Smoking Subjects Research Articles

Understanding complex effects on clinical outcomes and biomarker activities of food supplementation in heavy smokers: an approach using bayesian networks

BACKGROUND: Antioxidant administration can significantly alleviate smoking-mediated oxidative stress. In our previous research, using a concentrated mixed juice powder led to significant reduction in oxidative status markers and improved lung function among smokers. OBJECTIVE: To compare the effectiveness of different antioxidant formulations of the retail product Juice Plus+® on oxidative status and lung function in healthy smokers via a a Bayesian Network (BN) analysis. METHODS: At baseline and after 3 months’ supplementation, pulmonary function, cardiovascular risk factors, and oxidative status were assessed in 101 smokers, randomized into three groups: placebo (P), fruit/vegetable (FV), and fruit/vegetable/berry (FVB) group. BN analysis was performed via Monte Carlo simulations. Statistical significance was assigned as p < 0.05. RESULTS: No significant interaction was observed in P (network score –101.4, p = ns), whereas overall fit significantly improved in both FV (network score –185.7, p = 0.01) and FVB (–293.7, p = 0.003). Moreover, P group’s respiratory parameters appeared unrelated to the biochemical structure, whereas those of the FV and, to a greater extent, FVB groups were definitely related to it CONCLUSIONS: BN analysis demonstrated that the FV and FVB formulations contain nutraceutical compounds capable of synergistically acting and improving antioxidant modulation and respiratory function in smoking subjects

Depressive symptoms and smoking: Effect on mortality in a primary care cohort

ObjectiveDepressive symptoms have been suggested to increase mortality risk but causality remains unproven. Depressive symptoms increase likelihood of smoking which is thus a potential factor modifying the effect of depressive symptoms on mortality. This study aims to assess if the association of depressive symptoms and all-cause mortality is affected by smoking. MethodsA prospective cohort study in Finnish primary care setting was conducted among 2557 middle-aged cardiovascular disease (CVD) risk persons identified in a population survey. Baseline depressive symptoms were assessed by Beck's Depression Inventory (BDI) and current smoking by self-report. Data on mortality was obtained from the official statistics. Effect of depressive symptoms and smoking on all-cause mortality after 14-year follow-up was estimated. ResultsCompared to non-depressive non-smokers, the adjusted hazard ratio (HR) for all-cause mortality was 3.10 (95% CI 2.02 to 4.73) and 1.60 (95% CI 1.15 to 2.22) among smoking subjects with and without depressive symptoms, respectively. Compared to the general population, relative survival was higher among non-depressive non-smokers and lower among depressive smokers. Relative standardized mortality ratio (SMR) for all-cause mortality was 1.78 (95% CI 1.31 to 2.44) and 3.79 (95% CI 2.54 to 6.66) among non-depressive and depressive smokers, respectively, compared to non-depressive non-smokers. The HR for all-cause mortality and relative SMR of depressive non-smokers were not increased compared to non-depressive non-smokers. ConclusionCurrent smoking and increased depressive symptoms seem to additively contribute to excess mortality.

Effet du tabagisme sur le profil clinique et allergologique de la dermatite de contact

Several clinical and epidemiological data point to a possible link between smoking exposure and contact dermatitis (CD). To identify the clinical and epidemiological differences of CD in smoking and non-smoking subjects, and to determine the influence of smoking on the allergological profile of CD. Retrospective descriptive study who consulted the Department of Occupational Medicine and Occupational Pathology of the Farhat Hached University Hospital of Sousse (Tunisia) during a period of 8 years for exploration of CD and who were tested with the European Standard Battery (ESB). A total of 767 patients were enrolled during the study period, 40% of whom were smokers. The group of smokers was characterized by a male predominance (p=10-3) and a greater professional seniority compared to non-smokers (p=0.01). Personal history of atopy was predominant in non-smokers (p=0.02). Among the ESB allergens, there was a significant association between smoking and CD due to metals (chromium, cobalt) and conservatives. After binary logistic regression, the variables associated with smoking exposure were male gender (OR=12.12 ; 95% CI=[6.07 - 24.21]; p=10-3), Kathon CG allergy (OR=3.69 ; 95% CI=[1.24 - 10.81]; p=0.018), and right hand involvement (OR= 2.83; 95% CI=[1.29 - 6.17]; p=0.005). Our study revealed an effect of smoking on the clinical and allergological characteristics of CD.

