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CARDIAC MOLECULAR EFFECTS INDUCED BY AIR POLLUTION PARTICLES
Citation:
Dreher, K L., R Jaskot, J H. Richards, J. Lehmann, AND T. Knuckles. CARDIAC MOLECULAR EFFECTS INDUCED BY AIR POLLUTION PARTICLES. Presented at American Thoracic Society, Atlanta, GA, May 17-22, 2002.
Description:
Abstract Submitted to the American Thoracic Society 98th International Conference, May 17 - 22, 2002, Atlanta, GA
CARDIAC MOLECULAR EFFECTS INDUCED BY AIR POLLUTION PARTICLES
K. Dreher1, R. Jaskot1, J. Richards1, and T. Knuckles2. 1U. S. Environmental Protection Agency, Research Triangle Park, NC and 2North Carolina State University, Raleigh, NC
Epidemiology and clinical studies have shown the ability of particulate air pollution to alter cardiac physiology. Currently, it is not known whether specific types of air pollution particles are capable of producing potentially adverse cardiac molecular effects. This study examines the ability of fuel oil combustion particles, residual oil fly ash (ROFA), to produce cardiac molecular effects in vivo and in vitro. Rats were exposed by intratracheal instillation to ROFA and examined from 15 min to 24h post-exposure. Gene expression profiling detected an increase in mRNA levels for several cytokines and a matrix metalloproteinase within hearts recovered from ROFA-instilled rats at 1-6h and 24h post-exposure. Western blot analysis of proteins extracted from hearts recovered from ROFA exposed rats detected an increase in phosphotyrosine protein content as well as sustained activation of the mitogen activated protein kinase intracellular signaling pathway from 15 min to 6h post-exposure. Pulmonary exposure to ROFA was found not to increase plasma levels of IL-1 , TNF , IL-10 or endothelin-1. However, elevated plasma vanadium and nickel levels were observed in ROFA-exposed rats as early as 15 min post-exposure which remained elevated up to 6h post-exposure before decreasing towards control saline levels by 24h post-exposure. Exposure of primary cardiac cell cultures to a particle free ROFA leachate produced similar molecular responses as observed in vivo. Our results demonstrate the ability of ROFA to produce cardiac molecular effects that were temporally correlated with plasma metal content. ROFA-induced cardiac molecular effects occurred rapidly and prior to pulmonary inflammation and could be reproduced in vitro. These findings suggest that: (i) specific air pollution particles are capable of inducing cardiac molecular effects typically associated with heart disease; and (ii) bioavailable metal constituents were responsible for the observed cardiac molecular effects produced following exposure to fuel oil combustion particles. (This abstract does not necessarily represent US EPA policy)