Limited evidence exists on air pollution's systemic impact on lung function and mediating biomarkers. This study comprehensively evaluated associations between air pollution, COPD and lung function, while exploring biomarker mediation. A prospective analysis of 451 566 UK Biobank participants was conducted. Land use regression models estimated exposure to particulate matter (PM) ≤2.5 μm (PM2.5), PM ≤10 μm (PM10), PM with diameters between 2.5 and 10 μm, reflectance measured on PM2.5 filters and transformed into absorbance (PM2.5 absorbance), nitrogen dioxide (NO2) and nitrogen oxides (NOx). Linear and Cox regression assessed pollution effects on forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), FEV1:FVC ratio, peak expiratory flow (PEF) and COPD incidence. A meta-analysis synthesised results with prior cohorts (PROSPERO: CRD42023411304). Mediation analysis evaluated biomarkers. Elevated PM2.5, PM2.5 absorbance, NOx and NO2 correlated with reduced lung function (measured as FEV1, FVC, FEV1:FVC ratio and PEF) and higher COPD risk (hazard ratio: 1.08-1.15). Race-stratified analyses revealed interactions, with White populations showing greater COPD susceptibility. Meta-analysis confirmed air pollution-COPD links. Mediation analyses implicated plasma lipid metabolites, inflammatory cell counts and cytokines as mechanistic intermediaries. Air pollution associates with lung function decline and elevated COPD risk, with White populations disproportionately affected. Lipid, inflammatory and haematological biomarkers mediate this relationship. Findings underscore the urgency of air pollution control to mitigate respiratory harm and inform targeted preventive and therapeutic strategies.
Wang et al. (Tue,) studied this question.