Asthma–COPD overlap syndrome among smoker subjects with asthma: A cross-sectional study

This study aimed to assess the prevalence of asthma–chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS) in asthmatic outpatients with smoking exposure (smokers or ex-smokers with ≥10 pack-year history) and to evaluate quality of life (QoL) and adherence among the study sample. This cross-sectional study was conducted at outpatient respiratory clinics in governmental hospitals in Jordan. Asthmatic outpatients were interviewed to assess their spirometric readings, patients’ adherence, and patients’ QoL [using the Mini Asthma QoL questionnaire (MiniAQLQ)]. The prevalence of ACOS was found to be 33% among asthmatic smoker patients in the outpatient setting (n = 65 out of 200 subjects with asthma-diagnosed patients recruited into the study). For subjects with ACOS, 47.7% of them were older than 60 years old. Smoking history for more than 30 years was prevalent among most subjects with ACOS (67.7%). The MiniAQLQ average score was found to be low (mean ± SD = 3.23 ± 1.01, score out of 7) and similarly for patients’ adherence to their treatment modalities (mean ±SD = 1.76 ± 1.2, score out of 6). A significant positive relationship between adherence to treatment and QoL was found among subjects with ACOS (correlation coefficient = 0.171, p-value = 0.018). In conclusion, a moderate prevalence of ACOS was estimated among asthmatic smoker patients. Low levels of QoL and adherence to treatment were significantly correlated.

Tobacco exposure, but not aging, shifts the frequency of peripheral blood B cell subpopulations.

Several disturbances in T-cell mediated immunity have been described during aging, but immunosenescence of the B-cell compartment is less well elucidated. The peripheral blood B-cell compartment (CD19+) can be split into six main subpopulations according to the cell surface markers IgD, CD27, CD24, and CD38: Transitional, naïve, unswitched, switched, double negative and plasmablasts. We thus aimed to verify whether shifts in these subsets occur during healthy and pathological aging. We recruited three groups of aged people (> 60 years old), healthy, COPD patients, and smokers without altered pulmonary function test, and a fourth group of individuals 18-40 years old (youngs). Total B-cells percentage and absolute number were similar among the healthy aged, COPD patients, and youngs, but the smokers showed significantly higher absolute numbers. While all six B-cell subset percentages were comparable among the healthy aged, COPD patients, and youngs, smokers showed significantly higher percentages of switched B-cells and reduced naïve B-cells than the other three groups, resulting in an inverted naive:switched ratio. Analysis of the cell subset absolute numbers showed a similar trend. Overall, our results suggest that aging drives milder alterations in the distribution of peripheral blood B-cell subpopulations than in the T-cell compartment. We suggest that it is the T-cell immunosenescence that most contributes to the poor humoral immune responses in the elderly, vaccine responses included. Surprisingly it was the smokers who showed significant alterations when compared with the youngs, healthy aged, and aged COPD patients, probably as a result of the chronic immune stimulation described in active smoking subjects.

Single-cell immunophenotyping revealed the association of CD4+ central and CD4+ effector memory T cells linking exacerbating chronic obstructive pulmonary disease and NSCLC.

