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Bronchiectasis-Chronic Obstructive Pulmonary Disease Overlap Syndrome (BCOS) is a complex pulmonary condition that merges bronchiectasis and chronic obstructive pulmonary disease (COPD), presenting unique clinical challenges. Patients with BCOS typically exhibit a range of symptoms from both conditions, including a chronic productive cough, reduced lung function, frequent exacerbations, and diminished exercise tolerance. The etiology of BCOS involves multiple factors such as genetic predisposition, respiratory infections, tobacco smoke, air pollutants, and other inflammatory mediators. Accurate diagnosis requires a comprehensive approach, incorporating pulmonary function tests to evaluate airflow limitation, radiographic imaging to identify structural lung abnormalities, and blood eosinophil counts to detect underlying inflammation. Treatment strategies are tailored to individual symptom profiles and severity, potentially including bronchodilators, inhaled corticosteroids, and pulmonary therapy to improve lung function and quality of life. Patients with BCOS are also at an increased risk for cardiovascular complications, such as stroke, ischemic heart disease, and cor pulmonale. Additionally, medications like beta-agonists and muscarinic antagonists used in COPD treatment can further affect cardiac risk by altering heart rate. This paper aims to provide a thorough understanding of BCOS, addressing its development, diagnosis, treatment, and associated cardiovascular complications, to aid healthcare providers in managing this multifaceted condition and improving patient outcomes. [ABSTRACT FROM AUTHOR]

Simple Summary: Patients presenting with cystic metastasis in the neck lymph nodes and no obvious primary tumor, neck cancer of unknown primary (NCUP), represent a very complex management challenge, especially today in the Human Papillomavirus (HPV) era. Given the increasing incidence of HPV-related oropharyngeal squamous cell carcinoma (OPSCC), further detection methods other than p16 IHC (immunohistochemistry) for HPV testing are crucial. An HPV-positive status can localize the tumor to the oropharynx, a common site for occult primaries. Furthermore, up to 15% of p16 protein-positive tumors are actually HPV-negative. Failure to perform additional HPV testing can have dangerous prognostic and therapeutic implications such as de-escalation strategies that hesitate in an undertreatment. The other important topic faced in this study is the role of smoking and p53 mutations, especially their significance in HPV-positive cancers and the role of extranodal extension (ENE) in HPV-positive patients. In this paper, biomolecular, diagnostic, prognostic and therapeutical aspects are critically analyzed to make a precise diagnosis and accurately estimate the prognosis of such patients. Background: The incidence of patients showing neck metastasis and no obvious primary tumor at the initial diagnostic evaluation or neck cancer of unknown primary (NCUP) is rising. It is estimated that a relevant part of these tumors arises in the tonsillar crypts or base of the tongue and are p16+-related. However, today, the detection rate of the primary tumor is suboptimal. Identifying the primary tumor and its biomolecular characterization is essential since it influences the treatment administered, possibly reducing radiation fields and providing de-escalation to primary surgical management. However, p16 IHC (immunohistochemistry) might not be sufficient to diagnose HPV-related OPSCC. The other subset of patients discussed are the HPV-positive patients who have a history of tobacco exposure and/or p53 mutations. Possible factors that could negatively influence the outcomes of these patients are investigated and discussed below. So, this paper aims to analyze the diagnostic, bio-molecular, clinico-radiological, morphological, prognostic and therapeutical aspects of p16-positive OPSCC, highlighting the possible bias that can occur during the diagnostic and prognostic process. Methods: A narrative review was conducted to investigate the biases in the diagnostic and therapeutic process of two groups of patients: those who are p16-positive but HPV-negative patients, and those who are p16-positive and HPV-positive with exposure to traditional risk factors and/or p53 mutations. The keywords used for the literature research included the following: NCUP, OPSCC, p16IHC, HPV testing, p16 positive HPV negative OPSCC, p16 positive HPV positive OPSCC, tonsillectomy, tobacco exposure, p53 mutations, cystic neck metastasis, extranodal extension (ENE), radiotherapy, de-escalation and neck neck dissection. Results: HPV-positive OPSCC has specific clinico-radiological features. Bilateral tonsillectomy should be considered for the identification of the primary tumor. P16 IHC alone is not sufficient for diagnosing HPV-related OPSCC; additional detection methods are required. The role of tobacco exposure and p53 mutations should be investigated especially in cases of HPV-positive tumors. Extranodal extension (ENE) must be taken into consideration in the prognostic staging of HPV-positive tumors. Surgical primary treatment involving neck dissection (ND) and bilateral tonsillectomy followed by adjuvant radiation may represent the most appropriate approach for N3 cases. Diagnosis, prognosis and therapeutical implications must be addressed considering clinical, biomolecular and morphological aspects. At least today, the numerous biases that are still present influencing the diagnostic and prognostic process do not permit considering de-escalation protocols. Conclusions: A precise and accurate diagnosis is required in order to adequately stage and manage p16+ OPSCC, particularly with neck metastasis. The role of tobacco exposure and/or p53 mutations must be considered not only in p16+ OPSCC but especially in HPV-positive OPSCC. Until a more accurate diagnosis is possible, ENE should be considered even in p16+HPV+ OPSCC. Primary surgery with unilateral ND and bilateral tonsillectomy might be the treatment of choice given the numerous diagnostic and prognostic pitfalls. Therefore, it is inappropriate and risky to propose de-escalation protocols in routine clinical practice due to the risk of undertreatment. [ABSTRACT FROM AUTHOR]

