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By H. Netuka, J. V. Horak, A. W. Khair

"A general review of major problems concerning mathematical modelling of roof bolting problem is given. A mathematical model (MM) of interactive set Bolt - Resin - Rock and its discretization based on the Finite Element Method (FEM) is developed to calculate numerically course of displacement, stress and strain fields in this set. This new MM enables to get also course of the normal and tangential components of contact stress vector, normal displacement and then mutual tangential slip at the bolt - resin and resin - rock interfaces, respectively.Behavior of system on all interfaces is modelled in the MM as a ""unilateral contact"" governed by so called non-classical boundary condition of Signorini's type including Coulomb's law of friction between resin and rock, and ""a given friction"" law between bolt and resin (see Duvaut, Lions (1972) for mathematical formulation).Numerical example and some values of resulting stresses are shown and remarks on necessary and sufficient conditions for solvability of the problem are also given.IntroductionAs is well known roof bolting has become the primary support system in almost all underground coal mines. But the ""theoretical"" design criteria for roof bolt patterns are rather problematic because: "" ... real mechanisms by which the roof bolts reinforce the immediate roof of underground coal mine entry are still relatively unknown"", see Peng (1986).The aim of this contribution is to present brief description of fundamentals of mathematical theory (see Hlavacek et al., 1988) which could be, according to our opinion and knowledge, very helpful for numerical modelling of a such type of problems. For the sake of brevity we restrict ourselves here to just one of the simplest possible problem: analysis of the behavior of interactive set composed by only single full - length - grouted bolt, resin (or cement) and suitable part of domain of a ""immediate"" neighborhood of bolt which should represent physical action of real rock material."

Dec 1, 1995

By C. A. Pickles, J. M. Toguri

The refining of two molten Ag-Cu alloys, containing 7.5 and 11.2 mass% Cu, with a borosilicate slag was investigated using both air and pure O2 to determine the effects of the following variables: flow rate of oxidising gas; injection time; mass of sodium borosilicate flux; and injection of the oxidising gas into either the slag or the metal. The results demonstrate that more than 90% of the Cu can be removed with Ag losses of less than 5% and that refined metal with a Cu content of less than 0.5 mass% can be produced. Ag losses to the slag increased with the amount of Cu removed, and a mechanism is proposed to account for this

Dec 1, 1995

The deposit was discovered during systematic reconstruction of the geological history of glacial overburden, which averages 6 m in thickness over 80% of Sweden, by geochemical sampling and searching for small grains of eroded bedrock. The gold is mainly concentrated in and around high-grade quartz veins within a broad shear zone, though the correlation coefficient between quartz and gold in samples is not significant. Production from two pits, now connected, in the Central and Eastern orebodies has increased steadily from 1 238 kg Au in 1989 to 2 120 kg in 1994, the highest in Europe. The mine has adapted and improved its mining methods to achieve significant productivity increases and cost reductions. Most of the improvements have been achieved through a better understanding of the controls on mineralisation and of the implications of those controls for selective mining. Geostatistics has played an important role in the quantification of grade variability and gold occurrence. Better blasting and loading techniques have improved selectivity, grade control has been enhanced by a grade-control drilling programme, and significant improvements in mineral processing have been made

Dec 1, 1995

By R. L. Grayson, W. E. Wallace, J. W. Stephens, M. D. Attfield, P. S. Brower, V. Vallyathan, M. J. Keane, J. C. Harrison

Pure respirable quartz is a known pathogenic agent for lung disease. However, for mixed dusts, neither mineralogical nor in vitro cytotoxicity assays unequivocally predict the contribution of quartz to their pathogenic potential.First, although Coal Workers' Pneumoconiosis (CWP) and Progressive Massive Fibrosis (PMF) prevalence have been found to correlate with total respirable coal mine dust exposure, and with coal rank (Attfield and Morring, 1992), epidemiological studies generally have not found the quartz component of coal mine dust as measured by X-ray diffraction or infrared spectroscopy (each of which essentially measures the mass-percent quartz in a bulk sample) to be clear predictors of CWP prevalence or incidence (Walton et al., 1971). Second, the properties which distinguish the extreme fibrogenic potential of quartz are not revealed by conventional in vitro bioassay comparison with other silicate mineral dusts. As an example, quartz and kaolin (aluminosilicate) clay in vitro cytotoxicities are comparable for lavaged primary pulmonary macrophages.The studies discussed here address these two anomalies from a general hypothesis that the pathogenic activity of respired quartz particles is associated with properties of, and interactions with, the particle surfaces. One factor in the expression of toxic activity by a particle surface is the biological availability of that surface. Anomalous lack of correlation of disease prevalence with mass percent quartz in exposures to some mixed composition respirable-sized dusts suggests that individual particle surface features, invisible by bulk sample mass analysis, may alter the biological availability of a fraction of quartz particles in a dust. For pure-surfaced mineral particles, the comparably strong prompt membranolytic activities of quartz and kaolin in vitro suggest that upon deposition of such particles in the lung there must be other interactions with particle surfaces which distinguish quartz. This might be due to toxic surface-associated sites specific to silica, or to interactions of other sites on other mineral particles which affect the biological availability of their toxic functional groups. For example, alurninol groups on clays affect the availability or activity of adjacent silanol groups. Surface activities which distinguish quartz pathogenici ty might be manifest in one or more of the sequential interactions upon deposition in the lung; first with the pulmonary surfactant system, then with extracellular and phagolysosomal enzymatic digestive processes, or with subsequent cytotoxic processes.

