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Carbon Monoxide Toxicity
- On this page : Carbon Monoxide by
Edouard Bastarache, Introduction, Sources of
parameter, Hygiene &
Safety, Prevention, Protection
Aid, The Author
- Carbon monoxide (CO) is a colourless,
odourless gas that can be poisonous to humans. It is a product of
the incomplete combustion of carbon-containing fuels and is also
produced by natural processes or by biotransformation of
halomethanes within the human body. With external exposure to
additional carbon monoxide, subtle effects can begin to occur, and
exposure to higher levels can result in death. The health effects
of carbon monoxide are largely the result of the formation of
carboxyhemoglobin (COHb), which impairs the oxygen carrying
capacity of the blood.
- Carbon monoxide (CO) is an odourless gas
without irritating properties, which allows the inhalation of
significant and potentially lethal concentrations without warning
symptoms for the victim. CO intoxication is each year one of the
main causes of mortality by intoxication in industrialized
countries; 1000 to 2000 deaths per year are linked to carbon
monoxide in the United States.
- The frequency of non-lethal
intoxications by CO is probably much more significant, but
difficult to evaluate with precision because of the nonspecific
nature of the symptoms and clinical signs of the intoxication. It
is thus estimated that each year in the United States, more than
42 000 visits to emergency departments are due to intoxications by
CO with an annual rate of visits to the emergency for this of 16,5
by 100 000 inhabitants
- Given the universal use of fossil energy
sources in our modern society, all of the individuals are
potentially at risk of being exposed. The intoxication risk seems
higher in countries of northern latitude with a higher frequency
during the winter months, but many cases of intoxication to CO
occur each year in all of the industrialized countries
- Sources of exposure
- Carbon monoxide can be released in many
industrial, environmental and domestic situations.
- The main source of exposure to carbon
monoxide, without any doubt, is caused by its presence in the
exhaust fumes of internal combustion engines and in emission gases
during the incomplete combustion of combustible materials.
- Exposures to CO in confined places are
responsible for the very large majority of the potentially
dangerous exposures. The inappropriate use of heating systems also
represents one of the principal causes of exposure to carbon
- A-Uses and mission sources in the
- - the metallurgy of iron and various
other metals, their refining by their carbonyls (ex.:nickel
carbonyl), works by cutting and flamecutting;
- - chemical syntheses: the manufacture of
calcium carbide and metal carbonyls;
- - the use of explosives in mines and on
hydroelectric building sites;
- - in garbage incineration, cement
- - the use of lifting trucks
- - the use of heating appliances
operating on coal, gas or other hydrocarbons (stove, furnace,
defective gas appliances);
- - the endogenous metabolism of certain
xenobiotics can also lead to the production of CO as a metabolite:
methylene chloride, dibromomethane, diiodomethane and
- B-Main uses :
- - as a fuel;
- - as a reducing agent in metallurgy;
- - in the chemical industry for the
synthesis of many compounds: methanol, acetic acid, formic acid,
acrylic acid, phosgene, etc.
- C-Sources and concentrations of
carbon monoxide in the environment :
- Carbon monoxide is present in the
troposphere as traces which find their origin in natural processes
and certain human activities. Given that plants are able to
metabolize carbon monoxide and to produce some, it is considered
that as traces, this gas is a normal constituent of the natural
- The carbon monoxide concentration in the
air near urban agglomerations and industrial parks can be
appreciably higher than the normal natural concentration, but we
have yet to see a report of harmful effects on plants or
micro-organisms which would be attributable to the concentrations
measured in these conditions.
- It does remain that the presence of
carbon monoxide at these concentrations can be detrimental to
human health, according to the values reached in workplaces or in
residential zones, and in accordiance with the receptivity of the
subjects exposed to the potential harmful effects.
