Search Results (2,077)

Cigarette smoke is a major inducer of oxidative stress, promoting reactive oxygen species (ROS) accumulation and contributing to the pathogenesis of chronic obstructive pulmonary disease (COPD) and lung cancer. Heated tobacco products (HTP) and e-cigarettes are promoted as reduced-risk alternatives; however, their impact on cellular redox regulation remains unclear. Here, we investigated the effects of conventional cigarette smoke extract (CSE), HTP, and e-cigarette extracts on hydrogen peroxide (H₂O₂) permeability mediated by aquaporins (peroxiporins) and on the activity of key antioxidant enzymes (catalase, superoxide dismutase, and glutathione peroxidase) in ATII-like cells. Eight aquaporins were detected at the mRNA level, and seven were confirmed at the protein level. CSE markedly inhibited H₂O₂ permeability across plasma, mitochondrial, and nuclear membranes. HTP extract impaired H₂O₂ transport across the plasma membrane and nuclear envelope, while mitochondrial permeability was preserved. Both CSE and HTP extract reduced superoxide dismutase and glutathione peroxidase activities. In contrast, e-cigarette extract exerted minimal effects on membrane H₂O₂ permeability and selectively decreased superoxide dismutase activity. Overall, our findings identify a graded pattern of oxidative toxicity (CSE > HTP > e-cigarette) and highlight peroxiporins as critical regulators of intracellular redox homeostasis. Although less harmful than cigarettes, alternative nicotine delivery systems are not biologically inert. Full article

Background/Objectives: Non–small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality, driven by invasive behavior and frequent resistance to systemic therapies. Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) benefit patients with EGFR-mutant NSCLC, but their efficacy is often limited by tumor-intrinsic and environmental resistance mechanisms. Benzo[a]pyrene (BaP), a ubiquitous polycyclic aromatic hydrocarbon from tobacco smoke, combustion, and dietary sources, is a known carcinogen; however, its role in modulating therapeutic responses is poorly understood. Studies, including ours, implicate the platelet-activating factor-receptor (PAFR) pathway in mediating environmental pollutant and therapy-induced effects on tumor growth and microvesicle particle (MVP) release. We hypothesized that PAFR activation mediates BaP-induced NSCLC progression and influences EGFR-TKI responses. Methods: We assessed the effects of BaP, PAFR agonist CPAF, EGFR-TKIs, and their combinations on cell viability, proliferation, migration, anchorage-independent growth, and MVP secretion. Results: BaP did not alter cell survival but significantly increased migration, growth, colony formation, and MVP release, similar to CPAF, and these effects were blocked by a PAFR antagonist or acid sphingomyelinase inhibitor. Notably, BaP did not significantly reduce EGFR-TKI efficacy at tested concentrations. Conclusions: These results show that environmental carcinogens modulate NSCLC behavior through PAFR signaling without compromising EGFR-TKI responsiveness, highlighting PAFR as a potential therapeutic target. Full article

Background/Objectives: Methods of smoking have evolved over the years, including heated tobacco products. The impact of exposure to traditional tobacco smoke and heated/electronic tobacco products (IQOS) on biofilm formation has not been previously compared in vitro. Aims and objectives: The present study aimed to evaluate the impact of tobacco and electronic smoking on microbial biofilm formation on dental hard tissues. Materials and Methods: Thirty premolars were randomly assigned to six groups (n = 10 per group) according to tissue type and smoking exposure: Six experimental groups were defined: Group 1, non-exposed enamel; Group 2, enamel subjected to conventional cigarette smoke (CS); Group 3, enamel subjected to heated tobacco (HT); Group 4, non-exposed cementum; Group 5, cementum subjected to conventional cigarette smoke; and Group 6, cementum exposed to heated tobacco. Enamel and root discs were then immersed in 2 mL of an adjusted, standardized bacterial suspension of Streptococcus mutans (S. mutans) to allow bacterial biofilm adhesion after incubation for 48 h at 37 °C. The mean colony-forming unit (CFU) count was calculated, and the surface topography and roughness were assessed using scanning electron microscopy and ImageJ software with the SurfCharJ plugin, respectively. Results: Conventional cigarette smoking showed significantly higher S. mutans adhesion on the enamel and root discs compared with IQOS and control groups. Both IQOS and cigarette smoking increased roughness on enamel and root versus the control group, and cigarette smoking produced significantly higher roughness on the enamel surface when compared to IQOS; however, there were no significant differences in the roughness between the two smoking methods on the root surface. SEM analysis showed the most extensive enamel and root microtopography change in IQOS smoking. Conclusions: Aerosols from heated tobacco products (IQOS) alter the surface topography and roughness of enamel and root, while traditional cigarette smoking significantly increases bacterial colonization. Further in vivo studies are warranted to simulate the dynamic nature of the oral cavity. Full article

