Smoking-related Lung Disease Research Articles

Smoking-related interstitial lung disease : Radiological findings, histopathological correlations, and clinical observations

Identifying smoking-related interstitial lung diseases (SRILD) in smokers is challenging, as clinical manifestations can be nonspecific, and there is avariety of SRILD entities that not only interconnect but can also overlap. In diagnosing SRILD, imaging techniques such as high-resolution computed tomography (HRCT) allow the identification of characteristic features, serving as crucial pieces of the puzzle for definitive differentiation. Studies have demonstrated that HRCT exhibits asensitivity of approximately 80-90% in identifying SRILD, with aspecificity around 70-80%. The conclusive diagnosis often requires acorrelation between histopathological findings and clinical observations. Regular monitoring of smokers, especially when experiencing symptoms like shortness of breath and cough, coupled with acomprehensive diagnosis of SRILD, is crucial for accurate identification and individualized therapy.

Effects of Active Chronic Cigarette-Smoke Exposure on Circulating Fibrocytes

PurposeThis 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.MethodsFlow 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.ResultsA 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).ConclusionThe 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.

Cigarette smoke-induced dysbiosis: comparative analysis of lung and intestinal microbiomes in COPD mice and patients

BackgroundThe impact of cigarette smoke (CS) on lung diseases and the role of microbiome dysbiosis in chronic obstructive pulmonary disease (COPD) have been previously reported; however, the relationships remain unclear.MethodsOur research examined the effects of 20-week cigarette smoke (CS) exposure on the lung and intestinal microbiomes in C57BL/6JNarl mice, alongside a comparison with COPD patients’ intestinal microbiome data from a public dataset.ResultsThe study found that CS exposure significantly decreased forced vital capacity (FVC), thickened airway walls, and induced emphysema. Increased lung damage was observed along with higher lung keratinocyte chemoattractant (KC) levels by CS exposure. Lung microbiome analysis revealed a rise in Actinobacteriota, while intestinal microbiome showed significant diversity changes, indicating dysbiosis. Principal coordinate analysis highlighted distinct intestinal microbiome compositions between control and CS-exposed groups. In the intestinal microbiome, notable decreases in Patescibacteria, Campilobacterota, Defferibacterota, Actinobacteriota, and Desulfobacterota were observed. We also identified correlations between lung function and dysbiosis in both lung and intestinal microbiomes. Lung interleukins, interferon-ɣ, KC, and 8-isoprostane levels were linked to lung microbiome dysbiosis. Notably, dysbiosis patterns in CS-exposed mice were similar to those in COPD patients, particularly of Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 4 patients. This suggests a systemic impact of CS exposure.ConclusionIn summary, CS exposure induces significant dysbiosis in lung and intestinal microbiomes, correlating with lung function decline and injury. These results align with changes in COPD patients, underscoring the important role of microbiome in smoke-related lung diseases.

MicroRNA Monitoring in Human Alveolar Macrophages from Patients with Smoking-Related Lung Diseases: A Preliminary Study.

Chronic obstructive pulmonary disease (COPD) is a progressive lung disease that is commonly considered to be a potent driver of non-small cell lung cancer (NSCLC) development and related mortality. A growing body of evidence supports a role of the immune system, mainly played by alveolar macrophages (AMs), in key axes regulating the development of COPD or NSCLC phenotypes in response to harmful agents. MicroRNAs (miRNAs) are small non-coding RNAs that influence most biological processes and interfere with several regulatory pathways. The purpose of this study was to assess miRNA expression patterns in patients with COPD, NSCLC, and ever- or never-smoker controls to explore their involvement in smoking-related diseases. Bronchoalveolar lavage (BAL) specimens were collected from a prospective cohort of 43 sex-matched subjects to determine the expressions of hsa-miR-223-5p, 16-5p, 20a-5p, -17-5p, 34a-5p and 106a-5p by RT-PCR. In addition, a bioinformatic analysis of miRNA target genes linked to cancer was performed. Distinct and common miRNA expression levels were identified in each pathological group, suggesting their possible role as an index of NSCLC or COPD microenvironment. Moreover, we identified miRNA targets linked to carcinogenesis using in silico analysis. In conclusion, this study identified miRNA signatures in AMs, allowing us to understand the molecular mechanisms underlying smoking-related conditions and potentially providing new insights for diagnosis or pharmacological treatment.

