Pack-years Of Smoking Research Articles

Locus of control and breathlessness: a cross-sectional analysis of 28,730 people

BackgroundLong-term pathological breathlessness is a life-limiting symptom that risks taking control of the individual's life. We aimed to evaluate how locus of control (LOC), an individual's perceived control of present and past life events, relates to breathlessness in a middle-aged general population.MethodsA population-based, cross-sectional analysis of people 50–64 years in the Swedish CArdioPulmonary bioImage Study (SCAPIS). Breathlessness was measured using the modified Medical Research Council (mMRC) breathlessness scale. LOC was assessed using five-point scales related to work, life events, perceived future, treated by other people, past changes, and life improvements. The LOC factors were dichotomised as having an external or internal LOC. Logistic regression was used to examine the association between external LOC and presence of moderate/severe breathlessness (mMRC≥2). Associations between external LOC and higher breathlessness severity score (mMRC 0–4) were analysed using ordinal regression. The models were adjusted for age, sex, education level, pack-years of smoking, body mass index, lung function, depression, and cardiorespiratory diseases.ResultsOf 28 730 participants (52% women), 4% experienced breathlessness. Breathlessness was related to external LOC in relation to life events ([odds ratio] 1.47; [95% confidence interval] 1.26–1.71), future (1.89; 1.53–2.34), treated unfairly (1.73; 1.42–2.09), past changes (1.50; 1.30–1.74), and life improvements (2.91; 2.35–3.59). External LOC was associated with increased breathlessness severity.ConclusionExternal LOC is associated with experiencing worse breathlessness and the identified LOC factors can be considered in future intervention studies aiming to reduce the suffering from breathlessness.

Lung cancer screening in India: Preparing for the future using smart tools & biomarkers to identify highest risk individuals

There is a growing burden of lung cancer cases in India, incidence projected to increase from 63,708 cases (2015) to 81,219 cases (2025). The increasing numbers are attributed to smoking (India currently has nearly 100 million adult smokers) and environmental pollution. Most patients present with advanced disease (80-85% are incurable), causing nearly 60,000 annual deaths from lung cancer. Early detection through lung cancer screening (LCS) can result in curative therapies for earlier stages of lung cancer and improved survival. Annual low-dose computerized tomography (LDCT) is the standard method for LCS. Usually, high-risk populations (age>50 yr and >20 pack-years of smoking) are considered for LCS, but even such focused screening may be challenging in resource-limited countries like India. However, developing a smart LCS programme with high yield may be possible by leveraging demographic and genomic data, use of smart tools, and judicious use of blood-based biomarkers. Developing this model over the next several years will facilitate a structured cancer screening programme for populations at the highest risk of lung cancer. In this paper, we discuss the demographics of lung cancer in India and its relation to smoking patterns. Further, we elaborate on the potential applications and challenges of bringing a smart approach to LCS in high-risk populations in India.

Tobacco Smoking in Early Adulthood and Labor Market Performance: The Cardiovascular Risk in Young Finns Study.

Tobacco smoking has been associated with reduced success in the labor market, potentially due to its negative impact on labor productivity, especially in physically demanding jobs, as it affects physical fitness and performance adversely. This prospective study used data from the Cardiovascular Risk in Young Finns Study survey, linked to register information on labor market outcomes and education attainment, to examine the association between tobacco smoking and long-term labor market outcomes (earnings and employment, N = 1953). Smoking levels were determined by cigarette pack-years in 2001, as reported in the survey, whereas annual earnings and employment status were tracked from 2001 to 2019. A one-unit increase in pack-year of smoking was associated with a 1.8% decrease in earnings (95% confidence interval [CI]: -2.6% to -0.9%) and a 0.5% reduction in years employed (95% CI: -0.6% to -0.3%). This association was pronounced among participants with lower education levels. The earnings difference was evident among younger cohorts, whereas a negative correlation with employment was observed most strongly in older cohorts among individuals with lower education. Our findings suggest that smoking had a negative effect on earnings among the younger generation, particularly among the less well-educated. The finding of greater impacts on years of employment among the older age group, particularly among groups with low education levels, is consistent with the delayed onset of most health impacts, which may particularly affect productivity in physically demanding jobs that are more common among people with less education. Adverse consequences of smoking include reduced earnings and labor market participation, particularly among less well-educated groups. Tobacco control advocates should draw attention to these consequences in arguing for effective measures to reduce smoking initiation and increase cessation in order to achieve socially optimal outcomes.

