non-COPD Smokers Research Articles

The Risk Factors and Characteristics of COPD Among Nonsmokers in Korea: An Analysis of KNHANES IV and V.

Chronic obstructive pulmonary disease (COPD) is increasing in prevalence and mortality. This study evaluated the prevalence, risk factors, characteristics, and health-related quality of life (HRQoL) of COPD among nonsmokers in Korea. This was a population-based cross-sectional study using data obtained from the Fourth and Fifth Korean National Health and Nutrition Examination Survey, which was conducted from 2007 to 2011. A total of 15,063 participants completely answered the questionnaire and performed the spirometry. Among them, 59.6% were nonsmokers and 40.4% were smokers. The prevalence of nonsmoker COPD was 7.1%. On multivariate analysis, age ≥65years (OR, 2.93; 95% CI, 2.44-3.51), male sex (OR, 2.98; 95% CI, 2.40-3.71), living in rural area (OR, 1.26; 95% CI, 1.05-1.51), lower body mass index (BMI) (<18.5kg/m(2)) (OR, 3.00; 95% CI, 1.78-5.01), self-reported asthma (OR, 2.72; 95% CI, 2.05-3.60), and self-reported tuberculosis (OR, 4.73; 95% CI, 3.63-6.17) showed a significantly higher risk of nonsmoker COPD. Analysis of nonsmoker and smoker COPD revealed that there are more females in nonsmoker COPD patients (73.9 vs. 6.9%, P<0.001). Nonsmoker COPD patients presented with impaired mobility, pain/discomfort, and anxiety/depression functions as well as a lower mean EuroQol Five-Dimension Questionnaire utility score, which showed HRQoL. The burden of nonsmoker COPD was considerable. Older age, male sex, lower BMI, self-reported asthma, and self-reported tuberculosis were risk factors for nonsmoker COPD and there were differences between nonsmoker and smoker COPD in terms of sex, comorbidities, and HRQoL.

COPD in Nonsmokers: Reports from the Tunisian Population-Based Burden of Obstructive Lung Disease Study.

BackgroundIt’s currently well known that smoking and increasing age constitute the most important risk factors for chronic obstructive pulmonary disease (COPD). However, little is known about COPD among nonsmokers. The present study aimed to investigate prevalence, risk factors and the profiles of COPD among nonsmokers based on the Tunisian Burden of Obstructive Lung Disease (BOLD) study.Methods807 adults aged 40 years+ were randomly selected from the general population. We collected information about history of respiratory disease, risk factors for COPD and quality of life. Post-bronchodilator spirometry was performed for assessment of COPD. COPD diagnostic was based on the post-bronchodilator FEV1/FVC ratio, according to the Global Initiative for Obstructive Lung Disease (GOLD) guidelines. The lower limit of normal (LLN) was determined as an alternative threshold for the FEV1/FVC ratio.Results and ConclusionsAmong 485 nonsmokers, 4.7% met the criteria for GOLD grade I and higher COPD. These proportions were similar even when the LLN was used as a threshold. None of the nonsmokers with COPD reported a previous doctor diagnosis of COPD compared to 7.1% of smokers. Nonsmokers accounted for 45.1% of the subjects fulfilling the GOLD spirometric criteria of COPD. Nonsmokers were predominately men and reported more asthma problems than obstructed smokers. Among nonsmokers significantly more symptoms and higher co-morbidity were found among those with COPD. Increasing age, male gender, occupational exposure, lower body mass index and a previous diagnosis of asthma are associated with increased risk for COPD in nonsmokers. This study confirms previous evidence that nonsmokers comprise a substantial proportion of individuals with COPD. Nonsmokers with COPD have a specific profile and should, thus, receive far greater attention to prevent and treat chronic airway obstruction.

Prevalence and incidence of COPD in smokers and non-smokers: the Rotterdam Study.