Smoking-Related Interstitial Fibrosis and Smoker's Macrophages.

Smoking-related interstitial lung diseases (SRILDs) are a group of heterogeneous diffuse pulmonary parenchymal diseases associated with tobacco exposure. Smoking-related interstitial fibrosis (SRIF) is relatively recent, a pathologically defined form of SRILDs. SRIF is characterized by the accumulation of macrophages in the alveolar spaces, which is associated with interstitial inflammation and fibrosis. The macrophages frequently contain light brown pigment and are called 'smoker's macrophages'. Patients with SRIF who have clinical evidence of interstitial lung disease are most commonly relatively young, heavy smokers with abnormalities on chest computed tomography showing ground-glass opacities, peripheral consolidation, and reticulation. Although SRIF is caused by cigarette smoking, the exact pathophysiological mechanisms by which smoking causes this type of interstitial fibrosis remain unknown. The degree of fibrosis and appearance of macrophage aggregates are important points of distinction when evaluating and diagnosing SRIF. Macrophage heterogeneity, particularly the activation and function of monocyte-derived alveolar macrophages (Mo-AMs) and interstitial macrophages (IMs), has important implications for the pathogenesis of SRIF and developing treatments. Further researches focused on smoker's macrophages are needed to understand of the pathogenesis of SRIF.

Geographical location, cigarette risk perceptions, and current smoking among older US adults.

Cigarette smoking and smoking-related lung disease are more common in rural (vs urban) areas of the United States (US). This study examined relationships between geographical location, cigarette risk perceptions, and current smoking among older adults who are at greatest risk of developing smoking-related lung disease. The study was a secondary data analysis of 12126 respondents aged ≥40 years from Wave 5 of the Population Assessment of Tobacco and Health Study. Weighted descriptive statistics and Poisson regressions assessed current smoking (vs never or former) as a function of geographical location in a stepwise fashion, first unadjusted, then adjusting for sociodemographic characteristics, and finally for both sociodemographic characteristics and cigarette risk perceptions (4-item scale), in three separate models. Sensitivity analyses examined whether individual risk perceptions items had a greater impact on the association between geographical location and current smoking. Current smoking was more common among rural (20.6%) than urban (17.6%) residents. The risk ratio (RR) for rural (vs urban) residence on current smoking decreased from 1.17 (95% CI: 1.03-1.32) to 1.14 (95% CI: 1.01-1.29) to 1.08 (95% CI: 0.96-1.21) across the stepwise models. Lower cigarette risk perceptions confounded the rural-current smoking association and was an independent risk factor for smoking (adjusted RR, ARR=2.15; 95% CI: 1.94-2.18). In sensitivity analyses, believing that cigarettes are very or extremely (vs somewhat, slightly, or not at all) harmful to health and agreeing (vs not agreeing) that secondhand smoke causes lung disease in people who do not smoke, confounded the rural-current smoking association whereas beliefs about smoking causing lung cancer or lung disease in people who smoke did not. Lower cigarette risk perceptions among rural residents confounded the positive association between rural residence and current smoking. Results from sensitivity analyses highlight potential targets for communication campaigns aimed at promoting more accurate perceptions of the harmful health consequences of cigarette smoking.

Smoking-related interstitial lung disease: A narrative review.

Although smoking-related interstitial lung diseases (SR-ILD) are a relatively rare group of entities, they are a relevant public health problem of growing importance, both because they affect young adults and because of their increasing prevalence in recent years due to increased tobacco consumption. In patients who smoke and have non-specific respiratory symptoms, SR-ILD should be ruled out, a term that encompasses a group of different entities in which the basis for diagnosis is the smoking history together with compatible respiratory functional findings, radiology and/or histology. An association has been established between tobacco smoke and a group of diseases that include respiratory bronchiolitis-associated interstitial lung disease (2%-3% of all ILD), desquamative interstitial pneumonia (<1%), Langerhans cell histiocytosis (3%-5%) and acute eosinophilic pneumonia. Smoking is considered a risk factor for idiopathic pulmonary fibrosis which has also been called combined fibroemphysema (5%-10% of all ILD); however, the role and impact of smoking in its development, remains to be determined. The likely interconnection between the mechanisms involved in inflammation and pulmonary fibrosis in all these processes often results in an overlapping of clinical, radiological, and histological features. In the absence of robust scientific evidence on its management, smoking cessation is the first measure to be taken into account. Although most diseases have a benign clinical course after smoking cessation, some cases may progress to chronic respiratory failure.

