Concentrated ambient air particles induce vasoconstriction of small pulmonary arteries in rats.

The objective of this study was to determine whether short-term exposures to concentrated ambient particles (CAPs) alter the morphology of small pulmonary arteries in normal rats and rats with chronic bronchitis (CB). Sprague-Dawley male rats were exposed to CAPs, using the Harvard Ambient Particle Concentrator, or to particle-free air (sham) under identical conditions during 3 consecutive days (5 hr/day) in six experimental sets. CB was induced by exposure to 276 +/- 9 ppm of sulfur dioxide (5 hr/day, 5 days/week, 6 weeks). Physicochemical characterization of CAPs included measurements of particle mass, size distribution, and composition. Rats were sacrificed 24 hr after the last CAPs exposure. Histologic slides were prepared from random sections of lung lobes and coded for blinded analysis. The lumen/wall area (L/W) ratio was determined morphometrically on transverse sections of small pulmonary arteries. When all animal data (normal and CB) were analyzed together, the L/W ratios decreased as concentrations of fine particle mass, silicon, lead, sulfate, elemental carbon, and organic carbon increased. In separate univariate analyses of animal data, the association for sulfate was significant only in normal rats, whereas silicon was significantly associated in both CB and normal rats. In multivariate analyses including all particle factors, the association with silicon remained significant. Our results indicate that short-term CAPs exposures (median, 182.75 micro g/m3; range, 73.50-733.00 micro g/m3) can induce vasoconstriction of small pulmonary arteries in normal and CB rats. This effect was correlated with specific particle components and suggests that the pulmonary vasculature might be an important target for ambient air particle toxicity.

Lung inflammation induced by concentrated ambient air particles is related to particle composition.

The objectives of this study were (1) to determine whether short-term exposures to concentrated air particles (CAPs) cause pulmonary inflammation in normal rats and rats with chronic bronchitis (CB); (2) to identify the site within the lung parenchyma where CAPs-induced inflammation occurs; and (3) to characterize the component(s) of CAPs that is significantly associated with the development of the inflammatory reaction. Four groups of animals were studied: (1) air treated, filtered air exposed (air-sham); (2) sulfur dioxide treated (CB), filtered air exposed (CB-sham); (3) air treated, CAPs exposed (air-CAPs); and (4) sulfur dioxide treated, CAPs exposed (CB-CAPs). CB and normal rats were exposed by inhalation either to filtered air or CAPs during 3 consecutive days (5 hours/day). Pulmonary inflammation was assessed by bronchoalveolar lavage (BAL) and by measuring the numerical density of neutrophils (Nn) in the alveolar walls at the bronchoalveolar junction and in more peripheral alveoli. CAPs (as a binary exposure term) and CAPs mass (in regression correlations) induced a significant increase in BAL neutrophils and in normal and CB animals. Nn in the lung tissue significantly increased with CAPs in normal animals only. Greater Nn was observed in the central compared with peripheral regions of the lung. A significant dose-dependent association was found between many CAPs components and BAL neutrophils or lymphocytes, but only vanadium and bromine concentrations had significant associations with both BAL neutrophils and Nn in CAPs-exposed groups analyzed together. Results demonstrate that short-term exposures to CAPs from Boston induce a significant inflammatory reaction in rat lungs, with this reaction influenced by particle composition.