points and the frequent demonstration of associations of health and physiologic effects with ambient PM levels at or below the current U.S. NAAQS for PM10. The weight of epidemiologic evidence suggests that ambient PM exposure has affected the public health of U.S. populations (EPA, 1996, vol. 3, p. 13-30).

The majority of the studies reviewed in the 1996 criteria document were related to the association of acute health effects and exposure to particulates, mainly PM10 and TSP (total suspended particulates).

Prospective studies of chronic exposure have associated ambient air pollution with mortality (Dockery et al., 1993; Pope et al., 1995; Abbey et al., 1999). Respirable particles (PM2.5) have stronger correlations with health effects than other air pollutants (Dockery et al., 1993), and deaths were associated with cardiopulmonary diseases (Dockery et al., 1993; Pope et al., 1995). Indeed, one reason for the increased interest in the effects on cardiac function is that seven times as many individuals suffer from cardiac disease than from underlying pulmonary disease (Pope et al., 1995).

In recent epiderniologic studies, the contributions of copollutants (other pollutants present in addition to particulates) have received greater attention. Ozone (Loomis et al., 1996; Stieb et al., 1996; Hoek et al., 1997; Delfino et al., 1997, 1998; Burnett et al., 1997; Moolgavkar et al., 1997), nitrogen dioxide (Pantazopoulou et al., 1995; Dab et al., 1996; Moolgavkar et al., 1997), sulfur dioxide (Dab et al., 1996; Moolgavkar et al., 1997), and carbon monoxide (Moolgavkar et al., 1997; Burnett et al., 1998) have also been positively and significantly associated with adverse health effects. Uncertainties in epidemiologic studies include the magnitude of risk for PM, the attribution of observed health effects to specific PM constituents, the time intervals over which PM health effects are manifested, the extent to which findings in one location can be generalized to other locations, the nature and magnitude of the overall public health risk from ambient PM exposure, and the biologic mechanisms of the observed responses. Differentiating adverse responses in individuals, specific toxicity of ambient particle exposures, and the effects of the "pollution mix" may require comprehensive monitoring specifically related to individual human exposures, as well as sensitive measures of health effects, to reduce uncertainties in the definitions of health effects from ambient air pollution.

No epiderniologic study has identified a particular chemical constituent of PM as a causative agent. Indications are that physical characteristics of the particles may be important. PM2.5 relationships to health can differ from those of PM10 (EPA, 1996), and one study showed that ultrafine particles (< 0.1 μm) are more sensitive indicators of effect than fine particles (Peters et al., 1997a). Ultrafine particles as a potential cause of the observed health effects are the focus of several European epidemiologic studies and a component of the Atlanta-Based Aerosol Research Inhalation Epidemiology Study (ARIES), which is partly supported by the DOE-FE program (see Chapter 3). Many ongoing health studies are attempting to define the pollutants or components of PM that are the most important to health effects and the biological mechanisms that would establish causality.

In fact, new epidemiologic research has focused on the biologic mechanisms of response. A primary biological hypothesis is that inflammation is the underlying cause of adverse cardiopulmonary responses (Godleski and Clarke, 1999). Peters et al. (1997b) supported a systemic inflammatory response mechanism, based on increases in blood viscosity associated with elevated TSP and sulfur dioxide levels in Augsburg, Germany. Another biological hypothesis focused on autonomic nervous system mechanisms, assessing cardiac responses by electrocardiogram and variations in heart rate (Godleski, 1999), which have been associated with adverse health effects in the medical literature (Dougherty and Burr, 1992; Ewing et al., 1981; Lombardi et al., 1987; van Ravenswaaig-Arts et al., 1993; and Bigger and Schwartz, 1994). Recently, Pope et al. (1999) showed significant increases in sympathetic and parasympathetic influences on the heart associated with increases in ambient PM10 based on variable heart rates in seven elderly subjects. These studies, coupled with comprehensive assessments of exposure, could make a significant contribution to the understanding of morbidity and mortality associated with increases in PM.

In a recent study, the EPA reviewed toxicologic studies of primary and secondary particle emissions from power plants (EPA, 1996). Although a number of historical data sets exist, studies of coal fly ash using samples collected more than 20 years ago are unlikely to be applicable to emissions from current facilities. The health effects of sulfate have been debated for many years, but it appears that associated metal or hydrogen ions may be the bases of "sulfate toxicity." Pathologic responses to particles containing silicon vary with the surface composition of the particle. Silica

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