No abstract

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.

Background: Exposure to wood smoke has been shown to contribute to adverse respiratory health effects including airway infections, but the underlying mechanisms are yet unclear. A preceding study failed to confirm any acute inflammation or cell influx in bronchial wash (BW) or bronchoalveolar lavage (BAL) 24 h after wood smoke exposure but showed unexpected reductions in leukocyte numbers. The present study was performed to investigate responses at an earlier phase, regarding potential development of acute inflammation, as well as indications of cytotoxicity. Methods: In a double-blind, randomised crossover study, 14 healthy participants were exposed for 2h to filtered air and diluted wood smoke from incomplete wood log combustion in a common wood stove with a mean particulate matter concentration of 409 µg/m3. Bronchoscopy with BW and BAL was performed 6 hours after exposure. Differential cell counts, assessment of DNA-damage and ex vivo analysis of phagocytic function of phagocytosing BAL cells were performed. Wood smoke particles were also collected for in vitro toxicological analyses using bronchial epithelial cells (BEAS-2B) and alveolar type II cells (A549). Results: Exposure to wood smoke increased BAL lactate dehydrogenase (LDH) (p=0.04) and reduced the ex vivo alveolar macrophage phagocytic capacity (p=0.03) and viability (p=0.02) vs. filtered air. BAL eosinophil numbers were increased after woodsmoke (p=0.02), while other cell types were unaffected in BW and BAL. In vitro exposure to wood smoke particles confirmed increased DNA-damage, decreased metabolic activity and cell cycle disturbances. Conclusions: Exposure to wood smoke from incomplete combustion did not induce any acute airway inflammatory cell influx at 6 hours, apart from eosinophils. However, there were indications of a cytotoxic reaction with increased LDH, reduced cell viability and impaired alveolar macrophage phagocytic capacity. These findings are in accordance with earlier bronchoscopy findings at 24 h and may provide evidence for the increased susceptibility to infections by biomass smoke exposure, reported in population-based studies.

Background Exposure to wood smoke has been shown to contribute to adverse respiratory health effects including airway infections, but the underlying mechanisms are unclear. A preceding study failed to confirm any acute inflammation or cell influx in bronchial wash (BW) or bronchoalveolar lavage (BAL) 24 h after wood smoke exposure but showed unexpected reductions in leukocyte numbers. The present study was performed to investigate responses at an earlier phase, regarding potential development of acute inflammation, as well as indications of cytotoxicity. Methods In a double-blind, randomised crossover study, 14 healthy participants were exposed for 2 h to filtered air and diluted wood smoke from incomplete wood log combustion in a common wood stove with a mean particulate matter concentration of 409 µg/m3. Bronchoscopy with BW and BAL was performed 6 h after exposure. Differential cell counts, assessment of DNA-damage and ex vivo analysis of phagocytic function of phagocytosing BAL cells were performed. Wood smoke particles were also collected for in vitro toxicological analyses using bronchial epithelial cells (BEAS-2B) and alveolar type II-like cells (A549). Results Exposure to wood smoke increased BAL lactate dehydrogenase (LDH) (p = 0.04) and reduced the ex vivo alveolar macrophage phagocytic capacity (p = 0.03) and viability (p = 0.02) vs. filtered air. BAL eosinophil numbers were increased after wood smoke (p = 0.02), while other cell types were unaffected in BW and BAL. In vitro exposure to wood smoke particles confirmed increased DNA-damage, decreased metabolic activity and cell cycle disturbances. Conclusions Exposure to wood smoke from incomplete combustion did not induce any acute airway inflammatory cell influx at 6 h, apart from eosinophils. However, there were indications of a cytotoxic reaction with increased LDH, reduced cell viability and impaired alveolar macrophage phagocytic capacity. These findings are in accordance with earlier bronchoscopy findings at 24 h and may provide evidence for the increased susceptibility to infections by biomass smoke exposure, reported in population-based studies.