Quantitative assessment of the iron-catalyzed degradation of a polyamide nanofiltration membrane by hydrogen peroxide

Peracetic acid (PAA)/hydrogen peroxide (H2O2) is of interest as a substitute disinfectant and antifouling agent for chlorine in water treatment systems using reverse osmosis (RO) and nanofiltration (NF). To maximize disinfection while minimizing damage to membranes, it is necessary to understand the factors that govern the oxidation of the polyamide (PA) separation layer by peroxides. This study evaluated the tolerance of a NF membrane to H2O2 exposure and quantified the catalytic effect of different forms of iron on membrane oxidation and the inhibitory effect of radical quenching by methanol (MeOH) and tert-butanol (t-BuOH). The experimental approach involved exposing a swath of a nanofiltration membrane (NF90, Dow) to high concentrations of H2O2 (up to 102 g/L) without and with the presence of goethite and ferric oxide and colloidal iron. Membranes were tested by quantifying flux and rejection in a gas-pressured, non-metallic, 50 mL-stirred ultrafiltration cell (Amicon). Membranes oxidation was studied using X-ray photoelectron (XPS) and Fourier Transformed Infrared Spectroscopy (FTIR). In pure water without iron oxides, the membrane tolerated H2O2 concentrations of 3000 mM (102,000 mg/L) for more than 168 h (CTmax > 1.7 x 10(7) mg.h/L (ppm-h)). All forms of iron accelerated membrane oxidation causing PA hydrolysis and membrane failure. In the presence of 90 mg goethite (6.72 mg/cm(2)) at an exposure of 2 mM initial H2O2, goethite decreased the rejection of NaCl to 70% and ACE to 85% in 24 h. Rejection loss accelerated with increasing H2O2 concentration and goethite loading. If MeOH and t-BuOH concentration were two times that of the H2O2 concentration, membrane degradation was significantly inhibited apparently because the alcohols acted as a sink for center dot OH and other reactive species. Findings are in agreement with studies that indicated activation of H2O2 by iron oxides via a Fenton-like mechanism.