The air pollution to which individuals are exposed is multifaceted; there are no standardized approaches to characterize specific pollutant mixtures, which typically include hundreds of individual gaseous compounds and particles of complex physicochemical composition. Accordingly, indicator pollutants are often used to assess exposures for risk assessment and epidemiologic analysis. For such mixtures, the relative importance of different pollutants is a function of location-specific economic, developmental, social, and technological factors combined with meteorology, topography, geography and atmospheric transformations. Literature and measurement databases exist for a limited number of selected gaseous pollutants (ozone [O3], nitrogen oxides [NOx ≈ NO+NO2], sulfur dioxide [SO2], carbon monoxide [CO]) and one or more measures of PM such as Total Suspended Particles (TSP), or the mass concentration of particles with aerodynamic diameter smaller than 10 (PM10) or 2.5 (PM2.5) micrometers.
An extensive epidemiological literature relates PM2.5 to adverse health impacts (8 (link)-10 (link)). In epidemiologic cohort studies of long term exposure (which form the basis of the exposure-response functions used in health impact assessment) PM2.5 is the most robust indicator of adverse (mortality) impacts (11 (link)). The epidemiologic observations of adverse health impacts associated with elevated ambient PM2.5 concentrations is supported by toxicological experiments, epidemiologic analyses of acute exposures and controlled exposure studies. In populated regions, a large fraction of PM2.5 originates from combustion processes and includes both primary PM (direct emissions) and secondary PM (resulting from atmospheric transformations).
Ozone represents a pollutant mixture that is somewhat different from that associated with PM. This gaseous pollutant is derived from a series of atmospheric photochemical reactions of primary air pollutants, including nitrogen oxides and volatile organic compounds (VOCs). The seasonal, spatial and temporal patterns of surface ozone concentrations are often distinct from those of PM, as are the relative importance of emissions source categories of ozone precursors. Epidemiologic associations have been observed between elevated ozone concentrations and premature mortality that are independent of associations between PM and mortality (12 (link)-15 (link)). There is also an extensive literature on adverse respiratory impacts resulting from ozone exposure in randomized controlled exposure studies (16 (link)). As such, estimates of the global burden of disease attributable to outdoor air pollution are further enhanced by the inclusion of ozone in addition to PM2.5. By including both metrics, the GBD analysis is also compatible with recent national and regional analyses of air pollution health and economic impacts (e.g. (17 )).
An extensive epidemiological literature relates PM2.5 to adverse health impacts (8 (link)-10 (link)). In epidemiologic cohort studies of long term exposure (which form the basis of the exposure-response functions used in health impact assessment) PM2.5 is the most robust indicator of adverse (mortality) impacts (11 (link)). The epidemiologic observations of adverse health impacts associated with elevated ambient PM2.5 concentrations is supported by toxicological experiments, epidemiologic analyses of acute exposures and controlled exposure studies. In populated regions, a large fraction of PM2.5 originates from combustion processes and includes both primary PM (direct emissions) and secondary PM (resulting from atmospheric transformations).
Ozone represents a pollutant mixture that is somewhat different from that associated with PM. This gaseous pollutant is derived from a series of atmospheric photochemical reactions of primary air pollutants, including nitrogen oxides and volatile organic compounds (VOCs). The seasonal, spatial and temporal patterns of surface ozone concentrations are often distinct from those of PM, as are the relative importance of emissions source categories of ozone precursors. Epidemiologic associations have been observed between elevated ozone concentrations and premature mortality that are independent of associations between PM and mortality (12 (link)-15 (link)). There is also an extensive literature on adverse respiratory impacts resulting from ozone exposure in randomized controlled exposure studies (16 (link)). As such, estimates of the global burden of disease attributable to outdoor air pollution are further enhanced by the inclusion of ozone in addition to PM2.5. By including both metrics, the GBD analysis is also compatible with recent national and regional analyses of air pollution health and economic impacts (e.g. (17 )).
