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Abstract Background Chronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities. The main causes of COPD are Gene-environment interactions associated with tobacco smoking (COPD-TS) and biomass smoke (COPD-BS). It is well know that microRNAs (miRNAs) participate in the control of post-transcriptional regulation and are involved in COPD-TS; nevertheless, those miRNAS are participating in the COPD-BS are unidentified. Thus, we studied which miRNAs are involved in COPD-BS (GOLD stages I–II). Methods In the screening phase, the profile of the miRNAs was analyzed in serum samples (n = 3) by means of a PCR array. Subsequently, the miRNAs were validated with RT-qPCR (n = 25) in the corresponding study groups. Additionally, the serum concentration of Notch1 was measured comparing COPD-BS vs COPD-TS. Results miR-34a was down-regulated in COPD- BS vs COPD-TS. In the other study groups, three miRNAs were differentially expressed: miR-374a was down-regulated in COPD-BS vs C, miR-191-5p was up-regulated in COPD-BS vs H-BS, and miR-21-5p was down-regulated in COPD-TS compared to the C group. Moreover, the serum concentration of Notch1, one of the targets of miR-34a, was increased in COPD-BS compared to women with COPD-TS. Conclusions This is the first study in patients with COPD due to biomass that demonstrates miRNA expression differences between patients. The observations support the concept that COPD by biomass has a different phenotype than COPD due to tobacco smoking, which could have important implications for the treatment of these diseases.

Abstract Background The main causes of COPD are tobacco smoking (COPD-TS) and biomass smoke exposure (COPD-BS). COPD-TS is known to induce changes in adipokines, incretins, and peptide hormones, frequent biomarkers of inflammation; however, it is unknown if similar changes occur in COPD-BS. Methods Clinical and physiological characteristics, and serum concentration of C-peptide, ghrelin, GIP, GLP-1, glucagon, insulin, leptin, PAI-1, resistin, and visfatin were measured in women with COPD-BS, COPD-TS, and healthy controls. Data were compared with one-way ANOVA and Tukey’s post hoc test; nonparametric were expressed as median (interquartile ranges), with Kruskal-Wallis and Dunn’s post-hoc test. Multivariate analysis, age, BMI, MS, and FEV1% pred with levels of inflammatory mediators in COPD women. Results FEV1% pred, FVC% pred, and FEV1/FVC ratio were decremented in COPD. In COPD-TS increased C-peptide, ghrelin, GIP, GLP-1, and leptin, and reduced glucagon, PAI-1, resistin, and visfatin. In COPD-BS enlarged ghrelin, insulin, leptin, and PAI-1 comparatively with COPD-TS and control, while C-peptide and GLP-1 relatively with controls; conversely, glucagon, and resistin were reduced. Multivariate analysis showed association of ghrelin, insulin, PAI-1, and visfatin with BS exposure. Conclusions women with COPD-BS have a distinct profile of adipokines, incretins, and peptide hormones, and specifically with ghrelin, insulin, PAI-1, and visfatin related to BS exposure.

Biomass smoke exposure is a threat to child and maternal health in many resource-limited countries and is associated with poor pregnancy outcomes and serious lung diseases in the offspring. We aimed to assess the feasibility, acceptability and impact of a midwife-led education programme on biomass risks and prevention for women attending maternity clinics in Uganda. Education materials were co-developed through an iterative process by midwives and other stakeholders. The materials were serially tested and approved by the Ministry of Health and used by midwives and village health teams (VHTs). The district health team, 12 midwives and 40 VHTs were sensitised on biomass smoke. Two hundred and forty-four women were educated about biomass smoke by midwives; pre- and post-session questionnaires showed major improvements in knowledge of biomass smoke risks. Qualitative interviews with women three months after the sessions showed that they made behavioural changes such as avoiding smoke while cooking, using dry wood, solar power for lighting and improved ventilation. The major barrier to behavioural changes was poverty, but some improvements cost no money. The programme delivered by midwives was feasible and acceptable; implementing this programme has the potential to reduce exposure to smoke with major benefits to mother, foetus, and children throughout their lives. [ABSTRACT FROM AUTHOR]

