Pulmonary Function, Airway Responsiveness, and Respiratory Symptoms in Asthmatics Following Exercise in No₂

Abstract

Two experiments were conducted to determine respiratory responses of persons with asthma performing intermittent moderate exercise while exposed to low concentrations of NO2. In the first, preliminary experiment, 13 male subjects, aged 19-35, with mild asthma were exposed on separate days in a chamber (natural breathing, 20 degrees C, 40% RH) to 0.30 ppm NO2 and to a control or "clean air" exposure (0.0 ppm NO2). Exposure included three 10-min periods of moderate treadmill exercise (VE = 44.5 liter/min), each followed by symptom measurement and pulmonary function testing. The average decrease in FEV1 following the initial 10 min exercise in 0.30 ppm was 11% which was significantly greater (p less than 0.05) than that observed in clean air (7%). Differences in FVC and SRaw were not significantly different at this time. Slight cough and dry mouth and throat were apparent only after the first exercise in NO2. After the second and third exercises, decreases in FEV1 and FVC and increases in SRaw were significantly greater in 0.30 than in 0.0 ppm NO2. Individual subject responses were variable. These results suggested that some asthmatics who perform moderate exercise while exposed to 0.30 ppm NO2 may experience bronchoconstriction and reduction in spirometric performance. Because of these preliminary findings, a more comprehensive, concentration-response experiment was conducted. Twenty-one male volunteers with mild asthma were exposed for 75 min with natural breathing to 0.0, 0.15, 0.30, and 0.60 ppm NO2. Exposure included three 10-min periods of moderate treadmill exercise (VE = 43 liter/min), each exercise followed by symptoms measurement and pulmonary function testing. In addition, airway responsiveness was measured two hr after each exposure by methacholine bronchial challenge testing. In the control exposures (0.0 ppm NO2), the exercise alone caused substantial decrements in pulmonary function. These decrements (as measured by decreases in FEV1 and FVC, and increases in SRaw) were not increased relative to the control exposure after any exercise session in any concentration of NO2. Furthermore, there was no overall group-averaged indication of a concentration-related effect of the NO2 on pulmonary function. Likewise, symptoms reported after NO2 exposure were not significantly different from those reported in clean air. Group-averaged airway responsiveness after exercise in NO2 was also not different from responsiveness after exercise in clean air. For only two subjects was there any indication of a concentration-related increase in airway responsiveness due to exposure to NO2.(ABSTRACT TRUNCATED AT 400 WORDS)

Dose–response relationships between occupational exposure to potash, diesel exhaust and nitrogen oxides and lung function: cross-sectional and longitudinal study in two salt mines

“…EVects of the single substance on lung function and bronchial responsiveness were shown at concentrations above 1 ppm NO 2 in healthy persons (Blomberg et al , 1997Bylin 1993;Frampton 1991;Mohsenin 1988) and above 0.1-0.25 ppm in asthmatics (Folinsbee et al 1992;Strand et al 1996Strand et al , 1998Roger et al 1990) as well as COPD patients (Morrow et al 1992). In a previous study (Frampton et al 1989) it was found that alveolar macrophages obtained from healthy subjects by broncho-alveolar lavage when exposed to 0.60 ppm NO 2 for 3 h were less eVective when inactivating inXuenza virus in vitro as compared with alveolar macrophages obtained after air exposure.…”

Diesel exhaust enhances airway responsiveness in asthmatic subjects

“…Animal studies have provided evidence that the particulate fraction of DE is able to cause an increase in airway responsiveness [28], but to the best of the authors9 knowledge, there are no previous experimental data concerning particulate pollution and hyperresponsiveness in humans. Regarding the gaseous phase of DE, some studies have reported an immediate increase in airway responsiveness following exposure to NO 2 [29,30], whereas other studies have not [31]. Most studies have been designed to explore the immediate and early effects of NO 2 and it is not clear from the literature whether NO 2 is able to induce a sustained increase in airway responsiveness.…”

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

“…In asthmatics, the data on nonspecific hyperresponsiveness to NO 2 suggests a sensitizing effect between 0.2 ppm and 0.6 ppm, though the responses, where significant, were small and unlikely to be of clinical significance (Bylin et al, 1985;Mohsenin, 1987;Strand et al, 1996). A limited number of studies have evaluated airway hyperresponsiveness in asthmatics at multiple NO 2 concentrations, and the results of these studies do not support a clear concentration-response relationship between 0.1 ppm and 0.5ppm (Bylin et al, 1988;Roger et al, 1990;Tunnicliffe, Burge & Ayres, 1994). It should be noted that, in all of the studies cited, a range of responses were observed; and in many studies, subgroups of responders were identified.…”