Association Between Clinicopathological Parameters and S100A8/A9 Expression According to Smoking History in Patients With Non-small Cell Lung Cancer.

Lung cancer is a major cause of cancer-related deaths worldwide, and chronic inflammation caused by cigarette smoke plays a crucial role in the development and progression of this disease. S100A8/9 and RAGE are associated with chronic inflammatory diseases and cancer. This study aimed to investigate the expression of S100A8/9, HMBG1, and other related pro-inflammatory molecules and clinical characteristics in patients with non-small cell lung cancer (NSCLC). We obtained serum and bronchoalveolar lavage (BAL) fluid samples from 107 patients and categorized them as never or ever-smokers. We measured the levels of S100A8/9, RAGE, and HMGB1 in the collected samples using enzyme-linked immunosorbent kits. Immunohistochemical staining was also performed to assess the expression of S100A8/9, CD11b, and CD8 in lung cancer tissues. The correlation between the expression of these proteins and the clinical characteristics of patients with NSCLC was also explored. The expression of S100A8/A9, RAGE, and HMGB was significantly correlated with smoking status and was higher in people with a history of smoking or who were currently smoking. There was a positive correlation between serum and BAL fluid S100A8/9 levels. The expression of S100A8/A9 and CD8 in lung tumor tissues was significantly correlated with smoking history in patients with NSCLC. Ever-smokers, non-adenocarcinoma histology, and high PD-L1 expression were significant factors predicting high serum S100A8/9 levels in multivariate analysis. The S100A8/9-RAGE pathway and CD8 expression were increased in smoking-related NSCLC patients. The S100A8/9-RAGE pathway could be a promising biomarker for chronic airway inflammation and carcinogenesis in smoking-related lung diseases.

Bronchoalveolar cytokine profile differentiates Pulmonary Langerhans cell histiocytosis patients from other smoking-related interstitial lung diseases

BackgroundPulmonary Langerhans cell histiocytosis (PLCH) is a rare interstitial lung disease (ILD) associated with smoking, whose definitive diagnosis requires the exclusion of other forms of ILD and a compatible surgical lung biopsy. Bronchoalveolar lavage (BAL) is commonly proposed for the diagnosis of ILD, including PLCH, but the diagnostic value of this technique is limited. Here, we have analyzed the levels of a panel of cytokines and chemokines in BAL from PLCH patients, in order to identify a distinct immune profile to discriminate PLCH from other smoking related-ILD (SR-ILD), and comparing the results with idiopathic pulmonary fibrosis (IPF) as another disease in which smoking is considered a risk factor.MethodsBAL samples were collected from thirty-six patients with different ILD, including seven patients with PLCH, sixteen with SR-ILD and thirteen with IPF. Inflammatory profiles were analyzed using the Human Cytokine Membrane Antibody Array. Principal component analysis (PCA) was performed to reduce dimensionality and protein–protein interaction (PPI) network analysis using STRING 11.5 database were conducted. Finally, Random forest (RF) method was used to build a prediction model.ResultsWe have found significant differences (p < 0.05) on thirty-two cytokines/chemokines when comparing BAL from PLCH patients with at least one of the other ILD. Four main groups of similarly regulated cytokines were established, identifying distinct sets of markers for each cluster. Exploratory analysis using PCA (principal component analysis) showed clustering and separation of patients, with the two first components capturing 69.69% of the total variance. Levels of TARC/CCL17, leptin, oncostatin M (OSM) and IP-10/CXCL10 were associated with lung function parameters, showing positive correlation with FVC. Finally, random forest (RF) algorithm demonstrates that PLCH patients can be differentiated from the other ILDs based solely on inflammatory profile (accuracy 96.25%).ConclusionsOur results show that patients with PLCH exhibit a distinct BAL immune profile to SR-ILD and IPF. PCA analysis and RF model identify a specific immune profile useful for discriminating PLCH.

