Reduction of Acute Inflammatory Effects of Fumed Silica Nanoparticles in the Lung by Adjusting Silanol Display through Calcination and Metal Doping
The production of pyrogenic (fumed) silica is increasing worldwide at a 7% annual growth rate, including expanded use in food, pharmaceuticals, and other industrial products. Synthetic amorphous silica, including fumed silica, has been generally recognized as safe for use in food products by the Foo...
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| Published in | ACS nano Vol. 9; no. 9; pp. 9357 - 9372 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Chemical Society
22.09.2015
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| Subjects | |
| Online Access | Get full text |
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| Abstract | The production of pyrogenic (fumed) silica is increasing worldwide at a 7% annual growth rate, including expanded use in food, pharmaceuticals, and other industrial products. Synthetic amorphous silica, including fumed silica, has been generally recognized as safe for use in food products by the Food and Drug Administration. However, emerging evidence from experimental studies now suggests that fumed silica could be hazardous due to its siloxane ring structure, high silanol density, and “string-of-pearl-like” aggregate structure, which could combine to cause membrane disruption, generation of reactive oxygen species, pro-inflammatory effects, and liver fibrosis. Based on this structure–activity analysis (SAA), we investigated whether calcination and rehydration of fumed silica changes its hazard potential in the lung due to an effect on silanol density display. This analysis demonstrated that the accompanying change in surface reactivity could indeed impact cytokine production in macrophages and acute inflammation in the lung, in a manner that is dependent on siloxane ring reconstruction. Confirmation of this SAA in vivo, prompted us to consider safer design of fumed silica properties by titanium and aluminum doping (0–7%), using flame spray pyrolysis. Detailed characterization revealed that increased Ti and Al doping could reduce surface silanol density and expression of three-membered siloxane rings, leading to dose-dependent reduction in hydroxyl radical generation, membrane perturbation, potassium efflux, NLRP3 inflammasome activation, and cytotoxicity in THP-1 cells. The reduction of NLRP3 inflammasome activation was also confirmed in bone-marrow-derived macrophages. Ti doping, and to a lesser extent Al doping, also ameliorated acute pulmonary inflammation, demonstrating the possibility of a safer design approach for fumed silica, should that be required for specific use circumstances. |
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| AbstractList | The production of pyrogenic (fumed) silica is increasing worldwide at a 7% annual growth rate, including expanded use in food, pharmaceuticals, and other industrial products. Synthetic amorphous silica, including fumed silica, has been generally recognized as safe for use in food products by the Food and Drug Administration. However, emerging evidence from experimental studies now suggests that fumed silica could be hazardous due to its siloxane ring structure, high silanol density, and "string-of-pearl-like" aggregate structure, which could combine to cause membrane disruption, generation of reactive oxygen species, pro-inflammatory effects, and liver fibrosis. Based on this structure-activity analysis (SAA), we investigated whether calcination and rehydration of fumed silica changes its hazard potential in the lung due to an effect on silanol density display. This analysis demonstrated that the accompanying change in surface reactivity could indeed impact cytokine production in macrophages and acute inflammation in the lung, in a manner that is dependent on siloxane ring reconstruction. Confirmation of this SAA in vivo, prompted us to consider safer design of fumed silica properties by titanium and aluminum doping (0-7%), using flame spray pyrolysis. Detailed characterization revealed that increased Ti and Al doping could reduce surface silanol density and expression of three-membered siloxane rings, leading to dose-dependent reduction in hydroxyl radical generation, membrane perturbation, potassium efflux, NLRP3 inflammasome activation, and cytotoxicity in THP-1 cells. The