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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Final Progress Reports: Louisiana State University: Combustion-Generated EPFRs: Assessing Cardiovascular Risks of Exposure

Superfund Research Program

Combustion-Generated EPFRs: Assessing Cardiovascular Risks of Exposure

Project Leader: Tammy R. Dugas
Co-Investigators: Kurt J. Varner, Huijing Xia (LSU Health Sciences Center - New Orleans)
Grant Number: P42ES013648
Funding Period: 2011-2025
View this project in the NIH Research Portfolio Online Reporting Tools (RePORT)

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Final Progress Reports

Year:   2017 

Kurt Varner, Ph.D., leads a research team that has shown that inhalation of environmentally persistent free radicals (EPFRs) can produce cardiovascular toxicity in rodents. First, they showed that the EPFR DCB230 directly kills mouse and rat heart cells in culture by inducing oxidative stress, which in turn initiates an intrinsic, mitochondrial signaling pathway. In intact rats, they showed that nose-only inhalation of DCB230 decreases the hearts ability to pump blood in otherwise healthy animals and impairs the hearts ability to functionally compensate for a subsequent ischemic injury. This decrease in heart function appears to be due to incomplete filling of the heart due to increased pulmonary resistance. The researchers also examined the functional effects of DCB230 exposure in rats having preexisting ischemic disease. Three weeks after myocardial infarction, rats were exposed to DCB230, five days/week for three weeks. After two weeks of exposure, systolic arterial pressure was significantly greater in the infarcted rats exposed to DCB230 than in control rats. While infarcted rats could functionally compensate for the ischemic damage to the heart, rats exposed to DCB230 were unable to increase contractile function. The researchers are assessing heart rate variability to determine whether changes in autonomic function are responsible for the increased systolic blood pressure. The team's newest studies, performed in mice using their custom inhalation system, provided new evidence that inhaled EPFRs can produce vascular dysfunction via direct actions on the blood vessels independent of systemic or pulmonary disease. Taken together, their data may have important clinical implications for healthy individuals and those with pre-existing cardiovascular disease who are exposed to high concentrations of environmental EPFRs.

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