Dung biomass smoke exposure impairs resolution of inflammatory responses to influenza infection.

Epidemiological studies associate biomass smoke with an increased risk for respiratory infections in children and adults in the developing world, with 500,000 premature deaths each year attributed to biomass smoke-related acute respiratory infections including infections caused by respiratory viruses. Animal dung is a biomass fuel of particular concern because it generates more toxic compounds per amount burned than wood, and is a fuel of last resort for the poorest households. Currently, there is little biological evidence on the effects of dung biomass smoke exposure on immune responses to respiratory viral infections. Here, we investigated the impact of dung biomass exposure on respiratory infection using a mouse model of dung biomass smoke and cultured primary human small airway epithelial cells (SAECs). Mice infected with influenza A virus (IAV) after dung biomass smoke exposure had increased mortality, lung inflammation and virus mRNA levels, and suppressed expression of innate anti-viral mediators compared to air exposed mice. Importantly, there was still significant tissue inflammation 14 days after infection in dung biomass smoke-exposed mice even after inflammation had resolved in air-exposed mice. Dung biomass smoke exposure also suppressed the production of anti-viral cytokines and interferons in cultured SAECs treated with poly(I:C) or IAV. This study shows that dung biomass smoke exposure impairs the immune response to respiratory viruses and contributes to biomass smoke-related susceptibility to respiratory viral infections, likely due to a failure to resolve the inflammatory effects of biomass smoke exposure.

Wildfire Variable Toxicity: Identifying Biomass Smoke Exposure Groupings through Transcriptomic Similarity Scoring.

The prevalence of wildfires continues to grow globally with exposures resulting in increased disease risk. Characterizing these health risks remains difficult due to the wide landscape of exposures that can result from different burn conditions and fuel types. This study tested the hypothesis that biomass smoke exposures from variable fuels and combustion conditions group together based on similar transcriptional response profiles, informing which wildfire-relevant exposures may be considered as a group for health risk evaluations. Mice (female CD-1) were exposed via oropharyngeal aspiration to equal mass biomass smoke condensates produced from flaming or smoldering burns of eucalyptus, peat, pine, pine needles, or red oak species. Lung transcriptomic signatures were used to calculate transcriptomic similarity scores across exposures, which informed exposure groupings. Exposures from flaming peat, flaming eucalyptus, and smoldering eucalyptus induced the greatest responses, with flaming peat grouping with the pro-inflammatory agent lipopolysaccharide. Smoldering red oak and smoldering peat induced the least transcriptomic response. Groupings paralleled pulmonary toxicity markers, though they were better substantiated by higher data dimensionality and resolution provided through -omic-based evaluation. Interestingly, groupings based on smoke chemistry signatures differed from transcriptomic/toxicity-based groupings. Wildfire-relevant exposure groupings yield insights into risk assessment strategies to ultimately protect public health.

Disruptions in oral and nasal microbiota in biomass and tobacco smoke associated chronic obstructive pulmonary disease.

Chronic exposures to tobacco and biomass smoke are the most prevalent risk factors for COPD development. Although microbial diversity in tobacco smoke-associated COPD (TSCOPD) has been investigated, microbiota in biomass smoke-associated COPD (BMSCOPD) is still unexplored. We aimed to compare the nasal and oral microbiota between healthy, TSCOPD, and BMSCOPD subjects from a rural population in India. Nasal swabs and oral washings were collected from healthy (n = 10), TSCOPD (n = 11), and BMSCOPD (n = 10) subjects. The downstream analysis was performed using QIIME pipeline (v1.9). In nasal and oral microbiota no overall differences were noted, but there were key taxa that had differential abundance in either Healthy vs COPD and/or TSCOPD vs. BMSCOPD. Genera such as Actinomyces, Actinobacillus, Megasphaera, Selenomonas, and Corynebacterium were significantly higher in COPD subjects. This study suggests that microbial community undergoes dysbiosis which may further contribute to the progression of disease. Thus, it is important to identify etiological agents for such a polymicrobial alterations which contribute highly to the disease manifestation.