Both the gut and the lungs possess a microbiome, a community of commensal bacteria, archaea, fungi, and viruses that perform important housekeeping functions in those organs. The colonic microbiome primarily ferments indigestible dietary fibers into essential short-chain fatty acids, synthesizes essential vitamins, regulates the mucosal immune system, and forms a protective barrier against pathogenic colonization. The lung microbiome maintains respiratory health primarily by regulating mucosal immunity, providing a physical barrier against invading pathogens, and producing beneficial metabolites. Several colonic microbiota metabolites, including the short-chain fatty acids acetate, propionate, and butyrate, together with the tryptophan metabolites indole-3-acetate and indole-3-propionate, secondary bile acids, and the polyamines spermidine and putrescine, are transported to the lungs via the gut–lung axis. These colonic microbiota biomolecules suppress lung inflammation, strengthen immune homeostasis, and reduce the severity of respiratory diseases. In contrast, lung microorganisms and their metabolites can travel to the gut via the gut–lung axis, influencing intestinal immune responses and potentially leading to an imbalance of gut microorganisms or dysbiosis. This means that respiratory diseases may lead to digestive issues, intestinal inflammation and chronic diseases. Here, we have reviewed this crosstalk and its impact on the principal pulmonary diseases: asthma, chronic obstructive pulmonary disease, cystic fibrosis, bronchogenic carcinoma, COVID-19, interstitial lung diseases, pneumonia, and tuberculosis. It is concluded that the gut microbiome plays a significant part in lung health and disease. Diet, tobacco smoking and electronic cigarette vaping all impact both the gut and lung microbiomes. Full article

Indigenous women experience a disproportionate burden of adverse perinatal health outcomes, yet the extent and nature of health promotion interventions addressing modifiable behavioural and social determinants remain poorly synthesised. This scoping review mapped smoking, nutrition, alcohol, physical exercise, and social and emotional wellbeing (SNAPS(o))-related perinatal health promotion programs delivered through Australian Aboriginal Community Controlled Health Organisations (ACCHOs), supplemented by relevant peer-reviewed evidence identified across Australia, Aotearoa New Zealand, Canada, and the United States. A two-phase design looked at peer-reviewed literature from January 2010 to January 2025 across PubMed, CINAHL, and the Cochrane Library, followed by a structured review of Aboriginal Community Controlled Health Organisation (ACCHO) websites in Australia (n = 145). Data were extracted on program characteristics, SNAPS(o) components, implementation models, and evaluation outcomes. Findings were synthesised using content analysis. Thirty-four programs were identified in total, most delivered through ACCHOs (n = 26) and predominantly implemented in Australia (n = 29). Smoking was the most frequently addressed component (n = 18, 55%), while nutrition and social and emotional wellbeing were each included in 27% of programs (n = 9), physical exercise in 18% (n = 6), and alcohol in 15% (n = 5). Grey-literature programs more commonly reflected multi-component, holistic models compared with peer-reviewed studies and formal evaluations. Only 10 programs had identifiable formal evaluation evidence, including published or publicly reported evaluations, almost all of which were identified through academic sources. Evaluations focused primarily on tobacco-related behavioural outcomes, with limited reporting of sustained maternal or infant health endpoints. The perinatal SNAPS(o) intervention landscape for Indigenous women is characterised by strong community-controlled delivery but limited published evaluation, particularly of integrated models implemented within ACCHOs. The concentration of evidence on smoking cessation highlights a need to expand evaluation across broader domains of maternal wellbeing. Strengthening Indigenous-led evaluation frameworks and outcome measures that reflect holistic models of care is essential to advancing equitable and culturally grounded perinatal health systems. Full article

