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1
Hui, David S., Benny K. Chow, Thomas Lo, Owen T. Y. Tsang, Fanny W. Ko, Susanna S. Ng, Tony Gin, and Matthew T. V. Chan. "Exhaled air dispersion during high-flow nasal cannula therapy versus CPAP via different masks." European Respiratory Journal 53, no. 4 (January 31, 2019): 1802339. http://dx.doi.org/10.1183/13993003.02339-2018.
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BackgroundHigh-flow nasal cannula (HFNC) is an emerging therapy for respiratory failure but the extent of exhaled air dispersion during treatment is unknown. We examined exhaled air dispersion during HFNC therapy versus continuous positive airway pressure (CPAP) on a human patient simulator (HPS) in an isolation room with 16 air changes·h−1.MethodsThe HPS was programmed to represent different severity of lung injury. CPAP was delivered at 5–20 cmH2O via nasal pillows (Respironics Nuance Pro Gel or ResMed Swift FX) or an oronasal mask (ResMed Quattro Air). HFNC, humidified to 37°C, was delivered at 10–60 L·min−1 to the HPS. Exhaled airflow was marked with intrapulmonary smoke for visualisation and revealed by laser light-sheet. Normalised exhaled air concentration was estimated from the light scattered by the smoke particles. Significant exposure was defined when there was ≥20% normalised smoke concentration.ResultsIn the normal lung condition, mean±sd exhaled air dispersion, along the sagittal plane, increased from 186±34 to 264±27 mm and from 207±11 to 332±34 mm when CPAP was increased from 5 to 20 cmH2O via Respironics and ResMed nasal pillows, respectively. Leakage from the oronasal mask was negligible. Mean±sd exhaled air distances increased from 65±15 to 172±33 mm when HFNC was increased from 10 to 60 L·min−1. Air leakage to 620 mm occurred laterally when HFNC and the interface tube became loose.ConclusionExhaled air dispersion during HFNC and CPAP via different interfaces is limited provided there is good mask interface fitting.
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Phillips, Jeremy, Bruno Kluss, Audrey Richter, and Eian D. Massey. "Exposure of Bronchial Epithelial Cells to Whole Cigarette Smoke: Assessment of Cellular Responses." Alternatives to Laboratory Animals 33, no. 3 (June 2005): 239–48. http://dx.doi.org/10.1177/026119290503300310.
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Cigarette smoke is composed of approximately 5% particulate phase and 95% vapour phase by weight. However, routine in vitro toxicological testing of smoke normally only measures the activity of the particulate phase. This study describes a new system for exposing cells at an air–liquid interface to serial dilutions of gaseous smoke. Confluent monolayers of NCI-H292 human lung epithelial cells on semi-permeable membranes were placed in a purpose-designed Perspex chamber at an air–liquid interface. The cells were exposed to dilute whole mainstream cigarette smoke for 30 minutes, followed by a 20-hour recovery period. Firstly, high and low delivery cigarettes were compared, and cytotoxicity was determined by using the neutral red uptake assay. Clear differential cytotoxic responses were observed with the two cigarette types, which correlated positively with the concentrations of components in smoke, and particularly compounds in the vapour phase, such as aldehydes. Secondly, low doses of smoke were found to up-regulate mRNA levels of the secreted mucin, MUC5AC, and to stimulate the production of interleukin (IL)-6, IL-8 and matrix-metalloprotease-1, but had no effect on growth-related oncogene alpha. This system will facilitate further investigations into the toxicological mechanisms of cigarette smoke components, and may be useful for studying other gaseous mixtures or aerosols.
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Miller, Colton, Susan O’Neill, Miriam Rorig, and Ernesto Alvarado. "Air-Quality Challenges of Prescribed Fire in the Complex Terrain and Wildland Urban Interface Surrounding Bend, Oregon." Atmosphere 10, no. 9 (September 3, 2019): 515. http://dx.doi.org/10.3390/atmos10090515.
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Prescribed fires in forest ecosystems can negatively impact human health and safety by transporting smoke downwind into nearby communities. Smoke transport to communities is known to occur around Bend, Oregon, United States of America (USA), where burning at the wildland–urban interface in the Deschutes National Forest resulted in smoke intrusions into populated areas. The number of suitable days for prescribed fires is limited due to the necessity for moderate weather conditions, as well as wind directions that do not carry smoke into Bend. To better understand the conditions leading to these intrusions and to assess predictions of smoke dispersion from prescribed fires, we collected data from an array of weather and particulate monitors over the autumn of 2014 and spring of 2015 and historical weather data from nearby remote automated weather stations (RAWS). We characterized the observed winds to compare with meteorological and smoke dispersion models using the BlueSky smoke modeling framework. The results from this study indicated that 1–6 days per month in the spring and 2–4 days per month in the fall met the general meteorological prescription parameters for conducting prescribed fires in the National Forest. Of those, 13% of days in the spring and 5% of days in the fall had “ideal” wind patterns, when north winds occurred during the day and south winds did not occur at night. The analysis of smoke intrusions demonstrated that dispersion modeling can be useful for anticipating the timing and location of smoke impacts, but substantial errors in wind speed and direction of the meteorological models can lead to mischaracterizations of intrusion events. Additionally, for the intrusion event modeled using a higher-resolution 1-km meteorological and dispersion model, we found improved predictions of both the timing and location of smoke delivery to Bend compared with the 4-km meteorological model. The 1-km-resolution model prediction fell within 1 h of the observed event, although with underpredicted concentrations, and demonstrated promise for high-resolution modeling in areas of complex terrain.
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McCarthy, Claire E., Parker F. Duffney, Robert Gelein, Thomas H. Thatcher, Alison Elder, Richard P. Phipps, and Patricia J. Sime. "Dung biomass smoke activates inflammatory signaling pathways in human small airway epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 311, no. 6 (December 1, 2016): L1222—L1233. http://dx.doi.org/10.1152/ajplung.00183.2016.
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Animal dung is a biomass fuel burned by vulnerable populations who cannot afford cleaner sources of energy, such as wood and gas, for cooking and heating their homes. Exposure to biomass smoke is the leading environmental risk for mortality, with over 4,000,000 deaths each year worldwide attributed to indoor air pollution from biomass smoke. Biomass smoke inhalation is epidemiologically associated with pulmonary diseases, including chronic obstructive pulmonary disease (COPD), lung cancer, and respiratory infections, especially in low and middle-income countries. Yet, few studies have examined the mechanisms of dung biomass smoke-induced inflammatory responses in human lung cells. Here, we tested the hypothesis that dung biomass smoke causes inflammatory responses in human lung cells through signaling pathways involved in acute and chronic lung inflammation. Primary human small airway epithelial cells (SAECs) were exposed to dung smoke at the air-liquid interface using a newly developed, automated, and reproducible dung biomass smoke generation system. The examination of inflammatory signaling showed that dung biomass smoke increased the production of several proinflammatory cytokines and enzymes in SAECs through activation of the activator protein (AP)-1 and arylhydrocarbon receptor (AhR) but not nuclear factor-κB (NF-κB) pathways. We propose that the inflammatory responses of lung cells exposed to dung biomass smoke contribute to the development of respiratory diseases.
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Maunders, Heather, Sudhanshu Patwardhan, Jeremy Phillips, Aaron Clack, and Audrey Richter. "Human bronchial epithelial cell transcriptome: gene expression changes following acute exposure to whole cigarette smoke in vitro." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 5 (May 2007): L1248—L1256. http://dx.doi.org/10.1152/ajplung.00290.2006.
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Cigarette smoke is a complex mixture of more than 4,000 constituents. Its effects on cell biology are poorly understood, partly because whole smoke exposure in vitro is technically challenging. To investigate the effects of smoke on cell signaling and function, a three-dimensional air-liquid interface model of tracheobronchial epithelium, grown from primary human lung epithelial cells, was exposed to air or whole mainstream cigarette smoke for 1 h in a purpose-designed chamber. Gene expression profiles were then determined at 1, 6, and 24 h postexposure using Affymetrix HGU133-2 Plus microarrays. Cells from three different donors were used in the study, and the experiment was performed in triplicate for each donor. Genes significantly regulated by smoke, compared with the air control, in all experiments were determined. Genes exhibiting differential expression were assigned to functional categories and mapped to signaling pathways. Effects were observed on many cellular processes including xenobiotic metabolism, oxidant/antioxidant balance, and DNA damage and repair. Notably, there was marked downregulation of the transforming growth factor-β pathway, which has not been previously reported. This study provides important data on the acute effects of whole cigarette smoke on mucociliary epithelium and may be used to gain a greater understanding of smoke toxicity.
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Wang, Jian, Juan Gui, Jun Gao, and Xueli Hu. "Parametrization of the fire-smoke exhaust system for a large and high-rise atrium in Shanghai through salt-bath experiment." Indoor and Built Environment 26, no. 2 (July 28, 2016): 272–91. http://dx.doi.org/10.1177/1420326x16660600.
