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Exposure and effects assessment of persistent organohalogen contaminants in arctic wildlife and fish
Authors:Robert J. Letcher  Jan Ove Bustnes  Christian Sonne  Mathilakath M. Vijayan
Affiliation:a Wildlife and Landscape Science Directorate, Science and Technology, Branch, Environment Canada, Carleton University, Ottawa, ON, Canada K1A 0H3
b Norwegian Institute for Nature Research, Unit for Arctic Ecology, The Polar Environmental Centre, N-9296 Tromsø, Norway
c University of Aarhus, National Environmental Research Institute, Department of Arctic Environment, Roskilde, DK-4000, Denmark
d Department of Biology, Norwegian University of Science and Technology, Trondheim, NO-7491, Norway
e Norwegian College of Fishery Science, University of Tromsø, N-9037 Tromsø, Norway
f Department of Biology, University of Waterloo, Waterloo, Ontario, Canada
g Norwegian Polar Institute, Tromsø, NO-9296, Norway
h Norwegian Institute for Nature Research, Polar Environmental Centre, N-9096 Tromsø, Norway
Abstract:Persistent organic pollutants (POPs) encompass an array of anthropogenic organic and elemental substances and their degradation and metabolic byproducts that have been found in the tissues of exposed animals, especially POPs categorized as organohalogen contaminants (OHCs). OHCs have been of concern in the circumpolar arctic for decades. For example, as a consequence of bioaccumulation and in some cases biomagnification of legacy (e.g., chlorinated PCBs, DDTs and CHLs) and emerging (e.g., brominated flame retardants (BFRs) and in particular polybrominated diphenyl ethers (PBDEs) and perfluorinated compounds (PFCs) including perfluorooctane sulfonate (PFOS) and perfluorooctanic acid (PFOA) found in Arctic biota and humans. Of high concern are the potential biological effects of these contaminants in exposed Arctic wildlife and fish. As concluded in the last review in 2004 for the Arctic Monitoring and Assessment Program (AMAP) on the effects of POPs in Arctic wildlife, prior to 1997, biological effects data were minimal and insufficient at any level of biological organization. The present review summarizes recent studies on biological effects in relation to OHC exposure, and attempts to assess known tissue/body compartment concentration data in the context of possible threshold levels of effects to evaluate the risks. This review concentrates mainly on post-2002, new OHC effects data in Arctic wildlife and fish, and is largely based on recently available effects data for populations of several top trophic level species, including seabirds (e.g., glaucous gull (Larus hyperboreus)), polar bears (Ursus maritimus), polar (Arctic) fox (Vulpes lagopus), and Arctic charr (Salvelinus alpinus), as well as semi-captive studies on sled dogs (Canis familiaris). Regardless, there remains a dearth of data on true contaminant exposure, cause-effect relationships with respect to these contaminant exposures in Arctic wildlife and fish. Indications of exposure effects are largely based on correlations between biomarker endpoints (e.g., biochemical processes related to the immune and endocrine system, pathological changes in tissues and reproduction and development) and tissue residue levels of OHCs (e.g., PCBs, DDTs, CHLs, PBDEs and in a few cases perfluorinated carboxylic acids (PFCAs) and perfluorinated sulfonates (PFSAs)). Some exceptions include semi-field studies on comparative contaminant effects of control and exposed cohorts of captive Greenland sled dogs, and performance studies mimicking environmentally relevant PCB concentrations in Arctic charr. Recent tissue concentrations in several arctic marine mammal species and populations exceed a general threshold level of concern of 1 part-per-million (ppm), but a clear evidence of a POP/OHC-related stress in these populations remains to be confirmed. There remains minimal evidence that OHCs are having widespread effects on the health of Arctic organisms, with the possible exception of East Greenland and Svalbard polar bears and Svalbard glaucous gulls. However, the true (if any real) effects of POPs in Arctic wildlife have to be put into the context of other environmental, ecological and physiological stressors (both anthropogenic and natural) that render an overall complex picture. For instance, seasonal changes in food intake and corresponding cycles of fattening and emaciation seen in Arctic animals can modify contaminant tissue distribution and toxicokinetics (contaminant deposition, metabolism and depuration). Also, other factors, including impact of climate change (seasonal ice and temperature changes, and connection to food web changes, nutrition, etc. in exposed biota), disease, species invasion and the connection to disease resistance will impact toxicant exposure. Overall, further research and better understanding of POP/OHC impact on animal performance in Arctic biota are recommended. Regardless, it could be argued that Arctic wildlife and fish at the highest potential risk of POP/OHC exposure and mediated effects are East Greenland, Svalbard and (West and South) Hudson Bay polar bears, Alaskan and Northern Norway killer whales, several species of gulls and other seabirds from the Svalbard area, Northern Norway, East Greenland, the Kara Sea and/or the Canadian central high Arctic, East Greenland ringed seal and a few populations of Arctic charr and Greenland shark.
