SUMMARY Polar bears are uniquely adapted to life in the High Arctic and have undergone drastic physiological changes in response to Arctic climates and a hyperlipid diet of primarily marine mammal prey. We analyzed 89 complete genomes of polar bear and brown bear using population genomic modeling and show that the species diverged only 479–343 thousand years BP. We find that genes on the polar bear lineage have been under stronger positive selection than in brown bears; nine of the top 16 genes under strong positive selection are associated with cardiomyopathy and vascular disease, implying important reorganization of the cardio-vascular system. One of the genes showing the strongest evidence of selection, APOB, encodes the primary lipoprotein component of low-density lipoprotein (LDL); functional mutations in APOB may explain how polar bears are able to cope with life-long elevated LDL levels that are associated with high risk of heart disease in humans.

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We present new and revised data for the phocine distemper virus (PDV) epidemics that resulted in the deaths of more than 23 000 harbour seals Phoca vitulina in 1988 and 30 000 in 2002. On both occasions the epidemics started at the Danish island of Anholt in central Kattegat, and subsequently spread to adjacent colonies in a stepwise fashion. However, this pattern was not maintained throughout the epidemics and new centres of infection appeared far from infected populations on some occasions: in 1988 early positive cases were observed in the Irish Sea, and in 2002 the epidemic appeared in the Dutch Wadden Sea, 6 wk after the initiation of the outbreak at Anholt Island. Since the harbour seal is a rather sedentary species, such 'jumps' in the spread among colonies suggest that another vector species could have been involved. We discussed the role of sympatric species as disease vectors, and suggested that grey seal populations could act as reservoirs for PDV if infection rates in sympatric species are lower than in harbour seals. Alternatively, grey seals could act as subclinical infected carriers of the virus between Arctic and North Sea seal populations. Mixed colonies of grey and harbour seal colonies are found at all locations where the jumps occurred. It seems likely that grey seals, which show long-distance movements, contributed to the spread among regions. The harbour seal populations along the Norwegian coast and in the Baltic escaped both epidemics, which could be due either to genetic differences among harbour seal populations or to immunity. Catastrophic events such as repeated epidemics should be accounted for in future models and management strategies of wildlife populations. KEY WORDS: Epizootic · Harbour seal · Mass mortality · Phocine distemper virus Resale or republication not permitted without written consent of the publisherDis Aquat Org 68: [115][116][117][118][119][120][121][122][123][124][125][126][127][128][129][130] 2006 natural reductions in food supply driven by El Niño conditions have led to high levels of mortality (Trillmich & Dellinger 1991).There is also increasing evidence for mortality resulting from infectious disease. In 1988, up to 60% of North Sea harbour seals Phoca vitulina died during an outbreak of a then newly discovered distemper virus identified by inclusion bodies (e.g. Dietz et al. 1989a, Bergman et al. 1990. This virus was isolated and described as a morbillivirus, phocine distemper virus (PDV) (Osterhaus & Vedder 1988). Subsequently, related dolphin and porpoise morbilliviruses were isolated from cetaceans (Barrett et al. 1993), and widespread screenings suggest that many populations of pinnipeds, cetaceans and sirenians in the North Atlantic had been exposed to these viruses prior to and after the 1988 PDV outbreak (Dietz et al. 1989b, Duignan et al. 1995a,b,c, 1997a,b, Van Bressem et al. 2001. Clinical signs of disease were not recorded in many of the populations in which morbillivirus antibodies were detected (Duignan et al. 1995b, Nielsen et al. 20...

► Unpublished and published data were compiled for Arctic fish, birds, and mammals. ► These data were compared to available toxicological threshold limits. ► Toothed whales, polar bears, and some bird and fish species exceeded the limits. ► Increasing mercury concentrations are observed for some Arctic species. ► These exceeded thresholds and increasing Hg trends are of concern. a b s t r a c t a r t i c l e i n f o This review critically evaluates the available mercury (Hg) data in Arctic marine biota and the Inuit population against toxicity threshold values. In particular marine top predators exhibit concentrations of mercury in their tissues and organs that are believed to exceed thresholds for biological effects. Species whose concentrations exceed threshold values include the polar bears (Ursus maritimus), beluga whale (Delphinapterus leucas), pilot whale (Globicephala melas), hooded seal (Cystophora cristata), a few seabird species, and landlocked Arctic char (Salvelinus alpinus). Toothed whales appear to be one of the most vulnerable groups, with high concentrations Science of the Total Environment 443 (2013) [775][776][777][778][779][780][781][782][783][784][785][786][787][788][789][790]

Killer whales (Orcinus orca) are among the most highly polychlorinated biphenyl (PCB)–contaminated mammals in the world, raising concern about the health consequences of current PCB exposures. Using an individual-based model framework and globally available data on PCB concentrations in killer whale tissues, we show that PCB-mediated effects on reproduction and immune function threaten the long-term viability of >50% of the world’s killer whale populations. PCB-mediated effects over the coming 100 years predicted that killer whale populations near industrialized regions, and those feeding at high trophic levels regardless of location, are at high risk of population collapse. Despite a near-global ban of PCBs more than 30 years ago, the world’s killer whales illustrate the troubling persistence of this chemical class.