Background on Sources,
Symptoms, Biomarkers and Treatment of
Chronic Carbon Monoxide Poisoning
by Albert Donnay, MHS, Environmental
President, MCS Referral & Resource
"And have I not told you that what you mistake for madness is but overacuteness of the senses?"
Edgar Allan Poe, The Tell-Tale Heart, 1843
CO poisoning has long been known as the Great Imitator in medicine since its symptoms may mimic of those of many other disorders, including:
Alzheimer's · Addison's · Anemia · Asthma · Attention Deficit Disorder · Autism · Chronic Fatigue Syndrome · Depression · Dysautonomia · Fibromyalgia · Irritable Bowel Syndrome · Lupus (SLE) · Migraine · Multiple Chemical Sensitivity · Multiple Sclerosis · Neurally Mediated Hypotension · Panic Disorder · Parkinson's · Psychoses · Reactive Airways Dysfunction Syndrome · Reflex Sympathetic Dystrophy · Stress
Research into many of these disorders suggest that they may be caused by CO poisoning, and thus also possibly helped by CO treatments.
- Sources of Carbon Monoxide (CO)
- Symptoms of Chronic Low-Level CO Poisoning
- Biomarkers of Chronic Low-Level CO Poisoning
- Treatment of Chronic Low-Level CO Poisoning
Carbon monoxide is and has been the most common cause of both accidental
toxic poisoning and death in the United States for over 100 years. This
protocol is meant to assist physicians, respiratory therapists, and other
medical professionals in diagnosing and treating cases of chronic low-level
CO poisoning as defined by specific symptoms and objective biomarkers.
It should not be used for self-diagnosis or self-treatment, or as a substitute
for professional medical advice.
Note that pure oxygen can be obtained only by prescription except in the
case of emergencies.
October 2006, 10th edition.
(c) 2000-2006 MCS Referral & Resources, 410-889-6666
Physician referrals and patient testimonials available upon request. Comments and suggestions are welcome.
1. SOURCES OF CARBON MONOXIDE
Exogenous Sources of Carbon
Monoxide (from outside the body)
monoxide (CO) is produced from the incomplete combustion or burning of
any fuel. Indoor exposures obviously are of greater concern than outdoor
ones, as they are more likely to pose a risk to human health. The primary
sources inside US homes and apartment buildings are smoking, unvented
gas ranges and vehicles started in attached but unvented garages. Other
CO sources include gas and oil furnaces, water and space heaters, ovens,
wood and coal stoves, wood and coal fireplaces, gas-log inserts and explosives.
Even electric ovens can produce CO when cooking some foods and always
do so in self-cleaning mode when baking off spilled food.
human body also breaks down some inhaled and ingested chemicals into
CO, including ubiquitous dichloromethane (a common solvent especially
in paint strippers and the most common propellant used in consumer product
CO is odorless, colorless and tasteless, the only way to protect people
from potentially fatal exposures is with a CO Detector, Monitor or CO
Alarm (see Resources, below). While detectors and monitors can measure
CO down to 1ppm (monitors do so continuously), CO alarms are barred by
current UL and IAS standards from giving any digital readout below 30ppm
or alarming below 70ppm. While there are no legal limits for indoor exposure,
U.S. EPA regulations limit CO outdoors to an average 9 parts per million
over 8 hours and 35 ppm maximum over 1 hour.
Sources of Carbon Monoxide (from inside the body)
of any kind induces increased production of heme oxygenase-1 (HO-1),
the so-called "universal stress enzyme" found throughout the body, which
breaks down heme from heme proteins into iron, biliverdin (which is then
converted into bilirubin, a potent anti-oxidant), and carbon monoxide.
