Background: Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants associated with biological aging.??
Objectives: This study aimed to characterize a chromosome-arm-specific telomere damage profile and transcriptome atlas during polycyclic aromatic hydrocarbons (PAHs) exposure accelerate aging, and explore the target genes regulated by the telomere position effect (TPE)  underlying PAHs-induced telomere damage. 
Methods: A total of 2,089 coke oven workers were recruited, and biological age was assessed by KDM-based biological age (KDM-BA). Chromosome arm-specific RTL was evaluated by telomere quantitative fluorescence in situ hybridization. Multiple urinary hydroxylated PAHs were quantified using gas chromatography tandem mass spectrometry (GC-MS/MS). 
Results: Urinary levels of PAHs metabolites were significantly elevated in coke oven workers. Among these metabolites, 2-OHFlu was associated with accelerated biological age and telomere shortening. Mean RTL could mediate 2.3 % of the association between 2-OHFlu and KDM-BA. Quantile g-computation identified negative associations between the PAHs mixture and RTL on chromosomes 16q (β = -0.10, P = 0.033), 3p (β = -0.12, P = 0.013), 16p (β = -0.09, P = 0.042), 19p (β = -0.15, P = 0.045), and 21p?? (β = -0.12, P = 0.044). Four upregulated genes (ENSG00000275927 [16p], TMC5 [16p], UBA52 [19p], and RN7SL833P [19p]) were negatively correlated with their respective chromosome arm RTL, and upregulated genes involved in the cell mitotic cycle, chromosome segregation, nuclear structure regulation, glutathione metabolism, and mitophagy.
Conclusions: Coke oven workers with accelerated aging phenotypes have shortened telomere length on 16p and 19p, which could subsequently modulate the expression of proximal genes through TPE mechanism, thereby influencing critical aging-related processes such as the cell cycle, mitophagy, glutathione metabolism, and ribosome biogenesis.