摘要
Ocean acidification caused by oceanic uptake of anthropogenic carbon dioxide(CO_2) tends to suppress the calcification of some marine organisms. This reduced calcification then enhances surface ocean alkalinity and increases oceanic CO_2 uptake, a process that is termed calcification feedback. On the other hand, decreased calcification also reduces the export flux of calcium carbonate(Ca CO_3), potentially reducing Ca CO_3-bound organic carbon export flux and CO_2 uptake, a process that is termed ballast feedback. In this study, we incorporate a range of different parameterizations of the links between organic carbon export, calcification, and ocean acidification into an Earth system model, in order to quantify the long-term effects on oceanic CO_2 uptake that result from calcification and ballast feedbacks. We utilize an intensive CO_2 emission scenario to drive the model in which an estimated fossil fuel resource of 5000 Pg C is burnt out over the course of just a few centuries. Simulated results show that, in the absence of both calcification and ballast feedbacks, by year 3500, accumulated oceanic CO_2 uptake is2041 Pg C. Inclusion of calcification feedback alone increases the simulated uptake by 629 Pg C(31%), while the inclusion of both calcification and ballast feedbacks increase simulated uptake by 449–498 Pg C(22–24%), depending on the parameter values used in the ballast feedback scheme. These results indicate that ballast effect counteracts calcification effect in oceanic CO_2 uptake. Ballast effect causes more organic carbon to accumulate and decompose in the upper ocean, which in turn leads to decreased oxygen concentration in the upper ocean and increased oxygen at depths. By year 2600, the inclusion of ballast effect would decrease oxygen concentration by 11% at depth of ca. 200 m in tropics. Our study highlights the potentially critical effects of interactions between ocean acidification, marine organism calcification, and Ca CO3-bound organic carbon export on the ocean carbon and oxygen cycles.
Ocean acidification caused by oceanic uptake of anthropogenic carbon dioxide（CO2） tends to suppress the calcification of some marine organisms. This reduced calcification then enhances surface ocean alkalinity and increases oceanic CO2 uptake, a process that is termed calcification feedback. On the other hand, decreased calcification also reduces the export flux of calcium carbonate（Ca CO3）, potentially reducing Ca CO3-bound organic carbon export flux and CO2 uptake, a process that is termed ballast feedback. In this study, we incorporate a range of different parameterizations of the links between organic carbon export, calcification, and ocean acidification into an Earth system model, in order to quantify the long-term effects on oceanic CO2 uptake that result from calcification and ballast feedbacks. We utilize an intensive CO2 emission scenario to drive the model in which an estimated fossil fuel resource of 5000 Pg C is burnt out over the course of just a few centuries. Simulated results show that, in the absence of both calcification and ballast feedbacks, by year 3500, accumulated oceanic CO2 uptake is2041 Pg C. Inclusion of calcification feedback alone increases the simulated uptake by 629 Pg C（31%）, while the inclusion of both calcification and ballast feedbacks increase simulated uptake by 449–498 Pg C（22–24%）, depending on the parameter values used in the ballast feedback scheme. These results indicate that ballast effect counteracts calcification effect in oceanic CO2 uptake. Ballast effect causes more organic carbon to accumulate and decompose in the upper ocean, which in turn leads to decreased oxygen concentration in the upper ocean and increased oxygen at depths. By year 2600, the inclusion of ballast effect would decrease oxygen concentration by 11% at depth of ca. 200 m in tropics. Our study highlights the potentially critical effects of interactions between ocean acidification, marine organism calcification, and Ca CO3-bound organic carbon export on the ocean carbon and oxygen cycles.
基金
supported by the National Natural Science Foundation of China(Grant Nos.41675063,41422503&41276073)
the National Key Basic Research Program of China(Grant No.2015CB953601)
the Fundamental Research Funds for the Central Universities
