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To understand the smoke level and NOx emission characteristics of in-use construction machinery in Beijing, we selected 905 construction machines in Beijing from August 2022 to April 2023 to monitor the emission level of smoke and NOx. The exhaust smoke level and excessive emission situation of different machinery types were identified, and their NOx emission levels were monitored according to the free acceleration method. We investigated the correlation of NOx and smoke emission, and proposed suggestions for controlling pollution discharge from construction machinery in the future. The results show that the exhaust smoke level was 0-2.62 m-1, followed a log-normal distribution (µ = -1.73, δ = 1.09, R2 = 0.99), with a 5.64% exceedance rate. Differences were observed among machinery types, with low-power engine forklifts showing higher smoke levels. The NOx emission range was 71-1516 ppm, followed a normal distribution (µ = 565.54, δ = 309.51, R2 = 0.83). Differences among machinery types were relatively small. Engine rated net power had the most significant impact on NOx emissions. Thus, NOx emissions from construction machinery need further attention. Furthermore, we found a weak negative correlation (p < 0.05) between the emission level of smoke and NOx, that is the synergic emission reduction effect is poor, emphasizing the need for NOx emission limits. In the future, the oversight in Beijing should prioritize phasing out China Ⅰ and China Ⅱ machinery, and monitor emissions from high-power engine China Ⅲ machinery.

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Cigarette smoke, a complex mixture produced by tobacco combustion, contains a variety of carcinogens and can trigger DNA damage. Overactivation of c-MET, a receptor tyrosine kinase, may cause cancer and cellular DNA damage, but the underlying mechanisms are unknown. In this work, we investigated the mechanisms of cigarette smoke extract (CSE) induced malignant transformation and DNA damage in human bronchial epithelial cells (BEAS-2B). The results demonstrated that CSE treatment led to up-regulated mRNA expression of genes associated with the c-MET signaling pathway, increased expression of the DNA damage sensor protein γ-H2AX, and uncontrolled proliferation in BEAS-2B cells. ATR, ATR, and CHK2, which are involved in DNA damage repair, as well as the phosphorylation of c-MET and a group of kinases (ATM, ATR, CHK1, CHK2) involved in the DNA damage response were all activated by CSE. In addition, CSE activation promotes the phosphorylation modification of ATR, CHK1 proteins associated with DNA damage repair. The addition of PHA665752, a specific inhibitor of c-MET, or knock-down with c-MET both attenuated DNA damage, while overexpression of c-MET exacerbated DNA damage. Thus, c-MET phosphorylation may be involved in CSE-induced DNA damage, providing a potential target for intervention in the prevention and treatment of smoking-induced lung diseases.

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Magnesium is a combustible metal that poses various safety risks, including fires and explosions. However, there are limited safety measures available to prevent and respond to potential fires and explosion incidents in the metal industry. In this study, the combustion process of Mg fires was closely examined using infrared thermal imaging, focusing on the effects of Mg powder size. For the experiment, Mg powder was burned by increasing the temperature to approximately 967.4 K using an ignition unit and controller equipped with a tungsten heater. Moreover, combustion velocity measurement experiments for Mg particle sizes of 75, 100, and 150 µm were conducted using the combustion velocity measurement device presented in the NFPA 484 standard. On combustion of Mg, flames are observed; smoke is emitted as demonstrated by thermal and flow visualization experiments. The combustion velocity measurement experiment results demonstrated that the greater the slope value (combustion velocity) for the combustion length over time, the faster is the combustion velocity, with the 75 µm particle size having the fastest combustion velocity. The results of this experiment can be utilized as references for Mg fire control design and to gain a better understanding of the scope of smoke and fire hazard investigation measures.

