| Summary: | Deflocculation is a common upset event in biological wastewater treatment plants and causes significant problems in biosolids discharge and environmental management. However, fundamental understanding of deflocculation is limited. The overall objective of this work was to explore the fundamentals for deflocculation under transients of short-term low dissolved oxygen (DO). The investigation was carried out in a sequence of batch and continuous experiments on activated sludge, followed by batch experiments on E. coli suspensions.
Both batch and continuous experiments on activated sludge demonstrated deflocculation of bioflocs under the transients of low DO (< 0.5 mg/L). Under the short-term low DO (in hours), turbidity increased by 20 times in the batch system and by 1-2 times in the continuous system, concentrations of suspended solids increased by 1-2 times, number of small particles (< 12.5 mm) increased by 2 times, more soluble EPS (proteins and humic substances) were released into supernatant or treated effluents, the removal efficiency of organic compounds was reduced by 50-70%. A 40% of increase in bulk K+ but a 30% of decrease in bulk Ca2+ under the DO limitation were observed in the batch experiments. There were significant increases in bulk K+ and decreases in bulk Ca2+ in the continuous experiments. Reversible changes were observed within 24 hours once the DO stress was removed. Floc strength of the remaining bioflocs after deflocculation increased. Deflocculation under the short-term low DO was consistent with an erosion process. The addition of selected chemicals (i.e., Ca2+, tetraethylammonium chloride, glibenclamide, and valinomycin) did not prevent deflocculation under the short-term low DO.
It is proposed that a DO stress causes an efflux of cellular K+ but an influx of extracellular Ca2+, resulting in a decreasing ratio of Ca2+/K+ in extracellular solution and thereby causing deflocculation. The E. coli tests supported that increasing bulk K+ under the DO limit was due to the release of cellular K+ and was a stress response to the DO limitation.
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