SHORT-TERM EXPOSURE TO 0.3 PPM NITROGEN-DIOXIDE DOES NOT POTENTIATE AIRWAY RESPONSIVENESS TO SULFUR-DIOXIDE IN ASTHMATIC SUBJECTS

Whether short-term exposure to low levels of nitrogen dioxide (NO2) enhances airway responsiveness in asthmatic subjects is controversial. Because it is well established that asthma is associated with increased airway responsiveness to another common air pollutant, sulfur dioxide (SO2), we examined whether short-term exposure of asthmatic subjects to 0.3 ppm NO2 potentiates airway responsiveness to inhaled SO2. We exposed nine subjects with clinically stable asthma to 0.3 ppm NO2 or filtered air in an environmental room for 30 min on 2 separate days at least 1 wk apart in a double-blind, randomized fashion. A questionnaire about common symptoms related to inhaled irritants was completed before and immediately after each exposure. Each subject exercised (60 to 80 W) on a cycloergometer during the first 20 min of each exposure. We measured specific airway resistance (SRaw) and FEV1/FVC before, 5 min after, and 1 h after completion of the air or NO2 exposures. The single-breath nitrogen test (SBN2) was also performed before and 1 h after completion of the air or NO2 exposures and closing volume was determined; subsequently, SO2 dose-response curves (0.25 to 4.0 ppm) were performed via a mouthpiece. Each dose of SO2 was inhaled at a minute ventilation of 20 L/min for 4 min and was doubled until SRaw increased by at least 8 U above baseline. The dose of SO2 required to provoke an increase in SRaw of 8 U above baseline was determined by linear interpolation from the dose-response curve (PD(8Uso2)). We found that exposure to NO2 was not associated with any change in the reported symptoms or in the measured pulmonary function tests. The mean SRaw was 7.1 ± 2.2 before and 9.5 ± 2.6 L x cm H2O/L/s after air exposure, and 7.1 ± 2.2 before and 9.7 ± 3.5 L x cm H2O/L/s after NO2 exposure but FEV1/FVC did not change. Mean SRaw, FEV1/FVC, and closing volume measured 60 min after air or NO2 exposures did not differ from baseline. The mean PD(8Uso2) was similar after air (1.25 ± 0.70 ppm) and NO2 (1.31 ± 0.75 ppm) exposures. We conclude that in exercising individuals with clinically stable asthma, a controlled 30-min exposure to 0.3 ppm NO2 is not associated with a greater change in pulmonary function than that observed after exposure to filtered air and does not potentiate airway responsiveness to inhaled SO2.