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Overview of the PMHealth Effects Research Program

A. J. Ghio, J. Vadenberg, J. Soukup and S. Becker


 
ABSTRACT

We tested the hypothesis that exposure of healthy volunteers to concentrated ambient particles (CAPS) is associated with an influx of inflammatory cells into the lower respiratory tract. Thirty-eight volunteers were exposed to either filtered air or particles concentrated from the immediate environment of the EPA Human Studies Facility in Chapel Hill, NC. Particle concentrations in the chamber during the exposures ranged from 23.1 - 311.1 g/m3. Volunteers alternated between moderate exercise (15 minutes) and rest (15 minutes) for a total exposure time of 2 hours. There were no symptoms noted by volunteers after the exposure. Similarly, there were no decrements in pulmonary function. Eighteen hours after exposure, analysis of cells and fluid obtained by bronchoalveolar lavage showed an increase in neutrophils in both the bronchial and alveolar fractions in those individuals exposed to CAPS. Blood obtained after exposure to CAPS contained significantly more fibrinogen relative to samples obtained prior to exposure. Previous studies of cytokine induction by PM10 pollution particulates in alveolar macrophages have indicated that endotoxin is an active component in outdoor pollution. Collection of PM2.5 and PM2.5-10 particles of teflon filters here in Chapel Hill indicated that cytokine inducing activity was associated with a soluble component of the larger particles, but not the smaller ones. Inhibition of this activity by LPS binding protein or polymyxin B, but not a metal chelator, again implied that endotoxin was present and accounted for all actvitity. When exposing macrophages to the PM2.5-10 particles themselves, cytokines were induced at > 50 fold higher levels than with the soluble fraction, while PM2.5 particles increased cytokine production approx. 5 fold compared to control. Pretreating the particles with 10 ug/ml polymyxinB reduced the activity > 50%, but not completely, suggesting that other components in the course particles may contribute to cytokine production. Individual outdoor air filters collected daily over a month implied that while water extractable endotoxin levels were relatively low and ranged 0-1.2 EU/filter (cholorimetric limulus assay), bioactivities of the extracts were much more variable. Either environmental endotoxins vary in their activating potential or other components synergize with endotoxin for cytokine production. Furthermore, PM2.5-10 inhibit phagocytosis most likely by affecting the viability of macrophages, which undergo apoptosis upon exposure. We conclude that moderate levels of ambient air particles are capable of inducing an inflammation in the lower respiratory tract as well as an increased concentration of blood fibrinogen and some portion of this effect may be associated with endotoxin content.



Reprinted from Proceedings of the 2000 Beltwide Cotton Conferences pp. 212 - 219
©National Cotton Council, Memphis TN

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Document last modified Saturday, Jun 17 2000