Search Results (23)

Background: Chronic Obstructive Pulmonary Disease (COPD) exhibits some phenotypic differences between patients with biomass smoke inhalation (COPD-B) and tobacco smoking (COPD-T). COPD-B is characterized by less emphysema but more airway disease and vascular pulmonary remodeling, which are related to mast cells in lung tissues in COPD-T. Our objective was to describe the differences between the number of mast cells in COPD-B and COPD-T patients. Methods: A cross-sectional study was conducted on lung tissue resections for suspected cancer obtained between 2014 and 2021 from patients with documented COPD due to wood smoke or tobacco exposure. Histological samples were analyzed for mast cell count, CD34+ expression, and structural changes in lung tissue and pulmonary circulation. Results: A total of 20 histological samples were analyzed, with significant differences found in mast cell count [median 8 (p25-75, 5–11) vs. 2 (p75-25, 0–6), p = 0.016] and severe peribronchiolar fibrosis (60% vs. 10%, p = 0.04) between COPD-B and COPD-T patients. A positive correlation [Spearman rho = 0.879 (95% CI 0.71–0.96), p < 0.001] was observed between mast cell count and a gradual increase in pulmonary artery diameter. Conclusions: These preliminary findings suggest histological differences and the presence of mast cells between COPD-B and COPD-T, which should be confirmed in a larger number of samples and patients. Full article

COPD induced by biomass-burning smoke is a public health problem in developing countries. Biomass-based fuels are ineffective and deliver elevated levels of carbon monoxide, polycyclic aromatic hydrocarbons, and fine particulate matter. PRSS23 participates in extracellular matrix remodeling processes in COPD patients. Our objective was to estimate the DNA methylation levels of cg23771366 (PRSS23) and their clinical relevance in COPD caused by chronic exposure to biomass-burning smoke (BBS). We included 80 women with COPD (COPD-BBS) (≥200 h per year), 180 women with exposure to BBS (≥200 h per year) but without COPD (BBES), and 79 lung-healthy women (HW) without exposure to biomass-burning smoke. The DNA methylation analysis shows significant differences between the three groups included in this study (p < 0.001). HW had high methylation levels (100%) in cg23771366 (PRSS23). In comparison, COPD-BBS and BBES had low levels [0.91% vs. 9.17%, respectively], showing statistically significant differences (p = 0.011) between both groups, with the COPD-BBS presenting the lowest levels in the methylation of cg23771366. In conclusion, chronic biomass-burning smoke exposure is associated with decreased levels of DNA methylation at the CpG cg23771366 site in PRSS23, reinforcing the relationship between PRSS23 and particulate matter. Full article

Background: Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality globally, and factors such as biomass exposure, demographic characteristics, and comorbidities significantly influence patient outcomes during exacerbations. Aim: This study aims to clarify the impact of patient characteristics on key hospital outcomes, including ICU admissions, hospital length of stay, and in-hospital mortality, focusing on the contextual role of biomass exposure rather than its direct impact. Methods: Using a multicenter, retrospective cohort design, we analyzed the medical records of patients admitted with COPD exacerbations from January 2021 to December 2023. Eligible patients were over 40 years old with confirmed COPD exacerbation, excluding those with other significant lung conditions, severe organ dysfunction, or incomplete data. The collected data included demographics, smoking history, comorbidities, medications, laboratory results, and clinical outcomes, with smoking status categorized into current, former, or never smokers. Results: Our analysis comprised 334 patients with a mean age of 69 ± 8.8 years, including 52 (15.6%) females. Biomass exposure, observed in 22% of patients, was associated with a higher likelihood of being female (p < 0.001), lower smoking rates (p < 0.001), higher prevalence of diabetes mellitus type 2 (p = 0.020), lower peripheral blood eosinophilia (p = 0.001), increased intensive care unit (ICU) admissions (p = 0.034), and higher in-hospital mortality (p = 0.043). Non-survivors tended to be older and had a higher prevalence of hypertension, a history of childhood pneumonia, longer COPD duration, greater need for non-invasive ventilation (NIV) during hospitalization, and more frequent ICU admissions. Univariate Cox regression analysis revealed no significant associations between characteristics and outcomes. Conclusions: Patients with biomass exposure were more likely to be female and had higher rates of ICU admission and in-hospital mortality. Full article