Alveolar type II epithelial cell FASN maintains lipid homeostasis in experimental COPD.

Alveolar epithelial type II (AEC2) cells strictly regulate lipid metabolism to maintain surfactant synthesis. Loss of AEC2 cell function and surfactant production are implicated in the pathogenesis of the smoking-related lung disease chronic obstructive pulmonary disease (COPD). Whether smoking alters lipid synthesis in AEC2 cells and whether altering lipid metabolism in AEC2 cells contributes to COPD development are unclear. In this study, high-throughput lipidomic analysis revealed increased lipid biosynthesis in AEC2 cells isolated from mice chronically exposed to cigarette smoke (CS). Mice with a targeted deletion of the de novo lipogenesis enzyme, fatty acid synthase (FASN), in AEC2 cells (FasniΔAEC2) exposed to CS exhibited higher bronchoalveolar lavage fluid (BALF) neutrophils, higher BALF protein, and more severe airspace enlargement. FasniΔAEC2 mice exposed to CS had lower levels of key surfactant phospholipids but higher levels of BALF ether phospholipids, sphingomyelins, and polyunsaturated fatty acid-containing phospholipids, as well as increased BALF surface tension. FasniΔAEC2 mice exposed to CS also had higher levels of protective ferroptosis markers in the lung. These data suggest that AEC2 cell FASN modulates the response of the lung to smoke by regulating the composition of the surfactant phospholipidome.

Cadmium Toxicity Induces Pyroptosis In Macrophages

Cadmium (Cd) toxicity contributes to chronic obstructive pulmonary disease (COPD) and other smoking-related lung disease. Caspase-1, gasdermin D (GSDMD), and gasdermin E (GSDME) are key proteins responsible for the initiation of pyroptosis. We hypothesize Cd induces host immune and inflammatory cell death in a macrophage model (RAW 264.7).

A case report on pulmonary fibro-emphysema: an incorrectly framed case

This case report describes the combination of pulmonary fibrosis and emphysema (CPFE) as a possible new addition to the growing list of smoking-related lung diseases, which are characterised by the coexistence of usual interstitial pneumonia (UIP) or non-specific interstitial pneumonia (NSIP) with emphysema in tobacco smokers.

Cleavage of Occludin by Cigarette Smoke-Elicited Cathepsin S Increases Permeability of Lung Epithelial Cells.

Chronic obstructive pulmonary disease (COPD) is an irreversible disease mainly caused by smoking. COPD is characterized by emphysema and chronic bronchitis associated with enhanced epithelial permeability. Lung biopsies from smokers revealed a decreased expression level of occludin, which is a protein involved in the cohesion of epithelial tight junctions. Moreover, the occludin level correlated negatively with smoking history (pack-years), COPD grades, and cathepsin S (CatS) activity. Thus, we examined whether CatS could participate in the modulation of the integrity of human lung epithelial barriers. Cigarette smoke extract (CSE) triggered the upregulation of CatS by THP-1 macrophages through the mTOR/TFEB signaling pathway. In a co-culture model, following the exposure of macrophages to CSE, an enhanced level of permeability of lung epithelial (16HBE and NHBE) cells towards FITC-Dextran was observed, which was associated with a decrease in occludin level. Similar results were obtained using 16HBE and NHBE cells cultured at the air-liquid interface. The treatment of THP-1 macrophages by CatS siRNAs or by a pharmacological inhibitor restored the barrier function of epithelial cells, suggesting that cigarette smoke-elicited CatS induced an alteration of epithelial integrity via the proteolytic injury of occludin. Alongside its noteworthy resistance to oxidative stress induced by cigarette smoke oxidants and its deleterious elastin-degrading potency, CatS may also have a detrimental effect on the barrier function of epithelial cells through the cleavage of occludin. The obtained data emphasize the emerging role of CatS in smoking-related lung diseases and strengthen the relevance of targeting CatS in the treatment of emphysema and COPD.