COPD is the third leading cause of death in the world and its global burden is predicted to increase further. Even though the prevalence of COPD is well studied, only few studies examined the incidence of COPD in a prospective and standardized manner. In a prospective population-based cohort study (Rotterdam Study) enrolling subjects aged ≥45, COPD was diagnosed based on a pre-bronchodilator obstructive spirometry (FEV1/FVC < 0.70). In absence of an interpretable spirometry within the Rotterdam Study, cases were defined as having COPD diagnosed by a physician on the basis of clinical presentation and obstructive lung function measured by the general practitioner or respiratory physician. Incidence rates were calculated by dividing the number of incident cases by the total number of person years of subjects at risk. In this cohort of 14,619 participants, 1993 subjects with COPD were identified of whom 689 as prevalent ones and 1304 cases as incident ones. The overall incidence rate (IR) of COPD was 8.9/1000 person-years (PY); 95 % Confidence Interval (CI) 8.4–9.4. The IR was higher in males and in smokers. The proportion of female COPD participants without a history of smoking was 27.2 %, while this proportion was 7.3 % in males. The prevalence of COPD in the Rotterdam Study is 4.7 % and the overall incidence is approximately 9/1000 PY, with a higher incidence in males and in smokers. The proportion of never-smokers among female COPD cases is substantial.Electronic supplementary materialThe online version of this article (doi:10.1007/s10654-016-0132-z) contains supplementary material, which is available to authorized users.

Does SOD3 R213G Homozygosity Influence Morbidity, Mortality, and Lung Function in the General Population?

The extracellular superoxide dismutase (SOD3, EC-SOD) enzyme is a major extracellular scavenger of the superoxide anion, a free radical with the potential to cause oxidative damage. Previously, R213G heterozygosity has been associated with a decreased risk of chronic obstructive pulmonary disease (COPD) and an increased risk of ischemic heart disease (IHD). We questioned whether SOD3 R213G homozygosity (213GG) influences morbidity, mortality, and lung function. We found 14 R213G homozygotes (213GG) among 95,871 individuals (1/7000) from the Copenhagen General Population Study and the Copenhagen City Heart Study. The hazard ratio for homozygotes versus noncarriers (NC) (213RR) was 2.8 (95% confidence interval: 1.2-6.8, p = 0.02) for IHD, 1.8 (0.7-4.8, p = 0.25) for any form of cancer, and 2.3 (0.9-6.2, p = 0.10) for all-cause mortality. R213G heterozygosity was not associated with morbidity or mortality. Among never-smokers, we found a 20% lower forced expiratory volume in 1 s (FEV1)% predicted (p = 0.003), a 16% lower FVC% predicted (p = 0.01), and a 7% lower FEV1/FVC ratio (p = 0.02) in R213G homozygotes compared to NC. Our results lead to the hypotheses that the SOD3 enzyme plays a role in cardiovascular disease and in impairing and maintaining lung function in never-smokers. However, our findings should be retested in larger studies and in nonsmoking COPD patient cohorts. Antioxid. Redox Signal. 24, 884-891.

N-Acetylcysteine Combined with Home Based Physical Activity: Effect on Health Related Quality of Life in Stable COPD Patients- A Randomised Controlled Trial.

