Description
The U.S. Fish and Wildlife Service, Region 7 (Alaska) intends to award a sole source contract in accordance with the Federal Acquisition Regulation (FAR) Part 5, Section 5.203 and is supplemented with additional information contained within to the Wadsworth Center for conducting analysis of Sea Otter Livers for PBDE levels for up to 5 years. This study will examine the association between exposure to PBDEs and the disease status of the Alaskan sea otter. This will be accomplished by determining and comparing hepatic concentrations of PBDEs in sea otters that died of infectious diseases and those that died of noninfectious causes. The availability of large numbers of archived tissues of Alaskan sea otters, which had been systematically examined for evidence of disease during postmortem investigations and necropsy, provides an opportunity to evaluate the association between PBDE concentrations and cause of mortality. Negotiations are estimated to occur approximately 15 days following the posting of this notice, with the estimated contract award approximately May 18, 2009. The Government is contemplating award of a firm fixed price contract with four option years. This announcement is for information purposes only. No solicitation is available. This is NOT a request for competitive proposals. Information received in response to this notice will be used solely for the purpose of determining whether or not to compete this requirement. A determination by the Government to not compete this requirement, based upon responses to this notice and currently available information about the intended recipient, is solely within the discretion of the Government. Background: The sea otter, once an abundant species with a range spanning from California in the east across the Pacific Rim to the Kuril Islands north of Japan in the west, was hunted to near-extinction in the 18th and 19th centuries for its fur. It was not until 1911 that the surviving population was legally protected by international law. The result was several remnant sea otter populations. Data collected by both the Fish & Wildlife Service and the U.S. Geological Survey show that the Alaskan sea otter population in the Aleutians declined by 95% since the mid-1970s, when it numbered between 50,000 and 100,000. From 1992 to 2000 it may have declined by 70%. Today, as few as 6,000 otters may remain in the entire Aleutian chain.The causes of the sea otter decline have been explored by reviewing available data on seaotter reproduction, survival, distribution, habitat, and environmental contaminants. Estes et al.(1998) concluded that the observed sea otter declines were most likely caused by increased adultmortality. Disease, pollution, and starvation may all influence sea otter mortality. Although several studies have examined the association between exposure to immunosuppressive contaminants and health of sea otters in California (Kannan et al. 1998; Nakata et al. 1998; Kannan et al. 2004a; Kannan et al. 2006a; Kannan et al. 2006b), little is known regarding the accumulation and effects of toxic organic pollutants in sea otters from Alaska. In attempts to better understand the factors that contribute to high mortality and reduced immunocompetence in Alaskan sea otters, in this study, we propose to examine the concentrations of polybrominated diphenyl ethers (PBDEs) in otters that died of infectious and non-infectious diseases. A few earlier studies have compared residue levels of PCBs, PBDEs, and butyltins between healthy and diseased sea otters (Kannan et al. 1998; Nakata et al. 1998; Kannan et al., 2006).Thymic atrophy and splenic depletion were significantly correlated with increased PCB and PBDE levels in harbor porpoises from the North Sea and the Baltic Sea (Beineke et al. 2005). PBDEs are flame retardants and are used in many household consumer products ranging from television sets and computers to sofas, blankets, and building materials (Hites 2004). Studies have shown that the concentrations of PBDEs in marine mammals have increased significantly over the last decade (She et al. 2002; Ikonomou et al. 2002; Kajiwara et al. 2004; Johnson-Restrepo et al. 2005a). PBDEs are also known to affect thyroid hormone homeostasis.This study will examine the association between exposure to PBDEs and the disease status of the Alaskan sea otter. This will be accomplished by determining and comparing hepatic concentrations of PBDEs in sea otters that died of infectious diseases and those that died of noninfectious causes. The availability of large numbers of archived tissues of Alaskan sea otters, which had been systematically examined for evidence of disease during postmortem investigations and necropsy, provides an opportunity to evaluate the association between PBDE concentrations and cause of mortality. Sea otters are unique and valuable sentinels that allow us to evaluate the health of coastal aquatic environments. The narrow home range, top-level predator status, and voracious