Smoke and NOx emission characteristics of in-use construction machinery base on substantial field measurement: A case study in Beijing, China.

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.

Oridonin alleviates cigarette smoke-induced nasal polyp formation by promoting autophagy.

Previous studies have indicated that oridonin is a promising candidate for therapeutic intervention in a range of inflammatory diseases. The objective of this study was to investigate the protective mechanism of oridonin in chronic rhinosinusitis with nasal polyp (CRSwNP). In nasal polyp (NP) mice model, cigarette smoke (CS) induced polypoid changes compared to previous modeling methods. Compared with CS-treated mice, oridonin reduced polypoid changes, goblet cell count, and promoted the expression of tight junction proteins (ZO-1, occludin, claudin-1) and production of autophagosomes. Following treatment with oridonin, the levels of OVA-specific IgE, IL-6, IFN-γ, IL-5, IL-13 and IL-17A in serum were observed to decrease; the levels of TGF-ß1, matrix metalloproteinase 2 (MMP2), MMP7, MMP9 and MMP12 levels in nasal lavage fluid were reduced, while tissue inhibitor of metalloproteinase-1 (TIMP-1) levels were increased. Furthermore, the aforementioned alterations in the mouse model were reversed by 3-methyladenine (3-MA), an autophagy inhibitor. In vitro, cigarette smoke extract (CSE) was observed to decrease the expression of tight junction proteins, the production of autophagosomes, and to reduce the expression of LC3-II and Beclin-1, accompanied by an increase in P62 expression. In addition, oridonin was observed to reverse CSE-induced epithelial barrier damage, and was associated with autophagy and the PI3K/AKT/mTOR pathway. In conclusion, oridonin was demonstrated to improve the damage of the nasal epithelial barrier induced by CS through the promotion of autophagy, which may represent a novel therapeutic option for the treatment of CRSwNP.

Experimental Mouse Models and Human Lung Organoid Models for Studying Chronic Obstructive Pulmonary Disease.

Chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality throughout the world, is a highly complicated disease that includes chronic airway inflammation, airway remodeling, emphysema, and mucus hypersecretion. For respiratory function, an intact lung structure is required for efficient air flow through conducting airways and gas exchange in alveoli. Structural changes in small airways and inflammation are major features of COPD. At present, mechanisms involved in the genesis and development of COPD are poorly understood. Currently, there are no effective treatments for COPD. To develop better treatment strategies, it is necessary to study mechanisms of COPD using proper experimental models that can recapitulate distinctive features of human COPD. Therefore, this review will discuss representative established mouse models to investigate inflammatory processes and basic mechanisms of COPD. In addition, human COPD-mimicking human lung organoid models are introduced to help researchers overcome limits of mouse COPD models.

Recent evidence on rates and factors influencing smoking behaviours after release from smoke-free prisons: a scoping review.

PURPOSE: Smoke-free prison policies have been introduced in some countries, in part to address very high levels of tobacco use in people in prison. However, relapse rates post-release remain high. This papers aims to improve understanding of post-release smoking and/or vaping behaviour is necessary to inform support for a priority population. DESIGN/METHODOLOGY/APPROACH: The authors searched health, social science and criminal justice databases for studies about smoking/vaping behaviours among people released from smoke-free prisons. Studies were included if they reported primary data and were published between January 2017 and March 2024 in English; the population was adults/young people (16 yr+) imprisoned or formerly imprisoned, in prisons with comprehensive smoke-free policies; and at least one of the following was reported: pre-release intention to smoke, vape or remain abstinent post-release; smoking/vaping behaviour post-release and factors influencing smoking/vaping behaviour; attempts to quit again following post-release smoking/vaping relapse. FINDINGS: Nine studies met our criteria. The evidence base is small and mainly from the USA or Australia. Evidence continues to suggest that most people resume smoking after leaving a smoke-free prison. No new interventions have been successful in reducing relapse rates. No studies report on vaping post-release, although two studies report on perceived factors affecting smoking relapse post-release from prisons allowing vaping. RESEARCH LIMITATIONS/IMPLICATIONS: Given very high rates of relapse, there remains a significant need to better understand what approaches are feasible and acceptable for reducing return to smoking post-release. ORIGINALITY/VALUE: This review updates the limited evidence on smoking behaviours after leaving a smoke-free prison.

