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Objective: The relationship between smoking and onset of glaucoma has been inconsistent. However, there is a gap in understanding whether tobacco smoking is linked to a worse visual impairment in different glaucoma subtypes. The objective of this study was to examine the association between smoking behavior and vision-related disability in people who have different glaucoma subtypes. Methods: A total of 283 people with primary open-angle glaucoma (POAG), primary angle closure glaucoma (PACG), normal tension glaucoma (NTG), and pseudo-exfoliative (PEX) were included in this cross-sectional study. The recruitment of study participants was organized in one of two tertiary centers for eye diseases in Belgrade, Serbia, during their regular eye checks. Information about the duration and quantity of smoking was self-reported. Vision-related impairment was quantified using a validated Glaucoma Quality of Life-15 (GQL-15) questionnaire. Results: A series of multiple linear regression models adjusted for age, gender, severity of glaucoma, lifestyle, and mobility, intraocular pressure level, visual parameters, previous and current therapy, and chronic illnesses suggested that a higher quantity of cigarettes smoked per day was associated with poorer vision-related quality of life only among people with NTG subtypes. This association was absent when smoking duration was tested in the adjusted linear regression model. Conclusion: A higher number of cigarettes smoked daily was associated with poorer vision-related impairment among people who have NTG, but not other glaucoma subtypes. It is recommended that ophthalmologists and other health-care professionals work to improve their patients' understanding of harmful effects of tobacco smoke and quit smoking. [ABSTRACT FROM AUTHOR]

Background: In the rural regions of Telangana State, many women are actively involved in the occupation of beedi rolling. Cigarette smoke either active or passive exerts deleterious effects on reproductive organs and function by means of both direct toxic influences, termed ovotoxicity, and the reduction of hormone secretion. Methods: The study involved a cohort of 320 women employed as beedi rollers and 280 women with no occupational exposure to chemicals for comparison. Serum samples were used to estimate the levels of Estrogen, Progesterone, Testosterone, Follicle Stimulating Hormone, luteinizing hormone, T3, T4 and TSH using Sandwich and competitive ELISA methods. Conclusion: The findings of the current study unveiled compelling statistical significance in the levels of estrogen, progesterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), T3 and T4.In conclusion, our study reveals a noteworthy correlation between beedi rolling and alterations in hormonal profiles of rural women in Telangana. [ABSTRACT FROM AUTHOR]

Cigarette smoke (CS) is a major risk factor for chronic lung diseases and promotes activation of pattern recognition receptors in the bronchial epithelium. NOD‐like receptor family, pyrin domain‐containing 3 (NLRP3) is a pattern recognition receptor whose activation leads to caspase‐1 cleavage, maturation/release of IL‐1β and IL‐18, and eventually pyroptosis. Whether the NLRP3 inflammasome participates in CS‐induced inflammation in bronchial epithelial cells is still unclear. Herein, we evaluated the involvement of NLRP3 in CS‐induced inflammatory responses in human primary bronchial epithelial cells. To this purpose, human primary bronchial epithelial cells were stimulated with CS extracts (CSE) and lytic cell death, caspase activation (‐1, ‐8, ‐3/7), cytokine release (IL‐1β, IL‐18, and IL‐8), NLRP3, pro‐IL‐1β/pro‐IL‐18 mRNA, and protein expression were measured. The impact of inhibitors of NLRP3 (MCC950), caspases, and the effect of the antioxidant N‐acetyl cysteine were evaluated. We found that CSE increased pro‐IL‐1β expression and induced activation of caspase‐1 and release of IL‐1β and IL‐18. These events were independent of NLRP3 and we found that NLRP3 was not expressed. N‐acetyl cysteine reverted CSE‐induced caspase‐1 activation. Overall, our findings support that the bronchial epithelium may play a central role in the release of IL‐1 family cytokines independently of NLRP3 in the lungs of smokers. [ABSTRACT FROM AUTHOR]

Background: Tobacco smoking is the leading cause of preventable death and disease worldwide, with over 8 million annual deaths attributed to cigarette smoking. This study investigates the impact of cigarette smoke and heated tobacco products (HTPs) on microglial function, focusing on toxicological profiles, inflammatory responses, and oxidative stress using ISO standard and clinically relevant conditions of exposure. Methods: We assessed cell viability, reactive oxygen species (ROS) production, lipid peroxidation, mitochondrial function, unfolded protein response, and inflammation in human microglial cells (HMC3) exposed to cigarette smoke, HTP aerosol or nicotine. Results: Our findings show that cigarette smoke significantly reduces microglial viability, increases ROS formation, induces lipid peroxidation, and reduces intracellular glutathione levels. Cigarette smoke also alters the expression of genes involved in mitochondrial dynamics and biogenesis, leading to mitochondrial dysfunction. Additionally, cigarette smoke impairs the unfolded protein response, activates the NF-κB pathway, and induces a pro-inflammatory state characterized by increased TNF and IL-18 expression. Furthermore, cigarette smoke causes DNA damage and decreases the expression of the aging marker Klotho β. In contrast, HTP, exhibited a lesser degree of microglial toxicity, with reduced ROS production, lipid peroxidation, and mitochondrial dysfunction compared to conventional cigarettes. Conclusion: These results highlight the differential toxicological profile of cigarette smoke and HTP on microglial cells, suggesting a potential harm reduction strategy for neurodegenerative disease for smokers unwilling or unable to quit. [ABSTRACT FROM AUTHOR]

The modification of cigarette filters with nanozymes has gradually emerged as a promising strategy for reducing the harmful effects of smoking by eliminating excessive harmful free radicals and remediating oxidative stress‐induced pulmonary injury. However, currently, available nanozymes‐integrated filters usually ignore safety concerns and fail to address the pungent odor of smoke, making it challenging to develop an individual system with high safety and effectiveness while considering these important factors. Herein, a novel smoke purifier (CDs/ME@MOF) is developed by alternatively introducing carbon dots nanozymes with excellent free radicals scavenging activity and Menthone masking the miscellaneous gas into a biocompatible γ‐cyclodextrin‐based metal–organic framework. The CDs/ME@MOF can act as a profitable additive incorporated with cigarette filters to achieve over 90% scavenging efficiency for cigarette smoke radicals and reduce the odor irritation. In the mice model, the CDs/ME@MOF composites demonstrated the significant inflammation suppression, antioxidant levels promotion, and notable lung tissues protection effect through elimination of free radicals. This work highlights the potential of CDs/ME@MOF as a safe, environmentally friendly, and multipurpose additive for modifying cigarette filter. [ABSTRACT FROM AUTHOR]

The use of tobacco cigarettes produces locomotor muscle weakness and fatigue intolerance. Also, smokers and chronic obstructive pulmonary disease patients have a greater incidence of muscle injury and a deficient myogenic response. However, the effects of smoke exposure on the recovery from eccentric exercise‐induced muscle injuries are unknown. Mice were exposed daily to cigarette smoke (CS) or room air (Air) for 4 months; the anterior crural muscles from one limb were injured by a lengthening contractions protocol (LCP) and recovered for 7 days. Lung compliance was greater, and body weights were lower, in CS‐exposed than in the Air group. In LCP‐subjected limbs, CS exposure lowered tibialis anterior myofiber cross‐sectional area, decreased the size of centrally nucleated myofibers, and decreased extensor digitorum longus (EDL) mass, but did not affect EDL force from both limbs. CS exposure upregulated the mRNA levels of several myogenic (Pax7, Myf5, nNOS) genes in the EDL. The combination of CS exposure and LCP decreased Myf5 and nNOS mRNA levels and exacerbated pro‐inflammatory mRNA levels. These data suggest that smoke exposure leads to an excessive pro‐inflammatory response in regenerating muscle that is associated with a lower muscle mass recovery from a type of injury that often occurs during strenuous exercise. [ABSTRACT FROM AUTHOR]

