Reduced bronchoalveolar macrophage phagocytosis and cytotoxic effects after controlled short-term exposure to wood smoke in healthy humans.

IF 7.2 1区 医学 Q1 TOXICOLOGY
Alva Hansson, Gregory Rankin, Oskari Uski, Maria Friberg, Jamshid Pourazar, Robert Lindgren, Natxo García-López, Christoffer Boman, Thomas Sandström, Annelie Behndig, Ala Muala
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引用次数: 1

Abstract

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.

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健康人体短期受控暴露于木材烟雾后支气管肺泡巨噬细胞吞噬和细胞毒性作用的减少。
背景:暴露于木材烟雾已被证明有助于呼吸道健康的不良影响,包括气道感染,但潜在的机制尚不清楚。先前的一项研究未能证实木材烟雾暴露24小时后支气管洗涤(BW)或支气管肺泡灌洗(BAL)中有任何急性炎症或细胞内流,但白细胞数量意外减少。目前的研究是为了调查早期的反应,关于急性炎症的潜在发展,以及细胞毒性的适应症。方法:在一项双盲、随机交叉研究中,14名健康参与者在一个平均颗粒物浓度为409微克/立方米的普通柴炉中,暴露于过滤空气和稀释木材燃烧产生的烟雾中2小时。暴露后6小时行BW和BAL支气管镜检查。对吞噬BAL细胞进行细胞计数、dna损伤评估和体外吞噬功能分析。采集木烟颗粒,利用支气管上皮细胞(BEAS-2B)和肺泡ii型样细胞(A549)进行体外毒理学分析。结果:与过滤空气相比,暴露于木材烟雾中会增加BAL乳酸脱氢酶(LDH) (p = 0.04),降低肺泡巨噬细胞的体外吞噬能力(p = 0.03)和生存能力(p = 0.02)。木材烟熏后BAL嗜酸性粒细胞数量增加(p = 0.02),而其他细胞类型在BW和BAL中未受影响。体外暴露于木材烟雾颗粒证实增加了dna损伤,降低了代谢活性和细胞周期紊乱。结论:暴露于不完全燃烧的木材烟雾中,除了嗜酸性粒细胞外,在6小时内没有引起任何急性气道炎症细胞内流。然而,有迹象表明LDH升高、细胞活力降低和肺泡巨噬细胞吞噬能力受损是细胞毒性反应。这些发现与早期24小时的支气管镜检查结果一致,并可能为基于人群的研究报告的生物质烟雾暴露增加感染易感性提供证据。
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来源期刊
CiteScore
15.90
自引率
4.00%
发文量
69
审稿时长
6 months
期刊介绍: Particle and Fibre Toxicology is an online journal that is open access and peer-reviewed. It covers a range of disciplines such as material science, biomaterials, and nanomedicine, focusing on the toxicological effects of particles and fibres. The journal serves as a platform for scientific debate and communication among toxicologists and scientists from different fields who work with particle and fibre materials. The main objective of the journal is to deepen our understanding of the physico-chemical properties of particles, their potential for human exposure, and the resulting biological effects. It also addresses regulatory issues related to particle exposure in workplaces and the general environment. Moreover, the journal recognizes that there are various situations where particles can pose a toxicological threat, such as the use of old materials in new applications or the introduction of new materials altogether. By encompassing all these disciplines, Particle and Fibre Toxicology provides a comprehensive source for research in this field.
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