Pathogenic Mechanisms in Chronic Obstructive Pulmonary Disease Due to Biomass Smoke Exposure

Objective: Asthma-chronic obstructive pulmonary disease overlap (ACO) indicates that its characteristics with pulmonary exaggerated reactivity and airflow limitation chronically. We aimed to investigate the differences among women non smoker participants who have asthma, chronic obstructive pulmonary disease (COPD) and ACO with biomass smoke exposure. Method: Patients were examined at the outpatient clinic from September 2017 to March 2020. Non-smoker women patients aged ≥40 years, diagnosed with obstructive pulmonary disease were included in the study. pulmonary function tests (PFT), early reversibility testing (bronchodilator test), and sputum eosinophil analysis were performed to all patients. Results: A total of 102 patients were included. The mean age was 46.95±9.50 years. In the differential diagnosis, 65 patients (63.7%) had asthma and 37 patients (36.3%) had COPD. Among COPD patients, 10 (27.0%) were diagnosed with ACO. The actual prevalence rates of COPD and ACO were 26.5% and 9.8%, respectively. Poisson regression analysis showed that COPD compared to asthma, while holding the others variable constant in the model, are expected to have 2.976 times greater rate for exacerbations.( IRR, 95%CI ,2.976 (0.687 to 1.494), 5.296 (1.203 to 2.130), P<0.001, Coef. 1.091, 1.667 respectively). Logistic Regression analysis demonstrated that, the count of sputum, blood eosinophil and total IgE results were correlated with the exacerbation times. Conclusion: Biomass smoke exposure in the women population is revealed as a significant factor for the diagnosis of ACO.

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Indoor Biomass Fuel Smoke Exposure as a Risk Factor for Chronic Obstructive Pulmonary Disease (COPD) for Women of Rural Bangladesh

Chattagram Maa-O-Shishu Hospital Medical College Journal ◽

10.3329/cmoshmcj.v15i1.28753 ◽

2016 ◽

Vol 15 (1) ◽

pp. 8-11 ◽

Cited By ~ 2

Author(s):

Rajat Sanker Roy Biswas ◽

Sujat Paul ◽

Md Ridwanur Rahaman ◽

Md Abu Sayeed ◽

Mohammed Gofranul Hoque ◽

...

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Risk Factor ◽

Natural Gas ◽

Rural Women ◽

Smoke Exposure ◽

Biomass Fuel ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Biomass Smoke ◽

Biomass Smoke Exposure

Background: Chronic Obstructive Pulmonary Disease (COPD) is of public health importance. Indoor biomass (wood, cowdung etc) smoke exposure from cooking is associated with respiratory conditions and may predispose to COPD. The objective of this study was to evaluate the risk of biomass smoke exposure and COPD.Methods: A cross sectional study was conducted at a rural setting of Bangladesh. Rural women over 40 years and exposed to biomass fuel, liquid petroleum gas or natural gas smoke were evaluated using a questionnaire and their lung function was assessed using a portable spirometry.Results: The overall prevalence of COPD in the rural women was 20.4%. It was significantly higher in women using biomass fuel for cooking than in those using natural gas/LPG (p<0.001). Biomass smoke exposure was found significantly associated with COPD (OR= 3.385, CI=1.60-7.13, p<0.05). Lung function was significantly reduced (p<0.05) among women who were using biomass than those using natural gas/LPG.Conclusion: Biomass fuel smoke exposure is a risk factor for development of COPD.Chatt Shi Hosp Med Coll J; Vol.15 (1); Jan 2016; Page 8-11

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Eosinophilic Airway Inflammation in Patients with Stable Biomass Smoke- versus Tobacco Smoke-Associated Chronic Obstructive Pulmonary Disease

Journal of Health and Pollution ◽

10.5696/2156-9614-9.24.191209 ◽

2019 ◽

Vol 9 (24) ◽

Cited By ~ 1

Author(s):

Lalita Fernandes ◽

Shraddha Rane ◽

Suresh Mandrekar ◽

Anthony Menezes Mesquita

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Pulmonary Disease ◽

Tobacco Smoke ◽

Induced Sputum ◽

Biomass Fuel ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Biomass Smoke ◽

