Non-smoking Controls Research Articles

Persistently Increased Systemic ACE2 Activity Is Associated With an Increased Inflammatory Response in Smokers With COVID-19.

Background: Tobacco smoking is known to be involved in the pathogenesis of several cardiopulmonary diseases. Additionally, smokers are highly susceptible to infectious agents due to weakened immunity. However, the progression of lung injury based on SARS-CoV-2-mediated COVID-19 pathogenesis amongst smokers and those with pre-existing pulmonary diseases is not known. We determined the systemic levels and activity of COVID-19 associated proteins, cytokine/chemokines, and lipid mediators (lipidomics) amongst COVID-19 patients with and without a history of smoking to understand the underlying susceptible factor in the pathogenesis of COVID-19.Methods: We obtained serum from healthy (CoV−), COVID-19 positive (CoV+), and COVID-19 recovered (CoV Rec) subjects with and without a history of smoking. We conducted a Luminex multiplex assay (cytokine levels), LC/MS (eicosanoids or oxylipin panel), and ACE2 enzymatic activity assays on the serum samples to determine the systemic changes in COVID-19 patients.Results: On comparing the levels of serum ACE2 amongst COVID-19 (positive and recovered) patients and healthy controls, we found a pronounced increase in serum ACE2 levels in patients with COVID-19 infection. Furthermore, ACE2 enzyme activity was significantly increased amongst COVID-19 patients with a smoking history. Also, we analyzed the levels of Angiotensin 1–7 (Ang1–7) peptide, the product of enzymatic action of ACE2, in the serum samples. We found significantly high levels of Ang1–7 in the serum of both CoV+ and CoV Rec patients. Our data further demonstrated a smoking-induced increase in serum furin and inflammatory cytokine [IFNγ(p = 0.0836), Eotaxin (p < 0.05), MCP-1 (p < 0.05), and IL-9 (p = 0.0991)] levels in COVID-19 patients as compared to non-smoking controls. Overall, our results show that smoking adversely affects the levels of systemic inflammatory markers and COVID-19 associated proteins, thus suggesting that COVID-19 infection may have severe outcomes amongst smokers.

Environmental and Genetic Factors in the Pathogenesis of COPD in the Road-Working Population.

Background Chronic obstructive pulmonary disease (COPD) is a typical heterogeneous condition caused by environmental and genetic risk factors. Objectives We investigated extrinsic (environmental) and intrinsic (genetic) factors contributing to the development of COPD in a nonsmoker road-working population in Northeast China. Method The target population was divided into a COPD group and an exposed control group. Another healthy nonroad working nonsmoker control group was also included for environmental factor comparison. Peripheral blood was collected and analyzed using inductively coupled plasma mass spectrometry for inorganic elements of PM2.5, and microarray, rt-PCR, and Multiplex ELISA for genetic factors. Results Forty-three COPD road workers, thirty-nine non-COPD road workers, and 52 age and gender-matched healthy nonroad workers were enrolled. There were significantly higher levels in all 24 inorganic elements in the COPD group compared with the healthy control group except potassium and manganese, while the majority of inorganic elements were similar between the COPD group and the exposed control group except in aluminum and cobalt. There were 39 genes showing significant differences between the COPD group and the exposed control group. Collagen, type XV, alpha 1 (COL15A1), Meis homeobox 1 (MEIS1), carbonyl reductase 3 (CBR3), and amine oxidase, copper containing 3 (AOC3) were confirmed by rt-PCR to be differentially expressed. Their correlations with blood cytokines were also evaluated. Conclusions Aluminum might contribute to the development of COPD in the road-working population. CBR3 and AOC3 seem expressed in different patterns than previously reported, evidenced by their correlation with proinflammatory and anti-inflammatory cytokines.