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A significant consequence of climate change is the rising incidence of wildfires. When wildfires occur close to wine grape (Vitis vinifera) production areas, smoke-derived volatile phenolic compounds can be taken up by the grape berries, negatively affecting the flavor and aroma profile of the resulting wine and compromising the production value of entire vineyards. Evidence for the permeation of smoke-associated compounds into grape berries has been provided through metabolomics; however, the basis for grapevines' response to smoke at the gene expression level has not been investigated in detail. To address this knowledge gap, we employed time-course RNA sequencing to observe gene expression-level changes in grape berries in response to smoke exposure. Significant increases in gene expression (and enrichment of gene ontologies) associated with detoxification of reactive compounds, maintenance of redox homeostasis, and cell wall fortification were observed in response to smoke. These findings suggest that the accumulation of volatile phenols from smoke exposure activates mechanisms that render smoke-derived compounds less reactive while simultaneously fortifying intracellular defense mechanisms. The results of this work lend a better understanding of the molecular basis for grapevines' response to smoke and provide insight into the origins of smoke-taint-associated flavor and aroma attributes in wine produced from smoke-exposed grapes.

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This review delves into the molecular complexities underpinning the epithelial-to-mesenchymal transition (EMT) induced by cigarette smoke (CS) in human bronchial epithelial cells (HBECs). The complex interplay of pathways, including those related to WNT//ß-catenin, TGF-ß/SMAD, hypoxia, oxidative stress, PI3K/Akt, and NF-κB, plays a central role in mediating this transition. While these findings significantly broaden our understanding of CS-induced EMT, the research reviewed herein leans heavily on 2D cell cultures, highlighting a research gap. Furthermore, the review identifies a stark omission of genetic and epigenetic factors in recent studies. Despite these shortcomings, the findings furnish a consolidated foundation not only for the academic community but also for the broader scientific and industrial sectors, including large tobacco companies and manufacturers of related products, both highlighting areas of current understanding and identifying areas for deeper exploration. The synthesis herein aims to propel further research, hoping to unravel the complexities of the EMT in the context of CS exposure. This review not only expands our understanding of CS-induced EMT but also reveals critical limitations in current methodologies, primarily the reliance on 2D cell cultures, which may not adequately simulate more complex biological interactions. Additionally, it highlights a significant gap in the literature concerning the genetic and epigenetic factors involved in CS-induced EMT, suggesting an urgent need for comprehensive studies that incorporate these types of experiments.

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Although deterioration of silicone maxillofacial prostheses is severely accentuated in smoking patients, the phenomenon has not been systematically studied. To address a gap in the literature concerning the stability of maxillofacial prostheses during service, in this contribution, the effect of cigarette smoke on the aspect and physical properties of M511 silicone elastomer was evaluated. The aspect, surface, and overall properties of the silicone material, pigmented or not, were followed by AFM, color measurements, FTIR, water contact angle measurements, TGA-DTG and DSC, hardness and compression stress-strain measurements. The types of the contaminants adsorbed were assessed by XRF, ESI-MS, MALDI-MS, and NMR spectral analyses. Important modifications in color, contact angle, surface roughness, local mechanical properties, and thermal properties were found in the silicone material for maxillofacial prostheses after exposure to cigarettes smoke. The presence of lead, nicotine, and several other organic compounds adsorbed into the silicone material was emphasized. Slight decrease in hardness and increase in Young's modulus was found. The combined data show important impact of cigarette smoke on the silicone physical properties and could indicate chemical transformations by secondary cross-linking. To our knowledge, this is the first study making use of complementary physical methods to assess the effect of cigarette smoke on the aspect and integrity of silicone materials for maxillofacial prostheses.