- Upon examining air quality data provided
by fixed control stations, one notes a tendency to the decline of
the concentration of carbon monoxide which translates the
effectiveness of antipollution systems with which recent vehicles
are equipped. In the United States, the emissions due to motor
vehicles which run on highways represent approximately 50 % of the
total amount of carbon monoxide emitted, while 13% is due to
vehicles not running on highways. Among the other sources of
emission one can quote the use of other fuels than automobile
fuels, for example in boilers (12 %), various industrial processes
(8 %), solid waste disposal (3 %) and various other sources (14
- The concentrations to which the general
population is exposed for more or less long periods frequently
range from 29 to 57 mg of carbon monoxide per m3 (25-50 ppm);
under these circumstances, physical activity is generally reduced
and the resulting rate of carboxyhemoglobin does not exceed 1-2 %
- Inside buildings, the carbon monoxide
concentration depends on the concentration of the surrounding air,
on the presence of internal sources, the ventilation and air
mixing in each room, and from one room to the next. In dwellings
where there are no other sources, the carbon monoxide
concentration in the air is about the same as the average external
concentration. The highest concentrations occur in the presence of
interior sources of combustion, in particular in closed garages,
service stations and restaurants, for instance.
- It is in the air of the dwelling houses,
churches and health care establishments that the carbon monoxide
concentration is the lowest. Lastly, cigarette smoking represents
a significant source of exposure to CO in the general population.
The amount of absobed CO following the use of cigarette depends on
certain factors, such as for example the frequency and the
intensity of inhalations.
- The CO concentration is about 4,5 % (45
000 ppm) in cigarette smoke and will result among smokers in a
carboxyhaemoglobine varying from 3 to 8 %, although levels of up
to 15 % have already been reported.
- It has been shown that passive
nicotinism resulting from the exposure to cigarette smoke on
average increases the exposure of non-smokers to approximately 1,7
mg/m3 (1,5 ppm) and that the use of a gas stove increases the CO
content of the air to approximately 2,9 mg/m3 (2,5 ppm). Among
other sources of carbon monoxide in the intenal air of dwellings
one can mention chimneys, water-heaters as well as coal or wood
- Toxicological properties
- A-Toxicokinetics :
- 1-Absorption :
- Carbon monoxide is absorbed exclusively
by the respiratory tract. It diffuses through the
alveolo-capillary membrane in way similar to oxygen. In the
presence of a constant concentration during several hours, the
rate of absorbtion decreases regularly until the partial pressures
of carbon monoxide in the blood of the pulmonary capillaries and
the alveolar air reach a state of equilibrium.
- 2-Distribution :
- Most of the absorbed carbon monoxide
sets in a reversible way on the heme pigments of the body. At
least 80% bind to hemoglobin of the érythrocytes to form
carboxyhemoglobin. The affinity of hemoglobin for carbon monoxide
is approximately 240 to 250 times higher than that for oxygen.
- 10 to 15% reacts with the myoglobin of
the muscular cells. Myoglobin has a constant of affinity for
carbon monoxide approximately eight times weaker than that of
hemoglobin. The myocardial muscular cells retain more carbon
monoxide than the skeletal muscular cells (ratio 3:1).
- 5% can also react with other
heme-containing compounds (ex: cytochromes, metalloenzymes).
Carbon monoxide crosses the hematoencephalic and placental
- 3-Métabolism :
- Carbon monoxide is practically not
metabolized, less than 1% of the absorbed amount is oxidized to
- It is also produced in an endogenous way
by the body at the time of the catabolism of heme pigments.
- The blood level of human endogenous
carboxyhemoglobin varies from 0,1 à 1,2%.
- Principal mechanism of the toxic
- the link between carbon monoxide and
hemoglobin producing carboxyhemoglobin causes a decrease of the
capacity of oxygen blood transportation and interferes with the
release of oxygen at the tissular level..
- 4-Excretion :
- Carbon monoxide is excreted almost
entirely in the expired air.
- Elimination is done quickly at the
beginning, then becomes slower with time and when the
concentration of carboxyhemoglobin drops.
