Non-smoking Chronic Obstructive Pulmonary Disease Patients Research Articles

DACH1 Attenuates Airway Inflammation in COPD by Activating NRF2 Signaling.

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the airways, it is characterized by impaired lung function induced by cigarette smoke (CS). Reduced DACH1 expression has a detrimental role in numerous disorders. However, its role in COPD remains understudied. This study aims to elucidate the role and underlying mechanism of DACH1 in airway inflammation of COPD. DACH1 expression was measured in lung tissues of patients with COPD. Airway epithelium-specific DACH1 knockdown mice and AAV-transfected DACH1 overexpressed mice were used to investigate its role and potential for therapeutic targeting in experimental COPD caused by CS. Furthermore, we discovered a potential mechanism of DACH1 in inflammation induced by cigarette smoke extract simulation (CSE) in vitro. Compared to non-smokers and smokers without COPD, COPD patients had reduced DACH1 expression, especially in the airway epithelium. Airway epithelium-specific DACH1 knockdown aggravated mice airway inflammation and lung function decline caused by CS, whereas DACH1 overexpression protected mice from airway inflammation and lung function decline. DACH1 knockdown and overexpression promoted and inhibited IL-6 and IL-8 secretion in 16 HBE cells after CSE simulation, respectively. Nuclear factor erythroid 2-related factor 2 (NRF2) was discovered to be a novel downstream target of DACH1, which binds directly to its promoter. By activating NRF2 signaling, DACH1 induction reduced inflammation. DACH1 levels are lower in smokers and nonsmoking COPD patients when compared to nonsmokers. DACH1 has protective effects against inflammation induced by CS by activating NRF2 signaling pathway. Targeting DACH1 is a potentially viable therapeutic approach for COPD treatment.

A2M Serves as Promising Biomarker for Chronic Obstructive Pulmonary Disease.

Chronic obstructive pulmonary disease (COPD) often associated with cigarette smoking. However, increasing evidence suggests that non-smoking COPD is much higher than previously thought. This study aims to identify a nonsmoking COPD biomarker and examined its value in diagnosis and prediction of acute exacerbation. A total of 35 stable COPD patients, 70 acute exacerbation chronic obstructive pulmonary disease (AECOPD) patients and 35 healthy control subjects were included. Plasma α 2 macroglobulin (A2M) and matrix metalloproteinase-9 (MMP-9) levels were measured using the enzyme-linked immunosorbent assay (ELISA) method on all participants. Their association with clinical characteristics and lung function parameters were determined by regression analysis. Receiver operating characteristic (ROC) curve was used to determine the diagnostic sensitivity and specificity. Correlation coefficients were evaluated using Pearson's correlation. Plasma A2M concentration was decreased and MMP-9 concentration, MMP-9/A2M ratio were elevated in stable COPD patients compared with control groups. And MMP-9 expression was significantly higher in AECOPD patients. A2M level was increased in AECOPD patients with infection compared with those without. In addition, there was no statistical difference in A2M levels between smokers and nonsmokers COPD or healthy control subjects. Furthermore, A2M, MMP-9 and MMP-9/A2M were correlated with forced expiratory volume in one second (FEV1)%, FEV1/ forced vital capacity (FVC), CAT and mMRC score in COPD patients, but had no correlation with fraction of exhaled nitric oxide (FeNO) and concentration of alveolar nitric oxide (CaNO). A2M is altered in peripheral blood of COPD patients and correlated with severity and infection. Moreover, there was no significant correlation between the change in A2M and smoking, FeNO and CaNO, suggesting A2M may reflect the overall rather than local inflammation in COPD patients and serve as a potential biomarker for nonsmoking COPD patients.

A comparative study of lung functions in non-smoker COPD patients from various localities with healthy subjects

