Airway hyperresponsiveness in guinea pigs exposed to acid-coated ultrafine particles.

Although several epidemiological studies have provided evidence that airborne sulfate particles can produce adverse health effects in susceptible individuals, there is only limited data demonstrating respiratory effects in human volunteers and experimental animals at near ambient concentrations. We have demonstrated previously that the mixing of metal oxide particles with SO2 under humid conditions produces acid-coated particles that are significantly more potent in causing pulmonary function changes than pure acid droplets. The present study examined the nonspecific airway responsiveness to acetylcholine in guinea pigs exposed to acid-coated zinc oxide particles. One and a half hours after a 1-h exposure to the aerosols or a control atmosphere, pulmonary resistance (RL) was measured in awake, spontaneously breathing animals before and during a challenge with increasing doses of iv acetylcholine (Ach). The provocative infusion rate of Ach that resulted in a 100% increase in RL (PR100) was significantly decreased (p less than .05) in animals exposed to sulfuric acid-coated metal oxide particles (approximately 30 micrograms/m3 sulfate) compared to control animals exposed to furnace gases (79.6 +/- 19.4 vs. 179.6 +/- 16.2 micrograms/kg/min, mean +/- SE, respectively). The PR100 of animals exposed to SO2 (109.1 +/- 45.4) or metal oxide particles (106.7 +/- 38.1) alone was not significantly different from that of furnace gas control animals, indicating that the acid coating on the metal oxide particles and not the particles themselves or the SO2 was responsible for the decrease in the PR100. Moreover, a 10-fold greater amount of total sulfate as a pure aqueous sulfuric acid aerosol was necessary to produce a decrease in PR100 (88.6 +/- 11.0 micrograms/kg/min) equivalent to that produced by coated particles. These results suggest that acute exposure to near-ambient concentrations of sulfuric acid under conditions that promote the formation of acid as a surface coating in respirable particles can induce a nonspecific airway hyperresponsiveness. In a similar manner, a dose-dependent significant decrease in PR100 was also produced in animals exposed to sodium sulfite droplets. Thus a single exposure to different forms of sulfur oxide aerosols can induce an alteration in the responsiveness of airway smooth muscle in the guinea pig.