Oral microbiome dysbiosis among cigarette smokers and smokeless tobacco users compared to non-users.

Tobacco use significantly influences the oral microbiome. However, less is known about how different tobacco products specifically impact the oral microbiome over time. To address this knowledge gap, we characterized the oral microbiome of cigarette users, smokeless tobacco users, and non-users over 4 months (four time points). Buccal swab and saliva samples (n = 611) were collected from 85 participants. DNA was extracted from all samples and sequencing was carried out on an Illumina MiSeq, targeting the V3-V4 region of the 16S rRNA gene. Cigarette and smokeless tobacco users had more diverse oral bacterial communities, including a higher relative abundance of Firmicutes and a lower relative abundance of Proteobacteria, when compared to non-users. Non-users had a higher relative abundance of Actinomyces, Granulicatella, Haemophilus, Neisseria, Oribacterium, Prevotella, Pseudomonas, Rothia, and Veillonella in buccal swab samples, compared to tobacco users. While the most abundant bacterial genera were relatively constant over time, some species demonstrated significant shifts in relative abundance between the first and last time points. In addition, some opportunistic pathogens were detected among tobacco users including Neisseria subflava, Bulleidia moorei and Porphyromonas endodontalis. Overall, our results provide a more holistic understanding of the structure of oral bacterial communities in tobacco users compared to non-users.

FBXL19 Targeted STK11 Degradation Enhances Cigarette Smoke-Induced Airway Epithelial Cell Cytotoxicity.

Objective: To investigate the effects of cigarette smoke (CS) on Serine/Threonine Kinase 11 (STK11) and to determine STK11's role in CS-induced airway epithelial cell cytotoxicity.Methods: STK11 expression levels in the lung tissues of smokers with or without COPD and mice exposed to CS or room air (RA) were determined by immunoblotting and RT-PCR. BEAS-2Bs-human bronchial airway epithelial cells were exposed to CS extract (CSE), and the changes in STK11 expression levels were determined by immunoblotting and RT-PCR. BEAS-2B cells were transfected with STK11-specific siRNA or STK11 expression plasmid, and the effects of CSE on airway epithelial cell cytotoxicity were measured. To determine the specific STK11 degradation-proteolytic pathway, BEAS-2Bs were treated with cycloheximide alone or combined with MG132 or leupeptin. Finally, to identify the F-box protein mediating the STK11 degradation, a screening assay was performed using transfection with a panel of FBXL E3 ligase subunits.Results: STK11 protein levels were significantly decreased in the lung tissues of smokers with COPD relative to smokers without COPD. STK11 protein levels were also significantly decreased in mouse lung tissues exposed to CS compared to RA. Exposure to CSE shortened the STK11 mRNA and protein half-life to 4 h in BEAS-2B cells. STK11 protein overexpression attenuated the CSE-induced cytotoxicity; in contrast, its knockdown augmented CSE-induced cytotoxicity. FBXL19 mediates CSE-induced STK11 protein degradation via the ubiquitin-proteasome pathway in cultured BEAS-2B cells. FBXL19 overexpression led to accelerated STK11 ubiquitination and degradation in a dose-dependent manner.Conclusions: Our results suggest that CSE enhances the degradation of STK11 protein in airway epithelial cells via the FBXL19-mediated ubiquitin-proteasomal pathway, leading to augmented cell death.HIGHLIGHTSLung tissues of COPD-smokers exhibited a decreased STK11 RNA and protein expression.STK11 overexpression attenuates CS-induced airway epithelial cell cytotoxicity.STK11 depletion augments CS-induced airway epithelial cell cytotoxicity.CS diminishes STK11 via FBXL19-mediated ubiquitin-proteasome degradation.

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.

Cigarette Smoking Among Pregnant Women During the Perinatal Period: Prevalence and Health Care Provider Inquiries - Pregnancy Risk Assessment Monitoring System, United States, 2021.