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BACKGROUND/AIM: Cigarette smoke has been shown to induce a phenotype in humans known as "acquired cystic fibrosis". This occurs because the cystic fibrosis transmembrane conductance regulator (CFTR) functions are impaired systemically due to the deleterious effects of smoke components. Elucidation of cigarette smoke effects on the tracheal epithelium is important. The aim of this study was to develop an ex vivo sheep tracheal model to investigate tracheal ion function. In this model, the epithelial sodium channel (ENaC) is inhibited after exposure to cigarette smoke extract (CSE) as a proof of principle. MATERIALS AND METHODS: Tracheas were isolated from healthy sheep and the tracheal epithelium was surgically excised. Tissues were mounted in Ussing chambers and the short circuit current (Isc) was measured after incubation with 5% CSE in PBS or PBS alone for 30 min. The function of ENaC was investigated by the addition of amiloride (10-5M) apically. Western blot analysis was performed to assess differences in ENaC quantity after CSE exposure. Some specimens were stained with H&E for detection of histological alterations. RESULTS: The amiloride effect on normal epithelium led to a significant decrease in Isc [ΔI=33±5.92 µA/cm2; p<0.001 versus control experiments (ΔI=1.44±0.71 µA/cm2)]. After incubation with CSE, ENaC Isc was significantly reduced (ΔI=14.80±1.96 µA/cm2; p<0.001). No differences in αENaC expression were observed between CSE-exposed and normal tracheal epithelium. Histological images post CSE incubation revealed decreases in the height of the epithelium, with basal cell hyperplasia and loss of ciliated cells. CONCLUSION: Reduced ENaC inhibition by amiloride after CSE incubation could be due to alterations in the tracheal epithelium.

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Existing studies that assess the impact of cooking with dirty solid fuels on human beings tend to underestimate the adverse impact on welfare. This paper aims to address this research gap by examining the happiness benefits of transitioning from solid fuel to cleaner alternatives. Using an extensive panel dataset from China, which includes 150,248 observations collected from 43,251 survey respondents interviewed between 2010 and 2018, this study employs various complementary methodologies, such as the fixed-effect model, propensity score matching, and time-varying difference-in-differences, to overcome challenges related to treatment selection bias and unobserved time-invariant heterogeneity. Further, life satisfaction approach is used to evaluate the economic benefits of cooking energy transition. Our findings indicate that switching from firewood to LPG/natural gas/gas can significantly enhance individual subjective well-being (SWB). Although the improvement brought about by electricity is slightly lower than that of LPG/natural gas/gas, it remains substantial. Notably, the positive effect is more pronounced among specific demographic groups, including females, rural residents, and low-income families. Moreover, these well-being improvements can manifest quickly and persist many years before any noticeable enhancements in physical health. This effect further amplifies over time. However, biogas shows no significant effect on SWB. These findings underscore the importance of clean fuels that contribute to increased happiness, as they are more likely to be consistently adopted. Finally, we estimate that the economic benefits of the well-being improvements resulting from the use of LPG/natural gas/gas and electricity range between $5.15 and $5.44 per day.

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BACKGROUND: A major industrial fire accident occurred in a tire manufacturing factory in Daejeon, Korea, on 12 March 2023 and lasted for 3 d, generating air pollutant emissions. Although evidence regarding the health effects of urban fires is limited, residents near tire factory may have experienced health hazards due to smoke exposure from fire plumes. OBJECTIVES: Capitalizing on the timing of this fire incident as a natural experiment, we estimated the attributable excess air pollution exposure and associated disease development among residents living near the tire factory. METHODS: We used the generalized synthetic control method to estimate air pollution exposure and health burden attributable to the accident among residents living in smoke-exposed districts. Based on satellite images and air pollution monitoring results, three administrative districts (within 1.2km from the factory) were defined as smoke-exposed, and the other 79 districts of Daejeon were defined as controls. Among the 11 monitoring stations in Daejeon, the station located 500m from the factory was used to estimate excess air pollution exposure (PM10, PM2.5, NO2, O3, SO2, and CO) for residents in the exposed districts. The number of daily district-level disease-specific incidence cases were acquired from the National Health Insurance Database and used to estimate excess health burden resulting from the fire. RESULTS: During the first week following the factory fire, residents of exposed districts had an estimated excess exposure to 125.2 [95% confidence interval (CI): 44.9, 156.7] µg/m3 of PM10, 50.4 (95% CI: 12.7, 99.8) ppb of NO2, and 32.0 (95% CI: 21.0, 35.9) ppb of SO2. We also found an average increase in the incidence cases of other diseases of upper respiratory tract [20.6 persons (95% CI: 6.2, 37.4)], lung disease due to external agents [2.5 persons (95% CI: 2.1, 3.3)], urticaria and erythema [5.9 persons (95% CI: -0.6, 11.2)], and episodic and paroxysmal disorders [8.5 persons (95% CI: 3.7, 13.4)] in exposed districts. DISCUSSION: Excessive air pollution exposure and disease incidence were identified among residents living close to the tire factory. Preventive measures, such as a warning system, to avoid health impacts to people breathing fire-related pollution may be beneficial for communities impacted by such events. https://doi.org/10.1289/EHP14115.