Chronic Obstructive Pulmonary Disease (COPD) is a disease characterized by local and systemic inflammation independently of the risk factor; during the exacerbations, such inflammation is accentuated and amplified. A practical inflammatory marker and one with an applicable predictive value in the follow-up has been sought. FeNO has shown an excellent performance in that respect within the context of asthma and has also been studied in tobacco-smoke COPD (COPD-TS). In Biomass-smoke COPD (COPD-BS), this, to our knowledge, has not been evaluated. Objective: To measure FeNO levels in patients with COPD-BS and to compare these with those of patients with stable COPD-TS and in healthy controls. Methods: Transversal, observational, descriptive, comparative, and analytical study. A total of 57 patients, including 23 with COPD-BS, 17 with COPD-TS, and 17 healthy control subjects. The measurement of FeNO was carried out on all of these by means of the on-line chemiluminescence technique; the values were expressed in parts per billion (ppb) for their analysis. Results: It was observed that the FeNO values were similar between COPD-BS and COPD-TS and were significantly different between the healthy and stable COPD (both groups). No correlation was found between pulmonary function and symptoms with FeNO in any of the groups. Conclusions: The level of FeNO in stable COPD is found to be increased in a similar manner in COPD-BS and COPD-TS, with a significant difference on comparing it with that of the healthy subjects. Full article

Background: Chronic Obstructive Pulmonary Disease (COPD) is a major global health challenge, primarily driven by exposures to tobacco smoke and biomass smoke. While Tobacco-Smoke-Induced COPD (TSCOPD) has been extensively studied, the diagnostic challenges and distinct pathogenesis of Biomass-Smoke-Induced COPD (BSCOPD), particularly in low- and middle-income countries, remain underexplored. Objective: To explore the differences in clinical manifestations, pulmonary function, and inflammatory profiles between BSCOPD and TSCOPD and highlight the diagnostic complexities of BSCOPD. Methods: This review analyzes the current literature comparing BSCOPD with TSCOPD, focusing on distinctive pathophysiological mechanisms, inflammatory markers, and oxidative stress processes. Results: BSCOPD presents differences in clinical presentation, with less emphysema, smaller airway damage, and higher rates of pulmonary hypertension compared to TSCOPD. BSCOPD is also characterized by bronchial hyperresponsiveness and significant hypoxemia, unlike TSCOPD, which exhibits severe airflow obstruction and emphysema. Additionally, the inflammatory profile of BSCOPD includes distinct mucous hypersecretion and airway remodeling. Conclusions: The unique genetic, epigenetic, and oxidative stress mechanisms involved in BSCOPD complicate its diagnosis and management. Biomass smoke’s underrecognized impact on accelerated lung aging and exacerbation mechanisms emphasizes the need for targeted research to refine diagnostic criteria and management strategies for BSCOPD. Future directions: Further research should focus on identifying specific biomarkers and molecular pathways to enhance early diagnosis and improve clinical outcomes in populations exposed to biomass smoke. Full article

Outdoor air pollution and biomass smoke exposure are related to the prevalence of chronic obstructive pulmonary disease (COPD). Since Osorno, Chile, is saturated with fine particulate matter (PM_2.5), the aim of this work is to determine the prevalence distribution of COPD patients in the Primary Health Care (PHC) system in the city of Osorno, and its relationship with PM_2.5. A cross-sectional descriptive study was carried out on COPD patients enrolled in the six PHC centers (PHCCs) of the city to assess the adjusted prevalence (population over 40 years). Gender- and territory-associated odds ratios (ORs) were also determined. In addition, an urban analysis of the distribution of PM_2.5 and an exploratory analysis of the spatial behavior of enrolled COPD patients through featured binning were carried out. In 2018, the city of Osorno had 809 enrolled COPD patients in the PHC system (55.1% female), with a 1.3% age-adjusted prevalence (inhabitants over 40 years old), which was 11.7% after underdiagnosis correction. The COPD patients were mainly between 70 and 79 years old (34.3%). The urban area under the administration of the PHCC Rahue Alto (PHCC-RA) had a higher OR (1.98 [1.73–2.26]) compared to the situation of the city. Also, air pollution (PM_2.5) was the highest in the PHCC-RA area, which could account for the observed prevalence. The number of COPD patients in this area is the highest in the commune, which increases the risk of complications derived from the disease and air pollution. Thus, territories with the highest COPD prevalence have the largest OR, which could complicate patients’ condition due to the high levels of outdoor air pollution. Full article

