No prior studies have linked long-term air pollution exposure to incident sudden cardiac arrest (SCA) or its possible development trajectories. We aimed to investigate the association between long-term exposure to air pollution and SCA, as well as possible intermediate diseases. Based on the UK Biobank cohort, Cox proportional hazard model was applied to explore associations between air pollutants and SCA. Chronic obstructive pulmonary disease (COPD) and major adverse cardiovascular events (MACE) were selected as intermediate conditions, and multistate model was fitted for trajectory analysis. During a median follow-up of 13.7 years, 2884 participants developed SCA among 458 237 individuals. The hazard ratios (HRs) for SCA were 1.04–1.12 per interquartile range increment in concentrations of fine particulate matter, inhalable particulate matter, nitrogen dioxide, and nitrogen oxides. Most prominently, air pollutants could induce SCA through promoting transitions from baseline health to COPD (HRs: 1.06–1.24) and then to SCA (HRs: 1.16–1.27). Less importantly, SCA could be developed through transitions from baseline health to MACE (HRs: 1.02–1.07) and further to SCA (HRs: 1.12–1.16). This study provides novel and compelling evidence that long-term exposure to air pollution could promote the development of SCA, with COPD serving as a more important intermediate condition than MACE.

中文翻译：

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空气污染和心脏骤停：慢性阻塞性肺病比心脏事件更重要的中间作用

先前没有研究将长期空气污染暴露与心脏骤停（SCA）或其可能的发展轨迹联系起来。我们的目的是调查长期暴露于空气污染与 SCA 以及可能的中间疾病之间的关联。基于英国生物银行队列，应用 Cox 比例风险模型来探索空气污染物与 SCA 之间的关联。选择慢性阻塞性肺疾病（COPD）和主要不良心血管事件（MACE）作为中间条件，并拟合多状态模型进行轨迹分析。在中位随访 13.7 年期间，458,237 人中有 2884 名参与者出现了 SCA。细颗粒物、可吸入颗粒物、二氧化氮和氮氧化物浓度每增加四分位数，SCA 的危险比 (HR) 为 1.04-1.12。最突出的是，空气污染物可以通过促进从基线健康向慢性阻塞性肺病（HR：1.06-1.24）再向SCA（HR：1.16-1.27）的转变而诱发SCA。不太重要的是，SCA 可以通过从基线健康过渡到 MACE（HR：1.02-1.07）并进一步过渡到 SCA（HR：1.12-1.16）来发展。这项研究提供了新颖且令人信服的证据，表明长期暴露于空气污染可能会促进 SCA 的发展，其中 COPD 是比 MACE 更重要的中间病症。