Carbon Monoxide and Cabin Air Hazards

Carbon monoxide (CO) is a colourless, odourless and tasteless gas produced whenever carbon-based fuel burns without enough oxygen. It is the classic poison of the light-aircraft cockpit. A crack in an exhaust pipe or heater muff on a winter flight can feed it straight into the cabin with the warm air. Breathed even in small quantities over time, it seriously reduces the blood's ability to carry oxygen. Among the first faculties it dulls is the judgement the pilot needs to recognise the problem.

Carbon monoxide is one of several hazards carried in the air a crew breathes. In most jet transports the cabin air is compressed by the engines or the APU, so an oil leak can contaminate it in a fume event. At cruising levels the outside air is extremely dry, it contains ozone that must be removed, and the thin atmosphere above gives less protection from cosmic radiation. This article covers all of these hazards. The wider physiology of oxygen shortage is in hypoxia and hyperventilation.

Sources of carbon monoxide

Carbon monoxide comes from the incomplete combustion of carbon. ATPL texts put the CO content of piston-engine exhaust at up to 9 per cent, against less than 1 per cent for jet exhaust. Poisoning is therefore mainly a problem of piston aircraft, and above all of their cabin heating.

In most single-engine training aeroplanes, cabin heat is ram air passed through a heater muff, or shroud: a close-fitting jacket around the exhaust muffler. The air is warmed by the hot pipe wall without touching the exhaust gas. If the muffler or a pipe cracks, or a joint or seal leaks, exhaust gas mixes with the heated air and flows directly into the cabin (see cabin heaters). The FAA's Aeronautical Information Manual (AIM) states that heater leaks of this kind cause several fatal and non-fatal accidents every year. Exposure is most likely in cold weather with the heater on, which is why the exhaust system gets careful attention at every inspection.

Other sources include:

• combustion heaters, which burn fuel in a chamber of their own and are fitted with automatic fuel shut-off and overheat protection because a failure could put combustion gases into the cabin
• exhaust drawn in on the ground from the aircraft's own engines or from other traffic; the Airbus A320 procedure, for example, selects APU bleed on just before engine shutdown at the stand to keep engine exhaust fumes out of the air conditioning
• tobacco smoke, which loads the smoker's blood with carbon monoxide before the flight has even begun.

How carbon monoxide affects the blood

Oxygen travels in the blood bound to haemoglobin in the red cells (see circulatory system). Haemoglobin's affinity for carbon monoxide is about 200 to 250 times its affinity for oxygen, so even a small concentration in the inhaled air progressively takes it over. The compound formed, carboxyhaemoglobin (COHb), cannot carry oxygen. It releases the gas only slowly, so the effect builds up during a flight and over successive flights, and symptoms can persist for hours after the exposure ends.

The result is anaemic hypoxia (hypaemic; the FAA says hypemic hypoxia): the air in the lungs holds normal oxygen, but the blood cannot carry it. Three consequences follow.

• Descent does not cure it. Only fresh air and, where available, oxygen reduce the load, and even then slowly.
• It adds to altitude hypoxia. The mild hypoxia of a cabin altitude of 8,000 to 10,000 ft accentuates the effects of carbon monoxide, and FAA material warns that susceptibility increases with altitude.
• The usual warning signs mislead. Carboxyhaemoglobin is bright cherry red, so the skin and lips flush instead of turning blue. A pulse oximeter reads it as oxygenated haemoglobin, so a normal saturation reading does not rule out poisoning.

Smokers carry the problem with them. A pilot who smokes 20 cigarettes a day has about 7 per cent carboxyhaemoglobin before take-off. ATPL texts equate this with the loss of oxygen-carrying capacity at 4,000 to 5,000 ft, so in a cabin pressurised to 6,000 to 8,000 ft the smoker reacts as if at up to about 12,000 ft. The same habit degrades night vision by about 20 per cent (see the eye and vision).

Symptoms and detection

Carbon monoxide poisoning develops insidiously. The first symptoms are typically:

• headache, or a feeling of tightness across the forehead
• nausea
• dizziness and drowsiness.

As exposure continues they progress to impaired vision, lethargy, impaired judgement and memory, personality change, slowed breathing, a weakening pulse and loss of muscular power, then convulsions, unconsciousness and death. Passengers are affected at the same time, and a passenger's nausea may be the first clue.

The gas itself gives no warning. Where there is a smell of exhaust, it comes from other combustion products and is the only sensory clue; its absence proves nothing. The symptoms overlap with those of altitude hypoxia, so a pilot with a headache and drowsiness at 4,000 ft with the heater on should suspect carbon monoxide, since hypoxia is not credible at that level.

A carbon monoxide detector gives an objective warning. The cheapest type is a chemical spot or card mounted on the panel, whose sensing spot darkens towards grey or black as CO accumulates. It warns only if the pilot looks at it, and it must be replaced when it expires. Electronic detectors sound an aural or visual alarm at a set concentration and are more reliable. The FAA recommends a carbon monoxide detector in the cabin of general aviation aircraft, alongside regular inspection of the exhaust system.