Background: COPD due to exposure to combustible biomass is an increasingly recognized phenotype, particularly among women who use traditional ovens, known as ‘Tabouna’, for baking bread. This paper aims to investigate the clinical and functional characteristics of COPD in Tunisian female patients attributed to the use of ‘Tabouna’. Methods: A retrospective single-center cohort study was conducted on patients recruited from the Department of Respiratory Disease at A. Mami Hospital, who were diagnosed with COPD between January 2014 and December 2022. The diagnosis of COPD adhered to the standards defined in GOLD 2022. Results: Out of the 95 women included in the study, 48 (50.5%) were exposed to tobacco smoke, while 47 (49.5%) were exposed to the ‘Tabouna’. The median age was 70.4 ± 11.5 years, ranging from 40 to 95 years. Patients exposed to biomass were notably older, with a median age of 75.4 compared to 64.6 (p = 0.04). A significant association was observed between COPD and biomass smoke exposure, both in women residing in rural and urban areas (p = 0.006). The frequency of patients exposed to biomass with comorbidities was higher than in the group exposed to tobacco, but only hypertension showed statistically significant results (p = 0.01). Tobacco smoke induced more impairment in lung function than biomass in the group with FEV1 ≤ 30% (p = 0.04). Long-acting muscarinic antagonists were more commonly prescribed to smokers (p = 0.04). Serious complications such as chronic respiratory failure and intensive care admissions were similar in both groups (p = 0.8 and 0.4). Conclusions: COPD in women after exposure to the ‘Tabouna’ was observed in older patients and characterized by delayed diagnosis. Despite these clinical differences, poor COPD outcomes were similar in both groups. Full article

Background: Sex differences in symptoms exist in patients with COPD. Our aim is to measure the differences between men and women with COPD, focusing on risk factors, symptoms, quality of life and drug prescriptions. Methods: In this cross-sectional observational study, patients with COPD were collected in China; demographic characteristics, smoking history, occupational exposure, biomass exposure, lung function, dyspnea, quality of life, and prescriptions for inhaled medications were collected. The nearest neighbor algorithm was used to match female and male patients (ratio 2:1) on age, body mass index, and lung function. Results: Compared with 1462 men, the 731 women generally had lower educational levels and were married less (both p < 0.001). A total of 576 (90.0%) women did not smoke cigarettes. More men were exposed to occupational dust (539 (36.9%) vs. 84 (11.5%), p = 0.013), while more women were exposed to biomass smoke (330 (45.1%) vs. 392 (26.8%), p = 0.004). Except for phlegm and chest tightness, women had more complaints than men for cough, breathlessness, activities, confidence, sleep and energy (p < 0.05). In addition, more women were prescribed triple therapy than men (236 (36.3%) vs. 388 (31.0%), p = 0.020). Conclusions: There are obvious discrepancies in the quality of life and use of inhaled medications between male and female patients with COPD. Full article

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide; the main risk factors associated with the suffering are tobacco smoking (TS) and chronic exposure to biomass-burning smoke (BBS). Different biological pathways have been associated with COPD, especially xenobiotic or drug metabolism enzymes. This research aims to identify single nucleotide polymorphisms (SNPs) profiles associated with COPD from two expositional sources: tobacco smoking and BBS. One thousand-five hundred Mexican mestizo subjects were included in the study and divided into those exposed to biomass-burning smoke and smokers. Genome-wide exome genotyping was carried out using Infinium Exome-24 kit arrays v. 1.2. Data quality control was conducted using PLINK 1.07. For clinical and demographic data analysis, Rstudio was used. Eight SNPs were found associated with COPD secondary to TS and seven SNPs were conserved when data were analyzed by genotype. When haplotype analyses were carried out, five blocks were predicted. In COPD secondary to BBS, 24 SNPs in MGST3 and CYP family genes were associated. Seven blocks of haplotypes were associated with COPD-BBS. SNPs in the ARNT2 and CYP46A1 genes are associated with COPD secondary to TS, while in the BBS comparison, SNPs in CYP2C8, CYP2C9, MGST3, and MGST1 genes were associated with increased COPD risk. Full article

