non-COPD Smokers Research Articles

The relationship between acrolein and oxidative stress in COPD: in systemic plasma and in local lung tissue.

PurposeCigarette smoke produces a high level of acrolein, which is thought to be pathogenically involved in the development of chronic obstructive pulmonary disease (COPD). The present study investigated the pathological role of acrolein in the development of COPD.Patients and methodsAcrolein concentration was measured in plasmas obtained from 47 patients with COPD and 18 current smokers without COPD, and in supernatants of homogenized lung tissues obtained from 10 never-smokers, 8 current smokers, and 8 patients with COPD by high-performance liquid chromatography. Oxidant status and antioxidant activity were measured using derivatives of reactive oxygen metabolite (d-ROM) and bio-antioxidant power (BAP), respectively, in the Free Radical Elective Evaluation FRAS4 system. In addition, immunohistochemistry was used to evaluate the over-presentation of acrolein in lung tissues of patients with COPD.ResultsPlasma concentrations of acrolein were significantly higher in the patients with COPD than the non-COPD smokers (P<0.001), which significantly correlated with the oxidant status in patients with COPD (R=0.69, P<0.05). Similar pathological alterations in acrolein concentrations were found in the lung tissue supernatants of patients with COPD, which significantly correlated with the oxidant status in patients with COPD. Furthermore, acrolein was strongly expressed in the lung tissues of patients with COPD.ConclusionThe increased acrolein concentrations were highly involved in the pathogenesis of COPD through interference in the balance of oxidative stress versus antioxidant potentiality.

Muscle Dysfunction in Smokers and Patients With Mild COPD: A SYSTEMATIC REVIEW.

To describe and discuss the available evidence in the literature concerning muscle function and the association between smoking and muscle dysfunction in smokers and patients with mild chronic obstructive pulmonary disease (COPD). The literature search involved the following databases: PubMed, Pedro, CINAHL, Cochrane Library, Lilacs, and EMBASE. Studies were included if they investigated muscle strength and/or endurance and/or cross-sectional area (CSA) in smokers and/or patients with COPD classified as Global Initiative for Obstructive Lung Disease (GOLD) I and without lung cancer. Two authors screened and identified the studies for inclusion. Eighteen studies were identified. Some studies found lower values in a variety of muscle strength variables in smokers compared with nonsmoking controls, whereas others found similar values between these groups. When comparing patients with COPD classified as GOLD I with smokers, COPD patients showed lower muscle strength. Two studies found no differences in muscle CSA between smokers compared with nonsmoking controls. Some preliminary evidence also shows that patients with COPD classified as GOLD I had lower CSA in comparison with smokers. Results concerning muscle dysfunction in smokers are divergent, since some studies have shown worse results in a variety of muscle strength variables in smokers compared with nonsmoking controls, whereas other studies have not. Moreover, there is rather preliminary evidence indicating worse muscle dysfunction and lower CSA in patients with mild COPD in comparison with healthy (or non-COPD) smokers.

Difference in Long-Term Trends in COPD Mortality between China and the U.S., 1992⁻2017: An Age⁻Period⁻Cohort Analysis.

Complications due to chronic obstructive pulmonary disease (COPD) is a leading cause of death in China and the United States (U.S.). This study aimed to investigate the long-term trends in COPD mortality in China and the U.S. using data from the Global Burden of Disease Study 2017 (GBD 2017) and explore the age, period, and cohort effects independently by sex under the age–period–cohort (APC) framework. Taking the age group 40–44 years old, the period 1992–1996, and the birth cohort 1913–1917 as reference groups, we found that the age relative risks (RRs) of COPD mortality increased exponentially in both China and the U.S., the period RRs increased in the U.S. but decreased in China; and the cohort RRs showed an overall downward trend in both China and the U.S. with the year of birth. From 1992 to 2017, the increased RRs of COPD mortality in the U.S. was mainly attributable to the increased prevalence of smoking before 1965, while the decreased RRs of COPD mortality in China was mainly attributable to reduced air pollution as well as improvements in medical technology and more accessible health services. Reducing tobacco consumption may be the most effective and feasible way to prevent COPD in China. However, we also need to pay more attention to COPD in nonsmokers in the future.

