Symptomatic Bronchoconstriction after Short-Term Inhalation of Sulfur Dioxide

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Abstract
We studied the relationship between duration and concentration of exposure in SO2-induced bronchoconstriction in 8 asthmatic subjects. On separate days, we administered SO2 in humidified air through a mouthpiece at 2 concentrations (0.5 and 1.0 ppm) for 3 time periods (1, 3, and 5 min) during eucapnic hyperpnea (60 L/min). Humidified air was administered for 5 min as a control. Bronchoconstrictuion was assessed by measurement of specific airway resistance (SRaw). The magnitude of the bronchoconstrictor response to both concentrations of SO2 increased progressively over the 3 time periods studied. The mean (.+-. SE) increase in SRaw (in L .times. cm H2O/s) and percent increase above baseline (in parentheses) after each exposure to SO2 were as follows: 2.5 .+-. 0.3 (34%) after 0.5 ppm for 1 min; 7.5 .+-. 4.7 (93%) after 1.0 ppm for 1 min; 13 .+-. 3.2 (173%) after 0.5 ppm for 3 min; 31.4 .+-. 7.4 (395%) after 1.0 ppm for 3 min; 19.6 .+-. 4.0 (234%) after 0.5 ppm for 5 min; 44.1 .+-. 9.8 (580%) after 1.0 ppm for 5 min; 3.5 .+-. 1.5 (46%) after humidified air for 5 min. For the group, the increases in SRaw caused by inhalation of both concentrations of SO2 for 1 min were small. However, 2 of 8 subjects did develop large increases in SRaw and chest tightness after inhalation of 1.0 ppm for 1 min. Seven of 8 subjects developed wheezing, chest tightness, or hyspnea and used an inhaled bronchodilator after inhalation of 0.5 ppm for 3 and 5 min and 1.0 ppm for 3 minutes. Two subjects were unable to complete the 5-min exposure to 1.0 ppm because of symptomatic bronchoconstriction. These results suggest that short-term (i.e..ltoreq. 3 min) inhalation of near ambient concentrations of SO2 can cause clinically significant bronchoconstriction. If these effects are confirmed in freely breathing subjects, pollution control strategies may need to be devised to prevent such short-term peak concentrations of SO2 from occurring in ambient air.

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