Objective <p>The component‑specific toxicity of fine particulate matter (PM_2.5) and the underlying metabolic pathways driving airflow impairment in chronic obstructive pulmonary disease (COPD) remain unclear. We evaluated how specific PM_2.5 constituents alter circulating metabolites and mediate short‑term changes in peak expiratory flow (PEF) among COPD patients.</p> Methods <p>A panel study was conducted in 32 patients with stable COPD in Beijing (2018–2019). Participants were followed-up across four seasons, yielding 3363 daily PEF measurements and 208 serum samples for untargeted metabolomics. PM_2.5 components concentrations were obtained from a high-resolution (1&#xa0;km) dataset integrating ground observations, satellite retrievals, and model simulations. Linear mixed-effects models were used to estimate the associations between PM_2.5 components and PEF, and a meet-in-the-middle strategy was adopted to identify mediating metabolites and pathways.</p> Results <p>PEF declines were associated with interquartile range increase in several PM_2.5 components (lag0-7 days moving average), most notably for black carbon [-5.88 (-8.76 ~ -3.01) L/min] and sulfate [-4.78 (-8.82 ~ -0.73) L/min]. Metabolomic analysis identified 12 metabolites significantly linked to PEF (q &lt; 0.05). Pathway enrichment highlighted urea cycle/amino group metabolism (<i>P</i> = 0.041) and bile acid biosynthesis (<i>P</i> = 0.012) as key biological response routes. Five metabolites were identified as mediators of the associations between PM_2.5 components and PEF, notably Nb-arachidoyltryptamine and 6-nitrochrysene.</p> Conclusion <p>These findings highlight black carbon and sulfate as primary drivers of PM_2.5-related lung function impairment in COPD patients, likely acting through systemic metabolic perturbations. Our study supports targeted emission controls and suggests metabolic profiling as a potential approach for targeted prevention in vulnerable populations.</p>