Cigarette smoking during pregnancy increases the risk for pregnancy complications and adverse infant outcomes such as preterm delivery, restricted fetal growth, and infant death. Health care provider counseling can support smoking cessation. Data from the 2021 Pregnancy Risk Assessment Monitoring System were analyzed to estimate the prevalence of smoking before, during, and after pregnancy; quitting smoking during pregnancy; and whether health care providers asked about cigarette smoking before, during, and after pregnancy among women with a recent live birth. In 2021, the prevalence of cigarette smoking was 12.1% before pregnancy, 5.4% during pregnancy, and 7.2% during the postpartum period; 56.1% of women who smoked before pregnancy quit smoking while pregnant. Jurisdiction-specific prevalences of smoking ranged from 3.5% to 20.2% before pregnancy, 0.4% to 11.0% during pregnancy, and 1.0% to 15.1% during the postpartum period. Among women with a health care visit during the associated period, the percentage of women who reported that a health care provider asked about smoking was 73.7% at any health care visit before pregnancy, 93.7% at any prenatal care visit, and 57.3% at a postpartum checkup. Routine assessment of smoking behaviors among pregnant and postpartum women can guide the development and implementation of evidence-based tobacco control measures at the jurisdiction and health care-system level to reduce smoking among pregnant and postpartum women.

GPS2 ameliorates cigarette smoking-induced pulmonary vascular remodeling by modulating the ras-Raf-ERK axis.

BACKGROUND: Mitogen-activated protein kinase (MAPK)signaling-mediated smoking-associated pulmonary vascular remodeling (PVR) plays an important role in the pathogenesis of group 3 pulmonary hypertension (PH). And G protein pathway suppressor 2 (GPS2) could suppress G-protein signaling such as Ras and MAPK, but its role in cigarette smoking -induced PVR (CS-PVR) is unclear. METHODS: An in vivo model of smoke-exposed rats was constructed to assess the role of GPS2 in smoking-induced PH and PVR. In vitro, the effects of GPS2 overexpression and silencing on the function of human pulmonary arterial smooth cells (HPASMCs) and the underlying mechanisms were explored. RESULTS: GPS2 expression was downregulated in rat pulmonary arteries (PAs) and HPASMCs after CS exposure. More importantly, CS-exposed rats with GPS2 overexpression had lower right ventricular systolic pressure (RVSP), right ventricular hypertrophy index (RVHI), and wall thickness (WT%) than those without. And enhanced proliferation and migration of HPASMCs induced by cigarette smoking extract (CSE) can be evidently inhibited by overexpressed GPS2. Besides, GPS2siRNA significantly enhanced the proliferation, and migration of HPASMCs as well as activated Ras and Raf/ERK signaling, while these effects were inhibited by zoledronic acid (ZOL). In addition, GPS2 promoter methylation level in rat PAs and HPASMCs was increased after CS exposure, and 5-aza-2-deoxycytidine (5-aza) inhibited CSE-induced GPS2 hypermethylation and downregulation in vitro. CONCLUSIONS: GPS2 overexpression could improve the CS-PVR, suggesting that GPS2 might serve as a novel therapeutic target for PH-COPD in the future.

Tobacco policies and changes in the tendency of smoking cessation in cigarette users in Chile: a longitudinal cross-sectional study.

OBJECTIVE: To assess the impact of tobacco control regulations and policy implementation on smoking cessation tendencies in cigarette users born between 1982 and 1991 in Chile. DESIGN: Longitudinal cross-sectional study. SETTING: National level. PARTICIPANTS: Data from the National Survey of Drug Consumption (Service of Prevention and Rehabilitation for Drug and Alcohol Consumption). A pseudo-cohort of smokers born between 1982 and 1991 (N=17 905) was tracked from 2002 to 2016. PRIMARY AND SECONDARY OUTCOMES MEASURES: Primary outcome was the tendency to cease smoking conceptualised as the report of using cigarettes 1 month or more ago relative to using cigarettes in the last 30 days. The main exposure variable was the Tobacco Policy Index-tracking tobacco policy changes over time. Logistic regression, controlling for various factors, was applied. RESULTS: Models suggested a 14% increase in the smoking cessation tendency of individuals using cigarettes 1 month or more ago relative to those using cigarettes in the last 30 days (OR 1.14, CI 95% CI 1.10 to 1.19) for each point increment in the Tobacco Policy index. CONCLUSIONS: Our study contributes to documenting a positive impact of the implementation of interventions considered in the MPOWER strategy in the progression of smoking cessation tendencies in smokers born between 1982 and 1991 in Chile.

