Risk Of Chronic Obstructive Pulmonary Disease Research Articles

Urinary volatile organic compound metabolites and COPD among US adults: mixture, interaction and mediation analysis

BackgroundVolatile organic compounds (VOCs) encompass hundreds of high production volume chemicals and have been reported to be associated with adverse respiratory outcomes such as chronic obstructive pulmonary disease (COPD). However, research on the combined toxic effects of exposure to various VOCs on COPD is lacking. We aimed to assess the effect of VOC metabolite mixture on COPD risk in a large population sample.MethodsWe assessed the effect of VOC metabolite mixture on COPD risk in 5997 adults from the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2020 (pre-pandemic) using multivariate logistic regression, Bayesian weighted quantile sum regression (BWQS), quantile-based g-Computation method (Qgcomp), and Bayesian kernel machine regression (BKMR). We explored whether these associations were mediated by white blood cell (WBC) count and total bilirubin.ResultsIn the logistic regression model, we observed a significantly increased risk of COPD associated with 9 VOC metabolites. Conversely, N-acetyl-S-(benzyl)-L-cysteine (BMA) and N-acetyl-S-(n-propyl)-L-cysteine (BPMA) showed insignificant negative correlations with COPD risk. The overall mixture exposure demonstrated a significant positive relationship with COPD in both the BWQS model (adjusted odds ratio (OR) = 1.30, 95% confidence interval (CI): 1.06, 1.58) and BKMR model, and with marginal significance in the Qgcomp model (adjusted OR = 1.22, 95% CI: 0.98, 1.52). All three models indicated a significant effect of the VOC metabolite mixture on COPD in non-current smokers. WBC count mediated 7.1% of the VOC mixture associated-COPD in non-current smokers.ConclusionsOur findings provide novel evidence suggesting that VOCs may have adverse associations with COPD in the general population, with N, N- Dimethylformamide and 1,3-Butadiene contributing most. These findings underscore the significance of understanding the potential health risks associated with VOC mixture and emphasize the need for targeted interventions to mitigate the adverse effects on COPD risk.

Assessing the causal role of physical activity and leisure sedentary behaviours with chronic obstructive pulmonary disease: a Mendelian randomisation study

BackgroundObservational studies show that patients with chronic obstructive pulmonary disease (COPD) tend to be sedentary during leisure time. Physical activity (PA) may reduce the risk of COPD, but the causal...

Inflammation mediates the association between furan exposure and the prevalence and mortality of chronic obstructive pulmonary disease: National Health and Nutrition Examination Survey 2013-2018.

Although extensive research has established associations between chronic obstructive pulmonary disease (COPD) and environmental pollutants, the connection between furan and COPD remains unclear. This study aimed to explore the association between furan and COPD while investigating potential mechanisms. The study involved 7,482 adults from the National Health and Nutrition Examination Survey 2013-2018. Exposure to furan was assessed using blood furan levels. Participants were categorized into five groups based on quartiles of log10-transformed blood furan levels. Logistic regression and restricted cubic spline regression models were used to assess the association between furan exposure and COPD risk. Mediating analysis was performed to assess the contribution of inflammation to the effects of furan exposure on COPD prevalence. Cox regression was used to assess the association between furan exposure and the prognosis of COPD. Participants with COPD exhibited higher blood furan levels compared to those without COPD (P < 0.001). Log10-transformed blood furan levels were independently associated with an increased COPD risk after adjusting for all covariates (Q5 vs. Q1: OR = 4.47, 95% CI = 1.58-12.66, P = 0.006, P for trend = 0.001). Inflammatory cells such as monocytes, neutrophils, and basophils were identified as mediators in the relationship between furan exposure and COPD prevalence, with mediated proportions of 8.73%, 20.90%, and 10.94%, respectively (all P < 0.05). Moreover, multivariate Cox regression analysis revealed a positive correlation between log10-transformed blood furan levels and respiratory mortality in COPD patients (HR = 41.00, 95% CI = 3.70-460.00, P = 0.003). Exposure to furan demonstrates a positive correlation with both the prevalence and respiratory mortality of COPD, with inflammation identified as a crucial mediator in this relationship.

