Chronic traffic pollution exposure is associated with eosinophilic, but not neutrophilic inflammation in older adult asthmatics.
OBJECTIVE
Airway inflammatory patterns in older asthmatics are poorly understood despite high asthma-related morbidity and mortality. In this study, we sought to define the relationship between exposure to traffic pollutants, biomarkers in induced sputum, and asthma control in older adults.


METHODS
Induced sputum was collected from 35 non-smoking adults ≥65 years with a physician's diagnosis of asthma and reversibility with a bronchodilator or a positive methacholine challenge. Patients completed the Asthma Control Questionnaire (ACQ), and Elemental Carbon Attributable to Traffic (ECAT), a surrogate for chronic diesel particulate exposure, was determined. Equal numbers of subjects with high (≥0.39 µg/m(3)) versus low (<0.39 µg/m(3)) ECAT were included. Differential cell counts were performed on induced sputum, and myeloperoxidase (MPO) and eosinophil peroxidase (EPO) were measured in supernatants. Regression analyses were used to evaluate the relationship between sputum findings, ACQ scores, and ECAT.


RESULTS
After adjustment for potential confounders, subjects with poorly controlled asthma based on ACQ ≥ 1.5 (n = 7) had significantly higher sputum eosinophils (median = 4.4%) than those with ACQ < 1.5 (n = 28; eosinophils = 2.6%; β = 10.1 [95% CI = 0.1-21.0]; p = 0.05). Subjects with ACQ ≥ 1.5 also had significantly higher sputum neutrophils (84.2% versus 65.2%; β = 7.1 [0.2-14.6]; p = 0.05). Poorly controlled asthma was associated with higher sputum EPO (β = 2.4 [0.2-4.5], p = 0.04), but not MPO (p = 0.9). High ECAT was associated with higher eosinophils (β = 10.1 [1.8-18.4], p = 0.02) but not higher neutrophils (p = 0.6).


CONCLUSIONS
Poorly controlled asthma in older adults is associated with eosinophilic and neutrophilic inflammation. Chronic residential traffic pollution exposure may be associated with eosinophilic, but not neutrophilic inflammation in older asthmatics.
Department of Medicine, Division of Immunology, Allergy and Rheumatology, College of Medicine, University of Cincinnati, Cincinnati , OH , USA .
Tolly G
TG
Epstein
Banurekha
B
Kesavalu
Cheryl K
CK
Bernstein
Patrick H
PH
Ryan
Jonathan A
JA
Bernstein
Nives
N
Zimmermann
Zana
Z
Lummus
Manuel S
MS
Villareal
Andrew M
AM
Smith
Peter H
PH
Lenz
David I
DI
Bernstein
D000328:Adult; D000368:Aged; D000397:Air Pollution / Q000009:adverse effects*; D001249:Asthma / Q000201:enzymology / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D015331:Cohort Studies; D004804:Eosinophils / Q000166:cytology / Q000276:immunology* / Q000473:pathology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000201:enzymology / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D019570:Inhalation Exposure; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000166:cytology / Q000276:immunology* / Q000473:pathology; D009820:Ohio; D009195:Peroxidase / Q000032:analysis; D012044:Regression Analysis; D013183:Sputum / Q000166:cytology / Q000201:enzymology; D011795:Surveys and Questionnaires; D001335:Vehicle Emissions / Q000506:poisoning*
D001335:Vehicle Emissions; D009195:Peroxidase