Tobacco Induced Diseases最新文献

Introduction: Coronavirus disease (COVID-19) is a worldwide infection characterized by various symptoms. Few studies have examined its oral manifestations. However, there is insufficient information on the oral manifestations of patients with COVID-19 who use tobacco products. Therefore, this cross-sectional study investigated oral symptoms of tobacco-using patients with mild-to-moderate COVID-19.

Methods: This study used a convenience sample of non-hospitalized patients (aged ≥18 years) with mild-to-moderate COVID-19 diagnosed by polymerized chain reaction (PCR). This study excluded pregnant or lactating women or patients with serious COVID-19 complications, including those who required hospitalization or were on specific medications (antiviral, corticosteroid, antimicrobial, or immunosuppressive). Oral examinations were performed, including labial, buccal, and gingival mucosa, tongue, floor of the mouth, and palate, for any newly developed lesions associated with the onset of COVID-19. The salivary flow was determined using the passive drool collection technique.

Results: Lip dryness, gingivitis, tongue lesions, and taste loss were the most commonly reported oral symptoms in patients with mild-to-moderate COVID-19. The most common general symptoms were tiredness and headache (63.9%), followed by dry cough, myalgia, sore throat, and fever. This study found 139 occurrences of oral symptoms, of which 52 were dry lips (27 tobacco non-users, and 25 tobacco users), and 11 were gingivitis (five non-users, and six tobacco users), and 12 tongue changes (eight non-users, and four tobacco users). Ageusia, or loss of taste sensation, was most commonly reported with or without other oral COVID-19 symptoms (55 occurrences: 36 non-users and 19 tobacco users). No significant differences were found in oral symptoms between tobacco non-users and tobacco users.

Conclusions: There is a need to expand the routine examination protocol for patients during future respiratory pandemics, as monitoring oral health allows dentists to improve the management of oral sequelae during a pandemic.

Introduction: Although many countries, including Thailand, currently ban the sale of e-cigarettes, their use continues to rise, especially among young adults. Since the study of e-cigarette use among university students is limited, this study aimed to determine factors associated with e-cigarette use and explore university students' attitudes toward e-cigarettes, perceived risk, and opinion of e-cigarette policies.

Methods: This cross-sectional study was conducted among undergraduate students using convenience sampling in a university, in central Thailand from November 2022 to February 2023. A self-administered online questionnaire was distributed to 19 faculties representing health sciences, science and technology, social and arts faculties, and the International College.

Results: A total of 548 students completed the online questionnaire, and 20.4% reported ever using e-cigarettes, while 40% of e-cigarette users were unsure about the nicotine content. About 28% agreed, and 22% were unsure whether e-cigarettes could help quit smoking. Most students perceived that e-cigarettes are addictive and harmful, while about half of the participants agreed with the policy related to e-cigarettes in Thailand. Students with positive attitudes towards e-cigarettes were more likely to use e-cigarettes (AOR=1.15; 95% CI: 1.08-1.22), and those with lower perceived risk (AOR=0.89; 95% CI: 0.82-0.96) and who disagreed with e-cigarettes policy (AOR=0.93; 95% CI: 0.89-0.97) were more likely to use e-cigarettes. Personal income and having friends who use e-cigarettes were the significant predictors for e-cigarette use, while studying in the faculty of science and technology was a predictor of using e-cigarettes last month.

Conclusions: Although the perceived risk was high, about half of the students thought that e-cigarettes could help them quit smoking and were unsure or disagreed with e-cigarette banning policies. Attitude, perceived risk, policy opinions, personal income, and having friends who used e-cigarettes, were associated with e-cigarette use. Thus, correcting misunderstandings and increasing risk perceptions about e-cigarettes must be advocated among university students.

Introduction: China enacted an excise tax on e-cigarettes in November 2022, which offers a distinctive opportunity to examine the industry's reactions to this fiscal adjustment. This study delves into the industry's pricing strategies following the introduction of the excise tax, facilitating a thorough assessment of the subsequent impact on market dynamics and the government's revenue streams.

Methods: We developed a TaXSiM model specifically tailored for e-cigarettes in China by integrating the country's e-cigarette tax framework. Our approach involved leveraging market data obtained from a representative product, the RELX Phantom Series, to ensure the model's effectiveness and relevance.

Results: The excise implementation of 2022 significantly heightened the tax burden on e-cigarettes, marking an increase of approximately 150 RMB per device and 19 RMB per cartridge. Despite these financial pressures, electronic cigarette firms exemplified by RELX, strategically endeavored to sustain competitiveness. Their approach involved initially implementing a 'Razor blade model' and eventually a 'comprehensive under-shifting' strategy, which mitigated the health impact of the tax hike, resulting in a relatively minor decline in sales while amplifying the impact on tax revenue. However, this strategic pricing maneuver came at a cost, as it led to a substantial decrease in profits, and therefore expedited a reshuffling of the industry by compelling smaller brands to leave the market rapidly.

