BACKGROUND: The Smoking paradox has generated inconsistent findings concerning the clinical prognosis of acute ST-segment elevation myocardial infarction (STEMI) patients, while providing limited insights into coronary anatomy and function which are crucial prognostic factors. Therefore, this study aimed to further investigate the existence of smoking paradox in coronary anatomy and function.
METHODS: This study divided STEMI patients into smokers and non-smokers. Quantitative coronary angiography, angiography‑derived microcirculatory resistance (AMR) and quantitative flow ratio (QFR) were utilized to analyze coronary anatomy and function. These parameters were compared using multivariable analysis and propensity score matching. The clinical outcomes were evaluated using Kaplan-Meier curve and Cox regression.
RESULTS: The study included 1258 patients, with 730 in non-smoker group and 528 in smoker group. Smokers were significantly younger, predominantly male, and had fewer comorbidities. Without adjusting for confounders, smokers exhibited larger lumen diameter [2.03(1.45-2.57) vs. 1.90(1.37-2.49), P = 0.033] and lower AMR [244(212-288) vs. 260(218-301), P = 0.006]. After matching and multivariate adjustment, smokers exhibited inversely smaller lumen diameter [1.97(1.38-2.50) vs. 2.15(1.63-2.60), P = 0.002] and higher incidence of coronary microvascular dysfunction [233(53.9%) vs. 190(43.6%), P = 0.002], but showed similar AMR and clinical outcomes compared to non-smokers. There was no difference in QFR between two groups.
CONCLUSIONS: Smoking among STEMI patients undergoing pPCI was associated with smaller lumen diameter and higher occurrence of coronary microvascular dysfunction, although it had no further impact on clinical prognosis. The smoking paradox observed in coronary anatomy or function may be explained by younger age, gender, and lower prevalence of comorbidities.

Background Most of the data regarding prevalence and size distribution of solid lung nodules originates from lung cancer screening studies that target high-risk populations or from Asian general cohorts. In recent years, the identification of lung nodules in non-high-risk populations, scanned for clinical indications, has increased. However, little is known about the presence of solid lung nodules in the Northern European nonsmoking population. Purpose To study the prevalence and size distribution of solid lung nodules by age and sex in a nonsmoking population. Materials and Methods Participants included nonsmokers (never or former smokers) from the population-based Imaging in Lifelines study conducted in the Northern Netherlands. Participants (age ≥ 45 years) with completed lung function tests underwent chest low-dose CT scans. Seven trained readers registered the presence and size of solid lung nodules measuring 30 mm3 or greater using semiautomated software. The prevalence and size of lung nodules (≥30 mm3), clinically relevant lung nodules (≥100 mm3), and actionable nodules (≥300 mm3) are presented by 5-year categories and by sex. Results A total of 10 431 participants (median age, 60.4 years [IQR, 53.8-70.8 years]; 56.6% [n = 5908] female participants; 46.1% [n = 4812] never smokers and 53.9% [n = 5619] former smokers) were included. Of these, 42.0% (n = 4377) had at least one lung nodule (male participants, 47.5% [2149 of 4523]; female participants, 37.7% [2228 of 5908]). The prevalence of lung nodules increased from age 45-49.9 years (male participants, 39.4% [219 of 556]; female participants, 27.7% [236 of 851]) to age 80 years or older (male participants, 60.7% [246 of 405]; female participants, 50.9% [163 of 320]). Clinically relevant lung nodules were present in 11.1% (1155 of 10 431) of participants, with prevalence increasing with age (male participants, 8.5%-24.4%; female participants, 3.7%-15.6%), whereas actionable nodules were present in 1.1%-6.4% of male participants and 0.6%-4.9% of female participants. Conclusion Lung nodules were present in a substantial proportion of all age groups in the Northern European nonsmoking population, with slightly higher prevalence for male participants than female participants. © RSNA, 2024 Supplemental material is available for this article.

