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PubMed1996

Comparison of the clinical anticaries efficacy of a 1500 NaF silica-based dentifrice containing triclosan and a copolymer to a 1500 NaF silica-based dentifrice without those additional agents: a study on adults in Israel.

Recent years have seen much work in the development of dentifrices containing the antimicrobial agent triclosan, a broad spectrum antibacterial agent manufactured for use in oral products by the Ciba-Geigy Corporation. Studies have shown that the incorporation of this agent into dental products, in combination with a PVM/MA copolymer (the non-proprietary designation for a polyvinylmethyl ether/maleic acid copolymer), can provide several important dental therapeutic benefits, including an antigingivitis effect. A considerable amount of the research on the therapeutic benefits of such dentifrices has been reported in the literature. The present study is a component of a large-scale program of clinical research to investigate the anticaries effectiveness of fluoride dentifrices containing 0.3% triclosan and 2.0% PVM/MA copolymer. The study included two treatment groups, each consisting of adults living near the Kiryat Gat area in Israel, who were assigned to the use of one of the following sodium fluoride (NaF) dentifrices: 1) a dentifrice containing 0.3% triclosan and 2.0% PVM/MA copolymer in a 0.331% NaF/silica (1500 ppm F) base; or 2) a dentifrice containing 0.331% NaF/silica (1500 ppm F). Conducted in accordance with the guidelines for caries clinical studies published by the Council on Dental Therapeutics of the American Dental Association, the study employed clinical diagnostic criteria as described in the August, 1987 National Institute of Dental Research (NIH/NIDR) publication. Dental radiographs were not employed. Principal comparisons of the dentifrices tested were implemented through the construction of 90% confidence intervals for the ratio of mean 3-year caries increments using Fieller's Theorem. Of those subjects who met the initial inclusion/exclusion criteria for this study, 1,296 were available for the 36-month examination. DFS (resp., DFT) increments over this period were 5.21 (1.30) for the triclosan/copolymer dentifrice, and 5.23 (1.39) for the dentifrice without those additives. The confidence interval calculations for both incremental DFS and DFT support the conclusion that a dentifrice containing 0.3% triclosan and 2.0% PVM/MA copolymer in a 0.331% NaF/silica (1500 ppm F) base provides a level of anticaries efficacy which is "at least as good as" that provided by a dentifrice containing 1500 NaF/silica, without those additive agents. As such, the results of this clinical study clearly indicate that the addition of triclosan and a copolymer to a 1500 NaF/silica dentifrice does not compromise its anticaries efficacy.

Adult↗
PubMed2000

Pulmonary chemokine and mutagenic responses in rats after subchronic inhalation of amorphous and crystalline silica.

Chronic inhalation of crystalline silica can produce lung tumors in rats whereas this has not been shown for amorphous silica. At present the mechanisms underlying this rat lung tumor response are unknown, although a significant role for chronic inflammation and cell proliferation has been postulated. To examine the processes that may contribute to the development of rat lung tumors after silica exposure, we characterized the effects of subchronic inhalation of amorphous and crystalline silica in rats. Rats were exposed for 6 h/day, on 5 days/week, for up to 13 weeks to 3 mg/m(3) crystalline or 50 mg/m(3) amorphous silica. The effects on the lung were characterized after 6.5 and 13 weeks of exposure as well as after 3 and 8 months of recovery. Exposure concentrations were selected to induce high pulmonary inflammatory-cell responses by both compounds. Endpoints characterized after silica exposure included mutation in the HPRT gene of isolated alveolar cells in an ex vivo assay, changes in bronchoalveolar lavage fluid markers of cellular and biochemical lung injury and inflammation, expression of mRNA for the chemokine MIP-2, and detection of oxidative DNA damage. Lung burdens of silica were also determined. After 13 weeks of exposure, lavage neutrophils were increased from 0.26% (controls) to 47 and 55% of total lavaged cells for crystalline and amorphous silica, with significantly greater lavage neutrophil numbers after amorphous silica (9.3 x 10(7) PMNs) compared to crystalline silica (6.5 x 10(7) PMNs). Lung burdens were 819 and 882 microg for crystalline and amorphous silica, respectively. BAL fluid levels of LDH as an indicator of cytotoxicity were twice as high for amorphous silica compared to those of crystalline silica, at the end of exposure. All parameters remained increased for crystalline silica and decreased rapidly for amorphous silica in the 8-month recovery period. Increased MIP-2 expression was observed at the end of the exposure period for both amorphous and crystalline silica. After 8 months of recovery, those markers remained elevated in crystalline silica-exposed rats, whereas amorphous silica-exposed rats were not significantly different from controls. A significant increase in HPRT mutation frequency in alveolar epithelial cells was detected immediately after 13 weeks of exposure to crystalline, but not to amorphous silica. A significant increase in TUNEL staining was detected in macrophages and terminal bronchiolar epithelial cells of amorphous silica-exposed rats at the end of the exposure period; however, crystalline silica produced far less staining. The observation that genotoxic effects in alveolar epithelial cells occurred only after crystalline but not amorphous silica exposure, despite a high degree of inflammatory-cell response after subchronic exposure to both types of silica, suggests that in addition to an inflammatory response, particle biopersistence, solubility, and direct or indirect epithelial cell cytotoxicity may be key factors for the induction of either mutagenic events or target cell death.