Background and Aim: Increased oxidative stress within the airways is associated to epithelial damage and amplification of inflammatory responses that in turn contribute to Chronic Obstructive Pulmonary Disease (COPD) progression. This study was aimed to identify whether a new formulation of N-acetylcisteine (NAC), carnitine, curcumin and B2 vitamin could counteract oxidative stress and downstream pro-inflammatory events promoted by cigarette smoke extract (CSE) exposure in primary bronchial epithelial cells (PBEC), both submerged/ undifferentiated (S-PBEC) and cultured at the air-liquid interface (ALI-PBEC). Methods: PBEC were exposed to CSE with/without the new formulation or NAC alone and ROS production, IL-8 and IL-6 gene expression and protein release were evaluated. Results: CSE increased ROS, IL-8 and IL-6 gene expression and protein release and the new formulation counteracted these effects. NAC alone was not effective on IL-8 and IL-6 release. The effects of a similar nutraceutical formulation were evaluated in COPD patients treated for six months. The results showed that the treatment reduced the concentration of IL-8 in nasal wash and improved quality of life. Conclusion: The tested formulation, exerting antioxidant and anti-inflammatory effects, can preserve airway epithelial homeostasis and improve clinical symptoms in COPD. [ABSTRACT FROM AUTHOR]

A physiological mechanism of programmed cell death called eryptosis occurs in aged or damaged red blood cells (RBCs). Dysregulated eryptosis contributes to abnormal microcirculation and prothrombotic risk. Cigarette smoke extract (CSE) induces a p38 MAPK‐initiated, Fas‐mediated eryptosis, activating the death‐inducing signaling complex (DISC). Indicaxanthin (Ind) from cactus pear fruits, is a bioavailable dietary phytochemical in humans and it is able to incorporate into RBCs enhancing their defense against numerous stimuli. This in vitro work shows that Ind, at concentrations that mimic plasma concentrations after a fruit meal, protects erythrocytes from CSE‐induced eryptosis. CSE from commercial cigarettes was prepared in aqueous solution using an impinger air sampler and nicotine content was determined. RBCs were treated with CSE for 3 h in the absence or presence of increasing concentrations of Ind (from 1 to 5 μM). Cytofluorimetric measurements indicated that Ind reduced CSE‐induced phosphatidylserine externalization and ceramide formation in a concentration‐dependent manner. Confocal microscopy visualization and coimmunoprecipitation experiments revealed that Ind prevented both CSE‐triggered Fas aggregation and FasL/FADD/caspase 8 recruitment in the membrane, indicating inhibition of DISC assembly. Ind inhibited the phosphorylation of p38 MAPK, caspase‐8/caspase‐3 cleavage, and caspase‐3 activity induced by CSE. Finally, Ind reduced CSE‐induced ATP depletion and restored aminophospholipid translocase activity impaired by CSE treatment. In conclusion, Ind concentrations comparable to nutritionally relevant plasma concentrations, can prevent Fas‐mediated RBC death signaling induced by CSE, which suggests that dietary intake of cactus pear fruits may limit the deleterious effects of cigarette smoking. [ABSTRACT FROM AUTHOR]

Based on the results of research in Majalengka Regency, it is very clear that the community wants a clean and healthy environment without exposure to cigarette smoke. Therefore, the Regional Government of Majalengka Regency needs to do to create a healthy and clean environment, so this needs to be a step to secure cigarettes for the health of both active and passive smokers through the establishment of a Smoke-Free Zone (KTR). Based on the above background, the purpose of this writing is as follows: a) To be able to find out what is the cause of the lack of a Regional Regulation on Non- Smoking Areas (KTR) in Majalengka Regency. b) To be able to find out what are the implications of the establishment of the Regional Regulation of Non-Smoking Areas (KTR) on the protection of the right to health in Majalengka Regency. The research method used is sociological juridical, which is legal research by looking at law as human behavior in society and then studied and reviewed based on relevant laws and regulations as a reference to solve problems. From a health perspective, cigarettes are the cause of death and pain that cause human misery and a decrease in quality of life and are contrary to Indonesia's human development. From a social and economic point of view, bad behavior of cigarette consumption violates human rights and is a means of impoverishing people. Based on the legal aspect, cigarettes are addictive substances which need to be regulated for the security of both production, distribution and use. [ABSTRACT FROM AUTHOR]

Although the effects of cigarette smoke (CS) on the development of several intestinal diseases is well documented, the impact of e-cigarette aerosol (e-cig) on digestive health is largely unknown. To compare the effects of e-cig and CS on mouse ileum and colon, animals were chronically exposed for 6 months by nose-only inhalation to e-cig at 18 or 30 W power, or to 3R4F CS. Results showed that e-cig exposure decreased colon cell proliferation. Several other proliferative defects were observed in response to both e-cig and CS exposure, including up- and down-regulation of cyclin D1 protein levels in the ileum and colon, respectively. E-cig and CS exposure reduced myeloperoxidase activity in the ileum. In the colon, both exposures disrupted gene expression of cytokines and T cell transcription factors. For tight junction genes, ZO-1- and occludin-protein expression levels were reduced in the ileum and colon, respectively, by e-cig and CS exposure. The 16S sequencing of microbiota showed specific mild dysbiosis, according to the type of exposure. Overall, e-cig exposure led to altered proliferation, inflammation, and barrier function in both the ileum and colon, and therefore may be a gut hazard on par with conventional CS. [ABSTRACT FROM AUTHOR]

Notch-1 signaling plays a crucial role in stem cell maintenance and in repair mechanisms in various mucosal surfaces, including airway mucosa. Persistent injury can induce an aberrant activation of Notch-1 signaling in stem cells leading to an increased risk of cancer initiation and progression. Chronic inflammatory respiratory disorders, including chronic obstructive pulmonary disease (COPD) is associated with both overactivation of Notch-1 signaling and increased lung cancer risk. Increased oxidative stress, also due to cigarette smoke, can further contribute to promote cancer initiation and progression by amplifying inflammatory responses, by activating the Notch-1 signaling, and by blocking regulatory mechanisms that inhibit the growth capacity of stem cells. This review offers a comprehensive overview of the effects of aberrant Notch-1 signaling activation in stem cells and of increased oxidative stress in lung cancer. The putative role of natural compounds with antioxidant properties is also described. [ABSTRACT FROM AUTHOR]

Lung cancer remains a major contributor to cancer fatalities, with cigarette smoking known to be responsible for up to 80% of cases. Based on the ability of cigarette smoke to induce inflammation in the lungs and increased lung cancer incidence in smokers with inflammatory conditions such as COPD, we hypothesized that inflammation plays an important role in the carcinogenicity of cigarette smoke. To test this hypothesis, we performed multi-omic analyses of Type II pneumocytes of A/J mice exposed to cigarette smoke for various time periods. We found that cigarette smoke exposure resulted in significant changes in DNA methylation and hydroxymethylation, gene expression patterns, and protein abundance that were partially reversible and contributed to an inflammatory and potentially oncogenic phenotype. [ABSTRACT FROM AUTHOR]

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//β-catenin, TGF-β/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. [ABSTRACT FROM AUTHOR]