This narrative review aims specifically to explore the relationship between tobacco exposure and systemic sclerosis (SSc), idiopathic inflammatory myositis (IIM), and systemic lupus erythematosus (SLE). Relevant articles were obtained by searching key terms such as "tobacco," "smoking," "scleroderma," "myositis," "lupus," and "Sjögren's" in PubMed and Google Scholar databases. The selected articles ranged from the years 2010 to 2023. Inclusion criteria were based on the relevance and contribution to the field of study. Systemic sclerosis is a complex condition involving multiple immune cell lines that can be influenced by tobacco. However, the existing literature does not provide sufficient evidence to support an increased risk of SSc in smokers or the impact on treatment options. Cigarette smoking does increase the risk of skin ulcerations in SSc patients. In addition, cigarette smoking has been associated with IIM through genetic and molecular mechanisms. Smokers with dermatomyositis or polymyositis are at an elevated risk of atherosclerosis and interstitial lung disease. Similarly, smoking in patients with SLE increases the risk of organ damage, thrombosis, and disease severity compared with non-smokers. Smokers with SLE also have more difficulty in controlling disease flares compared with non-smokers. Tobacco exposure can lead to secondary complications in patients with IIM and SLE, although the course of treatment may not differ significantly. No definitive conclusions can be drawn to the clear relationship between tobacco smoking and Sjögren's's syndrome. [ABSTRACT FROM AUTHOR]

Background/purpose: We suspected that there might be an interaction between sugar intake and tobacco exposure on the risk of dental caries. The study aimed to investigate the associations of sugar intake or tobacco exposure with the risk of dental caries. Materials and methods: This cross-sectional study obtained data of 18804 participants from National Health and Nutrition Examination Survey (NHANES) between 2011 and 2018. Weighted univariable and multivariable logistic regression models were applied to explore the associations of total sugar intake or tobacco exposure with the risk of dental caries. The relative excess risk of interaction (RERI), attributable proportion of interaction (API), and synergy index (SI) evaluated the interaction between total sugar intake and tobacco exposure on the risk of dental caries. The effect size of odds ratio (OR), and 95% confidence interval (CI) was inputted. Results: The OR of dental caries in adults with cotinine >10 ng/mL was 1.59 (95%CI: 1.38–1.82). The increased risk of dental caries was found in people with total sugar >19.5%E compared to those with total sugar ≤19.5%E (OR = 1.55, 95%CI: 1.34–1.78). Compared to people with cotinine ≤10 ng/mL and total sugar ≤19.5%E, adults with cotinine >10 ng/mL and total sugar >19.5%E were correlated with elevated risk of dental caries (OR = 2.76, 95%CI: 2.29–3.33). The interaction indicators RERI was 0.980 (95%CI: 0.413–1.547), API was 0.355 (95%CI: 0.192–0.517), and SI was 2.250 (95%CI: 1.344–3.767). Conclusion: There might be interaction between sugar intake and tobacco exposure on the occurrence of dental caries in adults.

We suspected that there might be an interaction between sugar intake and tobacco exposure on the risk of dental caries. The study aimed to investigate the associations of sugar intake or tobacco exposure with the risk of dental caries. This cross-sectional study obtained data of 18804 participants from National Health and Nutrition Examination Survey (NHANES) between 2011 and 2018. Weighted univariable and multivariable logistic regression models were applied to explore the associations of total sugar intake or tobacco exposure with the risk of dental caries. The relative excess risk of interaction (RERI), attributable proportion of interaction (API), and synergy index (SI) evaluated the interaction between total sugar intake and tobacco exposure on the risk of dental caries. The effect size of odds ratio (OR), and 95% confidence interval (CI) was inputted. The OR of dental caries in adults with cotinine >10 ng/mL was 1.59 (95%CI: 1.38–1.82). The increased risk of dental caries was found in people with total sugar >19.5%E compared to those with total sugar ≤19.5%E (OR = 1.55, 95%CI: 1.34–1.78). Compared to people with cotinine ≤10 ng/mL and total sugar ≤19.5%E, adults with cotinine >10 ng/mL and total sugar >19.5%E were correlated with elevated risk of dental caries (OR = 2.76, 95%CI: 2.29–3.33). The interaction indicators RERI was 0.980 (95%CI: 0.413–1.547), API was 0.355 (95%CI: 0.192–0.517), and SI was 2.250 (95%CI: 1.344–3.767). There might be interaction between sugar intake and tobacco exposure on the occurrence of dental caries in adults. [ABSTRACT FROM AUTHOR]

BackgroundGallstones represent a prevalent health issue globally, resulting in significant annual healthcare costs. While tobacco exposure is recognized for its association with numerous diseases, its correlation with gallstones remains contentious. Serum cotinine, a metabolite of nicotine, serves as a widely utilized indicator for assessing tobacco exposure. Crucially, no research has yet examined the association between serum cotinine levels and the gallstones.MethodsThis study is designed as a cross-sectional analysis, utilizing data from the NHANES public database. The relationship between serum cotinine levels and gallstones was analyzed using multinomial logistic regression models and smooth curve fitting. Subgroup analyses and interaction tests were performed to examine the potential contributions of different populations and covariates to the findings.ResultsA total of 5,856 participants were included in this study. After adjusting for relevant covariates, the multiple logistic regression model results indicated that for each unit increase in serum cotinine concentration above 0.29 ng/mL, there was a 29% increase in the prevalence of gallstones. Furthermore, smooth curve fitting analysis revealed a positive correlation between these variables. These findings underscore the impact of tobacco exposure on gallstone prevalence.ConclusionThis study demonstrates a positive correlation between tobacco exposure, as measured by serum cotinine levels, and the prevalence of gallstones, thus adding to the body of existing research on this relationship.

Background: Tobacco exposure during pregnancy is associated with several adverse outcomes in infants. We investigated the association between tobacco exposure during pregnancy (both active and second-hand) and various infections in infants up to 1 year. Methods: This prospective cohort study used a fixed dataset (jecs-an-20180131) from the Japan Environment and Children’s Study of registered births in Japan during 2011–2014 that included 104,065 fetal records from enrolled pregnant women. Based on the participants’ responses to the questionnaire on smoking status, mothers were first divided into “never smoked,” “quit smoking,” and “current smoker” groups and then into “no second-hand smoking (SHS)” and “SHS” groups. Infectious diseases included central nervous system infection, otitis media (OM), upper respiratory tract infection (URTI), lower respiratory tract infection (LRTI), gastroenteritis (GI), and urinary tract infection. Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were calculated using logistic regression analysis and adjusted for maternal, socioeconomic, and postnatal confounding factors. Results: Among the 73,205 newborns enrolled, multivariable analysis revealed that the aOR of LRTI and GI was 1.20 (95% CI, 1.07–1.33) and 1.18 (95% CI, 1.04–1.35), respectively, for the “current smoker with/without SHS” group compared with the “never smoked without SHS” group. “Quit smoking without SHS” was not associated with the risk of LRTI. SHS was associated with an increased risk of OM, URTI, LRTI, and GI, especially with LRTI and GI. Conclusion: Exposure to tobacco smoke during pregnancy was associated with an increased risk of OM, URTI, LRTI, and GI in infants during their first year of life.

