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Although this article is related to camping, I found it to be the most descriptive of the physical and neurological damaging effects of CO.
SHootie
Carbon Monoxide Hazards with Backpacking Stoves
Carbon monoxide (CO) poisoning in tents is a real danger for those that use lanterns or stove in tents and snow caves. CO is an odorless, tasteless, colorless, nonirritating gas formed by the incomplete combustion of stove fuels and has a way of sneaking up on unsuspecting campers. This poisonous gas can cause minor symptoms such as headache, nausea and fatigue, but can also result in long-term cognitive impairment or death. Between 1990 and 1994, there was an annual reported average of 30 fatal CO poisonings in tents or campers in the USA. And judging from the frequency and amount of deaths caused by using stoves in enclosed spaces, it would seem that the deadly dangers of using a stove in a tent are not common knowledge.
Disclaimer on the following information -
The following information is based on educated speculation by a non-expert on information from many sources. Much of research supporting the following is based on experiments done in cardboard boxes on not on actual or realistic outdoors situations. The majority of the supporting documentation on this page seems creditable and authored by respected authorities but these authors may have limited knowledge of stove use, flame theory and little or no outdoors experience. References are provided so that you can research this matter further and come to your own conclusions.
If you would like to skip all of the technical mambo jumbo and get straight to the skinny - the Recommendations for Avoidance are straight and to the point.
Pathophysiology
Effects of CO Poisoning
CO Accumulation and Altitude
CO Poisoning and Campers
Recommendations for Avoidance
Holes in the Research
References
Pathophysiology
Your body uses blood to transport and remove various nutrients and waste products to and from the tissues of your body. One of the most important aspects of blood is it's ability to continuously deliver oxygen. This is done with red blood cells that are packed full of special proteins called hemoglobin. The hemoglobin are designed to "grab" on to oxygen molecules as they diffuses across the pulmonary capillary membrane in the lungs. It then holds on to oxygen as the blood flows through the body and is able to unload it where needed in your body.
CO can rapidly diffuse across the pulmonary capillary membrane in the lungs and like oxygen binds to hemoglobin. CO in fact is able to bind with hemoglobin about 200-250 times better than oxygen. When hemoglobin binds with CO it forms a complex called carboxyhemoglobin (COHb). And depending on how much carboxyhemoglobin is in your blood determines your level of carboxyhemoglobinemia (also referred to as COHb), the level of total CO bound to red blood cells. Non-smokers can have as much as a 3% COHb under normal environmental conditions, while smokers may have as much as 10-15%.
When CO binds to an oxygen binding site on hemoglobin it changes the shape of the other three oxygen binding sites on that protein, which makes it very difficult for oxygen to attach to it and to off-load oxygen to peripheral tissues. This drastically impairs the amount of oxygen that is delivered to your tissues and brain. The higher your COHb, the lower the amount of oxygen that can be delivered to your brain, heart and other tissues.
To make matters worse, about 10-15% of the CO in your body will bind to other molecules in your body such as myoglobin, cytochromes, and NADPH reductase. CO will stay bound to these molecules much longer than it does to hemoglobin and particularly affects the function of your bodies cells by impairing oxidative phosphorylation at the mitochondrial level. Because of this, high oxygen demand organs (i.e. heart, brain and lungs) with bound CO will be unable to perform at optimal levels even with clearing of CO from the blood and with good oxygen flow.
CO poisoning also may cause several other problems such as reperfusion injury from partially reduced oxygen species produced during hyperperfusion. Xanthine dehydrogenase is converted by CO to xanthine oxidase, which produces damaging oxygen radicals that basically raise hell in cells. Guanylyl cyclase is activated by CO to produce cyclic GMP, and nitric oxide synthase, which makes NO that in turn appears to affect regulation of diameter in resistance vessels and therefore causes perfusion problems.
A very small portion of CO (less than a percent) will remain in gaseous from in the blood and is believed to contributes to the neurocognitive manifestations of CO poisoning with possible direct damage to brain tissues. CO acts as a gaseous neurotransmitter that affects respiration rate, heart rate, vasodilation, learning, memory and long-lasting adaptation to sensory stimuli (esp. odors). Exposure to CO can also cause reversible demyelinization of central nervous system lipids due to lipid peroxygenation.
The effects of CO toxicity are not short lived. At sea level, it takes 4-5 hours of normal breathing to eliminate half of the CO bound to your hemoglobin and much longer to clear other tissue. At higher altitudes it takes much longer to breath off the build up CO in your blood. And since the effects of CO accumulation is cumulative, a trip spanning several days can easily lead to severe CO poisoning. There are also problems with long term and delayed toxicity that may last longer than a year.
Effects of CO Poisoning
The effects of CO poisoning varies greatly from person to person and is largely vague. The lips and skin can appear "cherry red" with high COHb levels, but this is a poor assessment tool to use.
