Sulfuric acid-layered ultrafine particles potentiate ozone-induced airway injury.

Urban air pollution in the United States is composed of a complex mixture of particles and gases. Among the most prominent products of the atmospheric pollutants are sulfur oxides and ozone. In this report, we use two exposure protocols to examine the interaction between exposure to these two pollutants. In the first exposure regimen, guinea pigs were exposed to sulfuric acid (pure sulfuric acid mist or sulfuric acid layered on ZnO) for 1 h. Each exposure is followed 2 h later by another exposure to 0.15 ppm ozone for 1 h. Pulmonary function parameters were measured immediately after the ozone exposure. In guinea pigs that were exposed to 300 micrograms/m3 pure sulfuric acid mist, subsequent exposure to 0.15 ppm ozone did not produce additional change in pulmonary functions. In guinea pigs that were exposed to 84 micrograms/m3 sulfuric acid layered on ZnO, subsequent exposure to 0.15 ppm ozone produced more than additive alterations in vital capacity and diffusing capacity. In the second exposure regimen, guinea pigs were exposed to 24 micrograms/m3 sulfuric acid layered on ZnO for 3 h/d for 5 d. On d 8 and 9, animals received two additional daily 3-h exposures to 24 micrograms/m3 sulfuric acid layered on ZnO, and pulmonary functions were measured at the end of the daily exposure. Greater reductions in lung volumes and diffusing capacity were observed in animals on d 9 than would be observed in animals that received no additional exposure. In the third exposure regimen, guinea pigs were exposed to 24 micrograms/m3 sulfuric acid layered on ZnO for 3 h/d for 5 d. On d 9, animals were exposed to 0.15 ppm ozone for 1 h and pulmonary functions were measured at the end of the ozone exposure. Ozone exposure on d 9 induced reductions in lung volumes and diffusing capacity that were not observed in animals receiving exposures to either ozone or sulfuric acid layered ZnO alone. We conclude that single or multiple exposure to sulfuric acid-layered ZnO sensitizes guinea pigs to subsequent sulfuric acid or ozone exposure.

Pulmonary effects of ultrafine coal fly ash inhaled by guinea pigs.

Guinea pigs were exposed to ultrafine coal fly ash produced in a laboratory furnace. The average mass median aerodynamic diameter and the average mass concentration of Illinois no. 6 fly ash produced in all exposure conditions were 0.21 microns and 5.8 mg/m3, respectively. In guinea pigs exposed to Illinois no. 6 fly ash, total lung capacity (TLC), vital capacity (VC), and diffusing capacity for carbon monoxide (DLco) were significantly reduced below the control values immediately, 2 h, and 8 h postexposure. The diffusing capacity was still 10% below the control 96 h after exposure. The total sulfate in the Illinois no. 6 fly ash as determined using ion chromatography is 1105 +/- 120 micrograms/m3. Animals exposed to the Montana lignite fly ash at comparable concentration and particle size did not show alteration in diffusing capacity. The data suggest that part of the sulfate present in the fly ash of Illinois no. 6 could be in the form of sulfuric acid and is responsible for the adverse effects observed in the exposed animals. The sulfuric acid in the fly ash of Montana lignite is neutralized by its high alkali content and produces no change in lung functions.

Functional changes in the lungs of guinea pigs exposed to sodium sulfite aerosols.

Guinea pigs were exposed head only for 1 hr to submicrometer sodium sulfite aerosols (mass median aerodynamic diameter = 0.36 micron, sigma g = 2.96) at 474, 669, and 972 micrograms SO3(2-)/m3. Respiratory mechanics were measured in unanaesthetized animals before, during, and after exposure. Dose-related increases in resistance and decreases in compliance were observed. At 972 micrograms SO3(2-)/m3, the sodium sulfite aerosol caused a 50% increase in resistance and a 19% decrease in compliance. These changes were still present 1 hr after the end of exposure. The results were used to assess the irritant potency of sodium sulfite aerosol. Another group of guinea pigs was exposed whole body for 1 hr to the same aerosol at 0, 204, 395, and 1152 micrograms SO3(2-)/m3. Immediately after the exposures, lung volume, diffusion capacity for carbon monoxide (DLCO), and wet lung weight were evaluated in anesthetized, tracheotomized animals. As compared to controls, total lung capacity, vital capacity, functional residual capacity, residual volume, and DLCO were all decreased with increasing concentrations of sodium sulfite. Dose-related increases in wet lung weights were also observed. These results were compared with the irritant responses of animals exposed to zinc oxide and sulfur dioxide mixed under different conditions of temperature and humidity.