Lung cancer remains the leading cause of cancer-related mortality worldwide, with non-small cell lung cancer (NSCLC) constituting 85% of cases. Among NSCLCs, squamous cell carcinoma (SqCC) is strongly associated with smoking. However, lung cancer in never smokers (LCINS) represents approximately 25% of lung cancer cases globally and shows increasing incidence, particularly in East Asia. LCINS-SqCC is less well-characterized, especially regarding its genomic alterations and their impact on clinical outcomes. We conducted a retrospective analysis over a 20-year period (July 2003-July 2023) at two major tertiary centers in the UK. The cohort included 59 patients with LCINS-SqCC who underwent radical surgical resection. Data collected included demographic information, comorbidities, histopathological details, and outcome metrics such as disease-free and overall survival. Molecular sequencing of tumor specimens was performed to identify genomic aberrations. The cohort had a median age of 71 years (IQR 62-77) and a median BMI of 25.4 (IQR 22.8-27.8), with a slight male predominance (53%). The majority of patients (93%) had a preoperative MRC of 1-2. Recurrent disease was observed in 23 patients (39%), and 32 patients (54%) had died at a median follow-up of 3 years. Median disease-free survival was 545 days (IQR 132-1496), and overall survival was 888 days (IQR 443-2071). Preoperative creatinine levels were higher in patients who experienced recurrence (p = 0.037). Molecular analysis identified biallelic SMARCB1 loss in two younger patients, associated with rapid disease progression despite R0 resection. These patients\' tumors were PDL1-negative, TTF-1-negative, and positive for cytokeratin, CD56, and p40. SMARCB1-deficient SqCC in never smokers represents a highly aggressive variant with poor disease-free survival, highlighting the importance of integrating advanced molecular diagnostics in clinical practice. This study underscores the necessity for personalized treatment strategies, including targeted therapies such as EZH2 inhibitors and immune checkpoint blockade, to address the unique molecular pathways in SMARCB1-deficient cancers. Further clinical trials are essential to optimize therapeutic approaches for this challenging subgroup of lung cancer.

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BACKGROUND: Tobacco use is one of the main risk factors for Lung Cancer (LC) development. However, about 10-20% of those diagnosed with the disease are never-smokers. For Non-Small Cell Lung Cancer (NSCLC) there are clear differences in both the clinical presentation and the tumor genomic profiles between smokers and never-smokers. For example, the Lung Adenocarcinoma (LUAD) histological subtype in never-smokers is predominately found in young women of European, North American, and Asian descent. While the clinical presentation and tumor genomic profiles of smokers have been widely examined, never-smokers are usually underrepresented, especially those of a Latin American (LA) background. In this work, we characterize, for the first time, the difference in the genomic profiles between smokers and never-smokers LC patients from Chile.
METHODS: We conduct a comparison by smoking status in the frequencies of genomic alterations (GAs) including somatic mutations and structural variants (fusions) in a total of 10 clinically relevant genes, including the eight most common actionable genes for LC (EGFR, KRAS, ALK, MET, BRAF, RET, ERBB2, and ROS1) and two established driver genes for malignancies other than LC (PIK3CA and MAP2K1). Study participants were grouped as either smokers (current and former, n = 473) or never-smokers (n = 200) according to self-report tobacco use at enrollment.
RESULTS: Our findings indicate a higher overall GA frequency for never-smokers compared to smokers (58 vs. 45.7, p-value < 0.01) with the genes EGFR, KRAS, and PIK3CA displaying the highest prevalence while ERBB2, RET, and ROS1 the lowest. Never-smokers present higher frequencies in seven out of the 10 genes; however, smokers harbor a more complex genomic profile. The clearest differences between groups are seen for EGFR (15.6 vs. 21.5, p-value: < 0.01), PIK3CA (6.8 vs 9.5) and ALK (3.2 vs 7.5) in favor of never-smokers, and KRAS (16.3 vs. 11.5) and MAP2K1 (6.6 vs. 3.5) in favor of smokers. Alterations in these genes are comprised almost exclusively by somatic mutations in EGFR and mainly by fusions in ALK, and only by mutations in PIK3CA, KRAS and MAP2K1.
CONCLUSIONS: We found clear differences in the genomic landscape by smoking status in LUAD patients from Chile, with potential implications for clinical management in these limited-resource settings.

OBJECTIVE: Omega-3 supplementation as an adjunct to nonsurgical periodontal treatment has been reported to have a positive effect on healing in periodontitis patients. However, there is a lack of information on the effects of periodontal healing in smokers with periodontitis. The aim of this retrospective study was to investigate the effect of omega-3 supplementation given as an adjunct to nonsurgical periodontal treatment on clinical parameters in smoker and non-smoker periodontitis patients.
METHODS: This study included a total of 80 periodontitis patients, 40 non-smokers and 40 smokers who were systemically healthy. In this study, patients were divided into 4 groups as follows: Group 1 (Subgingival instrumentation (SI) alone/nonsmoker), Group 2 (SI alone/smoker), Group 3 (SI + Omega-3/nonsmoker) and Group 4 (SI + Omega-3/smoker). Group 3 and 4 consumed 1320 mg Omega-3 capsule (640 mg EPA, 480 mg DHA) once a day for 3 months. Probing depth (PD), clinical attachment level (CAL), gingival index (GI), plaque index (PI) and bleeding on probing (BOP %) were recorded at baseline, 1 month and 3 months after treatment.
RESULTS: Significant improvement of all clinical parameters at 1 and 3 months was observed in all groups. Whole mouth CAL, GI and BOP% were significantly reduced in group 4 compared to group 2 at 1 and 3 months postoperatively (p < 0.05). For moderately deep pockets (4-6 mm) and deep pockets (7 mm≤), PD and CAL reductions were significantly greater in groups taking omega - 3 (group 3 and group 4) compared to groups not taking omega-3 (group 1 and group 2) between baseline and 1 month and between baseline and 3 months (p ˂ 0.05).
CONCLUSIONS: Omega-3 supplementation given as an adjunct to nonsurgical periodontal treatment provided significant benefit in the improvement of clinical parameters (especially for CAL and PD) in the short term in smokers and non-smokers with periodontitis.
CONCLUSIONS: Nonsurgical periodontal treatment with omega-3 supplementation resulted in significant improvements in clinical parameters in smokers and non-smokers with periodontitis.