Examining the Effect of Genes on Depression as Mediated by Smoking and Modified by Sex.

Depression is heritable, differs by sex, and has environmental risk factors such as cigarette smoking. However, the effect of single nucleotide polymorphisms (SNPs) on depression through cigarette smoking and the role of sex is unclear. In order to examine the association of SNPs with depression and smoking in the UK Biobank with replication in the COPDGene study, we used counterfactual-based mediation analysis to test the indirect or mediated effect of SNPs on broad depression through the log of pack-years of cigarette smoking, adjusting for age, sex, current smoking status, and genetic ancestry (via principal components). In secondary analyses, we adjusted for age, sex, current smoking status, genetic ancestry (via principal components), income, education, and living status (urban vs. rural). In addition, we examined sex-stratified mediation models and sex-moderated mediation models. For both analyses, we adjusted for age, current smoking status, and genetic ancestry (via principal components). In the UK Biobank, rs6424532 [LOC105378800] had a statistically significant indirect effect on broad depression through the log of pack-years of cigarette smoking (p = 4.0 × 10-4) among all participants and a marginally significant indirect effect among females (p = 0.02) and males (p = 4.0 × 10-3). Moreover, rs10501696 [GRM5] had a marginally significant indirect effect on broad depression through the log of pack-years of cigarette smoking (p = 0.01) among all participants and a significant indirect effect among females (p = 2.2 × 10-3). In the secondary analyses, the sex-moderated indirect effect was marginally significant for rs10501696 [GRM5] on broad depression through the log of pack-years of cigarette smoking (p = 0.01). In the COPDGene study, the effect of an SNP (rs10501696) in GRM5 on depressive symptoms and medication was mediated by log of pack-years (p = 0.02); however, no SNPs had a sex-moderated mediated effect on depressive symptoms. In the UK Biobank, we found SNPs in two genes [LOC105378800, GRM5] with an indirect effect on broad depression through the log of pack-years of cigarette smoking. In addition, the indirect effect for GRM5 on broad depression through smoking may be moderated by sex. These results suggest that genetic regions associated with broad depression may be mediated by cigarette smoking and this relationship may be moderated by sex.

A miRNA-21-Mediated PTEN/Akt/NF-κB Axis Promotes Chronic Obstructive Pulmonary Disease Pathogenesis.

Background: This study sought to explore the underlying mechanism of miR-21 mediated apoptosis and inflammation in chronic obstructive pulmonary disease (COPD) induced by cigarette smoke (CS). Methods: We detected levels and PTEN/Akt/NF-κB axis protein levels in peripheral lung tissues of COPD patients and CS-exposed mice and HBE cells. Western blotting assay was used to determine the expression of cleaved caspase-3. IL-6 and IL-8 protein was detected in cell supernatant from cells by ELISA. HBE cells were transfected with a miR-21 inhibitor, and co-culture with A549. Results: Increased miR-21 expression, reduced PTEN expression and following activation of Akt in in peripheral lung tissues of COPD patients and CS-exposed mice and HBE cells. Inhibition of miR-21 showed enhanced PTEN levels and reduced the expression of phosphorylated form of Akt and NF-κB. Decreased expression of cleaved caspase-3, IL-6 and IL-8 in A549 cells co cultured with HBE cells transfected with miR-21 inhibitor compared with transfected with miR-21 control inhibitor. Conclusion: MiR-21 contributes to COPD pathogenesis by modulating apoptosis and inflammation through the PTEN/Akt/NF-κB pathway. Targeting miR-21 may increase PTEN expression and inhibit Akt/NF-κB pathway, offering potential diagnostic and therapeutic value in COPD management.

