Background　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.　Methods　A　prospective　analysis　of　451　566　UK　Biobank　participants　was　conducted.　Land　use　regression　models　estimated　exposure　to　particulate　matter　(PM)　＜=　2.5　mu　m　(PM2.5),　PM　＜=　10　mu　m　(PM10),　PM　with　diameters　between　2.5　and　10　mu　m,　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.　Results　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.　Conclusion　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.