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BACKGROUND: Chronic obstructive pulmonary disease (COPD) is an inflammatory airway disease characterized by emphysema and chronic bronchitis and a leading cause of mortality worldwide. COPD is commonly associated with several comorbid diseases which contribute to exacerbated patient outcomes. Cigarette smoke (CS) is the most prominent risk factor for COPD development and progression and is known to be detrimental to numerous effector functions of lung resident immune cells, including phagocytosis and cytokine production. However, how CS mediates the various pathologies distant from the lung in COPD, and whether CS has a similar biological effect on systemic immune cells remains unknown. METHODS: C57BL/6 mice were exposed to 8 weeks of CS as an experimental model of COPD. Bone marrow cells were isolated from both CS-exposed and room air (RA) control mice and differentiated to bone marrow-derived macrophages (BMDMs). Airspace macrophages (AMs) were isolated from the same CS-exposed and RA mice and bulk RNA-Seq performed. The functional role of differentially expressed genes was assessed through gene ontology analyses. Ingenuity Pathway Analysis was used to determine the activation states of canonical pathways and upstream regulators enriched in differentially expressed genes in both cell types, and to compare the differences between the two cell types. RESULTS: CS induced transcriptomic changes in BMDMs, including an upregulation of genes in sirtuin signalling and oxidative phosphorylation pathways and a downregulation of genes involved in histone and lysine methylation. In contrast, CS induced decreased expression of genes involved in pathogen response, phagosome formation, and immune cell trafficking in AMs. Little overlap was observed in differentially expressed protein-coding genes in BMDMs compared to AMs and their associated pathways, highlighting the distinct effects of CS on immune cells in different compartments. CONCLUSIONS: CS exposure can induce transcriptomic remodelling in BMDMs which is distinct to that of AMs. Our study highlights the ability of CS exposure to affect immune cell populations distal to the lung and warrants further investigation into the functional effects of these changes and the ensuing role in driving multimorbid disease.

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Chronic airway inflammation induced by cigarette smoke (CS) plays an essential role in the pathogenesis of chronic obstructive pulmonary disease (COPD). MALAT1 is involved in a variety of inflammatory disorders. However, studies focusing on the interaction between MALAT1 and CS-induced airway inflammation remain unknown. The present study investigated the effects and mechanisms of MALAT1 in CS-induced airway inflammation in the pathogenesis of COPD. RT-qPCR was employed to determine the mRNA levels of MALAT1, miR-30a-5p and inflammatory cytokines. Protein concentrations of IL-1ß and IL-6 in cell culture supernatant and mouse bronchoalveolar lavage fluid (BALF) were assessed by ELISA assay kits. Dual-luciferase reporter assay was conducted to verify the interaction between MALAT1 and miR-30a-5p. The protein expression of JNK and p-JNK was determined by western blot (WB). MALAT1 was highly expressed in cigarette smoke extract (CSE)-treated human bronchial epithelial cells (HBECs) and COPD mice lung tissues. Knockdown of MALAT1 significantly alleviate CS-induced inflammatory response. MALAT1 directly interacted with miR-30a-5p and knockdown of miR-30a-5p significantly inhibit the protective effects of MALAT1 silencing after CS exposure. Additionally, our results showed that miR-30a-5p could regulate inflammation via modulating the activation of JNK signaling pathway. Moreover, our results demonstrated MALAT1 could activate JNK signaling pathway by sponging miR-30a-5p. Our results demonstrated MALAT1 promotes CS-induced airway inflammation by inhibiting the activation of JNK signaling pathway via sponging miR-30a-5p.

