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Clinical relevance of cellular mediators of inflammation in workers exposed to asbestos.

Authors
Schwartz-DA; Galvin-JR; Frees-KL; Dayton-CS; Burmeister-LF; Merchant-JA; Hunninghake-GW
Source
Am Rev Respir Dis 1993 Jul; 148(1):68-74
NIOSHTIC No.
00216225
Abstract
Possible associations between cellular markers of parenchymal inflammation and clinical expression of asbestos (1332214) induced lung disease were examined. The study group consisted of 93 male asbestos workers, mean age 60 years, who were being evaluated for asbestos related lung disease. The average length of asbestos exposure was 36 years. Chest X-rays were taken and interpreted according to 1980 International Labor Office criteria. High resolution computed tomography (HRCT) of the lung parenchyma was performed. Pulmonary function testing was conducted, bronchoalveolar lavage (BAL) was performed, and lavagate fibronectin concentrations were determined. Lavage fluid alveolar macrophages were recovered and their ability to release prostaglandin-E2 (PGE2), interleukin- 1beta (IL1b), and tumor-necrosis-factor-alpha (TNFa) spontaneously or in response to stimulation by bacterial lipopolysaccharide was evaluated. Associations between BAL fluid fibronectin concentration and macrophage release of PGE2, IL1b, and TNFa and the presence of interstitial fibrosis as indicated by the chest X-ray and HRCT examinations, restrictive lung function, and gas exchange abnormalities were examined by univariate comparison and regression techniques. Thirty subjects had evidence of interstitial fibrosis on chest X-ray films, 22 showed interstitial abnormalities on HRCT films, 11 had spirometric evidence of airway restriction, and 22 had abnormal gas exchange. Elevated lavagate fibronectin concentrations and impaired release of PGE2 by unstimulated macrophages were significantly associated with airway restriction. Impaired release of PGE2 was also associated with abnormal gas exchange. None of the other biomarkers were associated with the presence of interstitial fibrosis, restrictive lung function, or abnormal gas exchange. The authors conclude that in asbestos exposed persons, BAL fluid fibronectin concentration and unstimulated macrophage release of PGE2 appear to be associated with airway restriction. Macrophage release of IL1b and TNFa is not associated with lung function restriction. None of the lavagate markers are associated with radiographic or HRCT evidence of interstitial lung disease. Routine use of BAL cannot determine the severity of asbestos induced lung disease.
Keywords
NIOSH-Grant; Pulmonary-system-disorders; Asbestos-workers; Clinical-diagnosis; Clinical-techniques; Biochemical-indicators; Chest-X-rays; Alveolar-cells; Pulmonary-function-tests; Airway-resistance; Visual-images; Occupational-exposure
Contact
Internal Medicine University of Iowa Pulmonary Disease Division Iowa City, IA 52242
CODEN
ARDSBL
CAS No.
1332-21-4
Publication Date
19930701
Document Type
Journal Article
Funding Amount
122514
Funding Type
Grant
Fiscal Year
1993
NTIS Accession No.
NTIS Price
Identifying No.
Grant-Number-K01-OH-000093
Issue of Publication
1
ISSN
0003-0805
Priority Area
Pulmonary System Disorders
Source Name
American Review of Respiratory Disease
State
IA
Performing Organization
University of Iowa, Iowa City, Iowa
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