Ozone-induced decrements in FEV1 and FVC do not correlate with measures of inflammation.
In order to test the hypothesis that changes in lung function induced by ozone (O3) are correlated with cellular and biochemical indices of respiratory tract injury/inflammation, we exposed 20 healthy subjects, on separate days, to O3 (0.2 ppm) and filtered air for 4 h during exercise. Symptom questionnaires were administered before and after exposure, and pulmonary function tests (FEV1, FVC, and SRaw) were performed before, during, and immediately after each exposure. Fiberoptic bronchoscopy, with isolated left main bronchus proximal airway lavage (PAL) and bronchoalveolar lavage (BAL; bronchial fraction, the first 10 ml of fluid recovered) of the right middle lobe, was performed 18 h after each exposure. The PAL, bronchial fraction, and BAL fluids were analyzed for the following end points: total and differential cell counts, and total protein, fibronectin, interleukin-8 (IL-8), and granulocyte-macrophage colony-stimulating factor (GM-CSF) concentrations. The study population was divided into two groups, least-sensitive (n = 12; mean O3-induced change in FEV1 = -7.0%) and most-sensitive (n = 8; mean O3-induced change in FEV1 = -36.0%). We found a significant O3 effect on SRaw (p<0.001) and lower respiratory symptoms (p<0.001) for all subjects combined, but no significant differences between the least- and most-sensitive groups. Ozone exposure increased significantly percent neutrophils in PAL (p=0.01); percent neutrophils, total protein, and IL-8 in bronchial fraction (p<0.001, p<0.001, and p<0.01, respectively); and percent neutrophils, total protein, fibronectin, and GM-CSF in BAL (p<0.001, p<0.001, p<0.01, p=0.05, respectively) for all subjects combined; there were no significant differences, however, between least- and most-sensitive groups. Our results indicate that levels of O3-induced symptoms and respiratory tract injury/inflammation were not correlated with the magnitude of decrements in FEV1 and FVC.
Balmes
J R
JR
Center for Occupational and Environmental Health, Cardiovascular Research Institute, University of California, San Francisco 94143-0854, USA.
Chen
L L
LL
Scannell
C
C
Tager
I
I
Christian
D
D
Hearne
P Q
PQ
Kelly
T
T
Aris
R M
RM
D000328:Adult; D000403:Airway Resistance / Q000187:drug effects; D001706:Biopsy; D001991:Bronchitis / Q000473:pathology* / Q000503:physiopathology; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D001999:Bronchoscopy; D002452:Cell Count; D005260:Female; D005336:Fiber Optic Technology; D005353:Fibronectins / Q000032:analysis; D005541:Forced Expiratory Volume / Q000187:drug effects*; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000032:analysis; D006801:Humans; D016209:Interleukin-8 / Q000032:analysis; D007958:Leukocyte Count; D008297:Male; D009504:Neutrophils / Q000473:pathology; D010126:Ozone / Q000009:adverse effects*; D005082:Physical Exertion; D011506:Proteins / Q000032:analysis; D014797:Vital Capacity / Q000187:drug effects*
D005353:Fibronectins; D016209:Interleukin-8; D011506:Proteins; D010126:Ozone; D016178:Granulocyte-Macrophage Colony-Stimulating Factor