Assessment of the impact of smoke from thermal destruction of materials of different origins on soil health.

The results of the study of the influence of smoke from the thermal destruction of materials of vegetable and synthetic origin on the enzymatic activity of ordinary chernozem are presented. The decrease of activity of investigated indicators (catalase, peroxidase, polyphenol oxidase, invertase) from thermal destruction of pine sawdust, straw, coniferous and leaf fall, peat, and materials based on polystyrene, rubber, and polyvinyl chloride was revealed. A significant decrease in the activity of soil enzymes after exposure to gaseous products of combustion during 15-60 min of soil fumigation was found. Oxidoreductases turned out to be the most sensitive to smoke. Smoke from peat burning has minimal inhibitory effect, activity of catalase after 30 min of fumigation decreased only by 15%, and peroxidase and polyphenol oxidase - by 8 and 12%. While the activity of the same enzymes when exposed to smoke from thermal degradation of rubber-based materials decreased by 16-42%, and polyvinyl chloride - by 29-73%, to a lesser extent from polystyrene (decrease by 7-29%). All obtained data on changes in the enzymatic activity of soils are reliable with the level of statistical significance p < 0.05.

Diagnostic Challenges and Pathogenetic Differences in Biomass-Smoke-Induced versus Tobacco-Smoke-Induced COPD: A Comparative Review.

Background: Chronic Obstructive Pulmonary Disease (COPD) is a major global health challenge, primarily driven by exposures to tobacco smoke and biomass smoke. While Tobacco-Smoke-Induced COPD (TSCOPD) has been extensively studied, the diagnostic challenges and distinct pathogenesis of Biomass-Smoke-Induced COPD (BSCOPD), particularly in low- and middle-income countries, remain underexplored. Objective: To explore the differences in clinical manifestations, pulmonary function, and inflammatory profiles between BSCOPD and TSCOPD and highlight the diagnostic complexities of BSCOPD. Methods: This review analyzes the current literature comparing BSCOPD with TSCOPD, focusing on distinctive pathophysiological mechanisms, inflammatory markers, and oxidative stress processes. Results: BSCOPD presents differences in clinical presentation, with less emphysema, smaller airway damage, and higher rates of pulmonary hypertension compared to TSCOPD. BSCOPD is also characterized by bronchial hyperresponsiveness and significant hypoxemia, unlike TSCOPD, which exhibits severe airflow obstruction and emphysema. Additionally, the inflammatory profile of BSCOPD includes distinct mucous hypersecretion and airway remodeling. Conclusions: The unique genetic, epigenetic, and oxidative stress mechanisms involved in BSCOPD complicate its diagnosis and management. Biomass smoke's underrecognized impact on accelerated lung aging and exacerbation mechanisms emphasizes the need for targeted research to refine diagnostic criteria and management strategies for BSCOPD. Future directions: Further research should focus on identifying specific biomarkers and molecular pathways to enhance early diagnosis and improve clinical outcomes in populations exposed to biomass smoke.

A review of occupational exposures to carcinogens among wildland firefighters.

