Accelerated biocorrosion of stainless steel in marine water via extracellular electron transfer encoding gene phzH of Pseudomonas aeruginosa.

Microbiologically influenced corrosion (MIC) constantly occurs in water/wastewater systems, especially in marine water. MIC contributes to billions of dollars in damage to marine industry each year, yet the physiological mechanisms behind this process remain poorly understood. Pseudomonas aeruginosa is a representative marine electro-active bacterium, which has been confirmed to cause severe MIC on carbon steel through extracellular electron transfer (EET). However, little is known about how P. aeruginosa causes corrosion on stainless steel. In this study, the corrosivity of wild-type strain, phzH knockout, phzH complemented, and phzH overexpression P. aeruginosa mutants were evaluated to explore the underlying MIC mechanism. We found the accelerated MIC on 2205 duplex stainless steel (DSS) was due to the secretion of phenazine-1-carboxamide (PCN), which was regulated by the phzH gene. Surface analysis, Mott-Schottky test and H2O2 measurement results showed that PCN damaged the passive film by forming H2O2 to oxidize chromium oxide to soluble hexavalent chromium, leading to more severe pitting corrosion. The normalized corrosion rate per cell followed the same order as the general corrosion rate obtained under each experimental condition, eliminating the influence of the total amount of sessile cells on corrosion. These findings provide new insight and are meaningful for the investigation of MIC mechanisms on stainless steel. The understanding of MIC can improve the sustainability and resilience of infrastructure, leading to huge environmental and economic benefits.

Direct microbial electron uptake as a mechanism for stainless steel corrosion in aerobic environments.

Shewanella oneidensis MR-1 is an attractive model microbe for elucidating the biofilm-metal interactions that contribute to the billions of dollars in corrosion damage to industrial applications each year. Multiple mechanisms for S. oneidensis-enhanced corrosion have been proposed, but none of these mechanisms have previously been rigorously investigated with methods that rule out alternative routes for electron transfer. We found that S. oneidensis grown under aerobic conditions formed thick biofilms (∼50 µm) on stainless steel coupons, accelerating corrosion over sterile controls. H2 and flavins were ruled out as intermediary electron carriers because stainless steel did not reduce riboflavin and previous studies have demonstrated stainless does not generate H2. Strain ∆mtrCBA, in which the genes for the most abundant porin-cytochrome conduit in S. oneidensis were deleted, corroded stainless steel substantially less than wild-type in aerobic cultures. Wild-type biofilms readily reduced nitrate with stainless steel as the sole electron donor under anaerobic conditions, but strain ∆mtrCBA did not. These results demonstrate that S. oneidensis can directly consume electrons from iron-containing metals and illustrate how direct metal-to-microbe electron transfer can be an important route for corrosion, even in aerobic environments.

Corrosion behavior of high nitrogen nickel-free austenitic stainless steel in the presence of artificial saliva and Streptococcus mutans.

High nitrogen nickel-free austenitic stainless steels (HNSs) have great potentials to be used in dentistry owing to its exceptional mechanical properties, high corrosion resistance, and biocompatibility. In this study, HNSs with nitrogen of 0.88 wt% and 1.08 wt% displayed much lower maximum pit depths than 316L stainless steel (SS) after 21 d of immersion in abiotic artificial saliva (2.2 µm and 1.7 µm vs. 4.5 µm). Microbiologically influenced corrosion (MIC) evaluations revealed that Streptococcus mutans biofilms led to much severer corrosion of 316L SS than HNSs. Corrosion current densities of HNSs were two orders of magnitude lower than that of 316L SS after incubation of 7 d (37.5 nA/cm2 and 29.9 nA/cm2 vs. 5.63 µA/cm2). The pitting potentials of HNSs were at least 550 mV higher than that of 316L SS in the presence of S. mutans, confirming the better MIC resistance of HNSs. Cytotoxicity assay confirmed that HNSs were not toxic to MC3T3-E1 cells and allowed better sessile cell growth on them than on 316L SS. It can be concluded that HNSs are more suitable dental materials than the conventional 316L SS.

Accelerated corrosion of 2205 duplex stainless steel caused by marine aerobic Pseudomonas aeruginosa biofilm.

Microbiologically influenced corrosion (MIC) of 2205 duplex stainless steel (DSS) in the presence of Pseudomonas aeruginosa was investigated through electrochemical and surface analyses. The electrochemical results showed that P. aeruginosa significantly reduced the corrosion resistance of 2205 DSS. Confocal laser scanning microscopy (CLSM) images showed that the depths of the largest pits on 2205 DSS with and without P. aeruginosa were 14.0 and 4.9µm, respectively, indicating that the pitting corrosion was accelerated by P. aeruginosa. X-ray photoelectron spectroscopy (XPS) results revealed that CrO3 and CrN formed on the 2205 DSS surface in the presence of P. aeruginosa.

Microbiologically Influenced Corrosion of 2707 Hyper-Duplex Stainless Steel by Marine Pseudomonas aeruginosa Biofilm.

Microbiologically Influenced Corrosion (MIC) is a serious problem in many industries because it causes huge economic losses. Due to its excellent resistance to chemical corrosion, 2707 hyper duplex stainless steel (2707 HDSS) has been used in the marine environment. However, its resistance to MIC was not experimentally proven. In this study, the MIC behavior of 2707 HDSS caused by the marine aerobe Pseudomonas aeruginosa was investigated. Electrochemical analyses demonstrated a positive shift in the corrosion potential and an increase in the corrosion current density in the presence of the P. aeruginosa biofilm in the 2216E medium. X-ray photoelectron spectroscopy (XPS) analysis results showed a decrease in Cr content on the coupon surface beneath the biofilm. The pit imaging analysis showed that the P. aeruginosa biofilm caused a largest pit depth of 0.69 µm in 14 days of incubation. Although this was quite small, it indicated that 2707 HDSS was not completely immune to MIC by the P. aeruginosa biofilm.

Extracellular Electron Transfer Is a Bottleneck in the Microbiologically Influenced Corrosion of C1018 Carbon Steel by the Biofilm of Sulfate-Reducing Bacterium Desulfovibrio vulgaris.

Carbon steels are widely used in the oil and gas industry from downhole tubing to transport trunk lines. Microbes form biofilms, some of which cause the so-called microbiologically influenced corrosion (MIC) of carbon steels. MIC by sulfate reducing bacteria (SRB) is often a leading cause in MIC failures. Electrogenic SRB sessile cells harvest extracellular electrons from elemental iron oxidation for energy production in their metabolism. A previous study suggested that electron mediators riboflavin and flavin adenine dinucleotide (FAD) both accelerated the MIC of 304 stainless steel by the Desulfovibrio vulgaris biofilm that is a corrosive SRB biofilm. Compared with stainless steels, carbon steels are usually far more prone to SRB attacks because SRB biofilms form much denser biofilms on carbon steel surfaces with a sessile cell density that is two orders of magnitude higher. In this work, C1018 carbon steel coupons were used in tests of MIC by D. vulgaris with and without an electron mediator. Experimental weight loss and pit depth data conclusively confirmed that both riboflavin and FAD were able to accelerate D. vulgaris attack against the carbon steel considerably. It has important implications in MIC failure analysis and MIC mitigation in the oil and gas industry.