A clinical study of chronic obstructive pulmonary disease in non-smokers attending a tertiary care hospital

Background: Chronic Obstructive Pulmonary Disease (COPD) ranks third among the prime causes of death globally. To study the clinical profile of COPD in non-smokers. To identify the other risk factors (other than smoking) of COPD. Methodology: Data was collected meeting the objectives of the study with a pre-tested proforma. Detailed history was taken, clinical examination was done and necessary investigations were carried out. Continuous data was expressed as Mean + SD and categorical data was expressed as number and percentage (%). Results: In the present study it was observed that most of the non-smoker COPD patients belonged to older age group. In the present study the mean age of the patients was 55.06 + 8.87 years. study subjects 80 years were 0% females account for 68%, with a male to female ratio of 1: 2.125. Conclusions: In this study of COPD in non-smokers, females were predominant. Cough and sputum production were the most common clinical features. Environmental tobacco smoke exposure and biomass fuel usage were the most common risk factors. Most of the patients belonged to rural background. Most of the patients presented with less severe form of the disease. Keywords: COPD; Non-smoker; Cough; Biomass; Smoking.

Clinical, demographic and radiological profile of smoker COPD versus nonsmoker COPD patients at a tertiary care center in North India.

Introduction:Cigarette smoking is the most predominant risk factor for development of chronic obstructive pulmonary disease (COPD). However, a considerable amount of patients do develop COPD without exposure to cigarette smoking. We aimed to analyze the incidence, demographic and clinical profile of nonsmoker COPD subjects at a tertiary care center.Methods:In this prospective observational study, 410 patients were screened for dyspnea. On the basis of spirometry findings, 360 patients were diagnosed as COPD and enrolled into the study. Patients were categorized into 2 groups on the basis of smoking habits (smoker and nonsmoker COPD). Clinical and demographic attributes were compared in between these two groups. This study was conducted over a period of one year, from August 2014 to July 2015. All statistical analyses were performed using Statistical Package for the Social Sciences version 19.0 (SPSS Inc, Chicago, IL, USA). Values were considered to be statistically significant at P < 0.05.Results:Out of 360 COPD cases, about 2/3rd (60%) were smokers and the rest nonsmokers. Majority of the patients were in the age group of 51-70 years. The mean age of smokers with COPD was significantly higher than nonsmokers with COPD (59.29 ± 10.28 years vs. 53.90 ± 8.77 years; P = 0.0001). Overall, males were predominant (57.2%) but there were higher number of female patients in nonsmoker group (25% vs. 70%; P = 0.001). At presentation, majority of nonsmoker with COPD were in GOLD severity grade II while in the smoking cohort majority were in GOLD severity Grade III. Among the 144 nonsmoker COPD patients, the most important and statistically significant risk factor was exposure to biomass smoke (68.06%). Other risk factors were long-standing asthma (37.50%), lower respiratory tract infection in childhood (32.60%), exposure to outdoor air pollution (17.92%).Conclusion:Nonsmoker COPD is emerging as a distinctive phenotype. They have less impairment in airflow limitation, and a lower prevalence of emphysema, chronic cough, and sputum compared with their smoking counterparts.

Biomass smoke COPD has less tomographic abnormalities but worse hypoxemia compared with tobacco COPD.

Special attention has emerged towards biomass smoke-induced chronic obstructive pulmonary disease (COPD), providing new knowledge for prevention and therapeutic approach of non-smoker COPD patients. However, the understanding of biomass smoke COPD is still limited and somewhat controversial. The aim of the present study was to compare COPD exclusively caused by tobacco smoking with COPD exclusively caused by environmental or occupational exposures. For this cross-sectional study, COPD patients were recruited from outpatient clinics and formed two groups: non-smoker COPD group (n=16) with exposure to biomass smoke who did not smoke cigarette and tobacco smoker COPD group (n=15) with people who did not report biomass smoke exposure. Subjects underwent pulmonary function tests, thoracic high-resolution computed tomography, 6-min walk test, and sputum induction. The non-smoker COPD group had biomass smoke exposure of 133.3±86 hour-years. The tobacco COPD group smoked 48.5±27.4 pack-years. Women were 62.5 and 66.7%, respectively, of non-smokers and smokers. The non-smoker COPD group showed higher prevalence of dyspnea, lower arterial oxygen tension (PaO2), and lower arterial oxygen saturation (SaO2%) with similar spirometry results, lung volumes, and diffusion capacity. Regarding inflammatory biomarkers, differences were detected in sputum number of lymphomononuclear cells and in sputum concentrations of interleukin (IL)-6 and IL-8 with higher values in the smoker group. Emphysema was more prevalent in the tobacco smoker group, which also showed higher relative bronchial wall thickness and lower lung density by quantitative analysis. Biomass smoke induced more hypoxemia compared to tobacco in COPD patients with similar severity.

