The prospective relationship between a-priori intentions for and patterns of e-cigarette use among adults who smoke cigarettes.

BACKGROUND: Electronic (e-)cigarettes may help adult cigarette smokers achieve cigarette cessation, depending on patterns of e-cigarette use. Among cigarette smokers who do not use e-cigarettes, it is unclear if and how a-priori intentions for use are related to uptake patterns. Longitudinal studies have focused on established e-cigarette users or adolescent and young adult populations exclusively. METHODS: Within a nationwide randomized clinical trial (N = 638), adult cigarette smokers not currently using e-cigarettes were randomized (2:1) to receive (or not) one-month sampling of e-cigarettes. An exploratory factor analysis (EFA) was performed on an established 15-item measure assessing a-priori intentions for e-cigarette use to identify latent variables. Among those receiving e-cigarette products, regression models examined relationships between intentions and: 1) uptake (yes/no), 2) frequency (number of days per week), and 3) amount (puffing episodes per day) of e-cigarette use at one-month follow-up. RESULTS: Two factors emerged from the EFA: 1) cigarette-related intentions (e.g., cigarette cessation, no smell) and 2) novel appeal of e-cigarettes (e.g., flavors). Three items remained and were treated as separate intentions: "feels like cigarette smoking", "curiosity", and "affordability". In the final multivariable models, "feel like cigarette smoking" predicted more frequent e-cigarette use (ß = 0.187, SE = 0.086, p = 0.03); however, none of the five factors/intentions were significantly associated with uptake or amount of use. CONCLUSIONS: For adult cigarette smokers not currently using e-cigarettes, a-priori intentions for using e-cigarettes might not be predictive of if or how these products will be used in the future, suggesting that motives may not drive use behavior.

A Mendelian randomization study on the causal effects of cigarette smoking on liver fibrosis and cirrhosis.

Background: Liver fibrosis significantly impacts public health globally. Untreated liver fibrosis eventually results in cirrhosis. Cigarette smoking is the main etiologic factor for various diseases. However, the causal effects of cigarette smoking on liver fibrosis and cirrhosis have yet to be fully elucidated. Methods: In this study, Mendelian randomization (MR) analysis was performed to assess the association between cigarette smoking, liver fibrosis, and cirrhosis. Single-nucleotide polymorphisms (SNPs) were selected as instrumental variables from a genome-wide association study (GWAS) of European ancestry. Patients were divided into six exposure categories as follows: "ever smoked," "pack years of smoking," "age of smoking initiation," "smoking status: never," "smoking status: current," and "smoking status: previous." The outcomes of this study included liver fibrosis and cirrhosis. MR-Egger, weighted median, inverse variance weighted, simple mode, and weighted mode were selected as the analysis methods. Cochran's Q and the MR-PRESSO tests were conducted to measure heterogeneity. The MR-Egger method was performed to evaluate horizontal pleiotropy, while the "leave-one-out" analysis was performed for sensitivity testing. Results: The results of this study showed that having a smoking history increases the risk of liver fibrosis and cirrhosis ["ever smoked": odds ratio (OR) = 5.704, 95% CI: 1.166-27.910, p = 0.032; "smoking status: previous": OR = 99.783, 95% CI: 2.969-3.353e+03, p = 0.010]. A negative correlation was observed between patients who never smoked and liver fibrosis and cirrhosis ("smoking status: never": OR = 0.171, 95% CI: 0.041-0.719, p = 0.016). However, there were no significant associations between "smoking status: current," "pack years of smoking," and "age of smoking initiation" and liver fibrosis and cirrhosis. Cigarette smoking did not have a significant horizontal pleiotropic effect on liver fibrosis and cirrhosis. The "Leave-one-out" sensitivity analysis indicated that the results were stable. Conclusion: The study confirmed the causal effects of cigarette smoking on liver fibrosis and cirrhosis.

The effect of cigarette smoking on the oral microbiota in a South African population using subgingival plaque samples.

