Airborne fine-dust pollution poses a significant threat to both respiratory and skin health; however, the skin's wound-healing process in response to such exposure remains underexplored. Therefore, this study examined the effect of fine-dust-model compounds, specifically polycyclic aromatic hydrocarbons (PM(10)-PAHs) and trace-metal-containing particles (PM(10)-Trace), on the wound-healing process using human skin equivalents reconstructed with collagen-based biomaterials and human skin cells. Our findings revealed that fine-dust exposure significantly delayed wound closure by 2-3 times compared with unexposed controls, impairing re-epithelialization. Live imaging of wound-healing dynamics revealed that trace-metal-containing particles had a more pronounced inhibitory effect than polycyclic aromatic hydrocarbons. Furthermore, fine-dust exposure elevated protease-activated receptor-1 (PAR1) expression by up to 161%, indicating significant physiological disruption. Additionally, fine-dust exposure triggered inflammation and oxidative stress, leading to structural and functional damage in the reconstructed skin. These results provide critical insights into how airborne pollutants disrupt skin repair mechanisms and highlight the need for targeted strategies to mitigate their harmful effects.