Wildfires can negatively impact the health and well-being of wildland firefighters through a variety of exposure pathways. Many studies have measured acute health effects from occupational exposure to pollutants in wildfire smoke; however, research specifically examining cancer risks from exposure to carcinogens is limited. This review aimed to better understand cancer risk in this occupation by assessing the existing evidence of exposures and summarizing measured concentrations of carcinogens among wildland firefighters. A systematic search was conducted to identify scientific papers using the following databases: Medline(OVID), Embase(OVID), PsycINFO(OVID), Cochrane Library, CINAHL(EBSCOHost), EconLit(EBSCOHost), Scopus, Agricultural and Environmental Science Collect(ProQuest), and NIOSHTIC-2. Forty-nine papers were identified that met eligibility criteria. Across the papers, 31 carcinogens were identified and quantified using a variety of assessment methods. Papers measured particulate matter (N = 26), polycyclic aromatic hydrocarbons (N = 12), volatile organic compounds (N = 14), crystalline silica (N = 5), black carbon (N = 4), asbestos (N = 3), radionuclides (N = 7), and metals (N = 2). Most papers measured inhalation exposures through traditional air sampling methods, but a subset of exposures to polycyclic aromatic hydrocarbons (N = 8), as well as heavy metals (N = 1), were measured through urinary biomarkers and naphthalene was measured using dermal wipe samples (N = 2). Although the heterogeneity of exposure assessment methods made direct comparison of concentrations difficult, the papers provide consistent evidence that wildland firefighters are regularly exposed to carcinogens. All wildland fire personnel should continue to implement recommended mitigation strategies and support new mitigations to reduce exposure to carcinogens on the job.

Linear polydichlorophosphazene and Ti3C2Tx MXene nanohybrids: Synthesis and application to epoxy resin to improve the fire safety and mechanical properties.

Enhancing the fire safety of epoxy resins (EPs) typically requires a significant amount of flame retardants, which often results in considerable degradation of their mechanical properties. To address this issue, a novel flame retardant known as PDCP@DPA@MXene was synthesized and integrated into EP to achieve notable improvements in flame retardancy, smoke suppression, and mechanical strength. By incorporating 1.5 wt% PDCP@DPA@MXene, the impact strength, tensile strength, and elongation at break of the resulting PDM-1.5 %/EP composite reached 12.1 kJ/m2, 57.4 MPa, and 13.0, respectively, reflecting enhancements of 63.5 %, 18.4 %, and 17.1 % compared to the pure EP. The enhancement in tensile strength may be attributed to the high rigidity of Ti3C2Tx MXene, which reinforces the EP matrix. Additionally, the intertwined structure of PDCP@DPA@MXene chains effectively mitigates material fracturing and absorbs impact forces, thus toughening the EP. The presence of phosphorus, nitrogen, and titanate in PDCP@DPA@MXene contributes to the formation of a more compact char layer. The PDM-1.5 %/EP sample achieved a V-0 rating in the vertical UL-94 test and exhibited a high limiting oxygen index of 32.0. Furthermore, the sample containing 2 wt% PDCP@DPA@MXene showed a significant reduction in peak heat release rate (p-HRR) and total heat release (THR), recording values of 689 kW/m2 and 71.9 MJ/m2, which are decreases of 45.1 % and 26.9 %, respectively, compared to pure EP. Additionally, the incorporation of PDCP@DPA@MXene led to a reduction in CO production. These flame-retarded EPs demonstrate strong potential for various applications due to their elevated glass transition temperature and robust thermal stability.

Investigating antimicrobial and antioxidant activity of liquid smoke and physical-chemical stability of bacon subjected to liquid smoke and conventional smoking.

Liquid smoke, an alternative to traditional wood burning smoking, enhances product value by imparting desirable characteristics such as aroma, flavor, and color. Furthermore, it contains components with inherent antimicrobial and antioxidant properties. This study compares the effects of liquid smoke and conventional smoking methods in bacon processing. Over a 90-day storage period at 22°C, physical-chemical stability, sensory attributes, and microbiological characteristics of the bacon were evaluated. The antimicrobial and antioxidant properties of liquid smoke were assessed. Liquid smoke exhibited antioxidant activity, with an inhibitory concentration (IC50) value of 0.19 mg/mL, indicating the concentration of the extract needed to inhibit 50% of DPPH (2,2'-diphenyl-1-picrylhydrazyl) radicals. Moreover, it demonstrated antimicrobial effects against Escherichia coli, Salmonella choleraesius, Staphylococcus aureus, and Listeria monocytogenes, with a minimum bactericidal concentration ranging from 7.5% to 10%. Throughout the storage, bacon treated with liquid smoke showed no signs of rancid odor, supported by thiobarbituric acid reactive substances values below 0.85 mg MDA/kg (where MDA is malondialdehyde). The utilization of liquid smoke yielded visually attractive bacon with enhanced color attributes, including a distinct yellow and red hue, as well as increased luminosity and brightness, surpassing the effects of traditional smoke. Remarkably, liquid smoke application significantly reduced processing time from 30 h to approximately 5 h, leading to substantial cost savings in the processing phase.