The relationship between DRD2 TaqIA polymorphism and tobacco addiction

Objectives: In this study, the relationship between tobacco addiction levels, early smoking, and DRD2 TaqIA polymorphism was investigated. Materials and methods: The present study included 36 smokers and 12 non-smoking voluntary controls. Study groups were established as the non-smoking control group and addicted (less than 1 pack, between 1-2 packs, more than 2 packs per day) groups. Genotypes of the dopamine type-2 receptor (DRD2) gene TaqIA polymorphic region from genomic DNA isolated from oral swab samples were determined by PCR followed by Restriction Fragment Length Polymorphism (RFLP) analysis. Results: Presence of the DRD2 TaqIA homozygous polymorphic genotype in addicted individuals who smoked two or more packs per day and the absence of non-smoker control individuals may indicate that the polymorphic TaqIA allele of the DRD2 gene is associated with smoking. It was found that individuals carrying the polymorphic TaqIA allele in homozygous (~13 years) and heterozygous forms (~16.3 years) had a lower age of starting smoking compared to homozygous wild types (~18.6 years). Mean BMI (body mass index) of the study participants was 24.66 kg/m2 (normal weight), waist/hip ratio 0.82 (no abdominal obesity). Conclusion: The results of our study suggest that the TaqIA variant allele is related to early smoking condition. In addition, it was determined that there was a higher tendency of smoking addiction among children of addicted parents.

Endothelial dysfunction in COPD: a systematic review and meta-analysis of studies using different functional assessment methods.

BackgroundCardiovascular disease is a major cause of morbidity and mortality in COPD. Endothelial dysfunction is suggested to be one of the pathogenetic mechanisms involved. This is a systematic review and meta-analysis of studies using any available functional method to examine differences in endothelial function between patients with COPD and individuals without COPD (controls).MethodsLiterature search involved PubMed and Scopus databases. Eligible studies included adult patients and evaluated endothelial damage via functional methods. The Newcastle–Ottawa scale was applied to evaluate the quality of retrieved studies. Subgroup analyses were performed to explore heterogeneity across the studies. Funnel plots were constructed to evaluate publication bias.ResultsOf the 21 reports initially identified, 19 studies with a total of 968 participants were included in the final meta-analysis. A significantly impaired response in endothelium-dependent (weighted mean between-group difference (WMD) −2.59, 95% CI −3.75 to −1.42) and -independent vasodilation (WMD −3.13, 95% CI −5.18 to −1.09) was observed in patients with COPD compared to controls. When pooling all studies together, regardless of the technique used for assessment of vascular reactivity, pronounced endothelial dysfunction was observed in COPD compared to controls (standardised mean difference (SMD) −1.19, 95% CI −1.69 to −0.68). Subgroup analysis showed that the difference was larger when patients with COPD were compared with nonsmoking controls (SMD −1.75, 95% CI −2.58 to −0.92). Sensitivity analyses confirmed the results.ConclusionsPatients with COPD have significantly impaired endothelial function compared to controls without COPD. Future studies should delineate the importance of endothelial dysfunction towards development of cardiovascular disease in COPD.

Blood eosinophil count in patients with COPD on inhaled corticosteroids in comparison with healthy smoker and nonsmoker controls

Background Chronic obstructive pulmonary disease (COPD) is associated with acute and chronic pulmonary inflammation in the lung and as a systemic inflammation. The blood eosinophil counts are now recommended by the Global Initiative for the Management of Obstructive Lung Disease as a guide of inhaled corticosteroid use in clinical practice, as it can predict its effect on the rate of COPD exacerbation. The increasing peripheral blood eosinophilic count in patients with COPD could explain the systemic eosinophilia in COPD, which causes increased lung eosinophil count in these patients, especially those on inhaled corticosteroids (ICS). Patients and methods The study included 56 patients with COPD who were active smokers with pack-years beyond 10 as cases. The control group includes 60 patients as healthy nonsmokers (HNS) and 66 patients as healthy current smokers (HS), with pack-year beyond 10. Prebronchodilator and postbronchodilator spirometry was done in the pulmonary function unit of the Chest Department, Ain Shams University Hospital, to confirm or to exclude the COPD diagnosis. The COPD cases were categorized as per the Global Initiative for the Management of Obstructive Lung Disease severity assessment guideline and were receiving budesonide 800 μg/day and formoterol 24 μg/day or salmeterol 100 μg and fluticasone propionate 500 μg twice daily. Skin prick test and complete blood count for its differential and eosinophil count were done for all cases. Results The study included 56 patients with COPD who were active smokers and received ICS. The control group included 60 patients as HNS along with 66 patients as healthy current smokers. The HNS group showed the least total leukocytic count of 5588.33±1081.13/µl and the least eosinophilic count of 99.47±91.51/µl, whereas the COPD group showed the highest total leukocytic count. A statistically significant relation was found also between COPD patients’ eosinophil count and the use of ICS, with P value 0.000. Conclusion The peripheral blood eosinophil counts collected from patients with COPD on ICS are significantly higher than the patients with COPD who are not using ICS and the healthy smoker and nonsmoker control group.

