Oxidation of cyanobacterial neurotoxin beta-N-methylamino-L-alanine (BMAA) with chlorine, permanganate, ozone, hydrogen peroxide and hydroxyl radical.

Beta-N-methylamino-L-alanine (BMAA), a new cyanobacterial neurotoxin produced by more than 20 genera of cyanobacteria, has been associated with amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) or Alzheimer's disease. Although BMAA has been shown to be removed in drinking water treatment plants (DWTPs), studies regarding the reactions between BMAA and the commonly used oxidants in DWTPs are limited to chlorine under specific conditions. In this study, the reaction kinetics between BMAA and five oxidants commonly used in DWTPs, including chlorine, potassium permanganate, ozone, hydrogen peroxide and hydroxyl radical were investigated. The oxidation of BMAA by chlorine, ozone or OH radical followed the second order reaction rate law, and the reaction rate was in the order of OH radicals > ozone >> chlorine. The rate constants increased by 20 times from 2 × 10 Ms at pH 5.8 to 4.93 × 10 Ms at pH 7, and kept in a relatively stable level at pH 7-9.5; rate constants of OH radicals were 1.11 × 10 Ms at pH 6.5 and 5.51 × 10- 1.35 × 10 Ms at pH > 6.5. For both permanganate and HO only, the removal of BMAA was negligible. The pH dependency of chlorine and the OH radical may be attributed to the neutral form of BMAA with free lone pair electrons readily to be attacked by oxidants. However, for ozonation of BMAA, the rate constants were 1.88 × 10-3.72 × 10 Ms, with a linear dependency on pH, implying that the hydroxide concentration governs the reaction. In addition, the rate of BMAA degradation was found to be slower in natural water if compared with that in deionized water.