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NCBI Bookshelf. Geneva: World Health Organization; Carbon monoxide CO is a colourless, non-irritant, odourless and tasteless toxic gas. It is produced by the incomplete combustion of carbonaceous fuels such as wood, petrol, coal, natural gas and kerosene.

Its molecular weight is Its solubility in water at 1 atm is 3. The molecular weight of carbon monoxide is similar to that of air It mixes freely with air in any proportion and moves with air via bulk transport. It is combustible, may serve as a fuel source and can form explosive mixtures with air.

It reacts vigorously with oxygen, acetylene, chlorine, fluorine and nitrous oxide. Carbon monoxide is not detectible by humans either by sight, taste or smell. It is only slightly soluble in water, blood serum and plasma; in the human body, it reacts with haemoglobin to form carboxyhaemoglobin COHb. The relationship of carbon monoxide exposure and the COHb concentration in blood can be modelled using the differential Coburn-Forster-Kane equation 3which provides a good approximation to the COHb level at a steady level of inhaled exogenous carbon monoxide. Inhalation is the only exogenous exposure route for carbon monoxide.

Anthropogenic emissions are responsible for about two thirds of the carbon monoxide in the atmosphere and natural emissions for the remaining one third. Small amounts are also produced endogenously in the human body 45. Exposure to low levels of carbon monoxide can occur outdoors near ro, as it is also produced by the exhaust of petrol- and diesel-powered motor vehicles. Parking areas can also be a source of carbon monoxide 6. Carbon monoxide is produced indoors by combustion sources cooking and heating and is also introduced through the infiltration of carbon monoxide from outdoor air into the indoor environment 7.

In developed countries, the most important source of exposure to carbon monoxide in indoor air is emissions from faulty, incorrectly installed, poorly maintained or poorly ventilated cooking or heating appliances that burn fossil fuels. In homes in developing countries, the burning of biomass fuels and tobacco smoke are the most important sources of exposure to carbon monoxide. Clogged chimneys, wood-burning fireplaces, decorative fireplaces, gas burners and supplementary heaters without properly working safety features could vent carbon monoxide into indoor spaces.

Incomplete oxidation during combustion may cause high concentrations of carbon monoxide in indoor air. Tobacco smoke can be a major source of indoor exposure, as can exhaust from motor vehicles operating in attached garages 6. Combustion of low-grade solid fuel and biofuels in a small stove or fireplace can generate high carbon monoxide emissions, which may become lethal to occupants unless the flue gases are vented outdoors via a chimney throughout the entire combustion process.

At the beginning of combustion, the pollutants released are dominated by particulate matter elemental and organic carbon but carbon monoxide dominates towards the end. Combustion of high-grade fuels such as natural gas, butane or propane usually produces much less carbon monoxide, provided that sufficient air is supplied to ensure complete combustion.

Nevertheless, even devices using such fuels can cause lethal carbon monoxide intoxication if they are not properly maintained or vented or if air : fuel ratios are not properly adjusted. Incense burning in homes and public buildings such as stores and shopping malls can be a source of exposure to carbon monoxide.

Jetter et al. The authors estimated a peak concentration of 9. Incense burning might be a ificant contributor to carbon monoxide exposure in cultures where incense is burned frequently, for example in religious rituals. of recent studies on carbon monoxide concentrations in indoor air are summarized in Table 2. The studies are listed by continent.

Studies concerning accidental or peak exposures are presented separately in Table 2. Representativeness and data quality, as well as the form in which the data are presented, vary greatly between the studies and make detailed comparisons meaningless except when comparing data within the same study. The general levels of carbon monoxide, however, vary so much between the locations and studies that patterns are easily discernible. Indoor concentrations of carbon monoxide and indoor : outdoor I : O ratios.

In the absence of indoor sources, current concentrations of carbon monoxide in indoor air in European and North American cities are well below the levels of existing air quality guidelines and standards. In the s and s, carbon monoxide levels in urban air often approached or even exceeded these reference values, but drastic reductions in emissions from space heating and traffic have substantially reduced anthropogenic emissions in spite of the growing size of cities and increasing traffic 9 The highest reported non-accidental carbon monoxide levels are observed in public or residential garages and in primitive kitchens when cooking with open fires Guatemala.

Aside from open-fire cooking with solid fuels, the most common sources for elevated carbon monoxide concentrations in indoor air are unvented gas appliances, tobacco smoking and proximity to busy traffic. Carbon monoxide intoxication can be caused by single or repetitively generated high short-term peaks, and carbon monoxide poisoning is the leading cause of death from poisoning accidental and intentional.

