Dynamic modelling of nitrous oxide emissions from three Swedish sludge liquor treatment systems.

The objective of this paper is to model the dynamics and validate the results of nitrous oxide (N2O) emissions from three Swedish nitrifying/denitrifying, nitritation and anammox systems treating real anaerobic digester sludge liquor. The Activated Sludge Model No. 1 is extended to describe N2O production by both heterotrophic and autotrophic denitrification. In addition, mass transfer equations are implemented to characterize the dynamics of N2O in the water and the gas phases. The biochemical model is simulated and validated for two hydraulic patterns: (1) a sequencing batch reactor; and (2) a moving-bed biofilm reactor. Results show that the calibrated model is partly capable of reproducing the behaviour of N2O as well as the nitritation/nitrification/denitrification dynamics. However, the results emphasize that additional work is required before N2O emissions from sludge liquor treatment plants can be generally predicted with high certainty by simulations. Continued efforts should focus on determining the switching conditions for different N2O formation pathways and, if full-scale data are used, more detailed modelling of the measurement devices might improve the conclusions that can be drawn.

Carbon footprints of Scandinavian wastewater treatment plants.

This study estimates the carbon footprints of 16 municipal wastewater treatment plants (WWTPs), all situated in Scandinavian countries, by using a simple model. The carbon footprint calculations were based on operational data, literature emission factors (efs) and measurements of greenhouse gas emissions at some of the studied WWTPs. No carbon neutral WWTPs were found. The carbon footprints ranged between 7 and 108 kg CO2e P.E.(-1) year(-1). Generally, the major positive contributors to the carbon footprint were direct emissions of nitrous oxide from wastewater treatment. Whether heat pumps for effluents have high coefficient of performance or not is extremely important for the carbon footprint. The choice of efs largely influenced the carbon footprint. Increased biogas production, efficient biogas usage, and decreased addition of external fossil carbon source for denitrification are important activities to decrease the carbon footprint of a WWTP.

Prolonged attenuation of acetylcholine-induced phosphorylation of extracellular signal-regulated kinase 1/2 following sevoflurane exposure.

BACKGROUND: Volatile anaesthetics are known to affect cholinergic receptors. Perturbation of cholinergic signalling can cause cognitive deficits. In this study, we wanted to evaluate acetylcholine-induced intracellular signalling following sevoflurane exposure. METHODS: Pheochromocytoma12 PC12 cells were exposed to 4.6% sevoflurane for 2 h. Subsequently, Western blotting was used to measure acetylcholine-induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK) 1/2 and basal Protein kinase B (AKT) phosphorylation. RESULTS: After exposure, acetylcholine-induced ERK 1/2 phosphorylation was reduced to 58 ± 8% [95% confidence interval (CI): 38-77%, P = 0.003] compared with non-exposed controls. At 30 min after the end of sevoflurane administration [at 0.7% sevoflurane (0.102 mM)], ERK 1/2 phosphorylation remained reduced to 57 ± 7% (95% CI: 39-74%, P = 0.001) and was at 120 min [0.02% (0.003 mM] still reduced to 63 ± 10% (95% CI: 37-88%, P = 0.01), compared with control. At 360 min after exposure, acetylcholine-induced ERK 1/2 phosphorylation had recovered to 98 ± 16% (95% CI: 45-152%, P = 0.98) compared with control. In contrast, immediately after sevoflurane exposure, basal AKT phosphorylation was increased by 228 ± 37% (95% CI: 133-324%, P = 0.02) but had returned to control levels at 30 min after exposure, 172 ± 67% (95% CI: 0-356%, P = 0.34). CONCLUSION: Sevoflurane exposure has differential effects on different intracellular signalling pathways. On one hand, we observed a prolonged attenuation of acetylcholine-induced ERK 1/2 phosphorylation that persisted even when sevoflurane concentrations close to detection level. On the other hand, basal AKT phosphorylation was increased twofold during sevoflurane exposure, with a rapid return to baseline levels after exposure. We speculate that the effects on acetylcholine-induced intracellular signalling observed in our in vitro model could be of relevance also for cholinergic signalling in vivo following sevoflurane exposure.

Dynamics of nitrogen oxides emission from a full-scale sludge liquor treatment plant with nitritation.