Introduction: Chronic obstructive pulmonary disease (COPD) is a nonspecific chronic inflammatory lung disease with no known cure. Codonopsis Radix (CR) has been shown to exhibit anti-inflammatory and antioxidant effects. Therefore, this study aimed to investigate the potential anti-inflammatory effects of different CR varieties on COPD mice. Methods: Sixty male-specified pathogen-free grade C57BL/6J mice were randomly divided into 6 groups, 10 mice in each group. The COPD mice model was induced by cigarette smoke extract combined with lipopolysaccharide, and the mice in each group were given corresponding drugs. Lung function was assessed in all mice. Lung tissues were stained with hematoxylin-eosin, Masson, and periodic acid-Schiff stains, and serum levels of interleukin (IL)-8 and tumor necrosis factor (TNF)-α were detected using an ELISA. Further, serum and lung tissue levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were detected by colorimetric assay. Network pharmacology and molecular docking were used to predict signaling pathways, which were validated by Western blot analysis. Results: Compared with the COPD group, the mice in each dosing group of CR exhibited significant reductions in serum IL-8 and TNF-α levels, serum and lung tissue MDA levels, and pathological lung tissue damage, alongside elevations in lung function and SOD levels (p < 0.01). Western blot analysis also indicated significant downregulation of p-p65/p65 and p-IκB-α/IκB-α protein expression, alongside significant upregulation of Nrf2 protein expression in the lung tissues of mice treated with CR (p < 0.01). Conclusion: In summary, CR effectively enhances lung function, minimizes lung tissue damage, and inhibits inflammation and oxidative stress in mice with COPD. Additionally, these findings suggest that inhibition of the Nrf2/NF-κB axis may be a key mechanism of action of CR in the alleviation of COPD. [ABSTRACT FROM AUTHOR]

Background: Smoking remains the single most common cause of preventable deaths. The liver is affected by the process of smoking through various inflammatory pathways. This will lead to aggravation of pathogenic impact on the liver tissue. The present study was undertaken to determine the liver function parameters in cigarette smokers. Aims and Objectives: The objective was to estimate and compare the parameters of liver function -- alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), total bilirubin, total protein, albumin, and globulin in asymptomatic male smokers and non-smokers of the age group 25-50 years in the above two groups. Materials and Methods: A cross-sectional comparative study was conducted on 60 males with 30 smokers and 30 non-smokers of the age group 25-50 years. All the subjects who have satisfied the inclusion and exclusion criteria were incorporated in the study. Informed consent was taken before the conduct of the study. The participants were selected in a consecutive manner till the sample size was achieved. AST, ALT, ALP, total bilirubin, total protein, and albumin were estimated using ERBA EM 360 fully automatic analyzer. The difference between the total protein and albumin was used to calculate the level of globulin. The Statistical Package for the Social Sciences version 18 was used for data analysis. Results: The mean values of AST, ALT, and ALP were significantly elevated in smokers when compared to non-smokers. The mean values of total bilirubin, total protein, albumin, and globulin were significantly decreased in smokers. Conclusion: Smoking leads to the development of hepatic damage which increases the intensity of complications. The study reveals the importance of screening asymptomatic smokers for liver function parameters to avoid complications of hepatic diseases hence improving the quality of life. [ABSTRACT FROM AUTHOR]

Prescribed burns are used to maintain wildland ecosystems and decrease fuel loads and associated wildfire hazard. Prescribed burns may produce enough smoke to cause adverse health outcomes. The aim of this review is to understand what communication materials exist for disseminating health risk information related to prescribed burn smoke and challenges to developing such communication. We examined United States peer-reviewed literature from PubMed, Scopus, and Web of Science databases and conducted an environmental scan of grey literature including materials from federal, and several US state and local governments, organisations, and newspapers. While 63% of the included peer-reviewed literature focuses on wildfire health risk communication, the review suggests similar methods and messages can be adapted for prescribed burns. The environmental scan review indicates effective strategies use several communication modes, and reliable and timely messaging. There are state regulations for prescribed burn notification, but these do not require communication or education of health risks associated with smoke exposure. Smoke management guidelines often contain information about prescribed burn health risks, but these do not discuss health risk education. Opportunities to expand effective health risk communication include improving inconsistent messaging and inter-agency collaborations, and increasing public interactions, especially with vulnerable populations. This review identifies current health risk communications for prescribed burn smoke exposure in the United States. While this review highlights several effective communication strategies, further research is needed to better understand prevention and intervention approaches and the efficacy of communication strategies to minimise health risks of prescribed burns. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

This study was conducted to determine pregnant women’s exposure to third-hand smoke, beliefs and influencing factors. The study included 400 pregnant women in a tertiary care obstetrics and gynecology hospital in Turkey. Data were collected using personal information form, Beliefs About Third-Hand Smoke Scale (BATHS-T) and Fagerström Test for Nicotine Dependence. 13.5% of the pregnant women smoked during pregnancy. However, 78.8% of the pregnant women were exposed to cigarette smoke at home. The mean score of BATHS-T scale and sub-scales increased in those whose spouses had university education or higher, and in pregnant women and their spouses who were public employees. The mean scores of BATHS-T scale and sub-scales were higher in pregnant women in the first trimester of pregnancy and in pregnant women with higher income levels. Community-based awareness of the effects of first, second and third-hand exposure to cigarette smoke on maternal and fetal health should be increased. [ABSTRACT FROM AUTHOR]

Transforming Growth Factor Beta1 (TGF-β1) signaling is upregulated in Chronic Obstructive Pulmonary disease (COPD), smokers, and people living with HIV. Cigarette smoking and HIV are also independent risk factors for COPD. Chronic inflammation is a hallmark of COPD. However, the underlying mechanisms remain unknown. Previous research has suggested that TGF-β1 alters the airway epithelial microRNAome and transcriptome, potentially contributing to lung inflammation. The Lactoperoxidase (LPO) system is an integral component of innate immunity within the airway. LPO plays a crucial role in host defense by catalyzing the oxidation of thiocyanate to hypothiocyanite in the presence of hydrogen peroxide (H2O2), generating a potent antibacterial and antiviral agent. Additionally, the LPO system potentially aids in maintaining cellular redox balance by reducing the levels of H2O2, thus mitigating oxidative stress within the airway epithelium. LPO dysfunction can impair immune responses and exacerbate inflammatory processes in respiratory diseases. In this study, primary bronchial epithelial cells and bronchial cell lines were treated with TGF-β1 and exposed to cigarette smoke to characterize the effect of these factors on LPO and their downstream effects. RT-qPCR and Western Blot were applied to quantify mRNA and proteins' expression. The levels of H2O2 were detected using the Amplex Red Assay. Magnetofection and transfection were applied to probe the effect of miR-449b-5p. Staining procedures using the MitoTracker Green and C12FDG dyes were used to establish mitochondria mass and senescence. The levels of pro-inflammatory cytokines were measured via Luminex assays. We found that TGF-β1 and cigarette smoke suppressed airway LPO expression, increasing H2O2 levels. This increase in H2O2 had downstream effects on mitochondrial homeostasis, epithelial cellular senescence, and the pro-inflammatory cytokine response. We demonstrate for the first time that airway LPO is regulated by TGF-β1-induced miRNA-mediated post-transcriptional silencing through miR-449b-5p in the lungs. Further, we identify and validate miR-449-5p as the candidate miRNA upregulated by TGF-β1, which is involved in LPO suppression. This paper demonstrates a new mechanism by which TGF-β1 can lead to altered redox status in the airway. [ABSTRACT FROM AUTHOR]