Evaluating the effectiveness of Smoke-Free Home SafeCare, an integrated intervention, among families at risk for secondhand smoke exposure and child maltreatment in the United States: a study protocol for a hybrid type 1 trial.

BACKGROUND: Secondhand smoke exposure (SHS) and child maltreatment (CM) are preventable yet have negative lifelong impacts on health. When considered together, the risk for negative health outcomes may be compounded, especially for people living in low-resource settings. Evidence-based interventions exist for preventing CM and reducing SHS among families with low resources; however, no programs jointly target SHS exposure and maltreatment risk. METHODS: This study is a hybrid type 1 trial to examine the effectiveness of a systematically braided intervention to target CM risk and SHS in the home. Fifty SafeCare Providers will be randomized to deliver either standard SafeCare (i.e., the SafeCare model alone; active treatment control; n = 25) or Smoke-Free Home SafeCare (SFHSC; treatment condition; n = 25), the braided intervention that includes both SafeCare and the Smoke-Free Homes: Some Things are Better Outside intervention to N = 500 families. Aim 2 is to assess family-level outcomes. The primary outcome is a full home smoking ban, validated by air nicotine monitors; secondary outcomes include parenting and smoking outcomes. Aim 3 is to evaluate process and implementation outcomes, including cost-benefit. We will use multilevel models and ROC analyses to evaluate and validate the primary outcome. We will use tests of non-inferiority to evaluate secondary outcomes. Cost-effectiveness analyses will be used to assess cost-benefit of SFHSC. DISCUSSION: This study will be the first to document the outcomes of a multi-component intervention to address cumulative risk factors that impact cancer risk among children whose parents are at risk or involved in child-protective services. Integrating an evidence-based intervention that targets SHS exposure in the home with a broadly disseminated CM prevention intervention may be a sustainable way to help reduce the compounded effects of SHS in the home and CM. TRIAL REGISTRATION: Clinicaltrials.gov, NCT05000632. Registered on August 11, 2021.

Phytochemical Profiling and Wound Healing Activity of Gigantochloa apus Liquid Smoke in Mus Musculus.

Purpose: Rope bamboo (Gigantochloa apus) is traditionally used for medicinal purposes, and extracts from stem leaves and shoots have been shown to possess antioxidant and anti-inflammatory activity. Thus, this study looked at the potential compounds present in and the usefulness of Rope bamboo liquid smoke preparations in the wound healing process in mice. Methods: The fingerprinting of the liquid smoke was done by liquid chromatography-mass spectrometry. In-vivo experiments were conducted to observe the diameter and percentage of wound healing in mice for 14 days using topical formulations containing liquid smoke concentrations of 100%, 50%, 25%, positive control and negative control. Statistical analyses were conducted using the Kruskal-Wallis test and Spearman correlation. Results: The phytochemical fingerprint showed the presence of alkaloids, flavonoids, vitamins, phenols, and lipids. The 100% undiluted liquid smoke accelerated wound healing faster compared to 50% and 25% dilutions. The differences in wound diameters were statistically significant across treatments having a p-value of 0.020 and dose-dependent (p = 0.029). Conclusion: Liquid smoke acceleration of the wound healing process was dose-dependent compared to controls. This dose-dependency indicates that the wound healing effects were probably due to the anti-inflammatory, antioxidant, and antimicrobial activities of the elucidated constituents of Rope bamboo liquid smoke.