Tobacco smoking generates airway inflammation in chronic obstructive pulmonary disease (COPD), and its involvement in the development of lung cancer is still among the leading causes of early death. Therefore, we aimed to have a better understanding of the disbalance in immunoregulation in chronic inflammatory conditions in smoker subjects with stable COPD (stCOPD), exacerbating COPD (exCOPD), or non-small cell lung cancer (NSCLC). Smoker controls without chronic illness were recruited as controls. Through extensive mapping of single cells, surface receptor quantification was achieved by single-cell mass cytometry (CyTOF) with 29 antibodies. The CyTOF characterized 14 main immune subsets such as CD4+, CD8+, CD4+/CD8+, CD4-/CD8-, and γ/δ T cells and other subsets such as CD4+ or CD8+ NKT cells, NK cells, B cells, plasmablasts, monocytes, CD11cdim, mDCs, and pDCs. The CD4+ central memory (CM) T cells (CD4+/CD45RA-/CD45RO+/CD197+) and CD4+ effector memory (EM) T cells (CD4+/CD45RA-/CD45RO+/CD197-) were FACS-sorted for RNA-Seq analysis. Plasma samples were assayed by Luminex MAGPIX® for the quantitative measurement of 17 soluble immuno-oncology mediators (BTLA, CD28, CD80, CD27, CD40, CD86, CTLA-4, GITR, GITRL, HVEM, ICOS, LAG-3, PD-1, PD-L1, PD-L2, TIM-3, TLR-2) in the four studied groups. Our focus was on T-cell-dependent differences in COPD and NSCLC, where peripheral CD4+ central memory and CD4+ effector memory cells showed a significant reduction in exCOPD and CD4+ CM showed elevation in NSCLC. The transcriptome analysis delineated a perfect correlation of differentially expressed genes between exacerbating COPD and NSCLC-derived peripheral CD4+ CM or CD4+ EM cells. The measurement of 17 immuno-oncology soluble mediators revealed a disease-associated phenotype in the peripheral blood of stCOPD, exCOPD, and NSCLC patients. The applied single-cell mass cytometry, the whole transcriptome profiling of peripheral CD4+ memory cells, and the quantification of 17 plasma mediators provided complex data that may contribute to the understanding of the disbalance in immune homeostasis generated or sustained by tobacco smoking in COPD and NSCLC.

Influence of cigarette smoking on the Index of Cardiac Electrophysiological Balance in apparently healthy Angolans.

Background: Tobacco use accelerates atherosclerosis and is one of the predictors of death from ischemic heart disease, arrhythmias, heart failure, and sudden death. A new non-invasive parameter, the Index of Cardiac Electrophysiological Balance (iCEB) between depolarization and repolarization of the action potential, was considered a new biomarker for the identification of patients at increased arrhythmic risk. Objectives: We aimed to evaluate the iCEB in apparently healthy Angolans with habitual cigarette smoking compared to non-smokers. Subjects and methods: Data were obtained from the CardioBengo study, a cross-sectional community-based study in which a random sample of individuals aged between 15 and 84 years was selected. In total, 214 apparently healthy subjects, 102 smokers, and 112 non-smokers in the same age group were included in the final analysis. Results: The average age of the participants was 42.17±13.04 years old and 26.6% of the sample was female. Smoking subjects had higher iCEB and corrected Index of Cardiac Electrophysiological Balance (iCEBc) values compared with non-smoking controls (4.39 vs. 4.25; p = 0.024, respectively), and (4.74 vs. 4.57; p = 0.030, respectively). Conclusions: In summary, iCEB and iCEBc were significantly higher in habitual smokers than in nonsmokers, which represents an increased risk of ventricular arrhythmogenesis in healthy habitual smokers. To the best of our knowledge, this is the first study performed in Africa to evaluate iCEB in smokers, making this type of study very important in low- and middle-income countries in the context of epidemiological transition.

Caspase-8 activation by cigarette smoke induces pro-inflammatory cell death of human macrophages exposed to lipopolysaccharide