- 5-Half-life :
- At rest, the elimination half-life of
blood carbon monoxide is approximately 3 to 4 hours for a subject
inhaling air and approximately 20 to 60 minutes for subjects
inhaling oxygen. With the administration of hyperbaric oxygen, the
elimination half-life of CO decreases but the numerical values
vary according to authors:
- 23 minutes at 3 atm.
- 27 minutes at 1.58 atm.
- 22 minutes at 2.5 atm.
- It may increase with age and decrease
with physical activity.
- The half-life of carbon monoxide in
foetal blood is approximately 7 hours.
- Immediately Dangerous to Life or
Health : 1200 ppm.
- B- Physiopathology
- Carbon monoxide intoxication causes
lesions mainly to cardiovascular and neurological systems and its
physiopathology is relatively complex.
- 1-Cellular hypoxia :
- Carbon monoxide intoxication is
characterized initially by tissue hypoxia. It is a well-known fact
that carbon monoxide binds in a competitive way to hemoglobin to
form carboxyhemoglobin, an abnormal hemoglobin which cannot be
used to carry oxygen. The affinity of carbon monoxide for
hemoglobin is 240 to 250 times more significant than that of
oxygen and the ratio carboxyhemoglobin/oxyhemoglobin will be
proportional to the ratio of the partial pressures of carbon
monoxide and oxygen.
- Carbon monoxide also involves a
displacement towards the left and a modification of the shape of
the intra-tissular dissociation curve of oxyhemoglobin, which
contributes even more to limit the release of oxygen at the
tissular level. Cellular hypoxia resulting from the formation of
carboxyhemoglobin will have as a harmful effect, a reflex increase
of ventilation, which will increase pulmonary absorbtion of carbon
monoxide in the context of a persistent exposure.
- The link of carbon monoxide to
hemoglobin with secondary tissue hypoxia does not constitute
however the only physiopathological mechanism implied in CO
intoxication, and hypoxic stress cannot by itself explains the
development of neurological effects..
- It does not seem to exist a direct
correlation between the degree of neurological effect and the
level of carboxyhemoglobin measured when the patient is admitted
at the emergency ward. Moreover, the transfusion to animals of
blood saturated with carboxyhemoglobin does not allow, in the
absence of free CO, to reproduce clinical symptomatology
- 2-Intracellular toxicity :
- It seems that carbon monoxide can also
act as an intracellular toxin. It is estimated that about 15 % of
absorbed carbon monoxide will be bound to extravascular proteins.
Carbon monoxide binds to cardiac and musculoskeletal myoglobin
starting from levels of carboxyhemoglobin of the order of 2 %. and
could alter oxygen uptake to thus reduce the effectiveness of
oxydative phosphorylation at the myocardial level. Carbon monoxide
can also bind to cytochrome oxydase (cytochrome a3) which is the
final enzyme of the electron transport chain at the mitochondrial
- This link will have as a consequence a
deterioration in the ATP production and intracellular acidosis.
Persistent alteration of intracellular metabolism after cessation
of exposure could be explained by the bond of carbon monoxide to
cytochrome oxydase. A persistent inhibition of mitochondrial
cytochrome oxydase during several days was shown in human beings
following exposure to carbon monoxide producing levels of
carboxyhemoglobin varying from 11 to 22 %.
- Exposure to carbon monoxide can lead to
the formation of reactive oxidizing molecules being able to induce
a lipidic peroxidation and a variety of lesions in the central
nervous system. Several physiopathological mechanisms encountered
during CO intoxication are similar to post-ischaemic lesions of
reperfusion. Among patients poisoned with CO, there is a positive
correlation which can be shown in an experimental way between
mitochondrial dysfonction induced by CO exposure and of lipidic
- Exposure to carbon monoxide causes a
nitric oxide release (NO) from blood platelets and endothelial
vascular cells with a significant increase of NO in perivascular
and vascular tissues. NO is a major physiological mediator and a
free radical of very short lifespan and has a cytotoxic potential.
