A long-term study of the effects of inhaled air pollution particles on the cardiovascular system was conducted in Riverside California.  Animals with high blood pressure or normal blood pressure were exposed to concentrated ultrafine ambient particles (UFP) for 5 hours per day, 4 days per week for 3 months.  Blood pressure, heart rate variability and histological changes in the heart were measured.  PM samples were collected and analyzed for elemental carbon, trace metals, organic carbon and peroxides (as a measure of oxidant formation on particles).  During this long term exposure, there was an unplanned incursion of smoke from wild land fires into the exposure area.  Initially during the fires, winds from the northeast (Santa Ana wind conditions) prevented smoke from the fires from reaching the exposure site.  However, after about a week the meteorological conditions changed and offshore winds began fumigating the exposure site with ambient particles that were augmented with particles from the smoke.  NASA satellite imagery enabled us to pinpoint when the wind direction changed and when the maximum period of exposure occurred.  There was a significant acute effect on blood pressure and the data suggest that exposure to smoke from wildfires may alter homeostatic control of cardiac output which might be medically significant. Long term exposures were associated with progressive increases in all exposed animals which were likely to be age-related, however the rate of increase was greater in rats exposed to PM.  Chronic exposure to PM also caused histopathological changes in the hearts of all studied strains. The effects ranged from cardiac inflammation caused by 3 months of exposure to UFP in normal and hypertensive rats.  Acute changes in blood pressure were correlated with organic constituents of the PM and with peroxides.

Reactions on ambient particles may influence acute and chronic changes in the heart: Effects following exposures of animals with and without hypertension

248th National Meeting (2014)

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