Women with COPD from biomass smoke have reduced serum levels of biomarkers of angiogenesis and cancer, with EGFR predominating, compared to women with COPD from smoking.

The main causes of COPD are smoking (COPD-TS) and exposure to biomass smoke (COPD-BS), considered as different phenotypes. The association of COPD-TS with lung cancer (LC) is well established, but not in COPD-BS. Thus, we studied the serum concentration of cytokines that participate in inflammation, angiogenesis, and tumor progression, used frequently as LC biomarkers, in women with COPD-BS compared with COPD-TS (n = 70). Clinical and physiological characteristics and the serum concentration (multiplex immunoassay) of 16 cytokines were evaluated. The analysis revealed that women with COPD-BS were shorter and older, and had lower concentrations of 12 serum cytokines: 6 proinflammatory and angiogenic IL-6Rα, PECAM-1, leptin, osteopontin, prolactin, and follistatin; and 6 that participate in angiogenesis and in tumor progression FGF-2, HGF, sVEGFR-2, sHER2/neu, sTIE-2, G-CSF, and SCF. Notably, there was a significant increase in sEGFR in women with COPD-BS compared to women with COPD-TS. PDGF-AA/BB and sTIE-2 did not change. These findings suggest that women with COPD-BS have markedly decreased proinflammatory, angiogenic, and tumor progression potential, compared to women with COPD-TS, with sEGFR as the predominant mediator, which might reflect a differential pattern of inflammation in women exposed to BS, favoring the development of chronic bronchitis.

COVID-19 Susceptibility in chronic obstructive pulmonary disease.

In barely nine months, the pandemic known as COVID-19 has spread over 200 countries, affecting more than 22 million people and causing over than 786 000 deaths. Elderly people and patients with previous comorbidities such as hypertension and diabetes are at an increased risk to suffer a poor prognosis after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Although the same could be expected from patients with chronic obstructive pulmonary disease (COPD), current epidemiological data are conflicting. This could lead to a reduction of precautionary measures in these patients, in the context of a particularly complex global health crisis. Most COPD patients have a long history of smoking or exposure to other harmful particles or gases, capable of impairing pulmonary defences even years after the absence of exposure. Moreover, COPD is characterized by an ongoing immune dysfunction, which affects both pulmonary and systemic cellular and molecular inflammatory mediators. Consequently, increased susceptibility to viral respiratory infections have been reported in COPD, often worsened by bacterial co-infections and leading to serious clinical outcomes. The present paper is an up-to-date review that discusses the available research regarding the implications of coronavirus infection in COPD. Although validation in large studies is still needed, COPD likely increases SARS-CoV-2 susceptibility and increases COVID-19 severity. Hence, specific mechanisms to monitor and assess COPD patients should be addressed in the current pandemic.

Phenotypic comparison between smoking and non-smoking chronic obstructive pulmonary disease.

BACKGROUND: Although COPD among non-smokers (NS-COPD) is common, little is known about this phenotype. We compared NS-COPD subjects with smoking COPD (S-COPD) patients in a rural Indian population using a variety of clinical, physiological, radiological, sputum cellular and blood biomarkers. METHODS: Two hundred ninety subjects (118 healthy, 79 S-COPD, 93 NS-COPD) performed pre- and post-bronchodilator spirometry and were followed for 2 years to study the annual rate of decline in lung function. Body plethysmography, impulse oscillometry, inspiratory-expiratory HRCT, induced sputum cellular profile and blood biomarkers were compared between 49 healthy, 45 S-COPD and 55 NS-COPD subjects using standardized methods. Spirometric response to oral corticosteroids was measured in 30 female NS-COPD patients. RESULTS: Compared to all male S-COPD subjects, 47% of NS-COPD subjects were female, were younger by 3.2 years, had greater body mass index, a slower rate of decline in lung function (80 vs 130 mL/year), more small airways obstruction measured by impulse oscillometry (p < 0.001), significantly less emphysema (29% vs 11%) on CT scans, lower values in lung diffusion parameters, significantly less neutrophils in induced sputum (p < 0.05) and tended to have more sputum eosinophils. Hemoglobin and red cell volume were higher and serum insulin lower in S-COPD compared to NS-COPD. Spirometric indices, symptoms and quality of life were similar between S-COPD and NS-COPD. There was no improvement in spirometry in NS-COPD patients after 2 weeks of an oral corticosteroid. CONCLUSIONS: Compared to S-COPD, NS-COPD is seen in younger subjects with equal male-female predominance, is predominantly a small-airway disease phenotype with less emphysema, preserved lung diffusion and a slower rate of decline in lung function.

