Assessing the performance of polyphosphate accumulating organisms in a full-scale side-stream enhanced biological phosphorous removal.

Phosphorous (P) removal in wastewater treatment is essential to prevent eutrophication in water bodies. Side-stream enhanced biological phosphorous removal (S2EBPR) is utilized to improve biological P removal by recirculating internal streams within a side-stream reactor to generate biodegradable carbon (C) for polyphosphate accumulating organisms (PAOs). In this study, a full-scale S2EBPR system in a water resource recovery facility (WRRF) was evaluated for 5 months. Batch experiments revealed a strong positive correlation (r = 0.91) between temperature and C consumption rate (3.56-8.18 mg-COD/g-VSS/h) in the system, with temperature ranging from 14°C to 18°C. The anaerobic P-release to COD-uptake ratio decreased from 0.93 to 0.25 mg-P/mg-COD as the temperature increased, suggesting competition between PAOs and other C-consumers, such as heterotrophic microorganisms, to uptake bioavailable C. Microbial community analysis did not show a strong relationship between abundance and activity of PAO in the tested WRRF. An assessment of the economic feasibility was performed to compare the costs and benefits of a full scale WRRF with and without implementation of the S2EBPR technology. The results showed the higher capital costs required for S2EBPR were estimated to be compensated after 5 and 11 years of operation, respectively, compared to chemical precipitation and conventional EBPR. The results from this study can assist in the decision-making process for upgrading a conventional EBPR or chemical P removal process to S2EBPR. PRACTITIONER POINTS: Implementation of S2EBPR presents adaptable configurations, exhibiting advantages over conventional setups in addressing prevalent challenges associated with phosphorous removal. A full-scale S2EBPR WRRF was monitored over 5 months, and activity tests were used to measure the kinetic parameters. The seasonal changes impact the kinetic parameters of PAOs in the S2EBPR process, with elevated temperatures raising the carbon demand. PAOs abundance showed no strong correlation with their activity in the full-scale S2EBPR process in the tested WRRF. Feasibility assessment shows that the benefits from S2EBPR operation can offset upgrading costs from conventional BPR or chemical precipitation.

Vitamin D3 deficiency induced intestinal inflammatory response of turbot through nuclear factor-κB/inflammasome pathway, accompanied by the mutually exclusive apoptosis and autophagy.

Vitamin D3 (VD3) participated widely in the nuclear factor-κB (NF-κB)-mediated inflammation, apoptosis, and autophagy through the vitamin D receptor (VDR). However, the molecular mechanisms remain not understood in teleost. The present study investigated the functions of VD3/VDR on intestinal inflammation, autophagy, and apoptosis of turbot in vivo and in vitro. Triple replicates of 30 fish were fed with each of three diets with graded levels of 32.0 (D0), 1012.6 (D1), and 3978.2 (D2) IU/kg VD3. Obvious intestinal enteritis was observed in the D0 group and followed with dysfunction of intestinal mucosal barriers. The intestinal inflammatory response induced by VD3 deficiency was regulated by the NF-κB/inflammasome signalling. The promotion of intestinal apoptosis and suppression of intestinal autophagy were also observed in the D0 group. Similarly, VD3 deficiency in vitro induced more intense inflammation regulated by NF-κB/inflammasome signalling. The mutually exclusive apoptosis and autophagy were also observed in the group without 1,25(OH)2D3 in vitro, accompanied by similar changes in apoptosis and autophagy increased apoptosis. The gene expression of VDRs was significantly increased with the increasing VD3 supplementation both in vivo and in vitro. Moreover, VDR knockdown in turbot resulted in intestinal inflammation, and this process relied on the activation of inflammasome mediated by NF-κB signalling. Simultaneously, intestinal apoptosis was promoted, whereas intestinal autophagy was inhibited. In conclusion, VD3 deficiency could induce intestinal inflammation via activation of the NF-κB/inflammasome pathway, intestinal apoptosis, and autophagy formed a mutually exclusive relation in teleost. And VDR is the critical molecule in those processes.

Elemental copper nanoparticle toxicity to anaerobic ammonium oxidation and the influence of ethylene diamine-tetra acetic acid (EDTA) on copper toxicity.

Soluble ions released by elemental copper nanoparticles (Cu0 NP) are toxic to key microorganisms of wastewater treatment processes. However, their toxicity to anaerobic ammonium oxidation (anammox) has not yet been studied. Chelating agents occurring in wastewater may decrease copper ions (Cu2+) concentration and consequently, decrease copper toxicity. This study evaluated Cu0 NP and CuCl2 toxicity to anammox and the influence of ethylene diamine-tetra acetic acid (EDTA) on copper toxicity. Bioassays were supplemented with Cu0 NP or CuCl2 with and without EDTA. Anammox activities were used to calculate inhibition constants (Ki). Results showed that Cu0 NP are toxic to anammox. Ki constants with respect to added copper were 1.8- and 2.81-fold larger (less toxic) in EDTA-containing assays for Cu0 NP and CuCl2, respectively, compared to EDTA-free assays. Additionally, Ki constants calculated in EDTA-free assays with respect the measured dissolved copper concentration were 0.023 mM Cu0 NP and 0.014 mM CuCl2. The similarity of these Ki constants indicates that Cu0 NP toxicity to anammox is caused by the release of Cu2+. Finally, severe toxicity caused by 0.315 mM and Cu0 NP 0.118 mM CuCl2 was attenuated by 88-100% when 0.14 mM EDTA was supplied. Toxicity attenuation likely occurred because EDTA complexed Cu2+ ions, thus, decreasing their bioavailability. Overall, this study indicates that Cu0 NP and CuCl2 are toxic to anammox, and furthermore, that EDTA attenuates Cu0 NP and CuCl2 toxicity to anammox by complexing Cu2+ ions.