Cigarette smoking impairs the lung innate immune response making smokers more susceptible to infections and severe symptoms. Dysregulation of cell death is emerging as a key player in chronic inflammatory conditions. We have recently reported that short exposure of human monocyte-derived macrophages (hMDMs) to cigarette smoke extract (CSE) altered the TLR4-dependent response to lipopolysaccharide (LPS). CSE caused inhibition of the MyD88-dependent inflammatory response and activation of TRIF/caspase-8/caspase-1 pathway leading to Gasdermin D (GSDMD) cleavage and increased cell permeability. Herein, we tested the hypothesis that activation of caspase-8 by CSE increased pro-inflammatory cell death of LPS-stimulated macrophages. To this purpose, we measured apoptotic and pyroptotic markers as well as the expression/release of pro-inflammatory mediators in hMDMs exposed to LPS and CSE, alone or in combination, for 6 and 24 h. We show that LPS/CSE-treated hMDMs, but not cells treated with CSE or LPS alone, underwent lytic cell death (LDH release) and displayed apoptotic features (activation of caspase-8 and -3/7, nuclear condensation, and mitochondrial membrane depolarization). Moreover, the negative regulator of caspase-8, coded by CFLAR gene, was downregulated by CSE. Activation of caspase-3 led to Gasdermin E (GSDME) cleavage. Notably, lytic cell death caused the release of the damage-associated molecular patterns (DAMPs) heat shock protein-60 (HSP60) and S100A8/A9. This was accompanied by an impaired inflammatory response resulting in inhibited and delayed release of IL6 and TNF. Of note, increased cleaved caspase-3, higher levels of GSDME and altered expression of cell death-associated genes were found in alveolar macrophages of smoker subjects compared to non-smoking controls. Overall, our findings show that CSE sensitizes human macrophages to cell death by promoting pyroptotic and apoptotic pathways upon encountering LPS. We propose that while the delayed inflammatory response may result in ineffective defenses against infections, the observed cell death associated with DAMP release may contribute to establish chronic inflammation.CS exposure sensitizes human macrophages to pro-inflammatory cell death. Upon exposure to LPS, CS inhibits the TLR4/MyD88 inflammatory response, downregulating the pro-inflammatory genes TNF and IL6 and the anti-apoptotic gene CFLAR, known to counteract caspase-8 activity. CS enhances caspase-8 activation through TLR4/TRIF, with a partial involvement of RIPK1, resulting on the activation of caspase-1/GSDMD axis leading to increased cell permeability and DAMP release through gasdermin pores [19]. At later timepoints caspase-3 becomes strongly activated by caspase-8 triggering apoptotic events which are associated with mitochondrial membrane depolarization, gasdermin E cleavage and secondary necrosis with consequent massive DAMP release.

Impaired autophagy in the lower airways and lung parenchyma in stable COPD.

There is increasing evidence of autophagy activation in COPD, but its role is complex and probably regulated through cell type-specific mechanisms. This study aims to investigate the autophagic process at multiple levels within the respiratory system, using different methods to clarify conflicting results reported so far. This cross-sectional study was performed on bronchial biopsies and peripheral lung samples obtained from COPD patients (30 and 12 per sample type, respectively) and healthy controls (25 and 22 per sample type, respectively), divided by smoking history. Subjects were matched for age and smoking history. We analysed some of the most important proteins involved in autophagosome formation, such as LC3 and p62, as well as some molecules essential for lysosome function, such as lysosome-associated membrane protein 1 (LAMP1). Immunohistochemistry was used to assess the autophagic process in both sample types. ELISA and transcriptomic analysis were performed on lung samples. We found increased autophagic stimulus in smoking subjects, regardless of respiratory function. This was revealed by immunohistochemistry through a significant increase in LC3 (p<0.01) and LAMP1 (p<0.01) in small airway bronchiolar epithelium, alveolar septa and alveolar macrophages. Similar results were obtained in bronchial biopsy epithelium by evaluating LC3B (p<0.05), also increased in homogenate lung tissue using ELISA (p<0.05). Patients with COPD, unlike the others, showed an increase in p62 by ELISA (p<0.05). No differences were found in transcriptomics analysis. Different techniques, applied at post-transcriptional level, confirm that cigarette smoke stimulates autophagy at multiple levels inside the respiratory system, and that autophagy failure may characterise COPD.

Immunohistochemical Study of Airways Fibrous Remodeling in Smoking Mice.

The fibrotic remodeling in chronic obstructive pulmonary disease (COPD) is held responsible for narrowing of small airways and thus for disease progression. Oxidant damage and cell senescence factors are recently involved in airways fibrotic remodeling. Unfortunately, we have no indications on their sequential expression at anatomical sites in which fibrotic remodeling develops in smoking subjects. Using immunohistochemical techniques, we investigated in two strains of mice after cigarette smoke (CS) exposure what happens at various times in airway areas where fibrotic remodeling occurs, and if there also exists correspondence among DNA damage induced by oxidants, cellular senescence, the presence of senescence-secreted factors involved in processes that affect transcription, metabolism as well as apoptosis, and the onset of fibrous remodeling that appears at later times in mice exposed to CS. A clear positivity for fibrogenic cytokines TGF-β, PDGF-B, and CTGF, and for proliferation marker PCNA around airways that will be remodeled is observed in both strains. Increased expression of p16ink4A senescence marker and MyoD is also seen in the same areas. p16ink4A and MyoD can promote cell cycle arrest, terminal differentiation of myofibroblasts, and can oppose their dedifferentiation. Of interest, an early progressive attenuation of SIRT-1 is observed after CS exposure. This intracellular regulatory protein can reduce premature cell senescence. These findings suggest that novel agents, which promote myofibroblast dedifferentiation and/or the apoptosis of senescent cells, may dampen progression of airway changes in smoking COPD subjects.

