Role of Particle Resuspension in Maintaining Hypoxic Level in the Pearl River Estuary

Eutrophication-induced seasonal hypoxia in the coastal ocean has widely been attributed to the excessive oxygen consumption induced by settling and deposition of organic particles on sea floor. However, the role of particle resuspension in maintaining the hypoxic level has seldom been investigated based on field observations. Here, we carefully examined particle resuspension and its contribution to oxygen consumption in the Pearl River Estuary in July 2020. The bottom hypoxia was found to appear over the organic-rich mudbelt off the estuary. Concentrated particles in suspension near the bottom, which were induced by particle resuspension rather than by particle settling, occurred near the front created by shelf salinity intrusions where bottom hypoxia appeared in the summer. The total dissolved oxygen (DO) depletion responsible for bottom hypoxia can be exclusively estimated from the DO budget during the tidal cycle. The water DO depletion dominated by particle resuspension is larger than or at least comparable to sediment oxygen demand. This highlights that the DO budget in the absence of particle resuspension overestimates the DO level in coastal hypoxia. Overall, our results suggest that particle resuspension play a vital role in maintaining the DO level of bottom hypoxia. This finding will be helpful to understand the impact of particle resuspension on coastal hypoxia, as well as other marine environmental problems in estuary and coastal ocean.

Automated summary

This study investigates the role of particle resuspension in maintaining hypoxia levels in the Pearl River Estuary. It finds that suspended particles caused by resuspension, rather than settling, are concentrated near the front of shelf salinity intrusions where bottom hypoxia occurs. The depletion of dissolved oxygen (DO) caused by particle resuspension is comparable to sediment oxygen demand, highlighting the importance of considering particle resuspension in coastal hypoxia research.