Thermally induced asthma and airway drying.

The purpose of this study was to determine whether mucosal dehydration causes thermally induced asthma. To provide data on this point, we studied the effects on lung function of progressive water loss (WL) from the respiratory tract by having eight subjects perform isocapnic hyperventilation for 1, 2, 4, and 8 min at a constant level (V E = 57.5 +/- 6.3 L/min [mean +/- SEM]) while they breathed dry air at frigid (TI = -12.5 +/- 2.7 degrees C) (cold trial) and ambient (24.3 +/- 0.7 degrees C) (warm trial) temperatures. Expired temperatures (TE) were continuously monitored, and WL from the intrathoracic airways was calculated from published relationships. FEV1 was measured before and after each challenge. Each inspirate produced stimulus-response decrements in FEV1, but the effect of cold air was greater (% Delta cold8min = 30.0 +/- 4.7%, warm = 16.0 +/- 4.4%; p = 0.01). Water loss, however, was significantly less in the cold experiment because TE was lower (WL cold8min = 4.8 +/- 0.4 g, warm = 7.1 +/- 0.7 g; p = 0.001; TE cold8min = 22.8 +/- 2.3 degrees C, warm 30.9 +/- 1.5 degrees C; p = 0.003). The FEV1 decreased as WL rose, but the largest intrathoracic losses were associated with the smallest obstructive response (% DeltaFEV1 cold8min = 30%, WL = 4.7 mg; % DeltaFEV1 warm8min = 16%, WL = 7.1 mg; p = 0.002). These data show that removal of water from the lower respiratory tract, and by inference the development of a hyperosmolar periciliary fluid, do not appear to be the primary causes of thermally induced asthma.