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RECORD NUMBER: 33 OF 45

OLS Field Name OLS Field Data
Main Title Modulation of eicosanoid production by human alveolar macrophases exposed to silica 'in vitro'. {microfiche}
Author Koren, H.S. ; Joyce, M. ; Devlin, R. B. ; Becker, S. ; Driscoll., K.
CORP Author Health Effects Research Lab., Research Triangle Park, NC. ;North Carolina Univ. at Chapel Hill. School of Medicine. ;Procter and Gamble Co., Cincinnati, OH. Miami Valley Labs. ;ABB Environmental, Inc., Chapel Hill, NC.
Publisher US Environmental Protection Agency, Health Affects Research Laboratory,
Year Published 1991
Report Number EPA/600/D-90/196
Stock Number PB91-136630
Additional Subjects Silicon organic compounds ; Toxicity ; Dust ; Particles ; Respiration ; In vitro analysis ; Liquid chromatography ; Inflammation ; Lung ; Humans ; Laboratory animals ; Pulmonary alveoli ; Macrophages ; Eicosanoids ; Dose-response relationships ; Bronchoalveolar lavage fluid ; Lipoxygenases ; Prostaglandin synthase ; Cell survival ; Leukotrienes ; Radioimmunoassay
Holdings
Library Call Number Additional Info Location Last
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Status
NTIS  PB91-136630 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 01/01/1988
Collation 30 p. : ill. ; 29 cm.
Abstract
The objective of the study was to determine the eicosanoid production by human alveolar macrophages in response to silica exposure in vitro and to assess their contribution to silica-induced fibrosis and inflammation. Macrophages were obtained from healthy volunteers and were incubated for 3 or 24 hours in the presence of silica (100, 60, and 0 microgram/ml). Supernatants were removed for eicosanoid analysis. Eicosanoids were analyzed by both HPLC and RIA. The data suggested that silica caused an increased release of LTB4, LTC4/D4/E4, and 5-HETE after 3 hours; and decreases in PGE2 and TXB2 production after 24 hours exposure to 100 microgram/ml silica. In addition, 12-HETE and 15-HETE production remained unchanged at either time point. These opposing effects seen with the metabolites of lipoxygenase and cyclooxygenase pathways could contribute to silica-induced fibrosis. The pattern of eicosanoid production after exposure to silica was different from that obtained when macrophages were stimulated with LPS for 3 or 24 hrs, indicating that the response to the particles was not just due to general cellular activation.
Notes
"EPA 600/D-90/196."