Clinical and microbiological characteristics and inflammatory profile during an exacerbation of COPD due to biomass exposure. A comparison with COPD due to tobacco exposure

Sansores, Raúl H; Paulin-Prado, Paulina; Robles, Robinson E; Montiel-Lopez, Francisco; Bautista-Félix, Nora Edith; Guzmán-Bouilloud, Nicolás Eduardo; Falfán-Valencia, Ramcés; Pérez-Rubio, Gloría; Hernández-Zenteno, Rafael de Jesús; Flores-Trujillo, Fernando; Pérez-Bautista, Oliver; Ramírez‐Venegas, Alejandra

doi:10.1016/j.rmed.2022.107010

Cited by 3 publications

(4 citation statements)

References 36 publications

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“…In addition, DEP per se may act as allergen carriers that absorbed various allergens, such as pollen, dust mites and pathogens [ 49 , 50 ], which might enhance eosinophil recruitment to the peripheral lungs in DEP-exposed rats. Likewise, previous studies have shown that eosinophilic inflammation was evident in biomass smoke-related COPD, but the majority of cell population in the sputum was neutrophil [ 17 , 51 ], which is consistent with our current findings. In addition, the lack of neutrophil recruitment to the airway mucosa might be due to the rapid transition of this cell type from tissue to the airway lumen that has been observed in COPD patients [ 52 ].…”

Section: Discussionsupporting

confidence: 93%

Fine particulate matter contributes to COPD-like pathophysiology: experimental evidence from rats exposed to diesel exhaust particles

Fang,

Wang,

Chen

et al. 2024

Respir Res

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Background Ambient fine particulate matter (PM2.5) is considered a plausible contributor to the onset of chronic obstructive pulmonary disease (COPD). Mechanistic studies are needed to augment the causality of epidemiologic findings. In this study, we aimed to test the hypothesis that repeated exposure to diesel exhaust particles (DEP), a model PM2.5, causes COPD-like pathophysiologic alterations, consequently leading to the development of specific disease phenotypes. Sprague Dawley rats, representing healthy lungs, were randomly assigned to inhale filtered clean air or DEP at a steady-state concentration of 1.03 mg/m3 (mass concentration), 4 h per day, consecutively for 2, 4, and 8 weeks, respectively. Pulmonary inflammation, morphologies and function were examined. Results Black carbon (a component of DEP) loading in bronchoalveolar lavage macrophages demonstrated a dose-dependent increase in rats following DEP exposures of different durations, indicating that DEP deposited and accumulated in the peripheral lung. Total wall areas (WAt) of small airways, but not of large airways, were significantly increased following DEP exposures, compared to those following filtered air exposures. Consistently, the expression of α-smooth muscle actin (α-SMA) in peripheral lung was elevated following DEP exposures. Fibrosis areas surrounding the small airways and content of hydroxyproline in lung tissue increased significantly following 4-week and 8-week DEP exposure as compared to the filtered air controls. In addition, goblet cell hyperplasia and mucus hypersecretions were evident in small airways following 4-week and 8-week DEP exposures. Lung resistance and total lung capacity were significantly increased following DEP exposures. Serum levels of two oxidative stress biomarkers (MDA and 8-OHdG) were significantly increased. A dramatical recruitment of eosinophils (14.0-fold increase over the control) and macrophages (3.2-fold increase) to the submucosa area of small airways was observed following DEP exposures. Conclusions DEP exposures over the courses of 2 to 8 weeks induced COPD-like pathophysiology in rats, with characteristic small airway remodeling, mucus hypersecretion, and eosinophilic inflammation. The results provide insights on the pathophysiologic mechanisms by which PM2.5 exposures cause COPD especially the eosinophilic phenotype.

