Journal
Respiratory Research
Publisher
BMC
Record source
DOAJ Research Library
Abstract / Description
Abstract Objective The component‑specific toxicity of fine particulate matter (PM2.5) and the underlying metabolic pathways driving airflow impairment in chronic obstructive pulmonary disease (COPD) remain unclear. We evaluated how specific PM2.5 constituents alter circulating metabolites and mediate short‑term changes in peak expiratory flow (PEF) among COPD patients. Methods 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. PM2.5 components concentrations were obtained from a high-resolution (1 km) dataset integrating ground observations, satellite retrievals, and model simulations. Linear mixed-effects models were used to estimate the associations between PM2.5 components and PEF, and a meet-in-the-middle strategy was adopted to identify mediating metabolites and pathways. Results PEF declines were associated with interquartile range increase in several PM2.5 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