Disturbances in the oral microbiota may be due to several mechanisms and factors, such as smoking. An imbalance in oral bacteria may result in changes to the innate immune system and the development of periodontal disease. This study aimed to investigate the distribution of oral microbiota in smokers and non-smokers in a South African population using subgingival plaque samples. From the 128 recruited participants, 57 were identified as smokers (serum cotinine: >15 ng/ml). Analysis of 16S rRNA gene sequencing demonstrated significant differences between the two groups with a reduced abundance of Actinobacteria in smokers. Fusobacterium and Campylobacter were found in higher abundance, while a lower abundance of Leptotrichia, Actinomyces, Corynebacterium, and Lautropia were observed. This study highlighted significant differences in the oral microbiota of smokers, indicating an abundance of anaerobic gram-negative bacteria. These findings suggest that smoking allows certain oral microorganisms to gain dominance, thereby predisposing individuals to periodontal disease development and progression.

E-cigarette Use and Severe Coronavirus Disease 2019 (COVID-19) Outcomes: A Meta-Analysis.

E-cigarettes have been known to cause varied poor health outcomes prior to coronavirus disease 2019 (COVID-19), but after the impact of COVID-19, evidence came out that was, in some instances, not as expected regarding the severity of COVID-19 among e-cigarette users (vapers). A meta-analysis was performed on the available evidence to comprehensively find the effect of COVID-19 on existing or past e-cigarette users (vapers). The Meta-analysis of Observational Studies in Epidemiology (MOOSE) guidelines were used to perform this meta-analysis. PubMed was searched for observational studies that described outcomes after COVID-19 positivity from December 1, 2019, to December 2023. Medical Subject Headings (MeSH) keywords were used for searching the relevant studies highlighting the relationship between COVID-19 and e-cigarette users. Calculations for pooled prevalence, 95% confidence interval (95% CI), weights for current e-cigarette users and vapers, and outcomes (events) were made. To analyze the data, Review Manager V.5.4 was used. The I² statistic was used to assess statistical heterogeneity. The I² statistic of >50% was considered significant heterogeneity. The "leave-one-out" method was used for sensitivity analysis. Out of 3231 studies, four studies reported data on vaping and non-vaping status and composite outcomes, resulting in a sample size of 653 COVID-19-positive cases. The pooled prevalence of being COVID-19 positive, having symptoms, or visiting an emergency room was 7.78% (653/8392). COVID-19 patients with current vaping status had decreased odds of poor outcomes compared to non-smokers, with a pooled odds ratio (OR) of 0.09 (95% CI 0.00-2.42; p>0.05) with heterogeneity between studies (I²=99%, p=0.15). Because of difficulties related to data collection and other factors, this meta-analysis was unable to conclusively establish the correlation between e-cigarette usage and severe COVID-19 outcomes such as hospitalization, admission to the intensive care unit, and fatality. Additional research using more detailed data is necessary to fully understand this correlation.

Determination of pulmonary vessel alteration in Chinese male smokers by quantitative computed tomography measurements: a retrospective study.

