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RECORD NUMBER: 29 OF 49

OLS Field Name OLS Field Data
Main Title Effects of ozone exposure on lipid metabolism in human alveolar macrophages. /
Author Friedman, F. ; Madden, M. C. ; Samet, J. M. ; Koren, H. S.
CORP Author North Carolina Univ. at Chapel Hill. Center for Environmental Medicine and Lung Biology.;Health Effects Research Lab., Research Triangle Park, NC.
Publisher University of North Carolina for US Environmental Protection Agency, Office of Research and Development,
Year Published 1991
Report Number EPA-R-812738; EPA/600/D-91/046
Stock Number PB91-176982
OCLC Number 45712591
Additional Subjects Air pollution effects(Humans) ; Ozone ; Pulmonary alveoli ; Macrophages ; Lipids ; Metabolism ; Arachidonic acids ; Phospholipids ; Phospholipase A2 ; Phospholipase C ; Prostaglandins ; Platelet-activating factor ; Bronchoalveolar lavage fluid ; High pressure liquid chromatography ; Thin layer chromatography ; Statistical analysis ; Eicosanoids
Holdings
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Status
NTIS  PB91-176982 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 01/01/1988
Collation 29 pages : illustrations ; 29 cm
Abstract
Alveolar macrophages (AM) store arachidonic acid (AA) which is esterified in cellular phospholipids until liberated by phospholipase A2 or C after exposure to inflammatory stimuli. Following release, there can be subsequent metabolism of AA into various potent, biological active mediators including prostaglandins and platelet activating factor (PAF). To examine the possibility that these mediators may account for some of the pathophysiologic alterations seen in the lung following O3 exposure, human AM were collected by bronchoalveolar lavage of normal subjects, plated into tissue culture dishes, and the adherent cells were incubated with 3H-AA or 3H-lysoPAF. Human AM exposed 1.0 ppm O3 for 2 hr released 65 + or - 12% more tritium, derived from 3H-AA, than paired air-exposed controls into media supernatants. In other studies using a similar O3 exposure protocol, there was also a significant increase in human AM PGE2 production (2.0 + or - 0.5 fold-increase above air-exposure values, p<0.01, n=17). In additional studies, using a similar O3 exposure protocol (1.0 ppm for 1 hr), there was also a significant increase in human AM PAF content (1.7 + or - 0.2 fold-increase above air-exposure values, p<0.02, n=5).
Notes
"EPA 600/D-91/046." Includes bibliographical references. Microfiche.