REVIEWS
Aeromedical Aspects of Commercial Air Travel
Richard Harding
Humans are extremely sensitive to the effects of
hypoxia, and the physiologic consequences of lack of
oxygen in flight are dominated by the changes seen in
three main areas which are as follows:
Be with us, now, 0 Lord. And when
We’re told to breathe Thy Oxygen
From dangling masks, be with us then.
Be near us Lord. We know that flight
Is but a challenge to Thy might,
A privilege and not a right.
0 Lord, whose mercy we revere,
We know we shouldn’t be up here.
4
Punch Book of Travel
the respiratory and cardiovascular responses to
the hypoxia,
the neurologic effects of the hypoxia, and
the neurologic effects of the cardiorespiratory responses.’
The clinical consequences will reflect changes seen in
all three systems. Ascent to altitude is associated with
an exponential fall in total barometric pressure (with
parallel reductions in both air density and temperature) and also, therefore, in the partial pressures of
the component gases of the atmosphere. Above 10,000
feet, however, the partial pressure of oxygen in arterial blood falls to a level that stimulates respiration
via the arterial chemoreceptors, and so alveolar carbon dioxide tension decreases as alveolar ventilation
increases. Reaching an altitude of 10,000 feet is a crucial stage in the development of the physiologic
changes associated with an ascent, and a consideration of the oxyhemoglobin dissociation curve helps
to show why this should be. Thus, the relationship
between oxygen tension and the percentage saturation of hemoglobin with oxygen describes the familiar sigmoid curve. The plateau at the top of the curve
represents a physiologic reserve, whereby a fall in
oxygen tension (however produced) from the normal
100 mm Hg to about 60-70 mm Hg produces a
desaturation of only 5-10%. In healthy individuals,
a fall of this magnitude is seen during a n ascent from
sea level to 10,000 feet. Above this altitude, the steep
part of the dissociation curve takes effect, there is rapid
desaturation of hemoglobin, and hypoxia develops.
The overt symptoms and signs of hypoxia, compared
with those of hyperventilation are summarized in
Table 1. Note the marked similarity, particularly in
the early stages, which emphasizes the insidious nature of the former and the danger of misdiagnosing
the latter.
The speed with which this clinical picture develops will clearly be related to the altitude at which exposure occurs and to the duration of that exposure. It
The distinction of being the first balloonists to
take to the air belonged to a sheep, a cockerel, and a
duck, which had been dispatched from Versailles in a
Montgolfier in September 1783. The balloon descended after 8 minutes when the air inside it cooled.
The sheep and the duck were both in good health, but
the cockerel was “unwell”. Learned professors at first
attributed this to the effects of rarefied atmosphere,
but closer inspection revealed that it had been trodden on by the sheep.
Problems
Notwithstanding that physical trauma was the
real cause of this avian aviation pioneer’s illness,
hypoxia was a reasonable deduction, since lack of
oxygen was, and remains, a potentially serious hazard to anyone during flight at altitude. This article
explains in more detail the implications of hypobaric
hypoxia for the traveling public, as well as describing
some other physiologic problems associated with air
travel (such as hyperventilation, barotrauma, and decompression sickness) before discussing the solution
adopted in modern commercial aircraft. The increasingly topical matter of cabin air quality and passenger
comfort will also be discussed.
Wing Commander Richard Harding, BSc, MB, BS, PhD,
DAvMed, AFOM, MRAeS, RAF: RAF Consultant in Aviation
Medicine, Royal Air Force Farnborough, Farnborough,
Hampshire, United Kingdom.