Background & Objectives: Chronic Obstructive Pulmonary Disease (COPD) is the illness with airflow obstruction caused by emphysema, chronic bronchitis, or a combination of both the disorders. It is the third leading cause of death worldwide. Between 20 and 40% of all COPD patients across the globe are never smokers. The primary objective of this study was to evaluate Pulmonary Function Tests (PFTs) in non-smoker COPD patients and compare their results with normal healthy subjects. The study also intended to check the variations in lung function of COPD patients living in urban & rural areas.
 Materials & Methods: The study was conducted by performing PFTs in 50 non-smoker COPD patients (28 from urban & 22 from rural areas) & comparing them with 50 non-smoker healthy subjects of same age group excluding ex-smokers. Various parameters of PFTs like FVC, FEV1, FEV1/FVC, PEFR & MVV were assessed & compared. For statistical data analysis unpaired t-Test was applied.
 Results: The mean values of PFT parameters such as FVC, FEV1, FEV1/FVC, PEFR & MVV are very significantly differed between COPD patients & healthy subjects (p<0.01). Although the data is not statistically significant between total COPD patients, urban & rural COPD patients, mean values of above PFT parameters are higher in total COPD patients than urban while higher in rural compared to total COPD patients (p>0.05). The mean values of above PFT parameters are not significant statistically between urban & rural COPD patients (p>0.05).
 Conclusion: The study indicates that as compared to normal subjects, in patients of COPD there is great reduction in mean values for FVC, FEV1, PEFR, FEV1/FVC%, & MVV irrespective of their residing location which is suggestive of an increase air way obstruction with reduced values of various PFT parameters. The study also shows that there is no significant difference in mean values of various parameters between urban & rural areas.

ВЛИЯНИЕ КУРЕНИЯ НА ПОКАЗАТЕЛИ ОКИСИ УГЛЕРОДА И ОКСИДА АЗОТА В ВЫДЫХАЕМОМ ВОЗДУХЕ У ПАЦИЕНТОВ С ХРОНИЧЕСКОЙ ОБСТРУКТИВНОЙ БОЛЕЗНЬЮ ЛЕГКИХ

To date, points of view regarding the effect of smoking on the indicators of exhaled air are very contradictory, especially with regard to the examination of patients with chronic obstructive pulmonary disease (COPD) suffering from tobacco dependence. Basically, a comparative analysis is carried out by researchers solely on the fact of the presence of tobacco dependence, without taking into account the indicator of the smoking index (CI), as such, or the data obtained from the examination of smoking COPD patients and healthy volunteers are compared. Objective: to evaluate the change in the concentration of carbon monoxide (CO), nitric monoxide (NO) and carboxyhemoglobin (COHb) in the exhaled air of patients with COPD, depending on the status of smoking and CI. Material and research methods. 96 patients with COPD were examined, the average age of which was 54.6±5.9 years, the duration of the disease was 15±4.8 years. 70 patients (72.9%) who participated in the study suffered from tobacco dependence, while CI ≤10 pack-year was observed in 2.8% of them, 11-20 pack-year in 42.9%, 21-30 pack-year in 40.0% and >30 pack-year in 14.3%. As part of a comprehensive examination, all patients underwent determination of CO (ppm) and COHb (%) in exhaled air using the MicroCO device (Micro medica, UK) and the level of NO was assessed using the Niox Mino analyzer (Aerocline, Sweden). The results of the study. During the analysis of the obtained data, we noted an increase in the average concentration of CO in the exhaled air in all smoking patients, while the increase in the indicator was directly proportional to the CI. A similar picture was observed with respect to the COHb level. The concentration of NO in the exhaled air, on the contrary, showed a tendency to decrease with increasing CI. A comparative analysis of the obtained data was carried out in three groups: I - non-smoking patients with COPD (n=26), II - patients with COPD with an IC of 11-20 pack-years (n=30) and III – patients with COPD with an IC of 21-30 pack-years (n=28). In terms of peripheral blood saturation, significant differences compared with the group of non-smokers were found in patients with IC 11-20 pack-years and with IC 21-30 pack-years, while there were no statistically significant differences between these groups of smoking patients. The CO level in smokers, regardless of CI, was significantly higher than in non-smokers, while in COPD patients with CI 21-30 pack-year it was also significantly higher than in patients with CI 11-20 pack-year. The COHb index in smokers with COPD was also significantly higher than in non-smokers, but when comparing data in the group with IC 11-20 pack-years and IC 21-30 pack/years, no statistically significant differences were found. In terms of NO in exhaled air, statistically significant differences were noted when comparing data in the group of non-smoking patients with COPD with the results obtained in groups of patients with IC 11-20 pack-years and with IC 21-30 pack-years, as well as when comparing data in these groups of smokers among themselves. Conclusions. The study revealed a statistically significant increase in the level of CO in the exhaled air, depending on the status of smoking and CI. It was determined that the smoking factor in COPD patients affects the level of NO in the exhaled air, causing its significant decrease in COPD patients with CI >10 pack-year compared to non-smoking COPD patients.

Prediction of COPD acute exacerbation in response to air pollution using exosomal circRNA profile and Machine learning.

