Telomeres are located at the end of eukaryotic chromosomes and vulnerable to exogenous chemical compounds. Exposure to coke oven emissions (COEs) leads to a dose-related telomere damage, and such chromosomal damage might trigger the cGAS/STING signaling pathway which plays an important role in immune surveillance. However, the relationship between the genetic variations in the cGAS/STING signaling pathway and telomere damage in the COEs-exposure workers has not been investigated. Therefore, we recruited 544 coke oven workers and 238 healthy control participants, and determined the level of COEs exposure, concentration of urinary 1-hydroxypyrene (1-OHPYR), genetic polymorphisms and telomere length. The results showed that the telomere length significantly decreased from the control-to high-exposure groups as defined by the external exposure level (P < 0.05). The results also indicated that STING rs7447927 CC, cGAS rs34413328 AA, and cGAS rs610913 AA could inhibit telomere shortening in the exposure group (P < 0.05), and cGAS rs34413328, urine 1-OHPYR and cumulative exposure dose (CED) had a significant association with telomere length by generalized linear model. In conclusion, telomere shortening was a combined consequence of short-term exposure, long-term exposure, and genetic variations among the COEs-exposure workers.

端粒位于真核染色体的末端，容易受到外源性化合物的攻击。暴露于焦炉排放物（COE）会导致剂量相关的端粒损伤，而这种染色体损伤可能会触发cGAS / STING信号通路，在免疫监测中起重要作用。但是，cGAS / STING中遗传变异之间的关系尚未调查COEs暴露工人的信号传导途径和端粒损伤。因此，我们招募了544名炼焦炉工人和238名健康对照组参与者，并确定了COE暴露水平，尿中1-羟基py（1-OHPYR）浓度，遗传多态性和端粒长度。结果表明，根据外部暴露水平，端粒长度从对照组到高暴露组明显减少（P  <0.05）。结果还表明，STING rs7447927 CC，cGAS rs34413328 AA和cGAS rs610913 AA可以抑制暴露组的端粒缩短（P  <0.05），而cGASrs34413328，尿液1-OHPYR和累积暴露剂量（CED）通过广义线性模型与端粒长度显着相关。总之，端粒缩短是COEs暴露工人中短期暴露，长期暴露和遗传变异的综合结果。