Dec 1, 1995

By D. L. Nussear, W. E. Wallace, N. N. Clark, M. Gautam, G. Hong-Guang

"Results from a study directed towards identifying and measuring the mutagenicity of diesel exhaust particulate matter involved in mining exposures, especially those which may synergistically affect genotoxic hazard, are presented in this paper. Particulate matter emissions from a diesel engine, representative of the ones found in underground mines, were sampled and assayed to determine the genotoxic potential as a function of engine operating conditions. Diesel exhaust was diluted in a multi-tube mini-dilution tunnel and the particulate matter was collected on 70 mm fluorocarbon coated glass fiber filters as well as on 8"" x 10"" hi-volume filters. A six mode steady state duty cycle was used to relate engine operating conditions to the mutagenicity potential.Protocols developed for using a primary component of pulmonary surfactant as a medium for collecting and applying respirable particulate material to cells for mutagenicity testing offer a true representation of in-vivo delivery of such respired aerosols to pulmonary cells and the genetic material within . The surfactant dispersion technique is discussed in this paper. Methods have been developed to sample and assay the diesel soot and diesel soot/mineral dust complexes which would not compromise the surface and physical properties of the particulate material."

Nov 1, 1995

By D. E. Banks, J. K. H. Ma, Y. Rojanasakul, J. Y. C. Ma, C. J. Malanga

There is evidence to suggest that cell injury induced in alveolar macrophages (AM) following phagocytic activation by silica particles may be mediated through changes in intracellular free calcium [Ca 2+}. However, the mechanism of silicainduced cytotoxicity relative to [Ca2+], overloading is not yet clear. To provide a better insight into this mechanism, isolated rat AMs were exposed to varying concentrations of crystalline silica (particle size< 5 µm in diameter) and the fluctuation in their [Ca2+]; and cell integrity were quantitatively monitored with the fluorescent calcium probe, Fura-2 AM, and the membrane integrity indicator, propidium iodide (Pl). Results from this study indicate that silica can rapidly increase [Ca2+]; in a dose-dependent manner with a characteristic transient calcium rise at low doses (<0.1 mg/ml) and an elevated and sustained rise at high doses (>0.1 mg/ml). Depletion of extracellular calcium [Ca 2+]0 markedly inhibited the [Ca2+]; rise (˜90%), suggesting that Ca2+ influx from extracellular source is a major mechanism for silica-induced [Ca2+]; rise. When used at low doses but sufficient to cause a transient [Ca2+]; rise, silica did not cause significant increase in cellular Pl uptake during the time of study, suggesting the presevation of membrane integrity of AMs under these conditions. At high doses of silica, however, a marked increase in Pl nuclear fluorescence was observed. Depletion of [Ca 2+] 0 greatly inhibited cellular Pl uptake, induced by 0. 1 mg/ml or higher doses of silica. This suggests that Ca 2 + influx, as a result of silica activation, is associated with cell injury. Indeed, our results further demonstrated that the low dose effect of silica on Ca 2+ influx is inhibited by the Ca2+ channel blocker nifedipine. At high doses of silica (>0.1 mg/ml), cell injury was not prevented by nifedipine or extracellular Ca2+ depletion, suggesting that other cytotoxic mechanisms, i.e., nonspecific membrane damage due to lipid peroxidation, are also responsible for the silica-induced cell injury. Silica had no significant effect on cellular ATP content during the time course of the study, indicating that the observed silicainduced (Ca2 ... ); rise was not due to the impairment of Ca2 + -ATPase pumps, which restricts Ca2+ efflux. Pretreatment of the cells with cytochalasin B to block phagocytosis failed to prevent the effect of silica on [Ca2+]; rise. Taken together, these results suggest that the elevation of [Ca2+]; caused by silica is due mainly to Ca2+ influx through plasma membrane Ca2+,channels and nonspecific membrane damage (at high doses). Neither ATP depletion nor Ca2+ leakage during phagocytosis was attributed to the silica-induced [Ca2+]; rise.

