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<p>This study investigated the link between long-term exposure to PM<sub>2.5</sub> components and the risk of developing chronic obstructive pulmonary disease (COPD) using UK Biobank data. The exposure dataset, derived from the European Monitoring and Evaluation Program (EMEP) model, included elemental carbon (EC), organic matter (OM), ammonium (NH<sub>4</sub><sup>+</sup>), nitrate (NO<sub>3</sub><sup>−</sup>), and sulfate (SO<sub>4</sub><sup>2−</sup>). The risk of COPD was assessed using the Cox proportional hazards model, and the contribution of each component was evaluated with quantile g-computation. A polygenic risk score for COPD was used to explore genetic interactions with PM<sub>2.5</sub> constituents. Adjusted hazard ratios showed an increased risk for each component and the mixed exposure, with SO<sub>4</sub><sup>2−</sup> (40.8%) contributing the most. We observed synergistic effects between genetic risk and exposure to PM<sub>2.5</sub>, EC, NH<sub>4</sub><sup>+</sup>, and SO<sub>4</sub><sup>2−</sup>, accounting for 10–18% of total COPD risk. Prolonged exposure to PM<sub>2.5</sub>, especially SO<sub>4</sub><sup>2−</sup>, increased the risk of COPD, with genetic factors modifying the effect.</p>

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Association of fine particulate matter constituents with chronic obstructive pulmonary disease and the effect modification of genetic susceptibility

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月5日

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  • Meiqi Xing,
  • Feipeng Cui,
  • Lei Zheng,
  • Yudiyang Ma,
  • Jianing Wang,
  • Linxi Tang,
  • Ning Chen,
  • Xinru Zhao,
  • Yaohua Tian,
  • Binbin Su

摘要

This study investigated the link between long-term exposure to PM2.5 components and the risk of developing chronic obstructive pulmonary disease (COPD) using UK Biobank data. The exposure dataset, derived from the European Monitoring and Evaluation Program (EMEP) model, included elemental carbon (EC), organic matter (OM), ammonium (NH4+), nitrate (NO3−), and sulfate (SO42−). The risk of COPD was assessed using the Cox proportional hazards model, and the contribution of each component was evaluated with quantile g-computation. A polygenic risk score for COPD was used to explore genetic interactions with PM2.5 constituents. Adjusted hazard ratios showed an increased risk for each component and the mixed exposure, with SO42− (40.8%) contributing the most. We observed synergistic effects between genetic risk and exposure to PM2.5, EC, NH4+, and SO42−, accounting for 10–18% of total COPD risk. Prolonged exposure to PM2.5, especially SO42−, increased the risk of COPD, with genetic factors modifying the effect.