Atmospheric pressure

Total gas pressure falls with altitude in a regular manner, halving every 5500 m (18 000 ft) (Fig. 9.5.5.2). The oxygen content of the atmosphere (20.93%) is constant to very high altitudes, so the same curve can be used to obtain the ambient oxygen pressure by rescaling the ordinate (Fig. 9.5.5.2). The oxygen pressure of physiological importance is that which exists in ambient air when it is warmed and wetted on entering the bronchial tree. This raises water vapour pressure to about 47 mmHg, regardless of the total gas pressure outside. The oxygen pressure in moist inspired gas (Pio₂), fully saturated with water vapour at 37 °C, is given by the relationship:$$P{\text{io}}_{\text{2}}=F{\text{io}}_{\text{2}}\left(P_{\text{B}}-47\right)$$

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Fig. 9.5.5.2

The variations of barometric pressure (P_B) and ambient oxygen pressure (PO₂) with altitude.

where Fio₂, the fractional concentration of oxygen in the inspirate, is 0.2093 and PB is barometric pressure (mmHg).

Atmospheric temperature

The atmospheric temperature decreases at 1.98 °C/300 m (1000 ft) from the Standard sea level temperature of 15 °C, to the tropopause (12 200 m or 40 000 ft). It remains stable at –56 °C up to about 24 400 m (80 000 ft) and then rises to almost body temperature at about 46 000 m (150 000 ft), but by then air density is so low that its temperature is unimportant.

Atmospheric ozone

Atmospheric ozone is formed by ultraviolet irradiation of diatomic oxygen molecules, which dissociate into atoms. At very high altitudes, all oxygen exists in the monatomic form. Lower down, some of this monatomic oxygen combines with oxygen molecules to form the triatomic gas ozone, with concentrations up to 10 parts per million. The ozonosphere normally exists between 12 200 and 42 700 m (40 000 and 140 000 ft). Below 12 200 m (40 000 ft) the irradiation is normally too weak for significant amounts of ozone to form. Concentrations of 1 parts per million at sea level can cause lung irritation. However, modern passenger jet aircraft are fitted with catalytic converters in the environmental control system (ECS), which break down the ozone before it enters the pressurized cabin.

Cosmic radiation

Aircraft occupants are exposed to elevated levels of cosmic radiation of galactic and solar origin.

The Sun has a varying magnetic field, which reverses direction approximately every 11 years. Near the reversal, at ‘solar minimum’, there are few sunspots, and the Sun’s magnetic field extending throughout the solar system is relatively weak. At solar maximum, there are many sunspots and other manifestations of magnetic turbulence.

The Earth’s magnetic field has a larger effect than the Sun’s magnetic field on cosmic radiation approaching the atmosphere. The protective effect is greatest at the equator and least at the magnetic poles. At the altitudes at which jet aircraft operate, galactic cosmic radiation is 2.5 to 5 times more intense in polar regions than near the equator.

The Earth’s surface is shielded from cosmic radiation by the atmosphere, the ambient radiation decreasing with altitude by approximately 15% for each increase of around 600 m (2000 ft), dependent on latitude.

Hypoxia

Oxygen has a dual role in most animal cells, being simultaneously life-giving and extremely poisonous. In air, or dissolved in simple solution, it is benign and ionized only with difficulty. However, once an electron is successfully attached to an oxygen molecule it becomes a highly corrosive superoxide ion, forming a cascade of other very destructive oxygen radicals. This is an essential feature of oxygen toxicity. Superoxide dismutase and various peroxidases have evolved to protect most cells from the effects of spontaneous formation of oxygen radicals by quenching the ions as rapidly as they appear.

Other enzymes have evolved, which harness this property in a controlled way. There are three types: oxidases, oxygenases, and hydroxylases. Quantitatively, cytochrome a₃ oxidase (EC 1.9.3.1) is the most important because, using oxygen as the ultimate electron sink, it allows many metabolic processes to proceed, at the same time unlocking and trapping most of the energy the body needs (oxidative phosphorylation).

Oxygenases introduce an oxygen molecule into organic molecules, creating new compounds. Although these enzymes consume only a small fraction of the body’s total oxygen requirement, they are particularly important for production and dismemberment of many critical compounds, such as the amine transmitters of the brain.

Hydroxylases insert one atom of oxygen and another of hydrogen into organic molecules. They too are responsible for many critical metabolic processes and for the denaturation of many drugs in the liver, kidney, and elsewhere.