Nov 1, 1995

By P. R. Miles, J. K. H. Ma, J. Y. C. Ma, L. Bowman

"The bisbenzylisoquinoline alkaloids are compounds which can be isolated from plants and which exhibit a broad range of pharmacological activities. Perhaps the best known alkaloid of this group is tetrandrine (TT), a compound isolated from the root of a traditional Chinese medicinal herb, Stephania tetrandra. It has been tested for its effects on the cardiovascular system, tumors, and the lungs. For example, tetrandrine has been shown to act as a calcium entry blocker in cardiac sarcolemmal vesicles (King et a/., 1988) and has been used in China as a treatment for angina and hypertension. Its possible effects as a tumor-inhibitory substance have also been investigated (Kupchan and Atland, 1973). In addition, there are several lines of evidence to suggest that it is a possible therapeutic agent for the treatment of silicosis. Yu et a/. (1983) have shown that TT inhibits the development of experimental silicosis in rats when it is administered orally after intratracheal instillation of quartz. Other studies have shown that the alkaloid inhibits the synthesis of collagen by fibroblasts and the formation of silicotic nodules in rats exposed to silica (Huang et al., 1981; Liu et al., 1983). In fact, tetrandrine has been used clinically in China as an antifibrotic agent and has been shown to improve both the appearance of chest radiographs and the measurements of diffusing capacity in patients with silicosis (Li et al., 1981).Since tetrandrine may have a potential use as a therapeutic agent for fibrotic lung diseases, its effects on various pulmonary cells and tissues should be studied. Alveolar type II cells are located in the alveolar regions of the lungs and are important because they are responsible for the synthesis and secretion of pulmonary surfactant (Dobbs et al., 1982; King, 1984), regeneration of the alveolar epithelium after lung injury (Kauffman et al., 1974), and metabolism of foreign compounds (Bend et al., 1985). Furthermore, in silicosis, for which TT has been suggested as a treatment, there are increased amounts of pulmonary surfactant produced (Dethloff et al., 1986a,b) as a result of increased rates of surfactant synthesis by type II cells (Dethloff et a/., 1989; Miller et al., 1988). Because type II cells play a critical role in maintaining normal lung function and because type II cells are affected in silicosis, for which 'TT has been used as a treatment, we studied the effects of tetrandrine on energy metabolism in these cells in vitro. Energy metabolism was chosen because it is a basic cellular function which is neces-sary for other cellular processes to occur. Since type II cells depend on mitochondrial metabolism for energy production (Fisher et al., 1980), we examined the effects of tetrandrine on cellular and mitochondrial ATP production and oxygen consumption. Additional experiments were performed in an effort to determine if intracellular calcium levels may be involved in the TT-induced effects. A preliminary report of those results has appeared previously (Ma et al., 1991)."

Nov 1, 1995

By K. Clifton, K. Kar, M. Gautam, J. T. Jurewicz

"This paper describes the history of LDV measurements employed in research involving gas-solid flows. Much of the discussion deals with measurement techniques employed to obtain separate and simultaneous solid and gas phase velocities. Also, LDV based measurement techniques that arc used to obtain particle size and concentration information in conjunction with the velocity measurements arc presented.INTRODUCTIONThere are numerous examples of industrial processes in which the motion of a solid or droplet dispersed phase in a suspending gas phase is critically important. The applications range from spray droplets injected into combustion chambers to the understanding of the time release mechanisms of particles generated by dissolving pharmaceutical tablets. In many of these processes, the heat, mass, and/or momentum transfer between the dispersed phase and the suspending fluid arc the items of interest. In the past, much of the phenomena were characterized by empirical models derived from flow averaged measurements. Gradual developments in laser Doppler velocimetry (LDV), have provided researchers with an unobtrusive measurement technique capable of obtaining the particle size velocity and concentration with good spatial resolution.In the two decades that LDV instrumentation has been available, most of the uses have concentrated on single phase fluid flow measurements. The light scattered from seed particles small enough to follow complex fluid motions, including turbulence, is converted into velocity information. While the utility of this instrument in single phase flows has been demonstrated beyond question, the use of LDV in gas-solid multiphase flows has had a more gradual development. The measurements ·of interest in these flow regimes are usually the velocity of the suspending fluid as well as that of the dispersed particulate phase. Early investigators were quick to see the potential of this instrument for measurements in gas-solid flows. The interest soon expanded to the development of instruments that could also simultaneously measure particle size and concentration within a two-phase flow field.This paper tracks the historical development of LDV technology as applied to gas-solid flows. The techniques to measure particle velocity, size, and concentration arc treated in separate sections although much of the development occurred simultaneously. Finally, some unique applications conducted at West Virginia University and other locations will be discussed in the application section."

