农村固体燃料燃烧排放颗粒物的氧化潜势及其与体外肺细胞生物效应的关系

Solid fuel (coal and biomass) combustion can lead to serious particulate matter (PM) pollution in rural household, which poses severe health risk on rural residents. Oxidative stress and inflammation are widely recognized as toxic mechanisms of PM. Therefore, the oxidative potential of PM has become an effective index to evaluate the health risk of PM. So far, there is still a lack of systematic research on the oxidative potential of PM emitted from various solid fuel combustion and its impact on human health. In this project, the oxidative potential of PM emitted from different types of solid fuel and its size distribution will be determined by quantifying the reactive oxygen species (·OH and H2O2) induced by PM in a simulated lung fluid. The relative contribution of different components to the oxidative potential of PM will be apportioned by the means of separation of components. The synergistic or antagonistic effects of the interaction between the components on oxidative potential will be explored. The deposition of size-resolved PM in the human respiratory tract will be modeled. According to the deposition efficiency of the PM with different sizes, the oxidative potential of deposited PM in the respiratory tract will be estimated, and the main contributing species will be identified. Through the in vitro cellular model, the impact of the oxidative potential and main components of PM on the cellular biological effects such as oxidative stress, inflammation, cytotoxicity will be revealed. This project will help to prevent and control the health risk from indoor solid fuel combustion in rural areas. Moreover, it will also help to understand the mechanism of detrimental health effects of PM.

农村室内固体燃料（煤和生物质）燃烧会导致严重的颗粒物（Particulate matter, PM）污染，由此带来的健康问题不容忽视。氧化应激和炎症效应是被普遍认可的PM致毒机制，因而氧化潜势成为评估PM健康危害的有效指标。目前尚未系统研究不同类型固体燃料排放PM的氧化潜势及其与人体健康效应的关系。本项目通过定量PM在模拟肺液中诱导产生的活性氧（·OH和H2O2）表征氧化潜势，得到不同燃料排放PM的氧化潜势及其粒径分布；通过物质分离方式探究组分对氧化潜势的贡献，揭示组分之间的相互作用对氧化潜势的协同或拮抗效应；模拟得到不同粒径PM在人体呼吸道的沉降效率，估算呼吸道沉降颗粒物的氧化潜势并识别主要贡献组分；利用体外肺细胞探究氧化潜势和组分与PM导致的氧化应激、炎症、细胞毒性等细胞生物效应的关系。项目的实施将为防控农村室内固体燃料燃烧的健康风险提供依据，同时为认识PM健康危害作用机制提供线索。

固体燃料（煤和生物质）是重要的民用能源，其燃烧排放会带来严重的室内颗粒物污染，由此带来的居民健康风险问题不容忽视。目前，对家用炉灶固体燃料燃烧排放颗粒物的毒性及其导致的人体健康危害缺乏研究。氧化应激和炎症效应是普遍被认可的颗粒物致毒机制，颗粒物在人体内诱导产生活性氧自由基的能力（氧化潜势）可有效评估其毒性。本项目通过测定颗粒物在人工模拟肺液中·OH生成水平来表征其氧化潜势，获得了5种块煤、19种薪柴和6种秸秆燃烧排放颗粒物的氧化潜势数据及粒径分布规律。氧化潜势水平范围为0.69-12 ng/(ug·PM10)，不同燃料差别较大，成熟度较高的煤，单位质量PM10的氧化潜势也越高。氧化潜势峰值出现在0.1-0.18um和0.18-0.32um粒径段，粗颗粒物氧化潜势较低。通过组分物理分离的方式，测定不同组分的氧化潜势，水溶性部分的氧化潜势约占总体的59%，水溶性组分中亲水性金属是氧化潜势最主要的来源，疏水性HULIS也有一定贡献。煤炭取暖家庭居民呼吸道沉积颗粒物粒径分布与室内环境颗粒物不同。呼吸单位体积空气，胸腔沉积颗粒物的总·OH生成水平最高，其次是肺泡，气管内最低，但肺泡内氧化潜势主要来自于<1um的细颗粒物。人支气管上皮细胞系BEAS-2B暴露于颗粒物水溶物后，出现明显的细胞毒性。本项目的实施为认识不同燃料排放颗粒物的毒性及健康效应提供了依据。

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