Administration, Inhalation↗
PubMed2006

Silica deposition in abaxial epidermis before the opening of leaf blades of Pleioblastus chino (Poaceae, Bambusoideae).

UNLABELLED: BACKGROUND AND AIMS Silica deposition is one of the important characteristics of the family Poaceae. The distribution, deposition process and physiology of silica in this family have been extensively investigated. Bamboos among members of Poaceae have leaves with a fairly long life span, and the leaves continuously accumulate silica in their tissues throughout their life, not only during the course of leaf opening, but also after opening. It has been revealed that the silica deposition process in relation to ageing of the bamboo leaf after opening differed depending on the cell types comprising the tissues. However, silica deposition has never been examined during the development and maturation periods of bamboo leaves. Hence, to clarify the silica deposition process in a developmental stage of the bamboo leaf, distribution of silica was observed in the abaxial epidermis before the opening of the leaf blades of Pleioblastus chino. METHODS: Abaxial epidermal tissues of leaves were examined using a scanning electron microscope equipped with an energy dispersive X-ray microanalyser. KEY RESULTS: Among seven cell types comprising the abaxial epidermis, three types of cells, guard cells, prickle hairs and silica cells, deposited silica conspicuously, and another four types, cork cells, long cells, micro hairs and subsidiary cells, deposited only a little silica. Among the former group of cell types, silica cells and guard cells deposited silica over their entire surfaces, while prickle hairs deposited silica only in the point-tips. Silica deposition was detected firstly in prickle hairs, and then in silica cells and guard cells. Only silica cells were assumed to deposit silica conspicuously before leaf opening but not conspicuously after opening. CONCLUSIONS: Cell types in leaf epidermis of bamboo are classified into three groups according to the silica deposition pattern. Silica deposition in silica cells may be positive as a part of the physiological activities of leaves.

Cell Differentiation↗
PubMed1993

Altered calcium homeostasis and cell injury in silica-exposed alveolar macrophages.

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 [Ca2+]i. However, the mechanism of silica-induced cytotoxicity relative to [Ca2+]i 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 microns in diameter) and the fluctuation in their [Ca2+]i and cell integrity were quantitatively monitored with the fluorescent calcium probe, Fura-2 AM, and the membrane integrity indicator, propidium iodide (PI). Results from this study indicate that silica can rapidly increase [Ca2+]i 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 [Ca2+]o markedly inhibited the [Ca2+]i rise (approximately 90%), suggesting that Ca2+ influx from extracellular source is a major mechanism for silica-induced [Ca2+]i rise. When used at low doses but sufficient to cause a transient [Ca2+]i rise, silica did not cause significant increase in cellular PI uptake during the time of study, suggesting the preservation of membrane integrity of AMs under these conditions. At high doses of silica, however, a marked increase in PI nuclear fluorescence was observed. Depletion of [Ca2+]o greatly inhibited cellular PI uptake, induced by 0.1 mg/ml or higher doses of silica. This suggests that Ca2+ 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 Ca2+ 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 silica-induced [Ca2+]i rise was not due to the impairment of Ca(2+)-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+]i rise. Taken together, these results suggest that the elevation of [Ca2+]i caused by silica is due mainly to Ca2+ influx through plasma membrane Ca2+ channels and nonspecific membrane damage (at high doses).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2002

Health hazards due to the inhalation of amorphous silica.