The stresses that have been shown to induce HO-1 in animals and humans
include heat, light, sound, odors, electromagnetic fields, infection,
physical trauma and mental or psychological stress. Chronic stress in
any of these pathways thus results in chronic destruction of heme and
chronic low-level CO poisoning. The ability of so many different types
of physical, biological, chemical and mental stressors to induce HO-1
explains why the core symptoms of chronic stress are so similar to CO
poisoning regardless of the stressor (see Symptoms, below). Stress-induced
HO-1 activity and the relatively constant activity of another isozyme,
HO-2, that does not respond to stress, together account for about 75%
of the human body's CO production. Other sources of CO include the auto-oxidation
of phenols, flavenoids and halomethanes, the photo-oxidation of organic
compounds, and the lipid peroxidation of membrane lipids.
activity can be directly measured in blood and various organs but of
course varies widely, while endogenous CO levels, which also include
any exogenous contribution, can be measured directly in breath, blood
or muscle. The most commonly measured carboxyhemoglobin level (COHb) only
identifies the percent of hemoglobin that is bound to CO, but this is
normal in cases of chronic low-level CO poisoning, and even in acute
cases not consistently related to symptoms.
2. SYMPTOMS OF CHRONIC LOW-LEVEL CARBON MONOXIDE
arising from exogenous or endogenous sources, CO in the human body may
be used or stored in several different ways until it is finally exhaled.
CO binds much more aggressively than oxygen to all heme proteins, especially
to hemoglobin (Hb). In doing so, it reduces the number of Hb binding
sites available for carrying oxygen and makes the remaining oxygen bind
more tightly. In muscle, CO binds more aggressively than oxygen to myoglobin
(the main heme protein in muscle) and so interferes with oxygen use during
exercise, especially in cardiac muscle.
activates guanylyl cyclase, which produces cyclic GMP, and nitric oxide
synthase, which makes NO, but it also impairs mitochondrial energy metabolism
and the function of cytochromes needed for detoxification. CO also triggers
oxidative vascular stress (via endothelial cell production of NO and
peroxynitrite) and brain lipid peroxidation. Most significantly, CO acts
as a gaseous neurotransmitter in modulating many critical functions including
respiration rate, heart rate, vasodilation, learning, memory and long-lasting
adaptation to sensory stimuli (esp. odors).
chronic low-level CO poisoning impairs oxygenation of tissue, any organ
may be affected, with the brain, heart and lungs being most sensitive
to the effects of CO. The most common symptoms of chronic CO poisoning
are actually the same as those of acute poisoning, except that they may
vary considerably over time as they wax and wane in response to not just
exogenous CO exposures but also in response to any chronically stressful
stimuli, since all such stimuli induce HO-1 to breakdown heme proteins
into CO (see Endogenous Sources, above).
Symptoms of Carbon Monoxide Poisoning
- Fatigue, Weakness
- Muscle Pain, Cramps
- Nausea, Vomiting
- Upset Stomach, Diarrhea
- Confusion, Memory Loss
- Dizziness, Incoordination
- Chest Pain, Rapid Heartbeat
- Difficult or Shallow
- Changes in Sensitivity
of Hearing, Vision, Smell, Taste or Touch
these symptoms are common to so many disorders, no single one is considered
diagnostic of CO poisoning, but CO should be suspected whenever a majority
of these symptoms are reported together and no other cause is determinable,
especially if the same symptoms are reported by more than one occupant
of the enclosed space (building, vehicle, boat or plane).
A far more discriminating
set of 30 symptoms appears in Edgar Allan Poe's classic 1839 tale, The
Fall of The House of Usher, which we propose may be read as a literal
description of chronic CO poisoning. Poe most likely suffered CO poisoning
from his exposure to the coal gas that was used in the 1800s for indoor
lighting. People with chronic CO poisoning today report having an average
of 27 of these 30 symptoms in the last month, compared to healthy normal
controls who average 2.
Poe's 30 Chronic CO Symptoms
1. "ghastly pallor of the skin... a cadaverousness of complexion"
2. "miraculous lustre of the eye"
3. "gossamer texture" [of hair: soft,silky]
4. "nervous agitation"
5. "alternately vivacious and sullen"
6. "voiced varied from tremulous indecision to ..."
