Scholarlink

<p>Previous studies often focused on single pollutant source, failing to replicate real-world exposure scenarios for chronic respiratory disease (CRD) risk. We aimed to explore the mixed exposure patterns of CRD risk factors and investigate interactions with smoking and genetic risk. We identified air pollution exposure modes using latent class analysis (LCA) in the UK Biobank. Cox model assessed associations between exposure modes and lung cancer (LC), idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and asthma. Interactions among exposure modes, smoking and genetic risk were analyzed. LCA divided participants into five groups, and hazard ratios (HRs) for “High air pollution” group were 1.28 for LC (95% CI: 1.08–1.52), 1.23 for IPF (95% CI: 1.03–1.48), 1.28 for COPD (95% CI: 1.17–1.39) and 1.09 for asthma (95% CI: 1.01–1.18). Significant additive interactions between high air pollution and smoking were observed for LC and COPD. Individuals with high genetic risk exposed to both smoking and high air pollution showed the relative excess risk due to interaction (RERI) of 2.74 for LC, 3.93 for IPF, and 1.68 for COPD. Smoking and air pollution together accounted for over 40% of LC, IPF and COPD cases. Our findings highlight the complex interplay between environmental air pollution, smoking, and genetic risk in CRD development in real-world exposure scenarios.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Air pollution exposure modes, smoking and genetic risk with chronic respiratory diseases: a prospective study

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月5日

查看全文
  • Ting Wang,
  • Linfang Lyu,
  • Ru Yuan,
  • Lei Lei,
  • Fanqing Meng,
  • Meng Zhu,
  • Weiwei Duan

摘要

Previous studies often focused on single pollutant source, failing to replicate real-world exposure scenarios for chronic respiratory disease (CRD) risk. We aimed to explore the mixed exposure patterns of CRD risk factors and investigate interactions with smoking and genetic risk. We identified air pollution exposure modes using latent class analysis (LCA) in the UK Biobank. Cox model assessed associations between exposure modes and lung cancer (LC), idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and asthma. Interactions among exposure modes, smoking and genetic risk were analyzed. LCA divided participants into five groups, and hazard ratios (HRs) for “High air pollution” group were 1.28 for LC (95% CI: 1.08–1.52), 1.23 for IPF (95% CI: 1.03–1.48), 1.28 for COPD (95% CI: 1.17–1.39) and 1.09 for asthma (95% CI: 1.01–1.18). Significant additive interactions between high air pollution and smoking were observed for LC and COPD. Individuals with high genetic risk exposed to both smoking and high air pollution showed the relative excess risk due to interaction (RERI) of 2.74 for LC, 3.93 for IPF, and 1.68 for COPD. Smoking and air pollution together accounted for over 40% of LC, IPF and COPD cases. Our findings highlight the complex interplay between environmental air pollution, smoking, and genetic risk in CRD development in real-world exposure scenarios.