A field study of lignite as a drying aid in the superheated steam drying of anaerobically digested sludge.

Dried sludge is preferred when the sludge is either to be incinerated or used as a soil amendment. This paper focuses on superheated steam drying which has many benefits, because the system is totally enclosed, thereby minimising odours and particulate emissions. This work reports on field trials at a wastewater treatment plant where anaerobically digested sludge is dried immediately after being dewatered by belt press. The trials showed that unlike previous off-site tests, the sludge could be dried without the addition of a filter aid at a low production rate. However, the trials also confirmed that the addition of the lignite (brown coal) into the anaerobically digested sludge led to a more productive drying process, improved product quality and a greater fraction of the product being in the desired product size range. It is concluded that these results were achieved because the lignite helped to control the granule size in the dryer. Furthermore neither Salmonella spp or E coli were detected in the dried samples. Tests on spontaneous combustion show that this risk is increased in proportion to the amount of lignite used as a drying aid.

Mechanisms of leukotriene D4-induced constriction in human small bronchioles.

We examined the mechanisms underlying leukotriene D4- (LTD4) induced constriction of human small (300 - 500 micron i.d.) bronchioles, and the effect of LTD4 on ion currents and Ca2+ transients in smooth muscle cells (SMC) isolated from these bronchioles. LTD4 caused a concentration-dependent bronchoconstriction with an EC50=0.58+/-0.05 nM (n=7) which was not easily reversible upon washout. This bronchoconstriction was entirely dependent on extracellular Ca2+. Blockade of L-type Ca2+ channels with nifedipine (10 microM) reduced LTD4 response by 39+/-2% (n=8), whilst La3+, Gd3+ and SK&F 96,365 abolished LTD4-induced bronchoconstriction completely and reversibly, suggesting the majority of Ca2+ entry was via non-selective cation channels. Antagonists of PI-PLC (U73,122 and ET-18-OCH3), PLD (propranolol) and PKC (cheleretrine and Ro31-8220) were without any effect on LTD4-induced bronchoconstriction, whilst the PC-PLC inhibitor D609 caused complete relaxation. Inhibition of protein tyrosine kinase with tyrphostin A23 (100 microM) caused about 50% relaxation, although the inactive analogue tyrphostin A1 was without effect. In freshly isolated SMC from human small bronchioles LTD4 caused a slow increase of intracellular Ca2+ concentration, with a consequent rise of the activity of large conductance Ca2+-dependent K+ channels and the amplitude of depolarization-induced outward whole-cell current. Again, no effect of LTD4 could be observed in the absence of extracellular Ca2+. We conclude that LTD4 causes constriction of these small bronchioles primarily by activating Ca2+ entry via non-voltage gated channels, possibly by a PC-PLC mediated pathway.