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Section: Discussionsupporting

confidence: 93%

Fine particulate matter contributes to COPD-like pathophysiology: experimental evidence from rats exposed to diesel exhaust particles

Fang,

Wang,

Chen

et al. 2024

Respir Res

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“…A further limitation was that no patients with exposure to biomass smoke were included in the study. These patients present similar characteristics in acute exacerbations as those exposed to tobacco smoke 6. Thus, it was not possible to present a fully comprehensive representation of the burden of severe exacerbations in low-income and middle-income countries.…”

Section: Discussionmentioning

confidence: 99%

“…These patients present similar characteristics in acute exacerbations as those exposed to tobacco smoke. 6 Thus, it was not possible to present a fully comprehensive representation of the burden of severe exacerbations in low-income and middle-income countries. Additionally, as a retrospective data study, it relied on the accuracy/completeness of the data that were captured in the eCRFs, and may be subject to recall bias.…”

Section: Discussionmentioning

confidence: 99%

“…2 Epidemiological studies indicate that COPD is strongly associated with a history of exposure to tobacco smoke; however, a substantial proportion of patients with COPD (25-45%) report that they have never smoked. 3 Other risk factors for the development of COPD, which are particularly relevant in developing countries, include biomass smoke exposure, [4][5][6] poor lung growth and development, [7][8][9][10][11] inadequately treated childhood respiratory infections, 12 occupational air pollution, 13 chronic childhood asthma 11 and post-tuberculosis lung disease. 13 Exacerbations are clinically significant events as they accelerate lung function decline, [14][15][16][17] negatively impact patient quality of life, 18 19 and are associated with increased hospital admissions and mortality.…”

Section: Introductionmentioning

confidence: 99%

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Rate of severe exacerbations, healthcare resource utilisation and clinical outcomes in patients with COPD in low-income and middle-income countries: results from the EXACOS International Study

Athanazio,

Bernal Villada,

Avdeev

et al. 2024

BMJ Open Resp Res

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IntroductionTheEXAcerbations ofChronic obstructive lung disease (COPD) and theirOutcomeS(EXACOS) International Study aimed to quantify the rate of severe exacerbations and examine healthcare resource utilisation (HCRU) and clinical outcomes in patients with COPD from low-income and middle-income countries.MethodsEXACOS International was an observational, cross-sectional study with retrospective data collection from medical records for a period of up to 5 years. Data were collected from 12 countries: Argentina, Brazil, Chile, Colombia, Costa Rica, Dominican Republic, Guatemala, Hong Kong, Mexico, Panama, Russia and Taiwan. The study population comprised patients ≥40 years of age with COPD. Outcomes/variables included the prevalence of severe exacerbations, the annual rate of severe exacerbations and time between severe exacerbations; change in lung function over time (measured by the forced expiratory volume in 1 s (FEV1)); peripheral blood eosinophil counts (BECs) and the prevalence of comorbidities; treatment patterns; and HCRU.ResultsIn total, 1702 patients were included in the study. The study population had a mean age of 69.7 years, with 69.4% males, and a mean body mass index of 26.4 kg/m2. The mean annual prevalence of severe exacerbations was 20.1%, and 48.4% of patients experienced ≥1 severe exacerbation during the 5-year study period. As the number of severe exacerbations increased, the interval between successive exacerbations decreased. A statistically significant decrease in mean (SD) FEV1from baseline to post-baseline was observed in patients with ≥1 severe exacerbation (1.23 (0.51) to 1.13 (0.52) L; p=0.0000). Mean BEC was 0.198 x109cells/L, with 64.7% of patients having a BEC ≥0.1 x109 cells/L and 21.3% having a BEC ≥0.3 x109 cells/L. The most common comorbidity was hypertension (58.3%). An increasing number of severe exacerbations per year was associated with greater HCRU.DiscussionThe findings presented here indicate that effective treatment strategies to prevent severe exacerbations in patients with COPD remain a significant unmet need in low-income and middle-income countries.

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Biomass Smoke–Associated Lung Diseases

et al. 2023

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Clinical and microbiological characteristics and inflammatory profile during an exacerbation of COPD due to biomass exposure. A comparison with COPD due to tobacco exposure

Cited by 3 publications

References 36 publications

Fine particulate matter contributes to COPD-like pathophysiology: experimental evidence from rats exposed to diesel exhaust particles

Fine particulate matter contributes to COPD-like pathophysiology: experimental evidence from rats exposed to diesel exhaust particles

Rate of severe exacerbations, healthcare resource utilisation and clinical outcomes in patients with COPD in low-income and middle-income countries: results from the EXACOS International Study

Biomass Smoke–Associated Lung Diseases

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