Reprint requests: Wing Commander, Richard Harding, BSc,
MB, ES, PhD, DAvMed, AFOM, MRAeS, RAF: RAF Consultant
in Aviation Medicine, Royal Air Force Farnborough, Farnborough, Hampshire, United Kingdom, GU14 6TD
21 1
212
J o u r n a l o f T r a v e l M e d i c i n e , V o l u m e 1. N u m b e r 4
Table 1 Comparison of the Symptoms and Signs of Hypoxia with
Those of Hyperventilation
Hypoxia
Hyperventilation
Personality change
Lack of insight
Loss of judgment
Feelings of unreality
Loss of self criticism
Euphoria
Loss of memory
Dizziness
Mental incoordination
Muscular incoordination
Lightheadedness
Neuromuscular
Feelings of apprehension
irritability
Sensory loss
Carpopedal spasm
Paresthesia of face and
extremities
Cyanosis
Hyperventilation
Semiconsciousness
Unconsciousness
Death
is also important to appreciate that several additional
factors may influence an individual’s susceptibility to
hypoxia and so modify the pattern of symptoms and
signs produced. Such exacerbating factors include the
following: physical activity, cold environmental temperature, intercurrent illness, and drugs.’ With regard
to the last, many pharmacologically active substances
have effects similar to those of hypoxic hypoxia and
so mimic or aggravate the condition. Those proprietary preparations with antihistamine constituents are
particularly likely to cause problems, as is alcohol.
Acute hypobaric hypoxia is rapidly and completely reversed if oxygen is administered or if alveolar oxygen tension is elevated as a consequence of sufficiently increased environmental pressure. There are
no long-term sequelae.
As can be seen, hypobaric hypoxia will produce a
hyperventilation of a severity proportional to the degree of hypoxia. But the commonest cause of hyperventilation in flight is, as it is on the ground, emotional stress, and particularly anxiety.’ The familiar
clinical features of mild hypocapnia (lightheadedness,
dizziness, anxiety, which may therefore produce a vicious circle, and paresthesia of the extremities and
around the lips) may be seen in anxious passengers,
who should be strongly reassured and advised to control the rate and depth of their breathing.’ The traditional remedy of rebreathing from a paper bag will
also be of help, but caution in the use of this tech-
nique has recently been counseled on the grounds that
any associated hypoxia may be e~acerbated.~
The pressure changes associated with ascent to
altitude and descent from altitude will also have direct effects on the gas-containing cavities, since any
gas within closed or semiclosed body cavities will obey
Boyle’s law on ascent to altitude. So, for example, any
such gas will have doubled in volume, if it is free to
do so, at an altitude of about 18,000 feet where atmospheric pressure is half that at sea level. The lungs,
the teeth, and the gut may be affected during ascent,
whereas the middle ear cavities and sinuses are particularly affected during descent.’
Although potentially the most serious problem,
expansion of gas within the lungs does not usually
present a hazard on ascent since gas can easily vent
via the trachea. Aerodontalgia is pain in a tooth on
ascent and is now uncommon since it does not occur
in healthy or correctly restored teeth. The mechanism
of pain production is obscure: it may be a consequence
of irritation of diseased pulp by atmospheric pressure
changes or it may be the result of a neural or vascular
phenomenon responding to the relative increase in
pressure within a closed air space beneath a dental
filling or carious deposit.
Expansion of gas within the small intestine can
cause pain of sufficient severity to produce vaso-vagal
syncope, but this is most unlikely to occur during normal ascent rates in commercial aircraft. Gaseous expansion in the small bowel is, however, aggravated by
foods and drinks that produce gas: e.g., beans, curries, brassicas, carbonated beverages, and alcohol, and
passengers may be made aware of this phenomenon
during flight when waistbands become a little more
snug! Gas in the stomach and large intestine does not
usually cause problems since it can be released easily.
Expanding gas in the middle ear cavity vents
through the eustachian tube on ascent and only rarely
causes any discomfort. The symptoms of otic
barotrauma develop during descent because air cannot pass back up the tube so readily. Pain, which begins as a feeling of increased pressure on the tympanic
membrane, quickly becomes increasingly severe unless the eustachian tube is able to open and so equalize pressure between the middle ear cavity and the
pharynx (i.e., the atmosphere); an event colloquially
known as “clearing” the ears. Many people can
achieve such opening merely by swallowing, by yawning, or by moving the lower jaw from side to side.
Others have to perform a deliberate maneuver to open
the tube by raising the pressure within the p h a r y n ~ . ~
Some individuals have great difficulty in learning these
procedures and may be unable to do so even after much
coaching and practice. The most useful of these tech-
Harding, Aeromedical Aspects of Commercial Air Travel
niques is the Frenzel maneuver, which is carried out
with the mouth, nostrils, and epiglottis closed. Air in
the nasopharynx is then compressed by the action of
the muscles of the mouth and tongue. In the Toynbee
maneuver, pharyngeal pressure is raised by swallowing whilst the mouth is closed and the nostrils occluded.