These enzymes differ in their affinity for oxygen, described by the Michaelis constant (for oxygen). This constant (K_mo₂) is that partial pressure of oxygen which, when all other factors are equal, allows an oxygen-consuming reaction to proceed at half its maximum velocity. The major oxidase (cytochrome a₃), which is the cocatalyst of oxidative phosphorylation, has a very high oxygen affinity, and thus a very low K_mo₂ of 1 mmHg or less. Thus, this particular type of oxygen consumption, representing 80 to 90% of the whole, can proceed at high rates down to very low levels of oxygen supply. By contrast (Fig. 9.5.5.3), the other enzymes, which are quantitatively less important but qualitatively critical, have Michaelis constants for oxygen that vary from 5 to 250 mmHg. A fall in oxygen supply will influence these processes long before oxidative phosphorylation is affected, and at times when overall oxygen consumption is diminished little, if at all.

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Fig. 9.5.5.3

Curves of oxygen uptake (O₂) as a fraction of the theoretical maximum (O_2max) against the partial pressure of oxygen (Po₂) for a family of oxygen-handling enzymes with Michaelis constants for oxygen (K_mo₂) from 1 to 250 mmHg.

Although Figure 9.5.5.2 describes how ambient oxygen pressure is related to altitude, it does not convey the pressure of oxygen to be found in the lungs. That pressure is determined by two equations (Fig. 9.5.5.4). The alveolar ventilation equation states that alveolar CO₂ pressure (Paco₂) depends only on CO₂ excretion and alveolar ventilation (Va), so:$$P{\text{aCO}}_{\text{2}}=k\left({\text{CO}}_{\text{2}}/V\text{a}\right)$$

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Fig. 9.5.5.4

Graphical representations of the alveolar ventilation and alveolar air equations.

The alveolar air equation states that since at any one time there is a fixed trading ratio between oxygen uptake and CO₂ excretion (R = CO₂/O₂), alveolar oxygen pressure (Pao₂) can be calculated from the moist inspired oxygen pressure (Pio₂*) and alveolar Pco₂, so:$$P{\text{aCO}}_{\text{2}}=P{\text{io}}_{\text{2}}*-k\left(P{\text{aCO}}_{\text{2}}/R\right)$$

Progressive hypoxia leads to a mild hyperventilation (i.e. a rise in Va and fall in Paco₂). Thus, it is possible to plot alveolar oxygen pressure against altitude (Fig. 9.5.5.5a).

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Fig. 9.5.5.5

(a) Variations in moist inspired, alveolar, and arterial oxygen pressure (Po₂) with altitude in normal men. (b) The conventional oxygen–haemoglobin dissociation curve of whole blood plotted to the same pressure scale as the left-hand graph, so that arterial O₂ content can be read directly (at the same horizontal level as the Po₂ curve. It also emphasizes that the arteriovenous oxygen content difference (a – vΔ) is proportional to the ratio of oxygen uptake (Mo₂) to local blood flow (Q).

When arterialized blood leaves a healthy lung, the oxygen pressure is about 10 mmHg less than that in the alveoli, due to uneven matching of ventilation to perfusion, some anatomical shunting, and an almost nominal obstacle to diffusion. In resting people, the alveolar–arterial oxygen gradient does not change much with altitude, although the relative importance of the factors contributing to it alter considerably; so subtracting a further 10 to 15 mmHg describes the relation between arterial oxygen pressure and altitude (Fig. 9.5.5.5).

The most important change is the loss of pressure, driving oxygen from the alveoli to blood, as the fall in alveolar Po₂ is much greater than that in mixed venous Po₂ (because of the shape of the oxygen dissociation curve). As a result, the alveolar–venous gradient for oxygen diffusion is smaller and equilibration slower than at ground level.

People ascend to altitude in a matter of minutes, rather than over several days, and adapt to hypoxia by an increase in blood flow and a modest hyperventilation, limiting the effects of hypoxia. The effects are shown in Fig. 9.5.5.6.

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Fig. 9.5.5.6

A summary of the functional consequences of altitude hypoxia.

Individuals abruptly exposed to altitudes of 3000 m (10 000 ft) and above suffer mental and physical effects, and this is the ceiling over which aviators are provided with oxygen. To allow a margin of safety, the maximum certified cabin altitude in civilian passenger aircraft is 2440 m (8000 ft), at which barometric pressure is 565 mmHg and arterial oxygen pressure is around 55 mmHg (see Fig. 9.5.5.5b, the oxyhaemoglobin dissociation curve), and venous oxygen pressures have fallen by only 1 to 2 mmHg. Even at this altitude, there is a decrease in performance. The latest generation of passenger aircraft are manufactured from newer materials, which provide greater strength from a given mass, thus allowing a higher differential cabin pressure with a lower cabin altitude.

