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

Abstract

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.

Keywords: Hurricane Katrina; pulmonary dysfunction; respiratory toxicology.

Figure 1

Decreased viability of epithelial cells exposed to sediment samples. Human epithelial cells (HEp2) were exposed to various concentrations of sediment (30 or 300 μg/ml). After 24 h, cell viability was assessed. Data are shown as percentage of viable cells. The numbers in the abscissa refer to different sediment samples. For example, 12 represents sediment sample #12 (SS-12). All samples were assayed in duplicate and the experiment repeated two times.

Figure 2

Significant changes in airway resistance is observed in mice exposed to Katrina sediment. A) Whole body plethysmography was performed to examine airway responsiveness (Penh). **p < 0.01 vs. saline; ^^^p<0.001 vs. silica. In addition, measurements of specific airway mechanics in response to MeCh were performed using the forced oscillation technique (B). Mice exposed to silica (data not shown) were statistically no different than mice exposed to saline alone. Data are expressed as means ± SE, n=5-6. ***p < 0.001 vs. saline/SS-C/SS-13.

Figure 3

Exposure of mice to SS-12 increased leukocyte numbers in the BALF. Significant increases in BALF cellularity was observed only when mice were exposed to SS-12. The increase in total BALF cellularity correlated with elevated levels of neutrophils. Data are expressed as means ± SE, n=6-8. ***p < 0.001 vs. saline. **p < 0.01 vs. saline. *p < 0.05 vs. saline.

Figure 4

Histopathology associated with exposure to SS-12. Lung tissue sections were obtained from mice exposed to saline, silica, and SS-12. Mild inflammation was observed in the luμgs of mice exposed to silica. Moderate inflammation, diffuse alveolitis, and mild type II pneumocyte hyperplasia were observed in the lungs of mice exposed to SS-12. Lung tissue sections were stained with H&E and representative photomicrographs taken at lOO×.

Figure 5

The oxidative ability of SS-12 is elevated and SS-12 induces oxidative stress in the lungs of exposed mice. A) The DTT consumption of HK-PM after a thirty minute incubation at room temperature. Oxidative ability was measured in quadruplicate by use of the DTT assay. DTT consumption was normalized to vehicle control and expressed as the percent maximum consumption. B) The amount of ROS in HK-PM exposed lungs was assessed by DCF staining. The increase in DCF fluorescence was then calculated by normalizing the mean fluorescence intensity of the lung homogenates from HK-PM treated mice to that of saline treated mice. C) Lung microsomes were prepared and 25 μg of microsomal protein was used for western blot analysis of HO-1. Recombinant HO-1 (50 ng) was used as a positive control (Lane 0). Quantitative analysis of the western blot revealed that lung microsomes from mice exposed to SS-12 contained 4.5 ±0.60 μg HO-1 per ml of sample. Three separate samples (corresponding to three separate mice) were obtained for each exposure group: lanes 1, 4, and 7 are saline; lanes 2, 5, and 8 are silica; and lanes 3, 6, and 9 are SS-12. Values are shown as the mean ± SEM (n = 3).