Peat smoke inhalation alters blood pressure, baroreflex sensitivity, and cardiac arrhythmia risk in rats.

Wildland fires (WF) are linked to adverse health impacts related to poor air quality. The cardiovascular impacts of emissions from specific biomass sources are however unknown. The purpose of this study was to assess the cardiovascular impacts of a single exposure to peat smoke, a key regional WF air pollution source, and relate these to baroreceptor sensitivity and inflammation. Three-month-old male Wistar-Kyoto rats, implanted with radiotelemeters for continuous monitoring of heart rate (HR), blood pressure (BP), and spontaneous baroreflex sensitivity (BRS), were exposed once, for 1-hr, to filtered air or low (0.38 mg/m3 PM) or high (4.04 mg/m3) concentrations of peat smoke. Systemic markers of inflammation and sensitivity to aconitine-induced cardiac arrhythmias, a measure of latent myocardial vulnerability, were assessed in separate cohorts of rats 24 hr after exposure. PM size (low peat = 0.4-0.5 microns vs. high peat = 0.8-1.2 microns) and proportion of organic carbon (low peat = 77% vs. high peat = 65%) varied with exposure level. Exposure to high peat and to a lesser extent low peat increased systolic and diastolic BP relative to filtered air. In contrast, only exposure to low peat elevated BRS and aconitine-induced arrhythmogenesis relative to filtered air and increased circulating levels of low-density lipoprotein cholesterol, complement components C3 and C4, angiotensin-converting enzyme (ACE), and white blood cells. Taken together, exposure to peat smoke produced overt and latent cardiovascular consequences that were likely influenced by physicochemical characteristics of the smoke and associated adaptive homeostatic mechanisms.

Household air pollution from domestic combustion of solid fuels and health.

Inefficient cooking and heating with solid fuels in poorly ventilated homes are a major source of exposure to indoor air pollution in developing countries. Household air pollution from cooking and heating with solid fuels also is an important contributor to outdoor air pollution. The combustion of organically derived solid fuel is qualitatively similar to the burning of tobacco in terms of emissions of particulate matter and gases, and the mechanisms by which solid fuel smoke causes adverse health effects in human subjects are likely similar. The public health effect of domestic cooking and heating with solid fuels is great. The World Health Organization estimates that there are 3.8 million deaths globally per year attributable to household air pollution. This estimate is based on the strength of the evidence, primarily meta-analyses of epidemiologic studies of acceptable scientific quality, although for cardiovascular disease, the evidence is more inferential. The greatest burden of household air pollution-related premature deaths is in children with pneumonia exposed to biomass smoke. The greatest estimated burden in adults is cardiovascular disease, but chronic obstructive pulmonary disease and lung cancer are important causes of disability and premature death in women, who are the primary cooks and tend not to smoke tobacco in developing countries. Research gaps and opportunities for interventions to reduce effects of solid fuel smoke on public health are identified.

The role of fuel type and combustion phase on the toxicity of biomass smoke following inhalation exposure in mice.