Atherosclerosis inflammation and burden in young adult smokers and vapers measured by PET/MR

Background and aimsElectronic cigarette (EC) use is popular among youth, touted as a safer alternative to smoking and promoted as a tool to aid in smoking cessation. EC cardiovascular safety however is not well established. The aim of this study was to examine cardiovascular consequences of EC use by evaluating their effect on the entire atherosclerotic cascade in young adults using noninvasive combined positron emission tomography (PET)/magnetic resonance imaging (MR) and comparing EC use with age matched smokers of traditional cigarettes and nonsmoking controls. MethodsCarotid PET/MR was applied to look at vascular inflammation (18-fluorodeoxyglucose (FDG)-PET) and plaque burden (multi-contrast MR of vessel wall) from 60 18-30 year-old subjects (20 electronic cigarette users, 20 traditional smokers and 20 nonsmokers). ResultsGroups were reasonably well balanced in terms of age, gender, demographics, cardiovascular risk and most biomarkers. There were no differences in vascular inflammation as measured by 18-FDG-PET target to background ratios (TBR) between EC users, traditional cigarette smokers and nonsmokers. However, measures of carotid plaque burden − wall area, normalized wall index, and wall thickness − measured from MR were significantly higher in both traditional smokers and EC users than in nonsmokers. ConclusionsYoung adult EC users, smokers and nonsmokers in our study did not exhibit vascular inflammation as defined by 18-F-FDG-PET TBR max, but smokers and EC users had significantly more carotid plaque burden compared to matched nonsmokers. Results could indicate that vaping does not cause an increase in vascular inflammation as measured by FDG-PET.

Increased myofibroblasts in the small airways, and relationship to remodelling and functional changes in smokers and COPD patients: potential role of epithelial–mesenchymal transition

IntroductionPrevious reports have shown epithelial–mesenchymal transition (EMT) as an active process that contributes to small airway fibrotic pathology. Myofibroblasts are highly active pro-fibrotic cells that secrete excessive and altered extracellular matrix (ECM). Here we relate small airway myofibroblast presence with airway remodelling, physiology and EMT activity in smokers and COPD patients.MethodsLung resections from nonsmoker controls, normal lung function smokers and COPD current and ex-smokers were stained with anti-human α-smooth muscle actin (SMA), collagen 1 and fibronectin. αSMA+ cells were computed in reticular basement membrane (Rbm), lamina propria and adventitia and presented per mm of Rbm and mm2 of lamina propria. Collagen-1 and fibronectin are presented as a percentage change from normal. All analyses including airway thickness were measured using Image-pro-plus 7.0.ResultsWe found an increase in subepithelial lamina propria (especially) and adventitia thickness in all pathological groups compared to nonsmoker controls. Increases in αSMA+ myofibroblasts were observed in subepithelial Rbm, lamina propria and adventitia in both the smoker and COPD groups compared to nonsmoker controls. Furthermore, the increase in the myofibroblast population in the lamina propria was strongly associated with decrease in lung function, lamina propria thickening, increase in ECM protein deposition, and finally EMT activity in epithelial cells.ConclusionsThis is the first systematic characterisation of small airway myofibroblasts in COPD based on their localisation, with statistically significant correlations between them and other pan-airway structural, lung function and ECM protein changes. Finally, we suggest that EMT may be involved in such changes.

