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Lung inflammation, caused by acute exposure to ozone (O 3 ) - one of the six criteria air pollutants - is a significant source of morbidity in susceptible individuals. Alveolar macrophages (AMØs) are the most abundant immune cells in the normal lung and their number increases following O 3 exposure. However, the role of AMØs in promoting or limiting O 3 -induced lung inflammation has not been clearly defined. Here, we used a mouse model of acute O 3 exposure, lineage tracing, genetic knockouts, and data from O 3 -exposed human volunteers to define the role and ontogeny of AMØs during acute O 3 exposure. Lineage tracing experiments showed that 12, 24, and 72 h after exposure to O 3 (2 ppm) for 3h all AMØs were tissue-resident origin. Similarly, in humans exposed to FA and O 3 (200 ppb) for 135 minutes, we did not observe ~21h post-exposure an increase in monocyte-derived AMØs by flow cytometry. Highlighting a role for tissue-resident AMØs, we demonstrate that depletion of tissue-resident AMØs with clodronate-loaded liposomes led to persistence of neutrophils in the alveolar space after O 3 exposure, suggesting that impaired neutrophil clearance (i.e., efferocytosis) leads to prolonged lung inflammation. Moreover, depletion of tissue-resident AMØ demonstrated reduced clearance of intratracheally instilled apoptotic Jurkat cells, consistent with reduced efferocytosis. Genetic ablation of MerTK - a key receptor involved in efferocytosis - also resulted in impaired clearance of apoptotic neutrophils followed O 3 exposure. Overall, these findings underscore the pivotal role of tissue-resident AMØs in resolving O 3 -induced inflammation via MerTK-mediated efferocytosis.