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Present specifications in Building Codes in China lack design parameters for smoke exhaust for large and high-rise atrium in buildings. An investigation of natural smoke filling and parametrization of fire-smoke exhaust in an atrium building in Shanghai was conducted based on salt-bath experiment, due to dynamic analogy between thermal smoke movement in air and brine dispersion in water. To obtain a small, scaled-down version of an atrium with a high polyfoam fire up to 1 MW, the brine-bath experiment was conducted with calcium chloride for small strength fire in small-space rooms, to demonstrate the natural smoke filling within the atrium. The interface height and filling time derived was highly comparable to those obtained by empirical equations. The results of computational fluid dynamics simulations agreed well with the salt-bath experiments. The evacuation time was also calculated with a dimensionless interface height of 0.2 to determine whether there was sufficient time for occupants to escape. The smoke filling process under mechanical smoke exhaust was also investigated by experiments, to parametrize the fire smoke exhaust system in the atrium. The optimal smoke exhaust level, natural and mechanical make-up level were determined and were recommended as the design parameters for the construction of atrium in buildings.
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Adamson, Jason, David Thorne, John McAughey, Deborah Dillon, and Clive Meredith. "Quantification of Cigarette Smoke Particle DepositionIn VitroUsing a Triplicate Quartz Crystal Microbalance Exposure Chamber." BioMed Research International 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/685074.
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There are a variety of smoke exposure systems available to the tobacco industry and respiratory toxicology research groups, each with their own way of diluting/delivering smoke to cell cultures. Thus a simple technique to measure dosein vitroneeds to be utilised. Dosimetry—assessment of dose—is a key element in linking the biological effects of smoke generated by various exposure systems. Microbalance technology is presented as a dosimetry tool and a way of measuring whole smoke dose. Described here is a new tool to quantify diluted smoke particulate depositionin vitro. The triplicate quartz crystal microbalance (QCM) chamber measured real-time deposition of smoke at a range of dilutions 1 : 5–1 : 400 (smoke : air). Mass was read in triplicate by 3 identical QCMs installed into onein vitroexposure chamber, each in the location in which a cell culture would be exposed to smoke at the air-liquid interface. This resulted in quantification of deposited particulate matter in the range 0.21–28.00 μg/cm2. Results demonstrated that the QCM could discriminate mass between dilutions and was able to give information of regional deposition where cell cultures would usually be exposed within the chamber. Our aim is to use the QCM to support the preclinical (in vitro) evaluation of tobacco products.
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Bowman, David, Lori Daniels, Fay Johnston, Grant Williamson, W. Jolly, Sheryl Magzamen, Ana Rappold, Michael Brauer, and Sarah Henderson. "Can Air Quality Management Drive Sustainable Fuels Management at the Temperate Wildland–Urban Interface?" Fire 1, no. 2 (August 9, 2018): 27. http://dx.doi.org/10.3390/fire1020027.
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Sustainable fire management has eluded all industrial societies. Given the growing number and magnitude of wildfire events, prescribed fire is being increasingly promoted as the key to reducing wildfire risk. However, smoke from prescribed fires can adversely affect public health. We propose that the application of air quality standards can lead to the development and adoption of sustainable fire management approaches that lower the risk of economically and ecologically damaging wildfires while improving air quality and reducing climate-forcing emissions. For example, green fire breaks at the wildland–urban interface (WUI) can resist the spread of wildfires into urban areas. These could be created through mechanical thinning of trees, and then maintained by targeted prescribed fire to create biodiverse and aesthetically pleasing landscapes. The harvested woody debris could be used for pellets and other forms of bioenergy in residential space heating and electricity generation. Collectively, such an approach would reduce the negative health impacts of smoke pollution from wildfires, prescribed fires, and combustion of wood for domestic heating. We illustrate such possibilities by comparing current and potential fire management approaches in the temperate and environmentally similar landscapes of Vancouver Island in British Columbia, Canada and the island state of Tasmania in Australia.
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Nguyen, Piercen K., Yeongkwon Son, Juli Petereit, Andrey Khlystov, and Riccardo Panella. "Modeling Human Lung Cells Exposure to Wildfire Uncovers Aberrant lncRNAs Signature." Biomolecules 13, no. 1 (January 12, 2023): 155. http://dx.doi.org/10.3390/biom13010155.
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Emissions generated by wildfires are a growing threat to human health and are characterized by a unique chemical composition that is tightly dependent on geographic factors such as fuel type. Long noncoding RNAs (lncRNAs) are a class of RNA molecules proven to be critical to many biological processes, and their condition-specific expression patterns are emerging as prominent prognostic and diagnostic biomarkers for human disease. We utilized a new air-liquid interface (ALI) direct exposure system that we designed and validated in house to expose immortalized human tracheobronchial epithelial cells (AALE) to two unique wildfire smokes representative of geographic regions (Sierra Forest and Great Basin). We conducted an RNAseq analysis on the exposed cell cultures and proved through both principal component and differential expression analysis that each smoke has a unique effect on the LncRNA expression profiles of the exposed cells when compared to the control samples. Our study proves that there is a link between the geographic origin of wildfire smoke and the resulting LncRNA expression profile in exposed lung cells and also serves as a proof of concept for the in-house designed ALI exposure system. Our study serves as an introduction to the scientific community of how unique expression patterns of LncRNAs in patients with wildfire smoke-related disease can be utilized as prognostic and diagnostic tools, as the current roles of LncRNA expression profiles in wildfire smoke-related disease, other than this study, are completely uncharted.
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Valente, Joana, Ana I. Miranda, António G. Lopes, Carlos Borrego, Domingos X. Viegas, and Myriam Lopes. "Local-scale modelling system to simulate smoke dispersion." International Journal of Wildland Fire 16, no. 2 (2007): 196. http://dx.doi.org/10.1071/wf06085.
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The main purpose of this paper is to present a fire behaviour system, developed to estimate fire progression, smoke dispersion and visibility impairment, at a local scale, and to evaluate its performance by comparing results with measurements from the Gestosa 2004 experimental field fires. The system is an improvement of two already available numerical tools, DISPERFIRE (Miranda et al. 1994) and FireStation (Lopes et al. 2002), which were integrated. FireStation is a software system aimed at the simulation of fire spread over complex topography. DISPERFIRE is a real-time system developed to simulate the dispersion in the atmosphere of the pollutants emitted during a forest fire. In addition, a model for the estimation of visibility impairment, based on the relationship between air pollutants concentration and visibility, was included in DISPERFIRE. The whole system was developed using a graphical interface, previously created for FireStation, which provides user-friendliness and easily readable output to facilitate its application under operational conditions. The system was applied to an experimental field fire and the main results were compared with experimental air pollutant concentration measured values. The performance of the model in predicting pollutant concentrations was good, particularly for NO2 and PM10.
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Wohnhaas, Christian T., Julia A. Gindele, Tobias Kiechle, Yang Shen, Germán G. Leparc, Birgit Stierstorfer, Heiko Stahl, et al. "Cigarette Smoke Specifically Affects Small Airway Epithelial Cell Populations and Triggers the Expansion of Inflammatory and Squamous Differentiation Associated Basal Cells." International Journal of Molecular Sciences 22, no. 14 (July 16, 2021): 7646. http://dx.doi.org/10.3390/ijms22147646.
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Smoking is a major risk factor for chronic obstructive pulmonary disease (COPD) and causes remodeling of the small airways. However, the exact smoke-induced effects on the different types of small airway epithelial cells (SAECs) are poorly understood. Here, using air–liquid interface (ALI) cultures, single-cell RNA-sequencing reveals previously unrecognized transcriptional heterogeneity within the small airway epithelium and cell type-specific effects upon acute and chronic cigarette smoke exposure. Smoke triggers detoxification and inflammatory responses and aberrantly activates and alters basal cell differentiation. This results in an increase of inflammatory basal-to-secretory cell intermediates and, particularly after chronic smoke exposure, a massive expansion of a rare inflammatory and squamous metaplasia associated KRT6A+ basal cell state and an altered secretory cell landscape. ALI cultures originating from healthy non-smokers and COPD smokers show similar responses to cigarette smoke exposure, although an increased pro-inflammatory profile is conserved in the latter. Taken together, the in vitro models provide high-resolution insights into the smoke-induced remodeling of the small airways resembling the pathological processes in COPD airways. The data may also help to better understand other lung diseases including COVID-19, as the data reflect the smoke-dependent variable induction of SARS-CoV-2 entry factors across SAEC populations.
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Ramenzoni, Liza, Andreas Schneider, Stephan Fox, Michael Meyer, Mirko Meboldt, Thomas Attin, and Patrick Schmidlin. "Cytotoxic and Inflammatory Effects of Electronic and Traditional Cigarettes on Oral Gingival Cells Using a Novel Automated Smoking Instrument: An In Vitro Study." Toxics 10, no. 4 (April 6, 2022): 179. http://dx.doi.org/10.3390/toxics10040179.
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Information about the potential oral health effects of vaping from electronic cigarettes (e-cigs) is still sparse and inconsistent. The purpose of this study was to compare the safety and cytotoxicity of e-cig liquid aerosols versus traditional cigarette (t-cig) smoke on human epithelial oral cells. T-cig smoke and e-cig aerosols were generated by a newly developed automated smoking instrument in order to simulate realistic user puffing behaviors. Air–liquid interface transwell cell cultures were exposed to standardized puff topography (puff duration: 2 s, puff volume: 35 mL, puff frequency: 1 puff every 60 s) of reference t-cigs or commercially available e-cigs at different air dilutions. Cell viability, morphology, and death rate were evaluated with MTT and TUNEL assays. The inflammatory cytokine gene expression of inflammatory genes was assessed by quantitative RT-PCR. E-cigs and t-cigs indicated similar adverse effects by enhancing cytotoxicity and cell death in a dose-dependent manner. E-cig aerosol and t-cig smoke treatment expressed upregulation of inflammatory cytokines up to 3.0-fold (p < 0.05). These results indicate that e-cig smoking may contribute to oral tissue–cell damage and tissue inflammation. Our approach allows the production of e-cig aerosol and t-cig smoke in order to identify harmful effects in oral tissues in vitro.