Exploring spontaneous brain activity changes in high-altitude smokers: Insights from ALFF/fALFF analysis.

INTRODUCTION: This study aims to explore the impact of smoking on intrinsic brain activity among high-altitude (HA) populations. Smoking is associated with various neural alterations, but it remains unclear whether smokers in HA environments exhibit specific neural characteristics. METHODS: We employed ALFF and fALFF methods across different frequency bands to investigate differences in brain functional activity between high-altitude smokers and non-smokers. 31 smokers and 31 non-smokers from HA regions participated, undergoing resting-state functional magnetic resonance imaging (rs-fMRI) scans. ALFF/fALFF values were compared between the two groups. Correlation analyses explored relationships between brain activity and clinical data. RESULTS: Smokers showed increased ALFF values in the right superior frontal gyrus (R-SFG), right middle frontal gyrus (R-MFG), right anterior cingulate cortex (R-ACC), right inferior frontal gyrus (R-IFG), right superior/medial frontal gyrus (R-MSFG), and left SFG compared to non-smokers in HA. In sub-frequency bands (0.01-0.027 Hz and 0.027-0.073 Hz), smokers showed increased ALFF values in R-SFG, R-MFG, right middle cingulate cortex (R-MCC), R-MSFG, Right precentral gyrus and L-SFG while decreased fALFF values were noted in the right postcentral and precentral gyrus in the 0.01-0.027 Hz band. Negative correlations were found between ALFF values in the R-SFG and smoking years. CONCLUSION: Our study reveals the neural characteristics of smokers in high-altitude environments, highlighting the potential impact of smoking on brain function. These results provide new insights into the neural mechanisms of high-altitude smoking addiction and may inform the development of relevant intervention measures.

Locus of control and the long-term effects of parental smoking on mental health.

RATIONALE: Few studies take a life course perspective to explain if exposure to second-hand smoke in childhood influences mental health in adulthood. Importantly, no study provides empirical evidence on the pathways through which exposure to second-hand smoke in childhood influences mental health in adulthood. There is also limited evidence on the factors that moderate the relationship between second-hand smoke exposure and mental health. To inform policy, it is important to explore the pathways through which second-hand smoke influences mental health and understand factors that are likely to moderate this relationship. OBJECTIVES: The objective of this paper is to examine if exposure to parental smoking in childhood influences mental health in adulthood. The study examines general health and smoking status in later life as potential channels and if locus of control (LoC), a personality trait developed in childhood and adolescence, moderates the relationship between exposure to parental smoking in childhood and mental health in adulthood. METHODS: Using 21 waves of longitudinal data from the Household, Income and Labour Dynamics in Australia (HILDA), the study conducts regression analyses that adjust for the potential effects of confounders and other biases. RESULTS: The results show that exposure to parental smoking in childhood is associated with a decline in mental health in later life, and that general health status and smoking status in adulthood are channels through which exposure to parental smoking in childhood influences mental health in adulthood. Specifically, those who are exposed to parental smoking in childhood tend to have poorer general health and a higher probability of being smokers in adulthood, both of which negatively impact mental health. The findings point to the moderating role of LoC, such that being more internal on LoC dampens the negative effects of exposure to parental smoking on mental health. CONCLUSION: The findings from this study lend support to the need to address the long-term implications of behaviours that are harmful to health. The findings also suggest that LoC has implications for an individual's psychological resilience against the negative effects from exposure to parental smoking in childhood.

Inequalities in exposure to second-hand smoke among adolescent boys and girls in 122 countries: Evidence from the Global Youth Tobacco Survey.