Occupational exposure to crystalline silica dust is associated with an increased risk for pulmonary diseases such as silicosis, tuberculosis, chronic bronchitis, chronic obstructive pulmonary disease (COPD) and lung cancer. This review summarizes the current knowledge about the health effects of amorphous (non-crystalline) forms of silica. The major problem in the assessment of health effects of amorphous silica is its contamination with crystalline silica. This applies particularly to well-documented pneumoconiosis among diatomaceous earth workers. Intentionally manufactured synthetic amorphous silicas are without contamination of crystalline silica. These synthetic forms may be classified as (1) wet process silica, (2) pyrogenic ("thermal" or "fumed") silica, and (3) chemically or physically modified silica. According to the different physicochemical properties, the major classes of synthetic amorphous silica are used in a variety of products, e.g. as fillers in the rubber industry, in tyre compounds, as free-flow and anti-caking agents in powder materials, and as liquid carriers, particularly in the manufacture of animal feed and agrochemicals; other uses are found in toothpaste additives, paints, silicon rubber, insulation material, liquid systems in coatings, adhesives, printing inks, plastisol car undercoats, and cosmetics. Animal inhalation studies with intentionally manufactured synthetic amorphous silica showed at least partially reversible inflammation, granuloma formation and emphysema, but no progressive fibrosis of the lungs. Epidemiological studies do not support the hypothesis that amorphous silicas have any relevant potential to induce fibrosis in workers with high occupational exposure to these substances, although one study disclosed four cases with silicosis among subjects exposed to apparently non-contaminated amorphous silica. Since the data have been limited, a risk of chronic bronchitis, COPD or emphysema cannot be excluded. There is no study that allows the classification of amorphous silica with regard to its carcinogenicity in humans. Further work is necessary in order to define the effects of amorphous silica on morbidity and mortality of workers with exposure to these substances.

Air Pollutants, Occupational↗
PubMed2000

Oligomeric but not monomeric silica prevents aluminum absorption in humans.

BACKGROUND: Soluble silica, a ubiquitous component of the diet, may be the natural ligand for dietary aluminum and may prevent its accumulation and toxicity in animals. However, previous studies on the inhibition of aluminum absorption and toxicity by soluble silica have produced conflicting results. We recently identified a soluble silica polymer, oligomeric silica, that has a much higher affinity for aluminum than does monomeric silica and that may be involved in the sequestration of aluminum. OBJECTIVE: By using (26)Al as a tracer, we investigated the effects of oligomeric and monomeric silica on the bioavailability of aluminum (study 1) and compared the availability of silicon from oligomeric and monomeric silica in the human gastrointestinal tract (study 2). DESIGN: In study 1, three healthy volunteers each ingested aluminum alone (control), aluminum with oligomeric silica (17 mg), and aluminum with monomeric silica (17 mg). In study 2, five healthy volunteers ingested both the oligomeric and monomeric forms of silica (34 mg). Serum and urine samples were analyzed for aluminum and silicon. RESULTS: Oligomeric silica reduced the availability of aluminum by 67% (P = 0.01) compared with the control, whereas monomeric silica had no effect (P = 0.40). Monomeric silica was readily taken up from the gastrointestinal tract and then excreted in urine (53%), whereas oligomeric silica was not detectably absorbed or excreted. CONCLUSIONS: The oligomeric, high-aluminum-affinity form of soluble silica reduces aluminum availability from the human gastrointestinal tract. Its potential role in the amelioration of aluminum toxicity in other biological systems requires attention.

Adult↗
PubMed2000

Male systemic sclerosis and occupational silica exposure-a population-based study.

