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IN VITRO EFFECTS OF PARTICULATE MATTER ON AIRWAY EPITHELIAL CELLS ISOLATED FROM CONCENTRATED AIR PARTICLES-EXPOSED SPONTANEOUS HYPERTENSIVE RATS
Citation:
Pagan, I, U P. Kodavanti, P A. Evansky, D L. Costa, AND J A. Dye. IN VITRO EFFECTS OF PARTICULATE MATTER ON AIRWAY EPITHELIAL CELLS ISOLATED FROM CONCENTRATED AIR PARTICLES-EXPOSED SPONTANEOUS HYPERTENSIVE RATS. Presented at Society of Toxicology, Nashville, TN, March 17-21, 2002.
Description:
In vitro effects of particulate matter on airway epithelial cells isolated from concentrated air particles-exposed spontaneous hypertensive rats
Ines Pagan, Urmila Kodavanti, Paul Evansky, Daniel L Costa and Janice A Dye. U.S. Environmental Protection Agency, ORD, National Health and Environmental Effects Research Laboratory, RTP, NC.
Spontaneously hypertensive (SH) rats, a strain with the genetic tendency to develop pulmonary and cardiac disease, are being used as a model to study the health effects of particulate matter (PM). In the present studies male SH rats were subjected to multiple exposures (12 exposures, over a 6 week period, 4 hr/day,) of either filtered air (control), or concentrated air particles (CAPS) from the Research Triangle Park (RTP), NC. Then, primary rat tracheal epithelial (RTE) cell cultures were established from both control and CAPS-exposed rats using an air-liquid interface system. After reaching confluency and maturity, cells were exposed to saline control, or to RTP-PM (PM 1.7-3.7, collected in bulk using a high volume sampler) at either 3.5 or 35 ug/ cm2 of culture area. Toxicity and cell injury were evaluated by lactate dehydrogenase (LDH) released and albumin translocation (index of increased solute permeability). Cell metabolism changes were evaluated by measuring intracellular glutathione (GSH) and ATP levels. RTE cell exposure to RTP-PM did not induce significant changes in LDH released by RTE cells. However, exposure of RTE cells to RTP-PM at 35 ug/ cm2 induced a mild increase in apical albumin levels that was greater in cells originating from CAPS-exposed rats than in cells from control air-exposed rats. RTP-PM exposures also induced decreases in GSH levels in cells originated from either air- or CAPS- exposed SH rats. RTP-PM exposures induced increases in ATP levels in RTE cells from either air or CAPS-exposed SH rats. Alterations of cellular metabolism by CAPS could contribute to the enhanced responses of cardiopulmonary compromised animals to the effects of ambient air pollutants, however more studies are needed to elucidate the extent of these differences. (The contents of this abstract do not necessarily reflect the views and policies of the US EPA).