BACKGROUND: Secondhand smoke exposure (SHS) is a major modifiable risk factor for morbidity and premature mortality. No study has assessed inequalities by sex in SHS exposure among adolescents globally. This study aims to explore the variations in SHS exposure among adolescents globally based on sex. METHODS: Most recent data from 122 countries and territories that conducted the Global Youth Tobacco Survey between 1 January 2013 and 31 December 2020, comprising 557,332 respondents aged 11-17 years, were used to assess the prevalence of SHS exposure at home, in other enclosed public places, and at school. Multivariable Poisson regression models were performed to investigate the association between sex and SHS exposure in each country. RESULTS: A total of 195,299 (35.0 %) adolescents reported exposure to SHS at home, 256,938 (46.1 %) in other enclosed public places, 258,528 (46.4 %) at school, and 399,644 (71.7 %) in any place. There were important inequalities in the prevalence of SHS exposure between countries. More girls than boys reported exposure to SHS at home in 54 countries (vs. one country with prevalence higher in boys than girls) and in other enclosed public places in 50 countries (vs. six countries). In contrast, the prevalence of SHS exposure at school was significantly higher in boys than girls in 25 countries while the opposite was observed in 14 countries. CONCLUSIONS: These findings emphasize the disparities in SHS exposure between adolescent boys and girls and, hence, highlight the urgent need to strengthen smoke-free policies and adopt targeted policies to address them.

Maternal exposure to smoking and wheezing phenotypes in children: a cohort study of the Japan Environment and Children's Study.

BACKGROUND: Previous studies have shown that prenatal maternal smoking and maternal secondhand smoke exposure during pregnancy were associated with an increased risk of wheezing and asthma development. However, few studies have examined the influence of different sources of tobacco exposure in different perinatal timeframes (preconception, prenatal, and postnatal) on wheezing phenotypes in children. Using national survey data from Japan, we investigated the effects of exposure to tobacco smoke during pregnancy on wheezing phenotypes in children before the age of 3 years. METHODS: Pregnant women who lived in the 15 regional centers in the Japan Environment and Children's Study were recruited. We obtained information on prenatal and postnatal exposure to active and secondhand smoke (SHS) and wheeze development up to 3 years of age. Multiple logistic regression analysis was performed to determine the association between tobacco smoke exposure and wheezing phenotypes in children. RESULTS: We analyzed 73,057 singleton births and identified four longitudinal wheezing phenotypes: never wheezing; early transient wheezing (wheezing by age 1 year but not thereafter); late-onset wheezing (wheezing by age 2-3 years but not beforehand); and persistent wheezing. Maternal smoking during pregnancy was significantly associated with early transient and persistent wheezing in children compared with no maternal smoking [early transient wheezing: 1-10 cigarettes per day, adjusted odds ratio (aOR) 1.43, 95% confidence interval (CI) 1.23-1.66; ≥ 11 cigarettes per day, aOR 1.67, 95% CI 1.27-2.20; persistent wheezing: 1-10 cigarettes per day, aOR 1.64, 95% CI 1.37-1.97; ≥ 11 cigarettes per day, aOR 2.32, 95% CI 1.70-3.19]. Smoking cessation even before pregnancy was also significantly associated with increased risk of early transient wheezing, late-onset wheezing, and persistent wheezing in children. Moreover, maternal exposure to SHS during pregnancy was significantly associated with increased risk of early transient and persistent wheezing compared with no such exposure. CONCLUSIONS: Maternal smoking before and throughout pregnancy was associated with wheeze development in children up to 3 years of age. It appears that smoking is detrimental compared to never smoking, regardless of whether individuals quit smoking before or after becoming aware of the pregnancy.

The Punicalagin Compound Mitigates Bronchial Epithelial Cell Senescence Induced by Cigarette Smoke Extract through the PAR2/mTOR Pathway.