[A prospective study on the relationship between exposure to solid fuels for heating and its duration and the risk of morbidity of respiratory diseases among residents aged 30-79 years].

Objective: To research the association between exposure to solid fuels for heating and its duration and the risk of respiratory diseases morbidity. Methods: Data from the China Kadoorie Biobank project sited in Pengzhou City, Sichuan Province. Cox proportional hazard regression model was used to analyze the association between exposure to solid fuels for heating and its duration and the risk of total respiratory diseases and the association between exposure to solid fuels for heating and the risk of chronic obstructive pulmonary disease (COPD) and pneumonia among respiratory diseases. Results: A total of 46 082 participants aged 30-79 years were enrolled, with 11 634 (25.25%) heating during the winter, of whom 8 885 (19.28%) used clean fuels and 2 749 (5.97%) used solid fuels, of whom 34 448 (74.75%) did not heat. After controlling for multiple confounding factors, Cox proportional hazard regression model was used, which revealed that compared with clean fuels, unheating could reduce the risk of total respiratory disease (HR=0.81,95%CI:0.77-0.86), COPD (HR=0.86,95%CI:0.78-0.95) and pneumonia (HR=0.80,95%CI:0.74-0.86), respectively. Exposure to solid fuels increased the risk of total respiratory disease (HR=1.10, 95%CI:1.01-1.20) and were not associated with COPD and pneumonia. Compared with no solid fuel exposure, the risk of total respiratory disease (1-19 years:HR=1.23, 95%CI:1.10-1.37; 20-39 years:HR=1.25, 95%CI:1.16-1.35; ≥40 years:HR=1.26, 95%CI:1.15-1.39) and COPD (1-19 years: HR=1.21, 95%CI:1.03-1.42; 20-39 years: HR=1.30, 95%CI:1.16-1.46; ≥40 years:HR=1.35, 95%CI:1.18-1.54) increased with the length of exposure of solid fuels (trend test P<0.001). Solid fuels exposure for 1-19 years and 20-39 years increased the risk of COPD by 23% (HR=1.23,95%CI:1.02-1.49) and 16% (HR=1.16, 95%CI:1.00-1.35). Conclusion: Heating solid fuels exposure increases the risk of total respiratory disease, COPD, and pneumonia.

Mendelian randomization analysis identifies druggable genes and drugs repurposing for chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a prevalent condition that significantly impacts public health. Unfortunately, there are few effective treatment options available. Mendelian randomization (MR) has been utilized to repurpose existing drugs and identify new therapeutic targets. The objective of this study is to identify novel therapeutic targets for COPD. Cis-expression quantitative trait loci (cis-eQTL) were extracted for 4,317 identified druggable genes from genomics and proteomics data of whole blood (eQTLGen) and lung tissue (GTEx Consortium). Genome-wide association studies (GWAS) data for doctor-diagnosed COPD, spirometry-defined COPD (Forced Expiratory Volume in one second [FEV1]/Forced Vital Capacity [FVC] <0.7), and FEV1 were obtained from the cohort of FinnGen, UK Biobank and SpiroMeta consortium. We employed Summary-data-based Mendelian Randomization (SMR), HEIDI test, and colocalization analysis to assess the causal effects of druggable gene expression on COPD and lung function. The reliability of these druggable genes was confirmed by eQTL two-sample MR and protein quantitative trait loci (pQTL) SMR, respectively. The potential effects of druggable genes were assessed through the phenome-wide association study (PheWAS). Information on drug repurposing for COPD was collected from multiple databases. A total of 31 potential druggable genes associated with doctor-diagnosed COPD, spirometry-defined COPD, and FEV1 were identified through SMR, HEIDI test, and colocalization analysis. Among them, 22 genes (e.g., MMP15, PSMA4, ERBB3, and LMCD1) were further confirmed by eQTL two-sample MR and protein SMR analyses. Gene-level PheWAS revealed that ERBB3 expression might reduce inflammation, while GP9 and MRC2 were associated with other traits. The drugs Montelukast (targeting the MMP15 gene) and MARIZOMIB (targeting the PSMA4 gene) may reduce the risk of spirometry-defined COPD. Additionally, an existing small molecule inhibitor of the APH1A gene has the potential to increase FEV1. Our findings identified 22 potential drug targets for COPD and lung function. Prioritizing clinical trials that target these identified druggable genes with existing drugs or novel medications will be beneficial for the development of COPD treatments.

