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Carbon Monoxide Toxicity

On this page : Carbon Monoxide by Edouard Bastarache, Introduction, Sources of exposure, Toxicological properties, Biological parameter, Hygiene & Safety, Prevention, Protection measures, Exposure Standards, First Aid, The Author
Introduction :
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 monoxide.
A-Uses and mission sources in the workplace :
- 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 factories;
- 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 bromochloromethane.
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 environment.
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 % among nonsmokers.
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 stoves.
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 barriers.
3-Métabolism :
Carbon monoxide is practically not metabolized, less than 1% of the absorbed amount is oxidized to carbon dioxide.
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 action:
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 level.
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 peroxidation.
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 stress.
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 include:
- 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 good health.
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 effects,
- general health status of the exposed individual.
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 emergency department.
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 manifestations are:
- 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 tract,
- 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 :

Concentration (% carboxyhemoglobin)

Probable effects following acute exposure


Biological exposure index.


Light headache, dyspnea at the time of intense muscular exertion, reduction of mental acuity.


Severe headache, dyspnea at the time of moderated muscular exertion, nausea, giddiness.


Severe headache, nausea, vomiting, muscular weakness, confusion, eye and judgement troubles.


Convulsions, loss of consciousness.


Coma, sometimes fatal cardiac and respiratory depression.

plus de 66%




Probable effects following an acute exposure (ppm CO) in a person in good health

35 ppm

Valeur d'exposition moyenne pondérée (VEMP)

200 ppm

Valeur d'exposition de courte durée (VECD) Headache 2 to 3 hours after exposure.

400 ppm

Headache and nausea 1 to 3 hours after exposure

600-700 ppm

Headache and nausea 1 hour after exposure

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 after exposure

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 minutes

Effects of the increase in carboxyhemoglobin (COHb) in the severely impaired cardiac patient :

Concentration (% carboxyhemoglobin)

Normal individual

Individual suffering from a severe cardiac condition

< 1%

Engogenous production



Increase of the arterial flow in certain organs to compensate for the reduction in oxygen (O2). transportion.

If the cardiac condition is severe, the patient can decompensate.


Lowering of the luminous visual perception threshold.

Lowering of the required exertion to cause angina.


Headache, abnormal evoked visual reaction.

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 abnormal.
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 functions.
- certain specific psychometric tests can be used, such as "CO Neuropsychological Screening Battery" (CONSB).
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 useful:
- arterial gases,
- electrocardiogram,
- cardiac enzymes,
- carboxyhemoglobin which must be measured directly by a cooxymeter
using the wavelength adapted for this abnormal hemoglobin.
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 oxygenation
- 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 treatment.
The classical indications for hyperbaric oxygen therapy are:
- coma or a history of loss of consciousness,
- neuropsychological anomalies at physical examination,
- 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 way.
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 as:
- 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
E-Sensitization :
No data concerning respiratory and cutaneous sensitizing was found in the consulted documentary sources
F-Pregnancy :
1-Carbon monoxide intoxication and pregnancy :
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 mother.
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 air:
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 interpretation :
- 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 chloride;
- 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% and more.
- 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 physiological state:
-individuals working under particular conditions:
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 widespread use.
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 conditions
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 regulation
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 pondérée (VEMP)
35 ppm 40 mg/m³  
b-Valeur d'exposition de courte durée (VECD)
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
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 :
1-CSST-Québec, Répertoire Toxicologique, 2003
2-Toxicologie Industrielle et Intoxications Professionnelles, Lauwerys R. dernière édition.
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.

By Edouard Bastarache

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Typecodes Article by Edouard Bastarache
Edouard Bastarache is a well known doctor that has written many articles on the subject of toxicity of ceramic materials and books on technical aspects of ceramics. He writes in both English and French.
Oxides CO - Carbon Monoxide

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