To explore potential biological mechanisms underlying the UFP-associated TxB2 increase in the COPD group, we evaluated the associations between UFP levels and biomarkers of lipid peroxidation (HETEs) and inflammation (IL-1β, IL-8, MCP-1, MIP-1α, MIP-1β, and TNF-α) and conducted mediation analyses. The gene discussed is CCL3; the disease is chronic obstructive pulmonary disease.