ObjectivesPast research has not examined secondhand and thirdhand smoke (THS) exposure in children of cigar smokers. We examined hand nicotine and cotinine levels in children of cigar smokers to explore the contribution of cigar smoke to tobacco smoke exposure (TSE).MethodsParticipants were children (N = 24; mean (SD) age = 6.5 (3.6) years) whose parents smoked cigars only or poly-used cigars and/or cigarettes. Primary outcomes were hand nicotine and urinary cotinine levels.ResultsAll children had detectable hand nicotine (range: 7.6-312.5ng/wipe) and cotinine (range: 0.3-100.3ng/ml). Positive correlations were found between hand nicotine and cotinine (r = 0.693, p = .001), hand nicotine and parents who also smoked cigarettes (r = 0.407, p = .048), and hand nicotine and number of smokers around the child (r = 0.436, p = .03). Hand nicotine (r = -0.464, p = .02), but not cotinine (r = -0.266, p = .26), was negatively correlated with child age. Multiple regression results indicated a positive association between hand nicotine and cotinine (p = .002; semi-partial r2 = 0.415), irrespective of child age.ConclusionsThe significant association of hand nicotine with urinary cotinine suggests that THS pollution should be assessed in evaluating children's overall TSE to cigars and other tobacco products, and hand nicotine may be a proxy for overall TSE. Younger children may have increased THS pollutant uptake.

Introduction Direct and indirect smoking exposure is highly related to mental health in children. This study aimed to identify the association between exposure to smoking or secondhand smoke (SHS) and attention deficit hyperactivity disorder (ADHD). Methods We used data from the Korean National Health and Nutrition Examination Survey (KNHANES) from 2007 to 2019, including variables such as diagnosed ADHD, smoking status, SHS, and urine cotinine levels among children and adolescents. We estimated the risk of ADHD according to smoking or SHS exposure in various exposure groups using adjusted logistic or linear regression models. Results Among 16434 participants, 133 children were diagnosed with ADHD (0.8%). Of these, 58 (43.6%) were aged

Abstract Background Alcohol consumption and tobacco exposure during pregnancy are hazardous behaviours which are increasing significantly in low and middle-income countries, including sub-Saharan Africa. However, they have received little attention in Nigeria’s maternal health research and services. The prevalence, pattern and predictors of alcohol consumption and tobacco exposure among pregnant women in Ibadan, Nigeria, were investigated. Methods This is a part of a prospective cohort study among pregnant women in Ibadan, Nigeria (Ibadan Pregnancy Cohort Study (IbPCS), which investigated the associations between maternal obesity, lifestyle characteristics and perinatal outcomes in Ibadan. Alcohol consumption and tobacco exposure of 1745 pregnant women were assessed during enrollment by self-reports using an interviewer-administered questionnaire. Bivariate and multiple logistic regression analyses examined the associations at a 5% level of statistical significance. Results The prevalence of pre-pregnancy alcohol consumption and alcohol consumption during pregnancy were 551 (31.7%) and 222 (12.7%), respectively, i.e. (one in every eight pregnancies is exposed to alcohol). Palm wine (52%) and beer (12%) were the most common alcohol consumed among pregnant women. The predictors of alcohol consumption during were pre-pregnancy alcohol use [AOR = 10.72, 95% CI: 6.88–16.70) and religion i.e. Muslims were less likely to consume alcohol during pregnancy compared to Christians: [AOR = 0.60, 95% CI: 0.40–0.92). The prevalence of tobacco exposure in the index pregnancy was 64 (3.7%), i.e. one in every 27 pregnancies is exposed to tobacco. In contrast, cigarette smoking, second-hand smoke and smokeless tobacco were 0.4, 1.7 and 1.8%, respectively. Pre-pregnancy cigarette smoking was reported by 33(1.9%) and was the most significant predictor [AOR = 12.95; 95% CI: 4.93, 34.03) of tobacco exposure during pregnancy in our study population. Conclusions Alcohol consumption and tobacco exposure are not uncommon and have been an ongoing but neglected threat to maternal and child health in Nigeria. Alcohol and tobacco control policy and programmes to prevent the use among pregnant and reproductive-age women in Nigeria should be implemented primarily during antenatal care.

AimTo assess the individual effects of overweight/obesity and tobacco exposure, and their combined effects on hypertension in children.MethodsThis cross-sectional study included 6,339 children aged 6–17 years from National Health and Nutrition Examination Surveys 1999–2018. Participants’ height, weight and blood pressure (BP) were measured by trained technicians. Hypertension was defined as: mean systolic BP (SBP) and/or diastolic BP (DBP) ≥ 90th percentile for sex, age, and height (for children aged 1–13 years), and SBP ≥120 mmHg and/or a DBP ≥80 mmHg (for adolescents aged 13–17 years); or self-reported having been diagnosed with hypertension or taking antihypertensive medication. Gender- and age-specific body mass index (BMI) cut-points were used to define overweight/obesity: “overweight” was defined as a BMI > 1 standard deviation (SD); “obesity” was defined as BMI > 2SD; and “thinness” was defined as BMI 0.05 µg/L or reporting the presence of at least one smoker in the household. Weighted univariate and multivariate logistic regression models were used to assess overweight/obesity and tobacco exposure with the odds of hypertension, and the combined effects of overweight/ obesity and tobacco exposure on hypertension, followed by strata-specific analyses. Odds ratios (OR) with 95% confidence intervals (CI) were calculated.ResultsThe prevalence of overweight/obesity and tobacco exposure was significantly higher in the hypertension group than in the non-hypertension group. Overweight/obesity (OR = 1.67, 95%CI: 1.26–2.21/ OR = 2.38, 95%CI: 1.67–3.39) and tobacco exposure (OR = 1.58, 95%CI: 1.16–2.14) were associated with a higher odd of hypertension in children, respectively. Additionally, we also observed the combined effect between overweight (OR = 3.05, 95%CI: 1.96–4.75)/obesity (OR = 3.68, 95%CI: 2.24–6.03) and tobacco exposure were related to hypertension odds in children, with a significant effect in different populations.ConclusionThere may exist joint effect of overweight/obesity and tobacco exposure on the odds of hypertension in American children. These findings offer an insight that early weight control and reduction of tobacco exposure may be important to reduce odds of hypertension in children.