Prevalencia y características de la enfermedad pulmonar obstructiva crónica en no fumadores

ObjectiveThe objective of the study was to know the profile of patients diagnosed with chronic obstructive pulmonary disease (COPD) and who have never been smokers. DesignA transversal study. LocationPrimary Care Centre of Pla d’Urgell (Primary care setting in Lleida, Spain). Participants512 patients older than 40 years with COPD from Primary Care Centre of Pla d’Urgell with a compatible spirometry [forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) ratio <0.7) to the beginning of the study. Main measurementsThe dependent variable was de COPD in non-smokers and the independents were variables collected from the information on the respiratory clinical history, the risk factors of the patients and on quality of life. We designed a predictor model of COPD in non-smokers compared to smokers. Results33.2% of COPD patients had never been smokers, 59.4% of whom were women. The average FEV1 for non-smokers was 70.5 (SD=17.1), higher than 62.6 (SD=18.5) for smokers/former smokers (p<0.001). The coverage of pneumococcal vaccination 23V was better in non-smokers (75.3%), p<0.001. COPD in non-smokers (compared to smokers/former smokers) were: mostly women (OR=16.46), older (OR=1.1), with better FEV1 (OR=1.1), better perception of quality, EuroQoL-5D (OR=0.8), with lower prevalence of diabetes (OR=0.5), lower level of studies (OR=0.2), and with fewer previous hospitalizations (OR=0.3). ConclusionsThe study evidences a high proportion of non-smokers in COPD patients. Our study aims that older women with less severity would be associated with an increased risk of COPD in non-smokers. It seems to indicate that COPD in non-smokers would appear at later ages and would be milder than smoking-related COPD.

Varenicline for long term smoking cessation in patients with COPD

BackgroundQuitting smoking is key for patients with Chronic Obstructive Pulmonary Disease (COPD). Standard recommendations for quitting smoking are implemented for COPD as well. Varenicline Tartrate (VT) is the most effective drug to help quit smoking, but few studies have analysed its effectiveness.Aim of the study: To determine the Abstinence Rate (AR) at 12 months, in COPD and non-COPD smokers. MethodsObservational study in 31 COPD (post bronchodilator-BD FEV1/FVC <0.70) and in 63 non-COPD smokers, were invited to receive treatment with Varenicline Tartrate (VT). Fourteen subjects with COPD and 46 non-COPD subjects received additionally Cognitive-Behavioral Therapy (CBT). Abstinence rate (AR) was validated by exhaled carbon monoxide CO (COe), in addition to a phone or face-to-face interview. Motivation score was measured with a visual analogue scale (MS). ResultsDifferences between COPD and non-COPD, mean FEV1/FVC ratio 0.52 ± 0.10 vs. 0.90 ± 0.15, age 60 ± 10 vs. 47 ± 10 years, smoking pack-years 37 ± 3.5 vs. 22 ± 12, and COe 16 ± 11 vs. 12 ± 9 ppm were statistically significant (p < 0.05); for MS the score was 93 ± 11 vs. 93 ± 11 and for attempts to quit (AQ) 2 ± 2 vs. 2 ± 3 were not. AR was not significantly different at 12 months (61.2 vs. 42.8% p = 0.072). Motivation was the only significant one-year AR predictor. ConclusionsCOPD smokers had a similar response (higher tendency) to VT regardless of the presence of airflow obstruction and stronger nicotine addiction.

