Triclosan degradation in sludge anaerobic fermentation and its impact on hydrogen production

Triclosan (TCS), a widely used antibacterial agent, was accumulated at significant levels in waste activated sludge (WAS). To date, however, the interaction between TCS and sludge anaerobic fermentation was rarely reported. Hence, this work aimed to deeply understanding the degradation of TCS in sludge anaerobic fermentation and its impact on hydrogen production. Experimental results showed that similar to 45% of TCS was degraded in long-term anaerobic fermentation, with 2,4-dichlorophenol as its main intermediate. Based on the information from high performance liquid chromatography-mass spectrometry analysis, three pathways i.e., dechlorination, hydroxylation, and cleavage of ether bonds, were proposed for TCS degradation. It was found that the maximum hydrogen yield decreased from 18.6 to 12.8 mL/g VSS with the increase of TCS from 12 to 487 mg/kg TSS. One possible reason for the decreased hydrogen yield was that a part of hydrogen generated might serve as electron donors for TCS dechlorination. Besides, the presence of TCS significantly suppressed acidogenesis (an important step responsible for hydrogen generation). This inhibition to acidogenesis is likely due to that the high-affinity functional groups of TCS such as hydroxyl groups could bind to the active sites of acetate kinase (AK, a key enzyme in acidogenesis), which reduced the active sites available for original fermentation substrates. Microbial analysis revealed that TCS increased the relative abundances of potential contaminant decomposers such as Guggeheimella but inhibited the populations of hydrogen producers such as Proteiniborus, which was consistent with the results obtained by chemical analyses.

Automated summary

TCS undergoes degradation in sludge anaerobic fermentation, leading to a decrease in hydrogen yield, possibly due to hydrogen serving as electron donors for TCS dechlorination. Furthermore, the presence of TCS significantly inhibits acidogenesis, likely through binding of TCS's functional groups to active sites of acetate kinase.