Nicotine is the primary addictive component of cigarette smoke and is associated with various smoking-related diseases. However, recent research has revealed its broader cognitive-enhancing and antiinflammatory properties, suggesting its potential therapeutic applications in several conditions. This review aims to examine the double-edged nature of nicotine, encompassing its positive and negative effects. We provide a concise overview of the physiochemical properties and pharmacology of nicotine, including insights into nicotine receptors. Therefore, the article is divided into two main sections: toxicity and therapeutic potential. We comprehensively explored nicotine-related diseases, focusing on specific signaling pathways and the underlying mechanisms that contribute to its effects. Furthermore, we addressed the current research challenges and future development perspectives. This review aims to inspire future researchers to explore the full medical potential of nicotine, which holds significant promise for the clinical management of specific diseases. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Tobacco smoking, a significant public health concern globally, is associated with a rise in noncommunicable diseases (NCDs) and preventable deaths, with pronounced impacts in conflict zones like Gaza. A cross-sectional study, conducted in 2020, in Gaza focused on individuals over 40 years of age, aiming to identify predictors of tobacco use and its links to diseases like coronary artery disease (CAD), chronic lung disease (CLD), and stroke using regression analysis. The research, based on the Gaza NCD study data with 4576 participants and a 96.6% response rate, found an overall tobacco smoking prevalence of 19.4%, with higher rates among men. After adjusting for various factors, the study identified significant associations between cigarette smoking in men and adverse health outcomes, such as CAD and CLD, with adjusted odds ratios (OR) of 1.67, 95% CI (1.22–2.29) and 1.68, 95% CI (1.21–2.33) respectively. However, after adjusting for independent variables, shisha smoking in men showed no association with these health outcomes. The findings of this study could assist other researchers in designing interventions aimed at reducing smoking prevalence by utilizing the associated factors identified in our analysis, such as age, education level, physical activity, and body mass index among men in Gaza. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease is a common chronic lung disease with an ever-increasing incidence. Despite years of drug research and approvals, we are still not able to halt progress or restore normal lung function. Our previous studies have demonstrated that liver growth factor—LGF has an effect on the repair of the affected tissue in a mouse model of cigarette smoke exposure, but by what pathways it achieves this is unknown. The present study aimed to identify differentially expressed genes between emphysematous mice treated with LGF to identify potential therapeutic targets for the treatment of pulmonary emphysema. The emphysema mouse model was induced by prolonged exposure to cigarette smoke. To determine the gene expression profile of the lung in smokers treated or not with LGF, lung messenger RNA gene expression was assessed with the Agilent Array platform. We carried out differentially expressed gene analysis, functional enrichment and validated in treated mouse lung samples. The treated group significantly improved lung function (~35%) and emphysema level (~20%), consistent with our previous published studies. Microarray analysis demonstrated 290 differentially expressed genes in total (2.0-fold over or lower expressed). Injury repair-associated genes and pathways were further enhanced in the lung of LGF treated mice. The expression trends of two genes (Zscan2 and Bag6) were different in emphysematous lungs treated with LGF compared to untreated lungs. Therefore, Zscan2 and Bag6 genes could play a role in regulating inflammation and the immune response in the lung that undergoes partial lung regeneration. However, further studies are necessary to demonstrate this causal relationship. [ABSTRACT FROM AUTHOR]

In this study, graphene nanoplatelets were applied to polyester fabrics using the knife‐coating method at different concentrations (50, 100, and 150 g/kg). SEM, DSC, and TGA/DTG analyses were performed. The influence of graphene coating on hydrophobicity and surface roughness was examined by water contact angle (WCA) measurement and root mean square roughness, respectively. Abrasion resistance and tear strength tests were also performed. The effect of graphene used as a filler on the flammability of polyester fabric was evaluated for the first time according to the BS 5852 standard. No significant weight loss (only in the range of 0.4%–1.5%) was observed in the graphene‐coated samples even after 100,000 cycles. While the WCA value was 0 for the uncoated fabric, the blind coating and maximum graphene‐coated sample measured 86° and 95°, respectively. The coating process reduced the roughness of the base fabric, and the decrease continued with the increasing graphene ratio. The tear strength values that were 45.5 N in the warp and 53.6 N in the weft direction in the blind coating, increased to 52.2 and 59.1 N, respectively, at the maximum graphene concentration. Graphene coating enhanced thermal stability, increased hydrophobicity, and improved flame retardancy in the test using a smoldering cigarette. [ABSTRACT FROM AUTHOR]

Particulate matter (PM) is one of the most hazardous atmospheric pollutants. Several plant species show high potential to reduce air pollutants and are widely used as green belts to provide clean outdoor spaces for human well-being. However, high PM concentrations cause physiological changes and stress in plants. In this study, 11 species of Thai native perennial plants were exposed to PM generated from tobacco smoke. Wrightia religiosa (Teijsm. & Binn.) Benth. ex Kurz, Bauhinia purpurea DC. ex Walp. and Tectona grandis L.f. reduced PM effectively (which is in the typical range of 43.95 to 52.97%) compared to other plant species. In addition, the responses of perennial plants under PM stress at the proteomic level were also evaluated. Proteomic analysis of these three plant species showed that plants respond negatively to high PM concentrations, such as reducing several photosynthetic-related proteins and increasing plant stress response proteins. To improve PM phytoremediation efficiency and reduce plant stress from PM, perennial plant–microbe interactions were investigated. W. religiosa was inoculated with Acinetobacter indicus PS1, and high biosurfactant-producing strains clearly showed a higher PM removal efficiency than non-inoculated plants (9.48, 9.5 and 12.6% for PM1.0, PM2.5 and PM10, respectively). Inoculating W. religiosa with A. indicus PS1 maintained chlorophyll a and b concentrations. Moreover, the malondialdehyde (MDA) concentration of W. religiosa inoculated with A. indicus PS1 was lower than that of non-inoculated W. religiosa. The leaf wax content (µg/cm2) and biosurfactant (µg/cm2) of W. religiosa inoculated with A. indicus PS1 were also higher than those of non-inoculated W. religiosa. This study clearly showed that inoculating plants with A. indicus PS1 can help plants remediate PM and improve their PM stress response. [ABSTRACT FROM AUTHOR]

Although it is known (from the observations of medical professionals) that cigarette smoke negatively affects maxillofacial prostheses, especially through staining/discoloration, systematic research in this regard is limited. Herein, the color modifications of M511 maxillofacial silicone, unpigmented and pigmented with red or skin tone pigments, covered with mattifiers, or with makeup and mattifiers, and directly exposed to cigarette smoke, were investigated by spectrophotometric measurements in the CIELab and RGB color systems. The changes in color parameters are comparatively discussed, showing that the base silicone material without pigmentation and coating undergoes the most significant modifications. Visible and clinically unacceptable changes occurred after direct exposure to only 20 cigarettes. By coating and application of makeup, the material is more resistant to color changes, which suggests that surface treatments provide increased protection to adsorption of the smoke components. The dynamic water vapor sorption (DVS) measurements indicate a decrease of the sorption capacity in pigmented versus unpigmented elastomers, in line with the changes in color parameters. [ABSTRACT FROM AUTHOR]

Background: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease associated with high morbidity and mortality worldwide. Oxidative injury and mitochondrial dysfunction in the airway epithelium are major events in COPD progression. Methods and results: The therapeutic effects of Progesterone (P4) were investigated in vivo and in vitro in this study. In vivo, in a cigarette smoke (CS) exposure-induced COPD mouse model, P4 treatment significantly ameliorated CS exposure-induced physiological and pathological characteristics, including inflammatory cell infiltration and oxidative injury, in a dose-dependent manner. The c-MYC/SIRT1/PGC-1α pathway is involved in the protective function of P4 against CS-induced COPD. In vitro, P4 co-treatment significantly ameliorated H2O2-induced oxidative injury and mitochondrial dysfunctions by promoting cell proliferation, increasing mitochondrial membrane potential, decreasing ROS levels and apoptosis, and increasing ATP content. Moreover, P4 co-treatment partially attenuated H2O2-caused inhibition in Nrf1, Tfam, Mfn1, PGR-B, c-MYC, SIRT1, and PGC-1α levels. In BEAS-2B and ASM cells, the c-MYC/SIRT1 axis regulated P4's protective effects against H2O2-induced oxidative injury and mitochondrial dysfunctions. Conclusion: P4 activates the c-MYC/SIRT1 axis, ameliorating CS-induced COPD and protecting both airway epithelial cells and smooth muscle cells against H2O2-induced oxidative damage. PGC-1α and downstream mitochondrial signaling pathways might be involved. [ABSTRACT FROM AUTHOR]