Background: Chronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities. The main causes of COPD are Gene-environment interactions associated with tobacco smoking (COPD-TS) and biomass smoke (COPD-BS). It is well know that microRNAs (miRNAs) participate in the control of post-transcriptional regulation and are involved in COPD-TS; nevertheless, those miRNAS are participating in the COPD-BS are unidentified. Thus, we studied which miRNAs are involved in COPD-BS (GOLD stages I-II).Methods: In the screening phase, the profile of the miRNAs was analyzed in serum samples (n = 3) by means of a PCR array. Subsequently, the miRNAs were validated with RT-qPCR (n = 25) in the corresponding study groups. Additionally, the serum concentration of Notch1 was measured comparing COPD-BS vs COPD-TS.Results: miR-34a was down-regulated in COPD- BS vs COPD-TS. In the other study groups, three miRNAs were differentially expressed: miR-374a was down-regulated in COPD-BS vs C, miR-191-5p was up-regulated in COPD-BS vs H-BS, and miR-21-5p was down-regulated in COPD-TS compared to the C group. Moreover, the serum concentration of Notch1, one of the targets of miR-34a, was increased in COPD-BS compared to women with COPD-TS.Conclusions: This is the first study in patients with COPD due to biomass that demonstrates miRNA expression differences between patients. The observations support the concept that COPD by biomass has a different phenotype than COPD due to tobacco smoking, which could have important implications for the treatment of these diseases. [ABSTRACT FROM AUTHOR]

This study shows that exposure to air pollutants from indoor cooking fuel combustion may be associated with elevated Diastolic Blood Pressure (DBP), Systolic Blood Pressure (SBP), Heart rate and Body mass index (BMI) in rural women of India. 60 premenopausal women (using solely agriculture residues, wood, dung, straw, leaf) and 30 women (solely using clean fuel, LPG) were recruited for this study. An ethically approved questionnaire was used in the study and health parameters were measured by standard instruments. Eight pollutants were measured by calibrated instruments, applied both in the living room as well as kitchens of test-subjects. The Test-subjects were divided into two groups, LPG users, and biomass users, and the toxicological risk was assessed by measurement of PM 2.5 levels in the given indoor environments. The concentrations of all the pollutants were significantly (p < 0.001) higher in biomass users than in LPG using households, except in the case of O 3 (p < 0.40 3 ) at the time of cooking. Results highlighted that DBP (p < 0.070), SBP (p < 0.143), Heart rate (p < 0.002) and BMI (p < 0.052) were varied in the two fuel user groups. In the case of biomass fuel user toxicological risk was higher (5.21) than LPG users (0.69). Moreover, Symptoms like asthma (25%), cough (76.67%), dizziness (36.67%), eye irritation (88.33%), and shortness of breath (43.33%) were highly prevalent among biomass users than in LPG users. The study highlighted that Biomass using women are more prone to cardiovascular disease and policies should be formulated for their sustainable health. [ABSTRACT FROM AUTHOR]

Biomass is widely used for fuel in developing countries. Particles and gases of biomass burning may cause changes in the lung. In this prospective study we investigated histopathological changes in the lungs of 42 non-smoking women [mean age (59±10) years] caused by biomass smoke. We valuated exposure to biomass smoke, case histories, and the findings of physical examination, radiology, bronchoscopy, and lung histopathology. Mean exposure to biomass smoke was (28±9) hour-year (1 hour-year equals 365 hours of exposure per year with average exposure of 1 hour a day). The radiological findings were mass (42 %), reticulonodular opacities (31%), mediastinal lymphadenopathy (26 %), pleuro-parenchymal fibrotic banding (19 %), widening of the pulmonary artery (14 %), ground glass (11%), mosaic perfusion (9 %), consolidation (9 %), segmental or subsegmental atelectasis (7 %), and bronchiectasis (7 %). The patients were diagnosed with lung cancer (35 %), interstitial lung disease (31%), sarcoidosis (9 %), tuberculosis (9 %), chronic obstructive pulmonary disease (4 %), chronic bronchitis (9 %), and metastasis (4 %). Bronchoscopy showed pilies, oedema, erythema, bronchus narrowing, endobronchial turnout, mucosal irregularity, increased vascularisation, blue-black anthracotic plaques, mucosal oedema, and purulent secretion. Transbronchial biopsies revealed neutrophil and lymphocyte leucocytes in the perivascular, peribronchiolar, and interalveolar septa, slightly enlarged connective tissue, thickening of the basal membrane, thickening of interalveolar septa, intimal and medial thickening of the vascular wall and vascular lumen narrowing, anthracosis between the cells and in the bronchiole epithelium. These findings confirm that biomass smoke has important toxic effects on the lung parenchyma, interstitium, and pulmonary vessels that may result in malignancies. [ABSTRACT FROM AUTHOR]