国内科研人员首次观测到了PM2.5颗粒是如何入侵人体细胞，证实其显著的呼吸毒性。
中科院上海应用物理研究所的研究人员在《Carbon》期刊上发表论文，报告了PM2.5细颗粒物呼吸毒性机制研究中取得新进展，他们首次观测到了PM2.5颗粒是如何入侵人体细胞。
PM2.5等细颗粒物因小尺寸和大比表面积，容易吸附空气中多种其它污染物，导致和PM10等粗颗粒物完全不一样的毒理学效应。研究人员使用碳黑颗粒和金属离子作为PM2.5呼吸毒性研究的模式材料，在细胞和动物水平揭示了碳黑-金属复合物颗粒诱导自噬和溶酶体功能紊乱的生物学机制，建立了对大气细颗粒物毒理及健康危害机制的全新认识。他们利用同步X射线双能吸收衬度成像技术首次观察到碳黑颗粒能吸附并载带大量金属离子进入巨噬细胞，从而破坏了细胞内部的自噬平衡，导致了显著的毒性效应。利用同步X射线荧光显微成像技术，观察到碳黑-金属相互作用导致大量金属进入肺组织，破坏了肺组织内某些重要生命元素的平衡，并造成肺组织的自噬和溶酶体相关功能的紊乱，导致了显著的呼吸毒性。
上述内容来源：solidot.org，仅供参考。
参考文献：Autophagy and lysosomal dysfunction: A new insight into mechanism of synergistic pulmonary toxicity of carbon black-metal ions co-exposure，Huating Konga, 1, Kai Xiaa, 1, Liang Pana, Jichao Zhanga, Yan Luob, Yu Zhanga, Zhifen Cuia, Nahed Nasser El-Sayedc, Ali Aldalbahic, Nan Chena, Aiguo Lid, Renzhong Taid, Chunhai Fana, Ying Zhua,Carbon，Volume 111, January 2017, Pages 322–333
Fine particulate matter (PM 2.5) is the principal instigators of adverse health events, yet gaps still remain in understanding the mechanism mediating its toxic response. Similar to nanoparticles, PM 2.5, with large surface area to volume ratio, can absorb multipollutants in air, displaying toxicity profiles that are very different from those of coarse particles of the same composition. One particularly relevant interaction is that of PM 2.5 and the anthropogenic metals. In this study, we used carbon black nanoparticle (CBs) and metal ions as model materials to investigate the synergistic pulmonary toxicity and its mechanism. We demonstrated that excessive metal contaminants adsorbed on CBs contributed to the observed toxic effects both in vitro and in C57BL6 mice intratracheal instillation model. Significantly, we found that autophagy and lysosomal dysfunction accounted for the synergistic pulmonary toxic effect of co-exposure to CBs and metals. Our findings provide a new insight into understanding the toxicological and healthy effects of fine particles, which have potential to aid in mitigating their adverse health effect.