Perfluorooctane sulfonate (PFOS) inhibits methane production during sludge anaerobic digestion by breaking the carbon-transfer bridge between methanogenesis and acidogenesis
Per- or polyfluoroalkyl compounds (PFASs) are recognized as emerging contaminant, with perfluorooctane sulfonate (PFOS) being one of the most extensively utilized PFASs due to its great chemical stability. However, knowledge of the bio-chemical behavior, the toxicity of PFOS and its mechanisms of interfacial binding to microorganisms remain inadequately validated. In this study, the biotoxicity of PFOS and its molecular interfacial adsorption mechanism in anaerobic digestion were investigated. The results showed that although the tightly bound EPS (TB-EPS) of anaerobic microorganisms could defend against the biotoxicity of PFOS to some extent by physical adsorption and chemical binding, the exposure to PFOS might produce a greater disturbance to methanogenic archaea. With the increase of PFOS, acid-producing bacteria (APB) and methanogenic archaea showed different resistance to PFOS, with methanogenic archaea being almost completely inhibited. On the contrary, APBs were more tolerant, and fatty acids accumulated up to 2194.27 mg/L. Metagenomics analysis further confirmed that functional genes associated with fatty acid biosynthesis (fas, FAS2, fabK, etc.) were up-regulated (approximately 85.29%) whereas the genes associated with methanogenesis (acs, comA, mcrB, etc.) were down-regulated (up to 65.96%). Molecular docking results confirmed that a portion of PFOS could pass through the EPS by binding to ATP-binding cassette (ABC) transporter substrate-binding protein and interact with key functional enzymes, which led to the inhibition of methanogens. This study provides novel insights into the molecular blocking mechanism by which PFOS disrupts carbon metabolic flux through the selective inhibition of methanogenic archaea, rather than through a general suppression of acidogenic bacteria.