Airway inflammation following exposure to diesel exhaust: a study of time kinetics using induced sputum.
The adverse health effects of particulate matter pollution are of increasing concern. In a recent bronchoscopic study in healthy volunteers, pronounced airway inflammation was detected following exposure to diesel exhaust (DE). The present study was conducted in order to evaluate the time kinetics of the inflammatory response following exposure to DE using induced sputum from healthy volunteers. Fifteen healthy nonsmoking volunteers were exposed to DE particles with a 50% cut-off aerodynamic diameter of 10 microm 300 microg x m(-3) and air for 1 h on two separate occasions. Sputum induction with hypertonic saline was performed 6 and 24 h after each exposure. Analyses of sputum differential cell counts and soluble protein concentrations were performed. Six hours after exposure to DE, a significant increase was found in the percentage of sputum neutrophils (37.7 versus 26.2% p=0.002) together with increases in the concentrations of interleukin-6 (12.0 versus 6.3 pg x mL(-1), p=0.006) and methylhistamine (0.11 versus 0.12 microg x L(-1), p=0.024). Irrespective of exposure, a significant increase was found in the percentage of sputum neutrophils at 24 as compared to 6 h, indicating that the procedure of sputum induction itself may change the composition of sputum. This study demonstrates that exposure to diesel exhaust induces inflammatory response in healthy human airways, represented by an early increase in interleukin-6 and methylhistamine concentration and the percentage of neutrophils. Induced sputum provides a safe tool for the investigation of the inflammatory effects of diesel exhaust, but care must be taken when interpreting results from repeated sputum inductions.
Nordenhäll
C
C
Dept of Respiratory Medicine and Allergy, University Hospital, Umeå, Sweden.
Pourazar
J
J
Blomberg
A
A
Levin
J O
JO
Sandström
T
T
Adelroth
E
E
D000328:Adult; D000397:Air Pollution / Q000009:adverse effects; D054360:Chemokine CXCL1; D019743:Chemokines, CXC; D002630:Chemotactic Factors / Q000032:analysis; D018592:Cross-Over Studies; D005260:Female; D006133:Growth Substances / Q000032:analysis; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D007700:Kinetics; D007958:Leukocyte Count; D008297:Male; D008761:Methylhistamines / Q000032:analysis; D009195:Peroxidase / Q000032:analysis; D011014:Pneumonia / Q000139:chemically induced* / Q000276:immunology / Q000378:metabolism*; D016037:Single-Blind Method; D013183:Sputum / Q000737:chemistry / Q000166:cytology / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D001335:Vehicle Emissions / Q000009:adverse effects*
C475829:CXCL1 protein, human; D054360:Chemokine CXCL1; D019743:Chemokines, CXC; D002630:Chemotactic Factors; D006133:Growth Substances; D036341:Intercellular Signaling Peptides and Proteins; D015850:Interleukin-6; D016209:Interleukin-8; D008761:Methylhistamines; D014409:Tumor Necrosis Factor-alpha; D001335:Vehicle Emissions; D009195:Peroxidase