Salivary microRNAs as innovative biomarkers for early diagnosis of oral diseases: a comparison of conventional cigarette smokers and tobacco heating system 2.2 users.

MicroRNAs (miRNAs) are considered valid prognostic and diagnostic biomarkers. The different miRNA expression profiles in cancer cells compared to normal cells make them potential biomarkers used for the early diagnosis of oral diseases. Following exposure to cigarette smoking, miRNA altered profile expression is associated with resistance mechanisms against anticancer therapies. Cellular models showed a reduced human gingival epithelium alteration after exposure to THS2.2 and a lower pathogenicity than 3R4F CS. The aim of the study was to compare the expression of saliva miRNA profile of THS2.2 and 3R4F CS users compared to patients not exposed to the risk factor and to identify and study the modulation of miRNAs associated with the development of oral diseases. In particular, we will focus on the analysis of a group of miRNAs know to be involved in the development of smoking-related diseases. The study will be performed in 18 months and dentists and biochemists will be involved in the different phases. To perform the study, healthy volunteers, including smokers of THS2.2 or 3R4F CS, will be enrolled. The samples will be collected from 3 experimental groups, each consisting of 30 subjects: group 1 (no smoking subjects), group 2 (subjects exposed to THS2.2), group 3 (subjects exposed to 3R4F CS). The collection of the saliva sample will be conducted in a standardized way. Following the collection, saliva will be processed. Previous studies have suggested that miRNAs are prognostic biomarkers for various smoking-related diseases. Based on the post-transcriptional regulation of some mRNAs connected to different oral pathologies, we expect a specific miRNA-mRNA interaction, which could be a starting point for the development of new possible diagnostic, therapeutic and prognostic approaches.

Ameliorating Effects of Virgin Coconut Oil (VCO) on Nicotine Dependence and Quality of Life in Smokers.

Safer and effective alternatives to manage nicotine dependence are still required. Preliminary studies have shown the potential of virgin coconut oil (VCO) to be used in dependence treatment. to assess the VCO effect administered for 14 days on nicotine dependence and quality of life. Forty smoking subjects participated in an open-label, single-center, pre/post-intervention study, and were required to take 15 ml VCO twice daily for 14 days. They were evaluated with the Fagerstrom Test for Nicotine Dependence (FTND) for nicotine dependence intensity and EuroQol-visual analogue scales (EQ VAS) for quality of life. The VCO regimen improved FTND (0.53 points decrease, p<0.05) and EQ-VAS (5.85 points increase p<0.01) scores. Adverse events were all mild. Results of the present study suggest that VCO has the potential to be a safe and effective adjunct therapy for the management of nicotine dependence.

The effect of bradykinin 1 receptor antagonist BI 1026706 on pulmonary inflammation after segmental lipopolysaccharide challenge in healthy smokers