Two physiological features of altitude hypoxia are important in aviation. The first is the total lack of awareness of cerebral impairment. The second is the time of useful consciousness, describing how rapidly consciousness is lost thus dictating how quickly the condition must be recognized and corrective action taken.

The time of useful consciousness is the interval after the onset of hypoxia during which an individual can carry out some purposeful activity. The general relation between this time interval and the altitude of sudden exposure is shown in Fig. 9.5.5.7a. It diminishes from about 4 min at 7620 m (25 000 ft) to a minimum of roughly 15 s, which is reached at 10 700 to 12 200 m (35 000–40 000 ft). This asymptote represents the sum of the 7 s or so required for blood to travel from the lungs to the brain and the time needed for the brain to utilize the oxygen already dissolved in its substance.

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Fig. 9.5.5.7

(a) Variations in the time of useful consciousness with altitude. (b) One way of expressing the dose of hypoxia needed to bring about the loss of consciousness.

In trained and healthy men breathing normally (i.e. with an alveolar Pco₂ of 35–40 mmHg), the dose of hypoxia acceptable before loss of useful consciousness is equivalent on a curve of alveolar Po₂ against time, to an area of 150 mmHg s, where Po₂ is less than 38 mmHg (Fig. 9.5.5.7b). However, this is sensitive to many other factors, such as the degree of hyperventilation and the acceleration to which the individual is exposed at the time. Hyperventilation causes cerebral vasoconstriction, and positive headwards acceleration (+G_z) opposes the upward flow of blood to the brain. Sometimes deterioration in consciousness is quickened by vasovagal syncope, but more often there is tachycardia as consciousness is lost. Exertion also quickens loss of consciousness, because blood transits quickly through the lungs leaving insufficient time for oxygen equilibration.

The minimum cabin pressure of 565 mmHg (75.1 kPa) in commercial passenger aircraft (equivalent to 2440 m or 8000 ft), will bring a healthy individual’s arterial Po₂ along the plateau of the oxyhaemoglobin dissociation curve until just at the top of the steep part (Fig. 9.5.5.5), still saturated. At ground level, people with respiratory disease may have arterial oxygen pressures as low as 55 to 60 mmHg. As they ascend to 2440 m (8000 ft), their arterial Po₂ will fall further. If their hypoxaemia at ground level is due to a mismatch of ventilation to perfusion, as is usually the case, the drop in arterial Po₂ will not be as extensive as in healthy people (c.40 mmHg), but if it is due to diffusion defect associated with desaturation on exertion, as in some fibrotic conditions, it may be greater. However, in either event, it can be reversed completely by the administration of oxygen, 30% oxygen at 2440 m (8000 ft) being equivalent to breathing air at ground level. Given prior notice, most airlines can provide a personal oxygen supply for any passenger, although there may be a charge. (The altitudes of the patient’s destination and transit points en route should also be considered.)

Oxygen equipment and pressure cabins

Aircraft operating below 3000 m (10 000 ft) do not require oxygen equipment. Many sophisticated light aircraft that can cruise above 3000 m do not have pressurized cabins, so oxygen equipment must be provided.

Other aircraft that fly higher usually have reinforced cabins capable of holding a high differential pressure between inside and out. These are the high-differential type, seen in passenger and transport aircraft generally, and the low-differential variety found in military high-performance aircraft. The former, holding a high transmural pressure, maintain cabin pressure above 565 mmHg (the equivalent of 2440 m or 8000 ft). They provide an environment in which the occupants breathe cabin air. However, it is possible for the pressurization system to fail, allowing the cabin pressure to fall to the external ambient value. This can be limited by descent to a lower altitude, but it is not always possible to descend immediately, for reasons of structure or air traffic control. Similarly, it is not always practical to descend below 3000 m (10 000 ft) because, in mid-Atlantic, for example, there may be insufficient fuel for the aircraft to reach the nearest land through the denser air at lower altitudes. Thus, an emergency oxygen supply is available for passengers and crew.