Nov 1, 1995

By R. V. Ramani, R. L. Grayson, R. L. Frantz, V. A. Marple, W. R. Myers, K. L. Rubow, Mutmansky. J. M., T. J. Stobbe

"An investigation of protocols for research performed from 1953 to 1988 on pneumoconioses (with emphasis on diseases related to coal and silica) was conducted in the Generic Mineral Technology Center for Respirable Dust. In addition, interviews were conducted with prominent U.S. medical researchers, aerosol scientists and engineers in government, industry, and universities to determine dust sources, dust preparation methods, laboratory protocols, and determinant variables related to in vitro and in vivo research and assess the comparability of results.Since the original report on the protocol project, additional research regarding free radical existence in freshly produced dust particles and the shape and contamination of particles generated for research purposes has further heightened scientists' concerns. As indicated by current research, fresher dust particles and those with more angular shapes may have a different level of reactivity in biological systems than do older or more rounded particles. Therefore, research on dust preparation methods for biomedical studies was undertaken and will be outlined here.Results of protocol review and interviews are summarized. Research on size reduction methods and their particle characteristics plus some recommendations concerning dust preparation methods and reporting in biomedical publications are also presented. Recent evidence indicates that these recommendations may be of importance in comparing and interpreting research results."

Nov 1, 1995

By V. A. Marple, K. L. Rubow, B. A. Olson

"INTRODUCTION Inertial classification, gravitational sedimentation centrifugation, and thermal precipitation arc techniques that can be used to collect particles for subsequent analysis or for particle classification. The inertial classifiers, which include impactors, virtual impactors, and cyclones, are widely used in the sampling or particles. Settling chambers, which include centrifuges as well as gravitational settling devices, are less widely used. Thermal precipitators arc seldom used.Impactors, in particular, have been used extensively, studied both theoretically and experimentally, and arc the instrument or choice for the determination or aerosol mass size distributions. Many versions or impactors arc available commercially and many more have been designed, built, and used in special studies.Virtual impactors are a more recently developed inertial classifier and possess a feature not round in conventional inertial impactors; namely, that the particles remain airborne after classification compared to the conventional impactor, where the particles arc collected on a solid surface. The feature or keeping particles airborne is important for transporting the particles to other particle-analyzing instruments, or to filters, and in concentrating particles larger than the cutsize in a small fraction of the total now."

Nov 1, 1995

By R. H. Reist, R. D. Dey, V. Castranova, J. P. Durham, Y. Rojanasakul

"Silicosis is a fibrotic pulmonary disease produced by inhalation of silica-containing dusts (Peters, 1986). Chronic silicosis may develop 20-40 years after initial exposure to crystalline silica, and the disease may progress from a simple to a complicated form. Few symptoms are evident in simple silicosis with pulmonary function being relatively normal. However, chest radiographs reveal small rounded ·opacities in the upper lobes of the lungs. These silicotic nodules consist of collagen arranged in a distinctive circular pattern. As fibrotic changes become more severe, the disease progresses to complicated silicosis (progressive massive fibrosis). Complicated silicosis is associated with shortness of breath and decreases in pulmonary function characteristic ofrestrictive lung disease. Chest x rays reveal numerous large silicotic nodules which may be associated with scar emphysema. Several mechanisms have been proposed to explain the cellular events which result in silica-induced lung damage and fibrosis (Lapp and Castranova, 1993). They include: ( l) direct cytotoxicity of silica, (2) activation of oxidant and enzyme release from alveolar macrophages, (3) recruitment and activation of polymorphonuclear leukocytes, and (4) stimulation of fibroblast proliferation and collagen synthesis.Tetrandrine is a bisbenzylisoquinoline alkaloid derived from the Chinese herb Radix Stephania tetrandra. It has a molecular weight of 622.73 and an empirical formula of C38H420 6N2. The chemical structure of tetrandrine has been published previously by our laboratory (Castranova et al., 1991 a). Its structure is characterized by methoxy groups at C7 and C12 , uncharged nitrogens at N2 and N’2 and two 17-carbon ring members connected by a double oxygen bridge between Ca-C7 and C11-C12. Tetrandrine has been shown to reduce both silica-induced fibrosis and the elevation of lung collagen content in rats (Huang et al .. 1981; Yu et al., 1983; ldel, 1987). Furthermore, tetrandrine has been used as an antifibrotic agent in Chinese clinical trials (Li et al.. 1981 ). Preliminary results suggest that administration of tetrandrine to patients with silicosis results in substantial improvement of symptoms, increases in diffusion capacity, and decreases in the size of shadows on lung x rays."

