Abstract
Inflammation may play a key role in the development of lung disease (Hunninghake et al. 1981a; Wright et al. 1984; Cooper et al. 1986) and the severity of lung injury and may be directly related to the amount of subsequent chronic inflammation and fibrosis (Shen et al. 1988). The primary feature of the acute inflammatory response is an influx of neutrophils (PMN). An increase in PMN in the lower lung has been implicated in the development of emphysema (Janoff et al. 1977), idiopathic pulmonary fibrosis (Hunninghake et al. 1980), airway hyperactivity (Holtzman et al. 1983), and increased mucous secretion after irritant exposure (Harkema et al. 1988). Many air pollutants including ozone (O3) have already been shown to induce a lung inflammatory response in multiple animal species (Hunninghake et al. 1981b; Luciano 1982; Castleman et al. 1980), but the effect in humans has been less well studied due to the difficulty of obtaining adequate samples for analysis.
The research described in this article has been reviewed by the Health Effects Research Laboratory, United States Environmental Protection Agency, and approved for publication. Approval does not signify that the contents necessarily reflect the views and policies of the Agency nor does mention of trade names or commercial products constitute endorsement or recommendation for use.
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Koren, H.S., Becker, S., Bromberg, P.A., Devlin, R.B. (1993). Time- and Dose-Dependent Cellular and Biochemical Changes in Response to Ozone Exposure. In: Mohr, U., Bates, D.V., Fabel, H., Utell, M.J. (eds) Advances in Controlled Clinical Inhalation Studies. ILSI Monographs. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77176-7_17
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