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PubMed1998

Effect of silica on phospholipase D activity in rat alveolar macrophages.

Silica may act as a stimulator of pulmonary inflammation and fibrosis. The effect of silica on phospholipase D (PLD) activity assayed as accumulation of [3H]phosphatidylethanol ([3H]PtdEt) was examined in [3H]palmitic acid-labeled primary cultures of rat alveolar macrophages. Silica induced a rapid accumulation of [3H]PtdEt in a time (0, 15, 30 and 45 min)- and concentration (0.5, 1.0, 2.5 and 5.0 mg/ml)-dependent manner indicating PLD activation. This silica-stimulated PLD activity was attenuated by the pretreatment with calcium chelator ethylene glycol-bis(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid (EGTA) or/and 1,2-bis(2-aminophenoxy)ethane-N,N,N,N-tetraacetic acid acetoxymethyl ester (BAPTA/AM) (EGTA: 54.3 +/- 8.6%, BAPTA/AM: 67.5 +/- 7.8% and EGTA + BAPTA/AM: 35.8 +/- 2.9, respectively). Also, silica-induced PLD activation was partially inhibited by the pretreatment with nonspecific phospholipase C (PLC) and PLD inhibitor (neomycin; 66.4 +/- 4.8%) or specific PLC inhibitor (U73122; 70.8 +/- 4.6%). Sphingosine as a protein kinase C (PKC) inhibitor did not change silica-induced PLD activity indicating that PKC might not play a role in PLD activation by silica. Based on these results, we concluded that a silica-stimulated phospholipase D activity is present in the rat alveolar macrophages and is predominantly regulated by PLC-mediated intracellular calcium.

Analysis of Variance↗
PubMedDate not supplied

Silica increases tumor necrosis factor (TNF) production, in part, by upregulating the TNF promoter.

Silica causes release of tumor necrosis factor (TNF) from mononuclear phagocytes. One hypothesis is that silica increases TNF production, in part, by upregulating the TNF gene. To evaluate this hypothesis, THP-1 cells (a myelomonocytic cell line) were exposed to various amounts of silica and then the TNF gene transcription was evaluated. In this study silica caused a dose-dependent increase in TNF mRNA and the peak response occurred at 3 h following stimulation. A transient transfection assay also showed that silica upregulated expression of a TNF CAT construct in THP-1 cells. Furthermore, a nuclear run-on assay demonstrated that silica particles induce increased TNF gene transcription in exposed cells. THP-1 cells cultured for various periods of time in the presence of silica released TNF into the cell supernatants. These studies show that silica can upregulate the TNF gene, which results in the release of TNF protein from the cells.

Autoimmunity↗
PubMedDate not supplied

Silica deposition in the lung during epithelial injury potentiates fibrosis and increases particle translocation to lymph nodes.

Increased respiratory disease and daily mortality rates are associated with higher levels of fine particulate air pollutants. We examined the possibility that deposition of particles to previously injured lungs might accentuate pulmonary damage, by investigating how the lung handled silica deposited during a phase of epithelial injury. A low dose of intratracheal (i.t.) bleomycin (BL) was used to induce epithelial damage in mice; 3 days later, 0.2 mg silica was instilled. Lung injury, measured by cell numbers and protein levels in bronchoalveolar lavage, was increased at 1 week and many silica particles translocated to the interstitium. At 12 weeks, the silica plus BL group showed increased pulmonary fibrosis biochemically and morphologically, and had significantly higher retained-silica content in the lung. In addition, these mice showed enlarged hilar lymph nodes with many granulomas-containing macrophages and silica. The results indicate that instillation of fine particulates to the alveoli at a time of epithelial damage potentiates the lung injury and increases translocation of particles to the interstitium. In the case of silica, deposition of particles into injured lungs resulted in increased fibrosis. The demonstration of enhanced translocation of silica to lymph nodes suggests that inhaled fine particulates may induce more distal effects following transport across an injured epithelium and subsequent entrance to the lymphatic system.

Animals↗
PubMedDate not supplied

Depletion of iron and ascorbate in rodents diminishes lung injury after silica.