Severity Of Disease ◽

Inflammatory Profile

Background. Chronic obstructive pulmonary disease (COPD) is an inflammatory disease with predominant involvement of neutrophils, macrophages and CD8+ lymphocytes. Eosinophilic airway inflammations are reported in stable state and during acute exacerbations of tobacco smoke-associated COPD (TS-COPD). Women exposed to biomass fuel smoke are known to have eosinophils in sputum. However, little is known about the sputum cellular inflammatory profile in biomass fuel smoke-associated COPD (BMS-COPD). We therefore aimed to compare the sputum cellular inflammatory profile in tobacco smoke- and biomass smoke-associated COPD. Methods. The study was conducted in a tertiary care hospital in Goa, India. A total of 113 patients with stable COPD reporting to the outpatient pulmonary clinic were recruited. All participants were ≥ 40 years of age. Sputum induction studies were performed by the method of Pizzichini et al. after baseline subject characterization. Significant eosinophilia was defined as induced sputum eosinophils ≥ 3%. Results. There were 85 TS-COPD and 28 BMS-COPD patients. The mean age [standard deviation (SD)] was 64.7 (7.8) and 63.0 years (8.3), p = 0.32 in TS and BMS-COPD, respectively. Eighteen subjects (21.1%) were female smokers. The smoking pack-year median [interquartile range (IQR)] was 36 (20, 58) and hour-years of biomass smoke exposure mean (SD) was 192.4 (61). The TS-COPD and BMS-COPD cases showed a post-bronchodilator forced expiratory volume in one second (FEV1%) mean (SD) of 57.9 (17.1), and 62.6 (19.4), p= 0.22, respectively. Both groups had similar symptoms and severity of disease. Induced sputum total cell count per gram of sputum × 106 mean (SD) was 3.05 (1.53) for TS-COPD, and 2.55(1.37) for BMS-COPD p=0.12. The neutrophils % mean (SD) was 86.4 (16.5) and 87.9 (10.2), p = 0.64; eosinophils % median (IQR) was 2.5 (1, 10) and 8 (2, 12.8), p = 0.07; lymphocytes % median (IQR) was 0 (0, 0.75) and 0 (0, 1) p = 0.13; macrophages % median (IQR) was 2.5 (0.75, 5.7) and 1 (0, 4.7) p = 0.13; and significant eosinophilia (eosinophils ≥3%) was 42 (49.4%) and 20 (71%), p=0.04, for TS-COPD and BMS-COPD, respectively. Conclusions. For similar severity of disease and clinical symptoms, significant eosinophilic inflammation was observed in stable BMS-COPD, while both groups had similar neutrophilic inflammation. Participant Consent. Obtained. Ethics Approval. The study was approved by the Institutional Ethics Committee of the Goa Medical College, Goa, India. Competing Interests. The authors declare no competing financial interests.

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Chronic Cigarette Smoke Exposure Primes NK Cell Activation in a Mouse Model of Chronic Obstructive Pulmonary Disease

The Journal of Immunology ◽

10.4049/jimmunol.0903654 ◽

2010 ◽

Vol 184 (8) ◽

pp. 4460-4469 ◽

Cited By ~ 51

Author(s):

Gregory T. Motz ◽

Bryan L. Eppert ◽

Brian W. Wortham ◽

Robyn M. Amos-Kroohs ◽

Jennifer L. Flury ◽

...

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Mouse Model ◽

Pulmonary Disease ◽

Cigarette Smoke ◽

Cell Activation ◽

Nk Cell ◽

Smoke Exposure ◽

Cigarette Smoke Exposure ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease

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Putative Systemic Biomarkers of Biomass Smoke-Induced Chronic Obstructive Pulmonary Disease among Women in a Rural South Indian Population

Disease Markers ◽

10.1155/2018/4949175 ◽

2018 ◽

Vol 2018 ◽

pp. 1-11 ◽

Cited By ~ 1

Author(s):

Sangeetha Vishweswaraiah ◽

Tania Ahalya Thimraj ◽

Leema George ◽

Chaya Sindaghatta Krishnarao ◽

Komarla Sundararaja Lokesh ◽

...

