Zinc Beryllium Silicate Research Articles

The etiology of osteosarcoma. A review of current considerations.

Various agents have caused osteosarcoma in several experimental animal systems. These agents or initiators may be classified as chemicals, radiation, viruses, and miscellaneous. Zinc beryllium silicate with beryllium oxide in rabbits and FBJ virus in mice are two such initiating agents. The relevance of these animal experiments to the human situation is not known, but recent reports regarding a transmissible agent obtained from human osteosarcoma tissue suggest that a virus may be implicated. There is a theoretic indication that the various etiologic agents, including viruses, may affect the DNA of normal cells in such a way that further evolution and differentiation through several cell divisions may result in the clinical appearance of cancer.

Increased bone formation in rabbits following intravenous and intra-osseous injection of zinc beryllium silicate.

Increased bone formation in rabbits following intravenous and intra-osseous injection of zinc beryllium silicate.

The influence of splenectomy on the induction of osteogenic sarcoma in rabbits.

Following splenectomy, eleven healthy rabbits were given zinc beryllium silicate. Three animals died before sufficient time had elapsed for the production of osteogenic sarcoma. In seven of the remaining eight animals, osteogenic sarcoma developed, while in the eighth new-bone formation was found in the medullary cavity of the long bones at the time of death. This condition the authors have come to recognize as the forerunner of beryllium-induced osteogenic sareoma in rabbits. The incidence of tumor in these rabbits (100 per cent) is definitely higher than the incidence in rabbits in which splenectomy was not performed prior to the injection of beryllium (50 per cent)12. Obviously, further study of a larger number of splenectomized rabbits to which beryllium has been given will be necessary before it can be stated conclusively that the presence of the spleen in a rabbit provides protection against the development of berylium-induced osteogenic sarcoma. Nevertheless, the results of the present study do suggest that this is the case.

Reactions within the lungs of guinea pigs to the intratracheal administration of zinc beryllium silicate.

Abstract Zinc silicate and zinc beryllium silicate were injected intratracheally into two groups of guinea pigs. Serial sacrifice of the animals was made and the pathology of lesions of the lungs was studied. Zinc silicate produced lesions comparable to but less severe than those from zinc beryllium silicate. Lesions from zinc silicate reached maximal intensity in about eight weeks; thereafter, recovery was noted and at 14 months a normal pulmonary parenchyma was restored. The beryllium salt produced more advanced lesions in two weeks with progression for three or four months. At 15 months some residual injury remained.

A Transplantable Beryllium-Induced Chondrosarcoma of Rabbits

Intravenous injections of zinc beryllium silicate induced the formation of a chondrosarcoma in the tibia of a rabbit. This tumor metastasized to the lungs. Both the primary and the metastatic tumors were successfully transplanted to the anterior chamber of the eyes of six rabbits. The histological appearance of the primary tumors and of the transplanted tumors is described.

The Effect of Beryllium on Bone

A series of fourteen rabbits were studied by roentgenograms made twice a month after injection of zinc beryllium silicate. After death or sacrifice, twelve long bones from ten rabbits were studied by microradiography and celloidin-embedded contiguous sections stained by hematoxylin and eosin. Spalteholz preparations of bones from four additional rabbits were also studied after injection of the arterial tree with a mixture of gelatin and India ink. The following observations were made: Medullary formation of bone was detected from the roentgenograms made eight to sixteen weeks after the last injection in all fourteen rabbits. Microradiography disclosed that this bone had a higher mineral content than the surrounding normal bone. In certain areas in this medullary bone, the lacunar spaces were blurred or indistinct on microradiography. Contiguous histological sections revealed that similar areas in sections stained by hematoxylin and eosin were devoid of cells. Therefore, it is postulated that the blurred lacunae evident in the microradiograms represent areas where the cells have died and mineralization of the empty lacunar spaces has occurred. Part of this phenomenon may be due to the direct cytotoxic effect of the zinc beryllium silicate seen in marrow spaces adjacent to the apparently non-viable, acellular bone on the surface of viable trabecular bone. Also, this phenomenon may be due to a decrease in vascularity caused by blockage of the blood supply by the abnormal bone. The decrease in vascularity, however, could be due purely to the cytotoxic effect of beryllium. Osteogenic sarcoma made its appearance thirty to fifty-two weeks after the last injection of beryllium. The morphological appearance of this phase is commented on, particularly the differences between the timorous bone and the abnormal medullary bone of beryllium poisoning and the similarity between this tumor and human osteogenic sarcoma.

