The decisive role of biological factors in the corrosion of the D16T alloy. Review
Abstract
The biocorrosion of duralumin grade D16T has been studied and a mechanism has been proposed according to which the initiators of initial corrosion damage are reactive oxygen species (ROS) produced by icromycetes. An assumption was made about the participation of hydrogen peroxide in the mycological corrosion of the D16T alloy, which is formed both during the life of micromycetes and during the activation of oxygen by zero-valent aluminium (ZVAl). The mechanisms of intergranular, pitting and pitting corrosion of duralumin under the influence of microscopic fungi are proposed. Purpose: determination of the main biological factor initiating biocorrosion of the D16T alloy; assessment of the biological impact of the association of microscopic fungi on the alloy in order to develop scientifically grounded and effective methods of protecting aluminium and its alloys from biocorrosion by micromycetes.
The object of the study was an aluminium alloy D16T in accordance with state standard (GOST) 4784–2019 after hardening and natural ageing, which is widely used for the manufacture of load-bearing elements of structures and equipment of fuel systems of aircraft, car bodies, parts of various machines and assemblies operating at low temperatures, and in the food and pharmaceutical industries. The stages of initiation and development of biocorrosion of the D16T alloy under the influence of a consortium of moulds have been studied using a scanning electron microscope. The phase composition of the D16T corrosion products has been studied.
In the process of vital activity of microscopic fungi, reactive oxygen species are formed, initiating the biocorrosion of the D16T alloy. The initial stage of biocorrosion is caused by hydrolysis of the protective passive aluminium film. At the stage of intense biocorrosion, oxygen-containing aluminium compounds are formed in the form of a water-saturated gel. Further, as this corrosion product accumulates, its water permeability decreases. The gel undergoes “ageing” and turns into crystalline products. Conidia and hyphae of microscopic fungi adhere, are mechanically fixed on the metal surface and penetrate into the surface layers and deep into the metal, causing its corrosive destruction in the form of pitting, ulcers, and cavities. It
is possible that the initiation of metal biocorrosion is a consequence of the hyperproduction of reactive oxygen species by the cells of micromycetes as a result of oxidative stress. This may be their defensive strategy aimed at destroying xenobiotic material.
The development of intergranular and pitting corrosion of the D16T alloy under the action of micromycetes occurs at the sites of contact with the exudate, which, due to a cascade of reactions with the participation of ROS, is locally enriched in hydroxide ions. The origin and development of pitting on the duralumin surface occurs in defects of the passive oxide film due to the displacement of oxygen-containing surface aluminium compounds and their interaction with corrosive OH– and ROS anions. Hydrogen peroxide, as an intermediate product of the metabolism of micromycetes, on the surface of the D16T alloy can participate in the Fenton process or decompose heterogeneously, also provoking the development of aluminium biocorrosion.
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