Use of Menthol Cigarettes and Accessories Among Youth Who Smoked After the Menthol Cigarette Ban in England and Canada, 2021: Implications for Health Equity.

INTRODUCTION: This study examined menthol cigarette use among youth who smoked, after menthol cigarette bans were implemented in England (May 2020) and Canada (October 2017). AIMS AND METHODS: Cross-sectional data come from 2021 ITC Youth Tobacco and Vaping Survey respondents aged 16-19 who smoked in the past 30 d in England (N = 715) and Canada (N = 419). Adjusted logistic regression models, estimated separately for each country, examined sociodemographic correlates of usually smoking menthol cigarettes (reporting currently most often smoking menthol cigarettes) overall, and by past 30-d use of any menthol accessories (e.g., filters, capsules). Youth reported the cigarette variety they smoked most often, coded as menthol or nonmenthol. RESULTS: Almost no youth who smoked in the past 30 d reported most often smoking a cigarette variety coded as menthol. However, 34.5% (95% CI: 30.4% to 38.9%) of youth who smoke in England and 30.9% (26.0%-36.3%) in Canada reported usually smoking menthol cigarettes, with greater odds of use among those identifying as black, or other race/ethnicity, respectively, compared to white in England (60.0%, aOR = 3.08, p = .001; 47.4%, aOR = 2.27, p = .011) and Canada (43.6%, aOR = 2.44, p = .046; 51.2%, aOR = 2.92, p = .001). Among those who reported usually smoking menthol cigarettes in England (N = 223) and Canada (N = 108), 71.7% (64.0%-78.2%) and 51.5% (41.1%-61.7%) reported using menthol accessories. CONCLUSIONS: After menthol cigarette bans in England and Canada, approximately one-third of youth who smoked reported usually smoking menthol cigarettes, with disproportionately higher use among those identifying as black and other race/ethnicity. Menthol accessories accounted for most menthol cigarette use. Closing regulatory loopholes is critical to advancing public health equity. IMPLICATIONS: Use of menthol cigarette accessories (eg, filters, cards, capsules) among youth who smoked was prevalent after implementation of menthol cigarette bans in England and Canada, and there was disproportionately higher use among those who identified as black and any other race/ethnicity. Efforts are therefore required to close regulatory loopholes of menthol cigarette bans. Findings further support countries, such as the United States, proposing menthol cigarette bans which extend coverage to accessories. More comprehensive menthol bans that also restrict accessories are likely to be more effective in reducing flavored tobacco use among young people and in advancing health equity.

Smoking-Attributable Health Care Expenditures for US Adults With Chronic Lower Respiratory Disease.

Importance: Cigarette smoking is a primary risk factor for chronic lower respiratory disease (CLRD) and is associated with worse symptoms among people with CLRD. It is important to evaluate the economic outcomes of smoking in this population. Objective: To estimate smoking prevalence and cigarette smoking-attributable health care expenditures (SAHEs) for adults with CLRD in the US. Design, Setting, and Participants: This cross-sectional study used data from the 2014-2018 and 2020 National Health Interview Surveys (NHIS) and the 2020 Medical Expenditure Panel Survey. The final study population, stratified by age 35 to 64 years and 65 years or older, was extracted from the 2014-2018 NHIS data. The data analysis was performed between February 1 and March 31, 2024. Exposures: Cigarette smoking, as classified into 4 categories: current smokers, former smokers who quit less than 15 years ago, former smokers who quit 15 or more years ago, and never smokers. Main Outcomes and Measures: Smoking-attributable health care expenditures were assessed using a prevalence-based annual cost approach. Econometric models for the association between cigarette smoking and health care utilization were estimated for 4 types of health care services: inpatient care, emergency department visits, physician visits, and home health visits. Results: In the 2014-2018 NHIS study sample of 13 017 adults, 7400 (weighted 62.4%) were aged 35 to 64 years, 5617 (weighted 37.6%) were 65 years or older, and 8239 (weighted 61.9%) were female. In 2020, among 11 211 222 adults aged 35 to 64 with CLRD, 3 508 504 (31.3%) were current smokers and 3 496 790 (31.2%) were former smokers. Total SAHEs in 2020 for this age group were $13.6 billion, averaging $2752 per current smoker and $1083 per former smoker. In 2020, 7 561 909 adults aged 65 years or older had CLRD, with 1 451 033 (19.2%) being current smokers and 4 104 904 (54.3%) being former smokers. Total SAHEs in 2020 for the older age group were $5.3 billion, averaging $1704 per current smoker and $682 per former smoker. In sum, SAHEs for adults with CLRD aged 35 years or older amounted to $18.9 billion in 2020. Conclusions and Relevance: In this cross-sectional study of adults with CLRD, cigarette smoking was associated with a substantial health care burden. The higher per-person SAHEs for current smokers compared with former smokers suggest potential cost savings of developing targeted smoking cessation interventions for this population.