The cytotoxic effect of NO can be partly associated with the
production of peroxynitrite, a major oxidant generated by the
reaction between NO and the superoxyde ion.
- It seems that oxygenated free radicals
of the superoxyde type are produced in the context of a carbon
monoxide exposure by mitochondrial dysfonction induced by hypoxic
- 3-Neurological toxicity :
- The produced peroxynitrite will be able
to bind to tissular proteins to produce the typical vascular and
perivascular neuro-histological lesions associated with CO
intoxication. The oxydative stress will thus have as a consequence
an increase in capillary permeability at the neurological level as
well as an increase in adhesion of the polymorphonuclear
leucocytes at the level of the altered endothelium. The adhesion
of the leucocytes to the cerebro-vascular endothelium will
contribute to a reduction in the cerebral perfusion and to the
initiation of the process of lipidic peroxidation.
- It has been shown in experiments that
hyperbaric oxygen therapy can prevent the adhesion of leucocytes
to the endothelium in an animal model of exposure to carbon
monoxide. It thus seems probable that the neurological tissue
lesions associated with carbon monoxide intoxication are of
vascular origin. It seems also plausible that the cardiovascular
response to carbon monoxide intoxication is determining in the
importance of future neurological lesions.
- 4-Cardio-vascular toxicity
- Carbon monoxide is associated with
myocardial depression explainable partly by hypoxic stress, by the
mitochondrial bond of CO with cytochrome a3, and by a link with
myocardial myoglobin. The link to myoglobin could play a major
role in myocardial depression associated with an intoxication by
CO given the significant role that myoglobin has on the
intracellular diffusion of oxygen.
- The blocking of the function of
myoglobin is associated with a reduction in the uptake of oxygen
and a reduction in the production of ATP by the cardiac muscle.
Myocardial depression combined with peripheral vasodilatation
secondary to an increase in the concentrations of NO in the
vascular endothelium will have as a consequence arterial
hypotension with a reduction of the cerebral perfusion being able
to lead to a loss of consciousness and subsequently to ischaemic
lesions of reperfusion in the brain.
- A transitory loss of consciousness is
generally regarded as a factor of bad prognosis in a carbon
monoxide intoxication. The possible cardiac toxic effects of CO
- - flutter,
- - auricular fibrillation,
- - ventricular tachycardia,
- - ventricular fibrillation,
- - myocardial ischemia.
- It has been showed without ambiguity
that at the level of 5.0% carboxyhemoglobin, there was reduction
of oxygen binding and consecutive reduction in the physical
capacity under conditions of maximum exertion in young adults in
- However, certain cardiovascular effects
are to feared more in the event of exposure to more characteristic
ambient carbon monoxide concentrations (in particular, the
aggravation of angina during physical activity) among a smaller
proportion but nevertheless considerable of the population.
Individuals suffering from chronic angina pectoris are currently
considered as the most receptive group to the effects of an
exposure to carbon monoxide, according to the signs of aggravation
of the angor noted among patients having a level of
carboxyhemoglobin from 2,9 to 4,5 %.
- The lowest observed adverse effect level
(LOAEL) among patients suffering from exertional ischemia varies
between 3 and 4 % carboxyhemoglobin, i.e. a level higher than the
basic value by 1,5 to 2,2 %. One did not study the effects of
carbon monoxide on asymptomatic episodes of ischemia, which
represent in fact the majority of cases among these patients.
- It was shown that a sufficient exposure
to produce a carboxyhemoglobin level of 6 % at least, appreciably
increased the number and the complexity of exertional arrhythmias
in the event of coronaropathy and ectopia. Exposure to carbon
monoxide can involve an increased risk of sudden death among
patients suffering from coronaropathy.
- C-Acute clinical effects :
- Carbon monoxide is a chemical poisonous gas.
- The clinical manifestations of exposure
to carbon monoxide are multiple and nonspecific. The presence of
more than one affected person in the same physical place, of
nonspecific symptoms should make one suspect a CO intoxication.