7. "...that species of energetic concision --abrupt, weighty, unhurried, and hollow-sounding enunciation--that leaden, self-balanced, and perfectly modulated guttural utterance, which may be observed in the lost drunkard"
8. "it was, he said, a constitutional and a family evil, and one for which he despaired to find a remedy--a mere nervous affection, he immediately added, which would soon pass off"
9. "it displayed itself in a host of unnatural sensations"
10. "he suffered much from a morbid acuteness of the senses"
11. "insipid food was alone endurable"
12. "could wear only garments of certain texture"
13. "the odors of all flowers were oppressive"
14. "eyes were tortured by even a faint light"
15. "there were but peculiar sounds, and these from stringed instruments, which did not inspire him with horror"
16. "phantasmagoric conceptions ... wild fantasies"
18. "without having noticed my presence" [oblivious to comings and goings of others]
19. "he arrested and overawed attention ... an intensity of intolerable awe"
20. "radiation of gloom"
21. "painted an idea...pure abstractions"
22. "intense mental collectedness and concentration ...observable only in particular moments"
23. "roamed from chamber to chamber with hurried, unequal, and objectless step"
24. "sleep came not near my couch"
25. "gazing upon vacancy for long hours, in an attitude of the profoundest attention, as if listening to some imaginary sound"
26. "hysteria in his whole demeanor"
27. "struggled to reason off the nervousness which had dominion over me"
28. "irrepressible tremor gradually pervaded my frame"
29. "there sat upon my heart an incubus of utterly causeless alarm"
30. "overpowered by an intense sentiment of horror, unaccountable yet unendurable"
3. BIOMARKERS OF CHRONIC LOW-LEVEL CARBON MONOXIDE
There are several
biomarkers capable of identifying the impaired oxygen delivery associated
with CO exposure and tracking its response to 100% oxygen treatment. Qualitatively,
a SPECT scan of the brain shows the most dramatic evidence
of decreased blood flow in various areas of the brain that all improve
with oxygen treatment. Unfortunately, high-resolution 3-camera SPECT scans
are hard to find and expensive, with scans costing thousands of dollars
each and most health insurers unwilling to pay for them.
and much less expensively (for just $50 to $100), one can order standard
arterial and venous blood gases to compare the partial pressure
of oxygen in venous blood (PvO2) with that of oxygen in
arterial blood (PaO2). PaO2 is usually normal or low-normal in cases
of CO poisoning but PvO2 is abnormally high, indicating substantial impairment
of oxygen delivery from arterial blood plasma into tissue. Venous blood
for the PvO2 analysis should be drawn at the elbow without a tourniquet.
The optimum PvO2 level in healthy non-smoking adults is about 25mm Hg,
while levels in CO poisoning (and CFS/FMS/MCS) patients are commonly in
the range of 30 to 50. The optimum atereo-venous gap is 70 to 60mmHg: a
smaller P(a-v)O2 gap is clear evidence that oxygen delivery to tissues
and/or its uptake is impaired.
adults, the fastest, least invasive and least expensive biomarker to assess
is the concentration (in ppm) of CO in exhaled breath,
which measures the total rate of CO excretion from all sources and correlates
closely with COHb in healthy controls. This is commonly measured in smoking
cessation clinics and some emergency rooms using handheld, battery powered,
electro-chemical CO sensors with digital readouts designed for this purpose
(see Resources, below). Because a 23-second breath hold is optimal (to
allow time for CO exchange in the lungs), this test is not easily done
by young children or people with significant respiratory impairments.
In normal healthy adults, breathCO levels range from 0- 6ppm, while smokers
range from 7ppm (after 24 abstinence) to over 70ppm (immediately after
smoking). Elevated levels may be due to exogenous CO poisoning but are
also associated with a variety of chronic diseases, including asthma,
bronchitis, cystic fibrosis and diabetes. The amount of CO exhaled also
increases when breathing enriched oxygen, so recording this immediately
before and after 100% oxygen treatment provides a simple way to quantify
the impact of each session on CO elimination.
measured but least helpful is the carboxyhemoglobin level
that gives the percent of hemoglobin (Hb) binding sites occupied by CO,
arterial and venous COHb are the same because CO binds so tightly to Hb).
