Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Internet Explorer is no longer a supported browser.

This website may not display properly with Internet Explorer. For the best experience, please use a more recent browser such as the latest versions of Google Chrome, Microsoft Edge, and/or Mozilla Firefox. Thank you.

Your Environment. Your Health.

Louisiana State University

Superfund Research Program

Ultrafine Pollutant Exposure Alters Pulmonary Immunologic Homeostasis (ARRA Funded)

Project Leader: Stephania A. Cormier
Grant Number: P42ES013648
Funding Period: 2009-2011

Learn More About the Grantee

Visit the grantee's eNewsletter page Visit the grantee's eNewsletter page Visit the grantee's Twitter page Visit the grantee's Facebook page Visit the grantee's Video page

Project Summary (2009-2011)

Chronic Obstructive Pulmonary Disease (COPD) is major health problem with increasing prevalence and mortality. Hypotheses for the proliferation of COPD have focused on exacerbating factors such as viral infections, tobacco exposure, and air pollution. Although understanding of the cellular and molecular mechanisms of COPD is rudimentary, considerable amounts of data now suggest a link between oxidative stress, pulmonary inflammation, and COPD. Dr. Cormier’s data, and that of others, indicate that exposure to laboratory-generated surrogate pollutant/particle systems (UFP; < 0.1 µm diameter) increases oxidative stress in vitro and in vivo. Increasing evidence suggests that an imbalance between reactive oxygen species (ROS) and reactive nitrogen species (RNS) and the enzymes that regulate their bioavailability is associated with structural damage to the airways resulting in reduced gas exchange/blood oxygenation and thus functional damage. Dr. Cormier’s preliminary results show that UFP initiate an inflammatory response in the lung that parallels the immuno- and patho-physiology observed in COPD. These data led the research group to the overall hypothesis that persistent free radical-containing ultrafine pollutant/particle systems (PFR/UFP) initiate immunological changes that predispose to chronic lung diseases (CLD), such as COPD, by increasing oxidative stress and altering dendritic cell (DC) function. The following specific aims will critically address this hypothesis:

  1. determine the impact of exposure to UFP in the normal lung and in the exacerbation of pulmonary immune homeostasis and pathophysiology in a disease setting (i.e. COPD);
  2. characterize the impact of exposure to UFP on pulmonary DC responses; and
  3. elucidate the molecular events by which UFP induces immune dysfunction and document the role of free radicals in these responses.

This application represents a unique, multidisciplinary approach to characterize the role of ROS and RNS in UFP-induced pulmonary and immune dysfunction. Completion of the project will provide insight into how combustion/thermal degradation of Superfund wastes affects the development and progression of inflammatory airways disease with the expectation of valid extrapolation to human inflammatory airways disease (i.e. COPD) and should provide a rational framework for clinical studies of antioxidant usage during UFP-associated disease exacerbation. The outcome of these studies will also have important implications for public health and environmental policy, since currently there are no air quality standards for ultrafine particulates.

Back
to Top