but the cause
of death was inhalation of toxic gases resulting from postcrash fires.
Such victims usually have had significantly elevated carboxyhemoglobin
levels and many also have had an elevated blood hydrogen cyanide
concentration.

Here we report on cases involving general aviation aireraft in which
no evidence of fire was found and carbon monoxide was the only toxic
substance present in the specimens from the victims. These data are
compared to the data from all cases in which a mixture of toxic gases’
has been present in accident victims and-to information found at autopsy~

METHODS.

Carbon monoxide saturation is determined on all blood samples. When
blood is not available, fluid-containing sufficient hemoglobin can usually
be obtained from tissue by freezing arid thawing or by the gentle application

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Technical Report Documentotion Page

J) Report No. Fo Goveinment Recession No

FAA-AM-82~15

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“I

Io Recipient's Catalog No

me Mie 547

CARBON MONOXIDE IN-FLIGHT INCAPACITATION =
AN OCCASIONAL TOXIC PROBLEM IN AVIATION.

sar
* pelbert J. Laceficld, Patricia A. Roberts»

ST Report Dare
OCTOBER 1982

|
$. Berforming Orgonzation Code

_]E Porton

Origen tation Report No

anla_M._Grape —
7 Pevlorming Orgenizanen Name ond Address
FAA Civil Aeromedical Institute

P.O. Box 25082
Oklahoma City+ oklahoma 73125

TO. Work Unit No. (TRAIS)

Ty Contract or Grant No-

Ti. Tyae of Report and Pend Covered

TE Sponsaring Agency Name ond Address
office of Aviation Medicine
Federal Aviation Administration
800 Independence Avenuer s.W.
Washington, p.c. 20591

—
Ta, Sponsoring Agency Code

=

TS. Suppiementory Notes

AM-A-82-TOX-14~

Research leading to preparation of this report was
tasks AM-A-68-PHB-14 through AM-A-72-PHB-14 and AM-A-73-TOX-14 through

performed under

V6. Abstract
‘Results from the toxicological study
21 (0.5 percent}

of accidents caused
determined

cause of incapacitation in
presented that are typical
carbon monoxide, in that no cause was
examination of the victims was made.

pilots should be undertaken to make them
and symptoms produced by this highly toxic gas. .

of samples from 4,072 pilots killed in
general aviation accidents have revealed that carbon rionoxide has been the
of the cases.
by, incapacitation from

Since no su
to warn pilots of elevated carbon monoxide levels in the cabin,
aware of the hazards of exposure to

Two cases are

until after_ toxicological
itable system is available
education of

V7. Key Words
Pilot incapacitation
Carbon monoxide

General aviation e ! Service,

WW. Security Ch
unclassified

Tor Sacuiiny Clowail, (ol this reper’)

unclassified

Te. Drsvibution Statement

Document is available to the public
through the National Technical Information

fot this pose)

springfield, Virginia 22161

Fie Na, of Pages

7

Form DOT F 1700.7 (8-7)

Reproduction

of comploted page ovthorized


fuel. ignition by-products, supporting the contention that the crack
existed prior to the crash. The crack had allowed exhaust gas to
enter the aircraft cabin through the cabin air heater system. The
accident occurred when the CO in the occupants reached incapacitating
levels.

Case 2. The pilot, the only occupant of a Piper TriPacer,
departed a local airport at 1700 on a cold December afternoon for
the purpose of practicing’ touch-and-go procedures. The flight
before the fatal accident'was of 30-minutes' duration. The crash
occurred in a wooded area adjacent to a large open field. The
plane descended into the trees at a shallow angle paralleling the
border of the open field.’ No autopsy was performed on the pilot
but blood was submitted for toxicological analysis. A carboxyhemo-
globin level of 23 percent was found. The pilot had been thrown
free of the burned aircraft and gross injuries suggested that he
died immediately after the crash. The finding of an elevated CO
saturation prompted close inspection of the exhaust and heater
system. Investigators found a cracked exhaust muffler and staining
of the heat exchange shroud by the exhaust gases (Figure 1). The

Figure 1, Muffler from a single engine aircraft. Note the split
in the muffler and the discoloration caused by exhaust
gases as they contacted the wall of the cabin heat.
exchanger skroud.’ The pilot was incapacitated in flight
by carbon menoxide and killed in the crash that followed.

. :

‘



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general aviation aircraft because of cost. There are available, in general
aviation, paper discs, impregnated with a chemical that reacts and changes
color in relation to the concentration of carbon monoxide. The color may
be compared to a printed color scale. Under strict laboratory conditions
this. system is capable of detecting hazardous levels of carbon monoxide but
when used to monitor:cabin air it has proven unreliable because of inter-
ference from sunlight, varying humidity, other gases, and cigarette snoke.