Exposures of the lung to iron chelates can be associated with an injury. The catalysis of oxygen-based free radicals is postulated to participate in this injury. Such oxidant generation by mineral oxide particles can be dependent on availability of both iron and a reductant. We tested the study hypothesis that lung injury after silica is associated with the availability of both iron and ascorbate in the host by depleting this metal and reductant in the lungs of rats and guinea pigs, respectively. Rats were fed either a normal diet or a diet deficient of iron. After 30 days, animals were instilled with either saline or 1.0 mg Minusil-5 silica. Relative to saline, silica significantly increased neutrophils and lavage protein. Iron depletion significantly diminished both the cellular influx and injury but only at 1 week after silica exposure. Guinea pigs were provided either a normal diet supplemented with 1,000 ppm vitamin C or a diet deficient in ascorbate. After 14 days, the guinea pigs were instilled with either saline or 1.0 mg silica. Silica exposure significantly increased neutrophils and lavage protein. Ascorbate depletion significantly diminished the influx of inflammatory cells and injury at both 1 day and 1 week after silica exposure. We conclude that host concentrations of both iron and ascorbate can affect lung injury after silica exposure.

Animals↗
PubMed1989

Fibroblast inhibition and prostaglandin secretion by alveolar epithelial cells exposed to silica.

The possibility that the interaction of silica with the alveolar epithelium can produce factors that alter fibroblast activity in the lung is investigated. Isolated type 2 cells, which were attenuated after a few days in culture, were then exposed to doses of silica from 50 to 200 micrograms/ml for 24 hours. Silica particles were found in the epithelial cell cytoplasm without causing cell necrosis. Subsequently, serum-free supernatants of these epithelial cells were collected over 4 hours and tested on fibroblast growth and collagen production. Growth of quiescent fibroblasts was not stimulated, whereas proliferation of rapidly growing cells was inhibited by supernants of type 2 cells exposed to silica at doses of 100 micrograms/ml and above; proline incorporation into collagen was also significantly reduced. Silica exposure resulted in a 6-fold greater secretion of prostaglandin E2 by type 2 cells as shown by radioimmunoassay, and the fibroblast growth inhibition was eliminated by treating the epithelial cells with indomethacin at the time of silica exposure. These results demonstrate that, in response to silica, alveolar epithelial cells secrete a factor(s) that that inhibits fibroblast growth and collagen synthesis. The high level of prostaglandin E2 found in epithelial cell supernants after silica suggests that this molecule is involved in fibroblastic control in the lung.

Animals↗
PubMed1989

[Effect of filler system on the mechanical properties of light-cured composite resins. I. Effect of various types of silica fillers on the mechanical properties of the composite resins].

To investigate the effect of silica fillers on the mechanical properties of visible light-cured composite resins, Bis-GMA-based composites with four types of silica fillers were prepared. The mechanical properties of the composites with splinter-shaped silica fillers increased with increasing the filler fraction. Although the spherical silica filler could be filled more with resin monomer than the splinter-shaped silica filler, the mechanical properties of spherical silica-filled composite were relatively lower than those of the composite with splinter-shaped silica fillers. The micro particle silica-filled composite showed no obvious increase in the mechanical properties in either the dry or wet conditions. SEM observations of the fractured resin surface revealed that fracture occurred through the resin matrix as well as the resin/filler interface and the mechanical properties of each composite resin were correlated with the nature of crack propagation.

Composite Resins↗
PubMed1989

Effect of silica treatment on histopathology of intestinal & hepatic amoebiasis in murine model.

Histopathological changes in intestinal and hepatic amoebiasis were studied in Swiss albine mice with and without silica pretreatment. The intestinal infection rate was higher in silica treated mice (83%) as compared to non-silica treated mice (33%). Histologically all the silica treated mice had caecal ulceration which tended to spread across the muscularis propria into the serosal layer. The hepatic lesions were observed grossly in 100 and 60 per cent mice with and without silica treatment, respectively. However, the liver lesions in the silica treated mice were more severe, leading to satellite abscesses and in some cases the capsule ruptured leading to adhesions to the diaphragm and peritoneum. Histologically, the blockade of histiocytes with silica resulted in mainly a neutrophilic damage which was extensive and widespread. It also destroyed the amoeba and led to abundant fibrosis. In the non-silica group the damage was slow and devoid of neutrophils with quicker healing and lack of fibrosis resembling human hepatic lesions.