Biological treatment in wastewater treatment plants (WWTPs) is a source of nitrogen oxides (N2O, NO and NO2) emitted to the atmosphere. Aerobic ammonia-oxidising bacteria (AOB) have been suggested to be the main source of these emissions. In a full-scale sludge liquor treatment plant at Sjölunda WWTP, it was shown that significant emissions of N2O, NO and NO2 do occur. The plant is operated with nitritation alone, which gives an environment enriched in aerobic AOB. During normal operation, emissions of N2O, NO and NO2 were found to be 3.8%, 0.06% and 0.01% of the ammonium nitrogen load. The N2O emissions were larger than the recommended estimated figure of the Intergovernmental Panel on Climate Change (IPCC) for a complete wastewater treatment plant. The N2O emissions correlated positively with the length of the previous anoxic period, i.e., settling and decantation, and with the ammonium oxidation rate. The NO and NO2 emission profiles were similar and dependent on ammonium oxidation and DO level, but the NO2 concentrations were always lower.

Full-scale sludge liquor treatment for ammonium reduction with low carbon dosage.

The separate treatment of sludge liquor, produced by dewatering anaerobic digested sludge at wastewater treatment plants, gives rise to extreme environments for nitrogen removal. A full-scale sequencing batch reactor was operated with the aim of introducing and studying denitritation as a supplement to nitritation in order to reduce operating costs. Since the main plant only has problems with ammonium reduction capacity, the initial strategy was to have sufficient ammonium reduction with optimal alkalinity production by denitrifiers, i.e. low carbon dosage and minimum alkalinity and residual oxidized ammonium in the effluent. This strategy led to an unbalanced and sensitive process because the denitrifiers were often inhibited. High dissolved oxygen (DO) readings and no decrease in oxidation-reduction potential (ORP) during anoxic phases with simultaneous ethanol dosage indicated inhibition of denitrifiers, probably by the intermediate product NO, which may have interfered with the DO sensor. Nitric oxide production was believed to be favoured in the beginning of the anoxic phase as a result of low pH and high nitrite concentration. A stable nitritation-denitritation process could be achieved when the aerobic hydraulic retention time (HRT) was decreased to the same length as the anoxic HRT, which resulted in increased unused alkalinity.

Operation for nitritation of sludge liquor in a full-scale SBR.

At Sjölunda WWTP, a full-scale SBR for treatment of mesophilic sludge digester liquor has been operated almost a year with stable nitrite accumulation. Only nitritation of the sludge liquor is needed since the oxidized ammonium is denitrified in the first anoxic zone of the high-loaded activated sludge in the main plant. The process strategy was to have an ammonium set-point to end the aeration, a low DO concentration and a low pH set-point. An increase of pH set-point from 6.8 to 7.2 increased loss of alkalinity in the effluent and increased sodium hydroxide dosing. An increase of DO set-point from 1.1 mg O2 L(-1) to 1.3 mg O2 L(-1) markedly increased ammonia reduction rates and only slightly increased nitrate production. Today, an introduction of denitritation in the SBR will be a more cost-effective treatment of sludge liquor at Sjölunda WWTP. However, the choice of operation with only nitritation or nitritation/denitritation in sludge liquor treatment should always include a consideration of chemical costs and treatment capacity of both main plant and side-stream plant.

The effects of taipoxin and notexin on the function and fine structure of the murine neuromuscular junction.

The isolated neurotoxins taipoxin and notexin from the venoms of the Elapidae, Oxyuranus scutellatus and Notechis scutatus scutatus respectively cause a neuromuscular block when administered to the mouse in vivo or to the phrenic nerve-hemidiaphragm preparation in vitro. The block is preceded by a latency period during which the toxins bind irreversibly to the nerve. The period is shortened by nerve activity. The frequency of the miniature end-plate potentials is gradually reduced, almost to zero, and their amplitude distribution is altered; small and very large miniature endplate potentials appearing. Ultrastructurally the endplates are altered in the presynaptic portion but not in the postsynaptic part. In an early stage of poisoning the axolemma has an increased number of omega-shaped indentations similar in size to synaptic vesicles. At a later stage, when the animals die of respiratory paralysis, the axolemmal indentations are more numerous and the synaptic vesicles greatly reduced in number, the remaining vesicles having a variable and frequently larger than normal size. When impulse activity in the phrenic nerve is stopped by cutting the nerve before the administration of toxin there is no reduction in the number of synaptic vesicles, only the appearance of an increased number of axolemmal indentations. It is suggested that taipoxin and notexin irreversibly interfere with the formation of synaptic vesicles by arresting vesicle membrane recycling at the level of the axolemma. When the pre-existing store of vesicles is depleted, by nerve activity, a neuromuscular block results.