Per- and polyfluoroalkyl substances (PFASs) from aqueous film forming foams (AFFFs) can hinder bioremediation of co-contaminants such as trichloroethene (TCE) and benzene, toluene, ethylbenzene, and xylene (BTEX). Anaerobic dechlorination can require bioaugmentation of Dehalococcoides, and for BTEX, oxygen is often sparged to stimulate in situ aerobic biodegradation. We tested PFAS inhibition to TCE and BTEX bioremediation by exposing an anaerobic TCE-dechlorinating coculture, an aerobic BTEX-degrading enrichment culture, and an anaerobic toluene-degrading enrichment culture to n-dimethyl perfluorohexane sulfonamido amine (AmPr-FHxSA), perfluorohexane sulfonamide (FHxSA), perfluorohexanesulfonic acid (PFHxS), or nonfluorinated surfactant sodium dodecyl sulfate (SDS). The anaerobic TCE-dechlorinating coculture was resistant to individual PFAS exposures but was inhibited by >1000× diluted AFFF. FHxSA and AmPr-FHxSA inhibited the aerobic BTEX-degrading enrichment. The anaerobic toluene-degrading enrichment was not inhibited by AFFF or individual PFASs. Increases in amino acids in the anaerobic TCE-dechlorinating coculture compared to the control indicated stress response, whereas the BTEX culture exhibited lower concentrations of all amino acids upon exposure to most surfactants (both fluorinated and nonfluorinated) compared to the control. These data suggest the main mechanisms of microbial toxicity are related to interactions with cell membrane synthesis as well as protein stress signaling.

中文翻译：

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全氟烷基磺酰胺和多氟烷基磺酰胺物质会影响芳烃和三氯乙烯生物修复中使用的微生物


水成膜泡沫 (AFFF) 中的全氟烷基物质和多氟烷基物质 (PFAS) 会阻碍三氯乙烯 (TCE) 以及苯、甲苯、乙苯和二甲苯 (BTEX) 等共污染物的生物修复。厌氧脱氯可能需要对脱卤球菌进行生物强化，而对于苯系物，通常会喷射氧气以刺激原位需氧生物降解。我们通过将厌氧 TCE 脱氯共培养物、需氧 BTEX 降解富集培养物和厌氧甲苯降解富集培养物暴露于正二甲基全氟己烷磺酰胺胺 (AmPr-FHxSA)、全氟己烷磺酰胺 (AmPr-FHxSA) 来测试 PFAS 对 TCE 和 BTEX 生物修复的抑制作用。 FHxSA)、全氟己烷磺酸 (PFHxS) 或非氟化表面活性剂十二烷基硫酸钠 (SDS)。厌氧 TCE-脱氯共培养物对单独的 PFAS 暴露有抵抗力，但被 >1000 倍稀释的 AFFF 抑制。 FHxSA 和 AmPr-FHxSA 抑制需氧 BTEX 降解富集。 AFFF 或单独的 PFAS 不会抑制厌氧甲苯降解富集。与对照相比，厌氧 TCE-脱氯共培养物中氨基酸的增加表明了应激反应，而与对照相比，BTEX 培养物在暴露于大多数表面活性剂（氟化和非氟化）后表现出较低的所有氨基酸浓度。这些数据表明微生物毒性的主要机制与细胞膜合成以及蛋白质应激信号传导的相互作用有关。