Record Display for the EPA National Library Catalog


OLS Field Name OLS Field Data
Main Title Modulation of Human Alveolar Macrophage Properties by Ozone Exposure In vitro.
Author Becker, S. ; Madden, M. C. ; Newman, S. L. ; Devlin, R. B. ; Koren, H. S. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. ;ABB Environmental Services, Inc., Chapel Hill, NC. ;Cincinnati Univ. Medical Center, OH. ;North Carolina Univ. at Chapel Hill.
Publisher c1991
Year Published 1991
Report Number EPA/600/J-91/266;
Stock Number PB92-113281
Additional Subjects Ozone ; Air pollution effects(Human) ; Macrophages ; Toxicology ; Humans ; Pulmonary alveoli ; In vitro analysis ; Cryptococcus neoformans ; Prostaglandins ; Superoxide ; Complement ; Electrophoresis ; Cytokines ; Tetradecanoylphorbol acetate ; Growth ; Interleukin-1 ; Interleukin-6 ; Immunofluorescence techniques ; Reprints ;
Library Call Number Additional Info Location Last
NTIS  PB92-113281 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 02/24/1992
Collation 15p
The study investigated changes in human alveolar macrophage (HAM) function after exposure in vitro to ozone (O3)(0.1-1.0 ppm for 2-4 hr). The functions studied reflect concern that O3 is detrimental to host defense mechanisms in the bronchoalveolar spaces. Exposure of HAM to O3 caused a concentration-dependent increase in release of prostaglandin E2(PGE2), an important modulator of inflammation, phagocytosis, and oxidative burst. Although phagocytosis of particulate immune complexes was decreased by O3, the authors found no change in the quantity of Fc receptors and complement receptors on the HAM surface. Superoxide (O2) production in response to phorbol ester was reduced after exposure of HAM to O3 while the basal O2 release in response to plastic adherence was not affected. Growth inhibition of the opportunistic yeast Cryptococcus neoformans by HAM was not affected by O3 exposure. The production of inflammatory mediators and immune modulators such as tumor necrosis factor-alpha, interleukin 1, and interleukin 6 were not induced by exposure to O3. However, compared to controls, O3-exposed HAM produced significantly lower levels of these cytokines when simulated with bacterial lipopolysaccharide (LPS). (Copyright (c) 1991 by Academic Press, Inc.)