This review summarizes data and information which have been generated on mercury (Hg) in the marine environment of the Canadian Arctic since the previous Canadian Arctic Contaminants Assessment Report (CACAR) was released in 2003. Much new information has been collected on Hg concentrations in marine water, snow and ice in the Canadian Arctic. The first measurements of methylation rates in Arctic seawater indicate that the water column is an important site for Hg methylation. Arctic marine waters were also found to be a substantial source of gaseous Hg to the atmosphere during the ice-free season. High Hg concentrations have been found in marine snow as a result of deposition following atmospheric mercury depletion events, although much of this Hg is photoreduced and re-emitted back to the atmosphere. The most extensive sampling of marine sediments in the Canadian Arctic was carried out in Hudson Bay where sediment total Hg (THg) concentrations were low compared with other marine regions in the circumpolar Arctic. Mass balance models have been developed to provide quantitative estimates of THg fluxes into and out of the Arctic Ocean and Hudson Bay. Several recent studies on Hg biomagnification have improved our understanding of trophic transfer of Hg through marine food webs. Over the past several decades, Hg concentrations have increased in some marine biota, while other populations showed no temporal change. Marine biota also exhibited considerable geographic variation in Hg concentrations with ringed seals, beluga and polar bears from the Beaufort Sea region having higher Hg concentrations compared with other parts of the Canadian Arctic. The drivers of these variable patterns of Hg bioaccumulation, both regionally and temporally, within the Canadian Arctic remain unclear. Further research is needed to identify the underlying processes including the interplay between biogeochemical and food web processes and climate change.
The current study aims to shed light on the neurotoxicity of MeHg in fish (white seabream - Diplodus sargus) by the combined assessment of: (i) MeHg toxicokinetics in the brain, (ii) brain morphometry (volume and number of neurons plus glial cells in specific brain regions) and (iii) fish swimming behavior (endpoints associated with the motor performance and the fear/anxiety-like status). Fish were surveyed for all the components after 7 (E7) and 14 (E14) days of dietary exposure to MeHg (8.7μgg), as well as after a post-exposure period of 28days (PE28). MeHg was accumulated in the brain of D. sargus after a short time (E7) and reached a maximum at the end of the exposure period (E14), suggesting an efficient transport of this toxicant into fish brain. Divalent inorganic Hg was also detected in fish brain along the experiment (indicating demethylation reactions), although levels were 100-200 times lower than MeHg, which pinpoints the organic counterpart as the great liable for the recorded effects. In this regard, a decreased number of cells in medial pallium and optic tectum, as well as an increased hypothalamic volume, occurred at E7. Such morphometric alterations were followed by an impairment of fish motor condition as evidenced by a decrease in the total swimming time, while the fear/anxiety-like status was not altered. Moreover, at E14 fish swam a greater distance, although no morphometric alterations were found in any of the brain areas, probably due to compensatory mechanisms. Additionally, although MeHg decreased almost two-fold in the brain during post-exposure, the levels were still high and led to a loss of cells in the optic tectum at PE28. This is an interesting result that highlights the optic tectum as particularly vulnerable to MeHg exposure in fish. Despite the morphometric alterations reported in the optic tectum at PE28, no significant changes were found in fish behavior. Globally, the effects of MeHg followed a multiphasic profile, where homeostatic mechanisms prevented circumstantially morphometric alterations in the brain and behavioral shifts. Although it has become clear the complexity of matching brain morphometric changes and behavioral shifts, motor-related alterations induced by MeHg seem to depend on a combination of disruptions in different brain regions.
A snow cover can modify when, to what extent, and in what form atmospherically deposited mercury is released to the underlying surface media and/or back to the atmosphere. Investigations of mercury transport and transformation processes in snow packs are hampered by the difficulty in controlling experimental and melt conditions and due to the huge variability in the composition and physical structure of environmental snow packs. A method was developed that allows the detailed mechanistic investigation of mercury fate in snow that is made, aged and melted under controlled laboratory conditions. A number of control samples established that mercury in indoor air, scavenged during the snow making process, constitutes the dominant source of mercury in the artificial snow. No addition of mercury is required. The amount of mercury in fresh snow was quantitatively (102 and 106% in two experiments) recovered in the dissolved and particulate fractions of the melt water and the vessel head space, confirming a mass balance for mercury and the absence of unquantifiable mercury sources and sinks in the experimental system. In snow made from unmodified tap water, more than half of the mercury present in the snowpack was recovered from the bottom of the snow vessel after all of the snow had melted. Such late elution is indicative of mercury being mostly associated with particles that are filtered by, and retained in, the shrinking snowpack. Addition of salt to the snow-making water at an environmentally realistic pH notably shifted the distribution of mercury in the snowpack from the particulate to the dissolved phase, resulting in more than 60% of the mercury eluting in the dissolved phase of early melt water fractions.
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