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  • Title: Health effects of acute exposure to air pollution. Part II: Healthy subjects exposed to concentrated ambient particles.
    Author: Holgate ST, Devlin RB, Wilson SJ, Frew AJ.
    Journal: Res Rep Health Eff Inst; 2003 Dec; (112):31-50; discussion 51-67. PubMed ID: 14738209.
    Abstract:
    The purpose of this study was to assess the impact of short-term exposure to concentrated ambient particles (CAPs*) on lung function and on inflammatory parameters in blood and airways of healthy human subjects. Particles were concentrated from the ambient air in Chapel Hill, North Carolina, using a Harvard/EPA (US Environmental Protection Agency) ambient fine particle concentrator (HAPC). Each of 38 subjects was exposed either to filtered air (n = 8) or to CAPs (n = 30) for two hours, during which all subjects intermittently exercised. Blood was obtained immediately before and 18 hours after exposure. Also at 18 hours after exposure, viable bronchial biopsy tissues and lavage samples were obtained from 10 CAPs-exposed and 7 control subjects by fiberoptic bronchoscopy. To balance these two groups, additional biopsy tissues were obtained from 4 control subjects participating in an identical protocol for another study. For the CAPs-exposed group, the concentration of particulate matter measuring 2.5 microm or less in aerodynamic diameter (PM2.5) in the exposure aerosols varied from 23.1 to 311.1 microg/m3; for the filtered air group, mean particle concentration was 2.9 microg/m3. For comparative analyses, the CAPs-exposed subjects were separated into three tertiles on the basis of the final concentration of particles to which they were exposed. Lung function, assessed by spirometry and plethysmography before and immediately after exposure, was unaffected by CAPs. Of the inflammatory parameters studied in blood, subjects exposed to CAPs showed mean increases in fibrinogen of 40 to 48 mg/dL with no obvious differentiation by dose, whereas subjects exposed to filtered air showed no change; red and white blood cell counts were unaffected by CAPs exposure. In bronchoalveolar lavage fluid from CAPs-exposed subjects, neutrophils showed a dose-dependent increase both when analyzed as an absolute cell count and as a percentage of total lavaged cells. Bronchial biopsy tissues from 10 CAPs-exposed subjects and 11 control subjects did not show any consistent effect of CAPs exposure on cell counts or adhesion molecule expression. We conclude that CAPs induced a modest degree of airway inflammation as judged by lavage, but this effect was not reflected in biopsy tissues from proximal airways. This discrepant finding may mean that the inflammatory effect of CAPs occurs in more distal airways or that the health effects of PM are driven by processes other than those investigated in this study.
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