The characteristics of wildland fire smoke exposures which initiate or exacerbate cardiopulmonary conditions are unclear. We previously reported that, on a mass basis, lung toxicity associated with particulate matter (PM) from flaming smoke aspirated into mouse lungs is greater than smoldering PM. In this study, we developed a computer-controlled inhalation system which can precisely control complex biomass smoke emissions from different combustion conditions. This system was used to examine the toxicity of inhaled biomass smoke from peat, eucalyptus, and oak fuels generated under smoldering and flaming phases with emissions set to the same approximate concentration of carbon monoxide (CO) for each exposure (60-110 ppm), resulting in PM levels of ~ 4 mg/m3 for flaming and ~ 40 mg/m3 for smoldering conditions. Mice were exposed by inhalation 1 h/day for 2 days, and assessed for lung toxicity at 4 and 24 h after the final exposure. Peat (flaming and smoldering) and eucalyptus (smoldering) smoke elicited significant inflammation (neutrophil influx) in mouse lungs at 4 h with the peat (flaming) smoke causing even greater lung inflammation at 24-h post-exposure. A significant alteration in ventilatory timing was also observed in mice exposed to the peat (flaming) and eucalyptus (flaming and smoldering) smoke immediately after each day of exposure. No responses were seen for exposures to similar concentrations of flaming or smoldering oak smoke. The lung toxicity potencies (neutrophil influx per PM mass) agreed well between the inhalation and previously reported aspiration studies, demonstrating that although flaming smoke contains much less PM mass than smoldering smoke, it is more toxic on a mass basis than smoldering smoke exposure, and that fuel type is also a controlling factor.

Risk of acute exacerbations in chronic obstructive pulmonary disease associated with biomass smoke compared with tobacco smoke.

BACKGROUND: Risk of exacerbations in chronic obstructive pulmonary disease (COPD) associated with biomass smoke has not been well addressed, although biomass smoke is similar in composition to tobacco smoke. METHODS: To investigate whether the risk of exacerbations in COPD associated with biomass smoke differs from that in COPD associated with tobacco smoke, we recruited patients with COPD from two Korean multicenter prospective cohorts. In a multiple linear regression model, the standardized regression coefficient (ß) of biomass smoke exposure ≥25 years was most similar to that (ß') of tobacco smoke exposure ≥10 pack-years (ß = - 0.13 and ß' = - 0.14). We grouped patients with COPD into four categories based on the above cut-offs: Less Tobacco-Less Biomass, Less Tobacco-More Biomass, More Tobacco-Less Biomass, and More Tobacco-More Biomass. The main outcome was the incidence of moderate or severe exacerbations. RESULTS: Among 1033 patients with COPD, 107 were included in Less Tobacco-Less Biomass (mean age: 67 years, men: 67%), 40 in Less Tobacco-More Biomass (mean age: 70 years, men: 35%), 631 in More Tobacco-Less Biomass (mean age: 68 years, men: 98%), and 255 in More Tobacco-More Biomass (mean age: 69 years, men: 97%). The incidence rates of exacerbations were not significantly different between Less Tobacco-More Biomass and More Tobacco-Less Biomass (adjusted incidence rate ratio, 1.03; 95% confidence interval, 0.56-1.89; P = 0.921). No interaction between sex and tobacco and biomass smoke was observed. When propensity score matching with available covariates including age and sex was applied, a similar result was observed. CONCLUSIONS: Patients with COPD associated with biomass smoke and those with COPD associated with tobacco smoke had a similar risk of exacerbations. This suggests that patients with COPD associated with biomass smoke should be treated actively.

miR-34a in serum is involved in mild-to-moderate COPD in women exposed to biomass smoke.

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.

Exposure to biomass smoke is associated with an increased expression of circulating miRNA-126 and miRNA-155 in Mexican women: a pilot study.

