A PHYSIOLOGICAL MECHANISM FOR ACTIVATED SLUDGE DEFLOCCULATION CAUSED BY SHOCK LOADS OF TOXIC CHEMICALS

It is hypothesized that physiological bacterial stress response mechanisms are involved in activated sludge process upset caused by shock loads of toxic chemicals. The goal of this research was to determine whether the bacterial glutathione-gated, electrophile-induced potassium efflux system is responsible for deflocculation observed in response to shock loads of toxic electrophilic (thiol reactive) chemicals to activated sludge wastewater treatment systems. These results indicate significant K+ efflux from the activated sludge floc structure to the bulk liquid in response to shock loads of chloro-2,4-dinitrobenzene (CDNB), N-ethylmaleimide (NEM), 2,4-dinitrotoluene (DNT), benzoquinone (BQ), and cadmium (Cd) to a bench-scale sequencing batch reactor (SBR) system. In most cases, the stressor chemicals caused significant deflocculation, as measured by an increase in effluent volatile suspended solids (VSS), at concentrations much less than that required to reduce the maximum specific oxygen uptake rate by 50% (IC50). This suggests that toxin-induced activated sludge deflocculation may actually be caused by a protective bacterial stress mechanism and that the upset event may not be detectable by aerobic respirometry. More importantly, the amount of K+ efflux appeared to correlate well with the degree of deflocculation. The transport of other cations including sodium, calcium, magnesium, iron, and aluminum, either to or from the floc structure, was negligible as compared to K+ efflux. It was also determined that the K+ efflux occurred immediately (within minutes) after toxin addition and then was followed by an increase in effluent turbidity. Work is ongoing to further characterize the role of the electrophile-induced K+ efflux mechanism in activated sludge deflocculation. The current results are very promising and are the first to suggest that activated sludge upset (i.e. deflocculation) may be caused by a specific protective stress response in bacteria.