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Duffney, Parker F., Claire E. McCarthy, Aitor Nogales, Thomas H. Thatcher, Luis Martinez-Sobrido, Richard P. Phipps, and Patricia J. Sime. "Cigarette smoke dampens antiviral signaling in small airway epithelial cells by disrupting TLR3 cleavage." American Journal of Physiology-Lung Cellular and Molecular Physiology 314, no. 3 (March 1, 2018): L505—L513. http://dx.doi.org/10.1152/ajplung.00406.2017.
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Cigarette smokers and people exposed to second-hand smoke are at an increased risk for pulmonary viral infections, and yet the mechanism responsible for this heightened susceptibility is not understood. To understand the effect of cigarette smoke on susceptibility to viral infection, we used an air-liquid interface culture system and exposed primary human small airway epithelial cells (SAEC) to whole cigarette smoke, followed by treatment with the viral mimetic polyinosinic polycytidylic acid (poly I:C) or influenza A virus (IAV). We found that prior smoke exposure strongly inhibited production of proinflammatory (interleukin-6 and interleukin-8) and antiviral [interferon-γ-induced protein 10 (IP-10) and interferons] mediators in SAECs in response to poly I:C and IAV infection. Impaired antiviral responses corresponded to increased infection with IAV. This was associated with a decrease in phosphorylation of the key antiviral transcription factor interferon response factor 3 (IRF3). Here, we found that cigarette smoke exposure inhibited activation of Toll-like receptor 3 (TLR3) by impairing TLR3 cleavage, which was required for downstream phosphorylation of IRF3 and production of IP-10. These results identify a novel mechanism by which cigarette smoke exposure impairs antiviral responses in lung epithelial cells, which may contribute to increased susceptibility to respiratory infections.
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Geraghty, Patrick, Nathalie Baumlin, Matthias A. Salathe, Robert F. Foronjy, and Jeanine M. D’Armiento. "Glutathione Peroxidase-1 Suppresses the Unfolded Protein Response upon Cigarette Smoke Exposure." Mediators of Inflammation 2016 (2016): 1–16. http://dx.doi.org/10.1155/2016/9461289.
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Oxidative stress provokes endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) in the lungs of chronic obstructive pulmonary (COPD) subjects. The antioxidant, glutathione peroxidase-1 (GPx-1), counters oxidative stress induced by cigarette smoke exposure. Here, we investigate whether GPx-1 expression deters the UPR following exposure to cigarette smoke. Expression of ER stress markers was investigated in fully differentiated normal human bronchial epithelial (NHBE) cells isolated from nonsmoking, smoking, and COPD donors and redifferentiated at the air liquid interface. NHBE cells from COPD donors expressed heightened ATF4, XBP1, GRP78, GRP94, EDEM1, and CHOP compared to cells from nonsmoking donors. These changes coincided with reduced GPx-1 expression. Reintroduction of GPx-1 into NHBE cells isolated from COPD donors reduced the UPR. To determine whether the loss of GPx-1 expression has a direct impact on these ER stress markers during smoke exposure,Gpx-1−/−mice were exposed to cigarette smoke for 1 year. Loss ofGpx-1expression enhanced cigarette smoke-induced ER stress and apoptosis. Equally, induction of ER stress with tunicamycin enhanced antioxidant expression in mouse precision-cut lung slices. Smoke inhalation also exacerbated the UPR response during respiratory syncytial virus infection. Therefore, ER stress may be an antioxidant-related pathophysiological event in COPD.
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Chow, W. K. "Study on the Flashover Criteria for Compartmental Fires." Journal of Fire Sciences 15, no. 2 (March 1997): 95–107. http://dx.doi.org/10.1177/073490419701500202.
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Criteria on the possibility of having flashover in a compartment fire were reviewed. The heat balance equation in the compartment was studied. The zone model CFAST 2.0 was applied to study the fire environment in a small compartment with a door of different area. Important parameters including the average upper and lower layer temperature, the smoke layer interface height, and the mass flow rates for intake air and outgoing smoke were calculated. Those pre dicted results were substituted back to the heat balance equation for determining the possibility of having flashover. The analysis shows that it is possible to deter mine the likelihood for flashover by using a well-validated zone model. From the heat-temperature curves derived, effect of the sprinkler can also be studied.
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Amatngalim, Gimano D., Jasmijn A. Schrumpf, Fernanda Dishchekenian, Tinne C. J. Mertens, Dennis K. Ninaber, Abraham C. van der Linden, Charles Pilette, Christian Taube, Pieter S. Hiemstra, and Anne M. van der Does. "Aberrant epithelial differentiation by cigarette smoke dysregulates respiratory host defence." European Respiratory Journal 51, no. 4 (March 15, 2018): 1701009. http://dx.doi.org/10.1183/13993003.01009-2017.
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It is currently unknown how cigarette smoke-induced airway remodelling affects highly expressed respiratory epithelial defence proteins and thereby mucosal host defence.Localisation of a selected set of highly expressed respiratory epithelial host defence proteins was assessed in well-differentiated primary bronchial epithelial cell (PBEC) cultures. Next, PBEC were cultured at the air–liquid interface, and during differentiation for 2–3 weeks exposed daily to whole cigarette smoke. Gene expression, protein levels and epithelial cell markers were subsequently assessed. In addition, functional activities and persistence of the cigarette smoke-induced effects upon cessation were determined.Expression of the polymeric immunoglobulin receptor, secretory leukocyte protease inhibitor and long and short PLUNC (palate, lung and nasal epithelium clone protein) was restricted to luminal cells and exposure of differentiating PBECs to cigarette smoke resulted in a selective reduction of the expression of these luminal cell-restricted respiratory host defence proteins compared to controls. This reduced expression was a consequence of cigarette smoke-impaired end-stage differentiation of epithelial cells, and accompanied by a significant decreased transepithelial transport of IgA and bacterial killing.These findings shed new light on the importance of airway epithelial cell differentiation in respiratory host defence and could provide an additional explanation for the increased susceptibility of smokers and patients with chronic obstructive pulmonary disease to respiratory infections.
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Li, Xiang. "In vitro toxicity testing of cigarette smoke based on the air-liquid interface exposure: A review." Toxicology in Vitro 36 (October 2016): 105–13. http://dx.doi.org/10.1016/j.tiv.2016.07.019.
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Duffney, Parker, Aitor Nogales, Thomas Thatcher, Luis Martinez-Sobrido, Richard P. Phipps, and Patricia J. Sime. "TLR3 signaling is impaired in small airway epithelial cells following cigarette smoke exposure." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 203.14. http://dx.doi.org/10.4049/jimmunol.196.supp.203.14.
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Abstract Mainstream and second hand cigarette smoke exposures increase the risk of respiratory viral infections, especially in children and those with underlying lung disease. Epithelial cells are the primary targets for viral infection and recognize foreign pathogens through multiple Toll-like receptors (TLR). TLR3 recognizes double stranded RNA, a common intermediate in virus replication, and activates antiviral signaling pathways. We hypothesized that cigarette smoke exposure impairs TLR3 signaling in airway epithelial cells leading to an increase in susceptibility to viral infection. Primary human small airway epithelial cells were cultured at the air-liquid interface and exposed to whole cigarette smoke. Following cigarette smoke exposure, cells were treated with the TLR3 ligand polyinosinic-polycytidylic acid (poly I:C), a mimic of RNA viral infection. Levels of interferon gamma induced protein 10 (IP-10) and antiviral interferon bioactivity were measured in culture supernatants. TLR3 cleavage was investigated using the cathepsin inhibitor z-FA-FMK and protein lysates were analyzed by western blot. Our data shows that cigarette smoke exposure causes a decrease in the production of IP-10, as well as a decrease in the interferon bioactivity of culture supernatants. Western blot data indicates that cigarette smoke inhibits cleavage of TLR3. Inhibitor studies confirmed that cleavage of TLR3 was important for the production of IP-10 and interferons. These data show that cigarette smoke disrupts the production of anti-viral signaling molecules by disrupting cleavage and activation of TLR3, as well as provides a mechanistic explanation for increased susceptibility to viral infections in smokers.
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Amatngalim, Gimano D., Jasmijn A. Schrumpf, Almira Henic, Esther Dronkers, Renate M. Verhoosel, Soledad R. Ordonez, Henk P. Haagsman, et al. "Antibacterial Defense of Human Airway Epithelial Cells from Chronic Obstructive Pulmonary Disease Patients Induced by Acute Exposure to Nontypeable Haemophilus influenzae: Modulation by Cigarette Smoke." Journal of Innate Immunity 9, no. 4 (2017): 359–74. http://dx.doi.org/10.1159/000455193.