Kezdeti tapasztalatok a HUNCHEST – alacsony dózisú CT-tüdőrákszűrési pilotprogrammal

Lung cancer is the cause of death of around 8000 Hungarians each year. International studies have proved that low-dose CT (LDCT) screening lowers the lung cancer mortality of high risk patients. The HUNCHEST pilot study launched in 2014 studies the possibilities of a lung cancer screening programme in Hungary. The study is also aimed at showing whether there is an increased number of detected lung cancer in the subgroup with chronic obstructive pulmonary disease (COPD). COPD and nonCOPD subjects, smokers and non-smokers are screened with low-dose CT in the 50-79 age group. The study is still undergoing recruitement, but in the light of the first results, the principles of the screening programme at the National Korányi Institute of Pulmonology are also presented. Orv Hetil. 2018; 159(43): 1741-1746.

Etiology and clinical profile of COPD in non-smoker in urban area

Background: Smoking is established as a causative risk factor for COPD as early as 1950. However, in the past decade it is shown that, other risk factors like indoor and outdoor air pollutants, workplace exposure to dust and fumes, poor nourishment and poor socioeconomic status are also associated with COPD. COPD is a disease associated poor quality of life due to recurrent exacerbations. Till to date focus has been on smoking as a risk factor for COPD, but other factors also need to be taken into consideration.Methods: Study was conducted in 60 eligible patients from urban area for a period of 18 months. Individual patient was asked detailed personal demographic data, respiratory symptoms, exposure to passive smoking, family history of COPD. Detailed physical examination including Anthropometric measurements and other relevant general and systemic examination was carried out. Biochemical investigations, ECG, Chest X-ray, CT chest, spirometry and 2D echocardiography were carried out in all patients.Results: The mean age of the patient was 65.7±7.95 with male preponderance. Common symptoms were dyspnea and cough and common signs were rhonchi and hyper resonance note on percussion. Common risk factors were indoor air pollution and low socioeconomic class. Most of the patients has hypoxia and hypercapnia. X-ray chest and CT chest showed hyperinflation, air trapping. Majority of patients had moderate FEV/FVC ratio on spirometry.Conclusions: Non-smoker COPD patients usually present in old age. Common presentation is dyspnea followed by cough and rhonchi on examination. Most common risk factor for non- smoker COPD is indoor air pollution, low socioeconomic class and cotton mill workers. Amongst indoor pollution, LPG, kerosene and wood are the risk factors for non-smokers COPD in urban population.

Effect of Liuweibuqi capsules on CD4+CD25+Foxp3+ regulatory T cells, helper T cells and lung function in patients with stable chronic obstructive pulmonary disease complicated with lung Qi deficiency

Chronic obstructive pulmonary disease (COPD) is predicted to become the fifth leading cause of disability and the third leading cause of death around the world by 2020. Though it is potentially treatable and preventable, evidence of brain structural alterations in COPD remains sparse and conflicting. We aim to investigate the effect of Liuweibuqi capsules on CD4+CD25+ Forkhead box protein 3+ (Foxp3+) regulatory T cells (Tregs), helper T cells (Th) and lung function in patients with stable COPD complicated with lung Qi deficiency. COPD patients with lung Qi deficiency [458] were assigned into non-smoking COPD (NS-COPD), non-smoking control (NS-control), smoking COPD (S-COPD) and smoking control (S-control) groups, and healthy volunteers [245] into the non-smoking healthy (NSH) and smoking healthy (SH) groups. Levels of inflammatory cytokines were detected by Enzyme-linked immunoassay (ELISA). Contents of inflammatory cells, inflammatory marker, and CD4+CD25+Fox3+Tregs were measured by flow cytometry. FEV1/FVC (%) and FEV1 (%) were detected by pulmonary function test apparatus. Correlation between FEV1 (%) and Th1, Th2, Th17, Th1/Th2 or CD4+CD25+Fox3+Tregs was analyzed by Spearman rank correlation test. The related factors affecting treatment efficacy was assessed by logistic analysis. COPD patients and smoking people showed higher level of INF-γ, IL-4, IL-17, Th1, Th2, Th17 and Th1/Th2 but lower level of CD4+CD25+Fox3+Tregs. Liuweibuqi capsules could decrease level of inflammatory cells, cytokines, and markers (especially Th17 and IL-17), and increase level of CD4+CD25+Fox3+Tregs. FEV1 (%) negatively correlated with Th1, Th2, Th17 and Th1/Th2 but positively correlated with CD4+CD25+Fox3+Tregs, and smoking may strengthen their correlation, but Liuweibuqi capsules may weaker their correlation. Levels of inflammatory cytokines, cells, marker, CD4+CD25+Fox3+Tregs, FEV1/FVC (%), FEV1 (%), smoking and Liuweibuqi capsules are factors affecting efficacy. Taken together, our data support the notion that smoking is an important factor to induce and aggravate COPD. Liuweibuqi capsules could stimulate proliferation of CD4+CD25+Fox3+Tregs and decrease Th17 expression to improve the lung function in stable COPD patients with lung Qi deficiency, and it had obvious efficacy for smoking COPD patients.

