Early Diagenesis in Hypoxic Zones of the Northern Gulf of Mexico: a Disconnection Between Water Column and Sediment Reactivities

The Northern Gulf of Mexico (NGoM) near the Mississippi River mouth is one of the largest seasonal hypoxic zone of the coastal ocean. Coastal eutrophication associated with nutrient input from the Mississippi River watershed is responsible for the onset of hypoxia through increased primary production, organic matter sedimentation, and carbon remineralization in the stratified bottom waters. Oxic mineralization also generates ocean acidification by the production of metabolic CO₂ without alkalinity production. Yet the processes responsible for the maintenance and dynamics of the hypoxic conditions throughout the summer and, most notably, the role of sediment oxygen consumption on the hypoxic zone remain largely uncertain. According to NOAA data (Rabalais, 2017), the year 2017 showed the largest surface area of hypoxic waters ever recorded in the NGoM. In this study, we present pore water and sediment data from 4 shelf stations along a 20-30 meters depth east-west transect located in the hypoxic area or its edge collected in July-August 2017. By combining dissolved inorganic carbon (DIC), total alkalinity (TA), sulfate, and oxygen concentration profiles, we show that sediment diagenesis is generally weak, with limited sulfate depletion and DIC increase in the first 20 cm of pore waters, except near the Mississippi River mouth. On the contrary, oxygen consumption is rapid and oxygen is depleted within 1-2 mm, indicating substantial mineralization at the sediment-water interface at all stations. We thus hypothesize that a disconnection exists between the sediment surface containing substantial quantities of labile organic matter and sediment depths with limited labile substrate availability, possibly due to bioturbation inhibition during summer hypoxia. These findings overall indicate that NGoM shelf sediments may contribute to hypoxia and acidification through oxic respiration with little or no mitigation by TA production during anoxic diagenesis.