Having personally been badly poisoned by CO several times, I highly recommend your careful attention to this article and the under-appreciated risks of CO poisoning! Aeromedical issues are also a traditionally weak area on all FAA Flight Tests. To manage this silent killer, my personal recommendation is a pair of the new "Delta Zulu" Lightspeed Headsets (wearable technology). These literally saved my life. These headsets are especially valuable for CFIs climbing into so many unfamiliar aircraft! Manage risk: D.St.G.
Carbon Monoxide is a byproduct of combustion of fuels, wood, propane, and charcoal. All culprits we need to produce energy. One form of combustion in the powerplant is applied directly to the propellor in the form of thrust, while the other is in the form of heat. Lurking within the confines of these two is carbon monoxide, a colorless, odorless, and tasteless gas. Environmental carbon monoxide is a byproduct of incomplete combustion of any carbon-containing fuel. In an unventilated environment even on the ground, it is the cause of around 430 fatalities and 100,000 Emergency Room visits per year.
In General Aviation piston-powered aircraft, the cabin heating during winter or at altitude is done by ram air directed over the engine muffler (discontinued in automobiles years ago). Any poor-fitting components, cracks or holes, unsealed firewalls, and even poorly sealed wheel wells, will allow the carbon monoxide generated during the combustion process to escape and mix with the heated ram air and enter the cabin.
Limits
The established limit of exposure in most healthy individuals is 0 – 10 parts per million (ppm). Smokers carry a higher limit to 20 – 40 ppm. OSHA considers 100 ppm in unventilated spaces as unhealthy and/or prolonged exposure of 55 ppm for 8 hours or longer.
In 2022 based on 31 accidents of which 23 were fatal, between 1982 and 2020 the NTSB recommended to the FAA to require CO detectors in the cockpit. At the first instance of recognition, the pilot must use these common-sense recommendations; Turn the heat Off. Open fresh air ventilation to the cabin. Consider supplemental Oxygen if available. Land as soon as practicable. Advise ATC. If able run the engine Lean of Peak (to allow complete combustion of fuel). Seek medical attention upon landing and have the aircraft checked by a mechanic before the next flight.
A little Physiology
Hemoglobin is in the Red Blood Cells (RBC). It has two components; the oxygen transport protein (globin) attached to the iron (heme). The heme has an affinity for oxygen and sterically attaches and then dissociates to take in (oxygen from breathed air) and give out oxygen (delivered to the tissues) respectively. The hemoglobin gives blood its red color.
The Carbon Monoxide has a 200 – 300 times stronger binding ability to hemoglobin as compared to Oxygen. CO latches onto hemoglobin (selective binding) and that is called “carboxyhemoglobin.” This combination leads to a left shift of the “oxyhemoglobin dissociation curve,” which leads to less oxygen availability. In fact, at the 50% level of CO contamination, the Oxygen partial pressure is reduced from 28mmHg to 12 mmHg, hence the lowered oxygen-carrying capacity of the blood. The reduction of this partial pressure reduces the transport of oxygen across the membranes to the tissues. (Akin to high-pressure water across a screen versus low-pressure water source). In general, 40% CO levels are not associated with coma or death, but they can have long-standing pathological neuro-psychiatric as well as disabling pathological effects on humans. The individuals most affected by such hazards of moderate CO exposure are those with heart disease and lung ailments. It is important to remember that the elderly and those in poor physiological state, even those with <30% CO exposure can develop insidious long-term neuropsychiatric disorders 3 – 4 weeks after the acute exposure and these can be permanent in 10-30% of the exposed individuals.
The CO effect on Oxygen Dissociation Curve
CO poisoning is stealthy and quite misleading in terms of visible signs. The exposed individual can have the physiological manifestation of moderate to severe tissue hypoxia (low oxygen level) and yet present with normal PaO2, headache, fatigue, cherry red lips, confusion, shortness of breath and even seizures. Due to the normal PaO2 levels although at much lowered partial pressure, the pulse oximeter is not a reliable means to detect CO poisoning. The pulse oximeter detects light absorption based on the oxygen content of the tissues, which can be hampered by nail polish, low blood flow states etc. Therefore, it is an unreliable method to detect the difference between Oxyhemoglobin and carboxyhemoglobin! The only reliable means is a CO monitor with a functioning sensor.
