Sediment from hurricane katrina: potential to produce pulmonary dysfunction in mice

• Published in: International journal of clinical and experimental medicine Vol. 1; no. 2; pp. 130 - 144
• Main Authors: Wang, Kai, You, Dahui, Balakrishna, Shrilatha, Ripple, Michael, Ahlert, Terry, Fahmy, Baher, Becnel, David, Daly, Melissa, Subra, Wilma, McElduff, James S, Lomax, Larry G, Troxclair, Dana, Cormier, Stephania A
• Format: Journal Article
• Language: English
• Published: United States e-Century Publishing Corporation 01-01-2008
• Subjects: Original; pulmonary dysfunction; respiratory toxicology; Hurricane Katrina
• ISSN: 1940-5901; 1940-5901

On August 29, 2005, Hurricane Katrina made landfall along the Gulf Coast as a Category 3 hurricane. The associated storm surge and heavy rainfall resulted in major flooding throughout the New Orleans area. As the flood waters receded, thick sediment was left covering the ground and coating the interior of homes. This sediment was dispersed into the air and inhaled as dust by returning residents and workers. Our objective in this study was to evaluate the potential pulmonary effects associated with the respirable particulate matter (PM) derived from Hurricane Katrina (HK-PM) in mice. Samples of PM were collected from several locations along the Gulf Coast on September 30 and October 2, 2005 and had a mean aerodynamic diameter ranging from 3-5 mum). Chemical analysis and cytotoxicity assays were performed for all HK-PM samples. A few samples with varying levels of cytotoxicity were chosen for an acute inhalation exposure study. Airborne PM10 levels recorded in the New Orleans area post-Katrina were variable, ranging from 70 mug/m3 in Gentilly to 688 mug/m3 in Lakeview (residential areas). Mice exposed to one of these samples developed significant pulmonary inflammation and airways resistance and hyperresponsiveness to methacholine challenge. These studies demonstrate that dispersion of certain Katrina sediment samples through either natural (e.g., wind) or mechanical (e.g., vehicles) processes promotes airflow obstruction in mice.