Document Detail

Molecular markers of acute upper airway inflammation in workers exposed to fuel-oil ash.
MedLine Citation:
PMID:  9655727     Owner:  NLM     Status:  MEDLINE    
Biomarkers in nasal lavage (NL) fluid may be useful in determining the presence and severity of upper airway inflammation. We studied 18 boilermakers overhauling a large, oil-fired boiler and 11 utility workers who served as controls for 6 wk. NL was performed before (NL1), during (NL2), and after (NL3) the overhaul. We measured nasal fluid levels of interleukins 6 (IL-6) and 8 (IL-8), eosinophilic cationic protein (ECP), and myeloperoxidase (MPO) as markers of response to fuel-oil ash exposure. In boilermakers, MPO was elevated during boiler work versus preboiler work (mean = 33.8 versus 22.7 ng/ml, p < 0.05), and at the 2-wk postexposure lavage (NL3) it had declined to 24.2 ng/ml (p = 0.08). Mean IL-8 levels increased in boilermakers between NL1 and NL2 (mean = 83.8 versus 134.8 pg/ml, p < 0.05), then decreased at NL3 (mean = 134.8 versus 89.0 pg/ml, p < 0.05). Nasal fluid vanadium increased in boilermakers between NL1 and NL2 (median < 1.0 versus 4.7 ppb, respectively, p < 0.05), then decreased at NL3 (median, 4.7 versus < 1.0 ppb, respectively, p < 0. 05). Levels of IL-6 and ECP did not change significantly during the study. Utility workers showed no significant change in any marker during the study period. Particulate matter < 10 micro(m) (PM10) levels were higher for boilermakers than for utility workers before boiler work (geometric mean (GM) = 0.40 versus 0.10 mg/m3, p < 0.05). This difference was more significant during boiler work (GM = 0.47 versus 0.13 mg/m3, p < 0.001). Ozone levels were low during the study. These data suggest that exposure to fuel-oil ash results in acute upper airway inflammation, potentially mediated by increased IL-8 levels and the recruitment and activation of polymorphonuclear leukocytes. These changes were associated with significantly increased PM10 levels and concentrations of upper airway vanadium.
M A Woodin; R Hauser; Y Liu; T J Smith; P D Siegel; D M Lewis; D J Tollerud; D C Christiani
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of respiratory and critical care medicine     Volume:  158     ISSN:  1073-449X     ISO Abbreviation:  Am. J. Respir. Crit. Care Med.     Publication Date:  1998 Jul 
Date Detail:
Created Date:  1998-07-30     Completed Date:  1998-07-30     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9421642     Medline TA:  Am J Respir Crit Care Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  182-7     Citation Subset:  AIM; IM    
Department of Epidemiology and Department of Environmental Health (Occupational Health Program), Harvard School of Public Health, Boston, MA 02115, USA.
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MeSH Terms
Air Pollutants, Occupational / adverse effects*
Biological Markers
Blood Proteins / analysis
Cytokines / analysis*
Enzyme-Linked Immunosorbent Assay
Eosinophil Granule Proteins
Fuel Oils / adverse effects*
Inflammation Mediators / analysis*
Interleukin-6 / analysis
Interleukin-8 / analysis
Middle Aged
Nasal Lavage Fluid / chemistry
Occupational Diseases / chemically induced,  diagnosis*,  immunology
Occupational Exposure*
Peroxidase / analysis
Respiratory Tract Diseases / diagnosis*,  immunology
Vanadium Compounds / analysis
Grant Support
Reg. No./Substance:
0/Air Pollutants, Occupational; 0/Biological Markers; 0/Blood Proteins; 0/Cytokines; 0/Eosinophil Granule Proteins; 0/Fuel Oils; 0/Inflammation Mediators; 0/Interleukin-6; 0/Interleukin-8; 0/Vanadium Compounds; EC; EC 3.1.-/Ribonucleases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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