BACKGROUND: The continuing uncertainty about the silica-systemic sclerosis relationship led to the investigation of its role as a disease determinant in a large population-based study of systemic sclerosis. AIMS: To compare the frequency, socioeconomic and educational status, age-specific prevalence and duration of occupational silica exposure in males with and without systemic sclerosis. To assess the temporal relationship between exposure and disease onset. To estimate disease latency. To compare disease characteristics between silica-exposed and non-silica-exposed male cases. METHODS: The study was case-control in design. The exposure variable was occupational silica exposure as assessed by an occupational health officer blinded to case/control status and the outcome variable was systemic sclerosis. The employed instrument comprised either a standardised telephone questionnaire (interviewed cases and controls) or medical records (deceased or living-status-unknown cases). RESULTS: Sixty of 160 cases (37.5%) and 11 of 83 (13.3%) controls had occupational silica exposure (OR=3.93; 1.84-8.54). Comparison of data between 64 interviewed cases and all controls demonstrated initial occupational silica exposure occurring before age 40, comparable educational status but significantly different cumulative socioeconomic status with cases being over-represented in semi-skilled and unskilled occupations. Cross-sectional 'current' occupational data underestimated cumulative silica exposure by more than 50%. Silica exposure uniformly preceded onset of second disease symptoms and disease diagnosis. In most, it also preceded onset of first disease symptoms. Disease latency approximated two decades. No disease features distinguished silica-associated systemic sclerosis from idiopathic systemic sclerosis. The duration of silica exposure in the interviewed silica-exposed cases did not significantly exceed that of silica-exposed controls. CONCLUSIONS: Male systemic sclerosis displays socioeconomic dependence. Silica is a disease determinant in male systemic sclerosis, with disease features including a long latency and clinical characteristics indistinguishable from idiopathic disease. Cross-sectional 'current' occupational data underestimate cumulative occupational silica exposure.

Adolescent↗
PubMed2004

Estimation of diffusion coefficient of chromium in colloidal silica using digital photography.

In order to study the effectiveness of using colloidal silica, NYACOL DP5110, to stabilize chromium-contaminated soil, the diffusion of chromium in colloidal silica gel was estimated from laboratory experiments. To measure diffusion coefficients of chromium in the colloidal silica gel, a new measurement method based on digital photography was introduced. A series of experiments were designed and conducted to validate this new method and to estimate the diffusion coefficients of chromium in the colloidal silica gel. Accuracy of the proposed method was evaluated by several differentways. It was found that the apparent diffusion coefficient of chromium in colloidal silica gel ranged from 1.76 to 8.48 x 10(-10) m2/s depending mainly on the concentration of silica in the gel with chromium concentration less than 10(-2) M. Higher silica concentrations yielded lower diffusion coefficients due to the obstruction to the free movement of chromium. The adsorption isotherm of chromate to colloidal silica gel was found to be linear at pH 7; the partition coefficient was calculated to be 0.549 L/g. Mass balance calculations were performed to evaluate the accuracy of the proposed method and found that the measuring error was less than 6.5%. Based on the test data, the estimation of diffusion coefficients for chromium in colloidal silica gel using digital photography seems to be accurate and precise. This method is suitable for analyzing colored chemicals inside clear/white gels. From the results, it can be concluded that the gel behaves as a porous material with silica network forming continuous solid phase and its pore space saturated with water. The chromium ions diffuse in porous silica gel on a tortuous path. Therefore, the bulk diffusion dominates. Thus, the silica can be represented as a fix and impenetrable immersion in the solution. The presence of these motionless silica chains leads to an increase in the mean path of the diffusing molecules between two points in the system. On the basis of the test results, it can also be concluded that colloidal silica, NYACOL DP5110, for in-situ treatment of chromium-contaminated soils seems to be ineffective. Further research of more realistic simulation of diffusion and refined gel formulation with the capacity to convert the chromium to an immobile form is recommended.

Chromium↗
PubMed1996

Silica-induced apoptosis mediated via scavenger receptor in human alveolar macrophages.

