Superfund Research Program

Combustion-Generated Ultrafine Particles: Cardiovascular and Cardiac Effects (ARRA Funded)

Project Leader: Kurt J. Varner
Grant Number: P42ES013648
Funding Period: 2009-2011

Project-Specific Links

Final Progress Reports

Year:   2010 

Epidemiological data have consistently shown a positive correlation between increased airborne PM and hospitalizations for cardiovascular events including ischemic heart disease, cardiac arrhythmias, congestive heart failure, and death, especially in individuals with existing pulmonary disease. Dr. Varner’s research group is examining whether persistent free radical-ultrafine particle systems produced by the combustion/thermal degradation of hazardous wastes produces cardiac toxicity by increasing oxidative stress in the heart. They are comparing the cardiac/cardiovascular responses elicited by the acute and repeated administration of persistent free radical-ultrafine particle systems in control rats or rats with chronic obstructive pulmonary disease (COPD) and working to identify the mechanisms by which environmentally persistent free radicals-ultrafine particles produce oxidative stress and cardiac toxicity in vivo.

This year the researchers determined that ultrafine particles can decrease baseline ventricular function in vivo and are consistent with previous reports of particle-mediated functional deficits in isolated heart preparations. They also produced the first direct evidence that environmentally persistent free radicals produce oxidative stress and inflammation in rat hearts in vivo, resulting in the redox modification of cardiac proteins involved in energy production and contractile function.

The ability of particles to decrease baseline cardiac function and increase cardiac vulnerability to ischemia could have tremendous relevance regarding the clinical prognosis for individuals exposed to high ambient levels of particles, and/or those individuals suffering cardiac ischemia during, or shortly after exposure to high levels of airborne particulates. Identifying the roles oxidative stress and inflammation play in mediating the cardiac toxicity elicited by particles may provide the basis for preventative measures and/or treatments for individuals exposed to airborne particulates.