Background: The blood volume of intraparenchymal vessels is reported to be increased in smokers. However, the blood volume can be affected by many confounders besides tobacco exposure. This study aimed to investigate the association between cigarette smoking and pulmonary blood volume after adjusting the related factors in a large cohort of Chinese males. Methods: In this retrospective study, male participants admitted to the First Affiliated Hospital of Xi'an Jiaotong University for annual health assessment between February 2017 and February 2018 were enrolled. All subjects underwent non-contrast chest computed tomography (CT) scans, and 152 subjects underwent a review CT scan 2-3 years later. A three-dimensional approach was employed to segment the lung and intrapulmonary vessels and quantitative CT (QCT) measurements, including lung volume (LV), intrapulmonary vessel volume (IPVV), low-attenuation area <-950 Hounsfield unit (LAA-950 and LAA-950%), and mean lung density (MLD). Linear regression was used to estimate the association between IPVV and the smoking index (SI). A paired t-test was used to compare the QCT parameters between the initial and follow-up CT scans. Results: A total of 656 male participants were enrolled and classified into three subgroups: non-smokers (n=311), current smokers (n=267), and former smokers (n=78). The IPVV of current smokers (134.62±23.96 vs. 120.76±25.52 mL) and former smokers (130.79±25.13 vs. 120.76±25.52 mL) were significantly larger than that of non-smokers (P<0.05). A higher SI was associated with greater IPVV [non-standardized coefficient: 0.167, 95% confidence interval (CI): 0.086-0.248]. For current smokers, the IPVV of the follow-up scan significantly increased compared to its baseline scan (135.49±28.60 vs. 129.73±29.75 mL, t=-2.326, P=0.02), but for the non-smokers and former smokers, the IPVV of the follow-up scan did not increase or decrease compared to the baseline scan (P>0.05). Conclusions: Pulmonary vascular volumes detectable on non-contrast CT are associated with cigarette exposure, and smoking cessation may prevent pulmonary vasculature remodeling.

Using single-cell RNA sequencing and bulk RNA sequencing data to reveal a correlation between smoking and neutrophil activation in esophageal carcinoma patients.

BACKGROUND: Cigarette smoking is considered as a major risk factor for esophageal carcinoma (ESCA) patients. Neutrophil activation plays a key role in cancer development and progression. However, the relationship between cigarette smoking and neutrophils in ESCA patients remained unclear. METHODS: Single-cell RNA sequencing (scRNA-seq) and bulk RNA sequencing data were obtained from public databases. Uniform manifold approximation and projection (UMAP) was used to perform downscaling and clustering based on scRNA-seq data. The module genes associated with smoking in ESCA patients were filtered by weighted gene co-expression network analysis (WGCNA). Using the "AUCell" package, the enrichment of different cell subpopulations and gene collections were assessed. "CellChat" and "CellphoneDB" were used to infer the probability and significance of ligand-receptor interactions between different cell subpopulations. RESULTS: WGCNA was performed to screened module genes associated with smoking in ESCA patients from MEdarkquosie, MEturquoise, and MEgreenyellow. Next, eight cell clusters were identified, and using the AUCell score, we determined that neutrophil clusters were more active in the gene modules associated with smoking in ESCA patients. Two neutrophil subtypes, Neutrophils 1 and Neutrophils 2, exhibited greater enrichment in inflammatory response regulation, intercellular adhesion, and regulation of T cell activation. Furthermore, we found that neutrophils may pass through AMPT-(ITGA5 + ITGB1) and ICAM1-AREG in order to promote the development of ESCA, and that the expression levels of the receptor genes insulin-degrading enzyme and ITGB1 were significantly and positively correlated with cigarette smoking per day. CONCLUSION: Combining smoking-related gene modules and scRNA-seq, the current findings revealed the heterogeneity of neutrophils in ESCA and a tumor-promoting role of neutrophils in the tumor microenvironment of smoking ESCA patients.

Association of cigarette smoking with changes in macroeconomic conditions.

This study uses data from the 1987-2022 Behavioral Risk Factor Surveillance System and state-level employment rates from the US Bureau of Labor Statistics to estimate the association between macroeconomic conditions and cigarette smoking. Our finding suggests a positive association, which constantly declined with time after the 2001 recession. We find that a one percentage point increase in the employment rate is associated with a 1.4% higher likelihood of smoking cigarettes in the overall sample but declined to 0.4% among cohorts surveyed from 2011 to 2022. We also find strong positive and heterogeneous associations among sociodemographic groups, except among Blacks and persons aged 65 years and older, among whom there is no association; however, the positive associations consistently decreased among these sociodemographic groups. Consequently, the strong positive association disappeared in several sociodemographic groups in cohorts surveyed over the last decade.

Tobacco Quitline utilization compared with cigarette smoking prevalence in Virginia across rurality and Appalachian Status, 2011-2019.