Introduction: Cigarette smoke (CS) exacerbates the severity of diseases not only in lungs, but also in systemic organs having no direct contact with smoke. In addition, smoking during pregnancy can have severe health consequences for both the mother and the fetus. Therefore, our aim was to evaluate effects of prenatal exposure to CS on acetaminophen (APAP)-induced acute liver injury (ALI) in offspring. Methods: Female C57BL/6 mice on day 6 of gestation were exposed to mainstream CS (MSCS) at 0, 150, 300, or 600 µg/L for 2 h a day, 5 days a week for 2 weeks using a nose-only exposure system. At four weeks old, male offspring mice were injected intraperitoneally with a single dose of APAP at 300 mg/kg body weight to induce ALI. Results: Maternal MSCS exposure significantly amplified pathological effects associated with ALI as evidenced by elevated serum alanine aminotransferase levels, increased hepatocellular apoptosis, higher oxidative stress, and increased inflammation. Interestingly, maternal MSCS exposure reduced microRNA (miR)- 34a-5p expression in livers of offspring. Moreover, treatment with a miR-34a-5p mimic significantly mitigated the severity of APAP-induced hepatotoxicity. Overexpression of miR-34a-5p completely abrogated adverse effects of maternal MSCS exposure in offspring with ALI. Mechanistically, miR-34a-5p significantly decreased expression levels of hepatocyte nuclear factor 4 alpha, leading to down-regulated expression of cytochrome P450 (CYP)1A2 and CYP3A11. Discussion: Prenatal exposure to MSCS can alter the expression of miRNAs, even in the absence of additional MSCS exposure, potentially increasing susceptibility to APAP exposure in male offspring mice. [ABSTRACT FROM AUTHOR]

Introduction: NOD-like receptor protein 3 (NLRP3) is implicated in chronic obstructive pulmonary disease (COPD) pathogenesis. Here, we explored the role of NLRP3 in cigarette smoke (CS)-induced airway inflammation in COPD. Material and methods: NLRP3 expression level was assessed with the microarray data in GEO datasets and validated in serum by ELISA from a case-control cohort. Male C57BL/6J mice were randomly divided into: saline, CS, MCC950 (a specific NLRP3 inhibitor, 10 mg/kg) and CS + MCC950 (5 mg/kg and 10 mg/kg) groups (n = 5 per group). All mice were exposed to CS or air for 4 weeks. Then, broncho-alveolar lavage (BAL) fluid and lung tissues were collected for cell counting, ELISA, HE staining and RNA sequencing with validation by real-time qPCR. Results: Compared to non-smokers, NLRP3 expression was significantly elevated in the lung tissues and sera of COPD smokers. CS remarkably induced airway inflammation in mice, characterized by an increase of inflammatory cells and proinflammatory cytokines in BAL fluid and HE inflammatory score, which were ameliorated by MCC950 treatment dose-dependently. Subsequently, 84 candidate genes were selected following RNA sequencing, and five hub genes (Mmp9, IL-1a, Cxcr2, Cxcl10, Ccr1) were then identified by PPI and MCODE analyses, which were confirmed by real-time qPCR. GO and KEGG analysis suggested that the five genes were enriched in a complicated network of inflammatory processes and signaling pathways. Conclusions: NLRP3 expression is elevated in lungs and sera of COPD smokers. Inhibition of NLRP3 significantly attenuates CS-induced airway inflammation in mice via inactivation of multiple hub genes and their related inflammatory processes and signaling pathways. [ABSTRACT FROM AUTHOR]

Purpose: Recently, the detrimental effect of cigarette smoking on muscle metabolism has attracted much attention, but the relationship between cigarette smoking and muscle mass is poorly understood. Thus, this study investigated the association between exposure to cigarette smoke, defined based on serum cotinine, and muscle mass in the US population. Methods: We utilized National Health and Nutrition Examination Survey (NHANES) data between 2011 and 2018 for analysis. Data on serum cotinine, muscle mass (quantified by appendicular skeletal muscle mass index, ASMI), and covariates were extracted and analyzed. Weighted multivariate linear regression analyses and smooth curve fittings were performed to investigate the association between serum cotinine and ASMI. Subgroup analyses were stratified by gender, race and smoking status. When nonlinearity was detected, the threshold effects were analyzed using a two-piecewise linear regression model. Results: In total, 8004 participants were included for analysis. The serum level of cotinine was negatively associated with ASMI in the fully adjusted model. Furthermore, comparing participants in the highest vs. the lowest tertile of serum cotinine, we found that ASMI decreased by 0.135 Kg/m2. In subgroup analysis stratified by gender and race, the association between serum cotinine and ASMI remained significant in all genders and races. In addition, the association remained significant among current and former smokers, but not among those who never smoked. Smooth curve fittings showed nonlinear relationships between serum cotinine and ASMI, with the inflection points identified at 356 ng/mL. Conclusions: Our study revealed that serum cotinine was negatively related to muscle mass. This finding improves our understanding of the deleterious effects of cigarette smoking on muscle mass and highlights the importance of smoking cessation for muscle health. [ABSTRACT FROM AUTHOR]

The respiratory structure has a broad capacity to undergo the mechanism of regeneration. The recent study was intended to determine the efficacy of Withania somnifera (L.) Dunal and expression levels of IRS-1 and SOX-2 genes in the smoke-induced Pulmonary Injury. The present study included 3 groups (n = 9): Normal/negative control (NC), positive control/disease control (PC), and treatment group (TG; treated orally with 350 mg/kg of ethanol extract). Lung injury was induced in PC and TG groups in rats by cigarette smoke (4 CG/day). Decapitation (n = 3) was done on the 14th, 18th, and 21st day of treatment. Phenolic acid quantification by HPLC-UV/VIS showed a significant concentration of p-coumaric acid (130.2 mg/kg) that may also contribute to the extract's efficacy. Hematological parameters (leukocytes, hemoglobin, hematocrit) and serum oxidative parameters (total oxidant status and malondialdehyde) were significantly improved (P ≤ 0.05) in the TG compared to the PC group. Moreover, the total antioxidant capacity, total plasma protein, albumin, globulin, and platelet count significantly decreased in the PC while increasing in the treatment group (P ≤ 0.05). Histology showed damaged histological structures in the PC group, while there was obvious regeneration of architectural damage in the TG group. The IRS-1 and SOX-2 genes were up-regulated in the PC group, indicating the role of IRS-1 and SOX-2 gene expression in tissue homeostasis and regeneration in smoke-induced Pulmonary Injury. These results rationalize the traditional use of W. somnifera in pulmonary diseases and encourage further studies to exploit it in the pharmaceutical industry. [Display omitted] • Withania somnifera is a medicinal plant and provide relief in respiratory problems also. • Rat model of cigarette smoke-induced lung injury was used to investigate the effect of W.somnifera extract acute pulmonary pathophysiology. • Hematological parameters including leukocytes, hemoglobin, hematocrit, serum oxidative parameters, total plasma protein, albumin, globulin, and platelet count significantly improved in the treatment group (P ≤ 0.05). • The results further indicated the role of IRS-1 and SOX-2 gene expression in tissue homeostasis and regeneration in smoke-induced pulmonary injury. [ABSTRACT FROM AUTHOR]

