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Title: Co-Exposure to PM and O-3: Pulmonary C Fiber Platelet Activation in Decreased HRV

Principal Investigator / Author(s): Tablin, Fern

Contractor: UC Davis

Contract Number: 13-311

Research Program Area: Health & Exposure

Topic Areas: Health Effects of Air Pollution


Air pollution is composed of a variety of substances including ozone and particulate matter. Historically it has been shown that older people with pre-existing cardiovascular disease are particularly sensitive to air pollution exposure. This study used mature adult rats with and without pre-existing cardiovascular disease to understand the effects of combined pollutant (ozone and particulate matter) exposure on the cardiovascular and respiratory systems. The results demonstrated that both mature adult normal and spontaneously hypertensive animals were most significantly affected by co-pollutant exposures. In addition, adult animals with preexisting cardiovascular disease were more susceptible to oxidant stress and at greater risk with regard to alterations in the peripheral vasculature and heart and lung tissue as a result of exposure to either ozone or the combination of ozone and ultrafine particulate matter. In the peripheral blood, this was reflected in a greater number of platelet-white blood cell aggregates. Pathological changes, including edema, macrophage, and neutrophil infiltrates, as well as necrosis in the proximal airways and terminal bronchioles were present in the lungs of spontaneously hypertensive animals exposed either to ozone or combined ozone/ultrafine particulate matter. Similar lesions were seen in the normal Wistar rats but only for the combined pollutants. In both groups of animalís, lung injury and inflammation was associated with an increase in heart rate variability that was associated with increased number and severity of arrhythmias and an increase in parasympathetic outflow to the heart. Both strains of rats exposed to ozone + ultrafine particulate matter had significant differences in the severity of ventricular entropy, severity of arrhythmias and ventricular pre-contractions as well as total number of atrial-ventricular block events when compared to filtered air exposed animals. Only, in the spontaneously hypertensive rats were the changes in heart rate regulation and arrhythmias associated with acute myocardial cellular necrosis, hypercontractility and focal myocardial organized necrosis. When comparing the two strains of rats there were significantly greater severity scores for all myocardial histopathologic parameters in the spontaneously hypertensive animals exposed to combined pollutants. The data is consistent with the combined pollutant atmosphere being more toxic than would be expect from the responses elicited by ozone and ultrafine particulate matter alone and with chronic cardiovascular disease increasing the susceptibility to pollutant induced lung and heart injury. This information from this study provides a better understanding of the mechanisms responsible for increased deaths associated with older people with underlying cardiovascular disease in response to significant air pollution exposure.


For questions regarding this research project, including available data and progress status, contact: Research Division staff at (916) 322-3893

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