For the certification of transport aeroplanes, CS 25.831 and 14 CFR 25.831 regard a carbon monoxide concentration above 1 part in 20,000 parts of air (50 ppm) as hazardous. ATPL systems texts give the same figure as the limit of the British Civil Airworthiness Requirements (BCAR).

Actions for suspected CO poisoning

The AIM tells a pilot who smells exhaust, or who has a headache, drowsiness or dizziness while using the heater, to shut off the heater immediately and open the air vents. EASA and FAA training material gives the same sequence:

1. Cabin heat off, to stop further intake.
2. Fresh air on: all vents open, and a storm window if fitted, to flush the cabin.
3. No smoking.
4. Oxygen, if it is carried.
5. Land as soon as possible.

Because carboxyhaemoglobin clears slowly, the landing is still needed after the symptoms seem to ease. The AIM advises medical treatment if symptoms are severe or continue after landing. The aeroplane should not fly again until its exhaust system has been inspected.

Fume events and TCP

In most jet transports the cabin is supplied with bleed air taken from the engine or APU compressors. It is cooled in the air conditioning packs and then mixed with recirculated cabin air (see air conditioning packs). The compressor shafts run in oil-lubricated bearings behind seals. If a seal degrades, engine oil can leak into the compressor air and reach the cabin as smoke, haze or an oily or chemical smell. This is a fume event, also called cabin air contamination. Hydraulic fluid, de-icing fluid and exhaust ingested on the ground can contaminate the supply in the same way.

Synthetic turbine oils contain organophosphate anti-wear additives, commonly tricresyl phosphate (TCP). Hot oil fumes can therefore carry TCP and other decomposition products into the cabin. Reported crew symptoms include eye and throat irritation and impaired concentration. The long-term health effects of such exposure remain the subject of research.

The flight crew's first priority is to protect themselves so that they can keep flying the aircraft. They don their oxygen masks with the regulator at 100 per cent, which closes the air-dilution inlet so that no cabin air is breathed (see crew oxygen systems). They then follow the operator's smoke and fumes procedure. It typically identifies and isolates the source, for example the affected engine bleed or pack, and leads to a diversion if the fumes persist (see in-flight fire, smoke and fumes). The event is reported afterwards so that engineers can trace the source.

Ozone and cabin humidity

Ozone is a form of oxygen with three atoms in each molecule. It is toxic when breathed: it irritates the lungs, causes severe headaches and impairs night vision. Its concentration increases above about 40,000 ft. In winter, when the tropopause is low, ozone-rich air can reach normal cruising levels (see the atmosphere). Above 50,000 ft normal concentrations exceed tolerable limits, and the air must be treated before it enters the cabin. The heat of compression breaks much of the ozone down, and many jet transports also have catalytic converters in the air supply. Cabin ozone concentration is one of the cabin air standards transport aeroplanes are certificated against (CS 25.832 and 14 CFR 25.832).

Cabin humidity is low because the outside air at cruising levels holds almost no water: at 40,000 ft its relative humidity is only 1 to 2 per cent. The air conditioning removes still more, and the occupants' breath adds little. On long flights cabin relative humidity typically falls to 5 to 15 per cent. Human performance texts give 40 to 60 per cent as the range for comfort, while aircraft systems texts put the ideal cabin humidity nearer 30 per cent. Most aircraft do not regulate humidity at all. Some long-haul aircraft carry humidifiers that atomise drinking water into the supply air, and the Boeing 787 has cabin humidification.

The effects are discomfort more than danger:

• dry mucous membranes in the nose and throat
• sore eyes, as the tears evaporate
• a gradual loss of body water over a long duty.

Caffeine and alcohol add to the dehydration, so crews are advised to drink enough fluid during the flight.

Cosmic radiation and dose limits

Cosmic radiation is ionising radiation from space. Its steady component, galactic cosmic radiation, consists of high-energy particles from outside the solar system; the sun adds particles of its own during large solar eruptions. The atmosphere and the Earth's magnetic field are the shield. The magnetic field deflects most particles, giving the greatest protection at the equator and declining to almost none near the poles. The atmosphere above the aircraft thins with height. Dose rates therefore increase with altitude and with latitude, and are highest on polar and high-latitude routes flown at high cruising levels (see polar navigation).

The sievert (Sv) is the unit of effective dose, which weights the energy absorbed from radiation by its biological effect. Doses to aircrew are expressed in millisieverts (mSv), thousandths of a sievert. The International Commission on Radiological Protection (ICRP) is the independent international body whose recommendations underlie national and European radiation protection law. Its dose limits are:

In the European Union, aircrew exposure is regulated as occupational exposure under the Basic Safety Standards Directive, 2013/59/Euratom. For crew liable to receive more than 1 mSv a year, the operator must:

• assess their exposure
• take the assessed exposure into account when drawing up rosters, to reduce the doses of the most exposed crew
• inform them of the health risks their work involves
• give specific protection to pregnant crew members.

ATPL texts add that individual monitoring applies to crew likely to exceed 6 mSv a year. In the United States the FAA gives guidance rather than regulation, in Advisory Circular 120-61B.

Library articles are written for study and exam preparation. They do not replace your aircraft's approved documentation, your operator's procedures or the regulations themselves.