A study of hydrogen diffusion flames

Summary o (1) Both atomic sodium and atomic potassium are produced in a hydrogen diffusion flame by a reaction involving atomic hydrogen. (2) This reaction is sufficiently rapid to rea premixed flame stabilized by the presence of the main diffusion flame. (4) Measurements of the temperature along the axis of the diffusion flame yield data which favor an atom diffusion mechanism rather than a heat conduction mechanism for the stabilization of the inner cone. (5) Hydrogen atoms generated in a discharge tube will excite both a preparation of calcium oxide activated with bismuth and zinc beryllium silicate to luminescence. This luminescence is brighter at higher temperature. Zinc beryllium silicate will also luminesce when subjected to ions. (6) The luminescence of these materials is a valid test for hydrogen atoms in diffusion flames.

Beryllium-induced osteogenic sarcoma in rabbits.

The method of producing osteogenic sarcoma in rabbits by the injection of beryllium in the form of "zinc beryllium silicate" is presented. In five of ten animals which had such injections, osteogenic sarcomas developed several months later. There was new bone formation in the medullary cavities of the long bones before malignant changes were apparent. It is of particular interest to note that there was atrophy of the spleen in those animals in which bone tumours developed, whereas the spleen seemed to be quite normal in the rabbits which did not develop bone tumours. The tumours usually developed in the metaphysial regions. More than one tumour often developed in the same animal.

The Excitation Spectra of Various Silicate Phosphors

A description is given of the excitation spectra of a number of silicate phosphors when irradiated by ultraviolet energy. Phosphors described are (a) manganese‐activated zinc beryllium silicate, (b) lead‐ and manganese‐activated calcium silicate, (c) barium silicate activated by lead, and (d) barium silicate activated by lead and modified by the substitution of magnesium. For the manganese‐activated zinc beryllium silicates, the change of the excitation spectrum with the lattice constant is noted. For a number of the other phosphors, it is shown that the excitation spectra for the visible and ultraviolet bands are not the same. It is concluded that the mechanisms involved for the excitation of the two bands are different.

Variation of Emission Spectrum of Manganese-Activated Zinc Beryllium Silicate with Decay Time

Variation of Emission Spectrum of Manganese-Activated Zinc Beryllium Silicate with Decay Time

Effect of Thermal History on Color of Zinc Beryllium Silicate (Mn) Phosphors

The fluorescent colors at room temperature of various completely‐reacted manganese‐activated zinc beryllium silicate phosphors can be changed by reheating them to temperatures lower than the original firing temperature with subsequent cooling at a rate in effect similar to the original cooling rate. A radical change in the cooling rate, as by quenching in water, also produces color shifts apart from the change due to reheating alone.When a zinc beryllium silicate (Mn) phosphor is reheated at various temperatures from 700°C to 1200°C with subsequent normal cooling, shifts to the green occur in all cases with a maximum shift at 950°C. With increased time of retiring, especially at the higher temperatures, the colors shift back toward the original phosphor color.With reheating and subsequent water quenching, the color shift to the green increases almost linearly with temperature over the range 800°C to 1200°C and extrapolates to zero color shift at 700°C. The magnitude of the color shift is greater with quenching than with normal cooling.The data require two equilibrium approach rates for interpretation. The first or rapid change involves the equilibrium of manganese between its red‐emitting and green‐emitting states, with the green‐emitting structure predominating at high temperatures. The second or slow change involves the migration of beryllium between substitutional positions either for silicon or zinc in the crystal. The equilibrium favors the beryllium‐for‐zinc substitution more for higher temperatures.The beryllium position in turn modifies the manganese‐state distribution, and this third equilibrium between the primary equilibria accounts for the time dependence of the color shifts.