Exposure to silica dust can result in lung inflammation that may progress to fibrosis, for which there is no effective clinical treatment. The mechanisms involved in the development of pulmonary silicosis have not been well defined; however, most current evidence implicates a central role for alveolar macrophages (AM) in this process. We propose that the fibrotic potential of a particulate depends upon its ability to cause apoptosis in AM. In this study, human AM were treated with fibrogenic, poorly fibrogenic, and nonfibrogenic model particulates, such as silica (133 micrograms/ml), amorphous silica (80 micrograms/ml), and titanium dioxide (60 micrograms/ml), respectively. Cell were treated with these particulates in vitro for 6 and 24 hr and examined for apoptosis by morphological analysis, DNA fragmentation, and levels of cytosolic histone-bound DNA fragments (cell death ELISA assays). Treatment with silica resulted in morphological changes typical of apoptotic cells, enhanced DNA fragmentation (a characteristic feature of programmed cell death), and significant alveolar macrophage apoptosis as observed by cell death ELISA assays. In contrast, amorphous silica and titanium dioxide demonstrated no significant apoptotic potential. To elucidate the possible mechanism by which silica causes apoptosis, we investigated the role of the scavenger receptor (SR) in silica-induced apoptosis. Cells were pretreated with and without SR ligand binding inhibitor, polyinosinic acid (poly(I), 500 micrograms/ml), for 10 min prior to silica treatment. Pretreatment with poly(I) resulted in complete inhibition of silica-induced apoptosis as measured by cell death ELISA. Further, we examined the involvement of interleukin-converting enzyme (ICE) in silica-mediated apoptosis using an ICE inhibitor, Z-Val-Ala-Asp-fluoromethyl ketone. Z-Val-Ala-Asp-fluoromethyl ketone inhibited silica-induced apoptosis and IL-1 beta release. These results suggest that fibrogenic particulates, such as silica, caused apoptosis of alveolar macrophages and that this apoptotic potential of fibrogenic particulates may be a critical factor in initiating an inflammatory response resulting in fibrosis. Additionally, silica-induced apoptosis of alveolar macrophages may be due to the interaction of silica particulates with the SR, initiating one or a number of signaling pathways involving ICE, ultimately leading to apoptosis.

Adult↗
PubMed1993

Sandblasting and silica-coating of dental alloys: volume loss, morphology and changes in the surface composition.

Silica-coating alloys improves chemo-mechanical bonding. Sandblasting is recommended as pretreatment to thermal silica-coating or as part of a tribochemical silica-coating process. This study evaluated the effects of sandblasting and coating techniques on volume loss, surface morphology and compositional changes in noble (AuAgCu) and base alloys (NiCr and CoCr). Volume loss was statistically significantly higher in the noble as compared to the base alloys but does not seem to be critical for the clinical fit of restorations. Embedded alumina particles were found in all alloys after sandblasting and the alumina content increased to a range of 14 to 37 wt% as measured by EDS. Following tribochemical silica-coating, a layer of small silica particles remained on the surface, increasing the silica content to between 12 and 20 wt%. Ultrasonic cleaning removed loose alumina or silica particles from the surface, resulting in only slight decreases in alumina or silica contents, thus suggesting firm attachment of the major part of alumina and silica to the alloy surface. Clinically, ultrasonic cleaning of sandblasted and tribochemically silica-coated alloys might improve resin bonding as loose surface particles are removed without relevant changes in composition. Silica content following thermal silica-coating treatment increased only slightly from the sandblasted specimen. The silica layer employed by these silica-coating methods differs widely in both morphology and thickness. These results provide a basis for explanation of adhesive failure modes in bond strength tests which will possibly optimize resin bonding. Further research is needed to characterize the outermost surface layers after these treatments and the exact location of adhesive failures.

Analysis of Variance↗
PubMed1994

Effects of sandblasting and silica-coating procedures on pure titanium.