Symptomatology may occur following an exposure to a low level over
a prolonged period of time or following a significant exposure
over a short period. In both cases, neurological after-effects may
occur. It thus seems that the severity of the intoxication to
carbon monoxide will depend on several factors:
- - ambient carbon monoxide concentration,
- - duration of exposure,
- - individual susceptibility to CO
- - general health status of the exposed
- There is no reliable correlation between
the severity of the intoxication and the blood carboxyhemoglobin
(COHb) level measured at the time the patient is admitted in the
- 1- Acute general effects :
- Symptoms of general order are frequent :
- - headache,
- - nausea,
- - vomiting,
- - generalized weakness.
- Since CO intoxication frequently occurs
during winter, it is very frequent that the initial diagnosis is,
in an erroneous way, that of a viral infection. It was observed CO
exposure could be the unspecified cause of 5 to 19 % of the cases
of headaches in emergy departments.
- 2-Acute cardiovascular effects :
- The clinical manifestations of
cardiovascular nature are also significant:
- - thoracic pain,
- - tachypnea,
- - tachycardia,
- - hypotension with syncope,
- - convulsions,
- - pulmonary oedema,
- - cardiac arrhythmia and heart failure.
- 3-Acute neurological effects :
- The possible neurological clinical
manifestations are multiple :
- - ataxia,
- - dizzy spells,
- - disorders of memory,
- - concentration reduction,
- - convulsions,
- - coma.
- 4-Other acute clinical effects :
- The other significant clinical
- - metabolic acidosis,
- - retinal hemorrhages.
- Even if it does not constitute a
reliable marker of the severity of exposure, a significant rise in
COHb in a nonsmoker is useful for confirming the clinical
suspicion of an exposure.
- 5-Differential diagnosis :
- Often times, clinical symptomatology
could be confused with certain current clinical conditions:
- - infection of the higher respiratory
- - food poisoning,
- - cerebrovascular accident,
- - psychiatric disorders,
- - migraine,
- - myocardial ischemia.
- A serious intoxication can leave cardiac
after-effects (modifications of the electrocardiogram) and
neurological ones (reduction in the intellectual capacity,
personality disorders and behavior).
- 7-Dose-effects relationship
Probable effects following
Biological exposure index.
Light headache, dyspnea at the
time of intense muscular exertion, reduction of mental
Severe headache, dyspnea at the
time of moderated muscular exertion, nausea,
Severe headache, nausea,
vomiting, muscular weakness, confusion, eye and judgement
Convulsions, loss of
Coma, sometimes fatal cardiac
and respiratory depression.
plus de 66%
Probable effects following an
acute exposure (ppm CO) in a person in good
Valeur d'exposition moyenne
Valeur d'exposition de courte
durée (VECD) Headache 2 to 3 hours after
Headache and nausea 1 to 3 hours
Headache and nausea 1 hour after
1 200 ppm
Immediately dangerous to life
or health (IDLH)
1 600 ppm
Headache, nausea, giddiness in
20 minutes, loss of consciousness, coma and death 2 hours
3 200 ppm
Headache, giddiness in 5
minutes, coma and risk of death in 30 minutes
6 400 ppm
Headache, giddinesss in 1 to 2
minutes, coma and risk of death in15 minutes
20 000 ppm
Coma and death in 4
- Effects of the increase in
carboxyhemoglobin (COHb) in the severely impaired cardiac patient
Individual suffering from a
severe cardiac condition
Increase of the arterial flow in
certain organs to compensate for the reduction in oxygen
If the cardiac condition is
severe, the patient can decompensate.
Lowering of the luminous visual
Lowering of the required
exertion to cause angina.
Headache, abnormal evoked visual
Can cause death if the cardiac
function is very compromised.
- 8-Clinical evaluation :
- Given the nonspecific nature of the
symptoms and signs of CO intoxication, it is of primary importance
for the clinician to maintain a high level of suspicion when
confronted by a clinical picture compatible with this poison, even
if a history of exposure is lacking.