Animals↗
PubMed1982

Influence of silica and carrageenan on spleen colonies and colonies in murine peritoneal cell-coated cellulose acetate membranes.

Cellulose acetate (CA) discs placed in the peritoneum of mice become coated by a layer of peritoneal cells consisting primarily of macrophages (M). These CAM support the growth of hematopoietic colonies when syngeneic bone marrow cells are injected intraperitoneally. Most of these colonies are granulocytic and are recognizable by their peroxidase reaction. Since silica and carrageenan are known to reduce macrophage function, their effect on CAM granulocyte colony formation was tested. Carrageenan injected intraperitoneally before, concurrently, or after injection of marrow cells markedly reduced colony formation. Silica injected intraperitoneally concurrently or after injection of marrow cells reduced colony formation. Silica injected before marrow cells did not reduce colony formation. CAM produced in one mouse and exposed to carrageenan or silica in situ for 24 h before being transferred to sublethally irradiated recipients and seeded by injection of marrow cells had control levels of granulocytic colonies. Likewise, CAM produced in one mouse, removed, incubated in vitro with carrageenan or silica, carefully rinsed and transferred to sublethally irradiated recipients and seeded with marrow cells were able to support control levels of colony formation. Intravenous injection of silica or carrageenan had no consistent effect on colony formation. Spleen colonies (CFU-S) from marrow cells incubated in vitro with the agents, and given intravenously to lethally irradiated mice, were inhibited by silica, but not by carrageenan. Silica or carrageenan given intravenously to irradiated mice 3 h before or 3 h after intravenous marrow cell injection enhanced subsequent CFU-S formation.

Animals↗
PubMed1995

Differential pulmonary responses in rats inhaling crystalline, colloidal or amorphous silica dusts.

Pulmonary responses in rats were compared after short-term inhalation exposure to polymorphs of silica dust. Groups of CD rats were exposed 6 h a day for 3 d to crystalline silica or amorphous silica. Another group was exposed to Ludox colloidal silica for 6 h a day, 5 d a week for two or four weeks. Thereafter the groups were killed, and the lungs washed at several postexposure times. The crystalline silica produced persistent pulmonary inflammatory responses characterized by neutrophil recruitment and consistently elevated biomarkers of cytotoxicity in bronchoalveolar lavage fluids, and progressive histopathological lesions were observed within one month of the exposure. Amorphous silica produced a transient pulmonary inflammatory response, and Ludox elicited transient pulmonary inflammatory responses at 50 or 150 mg center dot m-3 but not at 10 mg center dot m-3. After three months most of the biochemical values of the Ludox-exposed animals had returned to the control level. These results demonstrate that crystalline silica dust is more potent in producing pulmonary toxicity when compared with amorphous or colloidal silica particles.

Administration, Inhalation↗
PubMed2001

Application of zirconium-modified silica gel as a stationary phase in the ion-exclusion chromatography of carboxylic acids. II. Separation of aliphatic carboxylic acids with pyromellitic acid as eluent and with suppressed conductimetric detection.

The application of zirconium-modified silica gels (Zr-Silica) as stationary phases for ion-exclusion chromatography with conductimetric detection (IEC-CD) for C1-C8 aliphatic carboxylic acids (formic, acetic, propionic, butyric, valeric, caproic, heptanoic and caprylic acids) was carried out using pyromellitic acid as the eluent. Zr-Silicas were prepared by the reaction of the silanol group on the surface of silica gel with zirconium tetrabutoxide [Zr(OCH2CH2CH2CH3)4] in ethanol solution. An ASRS-Ultra anion self-regenerating suppressor in the K+ form was used for the enhancement of conductimetric detector response of these aliphatic carboxylic acids. A Zr-Silica adsorbed on 10 mg zirconium g(-1) silica gel was the most suitable stationary phase in IEC-CD for the separation of these aliphatic carboxylic acids. Excellent simultaneous separation and highly sensitive detection for these aliphatic carboxylic acids were achieved in 25 min by IEC-CD with the Zr-Silica column (250x4.6 mm I.D.) and a 0.2 mM pyromellitic acid containing 0.15% heptanol as the eluent.

