Doctoral Dissertations

Date of Award

5-1991

Degree Type

Dissertation

Degree Name

Doctor of Philosophy

Major

Microbiology

Major Professor

David C. White

Committee Members

Howard Adler, James Chambers, Thomas Montie, Gary Sayler

Abstract

Microbial biofilms, formed on metal surfaces exposed to aqueous environments, and the metabolic activity of the attached bacteria, can cause corrosion and premature failure of metal structures. Most of the corrosion attributed to microbial activity is localized, and in the form of pitting corrosion. Studies on the mechanisms of microbiologically influenced corrosion (MIC) have lagged behind other corrosion studies. However, studies on mechanisms of MIC are essential in mitigation of MIC problems. MIC studies have been difficult due in part to the difficulties in analyzing local activities of bacteria, spatially and temporally. In addition, most electrochemical techniques for analyzing corrosion are destructive to biofilms, and provide only indirect information on localized corrosion. In this research, bacteria were isolated from corrosion tubercles. The isolates were characterized, and reexposed to steel samples in a laboratory test system to determine if corrosion observed in the field could be simulated in the laboratory. In this way, a test system was developed which could be used to study MIC under controlled laboratory conditions. Recently developed electrochemical techniques were evaluated to determine the usefulness of these techniques in MIC studies. Electrochemical impedance spectroscopy (EIS) was shown to be a useful technique for evaluating corrosion rates of individual metal samples over time. EIS was found to be nondestructive to bacterial biofilms. Potential applied during EIS analysis did not significantly alter the numbers of sessile bacteria, the numbers of sessile viable bacteria, or the activity of sessile bacteria. EIS was used to compare corrosion rates over time of steel exposed to bacteria and exposed to sterile medium. EIS was also used to study the corrosion rates of steel exposed to biofilms treated with oxidizing biocides. Results indicated that the bacterial isolates accelerated the rates of corrosion with respect to sterile controls. Oxidizing biocides increased the corrosion rates, even when most of the biofilm was removed. Although EIS provided a useful means for evaluating corrosion rates over time, in these studies, the technique did not provide a direct means to evaluate mechanisms of localized corrosion influenced by microbial biofilms and bacterial activity. The scanning vibrating electrode technique (SVET) was used to study nonuniform current densities over corroding steel samples. The SVET technique was used to determine corrosion rates at localized sites, under variable applied polarization. In addition, the SVET was used at open circuit potential to study localized corrosion without destruction to the biofilms. The results of the SVET studies demonstrated that although steel coupons appeared passive in sterile medium, small pits formed on the samples and subsequently became inactive (repassivated). In the presence of microbial biofilms, pits would initiate and repassivate for a certain amount of time, then would propagate rather than repassivate. Biofilms were necessary for pit propagation, since spent medium did not cause pit propagation. The time required for pit propagation was dependent on the viability of the bacteria as well as on the numbers of bacteria. SVET studies in sterile media demonstrated that phosphate and buffer promoted repassivation of pits. The bacterial biofilms interfered with this repassivation, either by maintaining an aggressive environment within pits, or by preventing inhibiting ions from reaching anodic sites. Incorporation of 14C-acetate into insoluble cell material, and exposure of the labelled bacteria to X-ray film was used to localize microbial biosynthetic activity. Microautoradiography was used to detect the individually labelled bacteria. These studies were combined with studies of localized corrosion using the SVET. Most of the label observed with the X-ray film was associated with the anodic sites of the steel. The 14C-acetate may have become chemically bound to the corrosion products. However, killed controls showed little label on the electrode surface. Alternatively, bacteria either caused initiation of pits by localized colonization, or bacteria preferentially attached to corrosion products, enabling pits, initiated by chemical corrosion, to propagate.

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