This study aimed to explore the combined effects of serum vitamin-D level and tobacco exposure on the risk of overweight and obesity in children. This cross-sectional study analysed the data of 11 636 children aged 2-17 years from the National Health and Nutrition Examination Surveys database between 2007 and 2018. Univariable and multivariate weighted logistic regression models were used to analyse the associations of serum vitamin-D or cotinine levels with overweight and obesity in children as well as the combined effects of serum vitamin-D and cotinine on the risk of overweight and obesity in children. Subgroup analysis was performed in terms of gender, age, race and household smokers. OR with corresponding 95 % CI was presented. The elevated risk of overweight and obesity in children was found in those with serum vitamin-D < 20 ng/ml (OR = 1·44, 95 % CI: 1·29, 1·61). Also, the odds of overweight and obesity in children was 1·14 (OR = 1·14, 95 % CI: 1·01, 1·29) in children with cotinine ≥ 0·05 ng/ml. Relative to participants with serum vitamin-D ≥ 20 ng/ml and cotinine < 0·05 ng/ml, increased risk of overweight and obesity was identified in those with serum vitamin-D < 20 ng/ml and cotinine < 0·05 ng/ml (OR = 1·45, 95 % CI: 1·26, 1·68) and serum vitamin-D < 20 ng/ml and cotinine ≥ 0·05 ng/ml (OR = 1·62, 95 % CI: 1·38, 1·91). Serum vitamin-D and cotinine exposure had combined effects on the risk of overweight and obesity in children.

Marjo Karvonen,1,2 Antti Saari,1,2 Reijo Sund,1 Ulla Sankilampi1,2 1School of Medicine, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland; 2Department of Pediatrics, Kuopio University Hospital, Kuopio, FinlandCorrespondence: Marjo Karvonen Email marjo.karvonen@kuh.fiBackground: Maternal smoking during pregnancy causes fetal growth retardation. Thereafter, it has been associated with excessive childhood weight gain and decreased linear growth in the offspring. However, it is not known whether head circumference (HC), the surrogate of brain size in childhood, is altered after intrauterine tobacco exposure. We assessed the association of maternal smoking during pregnancy with offspring HC growth up to age 6 years in comparison with length/height growth and weight gain.Methods: We combined data from Medical Birth Register and longitudinal growth data from primary care of 43,632 children (born 2004– 2017). Linear mixed effects models were used for modeling, adjusting for potential perinatal and socioeconomic confounders.Results: At birth, maternal smoking during pregnancy was associated with a mean deficit of 0.19 standard deviation score (SDS) (95% CI: − 0.25, − 0.12) in HC, − 0.38 SDS (95% CI: − 0.43, − 0.32) in length, and − 0.08 SDS (95% CI:− 0.14, − 0.02) in weight-for-length. HC in smokers’ children failed to catch up to that of non-smokers’ children. Height of smokers’ infants reached that of non-smokers’ infants by 12 months but declined thereafter. Weight-for-height of smokers’ infants exceeded the level of non-smokers’ infants at 3 months and remained significantly elevated thereafter. HC in the offspring of mothers who quit smoking in the first trimester was not deficient, but their weight-for-height was elevated.Conclusion: HC of smokers’ children is still deficient at age 6 years. Since most of the head growth occurs during the first 2 years of life, the defect may be permanent. In smokers’ children, weight gain was excessive up to 6 years and height was deficient at 6 years consistent with previous literature. Efforts should be made to encourage pregnant women to quit smoking in the beginning of the pregnancy.Keywords: maternal smoking, tobacco exposure, child growth, head circumference, weight, height

Objective: To investigate the possible subgroups of patients with Cluster Headache (CH) by using K-means cluster analysis. Methods: A total of 209 individuals (mean (SD) age: 39.8 (11.3) years), diagnosed with CH by headache experts, participated in this cross-sectional multi-center study. All patients completed a semi-structured survey either face to face, preferably, or through phone interviews with a physician. The survey was composed of questions that addressed sociodemographic characteristics as well as detailed clinical features and treatment experiences. Results: Cluster analysis revealed two subgroups. Cluster one patients (n = 81) had younger age at diagnosis (31.04 (9.68) vs. 35.05 (11.02) years; p = 0.009), a higher number of autonomic symptoms (3.28 (1.16) vs. 1.99(0.95); p < 0.001), and showed a better response to triptans (50.00% vs. 28.00; p < 0.001) during attacks, compared with the cluster two subgroup (n = 122). Cluster two patients had higher rates of current smoking (76.0 vs. 33.0%; p=0.002), higher rates of smoking at diagnosis (78.0 vs. 32.0%; p=0.006), higher rates of parental smoking/tobacco exposure during childhood (72.0 vs. 33.0%; p = 0.010), longer duration of attacks with (44.21 (34.44) min. vs. 34.51 (24.97) min; p=0.005) and without (97.50 (63.58) min. vs. (83.95 (49.07) min; p = 0.035) treatment and higher rates of emergency department visits in the last year (81.0 vs. 26.0%; p < 0.001). Conclusions: Cluster one and cluster two patients had different phenotypic features, possibly indicating different underlying genetic mechanisms. The cluster 1 phenotype may suggest a genetic or biology-based etiology, whereas the cluster two phenotype may be related to epigenetic mechanisms. Toxic exposure to cigarettes, either personally or secondarily, seems to be an important factor in the cluster two subgroup, inducing drug resistance and longer attacks. We need more studies to elaborate the causal relationship and the missing links of neurobiological pathways of cigarette smoking regarding the identified distinct phenotypic classes of patients with CH. [ABSTRACT FROM AUTHOR]