Factors Associated with Smoking Cessation of Participants in the National Lung Cancer Screening Program in Korea.

Smoking cessation interventions for participants in lung cancer screening are essential for increasing the effectiveness of screening to reduce lung cancer mortality. This study aimed to investigate the factors that lead to smoking cessation after lung cancer screening. The Korean National Lung Cancer Screening (KNLCS) Satisfaction Survey was conducted from 2021 to 2022 with 1,000 samples per year among participants in KNLCS targets 30 or more pack-year smokers. Factors associated with smoking cessation were analyzed based on the survey. Among 1,525 current smokers in the survey participants, 728 (47.7%) received screening result counseling from physician after screening and showed significantly higher smoking cessation rate than non-counselling participants [OR 2.17, 95% CI 1.27-3.70]. The participants who considered the counseling helpful were more likely to quit smoking [OR 3.53, 95% CI 2.00-6.22] and to reduce smoking amount [OR 2.05, 95% CI 1.54-2.71]. Similarly, those who received physicians' active recommendations to quit smoking were likely to quit smoking [OR 2.20, 95% CI 1.25-3.87] and to decrease smoking amount [OR 1.30, 95% CI 1.00-1.68]. In contrast, participants who had no abnormal findings from screening tended to have no significant change in smoking status despite the physicians' active recommendations to quit smoking. Physicians' active recommendations and effective counseling to quit smoking could be a key factor in increasing smoking cessation among lung cancer screening participants. Further research should be conducted to develop more effective strategies for smoking cessation to participants without abnormal findings in lung cancer screening.

Diverse clinical outcomes for the EGFR‑mutated and ALK‑rearranged advanced non‑squamous non‑small cell lung cancer.

EGFR and ALK are key driver mutations in non-small cell lung cancer (NSCLC). Tyrosine kinase inhibitors are recommended as the first-line treatment for advanced NSCLC with driving oncogenes because they have fewer side effects and provide better disease control than chemotherapy. The present retrospective analysis aimed to investigate how altered driver genes impact cancer outcomes and clinical presentation. A total of 628 patients with advanced-stage NSCLC and documented EGFR and ALK mutations were enrolled at Changhua Christian Hospital in Taiwan between August 2011 and January 2021. EGFR mutations were identified by PCR. ALK rearrangements were identified by immunostaining. Patients without EGFR or ALK mutations were labeled as wild-type (WT). EGFR mutation was detected in 446 (71.02%) patients, ALK rearrangement in 36 (5.73%) patients and WT in 146 (23.25%) patients. EGFR mutations resulted in higher frequency of lung, brain and multiple extrapulmonary metastases than ALK rearrangement. The ALK group exhibited the longest median overall survival (OS), followed by EGFR and WT groups (ALK: 51.60±13.32, EGFR: 24.03±1.22 and WT: 19.63±2.43 months, respectively; P=0.011). In patients with brain metastases, ALK group had a longer median OS than the EGFR group. Because there were few recruited patients with ALK rearrangement, the results were not significant. According to the results of Cox regression model analysis, driver mutations with EGFR and ALK, lower smoking pack-years, younger age, better performance status, no pleural metastasis and fewer extrapulmonary metastases were key prognostic factors. In conclusion, diverse clinical outcomes are driven by different driver mutations. EGFR mutation leads to more extrapulmonary metastases. Median OS was superior in ALK-rearranged NSCLC than EGFR-mutated NSCLC regardless of brain metastases.

Chemoradiation for human papillomavirus positive oropharyngeal cancer in smokers: A single-institutional experience.

To determine how smoking intensity impacts the prognosis of patients with human papillomavirus (HPV)-positive oropharyngeal cancer treated by chemoradiation. The medical records of 32 patients with histologically proven squamous cell carcinoma of the oropharynx and a prior smoking history were retrospectively reviewed. All patients were treated with intensity-modulated radiotherapy to a median dose of 70Gy (range 63 to 72Gy) with concurrent cisplatin. Seventeen patients (53%) had stage II disease; and 15 patients (47%) had stage III disease. Distribution of T-classification was: T1 8 (25%); T2 4 (13%); T3 10 (31%); and T4 10 (31%). Smoking history was categorized as follows: ≤10 pack-years (10 patients); 10-20 pack-years (6 patients); 20-30 pack-years (7 patients); >30 pack-years (9 patients). With a median follow-up of 40months (range, 6 to 121months), the 3-year overall survival for the entire population was 79%. Significant differences in 3-year overall survival (83% vs 54%, p=0.01), local-regional control (86% vs 62%, p<0.001), and progression-free survival (75% vs 52%, p=0.02) were observed when comparing patients with ≤30 pack-year versus those with >30 pack-year smoking histories. The deleterious effect of smoking seemed to be most impactful in those with heavy consumption (i.e., >30 pack-year history).

Smoking History and Nicotine Dependence Alter Sleep Features in Patients with Obstructive Sleep Apnea-Hypopnea Syndrome.

Introduction: There are many aspects in the relationship between smoking and sleep that have not been investigated thoroughly yet, especially in regards to obstructive sleep apnea-hypopnea syndrome (OSAHS). Methods: In this cross-sectional study, 2359 participants, who have visited the sleep clinic of our hospital during a 13-year period and were former or current smokers, were included. Their smoking history, measured in packyears of smoking, and their nicotine dependence, measured with the Fagerström scale, were correlated with various epidemiological and sleep-related variables. Results: Patients with respiratory, cardiovascular and metabolic comorbidities were older, more obese and presented a significantly greater history in packyears of smoking. Packyears were positively correlated with the Epworth sleepiness scale (ESS) (r = 0.06, p = 0.007), with %REM sleep time (r = 0.19, p = 0.042), apnea-hypopnea index (AHI) (r = 0.10, p < 0.001), oxygen desaturation index (ODI) (r = 0.10, p < 0.001), mean and maximum apnea duration (r = 0.10, p < 0.001 and r = 0.11, p < 0.001, respectively), while they were negatively correlated with mean and minimum SaO2 (r = -0.18, p < 0.001 and r = -0.13, p < 0.001, respectively). Furthermore, smoking history exhibited a significantly increasing trend with increasing OSA diagnosis and severity (p < 0.001). Patients with abnormal movements during sleep and those with restless sleep showed a significantly higher nicotine dependence, measured with the Fagerström scale, compared to those without abnormal movements or restless sleep (5.4 ± 2.8 vs. 4.7 ± 2.8, p = 0.002 and 5.1 ± 2.9 vs. 4.7 ± 2.7, p = 0.043). Conclusions: Smoking history in packyears probably affects OSAHS characteristics, while nicotine dependence seems to be related more with abnormal sleep behaviors.

Smoking, Genetic Susceptibility and Early Menopause: Unveiling Biological Mechanisms and Potential Therapy Targets.

To explore the association between smoking, genetic susceptibility and early menopause (EM) and clarify the potential mechanisms underlying this relationship. An observational and Transcriptome-wide association analysis (TWAS) study. UK Biobank and public summary statistics. 139 869 women with full baseline and menopause data, and no gynaecological surgery history. Adjusted modified Poisson regression models were developed to determine the smoking and genetic risk effects on EM. TWAS was used to identify gene expression between smoking and EM, with Mendelian randomisation (MR) to infer causality. Enrichment analysis explored regulatory networks of transcription factors, microRNAs and potential therapeutic targets. Small molecule drugs were predicted using drug-gene interaction analysis. EM prevalence and common gene expression patterns. Women with over 30 pack-years of smoking had about 1.5 times higher EM risk, with RRs of 1.39 (95%CI, 1.23-1.56), 1.45 (1.33-1.59) and 1.45 (1.36-1.55) in the low, intermediate and high genetic risk groups. TWAS identified hub genes such as IMMP2L, BMPR2 and HMGN1. MR confirmed daily cigarette consumption as a causal factor in early menopause. Several potential therapeutic targets (e.g., SP600125, INCB18424 and ruxolitinib) were identified. Smoking reduction significantly lowered the risk of EM. Hub genes and therapeutic targets identified provided new avenues for mitigating harmful effects of smoking.