OBSERVATIONS ON THE EFFECTS OF BERYLLIUM ON ALKALINE PHOSPHATASE

In the past 5 years a number of papers have dealt with the clinical aspects of exposure to various beryllium compounds (l-4). Because of these reports several laboratories (5) have attempted to reproduce in animals the lesions seen in the human cases but with only partial success. In 1946, Dr. Leroy Gardner (6) noted that the intravenous injection of zinc-beryllium silicate or beryllium oxide into rabbits resulted in the development of osteogenic sarcomas after a latent period as short as 5$ months or as long as 1 year. This observation has been confirmed in this laboratory and will be described in a later paper. Several authors (7-10) have reported that the addition of beryllium carbonate to the diet of young rats led to the development of rachitic changes which have been termed “beryllium rickets.” Extremely low levels of serum phosphate and a marked lowering of the alkaline phosphatase content of the kidney accompanied the development of this lesion. Furthermore, this lesion could not be prevented by cod liver oil or irradiated ergosterol, though Kay and Skill (10) were able to prevent it by the daily parenteral administration of glycerophosphate. These authors think that the lesion, at least in part, is due to the precipitation of beryllium phosphate in the intestine, making the phosphate unavailable for absorption. However, Sobel, Goldfarb, and Kramer (11) in studying in vitro the calcifying power of ordinary rachitic bone and beryllium rachitic bone in normal serum noted a markedly diminished calcifying power in the latter compared to the former. They also noted that, although the addition of viosterol to the beryllium rachitogenic diet produced a rise in the calcium and phosphorus product in the serum, the rickets was not prevented and the defect in the calcifying power in vitro was still present. This work suggested that in addition to the factor of poor absorption of phosphate from the intestine there was also a local factor which interfered with calcification. In 1943, Hyslop et al. (12) presented evidence that beryllium tends to be stored in bone.

CUTANEOUS GRANULOMA FROM ACCIDENTAL CONTAMINATION WITH BERYLLIUM PHOSPHORS

During the past ten years an appreciation of the peculiar properties of beryllium led to its utilization in a variety of industrial processes and products. 1 Unfortunately, in occasional persons exposed to a beryllium-contaminated atmosphere an illness developed characterized by a distinctive clinical course and a generalized granular pattern seen on roentgen examination of the lungs. 2 Despite the failure to produce generalized or pulmonary chronic granulomatosis 3 by exposure of experimental animals to beryllium compounds, clinical observations continue to emphasize the probable causative significance of zinc beryllium silicate in this disease. 4 Characteristic histologic changes and the presence of abnormal quantities of beryllium in the tissues and urine of such patients furnish further presumptive evidence incriminating these beryllium phosphors. Similar detailed observations in persons exposed to beryllium oxide and beryllium alloys 1a tend to single out beryllium as the principal known causative factor. Recent observations 5 that typical histologic

Temperature quenching and decay of fluorescence in zinc and zinc-beryllium silicates activated with manganese

Zinc silicate and zinc-beryllium silicate activated by manganese contain various types of fluorescence centres which differ in the wave length of the emitted radiation, the probability of the fluorescence transition, and the vibrational interaction with the surroundings which regulates the dissipation of energy of excitation. The centres are assumed to be manganese ions with different numbers of other manganese ions at neighbouring sites (clusters). Quenching of fluorescence is due to radiationless processes starting from the excited state of the centres (characteristic quenching). If particular conditions are fulfilled, however, quenching may also occur from (higher) éxcited states of a different type. In this case energy of excitation is transferred to centres especially suited for the dissipation of energy (quencher centres). This type of quenching is found in zinc silicates at medium manganese concentrations, and in zinc- and zinc-beryllium silicates containing foreign quenchers (iron). It is assumed that quencher centres are fluorescence centres with a low quenching point.

The Constitution of Zinc Beryllium Silicate Phosphors and its Effect on their Luminous Properties

The constitution of zinc beryllium silicates, prepared at temperatures in the neighborhood of the normal firing temperature, has been investigated. The limit of solubility of beryllium in zinc silicate at 1260°C. was found to be at about 25 molar per cent for phosphors containing 2.5 per cent manganese, as well as for unactivated products. This is only slightly below the value of 30 molar per cent found previously at the fusion temperature. No evidence could be found of a further reduction in solubility at temperatures below 1260°C. At 1260°C. the reaction between beryllia and silica alone is so slow that no appreciable amount of beryllium silicate could be detected until zinc oxide was added in addition, denoting that zinc silicate serves as a flux to catalyze the beryllia reaction. Firing at 1180°C was incapable of dissolving all the beryllia present, even for compositions below the saturation point.Maintenance of phosphors in lamps was somewhat better for a composition slightly higher in beryllia than corresponded to the saturation point. The maintenance was still better for phosphors prepared at 1180°C, a temperature at which not all of the beryllia introduced could be dissolved.The initial rate of decay of phosphorescence is exponential. The rate becomes greater as the concentration of either beryllium or manganese is increased. For a phosphor of standard color, the decay rate is smaller if this color is attained by the use of high beryllia and low manganese rather than the reverse.