This is the best technique to use when evaluating
eustachian function under physiologic conditions:
under direct vision, a slight inward movement of the
tympanic membrane is followed by a more marked
outward movement. Upper respiratory tract infections
(URTI) increase the likelihood of developing otic
barotrauma by causing inflammation and edema of
the eustachian lining, and passengers suffering from a
cold should be advised to take and use a topical nasal
decongestant.
The etiology of sinus barotrauma is the same as
that of its otic counterpart. On ascent, expanding air
vents easily from the sinuses through their ostia. On
descent, however, the ostia are readily occluded, especially if the victim has an URTI. A sudden, severe,
knife-like pain characteristically occurs in the affected
sinus. The pain continues if descent is not halted, and
epistaxis may result from submucosal hemorrhage.
The development of sinus barotrauma is related to
the rate of descent, and its prevention is part of the
rationale behind the slow rate of descent employed in
commercial aircraft (see below). The possibility of a
sinus problem cannot be predicted prior to flight, but
flying with a cold will clearly increase the risk and
having a nasal decongestant on hand is again sound
ad~ice.~
Finally, and thankfully infrequently, unprotected
ascent to altitude can give rise to decompression sickness (DCS).* The etiology of this illness, although
poorly understood, certainly involves supersaturation
of body tissues with nitrogen. Thus, ascent to altitude
is associated with a fall in inspired nitrogen and a corresponding fall in alveolar nitrogen. Nitrogen consequently starts to leave body stores but, since it is poorly
soluble in blood, tissue levels fall at a relatively slow
rate and the tissues therefore become supersaturated
with the gas. Bubbles begin to form around microscopic preexisting nuclei and then grow as blood gases
diffuse into them. Carriage of the bubbles to other
parts of the body may or may not be followed by clinical manifestations. The clinical features of DCS may
include any or all of the following: joint and limb pains
(“bendsyy)most commonly, respiratory disturbances
(“chokes”),skin manifestations (“creeps”),and visual
and neurologic disturbances rarely. Decompression
sickness is essentially never seen in healthy individuals at altitudes beIow 18,000 feet, but becomes increasingly common at altitudes above 25,000 feet
213
when it develops after at least 5 minutes at altitude.
As with susceptibility to hypoxia, certain preexisting
factors may increase the likelihood of developing the
illness, including drugs, alcohol, smoking, and
intercurrent illness, hypoxia itself, low environmental
temperatures, and increasing age. Of particular
relevance to the traveling public, however, is the increase in pressure sustained during diving (particularly to depths greater than 15 feet) which leads to
compression of additional nitrogen in the tissues with
consequently more available for bubble formation if
flying is subsequently undertaken. Medical guidance
should therefore be sought before flying after recreational diving.2
So, unprotected ascent to altitude can give rise to
many physiologic problems that are summarized in
Table 2.
Solution
The obvious way in which to prevent hypoxia is
to provide a personal source of breathing oxygen for
all aircraft occupants. This was the approach adopted
by early aviators and continues to be part of the routine solution for military aircrew. But breathing oxygen-enriched gas, or even 100% oxygen, will not overcome the problems of barotrauma or of decompression sickness. Encasement within a full pressure suit
will, and does, alleviate these difficulties (as well as
preventing hypoxia) and was the method adopted for
early high altitude military flights; one of the earliest
such suits being proposed, designed, and built by J. S.
Haldane. Such a solution is, however, clearly and totally impractical for the needs of mass public air transport.
The complete and elegant answer is, therefore, to
provide an environment within the aircraft cabin that
most closely approximates a terrestrial habitat: that
Table 2 Physical and Clinical Consequences of Changes in
Altitude.