Chronic exposure to indoor biomass smoke from the combustion of solid organic fuels is a major cause of disease burden worldwide. Almost 3 billion people use solid fuels such as wood, charcoal, and crop residues for indoor cooking and heating, accounting for approximately 50% of all households and 90% of rural households globally. Biomass smoke contains many hazardous pollutants, resulting in household air pollution (HAP) exposure that often exceeds international standards. Long-term biomass-smoke exposure is associated with Chronic Obstructive Pulmonary Disease (COPD) in adults, a leading cause of morbidity and mortality worldwide, chronic bronchitis, and other lung conditions. Biomass smoke-associated COPD differs from the best-known cigarette smoke-induced COPD in several aspects, such as a slower decline in lung function, greater airway involvement, and less emphysema, which suggests a different phenotype and pathophysiology. Despite the high burden of biomass-associated COPD, the molecular, genetic, and epigenetic mechanisms underlying its pathogenesis are poorly understood. This review describes the pathogenic mechanisms potentially involved in lung damage, the development of COPD associated with wood-derived smoke exposure, and the influence of genetic and epigenetic factors on the development of this disease. Full article

Acute exacerbations of COPD (AECOPD) are clinically significant events having therapeutic and prognostic consequences. However, there is a lot of variation in its clinical manifestations described by phenotypes. The phenotypes of AECOPD were categorized in this study based on pathology and exposure. In our cross-sectional study, conducted between 1 January 2016 to 31 December 2020, the patients were categorized into six groups based on pathology: non-bacterial and non-eosinophilic; bacterial; eosinophilic; bacterial infection with eosinophilia; pneumonia; and bronchiectasis. Further, four groups were classified based on exposure to tobacco smoke (TS), biomass smoke (BMS), both, or no exposure. Cox proportional-hazards regression analyses were performed to assess hazard ratios, and Kaplan–Meier analysis was performed to assess survival, which was then compared using the log-rank test. The odds ratio (OR) and independent predictors of ward admission type and length of hospital stay were assessed using binomial logistic regression analyses. Of the 2236 subjects, 2194 were selected. The median age of the cohort was 67.0 (60.0 to 74.0) and 75.2% were males. Mortality rates were higher in females than in males (6.2% vs. 2.3%). AECOPD-B (bacterial infection) subjects [HR 95% CI 6.42 (3.06–13.46)], followed by AECOPD-P (pneumonia) subjects [HR (95% CI: 4.33 (2.01–9.30)], were at higher mortality risk and had a more extended hospital stay (6.0 (4.0 to 9.5) days; 6.0 (4.0 to 10.0). Subjects with TS and BMS-AECOPD [HR 95% CI 7.24 (1.53–34.29)], followed by BMS-AECOPD [HR 95% CI 5.28 (2.46–11.35)], had higher mortality risk. Different phenotypes have different impacts on AECOPD clinical outcomes. A better understanding of AECOPD phenotypes could contribute to developing an algorithm for the precise management of different phenotypes. Full article

Secretoglobin family 1A member 1 (SCGB1A1) alternatively known as club cell protein 16 is a protective pneumo-protein. Decreased serum levels of SCGB1A1 have been associated with tobacco smoke induced chronic obstructive pulmonary disease (TS-COPD). Exposure to biomass smoke (BMS) is an important COPD risk factor among women in low and lower-middle income countries. Therefore, in a cross-sectional study (n = 50/group; total 200 subjects) we assessed serum SCGB1A1 levels in BMS-COPD subjects (11 male, 39 female) compared to TS-COPD (all male) along with TS-CONTROL (asymptomatic smokers, all male) and healthy controls (29 male, 21 female) in an Indian population. Normal and chronic bronchitis like bronchial mucosa models developed at the air–liquid interface using human primary bronchial epithelial cells (3 donors, and three replicates per donor) were exposed to cigarette smoke condensate (CSC; 0.25, 0.5, and 1%) to assess SCGB1A1 transcript expression and protein secretion. Significantly (p < 0.0001) decreased serum SCGB1A1 concentrations (median, interquartile range, ng/mL) were detected in both BMS-COPD (1.6; 1.3–2.4) and TS-COPD (1.8; 1.4–2.5) subjects compared to TS-CONTROL (3.3; 2.9–3.5) and healthy controls (5.1; 4.5–7.2). The levels of SCGB1A1 were positively correlated (r = 0.7–0.8; p < 0.0001) with forced expiratory volume in 1 s, forced vital capacity, their ratios, and exercise capacity. The findings are also consistent within the BMS-COPD sub-group as well. Significantly (p < 0.03) decreased SCGB1A1 concentrations were detected with severity of COPD, dyspnea, quality of life, and mortality indicators. In vitro studies demonstrated significantly (p < 0.05) decreased SCGB1A1 transcript and/or protein levels following CSC exposure. Circulating SCGB1A1 levels may therefore also be considered as a potent marker of BMS-COPD and warrant studies in larger independent cohorts. Full article

