Fly ash and lime-stabilized biosolid mixtures in mine spoil reclamation: simulated weathering.

The use of large quantities of neutral coal fly ash (NFA) may be facilitated by co-application with a lime-stabilized biosolid (LSB) for the reclamation of acid mine spoil (AMS). Although NFA may not aid in the mitigation of acid drainage, questions concerning the leachability and mineralogy of native and NFA- and LSB-born metals must be addressed. In this study, the potential long-term influence of LSB and NFA on AMS leachate chemistry and trace element mineralogy was evaluated using laboratory weathering and selective dissolution techniques. The application of LSB at a rate sufficient to neutralize the potential acidity of the AMS increased leachate pH from approximately 3 to 7.5 for the duration of the study. Fly ash rates (1X, 1.5X, and 2X LSB rate) did not affect leachate pH. The dominant electrolytes in all leachates were Ca and SO4, the concentrations of which were mirrored by solution electrical conductivity (EC). Leachate concentrations of Al, Fe, Mn, K, Cu, Ni, and Zn were significantly reduced by LSB application, whereas concentrations of Ca, SO4, Mg, Cl, F, B, and P were increased. Nitrate concentrations were not affected by LSB. With the exception of leachate B, which increased with increasing NFA rate and was regenerated during the weathering study, NFA did not affect leachate composition. Sequential selective dissolution indicated a transformation of Co, Cr, Cu, Ni, Pb, and Zn into less labile mineral pools with weathering. The results of these evaluations suggest that the application of NFA during AMS reclamation would have little effect on leachate chemistry or the mineralogy of trace elements. Thus, the high-volume application of NFA to AMS during reclamation may offer an additional opportunity for the use of this combustion by-product.

Time since death determinations of human cadavers using soil solution.

This study was conducted to collect data on specific volatile fatty acids (produced from soft tissue decomposition) and various anions and cations (liberated from soft tissue and bone), deposited in soil solution underneath decomposing human cadavers as an aid in determining the "time since death." Seven nude subjects (two black males, a white female and four white males) were placed within a decay research facility at various times of the year and allowed to decompose naturally. Data were amassed every three days in the spring and summer, and weekly in the fall and winter. Analyses of the data reveal distinct patterns in the soil solution for volatile fatty acids during soft tissue decomposition and for specific anions and cations once skeletonized, when based on accumulated degree days. Decompositional rates were also obtained, providing valuable information for estimating the "maximum time since death." Melanin concentrations observed in soil solution during this study also yields information directed at discerning racial affinities. Application of these data can significantly enhance "time since death" determinations currently in use.

Lipopolysaccharide and interleukin 1 inhibit interferon-gamma-induced Fc receptor expression on human monocytes.

The objectives of these studies were to study the effects of bacterial lipopolysaccharide (LPS) on interferon-gamma (IFN-gamma)-induced Fc receptor expression on human monocytes and to examine whether these effects were mediated through stimulation of interleukin 1 (IL-1) production. Fc receptor expression was determined by binding of monomeric monoclonal murine immunoglobulin (Ig)G2a and cytofluorographic analysis. IL-1 activity in monocyte supernatants and lysates was assayed by augmentation of mitogen-induced murine thymocyte proliferation. IFN-gamma induced the expression of Fc receptors on human monocytes that were specific for murine IgG2a. This induction was inhibited by the addition of LPS in amounts as low as 2 to 8 pg/ml. LPS inhibition of IFN-gamma-induced Fc receptor expression was paralleled by the appearance of IL-1 in monocyte lysates and supernatants. The addition of purified human or recombinant IL-1 beta at the initiation of culture similarly inhibited the expression of IFN-gamma-induced Fc receptors on the monocytes. LPS also inhibited Fc receptor expression on the human myelomonocytic cell line THP-1 after induction with IFN-gamma or phorbol myristate acetate alone or with both agents together. This inhibition also was paralleled by the production of IL-1 but the addition of exogenous IL-1 to the THP-1 cells had no effect on IFN-gamma-induced Fc receptor expression. Tumor necrosis factor (TNF) inhibited IFN-gamma-induced Fc receptor expression on human monocytes but was much less potent than comparable amounts of IL-1. TNF also did not inhibit Fc receptor expression on THP-1 cells. In fact, IL-1 or TNF led to an enhancement in IFN-gamma-induced Fc receptor expression on THP-1 cells. These results indicate that LPS can inhibit IFN-gamma-induced Fc receptor expression on human monocytes and that IL-1 and TNF may mediate these effects of LPS. Thus, an autocrine or paracrine role is suggested for these cytokines. The possibility exists that intracellular IL-1 resulting from LPS stimulation may be at least in part responsible for inhibition of Fc receptor expression.