BackgroundBradykinin 1 receptor (B1R) signalling pathways may be involved in the inflammatory pathophysiology of chronic obstructive pulmonary disease (COPD). B1R signalling is induced by inflammatory stimuli or tissue injury and leads to activation and increased migration of pro-inflammatory cells. Lipopolysaccharide (LPS) lung challenge in man is an experimental method of exploring inflammation in the lung whereby interference in these pathways can help to assess pharmacologic interventions in COPD. BI 1026706, a potent B1R antagonist, was hypothesized to reduce the inflammatory activity after segmental lipopolysaccharide (LPS) challenge in humans due to decreased pulmonary cell influx. MethodsIn a monocentric, randomized, double-blind, placebo-controlled, parallel-group, phase I trial, 57 healthy, smoking subjects were treated for 28 days with either oral BI 1026706 100 mg bid or placebo. At day 21, turbo-inversion recovery magnitude magnetic resonance imaging (TIRM MRI) was performed. On the last day of treatment, pre-challenge bronchoalveolar lavage fluid (BAL) and biopsies were sampled, followed by segmental LPS challenge (40 endotoxin units/kg body weight) and saline control instillation in different lung lobes. Twenty-four hours later, TIRM MRI was performed, then BAL and biopsies were collected from the challenged segments. In BAL samples, cells were differentiated for neutrophil numbers as the primary endpoint. Other endpoints included assessment of safety, biomarkers in BAL (e.g. interleukin-8 [IL-8], albumin and total protein), B1R expression in lung biopsies and TIRM score by MRI as a measure for the extent of pulmonary oedema. ResultsAfter LPS, but not after saline, high numbers of inflammatory cells, predominantly neutrophils were observed in the airways. IL-8, albumin and total protein were also increased in BAL samples after LPS challenge as compared with saline control. There were no significant differences in cells or other biomarkers from BAL in volunteers treated with BI 1026706 compared with those treated with placebo. Unexpectedly, neutrophil numbers in BAL were 30% higher and MRI-derived extent of oedema was significantly higher with BI 1026706 treatment compared with placebo, 24 h after LPS challenge. Adverse events were mainly mild to moderate and not different between treatment groups. ConclusionsTreatment with BI 1026706 for four weeks was safe and well-tolerated in healthy smoking subjects. BI 1026706 100 mg bid did not provide evidence for anti-inflammatory effects in the human bronchial LPS challenge model. Trial registrationThe study was registered on January 14, 2016 at ClinicalTrials.gov (NCT02657408).

Correlation Between Smoking and Il-1 Level and Arterial Stiffness as Measured By Cavi in the Young Adult Population Without other Cardiovascular Risk Factors.

Background: Recent studies have shown that arterial stiffness is a strong predictor of cardiovascular events and all-cause mortality, with CAVI (Cardio-Ankle Vascular Index) as a non-invasive arterial stiffness testing method in daily practice. Objective: This study was conducted to examine the relationship between smoking -as a risk factor for arterial stiffness- and CAVI values, as well as levels of IL-1β (Interleukin 1β) as a cytokine that plays a role in the pathophysiology of arterial stiffness. Methods: Eighty-four participants, including smokers and non-smokers without other cardiovascular risk factors, were included in the study. Demographic data, medical history, and smoking behavior were taken using a questionnaire, then IL-1β and CAVI levels were examined Results: The mean level of IL-1β in smoking subjects was significantly higher (15.09 ± 0.48) than in non-smoking subjects (5.53 ± 0.79; p=0.001). CAVI values in smoking subjects were also significantly higher (8.0 ± 0.06) than in non-smoking subjects (6.9 ± 0.02; p=0.001). Further analysis showed a strong positive correlation between smoking and IL-1β levels (r=+0.776; p=0.001) and CAVI values (r=+0.759; p=0.001). Conclusion: This study shows that smoking significantly correlates with IL-1β levels and CAVI values. The greater number of cigarettes used per day and the longer duration of smoking, there was a positive correlation between IL-1β levels and arterial stiffness as measured by CAVI.

Correlation between smoking and serum lipoprotein-associated phospholipase A2 level in overweight and obese men.

