打印机工作条件下室内二次有机气溶胶的形成机制与毒理效应

The formation and toxicological effect of indoor SOA is closely related to office gens’ health when a printer is in working condition. While little attention has been paid to indoor SOA, compared to SOA in the atmosphere. Secondary organic pollution from printer was not valued and researches on the formation, distribution and toxicity of SOA in the environment with printing have been less reported. Thus, more study need to be focused on the secondary organic pollution caused by printers, SOA formation, distribution as well as its toxicological effect. This project starts with simultaneous measurement for gas and particle organic compounds as well as other inorganic contaminants so as to master their distribution and features, physically and chemically. Based on the above mentioned measurement, smog chamber SOA generation simulation with single and multiple precursors are performed. Through the verification of the measured results, SOA yield function is formed, with precursor, physical factor and chemical factor as variables. In this way, inhibitory factor of indoor SOA formation can be studied as well as its formation mechanism can be revealed. Meanwhile，ultrafine SOA particles in the office with printer are collected to perform the double-cell co-cultured in vitro cytotoxicity test and chronic toxicity test of mice trachea in order to clarify biological toxicity and toxic mechanism of indoor SOA in the office with printer. To sum up, this project aims for a new approach to study SOA formation mechanism, inhibitory factor and its toxicological effect, which provides an important scientific basis for indoor SOA health effect assessment and pollution intervention as well as enriching SOA research methods.

打印机工作条件下室内二次有机气溶胶(SOA)的形成与毒理效应，与办公一族的健康息息相关。当前SOA研究多关注大气中的SOA，对室内SOA研究不足；打印带来的室内二次有机污染不被重视，打印工作室内SOA的形成、分布与毒理的研究鲜见。本研究拟开展打印工作室内气、粒相有机物和其它污染物的同步实测，掌握其分布与理化特征；在实测基础上,开展单一和多个前体物的烟雾箱SOA生成模拟，并与实测结果相互验证，建立以“前体物、物理因素和化学因素”为变量的SOA产率函数，明晰室内SOA生成的抑制因素,揭示形成机制；收集打印工作室内的超细SOA颗粒，开展2种细胞共培养的细胞体外毒性实验和小鼠气管慢性“喂毒”实验，阐明打印工作室内SOA的生物毒性和致毒机理。本研究旨在建立SOA研究新方法，揭示形成机制，明晰抑制因素，阐明毒理效应，为室内SOA的健康效应评估和污染干预提供重要科学依据，丰富、完善SOA研究方法。

研究了打印机工作条件下颗粒物的释放、粒径、化学组分、二次生成及其对机体的毒理效应与作用机理，为打印机的污染评价与防控提供基础数据和科学依据。主要研究成果：. （1）打印室内颗粒浓度变化与打印进程密切相关，HP1008、HP104W型打印机工作时PM2.5的平均排放速率分别为2.18、2.62mg/h；两种打印机若分别在30m3室内连续打印1h会使室内PM2.5浓度平均增加72.5、87.2μg/m3。. （2）颗粒中有机碳（OC）浓度为打印室＞寝室＞环境空气，元素碳（EC）浓度为打印室＞环境空气＞寝室，OC、EC浓度随粒径从0.006μm到10μm呈现“先增大，后减小”的规律，最大值出现在积聚模态0.256-0.382μm粒径段上。. （3）HP1008、HP104W型打印机打印排放的PM2.5中的碳组分占PM2.5的比重为5.42%、45.43%，OC/EC比值分别为10.87、83.87。打印结束后仓内PM2.5及碳组分的分布反映PM2.5的二次生成。. （4）打印机工作主要排放VOCs：乙苯、乙醇、丙酮、正己烷、苯乙烯、邻二甲苯、间，对-二甲苯、甲苯、萘、苯、六氯-1,3-丁二烯、十二烷、乙酸乙酯等;同时，打印机工作会造成室内臭氧浓度上升。. （5）打印室PM2.5使HUVEC、HBE细胞存活率下降，导致细胞氧化损伤和细胞凋亡；打印室PM2.5浓度越高，细胞存活率和SOD活性越低且MDA含量和凋亡通路中的Bax/Bcl-2蛋白表达也越高。. （6）打印室PM2.5上调小鼠体内磷酸化的蛋白激酶B(ｐ-AKT)、磷酸化的磷脂酰肌醇３-激酶（PI3K）蛋白表达量，而PI3K/ B(ｐ-AKT)信号通路的激活，促进基质金属蛋白酶-２(MMP-2)蛋白表达上调，MMP-2表达上调加剧肺部纤维化；血管内皮生长因子(VEGF)蛋白表达下调，B淋巴细胞瘤-2(Bcl-2)蛋白表达下调，Bcl-2同源水溶性蛋白(BAX)表达上调，激活凋亡启动子Caspase-8和执行子Caspase-3，打印室PM2.5的暴露加剧小鼠体内纤维化，长时间待在打印室的人员构成威胁。

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