Abstract
Although hypoxia has been well-studied in Chesapeake Bay, little attention has been given to the origin of the particulate organic matter (POM) that potentially contributes to early summer hypoxia. A combination of a high-resolution baroclinic physical model and a Lagrangian particle tracking model was used to study the sources of POM to the deep channel of the mesohaline Chesapeake Bay. The circulation model reasonably reproduced the salinity structure and circulation compared with observations. The particle tracking model was improved with a fast search algorithm, and a predict-correct method was developed in the backward tracking model to ensure a similar trajectory with the forward tracking. Backward tracking results revealed that the pathway of the POM has a strong dependence on the tracking initiation time and location of the particles, as well as the magnitude of the sinking speed. In general, the behavior of the POM trajectories can be explained by the three-dimensional residual circulation of the mesohaline mainstem Chesapeake Bay. The particles that accumulated in the deep channel of the upper mesohaline Chesapeake Bay where the onset of hypoxia occurs mainly come from downstream when particles stop tracking when they backtracked to the surface layer. Downstream sources accounted for roughly 83.5% of particles for a sinking speed of 1 m/day, and the proportion from the downstream decreased to 60.5% as the sinking speed increased to 25 m/day. In addition, the source from the eastern shore was larger than that from the western shore for particle sinking speed less than 8 m/day. Moreover, particles from the Potomac estuary with a sinking speed of 1 m/day can contribute 7.4% of the bottom POM accumulation in the upper mesohaline Chesapeake Bay. When particles were allowed to stay on the surface for a period before they sink, they backtracked to the upper Chesapeake Bay suggesting that more long-lived refractory organic particles originating from the upper Bay can contribute to organic matter accumulation in the deep channel. These results help to explain why hypoxia in the deep channel of the upper mesohaline Bay occurs to the north of the primary production maximum and also why hypoxia is earlier and more severe in this region compared to the rest of hypoxic zone. Overall, the model results suggest that more local sources of POM with relatively high sinking rates are most important in driving oxygen depletion. This study improves understanding of the origin and pathways of the POM that can potentially contribute to the development of hypoxia in the deep channel of the mesohaline Chesapeake Bay. Future studies need to be undertaken to better understand the relative importance of remote versus more local sources of organic matter in driving oxygen drawdown.
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