Ambient fine particulate matter (PM2.5) is linked to an increased risk of chronic obstructive pulmonary disease (COPD) exacerbations, which significantly increase the risk of mortality in COPD patients. Identifying the subtype of COPD patients who are sensitive to environmental aggressions is necessary. Using in vitro and in vivo PM2.5 exposure models, we demonstrate that exosomal hsa_circ_0005045 is upregulated by PM2.5 and binds to the protein cargo peroxiredoxin2, which functionally aggravates hallmarks of COPD by recruiting neutrophil elastase and triggering in situ release of tumor necrosis factor (TNF)-α by inflammatory cells. The biological function of hsa_circ_0005045 associated with aggravation of COPD is validated using exosome-transplantation and conditional circRNA-knockdown murine models. By sorting the major components of PM2.5, we find that PM2.5-bound heavy metals, which are distinguishable from the components of cigarette smoke, trigger the elevation of exosomal hsa_circ_0005045. Finally, using machine learning models in a cohort with 327 COPD patients, the PM2.5 exposure-sensitive COPD patients are characterized by relatively high hsa_circ_0005045 expression, non-smoking, and group C (mMRC 0-1 (or CAT<10) and≥2 exacerbations (or≥1 exacerbation leading to hospital admission) in the past year). Thus, our results suggest that environmental reduction in PM2.5 emission provides a targeted approach to protecting non-smoking COPD patients against air pollution-related disease exacerbation.

Gene-gene and gene-environment interactions of the inflammatory gene variants in the development of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a complex chronic inflammatory disease that is characterized by partly reversible airflow limitation, chronic inflammation, fibrosis of small airways, and destruction of lung parenchyma. We aimed to assess the association of the inflammatory gene loci singly and in combinations with COPD in smokers and non-smokers in ethnic Tatar from Russia to evaluate the gene-gene and gene-environment interactions in COPD development. Eleven loci of inflammatory genes, including IL19, IL20, IL24, PPBP, IL4, IL4RA, С5, FAS, FASLG, and TGFb1, were genotyped in 484 smoking COPD patients, 517 healthy smokers, 117 non-smoking COPD patients, and 100 healthy non-smokers. Significant associations with COPD in smokers were identified for IL19 (rs2243193), IL4 (rs2243250), IL4 (rs2070874), and PPBP (rs352010). In non-smokers, associations were established for IL24 (rs291107), IL4 (rs2070874), and PPBP (rs352010). Associations of inflammatory genes loci IL19 (rs2243193), IL4 (rs2070874), TGFb1 (rs1800469), PPBP (rs352010), and FASLG (rs763110) and smoking index were determined. Associations of FAS (rs1800682), FASLG (rs763110), IL4 (rs2243250), IL4RA (rs1805010), and PPBP (rs352010) loci with pulmonary function variables were observed. The results of gene-gene interactions analysis showed distinctive patterns of association of inflammatory gene loci with COPD in groups stratified by smoking status. The combination of A allele of IL19 (rs2243193), C allele of IL4 (rs2243250), and T allele of PPBP (rs352010) was the main component of the majority of protective gene-gene combination associated with COPD in smokers. The highest risk of COPD was conferred by TT genotype of PPBP (rs352010) in combination with A allele of FAS (rs1800682). While in non-smokers, the most commonly featured was IL24 (rs291107) C allele in protective patterns and IL24 (rs291107) T allele in predisposing combinations. The highest risk of COPD in non-smokers was detected in a gene-gene combination consisting of A allele of IL12RB2 (rs3762317) together with G allele of IL12A (rs2243115), C allele of IL4 (rs2070874), and A allele of IL4RA (rs1805010).

Clinical Characteristics of Non-Smoking Chronic Obstructive Pulmonary Disease Patients: Findings from the KOCOSS Cohort

ABSTRACT Chronic obstructive pulmonary disease (COPD) has been regarded as a disease of smokers, but the prevalence of non-smoking COPD patients have been reported to be considerable. We investigated differences in clinical characteristics between smoking and non-smoking COPD patients. We used data from the Korea COPD Subgroup Study (KOCOSS) database, which is a multicenter cohort that recruits patients from 54 medical centres in Korea. Comprehensive comparisons of smoking and non-smoking COPD patients were performed based on general characteristics, exacerbations, symptom scores, radiological findings, and lung-function tests. Of the 2477 patients included in the study, 8.1% were non-smokers and 91.9% were smokers. Non-smoking COPD patients were more likely to be female and to have a higher body mass index and lower level of education. Non-smoking COPD patients had more comorbidities, including hypertension, osteoporosis, and gastroesophageal reflux disease, and experienced more respiratory and allergic diseases. No significant differences in exacerbation rates, symptom scores, or exercise capacity scores were observed between the two groups. Smoking COPD patients had more emphysematous lung according to the radiological findings, and non-smoking patients had more tuberculosis-destroyed lung and bronchiectasis. Lung-function testing revealed no significant difference in the forced expiratory capacity in 1 sec between the two groups, but smokers had more rapid lung-function decline in the 5 years of follow-up data. We found differences in general characteristics and radiological findings between smoking and non-smoking COPD patients. No significant differences in exacerbation or symptom scores were observed, but decline in lung function was less steep in non-smoking patients. Supplemental data for this article is available online at https://doi.org/10.1080/15412555.2022.2053088 .