Introduction: While cigarette smoking rates have declined, rural and Appalachian populations in the United States have not seen similar decreases. Quitline programs are promising strategies in reducing disparities in these areas, but research on their usage is limited. Methods: We employed Small Area Estimation on the Virginia Behavioral Risk Factor Surveillance System (2011-2019) to estimate county-level smoking prevalence and utilized The Quit Now Virginia Quitline data (2011-2019) to estimate Quitline users. We analyzed differences in Quitline utilization by rurality and Appalachian status using statistical t-tests. Stepwise regression assessed the absolute estimate of county features, including poverty rate, tobacco retailer density, physician availability, coal mining industry, and tobacco agriculture, on Quitline usage. Results: While the average smoking rate overall was 15.3 %, only 7.4 % of smokers accessed Quitline services from 2011 to 2019. Appalachian regions exhibited higher smoking rates (20.9 %) and lower quitline usage (4.8 %) compared to non-Appalachian areas (14 % smoking prevalence, 8 % quitline usage). Rural regions had higher smoking prevalence (19.0 %) than urban areas (12.9 %), but no significant difference in Quitline utilization (7.6 % vs. 7.2 %, p = 0.7). Stepwise regression revealed counties with more tobacco agriculture had 3.2 % (p = 0.04) lower Quitline utilization. Also, more physicians availability in the county was associated with 3.9 % higher Quitline usage (p = 0.03) and Appalachian counties exhibited a 3.6 % lower Quitline usage rate compared to non-Appalachian counties. Conclusion: A significant gap exists between cigarette smoking prevalence and Quitline utilization, particularly in underserved rural and Appalachian areas, despite no clear barriers to accessing this remote cessation resource. Implication: The study underscores persistent disparities in smoking rates, with rural and Appalachian regions in the United States facing higher smoking prevalence and limited utilization of Quitline services. Despite no clear barriers to access, the gap between smoking prevalence and Quitline usage remains significant, particularly in underserved areas. Tailoring interventions to address regional disparities and factors like tobacco agriculture and physician availability is essential to reduce smoking rates and improve Quitline utilization in these communities.

Unhealthy Weight Control Behaviors according to the Status of Combustible Cigarette and Noncombustible Nicotine or Tobacco Product Use among Korean Adolescents with Experience Attempting to Reduce or Maintain Their Body Weight: The 15th Korea Youth Risk Behavior Survey, 2019.

Background: Noncombustible nicotine or tobacco product (NNTP) use, and cigarette smoking are associated with a high likelihood of unhealthy weight control behaviors (UWCBs) among adolescents. However, no study has addressed the differences in UWCBs among non-users, single users of combustible cigarettes (CCs) or NNTPs and dual users. This study compared the frequencies of weight control behaviors according to the status of CC and NNTP use among Korean adolescents. Methods: This was a cross-sectional study of 25,094 adolescents who had attempted to reduce or maintain their body weight during the past 30 days, using data from the 15th Korea Youth Risk Behavior Survey, 2019. Data on the status of CC and NNTP use, weight status, and weight control behaviors were obtained using self-report questionnaires. Subjects were categorized into four groups: non-users, cigarette-only users, NNTP-only users, and dual users. Results: Among boys and girls, current smokers and NNTP users were 8.9%±0.3% and 5.5%±0.3%, and 4.2%±0.2% and 1.7%±0.1%, respectively. Among boys, NNTP-only users were more likely to engage in extreme weight control behaviors than non-users. Among girls, users of either CCs or NNTPs were more likely to engage in extreme weight control behaviors and less extreme weight control behaviors than non-users. Conclusion: This study shows that users of either CCs or NNTPs are more likely to engage in UWCBs, and NNTP-only users are the most likely to do so.

Roles of glutamic pyruvate transaminase 2 in reprogramming of airway epithelial lipidomic and metabolomic profiles after smoking.