Quality of life is adversely affected in Chronic Obstructive Pulmonary Disease (COPD), due to irreversible, progressive nature of the disease and limitations of current treatment options available. One of the important aim of treatment of COPD is to improve Quality of Life (QoL). Cigarette smoke contains numerous free radicals and other oxidants. Oxidative stress has been implicated in pathogenesis, progression of disease and exacerbation in COPD. Pulmonary tuberculosis, outdoor and indoor air pollution and many others are aetiologies of COPD in non-smokers. N-Acetylcysteine (NAC) is a precursor of endogenous anti-oxidant, Glutathione (GSH) and both agents act as free radical scavengers. Exercise limitation results in poor physical performance and eventually poor QoL in COPD. To observe the combined effect of 600mg of NAC once daily and physical activity (home based) in addition to standard treatment for ten weeks, compared with placebo as control group with standard treatment. This randomised controlled trial was conducted at a tertiary care centre in Mumbai for two years from December 2011 to December 2013. Hundred patients diagnosed as stable COPD (as per Global Initiative against Obstructive Lung Disease (GOLD) 2010 guidelines) were enrolled in the study. There were 50 patients in study group and control group each. The QoL was assessed using Saint George Respiratory Questionnaire-C (SGRQ-C) initially and at the end of ten weeks. The study group was treated with NAC 600mg once a day combined with daily physical activity in addition to standard treatment. Control group patients were treated with placebo and standard treatment. At the end of 10 weeks, it was observed that, mean change in SGRQ-C was significant in "study group" as compared to "control group". Mean change in score among study group was 4.72 and the same in control was 1.32, p-value=0.007. There was significant improvement in SGRQ-C score at the end of 10 weeks and QoL in the study group (p-value-0.0001 i.e., <0.05) while improvement in SGRQ-C score and QoL score in control group was not significant (p-value=0.118 i.e., >0.05). Overall, there was statistically significant improvement in SGRQ-C score and QoL (p-value=0.03 i.e., <0.05) in the study group. From the current study, it can be concluded that N-acetylcysteine 600mg once a day and 20 minute daily walk in addition to regular treatment improves QoL in stable COPD patients.

Variability in proteinase-antiproteinase balance, nutritional status, and quality of life in stable chronic obstructive pulmonary disease due to tobacco and nontobacco etiology.

Context:Although the role of proteinase/antiproteinase imbalance in chronic obstructive pulmonary disease (COPD) due to tobacco is well established, information in COPD due to nontobacco etiology is sparse.Aims:To assess the variability in metalloproteinase activity in COPD related to tobacco and nontobacco causes.Settings and Design:This is a hospital-based, prospective, observational study.Subjects and Methods:Serum matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinases-1 (TIMP-1) were estimated in 200 subjects divided equally into four groups, i.e. COPD in tobacco smokers, COPD in nonsmokers but with exposure to biomass-related indoor air pollution, smokers without COPD, and nonsmoking healthy controls. Anthropometric skinfold measurements, quality of life (QOL) using St. George Respiratory Questionnaire, and exercise capacity using the 6-min walk test (6-MWT) were carried out. Groups were compared using analysis of variance and Kruskal–Wallis plus Mann–Whitney U-test to assess differences between groups. The Chi-square and Fisher's exact tests were used to evaluate associations among categorical variables. Spearman's rank correlation was calculated to assess the correlation between data.Results:Patients with COPD due to either tobacco or nontobacco etiology were older, more malnourished, had worse QOL, and poorer exercise capacity compared to non-COPD subjects. Triceps, subscapular, and suprailiac skinfold thicknesses were less in smokers with COPD than biomass-related COPD. MMP-9 and TIMP-1 levels were similar across all groups. TIMP-1 significantly correlated with 6-MWT among all groups.Conclusions:The protease-antiprotease balance in COPD is similar irrespective of the presence or absence of tobacco exposure but is related to poor exercise capacity.

Association of ET-1 gene polymorphisms with COPD phenotypes in a Caucasian population

The phenotypic expression of COPD consists of pulmonary emphysema and chronic bronchitis. An imprecise phenotypic definition may result in inconsistencies among genetic studies regarding COPD pathogenesis. Endothelin-1 gene polymorphisms have been linked to increased susceptibility of COPD development. The present study examined the involvement of +138 insA/delA and G198T ET-1 polymorphisms with emphysematous and bronchitic COPD phenotypes. In order to narrow down the phenotypic choices to either COPD-associated pulmonary emphysema or chronic bronchitis, a DLCO < 60% predicted threshold was chosen as an indicator of severe emphysema. 116 COPD smokers and 74 non-related, non-COPD smokers were evaluated. Statistical analysis showed that the 4A allele of the +138insA/delA SNP and the 4A:T haplotype were associated predominantly with a chronic bronchitis phenotype, whereas the TT genotype of the G198T SNP was found to be protective from emphysema development. The presence of both the 4A and T allele seems to modify the final expression of COPD towards a chronic bronchitis phenotype, since the G:3A haplotype was associated with a predominantly emphysematous phenotype in our study.

