Because ozone does not penetrate cells but leads to pulmonary and nonpulmonary events, a cascade mechanism has often been proposed to account for its toxicity. Human chamber and toxicologic studies have yielded strong evidence indicating that short-term exposure to ozone can exacerbate lung conditions, causing illness and hospitalization, and potentially lead to death. The available evidence on ozone exposure and exacerbation of heart conditions, which is less abundant, points to another concern.

Epidemiologic studies also have found that exposure to ozone (as an indicator of the broader mix of photochemical oxidants) is associated with those effects. Although methodologically somewhat different, the studies have been consistent in their use of large datasets with consistent diagnostic codes for health end points, nationally available ambient air measures, and data on adjustment for some potential confounders. The committee found that the four recent time-series analyses and meta-analyses of the relationship between exposure to ozone and premature mortality add to that evidence by providing robust statistical evidence of an association (Bell et al. 2004, 2005; Ito et al. 2005; Levy et al. 2005).

On the basis of the additional insights obtained from its review of the new time-series studies and its review of the broader evidence, the committee concludes that short-term exposure to ambient ozone is likely to contribute to premature deaths. Despite some continuing questions about the evidence, the committee concludes that it is strong enough to be used in the estimation of the expected mortality risk reduction that would result from reduction in exposure to ozone or the photochemical-oxidant mixture.

In its RIA for the finalized ozone national ambient air quality standards (NAAQS), EPA (2008b) analyzed a variety of assumptions about the association between ozone exposure and premature mortality. They included the assumption that the association is not causal (see Appendix B). Although it is rarely possible to exclude the possibility of zero effect in such analyses, the committee concludes that an absence of any effect is unlikely.


Those who evaluate regulatory benefits seek information from health researchers, for example,

  • To what extent is the relationship between ambient ozone concentration and mortality response due to ozone as opposed to copollutants that are quantified separately, such as airborne particulate matter (PM)?

  • Given that age and health status are important in estimating the quantity and quality of the remaining life expectancy, how dependent is the ozone-mortality relationship on those and other personal characteristics, such as socioeconomic status?

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