Subtle right ventricular dysfunction in asymptomatic chronic heavy cigarette smokers: a speckle tracking case-control study

BackgroundChronic heavy cigarette smoking can affect the right ventriclular function. The standard echocardiography may not show early right ventricular functional changes, and a more sensitive measure is needed. The aim of this work was to evaluate the subtle subclinical effects of chronic heavy cigarette smoking on the right ventricular function. The study included 55 healthy asymptomatic chronic heavy cigarette smokers (smoking history of at least 5 pack-years and a daily cigarette consumption of at least 1 pack) and 35 healthy non-smoking control subjects. Patients underwent a full clinical assessment and a conventional as well as a 2D-speckle tracking transthoracic echocardiography of the right ventricle and data was compared between the 2 groups.ResultsThe mean age was 32.9 ± 7.2 years in smokers and 30.9 ± 7.9 years in non-smokers (p = 0.227). The 2 groups showed comparable conventional right ventricular systolic and diastolic functions. Smokers showed a significantly lower (less negative) right ventricular global longitudinal strain (− 19.0 ± 3.2% vs. − 24.5 ± 3.5%, p < 0.001). Patients with a higher daily cigarette consumption showed a poorer right ventricular global longitudinal strain (p = 0.014).ConclusionChronic heavy cigarette smoking can adversely affect the right ventricular function, a finding that can be easily missed by conventional echocardiography and can be better detected by the right ventricular speckle tracking.

Affective disorders impact prevalence of Flavonifractor and abundance of Christensenellaceae in gut microbiota

BackgroundAffective disorders (AD) have been associated with a higher prevalence of the gut Flavonifractor genus and a lower abundance of the gut Christensenellaceae family.Objective and methodsBy pooling two independent study samples of patients with AD (n = 176), their unaffected first-degree relatives (n = 70) and healthy controls (n = 101) we aimed to replicate and extend our prior findings of differential Flavonifractor prevalence and Christensenellaceae abundance when comparing patients with AD and healthy controls. The gut microbiota was profiled using 16S rRNA gene amplicon sequencing.ResultsThe pattern of higher prevalence of Flavonifractor and lower Centered Log-Ratio (CLR) abundance of Christensenellaceae was associated with AD. In generalized linear models the CLR abundance of Christensenellaceae was lower in patients with AD (p = 0.024), and in smokers (p = 1.9*10−4), and inversely associated with increasing waist circumference (p = 0.031). The prevalence of Flavonifractor was higher in patients with AD (p = 0.033) and in smokers (p = 0.036). No impact of psychotropic medication was found. The CLR abundance of Christensenellaceae (p = 0.041), but not the prevalence of Flavonifractor (p = 0.20) could distinguish non-smoking patients with AD from non-smoking healthy controls, whereas no such associations were found in smokers. Unaffected relatives neither differed from patients with AD nor from healthy controls.ConclusionCompared with findings in healthy controls, AD was associated with a significantly lower CLR abundance of the health-linked Christensenellaceae and a significantly higher prevalence of Flavonifractor; findings that are associated with enhanced oxidative stress and systemic low-grade inflammation. If our observations are validated in future independent studies, they support the notion that parts of aberrant gut microbiota are shared by AD and states of dysmetabolism.

Salivary irisin: potential inflammatory biomarker in recurrent apthous stomatitis patients.

