Background: The exposure to environmental tobacco smoke (ETS) is considered as a risk factor for the development of various diseases including respiratory disorders. This study was performed to investigate the influence of ETS on allergic rhinitis by employing allergic nasal inflammation models in antigen-immunized and antigen-specific Th2 cell-transferred mice. Methods: BALB/c mice immunized with ovalbumin (OVA) and adoptively transferred with in vitro-differentiated OVA-reactive Th2 cells were exposed to ETS and were challenged with OVA. Then, the number of inflammatory cells in the nasal lavage fluids and nasal hyperresponsiveness (NHR) were examined. The influences of CSE and nicotine on the proliferative response and IL-4 production of Th2 cells induced by antigen stimulation were determined in vitro. Results: The significant suppression of antigen-induced NHR and eosinophil infiltration in the nasal mucosa was elicited by ETS exposure in both OVA-immunized and Th2 cell-transferred mice, whereas nasal neutrophil accumulation was rather enhanced. CSE and nicotine dose-dependently suppressed the proliferation and IL-4 production of Th2 cells, though the effect of nicotine on proliferation was relatively weak. Conclusions: Regardless of various harmful effects, ETS inhibits allergic nasal inflammaiton, probably via the down-regulation of Th2 cell responses by nicotine.