The CO bound to Hb is much less active biologically than the CO that is
less tightly bound to other heme proteins such as myoglobin and cytochromes
or that circulating freely in blood plasma. Although COHb is usually significantly
elevated in the hours immediately following an acute high level CO exposure--with
minor symptoms starting around 10% COHb according to most textbooks–it
usually normalizes within a few days of exposure (if not fatal) because
the biological half life of COHb is only 4 to 6 hours. COHb levels measured
weeks and months after a single acute CO exposure are usually normal (under
2% for non-smokers, under 10% for smokers) and rarely correlate with any
residual chronic symptoms. So while a high COHb level confirms significant
exposure to one or more sources of CO, a normal value cannot rule out
chronic low-level exposure. The symptoms in chronic cases are more
likely due to the myriad effects of CO in other more biologically active
pathways (binding with cytochromes, for example) than to its interference
with oxygen-binding on hemoglobin.
COHb can adjust
to great variation in CO exposure and oxygen demand, although it may take
weeks to habituate to new conditions. This is evident in how long it takes
non-smoking coast dwellers to habituate to the lower oxygen pressures
found at high altitudes compared to smokers, whose higher COHb levels
are more like those of people who live at high altitude year round and
who are more aerobically fit in such low-oxygen environments than visitors
with lower COHb levels.
4. TREATMENT OF CHRONIC LOW-LEVEL CARBON MONOXIDE
For the treatment
of chronic low-level CO poisoning evidenced by high PvO2 (regardless
of COHb level), MCS Referral & Resources recommends Extended
Normobaric Oxygen Therapy (ENOT). Three to four months of daily
2-hour sessions breathing 100% oxygen from a tank or concentrator while supine
via a nasal canulus at 6 to 10 liters per minute are usually sufficient
to normalize PvO2 and obtain lasting relief from the most common symptoms
of chronic CO poisoning. ENOT is less expensive and more widely available
than hyperbaric oxygen, which is the recommended treatment for acute CO
cases (for information on this option, contact the Undersea & Hyperbaric
Medicine Society, 301-942-2980). ENOT has fewer risks of adverse side effects
than hyperbaric therapy and may be carried on by the patient at home after
training by a respiratory therapist. Both Medicare and private insurers
are usually willing to pay for home delivery of supplemental oxygen regardless
of the source (compressed O2, liquid O2 or concentrator O2) as long as
the need is documented and consistent with a diagnosis of CO poisoning.
This protocol has not been evaluated in children (whose normal PvO2 range
is unknown) but they clearly are more sensitive to both CO and 100% oxygen.
was developed for treating adults with at least 5 of the 10 most common
symptoms of CO poisoning listed above (usually including chronic fatigue,
sensory changes and cognitive dysfunction) who also have an abnormally
elevated partial pressure of oxygen in venous blood. When drawn from the
antecubital fossa without a tourniquet, the optimal PvO2 in healthy controls
is about 25mmHg, so any PvO2 over 30, or a P(a-v)O2 gap of less than 60,
may be considered abnormal. These admittedly arbitrary cutoffs are primarily
for research purposes, however, and need not be strictly followed in clinical
practice, where physicians may want to consider other factors in assessing
the potential risks vs. benefits of oxygen treatment. Since PaO2 is rarely
significantly decreased in CO cases and more painful to obtain than venous
samples, arterial testing may be omitted unless documentation of the arterial-venous
oxygen gap is needed.
the initial PvO2 level, this should be rechecked weekly or biweekly during
treatment. Daily oxygen should continue until PvO2 either falls below
normal (25mmHg) and stays there or stops falling for two successive measurements.
Of course, if a patient is still reporting subjective improvements at
this point without adverse side effects, the treatments may be continued
until the patient no longer reports any additional benefit or need. While
no long-term studies have yet been done, anecdotal reports suggest PvO2
levels remain in the normal range and substantial symptom relief persists
for months with no need for further daily oxygen treatment. However,
physicians should consider prescribing a continuing supply of oxygen
for use as needed to relieve symptoms of any new CO exposures (most insurance
covers oxygen "as needed" for migraine if not for CO).
oxygen therapy should not be attempted in anyone who has reacted poorly
to 100% oxygen in the past. When first trying 100% oxygen, patients should
be monitored closely by their physician for sudden or dramatic changes
in heart rate, respiration, blood pressure and any reports of adverse
effects associated with oxygen toxicity (especially any respiratory,
neurologic or sensory complaints). If no adverse reactions are noted, patients
may be taught how to continue daily treatments at home on their own, with
a warning that they should immediately discontinue treatment and notify
their physician if they notice any poorly-tolerated effects.
