Wildlife populations are adversely affected in polluted environments. Nevertheless, a cause‐and‐effect relationship between excessive exposure to chlorinated hydrocarbons and induction of pathologic disorders in animals, is difficult to demonstrate without verification from experiments following the rationale of Koch's postulates. Deleterious effects of chlorinated chemicals such as DDT on songbird reproduction, as demonstrated by the clutch size of eggs in a nest, however, is an example, where exposure and causation are apparent. With amelioration of DDT pollution, clutch size increases, and the cause‐and‐effect relationship is established. Similar examples of exposure to DDT and PCBs inducing reproductive disorders and endocrine disruption among marine mammals have been documented in industrialized nations of northern Europe and in the upper latitudes of the Northern Hemisphere. Population declines in ringed, grey and harbor seals are apparently due to a rapid decrease in their rates of reproduction1. These latter observations are best interpreted in light of experiments conducted by Reijnders2. Reijnders exposed harbor seals to relatively high dietary levels of PCBs and induced PCB‐blood‐lipids among seals to an average of 25 mg/kg compared to 10 mg/kg among controls. The treated seals had a significantly reduced reproductive rate. A relationship between increased PCB‐blood‐levelsin vivoand the decrease in reproductive rates in this experiment is highly instructive for interpreting the decline of fertility in seal populations in polluted Baltic Sea waters. These linked observations are dependent upon demonstration of pathologic mechanisms associated with occlusion and stenosis of the uterine lumen among affected females in seal populations.