Causal Role of Immune Cells in Chronic Obstructive Pulmonary Disease: A Two-Sample Mendelian Randomization Study

Accumulating evidence has highlighted the importance of immune cells in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, the understanding of the causal association between immunity and COPD remains incomplete due to the existence of confounding variables. In this study, we employed a two-sample Mendelian randomization (MR) analysis, utilizing the genome-wide association study database, to investigate the causal association between 731 immune-cell signatures and the susceptibility to COPD from a host genetics perspective. To validate the consistency of our findings, we utilized MR analysis results of lung function data to assess directional concordance. Furthermore, we employed MR-Egger intercept tests, Cochrane’s Q test, MR-PRESSO global test, and "leave-one-out" sensitivity analyses to evaluate the presence of horizontal pleiotropy, heterogeneity, and stability, respectively. Inverse variance weighting results showed that seven immune phenotypes were associated with the risk of COPD. Analyses of heterogeneity and pleiotropy analysis confirmed the reliability of MR results. These results highlight the interactions between the immune system and the lungs. Further investigations into their mechanisms are necessary and will contribute to inform targeted prevention strategies for COPD.

Causal relationship between air pollution and chronic obstructive pulmonary disease in European and East Asian populations: a Mendelian randomization study

ABSTRACT Epidemiologic studies have suggested a possible association between air pollution and chronic obstructive pulmonary disease (COPD), but it is controversial and difficult to draw causal inferences. Five methods were adopted to evaluate the causal relationship between air pollution and COPD in European and East Asian populations by using MR Analysis. A statistically significant causal relationship between PM2.5 and COPD was observed in the European population (OR: 2.34; 95% CI: 1.06–5.05; p = 0.033). Statistical significance remained after adjustment for confounding factors (adjusted OR: 2.28; 95% CI: 1.01–5.20; p = 0.048). In East Asian populations, PM2.5 absorbance, a proxy for black carbon, was statistically associated with COPD (OR: 1.41; 95% CI: 1.09–1.81; p = 0.007). We did not adjust for confounders in East Asian populations, as the association was independent of known confounders (e.g. smoking, respiratory tract infections, etc.). In conclusion, increased concentrations of PM2.5 and PM2.5 absorbance were associated with an increased risk of COPD.

Association between Air Pollution Relating to Agricultural Residue Burning and Morbidity of Acute Cardiopulmonary Diseases in Upper Northern Thailand

In Northern Thailand, increasing seasonal agricultural residue burning has led to public concern about health risks. This study aimed to examine the associations between air pollutants related to agricultural residue burning and morbidity from acute cardiopulmonary diseases in upper Northern Thailand in 2018. An ecological study was conducted. Emergency room visits and hospitalizations for chronic obstructive pulmonary disease (COPD), stroke, myocardial infarction (MI), and asthma were extracted from the National Electronic Health Record database. We interpolated air pollution data to estimate weekly pollutant concentrations, including PM10, PM2.5, carbon monoxide, nitrogen dioxide, sulfur dioxide and ozone from 1 Jan to 31 Dec 2018. Associations between air pollution and health outcomes were analyzed using a mixed effect model incorporating different lag structures. Overall pollutant concentrations exceeded WHO air quality standard levels throughout March and April, which is the end of forest burning prohibition campaign. Morbidity from COPD, stroke, MI and asthma slightly increased over March–April. For every increase in PM2.5 level of 10 μg/m3, the relative risk of COPD, stroke, MI and asthma 1 week later was 1.10 (95% CI 1.09–1.12), 1.06 (1.05–1.08), 1.06 (1.04–1.08) and 1.06 (1.01–1.12), respectively. The effects of agricultural residue burning should be highlighted and policies should be developed to deter this practice.