Calcium Halophosphate Phosphors

Calcium halophosphates were prepared by firing together calcium chloride and calcium fluoride in various ratios with calcium phosphate containing antimony and manganese as activators, in an electric furnace at 1060°C. for 1 hour. The x‐ray diffraction studies gave patterns very similar to the mineral apatite. Spectral energy distribution measurements indicated that as the chlorine was replaced by equal mole fractions of fluorine, the peak of emission shifted from 5800 Å for all chlorine to 5550 Å when only fluorine was used. Calcium halophosphate activated with antimony alone has a peak of fluorescence at about 4800 Å. As the per centage of manganese is increased up to five per cent, the blue emission is entirely suppressed and a broad peak is obtained at about 5800 Å. The amount of antimony in the phosphor does not appreciably affect the fluorescent color. Excitation measurements of various calcium halophosphates reveal that there are two distinct peaks. A major one is located near 2500 Å and a minor one at 2200 Å. Replacing the chlorine by fluorine tends to shift the major peak toward the longer wavelengths. The effect of manganese seemed to be to enhance the minor excitation peak at 2200 Å. Fluorescent lamps made from this phosphor have been obtained that have outputs and color temperatures comparable to lamps made with zinc beryllium silicate and magnesium tungstate.

High Valent Manganese as Activator of Luminescence

In a previous letter (1) it was inferred from the analysis of the emission spectra of Mn‐activated zinc orthosilicate and zinc beryllium silicate phosphors, and from the extinction spectra of aqueous solutions of and , that the luminescence centers of these phosphors are essentially permanganate and manganate ions, respectively. In addition to this spectroscopic argument it is shown that several properties of various Mn‐activated phosphors can be explained from a common point of view with the assumption that their luminescent centers have or like configurations.

Emission Spectra of Silicate Phosphors with Manganese Activation

It is shown that the emission spectra of manganese activated zinc orthosilicate, zinc beryllium silicate and calcium silicate can be expressed as the sum of several Gaussian distribution curves. The observed distributions for zinc orthosilicate and for calcium silicate can be fully given as the sum of three bands, while that of zinc beryllium silicate requires five bands. In general, only the amplitude of the bands is affected by changes in composition with their location and sharpness remaining unchanged.Based on the hypothesis that transitions between energy levels of manganese ions in the crystal lattice are responsible for the emission of visible light, tentative assignments are given for the transitions responsible for each observed bands.The geometry of the crystal lattice is shown to influence the location of the bands as exemplified by the difference between zinc silicate and calcium silicate. Modifying ions, such as beryllium, are shown not to affect the band locations though they cause the development of new bands not previously observed in the unmodified phosphor. A hypothesis for this appearance of new bands is proposed in terms of a change in electron spin.

The CaSiO_3:(Pb+Mn) Phosphor

A calcium silicate phosphor, activated by lead and manganese, is described, and the conditions for its preparation are presented in detail. Under excitation by a low pressure mercury discharge, such as is employed in fluorescent lamps, this phosphor luminesces with an emission lying principally in the red end of the spectrum and with a high efficiency comparable to that of zinc beryllium silicate of the same luminescence color. Data are presented on the spectral emission of CaSiO3:Pb, CaSiO3:Mn, and CaSiO3:(Pb+Mn), both under cathode-ray and under 2537A excitation. It is shown that CaSiO3:Mn is excited to luminescence in the red end of the spectrum by cathode rays but not by ultraviolet light. The introduction of lead as an auxiliary impurity makes possible the excitation of this material by radiation in the neighborhood of the mercury resonance line. Qualitative absorption experiments indicate that the lack of response of CaSiO3:Mn to 2537A excitation is due to the absence of an absorption for this radiation; and that lead acts as a sensitizer for the manganese by introducing an absorption band in the vicinity of 2537A. The presence of a sensitizer is unnecessary under cathode-ray excitation, since in this case the energy is absorbed by the host crystal itself.

Causes of Early Loss of Light Output of Fluorescent Lamps

To determine the cause of loss of light output of fluorescent lamps the photo-decomposition of zinc silicate, zinc beryllium silicate, calcium tungstate, magnesium tungstate, and calcium cerium phosphate phosphors has been studied in a vacuum, air, and inert gases. The loss of light output has been shown to be caused by the photolysis of the commercial phosphors which is in contrast to the general theory in which the loss has been attributed to a film formation on the fluorescent particles. The photolysis of the silicate and tungstate phosphors is mainly caused by radiations less than 2000A. The calcium cerium phosphate is most sensitive to these radiations. The photochemically active center in the silicate phosphors appears to be the manganese atom. The tungsten and cerium atoms may be involved in the tungstate and phosphate phosphors, respectively.