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Background <p>Chronic obstructive pulmonary disease (COPD) is a leading cause of global morbidity, with aging and smoking as key risk factors. However, the mediating role of biological aging in the smoking-COPD relationship has been rarely examined in Chinese populations.</p> Methods <p>In this hospital-based cohort study, 1,269 Chinese adults aged 40–84&#xa0;years without COPD were enrolled. We developed Klemera-Doubal method-biological age (KDM-BA) using 11 routine clinical biomarkers. KDM-BA acceleration (KDM-BAAc) was calculated by regressing KDM-BA on chronological age (CA). Three Cox models were used to assess the association between KDM-BAAc and COPD risk. Restricted cubic spline models were used to evaluate the dose–response relationship between KDM-BAAc and COPD risk. Counterfactual mediation analysis was used to quantify BA acceleration’s mediating role in smoking-COPD association.</p> Results <p>Over a mean follow-up of 3.4&#xa0;years, 47 incident COPD cases occurred (incidence rate: 10.90/1000 person-years). Biological older was associated with higher COPD incidence [15.94 vs. 7.00/1,000 person-years; rate ratios (RR) = 2.28, 95% confidence intervals (95% CI) = 1.22–4.40]. Each 1-year increase in KDM-BAAc elevated COPD risk by 7% [fully adjusted hazard ratio (HR) = 1.07, 95% CI = 1.03–1.12]. Dose–response relationships were found between biological aging and COPD (fully adjusted<i> P</i> <sub>for overall</sub> = 0.003). KDM-BAAc mediated 14.3% (fully adjusted) of smoking's effect on COPD. Results remained robust across sensitivity analysis.</p> Conclusion <p>Accelerated biological aging is associated with increased COPD risk and serves as a significant mediator in the smoking-COPD relationship among Chinese adults.</p>

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Biological aging, a mediator between smoking and chronic obstructive pulmonary disease: evidence from a hospital-based cohort study in China

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月10日

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  • Dongming Xie,
  • Ao Lin,
  • Feng Luo,
  • Katie Lu,
  • Zhi Li,
  • Jinyi Huang,
  • Jinrong Zhang,
  • Jianjun Zou,
  • Houli Xiao,
  • Zhiyong Ren,
  • Dongsheng Huang,
  • Chenli Xie,
  • Cuiyi Chen,
  • Yibin Deng,
  • Jiachun Lu

摘要

Background

Chronic obstructive pulmonary disease (COPD) is a leading cause of global morbidity, with aging and smoking as key risk factors. However, the mediating role of biological aging in the smoking-COPD relationship has been rarely examined in Chinese populations.

Methods

In this hospital-based cohort study, 1,269 Chinese adults aged 40–84 years without COPD were enrolled. We developed Klemera-Doubal method-biological age (KDM-BA) using 11 routine clinical biomarkers. KDM-BA acceleration (KDM-BAAc) was calculated by regressing KDM-BA on chronological age (CA). Three Cox models were used to assess the association between KDM-BAAc and COPD risk. Restricted cubic spline models were used to evaluate the dose–response relationship between KDM-BAAc and COPD risk. Counterfactual mediation analysis was used to quantify BA acceleration’s mediating role in smoking-COPD association.

Results

Over a mean follow-up of 3.4 years, 47 incident COPD cases occurred (incidence rate: 10.90/1000 person-years). Biological older was associated with higher COPD incidence [15.94 vs. 7.00/1,000 person-years; rate ratios (RR) = 2.28, 95% confidence intervals (95% CI) = 1.22–4.40]. Each 1-year increase in KDM-BAAc elevated COPD risk by 7% [fully adjusted hazard ratio (HR) = 1.07, 95% CI = 1.03–1.12]. Dose–response relationships were found between biological aging and COPD (fully adjusted P for overall = 0.003). KDM-BAAc mediated 14.3% (fully adjusted) of smoking's effect on COPD. Results remained robust across sensitivity analysis.

Conclusion

Accelerated biological aging is associated with increased COPD risk and serves as a significant mediator in the smoking-COPD relationship among Chinese adults.