Kinetics and mechanism of ozonation to treat Microcystis-laden source waters affected by cell-viability

Abstract

Toxic cyanobacteria are challenging drinking water safety globally, and their cell-viability declines at decay stage of a succussive bloom. Ozone might be a more effective oxidant to treat both high- and low-viability cyanobacteria than other common oxidants (e.g., chlorine, potassium permanganate). However, previous studies only conducted ozonation experiments using high-viability cyanobacteria, and potential influences of cell-viability on ozonation process, remains unknown. In this study, kinetics of ozone decay, cell inactivation, membrane destruction, and cyanotoxin fate of high- and low-viability Microcystis (the most common genus), was investigated, and associated mechanism was discussed. Results showed that low-viability Microcystis exhibited a higher rate constant of membrane destruction (665–744 M−1 s−1) than high-viability Microcystis (364–600 M−1 s−1) by equal concentrations of ozone, ascribed to loosely gelatinous sheath comprised with fewer organic matters as oxidant scavengers. Meanwhile, a higher rate constant of photosynthetic inactivation induced by ozonation, was observed for low-viability Microcystis (312–364 M−1 s−1) than that for high-viability Microcystis (168–294 M−1 s−1). However, elevated aromatic organics competitively inhibited microcystin ozonation for low-viability Microcystis, and hydroxyl radicals for microcystin oxidation could be reduced by elevated organic loads and alkalinity. Moreover, elevated ozone exposure (>51 mg min L−1) did not totally oxidize microcystin with a residual of 30 μg L−1 for low-viability Microcystis. These findings suggested that elevated microcystin risk would be the great barrier to limit ozonation application for low-viability Microcystis, even with benefits of higher cell inactivation compared to high-viability Microcystis.