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PubMedDate not supplied

Influence of aluminum treatments on pulmonary retention of quartz in sheep silicosis.

Previous experiments with the sheep model of silicosis have demonstrated a reduction of the pathological activity of quartz after treatments with aluminum lactate (Al-lac), such as Al-lac pretreatment of intratracheally injected quartz or Al-lac inhalation of quartz-exposed animals. Preliminary data also suggested a more effective alveolar clearance of quartz treated with Al-lac. The present study was undertaken to fully document the effect of Al-lac treatments on the pulmonary retention of quartz. Sheep (on average, 27 per group) received a single injection in the tracheal lobe of either 100 mg/100 mL of alpha-quartz, 100 mg/100 mL of alpha-quartz followed by Al-lac inhalations at 1-month intervals, or 100 mg/100 mL of alpha-quartz Al-lac pretreated in vitro. Samples of lung parenchyma were analyzed at 2, 6, and 10 months after the injection. The quartz concentration in each sample was measured using the X-ray diffraction method. The concentrations were expressed in micrograms of quartz per milligram of dry lung parenchyma. The geometric mean concentrations in each of the three groups at 2 months were statistically different (ANOVA of the log values; p = .016) as well as at 6 months (ANOVA of the log values; p = .001). Al-lac clearly reduced the pulmonary retention of quartz. Both modalities of Al delivery were equally effective in clearing quartz up to 2 months, which may explain the documented reduction in pathological activities after in both forms of therapy. However, quartz soaked in Al-Lac solution was more effective than inhalation of Al-lac after quartz exposure. The half-life of both native quartz and quartz Al-lactate inhaled was 5.05 and 4.99 months, respectively, while it was 3.1 months for Al-treated quartz. Al-lac inhalations after the second month of exposure do not significantly affect the rate of clearance of deposited quartz.

Animals↗
PubMed2001

The quartz hazard: effects of surface and matrix on inflammogenic activity.

Modification of the quartz surface during the history of the particle is a powerful idea in understanding the variability of the quartz hazard. Interactions between quartz and other minerals are likely to occur in sediments, during industrial processing, or in matrix-bound quartz. We discuss new evidence regarding the basis of changes in the quartz surface that relate to changes in its ability to cause inflammation. Different samples of quartz were subjected to various biological assays. Endpoints included instillation of quartz into the tracheobronchial tree and measurement of PMN numbers in bronchoalveolar lavage (BAL) and in lung tissue, levels of the chemokine MIP-2 in BAL, and nuclear translocation of the transcription factor NF-kappaB in BAL cells. In vitro biological assays included cytotoxicity to epithelial cells, hemolytic activity, and radical activity of the particle surface as measured by electron spin resonance. Treatment of quartz with aluminium lactate impaired its ability to cause PMN recruitment, chemokine release, and NF-kappaB nuclear translocation in BAL. Workplace quartzes had no proinflammatory activity, which correlated with their ability to cause hemolysis but not their electron spin resonance (ESR) activity. Quartz in a matrix with coalmine dust or fly-ash showed different effects. In fly-ash, the toxicity was masked, but coalmine dusts were more toxic to epithelial cells than pure quartz in vitro; however, after instillation, the long-term inflammation was not related to the in vitro activity. Amelioration of quartz surface activity can occur in workplace samples of quartz and quartz samples whose surface is protected, to the extent that they have very little inflammogenic activity and display an inability to activate key subcellular pathways that lead to inflammation. Quartz from a workplace whose surface has been affected, or in a matrix such as coalmine dust or fly-ash, can have its toxicity modulated. These effects are due to minerals and organic compounds that can both decrease (e.g., aluminium salts) or enhance (e.g., coalmine dust matrix) biological activity and thus may contribute to toxicity in a complex way that is not easily predicted. Iron is a good example. There are reports that it can enhance quartz toxicity, or it may have little role to play in its toxicity, as shown here for almost pure quartz particles. A broad program of further research is needed before we have a sound understanding of the mechanisms of quartz toxicity.

Air Pollutants, Occupational↗
PubMed2002

Pulmonary inflammation in rats after intratracheal instillation of quartz, amorphous SiO2, carbon black, and coal dust and the influence of poly-2-vinylpyridine-N-oxide (PVNO).

