餐厨垃圾连续厌氧消化丙酸抑制机理及微量元素调控机制研究

The continuous anaerobic digestion of food waste is often unstable and inhibited by propionate accumulation, which is the bottleneck limiting the development and application this technology. This is the reason to initiate this study, where the mechanisms of propionate inhibition of long-term operated anaerobic system of food waste and enhancement of ecological functions of microbial community by trace elements supplementation are elucidated. In order to achieve above purposes, the issue of propionate inhibition of continuous anaerobic digestion of food waste is taken as the research target. The ecological functions of anaerobic microbial community and its nutritional requirement for trace elements are taken as the breakthrough points. On the one hand, effects of dynamic of microbial community structure and diversity on enzymatic activity, biochemical reaction rates, metabolic pathways of organics and ecological factors during long-term anaerobic digestion of food waste are investigated. During the phase of process imbalance, the responses of microbial community to propionate inhibition and consequent changes of environmental factors in terms of community structure, diversity, dynamic evolution, collaborative relationship and functional activity of anaerobic microorganism are explored. On the other hand, the mechanisms of enhancing enzymatic activity, adjusting anaerobic degradation pathways of organics, stimulating healthy succession of microbial community structure and diversity and enhancing ecological threshold of anaerobic system by trace elements are investigated. This study could provide the theoretical guidance for developing the high-efficiency control strategies for improving anaerobic digestion of food waste.

餐厨垃圾连续厌氧消化稳定性差，常发生丙酸抑制，是限制该技术发展和应用的瓶颈。本课题以餐厨垃圾连续厌氧消化丙酸抑制问题为研究对象，以微生物群落生态功能及其对微量元素的营养需求为切入点，解析丙酸抑制的微生物生态学机理和微量元素对微生物群落生态功能的调控机制。通过考察微生物群落结构和多样性随系统启动—稳定—丙酸累积—丙酸抑制—失败长期演化对关键酶活性、生化反应速率、有机物代谢路径和生态因子的影响、丙酸抑制胁迫及其引发的环境因子变化对微生物群落结构更替、多样性演化、种群进化、种间协作及功能活性调节的驱动效应，解析厌氧系统性能与微生物群落生态功能的交互作用，阐明丙酸抑制的微生物生态学机理；通过探究微量元素对关键酶活性、有机物降解途径、微生物群落结构和多样性演替、厌氧系统生态阈限四个方面的调控作用，揭示微量元素强化餐厨垃圾厌氧消化的微生物生态学机制。本研究可为高效调控餐厨垃圾厌氧系统性能提供理论支撑。

餐厨垃圾连续厌氧消化稳定性差，常发生丙酸抑制，是限制该技术发展和应用的瓶颈。本研究以餐厨垃圾连续厌氧消化丙酸抑制问题为研究对象，以微生物群落生态功能及其对微量元素的营养需求为切入点，解析丙酸抑制的微生物生态学机理和微量元素对微生物群落生态功能的调控机制。首先，揭示了不同条件下餐厨垃圾序批式和半连续式消化特性，解析了厌氧性能与微生物群落功能的交互作用。超高负荷（45 g VS/L）与pH控制（7.5）耦合影响下，序批式系统高稳定性与Methanosarcina显著生长密切相关，且调节pH能刺激互营细菌Syntrophomonadaceae生长，并维持氢营养型产甲烷菌较高活性，确保细菌与甲烷菌高效互营，避免酸累积。其次，揭示了连续系统丙酸抑制的微生物机理。失衡阶段Methanosaeta（丰度80.3%）取代Methanosarcina成为优势菌属，而主要氢型甲烷菌Methanoculleus、Methanobacterium丰度下降至0.2%和2.4%，同时甲烷群落多样性显著下降，H2/CO2产甲烷途径被阻断，氢分压上升引发丙酸代谢反馈抑制而累积。接着，揭示了基于微量元素的强化机制。微量元素对系统性能存在低促-高抑效应，且多元素表现出显著协同效应。Fe (100 mg/L) + Co (1 mg/L) + Mo (5 mg/L) + Ni (5 mg/L)效果最佳，辅酶F420、F430浓度达对照1.53和1.85倍，甲烷产量提高35.5%。添加微量元素的系统维持良好稳定性，刺激Methanosarcina始终优势生长（丰度67.2%-87.5%）并确保氢营养型甲烷菌丰度（10%左右）稳定，同时显著提高甲烷群落多样性，确保甲烷群落良好生态功能。最后，阐明了酸抑制下微量元素驱动系统微生态平衡重建的关键机制。酸抑制前期，添加微量元素能对系统实时恢复，而抑制中期则需补充微量元素和调节pH耦合调控，但抑制后期须同时补充微量元素、调节pH至7.5并补充活性良好的接种泥（接种比50%），才能恢复稳定。实时补充微量元素能刺激互营细菌Syntrophomonadaceae生长，丰度从1%升至16.4%，同时Methanosaeta丰度升至50%以上，产甲烷途径由H2还原CO2向解乙酸转化，强化有机酸互营代谢，驱动系统微生态平衡重建。本研究可为高效调控餐厨垃圾厌氧系统性能提供理论支撑。