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The problems inherent in studying the pathogenesis of chronic lung disease in human subjects in relation to inhaled air pollutants are discussed. The automatic rejection of findings of reversible airways changes as a significant health effect of acute pollutant inhalation is suggested to be unjustified, and an analogy with cigarette smoke inhalation is discussed. The author suggests that future clinical studies of air pollutant effects should emphasize response parameters, such as inflammation, which have amplifying potential. Recent studies of ozone effects are cited in this connection. The usefulness of nasal epithelium and of cultured human respiratory cells as models is noted. Finally, the hope is expressed that clinical air pollutant research will remain in the mainstream of our understanding of human lung biology.
air pollutant health effects, inhaled pollutant lung toxicity, mechanisms, ozone, arachidonate metabolism and oxidants, inflammation and oxidants, host factors, air pollution, inhalation toxicology
Professor of medicine, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC