Trends in the risk and burden of second primary malignancy among survivors of smoking-related cancers in the United States.

While there are a growing number of cancer survivors, this population is at increased risk of developing second primary malignancies (SPMs). We described the incidence, most common tumor sites, and trends in burden of SPM among survivors of the most commonly diagnosed smoking-related cancers. The current study was a population-based study of patients diagnosed with a primary malignancy from the top 10 smoking-related cancer sites between 2000 and 2014 from Surveillance, Epidemiology, and End Results data. SPM risks were quantified using standardized incidence ratios (SIRs) and excess absolute risks (EARs) per 10,000 person-years at risk (PYR). Trends in the burden of SPM were assessed using Joinpoint regression models. A cohort of 1,608,607 patients was identified, 119,980 (7.5%) of whom developed SPM (76% of the SPMs were smoking-related). The overall SIR of developing second primary malignancies was 1.51 (95% CI, 1.50-1.52) and the EAR was 73.3 cases per 10,000 PYR compared to the general population. Survivors of head and neck cancer had the highest risk of developing a SPM (SIR = 2.06) and urinary bladder cancer had the highest excess burden (EAR = 151.4 per 10,000 PYR). The excess burden of SPM for all smoking-related cancers decreased between 2000 and 2003 (annual percentage change [APC] = -13.7%; p = 0.007) but increased slightly between 2003 and 2014 (APC = 1.6%, p = 0.032). We show that 1-in-12 survivors of smoking-related cancers developed an SPM. With the significant increase in the burden of SPM from smoking-related cancers in the last decade, clinicians should be cognizant of long-term smoking-related cancer risks among these patients as part of their survivorship care plans.

Why making smoking cessation a priority for rare interstitial lung disease smokers?

This review aims to discuss the complex relationship between smoking and interstitial lung diseases (ILDs), emphasizing the significant morbidity and mortality associated with these conditions. While the etiology of ILDs remains multifactorial, cigarette smoking emerges as a prominent modifiable risk factor implicated in their pathogenesis and progression. This narrative review will provide insight into smoking-associated interstitial lung diseases and personalised approaches to smoking cessation. Epidemiological studies consistently link smoking to ILDs such as idiopathic pulmonary fibrosis (IPF), respiratory bronchiolitis-associated ILD (RB-ILD), and desquamative interstitial pneumonia (DIP), highlighting the urgent need for comprehensive tobacco cessation strategies. Despite the established benefits of smoking cessation, adherence to cessation programs remains challenging due to nicotine addiction, psychological factors, and social influences. The modest success rates of smoking cessation in ILD patients, emphasises the importance of tailored interventions and ongoing support is needed to overcome barriers and to improve outcomes of quitting smoking in this category of vulnerable patients.

Smoking-diseases correlation database: comprehensive analysis of the correlation between smoking and 422 diseases based on NHANES 2013-2018.

Background: Smoking is a risk factor for a wide range of diseases. Previous research has confirmed over 30 Smoking-Associated Diseases in diverse systems. There is limited research exploring the correlation among multiple diseases, with an absence of comprehensive investigations. Few studies concentrate on diseases exhibiting a negative correlation with smoking, wherein smokers demonstrate a lower prevalence. Objective: This study aimed to detect the correlation between smoking and other diseases using data from National Health and Nutrition Examination Surveys (NHANES) and construct a Smoking-Diseases Correlation Database (SDCD). The second aim is to obtain an extensive screening test for diseases that may be linked to smoking. Methods: 39,126 subjects' data from the NHANES 2013-2018 dataset were extracted. The baseline information, difference in blood routine and blood chemistry indicators between smokers and non-smokers, and diseases' correlation with smoking in four different models were analyzed by R. The data and statistics were aggregated into an online SDCD. Results: Our study reported 46 Smoking-Associated Diseases (SAD), including 29 Smoking Positively Associated Diseases (SPAD) and 17 Smoking Negatively Associated Diseases (SNAD). The SDCD of 422 diseases was constructed and can be accessed at https://chatgptmodel.shinyapps.io/sdcd/. Conclusion: Our findings revealed 46 SADs including 29 SPADs and 17 SNADs. We aggregated the statistics and developed online SDCD, advancing our understanding of the correlation between smoking and diseases.

How Risk Factors Affect Head and Neck Squamous Cell Carcinoma (HNSCC) Tumor Immune Microenvironment (TIME): Their Influence on Immune Escape Mechanisms and Immunotherapy Strategy.

Most head and neck squamous cell carcinomas (HNSCCs) are caused by lifestyle, such as cigarette smoking, or by viruses, such as human papillomavirus (HPV) and Epstein-Barr virus (EBV). HNSCC remains a clinical challenge, notwithstanding the improvements observed in the past years, involving surgery, radiotherapy, and chemotherapy. Recurrent/metastatic (R/M) disease represents an unmet clinical need. Immunotherapy has improved the prognosis of a small proportion of these patients, but most still do not benefit. In the last decade, several preclinical and clinical studies have explored the HNSCC tumor immune microenvironment (TIME), identifying important differences between smoking-associated and virus-associated HNSCCs. This review aims to present how different etiologies affect the HNSCC TIME, affecting immune escape mechanisms and sensitivity to immunotherapy.

Risk of second primary cancers in individuals diagnosed with index smoking- and non-smoking- related cancers.

PURPOSE: As the number of cancer survivors in the United States increases, quantifying the risks and burden of second primary cancers (SPCs) among cancer survivors will help develop long-term prevention and surveillance strategies. We describe the risk of developing a SPC among survivors of 10 cancer sites with the highest survival rates in the United States. METHODS: Adult patients diagnosed with an index smoking-related (urinary bladder, kidney and renal pelvis, uterine cervix, oral cavity and pharynx, and colon and rectum) and index non-smoking-related (prostate, thyroid, breast, corpus and uterus, and non-Hodgkin lymphoma) cancers were identified from Surveillance, Epidemiology, and End Results (2000-2015). SPC risks were quantified using standardized incidence ratios (SIRs) and excess absolute risks (EARs) per 10,000 person-years at risk (PYR). RESULTS: A cohort of 2,903,241 patients was identified and 259,685 (8.9%) developed SPC (7.6% of women and 10.3% of men). All index cancer sites (except prostate) were associated with a significant increase in SPC risk for women and men. Patients diagnosed with smoking-related index cancers (SIR range 1.20-2.16 for women and 1.12-1.91 for men) had a higher increased risk of SPC than patients with non-smoking-related index cancers (SIR range 1.08-1.39 for women and 1.23-1.38 for men) relative to the general population. CONCLUSION: We found that 1-in-11 cancer survivors developed a SPC. Given the increasing number of cancer survivors and the importance of SPC as a cause of cancer death, there is a need for increased screening for and prevention of SPC.

Association of Hemorrhoid Vascular Injuries with Cigarette Smoking-An Evaluation with Interesting Prospects.

Background Hemorrhoids are vascular structures in the anal canal which are seldom used to evaluate vascular diseases. Cigarette smoking is well-known to cause both arterial and venous vascular injuries. However, the impact of smoking on hemorrhoid vasculature is unknown. Objective Considering that vasculature in the hemorrhoids has the same anatomy and pathophysiology of vascular damage as other systemic vasculatures, we conducted this study to evaluate the relation between smoking and incidence of hemorrhoidal vascular injury. Design and Data Analysis Retrospective review of all the screening colonoscopies performed at our Department of Gastroenterology (predominantly serving urban minority population) over 3 years was conducted and patients with recorded smoking history were included in the study ( n = 242). Fisher's exact test with two-tailed p -value and odds ratio were used to evaluate for the association between smoking and incidence of hemorrhoids. Results We studied 242 subjects and found statistically significant association between smoking and hemorrhoids ( p < 0.05) with the risk of developing hemorrhoids among smokers being 2.4 times that of a nonsmoker. We further noted no significant difference in the incidence of hemorrhoidal vascular injuries between the past versus current smokers and male versus female smokers. Conclusion This is one of the first studies to establish an association between smoking and hemorrhoids. Our study shows that the hemorrhoidal vasculature is impacted by smoking similar to other vascular systems. This study sheds light on the possibility of evaluating hemorrhoids for clues of other systemic and gastrointestinal vascular damage. This correlation can add clinical value especially given the flexibility of assessing hemorrhoids as an outpatient in a cost effective and comfortable manner.

A cellular model to mimic exhaled cigarette smokeinduced lung microvascular endothelial cell injury and death.

Tobacco smoke exhaled from smokers is a key component of secondhand smoke, contributing to lung alveolar wall destruction seen in chronic lung diseases. Although mainstream and sidestream tobacco smoke are cyto-toxic to lung cells, it is unclear whether exhaled smoke induces lung cell injury or even death. We sought to establish an in vitro model to examine the effects of exhaled smoke on lung cells. Phosphate-buffered saline-conditioned cigarette smoke (CCS) derived from a blow-by system was used to mimic exhaled tobacco smoke exposure. Exposure of medium to CCS leads to dose-dependent increases in nicotine/cotinine levels. Scanning spectrophotometric analysis of the CCS-exposed medium reveals an absorption peak at 290 nm wavelength. The OD values at 290 nm are correlated with nicotine levels in the exposed medium, indicating that a simple measurement of OD at 290 nm can be used to monitor CCS exposure. Tobacco smoke contacts the microvascular endothelium located at lung alveoli, before it enters the blood stream. Hence, human lung microvascular endothelial cells (hMVEC) were exposed to CCS and assessed for cell injury and death. Exposure of hMVEC to CCS equivalent to burning 12-16 cigarettes leads to increased LDH release from the cells into the medium. This suggests that CCS can induce lung cell injury. CCS at a low level increases cell growth, whereas the high level of CCS decreases cell viability. In addition, CCS exposure induces cell detachment and morphological changes. Our results demonstrate that exposure of buffer-conditioned mainstream cigarette smoke leads to increased nicotine/cotinine levels and cell injury/death, which may contribute to the pathophysiology of passive smoking-associated lung diseases.