The ends of chromosomes shorten at each round of cell division, and this process is thought to be affected by occupational exposures. Occupational hazards may alter telomere length homeostasis resulting in DNA damage, chromosome aberration, mutations, epigenetic alterations and inflammation. Therefore, for the protection of genetic material, nature has provided a unique nucleoprotein structure known as a telomere. Telomeres provide protection by averting an inappropriate activation of the DNA damage response (DDR) at chromosomal ends and preventing recognition of single and double strand DNA (ssDNA and dsDNA) breaks or chromosomal end-to-end fusion. Telomeres and their interacting six shelterin complex proteins in coordination act as inhibitors of DNA damage machinery by blocking DDR activation at chromosomes, thereby preventing the occurrence of genome instability, perturbed cell cycle, cellular senescence and apoptosis. However, inappropriate DNA repair may result in the inadequate distribution of genetic material during cell division, resulting in the eventual development of tumorigenesis and other pathologies. This article reviews the current literature on the association of changes in telomere length and its interacting proteins with different occupational exposures and the potential application of telomere length or changes in the regulatory proteins as potential biomarkers for exposure and health response, including recent findings and future perspectives.

染色体末端在每轮细胞分裂时都会缩短，这一过程被认为受到职业暴露的影响。职业危害可能会改变端粒长度稳态，导致 DNA 损伤、染色体畸变、突变、表观遗传改变和炎症。因此，为了保护遗传物质，大自然提供了一种独特的核蛋白结构，称为端粒。端粒通过避免染色体末端 DNA 损伤反应 (DDR) 的不当激活并防止识别单链和双链 DNA（ssDNA 和 dsDNA）断裂或染色体端到端融合来提供保护。端粒及其相互作用的六种庇护蛋白复合体蛋白协同作用，通过阻断染色体上的 DDR 激活，充当 DNA 损伤机制的抑制剂，从而防止基因组不稳定、细胞周期扰乱、细胞衰老和细胞凋亡的发生。然而，不适当的 DNA 修复可能会导致细胞分裂过程中遗传物质分布不充分，最终导致肿瘤发生和其他病变。本文回顾了有关端粒长度及其相互作用蛋白的变化与不同职业暴露之间关系的现有文献，以及端粒长度或调节蛋白的变化作为暴露和健康反应的潜在生物标志物的潜在应用，包括最近的发现和未来的展望。