The rs74794265 SNP of the SREK1 Gene is Associated with COPD in Kashi, China.

BackgroundKashi city is situated near the Taklamakan desert and has a high incidence rate of chronic obstructive pulmonary disease (COPD). In this study, we aimed to explore the relationship between the SNP of the SREK1 gene locus rs74794265 and the susceptibility to COPD among the Uyghur population in Kashi, XinJiang, China.MethodsA total of 541 patients with COPD and 534 control subjects were included in this study. Sanger sequencing was used to analyze the SNP of the SREK1 gene locus rs74794265 site. The distribution of genotypes in different genetic models between the case and control group were analyzed by logistic regression analysis after adjusting for age, sex, and smoking history.ResultsThe SREK1 gene SNP locus rs74794265 included two genotypes, namely, C/C and C/T, of which C/C was the wildtype; The risk of COPD was significantly lower in patients with heterozygous C/T in rs74794265 [p=0.0236, OR=0.3677 (0.1547–0.8742)], and the allele frequency of T was also significantly lower in the patient group [p=0.0245, OR=0.3728 (0.1577–0.8811)]. The heterozygous C/T of rs74794265 among non-smoking COPD patients was significantly lower than other COPD patients [p=0.0298, OR=0.3217 (0.1156–0.8949)], and there was no significant correlation of the heterozygous C/T genotype in smokers.ConclusionWe found that the rs74794265 heterozygous C/T genotype significantly reduces the risk of COPD. The C/T genotype is likely a protective factor for COPD in the Kashi region. We speculate that the occurrence of COPD in this area is probably more related to desert climate condition and genetic factors than smoking status.

Role of NLRP3rs10754558 and NOS3rs1799983 genetic polymorphisms in smoking and nonsmoking COPD patients

Chronic Obstructive Pulmonary Disease (COPD) is a chronic inflammatory disease leading to structural abnormalities in the airways. Mortality and disability in COPD cases are high, causing an intense economic burden. This study aims to investigate the relationship between NLRP3 rs10754558 and NOS3rs1799983 polymorphisms and the risk of COPD. This work was carried out on 152 subjects classified into Group I, with 38 COPD patients who are smokers, Group II 38 nonsmoker COPD patients, Group III 38 healthy smokers, and Group IV with 38 healthy nonsmokers. Genotyping of NLRP3rs10754558C/G and NOS3rs1799983G/T polymorphisms was assayed by real-time PCR. For NLRP3rs10754558 polymorphism, significantly higher frequencies of G/G genotype versus C/C were evident in COPD patients more than controls (p ≤ 0.001). Also, G allele can increase the risk of COPD by (OR) 95% CI [2.498 (1.521–4.101)]. Higher frequencies of mutant G/T and T/T genotypes of NOS3 rs1799983 versus G/G in COPD patients (48.7% and 17.1%) were more than the values evident in controls (p = 0.004 and 0.005). T allele can also increase the risk of COPD by (OR) 95% CI [2.457 (1.491–4.049)]. Conceivable LD was evident between both polymorphisms in COPD patients and controls. No significant difference between the severity of COPD was detected by the GOLD staging and the studied polymorphisms variants in the COPD group (p = 0.441 and 0.83). Coding polymorphisms in NLRP3 and NOS3 can be associated with the hazard of COPD and the probability of cigarette smokers suffering the studied polymorphisms to develop COPD.

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.

Comparison of demographic, clinical, spirometry, and radiological parameters between smoking and non-smoking COPD patients in rural Gujarat, India.