Recurrent Aphthous Stomatitis (RAS) is the most common inflammatory condition of the oral mucosa characterised by recurrent onset of single or multiple painful ulcers mainly affecting the nonkeratinized oral mucosa. RAS mostly occurs in healthy individuals with no associated systemic diseases. Irisin is a newly identified adipomyokine and research has revealed that it has anti-inflammatory effects. The aim of this study was to investigate the significance of salivary irisin levels in patients with recurrent apthous stomatitis (RAS). In this investigation, 80 individuals were evaluated. The patient group included 30 patients diagnosed with RAS and each control group consisted of 25 smoker and non-smoker healthy individuals. Saliva samples were collected and salivary irisin, interleukin-2 (IL-2) and interferon-ɣ (IF-ɣ) levels were determined using enzyme-linked immunosorbent assay (ELISA). IL-2 and IF-ɣ levels in RAS patients were significantly higher than control smoker and non-smoker groups (p=0.0001, p=0.0001, respectively). Irisin level was higher in RAS patients than smoker controls and non-smoker controls. The level of irisin was found as sensitive and specific as IL-2 and more sensitive and specific than IF-ɣ. The salivary levels of pro-inflammatory cytokines IL-2 and IF-ɣ and irisin were higher in RAS group compared to controls. This is the first report evaluating the irisin an adipo-myokine as an inflammatory biomarker in RAS.

Effects of Smoking Status and State on Intrinsic Connectivity

BackgroundSmoking behavior during the first 24 hours of a quit attempt is a significant predictor of longer-term abstinence, yet little is known about the neurobiology of early tobacco abstinence. Specifically, the effects of acute tobacco deprivation and reinstatement on brain function—particularly at the level of large-scale network dynamics and assessed across the entire brain—remain incompletely understood. To address this gap, this study used a mixed within- and between-subjects design to assess the effects of smoking status (yes/no smoker) and state (deprived vs. satiated) on whole-brain patterns of intrinsic connectivity. MethodsParticipants included 42 tobacco smokers who underwent resting-state functional magnetic resonance imaging following overnight abstinence (deprived state) and following smoking reinstatement (satiated state, randomized order across participants). Sixty healthy control nonsmokers underwent a single resting-state scan using the same acquisition parameters. Functional connectivity data were analyzed using both a canonical network-of-interest approach and a whole-brain, data-driven approach, i.e., intrinsic connectivity distribution. ResultsNetwork-of-interest–based analyses indicated decreased functional connectivity within frontoparietal and salience networks among smokers relative to nonsmokers as well as effects of smoking state on default mode connectivity. In addition, intrinsic connectivity distribution analyses identified novel between-group differences in subcortical-cerebellar and corticocerebellar networks that were largely smoking state dependent. ConclusionsThese data demonstrate the importance of considering smoking state and the utility of using both theory- and data-driven analysis approaches. These data provide much-needed insight into the functional neurobiology of early abstinence, which may be used in the development of novel treatments.

IL-17F Gene rs763780 and IL-17A rs2275913 Polymorphisms in Patients with Periodontitis.

Background: Periodontitis (PD) is a chronic inflammatory disease that can eventually lead to tooth loss. Genetic and environmental factors such as smoking are involved in the pathogenesis of PD. The development of PD is potentiated by various pathogens that induce an immune response leading to the production of cytokines, such as interleukin (IL)-17. The synthesis of IL-17 is influenced genetically. The polymorphisms in IL-17 gene may affect the synthesis of IL-17. The aim of this study was to examine the association between the IL-17F rs763780 and IL-17A rs2275913 polymorphisms and PD in non-smoking and smoking patients to check if these polymorphisms could be a risk factor for PD. Methods: The study enrolled 200 patients with PD (130 non-smokers and 70 smokers) and 160 control subjects (126 non-smokers and 34 smokers). Periodontitis was diagnosed on the basis of 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. All samples were genotyped using allelic discrimination assays with TaqMan® probes on a Real-Time PCR Detection System. Results: There were no statistically significant differences in the distribution of the IL-17F rs763780 and IL-17A rs2275913 genotypes and alleles between patients with PD and control subjects, between smoking patients with PD and smoking control subjects, and between non-smoking patients with PD and non-smoking control subjects. Conclusions: The results of this study suggest a lack of statistically significant associations between IL-17F rs763780 and IL-17A rs2275913 polymorphisms and PD in Polish population.