BACKGROUND: Tobacco smoke is an important inducer of airway epithelial cell aging. Punicalagin(PCG) is a natural anti-aging compound. The effect of PCG on tobacco smoke-induced airway epithelial cell senescence is unknown. OBJECTIVE: Our study investigated whether PCG can treat the human bronchial epithelial cell line (BEAS-2B) aging by inhibiting the protease-activated receptor 2 (PAR2)/m- TOR pathway. METHODS: Bioinformatics techniques were used to analyze the potential biological functions of PAR2. Molecular dynamics evaluated the binding ability of PCG and PAR2. The CCK8 assay was used to detect the cytotoxicity of CSE and PCG. The activity of the PAR2/mTOR pathway and the expression of the characteristic aging markers p16, p21, and SIRT1 are detected by qRT-PCR and Western blotting. Cell senescence was observed by Senescence-associated ß-galactosidase (SA-ß-gal) staining. The senescence-associated secretory phenotype (SASP): concentrations of interleukin IL-6, IL-8, and TNF- α were detected by ELISA. RESULTS: The GSE57148 bioinformatics analysis dataset showed that PAR2 regulates lung senescence through the mTOR signaling pathway. Molecular dynamics results found that PCG and PAR2 had a strong and stable binding force. CSE induces BEAS-2B cell senescence and activates the PAR2/mTOR pathway. Inhibition of PAR2 mitigated the senescence changes. In addition, PCG's pretreatment can significantly alleviate CSE-induced BEAS-2B cell senescence while inhibiting the PAR2/mTOR pathway. CONCLUSION: PCG has a therapeutic effect on the senescence of airway epithelial cells.

Exposure to mixture particulate contaminants in the air and the risk of oral cancer: An updated systematic review and meta-analysis.

The mixture of contaminants in the air (e.g., PM2.5, smoke) is a part of air pollutants that has become a hot environmental issue. Previous epidemiological studies have reported the relationship between wood smoke and PM2.5 exposure and oral cancer, but findings have been inconsistent. Therefore, this work designed to find out the relationship between mixture contaminants in air exposure and oral cancer. Fourteen studies were included through research in three databases before February 2024. Before analysis, the Newcastle-Ottawa Scale was applied to examine the quality of all selected studies. Then, the meta-analysis was carried out by meta-regression analysis, sensitivity analysis and subgroup analysis. The results showed that exposure to PM2.5 may have a positive association with oral cancer (pooled OR = 1.13, 95 % confidence interval: 1.06, 1.20). In contrast, no significant association was found between indoor air pollution and oral cancer. However, the result of the subgroup analysis indicated there is a significant association of indoor air pollution and oral cancer in developing countries (pooled OR = 2.5, 95 % confidence interval: 1.7, 3.6). In addition, the heterogeneity among studies of indoor air pollution exposure and oral cancer may caused by studies carried out in developed countries according to the subgroup and meta-regression analyses. In conclusion, the studies about indoor air pollution exposure and oral cancer are discrepant. The effects of mixed air contaminants for people's health are not simple and more studies are demanded to find out it in the future.

A quantitative proteomic approach to evaluate the efficacy of carnosine in a murine model of chronic obstructive pulmonary disease (COPD).

The aim of the work was to study a dose-dependent effect of inhaled carnosine (10, 50 or 100 mg/kg/day) in mice exposed to cigarette smoke as a model of chronic obstructive pulmonary disease (COPD). A dose-dependent loading of the dipeptide in lung tissue and bronchoalveolar lavage (BAL) was firstly demonstrated by LC-ESI-MS analysis. Cigarette smoke exposure induced a significant lung inflammation and oxidative stress in mice which was dose-dependently reduced by carnosine. Inflammation was firstly evaluated by measuring the cytokines content in the BAL. All the measured cytokines were found significantly higher in the smoke group in respect to control, although the data are affected by a significant variability. Carnosine was found effective only at the highest dose tested and significantly only for keratinocyte-derived cytokine (KC). Due to the high variability of cytokines, a quantitative proteomic approach to better understand the functional effect of carnosine and its molecular mechanisms was used. Proteomic data clearly indicate that smoke exposure had a great impact on lung tissue with 692 proteins differentially expressed above a threshold of 1.5-fold. Protein network analysis identified the activation of some pathways characteristic of COPD, including inflammatory response, fibrosis, induction of immune system by infiltration and migration of leukocyte pathways, altered pathway of calcium metabolism and oxidative stress. Carnosine at the tested dose of 100 mg/kg was found effective in reverting all the pathways evoked by smoke. Only a partial reverse of the dysregulated proteins was evident at low- and mid-tested doses, although, for some specific proteins, indicating an overall dose-dependent effect. Regarding the molecular mechanisms involved, we found that carnosine upregulated some key enzymes related to Nrf2 activation and in particular glutathione peroxidase, reductase, transferase, SOD, thioredoxins, and carbonyl reductase. Such mechanism would explain the antioxidant and anti-inflammatory effects of the dipeptide.