- The measurement of COHb remains of
very great utility to confirm the exposure: a level higher than
2-3 % in a nonsmoker or 10 % in a smoker should be considered
- As mentioned previously, there is no
reliable correlation with the initial level of COHb and the future
evolution of the inoxication.
- a-Clinical examination :
- The following will have to be included
- - examination of the higher mental
- - certain specific psychometric tests
can be used, such as "CO Neuropsychological Screening Battery"
- Thus, the patient presenting, following
an exposure to CO, abnormal psychometric test results,
- can be at risk to develop persistent or
delayed neurological abnormalities. Lastly, the usefulnessl of
psychometric tests to predict the need for a hyperbaric oxygen
therapy remains a discussed issue.
- b-Paraclinical examinations
- The following examinations could be
- - arterial gases,
- - electrocardiogram,
- - cardiac enzymes,
- - carboxyhemoglobin which must be
measured directly by a cooxymeter
- using the wavelength adapted for this
- Following the confirmation of a CO
intoxication, it is important to identify as soon as possible the
exposure source in order to correct the problem and to prevent
later exposures among other individuals.
- a-Normobaric oxygen therapy
- The therapeutic method of choice for the
treatment of CO intoxication remains the delivery 100 % oxygen and
the suggested duration of treatment is 4 to 6 hours for the
majority of intoxications but certain sources suggest up to 48
hours of treatment.
- b-Hyperbaric oxygen therapy
- Since 1960, hyperbaric oxygen therapy is
used on a regular basis for the treatment of CO intoxication. In
theory, it comprises potential advantages for the treatment of CO
intoxication.These advantages include:
- - faster elimination of CO
- - improvement of tissue
- - faster dissociation of CO on its site
of intracellular binding at the cytochrome oxydase level
- - inhibition of leucocytic adhesion at
the vascular endothelium level
- - prevention of the process of lipidic
peroxidation at the central nervous system level (possibility)
- It is possible to obtain complete
recovery without after-effects following an intoxication to CO
without hyperbaric oxygen treatment and it is also possible to
find significant neurological anomalies after a hyperbaric oxygen
- The classical indications for hyperbaric
oxygen therapy are:
- - coma or a history of loss of
- - neuropsychological anomalies at
- - cardiovascular instability,
- - severe metabolic acidosis,
- - carboxyhemoglobin greater than 40 %.
- These indications are usually used in
clinical situations and represent a consensus among experts
without however having been validated in a rigorous scientific
- 10-Irritation et corrosion
- Carbon monoxide is not an irritating gas
for the respiratory tract and the eyes but contact with the liquid
gas can cause frostbites of the exposed tissues.
- D-Chronic effects :
- The presence of toxic effects associated
with a prolonged exposure to carbon monoxide is not yet clearly
elucidated in the consulted documentary sources.
- Some authors report effects such
- - headache,
- - asthenia,
- - giddiness,
- - insomnia,
- - irritability,
- - anorexia,
- - subtle neuropsychological disorders
such as memory disturbances, etc.
- Generally, there hardly exists data
indicating that atherogenic effects may occur in the population
due to exposure to carbon monoxide at the concentrations usually
met in ambient air
- No data concerning respiratory and
cutaneous sensitizing was found in the consulted documentary
- F-Pregnancy :
- 1-Carbon monoxide intoxication and
- Carbon monoxide intoxication during
pregnancy poses particular problems. It seems that a significant
risk of foetal death and neurological anomalies exist following
exposure to CO for the mother, with a risk of foetal death varying
from 36 to 67 %. Ventilation being increased during pregnancy, it
is possible that CO pulmonary absorbtion is greater in the
pregnant woman. The affinity of foetal hemoglobin for CO is
greater than that of maternal hemoglobin.