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Pulmonary Disease ◽

Tobacco Smoke ◽

Indian Population ◽

Chronic Obstructive ◽

South Indian Population ◽

Rural South ◽

Obstructive Pulmonary Disease ◽

Biomass Smoke ◽

South Indian

Rationale. Exposure to biomass smoke (BMS) has been implicated in chronic obstructive pulmonary disease (COPD). About 3 billion people worldwide use biomass fuel for cooking and heating. Women in rural communities of low- and lower-middle-income countries are disproportionately exposed to massive amounts of BMS during active cooking hours (4–6 h/day). Therefore, BMS exposure is considered as a risk factor for COPD in the same order of magnitude as tobacco smoke. In rural India, due to cultural reasons, women are the primary cook of the family and are mostly nonsmokers. Thus, BMS-induced COPD is predominant among rural Indian women. However, BMS-COPD remains a relatively unexplored health problem globally. Therefore, we investigated the serum chemokine and cytokine signatures of BMS-COPD and tobacco smoke-induced COPD (TS-COPD) patients compared to their control in a rural South Indian population for this field study. Methods. Concentrations of 40 serum chemokines and cytokines were measured using a multiplexed immunoassay. The study cohort consisted of BMS-COPD (female; n=29) and BMS-exposed subjects without COPD (BMS-CONTROL; female; n=24). For comparison, data from TS-COPD patients (male, n=23) and tobacco smokers without COPD (TS-CONTROL; male, n=22) were investigated. Subjects were matched for age, sex, and biomass exposure. Tobacco consumption was slightly higher in TS-COPD subjects compared to TS-CONTROL. BMS-exposed and TS-exposed subjects (currently exposed) were from the same locality with similar dwelling habits and socioeconomic status. A validated structured questionnaire-based survey and spirometry was performed. An additional control group with no tobacco and BMS exposure (TS-BMS-CONTROL; n=15) was included. Statistical significance was set at p≤0.01. Results. Serum median concentrations (pg/ml) of CCL15 [8799.35; 5977.22], CCL27 [1409.14; 1024.99], and CXCL13 [37.14; 26.03] were significantly higher in BMS-CONTROL compared to BMS-COPD subjects. Nine analytes exhibited higher concentrations in TS-CONTROL compared to TS-COPD subjects. Comparison of chemokine and cytokine concentrations among BMS-COPD versus TS-COPD and BMS-CONTROL versus TS-CONTROL subjects also revealed distinct molecular signatures. Conclusion. Our data identifies CCL27 and CXCL13 as putative, plausibly homeostatic/protective biomarkers for BMS-COPD within the investigated population that warrants validation in larger and multiple cohorts. The findings further indicate exposure-specific systemic response of chemokines and cytokines.

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DIFFERENCES IN PULMONARY HYPERTENSION IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE SECONDARY TO DIFFERENT TYPES OF SMOKE EXPOSURE

CHEST Journal ◽

10.1378/chest.136.4_meetingabstracts.89s-a ◽

2009 ◽

Vol 136 (4) ◽

pp. 89S

Author(s):

Khalil Ansarin ◽

Salehi Rezvaniieh ◽

Akram Motamaveleh

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Pulmonary Hypertension ◽

Pulmonary Disease ◽

Smoke Exposure ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Different Types

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Association of Clonal Hematopoiesis with Chronic Obstructive Pulmonary Disease

Blood ◽

10.1182/blood.2021013531 ◽

2021 ◽

Author(s):

Peter Miller ◽

Dandi Qiao ◽

Joselyn Rojas-Quintero ◽

Michael C. Honigberg ◽

Adam S. Sperling ◽

...

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Pulmonary Disease ◽

Somatic Mutations ◽

Hematopoietic Cells ◽

Smoke Exposure ◽

Smoking History ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Clonal Hematopoiesis ◽

Severe Copd

Chronic obstructive pulmonary disease (COPD) is associated with age and smoking, but other determinants of the disease are incompletely understood. Clonal hematopoiesis of indeterminate potential (CHIP) is a common, age-related state in which somatic mutations in clonal blood populations induce aberrant inflammatory responses. Patients with CHIP have an elevated risk for cardiovascular disease, but the association with COPD remains unclear. We analyzed whole-genome and exome sequencing data to detect CHIP in 48,835 subjects, of whom 8,444 had moderate-to-very-severe COPD, from four separate cohorts with COPD phenotyping and smoking history. We measured emphysema in murine models in which Tet2 was deleted in hematopoietic cells. In COPDGene, individuals with CHIP had a risk of moderate-to-severe and severe or very severe COPD 1.6 and 2.2 times greater than non-carriers, respectively (adjusted 95% confidence intervals [CI], 1.1 to 2.2 and 1.5 to 3.2). These findings were consistent observed in three additional cohorts and meta-analyses of all subjects. CHIP was also associated with decreased FEV1% predicted in COPDGene (mean between group difference -5.7%; adjusted 95% CI, -8.8 to -2.6), a finding replicated in additional cohorts. Smoke exposure was associated with a small but significant increased risk of having CHIP (OR 1.03 per ten pack-years, 95% CI 1.01-1.05) in the meta-analysis of all subjects. Inactivation of Tet2 in mouse hematopoietic cells exacerbated emphysema development and inflammation in cigarette smoke exposure models. Somatic mutations in blood cells are associated with the development and severity of COPD, independent of age and cumulative smoke exposure.

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