Metabolic abnormalities represent one of the pathological features of chronic obstructive pulmonary disease (COPD). Glutamic pyruvate transaminase 2 (GPT2) is involved in glutamate metabolism and lipid synthesis pathways, whilst the exact roles of GPT2 in the occurrence and development of COPD remains uncertain. This study aims at investigating how GPT2 and the associated genes modulate smoking-induced airway epithelial metabolism and damage by reprogramming lipid synthesis. The circulating or human airway epithelial metabolomic and lipidomic profiles of COPD patients or cell-lines explored with smoking were assessed to elucidate the pivotal roles of GPT2 in reprogramming processes. We found that GPT2 regulate the reprogramming of lipid metabolisms caused by smoking, especially phosphatidylcholine (PC) and triacylglycerol (TAG), along with changes in the expression of lipid metabolism-associated genes. GPT2 modulated cell sensitivities and survival in response to smoking by enhancing mitochondrial functions and maintaining lipid and energy homeostasis. Our findings provide evidence for the involvement of GPT2 in the reprogramming of airway epithelial lipids following smoking, as well as the molecular mechanisms underlying GPT2-mediated regulation, which may offer an alternative of therapeutic strategies for chronic lung diseases.

A Narrative Review on the Impact of Smoking on Female Fertility.

Understanding the significant impact of preventable factors, such as lifestyle decisions and bad habits like smoking, on female fertility has received a lot of attention. Pervasive smoking among fertile women is a serious public health concern. Smoking has well-documented negative impacts on general health, but it also has significant consequences on fertility. Many women of reproductive age still smoke, despite a wealth of data elucidating the effects of pregnancy and the health of the fetus as a result of prenatal exposure. This review attempts to investigate the consequences of smoking on female fertility, specifically focusing on how it affects the ovaries, oviducts, and uterus through a thorough examination of numerous studies. Important topics such as ovarian reserve, steroidogenesis, ovulation, controlling the menstrual cycle, oviductal function, uterine receptivity, and implantation will receive extra focus.

An intercontinental comparison of the influence of smoking on the occurrence of nonsyndromic cleft lip and palate: a meta-analysis and systematic review.

BACKGROUND: The influence of smoking on nonsyndromic clefts has been a topic of research for many years. However, few studies have investigated the effect of smoking on causing clefts in different gene pools. METHODS: A meta-analysis was conducted of case-control studies related to smoking. Keywords such as "clefts," "cleft lip," "cleft palate," "orofacial cleft," and "smoking" were used to search the MEDLINE, Embase, and Cochrane databases. RESULTS: In total, 51 articles were reviewed. The RevMan software was utilized for the analysis, and the Mantel-Haenszel method was employed to pool the odds ratios (ORs) and 95% confidence intervals. Although the overall OR, a measure of the association between exposure and outcome, was higher for smokers than for non-smokers, this association was significantly stronger in individuals from Asia and South America (1.73), and lowest in Europe (1.31). Among active and passive smokers in Asia, the OR was approximately 0.93, indicating an equivalent impact from both types of smoking. CONCLUSION: This analysis indirectly suggests that restriction measures targeting both active and passive smoking are crucial in Asia.

Anti-atherogenic role of green tea (Camellia sinensis) in South Indian smokers.

