Key points are not available for this paper at this time.
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.
Saldiva et al. (Sat,) studied this question.