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Antimicrobial proteins and peptides (AMPs) are a central component of the antibacterial activity of airway epithelial cells. It has been proposed that a decrease in antibacterial lung defense contributes to an increased susceptibility to microbial infection in smokers and patients with chronic obstructive pulmonary disease (COPD). However, whether reduced AMP expression in the epithelium contributes to this lower defense is largely unknown. We investigated the bacterial killing activity and expression of AMPs by air-liquid interface-cultured primary bronchial epithelial cells from COPD patients and non-COPD (ex-)smokers that were stimulated with nontypeable Haemophilus influenzae (NTHi). In addition, the effect of cigarette smoke on AMP expression and the activation of signaling pathways was determined. COPD cell cultures displayed reduced antibacterial activity, whereas smoke exposure suppressed the NTHi-induced expression of AMPs and further increased IL-8 expression in COPD and non-COPD cultures. Moreover, smoke exposure impaired NTHi-induced activation of NF-κB, but not MAP-kinase signaling. Our findings demonstrate that the antibacterial activity of cultured airway epithelial cells induced by acute bacterial exposure was reduced in COPD and suppressed by cigarette smoke, whereas inflammatory responses persisted. These findings help to explain the imbalance between protective antibacterial and destructive inflammatory innate immune responses in COPD.
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Foronjy, Robert F., Matthias A. Salathe, Abdoulaye J. Dabo, Nathalie Baumlin, Neville Cummins, Edward Eden, and Patrick Geraghty. "TLR9 expression is required for the development of cigarette smoke-induced emphysema in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 311, no. 1 (July 1, 2016): L154—L166. http://dx.doi.org/10.1152/ajplung.00073.2016.
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The expression of Toll-like receptor (TLR)-9, a pathogen recognition receptor that recognizes unmethylated CpG sequences in microbial DNA molecules, is linked to the pathogenesis of several lung diseases. TLR9 expression and signaling was investigated in animal and cell models of chronic obstructive pulmonary disease (COPD). We observed enhanced TLR9 expression in mouse lungs following exposure to cigarette smoke. Tlr9−/− mice were resistant to cigarette smoke-induced loss of lung function as determined by mean linear intercept, total lung capacity, lung compliance, and tissue elastance analysis. Tlr9 expression also regulated smoke-mediated immune cell recruitment to the lung; apoptosis; expression of granulocyte-colony stimulating factor (G-CSF), the CXCL5 protein, and matrix metalloproteinase-2 (MMP-2); and protein tyrosine phosphatase 1B (PTP1B) activity in the lung. PTP1B, a phosphatase with anti-inflammatory abilities, was identified as binding to TLR9. In vivo delivery of a TLR9 agonist enhanced TLR9 binding to PTP1B, which inactivated PTP1B. Ptp1b−/− mice had elevated lung concentrations of G-CSF, CXCL5, and MMP-2, and tissue expression of type-1 interferon following TLR9 agonist administration, compared with wild-type mice. TLR9 responses were further determined in fully differentiated normal human bronchial epithelial (NHBE) cells isolated from nonsmoker, smoker, and COPD donors, and then cultured at air liquid interface. NHBE cells from smokers and patients with COPD expressed more TLR9 and secreted greater levels of G-CSF, IL-6, CXCL5, IL-1β, and MMP-2 upon TLR9 ligand stimulation compared with cells from nonsmoker donors. Although TLR9 combats infection, our results indicate that TLR9 induction can affect lung function by inactivating PTP1B and upregulating expression of proinflammatory cytokines.
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Mathis, Carole, Carine Poussin, Dirk Weisensee, Stephan Gebel, Arnd Hengstermann, Alain Sewer, Vincenzo Belcastro, et al. "Human bronchial epithelial cells exposed in vitro to cigarette smoke at the air-liquid interface resemble bronchial epithelium from human smokers." American Journal of Physiology-Lung Cellular and Molecular Physiology 304, no. 7 (April 1, 2013): L489—L503. http://dx.doi.org/10.1152/ajplung.00181.2012.
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Organotypic culture of human primary bronchial epithelial cells is a useful in vitro system to study normal biological processes and lung disease mechanisms, to develop new therapies, and to assess the biological perturbations induced by environmental pollutants. Herein, we investigate whether the perturbations induced by cigarette smoke (CS) and observed in the epithelium of smokers' airways are reproducible in this in vitro system (AIR-100 tissue), which has been shown to recapitulate most of the characteristics of the human bronchial epithelium. Human AIR-100 tissues were exposed to mainstream CS for 7, 14, 21, or 28 min at the air-liquid interface, and we investigated various biological endpoints [e.g., gene expression and microRNA profiles, matrix metalloproteinase 1 (MMP-1) release] at multiple postexposure time points (0.5, 2, 4, 24, 48 h). By performing a Gene Set Enrichment Analysis, we observed a significant enrichment of human smokers' bronchial epithelium gene signatures derived from different public transcriptomics datasets in CS-exposed AIR-100 tissue. Comparison of in vitro microRNA profiles with microRNA data from healthy smokers highlighted various highly translatable microRNAs associated with inflammation or with cell cycle processes that are known to be perturbed by CS in lung tissue. We also found a dose-dependent increase of MMP-1 release by AIR-100 tissue 48 h after CS exposure in agreement with the known effect of CS on this collagenase expression in smokers' tissues. In conclusion, a similar biological perturbation than the one observed in vivo in smokers' airway epithelium could be induced after a single CS exposure of a human organotypic bronchial epithelium-like tissue culture.
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Heijink, Irene H., Harold G. de Bruin, Robin Dennebos, Marnix R. Jonker, Jacobien A. Noordhoek, Corry-Anke Brandsma, Maarten van den Berge, and Dirkje S. Postma. "Cigarette smoke-induced epithelial expression of WNT-5B: implications for COPD." European Respiratory Journal 48, no. 2 (April 28, 2016): 504–15. http://dx.doi.org/10.1183/13993003.01541-2015.
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Wingless/integrase-1 (WNT) signalling is associated with lung inflammation and repair, but its role in chronic obstructive pulmonary disease (COPD) pathogenesis is unclear. We investigated whether cigarette smoke-induced dysregulation of WNT-5B contributes to airway remodelling in COPD.We analysed WNT-5B protein expression in the lung tissue of COPD patients and (non)smoking controls, and investigated the effects of cigarette smoke exposure on WNT-5B expression in COPD and control-derived primary bronchial epithelial cells (PBECs). Additionally, we studied downstream effects of WNT-5B on remodelling related genes fibronectin, matrix metalloproteinase (MMP)-2, MMP-9 and SnaiI in BEAS-2B and air–liquid interface (ALI)-cultured PBECs.We observed that airway epithelial WNT-5B expression is significantly higher in lung tissue from COPD patients than controls. Cigarette smoke extract significantly increased mRNA expression of WNT-5B in COPD, but not control-derived PBECs. Exogenously added WNT-5B augmented the expression of remodelling related genes in BEAS-2B cells, which was mediated by transforming growth factor (TGF)-β/Smad3 signalling. In addition, WNT-5B upregulated the expression of these genes in ALI-cultured PBECs, particularly PBECs from COPD patients.Together, our results provide evidence that exaggerated WNT-5B expression upon cigarette smoke exposure in the bronchial epithelium of COPD patients leads to TGF-β/Smad3-dependent expression of genes related to airway remodelling.
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Klus, Hubert, Barbara Boenke-Nimphius, and Lutz Müller. "Cigarette Mainstream Smoke: The Evolution of Methods and Devices for Generation, Exposure and Collection." Beiträge zur Tabakforschung International/Contributions to Tobacco Research 27, no. 4 (October 1, 2016): 137–274. http://dx.doi.org/10.1515/cttr-2016-0015.
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SUMMARYThe objective of this review is to support tobacco scientists when evaluating information published on smoking machines, and on cigarette mainstream smoke (in vivoandin vitro) exposure systems and collection devices.The intriguing development of smoking machines (mainly for cigarettes) is followed for more than 170 years - from the first simple set-ups in the 1840s to the sophisticated and fully automated analytical smoking machines available today. Systems for the large-scale production of smoke (condensate) for preparative work are equally considered. The standardization of machine smoking methods and test pieces has solved several technical problems and produced sensible rules but, at the same time, given rise to new controversies like the compatibility of artificial and human smoking, and the implementation of more intense machine smoking regimes.Adequate space is allotted for the discussion of configurations forin vivosmoke exposure of rodent and non-rodent species and the machines generating the required smoke (condensate). Covered as well is the field ofin vitrotoxicity testing, including the increasingly informative new techniques of air-liquid interface exposure, which are becoming more and more refined with the use of organotypic cultures and genetic analyses.The review is completed by the examination of the considerable variety of mainstream smoke collection devices (filters and traps) developed over time - some for very specific purposes - and refers to the perpetual problem of artifact formation by aging.
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Ragbir, Prabhash, Ajith Kaduwela, David Passovoy, Preet Amin, Shuchen Ye, Christopher Wallis, Christopher Alaimo, Thomas Young, and Zhaodan Kong. "UAV-Based Wildland Fire Air Toxics Data Collection and Analysis." Sensors 23, no. 7 (March 29, 2023): 3561. http://dx.doi.org/10.3390/s23073561.