Background: Pre-Chronic Obstructive Pulmonary Disease (pre-COPD) and Preserved Ratio Impaired Spirometry (PRISm) phenotypes represent important components of the early obstructive lung disease spectrum, characterized by respiratory symptoms and structural lung abnormalities prior to the development of overt airflow limitation. Emphysema is considered one of the major structural phenotypes underlying airway disease and the COPD spectrum. Although cigarette smoking is the best recognized risk factor for these conditions, non-tobacco exposures may also contribute to early structural lung changes. In this study, we evaluated the radiological features, pulmonary function parameters, and dyspnea severity of CT-detected emphysema in symptomatic patients classified as having pre-COPD or PRISm, with particular attention paid to the potential influence of smoking status on disease characteristics. Methods: In this retrospective, single-center study, symptomatic patients aged 20–50 years classified as having pre-COPD or PRISm and in whom emphysema was detected on high-resolution computed tomography (HRCT) were evaluated. Only symptomatic patients who underwent HRCT for clinical indications and in whom emphysema was identified were included. Demographic characteristics, emphysema type and quantitative emphysema severity, pulmonary function parameters, and Modified Medical Research Council (mMRC) dyspnea scores were analyzed. The PRISm and pre-COPD groups were compared in terms of clinical and symptomatic characteristics. In addition, smoking-related clinical and radiological characteristics were also evaluated. Results: A total of 232 patients were included in the study. The median age was 43 years (38–48), and 84.1% of the participants were male. Among the study population, 68.5% were classified in the pre-COPD group and 31.5% in the PRISm group. The most frequently identified emphysema patterns were paraseptal (44.4%) and centrilobular (40.5%). The median total lung emphysema area was 18% (13–22). A weak negative correlation was observed between the degree of emphysema and FEV₁ (r = −0.185; p = 0.005), whereas a weak positive correlation was found between emphysema extent and the mMRC dyspnea score (r = 0.214; p = 0.001). Dyspnea severity was significantly higher in the PRISm group compared with the pre-COPD group (p < 0.001). In the smoking-status subgroup analysis, ever-smokers demonstrated significantly greater dyspnea severity and lower FEV₁ values, whereas never-smokers had a significantly higher proportion of emphysema extent > 18% (all p < 0.05). Conclusions: Radiologically detected emphysema in symptomatic patients without airflow limitation was associated with statistically significant but weak alterations in pulmonary function and dyspnea burden. Dyspnea severity was significantly higher in the PRISm phenotype. In a smoking-status subgroup analysis, ever-smokers had significantly greater dyspnea severity, whereas never-smokers showed a significantly higher proportion of extensive emphysema (>18%), despite similar functional impairment across groups. These findings underscore the importance of non-tobacco exposures in the development of emphysema within pre-obstructive spirometric phenotypes. Multicenter prospective studies incorporating healthy controls and systematic exposure documentation are needed to confirm these observations. Full article