Nov 1, 1995

By J. L. Stauffer, S. L. Lacey, L. J. Gaydos, L. M. Demers, D. C. Kuhn

"Tumor necrosis factor alpha (TNFa) and thromboxane A2 (TXA2) are major products of the activated alveolar macrophage and serve as key mediators of lung injury. In order to determine if the synthesis ofTXA2 and the release ofTNFa are associated, the production of these inflammatory agents by the human alveolar macrophage (AM), as a result of activation by lipopolysaccharide (LPS), was assessed in the absence and presence of the thromboxane synthase inhibitors UK 38,485 (Dazmegrel) and OKY 046. UK 38,485 and OKY 046 inhibited both LPS-stimulated TXA2 production and TNFa release in a dose-dependent manner. Prostaglandin E2 (PGE2) production was not increased by UK 38,485 or OKY 046. Neither LPS nor UK 38,485 had any effect on LT84 production by AM. Neither UK 38,485 or OKY 046 had any effect on LPS-stimulated interleukin-I beta release. However, the TXA2 mimetic, U46619, did not stimulate TNFa release by AM either in the absence or presence of UK 38,485. These findings suggest that 1) UK 38,485 and OKY 046 are inhibitors of both TXA2 production and TNFa release by activated human AM, 2) UK 38,485 probably does not exert its inhibitory action on TNFa release through effects on eicosanoid production and 3) the possibility that TNFa- and TXA2-induced lung injury may be subject to amelioration by imidazole-based compounds should be further evaluated.IntroductionTumor necrosis factor alpha (TNFa), produced by monocytes and macrophages, is a potent peptide mediator of lung injury (1,2). The exaggerated release of TNFa has been implicated in the etiology of acute lung reactions such as septic shock of bacterial or viral origin (3,4). The role of TNFa is expressed primarily through its ability to activate a variety of cell types within the lung environment including polymorphonuclear leukocytes (PMNs, ref. 5), type II epithelial cells (6) and fibroblasts (7). The role of lipid mediators in lung disease has also been extensively characterized (1). In particular, the relationship between pulmonary inflammation and fibrosis and the production of oxygenated derivatives of arachidonic acid (here termed ""eicosanoids"") appears to be a key factor in a variety of disease processes in the lung (8). The alveolar macrophage (AM) synthesizes primarily prostaglandin E2 (PGE2). thromboxane A2 (TXA2) and leukotriene 84 (LT84, ref. 9). These eicosanoids have been shown to produce a variety of effects in the lung including bronchial smooth muscle dilatation (PGE2, ref. 10), vascular smooth muscle contraction and platelet aggregation (TXA2, ref. 11) and oedema and immune cell extravasation (LT84, ref. 12)."

Nov 1, 1995

By N. S. Dalal, A. H. Hoffman, X. Shi, D. E. Banks, J. K. H. Ma, Y. Rojanasakul

Excessive production of reactive oxygen radicals by alveolar macrophages is proposed to play an important role in oxidative lung injury. A major product of oxygen radical formation is the highly reactive hydroxyl radical (•OH) generated via a biologic Fenton reaction. In addition to its known ability to induce lipid peroxidation, recent studies have suggested that the •OH may exert its cytotoxic effect through the alteration of [Ca2+], homeostasis. To test this potential mechanism as well as to investigate the relationship between •OH and Ca" overloading in cytotoxic injury, isolated rat alveolar macrophages were exposed to externally generated radical system, H2O2 (0.01 to 1 mM) and Fe (1 mM) and their [Ca2+] levels and cell injury were monitored using quantitative fluorescence microscopy with the aid of the specific Ca" indicator, Fura-2, and membrane integrity indicator, propidium iodide. Electron spin resonance measurements using the spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) confirmed the production of the .OH radical by this system. Upon the addition of the radicals, the macrophages displayed a rapid initial rise in [Ca2+] which was followed by a slower but more pronounced [Ca2+], elevation that reached a level 3 to 5 times higher than the basal level. This process preceded cell death as evident by nuclear propidium iodide fluorescence. Depletion of extracellular Ca" inhibited both the [Ca2+], response and cell injury. Preincubation of the cells with the Ca" channel blocker verapamil or .0H radical scavenger mannitol similarly inhibited the [Ca2+], rise and loss of viability. Firefly luciferase assay of cellular ATP content demonstrated that the alterations in [Ca2+], following .0H treatment preceded the depletion of ATP. Changes in membrane potential caused by Na* substitution with K* had no significant effect on either the unstimulated or stimulated [Ca"], levels. Taken together, these measurements indicate that .OH-induced injury in alveolar macrophages is associated with the alteration in [Ca2+], homeostasis. The mechanism of •OH-induced [Ca2+] loading is not due to nonspecific membrane damage or energy depletion, but mainly due to an increase in Ca2+ influx through Ca2+ selective channels. This Ca2+ over-load state as well as energy depletion caused by the oxidant may activate certain cellular degradative processes leading to cell injury and death.