Silica coating titanium improves chemomechanical bonding. Sandblasting is recommended as a pretreatment to thermal silica coating (Silicoater MD) or as part of a tribochemical silica coating process (Rocatec). This study evaluated the effects of sandblasting and coating techniques on volume loss, surface morphology and composition changes in pure titanium. Volume loss of titanium was similar to values reported for base alloys and does not seem to be critical for the clinical fit of restorations. Embedded alumina particles were found in the titanium after sandblasting and the alumina content increased to a range of 27.5-39.3 wt% as measured by EDS. Following tribochemical silica coating, a layer of small silica particles remained on the surface, increasing the silica content to a range of 17.9-19.5 wt%. Ultrasonic cleaning removed loose alumina or silica particles from the surface, resulting in only slight decreases in alumina or silica contents, suggesting firm attachment of most of the alumina and silica to the titanium surface. Silica content following thermal silica coating treatment increased only slightly from the sandblasted specimen to 1.4 wt%. The silica layer employed by these silica coating methods differs widely in both morphology and thickness. These results provide a basis for explanation of adhesive failure modes in bond strength tests and for developing methods to optimize resin bonding. Clinically, ultrasonic cleaning of sandblasted and tribochemically silica coated titanium should improve resin bonding as loose surface particles are removed without relevant changes in composition.

Aluminum Oxide↗
PubMed2006

Adsorption of organic molecules on silica surface.

The adsorption behaviour of various organic adsorbates on silica surface is reviewed. Most of the structural information on silica is obtained from IR spectral data and from the characteristics of water present at the silica surface. Silica surface is generally embedded with hydroxy groups and ethereal linkages, and hence considered to have a negative charged surface prone to adsorption of electron deficient species. Adsorption isotherms of the adsorbates delineate the nature of binding of the adsorbate with silica. Aromatic compounds are found to involve the pi-cloud in hydrogen bonding with silanol OH group during adsorption. Cationic and nonionic surfactants adsorb on silica surface involving hydrogen bonding. Sometimes, a polar part of the surfactants also contributes to the adsorption process. Styryl pyridinium dyes are found to anchor on silica surface in flat-on position. On modification of the silica by treating with alkali, the adsorption behaviour of cationic surfactant or polyethylene glycol changes due to change in the characteristics of silica or modified silica surface. In case of PEG-modified silica, adsolubilization of the adsorbate is observed. By using a modified adsorption equation, hemimicellization is proposed for these dyes. Adsorptions of some natural macromolecules like proteins and nucleic acids are investigated to study the hydrophobic and hydrophilic binding sites of silica. Artificial macromolecules like synthetic polymers are found to be adsorbed on silica surface due to the interaction of the multifunctional groups of the polymers with silanols. Preferential adsorption of polar adsorbates is observed in case of adsorbate mixtures. When surfactant mixtures are considered to study competitive adsorption on silica surface, critical micelle concentration of individual surfactant also contributes to the adsorption isotherm. The structural study of adsorbed surface and the thermodynamics of adsorption are given some importance in this review.

Journal Article↗
PubMed2002

Comparison of low doses of aged and freshly fractured silica on pulmonary inflammation and damage in the rat.

Most previous studies of silica toxicity have used relatively high exposure doses of silica. In this study, male rats received by intratracheal instillation either vehicle, aged or freshly fractured silica at a dose of either 5 microg/rat once a week for 12 weeks (total dose=60 microg) or 20 microg/rat once a week for 12 weeks (total dose=240 microg). One week after the last exposure, bronchoalveolar lavage (BAL) was conducted and markers of pulmonary inflammation, alveolar macrophage (AM) activation and pulmonary damage were examined. For rats exposed to a total of 60 microg silica, both aged and freshly fractured silica increased polymorphonuclear leukocytes (PMN) yield and AM activation above control to a similar degree, but no evidence of pulmonary damage, as measured by BAL fluid lactate dehydrogenase activity or albumin concentration, was detected. For rats exposed to 240 microg silica, aged or freshly fractured silica increased PMN yield and AM activation above control. However, zymosan-stimulated and L-NAME sensitive AM chemiluminescence was greater for rats exposed to freshly fractured silica compared to aged silica. Exposure to 240 microg aged or freshly fractured silica also resulted in pulmonary damage, but the extent of this damage did not differ between the two types of silica. The results suggest that exposure of rats to silica levels far lower than those previously examined can cause pulmonary inflammation. In addition, exposure to freshly fractured silica causes greater generation of reactive oxygen species from AM, measured as AM chemiluminescence, in comparison to aged silica, but there is an apparent threshold below which this difference does not occur.

