aeromedical aspects of commercial air travel

REVIEWS

Aeromedical Aspects of Commercial Air Travel Richard Harding

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.

Punch Book of Travel

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 de- scended 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 trod- den 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, Farnbor- ough, Hampshire, United Kingdom, GU14 6TD

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:

4 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 cru- cial stage in the development of the physiologic changes associated with an ascent, and a considera- tion of the oxyhemoglobin dissociation curve helps to show why this should be. Thus, the relationship between oxygen tension and the percentage satura- tion 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 na- ture 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

2 1 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 , Vo lume 1. Number 4

Table 1 Those of Hyperventilation

Comparison of the Symptoms and Signs of Hypoxia with

Hypoxia Hyperventilation

Personality change Lack of insight Loss of judgment Feelings of unreality Dizziness Loss of self criticism Euphoria Loss of memory Mental incoordination Lightheadedness Muscular incoordination Neuromuscular

Feelings of apprehension

irritability Carpopedal spasm Paresthesia of face and extremities

Sensory loss

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 propri- etary 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 suf- ficiently 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 de- gree of hypoxia. But the commonest cause of hyperventilation in flight is, as it is on the ground, emo- tional stress, and particularly anxiety.’ The familiar clinical features of mild hypocapnia (lightheadedness, dizziness, anxiety, which may therefore produce a vi- cious 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, cur- ries, 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 be- gins as a feeling of increased pressure on the tympanic membrane, quickly becomes increasingly severe un- less the eustachian tube is able to open and so equal- ize 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 yawn- ing, 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-

H a r d i n g , A e r o m e d i c a l A s p e c t s o f C o m m e r c i a l A i r T r a v e l 2 1 3

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, espe- cially 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 a d ~ i c e . ~

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 cor- responding fall in alveolar nitrogen. Nitrogen conse-

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 recrea- tional 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 over- come 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 to- tally 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

quently 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 micro- Changein Physical Clinical scopic preexisting nuclei and then grow as blood gases diffuse into them. Carriage of the bubbles to other Ascent 1 partial pressure Hypoxia 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 individu-

Table 2 Physical and Clinical Consequences of Changes in Altitude.

Consequence Consequence

of 0, (and hyperventilation)

1 Total pressure Barotrauma and decompression sickness

Variation in Thermal injury temperature

als at altitudes beIow 18,000 feet, but becomes increasingly common at altitudes above 25,000 feet Descent Total pressure Barotrauma

2 1 4 J o u r n a l o f T rave l Medic ine , Vo lume 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 mini- mized 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 remov- able 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 < 5,000-20,000 feet. min

descent < 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 nowa- days 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 circum- stances, 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 pre- warned.6

Emergencies are, understandably, the attention- grabbing 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-

H a r d i n g , A e r o m e d i c a l A s p e c t s o f C o m m e r c i a l A i r T r a v e l 2 1 5

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 pol- lution of recirculated cabin air with environmental tobacco smoke (ETS), together with increased aware- ness 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 envi- ronments are predominantly the consequence of hu- man 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, re- corded 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-

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 sur- mise 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 irn- provement; and indeed such measures are being ac- tively 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: Avia- tion medicine. 3rd ed. London: BMJ Publishing Group,

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 achieve- ments in aerospace. Maryland: Leeward Publications, 1979.

6. Harding RM, Mills RJ. Fitness to travel by air. In: Avia- tion 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:

9. National Academy of Science. The airliner cabin environment-air quality and safety. Washington DC: Na- tional Academy Press, 1986.

1993:58-72.

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aeromedical aspects of commercial air travel

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