Supplements and Diet
medications are needed to supplement extended normobaric oxygen therapy,
the treatment theoretically works best if the patient's exposures to
CO are minimized. This requires reducing exposures not just to exogenous
CO but also to all the many types of physical, biological, chemical and
mental stresses that increase endogenous CO production (via stress-induced
HO-1 catabolism of heme). Since medications and supplements are a source
of chemical stress and poorly tolerated by most people with chronic CO
poisoning and related syndromes (Autism, ADHD, CFS, FMS, MCS etc), the
protocol urges doctors to consider weaning their patients off all non-essential
supplements and medications prior to starting ENOT (including anti-depressants
except in potentially suicidal cases). While many of these patients have
significant deficiencies in vitamins (particularly the B series), minerals
(particularly magnesium and zinc) and hormones (particularly thyroid),
we recommend testing for but not treating these deficiencies until PvO2
has been normalized and the oxygen therapy concluded, as some may self-correct
with the improved oxygenation of tissue that ENOT provides. The only
exception is for buffered vitamin C or some other buffered anti-oxidant
which should be taken daily during oxygen treatment to boost the body's
ability to deal with the free radicals formed by oxidative metabolism.
Low plasma volume
should be treated concurrently with high water consumption (at least one
glass per hour except when sleeping). Since chlorinated water, alcohol,
caffeine and processed foods are all common sources of chemical stress
in these patients, they should be avoided as much as possible during the
oxygen treatment. If food intolerances have not already been identified
and eliminated, this should be done with a rotation diet prior to starting
ENOT. After their PvO2 normalizes, patients may try reintroducing a broader
range of foods one at a time.
100% oxygen has long been the standard therapy for the treatment of acute
CO poisoning (within hours or day of exposure), there are no published
studies on its extended use for the treatment of chronic CO symptoms as
described in this protocol. The references cited below address the biological
activity of CO, its role in sensory signaling, sensitization, and adaptation,
the clinical features of chronic CO poisoning, biomarkers of CO poisoning,
and oxygen treatment. They offer support for the protocol's working hypothesis,
which is that anyone with CO symptoms and impaired oxygen delivery (as
shown by high PvO2) may benefit from 100% oxygen therapy.
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S. Endothelial cell expression of vasoconstrictors and growth factors
is regulated by smooth muscle cell-derived carbon monoxide. J Clin
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RE: CO's Role
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AK, O'Dell TJ, Tonegawa S. Hippocampal long-term potentiation is normal
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and nonsmokers. Aviat.Space.Environ Med. 1988;59:928-31. [showing
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on the carbon monoxide/cGMP second-messenger system. J Neurosci. 1997;17:2703-12
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RE: Clinical Profile of Chronic Carbon Monoxide Poisoning (case series)
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Role of CO in the causation of myocardial disease. JAMA, 1938;110:1982-1986
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carbon monoxide upon the eye. Am J Opthamology, 1921; 73-90.
RE: COHb, Pulse Oximetry and pH as Unreliable Indicators of CO Poisoning
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(showing COHb is same in chronic CO cases v. controls)
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Stevenson DK, Van Kessel AL. Measurement of carboxyhemoglobin and total
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- Myers, R.A. and Britten,
J.S. Are arterial blood gases of value in treatment decisions for carbon
monoxide poisoning? Crit Care Med 1989 Feb;17(2):139-42.
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Agostini JC, Basu AP, Goldbaum LR, Absolon KB. Lack of toxicity of
transfused carboxyhemoglobin red blood cells and carbon monoxide inhalation.
Surg Forum. 1974;25:165-8.
