Abstract

The harbour porpoise is the only true native cetacean species in the German North Sea and Baltic Sea. Because of a decline of the population in recent decades a project was launched aiming to investigate the influence of pollutants on the endocrinium and immune system of harbour porpoises. Investigations are performed to find endocrine and immune disrupting effects on animals originating from the North and Baltic Seas and to compare these findings with observations from animals of Icelandic, Norwegian and Greenlandic waters.

Studies on the immune system revealed that several monoclonal and polyclonal antibodies from other species showed a specific reaction with cells of lymphoid tissues from harbour porpoises. Concanavalin A, pokeweed mitogen, phytohemagglutinin used in the lymphocyte transformation test showed a mitogen-induced induction of proliferation of peripheral blood lymphocytes. Using RT-PCR, cDNA of IL-2, IL-4, IL-6, IL-10 ,TGFβ und TNF-alpha was amplified in mitogen-stimulated lymphocytes and expression of iNOS mRNA was detected in lymphoid tissue.

Adrenal glands, hypophyses and thyroid glands represent major target organs of endocrine disruptors and were therefore investigated for possible pathological changes. The thyroid glands in animals from Germany, Iceland and Norway showed a significant difference in the degree of severity of fibrosis between the three groups. Minimal interfollicular fibrosis was observed in the thyroid glands of Icelandic animals. In contrast thyroid glands from German and Norwegian harbour porpoises showed a moderate to severe interfollicular fibrosis.

In addition polychlorinated biphenyls, DDT, toxaphene and polybrominated diphenylethers were analysed in blubber samples of the harbour porpoises. The PCB concentrations (sum of 15 congeners) ranged from 0.05 to 13 µg/g lipid and that the animals from Iceland had lower levels.

Summarizing the preliminary results suggest that thyroid glands of harbour porpoises are adversely affected by chemical endocrine disruptors, which might result in a thyroid disfunction.