Effects of poly-2-vinylpyridine-N-oxide (PVNO) were investigated in numerous in vivo and in vitro studies published in the nineteen sixties and seventies. These studies showed that PVNO inhibited development of fibrosis from quartz dust and improved lung clearance of quartz after inhalation exposure. Ameliorating effects of PVNO were observed also for pulmonary damage from colloidal SiO2 and organic substances, and the fibrogenic inflammation caused by carrageenan. Although it is not proven that silicosis is a precondition for quartz-induced lung tumours, we investigated the hypothesis that PVNO could reduce the lung tumour risk from quartz in rats. A carcinogenicity study was therefore started in rats with the main focus on the quantitative relationships among pulmonary inflammation, fibrosis and neoplasia caused by intratracheal instillation of 3 mg quartz DQ 12 with or without additional subcutaneous PVNO treatment. Other study groups were treated with multiple dust instillations, i.e. 30 instillations of 0.5 mg amorphous SiO2 at intervals of 2 weeks, 10 instillations of 0.5 mg of ultrafine carbon black or 1 mg coal at weekly intervals. The analyses of the bronchoalveolar lavage fluid (BALF) 9 months after start of the life-time study showed that the aim of producing similar levels of increased enzyme concentrations in the four groups treated with quartz/PVNO, amorphous SiO2, carbon black and coal was achieved. A 2.5- to 7.7-fold increase for lactate dehydrogenase (LDH), total protein, alkaline phosphatase and gamma-glutamyl transferase (gamma-GT) was found in these groups as compared to the control. In contrast, quartz treatment without PVNO increased the LDH level up to 24-fold and of total protein to 13-fold. However, the cell counts in the BALF were not so much different in all five groups, i.e. quartz without PVNO (leukocytes: 480.000, PMN: 190.000), quartz with PVNO (leukocytes: 300.000, PMN: 100.000), amorphous SiO2 (leukocytes: 570.000, PMN: 315.000), carbon black (leukocytes: 390.000, PMN: 150.000) and coal (leukocytes: 200.000, PMN: 65.000). Histopathological investigations after four weeks and three months revealed that the used PVNO sample was active in the quartz and amorphous SiO2 groups and markedly reduced the incidences or severity of several pulmonary changes such as macrophage accumulation, inflammatory cell infiltration, interstitial fibrosis, bronchiolo-alveolar hyperplasia, alveolar lipoproteinosis and amorphous SiO2 -induced granulomatous alveolitis/interstitial fibrotic granulomas. Also in the lung-associated lymph nodes (LALN), PVNO treatment significantly reduced the incidence and severity of inflammation in both quartz and amorphous SiO2 groups as evidenced by the presence of well-circumscribed aggregates of intact particle-laden macrophages without signs of degeneration and accompanying granulocytic infiltration and fibrosis. Immunological investigations at the 9 months timepoint on the in vitro production of reactive nitrogen (RNI) or oxygen (ROI) intermediates and tumour necrosis factor (TNF-alpha) from BALF-derived cells indicated a diminished responsiveness to LPS in all particle treatment groups. A diminished production of ROI was also found in the quartz, carbon black, and coal dust groups, respectively, as compared to the values seen in the quartz/PVNO- and amorphous SiO2 treated groups. Treatment with quartz plus PVNO restored the capability of the cells to respond to LPS as compared to the treatment with quartz alone. TNF-alpha production was diminished in the groups treated with quartz, carbon black, and coal dust alone whereas in the quartz/PVNO- and amorphous SiO2-treated groups an elevated TNF-alpha production was seen. These results led to the conclusion that only amorphous SiO2 did not affect the "normal" ability of the cells to respond to LPS and that PVNO protected the cells from a toxic effect of the quartz particles.

Animals↗
PubMed1990

Immunomodulation in mineral dust-exposed lungs: stimulatory effect and interleukin-1 release by neutrophils from quartz-elicited alveolitis.