Integrating genetic and clinical data to predict lung cancer in patients with chronic obstructive pulmonary disease

BackgroundChronic obstructive pulmonary disease (COPD) is closely linked to lung cancer (LC) development. The aim of this study is to identify the genetic and clinical risk factors for LC risk in COPD, according to which the prediction model for LC in COPD was constructed.MethodsThis is a case-control study in which patientis with COPD + LC as the case group, patientis with only COPD as the control group, and patientis with only LC as the second control group. A panel of clinical variables including demographic, environmental and lifestyle factors were collected. A total of 20 single nucleotide polymorphisms (SNPs) were genotyped. The univariate analysis, candidate gene study and multivariate analysis were applied to identify the independent risk factors, as well as the prediction model was constructed. The ROC analysis was used to evaluate the predictive ability of the model.ResultsA total of 503 patients were finally enrolled in this study, with 188 patients for COPD + LC group, 162 patients for COPD group and 153 patients for LC group. The univariate analysis of clincial data showed compared with the patients with COPD, the patients with COPD + LC tended to have significantly lower BMI, higher smoking pack-years, and higher prevalence of emphysema. The results of the candidate gene study showed the rs1489759 in HHIP and rs56113850 in CYP2A6 demonstrated significant differences between COPD and COPD + LC groups. By using multivariate logistic regression analysis, four variables including BMI, pack-years, emphysema and rs56113850 were identified as independent risk factors for LC in COPD and the prediction model integrating genetic and clinical data was constructed. The AUC of the prediction model for LC in COPD reached 0.712, and the AUC of the model for predicting LC in serious COPD reached up to 0.836.ConclusionThe rs56113850 (risk allele C) in CYP2A6, decrease in BMI, increase in pack-years and emphysema presence were independent risk factors for LC in COPD. Integrating genetic and clinical data for predicting LC in COPD demonstrated favorable predictive performance.

Comprehensive Mendelian Randomization Analysis of Smoking and Its Effects on Venous Thromboembolism.

An increasing number of Mendelian randomization (MR) studies have evaluated the causal link between smoking and venous thromboembolism (VTE). However, previous studies often rely on single genetic variants related to smoking quantity and exhibit various other shortcomings, making them prone to pleiotropy and potentially leading to imprecise causal estimates. Thus, the deeper causal mechanisms remain largely unexplored. This MR study reassessed the causal relationship between smoking and VTE, including its subtypes-deep vein thrombosis (DVT) and pulmonary embolism (PE). Data on VTE were sourced from the FinnGen consortium with nonoverlapping sample sizes. The smoking phenotypes analyzed included smoking initiation, lifetime smoking, the number of cigarettes smoked per day by both current and former smokers (CigDay), and total pack-years of smoking in adulthood. The primary analytical method was inverse-variance-weighted (IVW), supplemented by multiple verification methods to ensure robust results. Statistical rigor was ensured through LDtrait pruning and Steiger filtering for reverse causation, with comprehensive sensitivity analyses including RadialMR confirming the findings' robustness. After Bonferroni correction, this study demonstrates significant causal evidence linking lifetime smoking with the incidence of VTE (odds ratio [OR]IVW = 1.50, 95% confidence interval [CI] 1.21-1.85, p = 1.75 × 10-4) and PE (ORIVW = 1.69, 95% CI 1.25-2.28, p = 6.55 × 10-4), and suggestive evidence with DVT, consistent in direction with previous studies but showing considerable differences in effect sizes and significance. Additionally, CigDay (past and current) increases the risks of VTE and DVT, while no causal link was found between smoking initiation and VTE or its subtypes (p < 0.05), both directly contradicting previous conclusions. Furthermore, our study is the first to suggest a causal link between pack-years and an increased risk of VTE. This MR study employed rigorous statistical pruning of its instrumental variables, using the most comprehensive smoking phenotype to date. It successfully mitigated biases such as winner's curse, yielding causal effect results distinct from previous studies.

Incident Cardiometabolic Comorbidities in Smokers with/Without Chronic Obstructive Pulmonary Disease: A Long-Term Cohort Study.