Smoking-related interstitial lung disease

Exposure to smoke is associated with the development of diseases of the airways and lung parenchyma. Apart from chronic obstructive pulmonary disease (COPD), in some individuals, tobacco smoke can also trigger mechanisms of interstitial damage that result in various pathological changes and pulmonary fibrosis. A causal relation has been established between tobacco smoke and a group of entities that includes respiratory bronchiolitis-associated interstitial lung disease (RB-ILD), desquamative interstitial pneumonia (DIP), Langerhans cell histiocytosis (LCH), and acute eosinophilic pneumonia (AEP). Smoking is considered a risk factor for idiopathic pulmonary fibrosis (IPF); however, the role and impact of smoking in the development of this differentiated clinical entity, which has also been called combined pulmonary fibrosis and emphysema (CPFE) as well as nonspecific interstitial pneumonia (NIP), remains to be determined. The definition of smoking-related interstitial fibrosis (SRIF) is relatively recent, with differentiated histological characteristics. The likely interconnection between the mechanisms involved in inflammation and pulmonary fibrosis in all these processes often results in an overlapping of clinical, radiological, and histological features in the same patient that can sometimes lead to radiological patterns of interstitial lung disease that are impossible to classify. For this reason, a combined approach to diagnosis is recommendable. This combined approach should be based on the joint interpretation of the histological and radiological findings while taking the clinical context into consideration. This paper aims to describe the high-resolution computed tomography (HRCT) findings in this group of disease entities in correlation with the clinical manifestations and histological changes underlying the radiological pattern.

Hedgehog-interacting protein acts in the habenula to regulate nicotine intake

Hedgehog-interacting protein (HHIP) sequesters Hedgehog ligands to repress Smoothened (SMO)-mediated recruitment of the GLI family of transcription factors. Allelic variation in HHIP confers risk of chronic obstructive pulmonary disease and other smoking-related lung diseases, but underlying mechanisms are unclear. Using single-cell and cell-type-specific translational profiling, we show that HHIP expression is highly enriched in medial habenula (MHb) neurons, particularly MHb cholinergic neurons that regulate aversive behavioral responses to nicotine. HHIP deficiency dysregulated the expression of genes involved in cholinergic signaling in the MHb and disrupted the function of nicotinic acetylcholine receptors (nAChRs) through a PTCH-1/cholesterol-dependent mechanism. Further, CRISPR/Cas9-mediated genomic cleavage of the Hhip gene in MHb neurons enhanced the motivational properties of nicotine in mice. These findings suggest that HHIP influences vulnerability to smoking-related lung diseases in part by regulating the actions of nicotine on habenular aversion circuits.

Narrowing the Differential Diagnosis of Cystic Lesions in Smokers with Expiratory CT Acquisition Using the Cyst-Airway Communication Hypothesis.

The aim of this study was to assess percentage respiratory changes (δ) in the size of pulmonary cysts of different smoking-related etiologies. Retrospectively, we measured the cystic lesions due to histopathological-confirmed honeycombing from interstitial pulmonary fibrosis, pulmonary Langerhans cell histiocytosis (PLCH), and paraseptal emphysema, using paired inspiratory and expiratory CT scans. In a sample of 72 patients and 216 lesions, the mean diameter of PLCH and honeycombing decreased during expiration (PLCH, δ = 60.9%; p = 0.001; honeycombing, δ = 47.5%; p = 0.014). Conversely, paraseptal emphysema did not show any changes (δ = 5.2%; p = 0.34). In summary, our results demonstrated that cysts in smokers with PLCH and honeycombing fibrosis get smaller during expiratory CT scans, whereas the size of cystic-like lesions due to paraseptal emphysema and bullae tend to remain constant during respiratory cycles. These results support the hypothesis of cyst-airway communication in some cystic diseases, which could assist in the differential diagnosis in smoking-related lung diseases.

FIRE IN THE HOLE: GIANT BULLOUS LUNG DISEASE IN A VETERAN WITH BURN PIT EXPOSURE AND SMOKING

FIRE IN THE HOLE: GIANT BULLOUS LUNG DISEASE IN A VETERAN WITH BURN PIT EXPOSURE AND SMOKING

High-Resolution Computed Tomography Findings in Healthy Heavy Smokers and Correlation with Pulmonary Function Tests