Nov 1, 1995

By X. Shi, K. S. Kaspnak

"The generation of free radicals from reactions of nickel (Il)-thiol complexes with molecular oxygen and model lipid hydroperoxides was investigated by electron spin resonance (ESR) utilizing 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) as a spin trap. Incubation of nickel (II) [Ni(II)) with cysteine in an aerobic environment generated hydroxyl (·OH) radical, which then reacted with cysteine to generate a carbon-centered alkyl ( · R) radical. Radical generation was inhibited under a nitrogen atmosphere. Model lipid hydroperoxides, cumene hydroperoxide, and I-butyl hydroperoxide enhanced the yield of these radicals and also generated an alkoxyl (·OR) radical. Radical yield decreased by approximately half under a nitrogen atmosphere. Although histidine did not cause radical formation in the reaction between Ni(II) and cumene hydroperoxide under aerobic conditions, the addition of histidine to a mixture containing Ni(ll), cysteine, and cumene hydroperoxide under the same experimental conditions increased the yield of · R radical but lowered the yield of ·OR and ·OH radical adducts. It thus appears that histidine caused the ·OH attack to be more site-specific. Similar results were obtained utilizing 1-butyl hydroperoxide. Penicillamine or N-acetylcysteine yielded similar results except that under aerobic conditions, reaction between Ni(ll) and N-acetylcysteine without hydroperoxide did not generate a significant concentration of free radicals. Under the same experimental conditions, cystine did not generate any detectable free radicals, suggesting an important role of the -SH group in Ni(II)-mediated free radical generation. The results indicate that free radical generation from the reaction of Ni(Il)-thiol complexes and molecular oxygen, and/or lipid hydroperoxides, may play an important role in the mechanism(s) of Ni(II) toxicity and carcinogenesis. INTRODUCTIONWhile nickel is a well-recognized carcinogen [l, 2]. the underlying biochemical mechanisms remain unclear (3, 4). Recent studies suggest that these mechanisms may involve oxidative DNA damage through free radicals, especially the hydroxyl (•OH) radical [5-13]. The mechanisms of nickel carcinogenicity and toxicity may also involve lipid peroxidation [14-21]. Unlike ferrous ion [Fe(II)], the Ni(II) cation itself does not directly react with 02, H2O2, or lipid hydroperoxides to generate free radicals [12, 21]. However, it has been reported that Ni(II) complexes with certain synthetic oligopeptides, e.g., tetraglycine or glycylglycylhistidine, make Ni(II) reactive with 02. This reaction results in transitory formation of Ni(III) and degradation of the organic ligand via free radical reactions [22]. Such Ni(II)-peptide complexes are also capable of reacting with H2O2 to produce oxygen free radicals [11, 12]. Although the cellular environ¬ment may not contain these particular peptide ligands that are known to render Ni(II) redox active in vitro, it does contain a variety of oligopeptides that are capable of forming Ni(II) complexes at physiological pH, and thus may facilitate Ni(II) redox activity in vivo. These oligopeptides include glutathione (y-L glutamylycysteinylglycine), carnosine (homocarnosine (y aminobutyryl-L-histidine), and anserine ( B-alany1-3-methyl-L-histidine)."

