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Toxicity of 6:2 Chlorinated Polyfluorinated Ether Sulfonate (F-53B) to Escherichia coli: Growth Inhibition, Morphological Disruption, Oxidative Stress, and DNA Damage
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F-53B, a widely used PFOS substitute in electroplating, inhibited E. coli growth at 23.56 mg/L and caused membrane disruption, oxidative stress, and DNA damage through mechanisms distinct from classical PFAS toxicity. F-53B is increasingly detected across environmental matrices including those contaminated with microplastics, making understanding its toxicity critical for assessing combined exposure risks.
6:2 chlorinated polyfluoroalkyl ether sulfonic acid (F-53B), a substitute for perfluorooctane sulfonate (PFOS), is widely used as a mist suppressant in the electroplating industry. With the implementation of PFOS regulations, the use of F-53B has correspondingly increased, and it is now detected in various environmental matrices. However, toxicological information on F-53B remains incomplete and insufficient for environmental risk assessment. In this study, we systematically investigated, for the first time, the toxicity and underlying mechanisms of action of F-53B to Escherichia coli. The results showed that the 24 h half-maximal growth inhibition concentration (IC50) of F-53B was 23.56 mg/L, suggesting that F-53B may exhibit higher toxicity to E. coli than PFOS. Analyses of cell surface hydrophobicity, membrane permeability, membrane composition, and scanning electron microscopy (SEM) images showed that F-53B adsorbed onto the cell surface, altered membrane properties, and ultimately disrupted cell morphology. Increased intracellular levels of reactive oxygen species (ROS) and malondialdehyde (MDA), along with decreased activities of superoxide dismutase (SOD) and catalase (CAT), indicated enhanced oxidative stress induced by F-53B in E. coli. Furthermore, the alkaline comet assay demonstrated that F-53B exposure caused DNA damage. Taken together, the toxicity of F-53B to E. coli can be attributed to cell morphological disruption, oxidative stress, and DNA damage, ultimately leading to cellular inactivation or death. These findings advance our understanding of the cytotoxicity of F-53B in microorganisms.
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