Quartz deposition in the rat lung causes an intense and persistent neutrophil alveolitis leading to parenchymal fibrosis. Bronchoalveolar leucocytes (BAL) from quartz-exposed rat lungs were studied for their effects on splenic lymphocyte proliferation; titanium dioxide (TiO2) was used as a control, non-fibrogenic dust. Seven days after the intratracheal instillation of 1 mg of quartz or TiO2 suspended in phosphate-buffered saline (PBS), BAL were recovered by lavage; the effect of PBS alone was also studied. TiO2-elicited BAL (macrophages greater than 98%) inhibited splenocytes responding to suboptimal phytohaemagglutinin (PHA) more than PBS-elicited BAL (macrophages greater than 98%); the effect was dependent on the BAL:splenic lymphocyte ratio. Quartz-elicited whole BAL (macrophages 49%, neutrophils 51%), and an alveolar macrophage-enriched population with purity of 87% separated from it, were less inhibitory to splenocyte mitogenesis than PBS-elicited BAL. A neutrophil-enriched population, with a purity of 80%, markedly enhanced splenocyte response to PHA. In addition, whole quartz BAL and the macrophage-enriched population obtained from it enhanced the mitogenesis of T cell-enriched lymphocytes at a much lower BAL:lymphocyte ratio. The neutrophil-enriched quartz BAL enhanced mitogenesis substantially more than the whole or macrophage-enriched population from quartz-exposed lung. Supernatants from normal macrophages, PBS BAL, TiO2 BAL, quartz BAL and both alveolar macrophage and neutrophil-enriched quartz populations were assessed for interleukin-1 (IL-1) activity. Quartz-BAL, quartz macrophages and quartz neutrophils all produced significantly higher IL-1 levels than PBS BAL; the supernatants from quartz neutrophils, however, showed the highest IL-1 activity. These findings suggest that quartz-elicited bronchoalveolar leukocytes, especially neutrophils, enhance lymphocyte proliferation and that increased IL-1 secretion by these cells is likely to be the effector molecule involved. These findings have important implications for immune response in mineral dust-stimulated lung and for inflammatory lung disease in general.

Animals↗
PubMed1998

Quartz exposure in the slate industry in northern Norway.

In this study we have measured exposure levels to quartz in different parts of the slate industry in Alta, Northern Norway. Full shift personal samples were collected from the breathing zones of outdoor and indoor workers in the slate quarries and a slate factory. The quartz content of respirable dust was between 7 and 41%. The slate factory had the lower quartz levels although 41% of total and 73% of respirable samples were above the Norwegian TLV for quartz. The average concentration of total quartz in the slate factory was 0.27 mg/m3 and the average concentration of respirable quartz was 0.12 mg/m3. Outdoor in the quarries the average levels of quartz were 0.58 and 0.13 mg/m3 for total and respirable quartz, respectively. From the beginning of the last decade most of the quarry-workers have built quarry halls to protect themselves against a cold winter climate. Inside in these quarry halls the average levels were 1.74 mg/m3 total quartz and 0.46 mg/m3 respirable quartz. Assessment of historical exposure showed that 32 of totally 45 quarry workers with available exposure history had a lifetime inhaled quartz dose of more than 10 g. There is reason to fear that silicosis will be an increasing problem among quarry workers if efforts to reduce quartz exposure are not put into effect.

Air Pollution↗
PubMed2006

Pulmonary bioassay studies with nanoscale and fine-quartz particles in rats: toxicity is not dependent upon particle size but on surface characteristics.

Pulmonary toxicology studies in rats demonstrate that nanoparticles are more toxic than fine-sized particles of similar chemistry. This study, however, provides evidence to contradict this theory. The aims of the study were (1) to compare the toxicity of synthetic 50 nm nanoquartz I particles versus (mined) Min-U-Sil quartz ( approximately 500 nm); the toxicity of synthetic 12 nm nanoquartz II particles versus (mined) Min-U-Sil ( approximately 500 nm) versus (synthetic) fine-quartz particles (300 nm); and (2) to evaluate the surface activities among the samples as they relate to toxicity. Well-characterized samples were tested for surface activity and hemolytic potential. In addition, groups of rats were instilled with either doses of 1 or 5 mg/kg of carbonyl iron (CI) or various alpha-quartz particle types in phosphate-buffered saline solution and subsequently assessed using bronchoalveolar lavage fluid biomarkers, cell proliferation, and histopathological evaluation of lung tissue at 24 h, 1 week, 1 month, and 3 months postexposure. Exposures to the various alpha-quartz particles produced differential degrees of pulmonary inflammation and cytotoxicity, which were not always consistent with particle size but correlated with surface activity, particularly hemolytic potential. Lung tissue evaluations of three of the quartz samples demonstrated "typical" quartz-related effects--dose-dependent lung inflammatory macrophage accumulation responses concomitant with early development of pulmonary fibrosis. The various alpha-quartz-related effects were similar qualitatively but with different potencies. The range of particle-related toxicities and histopathological effects in descending order were nanoscale quartz II = Min-U-Sil quartz > fine quartz > nanoscale quartz I > CI particles. The results demonstrate that the pulmonary toxicities of alpha-quartz particles appear to correlate better with surface activity than particle size and surface area.

