Thermally induced asthma and airway drying

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