A little Chemistry
The difference between oxygen and carbon monoxide binding is illustrated simply based on the angle at which the two molecules bind. Oxygen binds sterically at an angle to the heme (carbon – iron-binding), while the CO binds perpendicularly to the plane of the (porphyrin) ring via the carbon – iron-binding) and this favors CO for hemoglobin binding. The two oxygen atoms create a hindrance (steric) with each other.
One might ask, what about Carbon Dioxide? Interestingly Carbon Dioxide does not compete with Oxygen because as Oxygen binds to the heme, Carbon Dioxide (CO2) binds non-competitively with the protein structure.
A Little Altered Physiology
Acute CO Poisoning leads to a rash of symptoms that include the following:
- Air hunger
- Confusion
- Chest pains (Angina) in compromised individuals.
- Dizziness
- Drowsiness
- Fainting
- Fatigue
- Lethargy
- Headache
- Irritability
- Palpitations (fast heart rate)
- Nausea and Vomiting
- Convulsions
- Cardiovascular Shock
- Coma
- Death
Important to remember that a low-level long long-duration exposure can lead to symptoms mistaken for an influenza or viral syndrome without fever.
The organs mostly affected by CO Poisoning are the ones we depend upon the most. The Heart and the Brain. The Heart has cells called Cardiomyocytes that possess cardio-myoglobin or heart muscle cells that have a high affinity for carbon monoxide. This affinity pushes away the oxygen required by the heart muscle to function and leads to heart muscle fatigue, cardiac dysfunction, and erratic electrical transmission through the heart, leading to an errant heartbeat and sudden death. In the brain, a similar result occurs where lack of oxygen in the brain cells leads to cellular collapse and the resultant loss of cognition, confusion, convulsions, and death as a final consequence. Long-term low exposure states can exhibit, memory loss, personality changes, and disorders of movement (gait etc.)
A Little Treatment
Remembering that CO forms a permanent non-dissociative complex with hemoglobin called carboxyhemoglobin, and the binding is irreversible with its 200 – 300 times affinity it overwhelms and limits the oxygen transport to organs, therefore the treatment must be immediate and “overwhelming” in nature. The half-life of carboxyhemoglobin is 74 minutes (based on the red cell turnover), hence the treatment must be sustained with…
- 100% Oxygen administration
- Hyperbaric Oxygen along with Carbon Dioxide.
- Intravenous Fluids
- Electrolyte replacement
- Arterial Oxygen level and lactic acid monitoring
- Electrocardiogram
- Chest X-Ray
- Medicines to treat symptoms.
The 100% Oxygen sustained use is based on the work of Haldane in 1895 who kept mice alive with 100% oxygen (hyperbaric) along with CO exposure, thus proving that sustained Oxygen use can allow enough of it to keep oxygen transport to the tissues.
The future might be a little different if Jeffery Long at the University of Berkley has his way. He has developed a MOF a metal-organic framework – an amazingly porous material with a growing list of applications – that incorporates chains of iron atoms tuned to attract CO and exclude other chemical compounds. Embedding the material in the cockpit of an aircraft might be a solution for saving potential lives in the future.
We are flying in the cold part of the year. Have an astute mechanic check your engine compartment for leaks, Buy a good CO Monitor (or those “Delta Zulus”). Have your current detector checked or serviced (if needed). Carry a pulse oximeter if you fly at altitudes. Always remain aware of the invisible hazard that lurks quietly with you in your airplane.
Here’s to Safe flying and looking forward to the future in aviation.
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REFERENCES:
- Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR. Carbon monoxide poisoning — a public health perspective.Toxicology 2000;145: 1-142
- Department of Health, London. Carbon Monoxide: the Forgotten Killer. Letter from the Chief Medical Officer, PL/CMO/98/5. London: DoH, 1998
- Haldane JS. The relation of carbonic oxide to oxygen tension. J Physiol (Lond) 1895;18: 201-7
- Meaden CW, Nelson LS. Inhaled toxins. In: Walls RM, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 10th ed. Philadelphia, PA: Elsevier; 2023:chap 148.
- Hampson NB. Pulse oximetry in severe carbon monoxide poisoning. Chest. 1998 Oct;114(4):1036-41.
- Lehninger Principles of Biochemistry 5th Edition