Albumins↗
PubMed2002

An improved method for production of silica from rice hull ash.

Rice hull ash (RHA) contains over 60% silica and can be an economically viable raw material for the production of silica based products. A previously published method for producing silica xerogel involved dissolving RHA silica with alkali solution to form sodium silicate solution and subsequently forming silica aquagel by adding hydrochloric acid to lower the pH from 11.8 to 7.0, followed by washing and drying aquagel to form xerogel. The silica xerogel had over 4% sodium as a contaminant. An improved method to produce silica xerogel with lower sodium is described in this study. The improved method involved production of silica aquagel by adding silicate solution to pH 1.5 hydrochloric, citric, or oxalic acid solutions until the pH 4.0 was reached. The aquagel was washed and dried to form silica xerogel. For comparison silica xerogels were also produced at pH 7.0 by the published method. X-ray photoelectron spectroscopy was used to determine the elemental content of silica xerogels. The silica, sodium, carbon and oxygen content of silica xerogels varied depending on the pH and the type of acid used for the production of these xerogels. Silica xerogels produced by the improved method using citric and oxalic acid had sodium content of 0.52% and 0.22%, respectively.

Acids↗
PubMed1994

Effect of short-term exogenous pulmonary surfactant treatment on acute lung damage associated with the intratracheal instillation of silica.

The objective of our study was to investigate whether coating the surface of silica with Survanta, a commercially available, bovine pulmonary surfactant, would reduce the in vitro cytotoxicity to alveolar macrophages (AMs), as well as attenuate lung damage in vivo following intratracheal instillation of silica. In the in vitro studies, alveolar macrophages from male Fischer 344 rats were incubated for 1 and 24 h with native or Survanta-treated silica (0.5 mg/ml). At both time points, the native, uncoated silica caused a dramatic loss of AM viability. The AMs were protected, however, when the silica was treated with the Survanta surfactant. This protective effect was significantly greater after 1 h when compared with 24 h. In the in vivo studies, a high dose of silica (10 mg/100 g body weight) was suspended in Survanta and intratracheally instilled into the lungs of male Fischer 344 rats. A number of biochemical and cellular parameters were measured within the bronchoalveolar lavage fluid (BALF) 1 and 14 d after the instillation exposures to assess lung damage. One day after the instillations, the suspension of silica in Survanta resulted in significant reductions in the silica-induced increases in total protein, beta-glucuronidase activity, and influx of neutrophils (PMNs) into the airspaces of the lungs. Fourteen days after the instillation exposures, this protective effect was lost. When Survanta was instilled into the lungs 15 min after the intratracheal instillation of silica, a significant reduction also was demonstrated in the silica-induced elevations in BALF total protein, beta-glucuronidase activity, and influx of PMNs 1 d after the instillation exposures. In an attempt to protect silica-exposed lungs over a longer period of time, Survanta was instilled into the lung 15 min after the silica instillation, and then every other day over a 7-d treatment period. Twenty-four hours after the last Survanta instillation, slight but significant decreases in the silica-induced elevations in BALF total protein and beta-glucuronidase activity were observed. The Survanta treatment, however, had no effect in preventing the infiltration of PMNs into the airspaces of the lungs. The results of this study indicate that artificially coating the silica with surfactant phospholipid offers short-term protection against its toxicity under both in vitro and in vivo conditions.

Analysis of Variance↗
PubMed2005

Nitric oxide and reactive oxygen species production causes progressive damage in rats after cessation of silica inhalation.

