Persistent organic pollutants (POPs) in Caspian seals of unusual mortality event during 2000 and 2001.

Persistent organic pollutants including organochlorine pesticides, PCBs, and PCDDs/DFs were determined in the blubber of Caspian seals, which died during an outbreak of canine distemper virus in 2000 and 2001. DDTs were the predominant contaminants that ranged from 3.1 to 560 microg/g lipid. A negative correlation was observed between concentration of contaminants and blubber thickness. During spring, as the blubber layer becomes thin after breeding and moulting, seals may face higher risk due to the increased concentration of organochlorines in their bodies. TEQs in the blubber of Caspian seals (10-340 pg TEQ/g) were lower than those in seals from other locations, suggesting that toxic effects of these contaminants are a deal less in the present population and they are unlikely to be linked to mass mortality. The levels of PCBs and pesticides in Caspian seals, however, comparable to those in other aquatic mammals that have suffered from epizootics, might pose a risk of immunosuppression.

Cytochrome P4501A expression, chemical contaminants and histopathology in roach, goby and sturgeon and chemical contaminants in sediments from the Caspian Sea, Lake Balkhash and the Ily River Delta, Kazakhstan.

Roach, goby and sturgeon were examined for cytochrome P4501A (CYP1A) expression and histopathology, in relation to contaminant burdens in fish and sediment. Gradients of induction of CYP1A were observed. Roach from the Ural and Ily River Deltas and roach and goby from the two stations nearest the Caspian Sea oil fields displayed higher levels of CYP1A expression in several organs than was observed in fish from further offshore. Great sturgeon and Russian sturgeon showed higher levels of CYP1A expression than was seen in starred sturgeon and gobies in the Ural delta. No fish showed evidence of contaminant-related histopathologies in the organs examined, despite the elevated CYP1A levels. Low levels of polychlorinated biphenyls and elevated levels of inshore and riverine petroleum hydrocarbons from these habitats suggest that this ongoing hydrocarbon exposure, and that from natural sources and long-term oil exploration on the Northeastern Caspian shore, contributed to the CYP1A induction observed.