Carbon monoxide is a relatively unreactive gas under ambient air conditions and is not absorbed by building materials or ventilation system filters. Therefore, in the absence of indoor carbon monoxide sources, the indoor air concentration is the same as the concentration of ventilated or infiltrating outdoor air. Under these conditions, the indoor : outdoor I : O carbon monoxide concentration ratio should be 1.

Since the time of Haldane 52it has been assumed that the effect of carbon monoxide exposure is due to hypoxic effects Carbon monoxide enters the body via inhalation and is diffused across the alveolar membrane with nearly the same ease as oxygen O 2.

Carbon monoxide is first dissolved in blood, but is quickly bound to haemoglobin Hb to form COHb, which is measured as the percentage of haemoglobin so bound. The binding of carbon monoxide to haemoglobin occurs with nearly the same speed and ease as with which oxygen binds to haemoglobin, although the bond for carbon monoxide is about times as strong as that for oxygen 54 — Thus carbon monoxide competes equivocally with oxygen for haemoglobin binding sites but, unlike oxygen, which is quickly and easily dissociated from its haemoglobin bond, carbon monoxide remains bound for a much longer time.

In this way, COHb continues to increase with continued exposure, leaving pro gressively less haemoglobin available for carrying oxygen. The result is arterial hypoxaemia. Another effect of COHb is to increase the binding strength of oxygen to haemoglobin, thus making release of oxygen into tissue more difficult The latter effect is quantitatively described as a leftward shift in the oxyhaemoglobin dissociation curve, proportional to the COHb level The model has also been tested under a wide variety of carbon monoxide exposure conditions and found to predict COHb more accurate ly than empirical methods 5459 — The most important variables in the formation of COHb are the concentration and duration of carbon monoxide in inhaled air and the rate of alveolar ventilation Alveolar ventilation, largely determined by body energy expenditure exercisecan vary over a wide range and is thus the major physiological determinant of the rate of COHb formation and elimination.

Carbon monoxide will also reduce the diffusion of oxygen into tissue via myoglobin by formation of carboxymyoglobin.

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The formation of carboxymyoglobin also acts as another sink for carbon monoxide. This process has been described by a multicompartmental physiological model 68 The models estimate the effects of carboxymyoglobin formation on carbon monoxide uptake, but the effect of carboxymyoglobin on tissue function is not clear.

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It is probable that such effects become important only for high levels of carbon monoxide exposure Binding of carbon monoxide to other proteins cytochrome P and cytochrome oxidase have also been demonstrated, but the dosimetry is unclear and the functional ificance appears to be limited to high levels of carbon monoxide exposure Carbon monoxide, in addition to being an environmental contaminant, is produced endogenously. Thus, it is not surprising that physiological mechanisms have evolved to compensate for its presence in mammalian blood and tissues.

These compensatory mechanisms must be considered when calculating the tissue dosimetry.

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For acute exposures, as COHb increases, arterial blood flow to the brain increases proportionally. Thus, even though the blood oxygen contents are decreased, in normal people the increased volume of blood tends to keep the amount of oxygen delivered to the brain constant, preventing hypoxia 71 — Thus it is apparent that the increased compensatory flow is sufficient to for the shift in the oxyhaemoglobin dissociation curve. This compensatory activity also occurs in neonates and fetuses 73 For chronic exposures to carbon monoxide, red cell volume increases or plasma volume decreases 70thus increasing the amount of oxygen that can be delivered.

An accumulating body of evidence indicates that direct carbon monoxide exposure not COHb can produce a of brain cellular events that could potentially lead to serious functional consequences see the section on health effects below. The direct effect of carbon monoxide on tissue has not been demonstrated in vivo, although such effects have been inferred by the observation of tissue effects in exposures in vivo that are very similar to such effects found with in vitro preparations.

It would appear that the presence of carbon monoxide in tissues from in vivo exposure would depend on carbon monoxide dissolved in blood, because it had not yet bound with haemoglobin or because there could be some level of dissociation due to chemical equilibrium reactions. The amount of such dissolved carbon monoxide and the diffusion into various tissues has not been described or modelled. Thus, the dosimetry for putative non-hypoxic effects of carbon monoxide exposure is not known. The amount of dissolved carbon monoxide in blood would seem to be highest for high-level carbon monoxide exposure.

