Telomeres are “protective messengers” at the ends of eukaryotic chromosomes that protect them from degradation, end to end fusion and recombination. Admittedly, telomeres progressively shorten with age that can also be significantly accelerated by pathological conditions, which are often considered as potential contributors for cellular senescence. It is commonly believed that constant accumulation of senescent cells may lead to dysfunctional tissues and organs, thereby accelerating aging process and subsequent occurrence of age-related diseases. In particular, epidemiological data has indicated a significant association between environmental pollutants exposure and a high incidence of age-related diseases. Moreover, there is growing evidence that environmental toxicity has a detrimental impact on telomere length. Overall, a consensus is emerging that environmental pollutants exposure could lead to accelerated telomere erosion and further induce premature senescence, which may be responsible for the acceleration of aging and the high morbidity and mortality rates of age-related diseases.

端粒是真核染色体末端的“保护信使”，可保护端粒免受降解，端对端融合和重组。诚然，端粒随着年龄的增长而逐渐缩短，而病理条件通常也被认为是导致细胞衰老的潜在因素，端粒的延长也可以大大加速。通常认为衰老细胞的不断积累可能导致组织和器官功能失调，从而加速衰老过程和随后与年龄有关的疾病的发生。尤其是，流行病学数据表明，环境污染物暴露与与年龄有关的疾病的高发病率之间存在重大关联。此外，越来越多的证据表明环境毒性对端粒长度有不利影响。总体，