Abstract This study investigated the link between long-term exposure to PM2.5 components and the risk of developing chronic obstructive pulmonary disease (COPD) using UK Biobank data. The exposure dataset, derived from the European Monitoring and Evaluation Program (EMEP) model, included elemental carbon (EC), organic matter (OM), ammonium (NH4 +), nitrate (NO3 −), and sulfate (SO4 2−). The risk of COPD was assessed using the Cox proportional hazards model, and the contribution of each component was evaluated with quantile g-computation. A polygenic risk score for COPD was used to explore genetic interactions with PM2.5 constituents. Adjusted hazard ratios showed an increased risk for each component and the mixed exposure, with SO4 2− (40.8%) contributing the most. We observed synergistic effects between genetic risk and exposure to PM2.5, EC, NH4 +, and SO4 2−, accounting for 10–18% of total COPD risk. Prolonged exposure to PM2.5, especially SO4 2−, increased the risk of COPD, with genetic factors modifying the effect.