Superfund Research Program

Oxidative Stress Core

Project Leader: Tammy R. Dugas
Grant Number: P42ES013648
Funding Period: 2011-2018

Project-Specific Links

Final Progress Reports

Year:   2017 

The Oxidative Stress Core worked with the biomedical projects to demonstrate that through a unique chemistry, environmentally persistent free radicals (EPFRs) produce damaging forms of reactive oxygen called reactive oxygen species (ROS). Once inhaled, this ROS production is maintained in a biologic environment such as the surface of the lung. Excessive ROS production is known to induce damage to cellular components and molecules through a process known as oxidative stress. Through interaction with the biomedical projects, the Core demonstrated that EPFR exposure induces oxidative stress in the lungs and heart. In cell culture models that mimic the interface between the air and the blood in the lungs, the research team found that EPFRs promote oxidative stress in epithelial cell and the cells that line the surface of the lungs, and that this oxidative stress promotes injury to the endothelial cells that line capillaries and blood vessels. These findings highlight the unique interrelationship between the lungs, the vasculature, and oxidative stress in determining the pathologic responses that occur after EPFR inhalation. This past year, the researchers worked to establish a dry particle dispersion system to facilitate chronic, whole-body exposure of mice to EPFRs. They also assisted the Environmentally Persistent Free Radicals Increase Cardiac Vulnerability to Ischemia Project in assessing cardiovascular effects, oxidative stress markers, and inflammatory cells in the lung and blood, to demonstrate that the vasculature is a primary target of EPFRs. The Core's work with the biomedical projects has demonstrated that through their unique chemistry, EPFR inhalation in and around Superfund Sites could potentially pose a human health risk.