Backgrounds: Despite the significant global health impact of cardiometabolic multimorbidity (CMM), our understanding of potential predictors associated with its development in smokers, remains limited. Objective: This study aimed to investigate whether a new COPD diagnosis and the rate of lung function decline serve as predictors for incident CMM (defined as having at least two of the following comorbidities: cerebro-cardiovascular diseases, hypertension, dyslipidemia, and diabetes mellitus) in smokers. Methods: An observational longitudinal analysis of prospectively collected data was conducted, including smokers without a previous COPD diagnosis and any cardiometabolic conditions. Sociodemographic and clinical data (body mass index, smoking history, respiratory symptoms, and hospital admissions) were collected at baseline. Lung function tests were performed at baseline and at the end of the follow-up period. The incidence of CMM, a new positive diagnosis of COPD, and the forced expiratory volume in 1 s (FEV1) annual rate of decline were prospectively registered. Adjusted Cox proportional hazard models were adopted to explore risk factors associated with the incidence of CMM. Results: From the 391 smokers included in the study, 207 (53%) were newly diagnosed with COPD, and 184 had a preserved spirometry at baseline (non-COPD group). After nearly a decade of follow-up, 34% (n = 133) of smokers developed CMM. This group was characterized by male predominance, older age, higher BMI and pack-years of smoking, lower post-FEV1, baseline COPD diagnosis, and a history of hospital admission. A positive diagnosis of COPD at baseline and a greater rate of lung function decline (ΔFEV1 ≥ 40 mL/year) were independent predictors for developing CMM. Conclusions: A new COPD diagnosis and an accelerated decline in lung function are significantly associated with the development of CMM in smokers.

The 2021 US Preventive Services Task Force lung cancer screening eligibility criteria disproportionately exclude younger Black patients with lung cancer.

The 2021 US Preventive Services Task Force (USPSTF) lung cancer screening guideline may continue to exclude many younger Black individuals who have not yet accumulated enough smoking pack-years to be eligible for screening. The objective of this study was to evaluate the proportions of Black and White patients with lung cancer, stratified by age at diagnosis, who would have been eligible for lung cancer screening. Incident lung cancer cases among Black and White individuals aged 50-80 years with a smoking history in the Southern Community Cohort Study (SCCS) were identified for analysis. The proportions of Black and White individuals, stratified by age at diagnosis, who would have qualified for screening under the 2013 and 2021 USPSTF guidelines were calculated. A total of 1856 individuals met inclusion criteria. Compared to the 2013 USPSTF guideline, the 2021 USPSTF guideline significantly increased the proportions of Black and White patients with lung cancer who would have qualified for screening in all age groups evaluated. However, under the 2021 USPSTF guideline, there remained a notable racial disparity in lung cancer screening eligibility, particularly among younger patients with lung cancer. Only 47.4% and 61.9% of Black patients aged 50-54 and 50-59 years, respectively, would have qualified for screening under the 2021 USPSTF guideline compared to 80.3% and 88.8% of White patients aged 50-54 and 50-59 years, respectively. With increasing age, the racial disparity in lung cancer screening eligibility between Black and White patients with lung cancer was reduced, and there were no longer any statistically significant differences in screening eligibility between Black and White patients with lung cancer aged 70-74 and 75-80 years. Of Black individuals aged 50-54 and 55-59 years who were ineligible for screening, 100% and 97.5% were ineligible because they had smoked fewer than 20 pack-years, respectively. This analysis of SCCS participants with lung cancer found that the 2021 USPSTF eligibility criteria disproportionately exclude many younger Black individuals with lung cancer, primarily because they have too few smoking pack-years.

Predictors of coronary atherosclerosis in middle-aged and older athletes: the MARC-2 study.