Diet behavior and nutrition are critical for maintaining health and improving quality of life. Cigarette smoking remains the leading cause of preventable death in the United States. Poor dietary choices, such as excessively frequenting restaurants, consuming ready-to-eat foods from grocery stores, and ingesting ultra-processed foods (like frozen meals and pizzas), can adversely impact health. Despite this, research comparing dietary behaviors between smokers and non-smokers is limited. Using data from the National Health and Nutritional Examination Survey 2017-2018, we analyzed diet behavior based on smoking status. Our findings reveal that smokers had a significant increase (90%) in the frequency of consuming frozen meals/pizzas in the past 30 days compared to non-smokers (coefficient: 1.9; 95% CI: 1.4, 2.6; p-value < 0.001). Additionally, over 70% of participants, regardless of their smoking status, were unaware of MyPlate, a nutritional guide created by the United States Department of Agriculture (USDA) to encourage Americans to make healthier food choices. There is an urgent need to increase public awareness of MyPlate and promote a better understanding of healthy dietary behaviors.

OBJECTIVE: This study aimed to evaluate the hypothesis that active smoking impacts upon mediators and abundance of circulating fibrocyte cells in smoking-related disease characterised by fibrosis.
METHODS: Flow cytometry and enzyme-linked immunosorbent assays were used to investigate blood from five patient groups: healthy never-smokers, healthy current smokers, stable chronic obstructive pulmonary disease (COPD) active smokers, idiopathic pulmonary fibrosis (IPF) never-smokers, and IPF active smokers.
RESULTS: A significant inverse dose-response relationship was observed in healthy smokers among cumulative smoking burden (pack-years) and fibrocyte abundance (p = 0.006, r = -0.86). Among serum profibrotic fibrocyte chemokines measured, CCL18 rose significantly alongside fibrocyte numbers in all five subject groups, while having an inverse dose-response relationship with pack-year burden in healthy smokers (p = 0.003, r = -0.89). In IPF, CCL2 rose in direct proportion to fibrocyte abundance irrespective of smoking status but had lower serum levels in those currently smoking (p =  < 0.001). For the study population, CXCL12 was decreased in pooled current smokers versus never-smokers (p = 0.03).
CONCLUSIONS: The suppressive effect of current, as distinct from former, chronic smoking on circulating fibrocyte abundance in healthy smokers, and modulation of regulatory chemokine levels by active smoking may have implications for future studies of fibrocytes in smoking-related lung diseases as a potential confounding variable.

Close associations among secondhand smoke (SHS) and metabolic syndrome (MetS) and its components have been demonstrated, however sex differences in these associations remain unclear. We collected 121,364 participants from the Taiwan Biobank, and excluded those with smoking history, the remaining 88,297 participants (male: 18,595; female: 69,702; mean age 50.1 ± 11.0 years) were included. SHS exposure was evaluated based on self-reported questionnaires. SHS was associated with MetS (odds ratio [OR], 1.268, p < 0.001 for males vs. 1.180, p < 0.001 for females), abdominal obesity (OR, 1.234, p < 0.001 for males vs. 1.199, p < 0.001 for females), low high-density lipoprotein cholesterol (OR, 1.183, p = 0.008 for males vs. 1.094, p = 0.011 for females), hyperglycemia (OR, 1.286, p < 0.001 for males vs. 1.234, p < 0.001 for females), but not with hypertriglyceridemia. SHS was associated with high blood pressure (BP) (OR, 1.278, p < 0.001) only in males, but not in females. Furthermore, significant interactions were found between sex x SHS on MetS (p = 0.023), abdominal obesity (p = 0.032), and elevated BP (p < 0.001). Moreover, the participants who were exposed to SHS for ≥1 hour per week were associated with a higher risk (OR = 1.316, p = 0.001 in males vs. OR = 1.220, p < 0.001 in females) of MetS compared to those with no exposure. These results showed an association between SHS and a high OR for MetS in both the males and females. Furthermore, sex differences were identified in the associations between SHS and MetS and its components, and SHS was more closely related to MetS, abdominal obesity, and high BP in males than in females.

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