Abstract

A number of epidemiological studies have attempted to assess the effect of recurrent ozone exposure in humans. For the most part, they have failed to document convincingly an association between chronic ozone exposure and differences in lung function performance or respiratory symptoms. This is not surprising given the small respiratory effects observed in animals chronically exposed to ozone and assuming that people with abnormal respiratory function resulting from other occupational or environmental exposures, such as tobacco smoke, would make up a much larger percentage of the population than people with respiratory effects attributable to ozone. Therefore, either more sensitive end points must be developed to detect subtle changes due to chronic ozone exposure, or ways of selecting subpopulations that are especially sensitive to ozone must be devised. It has been well documented that there are large and reproducible differences in the acute response of individuals to ozone as measured by pulmonary function tests. Recently, it has also been shown that there are large differences in the acute response of individuals to ozone as measured by inflammatory and other biochemical parameters. This paper discusses the problems of selecting individuals who are sensitive to ozone depending on the end point chosen. It also describes potential new sensitive end points that might be available for ozone epidemiology studies in the near future.

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