reduction of NLRP3 inflammasome activation was also confirmed in bone-marrow-derived macrophages. Ti doping, and to a lesser extent Al doping, also ameliorated acute pulmonary inflammation, demonstrating the possibility of a safer design approach for fumed silica, should that be required for specific use circumstances. Keywords: fumed silica; silanol groups; doping; NLRP3 inflammasome; IL-1 beta ; lung inflammation The production of pyrogenic (fumed) silica is increasing worldwide at a 7% annual growth rate, including expanded use in food, pharmaceuticals, and other industrial products. Synthetic amorphous silica, including fumed silica, has been generally recognized as safe for use in food products by the Food and Drug Administration. However, emerging evidence from experimental studies now suggests that fumed silica could be hazardous due to its siloxane ring structure, high silanol density, and “string-of-pearl-like” aggregate structure, which could combine to cause membrane disruption, generation of reactive oxygen species, pro-inflammatory effects, and liver fibrosis. Based on this structure–activity analysis (SAA), we investigated whether calcination and rehydration of fumed silica changes its hazard potential in the lung due to an effect on silanol density display. This analysis demonstrated that the accompanying change in surface reactivity could indeed impact cytokine production in macrophages and acute inflammation in the lung, in a manner that is dependent on siloxane ring reconstruction. Confirmation of this SAA in vivo, prompted us to consider safer design of fumed silica properties by titanium and aluminum doping (0–7%), using flame spray pyrolysis. Detailed characterization revealed that increased Ti and Al doping could reduce surface silanol density and expression of three-membered siloxane rings, leading to dose-dependent reduction in hydroxyl radical generation, membrane perturbation, potassium efflux, NLRP3 inflammasome activation, and cytotoxicity in THP-1 cells. The reduction of NLRP3 inflammasome activation was also confirmed in bone-marrow-derived macrophages. Ti doping, and to a lesser extent Al doping, also ameliorated acute pulmonary inflammation, demonstrating the possibility of a safer design approach for fumed silica, should that be required for specific use circumstances. The production of pyrogenic (fumed) silica is increasing worldwide at a 7% annual growth rate, including expanded use in food, pharmaceuticals, and other industrial products. Synthetic amorphous silica, including fumed silica, has been generally recognized as safe for use in food products by the Food and Drug Administration. However, emerging evidence from experimental studies now suggests that fumed silica could be hazardous due to its siloxane ring structure, high silanol density, and "string-of-pearl-like" aggregate structure, which could combine to cause membrane disruption, generation of reactive oxygen species, pro-inflammatory effects, and liver fibrosis. Based on this structure-activity analysis (SAA), we investigated whether calcination and rehydration of fumed silica changes its hazard potential in the lung due to an effect on silanol density display. This analysis demonstrated that the accompanying change in surface reactivity could indeed impact cytokine production in macrophages and acute inflammation in the lung, in a manner that is dependent on siloxane ring reconstruction. Confirmation of this SAA in vivo, prompted us to consider safer design of fumed silica properties by titanium and aluminum doping (0-7%), using flame spray pyrolysis. Detailed characterization revealed that increased Ti and Al doping could reduce surface silanol density and expression of three-membered siloxane rings, leading to dose-dependent reduction in hydroxyl radical generation, membrane perturbation, potassium efflux, NLRP3 inflammasome activation, and cytotoxicity in THP-1 cells. The reduction of NLRP3 inflammasome activation was also confirmed in bone-marrow-derived macrophages. Ti doping, and to a lesser extent Al doping, also ameliorated acute pulmonary inflammation, demonstrating the possibility of a safer design approach for fumed silica, should that be required for specific use circumstances.The production of pyrogenic (fumed) silica is increasing worldwide at a 7% annual growth rate, including expanded use in food, pharmaceuticals, and