Carbon monoxide (CO) is historically known as a deadly gas to humans. Although produced in small amounts in the human body, toxicity occurs predominately after inhalation of preformed CO. Exposure to CO can occur in occupational settings, in tobacco smoke, and in home settings whenever there is incomplete combustion of carbon-containing materials in an unventilated setting.

Uses

CO is used in industries as a feedstock for the production of methanol, acrylates, phosgene, and ethylene. It is also used in metallurgy applications and in industrial fuels. It is also recently being studied in preclinical stages for medicinal use. A major source of CO is the incomplete combustion of carboncontaining materials.

Environmental Fate

Exposure to this colorless, odorless gas occurs primarily though inhalation. CO exposure associated with the paint stripper methylene chloride is unique in that methylene chloride is biologically metabolized toCOin vivo. Dermal, oral, and inhalation exposure to methylene chloride can cause CO poisoning.

Aside from tobacco smoke, the most important sources of CO exposure for most individuals are the emissions created by internal combustion engines of vehicles and in household and occupational locations where combustion occurs. Specific sources of exposure include the burning of wood, charcoal, natural gas, or propane for heating and cooking, and propane-powered indoor equipment such as forklifts and ice rink resurfacers.
Average levels of CO in homes without gas stoves vary from 0.5 to 5 ppm. Levels near properly adjusted gas stoves are often 5–15 ppm, and those near poorly adjusted stoves may be 30 ppm or higher. CO exposures occur in a variety of occupational settings. The number of persons occupationally exposed to CO in the working environment is greater than for any other physical or chemical agent. The smoke of a cigarette contains approximately 14 mg of CO. The smoke of cigars ranges from approximately 38 mg for little cigars to almost 100 mg for large and premium cigars. CO in secondhand tobacco smoke has led to levels of CO as high as 50 ppm.

Mechanism of Toxicity 

CO has varied effects on multiple enzymatic reactions and processes. Most easily seen and measured via co-oximetry is its high affinity and binding to Hb. This results in an overall lack of oxygen carrying capacity along with a shift of the oxygen dissociation curve to the left so that even available oxyhemoglobin is less able to offload oxygen to tissue sites. This,coupled with CO’s ability to bind to and arrest cellular metabolism, results in global hypoxemia. The overall lack of tissue perfusion and energy production results in metabolic lactic acidosis.

CO also has the ability to bind to other globins, most importantly myoglobin. Significant myoglobin binding results in lack of tissue oxygenation to heart and myocardial damage.
The final high-risk organ system affected after CO exposure is the central nervous system. CO has the ability to cause delayed neuropsychiatric sequelae in addition to the acute effects seen as a result of hypoxemia. This is thought to be due to delayed lipid peroxidation achieved through the displacement of nitric oxide. A reperfusion-like injury occurs in these cases.