The aircraft environmental control system (ECS) automatically manages the internal cabin environment, providing healthy and comfortable surroundings for all occupants. There are regulatory requirements for minimum cabin air pressure, maximum levels of carbon monoxide, CO₂ and ozone, and minimum ventilation flow rates. The cabin air must also be free from harmful or hazardous concentrations of gases or vapours.

The cabin air supply is bled from the outside air entering the aircraft engine, or may be supplied from the outside air via electrically driven compressors. It is then passed through the air-conditioning packs and mixed with filtered recirculated air before distribution to the cabin. The system provides approximately 566 litres (20 cubic feet) of air per minute per passenger, of which about 50% is recirculated air (compared with up to 80% recirculated in buildings and other forms of public transport), giving a complete cabin air exchange every 2 to 3 min.

These high ventilatory flow rates maintain normal pressurization, as well as temperature control and the removal of odours and CO₂. The high flow rates also ensure that the volume of oxygen far exceeds the requirements of the aircraft occupants (0.34 litres/min at rest and 0.85 litres/min when walking).

The air is distributed to the cabin via overhead ducts and grills running the length of the cabin. The airflow circulates around the cabin rather than along the cabin and is continuously extracted through vents at floor level, as shown in Fig. 9.5.5.8.

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Fig. 9.5.5.8

Cabin air circulation and distribution.

The recirculated air is passed through high efficiency particulate air (HEPA) filters of the same specification used in hospital operating theatres, giving 99.99% efficiency in the removal of physical contaminants such as microbial particles. Aircraft cabin air has been demonstrated to be bacteriologically cleaner than the air in buildings, trains, or buses.

Although clean, the aircraft cabin air remains dry. During the flight, moisture is derived from the metabolism and activities of the cabin occupants as well as from the galleys and washrooms, giving a maximum relative humidity of the order of 10 to 20%. These levels are associated with surface drying of skin, mucous membranes, and cornea which may cause discomfort. Normal homeostatic mechanisms prevent dehydration and no harm to health has been demonstrated.

A high-differential cabin limits the vehicle’s range and manoeuvrability and increases the risk of catastrophic damage if the fuselage is punctured. So, military high-performance aircraft are fitted with low-differential cabins, which prevent cabin pressure falling below 280 mmHg (37.2 kPa) (equivalent to a pressure altitude of 7620 m or 25 000 ft). At this level, decompression illness becomes a potential hazard (see following paragraphs). In such aircraft, oxygen equipment is used routinely.

Mechanical effects of pressure change

In civilian passenger and transport aircraft, the climb to cruise altitude takes about 30 min and involves a maximum decrease of about 200 mmHg (26.6 kPa) in cabin pressure (to the equivalent of 2440 m or 8000 ft). Descent to land takes much the same time. Body fluids and tissues generally are virtually incompressible and do not alter shape to any important extent when such pressure changes are applied. The same is true of cavities such as the lungs, gut, middle ear, and facial sinuses that contain air, provided that they can vent easily. Gas-containing spaces that cannot vent easily behave differently.

The thoracoabdominal wall can develop transmural pressures of +100 mmHg or so briefly, but is normally flaccid and has a transmural pressure of a few millimetres of mercury. Gas within will usually be at a pressure very close to that outside, and must follow Boyle’s law. Ascent from ground level (760 mmHg) to 2440 m (8000 ft) (565 mmHg) will expand a given volume of trapped gas in a completely pliable container by about 35%. This may cause slightly uncomfortable gut distension in healthy people, but it is not an important problem.

Even very diseased lungs can vent themselves over a minute or so. In consequence, the risk of lung rupture in normal flight is extremely rare (Fig. 9.5.5.9).

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Fig. 9.5.5.9

A graphical summary of the factors determining lung rupture.

The cavity of the middle ear vents easily, but sometimes fails to fill because the lower part of the eustachian tube behaves as a nonreturn valve, especially when it is inflamed. As a result, the cavity equilibrates quite easily on ascent but does not refill on descent, and the eardrum bows inwards, causing pain that can be severe (otic barotrauma).

Altitude-induced decompression illness

If ambient pressure falls quickly to less than half its original value, the gas dissolved in blood and tissue fluids may come out of solution precipitously, forming bubbles and obstructing flow in small blood vessels. The time symptoms take to develop varies widely between individuals and shortens markedly as the altitude of exposure rises. A guide to these times and variability is given in Fig. 9.5.5.10. Symptoms usually resolve quickly after a descent of a few thousand feet and rarely persist after descent to ground level, breathing oxygen. Should they persist, treatment should be along the lines detailed in Chapter 9.5.4.