Animals↗
PubMed1995

Freshly fractured quartz inhalation leads to enhanced lung injury and inflammation. Potential role of free radicals.

Silicosis is a devastating pulmonary disease that continues to occur in industrial workplaces. Its pathogenesis is under critical evaluation, and this report provides new concepts on the possible early events that occur in lungs resulting from the inhalation of freshly fractured versus aged quartz in the development of two diverse disease entities. In this study, we evaluated the biochemical and pathologic changes in the lavagate and lungs of rats exposed to freshly fractured quartz (generated by jet milling), aged quartz (milled then aged for 2 mo prior to use), or clean air 5 h a day for 10 d over a 2-wk period. The concentration of crystalline quartz in the chambers averaged 20 mg/m3. Particle concentrations and particle size were similar for the freshly milled and aged quartz exposures. However, free radical concentrations associated with the freshly milled quartz samples were significantly higher than those for aged quartz. After a 2-wk exposure, animals were killed and studied by bronchoalveolar lavage and pulmonary histopathology. Inhalation of aged quartz increased the number of bronchoalveolar lavage cells, demonstrated histopathologic evidence of increased pulmonary infiltrates, showed enhanced concentrations of biochemical markers of lung injury, increased lipid peroxidation, and the ability of pulmonary phagocytes to produce more oxygen radicals. In general, all these pulmonary responses were significantly more pronounced after inhalation of freshly fractured quartz compared with aged quartz. In contrast, antioxidant enzymes showed decreased concentrations in the freshly fractured quartz-exposed group compared with the aged quartz-exposed animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Interleukin-10 regulates quartz-induced pulmonary inflammation in rats.

Interleukin-10 (IL-10) can downregulate expression of several proinflammatory cytokines including chemokines. This study investigated the role of IL-10 in the acute response of the rat lung to quartz particles. Intratracheal instillation of rats with 1 mg of quartz produced an inflammatory and cytotoxic response demonstrated by increased bronchoalveolar lavage (BAL) fluid neutrophils, lactate dehydrogenase, and protein. IL-10 was detected in rat lung, but IL-10 levels were not altered by quartz. In contrast, quartz increased lung levels of the chemokine macrophage inflammatory protein-2 (MIP-2). Treatment with recombinant murine IL-10 (rmIL-10) attenuated quartz-induced pulmonary inflammation and injury. Pretreatment with anti-IL-10 antiserum enhanced inflammatory responses to quartz. Consistent with effects on quartz-induced inflammation, rmIL-10 and anti-IL-10 serum decreased and increased, respectively, lung MIP-2 mRNA and protein in response to quartz. Additionally, rmIL-10 reduced production of hydrogen peroxide, superoxide anion, and nitric oxide by BAL cells from quartz-exposed and control rats. These results demonstrate that IL-10 is expressed in rat lung and downregulates quartz-induced inflammation and cell activation. The mechanism of the anti-inflammatory action of IL-10 after quartz administration involves, at least in part, attenuation of MIP-2 expression.

Animals↗
PubMed1997

Augmentation of pulmonary reactions to quartz inhalation by trace amounts of iron-containing particles.