Secondhand smoke increases the risk of developing chronic obstructive pulmonary disease

Smoking is the most important risk factor for chronic obstructive pulmonary disease (COPD), however evidence from large-scale studies on whether secondhand smoke (SHS) increases the risk of COPD is still lacking. We conducted this large longitudinal study to investigate the association between SHS and the development of COPD. This is a longitudinal study. Data on 6519 subjects who were never-smokers, had no history of COPD, and had complete lung function records were extracted from the Taiwan Biobank. They were divided into two groups according to SHS exposure: no exposure and exposure groups. Data were collected when participants enrolled in the study and during regular follow-up. Cox proportional hazards regression models were used to estimate the relative risk (RR) and 95% confidence interval (CI) for the association between SHS and the risk of developing COPD. At 48 months of follow-up, 260 (4%) participants in the no exposure group and 34 (7%) participants in the exposure group developed COPD. The RR of incident COPD development was significantly higher in the exposure group than that in the no exposure group after adjusting for confounders (RR = 1.49; 95% CI 1.04 to 2.14; P value = 0.031). There is a dose–response relationship between the duration of exposure to SHS and the risk of incident COPD, which demonstrates that an additional hour of exposure to SHS per week was associated with a 1.03-fold increased likelihood of developing COPD after adjusting for confounders (RR = 1.03; 95% CI 1.00 to 1.05; P value = 0.027). SHS exposure contributes to the development of COPD. This finding can help raise awareness of the harms of SHS and provide a reference for formulating anti-smoking policies.

Vessel and Airway Characteristics in One-Year CT-defined Rapid Emphysema Progression: SPIROMICS.

Rationale: Rates of emphysema progression vary in chronic obstructive pulmonary disease (COPD), and the relationship with vascular and airway pathophysiology remain unclear. Objective: We sought to determine if indices of peripheral (segmental and beyond) pulmonary arterial (PA) dilation measured via computed tomography (CT) are associated with a 1-year index of emphysema (EI: %voxels<-950HU) progression. Methods: 599 GOLD 0-3 former and never-smokers were evaluated from the SubPopulations and InterMediate Outcome Measures in COPD Study (SPIROMICS) cohort: rapid-emphysema-progressors (RP, n=188; 1-year ΔEI>1%), non-progressors (NP, n=301; 1-year ΔEI±0.5%) and never-smokers (NS: N=110). Segmental PA cross-sectional areas were standardized to associated airway luminal areas (Segmental : Pulmonary Artery-to-Airway Ratio: PAARseg). Full inspiratory CT scan-derived total (arteries + veins) pulmonary vascular volume (TPVV) was compared to vessel volume with radius smaller than 0.75mm (SVV.75/TPVV). Airway-to-lung ratios (an index of dysanapsis and COPD risk) were compared to TPVV-lung-volume-ratios. Results: Compared with NP, RP exhibited significantly larger PAARseg (0.73±0.29 vs. 0.67±0.23; p=0.001), lower TPVV-to-lung-volume ratio (3.21%±0.42% vs. 3.48%±0.38%; p=5.0 x 10-12), lower airway-to-lung-volume ratio (0.031±0.003 vs. 0.034±0.004; p=6.1 x 10-13) and larger SVV.75/TPVV (37.91%±4.26% vs. 35.53±4.89; p=1.9 x 10-7). In adjusted analyses, a 1-SD increment in PAARseg was associated with a 98.4% higher rate of severe exacerbations (95%CI: 29 to 206%; p = 0.002) and 79.3% higher in odds of being in the rapid emphysema progression group (95%CI: 24% to 157%; p = 0.001). At year-2 followup, the CT-defined RP group demonstrated a significant decline in post-bronchodilator-FEV1% predicted. Conclusion: Rapid one-year progression of emphysema was associated with indices indicative of higher peripheral pulmonary vascular resistance and a possible role played by pulmonary vascular-airway dysanapsis.