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Para estabelecer medidas equivalentes para o ensaio de produtos de tabaco em escala mundial é necessário que haja métodos consensuais de medição do conteúdo e das emissões específicas dos cigarros. Nenhum regime de fumar em máquina é capaz de representar plenamente o comportamento humano de fumar: os ensaios realizados em máquina de fumar são úteis para caracterizar as emissões de cigarro para fins de projeto e regulação, no entanto, a divulgação aos fumantes das medições em máquina pode provocar mal-entendidos a respeito das diferenças de exposição e risco existentes entre as diferentes marcas. Os dados de emissão de fumaça obtidos por medições em máquina podem ser usados como elementos para avaliar os perigos do produto, mas não são nem se destinam a ser medidas válidas de exposição ou risco para os seres humanos. A apresentação de diferenças nas medições em máquina como diferenças de exposição ou risco, constitui uso indevido do ensaio de acordo com os padrões da TobLabNet da OMS. Este documento foi preparado por membros da Rede de Laboratórios de Tabaco (TobLabNet) da Organização Mundial da Saúde (OMS) como um procedimento operacional padrão (POP) para o regime intenso de fumada de cigarro.

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Para estabelecer medidas equivalentes para o ensaio de produtos de tabaco em escala mundial é necessário que haja métodos consensuais de medição do conteúdo e das emissões específicas dos cigarros. Nenhum regime de tragada obtido por máquinas é capaz de representar plenamente o comportamento humano de fumar: os ensaios realizados em máquinas de fumar são úteis para caracterizar as emissões de cigarro para fins de design e regulação, mas a divulgação aos fumantes das medições em máquinas pode resultar em interpretações equivocadas a respeito das diferenças de exposição e risco existentes entre as marcas. Os dados de emissão de fumaça obtidos por medições em máquinas podem ser usados como elementos para a avaliação do perigo do produto, mas não são e nem se destinam a ser medidas válidas de exposição ou risco para os seres humanos. A apresentação de diferenças nas medições em máquina como diferenças de exposição ou risco constitui uso indevido dos resultados do ensaio com métodos recomendados da TobLabNet da OMS. Este documento foi preparado por membros da Rede de Laboratórios de Tabaco (TobLabNet) da Organização Mundial da Saúde (OMS) como um procedimento operacional padrão (POP) de método analítico para determinação de compostos orgânicos voláteis (COV) em corrente primária de cigarro em condições ISO e em regime intenso de fumada.

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Para estabelecer medidas equivalentes para o ensaio de produtos de tabaco em escala mundial é necessário que haja métodos consensuais de medição do conteúdo e das emissões específicas dos cigarros. Nenhum regime de tragada obtido por máquinas é capaz de representar plenamente o comportamento humano de fumar: os ensaios realizados em máquinas de fumar são úteis para caracterizar as emissões de cigarro para fins de design e regulação, mas a divulgação aos fumantes das medições em máquinas pode resultar em interpretações equivocadas a respeito das diferenças de exposição e risco existentes entre as marcas. Os dados de emissão de fumaça obtidos por medições em máquinas podem ser usados como elementos para a avaliação do perigo do produto, mas não são e nem se destinam a ser medidas válidas de exposição ou risco para os seres humanos. A apresentação de diferenças nas medições em máquina como diferenças de exposição ou risco constitui uso indevido dos resultados do ensaio com métodos recomendados da TobLabNet da OMS. Este documento foi preparado por membros da Rede de Laboratórios de Tabaco (TobLabNet) da Organização Mundial da Saúde (OMS) como um procedimento operacional padrão (POP) para medição de nicotina e monóxido de carbono na corrente primária do cigarro sob condições intensas de fumada.