Acute lung injury (ALI) and its more severe form acute respiratory distress syndrome (ARDS) is a critical respiratory condition characterized by a sudden respiratory collapse, accumulation of fluid in lungs leading to reduced blood oxygenation. ALI/ARDS management is mainly supportive, as no specific anti-inflammatory therapy exists for lung injury. Recently, several medicinal plants and natural products have gained attention for their antimicrobial, antioxidant, immunomodulation and anti-inflammatory activities. Cenchrus ciliaris L. (Buffel grass), is native to Africa and Asia where it is traditionally used for several inflammatory disorders, wounds and pain. Cigarette smoke induces inflammation and oxidative stress in respiratory system which can damage lungs and augment respiratory disorders that can progress to ALI/ARDS. We described antioxidant and anti-inflammatory potential of C. ciliaris L. which ameliorates acute lung injury induced by exposure to cigarette smoke. Total phenolic, flavonoid, tannin and saponin contents were quantified in 70 % methanolic extract of C. ciliaris (Cc.Cr). Phytochemical characterization was performed by UHPLC which indicated the presence of furoic acid, longistylin A, scandenin, salicylic acid, piscidic acid, 3-hydroxybenzaldehyde, pheophorbide and chrysoeriol reported for their antioxidant, anti-inflammatory and antimicrobial activities. ALI was induced in mice by exposure to cigarette smoke, followed by the collection of broncho alveolar lavage fluid (BALF) and lung tissues. Total inflammatory cells, differential leukocyte count, total protein contents, nitrite levels, interleukins, total oxidative stress and antioxidant capacity were assessed in BALF. MDA and catalase levels were assessed in lung tissue and histopathology was performed to assess the integrity of lung tissue architecture. Cc.Cr showed good antioxidant activity in CUPRAC and FRAP assays while it effectively scavenged free radicals in DPPH, ABTS and nitric oxide assay. Cc.Cr inhibited cycloxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) with IC 50 values 29.23 ± 9.73 μ g/ml and 24.12 ± 6.0 μ g/ml respectively. In mice, Cc.Cr improved total antioxidant capacity, lung tissue integrity, and hematological parameters while it reduced inflammation, oxidative stress, lung edema and tissue damage. Graphical abstract [Display omitted] • C. ciliaris L. possess good antioxidant and free radical scavenging activity. • It inhibits COX-2 and 5-LOX enzymes. • C. ciliaris L. improves total antioxidant capacity, lung tissue integrity and hematological parameters. • C. ciliaris L. reduced inflammation, oxidative stress, lung edema and tissue damage in acute lung injury. [ABSTRACT FROM AUTHOR]

Established risk factors for osteoarthritis (OA) include obesity, joint injury, age, race, and genetics. However, the relationship between cigarette smoking and OA has yet to be established. In the present study, we have employed the use of cigarette smoke extract (CSE), the water‐soluble vapor phase of cigarette smoke, with porcine cartilage explants to investigate the effects of cigarette smoking on cartilage catabolism at the tissue level. Articular cartilage explants were first exposed to 2.5%, 5%, and 10% CSE to assess its effects on cartilage homeostasis. Following, the effects of CSE on OA‐like inflammation was observed by culturing explants with a combined treatment of IL‐1β and TNF‐α and 10% CSE (CSE + OA). Cartilage explants were assessed for changes in viability, biochemical composition, extracellular matrix (ECM) integrity, and equilibrium mechanical properties (aggregate modulus and hydraulic permeability). CSE alone leads to both a time‐ and dose‐dependent decrease in chondrocyte viability but does not significantly affect sGAG content, percent sGAG loss, or the ECM integrity of cartilage explants. When IL‐1β and TNF‐α were combined with 10% CSE, this led to a synergistic effect with more significant losses in viability, significantly more sGAG loss, and significantly higher production of ROS than OA‐like inflammation only. Cartilage explant equilibrium mechanical properties were unaffected. Within the timeframe of this study, CSE alone does not cause OA but when combined with OA‐like inflammation leads to worsened articular cartilage degeneration as measured by chondrocyte viability, sGAG loss, proteoglycan staining, and ROS production. [ABSTRACT FROM AUTHOR]

Introduction: Although long-term macrolide antibiotics could reduce the recurrent exacerbation of chronic obstructive pulmonary disease (COPD), the side effect of bacterial resistance and the impact on the microbiota remain concerning. We investigated the influence of long-term erythromycin treatment on the airway and gut microbiota in mice with emphysema and patients with COPD. Methods: We conducted 16S rRNA gene sequencing to explore the effect of erythromycin treatment on the lung and gut microbiota in mice with emphysema. Liquid chromatography-mass spectrometry was used for lung metabolomics. A randomized controlled trial was performed to investigate the effect of 48-week erythromycin treatment on the airway and gut microbiota in COPD patients. Results: The mouse lung and gut microbiota were disrupted after cigarette smoke exposure. Erythromycin treatment depleted harmful bacteria and altered lung metabolism. Erythromycin treatment did not alter airway or gut microbial diversity in COPD patients. It reduced the abundance of pathogens, such as Burkholderia, in the airway of COPD patients and increased levels of symbiotic bacteria, such as Prevotella and Veillonella. The proportions of Blautia, Ruminococcus, and Lachnospiraceae in the gut were increased in COPD patients after erythromycin treatment. The time to the first exacerbation following treatment was significantly longer in the erythromycin treatment group than in the COPD group. Conclusion: Long-term erythromycin treatment reduces airway and gut microbe abundance in COPD patients but does not affect microbial diversity and restores microbiota balance in COPD patients by reducing the abundance of pathogenic bacteria. [ABSTRACT FROM AUTHOR]

There is a pressing need for novel pharmacological interventions and drug delivery innovations to attenuate the cigarette smoke-associated oxidative stress and lung disease. We report here on the attenuated total reflection–Fourier transform infrared spectroscopy (ATR-FTIR) and metabolomics of Wistar rats exposed to cigarette smoke for 28 days. The animals were treated for 15 days with plain cysteamine given orally or cysteamine as nanoemulsion given orally or via inhalation. The study design also included two control groups as follows: rats exposed to cigarette smoke but did not receive a treatment (diseased control group) and rats neither exposed to cigarette smoke nor a treatment (normal control group). The targeted metabolomics using Parallel Reaction Monitoring showed that in the diseased control group, ornithine, nicotinamide, xanthine, hypoxanthine, and caprolactam were increased compared with the normal control group. In addition, (±)8(9)-DiHET, which was initially downregulated in the diseased control group, exhibited a reversal of this trend with cysteamine nanoemulsion given via inhalation. The cysteamine nanoemulsion delivered by inhalation highlighted the importance of the route of drug administration for targeting the lungs. To the best of our knowledge, this is the first work to use ATR-FTIR and metabolomics in Wistar rat lung tissues, suggesting how cysteamine nanoemulsion can potentially reduce cigarette smoke-induced oxidative damage. The metabolites reported herein have potential implications for discovery of novel theranostics and, thus, to cultivate diagnostic and therapeutic innovation for early prevention and treatment of cigarette smoke-associated lung diseases. [ABSTRACT FROM AUTHOR]

Psoriasis is considered to be multifactorial, with both genetic and environmental factors contributing to its development. Polycyclic aromatic hydrocarbons (PAHs) are widespread in the environment, originating from sources such as cigarette smoke, exhaust emissions, grilled foods, smoked foods and urban air. Researchs have established a link between PAHs exposure and autoimmune disorders; however, specific effects of PAHs on psoriasis remain underexplored. This study aims to evaluate the correlation between PAHs exposure and susceptibility to psoriasis. We analysed eight monohydroxy PAHs (1‐Hydroxynaphthalene (1‐NAP), 2‐Hydroxynaphthalene (2‐NAP), 3‐Hydroxyfluorene (3‐FLU), 2‐Hydroxyfluorene (2‐FLU), 1‐Hydroxyphenanthrene (1‐PHE), 1‐Hydroxypyrene (1‐PYR), 2‐Hydroxyphenanthrene (2‐PHE) and 3‐Hydroxyphenanthrene (3‐PHE)) in 5996 participants from the National Health and Nutrition Examination Survey (NHANES). We employed multivariate logistic regression, trend analysis, weighted quantile sum (WQS) regression and restricted cubic spline (RCS) analysis to investigate the relationship between PAHs exposure and psoriasis risk. Multivariate logistic regression and trend analysis revealed that monohydroxy PAHs, including 2‐NAP, 3‐FLU, 2‐FLU and the mixture of 2‐PHE and 3‐PHE, are associated with an increased risk of psoriasis. Additionally, WQS regression showed a significant positive correlation between combined exposure to monohydroxy PAHs and psoriasis risk, with the mixture of 2‐PHE and 3‐PHE (47.3%) being the most influential factor. RCS regression further corroborated these findings. Specifically, 2‐FLU can increase the expression of psoriasis‐related inflammatory factors in HaCaT cells. In conclusion, PAHs exposure increases the risk of developing psoriasis. Efforts to reduce PAHs levels in the environment and minimise exposure are crucial for public health strategies aimed at preventing psoriasis. [ABSTRACT FROM AUTHOR]