Changein
Ascent
Physical
Consequence
1 partial pressure
of 0,
1 Total pressure
Descent
Clinical
Consequence
Hypoxia
(and hyperventilation)
Barotrauma
and decompression
sickness
Variation in
temperature
Thermal injury
Total pressure
Barotrauma
214
J o u r n a l o f T r a v e l M e d i c i n e , V o l u m e 1, N u m b e r 4
is, to pressurize the inside of the cabin. Thus, cabin
pressurization is the means by which the potential
hazards associated with ascent to altitude are minimized by maintaining the inside of an aircraft at a
higher pressure (and hence lower altitude) than that
to which the outside of the aircraft is exposed.*
The concept of cabin pressurization was developed toward the end of World War I, and by 1928,
Junkers in Germany had developed a two-man removable altitude cabin for fighter aircraft. In 1931, Auguste
Picard and Paul Kipfer flew a balloon to 51,961 feet
while suspended beneath it in a pressurized gondola;
and the first successful flight of an aircraft with an
integral pressurized cabin (the American X-C35, a
modified Lockheed Electra) took place 6 years later.
Pressurized Boeing 307 Stratoliners were in operation
with Transworld and Pan American airlines by 1939,
and from 1945 onwards, pressurized cabins were in
routine use for passenger aircraft.s
Clearly, the physiologically ideal situation would
be to pressurize the cabin to sea level at all times, but
this is not cost effective and therefore compromises
have to be made. Hence the maximum acceptable
cabin altitude will be determined by the risks of
hypoxia, decompression sickness, and gastrointestinal
distension; while the maximum rates of cabin ascent
and descent will be determined by effects on the middle ear cavities and sinuses (Table 3).
In large passenger-carrying transport aircraft
where comfort and mobility are important, and there
is little risk of rapid decompression, the cabin is pressurized to below 10,000 feet and commonly to a maximum of about 6,000 feet. Such aircraft are said to
have high differential pressure cabins since, when the
aircraft is flying at high altitudes, a large difference
exists between pressure within the cabin and the pressure outside.2
The cabin pressurization system is required to
control not only the pressure of air within the cabin,
but also its relative humidity, mass flow, volume flow
(ventilation), and temperature. In modern aircraft,
Table 3 Acceptable Limits of Cabin Altitude and Rates of
Ascent and Descent to Avoid Aeromedical Problems.
Problem
Acceptable Limits
Hypoxia
< 8,000 feet
Decompression sickness
< 22,000 feet
Gastrointestinal distension
c 6,000 feet
Middle ears
and sinuses:
ascent
descent
< 5,000-20,000 feet. min
< 500 feet. min -I
outside air enters the engines where it is compressed
and passes through cooling packs to a chamber to be
mixed with air that has been recirculated through high
efficiency filters. Air from this mixing chamber is then
continuously supplied to the cabin, the pressure of
which is controlled by sensors that govern a series of
valves responsible for normal discharge of air pressure, excess pressure relief, and inward pressure relief. The control schedule normally adopted in commercial aircraft is one whereby the cabin differential
pressure is allowed to increase slowly over a range of
aircraft altitudes. Such a schedule (which can usually
be controlled manually by the crew) is commonly used
from ground level since passenger comfort is thereby
improved.
The potential effects of rapid decompression to
high altitude upon the occupants of an aircraft are
entirely predictable and include hypoxia, decompression sickness, cold, and the problems of gas expansion. The movement of air and debris within the cabin
and through the defect will promote confusion and
difficulty with hearing and vision. Fortunately, such
dramatic events are very uncommon (and are nowadays most usually related to terrorist activity), but
cabin pressurization can be lost for other, technical,
reasons. Provided that the loss is not catastrophic, the
risks to the passengers and crew are slight. If the cabin
altitude exceeds about 14,000 feet, in such circumstances, passenger oxygen masks will be deployed
automatically, and everyone will have oxygen delivered continuously to their facepiece. The flight deck
crew, reassuringly, will be wearing more sophisticated
equipment while they fly the aircraft to a physiologically safe altitude.