To study the serum C-reactive protein level and its correlation with prognostic variables in stable COPD patients

Introduction: C-reactive protein is a stable and excellent biomarker of systemic inflammation which is easy to measure. COPD is an inflammatory disorder of lung with widespread Systemic manifestations and associated Systemic inflammatory response. C-reactive protein levels are increased in COPD patients. Present study investigated C-reactive protein level in stable COPD patients and its relation with clinically important outcome variable, exercise capacity. Method: Study included 56 stable COPD patients with mild to moderate severity in age group 40-70 years and 56 nonsmoking controls in the same age group. Clinical and physiological characteristics were determined and C-reactive protein levels were measured. Result: This study confirms the finding of higher C-reactive protein levels in smoker COPD patients (4.9 vs 4.0 mg-L-1) as compared to nonsmoker COPD patients. It also confirms that level of C-reactive protein in ex-smoker COPD population remains significantly higher than nonsmoker control group (4.9±0.5 vs 3.1mg/l). Conclusion: C-reactive protein level was strongly associated and correlated with 6 minute walk distance, FEV1 and GOLD stages, so C-reactive protein level can indirectly reflect prognosis of COPD patient and his exercise capacity. We recommend that measurement of C-reactive protein levels may be a useful tool to predict the prognosis and patient outcome in COPD patients. It also provides strong argument to develop therapies aimed at decreasing inflammation independent of smoking cessation.

Exhaled Breath Condensate pH in Lung Cancer, the Impact of Clinical Factors.

Lung cancer may be associated with airway acidification due to enhanced airway inflammation and oxidative stress. Exhaled breath condensate (EBC) pH is a non-invasive indicator of airway acidity; however, it is still unclear how EBC pH changes in lung cancer. The aim of the study was to investigate EBC pH in lung cancer together with clinical variables. Thirty-five patients with lung cancer and 37 control subjects (21 patients with stable COPD and 16 non-COPD smokers) were enrolled. EBC was collected for pH, which was determined with the argon-purging method, compared among the groups and correlated with clinical variables of patients with lung cancer. No difference was found in EBC pH between patients with lung cancer and control subjects. However, endobronchial tumour localisation, squamous-cell carcinoma subtype and gastro-oesophageal reflux were associated with low EBC pH values. No relationship was observed between EBC pH and the presence of COPD, lung function variables or smoking history. Although, EBC pH is unchanged in lung cancer, lower EBC pH values are associated with distinct phenotypes. Our findings could facilitate further research on airway acidity in lung cancer.

Epigenetic Repression of CCDC37 and MAP1B Links Chronic Obstructive Pulmonary Disease to Lung Cancer

Lung cancer and chronic obstructive pulmonary disease (COPD) share environmental risk factors. COPD also increases the risk of lung cancer; however, the molecular mechanisms are unclear. An epigenome-wide association study of lung tumors and cancer-free lung tissue (CFLT) pairs from non-small-cell lung cancer cases with (n = 18) or without (n = 17) COPD was conducted using the HumanMethylation450 beadchip (HM450K). COPD-associated methylation of top-ranked genes was confirmed in a larger sample set, independently validated, and their potential as sputum-based biomarkers was investigated. Methylation of CCDC37 and MAP1B was more prevalent in lung tumors from COPD than non-COPD cases [54 of 71 (76%) versus 20 of 46 (43%), p = 0.0013] and [48 of 71 (68%) versus 17 of 46 (37%), p = 0.0035], respectively, after adjustment for age, sex, smoking status, and tumor histology. HM450K probes across CCDC37 and MAP1B promoters showed higher methylation in tumors than CFLT with the highest methylation seen in tumors from COPD cases (p < 0.05). These results were independently validated using The Cancer Genome Atlas data. CCDC37 methylation was more prevalent in sputum from COPD than non-COPD smokers (p < 0.005) from two cohorts. CCDC37 and MAP1B expression was dramatically repressed in tumors and CFLT from COPD than non-COPD cases, p less than 0.02. The reduced expression of CCDC37 and MAP1B associated with COPD likely predisposes these genes to methylation that in turn, may contribute to lung cancer.

