Search

The activated sludge process within the pulp and paper industry is generally run to minimize the production of waste activated sludge (WAS), leading to high electricity costs from aeration and relatively large basin volumes. In this study, a pilot-scale activated sludge process was run to evaluate the concept of treating the wastewater at high rate with a low sludge age. Two 150 L containers were used, one for aeration and one for sedimentation and sludge return. The hydraulic retention time was decreased from 24 hours to 7 hours, and the sludge age was lowered from 12 days to 2–4 days. The methane potential of the WAS was evaluated using batch tests, as well as continuous anaerobic digestion (AD) in 4 L reactors in mesophilic and thermophilic conditions. Wastewater treatment capacity was increased almost four-fold at maintained degradation efficiency. The lower sludge age greatly improved the methane potential of the WAS in batch tests, reaching 170 NmL CH4/g VS at a sludge age of 2 days. In addition, the continuous AD showed a higher methane production at thermophilic conditions. Thus, the combination of high-rate wastewater treatment and AD of WAS is a promising option for the pulp and paper industry. Funding agencies: Swedish Energy Agency [32802-2]; Scan-dinavian Biogas Fuels AB; Poyry AB; BillerudKorsnas AB; SCA; Fiskeby Board AB; Purac AB

The pulp and paper industry is a large producer of wastewater and sludge, putting high pressure on waste treatment. In addition, more rigorous environmental legislation for pollution control and de ...

The production processes of the pulp and paper industry often run in campaigns, leading to large variations in the composition of wastewaters and waste sludges. During anaerobic digestion (AD) of these wastes, the viscosity or the production of extracellular polymeric substances (EPS) and soluble microbial products (SMP) may be affected, with the risk of foam formation, inefficient digester mixing or poor sludge dewaterability. The aim of this study was to investigate how viscosity and production of EPS and SMP during long-term AD of pulp and paper mill sludge is affected by changes in organic loading rate (OLR) and hydraulic retention time (HRT). Two mesophilic lab-scale continuous stirred tank reactors (CSTRs) were operated for 800 days (R1 and R2), initially digesting only fibre sludge, then co-digesting fibre sludge and activated sludge. The HRT was lowered, followed by an increase in the OLR. Reactor fluids were sampled once a month for rheological characterization and analysis of EPS and SMP. The production of the protein fraction of SMP was positively correlated to the OLR, implicating reduced effluent qualities at high OLR. EPS formation correlated with the magnesium content, and during sulphate deficiency, the production of EPS and SMP increased. At high levels of EPS and SMP, there was an increase in viscosity of the anaerobic sludges, and dewatering efficiency was reduced. In addition, increased viscosity and/or the production of EPS and SMP were important factors in sludge bulking and foam formation in the CSTRs. Sludge bulking was avoided by more frequent stirring. Electronic supplementary material The online version of this article (10.1007/s00449-019-02224-4) contains supplementary material, which is available to authorized users.

With the final aim of reducing the energy consumption and increase the methane production at Swedish pulp and paper mills, the methane potential of 62 wastewater effluents from 10 processes at seven pulp and/or paper mills (A-G) was determined in anaerobic batch digestion assays. This mapping is a first step towards an energy efficient and more sustainable utilization of the effluents by anaerobic digestion, and will be followed up by tests in lab-scale and pilot-scale reactors. Five of the mills produce kraft pulp (KP), one thermo-mechanical pulp (TMP), two chemical thermo-mechanical pulp (CTMP) and two neutral sulfite semi-chemical (NSSC) pulp. Both elementary and total chlorine free (ECF and TCF, respectively) bleaching processes were included. The effluents included material from wood rooms, cooking and oxygen delignification, bleaching (often both acid- and alkali effluents), drying and paper/board machinery as well as total effluents before and after sedimentation. The results from the screening showed a large variation in methane yields (percent of theoretical methane potential assuming 940 NmL CH4 per g TOC) among the effluents. For the KP-mills, methane yields above 50% were obtained for the cooking effluents from mills D and F, paper machine wastewater from mill D, condensate streams from mills B, E and F and the composite pre-sedimentation effluent from mill D. The acidic ECF-effluents were shown to be the most toxic to the AD-flora and also seemed to have a negative effect on the yields of composite effluents downstream while three of the alkaline ECF-bleaching effluents gave positive methane yields. ECF bleaching streams gave higher methane yields when hardwood was processed. All TCF-bleaching effluents at the KP mills gave similar degradation patterns with final yields of 10-15% of the theoretical methane potential for four of the five effluents. The composite effluents from the two NSSC-processes gave methane yields of 60% of the theoretical potential. The TMP mill (A) gave the best average yield with all six effluents ranging 40-65% of the theoretical potential. The three samples from the CTMP process at mill B showed potentials around 40% while three of the six effluents at mill G (CTMP) yielded 45-50%.

Type 2 diabetes originates in an expanding adipose tissue that for unknown reasons becomes insulin resistant. Insulin resistance reflects impairments in insulin signaling, but mechanisms involved are unclear because current research is fragmented. We report a systems level mechanistic understanding of insulin resistance, using systems wide and internally consistent data from human adipocytes. Based on quantitative steady-state and dynamic time course data on signaling intermediaries, normally and in diabetes, we developed a dynamic mathematical model of insulin signaling. The model structure and parameters are identical in the normal and diabetic states of the model, except for three parameters that change in diabetes: (i) reduced concentration of insulin receptor, (ii) reduced concentration of insulin-regulated glucose transporter GLUT4, and (iii) changed feedback from mammalian target of rapamycin in complex with raptor (mTORC1). Modeling reveals that at the core of insulin resistance in human adipocytes is attenuation of a positive feedback from mTORC1 to the insulin receptor substrate-1, which explains reduced sensitivity and signal strength throughout the signaling network. Model simulations with inhibition of mTORC1 are comparable with experimental data on inhibition of mTORC1 using rapamycin in human adipocytes. We demonstrate the potential of the model for identification of drug targets, e.g. increasing the feedback restores insulin signaling, both at the cellular level and, using a multilevel model, at the whole body level. Our findings suggest that insulin resistance in an expanded adipose tissue results from cell growth restriction to prevent cell necrosis.

Type 2 diabetes originates in an expanding adipose tissue that for unknown reasons becomes insulin resistant. Insulin resistance reflects impairments in insulin signaling, but mechanisms involved are unclear because current research is fragmented. We report a systems level mechanistic understanding of insulin resistance, using systems wide and internally consistent data from human adipocytes. Based on quantitative steady-state and dynamic time course data on signaling intermediaries, normally and in diabetes, we developed a dynamic mathematical model of insulin signaling. The model structure and parameters are identical in the normal and diabetic states of the model, except for three parameters that change in diabetes: (i) reduced concentration of insulin receptor, (ii) reduced concentration of insulin-regulated glucose transporter GLUT4, and (iii) changed feedback from mammalian target of rapamycin in complex with raptor (mTORC1). Modeling reveals that at the core of insulin resistance in human adipocytes is attenuation of a positive feedback from mTORC1 to the insulin receptor substrate-1, which explains reduced sensitivity and signal strength throughout the signaling network. Model simulations with inhibition of mTORC1 are comparable with experimental data on inhibition of mTORC1 using rapamycin in human adipocytes. We demonstrate the potential of the model for identification of drug targets, e.g. increasing the feedback restores insulin signaling, both at the cellular level and, using a multilevel model, at the whole body level. Our findings suggest that insulin resistance in an expanded adipose tissue results from cell growth restriction to prevent cell necrosis.