ETHNOPHARMACOLOGICAL RELEVANCE: Green tea (Camellia sinensis) is a popular beverage consumed all over the world due to its health benefits. Many of these beneficial effects of green tea are attributed to polyphenols, particularly catechins. AIM OF THE STUDY: The present study focuses on underlying anti-platelet aggregation, anti-thrombotic, and anti-lipidemic molecular mechanisms of green tea in South Indian smokers. MATERIALS AND METHODS: We selected 120 South Indian male volunteers for this study to collect the blood and categorised them into four groups; control group individuals (Controls), smokers, healthy control individuals consuming green tea, and smokers consuming green tea. Smokers group subjects have been smoking an average 16-18 cigarettes per day for the last 7 years or more. The subjects (green tea consumed groups) consumed 100 mL of green tea each time, thrice a day for a one-year period. RESULTS: LC-MS analysis revealed the presence of multiple phytocompounds along with catechins in green tea extract. Increased plasma lipid peroxidation (LPO), protein carbonyls, cholesterol, triglycerides, and LDL-cholesterol with decreased HDL-cholesterol levels were observed in smokers compared to the control group and the consumption of green tea showed beneficial effect. Furthermore, docking studies revealed that natural compounds of green tea had high binding capacity with 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA) when compared to their positive controls, whereas (-) epigallocatechin-3-gallate (EGCG) and (-) epicatechin-gallate (ECG) had high binding capacity with sterol regulatory element-binding transcription factor 1 (SREBP1c). Further, our ex vivo studies showed that green tea extract (GTE) significantly inhibited platelet aggregation and increased thrombolytic activity in a dose dependent manner. CONCLUSION: In conclusion, in smokers, catechins synergistically lowered oxidative stress, platelet aggregation and modified the aberrant lipid profile. Furthermore, molecular docking studies supported green tea catechins' antihyperlipidemic efficacy through strong inhibitory activity on HMG-CoA reductase and SREBP1c. The mitigating effects of green tea on cardiovascular disease risk factors in smokers that have been reported can be attributed majorly to catechins or to their synergistic effects.

A genome-wide meta-analysis of palmoplantar pustulosis implicates Th2 responses and cigarette smoking in disease pathogenesis.

BACKGROUND: Palmoplantar pustulosis (PPP) is an inflammatory skin disorder that mostly affects smokers and manifests with painful pustular eruptions on the palms and soles. While the disease can present with concurrent plaque psoriasis, TNF and IL-17/IL-23 inhibitors show limited efficacy. There is therefore a pressing need to uncover PPP disease drivers and therapeutic targets. OBJECTIVES: To identify genetic determinants of PPP and investigate whether cigarette smoking contributes to disease pathogenesis. METHODS: We performed a genome-wide association meta-analysis of three North-European cohorts (n=1,456 PPP cases and 402,050 controls). We then used the scGWAS program to investigate the cell-type specificity of the association signals. We also undertook genetic correlation analyses to examine the similarities between PPP and other immune-mediated diseases. Finally, we applied Mendelian randomization to analyze the causal relationship between cigarette smoking and PPP. RESULTS: We found that PPP is not associated with the main genetic determinants of plaque psoriasis. Conversely, we identified genome-wide significant associations with the FCGR3A/FCGR3B and CCHCR1 loci. We also observed 13 suggestive (P<5X10-6) susceptibility regions, including the IL4/IL13 interval. Accordingly, we demonstrated a significant genetic correlation between PPP and Th2-mediated diseases like atopic dermatitis and ulcerative colitis. We also found that genes mapping to PPP-associated intervals were preferentially expressed in dendritic cells and often implicated in T-cell activation pathways. Finally, we undertook a Mendelian randomization analysis, which supported a causal role of cigarette smoking in PPP. CONCLUSIONS: The first genome-wide association study of PPP points to a pathogenic role for deregulated Th2 responses and cigarette smoking.

Assessment of pulmonary physiological changes caused by aging, cigarette smoking, and COPD with hyperpolarized 129Xe magnetic resonance.