Keywords:ALB, thyroid hormone binding albumin   AMAP, Arctic Monitoring and Assessment Program   BDE-209, 2,2&prime  ,3,3&prime  ,4,4&prime  ,5,5&prime  -decabromodiphenyl ether   BFR, brominated flame retardant   BGS, brain growth spurt   BMD, bone mineral density   BMR, basal metabolic rate   CHL, chlordane   Con A, concanavalin   CP, chloroparaffin   CYP, cytochrome P450   CBz, chlorobenzene   DNA, deoxyribonucleic acid   E2, 17β-estradiol   EDC, endocrine disrupting compound   EFI, epithelial follicular index   EHV, herpes virus   EIV, influenza virus   FA, fluctuating asymmetry   FABP, fatty acid binding protein   FSH, follicle stimulating hormone   GH, growth hormone   GST, glutathione-S-transferase   HBCD, hexabromocyclododecane   HCH, hexachlorocyclohexane   Hg, mercury   HP, haptoglobin   HPT, hypothalamus-pituitary-thyroid   IGF-I, insulin-like growth factor I   IgG, immunoglobulin G   IgM, immunoglobin M   LH, luteinizing hormone   LOEL, lowest observed effect level   MeO-, methoxyl-   MeSO2-, methylsulfonyl-   mRNA, messenger ribonucleic acid   OC, organochlorine   OHC, organohalogen contaminant   25 OHD, 25-hydroxy-vitamin D3   OH-, hydroxyl-   4-OH-HpCS, 4-hydroxy-heptachlorostyrene   P4, progesterone   PAH, polycyclic aromatic hydrocarbon   PBDE, polybrominated diphenyl ether   PCB, polychlorinated biphenyl   PCDD, polychlorinated dibenzo-p-dioxin   PCDF, polychlorinated dibenzofuran   PCP, pentachlorophenol   PFC, perfluorinated compound   PFCA, perfluorinated carboxylic acid   PFOA, perfluorooctanoic acid   PFOS, perfluorooctane sulfonate   PFSA, perfluorinated sulfonate   PHA, phytohemagglufinin   POP, persistent organic pollutant   p,p&prime  -DDD, bis(p-chlorophenyl)-1,1-dichloroethane   p,p&prime  -DDE, bis(p-chlorophenyl)-1,1-dichloroethene   p,p&prime  -DDT, bis(p-chlorophenyl)-1,1,1-trichloroethane   PRC, prolactin   REO, reovirus   SLE, St. Lawrence river estuary   T, testosterone   T4, thyroxine   T3, 3,3&prime  ,5-triiodo-  smallcaps"  >l-thyronine   TBBPA, tetrabromobisphenol A   TBG, thyroid binding globulin   TCDD, 2,3,7,8-tetrachloro-dibenzo-p-dioxin   TEF, toxic equivalency factor   TEQ, toxic equivalent   TET, tetanus toxoid   TH, thyroid hormone   TTR, transthyretin
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