The role of Neutrophil counts, infections and Smoking in mediating the Effect of Bronchiectasis on Chronic Obstructive Pulmonary Disease: a mendelian randomization study.

The causality of the relationship between bronchiectasis and chronic obstructive pulmonary disease (COPD) remains unclear. This study aims to investigate the potential causal relationship between them, with a specific focus on the role of airway inflammation, infections, smoking as the mediators in the development of COPD. We conducted a two-sample Mendelian randomization (MR) analysis to assess: (1) the causal impact of bronchiectasis on COPD, sex, smoking status, infections, eosinophil and neutrophil counts, as well as the causal impact of COPD on bronchiectasis; (2) the causal effect of smoking status, infections and neutrophil counts on COPD; and (3) the extent to which the smoking status, infections and neutrophil counts might mediate any influence of bronchiectasis on the development of COPD. COPD was associated with a higher risk of bronchiectasis (OR 1.28 [95% CI 1.05, 1.56]). Bronchiectasis was associated with a higher risk of COPD (OR 1.08 [95% CI 1.04, 1.13]), higher levels of neutrophil (OR 1.01 [95% CI 1.00, 1.01]), higher risk of respiratory infections (OR 1.04 [95% CI 1.02, 1.06]) and lower risk of smoking. The causal associations of higher neutrophil cells, respiratory infections and smoking with higher COPD risk remained after performing sensitivity analyses that considered different models of horizontal pleiotropy, with OR 1.17, 1.69 and 95.13, respectively. The bronchiectasis-COPD effect was 0.99, 0.85 and 122.79 with genetic adjustment for neutrophils, respiratory infections and smoking. COPD and bronchiectasis are mutually causal. And increased neutrophil cell count and respiratory infections appears to mediate much of the effect of bronchiectasis on COPD.

Chronic obstructive pulmonary disease: Signs and symptoms, diagnosis, treatments, lifestyle risk factors and management

Chronic Obstructive Pulmonary Disease (COPD) is associated with increased health complications, leading to a rise in mortality rates. COPD remains a significant global health issue, underscoring the importance of recognizing symptoms, facilitating diagnosis, and implementing effective treatment strategies. However, information on lifestyle risk factors and the management of COPD remains fragmented. This review paper aims to understand the clinical pathophysiologic changes triggered by lifestyle practices and their management strategies. It is important to understand its symptoms, diagnostics criteria, and treatment to correlate with lifestyle risk factors and to identify effective lifestyle interventions. Lifestyle practices as defined by dietary practices such being anorexia and low fruit and vegetable intake, smoking habits, alcohol consumption, and physical inactivity have increased the risk of COPD. This review suggested lifestyle approaches for COPD treatment such as regular exercise, a healthy diet, and avoiding smoking. In this case, the development of the guided improved intervention is important for a better understanding of the mechanisms between COPD and its associated lifestyle practices. This information may help clinicians, health practitioners, and dietitians to guide patients to implement improved dietary interventions. To avoid the progression of COPD, lifestyle practice therapy could be the most effective strategies that aid with medications as prescribed by the physicians.