Background: Radon exposure is the second most important risk factor for lung cancer after tobacco smoking and represents a significant but often underestimated public health problem. Due to the absence of specific clinical manifestations at early stages, the identification of molecular biomarkers reflecting early radon-induced carcinogenic processes is of particular importance. The aim of this study was to identify protein biomarkers associated with radon exposure in lung cancer patients residing in settlements of the Akmola and North Kazakhstan regions of Kazakhstan. Methods: Indoor radon exposure was assessed using CR-39 detectors to measure radon concentrations in residential dwellings during summer and autumn periods. The study included 57 lung cancer patients and 73 control subjects residing in areas characterized by varying levels of radon exposure. Plasma samples were collected and analyzed using liquid chromatography–tandem mass spectrometry (LC–MS/MS) to identify differentially expressed proteins associated with lung cancer and radon exposure. Statistical analyses were performed to evaluate differences between groups and associations between radon exposure and molecular biomarkers. Results: Seasonal variability in indoor radon concentrations was observed, with several settlements demonstrating levels exceeding international reference values. Proteomic analysis identified multiple proteins differentially expressed between lung cancer patients and controls, as well as between radon-exposed and non-exposed lung cancer patients. Several proteins involved in inflammation, lipid metabolism, oxidative stress, and immune regulation pathways demonstrated significant differences in expression levels, suggesting potential associations with radon-induced carcinogenic mechanisms. LC–MS/MS proteomic profiling identified multiple differentially expressed proteins associated with lung cancer and radon exposure after false discovery rate correction. Proteins involved in inflammation, oxidative stress, immune regulation, and lipid metabolism, including ORM2, AZGP1, PRDX2, IRF7, and APOC3, demonstrated significant expression differences between radon-exposed and low-exposure groups. Conclusions: The identified protein biomarkers demonstrated significant associations with both radon exposure and lung cancer status, indicating their potential relevance for early detection and risk assessment of radon-induced lung cancer. The integration of environmental exposure assessment with proteomic profiling may provide new insights into the molecular mechanisms of radon-associated carcinogenesis and support the development of preventive strategies. Full article

Background and Aim: Passive smoking (PS) is a well-established risk factor associated with systemic and oral health impairments in children. However, its influence on perioperative physiological stability and recovery profiles during pediatric dental sedation remains insufficiently elucidated. This study investigated the association between PS exposure and perioperative vital parameters, recovery characteristics, and emergence behavioral outcomes in children undergoing dental extractions under sedation. Methods: This prospective cohort study (ClinicalTrials.gov: NCT06780189) included 100 ASA I children aged 4–6 years scheduled for primary molar extraction under midazolam-remifentanil-propofol sedation. Participants were stratified into three groups: no exposure, caregiver and household exposure, and household exposure only. An exposure-related relationship was evaluated based on daily household cigarette consumption. Perioperative vital signs (HR, blood pressure, and SpO₂) were continuously monitored. Postoperative recovery and emergence profiles were assessed using the Modified Aldrete Recovery Score (MASS), Richmond Agitation–Sedation Scale (RASS), and Pediatric Anesthesia Emergence Delirium (PAED) scale. Results: Children exposed to PS demonstrated significantly lower SpO₂ levels across all perioperative phases compared with non-exposed counterparts (p < 0.001), reflecting an exposure-related effect. In contrast, no statistically significant differences were observed in cardiovascular parameters (p > 0.05). Recovery time was significantly prolonged in PS-exposed children (p = 0.002). Furthermore, PS exposure was associated with significantly higher RASS and PAED scores, indicating increased agitation and emergence delirium (p < 0.001). Conclusions: Passive smoking adversely affects perioperative oxygenation, delays recovery, and exacerbates emergence neurobehavioral disturbances in children undergoing dental sedation. Environmental tobacco exposure must be integrated into preoperative risk assessments. Full article

