Background
Occupational exposure to complex chemical mixtures, such as polycyclic aromatic hydrocarbons (PAHs), benzene, toluene, xylene (BTX), and metals, is common in coke oven production. However, their combined effects on biological aging and systemic inflammation remain poorly understood.
Objectives
This study aimed to assess internal exposures to PAHs, BTX, and metals among coke oven workers, and to investigate their associations with biomarkers of biological aging (biological age acceleration and telomere length) and systemic inflammation.
Methods
We enrolled 1091 coke oven workers. Urinary metabolites of PAHs and BTX, along with metals, were quantified using GC-MS/MS, HPLC-MS/MS, and ICP-MS, respectively. Biological age acceleration (KDM-BA-Accel) and the systemic inflammatory response index (SIRI) were calculated from blood biomarkers. Relative telomere length (RTL) was measured by RT-qPCR. Associations were analyzed using generalized linear models (GLM), restricted cubic splines (RCS), and weighted quantile sum (WQS) regression for mixture effects.
Results
Workers showed significantly elevated urinary levels of eight PAH metabolites and three BTX metabolites (TTMA, SBMA, 3&4MHA), along with reduced levels of essential metals Mn and Cu. Biological aging was accelerated (increased KDM-BA-Accel and shortened RTL) in this population. GLM analysis revealed that TTMA was positively associated with KDM-BA-Accel (β = 0.16, Padj = 0.046), while several PAH/BTX metabolites (e.g., TTMA, SBMA, 3&4MHA) were negatively associated with RTL. SIRI was positively associated with 1-OHNap and 1-OH-Mnap. Essential metal Cu was positively correlated with RTL (β = 0.25, Padj = 0.009), whereas Mo was inversely associated with SIRI. WQS models indicated that combined exposure to metals was associated with lower KDM-BA-Accel and longer RTL, whereas combined exposure to PAHs/BTX or all 17 chemicals was associated with shorter RTL and higher SIRI. Interaction analysis suggested that metal exposure might attenuate the adverse effects of PAHs/BTX on aging biomarkers. KEGG pathway analysis implied that zinc may modulate inflammation-related aging pathways.
Conclusions
Occupational exposure to PAHs and BTX is associated with accelerated biological aging and increased systemic inflammation among coke oven workers, while essential metals like Cu may exert protective effects. These findings underscore the importance of monitoring combined chemical exposures in occupational health. Interventions aimed at reducing exposure to aromatic compounds and maintaining adequate essential metal levels could help mitigate accelerated aging in high-risk occupational populations. Policy measures should consider implementing holistic exposure surveillance and control strategies in similar industrial settings.