Household air pollution has been associated as a risk factor for cardiovascular diseases (CVD). Therefore, the aim of this study was to assess the expression of vascular inflammation regulators miR-126 and miR-155 in plasma from women that cook with wood and women that cook with liquid petroleum gas (LPG). A cumulative index of exposure to smoke (CIES) was estimated, urinary 1-hydroxypyrene (1-OHP) levels were quantified and miRNAs expression levels were determined by quantitative real-time PCR (qRT-PCR). Biochemical clinical parameters were also evaluated. The average values for CIES and 1-OHP were 140 ± 86.8 hours-years (12.0-270 hours-years) and 0.52 ± 0.45 µmol/mol creatinine, respectively. miR-126 and miR-155 expression levels were significantly higher (p < 0.01) in the wood users compared to LPG users. Besides, we found a significant association (p < 0.01) between miR-126 and miR-155 expression levels and CIES and urinary 1-OHP concentrations. These results contribute to the current evidence about the cardiovascular risk related to biomass smoke exposure, from an epigenetic level.

Comparative analysis of COPD associated with tobacco smoking, biomass smoke exposure or both.

BACKGROUND: Exposure to noxious gases and particles contained in both tobacco smoking (TS) and biomass smoke (BS) are well recognized environmental risk factors for chronic obstructive pulmonary disease (COPD). COPD is characterized by an abnormal inflammatory response, both in the pulmonary and systemic compartments. The differential effects of TS, BS or their combined exposure have not been well characterized yet. This study sought to compare the lung function characteristics and systemic inflammatory response in COPD patients exposed to TS, BS or their combination. METHODS: Sociodemographic, clinical and lung functional parameters were compared across 49 COPD patients with a history of smoking and no BS exposure (TS COPD), 31 never-smoker COPD patients with BS exposure (BS COPD), 46 COPD patients with a combined exposure (TS + BS COPD) and 52 healthy controls (HC) who have never been exposed neither to TS or BS. Blood cell counts, C-reactive protein (CRP), fibrinogen and immunoglobulin E (IgE) levels were quantified in all four groups. RESULTS: TS + BS COPD patients exhibited significantly lower oxygen saturation than the rest of groups (p < 0.01). Spirometry and diffusing capacity were significantly higher in BS than in TS or TS + BS patients. CRP levels were significantly higher in TS COPD patients than in BS COPD group (p < 0.05), whereas fibrinogen was raised in COPD patients with a history of smoking (TS and TS + BS) when compared to control subjects (p < 0.01). Finally, COPD patients with BS exposure (BS and BS + TS groups) showed higher IgE levels than TS and HC (p < 0.05). CONCLUSIONS: There are significant physiological and inflammatory differences between COPD patients with TS, BS and TS + BS exposures. The latter had worse blood oxygenation, whereas the raised levels of IgE in BS exposed patients suggests a differential Th2 systemic inflammatory pattern triggered by this pollutant.

Women with COPD by biomass show different serum profile of adipokines, incretins, and peptide hormones than smokers.

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.

Inflammation, oxidative stress, and higher expression levels of Nrf2 and NQO1 proteins in the airways of women chronically exposed to biomass fuel smoke.