Association between loneliness and cigarette smoking attitudes among university students in Iran: a cross-sectional study.

OBJECTIVES: During the last two decades, cigarette smoking witnessed a global increase in use, especially among youth. Loneliness is one of the possible psychosocial determinants of smoking. This study examined the association between loneliness and attitudes towards cigarette smoking among university students of Iran. DESIGN: Cross-sectional study. SETTING AND PARTICIPANTS: This study was conducted among 538 university students, who were recruited using the cluster random sampling method. Loneliness and smoking attitudes of the samples were assessed using the revised version of the University of California Los Angeles Loneliness Scale and the Scale of Cigarette Smoking Attitude (CSA). Descriptive statistics, Pearson's correlation coefficient and multivariable regression analysis were used to analyse the data. RESULTS: From a total of 538 participants, 301 (59.9%) students were young women. The mean age of the students was 22.2±2.9 years. Only 56 (10.4%) of the students were married and 370 (87.9%) of them were lived with their families. 131 (24.3%) students experienced cigarette smoking. In terms of university-related characteristics, 205 (38.1%) of the students studied in the faculty of medicine. Also, 30% of the students had a positive or indifferent attitude towards smoking, while 26.4% of the students reported feeling lonely. The mean scores for loneliness and CSA were 41.42±11.29 and 48.64±11.2, respectively. Statistically, a significant positive correlation was found between loneliness and CSA (r=0.289; p<0.001). After controlling for potential confounders by regression analysis, loneliness scores were also positively associated with CSA scores (B: 0.14; 95% CI 0.097 to 0.18). CONCLUSIONS: According to the positive association between loneliness and students' CSA, paying more attention to the state of loneliness in college students, examining situations and reasons that increase it and identifying the interventions that might reduce it are necessary. Reducing loneliness among college students can correct their attitudes towards smoking.

The interaction between diet quality and cigarette smoking on the incidence of hypertension, stroke, cardiovascular diseases, and all-cause mortality.

This study aimed to examine the interaction between diet quality indices (DQIs) and smoking on the incidence of hypertension (HTN), stroke, cardiovascular diseases, and all-cause mortality. We prospectively followed 5720 participants and collected dietary data via a validated food frequency questionnaire to calculate DQI-international (DQI-I) and DQI-revised (DQI-R). Considering an interaction analysis, we classified participants based on diet quality (median: higher/lower) and smoking status. Over 9 years of follow-up, higher diet quality scores were associated with a lower risk of stroke and mortality. While current smokers had a higher risk of stroke and mortality but had a lower risk of developing HTN. Compared to the current smokers with lower diet quality, nonsmokers with higher diet quality according to the DQI-I [HR 0.24; 95% CI (0.08, 0.66)], and DQI-R [HR 0.20; 95% CI (0.07, 0.57)] had a lower risk of stroke. Moreover, the lower risk of mortality was more evident in nonsmokers with higher DQI-I [HR 0.40; 95% CI (0.22-0.75)] and DQI-R scores [HR 0.34; 95% CI (0.18-0.63)] compared to nonsmokers with lower diet quality. While higher DQI-I and DQI-R scores were associated with a lower risk of stroke and mortality, this beneficial effect may be negated by smoking.

