Release and oxidation of cell-bound saxitoxins during chlorination of Anabaena circinalis cells.

Surface water sources are increasingly subject to proliferation of toxic cyanobacteria. Direct chlorination of source water containing toxic cyanobacterial cells for different treatment purposes might cause cell damage and toxin release. There is limited information available on chlorination of saxitoxins (STXs: saxitoxin, C-toxins, and gonyautoxins) produced by Anabaena circinalis. This work: (1) investigated the impact of chlorination on cell lysis and toxin/odor compound release in natural waters; (2) assessed the rates of chlorination of total STXs, and (3) estimated apparent rate constants for STX oxidation in ultrapure and natural waters. With a chlorine exposure (CT) value of 7.0 mg x min/L all cells lost viability causing toxin release. Cell-membrane damage occurred faster than released STXs oxidation. All saxitoxin and more than 95% of other STX analogues were subsequently oxidized. Kinetic analysis of the oxidation of STX analogues revealed significant differences in the susceptibility to chlorine, saxitoxin being the easiest to oxidize. Also, concentrations of trihalomethanes, haloacetic acids, and N-nitrosodimethylamine as chlorination byproducts were respectively <50 µg/L and 11 ng/L even at the highest CT value (50.3 mg x min/L).

Effect of chlorination on Microcystis aeruginosa cell integrity and subsequent microcystin release and degradation.

The proliferation of cyanobacteria in drinking water sources is problematic for water authorities as they can interfere with water treatment processes. Studies have shown that oxidants such as chlorine can enhance the coagulation of cyanobacteria; however, chlorine can potentially lyse cyanobacterial cells, releasing toxic metabolites. Chlorine also has the potential to effectively degrade these toxins. This study evaluated the effect of chlorine on the cell integrity of toxic Microcystis aeruginosa in reservoir water using flow cytometry. In addition, the effect of chlorine on the subsequent release and degradation of microcystin toxins was systematically assessed. Cell lysis occurred at chlorine exposure values between 7 and 29 mg min/L, which is within the range of normal disinfection practices. Intracellular toxin was shown to be released from damaged cells at a rate three times faster than it was degraded by chlorine. The degradation of extracellular microcystin by chlorine was found to be dependent upon the pH, chlorine exposure, and the presence of cyanobacterial cells.