ObjectiveTo investigate the possible subgroups of patients with Cluster Headache (CH) by using K-means cluster analysis.MethodsA total of 209 individuals (mean (SD) age: 39.8 (11.3) years), diagnosed with CH by headache experts, participated in this cross-sectional multi-center study. All patients completed a semi-structured survey either face to face, preferably, or through phone interviews with a physician. The survey was composed of questions that addressed sociodemographic characteristics as well as detailed clinical features and treatment experiences.ResultsCluster analysis revealed two subgroups. Cluster one patients (n = 81) had younger age at diagnosis (31.04 (9.68) vs. 35.05 (11.02) years; p = 0.009), a higher number of autonomic symptoms (3.28 (1.16) vs. 1.99(0.95); p < 0.001), and showed a better response to triptans (50.00% vs. 28.00; p < 0.001) during attacks, compared with the cluster two subgroup (n = 122). Cluster two patients had higher rates of current smoking (76.0 vs. 33.0%; p=0.002), higher rates of smoking at diagnosis (78.0 vs. 32.0%; p=0.006), higher rates of parental smoking/tobacco exposure during childhood (72.0 vs. 33.0%; p = 0.010), longer duration of attacks with (44.21 (34.44) min. vs. 34.51 (24.97) min; p=0.005) and without (97.50 (63.58) min. vs. (83.95 (49.07) min; p = 0.035) treatment and higher rates of emergency department visits in the last year (81.0 vs. 26.0%; p< 0.001).ConclusionsCluster one and cluster two patients had different phenotypic features, possibly indicating different underlying genetic mechanisms. The cluster 1 phenotype may suggest a genetic or biology-based etiology, whereas the cluster two phenotype may be related to epigenetic mechanisms. Toxic exposure to cigarettes, either personally or secondarily, seems to be an important factor in the cluster two subgroup, inducing drug resistance and longer attacks. We need more studies to elaborate the causal relationship and the missing links of neurobiological pathways of cigarette smoking regarding the identified distinct phenotypic classes of patients with CH.

Abstract Background Tobacco exposure (TE) is the major contributor for CVD mortality, but few published studies on CVD mortality attributable to TE have analyzed the potential reasons underlying long-term trends in China. Our studysought to find the potential reasons and compared CVD mortality attributable to TE in China, Japan, the United States of America (USA), and the world between 1990 and 2017. Methods The mortality data in China, Japan, the USA, and the world were obtained from Global Burden of Disease Study 2017(GBD 2017). Joinpoint regression was used to assess the trend magnitude and directions over time for CVD mortality, while the age-period-cohort method was used to analyzethe temporal trends of CVD mortality according to age, period, and cohort. Results A significant downward trend was found in the age-standardised mortality rate (ASMR) of CVD attributable to smoking in four regions. China had the smallest decline and the Chinese ASMR became the highest in 2017. All the annual net drifts in the four regions were negative and the local drifts were below zero. The longitudinal age curves of CVD mortality attributable to smoking increased in four regions,with China having the largest increase. The period or cohort RRs indicated a decline, and China had the smallest decline. The researchers further analyzed the IHD and stroke trends, finding that the morality and period or cohort RR of IHD in China was always at a high level. Conclusions CVD mortality attributable to TE declined in four regions, and was highest in China. The proportion of IHD mortality attributable to TE was similar to stroke, which significantly changed the traditional cognition of CVD composition, but the control measure was not sufficient for IHD in China.

The big percentage of lung adenocarcinomas (LUAD) arising in lifetime nonsmokers and the low sensitivities of known major tobacco biomarkers urgent the identification of real molecular signatures for corresponding personalized treatment. Moreover, cancer is presumed to have a symptomatology strongly dependent on modules of functionally-related genes rather than on a unique important gene. Our aims, therefore, are to identify signature genes by optimizing the tobacco exposure pattern (TEP) classification model and to uncover their interaction relationships at different molecular levels. A new method, TTZ, is proposed to extract features as input variables to TEP classification model. Based on the Z-curve method, TTZ is able to extract features not only from mutation frequencies but also from sequencing information of insertions and deletions. Two independent LUAD datasets, The Cancer Genome Atlas (TCGA) and Broad data, are downloaded to train and test the TEP classification model. Thirty-four genes are identified as tobacco related mutational signature genes with the accuracies of 93.55% and 92.65% for train and validation data, respectively. The inference of genetic and protein-protein interaction (PPI) networks uncover that LAMA1, EGFR, KRAS and TNN are the most connected core genes. Six signature genes are proved significantly involved in the cilium damage pathway, which is considered as one of the root causes of lung cancer. The identified signature genes may serve as potential drug targets for the precision medicine of LUAD. Most importantly, the TTZ feature extracting method can be easily extended to other disease or cancer related mutational signature identification issues.