Association between lipid profiles and cigarette smoke among adults in the Persian cohort (Shahedieh) study.

OBJECTIVES: Exposure to cigarette smoke introduces a large amount of nicotine into the bloodstream through the lungs. So, smoking can be a risk factor for many diseases. The present study was conducted to investigate the effect of active and passive cigarette smoke on the blood lipid profile and dyslipidemia. METHODS: This cross-sectional study was performed on 5052 individuals who participated in the recruitment phase of the Shahedieh cohort study. A logistic regression model was used to investigate the relationship between smoking exposure status and lipid profiles. RESULTS: The prevalence of abnormal low-density lipoprotein-cholesterol (LDL-C), abnormal HDL-C, abnormal total cholesterol (TC), abnormal triglyceride (TG), and dyslipidemia were 254 (5.00%), 562 (11.10%), 470 (9.30%), 1008 (20.00%), and 1527 (30.20%), respectively. Adjusting for confounders, it was observed that current smokers had higher odds of having abnormal HDL-C [OR (95% CI), 2.90 (2.28-3.69)], abnormal TG [OR (95% CI), 1.71 (1.38-2.13)] and dyslipidemia [OR (95% CI), 1.86 (1.53-2.25)]. Ex-smokers also had greater odds of abnormal HDL-C [OR (95% CI), 1.51 (1.06-2.16)] compared to non-smokers who were not exposed to cigarette smoke. CONCLUSIONS: The findings indicated that current smokers had higher TG and lower HDL. So, necessary measures should be taken to reduce smoking. The findings also showed that the prevalence of abnormal TG and HDL in ex-smokers was lower than in current smokers. Therefore, the existence of incentive policies to quit smoking seems necessary.

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.

An approach to identify gene-environment interactions and reveal new biological insight in complex traits.

There is a long-standing debate about the magnitude of the contribution of gene-environment interactions to phenotypic variations of complex traits owing to the low statistical power and few reported interactions to date. To address this issue, the Gene-Lifestyle Interactions Working Group within the Cohorts for Heart and Aging Research in Genetic Epidemiology Consortium has been spearheading efforts to investigate G × E in large and diverse samples through meta-analysis. Here, we present a powerful new approach to screen for interactions across the genome, an approach that shares substantial similarity to the Mendelian randomization framework. We identify and confirm 5 loci (6 independent signals) interacted with either cigarette smoking or alcohol consumption for serum lipids, and empirically demonstrate that interaction and mediation are the major contributors to genetic effect size heterogeneity across populations. The estimated lower bound of the interaction and environmentally mediated heritability is significant (P < 0.02) for low-density lipoprotein cholesterol and triglycerides in Cross-Population data. Our study improves the understanding of the genetic architecture and environmental contributions to complex traits.

Relationship between psychoactive substance, alcohol and cigarette use in nursing students. A cross-sectional study.

BACKGROUND: The increase in the use of psychoactive substances, alcohol and cigarettes in young people has become a public health problem. The identification of factors that increase or reduce the risk of exposure to these substances and the possible relationship between them is essential for planning strategies with a risk approach; hence the reason for this study. The objective was to establish the profile of use of psychoactive substances, alcohol and cigarettes and the factors associated with such use in nursing students of a higher education institution. METHODS: Quantitative, observational, analytical cross-sectional study. RESULTS: We included 310 students from 1 st to 9th semester of a Nursing programme from a private higher education institution in Bogotá. The prevalence of psychoactive substance use in the last year was 2.96% (95%CI, 1.36-5.54), with marijuana being the substance most used (55.55%). The prevalence of alcohol and cigarette use during the last 12 months was estimated at 86.64% (95%CI, 83.24-91.0) and 12.16% (95%CI, 8.43-15.88) respectively. A statistically significant association was found between the use of these substances: alcohol use was associated with cigarette use (OR = 3.22; P = 0.006) and smoking was associated with psychoactive substance use (OR = 15.4; P < 0.001). CONCLUSIONS: Alcohol use increases the likelihood of smoking cigarettes, and this in turn increases the likelihood of psychoactive substance use, in this university population.

