Information on ocean scale drivers of methylmercury levels and variability in tuna is scarce, yet crucial in the context of anthropogenic mercury (Hg) inputs and potential threats to human health. Here we assess Hg concentrations in three commercial tuna species (bigeye, yellowfin, and albacore, n = 1000) from the Western and Central Pacific Ocean (WCPO). Models were developed to map regional Hg variance and understand the main drivers. Mercury concentrations are enriched in southern latitudes (10°S–20°S) relative to the equator (0°–10°S) for each species, with bigeye exhibiting the strongest spatial gradients. Fish size is the primary factor explaining Hg variance but physical oceanography also contributes, with higher Hg concentrations in regions exhibiting deeper thermoclines. Tuna trophic position and oceanic primary productivity were of weaker importance. Predictive models perform well in the Central Equatorial Pacific and Hawaii, but underestimate Hg concentrations in the Eastern Pacific. A literature review from the global ocean indicates that size tends to govern tuna Hg concentrations, however regional information on vertical habitats, methylmercury production, and/or Hg inputs are needed to understand Hg distribution at a broader scale. Finally, this study establishes a geographical context of Hg levels to weigh the risks and benefits of tuna consumption in the WCPO.
The consumption of one meal of seafood containing domoic acid (DA) at levels high enough to induce seizures can cause gross histopathological lesions in hippocampal regions of the brain and permanent memory loss in humans and marine mammals. Seafood regulatory limits have been set at 20 mg DA/kg shellfish to protect human consumers from symptomatic acute exposure, but the effects of repetitive low-level asymptomatic exposure remain a critical knowledge gap. Recreational and Tribal-subsistence shellfish harvesters are known to regularly consume low levels of DA. The aim of this study was to determine if chronic low-level DA exposure, at doses below those that cause overt signs of neurotoxicity, has quantifiable impacts on cognitive function. To this end, female C57BL/6NJ mice were exposed to asymptomatic doses of DA (≈ 0.75 mg/kg) or vehicle once a week for several months. Spatial learning and memory were tested in a radial water maze paradigm at one, six and 25 weeks of exposure, after a nine-week recovery period following cessation of exposure, and at three old age time points (18, 24 and 28 months old). Mice from select time points were also tested for activity levels in a novel cage environment using a photobeam activity system. Chronic low-level DA exposure caused significant spatial learning impairment and hyperactivity after 25 weeks of exposure in the absence of visible histopathological lesions in hippocampal regions of the brain. These cognitive effects were reversible after a nine-week recovery period with no toxin exposure and recovery was sustained into old age. These findings identify a new potential health risk of chronic low-level exposure in a mammalian model. Unlike the permanent cognitive impacts of acute exposure, the chronic low-level effects observed in this study were reversible suggesting that these deficits could potentially be managed through cessation of exposure if they also occur in human seafood consumers.
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