OBJECTIVE: To comprehensively assess the impact of aging, cigarette smoking, and chronic obstructive pulmonary disease (COPD) on pulmonary physiology using 129Xe MR. METHODS: A total of 90 subjects were categorized into four groups, including healthy young (HY, n = 20), age-matched control (AMC, n = 20), asymptomatic smokers (AS, n = 28), and COPD patients (n = 22). 129Xe MR was utilized to obtain pulmonary physiological parameters, including ventilation defect percent (VDP), alveolar sleeve depth (h), apparent diffusion coefficient (ADC), total septal wall thickness (d), and ratio of xenon signal from red blood cells and interstitial tissue/plasma (RBC/TP). RESULTS: Significant differences were found in the measured VDP (p = 0.035), h (p = 0.003), and RBC/TP (p = 0.003) between the HY and AMC groups. Compared with the AMC group, higher VDP (p = 0.020) and d (p = 0.048) were found in the AS group; higher VDP (p < 0.001), d (p < 0.001) and ADC (p < 0.001), and lower h (p < 0.001) and RBC/TP (p < 0.001) were found in the COPD group. Moreover, significant differences were also found in the measured VDP (p < 0.001), h (p < 0.001), ADC (p < 0.001), d (p = 0.008), and RBC/TP (p = 0.032) between the AS and COPD groups. CONCLUSION: Our findings indicate that pulmonary structure and functional changes caused by aging, cigarette smoking, and COPD are various, and show a progressive deterioration with the accumulation of these risk factors, including cigarette smoking and COPD. CLINICAL RELEVANCE STATEMENT: Pathophysiological changes can be difficult to comprehensively understand due to limitations in common techniques and multifactorial etiologies. 129Xe MRI can demonstrate structural and functional changes caused by several common factors and can be used to better understand patients' underlying pathology. KEY POINTS: Standard techniques for assessing pathophysiological lung function changes, spirometry, and chest CT come with limitations. 129Xe MR demonstrated progressive deterioration with accumulation of the investigated risk factors, without these limitations. 129Xe MR can assess lung changes related to these risk factors to stage and evaluate the etiology of the disease.

Smoking-Related Interstitial Lung Disease: Historical Perspective and Advances in the Twenty-first Century.

In the twenty- first century, there is widespread agreement that in addition to lung cancer, emphysema, and chronic bronchitis, cigarette smoking causes accumulation of pigmented macrophages, interstitial fibrosis, and Langerhans cell proliferation in various permutations. These histologic changes remain subclinical in some patients and produce clinical manifestations and imaging abnormalities in others. Debate surrounds terminology of these lesions, which are often grouped together under the umbrella of "smoking-related interstitial lung disease." This review summarizes modern concepts in our understanding of these abnormalities and explains how the recognition of smoking-related interstitial fibrosis has advanced the field.

A systematic review and meta-analysis of the association between e-cigarette use among non-tobacco users and initiating smoking of combustible cigarettes.

INTRODUCTION: The rapid increase in e-cigarette use over the past decade has triggered an important public health question on the potential association between e-cigarette use and combustible cigarette smoking. Following AMSTAR 2 and PRISMA guidelines, this evidence synthesis sought to identify and characterize any associations between e-cigarette use among individuals not smoking cigarettes and initiation of cigarette smoking. METHODS: The protocol was registered on September 24, 2018 (PROSPERO 2018 CRD42018108540). Three databases were queried from January 01, 2007 to April 26, 2023. Search results were screened using the PICOS review method. RESULTS: Among 55 included studies (40 "good" and 15 "fair"; evidence grade: "high") that adjusted for gender, age, and race/ethnicity between groups, generally, there was a significant association between non-regular e-cigarette use and initiation of cigarette smoking, further supported by the meta-analytic results (AOR 3.71; 95% CI 2.86-4.81). However, smoking initiation was most often measured as ever/current cigarette smoking. Two studies (quality: 2 "good") evaluated progression to regular cigarette smoking among individuals with regular use of e-cigarettes, and generally found no significant associations. One study ("good") evaluated smoking initiation among individuals with regular use of e-cigarettes, finding an increasing probability of ever smoking cigarettes with increased e-cigarette use. Twelve studies (10 "good" and two "fair") examining progression to regular smoking among individuals with non-regular use of e-cigarettes reported inconsistent findings. CONCLUSIONS: Numerous methodological flaws in the body of literature limit the generalizability of these results to all individuals who are not smoking cigarettes with few studies measuring established/regular use/smoking of e-cigarettes and cigarettes. Further, studies did not control adequately for specific confounding variables representing common liabilities between e-cigarette use and cigarette smoking, nor did they account for sufficient follow-up durations. Collectively, these flaws limit the generalizability of findings to the question of an association between e-cigarette use and cigarette smoking initiation.