Our perception may not be reality: A longitudinal study of the relationship between perceived and actual change in smoking behavior.

INTRODUCTION: Results of the impact of lockdowns and stay-at-home orders during the COVID-19 pandemic on changes in cigarette smoking are mixed. Previous studies examining smoking changes during the early stages of the pandemic in 2020 have mainly focused on smoker's perception of changes in cigarette consumption. Such measure has not been widely used in other contexts, and therefore we aim to compare the discrepancy between smokers' perceived changes in cigarette smoking and the actual change in the number of cigarettes smoked, using repeated measurements. METHODS: We included 134 smokers from the French TEMPO cohort with repeated measurements of their perceived changes in smoking habits during the first phase of the COVID-19 pandemic and the number of cigarettes smoked repeatedly from March to May 2020. We used generalized estimation equations (GEE) to examine the association between changes in the number of cigarettes smoked and the odds of mismatched answers. RESULTS: The results suggest that at each study wave, 27-45% of participants provided mismatching answers between their perceived change in smoking habits and the actual change in the number of cigarettes smoked daily, measured repeatedly. Results from GEE analysis demonstrated that a mismatching assessment of smoking behavior was elevated among those who had an increase (OR = 2.52 [1.37;4.65]) or a decrease (OR = 5.73 [3.27;10.03]) in number of cigarettes smoked. DISCUSSION: Our findings highlight the possibility of obtaining different results depending on how changes in tobacco smoking are measured. This highlights the risk of underestimating the actual changes in cigarette smoking during the COVID-19 pandemic, but also more generally when validating public health interventions or smoking cessation programs. Therefore, objective measures such as the actual consumption of psychoactive substances should be utilized, preferably on a longitudinal basis, to mitigate recall bias.

Cigarette smoking and cardiovascular disease incidence and all-cause mortality: the modifying role of diet quality.

BACKGROUND: This study examines the potential long-term joint association between smoking and diet quality as modifiable risk factors concerning cardiovascular diseases (CVDs) incidence and all-cause mortality among current and former smokers. METHODS: The study followed 955 smokers from the third and fourth examinations of the Tehran Lipid and Glucose Study to March 2018. Dietary data was collected using a food frequency questionnaire. Three diet quality indices (DQIs) were computed at baseline: DQI-international (DQI-I), DQI-revised (DQI-R), and Mediterranean-DQI (Med-DQI). Cox proportional hazards regression models were used to determine the HR (95% CI) of the joint association between smoking and diet quality among heavy and light smokers, based on the number of cigarettes per day and pack-years, as well as between current and former smokers based on smoking habits. RESULTS: Over a follow-up period of almost eight years, 94 cases of CVDs (9.80%) and 40 cases of mortality (4.20%) were documented. The lower diet quality based on the Med-DQI was associated with a higher risk of mortality among current smokers (HR:3.45; 95%CI:1.12, 10.57). Light smokers with good diet quality, compared to heavy smokers with poor diet quality, had a lower risk of CVDs incident (HR:0.35; 95%CI: 0.15, 0.83) and all-cause mortality (HR:0.20; 95%CI:0.05, 0.77). Current smokers with good DQI had a lower risk of mortality compared to current smokers with poor DQI (HR:0.26; 95%CI:0.08, 0.80). However, this lower risk was more significant in former smokers with good DQI (HR:0.10; 95%CI:0.02, 0.45). CONCLUSIONS: Light and former smokers had a lower risk of developing CVDs and experiencing mortality. However, when coupled with a high-quality diet, this protective effect is even more pronounced.