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Smoke plumes emitted from wildland-urban interface (WUI) wildfires contain toxic chemical substances that are harmful to human health, mainly due to the burning of synthetic components. Accurate measurement of these air toxics is necessary for understanding their impacts on human health. However, air pollution is typically measured using ground-based sensors, manned airplanes, or satellites, which all provide low-resolution data. Unmanned Aerial Vehicles (UAVs) have the potential to provide high-resolution spatial and temporal data due to their ability to hover in specific locations and maneuver with precise trajectories in 3-D space. This study investigates the use of an octocopter UAV, equipped with a customized air quality sensor package and a volatile organic compound (VOC) air sampler, for the purposes of collecting and analyzing air toxics data from wildfire plumes. The UAV prototype developed has been successfully tested during several prescribed fires conducted by the California Department of Forestry and Fire Protection (CAL FIRE). Data from these experiments were analyzed with emphasis on the relationship between the air toxics measured and the different types of vegetation/fuel burnt. BTEX compounds were found to be more abundant for hardwood burning compared to grassland burning, as expected.
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Adamson, J., D. Azzopardi, and M. Gaça. "An exposure system for in vitro cell culture investigations of cigarette smoke toxicity at the air–liquid interface." Toxicology Letters 196 (July 2010): S135. http://dx.doi.org/10.1016/j.toxlet.2010.03.470.
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Hauser, Cindy DeForest, Ronnae Mailig, Hannah Stadtler, Jenna Reed, Shi Chen, Emilie Uffman, and Karen Bernd. "Waterpipe tobacco smoke toxicity: the impact of waterpipe size." Tobacco Control 29, Suppl 2 (September 6, 2019): s90—s94. http://dx.doi.org/10.1136/tobaccocontrol-2019-054960.
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IntroductionWaterpipe tobacco smoking continues to show increasing popularity, especially among individuals between 18 and 22 years old. Waterpipe tobacco smoke (WTS) is a mixture of particulates and gases formed from the combustion of the charcoal and volatilisation and humidification of the tobacco+humectant+flavouring substrate known as shisha or mu’assel. As such, variation in the configuration of the waterpipe may affect the particles produced. Our study focuses on the effects of waterpipe size on the physical properties and cytotoxicity of the smoke produced.MethodsShisha type and headspace volume were held constant and a modified Beirut puff protocol was followed while the size of the waterpipe was varied. Particle concentrations and size distributions were measured using a TSI Engine Exhaust Particle Sizer. Type II alveolar cells were exposed to smoke at the air-liquid interface and two metrics of cell health analysed.ResultsIn a 30 min session, we observed a decrease in total particle concentration (1014–1013) and mass (10 000–2800 mg/m3) and an increase in particle size (125–170 nm) as pipe height increases from 22 to 55 cm and bowl size from 300 to 1250 mL. Smoke from all pipe sizes caused decreases in lysosomal function (>40%) and membrane integrity (>60%) 24 hours post 57 min exposure, and meet the National Institutes of Health definition of a cytotoxic agent (≥30% decrease in cell viability).ConclusionSmoke from waterpipes of all sizes causes significant alveolar cellular harm, indicating that this device needs regulation as a hazard to human health.
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Moore, Martha M., Irene Abraham, Mark Ballantyne, Holger Behrsing, Xuefei Cao, Julie Clements, Marianna Gaca, et al. "Key Challenges and Recommendations for In Vitro Testing of Tobacco Products for Regulatory Applications: Consideration of Test Materials and Exposure Parameters." Alternatives to Laboratory Animals 51, no. 1 (January 2023): 55–79. http://dx.doi.org/10.1177/02611929221146536.
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The Institute for In Vitro Sciences (IIVS) is sponsoring a series of workshops to identify, discuss and develop recommendations for optimal scientific and technical approaches for conducting in vitro assays, to assess potential toxicity within and across tobacco and various next generation nicotine and tobacco products (NGPs), including heated tobacco products (HTPs) and electronic nicotine delivery systems (ENDS). The third workshop (24–26 February 2020) summarised the key challenges and made recommendations concerning appropriate methods of test article generation and cell exposure from combustible cigarettes, HTPs and ENDS. Expert speakers provided their research, perspectives and recommendations for the three basic types of tobacco-related test articles: i) pad-collected material (PCM); ii) gas vapour phase (GVP); and iii) whole smoke/aerosol. These three types of samples can be tested individually, or the PCM and GVP can be combined. Whole smoke/aerosol can be bubbled through media or applied directly to cells at the air–liquid interface. Summaries of the speaker presentations and the recommendations developed by the workgroup are presented. Following discussion, the workshop concluded the following: that there needs to be greater standardisation in aerosol generation and collection processes; that methods for testing the NGPs need to be developed and/or optimised, since simply mirroring cigarette smoke testing approaches may be insufficient; that understanding and quantitating the applied dose is fundamental to the interpretation of data and conclusions from each study; and that whole smoke/aerosol approaches must be contextualised with regard to key information, including appropriate experimental controls, environmental conditioning, analytical monitoring, verification and performance criteria.
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Burke, Marshall, Anne Driscoll, Sam Heft-Neal, Jiani Xue, Jennifer Burney, and Michael Wara. "The changing risk and burden of wildfire in the United States." Proceedings of the National Academy of Sciences 118, no. 2 (January 11, 2021): e2011048118. http://dx.doi.org/10.1073/pnas.2011048118.
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Recent dramatic and deadly increases in global wildfire activity have increased attention on the causes of wildfires, their consequences, and how risk from wildfire might be mitigated. Here we bring together data on the changing risk and societal burden of wildfire in the United States. We estimate that nearly 50 million homes are currently in the wildland–urban interface in the United States, a number increasing by 1 million houses every 3 y. To illustrate how changes in wildfire activity might affect air pollution and related health outcomes, and how these linkages might guide future science and policy, we develop a statistical model that relates satellite-based fire and smoke data to information from pollution monitoring stations. Using the model, we estimate that wildfires have accounted for up to 25% of PM2.5 (particulate matter with diameter <2.5 μm) in recent years across the United States, and up to half in some Western regions, with spatial patterns in ambient smoke exposure that do not follow traditional socioeconomic pollution exposure gradients. We combine the model with stylized scenarios to show that fuel management interventions could have large health benefits and that future health impacts from climate-change–induced wildfire smoke could approach projected overall increases in temperature-related mortality from climate change—but that both estimates remain uncertain. We use model results to highlight important areas for future research and to draw lessons for policy.
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Rayner, Rachael E., Patrudu Makena, Gaddamanugu L. Prasad, and Estelle Cormet-Boyaka. "Cigarette and ENDS preparations differentially regulate ion channels and mucociliary clearance in primary normal human bronchial 3D cultures." American Journal of Physiology-Lung Cellular and Molecular Physiology 317, no. 2 (August 1, 2019): L295—L302. http://dx.doi.org/10.1152/ajplung.00096.2019.
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Cigarette smoking is known to disrupt the normal mucociliary function of the lungs, whereas the effect of electronic nicotine delivery systems (ENDS) is not completely understood. This study aimed to compare the effects of acute exposure of primary normal human bronchial epithelial (NHBE) 3D cultures at air-liquid interface to combustible cigarette and ENDS preparations on mucociliary function, including ion channel function, ciliary beat frequency (CBF), and airway surface liquid (ASL) height. Differentiated NHBE cultures were exposed to whole smoke-conditioned media (WS-CM) or total particulate matter (TPM) prepared from 3R4F reference cigarettes, whole aerosol-conditioned media (ACM) or e-TPM generated from a marketed ENDS product, or nicotine alone. We found that a dose of 7 μg/mL equi-nicotine units of cigarette TPM and WS-CM significantly decreased cystic fibrosis transmembrane conductance regulator (CFTR) and the epithelial sodium channel (ENaC) function, which regulates fluid homeostasis in the lung. Conversely, higher (56 µg/mL) equi-nicotine units of ENDS preparations or nicotine alone had no effect on CFTR and ENaC function. Despite a significant decrease in ion channel function, cigarette smoke preparations did not alter CBF and ASL. Similarly, ENDS preparations and nicotine alone had no effect on ASL and CBF. This study demonstrates that acute exposures of cigarette smoke preparations exert a notable inhibitory effect on CFTR and ENaC function compared with ENDS preparations. In summary, the functional assays described herein are potentially useful for tobacco product evaluations.
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Purnamasari, Prima Dewi, Evan G. Sumbayak, Vicky Dwi Kurniawan, and RR Wulan Apriliyanti. "CO Pollution Warning System for Indoor Parking Area Using FPGA." International Journal of Reconfigurable and Embedded Systems (IJRES) 2, no. 2 (July 1, 2013): 64. http://dx.doi.org/10.11591/ijres.v2.i2.pp64-75.
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From some compounds used as parameters in air pollution-such as O3, Particulate Materials, CO, NO2, SO2 and Pb-CO is the most common cause of poisoning accidents. Indoor parking area is one sample of potential area for CO pollution. However, according to the scientific nature of CO-tasteless, colorless, and odorless-people exposed to CO are usually not aware that s/he exposed to dangerous levels of CO. This research aimed to make a prototype of an embedded system that can monitor air pollution, give an effective warning and it should be affordable. The prototype of CO air pollution alert system has been successfully built using FPGA Xilinx Spartan 3E as the major component. Sensor Hanwei MQ7 used in this prototype has been tested in a simulation box using cigarette smoke as CO pollutant and the reading result has met the characteristic curve in the datasheet. The system interface has met user satisfaction with MOS value 4.31 from 5 scales. Based on the response time testing, we conclude that FPGA is suitable to be used in a system that performs fast parallel processing based on logical actions from the input given.