Nov 1, 1995

By R. V. Ramani

"The importance of adequate mine ventilation for good health and safety conditions has been recognized since miners first ventured underground. All over the world, governmental actions on mine health and safety arc directly connected with mine atmospheric environments their assessment and control. These governmental actions have been, and continue to be, motivated by the repeated experience that potential threats from inadequate control can evolve, either suddenly or in the long-term, into unpleasant reality, with catastrophic health and safety consequences. These governmental actions arc also an indication of the remarkable professional progress being made in the field of mine ventilation.Surely, no developed country allows underground mines to operate without strong measures for the control of ventilation under legislation specific to the mining industry. In the United States, the federal government's responsibility for mine safety has evolved over the years through a series of legislative actions beginning in 1865 and continuing through 1910, 1941, 1947 and 1952.The passage of the Federal Metal and Nonmetallic Mine Safety Act of 1966 (the 1966 Metal Act), the Federal Coal Mine Health and Safety Act of 1969 (the 1969 Coal Act) and the Federal Mine Safety and Health Amendments Act of 1977 (the 1977 Mine Act) arc the most important milestones in this long legislative history. The 1977 Mine Act adopted many of the stronger features of the Occupational Health and Safety Act of 1970, perhaps the most significant piece of legislation on workers' occupational health and safety in US history.It is worthwhile to ask, ""How far has the United States come in mine ventilation since the enactment of the 1969 Coal Mine Health and Safety Act?"" This Act and its associated regulations defined in great specificity many standards for healthful and safe operation of a mine and. in some cases, what constitutes good ventilation practice."

Nov 1, 1995

By N. S. Dalal, X. Shi

It has been known for more than a decade that vanadium (V) stimulates the oxidation of NADH by plasma membranes (1) but the underlying mechanism is still not fully understood. This effect has been attributed to a membrane-associated NADH-dependent vanadium (V) oxidoreductase (1). Subsequent studies suggest that vanadium ( V) can accept an electron from fiavoprotein dehydrogenase that oxidizes NADH (2). The phenomenon ofNAD(P)H oxidation coupled to vanadium(V) reduction has also been demonstrated in other biological systems (3-6). A recent electron spin resonance (ESR) study from our laboratory reported on the accumulation of vanadium (IV) duringthe reduction ofvanadate (vanadium(V)) by the ftavoenzymes glutathione reductase (GSSG-R),4 lipoyl dehydrogenase, and ferredoxin-NADP+ oxidoreductase in the presence of NAD(P)H (7). It was concluded therein (7) that these ftavoenzymes function as NAD(P)H-dependent vanadium(V) reductases. More recently, however, Liochev and Fridovich (8) have argued that the ESR data (7) do not demonstrate that the investigated fiavoenzymes act as vanadate reductases. They suggest an alternative mechanism in which the fiavoenzyme simply serves as a generator ofsuperoxide (02) radical, which acts as a propagator of the radical chain reaction leading to NAD(P)H oxidation (9, 10), as summarized below:

Nov 1, 1995

By C. W. Lee

"Introduction of diesel engines in underground mines may generate severe health hazards associated with exhaust contaminants. One of the most important parameter in determining the optimal air quantity for hazard reduction is the exhaust dispersion. Through analyzing the exact solution of the diffusion equation and its approximation by finite difference method(FDM) , this paper aims at doing a fundamental research to find an efficient dispersion model suitable to the domestic mines. Diffusion coefficients are likely to be small in the underground airways with high ventilation resistance. This makes concentration profiles similar to the convection-based step functions. It is the case for fixed as well as moving engines. Concentration estimation by exact solution is almost impossible in the case of either a single engine moving at a variable speed or the existence of multiple engines. Application of FDM to the diffusion equation including turbulent dispersion results in the various problems; unstable concentration profiles depending on the engine location, nuctuating concentrations near the engine, and overestimation of the dispersion region of which error grows with waning diffusion coefficient.Convection-based dispersion model is found to fit well for dynamic simulation of exhaust dispersion from multiple diesel engines in the airways showing low diffusion coefficients. Its suitability is more likely in the regions with frequent equipment passage. Published"

