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Climate change and overfishing increase neurotoxicant in marine predators

机译：气候变化和过度捕捞增加海洋捕食者的神经毒性

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摘要

More than three billion people rely on seafood for nutrition. However, fish are the predominant source of human exposure to methylmercury (MeHg), a potent neurotoxic substance. In the United States, 82% of population-wide exposure to MeHg is from the consumption of marine seafood and almost 40% is from fresh and canned tuna alone(1). Around 80% of the inorganic mercury (Hg) that is emitted to the atmosphere from natural and human sources is deposited in the ocean(2), where some is converted by microorganisms to MeHg. In predatory fish, environmental MeHg concentrations are amplified by a million times or more. Human exposure to MeHg has been associated with long-term neurocognitive deficits in children that persist into adulthood, with global costs to society that exceed US$20 billion(3). The first global treaty on reductions in anthropogenic Hg emissions (the Minamata Convention on Mercury) entered into force in 2017. However, effects of ongoing changes in marine ecosystems on bioaccumulation of MeHg in marine predators that are frequently consumed by humans (for example, tuna, cod and swordfish) have not been considered when setting global policy targets. Here we use more than 30 years of data and ecosystem modelling to show that MeHg concentrations in Atlantic cod (Gadus morhua) increased by up to 23% between the 1970s and 2000s as a result of dietary shifts initiated by overfishing. Our model also predicts an estimated 56% increase in tissue MeHg concentrations in Atlantic bluefin tuna (Thunnus thynnus) due to increases in seawater temperature between a low point in 1969 and recent peak levels-which is consistent with 2017 observations. This estimated increase in tissue MeHg exceeds the modelled 22% reduction that was achieved in the late 1990s and 2000s as a result of decreased seawater MeHg concentrations. The recently reported plateau in global anthropogenic Hg emissions(4) suggests that ocean warming and fisheries management programmes will be major drivers of future MeHg concentrations in marine predators.
机译：超过30亿人依靠海鲜获取营养。但是，鱼类是人类接触甲基汞（MeHg）（一种有效的神经毒性物质）的主要来源。在美国，全甲基汞的人口中有82％来自海洋海鲜的消费，而几乎40％来自仅新鲜和罐装金枪鱼（1）。从自然和人为源排放到大气中的无机汞（Hg）大约有80％沉积在海洋中（2），其中的一部分被微生物转化为MeHg。在掠食性鱼类中，环境中的MeHg浓度被放大一百万倍或更多。人体暴露于MeHg与儿童成年后长期存在的神经认知缺陷有关，全球社会成本超过200亿美元（3）。第一项减少人为汞排放的全球条约（《水am水Min公约》）于2017年生效。但是，海洋生态系统持续变化对人类经常食用的捕食性动物（例如金枪鱼）中甲基汞的生物蓄积的影响，鳕鱼和箭鱼）在设定全球政策目标时尚未考虑。在这里，我们使用了30多年的数据和生态系统模型，结果表明，由于过度捕捞引起的饮食变化，大西洋鳕鱼（Gadus morhua）中的MeHg浓度在1970年代至2000年代之间增加了高达23％。我们的模型还预测，由于海水温度在1969年的低点与最近的峰值之间升高，大西洋蓝鳍金枪鱼（Thunnus thynnus）中的组织MeHg浓度估计会增加56％，这与2017年的观察结果一致。由于海水中甲基汞浓度的降低，估计的组织中甲基汞的增加量超过了1990年代末和2000年代末所模拟的22％的降低。最近报告的全球人为汞排放的平稳期（4）表明，海洋变暖和渔业管理计划将成为未来海洋捕食者中甲基汞浓度的主要驱动力。

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  • 来源
    《Nature》 |2019年第7771期|648-650|共3页
  • 作者

    Schartup Amina T.; Thackray Colin P.; Qureshi Asif; Dassuncao Clifton; Gillespie Kyle; Hanke Alex; Sunderland Elsie M.;

  • 作者单位

    Harvard Univ, Harvard John A Paulson Sch Engn & Appl Sci, Cambridge, MA 02138 USA|Harvard Univ, Harvard TH Chan Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA;

    Harvard Univ, Harvard John A Paulson Sch Engn & Appl Sci, Cambridge, MA 02138 USA;

    Indian Inst Technol Hyderabad, Dept Civil Engn, Kandi, India;

    Harvard Univ, Harvard John A Paulson Sch Engn & Appl Sci, Cambridge, MA 02138 USA|Harvard Univ, Harvard TH Chan Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA;

    Fisheries & Oceans Canada, St Andrews Biol Stn, St Andrews, NB, Canada;

    Fisheries & Oceans Canada, St Andrews Biol Stn, St Andrews, NB, Canada;

    Harvard Univ, Harvard John A Paulson Sch Engn & Appl Sci, Cambridge, MA 02138 USA|Harvard Univ, Harvard TH Chan Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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