CONTROLLING THE ACIDOGENIC METABOLIC PATHWAYS TOWARDS THE PRODUCTION OF TARGET PRODUCTS DURING TWO-PHASE ANAEROBIC DIGESTION OF FOOD WASTE

摘要

Hydrolysis/acidogenesis of food waste (FW) under different hydrogen partial pressure (PH2) influences the gas and acid production pathways, which is poorly understood. Therefore, the present study aimed to study the positive effects of four different PH2 on volatile acid production (VFA) and mircbial community shifts in LBR treating FW. Subsequently, the acidified product from LBRs fed into upflow anaerobic sludge blanker reactors (UASB) for CH4 production in a two-phase hybrid anaerobic solid-liquid system. One LBR was operated as control without regulation of headspace PH2, while other three LBRs were operated under different H2 levels as 80% (T2), 50-60% (T3) and 0.04 % (T4) with CO2 as mixing gas (but at constan headspace pressure ~3.3 psi). The two-phase systems were incubated under 35oC and monitored over the period of 20 days. Very low PH2 and high CO2 concentrations in headspace from T4 favoured the hydrolysis/acidogenesis rate resulting with high organic solubilization and butyric acid accumulations (~ 80% of total VFA). In subsequent treatment in UASB yielded 0.30 L/g VSadded within the residence time of 24h. The possible reasons could be that the more of electrons may channelled towards the butyric acid production pathways in T4, while the electrons shunted towards mixed VFA production in T1-T3. Further analysis of microbial community structures showed that the dominance of fermentative bacteria Clostridium sp., and Bifidobacters sp., in T4, while Lactobacillus sp., were predominant in T1. Although the microbial composition from T2 found similar that of T4, the acidification rate and the volatile organic acid profiles were different that might be linked with the differences in population size that required investigation. Overall, the present study results found to be very significant and proved that the regulation PH2 and CO2 concentraion could be used to manipulate the acidogenesis pathway in LBRs treating FW.