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The interactions between immune cells and epithelial cells influence the progression of many respiratory diseases, such as chronic obstructive pulmonary disease (COPD). In vitro models allow for the examination of cells in controlled environments. However, these models lack the complex 3D architecture and vast multicellular interactions between the lung resident cells and infiltrating immune cells that can mediate cellular response to insults. In this study, three complementary microphysiological systems are presented to delineate the effects of cigarette smoke and respiratory disease on the lung epithelium. First, the Transwell system allows the co‐culture of pulmonary immune and epithelial cells to evaluate cellular and monolayer phenotypic changes in response to cigarette smoke exposure. Next, the human and mouse precision‐cut lung slices system provides a physiologically relevant model to study the effects of chronic insults like cigarette smoke with the dissection of specific interaction of immune cell subtypes within the structurally complex tissue environment. Finally, the lung‐on‐a‐chip model provides an adaptable system for live imaging of polarized epithelial tissues that mimic the in vivo environment of the airways. Using a combination of these models, a complementary approach is provided to better address the intricate mechanisms of lung disease. [ABSTRACT FROM AUTHOR]

Adequate lung epithelial repair relies on supportive interactions within the epithelial niche, including interactions with WNT-responsive fibroblasts. In fibroblasts from patients with chronic obstructive pulmonary disease (COPD) or upon in vitro cigarette smoke exposure, Wnt/ß-catenin signalling is distorted, which may affect interactions between epithelial cells and fibroblasts resulting in inadequate lung repair. We hypothesized that cigarette smoke (CS), the main risk factor for COPD, interferes with Wnt/ß-catenin signalling in fibroblasts through induction of cellular stress responses, including oxidative- and endoplasmic reticulum (ER) stress, and thereby alters epithelial repair support potential. Therefore, we assessed the effect of CS-exposure and the ER stress inducer Thapsigargin (Tg) on Wnt/ß-catenin signalling activation in MRC-5 fibroblasts, and on their ability to support lung epithelial organoid formation. Exposure of MRC-5 cells for 15 min with 5 AU/mL CS extract (CSE), and subsequent 6 h incubation induced oxidative stress (HMOX1). Whereas stimulation with 100 nM Tg increased markers of both the integrated stress response (ISR - GADD34/PPP1R15A, CHOP) and the unfolded protein response (UPR - XBP1spl, GADD34/PPP1R15A, CHOP and HSPA5/BIP), CSE only induced GADD34/PPP1R15A expression. Strikingly, although treatment of MRC-5 cells with the Wnt activator CHIR99021 upregulated the Wnt/ß-catenin target gene AXIN2, this response was diminished upon CSE or Tg pre-exposure, which was confirmed using a Wnt-reporter. Furthermore, pre-exposure of MRC-5 cells to CSE or Tg, restricted their ability to support organoid formation upon co-culture with murine pulmonary EpCam+ cells in Matrigel at day 14. This restriction was alleviated by pre-treatment with CHIR99021. We conclude that exposure of MRC-5 cells to CSE increases oxidative stress, GADD34/PPP1R15A expression and impairs their ability to support organoid formation. This inhibitory effect may be restored by activating the Wnt/ß-catenin signalling pathway. [ABSTRACT FROM AUTHOR]

Background: Bone healing is a complex process controlled by various mechanisms. It is known that cigarette smoking (CS) negatively affects bone healing by disrupting many of these mechanisms. In an effort to find ways to eliminate these negative effects caused by CS, studies have been conducted on various vitamins, antioxidants, and medications. Since high doses and repeated injections are required to increase the therapeutic effect of conventional drug applications, controlled drug delivery systems have been developed to avoid such problems. This study aimed to investigate the effects of resveratrol (RES), which has been made into a controlled drug delivery system, on bone healing in rats that were experimentally exposed to cigarette smoke to create a chronic smoking model. Methods: After establishing a chronic CS model by exposing the subjects to cigarette smoke of six cigarettes/day for four weeks, monocortical critical size defects of 3 mm (SD ± 0.02 mm) in diameter were created in the femur using a trephine bur. During the operation, the defects in RES groups were filled locally with a gel-formed solution of RES (50 µM) and Pluronic F-127 (14 µL). CS exposure was continued during the bone healing period after surgery. All groups were sacrificed one month after the operation, and femur samples were taken. Results: The obtained samples were examined by histomorphometric and immunohistochemical techniques; osteoblast count, new bone area, macroscopic filling score, vascularization, and proliferation were evaluated. Conclusion: The results of this study indicate that CS negatively affects bone healing and that local application of RES reduces this effect. [ABSTRACT FROM AUTHOR]

Background and Objectives: Formaldehyde induces oxidative stress and is carcinogenic, particularly squamous cell carcinoma of the nasopharyngeal area. Around us, in exhaust gases, cigarette smoke, and various industrial products, FA primarily affects the respiratory tract and other organs like the cornea, liver, kidneys, brain, and cardiovascular system. This study aims to determine if antioxidants can mitigate FA's harmful effects. Materials and Methods: Several databases, including PubMed, Science Direct, Springer, and Wiley, were systematically searched. Research publications on antioxidants mitigating FA-induced oxidative damage were included, but reviews and articles lacking complete texts were excluded. SYRCLE's risk of bias tool for animal studies has been used. Tables were used for data synthesis. Out of 8790 articles, 35 publications detailing tissue homogenate for biochemical analysis, standard hematoxylin–eosin staining, and immunohistochemistry markers for histopathological and immunohistochemical diagnosis were selected. Most studies were case–control studies, utilizing rat or mouse models. Additionally, one cohort study on industrial workers was analyzed. Conclusions: Antioxidants, including plant extracts, vitamins, and pigments, can prevent or heal FA-induced lesions. However, human studies, particularly biopsies, remain challenging, and animal trials are limited. Further research is needed to confirm FA's long-term effects and optimize antioxidant dosages. [ABSTRACT FROM AUTHOR]

Lung cancer remains the leading cause of cancer‐related deaths, with cigarette smoking being the most critical factor, linked to nearly 90% of lung cancer cases. NNK, a highly carcinogenic nitrosamine found in tobacco, is implicated in the lung cancer‐causing effects of cigarette smoke. Although NNK is known to mutate or activate certain oncogenes, its potential interaction with p27 in modulating these carcinogenic effects is currently unexplored. Recent studies have identified specific downregulation of p27 in human squamous cell carcinoma, in contrast to adenocarcinoma. Additionally, exposure to NNK significantly suppresses p27 expression in human bronchial epithelial cells. Subsequent studies indicates that the downregulation of p27 is pivotal in NNK‐induced cell transformation. Mechanistic investigations have shown that reduced p27 expression leads to increased level of ITCH, which facilitates the degradation of Jun B protein. This degradation in turn, augments miR‐494 expression and its direct regulation of JAK1 mRNA stability and protein expression, ultimately activating STAT3 and driving cell transformation. In summary, our findings reveal that: (1) the downregulation of p27 increases Jun B expression by upregulating Jun B E3 ligase ITCH, which then boosts miR‐494 transcription; (2) Elevated miR‐494 directly binds to 3′‐UTR of JAK1 mRNA, enhancing its stability and protein expression; and (3) The JAK1/STAT3 pathway is a downstream effector of p27, mediating the oncogenic effect of NNK in lung cancer. These findings provide significant insight into understanding the participation of mechanisms underlying p27 inhibition of NNK induced lung squamous cell carcinogenic effect. [ABSTRACT FROM AUTHOR]

