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EFFECTS OF SUBCHRONIC EXPOSURE TO CONCENTRATED AMBIENT PARTICULATES ON ELECTROCARDIOGRAM AND HEART RATE VARIABILITY IN SPONTANEOUSLY HYPERTENSIVE RATS
Citation:
Rowan, W. H., L. B. Wichers, J. P. Nolan, D L. Costa, AND W P. Watkinson. EFFECTS OF SUBCHRONIC EXPOSURE TO CONCENTRATED AMBIENT PARTICULATES ON ELECTROCARDIOGRAM AND HEART RATE VARIABILITY IN SPONTANEOUSLY HYPERTENSIVE RATS. Presented at American Thoracic Society, Orlando, FL, May 21-26, 2004.
Description:
Epidemiological studies have linked air pollution exposure to adverse respiratory health effects, especially in individuals with inflammatory airways disease. Symptomatic asthmatics appear to be at greatest risk. We previously demonstrated that exposure of rats to particulate matter (PM)-derived samples containing certain metals [i.e., copper (Cu) and zinc (Zn)] resulted in acute lung injury, neutrophilic inflammation, and alveolitis. Herein, we investigated specific Cu- and/or Zn-induced alveolar epithelial effects to examine whether metal-induced effects may be exaggerated under inflammatory conditions. Using Cu or Zn exposures that individually were noncytotoxic in confluent RLE-6TN (rat type II alveolar) cells, results indicated that Cu+Zn exposure resulted in minor epithelial injury and increased MIP-2 (2.0-fold) production; while Zn or Cu+Zn exposure resulted in 1.5- and 2.0-fold increases in RANTES. Thereafter, to simulate the inflamed lungs of symptomatic asthmatics, cells were exposed to metals a combination of TNF , IL-1 , and IFN (cytomix). Simultaneous exposure of cells to cytomix + Cu+Zn x 24h did not augment cell injury or MIP-2 production, and RANTES production was reduced. Exposure to cytomix x 48h with Cu+Zn during the latter 24h also failed to amplify epithelial injury and was associated with decreased MIP-2 and RANTES release. Of interest, however, pre-exposure of cells to cytomix x 24h and then Cu+Zn x 24h resulted in significantly greater RANTES release; with negligible effects on injury or MIP-2. Similar results were obtained in cells pre-inflamed with IL-1 or IFN followed by Zn or Cu+Zn exposure. Results support the possibility that exposure of individuals with pre-existing lung inflammation to Zn-containing PM may enhance chemokine production thus amplifying eosinophilic inflammation, potentially exacerbating asthmatic symptoms and disease. (Abstract does not reflect USEPA policy).