The goal of the present study was twofold: to rapidly assess the potential environmental toxicological response following the storm surge and flooding caused by Hurricane Katrina along the Gulf Coast of Mississippi, USA, in August 2005, and to establish post-Katrina baseline toxicological profiles for three environmental matrices (water, suspended sediments, and sediments) within the intertidal zone. Sediment and water samples were collected monthly from September 2005 to 2006 from 10 sites along the Gulf Coast from Gulfport, Mississippi, to Mobile Bay, Alabama. Water samples and suspended sediment matrices were extracted, assayed, and toxic equivalent values calculated for compounds with estrogenic potential, using the yeast estrogen screen, and CYP1A induction potential, using the H4IIE rat hepatoma ethoxyresorufin-O-deethylase assay. Polycyclic aromatic hydrocarbons (PAHs) were measured in surface sediments. It was hypothesized that the more heavily storm impacted sites, those closest to Katrina's path and time of landfall (e.g., Gulfport, September-October 2005), would elicit higher bioassay responses and PAH concentrations compared to those further east or approximately a year post-Katrina (e.g., Mobile Bay, August- September 2006). Benzo[a]pyrene equivalents decreased along spatial and temporal storm intensity gradients, but estrogenic compounds and sediment PAHs did not. Estrogen equivalents (approximately 1 ng/L) from water and suspended sediment samples occurred primarily in samples collected within a few months post-Katrina. Site-averaged surface sediment total PAHs varied significantly between sites and were higher than the U.S. National Oceanic and Atmospheric Administration's probable effects level at the Gulfport Marina and Back Biloxi Bay, Mississippi, sites. Results from the present study suggest that CYP1A inducing compounds elicited a short-term bioassay response in the water matrix shortly (within weeks) after Katrina's passing but were quickly reduced.

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