Tobacco use remains a major public health challenge in Jordan, where cigarette smoking and waterpipe use are both common and dual use is increasingly prevalent. Community pharmacies are highly accessible healthcare settings, yet structured smoking-cessation services remain underutilized. This study evaluated the clinical effectiveness and implementation of Dual-Quit Digital, a pharmacist-delivered cessation counseling program tailored to the type of tobacco used, paired with a 6-month automated WhatsApp^® (Menlo Park, CA, USA) follow-up system. We conducted a pragmatic, two-arm, parallel-group, Hybrid Type 2 cluster randomized controlled trial in 16 community pharmacies in Jordan, randomized 1:1 to intervention or usual care. A total of 320 adult tobacco users were enrolled (160 per arm). The intervention combined a structured in-pharmacy pharmacist consultation, tailored behavioral support, phenotype-stratified pharmacotherapy support, and 6 months of semi-automated WhatsApp^® follow-up with telepharmacy escalation for predefined red-flag responses. The control arm received usual care, consisting of opportunistic brief advice and standard over-the-counter sales without proactive follow-up. The primary outcome was biochemically verified continuous abstinence at 6 months, defined as exhaled carbon monoxide (CO) < 10 ppm and analyzed using intention-to-treat principles. Secondary outcomes included 7-day point prevalence abstinence (PPA) at 3 and 6 months, 30-day PPA at 6 months, both-product abstinence among baseline dual users, pharmacotherapy uptake and adherence, and implementation-relevant outcomes, including service reach, feasibility of recruitment, and digital engagement metrics. All 16 pharmacies were retained, and all 320 randomized participants were included in the intention-to-treat analysis. At 6 months, CO-verified continuous abstinence was achieved by 26.3% of participants in the intervention arm compared with 11.3% in the control arm (adjusted odds ratio [aOR] 2.84, 95% CI 1.55–5.18; p < 0.001). The intervention also improved 7-day PPA at 3 months (33.1% vs. 15.6%; aOR 2.68, 95% CI 1.56–4.60; p < 0.001), 7-day PPA at 6 months (30.6% vs. 14.4%; aOR 2.62, 95% CI 1.48–4.62; p = 0.001), and 30-day PPA at 6 months (28.1% vs. 11.9%; aOR 2.89, 95% CI 1.59–5.24; p < 0.001). Among baseline dual users, both-product abstinence was higher in the intervention arm (21.9% vs. 7.8%; aOR 3.30, 95% CI 1.12–9.75; p = 0.026). Pharmacotherapy initiation was more frequent in the intervention arm (72.5% vs. 28.1%; p < 0.001), as was self-reported adherence for at least 8 weeks among initiators (56.0% vs. 26.7%; p = 0.002). In the intervention arm, active patient response rates to scheduled WhatsApp^® messages remained substantial, with 88.1% responding at Week 1, 73.8% at Week 4, 67.5% at Month 3, and 61.3% at Month 6; 145 red-flag triggers were captured from 62 participants, and 84.1% of escalations resulted in successful pharmacist follow-up within 48 h. The Dual-Quit Digital model significantly improved smoking-cessation outcomes compared with usual care and proved operationally feasible. These findings support integrating phenotype-stratified pharmacist counselling, pharmacotherapy support, and low-burden digital follow-up as a pragmatic cessation model for Jordan and similar settings. Full article

Background: Long-term survivors (LTS) after gynecological cancer may be cured but still face physical and psychological challenges. This multicenter study aimed to assess the long-term side effects, the received follow-up care, and the personal perspectives of survivors. Methods: Between 2019 and 2025, LTS from four European countries within the ENGOT (European Network of Gynecological Oncological Trial Groups) and GCIG (Gynecologic Cancer InterGroup) networks were recruited. Long-term survival was defined as surviving at least five years after the first diagnosis. LTS completed a questionnaire with 81 questions (patient’s characteristics, oncological history, current health status, lifestyle factors). Analyses were mainly descriptive. Results: A total of 677 LTS were enrolled, with a median age of 64.0 years (range: 26–92) and a median survival time of 7 years (range: 5–38). A total of 46.6% were diagnosed with cervical cancer, 32.9% with endometrial cancer, 4.4% with ovarian cancer, and 16.1% with other types of gynecological cancer. Moreover, 36.9% still suffer from physical and psychological symptoms, most frequently being lymphedema (36.2%), hot flashes (22.4%), difficulties with concentration (21.1%), fatigue (20.9%), vaginal dryness (20.1%), and urinary incontinence (18.9%). Median overall health status was ranked (scale 1–5; 1 = very good, 5 = very poor) as 2, while 13.5% rated their health as poor/very poor. Current symptoms were associated with poorer health status (p < 0.001) and a history of recurrent disease (p = 0.001). In addition, 13.6% reported not receiving follow-up care. CA-125 was determined in 80.8% of ovarian LTS, as well as in 30.7% of cervical and 28.9% of endometrial LTS. Pap smear follow-up was reported by 50.5% of endometrial LTS. A total of 33.7% did not exercise at all or exercised less than an hour per week, 13.4% smoke tobacco, and 51.2% drink alcohol more often than once a month. Conclusions: Our findings highlight the need for patient-centered follow-up care, addressing both long-term side effects and education on lifestyle and prevention. Follow-up procedures that do not follow guidelines should be avoided. Full article