The emergency oxygen system is, of course, also
available for those passengers who may become ill in
flight; a development most frequently seen in those
who already have compromised cardiorespiratory
function. It cannot be over emphasized that such people should seek medical advice before traveling by air,
and should be sure that the airline has been prewarned.6
Emergencies are, understandably, the attentiongrabbing events of air travel. But they are also, thankfully, exceptions to the rule: almost all air travel is
undertaken completely without incident. For most
people, therefore, the hazards of commercial flight are
no more irritating than boredom and the problems
surrounding personal comfort. Cabin pressurization
allows freedom of movement and action within the
cabin, unencumbered by complex life support equipment, but passenger comfort and cabin air quality are
increasingly of concern to aircraft manufacturers, to
airlines and, of course, to passengers.’J This height-
Harding, A e r o m e d i c a l A s p e c t s of Commercial Air Travel
ened interest follows reports that headaches, nausea,
and upper respiratory tract irritation are common, that
poor ventilation of cabins may cause disease amongst
passengers, and that tobacco smoke and other environmental contaminants may increase the risk of respiratory illness. Many relate these problems to a
change in the way in which air is delivered to the cabins of modern commercial aircraft. Thus, until the late
1980s, about 20 cubic feet per minute offresh air were
delivered to the cabin per person per minute. Today,
this figure has been reduced to about 10 cubic feet per
minute per person, although the total requirement for
ventilation remains the same: consequently, the rest is
recirculated air (see above). It was concern about pollution of recirculated cabin air with environmental
tobacco smoke (ETS), together with increased awareness of the health risks associated with passive smoking that led, in part, to the widespread ban on smoking in aircraft during the late 1980s. Commercial pressure from nonsmoking customers was also relevant.
Studies of potential contaminants of cabin air (carbon dioxide, microbial aerosols, ozone, and ETS) have
shed some light on the subject, but not
Thus, raised carbon dioxide levels in closed environments are predominantly the consequence of human metabolism, so that the presence and removal of
carbon dioxide will be functions of the number of
people present and the ventilation rate. The level of
carbon dioxide can therefore be used as an indication
of efficiency of ventilation: as the fresh air component
declines so the carbon dioxide level may be expected
to rise. Not surprisingly, levels in modern aircraft have
been found to be significantly higher than those normally associated with comfort, although they have
remained well below mandated limits. Similarly, recorded levels of microbial aerosols appear never to
approach those normally associated with a risk of ill
health. Ozone levels well in excess of the required limits
have been reported in some studies, but have remained
well below them in others. In any event, catalytic ozone
converters are now required if the flight profile indi-
215
cates that statutory levels for ozone will be exceeded.
Finally, as well as being a source of nuisance, ETS has
been cited as the cause of in-flight headaches, eye nose
and throat irritation, and breathing difficulties. It could
be argued, however, that coexisting factors such as
low relative humidity, high ozone levels, and even
hypoxia, may also be to blame.
In conclusion, although it is reasonable to surmise that ETS and other cabin pollutants do not appear to represent a great threat to health, and that
their effects may in any case be confounded by other
factors, there is no doubt that a total ban on smoking
on all aircraft would instantly lead to subjective irnprovement; and indeed such measures are being actively considered by some airlines.
References
1. Harding RM. Hypoxia and hyperventilation. In:
Ernsting J, King PF, eds. Aviation medicine. 2nd ed.
London: Butterworths. 1988:45-59.
2. Harding RM, Mills FJ. Problems of altitude. In: Aviation medicine. 3rd ed. London: BMJ Publishing Group,
1993:58-72.
3. Callahan M. Hypoxic hazards of traditional paper bag
rebreathing in hyperventilating patients. Ann Ernerg
Med 1989; 18:622-628.
4. Harding RM. ENT problems and the air traveller. Travel
Med Int 1992; 10:98-100.
5 . Engle E, Lott AS. Man in flight-biomedical achievements in aerospace. Maryland: Leeward Publications,
1979.
6. Harding RM, Mills RJ. Fitness to travel by air. In: Aviation medicine. 3rd ed. London: BMJ Publishing Group,
1993:30-42.
7. Harding RM. Cabin air quality in aircraft. BMJ 1994;
308:427-428.
8. Space D. Cabin Air quality. Airliner 1993; Oct-Dec:
19-24.
9. National Academy of Science. The airliner cabin environment-air quality and safety. Washington DC: National Academy Press, 1986.