Fucosylated surfactant protein-D is a biomarker candidate for the development of chronic obstructive pulmonary disease

We previously reported that knockout mice for α1,6-fucosyltransferase (Fut8), which catalyzes the biosynthesis of core-fucose in N-glycans, develop emphysema and that Fut8 heterozygous knockout mice are more sensitive to cigarette smoke-induced emphysema than wild-type mice. Moreover, a lower FUT8 activity was found to be associated with a faster decline in lung function among chronic obstructive pulmonary disease (COPD) patients. These results led us to hypothesize that core-fucosylation levels in a glycoprotein could be used as a biomarker for COPD. We focused on a lung-specific glycoprotein, surfactant protein D (SP-D), which plays a role in immune responses and is present in the distal airways, alveoli, and blood circulation. The results of a glycomic analysis reported herein demonstrate the presence of a core-fucose in an N-glycan on enriched SP-D from pooled human sera. We developed an antibody–lectin enzyme immunoassay (EIA) for assessing fucosylation (core-fucose and α1,3/4 fucose) in COPD patients. The results indicate that fucosylation levels in serum SP-D are significantly higher in COPD patients than in non-COPD smokers. The severity of emphysema was positively associated with fucosylation levels in serum SP-D in smokers. Our findings suggest that increased fucosylation levels in serum SP-D are associated with the development of COPD. Biological significanceIt has been proposed that serum SP-D concentrations are predictive of COPD pathogenesis, but distinguishing between COPD patients and healthy individuals to establish a clear cut-off value is difficult because smoking status highly affects circulating SP-D levels. Herein, we focused on N-glycosylation in SP-D and examined whether or not N-glycosylation patterns in SP-D are associated with the pathogenesis of COPD. We performed an N-glycomic analysis of human serum SP-D and the results show that a core-fucose is present in its N-glycan. We also found that the N-glycosylation in serum SP-D was indeed altered in COPD, that is, fucosylation levels including core-fucosylation are significantly increased in COPD patients compared with non-COPD smokers. The severity of emphysema was positively associated with fucosylation levels in serum SP-D in smokers. Our findings shed new light on the discovery and/or development of a useful biomarker based on glycosylation changes for diagnosing COPD.This article is part of a Special Issue entitled: HUPO 2014.

Identification of MMP-9 as a biomarker for detecting progression of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a complex immunological disease with multiple pathological features that is primarily induced by smoking together with additional genetic risk factors. COPD is frequently underdiagnosed; forced expiratory volume in the first second (FEV1) is considered to be the main diagnostic measure for COPD, yet it is insufficiently sensitive to monitor disease progression. Biomarkers capable of monitoring COPD progression and severity are needed. In this report, we evaluated matrix metalloproteinase-9 (MMP-9) as an early marker for the detection and staging of COPD, by assessing the mRNA levels of MMP-9 in peripheral blood samples collected from 22 COPD patients, 6 asymptomatic smokers, and 5 healthy controls. Our results demonstrate that the mRNA levels of MMP-9 increased more than two-fold in severe COPD relative to non-COPD smokers or moderate COPD groups. Moreover, in the very severe COPD group, MMP-9 mRNA levels showed a 4-fold increase relative to the non-COPD smokers or the moderate COPD groups, while there was a mild increase (∼40%) when compared to the severe COPD group. Taken together, our results suggest that MMP-9 serves as a biomarker for the grade and severity of COPD.

Expression of Nitric Oxide Synthase Isoenzyme in Lung Tissue of Smokers with and without Chronic Obstructive Pulmonary Disease.

