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Oxidative damage mediates the association between polycyclic aromatic hydrocarbon exposure and lung function.

Limin Cao1,2, Yun Zhou1,2, Aijun Tan3

  • 1Department of Occupational & Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.

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Polycyclic aromatic hydrocarbon (PAH) exposure is linked to reduced lung function, potentially mediated by oxidative DNA damage. This study found that oxidative DNA damage plays a role in the association between high-molecular-weight PAH exposure and decreased forced vital capacity (FVC).

Keywords:
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Area of Science:

  • Environmental Health
  • Toxicology
  • Pulmonary Medicine

Background:

  • Polycyclic aromatic hydrocarbons (PAHs) exposure is associated with reduced lung function.
  • The role of oxidative damage in this association is not fully understood.
  • This study investigates oxidative DNA and lipid damage as potential mediators.

Purpose of the Study:

  • To explore the mediating role of oxidative DNA or lipid damage in the association between PAH exposure and lung function.
  • To quantify the relationship between urinary PAH metabolites, oxidative stress markers, and lung function parameters.

Main Methods:

  • Measured urinary monohydroxy polycyclic aromatic hydrocarbon metabolites (OH-PAHs), 8-hydroxy-2'-deoxyguanosine (8-OHdG), and 8-isoprostane (8-iso-PGF2α) in 3367 participants.
  • Assessed lung function parameters including FEV1 and FVC.
  • Utilized linear mixed models and mediation analysis to examine associations and mediation effects.

Main Results:

  • Increased urinary OH-PAHs were associated with decreased FEV1 and FVC.
  • Positive dose-response relationships were observed between OH-PAHs and oxidative damage markers (8-OHdG, 8-iso-PGF2α).
  • Urinary 8-OHdG mediated 14.22% of the association between high-molecular-weight OH-PAHs and FVC.

Conclusions:

  • Oxidative DNA damage may mediate the adverse effects of high-molecular-weight PAH exposure on lung function.
  • Findings suggest a mechanism linking PAH exposure to lung function decline through oxidative stress.