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Fig. 9.5.5.10

The incidence of decompression sickness (%) at the end of 2 h of exposure to various altitudes in men at rest, or exerting themselves.

Atmospheric pressure halves at 5000 m (18 000 ft) and decompression illness occurs rarely, if at all, below this altitude. It is very rare below 7600 m (25 000 ft) and therefore is normally of no concern at normal passenger aircraft cabin altitudes, although the risk continues to be significant in some military flights. However, it does occasionally occur in those passengers who have been exposed to a hyperbaric environment prior to flight, such as divers and tunnel workers. Subaqua divers (see Chapter 9.5.6) are advised to allow a minimum of 12 h to elapse between diving and flight, or 24 h if the dive required decompression stops.

Jet lag

Besides sleep, the major influence on waking performance and alertness is the internal circadian clock. Circadian rhythms fluctuate on a regular cycle which lasts something over 24 h. The circadian rhythms are controlled by the suprachiasmatic nucleus of the hypothalamus. Many body functions have their own circadian rhythm and they are synchronized to a 24-h pattern by ‘zeitgebers’ (time givers), light being among the most powerful.

Moving to a new light/dark schedule (as in changing time zones) leads to a discrepancy between internal suprachiasmatic nucleus timing and external environmental cues. The internal clock can take days or weeks to readjust, depending on the number of time zones crossed (desynchronosis). Some preventive measures are listed in Box 9.5.5.1.

Fatigue is defined as the likelihood of falling asleep. Therefore, in practical terms, there is little difference between chronic fatigue and acute tiredness. Fatigue can be caused by sleep loss and circadian desynchronosis, but it can also result from low motivation and low levels of external stimulation.

Caffeine consumption may be used to increase alertness. A cup of coffee usually takes about 15 and 30 min to become effective, and the effect lasts for between 3 and 4 h. However, this is less effective for individuals who regularly drink large amounts of caffeine-containing beverages.

Bright light (>2500 lux), used at the appropriate time in the circadian cycle, can help to reset the circadian clock.

After flying east, the traveller should be exposed to evening light, but morning light avoided. Conversely, when travelling west, morning light should be sought and evening light avoided. This makes the best use of the natural zeitgebers in resetting the body clock.

Temazepam is a short-acting benzodiazepine with a short half-life. Many people find this drug helpful in promoting sleep, and if used for two or three days after travel, can assist in resetting the sleep cycle.

Melatonin is secreted by the pineal gland with a rhythm linked to the light/dark cycle through the suprachiasmatic nucleus. It is effective in inducing sleep when taken at the appropriate stage in the circadian cycle. However, if taken at the wrong stage, it can disrupt the sleep/wake cycle and destabilize sleep patterns. This limits its usefulness in treating jet lag.

There is no simple or single solution for combating the effects of jet lag. Individual have to evolve strategies to suit their particular needs.

Traveller’s thrombosis (DVT/VTE)

Longhaul travel is associated with prolonged periods of immobility, a recognized risk factor for DVT, first described by Virchow in 1856. However, there have been concerns as to whether there are other factors specific to air travel that further increase the risk.

In the general population, DVT occurs in 1 to 3 per 1000 people per year, of which 20% give rise to pulmonary embolism. Increasing age is known to be a strong risk factor, possibly due to decreased mobility and reduced muscular tone.

The pathogenesis of thrombosis still relies on the basic premise of Virchow, who identified circulatory stasis, hypocoagulability, and endothelial injury as the risk factors.

Several clinical studies have shown an association between air travel and the risk of DVT, with the risk of VTE in travellers increasing with the distance travelled. A recent case–control study showed that all modes of travel increased the risk of venous thrombosis about twofold, with an absolute risk of 1 thrombosis per 6000 journeys.

It has been found that combinations of risk factors synergistically increase the risk of thrombosis. In people with factor V Leiden, the risk of thrombosis after flying was about 14 times increased and in women using oral contraceptives it was around 20-fold increased.

It has also been shown that the risk rises with the number of flights taken in a short time-frame as well as with the duration of the flight. The majority of these clots are asymptomatic and disperse naturally.

Thus, even though the overall risk of venous thrombosis after air travel is only moderately increased, clear subgroups can be identified in whom the risk is higher.

The low humidity of the aircraft cabin does not in itself lead to dehydration. Excessive alcohol consumption may cause dehydration, but there is no evidence that this is a significant risk factor leading to DVT.