Alkylating and oxidative stresses in smoking and non-smoking patients with COPD: Implications for lung carcinogenesis

Chronic obstructive pulmonary disease (COPD) is a disease characterized by chronic inflammation and irreversible airway obstruction. Cigarette smoking is the predominant risk factor for developing COPD. It is well-known that the COPD is also strongly associated with an increased risk of developing lung cancer. Cigarette smoke contains elevated concentrations of oxidants and various carcinogens (e.g., tobacco-derived nitrosamines) that can cause oxidative and alkylating stresses, which can also arise from inflammation. However, it is surprising that, except for oxidative stress, little information is available on the burden of alkylating stress and the detoxification efficiency of tobacco-derived carcinogens in COPD patients. In this study, we used LC-MS/MS to measure the archetypical tobacco-specific carcinogenic 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), its major metabolite, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), three biomarkers of oxidative stress (8-oxo-7,8-dihydroguanine, 8-oxoGua; 8-oxo-7,8-dihydro-2′-deoxyguanosine, 8-oxodGuo; 8-oxo-7,8-dihydroguanosine, 8-oxoGuo) and two biomarkers of alkylating stress (N7-methylguanine, N7-MeGua and N3-methyladenine, N3-MeAde), in the urine of smoking and non-smoking COPD patients and healthy controls. Our results showed that not only was oxidative stress significantly elevated in the COPD patients compared to the controls, but also alkylating stress. Significantly, levels of alkylating stress (i.e., N7-MeGua) were highly correlated with the COPD severity and not affected by age and smoking status. Furthermore, COPD smokers had significantly higher ratios of free NNAL to the total NNAL than control smokers, implying a lower detoxification efficiency of NNK in COPD smokers. This ratio was even higher in COPD smokers with stages 3–4 than in COPD smokers with stages 1–2. Taken together, our results demonstrated that the detoxification efficiency of tobacco-derived carcinogens (e.g., NNK) was associated with the pathogenesis and possibly the progression of COPD. In addition to oxidative stress, alkylating stress derived from chronic inflammation appears to be also dominant in COPD patients.

Co-occurring tobacco and cannabis use in adolescents: Dissociable relationships with mediofrontal electrocortical activity during reward feedback processing

Differences in corticostriatal neural activity during feedback processing of rewards and losses have been separately related to cannabis and tobacco use but remain understudied relative to co-use in adolescents. Using high-density EEG (128 electrode system, 1000 Hz sampling), we examined event-related potentials (ERPs) elicited by monetary reward, neutral, and loss feedback during performance on a non-learning four-choice guessing task in a sample of non-deprived daily-cigarette-smoking adolescents (n = 36) who used tobacco and cannabis regularly (TC adolescents), and non-smoking healthy control adolescents (HCs) (n = 29). Peak amplitudes and latencies of mediofrontal ERPs indexing feedback-related negativities (FRNs) were used as outcomes in repeated-measures ANOVAs. No differences in FRNs were observed between TC and HC adolescents. Within TC adolescents, cannabis-use and tobacco-use variables had distinct relationships with the FRN, with cannabis-related problem severity being positively correlated with FRN amplitude during reward feedback and tobacco-related problem severity being negatively correlated with FRN latency during non-loss feedback (i.e., reward and neutral). These findings suggest that co-occurring cannabis and tobacco use may have dissociable relationships with feedback processing relating to each drug and support an incentive salience model of addiction severity related to cannabis use in adolescents.

The effects of smoking Haschich on blood parameters in young people from the Beni Mellal region Morocco