The interplay between the environmental exposome and the cancer genome remains a critical gap in precision oncology. While somatic mutational signatures—genomic fossils imprinted by exposures such as ultraviolet radiation; tobacco smoke; and industrial pollutants—are well characterised for their etiological significance; their functional impact on therapeutic efficacy remains largely unexplored. We hypothesised that these environmental genomic scars induce distinct pharmacogenomic vulnerabilities and resistance mechanisms that vary by geographical exposure patterns. This study employs two complementary analytical frameworks. First, a linear regression-based pharmacogenomic screen across four datasets (GDSC1, GDSC2, CTRP, CCLE; 1001 cell lines, 31 cancer types) identified 608 statistically significant (p < 0.01) mutational signature–drug interactions, revealing that UV-associated signature SBS7a is associated with broad-spectrum therapeutic resistance, including to BRAF inhibitors (PLX-4720, p < 10⁻⁴), while pollution-driven oxidative stress (SBS18) is associated with sensitivity to p38 MAPK inhibition (VX-702, r = −0.45, p < 10⁻⁹). Second, an XGBoost predictive model trained exclusively on 33,679 GDSC2 records using a 1265-feature matrix integrating 40 SBS signatures, drug chemistry descriptors, proteomic features, and two satellite-derived environmental variables (NASA PM_2.5 and UV)—achieved R² = 0.7973 on a 20% holdout set (grouped cross-validation R² = 0.7296). SHAP analysis revealed that satellite-derived PM_2.5 (Zone_PM25) ranked 7th of 1265 features, exceeding all 40 individual SBS mutational signatures. Synthesising these findings with satellite-derived atmospheric data, we constructed an exploratory spatially interpolated risk surface spanning 122 nations, generating the hypothesis that uniform drug efficacy assumptions may not apply globally. These findings suggest that a patient’s environmental exposure history may constitute a measurable pharmacogenomic variable. This exploratory framework warrants validation in independent datasets and with individual-level geographic data before clinical application. Full article

Background/Objectives: Lung cancer remains the leading cause of cancer-related mortality in Central and Eastern Europe (CEE), where late-stage diagnosis, structural healthcare limitations, and regional epidemiological confounders complicate early detection. This review aimed to synthesize the evidence from Romania, Poland, Hungary, and Bulgaria and to outline a context-adapted multimodal screening strategy for CEE settings. Methods: A structured review of PubMed-, Scopus-, and Web of Science-indexed literature published from 2010 through 27 December 2025 was performed, focusing on lung cancer epidemiology, screening, implementation barriers, risk stratification, and adjunctive diagnostic approaches in the four selected CEE countries. A total of 297 articles were included. Results: The evidence confirms a persistently high burden of late-stage lung cancer across CEE, driven by tobacco exposure, air pollution, radon, comorbidities, diagnostic delays, fragmented registries, workforce shortages, and marked socioeconomic and geographic inequalities. In addition, tuberculosis-related granulomatous lesions and chronic inflammatory lung disease complicate nodule interpretation and reduce screening specificity in parts of the region. Screening experience from Poland and Hungary supports the feasibility of low-dose computed tomography (LDCT) when paired with volumetric assessment and structured follow-up. Risk-prediction models may improve participant selection, while biological triage may help reduce unnecessary invasive procedures, although prospective validation remains limited. Conclusions: In CEE, lung cancer screening should be implemented as a multimodal, context-adapted program combining risk-based enrollment, volumetric LDCT, selective biological triage, smoking-cessation support, and centralized multidisciplinary delivery. Full article