Long-term exposure to third-hand smoke could accelerate biological aging via mitochondrial dysfunction: Evidence from population and animal studies.

The relationship between third-hand smoke (THS) exposure and lifespan remains inadequately explored. Our study sought to clarify the effects of THS on aging and lifespan. In this pursuit, our cross-sectional analysis assessed hematological aging markers in 986 non-smokers and examined lifespan alterations using a Drosophila model. THS exposure levels were quantified through survey metrics consistent with the Global Adult Tobacco Survey. The findings revealed that THS exposure significantly accelerated biological aging, with exposed individuals exhibiting an average increase in biological age of 3.04 years compared to their unexposed counterparts (p < 0.05). Correspondingly, the Drosophila model reflected these outcomes, showing a reduction in lifespan by 16.07 days (p < 0.01). Proteomic analyses identified MRPL2 as a pivotal protein in THS-induced aging, linking its expression to mitochondrial dysfunction and oxidative stress. Further metabolomic profiling highlighted disruptions in energy metabolism pathways. Follow-up in vitro experiments confirmed the role of MRPL2 in the aging processes at the cellular level. Overall, our results indicate that THS exposure is a significant accelerant of aging, providing new perspectives on the health consequences of environmental smoke residues.

DNA methylation at AHRR as a master predictor of smoke exposure and a biomarker for sleep and exercise.

BACKGROUND: DNA methylation profiling may provide a more accurate measure of the smoking status than self-report and may be useful in guiding clinical interventions and forensic investigations. In the current study, blood DNA methylation profiles of nearly 800 Polish individuals were assayed using Illuminia EPIC and the inference of smoking from epigenetic data was explored. In addition, we focused on the role of the AHRR gene as a top marker for smoking and investigated its responsiveness to other lifestyle behaviors. RESULTS: We found > 450 significant CpGs associated with cigarette consumption, and overrepresented in various biological functions including cell communication, response to stress, blood vessel development, cell death, and atherosclerosis. The model consisting of cg05575921 in AHRR (p = 4.5 × 10-32) and three additional CpGs (cg09594361, cg21322436 in CNTNAP2 and cg09842685) was able to predict smoking status with a high accuracy of AUC = 0.8 in the test set. Importantly, a gradual increase in the probability of smoking was observed, starting from occasional smokers to regular heavy smokers. Furthermore, former smokers displayed the intermediate DNA methylation profiles compared to current and never smokers, and thus our results indicate the potential reversibility of DNA methylation after smoking cessation. The AHRR played a key role in a predictive analysis, explaining 21.5% of the variation in smoking. In addition, the AHRR methylation was analyzed for association with other modifiable lifestyle factors, and showed significance for sleep and physical activity. We also showed that the epigenetic score for smoking was significantly correlated with most of the epigenetic clocks tested, except for two first-generation clocks. CONCLUSIONS: Our study suggests that a more rapid return to never-smoker methylation levels after smoking cessation may be achievable in people who change their lifestyle in terms of physical activity and sleep duration. As cigarette smoking has been implicated in the literature as a leading cause of epigenetic aging and AHRR appears to be modifiable by multiple exogenous factors, it emerges as a promising target for intervention and investment.