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Aufderheide, Michaela, Shigeaki Ito, Shinkichi Ishikawa, and Makito Emura. "Metaplastic phenotype in human primary bronchiolar epithelial cells after repeated exposure to native mainstream smoke at the air-liquid interface." Experimental and Toxicologic Pathology 69, no. 5 (June 2017): 307–15. http://dx.doi.org/10.1016/j.etp.2017.01.015.
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Azzopardi, David, Linsey E. Haswell, Geoff Foss-Smith, Katherine Hewitt, Nathan Asquith, Sarah Corke, and Gary Phillips. "Evaluation of an air–liquid interface cell culture model for studies on the inflammatory and cytotoxic responses to tobacco smoke aerosols." Toxicology in Vitro 29, no. 7 (October 2015): 1720–28. http://dx.doi.org/10.1016/j.tiv.2015.06.016.
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Aminu, Muhammad, Ali Yerima, Abubakar Salisu, and Abbas Adamu. "Design and Implementation of an IOT Based Smart Home Monitoring and Control System Using NodeMCU." Journal of Engineering Research and Reports 25, no. 2 (May 19, 2023): 78–88. http://dx.doi.org/10.9734/jerr/2023/v25i2881.
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This paper presents the design and implementation of an IoT-based smart home monitoring and control system using a NodeMCU firmware and prototyping board. The system allows the user to remotely control electrical appliances through a web-based user interface dashboard. The system uses sensors DHT11 to monitor the temperature and humidity of the home and MQ 2 to monitor the air quality and alerts the user in case smoke or fire is detected. Various HTML scripts are executed to develop a web-based dashboard interface where the user interacts with the system. When connected to the internet, the system generates an IP address that is used to assess the web page for monitoring and control of various house appliances. A maximum coverage range of up to 42.05 meters indoors was achieved by the system using the onboard Wi-Fi module on the NodeMCU. In addition, a correlation was observed between the Wi-Fi coverage distance and the response time to a command signal from the web-based dashboard. The system provides energy efficiency, home security, and centralized remote control of appliances thereby minimizing human efforts and energy losses and providing a friendly and secure home.
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Knabe, Lucie, Aurélie Petit, Charlotte Vernisse, Jérémy Charriot, Martine Pugnière, Corinne Henriquet, Souphatta Sasorith, et al. "CCSP counterbalances airway epithelial-driven neutrophilic chemotaxis." European Respiratory Journal 54, no. 1 (April 25, 2019): 1802408. http://dx.doi.org/10.1183/13993003.02408-2018.
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Club cell secretory protein (CCSP) knockout mice exhibit increased airway neutrophilia, as found in chronic obstructive pulmonary disease (COPD). We therefore investigated whether treating COPD airway epithelia with recombinant human CCSP (rhCCSP) could dampen exaggerated airway neutrophilia.Control, smoker and COPD air–liquid interface (ALI) cultures exposed to cigarette smoke extract (CSE) were treated with and without rhCCSP. The chemotactic properties of the supernatants were assessed using Dunn chambers. Neutrophil chemotaxis along recombinant human interleukin 8 (rhIL8) gradients (with and without rhCCSP) was also determined. rhCCSP–rhIL8 interactions were tested through co-immunoprecipitation, Biacore surface plasmon resonance (SPR) andin silicomodelling. The relationship between CCSP/IL8 concentration ratios in the supernatant of induced sputum from COPD patientsversusneutrophilic airway infiltration assessed in lung biopsies was assessed.Increased neutrophilic chemotactic activity of CSE-treated ALI cultures followed IL8 concentrations and returned to normal when supplemented with rhCCSP. rhIL8-induced chemotaxis of neutrophils was reduced by rhCCSP. rhCCSP and rhIL8 co-immunoprecipitated. SPR confirmed thisin vitrointeraction (equilibrium dissociation constant=8 µM).In silicomodelling indicated that this interaction was highly likely. CCSP/IL8 ratios in induced sputum correlated well with the level of small airway neutrophilic infiltration (r2=0.746, p<0.001).CCSP is a biologically relevant counter-balancer of neutrophil chemotactic activity. These different approaches used in this study suggest that, among the possible mechanisms involved, CCSP may directly neutralise IL8.
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Åstrand, Annika B. M., Martin Hemmerling, James Root, Cecilia Wingren, Jelena Pesic, Edvin Johansson, Alaina L. Garland, Arunava Ghosh, and Robert Tarran. "Linking increased airway hydration, ciliary beating, and mucociliary clearance through ENaC inhibition." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 1 (January 1, 2015): L22—L32. http://dx.doi.org/10.1152/ajplung.00163.2014.
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Airway dehydration causes mucus stasis and bacterial overgrowth in cystic fibrosis and chronic bronchitis (CB). Rehydration by hypertonic saline is efficacious but suffers from a short duration of action. We tested whether epithelial sodium channel (ENaC) inhibition would rehydrate normal and dehydrated airways to increase mucociliary clearance (MCC) over a significant time frame. For this, we used a tool compound (Compound A), which displays nanomolar ENaC affinity and retention in the airway surface liquid (ASL). Using normal human bronchial epithelial cultures (HBECs) grown at an air-liquid interface, we evaluated in vitro potency and efficacy using short-circuit current ( Isc) and ASL height measurements where it inhibited Isc and increased ASL height by ∼50% (0.052 μM at 6 h), respectively. The in vivo efficacy was investigated in a modified guinea pig tracheal potential difference model, where we observed an effective dose (ED50) of 5 μg/kg (i.t.), and by MCC measures in rats and sheep, where we demonstrated max clearance rates at 100 μg/kg (i.t.) and 75 μg/kg (i.t.), respectively. Acute cigarette smoke-induced ASL height depletion in HBECs was used to mimic the situation in patients with CB, and pretreatment prevented both cigarette smoke-induced ASL dehydration and lessened the decrease in ciliary beat frequency. Furthermore, when added after cigarette smoke exposure, Compound A increased the rate of ASL rehydration. In conclusion, Compound A demonstrated significant effects and a link between increased airway hydration, ciliary function, and MCC. These data support the hypothesis that ENaC inhibition may be efficacious in the restoration of mucus hydration and transport in patients with CB.
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Bigot, Paul, Simon Chesseron, Ahlame Saidi, Damien Sizaret, Christelle Parent, Agnès Petit-Courty, Yves Courty, Fabien Lecaille, and Gilles Lalmanach. "Cleavage of Occludin by Cigarette Smoke-Elicited Cathepsin S Increases Permeability of Lung Epithelial Cells." Antioxidants 12, no. 1 (December 21, 2022): 5. http://dx.doi.org/10.3390/antiox12010005.
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Background. Chronic obstructive pulmonary disease (COPD) is an irreversible disease mainly caused by smoking. COPD is characterized by emphysema and chronic bronchitis associated with enhanced epithelial permeability. Hypothesis. Lung biopsies from smokers revealed a decreased expression level of occludin, which is a protein involved in the cohesion of epithelial tight junctions. Moreover, the occludin level correlated negatively with smoking history (pack-years), COPD grades, and cathepsin S (CatS) activity. Thus, we examined whether CatS could participate in the modulation of the integrity of human lung epithelial barriers. Methods and results. Cigarette smoke extract (CSE) triggered the upregulation of CatS by THP-1 macrophages through the mTOR/TFEB signaling pathway. In a co-culture model, following the exposure of macrophages to CSE, an enhanced level of permeability of lung epithelial (16HBE and NHBE) cells towards FITC-Dextran was observed, which was associated with a decrease in occludin level. Similar results were obtained using 16HBE and NHBE cells cultured at the air–liquid interface. The treatment of THP-1 macrophages by CatS siRNAs or by a pharmacological inhibitor restored the barrier function of epithelial cells, suggesting that cigarette smoke-elicited CatS induced an alteration of epithelial integrity via the proteolytic injury of occludin. Conclusions. Alongside its noteworthy resistance to oxidative stress induced by cigarette smoke oxidants and its deleterious elastin-degrading potency, CatS may also have a detrimental effect on the barrier function of epithelial cells through the cleavage of occludin. The obtained data emphasize the emerging role of CatS in smoking-related lung diseases and strengthen the relevance of targeting CatS in the treatment of emphysema and COPD.
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Hargrave, Chad, Lance Munday, Gareth Kennedy, and André de Kock. "Mine Machine Radar Sensor for Emergency Escape." Resources 9, no. 2 (February 4, 2020): 16. http://dx.doi.org/10.3390/resources9020016.
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This paper presents the results of recent work to develop and trial a mine machine radar sensor for underground coal mine vehicles. There is an urgent industry need for an integrated solution to the problem of operating an underground vehicle in conditions of dense ambient dust and/or smoke, such as may occur in underground coal mines after a fire or explosion. Under these conditions, sensors such as cameras and lidar offer limited assistance due to their inability to penetrate thick dust. Thermal infrared can penetrate dust but still results in poor vision, as there is insufficient temperature contrast between the tunnel walls and the ambient air. Microwave radar sensors are able to penetrate the dust, and suitable radar sensors have been developed for use in the automation industry. Adapting such sensors for use in an underground coal mining environment was the focus of this research effort, and involved trialing a suitable sensor in dust and smoke chambers as well as trials in an underground coal mine with introduced dust. Data processing and the development of a suitable user interface were key aspects of the research. Since any sensor would have to operate in an explosive atmosphere, a related research work developed a flameproof dielectric enclosure to allow the use of the radar in the mine environment.