Exercise improves cardiovascular health, but high-volume high-intensity exercise is associated with increased coronary artery atherosclerosis and calcification (CAC). We aimed to identify predictors of CAC in athletes. We assessed the association of traditional and non-traditional cardiovascular risk factors with CAC using linear and logistic regression. 289 male athletes from the MARC-2 study were included, with a median age of 60 [Q1-3 56-66] years, lifelong weekly training load of 26 [17-35] MET-hours, BMI of 24.5 [22.9-26.6] kg/m2, systolic blood pressure of 139±18 mmHg, and reported 0.0 [0.0-8.0] smoking pack years. Thirty-one percent had a CAC score >100 and 13% >400. Among traditional cardiovascular risk factors, higher age, systolic blood pressure, smoking pack years, and family history of coronary artery disease independently predicted greater CAC scores, while body mass index, LDL cholesterol, and diabetes mellitus did not. Among non-traditional risk factors, higher training loads, serum phosphate, and lower adjusted energy intake and fat percentage of energy intake independently predicted greater CAC scores. The full model with all traditional and non-traditional risk factors had higher accuracy in predicting CAC>100 (ROC-AUC 0.76, 95%CI [0.70-0.82]) and CAC>400 (0.85 [0.77-0.92]) than traditional cardiovascular risk factors alone (0.72 [0.65-0.78], p=0.012, and 0.81 [0.74-0.90], p=0.038, respectively). Non-traditional risk factors, including training load, dietary patterns, and serum phosphate, were independently associated with CAC in aging male athletes. Prediction accuracy for CAC increased when including these variables in a prediction model with traditional risk factors.

Smoking status and edentulism among older Chinese: a cohort study.

The harmful impact of tobacco smoke on health is widely recognized, linking it to various diseases. However, the link between tobacco smoke and edentulism in China's population hasn't been fully investigated. This study aims to fill this gap by exploring smoking habits and the possible connection between tobacco smoke and edentulism in a nationally representative Chinese cohort. This study used data from the 2011 China Longitudinal Study of Health and Retirement (CHARLS) and included 17,705 participants aged 45years and older, and linked with follow-up data (2018). Smoking status (non-smoker, ex-smoker, smoker, pack-years of smoking, age at starting and ceasing smoking) was used as an independent variable, and edentulism was used as a dependent variable. Multivariable logistic regression analysis and curve fitting were used to evaluate the association between smoke status and edentulism. Subgroup analyses were then employed to examine the impact of subgroup factors on the link between smoking status and edentulism. A total of 13,720 people were included in the study, 2,029 of whom were edentulism patients. The association between smoking duration (OR = 1.038, 95%CI = 1.031, 1.045) /Age at quitting smoking (OR = 1.026, 95%CI = 1.013, 1.039)/Smoking pack years (OR = 1.005, 95%CI = 1.002, 1.007) and risk of edentulism was significant, while Age start smoking (OR = 1.003, 95%CI = 0.995, 1.012) and Cigarettes consumed per day (OR = 0.998, 95%CI = 0.991, 1.006) was not associated with risk of edentulism. Compared with non-smokers, current smoker had a higher risk of edentulism (OR 1.274, 95% CI = 1.108, 1.465). Additionally, our results also revealed that there was a nonlinear trend between Smoking duration/Cigarettes consumed per day/Age at quitting smoking/ Age at starting smoking/pack-years of smoking and edentulism (P > 0.05). The research found a significant link between smoking habits and edentulism in nationally representative Chinese population. This study in China found a complex link between tobacco use and tooth loss among middle-aged and elderly individuals, highlighting the need for personalized smoking cessation strategies to improve dental health in this population.

Plasma Proteomic Markers of Iron and Risk of Diabetes in a Cohort of African American and White American Current and Former Smokers.

Little information is available on iron with diabetes risk among African Americans, a population where both anemia and elevated ferritin are common. We tested whether plasma proteomic measurements of ferritin and transferrin were associated with increased diabetes risk in a cohort of current and former African American (NHB) and Non-Hispanic White (NHW) smokers. NHB and NHW participants from the COPDGene study who were free of diabetes (n = 4693) at baseline were followed for incident diabetes. The SomaScan was used to determine the relative amounts of natural log-transformed ferritin, transferrin, and hepcidin. During an average of 5.6 years of follow-up, diabetes incidence was 7.9%. Ferritin at follow-up was higher in NHB than NHW participants (p = <0.0001). Ferritin at follow-up was associated with increased diabetes risk (OR = 1.36, 95% CI = 1.08-1.70), while transferrin was associated with decreased risk (OR = 0.25, 95% CI = 0.08-0.77) controlling for age, sex, BMI, smoking pack-years, hepcidin, CRP, and Il-6. Race-specifically, increased risk associated with higher ferritin levels among NHB (OR = 1.56, 95% CI = 1.13-2.16) but not NHW (OR = 1.22, 95% CI = 0.89-1.68) participants. Sex-specifically, ferritin's relationship was similar among NHB men and women and NHW women (ORs ranging from 1.41-1.59); but not NHW men (OR = 0.98, 95% CI = 0.64-1.49). Similarly, transferrin ORs non-significantly ranged from 0.19-0.30 for NHB men and women and NHW women, but was significant for NHW men (OR = 0.07, 95% CI = 0.01-0.63). Higher body iron stores is associated with increased diabetes risk among both NHB and NHW people. Unsuspected elevated iron stores may increase diabetes risk in NHB patients and should be monitored.