Comprehensive Analysis of miRNA-mRNA-lncRNA Networks in Non-Smoking and Smoking Patients with Chronic Obstructive Pulmonary Disease

Background/Aims: Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. This study aimed to identify overlapping or diverging dysregulated genes, lncRNAs, miRNAs and signaling pathways in smoking and non-smoking chronic obstructive pulmonary disease (COPD). Methods: Compared to normal controls, we identified the shared and divergent differentially expressed mRNAs (DEmRNAs), miRNAs (DEmiRNAs) and lncRNAs (DElncRNAs) in smoking and non-smoking COPD by RNA-sequencing and bioinformatics analysis. Functional annotation of DEmRNAs were performed. Both cis and trans-target DEmRNAs of DElncRNAs were identified. The target DEmRNAs of DEmiRNAs were identified as well. The DEmiRNA-DEmRNA-DElncRNA interaction network was constructed. QRT-PCR was performed to validat the selected DEmiRNAs, DEmRNA and DElncRNAs in COPD. Results: Compared to normal control, 1234 DEmRNAs, 96 DElncRNAs and 151 DEmiRNAs were identified in non-smoking patients with COPD; 670 DEmRNAs, 44 DElncRNAs and 63 DEmiRNAs were identified in smoking patients with COPD. Leukocyte transendothelial migration and pathways in cancer were significantly enriched pathways in non-smoking and smoking COPD, respectively. MiR-122-5p-A2M-LINC00987/A2M-AS1/ linc0061 interactions might play key roles in COPD irrespective with the smoking status. Let-7-ADRB1-HLA-DQB1-AS1 might play a key role in the pathogenesis of smoking COPD while miR-218-5p/miR15a-RORA-LOC101928100/LINC00861 and miR-218-5p/miR15a-TGFβ3-RORA-AS1 interactions might involve with non-smoking COPD. Conclusion: We identified the shared and diverging genes, lncRNAs, miRNAs and their interactions and pathways in smoking and non-smoking COPD which provided clues for understanding the mechanism and developing novel diagnostic and therapeutic strategies for COPD.

The Lipid Profile Parameter in Chronic Obstructive Pulmonary Disease Patients and Correlation with Severity of Disease