Association between per- and polyfluoroalkyl substances exposure and prevalence of chronic obstructive pulmonary disease: The mediating role of serum albumin

BackgroundNo study has examined the association between per- and polyfluoroalkyl substances (PFAS) exposure and chronic obstructive pulmonary disease (COPD) risk. This study aims to explore this relationship. MethodsThis study enrolled 4541 individuals who had available data on PFAS, COPD, and covariates from NHANES 2007–2018. Serum PFAS including perfluorohexane sulfonate (PFHxS), perfluorononanoic acid (PFNA), perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS) were analyzed, because of high detective rates. Considering the skew distribution of PFAS levels, the natural logarithm-transformed PFAS (Ln-PFAS) was used. Logistic regression analysis, restricted cubic spline (RCS), and weighted quantile sum (WQS) regression were performed to explore the single, nonlinear, and mixed effects. A mediating analysis was used to evaluate the mediated effects of albumin. ResultsIndividuals with COPD had higher levels of PFHxS, PFNA, PFOA, and PFOS compared to those without COPD. Ln-PFNA (OR males: 1.92, 95 % CI:1.31 to 2.80, P: <0.001; OR females: 1.07, 95 % CI: 0.81 to 1.40, P: 0.636) and ln-PFOA (OR males: 2.17, 95 % CI:1.38 to 3.41, P: <0.001; OR females: 1.49, 95 % CI: 1.08 to 2.05, P: 0.016) were associated with COPD risk especially in males. The interaction between PFNA exposure and sex on COPD risk was significant (P interaction: <0.001). The RCS curve demonstrated the nonlinear relationship between the ln-PFOA (P nonlinear:0.001), ln-PFNA (P nonlinear:0.045), and COPD risk in males. WQS analysis showed mixed PFAS exposure was correlated with COPD risk in males (OR: 1.44, 95 % CI:1.18 to 1.75, P: <0.001). Albumin mediated the relationship between PFOA and COPD (mediated proportion: −17.94 %). ConclusionThis study concludes PFOA and PFNA are linked to a higher COPD risk in males, and serum albumin plays a mediating role in the relationship between PFOA and COPD. Thess findings are beneficial for the prevention of COPD. Further studies are required to explore potential mechanisms.

[A prospective study on association between sleep duration and the risk of chronic obstructive pulmonary disease in adults in Suzhou].

Objective: To investigate the prospective association of sleep duration with the development of chronic obstructive pulmonary disease (COPD) in adults in Suzhou. Methods: The study used the data of 53 269 participants aged 30-79 years recruited in the baseline survey from 2004 to 2008 and the follow-up until December 31, 2017 of China Kadoorie Biobank (CKB) conducted in Wuzhong District, Suzhou. After excluding participants with airflow limitation, self-reported chronic bronchitis/emphysema/coronary heart disease history at the baseline survey and abnormal or incomplete data, a total of 45 336 participants were included in the final analysis. The association between daily sleep duration and the risk for developing COPD was analyzed by using a Cox proportional hazard regression model, and the hazard ratio (HR) values and their 95%CI were calculated. The analysis was stratified by age, gender and lifestyle factors, and cross-analysis was conducted according to smoking status and daily sleep duration. Results: The median follow-up time was 11.12 years, with a total of 515 COPD diagnoses in the follow-up. After adjusting for potential confounders, multifactorial Cox proportional hazard regression analysis showed that daily sleep duration ≥10 hours was associated with higher risk for developing COPD (HR=1.42, 95%CI: 1.03-1.97). The cross analysis showed that excessive daily sleep duration increased the risk for COPD in smokers (HR=2.49, 95%CI: 1.35-4.59, interaction P<0.001). Conclusion: Longer daily sleep duration (≥10 hours) might increase the risk for COPD in adults in Suzhou, especially in smokers.

