Despite the similar BAL neutrophilic and eosinophilic response to ozone exposure between subjects with and without asthma, those with asthma had distinct higher up-regulation of many of DEGs involved in wounding, adhesion, and extracellular processes, with an increased pro-inflammatory signal (PLA2G7, S100A12, CORO1A, PLXNC1, SELL, and SIGLEC10), a predilection for M1 macrophage phenotype (CCR2 and CCL22), and augmented matrix degradation and remodeling (MMP8, MMP9, and SULF2). Here, MMP9 is linked to asthma.