Molecular markers of acute upper airway inflammation in workers exposed to fuel-oil ash.
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.
Woodin
M A
MA
Department of Epidemiology and Department of Environmental Health (Occupational Health Program), Harvard School of Public Health, Boston, MA 02115, USA.
Hauser
R
R
Liu
Y
Y
Smith
T J
TJ
Siegel
P D
PD
Lewis
D M
DM
Tollerud
D J
DJ
Christiani
D C
DC
D000328:Adult; D000395:Air Pollutants, Occupational / Q000009:adverse effects*; D015415:Biomarkers; D001798:Blood Proteins / Q000032:analysis; D016207:Cytokines / Q000032:analysis*; D004797:Enzyme-Linked Immunosorbent Assay; D047091:Eosinophil Granule Proteins; D005648:Fuel Oils / Q000009:adverse effects*; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000032:analysis*; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D008875:Middle Aged; D017817:Nasal Lavage Fluid / Q000737:chemistry; D009784:Occupational Diseases / Q000139:chemically induced / Q000175:diagnosis* / Q000276:immunology; D016273:Occupational Exposure; D009195:Peroxidase / Q000032:analysis; D012140:Respiratory Tract Diseases / Q000175:diagnosis* / Q000276:immunology; D012260:Ribonucleases; D017968:Vanadium Compounds / Q000032:analysis
D000395:Air Pollutants, Occupational; D015415:Biomarkers; D001798:Blood Proteins; D016207:Cytokines; D047091:Eosinophil Granule Proteins; D005648:Fuel Oils; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D017968:Vanadium Compounds; D009195:Peroxidase; D012260:Ribonucleases