Impact of electronic cigarette usage on the onset of respiratory symptoms and COPD among Chinese adults

The prevalence of dual usage and the relatively low cessation rate among e-cigarette (EC) users suggest that ECs have not demonstrated significant effectiveness as a smoking cessation tool. Furthermore, there has been a substantial increase in the prevalence of EC usage in recent years. Therefore, the objective of this study is to investigate the association between EC use and the incidence of respiratory symptoms and chronic obstructive pulmonary disease (COPD). A total of 10,326 participants aged between 20 and 55 years, without any respiratory diseases or COPD, were recruited for the study. These individuals attended employee physical examinations conducted at 16 public hospitals in Hebei province, China from 2015 to 2020. Logistic regression models were utilized to assess the association between EC use and the risk of respiratory symptoms and COPD using risk ratios along with their corresponding 95% confidence intervals. Restricted cubic spline functions were employed to investigate the dose–response non-linear relationship. The robustness of the logistic regression models was evaluated through subgroup analyses, and sensitivity analyses. During the 5-year follow-up period, a total of 1071 incident cases of respiratory symptoms and 146 incident cases of COPD were identified in this cohort study. After adjusting for relevant confounding factors, EC users demonstrated a respective increase in the risk of reporting respiratory symptoms and COPD by 28% and 8%. Furthermore, dual users who used both ECs and combustible cigarettes exhibited an elevated risk of incident respiratory symptoms and COPD by 41% and 18%, respectively, compared to those who had never used non-users of any cigarette products. The association between daily EC consumption and the development of respiratory symptoms, as well as COPD, demonstrated a significant J-shaped pattern. The potential adverse association between the consumption of ECs, particularly when used in combination with combustible cigarettes, and the development of respiratory symptoms and COPD necessitates careful consideration. Policymakers should approach ECs cautiously as a prospective smoking cessation tool.

Association of the oxidation balance score with the prevalence of chronic obstructive pulmonary disease from the NHANES 2007–2012: A large-scale cross-sectional study

BackgroundThe occurrence of chronic obstructive pulmonary disease (COPD) is associated with oxidative stress. Oxidation Balance Score (OBS) can evaluate the oxidation and antioxidant status of the body. However, we found no studies that examined the association between the two. ObjectiveTo assess the association between OBS and COPD prevalence, and to explore dietary and lifestyle patterns aimed at preventing and delay COPD in adults. MethodWe included 13,909 participants using data from the NHANES. Weighted logistic regression model and weighted restricted cubic spline curve were used to explore the relationship between OBS and COPD. Subgroup analysis and sensitivity analysis were used to determine the stability of results. Mediation analysis was employed to assess the effect of inflammatory factors. ResultIn logistic regression model, compared with the lowest quartile of OBS, the highest quartile of OBS, diet OBS, lifestyle OBS and COPD had odd ratios OR(95%CI)=0.67 (0.51, 0.89), OR (95% CI) = 0.71 (0.55, 0.93), and OR (95% CI) = 0.39 (0.26, 0.58) respectively. The restricted cubic spline curve reveals that OBS and dietary OBS exhibit an L-shaped curve in relation to COPD prevalence, while lifestyle OBS shows a negative correlation curve with COPD prevalence. Subgroup analysis and sensitivity analysis proved the robustness of the association. Mediation analysis demonstrated that inflammatory factors mediate the association of OBS on the prevalence of COPD. ConclusionThe increase of OBS, dietary OBS, and lifestyle OBS was associated with a decrease in the prevalence of COPD, but excessive OBS and dietary OBS were associated with an inapparent decrease or even increased risk of COPD.