Conclusions: To effectively curb the use of e-cigarettes through tax policies, it is advisable to relocate the imposition of excise taxes on electronic cigarettes to the retail stage. This shift aims to narrow the scope for industry-level pricing strategies. Furthermore, this approach should be coupled with the introduction of an additional specific tax, strategically crafted to accentuate the health-related benefits associated with the excise taxation on electronic cigarettes.

Introduction: Cigarette smoking is one of the most important causes of COPD and could induce the apoptosis of pulmonary microvascular endothelial cells (PMVECs). The conditional knockout of LRG1 from endothelial cells reduced emphysema in mice. However, the mechanism of the deletion of LRG1 from endothelial cells rescued by cigarette smoke (CS) induced emphysema remains unclear. This research aimed to demonstrate whether LRG1 promotes the apoptosis of PMVECs through KLK10 in COPD.

Methods: Nineteen patients were divided into three groups: control non-COPD (n=7), smoker non-COPD (n=7), and COPD (n=5). The emphysema mouse model defined as the CS exposure group was induced by CS exposure plus cigarette smoke extract (CSE) intraperitoneal injection for 28 days. Primary PMVECs were isolated from the mouse by magnetic bead sorting method via CD31-Dynabeads. Apoptosis was detected by western blot and flow cytometry.

Results: LRG1 was increased in lung tissue of COPD patients and CS exposure mice, and CSE-induced PMVECs apoptosis model. KLK10 was over-expressed in lung tissue of COPD patients and CS exposure mice, and CSE-induced PMVECs apoptosis model. LRG1 promoted apoptosis in PMVECs. LRG1 knockdown reversed CSE-induced apoptosis in PMVECs. The mRNA and protein expression of KLK10 were increased after over-expressed LRG1 in PMVECs isolated from mice. Similarly, both the mRNA and protein levels of KLK10 were decreased after LRG1 knockdown in PMVECs. The result of co-immunoprecipitation revealed a protein-protein interaction between LRG1 and KLK10 in PMVECs. KLK10 promoted apoptosis via the down-regulation of Bcl-2/Bax in PMVECs. KLK10 knockdown could reverse CSE-induced apoptosis in PMVECs.

Conclusions: LRG1 promotes apoptosis via up-regulation of KLK10 in PMVECs isolated from mice. KLK10 promotes apoptosis via the down-regulation of Bcl-2/Bax in PMVECs. There was a direct protein-protein interaction between LRG1 and KLK10 in PMVECs. Our novel findings provide insights into the understanding of LRG1/KLK10 function as a potential molecule in COPD.

Introduction: Tobacco smoke is a major health risk factor for smokers but also for non-smokers due to passive smoking. These risks come from conventional cigarette smoke but also from aerosol produced by electronic cigarettes and heated tobacco products (HTPs). The aim of this study was to investigate population knowledge about the adverse effects of passive smoking from traditional cigarettes, electronic cigarettes, and HTPs.

Methods: Between February and October 2023, 504 subjects among the general population responded to a questionnaire with 8 questions in Italian, via a link to the Google Forms platform. The questions related to the oral health effects of active and passive smoking. Descriptive analyses of all variables in the questionnaire were performed, and statistical analyses between variables were carried out using the chi-squared test and Fisher's exact test.

Results: A large subset of individuals interviewed stated that active smoking is harmful to health and consider active smoking more damaging compared with passive smoking (86.3%). The majority believed that passive smoking of cigarettes is more harmful to oral health than passive smoking of HTPs (79.4%) or electronic cigarettes (e-cigarettes) (84.9%).

Conclusions: Results suggest that most people in this study had good knowledge about the adverse effects of active or passive smoking on health; however, knowledge regarding e-cigarettes and HTPs was poor and confused. These results reveal the complexity of perceptions regarding different types of smoking and the need for further research to fully understand the risks associated with each type of passive smoking.

Introduction: We aim to assess the association between smoking behavior and intracranial aneurysms (IAs) and the effect of smoking cessation medications on IAs at the genetic level.

Methods: Causal effects of four phenotypes: 1) age at initiation of regular smoking, 2) cigarettes smoked per day, 3) smoking cessation, and 4) smoking initiation on IAs, were analyzed using two-sample inverse-variance weighted Mendelian randomization analyses. The effects of genes interacting with the smoking cessation medications were analyzed using cis-expression quantitative trait loci genetic instruments on IAs using summary statistics-based Mendelian randomization analyses. Colocalization analyses were then used to test whether the genes shared causal variants with IAs. The role of confounding phenotypes as potential causative mechanisms of IAs at these gene loci was tested.