Context: In India, despite implementation of the strategies under National Tobacco Control Programme [NTCP], women are easily exposed to tobacco consumption that is smokeless (SLT) and smoking tobacco along with second-hand smoke [SHS], making them highly susceptible to tobacco hazards. Aims: This study aimed to assess the exposure of women to tobacco use and SHS at home and to elicit predictors of tobacco exposure in a rural community of West Bengal. Methodology: A community based, cross-sectional study was conducted among 176 women aged 18 years and above. Data was collected by cluster sampling technique (16*11) using predesigned pretested structured schedule. Tobacco exposure was measured using a composite score including tobacco consumption and SHS at home. Results: Tobacco use (SLT and smoking tobacco) was significantly associated with educational attainment [AOR = 2.12], occupation [AOR = 2.13] and knowledge [AOR = 1.22]. There was significant association between SHS at home with knowledge [AOR = 1.16] and attitude of the study subjects. [AOR = 1.93]. Overall tobacco exposure (SLT, smoking tobacco, and SHS), was found to be 79.5%. Significant association was found between high tobacco exposure with age group [AOR = 3.82], educational attainment [AOR = 1.74] and knowledge regarding hazards of tobacco [AOR = 1.31]. Conclusion: Prevalence of SLT use as well as exposure of women to SHS at home is unexpectedly high in the study population. Women specific information and education campaigns focusing on tobacco hazards (both tobacco use and SHS) through existing primary health care infrastructure should be strategized under NTCP.

Background: Gallstones represent a prevalent health issue globally, resulting in significant annual healthcare costs. While tobacco exposure is recognized for its association with numerous diseases, its correlation with gallstones remains contentious. Serum cotinine, a metabolite of nicotine, serves as a widely utilized indicator for assessing tobacco exposure. Crucially, no research has yet examined the association between serum cotinine levels and the gallstones., Methods: This study is designed as a cross-sectional analysis, utilizing data from the NHANES public database. The relationship between serum cotinine levels and gallstones was analyzed using multinomial logistic regression models and smooth curve fitting. Subgroup analyses and interaction tests were performed to examine the potential contributions of different populations and covariates to the findings., Results: A total of 5,856 participants were included in this study. After adjusting for relevant covariates, the multiple logistic regression model results indicated that for each unit increase in serum cotinine concentration above 0.29 ng/mL, there was a 29% increase in the prevalence of gallstones. Furthermore, smooth curve fitting analysis revealed a positive correlation between these variables. These findings underscore the impact of tobacco exposure on gallstone prevalence., Conclusion: This study demonstrates a positive correlation between tobacco exposure, as measured by serum cotinine levels, and the prevalence of gallstones, thus adding to the body of existing research on this relationship., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Liu, Zhang, Wang, Faisal, He, Tai and Lin.)

Although different trajectories in lung function decline have been identified in patients with COPD associated to tobacco exposure (TE-COPD), genetic, environmental, and infectious factors affecting lung function throughout life have not been fully elucidated in patients with COPD associated to biomass (BE-COPD). In this review, we present current epidemiological findings and notable advances in the natural history of lung decline in BE-COPD, as well as conditions modeling the FEV1 trajectory, such as health insults, during the first years of childhood. Evidence shows that women exposed to biomass smoke reach adult life with a lower FEV1 than expected. However, in contrast to the “horse racing effect” predicting an excessive lung-function decline in forthcoming years, as observed in smokers, this decline is slower in non-smokers, and no rapid decliners are observed. Accordingly, BE-COPD might be considered another phenotype of COPD based on assessments of lung function decline. Likewise, other functional and clinical aspects described in this review suggest that this condition might be similar to TE-COPD. More research is needed to fully characterize this subgroup of variants of COPD.

Background and aimsPrenatal exposure to maternal cigarette smoking (PEMCS) is associated with a higher probability of substance use in adolescence. We explore if externalizing behavior mediates this relationship, while controlling for a number of potential covariates of this mediation process.MethodsWe used data obtained in two geographically distinct community samples of adolescents. The first (cross-sectional) sample consisted of 996 adolescents (12-18 years of age) recruited from the Saguenay Youth Study (SYS) in Canada (47% with PEMCS). The second (longitudinal) sample consisted of 1141 adolescents (49% with PEMCS) from the Northern Finland Birth Cohort (NFBC1986). In both samples, externalizing behavior and substance use were assessed during adolescence. In the NFBC1986 cohort, externalizing behavior was also assessed in childhood.ResultsIn both populations, PEMCS is associated with a higher likelihood of adolescent drug experimentation. In the NFBC1986 cohort, exposed (versus non-exposed) adolescents experiment with an extra 1.27 [B = 0.24, 95% confidence intervals (CI) = 0.15, 0.33 P

Abstract Background Primary mucosal melanoma (MM) is a rare subtype of melanoma that arises from melanocytes in the mucosa. MM has not been well profiled for mutations and its etiology is not well understood, rendering current treatment strategies unsuccessful. Hence, we investigated mutational landscape for MM to understand its etiology and to clarify mutations that are potentially relevant for MM treatment. Methods Forty one MM and 48 cutaneous melanoma (CM) tissues were profiled for mutations using targeted deep next-generation sequencing (NGS) for 89 cancer-related genes. A total of 997 mutations within exons were analyzed for their mutational spectrum and prevalence of mutation, and 685 non-synonymous variants were investigated to identify mutations in individual genes and pathways. PD-L1 expression from 21 MM and 18 CM were assessed by immunohistochemistry. Results Mutational spectrum analysis revealed a lower frequency of UV-induced DNA damage in MM than in CM (p = 0.001), while tobacco exposure was indicated as a potential etiologic factor for MM. In accordance with low UV damage signatures, MM demonstrated an overall lower number of mutations compared to CM (6.5 mutations/Mb vs 14.8 mutations/Mb, p = 0.001), and less PD-L1 expression (p = 0.003). Compared to CM, which showed frequent mutations in known driver genes (BRAF 50.0%, NRAS 29.2%), MM displayed lower mutation frequencies (BRAF; 12.2%, p

