Pulmonary performance of elderly normal subjects and subjects with chronic obstructive pulmonary disease exposed to 0.3 ppm nitrogen dioxide.

Symptoms and changes in pulmonary function of subjects with chronic obstructive pulmonary disease (COPD) and elderly normal subjects, induced by a 4-h exposure to 0.3 ppm NO2, were investigated using a double-blind, crossover design with purified air. The 5-day experimental protocol required approximately 2 wk with at least a 5-day separation between randomized 4-h exposures to either NO2 or air which included several periods of exercise. Over a 2-yr period, COPD subjects, all with a history of smoking, consisting of 13 men and 7 women (mean age of 60.0 yr) and 20 elderly normal subjects of comparable age and sex were evaluated. During intermittent light exercise, COPD subjects demonstrated progressive decrements in FVC and FEV1 compared with baseline with 0.3 ppm NO2, but not with air. Differences in percent changes from baseline data (air-NO2) showed an equivocal reduction in FVC by repeated measures of analysis of variance and cross-over t tests (p less than 0.10). Subgroup analyses suggested that responsiveness to NO2 decreased with severity of COPD; in elderly normal subjects, NO2-induced reduction in FEV1 was greater among smokers than never-smokers. A comparison of COPD and elderly normal subjects also revealed distinctions in NO2-induced responsiveness.

Effects of nitrogen dioxide exposure on bronchoalveolar lavage proteins in humans.

Nitrogen dioxide (NO2) is a pollutant of both outdoor and indoor atmospheres that has the potential to alter alveolar epithelial permeability. In order to assess alterations in the protein content of alveolar lining fluid induced by brief (3-h) exposures to low-level NO2, normal volunteers were exposed sequentially to air and NO2, separated by at least 2 wk, in an environmental chamber. Bronchoalveolar lavage (BAL) was performed after exposure. Four experimental protocols were used: (1) continuous 0.60 ppm NO2 with BAL performed 3.5 h after exposure (n = 8), (2) background 0.05 ppm NO2 with three 15-min peaks of 2.0 ppm followed by BAL 3.5 h after exposure (n = 15), (3) continuous 0.60 ppm NO2 with BAL performed 18 h after exposure (n = 8), and (4) continuous 1.5 ppm NO2 with BAL 3.5 h after exposure (n = 15). No changes in lavage fluid levels of total protein or albumin were observed in response to NO2. However, exposure to continuous 0.60 ppm NO2 was associated with increases in lavage fluid levels of the antiprotease alpha-2-macroglobulin (alpha 2M) when assessed 3.5 h after exposure (air versus NO2: 20 +/- 1 versus 29 +/- 2 ng/ml, P = 0.01). No significant changes in levels of alpha 2M in BAL fluid were observed in the other exposure protocols. Lavaged cell numbers, differential counts, and viability were not altered by exposure to the pollutant.(ABSTRACT TRUNCATED AT 250 WORDS)

Nitrogen dioxide exposure in vivo and human alveolar macrophage inactivation of influenza virus in vitro.

Epidemiologic studies have reported an increased incidence of respiratory infections and illness in association with elevated indoor levels of nitrogen dioxide (NO2). Animal exposure studies have found that brief exposures to peak levels of NO2 produce greater morbidity than continuous lower level exposure. In order to examine the effect of NO2 inhalation on human alveolar macrophages, normal volunteers were exposed sequentially to air or NO2, by double-blind randomization, in an environmental chamber. Two exposure protocols with comparable concentration x time products were used: (a) continuous 0.60 ppm NO2 (n = 9), and (b) background 0.05 ppm NO2 with three 15-min peaks of 2.0 ppm (n = 15). Inhalation of NO2 caused no significant changes in pulmonary function or airway reactivity in either exposure protocol. Alveolar macrophages obtained by bronchoalveolar lavage 3 1/2 hr after exposure to continuous 0.60 ppm NO2 tended to inactivate influenza virus in vitro less effectively than cells collected after air exposure (1.96 vs 1.25 log10 plaque-forming units on Day 2 of incubation, P less than 0.07). Four of nine subjects accounted for the observed impairment in virus inactivation; cells from these four subjects demonstrated an increase in interleukin-1 (IL-1) production after NO2 vs air, whereas the five remaining subjects decreased IL-1 production after NO2. In contrast, intermittent peak exposure did not alter the rate of viral inactivation or IL-1 production. This methodology has the potential to identify pollutant effects on mechanisms of respiratory defense in humans.