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*GAS-PHASE AND PARTICULATE COMPONENTS OF DIESEL EXHAUST PRODUCE DIFFERENTIAL CARDIOPHYSIOLOGICAL IMPAIRMENTS IN HEALTHY RATS
Citation:
GORDON, C. J., Q. T. KRANTZ, P. ROWSEY, M. SCHLADWEILER, A. D. LEDBETTER, AND U. P. KODAVANTI. *GAS-PHASE AND PARTICULATE COMPONENTS OF DIESEL EXHAUST PRODUCE DIFFERENTIAL CARDIOPHYSIOLOGICAL IMPAIRMENTS IN HEALTHY RATS. Presented at Society of Toxicology (SOT) Annual Meeting, Washington, DC, March 06 - 10, 2011.
Impact/Purpose:
The data suggest that particulate but not gas-phase components of DE selectively impairs cardiac contractility in a persistent manner in healthy normotensive rats, while causing acute and transient reduction in blood pressure, possibly mediated by gas phase components (Abstract does not represent USEPA policy).
Description:
We recently showed that inhalation exposure of normotensive Wistar Kyoto (WKY) rats to whole diesel exhaust (DE) elicited changes in cardiac gene expression pattern that broadly mimicked gene expression in non-exposed spontaneously hypertensive rats. We hypothesized that healthy WKY rats would develop hypertension when exposed to whole DE but not gas-phase components which includes carbon monoxide, a known inhibitor of blood pressure. Male WKY rats (12-14 wk old) were implanted with radiotelemetry units (Data Sciences) to monitor blood pressure (BP), heart rate (HR), core temperature (CT), QA interval, and motor activity (MA). Rats were placed unrestrained in chambers and exposed for 5 h/d, 5d/wk for 4 wks to filtered air (CON), gas-phase components of filtered DE (FOE), or whole DE consisting of 1.81 mg/m3 of ultrafine particles plus gas-phase components (N=4 per exposure condition). Telemetry parameters were monitored continuously at 10 min intervals during exposure and between exposures while rats were housed in their home cages. DE and FDE led to mild reductions in BP and HR during the first week of exposure. CT and MA were unaffected. QA interval was elevated in DE but not FDE during all four wks of exposure. Telemetry parameters recovered during the recovery phase each night. However, QA interval showed a tendency to remain elevated during recovery from DE. An increase in QA interval is an indication of reduction in cardiac contractility. The data suggest that particulate but not gas-phase components of DE selectively impairs cardiac contractility in a persistent manner in healthy normotensive rats, while causing acute and transient reduction in blood pressure, possibly mediated by gas phase components (Abstract does not represent USEPA policy).