细胞衰老是个体衰老的关键原因，受遗传、表观遗传、生存状态及环境因素的共同影响。随化工、电子类用品的普遍使用，导致其生产、使用和废弃处理过程中所产生的持久性有机污染物（POPs）造成的环境污染日益严重，对人类健康所造成的不利影响更备受关注。项目组前期队列研究（n=7318）发现，POPs暴露人群出现严重的细胞凋亡及生殖器官衰老、免疫退化等组织退行性改变。同时，现有数据显示暴露人群DNA损伤增加、端粒长度缩短、衰老相关炎性反应通路激活、孕产妇胎盘组织衰老进程加快，证实POPs与细胞和机体衰老密切相关。本项目将系统地研究POPs暴露对染色体稳定性、基因组表观修饰、端粒损伤、炎症反应的影响，明确POPs诱导器官衰老及组织退行性变化的分子机制和信号通路，发现、鉴定个体衰老的预警标志物，为环境诱发的衰老相关疾病的干预方案提供指导，为制定工业生产和固体废弃物无害化处理的标准提供依据。

Cellular senescence does contribute to a numbers of organismal aging, can be affected by genetic, epigenetic, environmental factors. Persistent organic pollutants (POPs), which are chemical substances that do not break down in the environment attracted great attention to its effect on environmental pollution and human disease, since man-made chemicals are extensively used recently. Our previous ambispective cohort study showed that, POPs exposure could cause a series of degenerative changes including cells apoptosis, aging of reproductive organs and dysfunction of immune system et.al (n = 7318). At the meanwhile, our data also demonstrated that populations from POPs exposed region have a significantly higher level of DNA damage, increased incidence of telomere shortening and the activation of senescence-associated inflammatory pathway. Moreover, the placenta tissues from the pregnant woman have more SA-β-Gal staining compared to the people from the control area, suggesting that POPs exposure plays an important role in cell senescence and individuals aging. The currently study will explore relationship between POPs exposure and chromosome stability, telomere damage, inflammation, to further clarify the reason why POPs leading to organismal aging and degenerative changes in different tissues, which could finally provide a guide for the therapy involved in environment induced age-related diseases, as well as industrial production and the solid chemical waste disposal.