Background: Environmental pollutants such as diesel exhaust particles (DEP) have been implicated in exacerbating allergic airway inflammation. However, the precise immune cell dynamics triggered by DEP inhalation remain poorly understood. This study aimed to investigate the immunological mechanisms underlying DEP-induced airway inflammation, focusing on the recruitment and activation of monocyte-derived cells and their role in promoting asthma-like responses. Methods: Mice were exposed to DEP via inhalation. Lung immune cells were analyzed using single-cell RNA sequencing (scRNA-seq) and flow cytometry, while histological analysis was used to localize DEP within the lungs. Bronchoalveolar lavage fluid (BALF) and lung homogenates were assessed for cytokine levels, and reactive oxygen species (ROS) production was measured in alveolar macrophages (AMs). The role of CCR2 ⁺ monocytes was further evaluated using CCR2-deficient mice in an ovalbumin (OVA)-induced asthma model. Results: scRNA-seq analysis revealed increased infiltration of classical monocytes in DEP-exposed lungs, with monocyte-derived AMs contributing to enhanced MCP-1 production. DEP localized predominantly in AMs, driving MCP-1 synthesis via ROS-dependent pathways. DEP exposure aggravated eosinophilic airway inflammation in OVA-challenged mice, with significant CCR2 ⁺ monocyte recruitment and elevated cytokine levels, including MCP-1, MIP-1α, MIP-1β, and RANTES. In CCR2-deficient mice, DEP-induced monocyte recruitment and asthma exacerbation were markedly reduced, highlighting the critical role of CCR2 in these processes. Conclusions: DEP exposure promotes airway inflammation through ROS-driven MCP-1 production in AMs, leading to CCR2-dependent recruitment of classical monocytes. These findings offer novel insights into the immune mechanisms underlying DEP-induced respiratory diseases and suggest potential therapeutic targets for intervention.