appetite make the sea otter a suitable surrogate for human exposure to aquatic sources of environmental contaminants (Kajiwara et al. 2001; Kannan et al. 2004a). A subset of samples from adult female sea otters will be selected from an archived sample set of >300 beached Alaskan sea otters found freshly dead or dying between 1992 and 2008, along south-central Alaska. The otters were found terminally ill or dead and carcasses were in good postmortem condition. Necropsies of sea otters were performed at U.S. Fish and Wildlife Service in Anchorage, AK, for the determination of cause of death. Sample selection will be based on gender and age, to eliminate these variables as confounding factors. Additionally, female sea otters will be chosen, because their more localized movement patterns make them more suitable indicators of local sources of pollution. Based on the cause of death, samples are classified as emaciation, infectious disease and trauma. Liver will be chosen for analysis for the following reasons. First, this organ plays a significant role in toxicant processing. Depending on the availability of brain tissues, we also propose to analyze brain tissues. Liver samples (~5 g) will be homogenized with anhydrous sodium sulfate (120 g), spiked with the internal standards PCB-30 and PCB-204 (25 ng), and extracted with mixed solvents dichloromethane (300 mL) and hexane (100 mL) using a Soxhlet apparatus for 20 h (Kannan et al. 2004a). The solvent will be concentrated (11 mL), and an aliquot (1 mL) will be taken for gravimetric determination of fat content. A second aliquot (5 mL) will be spiked with 13C-labeled PBDEs (10 ng each congener; EO5100; Cambridge Isotope Laboratories, Andover, MA) and subjected to column chromatography for removal of lipids. Columns (10 mm i.d.) will be prepared by layering silica gel (2 g, 100-200 mesh), 40% acidic silica gel (1 g), silica gel (1 g), 40% acidic silica gel (1 g), and silica gel (1 g). Sample extracts will be eluted with 15% dichloromethane in hexane (150 mL). Samples will be further subjected to lipid removal by treatment with concentrated sulfuric acid, if and when needed. Sample extracts (2 uL) are injected into a Hewlett-Packard 6890 gas chromatograph interfaced with a Hewlett-Packard 5973 mass spectrometer (GC-MS). Injections are made in the splitless mode, and samples are separated on a 30 m DB-5 (5 % diphenyl /dimethylpolysiloxane) analytical capillary column with a 250 m i.d. and a 0.25 m film thickness. The oven temperature program is set to 100 C for 1 min, 10 C/min to 160 C, hold 3 min, and 2.5 C/min to 260 C, hold for 10 min. The inlet and interface temperatures are set to 270 C and 300 C, respectively. The MS is operated in an electron impact mode (70 eV) and selected ion monitoring mode (SIM). PBDE congeners are identified and quantified by SIM at m/z 406, 408; 486, 484; 564, 566; and 642, 644 for tri-; tetra-; penta-; and hexa-BDEs, respectively. Quantification is based on external calibration standard. PBDE congener 209 will be analyzed using GC with electron capture detection.In order to assure the quality of the measurements, several steps will be taken. 13C-labeled-PBDEs, one from each homologue group will be spiked into every sample for the calculation of recoveries. Recoveries of PCB-30 and PCB-204, spiked as surrogate standards prior to extraction will be monitored. A quantitation limit (LOQ) of 1 ng/g, wet weight, for total PBDEs is determined using this method. Procedural blanks will be analyzed simultaneously with every batch of five samples as a check for interferences or contamination arising from solvents and glassware. Total PBDEs represent the sum of BDE congeners 47,99,100,153, and 154, 183 and 209. Goals: To investigate the potential role of Polybrominated Diphenyl Ethers (PDBEs) in Alaskan Sea Otters that Died of Infectious Diseases and Noninfectious Causes; and to monitor marine pollution in coastal Alaska by means of a sentinel species Objectives: The objectives of this study are to (1) establish baseline levels of PBDEs in Alaskan sea otters (2) to compare concentrations of PBDEs in sea otters by location, nutritive condition, and through time and (3) to establish an association of PBDE concentrations with infectious and noninfectious mortality categories in sea otters. Tasks: The contractor shall analyze 50 liver tissues of northern sea otters collected since 1992 through 2009 to further determine the concentrations of PBDEs. Deliverables:1. Results of PBDE analysis in an Excel Spreadsheet. 2. Interpretation of PBDE results in manuscript form.3. Guidance on any follow-up analytical work. Period of Performance for Task order #1: 1 June 2009 through 1 June 2010. Upon Government acceptance of all deliverables, the contractor can submit their invoice. This notice of intent is not a request for competitive proposals and the Government does not intend to accept proposals received. Award will be made 15 days after publication of this notice. See Numbered Note 22.