Benzoates↗
PubMedDate not supplied

Thermal analysis of the plant encapsulation-dehydration cryopreservation protocol using silica gel as the desiccant.

The encapsulation-dehydration cryopreservation protocol is critically dependent upon the evaporative desiccation step, which must optimise survival with the retention of glass stability on sample cooling and rewarming. Desiccation is usually achieved evaporatively by drying in a sterile airflow. However, chemical desiccation using silica gel has advantages for laboratories that do not have environmental control and/or which are exposed to high relative humidities and risks of microbial contamination. This study characterised thermal profiles of silica gel-desiccated encapsulated shoot-tips of two Ribes species using Differential Scanning Calorimetry. For both species silica gel-desiccation at 16 degrees C for 5 h decreased bead water content from ca. 75 to 28% fresh weight (3.8 to 0.4 g x g(-1) dry weight); further desiccation (for 6 and 7 h) reduced the bead water content to 21% (0.3 g x g(-1) dry weight). These changes in water status altered the thermal properties of beads for both species. After 7 h desiccation over silica gel stable glass transitions were observed on both cooling and rewarming of beads containing meristems. Tg mid-point temperatures ranged from -78 to -51 degrees C (cooling) and from -88 to -54 degrees C (warming) [at cooling and warming rates of 10 and 5 degrees C min(-1), respectively] after 5 to 7 h silica gel-desiccation. Post-cryopreservation viability of both species was ca. 63%. Thermal analysis studies revealed that an encapsulation/dehydration protocol using silica gel as a desiccant should comprise a minimum 5 h drying (at 16 degrees C). This reduces bead moisture content to a critical point (ca. 0.4 g x g(-1) dry weight) at which stable glasses are formed on cooling and rewarming. It is concluded that silica gel has advantages for use as a desiccant for alginate-encapsulated plant meristems by promoting stable vitrification and is useful in laboratories and/or geographical locations where environmental conditions are not under stringent control.

Cell Survival↗
PubMed1997

Molecular orbital models of ring expansion mechanisms in the silica-carbon monoxide system.

The development of a zero net shrinkage dental restorative material based upon a polymer-bioactive glass composite requires a second-phase material that expands. This study details the mechanisms of silica ring expansion by reaction with carbon monoxide. Carbon monoxide was used as a model adduct to represent potentially active sites on the polymer phase of the dental restorative. Silica rings were used to model the bioactive-glass phase of the composite. The 3-, 4-, 5-, and 6-"member" silica rings have been modeled using the Austin Method (AM1) semi-empirical molecular orbital calculations. The reaction pathways were determined for carbon monoxide (CO) reaction addition to each of the rings. The activation barriers (Ea) for the ring expansions were determined from the transition state geometries wherein only one imaginary eigenvalue in the vibration spectrum existed (a true saddle point). In each case the reaction pathway included the hydrogen bonding of CO with a silicon, exothermic pentacoordinate bonding to silicon by the CO and weakening of the Si-O bridging bonds of the ring, and, finally, the incorporation of CO into the ring, forming a silica-carbonate ring. The activation for the ring expansions are +4.3, +6.1, +7.0, and -2.9 Kcal/mol for 3-, 4-, 5-, and 6-"member" silica rings, respectively. The volumetric expansion of the silica was estimated based upon the dilation of adjacent silicon-silicon atomic distances. The dimensional change was calculated to be 3.9%, 21.3%, 19.4%, and 24.2% for 3-, 4-, 5-, and 6-membered silica-carbonate rings, respectively.

Biocompatible Materials↗
PubMed1999

Sol-gel-processed sintered silica xerogel as a carrier in controlled drug delivery.