Lung structure and longitudinal change in cardiac structure and function: the MESA COPD Study.

Lung structure and cardiac structure and function are associated cross-sectionally. The classic literature suggests relationships of airways disease to cor pulmonale and emphysema to reduced cardiac output (CO) but longitudinal data are lacking. The Multi-Ethnic Study of Atherosclerosis (MESA) COPD Study was a multicentre longitudinal COPD case-control study of participants 50-79 years with ≥10 pack-years smoking without clinical cardiovascular disease. Segmental airway wall area (WA) and percent emphysema were measured on computed tomography. Right and left ventricle parameters were assessed on cardiac magnetic resonance imaging (cMRI) in exams 6 years apart. Longitudinal and period cross-sectional associations were evaluated with mixed models adjusted for demographics, body size and smoking. The 187 participants with repeated cMRI were 67±7 years old; 42% had COPD; 22% currently smoked; and the race/ethnicity distribution was 54% White, 30% Black, 14% Hispanic and 3% Asian. Greater WA at enrolment was associated with longitudinal increase in right ventricular (RV) mass (3.5 (95% CI 1.1-5.9) g per 10 mm2 WA). Greater percent emphysema was associated with stably lower left ventricular (LV) end-diastolic volume (-7.8 (95% CI -10.3- -3.0) mL per 5% emphysema) and CO (-0.2 (95% CI -0.4- -0.1) L·min-1 per 5% emphysema). Cardiac associations varied by lung structure over 6 years in this multi-ethnic study. Greater WA at enrolment was associated with longitudinal increases in RV mass, whereas greater percent emphysema was associated with stable decrements in LV filling and CO.

Association between smoking status, toxicity and survival in the checkpoint inhibitor immunotherapy.

Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy by enhancing T-cell-mediated immune responses against tumors. However, their use can lead to immune-related adverse events (irAEs), impacting patient outcomes. This single-center, observational study investigates the relationship between immune-related adverse events (irAEs) and survival outcomes in 151 patients treated with ICIs, with or without chemotherapy, at the Department of Clinical Oncology and Chemotherapy in the Independent Public Hospital No. 4 in Lublin. Statistical analyses were performed using the log-rank test, and multivariable Cox proportional hazard model (p < 0.05). IrAEs were observed in 38% of patients, with the most common being thyroid dysfunction (11.9%) and dermal toxicity (6.6%). Individual toxicity groups presented similar median values of "pack-years", suggesting that smoking did not have a direct impact on the degree of toxicity. No relationship between the number of "pack-years" and the time of occurrence of toxicity symptoms and the number of toxicity sites was found. Smoking status did not have a moderating effect on the toxicity parameter in survival analysis (OS) and progression free survival analysis (PFS). Pack-years of smoking significantly impacted both OS (HR = 1.01, p = 0.014) and PFS (HR = 1.01, p = 0.011). The results suggested that smoking, measured in pack-years, had no appreciable effect on the amount of toxicity experienced by patients and no correlation between smoking status, irAEs and efficiency of the treatment was found. Despite results not reaching statistical significance, other potential mechanisms by which smoking may influence cancer treatment cannot be ruled out.

Prevalent findings on low-dose CT scan lung cancer screening: a French prospective pilot study.

