Persistent airway inflammation but accommodated antioxidant and lung function responses after repeated daily exposure to nitrogen dioxide

Citation
A. Blomberg et al., Persistent airway inflammation but accommodated antioxidant and lung function responses after repeated daily exposure to nitrogen dioxide, AM J R CRIT, 159(2), 1999, pp. 536-543
Citations number
35
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
ISSN journal
1073449X → ACNP
Volume
159
Issue
2
Year of publication
1999
Pages
536 - 543
Database
ISI
SICI code
1073-449X(199902)159:2<536:PAIBAA>2.0.ZU;2-6
Abstract
Nitrogen dioxide (NO2) is a common indoor and outdoor air pollutant that ma y induce deterioration of respiratory health. In this study the effects of repeated daily exposure to NO2 on airway antioxidant status, inflammatory c ell and mediator responses, and lung function were examined. Healthy nonsmo king subjects were exposed under controlled conditions to air (once) and to 2 ppm of NO2 for 4 h on four consecutive days. Lung function measurements were made before and immediately after the end of each exposure. Bronchosco py with endobronchial biopsies, bronchial wash (BW), and bronchoalveolar ra vage (BAL) was carried out 1.5 h after the air exposure and after the last exposure to NO2. Repeated NO2 exposure resulted in a decrease in neutrophil numbers in the bronchial epithelium. The BW revealed a twofold increase in content of neutrophils (p < 0.05) and a 1.5-fold increase in myeloperoxida se (MPO) (p < 0.01) indicative of both migration and activation of neutroph ils in the airways. After the fourth NO2 exposure, antioxidant status of th e airway fluid was unchanged. Significant decrements in FEV1 and FVC were f ound after the first exposure to NO2, but these attenuated with repeated ex posures. Together, these data indicate that four sequential exposures to NO 2 result in a persistent neutrophilic inflammation in the airways, whereas changes in pulmonary function and airway antioxidants are resolved. We conc lude that NO2 is a proinflammatory air pollutant under conditions of repeat ed exposure.