other industrial products. Synthetic amorphous silica, including fumed silica, has been generally recognized as safe for use in food products by the Food and Drug Administration. However, emerging evidence from experimental studies now suggests that fumed silica could be hazardous due to its siloxane ring structure, high silanol density, and "string-of-pearl-like" aggregate structure, which could combine to cause membrane disruption, generation of reactive oxygen species, pro-inflammatory effects, and liver fibrosis. Based on this structure-activity analysis (SAA), we investigated whether calcination and rehydration of fumed silica changes its hazard potential in the lung due to an effect on silanol density display. This analysis demonstrated that the accompanying change in surface reactivity could indeed impact cytokine production in macrophages and acute inflammation in the lung, in a manner that is dependent on siloxane ring reconstruction. Confirmation of this SAA in vivo, prompted us to consider safer design of fumed silica properties by titanium and aluminum doping (0-7%), using flame spray pyrolysis. Detailed characterization revealed that increased Ti and Al doping could reduce surface silanol density and expression of three-membered siloxane rings, leading to dose-dependent reduction in hydroxyl radical generation, membrane perturbation, potassium efflux, NLRP3 inflammasome activation, and cytotoxicity in THP-1 cells. The reduction of NLRP3 inflammasome activation was also confirmed in bone-marrow-derived macrophages. Ti doping, and to a lesser extent Al doping, also ameliorated acute pulmonary inflammation, demonstrating the possibility of a safer design approach for fumed silica, should that be required for specific use circumstances. The production of pyrogenic (fumed) silica is increasing worldwide at a 7% annual growth rate, including expanded use in food, pharmaceuticals and other industrial products. Synthetic amorphous silica, including fumed silica, has been generally recognized as safe (GRAS) for use in food products by the Food and Drug Administration (FDA). However, emerging evidence from experimental studies now suggests that fumed silica could be hazardous due to its siloxane ring structure, high silanol density, and “string-of-pearl-like” aggregate structure, which could combine to cause membrane disruption, generation of reactive oxygen species, pro-inflammatory effects, and liver fibrosis. Based on this structure-activity analysis (SAA), we investigated whether calcination and rehydration of fumed silica changes its hazard potential in the lung due to an effect on silanol density display. This analysis demonstrated that the accompanying change in surface reactivity could indeed impact cytokine production in macrophages and acute inflammation in the lung, in a manner that is dependent on siloxane ring reconstruction. Confirmation of this SAA in vivo, prompted us to consider safer design of fumed silica properties by titanium (Ti) and aluminum (Al) doping (0–7%), using flame spray pyrolysis (FSP). Detailed characterization revealed that increased Ti and Al doping could reduce surface silanol density and expression of three-membered siloxane rings, leading to dose-dependent reduction in hydroxyl radical generation, membrane perturbation, potassium efflux, NLRP3 inflammasome activation and cytotoxicity in THP-1 cells. The reduction of NLRP3 inflammasome activation was also confirmed in bone marrow-derived macrophages (BMDMs). Ti- and to a lesser extent Al-doping, also ameliorated acute pulmonary inflammation, demonstrating the possibility of a safer design approach for fumed silica, should that be required for specific use circumstances. |
| Author | Brinker, C. Jeffrey Sun, Bingbing Wang, Meiying Liao, Yu-Pei Chang, Chong Hyun Dong, Juyao Nel, André E Dunphy, Darren R Wang, Xiang Mädler, Lutz Ji, Zhaoxia Pokhrel, Suman Li, Ruibin Xia, Tian Zhang, Haiyuan |
| AuthorAffiliation | Chinese Academy of Sciences Laboratory of Chemical Biology, Changchun Institute of Applied Chemistry University of Bremen Self-Assembled Materials Department Division of NanoMedicine, Department of Medicine University of California Department of Molecular Genetics and Microbiology Sandia National Laboratories Department of Chemistry California NanoSystems Institute Foundation Institute of Materials Science (IWT), Department of Production Engineering Department of Chemical and Nuclear Engineering University of New Mexico |
