Background Allergic rhinitis(AR) is an increasing challenge to public health worldwide. Exposure to environmental black carbon (BC) is associated with increased risk of allergic rhinitis, but the molecular mechanisms underlying its toxicity have not been fully elucidated. The aims of the present study were therefore to determine the effect of BC on the expression of interleukin 1 beta (IL-1 beta) and to investigate the mechanism underlying BC-induced IL-1 beta production in pollen-sensitized human nasal epithelial cells (hNECs). Methods Nasal mucosal samples collected from 10 patients undergoing nasal surgery were used to isolate and culture epithelial cells as air-liquid interface (ALI) cultures. Cultures exposed to BC +/- pollen allergen for 24 hours were assessed for the presence of IL-1 beta, the production of reactive oxygen species (ROS), and activation of the nucleotide-binding, oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome. Furthermore, the mechanisms underlying BC +/- pollen allergen-induced IL-1 beta in hNECs were evaluated. Results Exposure to BC significantly increased the production of IL-1 beta and ROS and the expression of NLRP3 in hNECs, compared with control, all of which were significantly increased further by exposure to a combination of BC and pollen. Incubation of hNECs with N-acetyl-L-cysteine (NAC) significantly attenuated BC +/- pollen-induced expression of ROS, NLRP3, and IL-1 beta. NLRP3 and Caspase-1 inhibitors (MCC950 and YVAD) significantly inhibited IL-1 beta expression and NLRP3 activation, but not NLRP3 expression following exposure to BC +/- pollen. Conclusion These findings suggest that exposure to BC and pollen can exaggerate oxidative stress and significantly increase the expression of IL-1 beta in hNECs, and that this may involve a pathway integrating ROS-NLRP3-Caspase-1-IL-1 beta signaling.