Background: Chronic Obstructive Pulmonary Disease (COPD) is an inflammatory disease characterized by airflow obstruction, commonly present in smokers and subjects exposed to noxious particles product of biomass-burning smoke (BBS). Several association studies have identified single-nucleotide polymorphisms (SNP) in coding genes related to the heat shock proteins family-genes that codify the heat shock proteins (Hsp). Hsp accomplishes critical roles in regulating immune response, antigen-processing, eliminating protein aggregates and co-activating receptors. The presence of SNPs in these genes can lead to alterations in immune responses. We aimed to evaluate the association of SNPs in the HSP90 gene complex and COPD. Methods: We enrolled 1549 participants, divided into two comparison groups; 919 tobacco-smoking subjects (cases COPD-TS n = 294 and, controls SWOC n = 625) and 630 chronic exposed to BBS (cases COPD-BBS n = 186 and controls BBES n = 444). We genotyped 2 SNPs: the rs13296 in HSP90AB1 and rs2070908 in HSP90B1. Results: Through the dominant model (GC + CC), the rs2070908 is associated with decreased risk (p < 0.01, OR = 0.6) to suffer COPD among chronic exposed BBS subjects. We found an association between rs13296 GG genotype and lower risk (p = 0.01, OR = 0.22) to suffer severe COPD-TS forms in the severity analysis. Conclusions: single-nucleotide variants in the HSP90AB1 and HSP90B1 genes are associated with decreased COPD risk in subjects exposed to BBS and the most severe forms of COPD in tobacco-smoking subjects. Full article

Chronic obstructive pulmonary disease (COPD), the frequently fatal pathology of the respiratory tract, accounts for half a billion cases globally. COPD manifests via chronic inflammatory response to irritants, frequently to tobacco smoke. The progression of COPD from early onset to advanced disease leads to the loss of the alveolar wall, pulmonary hypertension, and fibrosis of the respiratory epithelium. Here, we focus on the epidemiology, progression, and biomarkers of COPD with a particular connection to lung cancer. Dissecting the cellular and molecular players in the progression of the disease, we aim to shed light on the role of smoking, which is responsible for the disease, or at least for the more severe symptoms and worse patient outcomes. We summarize the inflammatory conditions, as well as the role of EMT and fibroblasts in establishing a cancer-prone microenvironment, i.e., the soil for ‘COPD-derived’ lung cancer. We highlight that the major health problem of COPD can be alleviated via smoking cessation, early diagnosis, and abandonment of the usage of biomass fuels on a global basis. Full article

Chronic obstructive pulmonary disease (COPD), the leading cause of mortality and morbidity worldwide, is characterized by abnormal activation of inflammatory cells. The increased pro-inflammatory cytokines, such as tumour necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β), further amplify the inflammation. We evaluated the dose response relationship of IL-1β and TNF-α levels and severity of airflow limitation, and differential responses in IL-1β and TNF-α between biomass COPD (BMS-COPD) and tobacco smoke COPD (TS-COPD) using a case control design in 160 subjects. Patients with COPD had higher serum levels of both IL-1β and TNF-α compared to healthy controls. A large difference in TNF-α was observed between TS-COPD and BMS-COPD, where TS-COPD patients had much higher levels. Serum IL-1β levels were higher in BMS-COPD. Levels of IL-1β correlated better with severity of airflow limitation than TNF-α levels. Both TNF-α and IL-1β levels had a negative linear relationship with Forced Expiratory Volume in 1st second (FEV1) and six-minute walk distance. The correlations were stronger with FEV1 than six-minute walk distance. The correlations of TNF-α and IL-1β with St George Respiratory Questionnaire (SGRQ) scores and body mass index (BMI) were not significant. In conclusion, the levels of pro-inflammatory cytokines TNF-α and IL-1β are differently elevated in TS-COPD and BMS-COPD, respectively. Full article