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P., Felt, B., Greene, M., Lacovara, J. and Hackett, F. Carbon monoxide
poisoning due to automobile exposure: disparity between carboxyhemoglobin
levels and symptoms of victims. Pediatrics 1988, 82(4):663-6.
- Seger D, and Welch L.
Carbon monoxide controversies: neuropsychologic testing, mechanism
of toxicity, and hyperbaric oxygen. Ann Emerg Med 1994;24(2):242-8
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Gaydos JC. Errors in derivations of the Coburn-Forster-Kane equation
for predicting carboxyhemoglobin. Am Ind Hyg Assoc J. 1996;57:621-5.
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concentrations in various conditions of single acute exposure to carbon
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- Tikuisis P, Madill HD,
Gill BJ, Lewis WF, Cox KM, Kane DM. A critical analysis of the use
of the CFK equation in predicting COHb formation. Am Ind Hyg Assoc
RE: CO In Breath and Other
Sensitive But Non-Specific Indicators of CO Exposure or Disease
- Chan GC, Lau YL, Yeung
CY. End tidal carbon monoxide concentration in childhood haemolytic
disorders. J Paediatr.Child Health. 1998;34:447-50.
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Carbon monoxide levels in the breath of smokers and nonsmokers: effect
of domestic heating systems. J Epidemiol Community.Health. 1985;39:75-8.
- TJ, MacDonald MJ, Zerbe
GO, Petty TL. Reinforcing breath carbon monoxide reductions in chronic
obstructive pulmonary disease. Drug Alcohol Depend. 1991;29:47-62.
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I, et al. A positron emission tomography study of patients with acute
carbon monoxide poisoning treated by hyperbaric oxygen. J Neurol. 1993;240:430-4.
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I, Bell CW, Wass A. Immediate carbon monoxide estimates and self-reported
smoking. Percept.Mot.Skills. 1979;49:675-8.
- He F, Liu X, Yang S, et
al. Evaluation of brain function in acute carbon monoxide poisoning
with multimodality evoked potentials. Environ Res. 1993;60:213-26.
- Horvath I, Loukides S,
Wodehouse T, Kharitonov SA, Cole PJ, Barnes PJ. Increased levels of
exhaled carbon monoxide in bronchiectasis: a new marker of oxidative
stress. Thorax. 1998;53:867-70.
- Horvath I, Donnelly LE,
Kiss A, Paredi P, Kharitonov SA, Barnes PJ. Raised levels of exhaled
carbon monoxide are associated with an increased expression of heme
oxygenase-1 in airway macrophages in asthma: a new marker of oxidative
stress. Thorax. 1998;53:668-72.
- Horvath I, Barnes PJ.
Exhaled monoxides in asymptomatic atopic subjects. Clin Exp Allergy.
- Hunter K, Mascia M, Eudaric
P, Simpkins C. Evidence that carbon monoxide is a mediator of critical
illness. Cell Mol.Biol (Noisy.-le.-grand.). 1994;40:507-10.
- Jalukar V, Penney DG,
Crowley M, Simpson N. Magnetic resonance imaging of the rat brain following
acute carbon monoxide poisoning. J Appl Toxicol. 1992;12:407-14.
- Kirkham AJ, Guyatt AR,
Cumming G. Alveolar carbon monoxide: a comparison of methods of measurement
and a study of the effect of change in body posture. Clin Sci. 1988;74:23-8.
[showing supine CO greater than erect CO]
- Kurt TL, Anderson RJ,
Reed WG. Rapid estimation of carboxyhemoglobin by breath sampling in
an emergency setting. Vet Hum Toxicol. 1990;32:227-9.
- Paredi P, Biernacki W,
Invernizzi G, Kharitonov SA, Barnes PJ. Exhaled carbon monoxide levels
elevated in diabetes and correlated with glucose concentration in blood:
a new test for monitoring the disease? Chest. 1999;116:1007-11.
- Paredi P, Shah PL, Montuschi
P, et al. Increased carbon monoxide in exhaled air of patients with
cystic fibrosis. Thorax. 1999;54:917-20.