Physical activity and the risk of chronic obstructive pulmonary disease: A longitudinal follow-up study in Taiwan

BackgroundThis study aimed to investigate whether physical activity (PA) is associated with a lower risk of subsequently developing chronic obstructive pulmonary disease (COPD). MethodsWe conducted this population-based longitudinal follow-up study in a community in Taiwan. This study recruited 61,446 subjects who had participated in the Keelung Community-based Integrated Screening Program (KCIS) between 2005 and 2012. During their participation in KCIS, they were provided with structured questionnaires to collect their baseline characteristics, including weekly PA time. After excluding subjects diagnosed with COPD before they joined KCIS and/or who provided incomplete lifestyle data, 59,457 subjects remained, and were classified into three groups based on their weekly PA time: i.e., as NPA (no regular PA), LPA (low PA, <90 min/week) and HPA (high PA, ≥90 min/week). The primary outcome was a new diagnosis of COPD, followed up until the end of 2015 or their death. Cox proportional-hazard regression was used to assess the impact of PA on the risk of COPD. ResultsThe risk of COPD was more than 20% lower in the LPA and HPA groups than in the NPA group. Specifically, the adjusted hazard ratio for the risk of COPD was 0.72 in the LPA group (95% CI, 0.61-0.85, p < 0.001) and 0.79 in the HPA group (95% CI, 0.69-0.90, p < 0.001). ConclusionsOur research uncovered an inverse relationship between PA and COPD. The findings suggest that PA might be useful as a strategy for the primary prevention of COPD.

Effects of triple therapy on disease burden in patients of GOLD groups C and D: results from the observational COPD cohort COSYCONET

BackgroundRandomized controlled trials described beneficial effects of inhaled triple therapy (LABA/LAMA/ICS) in patients with chronic obstructive pulmonary disease (COPD) and high risk of exacerbations. We studied whether such effects were also detectable under continuous treatment in a retrospective observational setting.MethodsData from baseline and 18-month follow-up of the COPD cohort COSYCONET were used, including patients categorized as GOLD groups C/D at both visits (n = 258). Therapy groups were defined as triple therapy at both visits (triple always, TA) versus its complement (triple not always, TNA). Comparisons were performed via multiple regression analysis, propensity score matching and inverse probability weighting to adjust for differences between groups. For this purpose, variables were divided into predictors of therapy and outcomes.ResultsIn total, 258 patients were eligible (TA: n = 162, TNA: n = 96). Without adjustments, TA patients showed significant (p < 0.05) impairments regarding lung function, quality of life and symptom burden. After adjustments, most differences in outcomes were no more significant. Total direct health care costs were reduced but still elevated, with inpatient costs much reduced, while costs of total and respiratory medication only slightly changed.ConclusionWithout statistical adjustment, patients with triple therapy showed multiple impairments as well as elevated treatment costs. After adjusting for differences between treatment groups, differences were reduced. These findings are compatible with beneficial effects of triple therapy under continuous, long-term treatment, but also demonstrate the limitations encountered in the comparison of controlled intervention studies with observational studies in patients with severe COPD using different types of devices and compounds.

Haemodynamic compensations for exercise tissue oxygenation in early stages of COPD: an integrated cardiorespiratory assessment study

BackgroundCardiovascular comorbidities are increasingly being recognised in early stages of chronic obstructive pulmonary disease (COPD) yet complete cardiorespiratory functional assessments of individuals with mild COPD or presenting with COPD risk...

Bidirectional relationship between chronic obstructive pulmonary disease and oral disease

Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease that has various comorbid conditions and systemic complications. One of the complications is dental and oral disease, which can occur through systemic inflammatory mechanisms and the long-term side effects of inhaled drugs. Dental and oral diseases can also cause COPD progression, increase the risk of exacerbations, and affect the patient's quality of life. Some mechanisms that may play a role include aspiration of oral pathogens, aspiration of inflammatory proteins, and systemic inflammation. Dysbiosis of the lung microbiome can result from dental and oral conditions, increasing the risk of COPD and pulmonary infections. The association between COPD and oral disease includes the presence of systemic inflammatory conditions, the risk factor of smoking, and the indirect effects of inhaled medication use. Comprehensive management of COPD patients regarding dental and oral health is needed, which includes prevention of dental and oral disease, routine assessment of dental and oral health, provision of specific dental therapy, and personalized treatment in selecting COPD therapy.