Despite significant therapeutic advances, lung cancer remains the biggest killer among cancers. In France, there is no national screening program against lung cancer. Thus, in this perspective, the Foch Hospital decided to implement a pilot and clinical low-dose CT screening program to evaluate the efficiency of such screening. The purpose of this study was to describe the prevalent findings of this low-dose CT screening program. Participants were recruited in the screening program through general practitioners (GPs), pharmacists, and specialists from June 2023 to June 2024. The inclusion criteria included male or female participants aged 50 to 80 years, current smokers or former smokers who had quit less than 15 years prior, with a smoking history of over 20 pack-years. Chest CT scans were conducted at Foch Hospital using a low-dose CT protocol based on volume mode with a multi-slice scanner (≥60 slices) without contrast injection. In total, 477 participants were recruited in the CT scan screening, 235 (49%) were males with a median age of 60 years [56-67] and 35 smoke pack-years [29-44] and 242 females (51%) with a median age of 60 years [55-60] and 30 smoke pack-years [25-40]. Eight participants showed positive nodules on CT scan, as a 1.7% rate. 66.7% of diagnosed cancers were in early stages (0-I). It is feasible to implement structured lung cancer screening using low-dose CT in a real-world setting among the general population. This approach successfully identifies most early-stage cancers that could be treated curatively.

Impact of Smoking on MicroRNAs in Significant Coronary Artery Disease.

Given the importance of coronary artery disease (CAD) and the range of cardiovascular disease phenotypes in smokers, as well as the potential genetic and epigenetic factors, we were motivated to explore the impact of smoking on some selected microRNAs associated with significant CAD. A total of 60 individuals were selected in four groups including non-smoker without significant CAD (S-A-), non-smokers with significant CAD (S-A+), smokers without significant CAD (S+A-) and smokers with significant CAD (S+A+). Micro-RNA expression was investigated using real-time PCR. General linear model was used to calculate fold change (FC) considering SA- as the reference group. For mir-34a, down-regulation was observed in S+A- (FC =0.13, P =0.007) and S+A+ (FC =0.23, P =0.036) groups. For mir-126-3p, down-regulation was observed in S-A+ group (FC =0.05, P =0.024). For mir-199, up-regulation was observed for S+A- group (FC =9.38, P =0.007). The only significant interaction between pack-years of smoking and number of significantly narrowed vessels (≥75% stenosis) was for mir-199 which was in favor of down-regulation (P =0.006), while the main effects were in favor of up-regulation (P <0.05). Mir-34a expression may be affected by smoking, whereas mir-126-3p expression may be affected by atherosclerosis, the most common reason of CAD. The significant down-regulation of mir-199 for the interaction of smoking dose and severity of CAD was a notable finding showing the harmful consequence of this interaction. Further studies are needed for this micro-RNA.

Effect of Smoking Duration and Pack-Year History on Histological Subtypes of Lung Cancer

Background: Lung cancer is the leading cause of cancer-related mortality worldwide, with smoking as the principal risk factor. The histological subtypes of lung cancer, including adenocarcinoma, squamous cell carcinoma, and small cell carcinoma, vary according to smoking history and intensity. This study investigates the effect of smoking duration and pack-year history on the histological subtypes of lung cancer in Bangladesh. Methods: A cross-sectional study was conducted at the National Institute of Diseases of the Chest and Hospital (NIDCH) from July 2007 to June 2008. A total of 98 patients with confirmed primary lung cancer were included, comprising 81 smokers and 17 non-smokers. Results: Among the 98 patients, 45% had adenocarcinoma, 28.6% squamous cell carcinoma, 16.3% small cell carcinoma, 6.1% large cell carcinoma, and 3.1% other subtypes. Smokers exhibited a higher incidence of squamous cell carcinoma (33.3%) and small cell carcinoma (19.8%), while adenocarcinoma was more common in non-smokers (88.2%). Majority (94.1%) of the patients with lesions in the upper lobe was smokers compared to 56.7% of patients with lesions in the lower lobe (p &lt; 0.001) Ratio of upper and lower lobe tumour among smoker was roughly of 4:1. A significant association was found between smoking duration, pack-years, and the occurrence of squamous and small cell carcinoma (p &lt; 0.001). Conclusion: Smoking duration and pack-years have a significant impact on the histological subtypes of lung cancer. Squamous cell carcinoma and small cell carcinoma are more prevalent in smokers, while adenocarcinoma is more common in non-smokers.