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Salt stress is a serious problem, because it reduces the plant growth and seed yield of wheat. To investigate the salt-tolerant mechanism of wheat caused by plant-derived smoke (PDS) solution, metabolomic and proteomic techniques were used. PDS solution, which repairs the growth inhibition of wheat under salt stress, contains metabolites related to flavonoid biosynthesis. Wheat was treated with PDS solution under salt stress and proteins were analyzed using a gel-free/label-free proteomic technique. Oppositely changed proteins were associated with protein metabolism and signal transduction in biological processes, as well as mitochondrion, endoplasmic reticulum/Golgi, and plasma membrane in cellular components with PDS solution under salt stress compared to control. Using immuno-blot analysis, proteomic results confirmed that ascorbate peroxidase increased with salt stress and decreased with additional PDS solution; however, H+-ATPase displayed opposite effects. Ubiquitin increased with salt stress and decreased with additional PDS solution; nevertheless, genomic DNA did not change. As part of mitochondrion-related events, the contents of ATP increased with salt stress and recovered with additional PDS solution. These results suggest that PDS solution enhances wheat growth suppressed by salt stress through the regulation of energy metabolism and the ubiquitin-proteasome system related to flavonoid metabolism.

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Increased frequency, intensity, and duration of wildfires are intensifying exposure to direct and smoke-related hazards in many areas, leading to evacuation and smoke-related effects on health and health systems that can affect regions extending over thousands of kilometres. Effective preparation and response are currently hampered by inadequate training, continued siloing of disciplines, insufficient finance, and inadequate coordination between health systems and governance at municipal, regional, national, and international levels. This Review highlights the key health and health systems considerations before, during, and after wildfires, and outlines how a health system should respond to optimise population health outcomes now and into the future. The focus is on the implications of wildfires for air quality, mental health, and emergency management, with elements of international policy and finance also addressed. We discuss commonalities of existing climate-resilient health care and disaster management frameworks and integrate them into an approach that addresses issues of financing, leadership and governance, health workforce, health information systems, infrastructure, supply chain, technologies, community interaction and health-care delivery, before, during, and after a wildfire season. This Review is a practical briefing for leaders and health professionals facing severe wildfire seasons and a call to break down silos and join with other disciplines to proactively plan for and fund innovation and coordination in service of a healthier future.

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Fuchs endothelial corneal dystrophy (FECD), a degenerative corneal condition, is characterized by the droplet-like accumulation of the extracellular matrix, known as guttae and progressive loss of corneal endothelial cells ultimately leading to visual distortion and glare. FECD can be influenced by environmental stressors and genetic conditions. However, the role of mitochondrial dysfunction for advancing FECD pathogenesis is not yet fully studied. Therefore, in the present study we sought to determine whether a combination of environmental stressors (ultraviolet-A (UVA) light and cigarette smoke condensate (CSC)) can induce mitochondrial dysfunction leading to FECD. We also investigated if MitoQ, a water-soluble antioxidant, can target mitochondrial dysfunction induced by UVA and CSC in human corneal endothelial cells mitigating FECD pathogenesis. We modeled the FECD by increasing exogenous oxidative stress with CSC (0.2%), UVA (25J/cm2) and a combination of UVA + CSC and performed a temporal analysis of their cellular and mitochondrial effects on HCEnC-21T immortalized cells in vitro before and after MitoQ (0.05 µM) treatment. Interestingly, we observed that a combination of UVA + CSC exposure increased mitochondrial ROS and fragmentation leading to a lower mitochondrial membrane potential and increased levels of cytochrome c release leading to apoptosis and cell death. MitoQ intervention successfully mitigated these effects and restored cell viability. The UVA + CSC model could be used to study stress induced mitochondrial dysfunction. Additionally, MitoQ can serve as a viable antioxidant in attenuating mitochondrial dysfunction, underscoring its potential as a molecular-focused treatment approach to combat FECD pathogenesis.

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This Medical News article is an interview about the latest findings presented at the recent Alzheimer's Association International Conference.

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