scholarly journals Wood smoke exposure and risk of chronic obstructive pulmonary disease

2006 ◽  
Vol 27 (3) ◽  
pp. 542-546 ◽  
Author(s):  
M. Orozco-Levi
2003 ◽  
Vol 29 (2) ◽  
pp. 64-68 ◽  
Author(s):  
Mateo Sainz Yaksic ◽  
Mauro Tojo ◽  
Alberto Cukier ◽  
Rafael Stelmach

Chronic obstructive pulmonary disease (COPD) is a public health problem. Tobacco smoking is the major cause, but not the only one. Air pollution, exposure to chemicals, environmental smoke exposure, and passive smoking are among other contributing causes; being viral and bacterial infections also risk factors. Gender and weight are associated to the severity of the disease. Co-morbidity is frequent. OBJECTIVE: To characterize a population of COPD outpatients followed at an outsourced medical service. METHODS: Questionnaires were applied to patients with COPD. The data included gender, age, weight, body mass index (BMI), oxygen delivery users, and FEV1, exposure to tobacco smoke, exposure to wood smoke, history of tuberculosis and co-morbid diseases. RESULTS: Of the 70 patients enrolled in the study, 70% (49) were men with an average age of 64 ± 10 years, average weight of 63 ± 16 kg and average BMI of 22 ± 5 kg/m². Mean FEV1 was 35 ± 14% and 45.7% were oxygen dependent. Nine (12.8%) patients never smoked, while 78.8% had quit tobacco smoking, (38 ± 11 pack/years was the average). Nine (12.8%) smoked corn husk cigarettes. Eighteen (25.7%) were exposed to wood smoke. Eleven (15.7%) patients had tuberculosis, 5.7% complained of asthma symptoms, 2.8% had bronchiectasis, 11.4% diabetes mellitus, 51.4% hypertension, and 20% Cor pulmonale. CONCLUSION: Other possible COPD etiologies must be investigated. Determinants of the pulmonary injury could be environmental smoke exposure associated to former infections. Men with low BMI are typically representative of this severe patient population. Hypertension and Cor Pulmonale are frequent co-morbidity factors.


2011 ◽  
Vol 59 (3) ◽  
pp. 587-592 ◽  
Author(s):  
Alberto Guzmán-Grenfell ◽  
Nayeli Nieto-Velázquez ◽  
Yessica Torres-Ramos ◽  
Araceli Montoya-Estrada ◽  
Alejandra Ramírez-Venegas ◽  
...  

2010 ◽  
Vol 184 (8) ◽  
pp. 4460-4469 ◽  
Author(s):  
Gregory T. Motz ◽  
Bryan L. Eppert ◽  
Brian W. Wortham ◽  
Robyn M. Amos-Kroohs ◽  
Jennifer L. Flury ◽  
...  

Blood ◽  
2021 ◽  
Author(s):  
Peter Miller ◽  
Dandi Qiao ◽  
Joselyn Rojas-Quintero ◽  
Michael C. Honigberg ◽  
Adam S. Sperling ◽  
...  

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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