Sol-gel-processed sintered silica xerogel was studied as a controllable, dissolvable, implantable material. The erosion of the matrix and the release of the preadsorbed drug toremifene citrate was investigated both in vitro and in vivo using mice. In an in vitro dissolution study, 50 to 60% of the drug was released after 24 h, according to the square root of time kinetics, and the weight loss of the silica was 24 wt %. Silica xerogel with tritium-labeled toremifene was implanted subcutaneously in mice for 56 days. To determine the amount of tritiated drug remaining in the silica disks at the implantation site, the disks were excised periodically and the radioactivity measured. About 40% of the radioactivity was released during the first 4 days and all of it within 28 days. Radioactivity also was measured in the liver, lungs, kidneys, uterus, and blood. The radioactivity reached a maximum level after 4 days in the liver, kidneys, and lungs and slowly decreased until all of the drug had been released from the matrix after 28 days. After release of the drug (28 days) the amount of remaining silica xerogel implant was 45 wt %, and at the end of the study (56 days) it was 24 wt %. In the histopathological study, sintered silica xerogel did not show any tissue toxicity at the site of the implantation, in the liver, or in the kidneys. It was concluded that sintered silica xerogel is a biocompatible and controllably resorbable material and therefore is a promising matrix for use in the sustained delivery of drugs.

Animals↗
PubMedDate not supplied

Separation of porphyrins by capillary electrophoresis in fused-silica and ethylene vinyl acetate copolymer capillaries with visible absorbance detection.

A mixture of 5 porphyrins were separated by capillary electrophoresis. A UV-VIS detector was used to detect the separated components. Separation was performed in 2 types of capillaries, i.e. fused-silica and ethylene vinyl acetate copolymer (EVA) plastic capillaries. The concentration limit of detection (CLOD), mass limit of detection (MLOD), and relative standard deviations (RSD) of migration time and area were investigated. LOD was comparable to that of epi-fluorescence detection. LOD was lower when separation was performed in EVA capillary compared to fused-silica capillary. RSD of migration times of the porphyrins when separated in fused-silica capillary ranges between 0.5 to 1.6% and in EVA capillary ranges between 0.3 to 1.2%. Area RSD in fused-silica capillary ranges between 7 to 20% and in EVA capillary ranges between 4.7 to 12.3%. Urine spiked with porphyrins was also analysed by CE using fused-silica and EVA capillaries. Analysis of urine sample spiked with porphyrins showed that stacking effect of porphyrins was observable only in fused-silica and not in EVA capillary. This led to similar LOD in fused-silica capillary to those for EVA capillary.

Electrophoresis, Capillary↗
PubMed2001

Respiratory effects of exposure to low levels of concrete dust containing crystalline silica.

BACKGROUND: Dusts containing crystalline silica are generated in mining, construction, glass, granite and concrete production industries. The association between exposure to low levels of concrete dust containing crystalline silica and reduction in lung function, was evaluated in a cross-sectional study. METHODS: The study was carried out among 144 concrete workers, from two factories, with exposure assessment of respirable dust and silica by personal samplers. Results of respiratory questionnaires and standardized measurements of lung function were compared with the results in a control population. Multiple linear regression analysis was used in selecting factors that predict (age and standing height standardized residual) lung function. RESULTS: The average concentration of respirable dust in both factories was 0.8 mg/m(3) and 0.06 mg/m(3) for respirable silica. The average silica content of the dust was 9%. The average cumulative dust exposure was 7.0 mg/m(3) year and cumulative silica exposure was 0.6 mg/m(3) year. Significant associations between exposure to concrete dust and a small lung function (FEV(1)/FVC ratio, MMEF) loss were found, independent of smoking habits and of a history of allergy. CONCLUSIONS: Our results indicate that, concrete workers with chronic obstructive pulmonary symptoms and/or work-related lower respiratory symptoms are at risk of having a reduction in lung function (FEV&(1)/FVC ratio) outside the 5th percentile of the external reference population, and therefore, of mild chronic obstructive pulmonary disease, at respirable concrete dust levels below 1 mg/m(3) with a respirable crystalline silica content of 10% (TWA, 8 hr).

Adult↗
PubMed2005

Risk of silicosis in cohorts of Chinese tin and tungsten miners and pottery workers (II): Workplace-specific silica particle surface composition.