Background: Despite well-documented adverse impact on both systemic and oral health, tobacco smoking remains a persistent issue in military populations. It contributes to the global burden of tobacco use and is often perceived as a means of coping with stress in military settings. Purpose: This study aimed to assess the prevalence of tobacco use among military marines, its impact on oral health, and their level of knowledge regarding smoking, as well as to identify variables associated with their smoking habits. Thus, it provides a basis for implementing appropriate tobacco cessation and harm reduction strategies, particularly within the military. This study demonstrated a high prevalence of tobacco use among military marines, despite generally high levels of knowledge regarding tobacco smoking. A knowledge gap was still evident in relation to smoking behavior. The most frequently reported oral health impacts among smokers were tooth staining, halitosis, and taste impairment. Duration of military service and level of knowledge were significantly associated with smoking behavior. Materials and Methods: A validated and reliable online survey was administered to collect socio-demographic data, including age, education level, and length of military service. The survey also assessed smoking status, smoking behavior, its impact on oral health, and participants’ knowledge of smoking-related risks. Data were analyzed descriptively, and associated factors were examined using multivariate analysis. Results: A total of 475 military marines participated in the study. Of these, 44.8% were current smokers, 25.7% were former smokers, and 29.5% had never smoked. Overall, 71% of participants demonstrated good knowledge of smoking-related risks. The most commonly reported oral health impacts were halitosis, tooth staining, and impaired taste. Smoking status did not differ significantly by age (p = 0.095) or education level (p = 0.610), but differed significantly by length of military service (p < 0.05) and level of knowledge (p < 0.05). Multivariate analysis using multinomial logistic regression indicated that length of military service was a significant predictor of smoking behavior (p = 0.005; 95% CI: 0.282–0.800), with 1–5 years of service emerging as the most influential category. Based on the odds ratio, individuals with 11–15 years of service had a 1.8-fold higher likelihood of smoking. Conclusions: Despite a generally good level of knowledge regarding the health risks of smoking, the prevalence of tobacco use remains high among military marines. The most commonly reported oral health impacts were tooth staining, halitosis, and impaired taste. Length of military service and level of knowledge regarding smoking were identified as significant factors associated with smoking status. Full article

Radon-222, a naturally occurring radioactive gas, is the second leading cause of lung cancer globally, after tobacco use. When inhaled, its decay products, especially polonium-218 and polonium-214, emit high-energy alpha particles that induce dense DNA damage in the bronchial epithelium. Because ambient radon measurements often vary significantly over time and across locations, they provide limited insight into individual exposure levels. This suggests the urgent need for biological markers that can accurately indicate internal dose and early signs of lung cancer development. This review offers an extensive overview of biomarkers associated with radon exposure, from internal dosimetry to early biological responses. It covers internal dose markers (e.g., radon progeny in air and ²¹⁰Po/²¹⁰Pb in bones and teeth), molecular and cytogenetic indicators of effective dose (such as chromosomal aberrations, γ-H2AX foci, and DNA adducts), and early effect markers (including somatic mutations, epigenetic changes, miRNA profiles, and autoantibody signatures). The review highlights translocations detected via FISH, discussing those that are stable over time versus those that are transient. It also evaluates the reliability and practicality of these biomarkers in occupational and residential settings, noting how smoking complicates causal inference due to overlapping mutation pathways. Finally, it suggests that integrating multi-omics technologies could improve the precision of biomarker panels. Full article

The oral cavity is home to a diverse community of microbiota comprising bacteria, viruses, protozoa, and fungi. These microorganisms inhabit several oral niches and play a significant role in supporting both oral and systemic health. The fine balance between the microbial communities can be influenced by genetics and environmental factors, potentially leading to dysbiosis. Alterations in the oral microbiota have been implicated in periodontitis, chronic inflammation, and systemic disease. Tobacco has been identified as a major player in altering the oral microenvironment and disturbing the balance between potentially pathogenic and beneficial commensals. The resulting dysbiosis promotes inflammation and assists in the passage of pathogenic microorganisms into the blood system. This narrative review examines current evidence linking the use of tobacco with the dominance of pathogenic oral bacteria and a dysfunctional immune response. We explore how the chemicals and toxins in cigarettes promote a reduction in oxygen and cause changes in the abundance of anaerobic bacteria. After discussing the mechanistic pathways leading to periodontitis and the entry of microorganisms into the circulation, the review will interrogate previous studies and identify opportunities and priorities for future research. Full article