Background:It has been demonstrated that only 10%–20% cigarette smokers finally suffer chronic obstructive pulmonary disease (COPD). The underlying mechanism of development remains uncertain so far. Nitric oxide (NO) has been found to be closely associated with the pathogenesis of COPD, the alteration of NO synthase (NOS) expression need to be revealed. The study aimed to investigate the alterations of NOS isoforms expressions between smokers with and without COPD, which might be helpful for identifying the susceptibility of smokers developing into COPD.Methods:Peripheral lung tissues were obtained from 10 nonsmoker control subjects, 15 non-COPD smokers, and 15 smokers with COPD. Neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS) mRNA and protein levels were measured in each sample by using real-time polymerase chain reaction and Western blotting.Results:INOS mRNA was significantly increased in patients with COPD compared with nonsmokers and smokers with normal lung function (P < 0.001, P = 0.001, respectively). iNOS protein was also higher in COPD patients than nonsmokers and smokers with normal lung function (P < 0.01 and P = 0.01, respectively). However, expressions of nNOS and eNOS did not differ among nonsmokers, smokers with and without COPD. Furthermore, there was a negative correlation between iNOS protein level and lung function parameters forced expiratory volume in 1 s (FEV1) (% predicted) (r = −0.549, P = 0.001) and FEV1/forced vital capacity (%, r = −0.535, P = 0.001).Conclusions:The expression of iNOS significantly increased in smokers with COPD compared with that in nonsmokers or smokers without COPD. The results suggest that iNOS might be involved in the pathogenesis of COPD, and may be a potential marker to identify the smokers who have more liability to suffer COPD.

Effect of threshold on the correlation between airflow obstruction and low attenuation volume in smokers assessed by inspiratory and expiratory MDCT

The estimation of emphysematous changes is very sensitive to computed tomography (CT) threshold level. In clinical practice, the predetermined threshold is usually set at -950 Hounsfield units (HU) for the detection of low attenuation volume (LAV). However, threshold levels that are tightly connected to pulmonary function abnormalities have not been determined. To determine the threshold level for calculating an LAV that closely reflects airflow limitation in patients with chronic obstructive pulmonary disease (COPD). Seventy-six consecutive non-COPD smokers and COPD patients underwent paired inspiratory and expiratory multidetector CT (MDCT). LAV% was segmented every 10 HU between -1000 and -750 HU to examine the correlation between LAV% and indexes of obstructive impairment. LAV% gradually increased as the threshold level increased on both inspiratory and expiratory images. LAV% on inspiratory images was higher than that on expiratory images at all threshold levels between -1000 and -750 HU. The threshold level that correlated with obstructive impairment differed between the two images: -930 HU on inspiratory and -870 or -880 HU on expiratory images. LAV% dramatically changed according to the threshold level on both inspiratory and expiratory images, indicating that LAV% is dependent on the attenuation threshold level in patients with COPD. The threshold linking LAV% to airflow limitation was higher on expiratory than on inspiratory images.

Chronic obstructive pulmonary disease in treated pulmonary tuberculous patients

Abstract Background/Aim To detect the prevalence of chronic obstructive pulmonary disease (COPD) as a sequel of treated pulmonary tuberculosis (PTB). Materials and methods A total of 50 adults, 28 men and 22 women, with a definite diagnosis of PTB and complete antituberculous therapy, with subsequent presentation of exertional dyspnea and/or cough, and expectorations for which no other alternative cause was found, were included in our study. All the patients underwent full history taking, full clinical examination, chest radiography, erythrocyte sedimentation rate, prebronchodilator and postbronchodilator forced vital capacity (FVC%), and forced expiratory volume (FEV1%) in the first second of FEV1/FVC%. Results Pulmonary function testing showed 22 patients (44%) with irreversible obstructive pattern denoting chronic obstructive pulmonary disease (COPD), seven patients had restrictive ventilatory defect, and three patients had mixed obstructive and restrictive pattern. Of those 22 patients with irreversible obstructive pattern (COPD), 11 patients (50%) had mild obstruction, nine patients (40.9%) had moderate obstruction, and two patients (9.1%) had severe obstruction. There is a positive correlation between dyspnea and post-tuberculous COPD patients, and a negative correlation between cough and post-tuberculous COPD patients. There is no correlation between the duration since the completion of antituberculous therapy and development of COPD. Conclusion COPD can be a sequel of PTB and should be overlooked, especially in those patients complaining of dyspnea even in the absence of any history of smoking. Post-tuberculous COPD as a cause of COPD in nonsmokers should be now more recognized in countries where the prevalence of PTB is still high.