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a vaso-specific inflammatory marker that exacerbates atherosclerotic through inflammatory responses. It can be used to predict the occurrence of adverse cardiovascular events and to assess the residual risk of cardiovascular diseases. This study aims to investigate the correlation between smoking and serum Lp-PLA2 levels in overweight and obese men, and to provide evidence for preventing the cardiovascular diseases. Male subjects, who participated in health examination at the Health Management Center, Third Xiangya Hospital, Central South University from May 1, 2020 to April 30, 2021, were selected. The smoking status and other information were collected by the Self-test Scale of Physical Examination. According to the smoking status, they were divided into a never-smoking group, a current smoking group, a quit smoking group and a passive smoking group. According to the daily smoking amount, the current smoking subjects were divided into a <10 cigarettes group, a 10 to 20 cigarettes group, a 21 to 30 cigarettes group, and a >30 cigarettes group. According to the smoking years, the current smoking subjects were divided into a <5 years group, a 5 to 10 years group, a 11 to 20 years group, and a >20 years group.Serum Lp-PLA2 levels and other clinical indexes in different smoking groups were measured and compared, the correlation between smoking and serum Lp-PLA2 levels in overweight and obese men was analyzed by logistic regression analysis. Serum Lp-PLA2 levels were significantly different between the never-smoking group and the current smoking group (P<0.05). Logistic regression analysis showed that, before adjusting other influencing factors and in terms of smoking status, the current smoking group (OR=1.81, 95% CI 1.27 to 2.58, P<0.01) and the quit smoking group (OR=2.09, 95% CI 1.12 to 3.90, P<0.05) were positively correlated with serum Lp-PLA2 levels compared with the never-smoking group, while the passive smoking group had no correlation with serum Lp-PLA2 levels (OR=1.27, 95% CI 0.59 to 2.73, P>0.05). In terms of daily smoking amount, the 10 to 20 cigarettes group (OR=2.09, 95% CI 1.40 to 3.12, P<0.001) and the 21 to 30 cigarettes group (OR=1.98, 95% CI 1.22 to 3.20, P<0.01) were positively correlated with serum Lp-PLA2 levels compared with the never-smoking group, while the <10 cigarettes group (OR=1.45, 95% CI 0.81 to 2.60, P>0.05) and the >30 cigarettes group (OR=1.17, 95% CI 0.60 to 2.28, P>0.05) had no correlation with serum Lp-PLA2 levels. In terms of smoking years, the 5 to 10 years group (OR=1.94, 95% CI 1.07 to 3.53, P<0.05), the 11 to 20 years group (OR=2.06, 95% CI 1.33 to 3.18, P<0.01), and the >20 years group (OR=1.66, 95% CI 1.11 to 2.47, P<0.05) were positively correlated with serum Lp-PLA2 levels compared with the never-smoking group, while the <5 years group had no correlation with serum Lp-PLA2 levels (OR=1.12, 95% CI 0.38 to 3.33, P>0.05). After adjusting for age and other indicators, the correlation between smoking years and serum Lp-PLA2 levels was the same as before adjustment among the above smoking groups, except that the correlation between the smoking 5 to 10 years group and serum Lp-PLA2 levels was not significant (OR=1.77, 95% CI 0.95 to 3.29, P>0.05). Smoking is correlated with serum Lp-PLA2 levels in overweight and obese men.

Association of ABCB1, ABCG2 drug transporter polymorphisms and smoking with disease risk and cytogenetic response to imatinib in chronic myeloid leukemia patients

BackgroundDespite acceptable results of imatinib in the treatment of chronic myeloid leukemia (CML), some patients fail to acquire a complete cytogenetic response (CCyR), which may be caused by polymorphisms in the pharmacogenetic genes. The study aimed to evaluate the association of two polymorphisms in the ABCB1 and ABCG2 genes with cytogenetic response to imatinib and the risk of CML development. MethodsWe genotyped ABCB1 (c .2677G/T/A) and ABCG2 (c .421C/A) polymorphisms by PCR-RFLP, T-ARMS-PCR methods in 111 patients with CML and 102 sex- and age-matched healthy subjects. CCyR was determined by standard chromosome banding analysis (CBA). ResultsAnalysis of polymorphisms showed significant association of ABCG2 c.421CA genotype (p < 0.0001; OR = 0. 17), and ABCG2c.421A allele (p < 0.0001; OR = 0.31) with decreased risk of CML. Moreover, ABCB1c.2677GT- ABCG2c.421CC combined genotype (p = 0.017; OR = 4.20) was associated with increased risk of CML. Analysis of the joint effect of SNP-smoking combination showed that smoker subjects with the ABCB1c.2677GG/GT (p = 0.001; OR = 15.96, p = 0.001; OR = 8.13, respectively) or ABCG2c.421CC genotypes (p = 0.001; OR = 5.82) had the increased risk of CML, while the risk of the CML in non-smokers carrying the ABCG2c.421CA (p < 0.0001; OR = 0. 18) genotype was strongly decreased compared with reference group. Regarding drug response, ABCG2c.421 CC/CA genotypes in the smoker patients were associated with an increased risk of resistance to imatinib (p < 0.0001; OR = 7.02, p = 0.018; OR = 4.67, respectively). ConclusionOur results suggest the impact of ABCG2c .421C/A polymorphism on CML development, and smoking may have a synergistic role in the risk of CML and resistance to imatinib.