| AuthorAffiliation_xml | – name: Self-Assembled Materials Department – name: Department of Chemistry – name: Chinese Academy of Sciences – name: Department of Molecular Genetics and Microbiology – name: Division of NanoMedicine, Department of Medicine – name: Laboratory of Chemical Biology, Changchun Institute of Applied Chemistry – name: California NanoSystems Institute – name: University of California – name: University of New Mexico – name: Department of Chemical and Nuclear Engineering – name: Sandia National Laboratories – name: Foundation Institute of Materials Science (IWT), Department of Production Engineering – name: University of Bremen – name: 6 Department of Chemistry, University of California, Los Angeles, CA 90095, United States – name: 3 Department of Chemical and Nuclear Engineering, University of New Mexico, Albuquerque, New Mexico 87131, United States – name: 8 Self-Assembled Materials Department, Sandia National Laboratories, PO Box 5800 MS1349, Albuquerque, New Mexico 87185, United States – name: 5 California NanoSystems Institute, University of California, Los Angeles, CA 90095, United States – name: 1 Division of NanoMedicine, Department of Medicine, University of California, Los Angeles, CA 90095, United States – name: 4 Laboratory of Chemical Biology, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun, Jilin, China – name: 7 Department of Molecular Genetics and Microbiology, University of New Mexico, Albuquerque, New Mexico 87131, United States – name: 2 Foundation Institute of Materials Science (IWT), Department of Production Engineering, University of Bremen, Germany |
| Author_xml | – sequence: 1 givenname: Bingbing surname: Sun fullname: Sun, Bingbing – sequence: 2 givenname: Suman surname: Pokhrel fullname: Pokhrel, Suman – sequence: 3 givenname: Darren R surname: Dunphy fullname: Dunphy, Darren R – sequence: 4 givenname: Haiyuan surname: Zhang fullname: Zhang, Haiyuan – sequence: 5 givenname: Zhaoxia surname: Ji fullname: Ji, Zhaoxia – sequence: 6 givenname: Xiang surname: Wang fullname: Wang, Xiang – sequence: 7 givenname: Meiying surname: Wang fullname: Wang, Meiying – sequence: 8 givenname: Yu-Pei surname: Liao fullname: Liao, Yu-Pei – sequence: 9 givenname: Chong Hyun surname: Chang fullname: Chang, Chong Hyun – sequence: 10 givenname: Juyao surname: Dong fullname: Dong, Juyao – sequence: 11 givenname: Ruibin surname: Li fullname: Li, Ruibin – sequence: 12 givenname: Lutz surname: Mädler fullname: Mädler, Lutz – sequence: 13 givenname: C. Jeffrey surname: Brinker fullname: Brinker, C. Jeffrey – sequence: 14 givenname: André E surname: Nel fullname: Nel, André E email: txia@ucla.edu, anel@mednet.ucla.edu – sequence: 15 givenname: Tian surname: Xia fullname: Xia, Tian email: txia@ucla.edu, anel@mednet.ucla.edu |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26200133$$D View this record in MEDLINE/PubMed |
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| Snippet | The production of pyrogenic (fumed) silica is increasing worldwide at a 7% annual growth rate, including expanded use in food, pharmaceuticals, and other... The production of pyrogenic (fumed) silica is increasing worldwide at a 7% annual growth rate, including expanded use in food, pharmaceuticals and other... |
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| SubjectTerms | Calcium - metabolism Cell Line Density Doping Foods Fumed silica Humans Liver Cirrhosis - chemically induced Liver Cirrhosis - pathology Lung - drug effects Lung - pathology Lungs Nanoparticles - adverse effects Nanoparticles - chemistry Pneumonia - chemically induced Pneumonia - pathology Reactive Oxygen Species - toxicity Reduction Silanes - chemistry Silicon Dioxide - adverse effects Silicon Dioxide - chemistry Siloxanes Structure-Activity Relationship Titanium United States United States Food and Drug Administration |
| Title | Reduction of Acute Inflammatory Effects of Fumed Silica Nanoparticles in the Lung by Adjusting Silanol Display through Calcination and Metal Doping |
| URI | http://dx.doi.org/10.1021/acsnano.5b03443 https://www.ncbi.nlm.nih.gov/pubmed/26200133 https://www.proquest.com/docview/1715914022 https://www.proquest.com/docview/1770332999 https://pubmed.ncbi.nlm.nih.gov/PMC4687969 |
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