Scientific basis for an air quality standard for carbon monoxide

Report no. 97/51: Carbon Monoxide (CO) is emitted into the atmosphere mainly as a product of the incomplete combustion of carbonaceous material. The major sources of CO exposure for the general, non-smoking population are exhaust emissions from combustion engines and the burning of fossil fuels. Smoking provides an additional source of CO for the non-smoking as well as the smoking public. In addition to these exogenous sources, CO is generated endogenously mainly from the breakdown of haem proteins. Healthy individuals can tolerate low level exposures to CO but it can be hazardous at higher concentrations and even at low concentrations for those with unusual susceptibility. The primary toxic action of carbon monoxide is the inhibition of cell oxidation following exposure by inhalation.

The brain, heart, and embryo/foetus have critical needs for oxygen. It follows that the major health effects associated with CO exposure include cardiovascular, central nervous system, and developmental toxicities. Of these, the most critical target of carbon monoxide is the cardiovascular system. Furthermore, the most susceptible populations are those individuals with pre-existing cardiovascular disease. The absorption and elimination of CO from the body is influenced by concentration,duration of exposure and pulmonary ventilation. Most absorbed CO binds reversibly with haemoglobin (Hb) forming carboxyhaemoglobin (COHb), reducing the oxygen carrying capacity of the blood. The relationship between CO exposure and the formation of COHb has been mathematically described. The extent of COHb saturation may be used as a biological marker of exposure. In addition, specific adverse health effects have been linked to characteristic COHb levels, which have in turn been associated with CO exposure levels, and these relationships can serve as a basis for an Air Quality Standard (AQS).

Chronic angina patients are presently viewed as the most sensitive group at risk after exposure to CO, and the most sensitive health endpoint is earlier onset of angina with exercise. A COHb saturation of 2.5% posed no significant health effect to the non-smoking population including those with angina. This COHb level corresponds to continuous CO exposures at 15 ppm. A safety factor was applied to the CO exposure conditions to adjust for the uncertainty associated with person shaving other pre-existing disease conditions, e.g., anaemia or pulmonary disease.This adjustment resulted in a predicted COHb concentration of 1.6%, corresponding to continuous CO exposure at 10 ppm. [Thus, an 8 hour running average of 10 ppm is a scientifically supportable AQS for carbon monoxide.]