Introduction: More than 90% of the deaths caused by chronic obstructive pulmonary disease (COPD) occur in the low- and middle -income countries. The main aim of this study was to investigate the lipid profile levels in COPD patients and examine the correlation of total cholesterol, triglycerides, low-density lipoproteins, high density lipoproteins, and LDL/HDL risk ratio with COPD stages that are developed by the global initiative for chronic obstructive lung disease (GOLD) Materials & Methods: A total of 100 COPD patients including 25 COPD non-smokers were enrolled in this study. The diagnosis of COPD was carried out by using the spirometry following the GOLD guidelines (post-bronchodilator forced expiratory volume (FEV1)/forced vital capacity (FVC) ratio < 70% predicted). Accordingly, the patients were divided into four groups based on the severity of their disease in accordance with the GOLD guidelines, including mild COPD (stage I, FEV1 ≥ 80% predicted), moderate COPD (stage II, 50% ≤ FEV1 < 80% predicted), severe COPD (stage III, 30% ≤ FEV1 < 50% predicted), and very severe COPD (stage IV, FEV1 < 30% predicted). The fasting blood samples of lipid profile were collected. The four COPD groups were compared using the ANOVA test. Results: According to the results, the majority 53 patients (53%) were in age group 40 to 60 years with mean age of 60.46 +/-11.56. Most of the patients had moderate to severe airflow obstruction (GOLD stages II and III). The severity of COPD had no significant correlation with the triglycerides, LDL, HDL, and LDL/HDL risk ratio. The mean total cholesterol levels in the stages I and IV were 151.92±32.82 and 128.50 ±21.46 mg/dL, respectively, which was statistically significant (P=0.04). Conclusion: The present study indicates that there was no significant correlation between various lipid profile parameters and severity of COPD.

Serum cytokine levels related to exposure to volatile organic compounds and PM2.5 in dwellings and workplaces in French farmers - a mechanism to explain nonsmoking COPD.

Although French farmers smoke less on average than individuals from the general population, they suffer more from COPD. Exposure to biological and chemical air pollutants in the farm may be the cause of these higher COPD rates. This study investigates the role of bio-contaminants, including the relationship of exposure to volatile organic compounds (VOCs) and fine particulate matter (of diameter of 2.5 µm [PM2.5]) objectively measured in the farm settings (dwellings and workplaces) to serum cytokines involved in COPD, in a sample of 72 farmers from 50 farms in the Auvergne region, France. Mean concentrations of VOCs were highest inside the home, while levels of PM2.5 were highest in workplaces (stables and granaries). After adjusting for confounders, high exposure to PM2.5 was significantly associated with a decreased level of serum cytokines (among others, IL13: β: −0.94, CI: −1.5 to −0.2, P-value =0.004; IL8: β: −0.82, CI: −1.4 to −0.2, P-value =0.005) and high exposure to VOCs according to a VOC global score with a decreased IL13 level (β: −0.5, CI: −0.9 to −0.1, P-value =0.01). Moreover, respiratory symptoms and diseases, including COPD, were associated with a decreased level of serum cytokines significantly in the case of IL5. An alteration of immune response balance in terms of cytokine levels in relation to indoor chemical air pollution exposure may contribute to respiratory health impairment in farmers.

Telomere shortening and accelerated aging in COPD: findings from the BODE cohort

BackgroundChronic Obstructive Pulmonary Disease (COPD) may be associated with accelerated aging. Telomere shortening is a biomarker of aging. Cross-sectional studies describe shorter telomeres in COPD compared with matched controls. No studies have described telomere length trajectory and its relationship with COPD progression. We investigated telomere shortening over time and its relationship to clinical and lung function parameters in a COPD cohort and smoker controls without COPD.MethodsAt baseline leukocyte telomere length was measured by qPCR in 121 smokers with COPD and 121 without COPD matched by age (T/S0). The measurements were repeated in 70 of those patients with COPD and 73 non-COPD smokers after 3 years of follow up (T/S3).ResultsAt initial measurement, telomeres were shorter in COPD patients when compared to smoker controls (T/S = 0.68 ± 0.25 vs. 0.88 ± 0.52, p = 0.003) independent from age and sex. During the follow-up period, we observed an accelerated telomere shortening in individuals with COPD in contrast to smoker controls (T/S0 = 0.66 ± 0.21 vs. T/S3 = 0.46 ± 0.16, p < 0.001, for the patients with COPD and T/S0 = 0.83 ± 0.56 vs. T/S3 = 0.74 ± 0.52, p = 0.023 for controls; GLIM, p = 0.001). This shortening was inversely related to the baseline telomere length (r = −0.49, p < 0.001). No significant relationship was found between the rate of change in telomere length and change in lung function in the patients with COPD (p > 0.05).ConclusionsCompared with smokers, patients with COPD have accelerated telomere shortening and this rate of attrition depends on baseline telomere length. Furthermore, the telomere length and its rate of shortening did not relate to clinical and lung function parameters changes over 3 years of follow-up.

