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In this study, ash transformation and release of critical ash-forming elements during single-pellet combustion of different types of agricultural opportunity fuels were investigated. The work focused on potassium (K) and phosphorus (P). Single pellets of poplar, wheat straw, grass, and wheat grain residues were combusted in a macro-thermogravimetric analysis reactor at three different furnace temperatures (600, 800, and 950 °C). In order to study the transformation of inorganic matters at different stages of the thermal conversion process, the residues were collected before and after full devolatilization, as well as after complete char conversion. The residual char/ash was characterized by scanning electron microscopy-energy-dispersive X-ray spectroscopy, X-ray diffraction, inductively coupled plasma, and ion chromatography, and the interpretation of results was supported by thermodynamic equilibrium calculations. During combustion of poplar, representing a Ca-K-rich woody energy crop, the main fraction of K remained in the residual ash primarily in the form of K2Ca(CO3)2 at lower temperatures and in a K-Ca-rich carbonate melt at higher temperatures. Almost all P retained in the ash and was mainly present in the form of hydroxyapatite. For the Si-K-rich agricultural biomass fuels with a minor (wheat straw) or moderate (grass) P content, the main fraction of K remained in the residual ash mostly in K-Ca-rich silicates. In general, almost all P was retained in the residual ash both in K-Ca-P-Si-rich amorphous structures, possibly in phosphosilicate-rich melts, and in crystalline forms as hydroxyapatite, CaKPO4, and calcium phosphate silicate. For the wheat grain, representing a K-P-rich fuel, the main fraction of K and P remained in the residual ash in the form of K-Mg-rich phosphates. The results showed that in general for all studied fuels, the main release of P occurred during the devolatilization stage, while the main release of K occurred during char combustion. Furthermore, less than 20% of P and 35% of K was released at the highest furnace temperature for all fuels.

Over 640 million people in Africa are expected to rely on solid-fuels for cooking by 2040. In Western Kenya, cooking inefficiently persists as a major cause of burden of disease due to household air pollution. Efficient biomass cooking is a local-based renewable energy solution to address this issue. The Life-Cycle Assessment tool Simapro 8.5 is applied for analyzing the environmental impact of four biomass cooking strategies for the Kisumu County, with analysis based on a previous energy modelling study, and literature and background data from the Ecoinvent and Agrifootprint databases applied to the region. A Business-As-Usual scenario (BAU) considers the trends in energy use until 2035. Transition scenarios to Improved Cookstoves (ICS), Pellet-fired Gasifier Stoves (PGS) and Biogas Stoves (BGS) consider the transition to wood-logs, biomass pellets and biogas, respectively. An Integrated (INT) scenario evaluates a mix of the ICS, PGS and BGS. In the BGS, the available biomass waste is sufficient to be upcycled and fulfill cooking demands by 2035. This scenario has the lowest impact on all impact categories analyzed followed by the PGS and INT. Further work should address a detailed socio-economic analysis of the analyzed scenarios.

Introduction: Biomass combustion emissions contribute to indoor and outdoor air pollution. Exposure to wood smoke has been associated with development and worsening of respiratory diseases such as asthma and COPD, but also increases in airway infections. The mechanisms behind these effects are not fully clear. Aim and Objectives: To evaluate effects on lymphocyte subtypes and activity markers in peripheral blood from healthy subjects by controlled wood smoke exposure. Methods: Fourteen healthy subjects participated in a randomized, double-blind crossover study with exposures to sooty wood smoke and filtered air for two hours, on two occasions. Blood sampling for flow cytometry was performed 6 hours after each exposure. Peripheral blood cells were stained with fluorochrome-conjugated antibodies for CD3, CD4, CD8, CD25, CD127, CD69, CD56 and CD16. Results: Total lymphocyte numbers were increased 6 hours post wood smoke exposure, as were CD3+, CD4+ and CD8+ cells, along with the numbers of CD8+ cells expressing CD56CD16 vs filtered air. On CD4+ and CD8+ cells the CD69 and CD25 activation marker expressions were increased after wood smoke exposure, as were regulatory T cells. Conclusions: Short-term exposure to wood smoke recruited and activated CD4 and CD8 cells to the peripheral blood as a systemic response to the noxious challenge. These findings may be of importance for adverse health effects by wood smoke, especially after long-term exposure.

Background: Biomass smoke is associated with adverse health effects on the respiratory system, including increased asthma morbidity and worsening of symptoms leading to emergency room visits. Aims and Objectives: The aim of this study was to investigate whether controlled exposure to wood smoke generated from incomplete soot-rich combustion would increase small airway resistance and reactance. Methods: Fifteen healthy subjects (20-45 ys) underwent controlled chamber exposure on two occasions to filtered air and to sooty wood smoke (PM1 ~ 450 μg/m3), generated by a common Swedish wood stove firing birch logs. The study was performed in a double-blind, randomized cross-over fashion and the subjects alternated between exercise (VE=20 L/min/m2) and rest at 15-minute intervals for 2 hours. Forced Oscillation Technique (FOT) (tremoFlo®, THORASYS) was used to determine airway resistance and reactance before and after exposure to wood smoke as well as before and after exposure to filtered air. Results: Both airway reactance (P Conclusions: Short term exposure to sooty wood smoke did not affect small airways resistance or reactance as determined using FOT in healthy subjects. Further research should study the effects in asthmatic populations, and also whether repeated exposures are needed to cause the small airways effects indicated by population-based studies.

Background: Exposure to emissions from biomass burning contributes to respiratory diseases, including obstructive airway diseases, acute lower respiratory tract infections and tuberculosis. The underlying mechanisms effects are not well understood. Aims and Objectives: To determine if exposure to wood smoke from incomplete combustion would elicit DNA damage on airway cells and epithelial cell lines. Methods: Fourteen healthy subjects underwent controlled chamber exposure on two occasions to filtered air and to sooty wood smoke (PM1 ~ 450 μg/m3), generated by a Swedish wood stove firing birch logs, according to double-blind randomized cross-over design. The subjects alternated exercise (VE=20 L/min/m2) and rest at 15-minute intervals for 2 hours. Bronchoscopies with sampling of bronchial wash (BW) and bronchoalveolar lavage (BAL) were performed 6 hours after exposure. Furthermore, alveolar type II cell line A549 and bronchial epithelial cell line BEAS-2B were exposed to wood smoke particles at four different doses. DNA damage was examined with the Comet assay and olive tail moment (OTM) was quantified. Results: Eosinophil numbers was increased in BAL after exposure to wood smoke, with no changes in other cells. Moreover, there was a dose-dependent increase in DNA damage in vitro when comparing PM concentrations above 75µg ml-1 to air. Conclusion: Short term exposure to sooty wood smoke induced a bronchoalveolar eosinophilic insult. This may link with the development and worsening of asthma after chronic exposure to wood smoke. Moreover, the observed DNA damage in vitro may explain the previously shown reduction in airway cells, which in turn may causally affect cellular immunity and increase the incidence of respiratory infection