Relationship between the airway response to inhaled sulfur dioxide, isocapnic hyperventilation, and histamine in asthmatic subjects.

To determine whether bronchoconstriction induced by sulfur dioxide can be predicted by the airway response to inhaled histamine, we exposed on two days 46 patients with asthma to air or 0.5 ppm SO2. The exposure protocol consisted of 10 min of tidal breathing followed by 10 min of isocapnic hyperventilation at a rate of 30 l/min. Airway response was measured before (baseline) and after hyperventilation in terms of specific airway resistance, SRaw. Exposure to air increased baseline mean (SD) SRaw from 6.27 (2.12) to mean (SD) maximum post-hyperventilation SRaw of 9.10 (4.38) cmH2O*s (P less than 0.0001). Exposure to SO2 increased mean (SD) baseline SRaw from 6.93 (3.29) to mean (SD) maximum post-hyperventilation SRaw of 18.21 (18.69) cmH2O*s (P less than 0.0001). Mean (SD) effect of SO2 defined as difference between maximum post-hyperventilation SRaw after SO2 versus air was 9.11 (16.14) cm H2O*s. When evaluated individually, 26 and 34 of the 46 patients showed an airway response to hyperventilation of air and SO2, respectively. Airway response to histamine was determined as the histamine concentration necessary to increase specific airway resistance by 100%, PC100SRaw. The airway response after SO2 and PC100SRaw showed a weak but significant correlation (R = -0.48), whereas the responses to hyperventilation and SO2 did not correlate. We suggest that the mechanisms by which histamine and SO2 exert their bronchomotor effects are different and that in asthmatic patients the risk of pollutant-induced asthmatic symptoms can be poorly predicted by histamine responsiveness.