Toxic shock-induced deflocculation was examined for activated sludge exposed to six different classes of industrially relevant chemical toxins: an electrophilic solvent (1-chloro-2,4-dinitrobenzene, CDNB), a heavy metal (cadmium), a hydrophobic chemical (1-octanol), an uncoupling agent (2,4-initrophenol, DNP), alkaline pH, and weakly complexed cyanide. The concentrations required to inhibit respiration by 50% were used to shock sequencing batch reactors (SBRs) containing a nitrifying (10-day solids retention time (SRT)) and a non-nitrifying (2-day SRT) biomass. Effluent total suspended solids (TSS) and soluble potassium were monitored to examine deflocculation caused by a bacterial stress response mechanism called glutathione-gated potassium efflux (GGKE). Reactors were monitored for recovery over a period of 3 SRTs or less. At the concentrations tested, CDNB, cadmium and pH 11 were found to cause significant increases in effluent TSS concentrations and showed elevated levels of potassium. In contrast, octanol, DNP and cyanide did not induce severe deflocculation and showed moderate increases in effluent potassium levels. Recovery of effluent TSS and potassium concentrations to control levels generally did not correlate, supporting the hypothesis that reflocculation requires regrowth of biomass. These results suggest that different chemicals induce deflocculation in SBRs, but deflocculation is not necessarily caused by the GGKE mechanism in all cases.

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