- An equilibrium state will be reached in
the foetus and the elimination of CO is slower for the foetal
circulation. The maximum level of carboxyhemoglobin reached during
the intoxication could be greater in the foetus than in the
- On the basis of retrospective data, it
seems that oxygen therapy is safe for the foetus and the mother.
Precise information on hyperbaric is not established in a final
manner but a carboxyhemoglobin of 15 % is often used by several
experts as a critical value because of the greatest
physiopathological sensitivity of the foetal circulation.
- 2-Data on the mother's milk:
- There is no data concerning its
excretion or detection in mother's milk.
- G-Carcinogenic effects:
- No data concerning a carcinogenic effect
was found in the consulted documentary sources.
- Biological parameter,
biological exposure index and time of sampling:
- A-Main exposure index
- Carboxyhemoglobin: 3.5% ( end of break)
- B-Other exposure index
- Carbon monoxide in the expired
- ACGIH proposes a biological exposure
index of 20 ppm for a sample taken at the end of the workshift
This biological exposure index corresponds to a concentration
expected following an exposure to 25 ppm for
- 8 hours.
- C-Factors to consider in the
- - carboxyhemoglobin is not a specific
indicator of exposure to carbon monoxide;
- - the biological exposure index does not
apply to smokers or to the people exposed to methylene
- - this biological index of exposure
corresponds to an exposure of 25 ppm. carbon monoxide.
- D-Comments :
- a-Biological values of
carboxyhemoglobin for a non- professionally exposed population
- - Endogenous formation : less than 1%.
- - Pregnant woman : 0,4 to 2,6 %.
- - Patient suffering from hemolytic
anaemia : 4 to 6%.
- - Urban population : 1 to 2%.
- - Travellers on congested motorways : 5%
- - Smokers : 1 package per day 5 to 6%, 2
to 3 packages per day 7 to 9%, cigar up to 20%.
- - Exposure to 50 ppm of methylene
chloride during 8 hours: 1,5 to 2,5%.
- b-Sensitive population :
- Any individual who has an impaired
pulmonary function or a disease capable of affecting the blood
transportion capacity of oxygen or its availability :
- - workers having respiratory diseases
(ex: emphysema, fibrosis).
- - those who suffer from other diseases
(ex: a cardiopathy, arteriosclerosis, anemia).
- - individuals having a particular
- the pregnant woman,
- the embryo or the foetus.
- -individuals working under particular
- heavy work,
- high temperature
- high altitude (5 000 feet above the sea
- Hygiene and safety
- A-Appearance :
- At normal temperature and pressure,
carbon monoxide is a colourless and odourless gas.
- B-Exposure characteristics :
- The exposure to carbon monoxide in the
work environment, is done mainly by the gas. The exposure to
liquid gas generates an important carbon monoxide concentration
because of its very low boiling point and its high volatility. The
exposure to liquid gas is less frequent because of its less
- C-Exposure to the gas
- The absence of odor on the part of
carbon monoxide makes it so that it is impossible to identify its
presence before or after the VEMP (35 ppm or 40 mg/m³), or
the VECD (200 ppm or 230 mg/m³) are reached. The odor cannot
thus be an adequate sign of warning of a dangerous exposure.
Because of its density close to that of air, it mixes easily with
air and quickly can, in the event of leakage or of incomplete
organic matter combustion, reach dangerous concentrations.
- The value of IDLH (Immediately Dangerous
to Life or Health, 1 200 ppm or 1 375 mg/m³) being
sufficiently low compared to the LLE (Lower Limit of Explosivity,
12, 5 % or 125 000 ppm), the risk of intoxication will occur well
before the risk of explosion.
- Detectors are thus recommended where
exists the possibility of exposure to carbon monoxide
- D-Exposure to the liquified gas :
- Carbon monoxide in the liquid state, is
a cryogenic liquid at -191,5°C, it is thus necessary to hold
account of all the aspects which comprise the exposure to a liquid
at very low temperature.
- E-Inflammability and explosiveness
- 1-Inflammability :
- Carbon monoxide is a flammable gas; the
fire hazard is very high with strong concentrations and in the
presence of a source of ignition.