Prevalence and etiological profile of chronic obstructive pulmonary disease in nonsmokers.

Background:Tobacco smoking has been recognized as the most important risk factor for chronic obstructive pulmonary disease (COPD) for a long time, but recent studies have shown that nonsmokers also contribute to a significant proportion of COPD. This study was performed to find out the proportion of nonsmoker individuals among COPD patients and to determine various etiologies in nonsmoker COPD patients.Materials and Methods:This study was an observational cross-sectional study conducted in Department of Pulmonary Medicine, MLN Medical College, Allahabad. A total of 200 COPD patients, aged >18 years of either gender with COPD, diagnosed by clinical and spirometric criteria (GOLD guideline) were included in the study.Results:Of the 200 COPD patients, the proportion of nonsmoker patients was 56.5%, and the smoker was 43.5%. Among 113 nonsmoker COPD patients, maximum number of patients (69.03%) belonged to low socioeconomic status but most important and statistically significant risk factor was exposure to biomass smoke (53.98%), other significant risk factors were treated pulmonary tuberculosis (32.74%), and long-standing asthma (14.16%). Risk factors that were not statistically significant were occupational exposure (9.73%), exposure to outdoor air pollution (3.54%), and lower respiratory tract infection during childhood (1.77%). The patients who were exposed to more than one risk factors, developed COPD at an earlier age.Conclusions:This study revealed that nonsmokers contribute a significant proportion of COPD patients. Multiple risk factors other than smoking also play a major role in the development of COPD, particularly exposure to biomass smoke, treated pulmonary tuberculosis, and long-standing asthma.

Antibacterial Defense of Human Airway Epithelial Cells from Chronic Obstructive Pulmonary Disease Patients Induced by Acute Exposure to Nontypeable Haemophilus influenzae: Modulation by Cigarette Smoke

Antimicrobial proteins and peptides (AMPs) are a central component of the antibacterial activity of airway epithelial cells. It has been proposed that a decrease in antibacterial lung defense contributes to an increased susceptibility to microbial infection in smokers and patients with chronic obstructive pulmonary disease (COPD). However, whether reduced AMP expression in the epithelium contributes to this lower defense is largely unknown. We investigated the bacterial killing activity and expression of AMPs by air-liquid interface-cultured primary bronchial epithelial cells from COPD patients and non-COPD (ex-)smokers that were stimulated with nontypeable Haemophilus influenzae (NTHi). In addition, the effect of cigarette smoke on AMP expression and the activation of signaling pathways was determined. COPD cell cultures displayed reduced antibacterial activity, whereas smoke exposure suppressed the NTHi-induced expression of AMPs and further increased IL-8 expression in COPD and non-COPD cultures. Moreover, smoke exposure impaired NTHi-induced activation of NF-κB, but not MAP-kinase signaling. Our findings demonstrate that the antibacterial activity of cultured airway epithelial cells induced by acute bacterial exposure was reduced in COPD and suppressed by cigarette smoke, whereas inflammatory responses persisted. These findings help to explain the imbalance between protective antibacterial and destructive inflammatory innate immune responses in COPD.

Study of Role of Surfactant Protein-D, Malondialdehyde, Protein Carbonyl and its Correlation with Airflow Obstruction (FEV1% Predicted) in Patients with Smoker Chronic Obstructive Pulmonary Disease (COPD)

Background: Smokers lungs are exposed to rich amounts of oxidants. Oxidative stress and inflammation are hallmarks of chronic obstructive pulmonary disease. SP-D is lung specific protein play important role in the lungs including regulation of surfactant homeostasis in the alveoli and modulation of host defense system in the lung. The aim of this study was to examine role of surfactant protein-D, malondiladehyde and protein carbonyl in smoker COPD patients and to see whether there is any correlation between pulmonary function test with MDA, PC and SP-D in COPD patients. Materials and methods: We measured serum SP-D, MDA and PC in 30 smoker COPD patients, 30 non-smoker COPD patients and in 30 healthy controls by ELISA and spectrophotometric methods respectively. Results: Serum levels of SP-D, MDA and PC were significantly higher in smoker COPD patients than non-smoker COPD patients. SP-D, MDA and PC were significantly increased in smoker COPD patients as compared to healthy controls. We found inverse correlation between FEV1% predicted with SP-D, MDA and PC in COPD patients. MDA and PC were directly correlated with SP-D in COPD patients. Conclusion: From these findings we conclude that deleterious effect tobacco smoke causes lipid and protein oxidation and lung tissue damage. Lung tissue injury causes release of SP-D in the blood stream. This is directly related with extent of injury and pulmonary function in COPD patients.