Results: Cigarettes smoked per day (OR=2.89; 95% CI:1.85-4.51) and smoking initiation on IAs (OR=4.64; 95% CI: 2.64-8.15) were significantly associated with IA risk. However, age at initiation of regular smoking (OR=0.54; 95% CI: 0.10-2.8) and smoking cessation (OR=6.80; 95% CI: 0.01-4812) had no overall effect on IAs. Of 88 genes that interacted with smoking cessation medications, two had a causal effect on IA risk. Genetic variants affecting HYKK levels showed strong evidence of colocalization with IA risk. Higher HYKK levels in the blood were associated with a lower IA risk. Gene target analyses revealed that cigarettes/day could be a main mediator of HYKK's effect on IA risk.

Conclusions: This study provides evidence supporting that smoking initiation on IAs and cigarettes/day may increase IA risk. Increased HYKK gene expression may reduce IA risk. This can be explained by the increased number of cigarettes consumed daily. HYKK could also reduce IA risk due to the positive effect of continuous abstinence and varenicline therapy on smoking cessation.

Introduction: This study aimed to investigate the effects of nicotine on the activation of pancreatic stellate cells (PSCs) and pancreatic fibrosis in chronic pancreatitis (CP), along with its underlying molecular mechanisms.

Methods: This was an in vivo and in vitro study. In vitro, PSCs were cultured to study the effects of nicotine on their activation and oxidative stress. Transcriptome sequencing was performed to identify potential signaling pathways involved in nicotine action. And the impact of nicotine on mitochondrial Ca²⁺ levels and Ca²⁺ transport-related proteins in PSCs was analyzed. The changes in nicotine effects were observed after the knockdown of the mitochondrial calcium uniporter (MCU) in PSCs. In vivo experiments were conducted using a mouse model of CP to assess the effects of nicotine on pancreatic fibrosis and oxidative stress in mice. The alterations in nicotine effects were observed after treatment with the MCU inhibitor Ru360.

Results: In vitro experiments demonstrated that nicotine promoted PSCs activation, characterized by increased cell proliferation, elevated α-SMA and collagen expression. Nicotine also increased the production of reactive oxygen species (ROS) and cellular malondialdehyde (MDA), exacerbating oxidative stress damage. Transcriptome sequencing revealed that nicotine may exert its effects through the calcium signaling pathway, and it was verified that nicotine elevated mitochondrial Ca2+ levels and upregulated MCU expression. Knockdown of MCU reversed the effects of nicotine on mitochondrial calcium homeostasis, improved mitochondrial oxidative stress damage and structural dysfunction, thereby alleviating the activation of PSCs. In vivo validation experiments showed that nicotine significantly aggravated pancreatic fibrosis in CP mice, promoted PSCs activation, exacerbated pancreatic tissue oxidative stress, and increased MCU expression. However, treatment with Ru360 significantly mitigated these effects.

Conclusions: This study confirms that nicotine upregulates the expression of MCU, leading to mitochondrial calcium overload and exacerbating oxidative stress in PSCs, and ultimately promoting PSCs activation and exacerbating pancreatic fibrosis in CP.

Introduction: Despite the existence of numerous studies highlighting the adverse effects of smoking on kidney function, the investigation of the correlation between serum cotinine and chronic kidney disease (CKD) remains inconclusive due to insufficient evidence. Consequently, the primary objective of this study was to ascertain the association between serum cotinine levels and CKD.

Methods: This study analyzed data from 10900 Americans participating in the National Health and Nutrition Examination Survey between 2005 and 2016. The independent variable under investigation was log serum cotinine, while the dependent variable was the presence of CKD. To investigate the potential linear and non-linear correlations between serum cotinine and CKD, logistic regression models and generalized additive models (GAM) were employed. Furthermore, stratified analyses and interaction tests were conducted to evaluate potential disparities in the relationship between serum cotinine and CKD, based on sex.

Results: The median age in the study participants was 49.28 ± 17.96 years, and the median log serum cotinine (ng/mL) was -0.54 ± 1.68. The prevalence of CKD was found to be 17.04%. Multifactorial regression analysis did not show a statistically significant association between log serum cotinine and CKD (OR=1.02; 95% CI: 0.98-1.06, p=0.4387). A statistically significant non-linear association between log serum cotinine and CKD was also not observed in the GAM analysis (p non-linear value=0.091). Subgroup analyses revealed sex differences in the association between log serum cotinine and CKD. Briefly, males had a positive association between log serum cotinine and incident CKD (OR=1.08; 95% CI: 1.02-1.15, p=0.0049). In females, there was a U-shaped association between log serum cotinine and CKD, with an optimal inflection point for log serum cotinine of -0.30 (serum cotinine=0.5 ng/mL).

Conclusions: Cross-sectional analyses of NHANES data showed gender differences in the association between serum cotinine and the development of CKD.