Breath carbon monoxide

An experimental human exposure study titled Tetrachloroethylene Development of a biologic standard for the industrial worker by breath analysis, completed by Stewart and colleagues, was first published by NIOSH in 1974. This publication can now be obtained from the National Technical Information Service (NTIS) with a 1981 date, and is cited as Stewart et al. (1981) throughout this Profile. In this study, four male volunteers were sequentially exposed to 0, 20, 100, or 150 ppm tetrachloroethylene vapor for 7.5 hours/day, 5 days/week (Stewart et al. 1981). The men were exposed to each concentration for 1 week. Once each week, pulmonary function was assessed at both rest and during two levels of exercise with forced maximum expiratory flow measurements, while alveolar-capillary gas exchange was measured by single breath carbon monoxide diffusion. The exposures to tetrachloroethylene at these vapor concentrations and time intervals had no effect on the pulmonary function measurements. 

American Association for Respiratory Care, 1999, Clinical Practice Guideline Single-breath Carbon Monoxide Diffusing Capacity, Respir. Care, 44(5) 539-546. 

American Thmacic Society, 1995, Single Breath Carbon Monoxide Diffusing Capacity (transfer factor), Am. Rev. Respir. Dis., 152 2185-2198. 

Carbon monoxide is about the same size and shape as O2, but CO binds more tightly than O2 to iron. In addition, once a hemoglobin molecule has bound two CO molecules, it can no longer achieve the configuration necessary to bind O2. Consequently, breathing carbon monoxide can be fatal because it interferes with the transport of oxygen through the bloodstream. 

The equilibrium constant for the formation of carboxyhemoglobin is about 250 times larger than that for oxyhemoglobin. The result is that breathing carbon monoxide deprives the cells of oxygen, and the victim is ultimately asphyxiated. A few hemoglobin... 

Prevention of carbon monoxide poisoning is best accompHshed by providing good ventilation where contamination is a problem. If good ventilation is not possible, a self-contained breathing apparatus, such as a Scott Air-Pak, must be used. The use of gas masks containing an adsorbent is generally not recommended since it is difficult to know when the adsorbent is exhausted. 

The toxic symptoms from inhalation of nickel carbonyl are beUeved to be caused by both nickel metal and carbon monoxide. In many acute cases the symptoms ate headache, di22iQess, nausea, vomiting, fever, and difficulty in breathing. If exposure is continued, unconsciousness follows with subsequent damage to vital organs and death. Iron pentacarbonyl produces symptoms similar to nickel carbonyl but is considered less toxic than nickel carbonyl. 

Carbon monoxide 30 ppm carbon monoxide in end-tidal breath (HGV) Post shift... 

Asphyxiant Simple asphyxiants are inert gases which deplete the oxygen supply in the breathing air to below the critical value of J8% by volume, such as gaseous fuels or nitrogen. Chemical asphyxiants, such as carbon monoxide and hydrogen cyanide, have a direct biological effect. 

Not only 02 molecules but also other groups can be bound to the iron atom of hemoglobin. Specifically, carbon monoxide molecules can be so attached and, in fact, CO is more firmly bound to hemoglobin than is O2. This is one detail of the carbon monoxide poisoning mechanism. If we breathe a mixture of CO and 02 molecules, the CO molecules are preferentially picked up by the red blood cells. Since the sites... 

Carbon monoxide poisoning is particularly insidious. An individual exposed to carbon monoxide is usually unaware of it because this gas is odorless, colorless, and tasteless. Furthermore, it does not elicit any irritant reflexes that result in sneezing, coughing, or feelings of dyspnea (difficulty in breathing). Finally, carbon monoxide does not stimulate ventilation. As will be discussed in a subsequent section, the peripheral chemoreceptors are sensitive to decreases in P02, not oxygen content. 

Unfortunately, most fatalities in fires occur by inhalation of toxic vapours. These can be carbon monoxide (which arises from incomplete combustion), cyanides (from nitrogen-containing polymers) and chlorides (from chloropoly-mers). These are the adverse consequences of flammable polymer combustion. They can be overcome by using breathing apparatus, face masks, etc. 

Use a self-contained breathing apparatus (SCBA). Air purifying respirators (APRs) are not recommended for use in an atmosphere containing carbon monoxide or metal carbonyls because of poor warning properties and the unknown effectiveness of sorbents used in the filters. 

A casualty with known exposure to carbon monoxide blood agents, who was initially unconscious but has regained consciousness or a casualty who shows neurological abnormalities such as dizziness, confusion, or hallucinations, has cardiac arrhythmias, bronchospasm or complains of severe headache, difficulty in breathing or chest pain. If available, breath measurement indicates that the blood carbon monoxide level exceeds 20%. 

Small, portable sensors are now available to monitor the air we breathe for such toxins as carbon monoxide, CO. As soon as the air contains more than a critical concentration of CO, the sensor alerts the householder, who then opens a window or identifies the source of the gas. 

Carboxyhemoglobin Concentration [HbCO] This can be estimated with the method of Jones and co workers. The subject holds a deep breath for 20 s to allow equilibration of carbon monoxide between alveolar air and blood and then expires a sample of that air into a container. The air carbon monoxide concentration may be directly related to carboxyhemoglobin concentration [HbCO]. The test can be performed before exposure in an environmental chamber to help to verify that the subject has not received inordinate ambient pollutant exposure. 

Carbon dioxide (CO ) in its pure form will suffocate you by preventing oxygen from entering your lungs. Carbon monoxide (CO) is deadly, even in small amounts once breathed into the lungs, it replaces the oxygen in the bloodstream. 

Lead aerosol in the air is poisonous to breathe, especially for young children. Many people called for the abolition of lead in gasoline. In the 1970s, the photochemical smog in California was attributed to unburned hydrocarbons and carbon monoxide from automobile tailpipes, and the best solution was the catalytic converter which works with finely divided platinum particles deposited on alumina monoliths. When leaded gasoline is used, these platinum atoms would be quickly covered by a barrage of lead aerosols. This finally led to the abolishment of TEL as a gasoline additive. 

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