Nov 1, 1995

By M. S. Seehra, V. S. Babu

"INTRODUCTION The accurate determination of the free silica index in coal mine dusts is an important requirement because severe health hazards are believed to be associated with the inhalation of respirable-sized silica particles.1-6 Free silica refers to the three polymorphs of silica (Si02)viz., quartz, cristobalite, and tridymite-although quartz is usually the dominant form in most mine dusts.6 The free silica index is the concentration in micrograms of free silica in air per m3 of air sampled corrected to standard conditions of 25°C and 760 mm/Hg, the present MSHA (Mine Safety and Health Administration) limit on time-averaged basis being 100 µ.g/m 3 for coal mines. A recent review7 has concluded that quartz, cristobalite, and tridymite particles impart nearly equal long-term hemolytic damage when compared on a per unit surface area basis.At present, two experimental methods-viz., transmission infrared spectroscopy (TIRS) and x-ray diffraction (XRD)-are commonly used for the determination of silica concentrations in mine dusts. In TIRS, which has been adopted by MSHA and is commonly called the P7 method, the silica absorption band near 800 cm - 1 is used for quantification. However the mineral kaolinite, which is commonly present in mine dusts, also has absorption band, albeit weaker, at 800 cm- 1• To correct for this interference, one uses the stronger 915-cm -1 band of kaolinite to determine the concentration of kaolinite, and the kaolinite contribution to the absorbance at 800 cm-1 is then determined from a calibration curve, leading to the determination of silica by subtraction. In the XRD technique, usually an internal standard such as CaF 2 is used to determine the concentration of silica from line intensity measurements. XRD has the added advantage that concentrations of quartz, cristobalite, and tridymite can be determined.8•9 In an exhaustive study on the precision of the techniques ofTIRS and XRD for monitoring worker exposure,9 the conclusion has been reached that both methods measure silica within 253 of the ""true"" value 953 of the time in a single laboratory."

Nov 1, 1995

By L. D. Gehi, A. W. Khair, M. Ahmad

"Bit wear presents problems to mining operations because it affects both productivity and economics. Most bit research deals with energy requirements and energy dissipation mechanics for ideal fragmentation during the cutting process.Mechanical cutting leads to dust generation. Past studies involving dust generation due to bit wear concluded that dust concentrations increased considerably after a 7% bit weight loss: leading researchers recommend that the bits be changed at that point.Bit wear is affected by three factors: machine operating parameters in-situ mining conditions and rock properties. Operating parameters such as the depth of cut tool material spray position and the drum's rotating velocity are very important and have a definite impact on bit wear.During the mining process the amount of rock in coal and the strength of that rock is important as abrasion and adhesion take affect. Diffusive wear or deformation becomes dominant only when the temperatures exceed critical. Temperatures rise as a function of drum velocity rock properties and the cutting tool itself.Miner bit surveyIn this study, 15 mines were surveyed, and of those six responded for nine seams. The survey reflected a wide range of information about coal production and bit consumption from continuous miner sections. Also used bits were collected to get first-hand information to analyze wear."

Nov 1, 1995

By C. Van Dyke, K. Van Dyke, J. Gutierrez, C. Nowack

"Using propidium assay and flow cytometry, we examined how silica exerts its toxicity toward phagocytic cells employing the human neutrophil as a model. This toxicity appears to be associated with calcium bound to silica. Once the silica with calcium is phagocytized, the extra calcium causes the death of the cell. Using ""Ca we found that 6 to 10% of millimolar calcium is bound to milligram amounts of respirable-sized silica (diameter of 5 µ.m or less) at physiological pH. If the silica particles arc coated with an organosilanc (Prosil 28). calcium binding is decreased by 60% as is cell death. Pretreating with INDO IAM (a chelator of intracellular calcium) reduces the cellular death by 80%. Nonfibrogcnic particles- polystyrene beads or coal dust-produced 10% or less cell death in a 4-h period. Silica with no added, external calcium appears to exert toxicity to neutrophils; however, pretreating cells with EDT A decreases cellular death to the level of nonfibrogcnic particles. Chronic toxicity with silica-calcium appears similar to the chronic toxicity in gout where particles cause a cycle of inflammation. c 1993 Academic Press, Inc.Silicosis is an occupational disease caused by the inhalation of fine particles of silica, usually between 0.1 and 5 µ.m in diameter (1). A recent hypothesis explaining silica's toxicity suggested that surface free radicals caused damage to cells (2). This explanation appears doubtful, however, since the addition of silica to water, such as that found in biological systems, quenches free radicals; also, such a hypothesis does not provide basis for a persistent inflammatory pattern that lasts for years. Kane et al. (3) proposed that silica's toxicity resulted from an excessive concentration of calcium ions within the phagocytic cell (macrophages). However, the mechanism that was capable of linking silica to an excess of intracellular, ionic calcium was not explained. The surface of silica is certainly involved because covering the surface with polymers or phospholipids decreases silica's toxicity (4-6).When silica is engulfed by macrophages platelet activating factor and leukotrienes are produced (7, 8). This is the same inflammatory pattern produced by phagocytic cells exposed to the calcium ionophore A23187 and ionic calcium. How could silica be acting like A23187? Perhaps calcium binds to silica extracellulary and then is released intracellulary following phagocytosis; the latter process, in a sense a ""piggy back"" process, would permit activation of inflammation and cell death mechanisms."

Nov 1, 1995