The roles of anoxia, H2S, and storm events in fish kills of dead-end canals of Delaware inland bays

Abstract

In 2001, the development of seasonal anoxia was studied in two waterways located at the head of Delaware’s northern inland bay, Rehoboth Bay. Bald Eagle Creek is a northern tributary of the bay, which has tidal exchange with Torquay Canal (a dead-end canal) via a short channel with a 1.4 m sill. Mean low water depth in Torquay Canal is about 2 m, but dredging produced over a dozen depressions with a total water depth of 5.5 m. During the summer of 2000, four major fish kills were reported in Torquay Canal and Bald Eagle Creek with more than 2.5 million juvenile menhaden (Brevoortia tyrannus) killed. Low O2 concentration was assumed to be the problem but production of toxic H2S is more likely. From late spring 2001, we conducted in situ determination of temperature, salinity, pH, dissolved O2, and H2S in Torquay Canal and Bald Eagle Creek. During spring, water column stratification began in the depressions with warmer and less salty water observed in the upper layer, and cooler, saltier water below 2 m. O2 was at saturation levels in the surface waters but was not detectable below 2 m by the end of May. The depressions were anoxic with H2S accumulating to mM concentrations in June. A storm event prior to July 12 mixed these two layers with a subsequent loss of H2S. The H2S levels again increased in the deep water due to stratification and reached another maximum in late August. Another storm event occurred at this time resulting in no detectable O2 and up to 400 μM H2S in surface waters. H2S appears to be the primary reason for fish kills in these tributaries. Aerators installed in Torquay Canal on June 21 had no significant effect on abating stratification and anoxic conditions beyond their immediate area.