Our laboratory has previously reported results from a rat silica inhalation study which determined that, even after silica exposure ended, pulmonary inflammation and damage progressed with subsequent fibrosis development. In the present study, the relationship between silica exposure, nitric oxide (NO) and reactive oxygen species (ROS) production, and the resultant pulmonary damage is investigated in this model. Rats were exposed to silica (15 mg/m3, 6 h/day) for either 20, 40, or 60 days. A portion of the rats from each exposure were sacrificed at 0 days postexposure, while another portion was maintained without further exposure for 36 days to examine recovery or progression. The major findings of this study are: (1) silica-exposed rat lungs were in a state of oxidative stress, the severity of which increased during the postexposure period, (2) silica-exposed rats had significant increase in lung NO production which increased in magnitude during the postexposure period, and (3) the presence of silica particle(s) in an alveolar macrophage (AM) was highly associated with inducible nitric oxide synthase (iNOS) protein. These data indicate that, even after silica exposure has ended, and despite declining silica lung burden, silica-induced pulmonary NO and ROS production increases, thus producing a more severe oxidative stress. A quantitative association between silica and expression of iNOS protein in AMs was also determined, which adds to our previous observation that iNOS and NO-mediated damage are associated anatomically with silica-induced pathological lesions. Future studies will be needed to determine whether the progressive oxidative stress, and iNOS activation and NO production, is a direct result of silica lung burden or a consequence of silica-induced biochemical mediators.

Administration, Inhalation↗
PubMed1993

Lavage phospholipid concentration after silica instillation in the rat is associated with complexed [Fe3+] on the dust surface.

The basis for surfactant accumulation after silica exposure is not known. As a result of an association between elevations in extracellular surfactant and oxidant exposures, we tested the hypothesis that (1) surfactant-enriched material can function as an in vitro target for oxidants catalyzed by Fe3+ complexed to the surface of silica, and (2) in vivo alveolar accumulation of surfactant after exposure of the lower respiratory tract to silica is associated with the concentration of Fe3+ complexed to the dust surface. Surfactant-enriched material was incubated in both chemical and cellular systems with either Gey's balanced salt solution, acid-washed silica, deferoxamine-treated silica, wetted silica, or iron-loaded silica. The absorbance of oxidized products was associated with concentrations of complexed iron on the surface of the silica dust. Rats (n = 10/group) were intratracheally instilled with either normal saline, 6.0 mg acid-washed silica, 6.0 mg deferoxamine-treated silica, 6.0 mg wetted silica, or 6.0 mg iron-loaded silica. Ninety-six hours after tracheal instillation, silica significantly increased extracellular surfactant as reflected by lipid phosphorous in the total lavage fluid. Lipid accumulation was associated with concentrations of surface complexed iron on the surface of the silica.

Animals↗
PubMedDate not supplied

Silica exposure induces cytotoxicity and proliferative activity of type II pneumocytes.

The contribution of the type II pneumocyte to the pathogenesis of silicosis is largely unknown. Prominent features of silicosis are hyperplasia and hypertrophy of type II epithelial cells, often accompanied by phospholipid accumulation in the lung. The biologic regulation of these events is poorly understood. This study addresses the question of a direct effect of silica on type II pneumocytes, since direct contact of the inhaled silica dust can occur in vivo. Type II cells were isolated from fetal rat lungs and their epithelial specificity was verified. Experiments were performed on 2nd passage monolayers in 2% serum. Repair, replication, and growth activity was evaluated by the incorporation of [3H]thymidine. Cytotoxicity was measured by quantitating the release of [14C]adenine and expressed as a cytotoxicity index (CI). Type II cell proliferation and cytotoxicity were evaluated for the mineral dusts silica (SiO2), aluminum-treated silica (SiO2AlK), and titanium (TiO2). Of these mineral dusts, only low concentrations of silica increased type II cell [3H]thymidine incorporation (silica 2.5 micrograms/mL: 52% above control, P less than .05; silica 20 micrograms/mL: 57% above control, P less than .02). In addition, silica increased the cell number significantly, although to a lesser degree. Exposure of the type II epithelial cells to silica dust for 24 h resulted in dose-dependent cytotoxicity (silica 10 micrograms/mL, CI = 9.1%, P less than .0002; 250 micrograms/mL, CI = 45.1%, P less than .0001). SiO2Al completely suppressed these proliferation and cytotoxicity effects, which were then similar to those of the inert dust, TiO2. These data suggest that direct exposure and contact of the type II pneumocytes to low-dose silica dust initiated repair, replication, and growth activity, while exposure to higher silica concentrations resulted in marked cytotoxicity. Both the repair, replication, and growth and the cytotoxic responses of the type II epithelial cells to silica exposure are related to the surface properties of silica.

Animals↗