Biosolids management--sustainable development status and future direction.

The role of biosolids management continues to gain priority in terms of holistic waste management/reuse. Recommended options should lead to simple and safe management alternatives that stress reclamation of resources. This paper addresses current sustainability strategies, priorities and future direction of waste management as it relates to residuals and in particular to sludges/biosolids. Sludge management and resource recovery approaches must be diversified and flexible. They should be based on actual needs of the affected society and community. It is also important that the chosen strategy be appropriate to the conditions of the site under consideration. Processes which promote sustainability will become viable options for resource management if conversion into a "value-added product" can be realized.

Production of class A biosolids with anoxic low dose alkaline treatment and odor management.

The feasibility of full-scale anoxic disinfection of dewatered and digested sludge from Winnipeg, Manitoba with low lime doses and lagoon fly ash was investigated to determine if a class A product could be produced. Lime doses of 50 g, 100 g, and 200 g per kg of biosolids (dry) were used along with fly ash doses of 500 g, 1,000 g, and 1,500 g per kg of biosolids (dry). The mixed product was buried in eight-10 cubic metre trenches at the West End Water Pollution Control Center in Winnipeg. The trenches were backfilled with dirt and trapped to simulate anoxic conditions. Sampling cages were packed with the mixed product and pathogens non-indigenous to Winnipeg's biosolids. The cages were buried amongst the mixed biosolids in the trench. The non-indigenous pathogens spiked in the laboratory were the helminth Ascaris suum and the enteric virus reovirus. Samples were removed at days 12, 40, 69, 291, and 356 and were tested for the presence of fecal Coliform, Clostridium perfringens spores, Ascaris suum eggs, and reovirus. The pH, total solids, and free ammonia content of the mixed product were also determined for each sample. Odor was quantified for samples at both 291 and 356 days. Fecal Coliform bacteria and reovirus were completely inactivated for doses as low as 100 g lime per kg biosolids (dry) and 50 g lime + 500 g fly ash per kg biosolids (dry). Spores of the bacteria C. perfringens experienced a 4-log reduction when treated with 100 g lime per kg biosolids and a 5-log reduction when treated with doses as low as 50 g lime + 500 g fly ash per kg biosolids (dry) after 69 days. Ascaris eggs were completely inactivated in 5 gram packets for all treatments involving 100 g lime per kg biosolids (dry) after 69 days. Class A pathogen requirements were met for all treatments involving a lime dose of at least 100 g per kg biosolids. The odor potential from the produced biosolids is also assessed.

Potentiation by red blood cells of shear-induced platelet aggregation: relative importance of chemical and physical mechanisms.

Evidence has been reported to indicate that red blood cells (RBCs) may potentiate platelet adherence and platelet aggregation (PAG) in different flow systems in vitro as well as hemostatic platelet plug formation in response to vascular injury. In this study, we demonstrate that RBCs enhance PAG induced by well-defined, low-intensity, uniform, laminar shear stress. Potentiation by RBCs of shear-induced PAG was associated with appreciable loss of adenine nucleotides from 14C-adenine-labeled RBCs, the extent of which increased with increasing RBC concentration. The concentrations of RBC-derived ADP measured in the medium after shear, as determined by both high pressure liquid chromatography and the luciferin/luciferase system, were within the range of concentrations of ADP which may trigger PAG or potentiate PAG induced by low concentrations of other platelet agonists in the aggregometer. To assess the relative contribution of chemical (ADP) and physical (platelet surface transport) mechanisms in the RBC-mediated potentiation of shear-induced PAG, aliquots of citrated platelet-rich plasma (C-PRP) were exposed to shear stress in the presence of untreated RBCs or RBCs exposed to an antihemolytic concentration (5 mumol/L) of the membrane stabilizing agent, chlorpromazine (CPZ). Potentiation of shear-induced PAG in the RBC-CPZ system was significantly less than that in the untreated RBC system. However, CPZ-induced reduction of PAG potentiation was associated with an increase rather than a decrease in loss of adenine nucleotides from RBC. Furthermore, shear-induced PAG in C-PRP as well as ADP- and collagen-induced PAG in C-PRP in the aggregometer was significantly inhibited by 5 mumol/L CPZ, indicating that the observed reduced potentiation of shear-induced PAG by RBCs in the presence of CPZ was due to a direct inhibitory effect of the drug on platelets rather than a reduction of shear-induced liberation of ADP from RBCs. When aliquots of C-PRP were exposed to shear stress in the presence of RBCs completely depleted of ADP by fixation in 1% glutaraldehyde, potentiation of PAG was approximately half of that observed with intact RBCs. These findings indicate that both RBC-derived ADP and RBC-mediated platelet surface transport are involved in the potentiation by RBCs of PAG induced by laminar shear stress.

