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INCREASED AIRWAYS INFLAMMATION AND MODIFIED BAL CELL SURFACE PHENOTYPES IN ASTHMATICS EXPOSED TO COARSE SIZE (PM2.5-10) CONCENTRATED AMBIENT PARTICLES (CAPS)
Citation:
LAY, J., N. ALEXIS, D. PEDEN, A. J. GHIO, Y. T. HUANG, AND R. B. DEVLIN. INCREASED AIRWAYS INFLAMMATION AND MODIFIED BAL CELL SURFACE PHENOTYPES IN ASTHMATICS EXPOSED TO COARSE SIZE (PM2.5-10) CONCENTRATED AMBIENT PARTICLES (CAPS). Presented at American Thoracic Society Annual Meeting, San Diego, CA, May 19 - 24, 2006.
Description:
Although associations between inhalation of PM10 and disease morbidity and mortality appear stronger for fine (PM2.5) vs coarse (PM2.5-10) or ultrafine/UF (PM<0.1) PM. In vitro studies suggest that PM2.5-10 are more potent in inducing pro-inflammatory cytokine responses from alveolar macrophages and airway epithelial cells. Evidence suggests that asthmatics may be particularly susceptible to the health effects of PM2.5-10. Airways inflammation and potentially impaired innate host defense capabilities may heighten sensitivity of asthmatics to inhaled PM2.5-10. We exposed mild-moderate asthmatics to coarse concentrated ambient particles (CAPS) (mean + SD = 91 + 15 ug/m3) and filtered air (FA) on two separate occasions. Bronchoalveolar lavage (BAL) and bronchial wash (BW) were obtained 20 hrs. after exposure. Flow cytometry was performed on BAL leukocytes and assessed for cell-surface phenotypes associated with innate host defense (CD 11 b, mCD14, CD64), antigen presentation/T-cell interaction (HLA-DR, CD86, CD80, CDla, CD40) and inflammation (CD16). Preliminary data (N=5) shows that CAPs (vs FA) caused a moderate increase in BW %PMN in 4 of 5 subjects. No changes in %PMNs were noted in BAL. All surface markers on monocytes were modified by CAPs, but only mono CD16 (72 +26 vs. 23 + 5) and macrophage HLA-DR (123 + 23 vs. 58 + 14) were significantly (p<0.05) elevated. This suggests that CAPs induce inflammation in the lungs of asthmatics and up-regulate surface receptors that mediate pathogen recognition and antigen presentation, responses that can lead to increased sensitivity to inhaled allergic stimuli. This abstract does not necessarily reflect the views of the US-EPA and no official endorsement should be inferred.