Long COVID among US adults from a population-based study: Association with vaccination, cigarette smoking, and the modifying effect of chronic obstructive pulmonary disease (COPD).

OBJECTIVE: Post-COVID Conditions (or Long COVID) have been widely reported, but population-based studies exploring the relationship between its risk factors are lacking. We examined the associations between Long COVID, chronic obstructive pulmonary disease [COPD], vaccination status, and cigarette smoking. We also tested for the modifying effect of COPD status. METHODS: Data from the 2022 US nationwide Behavioral Risk Factor Surveillance System (BRFSS) were analyzed. Our primary outcome was Long COVID (Yes/No) after a positive COVID-19 diagnosis. Predictor variables were COPD, coronary heart disease (CHD), diabetes, asthma, body mass index, cigarette smoking status, and number of COVID-19 vaccinations (0-4). Weighted multivariable logistic regression models were used and adjusted for sociodemographic factors. Regression models were used to explore the modifying effects of COPD status. RESULTS: The weighted prevalence of Long COVID among survivors (N = 121,379) was 21.8% (95%CI: 21.4, 22.3), with tiredness/fatigue (26.2% [95%:25.1, 27.2]) as the most common symptom. Respondents with COPD (aOR: 1.71 [95%CI: 1.45, 2.02]), current daily smokers (aOR: 1.23 [95%CI:1.01, 1.49]), and former smokers (aOR: 1.24 [95%CI:1.12, 1.38]) (vs. never established smokers) had higher odds of Long COVID. However, respondents who had received three (aOR: 0.75 [95%CI:0.65, 0.85]) and four (aOR: 0.71 [95%CI:0.58, 0.86]) vaccine doses (vs. no vaccine) had lower odds of Long COVID. COPD had a modifying effect on the relationship between cigarette smoking and Long COVID (p-value: 0.013). CONCLUSION: Our findings underscore a complex interaction between COPD, cigarette smoking, and Long COVID. Further, COVID-19 vaccination may be protective against Long COVID.

Cigarette smoke impairs the hematopoietic supportive property of mesenchymal stem cells via the production of reactive oxygen species and NLRP3 activation.

BACKGROUND: Mesenchymal stem cells (MSCs) play important roles in tissue homeostasis by providing a supportive microenvironmental niche for the hematopoietic system. Cigarette smoking induces systemic abnormalities, including an impeded recovery process after hematopoietic stem cell transplantation. However, the role of cigarette smoking-mediated alterations in MSC niche function have not been investigated. METHODS: In the present study, we investigated whether exposure to cigarette smoking extract (CSE) disrupts the hematopoietic niche function of MSCs, and pathways impacted. To investigate the effects on bone marrow (BM)-derived MSCs and support of hematopoietic stem and progenitor cells (HSPCs), mice were repeatedly infused with the CSE named 3R4F, and hematopoietic stem and progenitor cells (HSPCs) supporting function was determined. The impact of 3R4F on MSCs at cellular level were screened by bulk-RNA sequencing and subsequently validated through qRT-PCR. Specific inhibitors were treated to verify the ROS or NLRP3-specific effects, and the cells were then transplanted into the animal model or subjected to coculture with HSPCs. RESULTS: Both direct ex vivo and systemic in vivo MSC exposure to 3R4F resulted in impaired engraftment in a humanized mouse model. Furthermore, transcriptomic profile analysis showed significantly upregulated signaling pathways related to reactive oxygen species (ROS), inflammation, and aging in 3R4F-treated MSCs. Notably, ingenuity pathway analysis revealed the activation of NLRP3 inflammasome signaling pathway in 3R4F-treated MSCs, and pretreatment with the NLRP3 inhibitor MCC950 rescued the HSPC-supporting ability of 3R4F-treated MSCs. CONCLUSION: In conclusion, these findings indicate that exposure to CSE reduces HSPCs supportive function of MSCs by inducing robust ROS production and subsequent NLRP3 activation.