Inflammatory response in humans exposed to 2.0 ppm nitrogen dioxide.

Nitrogen dioxide (NO2) is a common indoor air pollutant, especially in homes with unvented combustion appliances. Epidemiological studies suggest that children living in homes with unvented heating sources are more prone to respiratory infections than children living in homes with lower levels of NO2. However, experimental studies in which human volunteers were exposed acutely to moderate levels of NO2 (0.5-2.0 ppm) have shown little evidence of lung inflammation or decreased host resistance capacity. In the study reported here, 8 healthy volunteers were exposed to 2.0 ppm NO2 and to filtered air for 4 h while undergoing intermittent moderate exercise. Bronchoalveolar lavage was performed the following morning. The lavage was divided into a predominantly bronchial washing (first 20 ml of lavage; BL) and a predominantly alveolar washing (BAL). In the BL, NO2 exposure caused increases in polymorphonuclear neutrophils (PMNs), interleukin 6 (IL-6), IL-8, alpha1-antitrypsin, and tissue plasminogen activator, and decreases in epithelial cells. In the BAL, there were no NO2-induced changes in either cell numbers or soluble mediators. On the other hand, alveolar macrophages from BAL showed a decrease in the ability to phagocytose unopsonized Candida albicans and a decrease in superoxide production. No difference in susceptibility to virus infection was found between the NO2- and air-exposed macrophages. No changes in lung function were observed, but the aerosol bolus recovery technique revealed a statistically significant (p <.05) decrease in the fraction of aerosol recovered following nitrogen dioxide exposure, which is suggestive of small obstructive changes induced by NO2.

Bronchoscopic determination of ozone uptake in humans.

Measurements of ozone uptake efficiency in the human respiratory tract provide critical information toward understanding ozone dose-response characteristics. We measured ozone uptake efficiency by different regions of the respiratory tract between the mouth and bronchus intermedius in 10 healthy, resting, nonsmoking male and female subjects. The distal end of a bronchoscope was sequentially positioned at the bronchus intermedius (BI), main carina (CAR), upper trachea, and above the vocal cords. Ozone concentration was measured continuously at each sight using a rapid-responding ozone analyzer. During sampling subjects breathed through a mouthpiece connected to a pneumotachograph at a paced rate of 12 breaths/min. Integration of the product of the flow and ozone concentrations during inspiration and expiration provided the ozone mass passing each anatomic location during each phase of respiration. On inspiration the uptake efficiencies of ozone by structures between the mouth and each location j (Em-j) were 0.176 +/- 0.037 (SE), 0.271 +/- 0.024, 0.355 +/- 0.030, and 0.325 +/- 0.031 for above the vocal cords, upper trachea, CAR, and BI, respectively. A significant effect of location on Em-j was found by analysis of variance (P < 0.0002). Pairwise comparisons showed that Em-j increased as the lung penetration increased except between CAR and BI, which was not significantly different.