Conceptual framework for assessing the response of delta channel networks to Holocene sea level rise

Recent research has identified two fundamental unit processes that build delta distributary channels. The first is mouth-bar deposition at the shoreline and subsequent channel bifurcation, which is driven by progradation of the shoreline; the second is avulsion to a new channel, a result of aggradation of the delta topset The former creates relatively small, branching networks such as Wax Lake Delta; the latter generates relatively few, long distributaries such as the Mississippi and Atchafalaya channels on the Mississippi Delta. The relative rate of progradation to aggradation, and hence the creation of accommodation space, emerges as a controlling parameter on channel network form. Field and experimental research has identified sea level as the dominant control on Holocene delta growth worldwide, and has empirically linked channel network changes to changes in the rate of sea level rise. Here I outline a simple modeling framework for distributary network evolution, and use this to explore large-scale changes in Holocene channel pattern that have been observed in deltas such as the Rhine-Meuse and Mississippi. Rapid early- to mid-Holocene sea level rise forced many deltas into an aggradational mode, where I hypothesize that avulsion and the generation of large-scale branches should dominate. Slowing of sea level rise in the last similar to 6000 yr allowed partitioning of sediment into prograidation, facilitating the growth of smaller-scale distributary trees at the shorelines of some deltas, and a reduction in the number of large-scale branches. Significant antecedent topography modulates delta response; the filling of large incised valleys, for example, caused many deltas to bypass the aggradational phase. Human effects on deltas can be cast in terms of geologic controls affecting accommodation: constriction of channels forces rapid local progradation and mouth-bar bifurcation, while accelerated sea level rise increases aggradation and induces more frequent channel avulsion. (C) 2009 Elsevier Ltd. All rights reserved.