Osman Savran,1 Charlotte Suppli Ulrik1,2 1Department of Respiratory Medicine, Hvidovre Hospital, Hvidovre, Denmark; 2Institute of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark Background: Early life events may predispose to the development of chronic lung disease in adulthood.Aim: To provide an update on current knowledge of early nongenetic origins of COPD.Materials and methods: Systematic literature review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines.Results: A total of 16 studies, comprising 69,365 individuals, met the predefined criteria and were included in the present review. Studies have shown that in utero tobacco exposure, low birth weight, preterm birth, and respiratory diseases, primarily asthma and pneumonia, in early childhood are associated with lung function impairment later in childhood, and by that predispose to subsequent development of COPD, although the causal association between childhood respiratory diseases and COPD has been questioned in one study. Environmental tobacco exposure has also been shown to have negative impact on lung function in childhood possibly leading to COPD in adulthood, although it is at present not possible to clearly distinguish between the impact of active and the environmental tobacco exposure on subsequent development of COPD.Conclusion: Tobacco exposure in utero and early life is a risk factor for subsequent development of COPD. Furthermore, low birth weight, lower respiratory tract infections and asthma, including wheezy bronchitis, in childhood also seem to be important determinants for later development of COPD. Early life insults may, therefore, be crucial to COPD development. Keywords: COPD, respiratory infections, obstructive lung disease, preterm birth, tobacco exposure, early life, secondhand smoke

Context: In India, despite implementation of the strategies under National Tobacco Control Programme [NTCP], women are easily exposed to tobacco consumption that is smokeless (SLT) and smoking tobacco along with second-hand smoke [SHS], making them highly susceptible to tobacco hazards. Aims: This study aimed to assess the exposure of women to tobacco use and SHS at home and to elicit predictors of tobacco exposure in a rural community of West Bengal. Methodology: A community based, cross-sectional study was conducted among 176 women aged 18 years and above. Data was collected by cluster sampling technique (16*11) using predesigned pretested structured schedule. Tobacco exposure was measured using a composite score including tobacco consumption and SHS at home. Results: Tobacco use (SLT and smoking tobacco) was significantly associated with educational attainment [AOR = 2.12], occupation [AOR = 2.13] and knowledge [AOR = 1.22]. There was significant association between SHS at home with knowledge [AOR = 1.16] and attitude of the study subjects. [AOR = 1.93]. Overall tobacco exposure (SLT, smoking tobacco, and SHS), was found to be 79.5%. Significant association was found between high tobacco exposure with age group [AOR = 3.82], educational attainment [AOR = 1.74] and knowledge regarding hazards of tobacco [AOR = 1.31]. Conclusion: Prevalence of SLT use as well as exposure of women to SHS at home is unexpectedly high in the study population. Women specific information and education campaigns focusing on tobacco hazards (both tobacco use and SHS) through existing primary health care infrastructure should be strategized under NTCP. [ABSTRACT FROM AUTHOR]

Background: Tobacco exposure (TE) is the major contributor for CVD mortality, but few published studies on CVD mortality attributable to TE have analyzed the potential reasons underlying long-term trends in China. Our studysought to find the potential reasons and compared CVD mortality attributable to TE in China, Japan, the United States of America (USA), and the world between 1990 and 2017.Methods: The mortality data in China, Japan, the USA, and the world were obtained from Global Burden of Disease Study 2017(GBD 2017). Joinpoint regression was used to assess the trend magnitude and directions over time for CVD mortality, while the age-period-cohort method was used to analyzethe temporal trends of CVD mortality according to age, period, and cohort.Results: A significant downward trend was found in the age-standardised mortality rate (ASMR) of CVD attributable to smoking in four regions. China had the smallest decline and the Chinese ASMR became the highest in 2017. All the annual net drifts in the four regions were negative and the local drifts were below zero. The longitudinal age curves of CVD mortality attributable to smoking increased in four regions,with China having the largest increase. The period or cohort RRs indicated a decline, and China had the smallest decline. The researchers further analyzed the IHD and stroke trends, finding that the morality and period or cohort RR of IHD in China was always at a high level.Conclusions: CVD mortality attributable to TE declined in four regions, and was highest in China. The proportion of IHD mortality attributable to TE was similar to stroke, which significantly changed the traditional cognition of CVD composition, but the control measure was not sufficient for IHD in China. [ABSTRACT FROM AUTHOR]

Levels of biomarkers of exposure to selected harmful and potentially harmful smoke constituents found in cigarette smoke, in addition to nicotine were measured in 160 smokers randomized for 5 days to continuing smoking conventional cigarettes (41 participants), switching to Tobacco Heating System 2.2 (THS 2.2) (80 participants), or abstaining from smoking (39 participants). The data reported here are descriptive statistics of the levels of each biomarker of exposure expressed as concentrations adjusted to creatinine; at baseline, and at the end of the study, and their relative change from baseline. Reductions in the levels of biomarkers of exposure when expressed as quantity excreted, are also reported. Detailed descriptions of bioanalytical assays used are also provided. The data presented here are related to the article entitled “Evaluation of the Tobacco Heating System 2.2. Part 8: 5-Day randomized reduced exposure clinical study in Poland” (Haziza et al., 2016) [1].

Objective Numerous Chinese-language movies have gained considerable popularity among international movie markets and audiences. For example, there are 700 foreign movies imported into Taiwan. Among these movies, there are 80 percent import from the Western world. In the past, there are many studies confirm that the smoking scenes or behaviors could affect teenagers’ smoking behavior (Charlesworth et al., 2005). Methods Content Analysis. Results Tobacco Messages Exposure (1) In 100 movies that were analyzed, half of them (49%) exposed tobacco messages. (2) In 49 movies that were exposed tobacco messages, the number of foreign-language movies (41movies) was five times as Chinese-language (8 movies). However, every Chinese-language movie average exposed tobacco messages 40.13 times, more than foreign movies (23.00 times) as 1.74 times. Conclusions There are some important discoveries in 2018, for example, in the popular 100 movies, there is one out of every two movies exposed tobacco messages. In addition, the tobacco messages appear in the G-rated movies that are suitable for children (13.17 times) are more than the tobacco messages that appear in the PG12-rated movie (10.14 times). In particular, the tobacco messages exposed in Chinese-language movies are more than Hollywood movies, and also illustrate the phenomenon that young people are exposed to the risk of smoke, not just Hollywood movies.