Context:A total of 20% of Chronic Obstructive Pulmonary Disease(COPD) patients are non-smokers due to preventable causes, such as biomass fuel exposure, post tuberculous sequelae, occupational exposure, air pollution, persistent chronic asthma, and genetic predisposition.Aims:To compare smokers and non-smokers with COPD.Settings and Design:An observational study was conducted at a tertiary care hospital on 60 patients diagnosed with COPD, (GOLD criteria), who were divided into smoker and non-smoker groups.Subjects and Methods:Demographic data, clinical profile, smoking history, and radiological data were collected and compared. Exclusion criteria were individuals having active pulmonary tuberculosis and reversible air flow limitations.Statistical Analysis Used:Using STATA 14.2, quantitative and qualitative data were presented using descriptive statistics.Results:A total of 100% of smokers were male, whereas 70% of non-smokers were female. Compared to non-smokers (16.67%), smokers (26.6%) presented with higher grade of dyspnea. A statistically significant difference was seen with more smokers diagnosed as severe (40%) and very severe (30%) COPD compared to non-smokers with mild (16.67%) and moderate (46.67%) COPD (P < 0.012), Post bronchodilator FEV1 among smokers (42.63) compared to non-smokers (56.63) (P < 0.01) and decrease in FEV1 as the grade of dyspnea increased (P < 0.002). Compared to 36.67% in non-smokers, 70% smokers showed emphysematous x-rays.Conclusions:In our study we found majority of non-smokers to be female, and smokers had a higher grade of dyspnea, more severe COPD, lower post bronchodilator FEV1, and more emphysematous changes on x-rays.

Impact of Education on COPD Severity and All-Cause Mortality in Lifetime Never-Smokers and Longtime Ex-Smokers: Results of the COSYCONET Cohort.

BackgroundBeyond smoking, several risk factors for the development of chronic obstructive pulmonary disease (COPD) have been described, among which socioeconomic status including education is of particular interest. We studied the contribution of education to lung function and symptoms relative to smoking in a group of never-smokers with COPD compared to a group of long-time ex-smokers with COPD.MethodsWe used baseline data of the COSYCONET cohort, including patients of GOLD grades 1–4 who were either never-smokers (n=150, age 68.5y, 53.3% female) or ex-smokers (≥10 packyears) for at least 10 years (n=616, 68.3y, 29.9% female). Socioeconomic status was analyzed using education level and mortality was assessed over a follow-up period of 4.5 years. Analyses were performed using ANOVA and regression models.ResultsSpirometric lung function did not differ between groups, whereas CO diffusing capacity and indicators of lung hyperinflation/air-trapping showed better values in the never-smoker group. In both groups, spirometric lung function depended on the education level, with better values for higher education. Quality of life and 6-MWD were significantly different in never-smokers as well as patients with higher education. Asthma, alpha-1-antitrypsin deficiency, and bronchiectasis were more often reported in never-smokers, and asthma was more often reported in patients with higher education. Higher education was also associated with reduced mortality (hazard ratio 0.46; 95% CI 0.22–0.98).ConclusionOverall, in the COSYCONET COPD cohort, differences in functional status between never-smokers and long-time ex-smokers were not large. Compared to that, the dependence on education level was more prominent, with higher education associated with better outcomes, including mortality. These data indicate that non-smoking COPD patients’ socioeconomic factors are relevant and should be taken into account by clinicians.

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.

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 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.

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.

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.

Association of the CYP1A1 MspI and TNFα-308 polymorphisms with chronic obstructive pulmonary disease in Inner Mongolia.

Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by persistent airflow limitation. Smoking, occupational exposures, air pollution, and genetics are all risk factors. In the present study, we detected the cytochrome P4501A1 gene (CYP1A1) MspI polymorphism and the tumor necrosis factor alpha (TNFα)-308 single nucleotide polymorphism in COPD patients, and investigated their associations with smoking and COPD susceptibility in Inner Mongolia. A total of 101 COPD patients and 80 controls were enrolled in the study. The polymorphisms were analyzed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). CYP1A1 MspI allele frequencies were significantly different between COPD patients and controls (P=0.033). COPD susceptibility was higher in subjects with the m2 allele compared to subjects with the m1 allele [odds ratio (OR)=2.531, 95% confidence interval (CI)=1.297-4.940, P=0.006]. Significant differences were observed in the TNFα-308 genotype and allele distributions between COPD patients and controls (P=0.006 and P=0.003, respectively). Compared to subjects with the GG genotype, subjects with GA+AA genotypes had higher COPD risk (OR=3.639, 95%CI=1.576-8.403, P=0.002). The TNFα-308 polymorphism differed between smoking and non-smoking COPD patients and controls (P=0.047 for genotype and P=0.030 for allele). In conclusion, the CYP1A1 MspI and TNFα-308 polymorphisms were associated with COPD susceptibility. Furthermore, of the two polymorphisms, only TNFα-308 may exert an interaction with smoking.