The final dose for carbon-monoxide-induced hypoxic effects is thus seen to be some measure of tissue oxygenation. This is an inverse measure in the sense that, as tissue oxygen increases towards the normal, function improves. As shown above, tissue oxygenation is determined by a the blood oxygen content inversely proportional to COHb levelb the ease of dissociation from blood to tissue the oxyhaemoglobin dissociation curvec the volume of blood delivered to tissue and d the ability of tissue to utilize the oxygen tissue respiration.

To these we must add the rate of oxygen utilization by the tissue. The final criterion of tissue function is the energy metabolism rate in the tissue. The issue of dosimetry is complex, but there exist physiologically based mathematical models to estimate many of the above variables and thus to predict tissue function. They are not mathematically trivial, but with modern computation tools the necessary calculations are readily performed 3 The information required for regulatory guidance setting is some measure of the biologically critical concentration and duration of carbon monoxide exposure in inhaled air.

To estimate environmental guidelines that provide reasonable protection against adverse health effects, information is required about what tissue dose produces what health effects. Given this critical tissue dose, one can estimate the various environmental concentrations, subject characteristics and subject activities that will produce the critical tissue dose.

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Thus for a specific environmental case of interest, mathematical simulations can be done to estimate protective regulatory decisions. Therefore, for each health effect of interest, critical tissue oxygenation must be known. It might be argued that the critical tissue dose is obtained from experimental evidence in which environmental exposure is given in the first place. Experiments, however, are not usually good simulations of actual scenarios of interest. The purpose of the simulations is to be able to simulate any environment of interest without having direct experimental evidence. Unfortunately, in the absence of adequate dosimetric information, and therefore dosimetric models, simulation by models is not possible.

Thus for non-hypoxic effects, it is frequently necessary to use less general evidence from empirical environmental data to make estimates of critical exposures. To preserve exposure data from experiments and literature reviews, it would seem to be important to report both COHb and exposure concentration and duration. This would potentially permit calculation of tissue dose for non-hypoxic tissue effects when the dosimetry models are developed. It should be kept in mind that the tissue dose and the eventual health effect are not necessarily contemporaneous.

Delayed sequelae may occur and cumulative exposure may be needed to become effective. These are really questions of physiological mechanisms. For the acute health effects, the literature search was conducted in the PubMed and Web of Science databases, searching the keywords carbon monoxide and health. Similar search statements were used for physiological and mechanistic articles. From these searches, articles were found and, from these, 52 were deemed relevant and used in the review. The references in each of the relevant articles were searched to find any other articles that might have been missed by the automated searches.

A similar strategy was followed for a review of the health effects of chronic exposure. From these articles, were deemed relevant and were used. This review will discuss concisely and briefly human exposure to carbon monoxide in enclosed i. Since outdoor air inevitably becomes indoor air, some consideration of carbon monoxide levels in outdoor air and their effects on humans are required.

To that end, there will be some discussion of epidemiological studies involving ultra-low-level carbon monoxide found in outside air. Because animal studies cannot at present provide much useful data about many aspects of the carbon monoxide poisoning syndrome 76they have been considered only in order to understand basic mechanisms by which carbon monoxide may impair human health. This review extends the discussion of those issues involving carbon monoxide exposure in humans summarized in the WHO and European Union reports 77 There has been no major attempt to recapitulate the review of most studies before roughly Other recent reviews on carbon monoxide exposure are available in monographs by Penney 79 — 81 and Kleinman 6.

Recourse to these works is strongly encouraged. Tikuisis 82 reviewed human carbon monoxide uptake and elimination in Flachsbart 84 reviewed ambient and very low concentrations of carbon monoxide on humans more recently. Penney 81 recently reviewed pitfalls in making diagnoses of carbon monoxide poisoning, especially chronic poisoning.

Penney 85 reviewed the effects of carbon monoxide exposure on developing animals and humans in White 86 reviewed carbon monoxide poisoning in children in Public perceptions about carbon monoxide in the northern and southern regions of the United States, some relevant to indoor air, were investigated by Penney and published in Penney reviewed the general characteristics of chronic carbon monoxide poisoning in humans in 80 and 88as did Hay et al. InHazucha 92 reviewed the effects of carbon monoxide on work and exercise capacity in humans.

McGrath 93 reviewed the interacting effects on humans of altitude and carbon monoxide.

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Chapter 5: Indoor Air Pollutants and Toxic Materials