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Nara, Hidenori, Yasuo Fukano, Tomoki Nishino, and Michaela Aufderheide. "Detection of the cytotoxicity of water-insoluble fraction of cigarette smoke by direct exposure to cultured cells at an air–liquid interface." Experimental and Toxicologic Pathology 65, no. 5 (July 2013): 683–88. http://dx.doi.org/10.1016/j.etp.2012.08.004.
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Chen, Rui, Yingmin Liang, Mary Sau Man Ip, Kalin Yanbo Zhang, and Judith Choi Wo Mak. "Amelioration of Cigarette Smoke-Induced Mucus Hypersecretion and Viscosity by Dendrobium officinale Polysaccharides In Vitro and In Vivo." Oxidative Medicine and Cellular Longevity 2020 (October 20, 2020): 1–10. http://dx.doi.org/10.1155/2020/8217642.
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Chronic obstructive pulmonary disease (COPD), characterized by oxidative stress and inflammation, is one of the leading causes of death worldwide, in which cigarette smoke (CS) is the major risk factor. Dendrobium officinale polysaccharides (DOPs) are the main active ingredients extracted from Dendrobium officinale, which have been reported to have antioxidant and anti-inflammatory activity as well as inhibition of mucin gene expression. This study is aimed at investigating the effect of DOPs on CS-induced mucus hypersecretion and viscosity in vitro and in vivo. For in vitro study, primary normal human bronchial epithelial cells (HBECs) differentiated at the air-liquid interface (ALI) culture for 28 days were stimulated with cigarette smoke medium (CSM) in the absence or presence of various concentrations of DOPs or N-acetylcysteine (NAC) for 24 hours. For in vivo study, male Sprague-Dawley rats were randomized to sham air (SA) as control group or CS group for 56 days. At day 29, rats were subdivided and given water as control, DOPs, or NAC as positive control as a mucolytic drug via oral gavage for the remaining duration. Samples collected from apical washing, cell lysates, bronchoalveolar lavage (BAL), and lung tissues were evaluated for mucin gene expression, mucus secretion, and viscosity. DOPs ameliorated the CS-induced mucus hypersecretion and viscosity as shown by the downregulation of MUC5AC mRNA, MUC5AC secretary protein, and mucus viscosity via inhibition of mucus secretory granules in both in vitro and in vivo models. DOPs produced its effective effects on the CS-induced mucus hypersecretion and viscosity via the inhibition of the mucus secretory granules. These findings could be a starting point for considering the potential role of DOPs in the management of the smoking-mediated COPD. However, further research is needed.
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Mathis, Carole, Stephan Gebel, Carine Poussin, Vincenzo Belcastro, Alain Sewer, Dirk Weisensee, Arnd Hengstermann, et al. "A Systems Biology Approach Reveals the Dose- and Time-Dependent Effect of Primary Human Airway Epithelium Tissue Culture after Exposure to Cigarette Smoke in Vitro." Bioinformatics and Biology Insights 9 (January 2015): BBI.S19908. http://dx.doi.org/10.4137/bbi.s19908.
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To establish a relevant in vitro model for systems toxicology-based mechanistic assessment of environmental stressors such as cigarette smoke (CS), we exposed human organotypic bronchial epithelial tissue cultures at the air liquid interface (ALI) to various CS doses. Previously, we compared in vitro gene expression changes with published human airway epithelia in vivo data to assess their similarities. Here, we present a follow-up evaluation of these in vitro transcriptomics data, using complementary computational approaches and an integrated mRNA-microRNA (miRNA) analysis. The main cellular pathways perturbed by CS exposure were related to stress responses (oxidative stress and xenobiotic metabolism), inflammation (inhibition of nuclear factor-kB and the interferon gamma-dependent pathway), and proliferation/differentiation. Within post-exposure periods up to 48 hours, a transient kinetic response was observed at lower CS doses, whereas higher doses resulted in more sustained responses. In conclusion, this systems toxicology approach has potential for product testing according to “21st Century Toxicology”.
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Veerapaneni, Vivek Vardhan, Swapna Upadhyay, Tania A. Thimraj, Jayaraj Biligere Siddaiah, Chaya Sindaghatta Krishnarao, Komarla Sundararaja Lokesh, Rajesh Thimmulappa, Lena Palmberg, Koustav Ganguly, and Mahesh Padukudru Anand. "Circulating Secretoglobin Family 1A Member 1 (SCGB1A1) Levels as a Marker of Biomass Smoke Induced Chronic Obstructive Pulmonary Disease." Toxics 9, no. 9 (August 31, 2021): 208. http://dx.doi.org/10.3390/toxics9090208.
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Secretoglobin family 1A member 1 (SCGB1A1) alternatively known as club cell protein 16 is a protective pneumo-protein. Decreased serum levels of SCGB1A1 have been associated with tobacco smoke induced chronic obstructive pulmonary disease (TS-COPD). Exposure to biomass smoke (BMS) is an important COPD risk factor among women in low and lower-middle income countries. Therefore, in a cross-sectional study (n = 50/group; total 200 subjects) we assessed serum SCGB1A1 levels in BMS-COPD subjects (11 male, 39 female) compared to TS-COPD (all male) along with TS-CONTROL (asymptomatic smokers, all male) and healthy controls (29 male, 21 female) in an Indian population. Normal and chronic bronchitis like bronchial mucosa models developed at the air–liquid interface using human primary bronchial epithelial cells (3 donors, and three replicates per donor) were exposed to cigarette smoke condensate (CSC; 0.25, 0.5, and 1%) to assess SCGB1A1 transcript expression and protein secretion. Significantly (p < 0.0001) decreased serum SCGB1A1 concentrations (median, interquartile range, ng/mL) were detected in both BMS-COPD (1.6; 1.3–2.4) and TS-COPD (1.8; 1.4–2.5) subjects compared to TS-CONTROL (3.3; 2.9–3.5) and healthy controls (5.1; 4.5–7.2). The levels of SCGB1A1 were positively correlated (r = 0.7–0.8; p < 0.0001) with forced expiratory volume in 1 s, forced vital capacity, their ratios, and exercise capacity. The findings are also consistent within the BMS-COPD sub-group as well. Significantly (p < 0.03) decreased SCGB1A1 concentrations were detected with severity of COPD, dyspnea, quality of life, and mortality indicators. In vitro studies demonstrated significantly (p < 0.05) decreased SCGB1A1 transcript and/or protein levels following CSC exposure. Circulating SCGB1A1 levels may therefore also be considered as a potent marker of BMS-COPD and warrant studies in larger independent cohorts.
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Swidinsky, Andrei, and Misac Nabighian. "Transient electromagnetic fields of a buried horizontal magnetic dipole." GEOPHYSICS 81, no. 6 (November 1, 2016): E481—E491. http://dx.doi.org/10.1190/geo2016-0136.1.
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Electromagnetic surveys using a vertical transmitter loop are common in land, marine, and airborne geophysical exploration. Most of these horizontal magnetic dipole (HMD) systems operate in the frequency domain, measuring the time derivative of the induced magnetic fields, and therefore a majority of studies have focused on this subset of field measurements. We examine the time-domain electromagnetic response of a HMD including the electric fields and corresponding smoke rings produced in a conductive half-space. Cases of a dipole at the surface and buried within the earth are considered. Results indicate that when the current in the transmitter is rapidly switched off, a single smoke ring is produced within the plane of the vertical transmitter loop, which is then distorted by the air-earth interface. In this situation, the circular smoke ring, which would normally diffuse symmetrically away from the source in a whole space, is approximately transformed into an ellipse, with a vertical major axis at an early time and a horizontal major axis at a late time. As measured from the location of the transmitter, the depth of investigation and lateral footprint of such a system increases with burial depth. It is also observed that the electric field measured in the direction of the magnetic dipole only contains a secondary response related to the charge accumulation on any horizontal conductivity boundaries because the primary field is always absent. This field component can be expressed analytically in terms of a static and time-varying field, the latter term adding spatial complexity to the total horizontal electric field at the earth surface at early times. Applications of this theoretical study include the design of time-domain induction-logging tools, crossborehole electromagnetic surveys, underground mine expansion work, mine rescue procedures, and novel marine electromagnetic experiments.
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Leigh, Noel J., Phillip L. Tran, Richard J. O’Connor, and Maciej Lukasz Goniewicz. "Cytotoxic effects of heated tobacco products (HTP) on human bronchial epithelial cells." Tobacco Control 27, Suppl 1 (September 5, 2018): s26—s29. http://dx.doi.org/10.1136/tobaccocontrol-2018-054317.
