cally significantly associated with strongly acidic PM (relative odds, 1.7; 95% confidence interval, 1.1-2.4). It was also found in the “24-city Study” that mean forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) were lower in communities that had high concentrations of strongly acidic PM (Raizenne et al. 1996). Thus, chronic exposures to highly acidic PM have been associated with adverse effects on measures of respiratory health in children.

Asthmatic subjects appear to be more sensitive than healthy subjects to the effects of acidic aerosols on lung function, but reported effective concentrations differ widely among studies (EPA 1986b). Adolescent asthmatics might be more sensitive than adult asthmatics and might experience small decrements in lung function in response to H2SO4 at concentrations only slightly above peak ambient concentrations (for example, less than 100 µg/m3 H2SO4, or 2,000 nmol/m3) (Koenig et al. 1983, 1989). Even in studies reporting an overall absence of statistically significant effects on lung function, individual asthmatic subjects appear to demonstrate clinically important effects (Avol et al. 1990). Two studies from different laboratories have suggested that responsiveness to acidic aerosols correlates with the degree of baseline airway hyperresponsiveness (Utell et al. 1983; Hanley et al. 1992).

Studies have also examined the effects of exposure to both H2SO4 and ozone on lung function in healthy and asthmatic subjects (Frampton et al. 1995). Two recent studies found evidence that H2SO4 at 100 µg/m3 potentiates the ozone response, in contrast with previous studies. Animal studies support the hypothesis of a synergism between acidic aerosols and ozone (e.g., Last et al. 1986). Overall, acidic aerosols appear to be a contributing factor in the toxicity of PM at present-day ambient levels, either alone or in conjunction with ozone exposure. Thus, to the extent that incineration emissions increase the acidity (i.e., lowers the pH) of ambient PM, they may be expected to also increase the toxicity of those ambient aerosols.

Carbon Monoxide

Carbon monoxide (CO) is a colorless, odorless, poisonous gas formed during combustion processes as a result of carbon not being completely oxidized to carbon dioxide (CO2).

CO binds strongly to hemoglobin, with an affinity over 200 times that of oxygen. The binding of CO with hemoglobin is not readily reversible, so it reduces the oxygen-carrying capacity of the blood significantly. CO concentrations above 25 ppm might lead to carboxyhemoglobin (COHb) concentrations of 5%, which has been associated with cardiovascular and respiratory disease and can interfere with pregnancy. Major damage to brain and lung occurs at 50% COHb, and death at 70%.

The body's natural production of CO results in a normal background COHb saturation concentration of 0.4-0.7%. In the nonsmoking population, COHb

The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement