Li Guoxing, Zhang Ke, Yang Teng, Jin Jianbo, Guo Xinbiao, Cai Yutong Samuel, Huang Jing
Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, Beijing, China.
Environmental Research Group, School of Public Health, Imperial College London, London, UK.
Thorax. 2025 Jul 21. doi: 10.1136/thorax-2024-222871.
In the UK, an estimated 15% of asthma patients have concurrent chronic obstructive pulmonary disease (COPD), yet the underlying causes and mechanisms remain largely unexplored. This study aimed to investigate the roles of both ambient air pollution and genetic susceptibility in the progression from asthma to COPD.
46 832 participants with asthma were recruited from the UK Biobank during the baseline period (2006-2010). Particulate matter with a diameter of 2.5 μm (PM) and nitrogen dioxide (NO) were estimated at baseline address using land-use regression models. Air pollution score reflected joint exposure to air pollution. Polygenic risk score was calculated using novel genetic signals identified for coexistence of asthma+COPD. Cox proportional hazards regression analysis was employed to quantify the risks of both ambient air pollution and genetic scores on incident COPD among asthmatics, adjusting for covariates.
Over a median follow-up of 10.84 years, 3759 participants with asthma at baseline developed COPD. For an IQR increase in PM and NO, the HR for developing COPD was 1.07 (95% CI: 1.02 to 1.11) and 1.10 (95% CI: 1.04 to 1.15), respectively. Adverse effects could be observed at concentrations as low as 8 µg/m for PM and 12 µg/m for NO. A significant multiplicative interaction was identified between ambient air pollution and genetic susceptibility. Individuals with the highest genetic risk score exhibited the greatest risk, with an HR of 1.13 (95% CI: 1.05 to 1.22) per IQR increase in air pollution score (P <0.05).
Ambient air pollution is strongly associated with progression from asthma to comorbidity COPD, particularly among individuals with high genetic risk.
在英国，估计15%的哮喘患者同时患有慢性阻塞性肺疾病（COPD），但其潜在原因和机制在很大程度上仍未得到探索。本研究旨在调查环境空气污染和遗传易感性在从哮喘进展为COPD过程中的作用。
在基线期（2006 - 2010年）从英国生物银行招募了46832名哮喘患者。使用土地利用回归模型在基线住址处估计直径为2.5μm的颗粒物（PM）和二氧化氮（NO）。空气污染评分反映了空气污染的联合暴露情况。使用为哮喘 + COPD共存确定的新遗传信号计算多基因风险评分。采用Cox比例风险回归分析来量化环境空气污染和遗传评分对哮喘患者发生COPD的风险，并对协变量进行调整。
在中位随访10.84年期间，3759名基线时患有哮喘的参与者发展为COPD。PM和NO每增加一个四分位间距，发生COPD的风险比（HR）分别为1.07（95%置信区间：1.02至1.11）和1.10（95%置信区间：1.04至1.15）。对于PM浓度低至8μg/m³和NO浓度低至12μg/m³时即可观察到不良影响。在环境空气污染和遗传易感性之间发现了显著的相乘交互作用。遗传风险评分最高的个体风险最大，空气污染评分每增加一个四分位间距，HR为1.13（95%置信区间：1.05至1.22）（P<0.05）。
环境空气污染与从哮喘进展为合并COPD密切相关，尤其是在遗传风险高的个体中。