The prevalence and patient characteristics of chronic obstructive pulmonary disease in non-smokers in Vietnam and Indonesia: An observational survey.

An estimated 25-40% of patients with chronic obstructive pulmonary disease (COPD) have never smoked. We investigated the prevalence and patient characteristics of COPD in non-smokers from Vietnam and Indonesia. This population-based cross-sectional survey of participants from urban and rural Vietnam and Indonesia used a stratified multistage cluster sampling design, with sample and population weights applied to ensure representativeness. Participants were female or male (recruited in the ratio 2:1) non-smokers, 40 years or older and able to perform a spirometry test. Spirometry was performed at a single study visit. Other clinical information was collected via standardized questionnaires. The 1506 evaluable participants were approximately equally distributed between Vietnam and Indonesia, and rural and urban areas. Overall prevalence of COPD was found to be 6.9% (95% confidence interval (CI): 5.7-8.3), with almost three times higher prevalence in men than women (12.9% (95% CI: 9.1-18.0) vs 4.4% (95% CI: 3.0-6.5)). We found higher rates of COPD in Vietnam than Indonesia (8.1% (95% CI: 5.8-11.3) vs 6.3% (95% CI: 4.8-8.3)), with a particularly high prevalence in urban Vietnam (11.1% (95% CI: 8.1-15.1)). Very few participants (6%) diagnosed to have COPD during the study had been previously diagnosed with COPD. Respiratory symptoms and lower health-related quality of life were more common in participants with COPD. The prevalence of COPD in non-smoking individuals from rural and urban Vietnam and Indonesia was 6.9%, of which a significant proportion (94%) were previously undiagnosed.

Chronic bronchitis and current smoking are associated with more goblet cells in moderate to severe COPD and smokers without airflow obstruction.

BackgroundGoblet cell hyperplasia is a classic but variable pathologic finding in COPD. Current literature shows that smoking is a risk factor for chronic bronchitis but the relationship of these clinical features to the presence and magnitude of large airway goblet cell hyperplasia has not been well described. We hypothesized that current smokers and chronic bronchitics would have more goblet cells than nonsmokers or those without chronic bronchitis (CB), independent of airflow obstruction.MethodsWe recruited 15 subjects with moderate to severe COPD, 12 healthy smokers, and 11 healthy nonsmokers. Six endobronchial mucosal biopsies per subject were obtained by bronchoscopy and stained with periodic acid Schiff-Alcian Blue. Goblet cell density (GCD) was quantified as goblet cell number per millimeter of basement membrane. Mucin volume density (MVD) was quantified as volume of mucin per unit area of basement membrane.ResultsHealthy smokers had a greater GCD and MVD than nonsmokers and COPD subjects. COPD subjects had a greater GCD than nonsmokers. When current smokers (healthy smokers and COPD current smokers, n = 19) were compared with all nonsmokers (nonsmoking controls and COPD ex-smokers, n = 19), current smokers had a greater GCD and MVD. When those with CB (n = 12) were compared to those without CB (n = 26), the CB group had greater GCD. This finding was also seen in those with CB in the COPD group alone. In multivariate analysis, current smoking and CB were significant predictors of GCD using demographics, lung function, and smoking pack years as covariates. All other covariates were not significant predictors of GCD or MVD.ConclusionsCurrent smoking is associated with a more goblet cell hyperplasia and number, and CB is associated with more goblet cells, independent of the presence of airflow obstruction. This provides clinical and pathologic correlation for smokers with and without COPD.