- 2-Explosiveness :
- Carbon monoxide may form explosive
mixtures with air.
- F-Combustion products
- Carbon dioxide.
- G-Reactivity :
- 1-Stability :
- Stable at normal pressure and
temperature, carbon monoxide becomes reactive at high temperature
and can act as a powerful reducing agent.
- 2-Incompatibility :
- Carbon monoxide is a strong reducing
agent which violently reacts with strong oxidants such as
halogens. It is incompatible with oxygen
- 3-Decomposition products :
- It does not decompose under normal
- Prevention :
- Information campaigns should be
undertaken in a periodic way at the beginning of winter to inform
the public on the dangers of the potential sources of CO.
- Several simple means to prevent CO
intoxications can be easily applied:
- - the routine inspection and maintenance
of combustion devices and chimneys;
- - the banning of letting car engines run
in closed garages at idle even when the door is open;
- - the banning of the use of
non-ventilated cooking devices inside dwellings;
- - the generalized use of CO detectors
- Many CO intoxications can be explained
by the public's ignorance about its harmful effects
- Protection measures :
- Laws on Occupational health and Safety
aim at the elimination of hazaerds at the source. When engineering
measures and modifications of the working methods are not
sufficient enough to reduce the exposure to this substance, the
wearing of individual protection equipment may prove to be
necessary. The protection gears must be in conformity with
- A-Respiratory tract :
- Wear a suitable apparatus of respiratory
protection if the concentration in the work environment is greater
than the VEMP (35 ppm or 40 mg/m³) or than the VECD (200 ppm
or 230 mg/m³).
- B-Skin :
- Wear a suitable device of skin
protection if there is a hazard of splashes with the liquid gas.
The selection of protection equipement for the skin depends on the
nature of the work to carry out.
- C-Eyes :
- Wear a suitable protection device for
the eyes if there is a hazard of splashes with liquid gas. The
selection of an ocular protection gear depends on the nature of
work to carry out and, if it is necessary, on the type of device
of respiratory protection used.
- Exposure standards
- A-Workplace :
- 1-Quebec's exposure limits
- a-Valeur d'exposition moyenne
- 35 ppm 40 mg/m³
- b-Valeur d'exposition de courte
- 200 ppm 230 mg/m³
- B-Environment :
- 1-WHO :
- -25 ppm/1 h
- -9 ppm/8 h
- 2-EPA United Kingdom :
- 10 ppm/8 h
- 3-EPA USA :
- 35 ppm/1 h
- 9 ppm/8h
- 4-Japan :
- -20 ppm/2 h
- -10 ppm/8 h
- 5-Finland :
- -25 ppm/1 h
- -9 ppm/8 h
- C-Dwellings air quality
- Health Canada :
- - < 11 ppm for 8 heures,
- - < 25 ppm for 1 heure.
- First Aid
- A-Inhalation :
- In the event of inhalation of the gas,
bring the person into a ventilated place. If she/he does not
breathe any- more, artificial respiration should be given. Give
oxygen, maintain the victim warm and tranfer she/he to the nearest
medical emergency department.
- B-Frostbite :
- In the case of frostbite, apply lukewarm
water and see a physician.
- References :
Répertoire Toxicologique, 2003
- 2-Toxicologie Industrielle et
Intoxications Professionnelles, Lauwerys R. dernière
- 3-Bulletin d'Information
Toxicologique du Québec, Vol 17, No.3.
- 4-IPCS No.213, Carbon Monoxide (2nd
edition), OMS, 1999.
- 5-Règlement sur la
qualité et la sécurité du travail,
Gouvernement du Québec, 2001.
Out Bound Links
In Bound Links
CO - Carbon Monoxide
Edouard Bastarache M.D.
Occupational & Environmental Medicine
Author of "Substitutions for Raw Ceramic Materials"
Tracy, QuÃ©bec, CANADA