The follow table shows some of the symptoms associated with certain serum levels of COHb, and real life situations will vary greatly from person to person and situation to situation.
General Effects of Various COHb levels at sea level
0-10%
Generally does not cause symptoms for health folks.
10-20%
Mild frontal headache, malaise, nausea, vomiting, dizziness and loss of manual dexterity
20-30%
Headache with rapid heartbeat, confusion, lethargy, visual disturbances.
This level may lead to death as the victim loses both the interest and the ability to leave a danger area (such as fire)
30-40%
Collapse
40-50%
Seizures
50-60%
Coma
60-70%
Death in 2 hours
80-90%
Death in less than 1 hour
90-100%
Death in minutes
Leigh-Smith S. Carbon monoxide poisoning in tents--a review. Wilderness and Environmental Medicine. 2004 Fall;15(3):157-63. and other sources
The level of CO exposure considered safe varies from guideline to guideline. OSHA in the States now sets the limit at 50 ppm over an 8 hour work day while other countries set limits at 30-35 ppm. The maximum amount of CO allowable in the work area (for short term exposure) is generally between 100-200 ppm, again dependant on regulating agency. The following graph depicts predicted levels of COHb vs. duration of various levels of CO for a sedentary (not breathing hard) male at sea level.
Log(%COHb) = 0.858log[CO] + 0.63log(t) - 2295 (Peterson JE, Stewart RD: Predicted the carboxy-hemoglobin levels result from carbon monoxide exposure. J Appl Physiol 1975;39:633-638.)
This chart is a bit misleading since it appears that the CO concentrations that you are likely to experience in a tent (up to 600 ppm) will only cause nausea and headaches. Note that the amount of COHb at sea level it takes to give you a headache, is the same level that will cause you to collapse at higher altitudes. It is also important to note that COHb levels are also accumulative and will build up over time with each exposure to CO.
Delayed Neurologic Sequelae
There is also a risk of delayed neurologic sequelae (DNS) 3-240 days after apparent recovery of 40% of patients with significant CO exposure. DNS includes various degrees of impaired cognition, memory dysfunction, vertigo, ataxia, parkinsonism, muscle rigidity, gait disturbance, disorientation, mutism, urinary incontinence, fecal incontinence, cortical blindness, hearing loss, tinnitus, nystagmus, seizures, coma, electroencephalographic abnormalities, cerebral edema, leukoencephalopathy, diabetes insipidus and globus pallidus necrosis. These deficits may persist for a year or longer.
Brain Syndrome associated with Delayed Neurologic Sequelae
Psychiatric Symptoms
% of Patients
Apathy
100
Disorientation
100
Amnesia
100
Hypokinesia
95
Mutism
95
Irritability, distractibility
91
Apraxia
76
Bizarre Behaviors - silly smiles or frowning
70
Mannersitic Behavior
41
Irrational Confabulatory Talking
30
Insomnia
19
Depressed Mood
15
Delusions
12
Echolalia
2
Elated Mood
2
Neurological Symptoms
Urinary and/or fecal incontinence
93
Gait disturbance
91
Glabella sign
91
Grasp reflex
87
Increased muscle tone
86
Retropulsion
72
Increased DTR
22
Placid paralysis
19
Tremor
14
Dysarthria
9
Min SK. A brain syndrome associated with delayed neuropsychiatric sequelae following acute carbon monoxide intoxication. Acta Psychiatr Scand. 1986 Jan;73(1):80-6.
Chronic Carbon Monoxide Poisoning
People exposed to low levels of carbon monoxide for long periods can develop chronic CO poisoning, which can be a very serious problems. Fatigue, headache and dizziness are the three most common symptoms, but chronic symptoms also include flu-like illness, headaches, tearfulness, depression, agitation, anxiety, decreased memory, attention and concentration skills, poor reasoning skills, irritability, euphoria, and overall personality changes.
Chronic CO poisoning can be extremely difficult to diagnose and is often confused with chronic fatigue syndrome, multiple chemical sensitivity, fibromyalgia, malingering, anxiety and depression. Since symptoms are vague and COHb levels are often unremarkable, psychometric testing may be required to identify problems. An MRI, CT or SPECT scan may demonstrate abnormalities, but may not demonstrate any problems early on in poisoning.
English Translation
Carbon monoxide binds to blood cells and cause people to asphyxiate. If you don't die from it right away, carbon monoxide can cause a lot of other long term problems like pooping in your pants.