A brief review of the current status of alternatives to chlorine disinfection of water.

This paper briefly outlines some of the alternative disinfectants being considered in lieu of chlorination. Methods currently in use as well as those in the research stage are included. Each method is assessed with respect to disinfection efficiency and environmental impact. (Am J Public Health 1982; 72:1290-1293.)

Role of cytoplasmic and releasable ADP in platelet aggregation induced by laminar shear stress.

We examined the extent of lytic and sublytic platelet injury after exposure of platelets to shear stress and the role in shear-induced PAG of ADP liberated from platelets as a result of shear-induced platelet dense body release and/or platelet damage. Platelets in C-PRP or TAS were subjected to well-defined, laminar shear stress in a rotational viscometer, and PAG (loss of single, nonaggregated platelets), 14C-serotonin release, and loss from platelets of LDH and 51Cr were determined. Increased PAG with increasing shear stresses was associated with progressive loss of LDH and 51Cr. Loss of 51Cr was consistently in excess of that of LDH, indicating sublytic platelet injury, which was confirmed by electron microscopy. At the lowest shear stress used (50 dynes/cm2), PAG in C-PRP was observed in the absence of detectable loss of 51Cr or LDH. When platelets in TAS were sheared in the presence of CP/CPK, an enzyme system capable of removing extracellular ADP, PAG was only partially (approximately 40%) inhibited. However, when platelets were preincubated with CP/CPK and ATP (to saturate platelet ADP receptors), shear-induced PAG was almost completely suppressed. Similar results were obtained with PAG induced by collagen in the aggregometer. The findings indicate that (1) shear-induced PAG in this system may occur without measurable lytic or sublytic platelet damage and (2) ADP liberated from platelets as a result of shear-induced release or damage may represent the major if not sole mediator of shear-induced PAG.

Lymphocyte proliferative response and tissue distribution of methylmercury sulfide and chloride in exposed rats.

The immunotoxic effects and tissue distribution of different forms of methylmercury compounds were studied in rats. Methylmercury sulfide or methylmercury chloride was fed to rats at concentrations of 5 or 500 microg/L in drinking water for 8 wk. T-cell lymphocyte proliferative response to phytohemagglutinin (PHA) and determination of tissue distribution of mercury by gas chromatography using electron capture were assayed. Four different forms of mercury compounds were employed: MeHgS-, (MeHg)2S, (MeHg)3S+, and MeHgCl. Results indicated that exposure to methylmercury significantly enhanced lymphocyte responsiveness in most of the exposed groups at the low concentration of 5 microg/L, with the highest proliferative response (fourfold increase) in the MeHgCl group. At 500 microg/L, a significant decrease in the lymphocyte proliferative response was observed in the (MeHg)3S+ and MeHgCl groups; conversely, the MeHgS(-)- and (MeHg)2S-exposed animals had a modest increase of the lymphocyte proliferative response. The largest concentrations of all four mercury forms were detected in the kidney and spleen. The levels of mercury found in kidney, spleen, liver, brain, and testis were lower in the MeHgCl group than in those exposed to (MeHg)2S and (MeHg)3S+. These data indicate that the organ distribution of mercury and immune alteration may vary according to the chemical structure of the compound. This observation may have important implications in humans potentially exposed to low levels of methylmercury present in the environment, since the immune system plays an important regulatory role in the host-defense mechanisms.