- Pracyk JB, Stolp BW, Fife
CE, Gray L, Piantadosi CA. Brain computerized tomography after hyperbaric
oxygen therapy for carbon monoxide poisoning. Undersea.Hyperb.Med.
- Risser NL, Belcher DW.
Adding spirometry, [breath] carbon monoxide, and pulmonary symptom
results to smoking cessation counseling: a randomized trial. J Gen
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- Stewart, R.D., Stewart,
R.S., Stamm, W., and Seelen, R.P. Rapid estimation of carboxyhemoglobin
level in fire fighters. JAMA, 235,390-392,1976.Uasuf CG, Jatakanon
A, James A, Kharitonov SA, Wilson NM, Barnes PJ. Exhaled carbon monoxide
in childhood asthma. J Pediatr. 1999;135:569-74.
- Verhoeff AP, van der Velde
HC, Boleij JS, Lebret E, Brunekreef B. Detecting indoor carbon monoxide
(CO) exposure by measuring CO in exhaled breath. Int Arch Occup Environ
- Vreman HJ, Baxter LM,
Stone RT, Stevenson DK. Evaluation of a fully automated end-tidal carbon
monoxide instrument for breath analysis. Clin Chem. 1996;42:50-6.
- Wickramatillake HD. Validation
of the end-expired method for measuring carboxyhaemoglobin levels for
the use in occupational and environmental exposure studies. Occup Med
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Ishizuka S, Monma M, Mizuta K, Sasaki H. Increased carbon monoxide
in exhaled air of subjects with upper respiratory tract infections.
Am J Respir Crit Care Med.1998;158:311-4
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Okinaga S, Yamaya M, Ohrui T, Sasaki H. Increased carbon monoxide in
exhaled air of asthmatic patients. Am J Respir Crit Care Med. 1997;156:1140-3.
RE: Effect of 100% Oxygen (O2) on Blood O2 Content, O2 Pressure (PO2)
and O2 Delivery
- Fox, S.I., Human Physiology
[5th Edition] Dubuque, IA: William C. Brown Publishers, 1996, page 478:
in blood P[a]O2 -- produced, for example, by breathing 100% oxygen from
a gas tank -- thus cannot significantly increase the amount of oxygen
contained in the red blood cells. It can, however, significantly increase
the amount of oxygen dissolved in the [arterial] plasma because the amount
dissolved is directly determined by the PO2. If the PO2 doubles, the amount
of oxygen dissolved in the plasma also doubles, but the total oxygen content
of whole blood increases only slightly, since most of the oxygen by far
is not in plasma but in the red blood cells [tightly bound to hemoglobin].
Since the oxygen carried by red blood cells must first dissolve in plasma
before it can diffuse to the tissue cells, however, a doubling of [arterial]
blood PO2 [or a halving of the venous PO2] means that the rate of oxygen
diffusion to the tissues would double under these conditions. For
this reason, breathing from a tank of 100% oxygen would signifi-cantly
increase oxygen delivery to the tissues, although it would have little
effect on the total oxygen content of blood." [comments and
RE: Treatment of Carbon Monoxide Poisoning with Normobaric 100% Oxygen
- Hardy, K.R. and Thom,
S.R. Pathophysiology and treatment of carbon monoxide poisoning. J
Toxicol Clin Toxicol 1994;32(6):613-29.
- Kirkham, A.J., Guyatt,
A.R. and Cumming, G. Alveolar carbon monoxide: a comparison of methods
of measurement and a study of the effect of change in body posture [showing
that the level of expired CO increases as the concentration of inhaled
oxygen increases]. Clin Sci 1988, 74:23-28.
- Meert, K.L., Heidemann,
S.M., and Sarnaik, A.P. Outcome of children with carbon monoxide poisoning
treated with normobaric oxygen. J Trauma 1998, 44(1):149-54.
- Scheinkestel, C.D., Bailey,
M., Myles, P.S., Jones, K., Cooper, D.J., Millar, I.L., et al. Hyperbaric
or normobaric oxygen for acute carbon monoxide poisoning: a randomized
controlled clinical trial. Med J Australia 1999; 170: 203-210.