Fracturing quartz produces silica-based radicals on the fracture planes and generates hydroxyl radicals (.OH) in aqueous media. .OH production has been shown to be directly associated with quartz-induced cell damage and phagocyte activation in vitro. This .OH production in vitro is inhibited by desferrioxamine mesylate, an Fe chelator, indicating involvement of a Fenton-like reaction. Our objective was to determine if Fe contamination increased the ability of inhaled quartz to cause inflammation and lung injury. Male Fischer 344 rats were exposed 5 hr/day for 10 days to filtered air, 20 mg/m3 freshly milled quartz (57 ppm Fe), or 20 mg/m3 freshly milled quartz contaminated with Fe (430 ppm Fe). High Fe contamination of quartz produced approximately 57% more reactive species in water than quartz with low Fe contamination. Compared to inhalation of quartz with low Fe contamination, high Fe contamination of quartz resulted in increases in the following responses: leukocyte recruitment (537%), lavageable red blood cells (157%), macrophage production of oxygen radicals measured by electron spin resonance or chemiluminescence (32 or 90%, respectively), nitric oxide production by macrophages (71%), and lipid peroxidation of lung tissue (38%). These results suggest that inhalation of freshly fractured quartz contaminated with trace levels of Fe may be more pathogenic than inhalation of quartz alone.

Administration, Inhalation↗
PubMed1987

Sustained efficacy of aluminum to reduce quartz toxicity in the lung.

In a recent study of the sheep tracheal lobe model, we have demonstrated that surface chemistry modification of quartz by aluminum lactate significantly alters the biological activity of quartz for at least 2 months after exposure. In the present study, we have extended our observations of the biological reaction of the lung tissue to aluminum treated quartz and to untreated quartz, added lung lavage analyses of surfactant and glycosaminoglycans as additional indicators of activity of the quartz-induced lung injury and analyzed lung lavage and tissue retention of the minerals. The tracheal lobe of 8 sheep was exposed to either 11 mg of aluminum lactate in 100 ml saline (Al group), 100 mg of quartz (Minusil-5) in 100 ml saline (Si group) or 100 mg of quartz treated with 11 mg of Al lactate in 100 ml saline (Si-Al group). The 24 sheep were studied by lung lavage at month 9, 0.13, 1, 2, 3, 5, 7, 9, and 10 and by autopsy at month 10. In the Al group, we found no significant change over time, the pathologic score was 0.38 +/- 0.15 and Si undetectable. In the Si group, we found significant sustained increases in total lavage cells, macrophages, lymphocytes, neutrophils, glycosaminoglycans, lactate dehydrogenase, phosphatidylcholine and phosphatidylglycerol. Histologically we found a macrophagic lymphocytic alveolitis with early nodular silicotic lesions; the pathological score was 3.0 +/- 0.8 at month 10 with an average quartz tissue level of 1.4 +/- 0.4 micrograms/mg. In the Si-Al group, all these changes were significantly reduced early and remained so up to 10 months after exposure; the pathological score was 1.1 +/- 0.4 and lung levels of quartz were undetectable. The data thus demonstrated that Al treatment of quartz significantly reduces the biological activity of quartz and increases its clearance with essentially no detectable particle retention in the lung 10 months after exposure.

Aluminum↗
PubMed1993

Quartz selectively down-regulates CR1 on activated human granulocytes.

We have investigated the interaction between quartz and granulocytes with respect to complement receptor expression. When N-formylmethionyl-leucyl-phenylalanine (fMLP)-stimulated leukocytes were exposed to quartz at 37 degrees C, CR1 was down-regulated but CR3 was not affected. This was a direct effect on granulocytes because it occurred in a similar fashion when mixed leukocyte suspensions and isolated granulocyte populations were used as targets for quartz. The observed down-regulation by quartz was not affected by the microfilament-disrupting agent cytochalasin B and the total detectable pool of CR1 was reduced after quartz exposure. When protease inhibitors, such as aprotinin or phenylmethanesulfonyl fluoride, were present during quartz exposure, the down-regulation of CR1 was less pronounced, but this was not the case not when protease inhibitors such as EDTA-Na2 and pepstatin were present. Exposure to quartz was not accompanied by a pronounced release of beta-glucuronidase (marker for the primary granules) or vitamin B12 binding protein (marker for the secondary granules). In contrast to quartz, exposure to alumina did not affect the expression of CR1 and CR3. The spontaneous mobilization of CR1 at 37 degrees C was reduced when quartz was present but the CR3 mobilization was unaffected. Our results indicate that quartz induces a granule protease-dependent selective shedding of CR1 but not CR3 despite a low degree of degranulation.

Aprotinin↗