Investigating a mechanistic cause for activated-sludge deflocculation in response to shock loads of toxic electrophilic chemicals.

It is hypothesized that a physiological bacterial stress response mechanism, called the glutathione-gated potassium efflux system, is a significant contributor to activated-sludge deflocculation caused by shock loads of toxic electrophilic chemicals. The results show significant potassium (K+) efflux from activated sludge flocs to the bulk liquid in response to sublethal (concentrations less than that required to reduce the specific oxygen uptake rate by 50%) shock loads of chloro-2,4-dinitrobenzene, N-ethylmaleimide, 2,4-dinitrotoluene, benzoquinone, and cadmium in a bench-scale sequencing batch reactor system. Electrophile-induced K+ efflux was correlated with significant deflocculation, as measured by an increase in effluent volatile suspended solids. The K+ efflux occurred immediately (within minutes) after toxin addition and preceded the observed increase in effluent turbidity. The transport of other cations, including sodium, calcium, magnesium, iron, and aluminum, either to or from the floc structure, was negligible as compared with K+ efflux, and cell lysis was determined to be minimal at the chemical shock loads applied. The current results are the first to suggest that activated-sludge upset (i.e., deflocculation) may be caused by a specific protective stress response in bacteria.