CO Accumulation and Altitude
The higher you go above sea level, the lower the barometric and oxygen pressures become. Since our lungs are designed to utilize the gradient created by the greater oxygen pressures outside of our body than inside, a drop in inhaled oxygen pressures has a detrimental affect on how much oxygen gets in to our blood and to our tissues. A decrease in the amount of oxygen diffusing into the blood, and therefore being transported throughout your body, can have severe effects on high oxygen dependant tissues and organs, such as the brain and heart. To further complicate things, burning a stove in an enclosed space consumes oxygen, which in turn lowers the partial pressure of oxygen and amplifies the decreased oxygen (hypoxia) that may already be present at altitude.
Model Atmosphere equation: PB = exp(6.63268 - 0.1112 h - 0.00149hh), where PB is barometric pressure in Torr and h is altitude in km
It is true that there are people who have summited the highest point of the world without supplemental oxygen, but this is far from the normal abilities of the human body and not without ill and long term consequences - such as the far greater occurrence of death during decent compared to those using oxygen. Even at altitudes of just 10,000 feet (3000 meters), people start to feel the effects of altitude and may suffer from the affects of lack of oxygen (hypoxia). At and above these altitudes, one should be concerned with the many problems directly associated with this drop in atmospheric pressures (i.e. acute mountain sickness, high altitude pulmonary edema and high altitude cerebral edema).
Data Plotted from study of 11male and 2 female acclimated mountain climbers by Tannheimer M, Thomas A, Gerngross H. Oxygen saturation course and altitude symptomatology during an expedition to broad peak (8047 m). Int J Sports Med. 2002 Jul;23(5):329-35.
Since the CO bound to your hemoglobin decreases the amount of available O2 you can pull out of the air, the higher your COHb, the lower your body's blood oxygen level. Even small amounts of CO in your body can have severe affects on your ability to function at higher altitudes. COHb levels that may only cause slightly noticeable problems at sea level can be very deadly at high altitudes. In one experiment (Forbes WH, Sargent F, Houghton FJW. The rate of carbon monoxide uptake by normal men. Am J Physiol. 1945;143: 594-608.) four out of seventeen healthy subjects at a simulated altitude of 4725 meters (15,500') collapsed when their COHb reached between 9-19%.
Predicted COHb and O2Hb saturation in regards to altitude calculated from oxygen blood saturation findings of 11male and 2 female acclimated conditioned mountain climbers by Tannheimer M, Thomas A, Gerngross H. Oxygen saturation course and altitude symptomatology during an expedition to broad peak (8047 m). Int J Sports Med. 2002 Jul;23(5):329-35.
Note: graph doesn't take into account several variables such as increased basilar CO production, lack of attitude acclimation, erratic respiratory cycles at high elevations, inability to compensate even with 100% O2 and factors that may only be applicable to high altitudes. In fact, the formula used to make this chart may not reflect real life oxygen saturation levels.
Increases in altitude amplify the dangers of CO exposure several ways. First off, the decreased levels of oxygen pressures at higher altitudes will further decrease the amount of oxygen the blood can hold in a CO taxed system. Decreased oxygen pressures also CO to take longer to clear from your body. At higher altitudes, you also create more CO and breath faster, which causes you to inhale more CO from a burning lantern or stove.
Those who have been at high altitudes for long periods should develop more red blood cells and hemoglobin and will therefore accumulate more CO than someone not acclimated to higher elevations. This allows for the built up of higher amounts of CO in the blood which increases the half-life of COHb, causing it to linger in the body longer.
Those at high altitudes are also more likely to be subjected to harsh cold (the lack of oxygen adds to this), hazardous precipitation and wind which increased the likelihood that these travelers will zip up their tents or block off ventilation to snow caves. Tents at higher altitudes are also subject to icing over or being covered in snow. All of these factors decrease the ventilation and increase concentrations of CO in shelters. At higher altitudes, climbers may opt to use snow caves in lieu of tents, which provide even worse ventilation than tents. The dehydration and cold experienced in many high altitude settings may also increase the frequency of firing up a stove for a brew or heat.
People at high altitudes act weird anyways due to the lack of oxygen and fatigue, and the signs of CO poisoning are often dismissed as just fatigue and/or acute mountain sickness. This is a problem as CO intoxicated individuals may not realize their condition and continue to expose themselves to high levels CO. It's also important to note that it's not only affixation caused by CO poisoning that will kill you. CO poisoning can create various neurological problems and premature fatigue that could cause a climber to fall off of a cliff and plummet to his death, scattering body parts and very expensive mountaineering gear across the white jagged landscape.
One Norwegian study (see Thomassen below) exposed 7 healthy young nonsmoking male subjects to 2 hours of melting snow with an Optimus 111 stove in three different tents at a campsite 200m (650') above sea level . They all ended up with COHb levels of greater than 20%. At that low elevation the subjects were already experiencing signs of CO poisoning from their burning stove and were subject to the possible long term neurologic damage and potentially deadly CO levels. Exposure to similar levels of CO at greater elevations is a sure invitation to a very dreary death. |
