POLARIS Research Centre, Department of Earth and Environmental Sciences, University of Milano-Bicocca, Piazza della Scienza 1, 20126 Milano, Italy.
POLARIS Research Centre, Department of Earth and Environmental Sciences, University of Milano-Bicocca, Piazza della Scienza 1, 20126 Milano, Italy.
Sci Total Environ. 2019 Feb 1;649:1422-1433. doi: 10.1016/j.scitotenv.2018.08.249. Epub 2018 Aug 20.
Biomass combustion significantly contributes to indoor and outdoor air pollution and to the adverse health effects observed in the exposed populations. Besides, the contribution to toxicity of the particles derived from combustion of different biomass sources (pellet, wood, charcoal), as well as their biological mode of action, are still poorly understood. In the present study, we investigate the toxicological properties of PM10 particles emitted indoor from a stove fueled with different biomasses. PM10 was sampled by gravimetric methods and particles were chemically analyzed for Polycyclic Aromatic Hydrocarbons (PAHs) and elemental content. Human lung A549 cells were exposed for 24 h to 1-10 μg/cm PM and different biological endpoints were evaluated to comparatively estimate the cytotoxic, genotoxic and pro-inflammatory effects of the different PMs. Pellet PM decreased cell viability, inducing necrosis, while charcoal and wood ones mainly induced apoptosis. Oxidative stress-related response and cytochrome P450 enzymes activation were observed after exposure to all the biomasses tested. Furthermore, after pellet exposure, DNA lesions and cell cycle arrest were also observed. The severe genotoxic and pro-necrotic effects observed after pellet exposure were likely the consequence of the high metal content. By administering the chelating agent TPEN, the genotoxic effects were indeed rescued. The higher content in PAHs measured in wood and charcoal PMs was likely the reason of the enhanced expression of metabolizing and oxidative stress-related enzymes, like CYP1B1 and HO-1, and the consequent increase in apoptotic cell death. These data suggest that combustion particles from different biomass sources may impact on lung cells according to different pathways, finally producing different toxicities. This is strictly related to the PM chemical composition, which reflects the quality of the combustion and the fuel in particular. Further studies are needed to clarify the role of particle dimension and the molecular mechanisms behind the harmful effects observed.
生物质燃烧会显著导致室内和室外空气污染,并对暴露人群的健康产生不利影响。此外,燃烧不同生物质(颗粒、木材、木炭)产生的颗粒的毒性贡献及其生物学作用模式仍知之甚少。在本研究中,我们研究了由不同生物质燃料的炉子室内排放的 PM10 颗粒的毒理学特性。通过重量法采集 PM10 颗粒,并对其进行多环芳烃(PAHs)和元素含量的化学分析。将人肺 A549 细胞暴露于 1-10μg/cm³ PM 下 24 小时,评估不同的生物学终点,以比较评估不同 PM 的细胞毒性、遗传毒性和促炎作用。颗粒 PM 降低了细胞活力,诱导了坏死,而木炭和木材 PM 主要诱导了细胞凋亡。暴露于所有测试的生物质后,观察到氧化应激相关反应和细胞色素 P450 酶的激活。此外,在颗粒暴露后还观察到了 DNA 损伤和细胞周期停滞。在颗粒暴露后观察到的严重遗传毒性和促坏死作用可能是由于金属含量高所致。通过给予螯合剂 TPEN,遗传毒性作用确实得到了挽救。在木材和木炭 PM 中测量到的较高 PAHs 含量可能是代谢和氧化应激相关酶(如 CYP1B1 和 HO-1)表达增强以及随后的凋亡细胞死亡增加的原因。这些数据表明,来自不同生物质源的燃烧颗粒可能根据不同的途径对肺细胞产生影响,最终产生不同的毒性。这与 PM 的化学成分密切相关,反映了燃烧的质量和燃料的质量。需要进一步的研究来阐明颗粒尺寸和观察到的有害影响背后的分子机制的作用。