&lt;abstract&gt;&lt;sec&gt; &lt;title&gt;Objective&lt;/title&gt; &lt;p&gt;The objective of this work is to evaluate the effects of smoking hashish on some blood parameters (Red blood cells, Hemoglobins, Hematocrits, MCV, MCH, MCHC, White blood cells, Urea, Creatinine, Cholesterol, Triglycerides, Liver Aminotransferases) among young people from the Beni Mellal region, Morocco.&lt;/p&gt; &lt;/sec&gt;&lt;sec&gt; &lt;title&gt;Methods&lt;/title&gt; &lt;p&gt;Blood samples are collected from 30 male, fasting, voluntary and anonymous individuals in three groups; 10 non-smokers (controls), 10 moderate chronic smokers (5 joints/day (5 j/d) or less for a period not exceeding 3 years) and 10 intense chronic smokers (15 joints/day or more for a period equal to or greater than 5 years).&lt;/p&gt; &lt;/sec&gt;&lt;sec&gt; &lt;title&gt;Results&lt;/title&gt; &lt;p&gt;The results obtained show that with the duration and number of joints consumed, a decrease in the level of HB, RBCs, HT, platelets, urea, cholesterol, triglycerides, SGOT and SGPT while there is an increase in MCH, MCHC, eosinophils and creatinine.&lt;/p&gt; &lt;/sec&gt;&lt;sec&gt; &lt;title&gt;Conclusion&lt;/title&gt; &lt;p&gt;These results could be explained by the impact of the active ingredients in the joints, including THC in cannabis and the components of smoked cigarettes in conjunction with cannabis resin on consumer nutrition.&lt;/p&gt; &lt;/sec&gt;&lt;/abstract&gt;

Analysis of serum lipid profile in adult female smokers in Erbil city, Kurdistan region of Iraq

Background: There are few studies demonstrated the association between smoking and lipid profile in female adult smokers. Materials and Methods: This study conducted to determine and compare the serum lipid profile of female adult smokers with non-female smokers, known as controls. In 180 female subjects, the level of serum lipid profile measured. Results: Of these, 110 were smokers and 70 non-smokers (control) aged between 25 and 50 years. The study involved only smokers who had smoked for more than 5 years. Our result revealed that mean serum of total cholesterol (275.2 ± 32.6 mg/dl), triacylglycerol (188.4 ± 56.42 mg/dl), very low density lipoprotein (36.6 ± 14.2 mg/dl), low density lipoprotein (133.21 ± 9.81 mg/dl) were significantly higher in female smokers as compared to non-female smokers with mean of serum total cholesterol (172.3 ± 18.6 mg/dl), very low density lipoprotein (21.8 ± 9.6 mg/dl), triglyceride (108 ± 8.84 mg/dl), low density lipoprotein (94.54 ± 8.5 mg/dl). However, the mean of serum value for high density lipoprotein cholesterol in chronic female smokers was lower (44.6 ± 4.6 mg/dl) than in non-female smokers (55.3 ± 8.2 mg/dl). Conclusion: This study indicated that smoking cigarettes in female cause’s dyslipidemia, resulting in increased risk of cardiovascular disease among smokers.

Effect of cigarette smoking on serum testosterone level among male smokers

Objective Smoking is considered as a growing epidemic worldwide, and it was found to have negative influence on health, causing a variety of diseases in both sexes, such as pulmonary fibrosis, chronic obstructive pulmonary disease, cerebrovascular and cardiovascular disorders, pulmonary and extrapulmonary malignancies, infertility, erectile dysfunction, recurrent abortions, and teratogenicity. In addition, several studies have been conducted owing to concerns on its effect on the endocrinal system in males, especially its effects on testosterone levels; however, this concern is still debatable, and all reported results were conflicting. Patients and methods Herein, the cohort study was conducted on a subgroup of smoking males (n=155) to evaluate its effect on serum total testosterone (T), estradiol (E2), as well as T/E2 ratio compared with a non-smoking control group (n=134). Results Our results have shown that there was a significant statistical difference between smoker and non-smoker groups concerning serum total testosterone (T), estradiol (E2), and subsequently T/E2 ratio, with P values of 0.002, less than 0.001, and less than 0.001, respectively. In addition, there was a statistically significant negative correlation between the duration of smoking and T. However, there was no correlation between duration of smoking and either E2 or T/E2 ratio. Conclusion Thus, the current study added further evidence to the unsettled debate suggesting negative harmful effects of smoking on serum testosterone level.