The study was carried out to examine whether chronic exposure to smoke during daily household cooking with biomass fuel (BMF) elicits changes in airway cytology and expressions of Nrf2 (nuclear factor erythroid 2 [NF-E2]-related factor 2 [Nrf2]), Keap1 (Kelch-like erythroid-cell-derived protein with CNC homology [ECH]-associated protein 1), and NQO1 (NAD(P)H:quinone oxidoreductase 1) proteins in the airways. For this, 282 BMF-using women (median age 34 year) and 236 age-matched women who cooked with liquefied petroleum gas (LPG) were enrolled. Particulate matter with diameters of < 10 µm (PM10) and < 2.5 µm (PM2.5) were measured in indoor air with real-time laser photometer. Routine hematology, sputum cytology, Nrf2, Keap1, NQO1, and generation of reactive oxygen species (ROS) along with the levels of superoxide dismutase (SOD) and catalase were measured in both groups. PM10 and PM2.5 levels were significantly higher in BMF-using households compared to LPG. Compared with LPG users, BMF users had 32% more leukocytes in circulation and their sputa were 1.4-times more cellular with significant increase in absolute number of neutrophils, lymphocytes, eosinophils, and alveolar macrophages, suggesting airway inflammation. ROS generation was 1.5-times higher in blood neutrophils and 34% higher in sputum cells of BMF users while erythrocyte SOD was 31% lower and plasma catalase was relatively unchanged, suggesting oxidative stress. In BMF users, Keap1 expression was reduced, the percentage of AEC with nuclear expression of Nrf2 was two- to three-times more, and NQO1 level in sputum cell lysate was two-times higher than that of LPG users. In conclusion, cooking with BMF was associated with Nrf2 activation and elevated NQO1 protein level in the airways. The changes may be adaptive cellular response to counteract biomass smoke-elicited oxidative stress and inflammation-related tissue injury in the airways.

Cardiovascular Studies in Patients with Chronic Obstructive Pulmonary Disease Due to Biomass Smoke or Tobacco.

BACKGROUND AND OBJECTIVE: The cardiovascular effects of biomass smoke exposure in patients with chronic obstructive pulmonary disease are not well characterized, and few studies have assessed the possible differences between patients with disease caused by biomass smoke and tobacco. The aim of this study was to search for differences in cardiovascular variables between both types of the disease. METHODS: Twenty subjects (15 men, 5 women) with chronic obstructive pulmonary disease caused by tobacco were matched one to one for sex, age, and forced expiratory volume in 1 s to 20 patients with biomass-related disease. Echocardiography and carotid ultrasound studies were performed. Flow-mediated endothelium-dependent vasodilatation and endothelium-independent vasodilatation were also measured. RESULTS: There were no significant differences between groups in any of the echocardiographic variables, nor in the intima-media carotid thickness, the number of carotid plaques, or the percentage of endothelium-dependent or endothelium-independent vasodilation. A high percentage of patients in both groups showed an abnormal flow-mediated endothelium-dependent vasodilatation pattern. CONCLUSION: The study does not support the hypothesis of a different cardiovascular effect of biomass or tobacco smoke exposure in patients with chronic obstructive pulmonary disease. Cardiovascular comorbidity should be assessed in patients with biomass-associated disease, similarly to subjects with tobacco-related disease.

Hypertensive and toxicological health risk among women exposed to biomass smoke: A rural Indian scenario.

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 PM2.5 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 O3 (p < 0.403) 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.

Dung biomass smoke activates inflammatory signaling pathways in human small airway epithelial cells.

Animal dung is a biomass fuel burned by vulnerable populations who cannot afford cleaner sources of energy, such as wood and gas, for cooking and heating their homes. Exposure to biomass smoke is the leading environmental risk for mortality, with over 4,000,000 deaths each year worldwide attributed to indoor air pollution from biomass smoke. Biomass smoke inhalation is epidemiologically associated with pulmonary diseases, including chronic obstructive pulmonary disease (COPD), lung cancer, and respiratory infections, especially in low and middle-income countries. Yet, few studies have examined the mechanisms of dung biomass smoke-induced inflammatory responses in human lung cells. Here, we tested the hypothesis that dung biomass smoke causes inflammatory responses in human lung cells through signaling pathways involved in acute and chronic lung inflammation. Primary human small airway epithelial cells (SAECs) were exposed to dung smoke at the air-liquid interface using a newly developed, automated, and reproducible dung biomass smoke generation system. The examination of inflammatory signaling showed that dung biomass smoke increased the production of several proinflammatory cytokines and enzymes in SAECs through activation of the activator protein (AP)-1 and arylhydrocarbon receptor (AhR) but not nuclear factor-κB (NF-κB) pathways. We propose that the inflammatory responses of lung cells exposed to dung biomass smoke contribute to the development of respiratory diseases.