- Tibbles, P.M., Perrotta,
P.L. Treatment of carbon monoxide poisoning: a critical review of human
out-come studies comparing normobaric oxygen with hyperbaric oxygen.
Ann Emerg Med 1994; 24:269-276.
- Weaver, L.K. Carbon monoxide
poisoning. Crit Care Clin 1999, 15(2):297-317.
of MCS Referral & Resources with link to the Poe- Awareness poster)
(links to CO webpages and discussion lists)
(Dr. Penney's CO Headquarters)
or Concentrators (capable of generating 90% oxygen at 6 liters per minute)
For home delivery
of compressed or liquid oxygen or to rent an oxygen concentrator–each
available only by prescription--check in your local yellow pages under
"oxygen" for accredited suppliers. Most accept Medicare and private insurance
as full payment, but if paid out of pocket, the total cost for oxygen,
tubing, setup, and service should be less than the $225 per month that
Medicare pays for continuous supplemental oxygen, regardless of modality
(liquid is most common). Oxygen concentrators that reach 90% O2 at 6
liters per minute–sufficient for this protocol--can be bought new for
$1000 to $2000 or used from MCS R&R for $500 (refurbished by factory
certified technicians with a full 3-year warranty, call 410-889-6666 for
details). Regardless of which option is selected, be sure a respiratory
therapist comes to the patient's home to set up and demonstrate the equipment.
This should include a regulator valve that can adjust the flow to at
least 6 liters per minute connected via flexible tubing to a cannulus
(or to a non-rebreather plastic or ceramic mask if prefered). The
flow rate, percent oxygen, and all these components should be specified
in the physician's prescription.
and Non-Rebreather Masks
cannot tolerate using standard oxygen tubing and masks because of the
chemicals these give off when new. In such cases, patients should try
using stainless steel tubing and a ceramic canulus or mask. These, and cellophane
non-rebreather bags, are available from the American Environmental Health
Fdn (800-428-2343). For those who also cannot tolerate ceramic
masks, Dr. Trep Piamonte of the Dallas Environmental Health Center makes
a small aluminum one ($35, available from him directly, 214-373-5126.
Low-Level Carbon Monoxide
Monitors for People at Greater Risk of CO Poisoning
& Resources used to distribute the IST-AIM 935 digital CO Monitor
designed by Albert Donnay, the only CO detector that displays from 5ppm
and provides instantaneous warnings above the US EPA limits of 9 and 35ppm.
Unfortunately it is no longer in production, but two other portable CO detectors
that can display below 30ppm (one from 0 and the other from 10ppm) are available
for approx. $130 each from www.aeromedix.com
. In comparison, regular CO Alarms do not display CO levels under
30ppm and do not go off until over 70ppm for one to four hours.
Breath Analyzers (displays from 0 - 999ppm, gives warning above 35ppm)
100% oxygen increases the concentration of exhaled CO, physicians may
want to monitor both exhaled O2 and CO levels before and after treatment.
MCS R&R director Albert Donnay has worked with Biosystems to customize
an air monitorning instrument for breath analysis. The MultiPro, which
is the size of a fat cell phone, not only measures both O2 and CO, it also
detects hydrogen sulfide down to 0.1ppm. H2S, like CO, is made endogenously
and acts as a sensory neurotransmitter.
Poe Carbon Monoxide Awareness Poster
offers an 11x17 inch poster entitled "The Tell-Tale Signs of Carbon Monoxide
Poisoning" featuring the face of Edgar Allan Poe and information about
symptoms, sources, effects, populations at risk and treatment. Designed
for display in physician offices and emergency rooms. Single copies are
free, rolled copies mailed in protective tubes are $1 each (minimum 5).
could not have been written without the invaluable input of many physicians,
respiratory therapists and their patients. Special thanks are due to Dr.
William Rea and Dr. Amado Piamonte at the Dallas Environmental Health
Center, Dr. Ann McCampbell, and Dr. Larry Plumlee -- although final responsibility
for the protocol rests with MCS Referral & Resources, to whom any
comments should be addressed: 410-889-6666, fax 410-889-4944,
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