Background: Tobacco exposure during pregnancy is associated with several adverse outcomes in infants. We investigated the association between tobacco exposure during pregnancy (both active and second-hand) and various infections in infants up to 1 year., Methods: This prospective cohort study used a fixed dataset (jecs-an-20180131) from the Japan Environment and Children's Study of registered births in Japan during 2011-2014 that included 104,065 fetal records from enrolled pregnant women. Based on the participants' responses to the questionnaire on smoking status, mothers were first divided into "never smoked," "quit smoking," and "current smoker" groups and then into "no second-hand smoking (SHS)" and "SHS" groups. Infectious diseases included central nervous system infection, otitis media (OM), upper respiratory tract infection (URTI), lower respiratory tract infection (LRTI), gastroenteritis (GI), and urinary tract infection. Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were calculated using logistic regression analysis and adjusted for maternal, socioeconomic, and postnatal confounding factors., Results: Among the 73,205 newborns enrolled, multivariable analysis revealed that the aOR of LRTI and GI was 1.20 (95% CI, 1.07-1.33) and 1.18 (95% CI, 1.04-1.35), respectively, for the "current smoker with/without SHS" group compared with the "never smoked without SHS" group. "Quit smoking without SHS" was not associated with the risk of LRTI. SHS was associated with an increased risk of OM, URTI, LRTI, and GI, especially with LRTI and GI., Conclusion: Exposure to tobacco smoke during pregnancy was associated with an increased risk of OM, URTI, LRTI, and GI in infants during their first year of life.

Background: Primary mucosal melanoma (MM) is a rare subtype of melanoma that arises from melanocytes in the mucosa. MM has not been well profiled for mutations and its etiology is not well understood, rendering current treatment strategies unsuccessful. Hence, we investigated mutational landscape for MM to understand its etiology and to clarify mutations that are potentially relevant for MM treatment.Methods: Forty one MM and 48 cutaneous melanoma (CM) tissues were profiled for mutations using targeted deep next-generation sequencing (NGS) for 89 cancer-related genes. A total of 997 mutations within exons were analyzed for their mutational spectrum and prevalence of mutation, and 685 non-synonymous variants were investigated to identify mutations in individual genes and pathways. PD-L1 expression from 21 MM and 18 CM were assessed by immunohistochemistry.Results: Mutational spectrum analysis revealed a lower frequency of UV-induced DNA damage in MM than in CM (p = 0.001), while tobacco exposure was indicated as a potential etiologic factor for MM. In accordance with low UV damage signatures, MM demonstrated an overall lower number of mutations compared to CM (6.5 mutations/Mb vs 14.8 mutations/Mb, p = 0.001), and less PD-L1 expression (p = 0.003). Compared to CM, which showed frequent mutations in known driver genes (BRAF 50.0%, NRAS 29.2%), MM displayed lower mutation frequencies (BRAF; 12.2%, p < 0.001, NRAS; 17.1%), and was significantly more enriched for triple wild-type (no mutations in BRAF, RAS, or NF1, 70.7% vs 25.0%, p < 0.001), IGF2R mutation (31.7% vs 6.3%, p = 0.002), and KIT mutation (9.8% vs 0%, p = 0.042). Of clinical relevance, presence of DCC mutations was significantly associated with poorer overall survival in MM (log-rank test, p = 0.02). Furthermore, mutational spectrum analysis distinguished primary anorectal MM from CM metastasized to the bowel (spectrum analysis p < 0.001, number of mutations p = 0.002).Conclusions: These findings demonstrated a potential etiologic factor and driver mutation for MM and strongly suggested that MM initiation or progression involves distinct molecular-mechanisms from CM. This study also identified mutational signatures that are clinically relevant for MM treatment. [ABSTRACT FROM AUTHOR]

Aim of the study was to present available data on biomarkers of tobacco exposure and to inform about their utility in daily practice, focusing on expertise in the field in the Clinic of Pulmonary Diseases of Iasi, Romania. Data overview Smoking status declared by patients must be objectively validated by biochemical tests to determine biomarkers of tobacco exposure. The main biomarkers utilized by practitionners are: carbon monoxide in expired air and plasma, saliva, urine, hair and intranasal cotinine. More recently, researchers have studied also the role of some new biomarkers: anatabine, anabasine, thyocianate, serum uric acid and nitric oxide in expired air. We present up to date data about advantages and disadvantages of each such biomarker and practical details on clinical use, as some of them are also markers of chronic airway inflammation. Conclusions Laboratory tests for tobacco biomarkers offer the opportunity to measure constituents of tobacco smoke and to show exposing to toxicants in tobacco, regardless smoking behavior. In daily clinical practice of the Clinic of Pulmonary Diseases of Iasi have been succesfully introduced carbon monoxide and nitric oxide in exhaled air, serum uric acid and urinary cotinine determinations.

Introduction and objectives. Studies analyzing risk factors, multiple indoor and outdoor factors related to asthma and/or allergic rhinitis (AR) in childhood, are very rare. The presented study was carried out to simultaneously assess host-related, indoor and particulate matter exposure with current allergic rhinitis (AR) and/or asthma in children (6–7 years) and adolescents (13–14 years). Material and methods. The method was a cross-sectional population-based study in which participants were diagnosed by means of the International Study of Asthma and Allergies in Childhood (ISAAC) written questionnaire. Results. Exposure to indoor risk factors were verified in 1,302 individuals, in which the prevalence of AR, asthma and ARasthma comorbidity were 37.3%, 28.4%, and 16%, for children and 31.5%, 16.2%, and 10.5% for adolescents, respectively. Smoking during pregnancy was associated with current asthma (OR=1.5), second-hand smoking with AR-asthma comorbidity (OR=1.4) and visible mold on the walls with current AR, asthma, and AR-asthma comorbidity (OR=1.6). In a subgroup of 590 children, in addition to the indoor risk factors, exposure to PM10 was assessed. In this joint analysis, there was association with the same previously mentioned risk factors (p values ≤ 0.5) and a negative association to PM10 (p ≤ 0.002). Conclusion. The results suggest that avoidance of smoking during pregnancy, second-hand smoking and exposure to mould at home can contribute to reducing current AR and/or current asthma. Exposure to PM10 was not associated with the prevalence rate of these diseases.