BACKGROUND: It is hypothesized that surface occlusion by alumino-silicate affects the toxic activity of silica particles in respirable dust. In conjunction with an epidemiological investigation of silicosis disease risk in Chinese tin and tungsten mine and pottery workplaces, we analyzed respirable silica dusts using a multiple-voltage scanning electron microscopy-energy dispersive X-ray spectroscopy (MVSEM-EDS). METHODS: Forty-seven samples of respirable sized dust were collected on filters from 13 worksites and were analyzed by MVSEM-EDS using high (20 keV) and low (5 keV) electron beam accelerating voltages. Changes in the silicon-to-aluminum X-ray line intensity ratio between the two voltages are compared particle-by-particle with the 90th percentile value of the same measurements for a ground glass homogeneous control sample. This provides an index that distinguishes a silica particle that is homogeneously aluminum-contaminated from a clay-coated silica particle. RESULTS: The average sample percentages of respirable-sized silica particles alumino-silicate occlusion were: 45% for potteries, 18% for tin mines, and 13% for tungsten mines. The difference between the pottery and the metal mine worksites accounted for one third of an overall chi-square statistic for differences in change in measured silicon fraction between the samples. CONCLUSION: The companion epidemiological study found lower silicosis risk per unit cumulative respirable silica dust exposure for pottery workers compared to metal miners. Using these surface analysis results resolves differences in risk when exposure is normalized to cumulative respirable surface-available silica dust.

Ceramics↗
PubMed2006

Continued exposure to silica after diagnosis of silicosis in Brazilian gold miners.

BACKGROUND: There is a paucity of studies analyzing the effect of continued silica exposure after the onset of silicosis with regard to disease progression. The present study investigates differences in clinical and radiological presentation of silicosis among former workers with a diagnosis of silicosis, and compares workers who continued to be exposed to silica with those who stopped silica exposure after having received their diagnosis. METHODS: A sample of 83 former gold miners with a median of 21 years from the first diagnoses of silicosis, had their clinical and occupational histories taken and underwent both chest radiography (International Labor Organization standards) and spirometry. Their silica exposure was assessed and an exposure index was created. The main outcome was the radiological severity of silicosis and tuberculosis (TB). The statistical analysis was done by multiple logistic regression. RESULTS: Among the 83 miners, 44 had continued exposed to silica after being diagnosed with silicosis. Continuation of silica exposure was associated with advanced radiological images of silicosis (X-ray classification in category 3, OR = 6.42, 95% CI = 1.20-34.27), presence of coalescence and/or large opacities (OR = 3.85, CI = 1.07-13.93), and TB (OR = 4.61, 95% CI = 1.14-18.71). CONCLUSIONS: Differential survival is unlikely to explain observed differences in silicosis progression. Results reinforce the recommendation that silica exposure should be halted at an early stage whenever X-ray is suggestive of the disease.

Adult↗
PubMed2002

Occupational exposure to crystalline silica and risk of systemic lupus erythematosus: a population-based, case-control study in the southeastern United States.

OBJECTIVE: Crystalline silica may act as an immune adjuvant to increase inflammation and antibody production, and findings of occupational cohort studies suggest that silica exposure may be a risk factor for systemic lupus erythematosus (SLE). We undertook this population-based study to examine the association between occupational silica exposure and SLE in the southeastern US. METHODS: SLE patients (n = 265; diagnosed between January 1, 1995 and July 31, 1999) were recruited from 4 university rheumatology practices and 30 community-based rheumatologists in 60 contiguous counties. Controls (n = 355), frequency-matched to patients by age, sex, and state of residence, were randomly selected from driver's license registries. The mean age of the patients at diagnosis was 39 years; 91% were women and 60% were African American. Detailed occupational and farming histories were collected by in-person interviews. Silica exposure was determined through blinded assessment of job histories by 3 industrial hygienists, and potential medium- or high-level exposures were confirmed through followup telephone interviews. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated by logistic regression. RESULTS: More patients (19%) than controls (8%) had a history of medium- or high-level silica exposure from farming or trades. We observed an association between silica and SLE (medium exposure OR 2.1 [95% CI 1.1-4.0], high exposure OR 4.6 [95% CI 1.4-15.4]) that was seen in separate analyses by sex, race, and at different levels of education. CONCLUSION: These results suggest that crystalline silica exposure may promote the development of SLE in some individuals. Additional research is recommended in other populations, using study designs that minimize potential selection bias and maximize the quality of exposure assessment.

Adolescent↗