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<p>Chronic obstructive pulmonary disease (COPD) is one of the leading causes of mortality worldwide. However, whether air pollutants can cause COPD remains unknown. Summary data for the genome-wide association study of each phenotype were obtained from the publicly available datasets. Using single-nucleotide polymorphisms as instrumental variables, we performed Mendelian randomization (MR) to assess the relationship among PM2.5, smoking and early-onset COPD. A large-scale genetic analysis is performed to investigate the biological pathways. In MR, exposure to higher PM2.5 increased the risk of early-onset COPD (IVW, OR (95% CI) = 1.63 (1.15, 2.31), <i>p</i> = 5.60E−03) but had no association with later-onset COPD. In addition, cigarettes per day (IVW, OR (95% CI) = 1.71 (1.46, 1.99), <i>p</i> = 1.60E−11) was positively associated with the risk of early-onset COPD, while age of smoking initiation (IVW, OR (95% CI) = 0.39 (0.27, 0.57), <i>p</i> = 1.21E−06) had a negative effect. In addition, two smoking behaviors could be mediators between PM2.5 and early-onset COPD (<i>p</i> &lt; 0.05). Furthermore, 136 significantly enriched biological pathways of PM2.5 potentially causing early-onset COPD were identified in a large-scale genetic analysis. This study provides strong evidence that exposure to higher PM2.5 was causally associated with smoking behavior and early-onset COPD. Smoking behavior acted as a mediator between PM2.5 and early-onset COPD. More attention should be given to people exposed to higher PM2.5 for the prevention of smoking and COPD.</p>

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PM2.5 increases the risk of early-onset COPD mediated by smoking and shared genes: a large-scale genetic analysis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月12日

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  • Jie Wen,
  • Yanlin Yang,
  • Hao Zhang,
  • Wantao Wu,
  • Ziyu Dai,
  • Xisong Liang,
  • Shuyuan Chen

摘要

Chronic obstructive pulmonary disease (COPD) is one of the leading causes of mortality worldwide. However, whether air pollutants can cause COPD remains unknown. Summary data for the genome-wide association study of each phenotype were obtained from the publicly available datasets. Using single-nucleotide polymorphisms as instrumental variables, we performed Mendelian randomization (MR) to assess the relationship among PM2.5, smoking and early-onset COPD. A large-scale genetic analysis is performed to investigate the biological pathways. In MR, exposure to higher PM2.5 increased the risk of early-onset COPD (IVW, OR (95% CI) = 1.63 (1.15, 2.31), p = 5.60E−03) but had no association with later-onset COPD. In addition, cigarettes per day (IVW, OR (95% CI) = 1.71 (1.46, 1.99), p = 1.60E−11) was positively associated with the risk of early-onset COPD, while age of smoking initiation (IVW, OR (95% CI) = 0.39 (0.27, 0.57), p = 1.21E−06) had a negative effect. In addition, two smoking behaviors could be mediators between PM2.5 and early-onset COPD (p < 0.05). Furthermore, 136 significantly enriched biological pathways of PM2.5 potentially causing early-onset COPD were identified in a large-scale genetic analysis. This study provides strong evidence that exposure to higher PM2.5 was causally associated with smoking behavior and early-onset COPD. Smoking behavior acted as a mediator between PM2.5 and early-onset COPD. More attention should be given to people exposed to higher PM2.5 for the prevention of smoking and COPD.