Rats were exposed for up to 3.75 h to 0.20-0.80 ppm O3 under conditions of rest and treadmill exercise up to 30 m/min, 20% grade, to assess the importance of exposure duration, O3 concentration, and exercise on lung tissue injury. Focal lung parenchymal lesions increased in abundance and severity in response to the three variables; however, exercise was the most important. Lesion response to exercise was greater than that predicted by a simple proportion to estimated effective dose of O3. The results emphasize the importance of including exercise in assessment of possible adverse health effects of exposure to airborne pollutants.

The objective of this study was to evaluate the toxicity of inhaled diesel engine–generated fine carbon particles, when an acid mixture of the type found in California's air was also present. Rats were exposed nose–only for 5 hours per day for 5 consecutive days. The target concentrations of the pollutants in the three atmospheres studied were: (a) 0.5 mg/m3 diesel exhaust soot, (b) 0.35 mg/m3 nitric acid + 0.15 mg/m3 sulfuric acid, and (c) 0.5 mg/m3 diesel exhaust soot + 0.35 mg/m3 nitric acid + 0.15 mg/m3 sulfuric acid. Control rats were exposed using the same schedule to purified air. The evaluation of potential toxic effects in exposed rats included: (a) measurement of respiratory tract clearance of insoluble tracer particles; (b) histopathologic examination of respiratory tract tissues, including autoradiographic measures of cell turnover as an index of cell killing; and (c) measurement of functional effects on pulmonary alveolar macrophages. Biological effects were observed for each of the atmospheres studied. None of the atmospheres produced significant lung cell damage, but retained soot deposits were seen in the lung after exposure to atmospheres that contained soot. Although the diesel soot + acids atmosphere did not alter early or late clearance of tracer particles, this atmosphere – and the other two atmospheres studied – depressed pulmonary macrophage functions. This interference with macrophage functions may have significant implications to human health. © 1991, Mary Ann Liebert, Inc. All rights reserved.

Although photochemical air pollutants are believed to be associated with respiratory illness, there is also a need to consider their possible effects on postnatal lung maturation. The purpose of this study was to determine whether the maturation of lungs of young beagle dogs might be altered by an inhalation exposure to ozone that represents a severe 5-d episode of photochemical oxidant air pollution. Exposures were at 6 wk of age to purified air, 1 or 2 ppm ozone for 4 h/d on 5 consecutive days. After holding for 6 wk in clean air, lungs were removed and weighed, and the left lung was fixed both by inflation at 30 cm pressure and immersion using buffered formalin. Histologic sections were used for morphometric measurements. Statistical analysis showed that the mean linear intercept (inversely related to lung surface area) was greater than controls (up to about 5%) in the 1 ppm ozone-exposed group. This effect was not seen at 2 ppm ozone, apparently due to large variations in mean linear intercept. No significant differences were seen in body weight, chest girth, lung weight, or volumes of the fixed, inflated lungs. It is concluded that if anatomic maturation of the lung was retarded by this brief regimen of ozone exposure, the effect was small and not likely to have major health consequences.

Several inhaled atmospheres were tested for effects on the rat respiratory defense system. Materials studied included ozone and aerosols of ammonium sulfate, ferric sulfate, and sulfuric acid; relative humidity was also a controlled experimental variable. Each sulfate was studied alone as a submicrometer aerosol at a concentration of 3.5 mg/m3 in air and combined with ozone at 0.8 ppm. Results were compared with those for sham-exposed animals and for rats exposed to ozone alone. Air pollutant exposures, inside stainless steel chambers, were one time only for 4 h. The end points for evaluation of effects were measurements of early and late rates of clearance of radiolabeled insoluble tracer particles. Tracer particles were inhaled before air pollutant exposures and particle clearance was followed for about 2 wk. Ozone alone slowed the early (0-50 h after exposure) particle clearance and stimulated clearance during the later phase (2-17 d). High humidity usually amplified these effects of ozone as well as many of the other atmospheres studied. Sulfate aerosols alone tended to produce relatively small effects on early or late clearance. Combinations of ozone and aerosols resulted in effects that were similar to those of ozone alone. The data do not support the hypotheses that sulfate aerosols synergize with ozone in altering respiratory tract clearance, sulfuric acid being a probable exception. These data alone cannot be used to predict the overall health effects of the materials studied.