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| Block 8: Environmental Issues and Public Health - Air Pollution Chapter 3: The Main Air Pollutants; Their Health Impacts; Exposure - Response Relationships (Continued) |
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Carbon monoxide is a colorless, odorless, poisonous gas formed when carbon in fuels is not burned completely. It is a byproduct of highway vehicle exhaust, which contributes about 60 percent of all CO emissions. In cities, vehicle exhaust can cause as much as 95 percent of all CO emissions. These emissions can result in high concentrations of CO, particularly in local areas with heavy traffic congestion. Other sources of CO emissions include industrial processes and fuel combustion in sources such as boilers and incinerators.
Carbon monoxide enters the bloodstream and reduces oxygen delivery to the body's organs and tissues. The health threat from exposure to CO is most serious for those who suffer from cardiovascular disease. Healthy individuals are also affected, but only at higher levels of exposure. Exposure to elevated CO levels is associated with visual impairment, reduced work capacity, reduced manual dexterity, poor learning ability, and difficulty in performing complex tasks.
CO diffuses rapidly across alveolar, capillary and placental membranes. Approximately 80-90% of the absorbed CO binds with hemoglobin to form carboxyhemoglobin (COHb), which is a specific biomarker of exposure in blood. The affinity of hemoglobin for CO is 200-250 times that for oxygen. During exposure to a fixed concentration of CO, the COHb concentration increases rapidly at the onset of exposure, starts to level off after 3 hours, and reaches a steady-state after 6-8 hours of exposure. It is noted that the elimination half-life in the fetus is much longer than in the pregnant mother.
The binding of CO with hemoglobin to form COHb reduces the oxygen-carrying capacity of the blood and impairs the release of oxygen from hemoglobin. These are the main causes of tissue hypoxia produced by CO at low exposure levels. At higher concentrations, the rest of the absorbed CO binds with other heme proteins such as myoglobin and with cytochrome oxidase and cytochrome P-450. The toxic effects of CO first become evident in organs and tissues with high oxygen consumption, such as the brain, heart, exercising skeletal muscle and the developing fetus.
Severe hypoxia due to acute CO poisoning may cause both reversible, short-lasting, neurological deficits and severe, often delayed, neurological damage. The neurobehavioural effects include impaired coordination, tracking, driving ability, vigilance and cognitive performance at COHb levels as low as 5.1-8.2%. In apparently healthy subjects, the maximal exercise performance decreases at COHb levels as low as 5%. The regression between the percentage decrease in maximal oxygen consumption and the percentage increase in COHb concentration appears to be linear, with a fall in oxygen consumption of approximately 1% for each 1% rise in COHb level above 4%.
In controlled studies involving patients with documented coronary artery disease, mean pre-exposure COHb levels of 2.9-5.9% (corresponding to post-exercise COHb levels of 2.0-5.2%) have been associated with a significant shortening in the time to onset of angina, with increased electrocardiographic changes and with impaired left ventricular function during exercise. In addition, ventricular arhythmias may be increased significantly at the higher range of mean post-exercise COHb levels. Epidemiological and clinical data indicate that CO from smoking and environmental or occupational exposures may contribute to cardiovascular mortality and to the early course of myocardial infarction. Current data from epidemiological studies and experimental animal studies indicate that common environmental exposures to CO in the developed world would not have atherogenic effects on humans (WHO 1999a).
During pregnancy, endogenous production of CO is increased so that maternal COHb levels are usually about 20% higher than the non-pregnant values. At steady-state, the fetal COHb levels are as much as 10-15% higher than the maternal COHb levels. There is a well-established and probably causal relationship between maternal smoking and low birth weight at fetal COHb levels of 2-10%. In addition, maternal smoking seems to be associated with a dose-dependent increase in perinatal deaths and with behavioural effects in infants and young children.
