Localized hypoxia may have caused coral reef mortality at the Flower Garden Banks
Localized hypoxia may have caused coral reef mortality at the Flower Garden Banks
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DOI：
10.1007/s00338-019-01883-9
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发表时间：
2020-02-01
期刊：
影响因子：
3.5
通讯作者：
DiMarco, Steven F.
中科院分区：
文献类型：
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作者：
Kealoha, Andrea K.;Doyle, Shawn M.;DiMarco, Steven F.
2016年7月25日，在花园银行（FGB）国家海洋保护区的东岸（EB）发现了浑浊的水和死亡的珊瑚，海绵和其他无脊椎动物。死亡范围超过0.06 km（2），在某些地区报告的珊瑚死亡率高达80%。几天之内，应对工作正在进行中，以调查导致死亡事件的潜在机制。水文调查，系泊浮标数据，和区域水动力学模型被用来表征水化学，水文，和微生物群落内的FGB。在EB和东部监测站的地表沃茨中检测到低盐度（~ 31-33）、总碱度（~ 2284-2330 μ mol kg（-1））和溶解无机碳（DIC，~ 1968-2011 μ mol kg（-1）），表明存在河水。密西西比河/阿查法拉亚河是事件期间淡水的主要来源，尽管德克萨斯州的河流在2016年期间都有异常高的排放量，贡献了大约五分之一的淡水总量。在75米深度，高密度，盐度，DIC，铵，和丰富的微生物类群与深沃茨一致的低温和文石饱和状态在北方和东部站，表明在这些站更深的源水。横坡密度梯度也符合上升流环流模式。利用这些观察结果和数据，我们假设死亡事件最有可能是由两个过程的组合引起的。浑浊的淡水层抑制了光合作用，导致珊瑚礁有机物的净呼吸。此外，深层密集的沃茨涌上岸边，形成分层的底层，阻止了上覆水柱的再氧化，导致珊瑚礁上的局部缺氧。缺氧可能在两天内迅速形成。展望未来，氧气和碳酸盐化学的高频时间测量对于监测风险至关重要（例如，（c）与淡水排放和上升流有关的海洋环境变化（如缺氧和酸化），因为这些过程可能对珊瑚礁的健康产生不利影响。
On July 25, 2016, turbid water and dead corals, sponges and other invertebrates were discovered at the East Bank (EB) of the Flower Garden Banks (FGB) National Marine Sanctuary. Mortality was spread over 0.06 km(2), with up to 80% coral mortality reported in some areas. Within days, response efforts were underway to investigate the potential mechanisms leading to the mortality event. Hydrographic surveys, moored buoy data, and a regional hydrodynamic model were used to characterize water chemistry, hydrography, and microbial communities within the FGB. Low salinity (~ 31-33), total alkalinity (~ 2284-2330 mu mol kg(-1)), and dissolved inorganic carbon (DIC, ~ 1968-2011 mu mol kg(-1)) were detected in surface waters over the EB and eastern stations, revealing the presence of river-derived water. The Mississippi/Atchafalaya rivers were the primary sources of freshwater during the event, although Texas rivers, all of which had unusually high discharge during 2016, contributed approximately one-fifth to the total freshwater mass. At 75 m depth, high density, salinity, DIC, ammonium, and abundance of microbial taxa associated with deep waters were coincident with low temperature and aragonite saturation state at the northern and eastern stations, indicating a deeper source water at these stations. Cross-slope density gradients were also consistent with an upwelling circulation pattern. Using these observations and data, we hypothesize that the mortality event was most likely caused by the combination of two processes. The turbid freshwater layer inhibited photosynthesis, leading to net respiration of coral reef organic matter. Additionally, deep, dense waters upwelled onto the bank and formed a stratified bottom layer, which prevented re-oxygenation from the overlying water column and led to localized areas of hypoxia within pockets on the reef. Hypoxia likely formed rapidly, within two days. Moving forward, high-frequency temporal measurements of oxygen and carbonate chemistry are critical for monitoring risks (e.g., hypoxia and acidification) associated with freshwater discharge and upwelling, since these processes may adversely affect coral reef health.