Although the impact of smoking tobacco on human health is well understood, less is known about the effects of tobacco smoke on cotton, viscose and polyamide fabrics. In this study, tobacco smoke was applied to fabric samples to investigate the effects of tobacco smoke on their mechanical and colour properties. For this purpose, tobacco smoke was pumped into a mechanism consisting of a glass box, in which cotton, viscose and polyamide fabrics were placed in a suspended position. The fabric samples were treated with tobacco smoke for 1 or 2 months. The samples were evaluated in terms of tensile and tear strength, elongation at break, as well as pilling and abrasion resistance values. A colour measurement test was used to investigate the withering effect of tobacco smoke, and Fourier Transfer–Infrared analysis was performed to examine the chemical changes. The tensile strength values in the warp direction were 419.34, 404.62 and 421.78 N without treatment and after 1 and 2 months of tobacco smoke treatment, respectively, for the cotton woven fabric. Furthermore, for woven cotton fabric, the L* value decreased from 93.8 to 78.7 after being treated with tobacco smoke for 2 months. As a result of this study, it was determined that tobacco smoke has no effect on the tensile strength properties of fabrics, causes changes to pilling and abrasion resistance values, and adversely affects the colour properties of fabrics. [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to evaluate and compare the impact of cigarette smoking (CS) and heated tobacco (HT) on the alteration of color and ultrastructural characteristics of human enamel and cementum. Background: According to tobacco companies, a less harmful substitute for CS is HT products. Nevertheless, comprehensive research on the effects of HT on tooth structures has been lacking. This study aimed to evaluate and compare the impact of CS and HT on the alteration of color and ultrastructural characteristics of human enamel and cementum. Materials and Methods: Thirty intact and noncarious human maxillary premolars extracted for orthodontic treatment purposes, previously disinfected, were used in the study. The specimens were randomly separated into six groups (n = 10), as follows: Group 1: enamel without smoking exposure; Group 2: enamel exposed to CS; Group 3: enamel exposed to HT; Group 4: cementum without smoking exposure; Group 5: cementum exposed to CS; and Group 6: cementum exposed to HT. The measurement of color change was conducted using a spectrophotometer. The surface alterations and mineral composition of enamel and cementum were evaluated using scanning electron microscopy and energy‐dispersive X‐ray spectroscopy. ANOVA test followed by Tukey's post hoc test was used to determine significant differences between groups. Results: Results showed that CS had a more pronounced effect on enamel and cementum color changes than HT. The impact of CS and HT on color changes was more evident in cementum than in enamel. Surface morphology of enamel and cementum showed alterations in histology following exposure to both smoking types. Moreover, the mineral content experienced a significant reduction after using CS and HT. The reduction in calcium content after CS and HT exposure was similar. However, HT led to a significant decrease in the phosphorus content of enamel when compared with CS. At the same time, CS exposure in cementum resulted in a more significant reduction in Ca/P ratio than HT. Conclusions: Although HT may appear to present a lower danger to hard dental tissues than CS, it is not entirely harmless. CS results in more color changes on the enamel and cementum of teeth. Both smoking methods affected the mineral content of teeth, with CS having a significant effect on the roots, while HT significantly affected the crowns' mineral composition. Clinical Relevance: The study addresses a knowledge gap on how smoking and HT products affect hard tooth tissues. Few studies compared the histological and colorimetric effects of these two smoking strategies before this study. Our research shows that cigarette smoke and HT products affect dental enamel and cementum differently, revealing their potential tooth harm. The use of HT products may cause tooth cavities and periodontal disease. This research can help clinicians advise patients on the oral health effects of these smoking alternatives. This will help improve preventive and corrective dental procedures as HT products become more prevalent. [ABSTRACT FROM AUTHOR]

Abstract Transforming Growth Factor Beta1 (TGF-β1) signaling is upregulated in Chronic Obstructive Pulmonary disease (COPD), smokers, and people living with HIV. Cigarette smoking and HIV are also independent risk factors for COPD. Chronic inflammation is a hallmark of COPD. However, the underlying mechanisms remain unknown. Previous research has suggested that TGF-β1 alters the airway epithelial microRNAome and transcriptome, potentially contributing to lung inflammation. The Lactoperoxidase (LPO) system is an integral component of innate immunity within the airway. LPO plays a crucial role in host defense by catalyzing the oxidation of thiocyanate to hypothiocyanite in the presence of hydrogen peroxide (H2O2), generating a potent antibacterial and antiviral agent. Additionally, the LPO system potentially aids in maintaining cellular redox balance by reducing the levels of H2O2, thus mitigating oxidative stress within the airway epithelium. LPO dysfunction can impair immune responses and exacerbate inflammatory processes in respiratory diseases. In this study, primary bronchial epithelial cells and bronchial cell lines were treated with TGF-β1 and exposed to cigarette smoke to characterize the effect of these factors on LPO and their downstream effects. RT-qPCR and Western Blot were applied to quantify mRNA and proteins’ expression. The levels of H2O2 were detected using the Amplex Red Assay. Magnetofection and transfection were applied to probe the effect of miR-449b-5p. Staining procedures using the MitoTracker Green and C12FDG dyes were used to establish mitochondria mass and senescence. The levels of pro-inflammatory cytokines were measured via Luminex assays. We found that TGF-β1 and cigarette smoke suppressed airway LPO expression, increasing H2O2 levels. This increase in H2O2 had downstream effects on mitochondrial homeostasis, epithelial cellular senescence, and the pro-inflammatory cytokine response. We demonstrate for the first time that airway LPO is regulated by TGF-β1-induced miRNA-mediated post-transcriptional silencing through miR-449b-5p in the lungs. Further, we identify and validate miR-449-5p as the candidate miRNA upregulated by TGF-β1, which is involved in LPO suppression. This paper demonstrates a new mechanism by which TGF-β1 can lead to altered redox status in the airway.

Abstract 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.

Abstract Purpose Recently, the detrimental effect of cigarette smoking on muscle metabolism has attracted much attention, but the relationship between cigarette smoking and muscle mass is poorly understood. Thus, this study investigated the association between exposure to cigarette smoke, defined based on serum cotinine, and muscle mass in the US population. Methods We utilized National Health and Nutrition Examination Survey (NHANES) data between 2011 and 2018 for analysis. Data on serum cotinine, muscle mass (quantified by appendicular skeletal muscle mass index, ASMI), and covariates were extracted and analyzed. Weighted multivariate linear regression analyses and smooth curve fittings were performed to investigate the association between serum cotinine and ASMI. Subgroup analyses were stratified by gender, race and smoking status. When nonlinearity was detected, the threshold effects were analyzed using a two-piecewise linear regression model. Results In total, 8004 participants were included for analysis. The serum level of cotinine was negatively associated with ASMI in the fully adjusted model. Furthermore, comparing participants in the highest vs. the lowest tertile of serum cotinine, we found that ASMI decreased by 0.135 Kg/m2. In subgroup analysis stratified by gender and race, the association between serum cotinine and ASMI remained significant in all genders and races. In addition, the association remained significant among current and former smokers, but not among those who never smoked. Smooth curve fittings showed nonlinear relationships between serum cotinine and ASMI, with the inflection points identified at 356 ng/mL. Conclusions Our study revealed that serum cotinine was negatively related to muscle mass. This finding improves our understanding of the deleterious effects of cigarette smoking on muscle mass and highlights the importance of smoking cessation for muscle health.