Introduction: Chest radiographs and pulmonary function tests (PFTs), may show the adverse effects of smoking on the lungs, but in some cases these methods are inadequate and interpreted as normal. High-resolution computed tomography (HRCT) provides more sensitive and specific imaging features to identify parenchymal-interstitial abnormalities in the early stages of the disease related with smoking. The purpose of this study is to recognize lung HRCT findings of smoking in cigarette smokers and non-smokers and investigate whether there is a relationship with airway obstruction on PFTs. Methods: A total of 155 subjects (110 heavy smokers, 45 non-smokers) who performed both HRCT and PFTs were included in the study. Two radiologists independently evaluated the CT findings for the following characteristics: bronchiectasis, bronchial wall thickening, emphysema, atelectasis, interstitial patterns, and fibrotic changes. Afterwards, the relationship between the HRCT findings and PFTs of the heavy smokers and non-smokers was presented statistically. Results: There were statistically significant differences regarding emphysema and bronchial wall thickening between the heavy smokers and non-smokers (p = 0.001 and p = 0.000, respectively) on HRCT. Emphysema and bronchial wall thickening were more common in patients who had obstructive PFTs. Fibrotic changes, atelectasis, bronchial wall thickening, and emphysema were the most common imaging findings although normal PFTs. Conclusion: It is crucial to recognize the common imaging findings on HRCT of heavy smokers for diagnosis and treatment of smoking related lung disease. HRCT is vital in detecting the early stages of parenchymal-interstitial abnormalities of the lungs due to smoking, despite normal chest radiograms and PFTs.

Smoking-related interstitial lung diseases

Klinisches ProblemRaucherassoziierte interstitielle Lungenerkrankungen umfassen heterogene pulmonale Pathologien, deren korrekte Diagnostik prognostische und therapeutische Konsequenzen hat. In diesem Artikel werden die gängigsten raucherassoziierten interstitiellen Lungenerkrankungen beschrieben sowie eine strukturierte Herangehensweise präsentiert, welche den diagnostischen Arbeitsprozess erleichtern kann.Empfehlungen für die PraxisDie Computertomographie (CT) besitzt einen hohen Stellenwert in der Diagnose der raucherassoziierten interstitiellen Lungenerkrankungen und kann dazu beitragen, Lungenbiopsien zu verhindern. Um eine hohe diagnostische Genauigkeit zu erreichen, sollten standardisierte Untersuchungsprotokolle sowie eine strukturierte Herangehensweise in der Befundung zur Anwendung kommen. In den entzündlich dominierten Stadien der respiratorischen Bronchiolitis (RB), der respiratorischen Bronchiolitis mit interstitieller Lungenerkrankung (RB-ILD) sowie der desquamativen interstitiellen Pneumonie (DIP) haben die Beendigung des Rauchens sowie Steroide den größten therapeutischen Effekt. Bei fibrotischen Veränderungen (z. B. im Rahmen einer idiopathischen pulmonalen Fibrose [IPF]) können antifibrotische Therapien mit Pirfenidon und Nintedanib zum Einsatz kommen. Patienten mit dem Verdacht auf raucherassoziierte interstitielle Lungenerkrankung sollten in multidisziplinären Boards abgeklärt und behandelt werden.

Association between Low-Dose Computed Tomography Results and 1-Year Smoking Cessation in a Residential Smoking Cessation Program.

The COVID-19 pandemic is a global health threat. Smoking and smoking-related lung diseases are risk factors for severe COVID-19 infection. This study investigated whether low-dose computed tomography (LDCT) scan results affected the success of 1-year smoking cessation. The Gyeonggi Southern Smoking Support Center performed the residential smoking cessation program from January to December 2018. During the program, LDCT was performed on 292 participants; 6 months later, follow-up via telephone or visit was conducted. Among the 179 participants who succeeded in smoking cessation for 6 months, telephone follow-up was conducted to determine whether there was a 12-month continuous smoking cessation. In order to evaluate the association between LDCT results and 12-month continuous abstinence rate (CAR), logistic regression was used to estimate the odds ratio (OR) and 95% confidence interval (CI). The CARs at 6 and 12 months were 61.3% and 31.5%, respectively. Indeterminate or suspicious malignant lung nodules were associated with a higher 12-month CAR (OR, 3.02; 95% CI, 1.15–7.98), whereas psychiatric history was associated with a lower 12-month CAR (OR, 0.06; 95% CI, 0.03–0.15). These results suggest that abnormal lung screening results may encourage smokers to quit smoking.