are associated with more than a 1-year shortening of expected lifespan for the entire population (WHO 1995).

Dockery and Pope (1994) have reviewed the effects of PM10 on both respiratory mortality and morbidity. They considered five primary health end points: mortality, hospital use, asthma attacks, respiratory symptoms, and lung function. They concluded that there was a coherence of effects across the end points, with most end points showing a 1-3% change per 10 µg/m3. A later analysis by Thurston (1996) indicated that those PM-effect estimates are reduced somewhat if the influences of copollutants are addressed.

Hospitalization data can provide an especially useful measure of the morbidity status of a community during a specified period. Hospitalization data on respiratory-illness diagnosis, or more specifically for chronic obstructive pulmonary disease (COPD) and pneumonia, give a measure of respiratory status. Both COPD and pneumonia hospitalization studies show moderate but statistically significant relative risks, in the range of 1.06-1.25, associated with an increase of 50 µg/m3 in PM10. Table 5-1 presents results of several studies of short-term exposure-response relationships of fine-particle sulfates, PM2.5, and PM10 with different health-effect indicators, as developed by the World Health Organization. The data provide quantitative estimates of the effect of PM (per unit of increment) for each outcome considered.

Acidic Gases and Acidic Aerosols
Nitrogen Oxides

Nitric oxide (NO) is the major nitrogenous pollutant emitted from incineration facilities. Although NO itself is not thought to result in any deleterious health effects at the concentrations surrounding combustion sources, it is readily oxidized in the ambient environment to nitrogen dioxide (NO2), which is the most biologically significant of the nitrogen oxides. NO2 exerts its health effects via two primary pathways. One pathway is directly through interactions with the respiratory system when breathed. The other pathway is indirectly through the photochemical formation of atmospheric ozone, a secondary pollutant with much greater respiratory effects than NO2 itself. Collectively, nitrogen oxides are often assessed as a group known as NOx.

NO2 is water-soluble and, when breathed, is efficiently absorbed in the mucous lining of the nasopharyngeal cavity and lung, where it converts to nitrous acid, HNO2, and nitric acid, HNO3, which can then react with the pulmonary and extrapulmonary tissues. NO2 has been shown in occupational settings to be rapidly fatal at extremely high concentrations (i.e., 150,000 ppb and above) because of pulmonary edema, bronchial pneumonia, or bronchiolitis fibrosa obliterans (NRC 1977, Ellenhorn and Barceloux 1988), but these exposures are 10,000 times in excess of ambient concentrations found near sources such as

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