The two cases presented are typical of accidents caused by .icapacitation
from carbon monoxide in that no cause was determined until after toxicological
examination of the victims was made. Both defective exhaust systems were
found after the field investigator had been advised of the laboratory findings.
Although the exhaust system has been found to be the culprit in most of the
21 cases, other routes of entry of carbon monoxide into the cabin have been
found in this and other series (7,9).

Not all in-flight exposures to carbon monoxide result in accidents.
Four members of a family, on a cross-country flight, developed headaches
and the pilot-father became nauseated. The plane was safely landed at
Wichita, Kansas, and the occupants were admitted to a hospital. Laboratory
analysis revealed elevated carboxyhemoglobin levels. They were observed
and released in a few hours. Inspection of the aireraft turned up a leaky
manifold and a firewall that was not airtight. In this instance a problem
was recognized in time to prevent a tragedy.

Carbon monoxide, though odorless, occurs with other products of combus-
tion in exhaust gases. Most people are able to detect an odor when exposed
to exhaust from an internal combustion engine. Wher any of the symptoms of *
carbon monoxide poisoning such as headache, drowsiness, nausea, or blurred
vision occur in a pilot or passengers, use of the cabin heater, if in opera~
tion, should be discontinued. Fresh outside air vents should be opened and,
if possible, descent should be made to a lower altitude. The aircraft should
be landed as soon as safely possible and inspected for exhaust leaks.

Although less than 0.5 percent of fatal general aviation accidents can
be attributed to pilot incapacitation from carbon monoxide, pilots should
know of the hazards and symptoms of exposure to carbon monoxide. Only by
early recognition can a pilot take the necessary actions to prevent incapaci-
tation and a possible serious crash.

Of course, prevention of exposure to carbon monoxide is the best safety
measure; prevention mandates an intact engine exhaust system. At periodic
checks exhaust systems should be inspected to assure that exhaust fumes
cannot enter the cabin.


“That exposure to carbon monoxide in the cabins of aircraft can lead

to incapacitation has been recognized for many years. in 1964, Slusher

{7) reported that although engine exhaust system failures in general

aviation aircraft were not frequent, in 70 percent of the failures a

carbon monoxide hazard was created in the cabin atmosphere. Exhaust:

gases from internal combustion engines may contain as much as 5 to 7

percent carbon monoxide. After mixing with other air, a much lower concentra~
tion would be found in the cabin air.

The FAA limits levels of carbon monoxide in cabin air to 0.005
percent or 50 parts per million (ppm). The OSHA permissible exposure
limit is 50 ppm of air averaged over an 8-hour work shift. The National
Institute for Occupational Safety and Health {NIOSH) has recommended
that the permissible exposure limit be reduced to 35 ppm, averaged over
a@ work shift of up to 10 hours per day, 40 hours per week, with a ceiling
of 200 ppm (8). Work done at the FAA'S Aviation Toxicology Laboratory by
Crane (3) has led to a mathematical expression of the relationship between
respiration rate, body weight, carbon monoxide content of inspired air,
and time-to-incapacitation (T,) and time-to-death (Tg). Table 1 was
derived from this relationship and shows the time-to-incapacitation for
man as a function of carbon monoxide concentration (at near sea level).

Table 1. Carbon Monoxide in Air Versus Time to Incapacitation |

Carbon Monoxide Concentration Time to Incapacitation
* ppm minutes
0.05 500 220
0.10 1000 . 110
0.20 2000 55
0.30 3000 37
0.40 4000 27
0.50 5000 22

As noted in the OSHA summary above, serious decrements in vision,
judgment, and motor skills are reached long before total incapacitation
(unconsciousness). Such degradations in function occur more quickly at
increased altitudes because of the diminishing oxygen. transport to periph-
eral tissues.

A carbon monoxide detector has been developed and is used by the
United States Air Force. The apparatus draws air from a preselected loca-
tion in the aircraft and illuminates a warning light when concentrations of
CO exceed 0.005 to 0.007 percent. — This instrument has not been used in

5.


of pressure. Hemoglobin is determined by the standard cyanmethemoglobin
method or by an alkaline hematin method. Samples containing more than

For confirmation, or when greater sensitivity and Specificity are needed,
carboxybemoglobin content is determined by a gas chromatographic method
utilizing a flame ionization detector after the catalytic conversion of
carbon monoxide to methane (6). The instrument and its Operating condi~
tions are as follows: Varian Aerograph 1400; columns (1/8 in x 6 ft)
Carbosphere, 80-100 mesh; flame ionization detector; carrier gas, hydrogen,
30 mi/min; injection Port 200°C, column 30°c, followed by a nickel-on~
firebrick column Q/8 in x 1 ft) maintained at 370°C; and a Hewlett Pachard
3390A reporting integrator. Blood and bloody fluids are diluted 1 to 1
with distilled water, This system may be used to determine as little as

and ‘trapped in sodium hydroxide. The trapped cyanide is then measured : -
colorimetrically (5).

FINDINGS.

from a series of 4,072 fatal general aviation accidents, In 21 of these
cases it was established that postcrash fire could not have contributed to
the elevated carboxyhemoglobin levels and that the co must have been .ac-
quired prior to, or during, flight. The following two cases illustrate
this occasional cause of fatal aircraft accidents. In both cases the source
Of the cockpit air contamination was found.

Case l. A Piper Cherokee departed Savannah, Georgia, at
2150°on a rainy September night with three Persons. aboard a VFR
flight. the flight continued for 1 hour and 20 minutes at an
altitude of 2,500 feet. During the last 15 minutes of the flight
the pilot was in contact with the Macon, Georgia, radar approach
control and was vectored around thunderstorms that were in the
area. The last communication with the flight occurred 4 minutes
before radar contact was lost. The wreckage was found shortly
after the accident and there were no survivors. The aircraft
impacted in a near vertical attitude as evidenced by damage to
only one tall pine tree from near the top to the ground. The
engine and Propeller were almost completely buried at the base of
the tree. Hoth front seat occupants were Partially decapitated.
Carboxyhemoglobin levels in two victims were 43 percent and 47
percent. Samples were not obtained on the third occupant. After
the laboratory analysis revealed high CO levels with no hydrogen
cyanide, and the autopsy evidence indicated that the occupants
could not have survived the impact to acquire co from the posterash
fire, investigators carefully examined the cabin heating system.
They found a crack in the exhaust muffler. Analysis of scrapings
from the inner wall of the heater duct confirmed the presence of


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DTG FILE COPY

/0

FAA-AM-82-15

CARBON MONOXIDE IN-FLIGHT INCAPACITATION:
AN OCCASIONAL TOXIC PROBLEM IN AVIATION

Delbert J. Lacefield
Patricia A. Roberts
Paula M. Grape

Civil Aeromedical Institute
Federal Aviation Administration
Oklahoma City, Okiahoma

OCTOBER 1982

Document is available to the public through the
National Technical Information Service
Springfield, Virginia 22161

Prepared for
U.S. DEPARTMENT OF TRANSPORTATION l Cc

Federal Aviation Administration ELECTE
Office of Aviation Medicine ; aN
Washington, D.C. 20591 JAN2 7 1983 ¢ 2

B


JACK R. HUNT MEMORIAL LIBRARY
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MICROCOPY RESOLUTION TEST CHART
WATONAL BUKEAU OF STANDARDS-1965.4



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REFERENCES

Stewart, R. D., E. D. Baretta, and L. R. Platte: Carboxyhemoglobin
levels in American blood donors. J. AM. MED. ASSOC., 229:1187-1195,
1974.

Seppanen, A., V. Hakkinen, and M. Tenkku: Effects of gradually
increasing carboxyhemoglobir, saturation on visual perception and
psychomotor performance of smoking and nonsmoking subjects. ANN.
CLIN. RES., 9:284-289, 1977.

Crane, C..R.: The prediction of human incapacitation Ly the combustion
products carbon monoxide and hydrogen cyanide using a small animal test
protocol. Paper presented at the Annual Meeting of Aerospace Medical
Society, Washington, D.C., May 14-17, 1979.

Lacefield, D. J., BP. A. Roberts, and C. W. Blossom: Toxicological
findings in fatal civil aviation accidents, fiscal years 1968-1974.
AVIAT. SPACE ENVIRON. MED., -46:1030-1032, 1975.

Feldstein, M.: Microdiffusion analysis as applied to toxicology.
In Cc. P. Stewart and A. Stolman (Ed.).. Toxicology: Mechanisms and
Methods, Vol. 1, Academic Press, New York. pp 653-656, 1960.

Lafarge, J. P., M. Laplace, and J, Lebbe: Determination of carboxy-
hemoglobin without prior extraction. ARCH. MAL. PROF. HYG. TOXICOL.
IND., 31:201-208, 1970.

Slusher, G. R.: Analysis of engine exhaust system failures in general
aviation aircraft. Federal Aviation Agency, Aircraft Development
Service, September 1964. FAA ADS 29.

U. S. Department. of Labor, Occupational Safety and Health Administration,
Occupational Health Guidelines for Carbon Monoxide, September 1978.

Dille, J. R., and M. K. Linder: The effects of tobacco on aviation
safety. AVIAT. SPACE ENVIRON. MED., 52:112-115, 1981.