A cross-sectional study of pulmonary function tests among the municipal street sweepers of Chitradurga District, Karnataka

Municipal street sweepers are exposed to large amount of dusts, microorganisms, toxins and automobile exhaust pollution. Chronic inhalation of such particulate matter has the potential to impair their pulmonary functions. The strict adherence to the standards and norms for the management of municipal solid wastes to reduce occupational health hazards in developing countries India is still a matter of concern. This study conducted among the municipal sweepers of Chitradurga district, compared the effects of chronic exposure to dust on the pulmonary function using spirometry test. This study also assessed the effects of smoking and irregular usage of protection masks, and compared the results with the healthy controls. Respiratory symptoms of cough (30%), chest pain (17.5%), catarrah and sneezing (21.5%) were found to be in higher percentage among the municipal street sweepers than the controls. Only 20% of participants municipal street sweepers used personal protective measures, wearing protective masks, regularly in the past 1 year, during sweeping streets. It was found that FEV1, FEV1/FVC, PEFR and FEF 25%-75% were significantly lesser among non-smoker street sweepers, when compared with that of non-smoking controls. Similarly these PFT values were significantly reduced among the smoker street sweepers and among the sweepers who didn’t use protective masks while sweeping. This study highlights the occupational hazard faced by municipal sweepers and attempts to emphasize on importance of usage of protective masks. Keywords: Street sweepers; Personal Protective Measures; Dust; Spirometry.

Serum high-density lipoprotein and triglycerides in patients with chronic obstructive pulmonary disease

Background: Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation and inflammation. It is now recognized to have systemic consequences that may affect morbidity and mortality. In patients with COPD, smoking is the major risk factor which affects the lipid profile. The objective of this study was to evaluate serum levels of high-density lipoprotein (HDL) and triglycerides (TG) in patients with COPD and compare them with healthy non-smoking controls. Methodology: This study was conducted in COPD patients with age and gender matched healthy controls. Both cases and controls were evaluated to obtain relevant history and clinical data. Spirometry and fasting lipid profile were performed in cases and controls; staging of COPD was based on Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2011 guidelines. Results: Fifty one subjects diagnosed with COPD and an equal number of controls were recruited; this included 43 males and 8 females with a mean age of 57.3 years. The mean smoking index of COPD patients was 316.8. Seven (13.7%) patients had mild, 30(58.8%) had moderate, 12(23.5%) had severe and 2(3.9%) had very severe COPD. Twelve (23.5%) patients each in the COPD and control group had elevated triglycerides; the mean level being 141.6 mg/dl in COPD patients and 136.3 mg/dl in controls. (p=0.53).Thirty one (60.7%) patients with COPD and 22(43.1%) controls had decreased HDL; mean level was 41.2mg/dl in COPD patients and 47.6mg/dl in controls. A statistically significant difference was found in serum HDL level between cases and controls. (p=0.009) Conclusions: It can be concluded from this study that lipid profile derangements are common in patients with COPD compared to healthy non-smoking controls. Further, the hypothesis that COPD is a systemic disease is supported by our study. Keywords: HDL; High density lipoprotein, LDL, Low density lipoprotein.

E-cig might cause cell damage of oral mucosa

The aim of this study was to investigate cytogenetic and cytotoxic damage through the evaluation of micronuclei (MN) and metanuclear anomalies in the oral mucosa of electronic cigarette (e-cig) users. The patients were recruited into 4 groups: e-cig users, smokers, former smokers, and nonsmokers (control). The samples were collected by means of exfoliative cytology of the lateral region of the tongue and the floor of the mouth. The smears obtained were fixed and stained by the Feulgen method for investigation of MN and metanuclear anomalies. A significant difference was observed for MN frequency only between the smoker and control groups. As for metanuclear anomalies, significant differences were observed: karyolysis between: smokers and control, e-cig and control, as well as former smokers; karyorrhexis: between smoker and control; binucleation: between e-cig and former smoker, as well as control; broken eggs: between e-cig and all other groups; nuclear bud: between e-cig and former smokers, as well as control. E-cig and alcohol users presented genotoxicity and cytotoxicity in the oral mucosa cells. The use of e-cigs and alcohol by former smokers can cause more damage to the cells of the oral mucosa compared to those who have not used e-cigs.