The Study of Aetiology of Chronic Obstructive Pulmonary Disease (COPD) in Non-Smokers

Although COPD occurs predominantly in smokers, non-smokers also develop COPD. In the past decade and especially the past 5 years, results from a growing number of published studies have suggested that risk factors other than smoking are strongly associated with COPD. The aim of the present study is to explore the different causes of non-smoker COPD patients getting treatment from Pulmonary Medicine department and to compare the demographic incidence of COPD in non-smokers in rural & urban areas. It’s a study of 126 patients who came to pulmonary medicine department with breathlessness and cough. Every patient underwent spirometry and diagnosis of COPD got confirmed by post bronchodilator FEV1/FVC. Detailed history was taken regarding various risk factors leading to COPD, like biomass exposure, environmental tobacco smoke exposure, occupational exposure, outdoor and indoor air pollution, long standing bronchial asthma, history of pulmonary tuberculosis and associated co-morbidities. In this study we found out that the exposure to biomass smoke is the most common aetiology of non-smoker COPD, followed by environmental tobacco smoke. Females are affected more than males. Non smoker COPD is more common in rural population than urban population.

Alpha – 1 antitrypsin in smokers and non smokers chronic obstructive pulmonary disease

Aim: The aim of the present study is to correlate and compare alpha-1 antitrypsin level in smoker and non smoker chronic obstructive pulmonary disease patients. Material and Methods: A comparative study was carried out in 200 subjects, more than 40 years of age and having chronic obstructive pulmonary disease for more than 1 year with a history of smoking at least 20 cigarettes per day (Group A) and without a history of smoking (Group B). Pulmonary function tests were used to diagnose the disease as per the Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification. Alpha-1 antitrypsin level was done by turbidimetry method on fully auto analyzer I-Lab 650 (Instrumentation Laboratory, USA) at Clinical Biochemistry Section, Laboratory Services Sir Takhtsinhji Hospital, Bhavnagar. Statistical analysis was done by using unpaired t-test and Pearson’s correlation coefficient. Results: Results of present study shows that alpha-1 antitrypsin level was decreased in smoker chronic obstructive pulmonary disease patients (150.83±18.853) when compared to non smokers (183.97±29.383). There was statistically significant difference in alpha-1 antitrypsin level between the two groups with ‘p’ value of <0.0001. Pearson’s correlation test show negative correlation between smoker and nonsmoker chronic obstructive pulmonary disease patients. Conclusion: The values of serum alpha-1 antitrypsin levels were more significantly decreased in smokers indicating an important role of smoking in pathogenesis of chronic obstructive pulmonary disease. Alpha-1 antitrypsin can act as a predictor for future development of chronic obstructive pulmonary disease in smokers and in nonsmokers.

Impairment of Pulmonary Vasoreactivity in Response to Endothelin-1 In Patients With Chronic Obstructive Pulmonary Disease (COPD)

Background: Pulmonary hypertension secondary to COPD is characterized principally by impairment of vasoreactivity and vascular remodeling. While the structural changes have been described in all stages of COPD, the impairment of vasoreactivity in response to ET-1, a potent vasoconstrictor, has not been well understood. Materials and methods: Proximal pulmonary arteries were obtained from non-smokers, smokers with normal lung function, and COPD patients who underwent lung resection for other diseases (n=6 in each group). Pulmonary arterial contraction induced by ET-1 was assessed without or with the presence of ET-1 receptor antagonists (BQ- 123 and BQ-788). Expressions of ET-1 receptors were measured by immunohistochemistry, western blot, and qRTPCR. Results: ET-1-induced pulmonary arterial contraction increased significantly in COPD patients in comparison with control subjects and non-COPD smokers (P<0.05) and the use of ET-1 receptor antagonists could not prevent this contraction. The hypercontraction was not associated with the increase of ET-1 and ET-1 receptors expression in pulmonary arterial vessels. Conclusion: In patients with COPD, pulmonary arterial contraction induced by ET-1 has increased significantly and could not be prevented by using ET-1 receptor antagonist alone. This alteration might be related to the upreguation of other signalling pathways in pulmonary arterial vessels of COPD patients.