Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.
Thermochemical Energy Conversion Laboratory, Department of Applied Physics and Electronics, Umeå University, Umeå, Sweden.
Part Fibre Toxicol. 2023 Jul 31;20(1):30. doi: 10.1186/s12989-023-00541-x.
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.
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/m. 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).
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.
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.
已证实，暴露于木柴烟雾会导致不良的呼吸道健康影响，包括气道感染，但潜在机制尚不清楚。先前的一项研究未能确认在暴露于木柴烟雾后 24 小时支气管灌洗液（BW）或支气管肺泡灌洗（BAL）中出现任何急性炎症或细胞浸润，但显示白细胞数量出人意料地减少。本研究旨在更早阶段研究潜在的急性炎症发展以及细胞毒性的迹象。
在一项双盲、随机交叉研究中，14 名健康参与者在一个普通的燃木炉中暴露于过滤空气和不完全燃烧木柴产生的稀释烟雾 2 小时，平均颗粒物浓度为 409μg/m。暴露后 6 小时进行支气管镜检查和 BW 及 BAL。进行了差异细胞计数、DNA 损伤评估以及吞噬 BAL 细胞的体外吞噬功能分析。还收集了木柴烟雾颗粒，用于支气管上皮细胞（BEAS-2B）和肺泡 II 型样细胞（A549）的体外毒理学分析。
暴露于木柴烟雾会增加 BAL 乳酸脱氢酶（LDH）（p=0.04），并降低体外肺泡巨噬细胞的吞噬能力（p=0.03）和活力（p=0.02），与过滤空气相比。暴露于木柴烟雾后 BAL 嗜酸性粒细胞数量增加（p=0.02），而 BW 和 BAL 中的其他细胞类型不受影响。体外暴露于木柴烟雾颗粒证实会导致 DNA 损伤增加、代谢活性降低和细胞周期紊乱。
暴露于不完全燃烧的木柴烟雾在 6 小时内并未引起任何急性气道炎症细胞浸润，除了嗜酸性粒细胞。然而，有证据表明存在细胞毒性反应，表现为 LDH 增加、细胞活力降低和肺泡巨噬细胞吞噬能力受损。这些发现与 24 小时支气管镜检查结果一致，可能为人群研究中报告的生物质烟雾暴露增加感染易感性提供证据。
