INFLAMMATORY RESPONSE IN HUMANS EXPOSED TO 2.0 PPM NITROGEN DIOXIDE
Authors: Devlin, Robert B.; Horstman, Donald P.; Gerrity, Timothy R.; Becker, Susanne; Madden, Michael C.; Hatch, Gary E.; Koren, Hillel S.
Source: Inhalation Toxicology, Volume 11, Number 2, 1 February 1999 , pp. 89-109(21)
Publisher: Informa Healthcare
Abstract: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, 1-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 NO2 exposure, which is suggestive of small obstructive changes induced by NO2.
Document Type: Research article
Publication date: 1999-02-01