效应导向的典型共存污染对大气细颗粒物环境持久性自由基毒性影响的化学机制研究

Environmentally persistent free radicals (EPFRs) in airborne fine particulate matters (PM2.5) possess relatively high bioactivity. Owing to the unique pollution situation in China, coexistent air pollutants of high reactivity, like NOx, may present at high concentration during regional haze episode. Therefore, a working hypothesis has been proposed that such coexistent air pollutants may directly interact with EPFRs or their precursors in PM2.5 to transform the original speciations into possibly more/less toxic components. In this project, typical PM2.5 organic components such as polycyclic aromatic hydrocarbon and chlorophenols will be chosen as model compounds for precursors from different sources like coal-combustion or vehicle exhaust, while representative solid phase such as Fe(III)2O3, Zn(II)O and Cu(II)O will be used for modeling the surface of airborne fine particulate matters. Major efforts will be made to reveal the influencing mechanism of PM2.5-EPFRs toxicity by classical coexistent air pollutants which prevail in the haze events. By using the integrated approach based on computational simulation methods and effect-directed toxic component identification techniques, the applicant believes that both theoretical prediction and experimental results would provide valuable information for elucidating the molecular mechanism of the change in toxicity for PM2.5-EPFRs in the primary particulate matters and revealing the chemical nature of toxic component transformation for PM2.5-EPFRs in the secondary particulate matters. The progress made in the project not only may help understanding the environmental transformation of toxic components in PM2.5, but also can provide theoretical support to the emission control of air pollutants capable of component activation.

大气细颗粒物(PM2.5)环境持久性自由基(EPFRs)是一种高活性组分。我国特有大气污染状况导致灰霾发生时氮氧化物等高反应性组分与细颗粒物污染共存，其能通过与EPFRs或其前体分子反应而改变PM2.5体系生物活性与毒性效应。本项目拟采用计算模拟与实验测试相结合的方法，选取多环芳烃、氯代苯酚、氯代苯等作为煤烟型污染、汽车尾气等一次气溶胶有机组分的模型分子，以我国PM2.5中含量较多的Fe(III)2O3、Zn(II)O和Cu(II)O等为典型细颗粒物固相组成，重点开展效应导向的典型大气共存组分对PM2.5中EPFRs毒性影响的化学机制研究工作，以期揭示一次细颗粒物EPFRs毒性变化的分子机制，阐明二次细颗粒物生成过程EPFRs体系毒性组分演化的化学本质，为科学认识灰霾有害成分的环境演化并从源头上有效减少和控制能使组分活化的污染排放提供理论依据与方法储备。

环境持久性自由基(EPFRs)是一种典型大气细颗粒物(PM2.5)毒性组分。项目从3方面回答了共存污染影响PM2.5上EPFRs毒性化学机制这一核心科学问题：(1)指出污染物在一次颗粒物表面原位形成EPFRs的化学实质是表面催化组分与前驱体间的电荷转移，诠释了固相组成影响EPFRs生成和前驱体赋存形态的结构基础是其金属离子的得失电子能力，而氧缺位等也会影响这一能力。具有空d轨道的金属离子越容易接受前驱体的电子，就越可加速酚类、多环芳烃等前体分子向相应EPFRs的转化。基于金属离子氧化还原势成功构建了不同表面EPFRs生成性能的定量预测模型以评价不同体系EPFRs相关毒性的差异。(2)阐明了大气EPFRs前驱体结构和其对应EPFRs类型的差异决定了一次细颗粒物EPFRs的毒性变化。酚类生成氧中心EPFRs经历界面吸附和催化转化两个步骤，而多环芳烃生成碳中心自由基阳离子则是无能垒反应。基于此，成功构建了不同类型污染物EPFRs生成性能的预测模型。(3)以O2、白天氧化剂·OH和夜间氧化剂NO3等为典型大气共存反应性组分，揭示了一次气溶胶向二次气溶胶转化中EPFRs体系毒性受共存组分影响而发生演化的化学本质是共存污染对体系稳定性和化学形态的调控。酚氧型EPFRs在O2存在时仍稳定，但·OH和NO3会使其发生氧化。反之，O2就会使得碳中心EPFRs快速向氧中心自由基转化。灰霾发生时污染水平显著升高的氮氧化物和大气湿度可使得原始形态EPFRs寿命显著缩短，但其产物毒性并不一定降低。此外，项目在界面体系模拟、污染混合物联合毒性预测和机制解析等方法学方面亦取得进展，申请了专利并研发了工具软件。项目在ES&T等发表SCI论文24篇(12篇IF>9)，参编1本专著«大气细颗粒物的毒理与健康效应»；申请5项国家发明专利，1项已经获得授权; 3项专业软件取得国家计算机软件著作权。