Background/Aims: Ambient ozone (O3) pollution exposure triggers airway inflammation and is linked to the development and exacerbation of pulmonary diseases. In vivo exposure studies with human volunteers documented significant variation in molecular markers of O3-induced airway inflammation between individuals and demonstrated that a given individual’s molecular response was replicable across independent O3 exposures. Response variation and replicability imply a level of genomic control over the inflammatory reaction to O3, though relevant loci are largely unknown. We aim to identify loci using a response eQTL (reQTL) approach, utilizing primary human bronchial epithelial cells (HBECs). Well-differentiated HBEC cultures mimic the in vivo bronchial epithelium structure and are held at an air-liquid interface which permits exposure to air pollutants. Here, we tested whether HBEC cultures recapitulated in vivo inter-individual variation in the pro-inflammatory response at multiple O3 concentrations. The magnitude of response was concentration-dependent as measured via expression of two hallmark O3 response genes, CXCL8 and HMOX1. Further, the interaction effect between concentration and donor was statistically significant for both genes. Inter-donor variation in gene expression was maximized at 0.4 parts per million (ppm) O3, using the coefficient of variation. To determine replicability, we repeated the 0.4 ppm exposure in a second independent set of 17 donors, where the interaction between exposure (either O3 or filtered air) and donor was again significant.