Evaluation of Exhaled Carbon Monoxide Levels in Smokers and Non-Smokers-A Comparative Study

Background: Cigarette smoke causes both acute and chronic changes of the immune system. Carbon monoxide (CO) exhaled through breath of an individual is an easiest, immediate and non-invasive method to assess smoking status. Aim: The aim of the study is to compare the exhaled CO levels in smokers and non-smokers using portable CO monitor. Material &amp; Methods: The exhaled CO levels were measured in 100 subjects (50 smokers, 50 non-smokers) who were examined during the OPD. Exhaled CO concentration was measured using the Micro+ Smokerlyser. Results: The mean carbon monoxide in the smokers was 6.34 PPM and the mean carbon monoxide in non-smokers was 1.26 PPM. There was statistically very highly significant difference of mean CO among smokers and non-smokers (P&lt;0.001). Conclusion: The exhaled CO levels successfully distinguished smokers from nonsmokers and it provides an easy and non-invasive mode of assessing a subject's smoking status. This will be beneficial for healthcare providers to examine the effectiveness of tobacco cessation and prevention programs.

Prevalence of reduced lung diffusing capacity and CT scan findings in smokers without airflow limitation: a population-based study

BackgroundPopulation distribution of reduced diffusing capacity of the lungs for carbon monoxide (DLCO) in smokers and main consequences are not properly recognised. The objectives of this study were to describe...

The interaction of persistent antiphospholipid antibodies positivity and cigarette smoking is associated with an increased risk of cardiovascular events: Cross-sectional and longitudinal analysis

BackgroundThe antiphospholipid antibody (aPL)-positivity was suggested as a nontraditional risk of coronary artery disease (CAD) and it was associated with cigarette smoking. The co-occurrence of them was usually reported in individuals with cardiovascular diseases. This study was to demonstrate their interaction on the increasing risk of cardiovascular events. Methods and resultsA total of 826 consecutive male individuals who underwent coronary angiography (CAG) /percutaneous coronary intervention (PCI) were prospectively followed and classified into three groups based on different smoking statuses. The current smoking subjects had the highest occurrence of aPL-positivity, including aCL IgM (20.1%) and aβ2GP1 IgM (15.5%). IgM isotype positivity was an independent risk factor of CAD in the multivariate model, OR: 2.70 (1.52–4.80) for aCL IgM and OR:2.50 (1.35–4.63) for aβ2GP1 IgM.The interaction of current smoking and IgM isotype positivity was significantly associated with increased risk of CAD, OR: 8.75(4.59–16.66) for aCL IgM and OR: 8.78(4.28–17.98) for aβ2GP1 IgM. During about 3 years of follow-up, the smoking patients carrying persistent aPL positivity had the highest cumulative incidence of recurrent myocardial infarction and in-stent restenosis after CAD. ConclusionThe interaction of current smoking and IgM isotype positivity was significantly associated with the increased risk of CAD, including positive aCL IgM and aβ2GP1 IgM. Cigarette smoking elevated the risk of subsequent cardiovascular events in the presence of IgM isotype positivity, including recurrent myocardial infarction and in-stent restenosis.

Red Cell Microparticles Suppress Hematoma Growth Following Intracerebral Hemorrhage in Chronic Nicotine-Exposed Rats

Spontaneous intracerebral hemorrhage (sICH) is a disabling stroke sub-type, and tobacco use is a prominent risk factor for sICH. We showed that chronic nicotine exposure enhances bleeding post-sICH. Reduction of hematoma growth is a promising effective therapy for sICH in smoking subjects. Red-blood-cell-derived microparticles (RMPs) are hemostatic agents that limit hematoma expansion following sICH in naïve rats. Considering the importance of testing the efficacy of experimental drugs in animal models with a risk factor for a disease, we tested RMP efficacy and the therapeutic time window in limiting hematoma growth post-sICH in rats exposed to nicotine. Young rats were chronically treated with nicotine using osmotic pumps. sICH was induced in rats using an injection of collagenase in the right striatum. Vehicle/RMPs were administered intravenously. Hematoma volume and neurological impairment were quantified ≈24 h after sICH. Hematoma volumes in male and female nicotine-exposed rats that were treated with RMPs at 2 h post-sICH were significantly lower by 26 and 31% when compared to their respective control groups. RMP therapy was able to limit hematoma volume when administered up to 4.5 h post-sICH in animals of both sexes. Therefore, RMPs may limit hematoma growth in sICH patients exposed to tobacco use.