Prevalence and Risk Factors of Chronic Obstructive Pulmonary Disease among Nonsmokers: Fifth Korea National Health and Nutrition Examination Survey (2010–2012)

ObjectivesThe purpose of this study was to determine the prevalence of COPD among non-smoking adults, and to investigate the risk factors that affect disease occurrence. MethodsThe data from the 5th Korea national health and nutrition examination survey (KNHNES) has been used, and 5,489 non-smoking adults aged between 40 to 79 years with diagnosable FEV1/FVC were selected therefrom as the subjects of this study. ResultsThe prevalence of COPD in non-smokers was observed to be 6.9%. The development of the COPD showed statistically significant difference among groups; males showed about 2.54 times (95% CI: 1.410∼146.612) higher rates compared to females, subjects aged 70–79 showed about 3.08 times (95% CI: 1.823∼11.437) higher rates compared to those aged 40–49, subjects whose education level was elementary school or less showed about 5.36 times (95% CI: 1.341∼21.393) higher rates compared to those who are college or more, and subjects who are middle school showed about 4.72 times (95% CI: 1.374∼16.217) higher rates compared to the college or more. ConclusionIt is confirmed that development of the COPD in non-smokers reach significance. For the prevention of the disease, there is a need to identify COPD-related risk factors in males and the elderly and provide appropriate nursing intervention, and to develop health-related education programs for those with low educational background to take in order to promote the improvement of lung health.

Interleukin-17 expression and clinical significance in the lung tissue of patients with stable chronic obstructive pulmonary disease

To observe the interleukin-17 (IL-17) expression in lung tussiue of patients with stable chronic obstructive pulmonary disease (COPD) and investigate the clinical significance. A total of 50 patients receiving lung resections in General Hospital, Tianjin Medical University for lung cancer from October 2010 to October 2011 were included and divided into non-smoking COPD group (NS group), smoking non-COPD group (S group), smoking COPD group (COPD group) according to smoking status and 2013 COPD diagnosis standard. The expression of IL-17 was detected by immumohistochemical staining. The volume of IL-17 in the airway and lung parenchyma was calculated by immumohistochemical staining scores which was product of dyeing cells positive rate and intensity. Pearson correlation analysis was used to analyze the relationships between expression of IL-17 in the airway and lung parenchyma and forced expiratory volume in 1 second/predicted value (FEV1%pred), carbon monoxide diffusion amount accounting for the percentage of the expected value (DLCO%pred), COPD assessment test (CAT) score, body mass index (BMI). The expressions of IL-17 in airway and lung parenchyma in S group (5.6±3.1, 6.4±2.5) were higher than those in NS group (1.6±1.4, 1.4±1.2) (both P<0.05), while expressions in COPD group (7.3±2.5, 7.8±2.1) were further higher than S group (both P<0.05). In the S group and COPD group, the expressions of IL-17 in the airway and lung parenchyma were positively correlated with smoking (r=0.453, P=0.007 and r=0.573, P<0.001); In the COPD group, the expressions of IL-17 in the airway and lung parenchyma were negatively correlated with FEV1%pred (r=-0.729, P=0.001 and r=-0.489, P=0.039), negatively related with DLCO%pred (r=-0.493, P=0.038 and r=-0.520, P=0.027), positively correlated with COPD CAT score (r=0.730, P=0.001 and r=0.644, P=0.004) and negatively related with BMI (r=-0.653, P=0.003 and r=-0.485, P=0.041). Smoking increases inflammation of lung tissue, increases IL-17 expression in airway and lung parenchyma; the expression of IL-17 is closely related to the severity of disease, the quality of life and prognosis in COPD patients.