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BackgroundHeated tobacco product(s) (HTP), also called heat-not-burn products, are a re-emerging class of tobacco products that purport to reduce health risk compared with smoking combustible tobacco products. This study examined the potential toxic effects of inhaling emissions from an HTP in comparison with electronic and combustible tobacco cigarettes.MethodsInhalation toxicity of HTP (IQOS; tobacco flavour), e-cigarette (MarkTen; tobacco flavour) and tobacco cigarette (Marlboro Red) was examined in vitro using an air–liquid interface with human bronchial epithelial cells (H292). Cells were exposed directly to 55 puffs from the e-cigarette, 12 puffs from the HTP and 8 puffs from the tobacco cigarette to equilibrate nicotine delivery to the cells across products. Cytotoxicity was measured using neutral red uptake and trypan blue assays. Cytotoxic effects of each tested product (HTP, e-cigarette and tobacco cigarette) were compared with an air control. Release of inflammatory markers (cytokines) was measured using ELISA.ResultsThe HTP showed higher cytotoxicity compared with the air controls using the neutral red assay. The HTP also showed higher cytotoxicity than the e-cigarette, but lower cytotoxicity than the combustible cigarettes using the same assay. A significant increase in cytokines levels, compared with air controls, was observed postexposure to tobacco smoke but not to emissions from HTP or e-cigarette aerosol.DiscussionUsing limited cytotoxic measures, the HTP showed reduced cytotoxicity relative to a combustible cigarette but higher toxicity than an e-cigarette. More comprehensive testing is needed to determine long-term effects of inhaling emissions from HTP.
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Weber, S., M. Hebestreit, T. Wilms, and B. Kurkowsky. "Validation of the in vitro comet assay in conjunction with an air–liquid interface exposure of cigarette smoke in human lung epithelial cells." Toxicology Letters 196 (July 2010): S134. http://dx.doi.org/10.1016/j.toxlet.2010.03.467.
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Wilkinson, S. L., A. K. Furukawa, B. M. Wotton, and J. M. Waddington. "Mapping smouldering fire potential in boreal peatlands and assessing interactions with the wildland–human interface in Alberta, Canada." International Journal of Wildland Fire 30, no. 7 (2021): 552. http://dx.doi.org/10.1071/wf21001.
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Treed peatlands exhibit both crown and smouldering fire potential; however, neither are included in Canadian wildfire management models and, as such, they are not formally represented in management decision-making. The lack of smouldering fire risk assessment is a critical research gap as these fires can represent heavy resource draws and are predominant sources of smoke, air pollutants and atmospheric carbon. Here, for the first time, we combine existing knowledge of the controls on smouldering peat fire with expert opinion-based weightings through a multi-criteria decision analysis, to map the smouldering fire potential (i.e. hazard) of treed peatlands in the Boreal Plains, Alberta, Canada. We find that smouldering potential varies considerably between treed peatlands and that areas of sparser peatland coverage may contain high smouldering-potential peatlands. Further, we find that treed peatlands are a common feature in the wildland–human interface and that proportionally, the area of high smouldering potential is greater closer to roads compared with farther away. Our approach enables a quantitative measure of smouldering fire potential and evidences the need to incorporate peatland–wildfire interactions into wildfire management operations. We suggest that similar frameworks could be used in other peatland dominated regions as part of smouldering fire risk assessments.
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Su, Kuo Lan, Sheng Wen Shiau, Yi Lin Liao, and J. H. Guo. "Bayesian Estimation Algorithm Applying in Gas Detection Modules." Applied Mechanics and Materials 284-287 (January 2013): 1764–69. http://dx.doi.org/10.4028/www.scientific.net/amm.284-287.1764.
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The paper develops gas detection modules for the intelligent building. The modules use many gas sensors to detect environment of the home and building. The gas sensors of the detection modules are classified two types. One is competitiveness gas detection module, and uses the same sensors to detect gas leakage. The other is complementation gas detection module, and uses variety sensors to classify multiple gases. The paper uses Bayesian estimation algorithm to be applied in competitiveness gas detection module and complementation gas detection module, and implement the proposed algorithm to be nice for variety gas sensor combination method. In the competitiveness gas detection module, we use two gas sensors to improve the proposed algorithm to be right. In the complementation gas detection module, we use a NH3 sensor, an air pollution sensor, an alcohol sensor, a HS sensor, a smoke sensor, a CO sensor, a LPG sensor and a nature gas sensor, and can classify variety gases using Bayesian estimation algorithm. The controller of the two gas detection modules is HOLTEK microchip. The modules can communicate with the supervised computer via wire series interface or wireless RF interface, and cautions the user by the voice module. Finally, we present some experimental results to measure know and unknown gas using the two gas detection modules on the security system of the intelligent building.
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Muñoz, Carlos, Juan Huircan, Francisco Jaramillo, and Álex Boso. "Calibration of Sensor Network for Outdoor Measurement of PM2.5 on High Wood-Heating Smoke in Temuco City." Processes 11, no. 8 (August 3, 2023): 2338. http://dx.doi.org/10.3390/pr11082338.
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In order to ascertain the spatial and temporal changes in the air quality in Temuco City, Chile, we created and installed a network of inexpensive sensors to detect PM2.5 particulate matter. The 21 measurement points deployed were based on a low-cost Sensiron SPS30 sensor, complemented with temperature and humidity sensors, an Esp32 microcontroller card with LoRa and WiFi wireless communication interface, and a solar charging unit. The units were calibrated using an airtight combustion chamber with a Grimm 11-E as a reference unit. The calibration procedure fits the parameters of a calibration model to map the raw low-cost particle-material measurements into reliable calibrated values. The measurements showed that the concentrations of fine particulate material recorded in Temuco present a high temporal and spatial variability. In critical contamination episodes, pollution reaches values as high as 354 µg/m3, and at the same time, it reaches 50 µg/m3 in other parts of the city. The contamination episodes show a similar trend around the city, and the peaks are in the time interval from 07:00 PM to 1:00 AM. In the winter, this time of day coincides with when families are usually home and there are low temperatures outside.
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Karuna, G., R. P. Ram Kumar, Steven Gopaldas, Vasista Parvathaneni, and Teddu Lokesh. "Air Quality and Hazardous Gas Detection using IoT for Household and Industrial Areas." E3S Web of Conferences 391 (2023): 01146. http://dx.doi.org/10.1051/e3sconf/202339101146.
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The detection and monitoring of hazardous gases is essential for ensuring the safety of individuals in various settings, such as industrial environments and residential areas. gas detectors detect gases like LPG, NH3, alcohol, NOx, Benzene, CO2, Alcohol, Propane, Hydrogen, Methane, Carbon Monoxide, and smoke in the area around them. In this study, we present a system for real-time detection and monitoring of hazardous gases using MQ135 and MQ2 sensors. The system consists of a monitor that is placed in a fixed location and a mobile device that can be carried by the user. The MQ135 sensor is used to detect gases such as ammonia, while the MQ2 sensor is used to detect gases such as carbon monoxide and hydrocarbons. Each of these gases is known through the Parts per Million (PPM) values and can be determined which gas it is. The system utilises a microcontroller to process the sensor data and display the gas concentrations on a user interface. The mobile device also has the capability to alert the user and send notifications through an accompanying App if the gas concentrations exceed a predetermined threshold. The system is reliable, accurate, and easy to use, making it an ideal solution for detecting and mitigating the risks associated with hazardous gases in various settings. The system was tested in various environments and was able to accurately detect and monitor the presence of hazardous gases and it is a reliable and convenient solution for detecting and monitoring hazardous gases in real-time.
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Weber, Susanne, Marco Hebestreit, Torsten Wilms, Lynda L. Conroy, and Gregory Rodrigo. "Comet assay and air–liquid interface exposure system: A new combination to evaluate genotoxic effects of cigarette whole smoke in human lung cell lines." Toxicology in Vitro 27, no. 6 (September 2013): 1987–91. http://dx.doi.org/10.1016/j.tiv.2013.06.016.
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Jaunky, Tomasz, David Thorne, Andrew Baxter, Simone Hadley, Justin Frosina, Damien Breheny, James Murphy, and Marianna Gaça. "An Experimental Analytical and In Vitro Approach to Bridge Between Different Heated Tobacco Product Variants." Contributions to Tobacco & Nicotine Research 31, no. 1 (March 1, 2022): 1–9. http://dx.doi.org/10.2478/cttr-2022-0001.
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Summary Tobacco heating products (THPs) have reduced toxicant emissions relative to cigarettes. THPs are continually evolving, but safety and efficacy studies on each new variant involve considerable resources. As employed by the pharmaceutical industry, a “bridging” process could be used to demonstrate product equivalence. Therefore, we investigated the feasibility of a bridging approach by evaluating aerosol emissions and in vitro cytotoxicity of five variant THPs in relation to a base product. All products were compared to a reference cigarette and a commercial benchmark. Relative to smoke, chemical reductions in THP aerosols were comparable among the THPs at 94–97%. The aerosols showed similar cytotoxicity in human lung tissues exposed at the air-liquid interface (p = 0.8378) but were significantly less toxic than smoke (p = 0.04). Relative to the THP benchmark, variant THPs showed lower cytotoxicity (p = 0.0141). Emissions and cytotoxicity data demonstrated that the variant THPs were comparable to the base THP, irrespective of consumable format or flavour. This dataset demonstrates the feasibility of a bridging approach and can inform an evidence-based strategy in developing sufficient data to predict similarity against an already established dataset. Therefore, avoiding repetition of vast data generation could ease authorisation requirements of newer products. Finally, we propose that more work is required to understand chemical, biological (in vitro), human consumption, and clinical data before the equivalence of these products (and others) can be definitively demonstrated. Future studies maybe needed to assess additional chemical and biological outputs and all data will need to be contextualised against human consumption data in terms of a bridging framework.