Two recent studies of reduced oxygen partial pressure with nonhypoxic control groups found no evidence of coagulation. There is no evidence that hypoxia or the hypobaric environment of an aircraft cabin is a significant risk factor for the development of DVT.

Although there is good evidence for the value of aspirin in preventing arterial thromboembolic disease, its role in the prevention of venous thromboembolic disease is much less clear. The side effect profile is significant.

There is no evidence to support the use of aspirin in preventing the development of DVT during flight.

For those travellers at medium to high risk of DVT, there is evidence that the use of compression stockings appears to substantially lower the risk of asymptomatic DVT, but it remains unclear as to whether this reduction is clinically significant. One study has shown that for 20 to 40% of travellers, the commercially available stockings do not fit adequately. It is essential for stockings to be correctly fitted so as to provide adequate compression to stimulate venous return.

Although the use of low molecular weight heparin for the prevention of DVT in the aviation setting is not supported by direct evidence, in a high-risk traveller consideration may be given to a single prophylactic dose prior to flying.

While the relative risk of developing venous thrombosis when flying is significant, the absolute risk of developing symptomatic DVT is very low. The absolute risk of developing a pulmonary embolus during or after a flight between the United Kingdom and the east coast of the United States of America has been calculated as less than 1 in 10⁶.

Medical practitioners need to be circumspect in advising any preventive measures, taking careful account of efficacy and risk profile of the preventive method.

Passenger fitness to fly

Medical clearance is required when:

• ◆ Fitness to travel is in doubt as a result of recent illness, hospitalization, injury, surgery, or instability of an acute or chronic medical condition.

• ◆ Special services are required (e.g. oxygen, stretcher or authority to carry or use accompanying medical equipment such as a ventilator or a nebulizer).

Medical clearance is not required for carriage of an invalid passenger outside these categories, although special needs (such as a wheelchair) must be reported to the airline at the time of booking.

It is vital that passengers remember to carry with them any essential medication, and not pack it in their checked baggage.

Deterioration on holiday or on a business trip of a previously stable condition, or an accident, can often give rise to the need for medical clearance for the return journey. A stretcher may be required, together with medical support, and this can incur considerable cost. It is important for all travellers to have adequate travel insurance.

Spread of infectious disease

There is no evidence that the pressurized cabin itself makes transmission of disease any more likely, and it has been shown that recirculation of cabin air is not a risk factor for contracting symptoms of upper respiratory tract infection. Data suggest that risk of disease transmission to susceptible passengers, by person-to-person droplet spread within the aircraft cabin, is associated with sitting within two rows of a contagious passenger for a flight time of more than 8 h.

Newly emerging infectious disease

SARS is an atypical pneumonia caused by a novel coronavirus, which first appeared in eastern Asia in 2003.

Thousands of flights took place to and from what the World Health Organization defined as ‘affected areas’ during the outbreak, but transmission occurred only on 5 flights involving 29 secondary cases (24 cases on 1 flight). In addition, a further 40 flights were identified on which one or more probable cases (i.e. symptomatic at the time of travel) travelled but where no secondary cases developed. Thus the risk of transmission on board an aircraft is thought to be low.

Avian influenza (‘bird flu’) is a highly pathogenic strain A/H5N1 causing an epidemic amongst birds in Asia, Europe, and Africa. Human infection is very rare, but serious when it occurs. During 2006, the World Health Organization reported a total of 109 cases of which 79 died. None of the reported cases occurred within Europe, and air travel is not thought to be a risk factor.

On the other hand, pandemic influenza causes major morbidity and mortality in humans, with serious economic and social consequences. It usually affects a large proportion of the global population due to the absence of immunity, and spreads very rapidly throughout the world. Influenza pandemics occurred in 1918 (‘Spanish flu’), 1957 (‘Asian flu’), 1968 (‘Hong Kong flu’) and in 2009 (‘Swine flu’), all with high mortality.

The World Health Organization’s strategy for rapid containment of an emerging influenza pandemic aims to interrupt disease transmission by isolating and treating infectious individuals, treating and quarantining exposed people, and minimizing the exposure of uninfected persons. Modelling suggests that restricting air travel will not prevent the global spread of pandemic influenza, but might delay the spread sufficiently to allow countries time to prepare. Guidelines can be accessed from http://www.who.int or http://www.cdc.gov.

It is important that individuals should not travel on commercial aircraft with a febrile illness.