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Lake Erie is one of the five great lakes of North America. It is the shallowest, the warmest, and the most biologically productive of the Great Lakes producing more fish than all of the other four lakes combined. It is also a source of drinking water for 11 million people and a recreational asset. On the flipside, it is also very vulnerable and troubled with environmental challenges because it has the smallest water volume, but the greatest pressures from the human settlement. One of the many issues faced by the Lake is pollution. It receives larger loads of many pollutants than any other Great Lake. Even with the best pollution controls many pesticides and organohalogens continue to enter the lake. Polybrominated diphenyl ethers (PBDEs) are a class of flame-retardants that have been used in a variety of consumer products since the 1970s. They are added to many commercial and household products such as computers, foam mattresses, carpets, etc. Being largely non-polar and chemically stable, these chemicals are extremely lipophilic and resist degradation in the environment, thus giving them a high affinity for their bioaccumulation. Due to these properties PBDEs have become ubiquitous environmental contaminants. These compounds are reported to be endocrine disruptors and could cause oxidative damage. This report presents the sample preparation protocol, the GC-MS analysis of PBDEs in Lake Erie sediment samples.

Brominated flame retardants (BFRs) are synthetic organobromide compounds which inhibit ignition and combustion processes. Because of their immense ability to retard fire and save life and property, they have been extensively used in many products such as TVs, computers, foam, plastics etc. The five major classes of BFRs are tetrabromobisphenol-A (TBBPA), hexabromocyclododecane (HBCD), pentabromodiphenyl ether, octabromodiphenyl ether, and decabromodiphenyl ether. The last three are also commonly called PBDEs. BDE-85 and BDE-209 are the two prominent congeners of PBDEs and this study reports the adverse effects of these congeners in rodents. Exposure of rat sciatic nerves to 5 g/mL and 20 g/mL of BDE-85 and BDE-209 respectively lead to significant, concentration dependent reduction in nerve conduction function. Glucose absorption in the rat intestinal segments exposed to 5 g/mL of BDE-85 and BDE-209 was significantly reduced for both the compounds tested. Lastly, mice when exposed to 0.25 mg/kg body weight for four days showed a disruption in oxidant and antioxidant equilibrium. The tissues namely liver and brain have shown increase in the levels of lipid hydroperoxides indicating oxidative stress. Moreover, all the protective enzymes namely superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase, and glutathione S transferase (GST) have shown tissue specific alterations indicating the induction of damaging oxidative stress and setting in of lipid peroxidation in exposed animals. The results indicate monitoring of PBDEs in the environment is essential because levels as low as 5 g/mL and 0.25 mg/kg body weight were able to cause damage to the functions of rodents.