Changes in RANKL and osteoprotegerin expression after chronic exposure to indoor air pollution as a result of cooking with biomass fuel.

The impact of indoor air pollution as a result of cooking with unprocessed biomass on membrane-bound and serum receptor activator of nuclear factor-kappa ligand 1 (RANKL), its soluble decoy receptor osteoprotegerin (OPG) and osteoclast precursor CD14(+) CD16(+) monocytes was investigated. Seventy-four pre-menopausal women from eastern India using biomass and 65 control women who cooked with cleaner liquefied petroleum gas were enrolled. PM10 and PM2.5 levels in their indoor air were measured with real-time aerosol monitors. The levels of membrane-bound RANKL on leukocytes and percentage CD14(+) CD16(+) monocytes in the subjects' blood were assayed by flow cytometry. Soluble RANKL and OPG in serum were measured by ELISA. The results showed that PM10 and PM2.5 levels were significantly higher in the indoor air of biomass-using households. Compared with the control women, the levels of CD4(+) and CD19(+) lymphocytes and circulating granulocytes with elevated levels of membrane-bound RANKL were higher in biomass users. The serum levels of RANKL were increased by 41% whereas serum OPG was reduced by 22% among biomass users. The absolute number of CD14(+) CD16(+) monocytes was significantly increased in biomass users than the control women. After controlling for potential confounders, PM10 and PM2.5 levels were found to be positively associated with leukocyte and serum RANKL and CD14(+) CD16(+) monocyte levels, but negatively with serum OPG. From these results, we can conclude that chronic exposure to biomass smoke increased membrane-bound and soluble RANKL and circulating osteoclast precursors but decreased OPG, suggesting an increased risk of bone resorption and consequent osteoporosis in biomass-exposed women of a child-bearing age. Copyright © 2015 John Wiley & Sons, Ltd.

Biomass Smoke Exposure Enhances Rhinovirus-Induced Inflammation in Primary Lung Fibroblasts.

Biomass smoke is one of the major air pollutants and contributors of household air pollution worldwide. More than 3 billion people use biomass fuels for cooking and heating, while other sources of exposure are from the occurrence of bushfires and occupational conditions. Persistent biomass smoke exposure has been associated with acute lower respiratory infection (ALRI) as a major environmental risk factor. Children under the age of five years are the most susceptible in developing severe ALRI, which accounts for 940,000 deaths globally. Around 90% of cases are attributed to viral infections, such as influenza, adenovirus, and rhinovirus. Although several epidemiological studies have generated substantial evidence of the association of biomass smoke and respiratory infections, the underlying mechanism is still unknown. Using an in vitro model, primary human lung fibroblasts were stimulated with biomass smoke extract (BME), specifically investigating hardwood and softwood types, and human rhinovirus-16 for 24 h. Production of pro-inflammatory mediators, such as IL-6 and IL-8, were measured via ELISA. Firstly, we found that hardwood and softwood smoke extract (1%) up-regulate IL-6 and IL-8 release (p ≤ 0.05). In addition, human rhinovirus-16 further increased biomass smoke-induced IL-8 in fibroblasts, in comparison to the two stimulatory agents alone. We also investigated the effect of biomass smoke on viral susceptibility by measuring viral load, and found no significant changes between BME exposed and non-exposed infected fibroblasts. Activated signaling pathways for IL-6 and IL-8 production by BME stimulation were examined using signaling pathway inhibitors. p38 MAPK inhibitor SB239063 significantly attenuated IL-6 and IL-8 release the most (p ≤ 0.05). This study demonstrated that biomass smoke can modulate rhinovirus-induced inflammation during infection, which can alter the severity of the disease. The mechanism by which biomass smoke exposure increases inflammation in the lungs can be targeted and inhibited via p38 MAP kinase pathway.