Kinetic passivation effect of localized differential aeration on brass

The formation of a localized differential aeration cell on metals, susceptible to both anodic and cathodic corrosion, is a serious threat because of multiple degradation processes commencing with the passivation layer destruction. By using local electrochemical and X-ray dispersive techniques, it has been demonstrated that the differential aeration cell formed on high brass (α-brass, Cu65-Zn35) in the presence of 1H-benzotriazole or 5-methyl-1H-benzotriazole plays both corrosion-inhibiting and accelerating roles, depending on the inhibitor exposure time. Alternating-current scanning electrochemical microscopy was used to image local electrochemical activity, whereas energy-dispersive X-ray spectroscopy provided evidence for the mechanism of the observed phenomena. Short-term exposure to the inhibitor (5 min) promotes the formation of a passivation layer in the waterline region. In contrast, after prolonged exposure (45 min), a deficient passivation layer develops for both inhibitors. An excess of zinc(II)-inhibitor complexes in the passivation layer is accountable for the corrosion resistance of the region with high differential aeration. Rapid dezincification and local alkalinization facilitate the initial rapid formation of a passivation layer in the area under differential aeration to preserve its composition upon further modification. Waterline passivation: A differential aeration cell formed at the meniscus between air and electrolyte invokes local corrosion of brass. In the presence of inhibitors, a short-term passivation effect takes place that can be analyzed by spectroscopic and local electrochemical techniques (see figure). Simultaneous rapid cathodic alkalinization and dezincification lead to the rapid formation of a barrier layer that is temporarily superior to the bulk layer.