One of the most common outdoor air pollutants is Ozone (O3) that forms in the Earth's atmosphere, both naturally and by reactions of man-made air pollutants. A growing set of data have demonstrated a close correlation between exposure to different air pollutants and multiple adverse effects in different organs and tissues, such as lung, cardiovascular system, skin and central nervous system (CNS). We examined in two species of male mice, whether O3 could alters olfactory behavior and cellular properties in the olfactory system. For this purpose, mice were exposed to O3 at a concentration found in highly polluted city air [0.8 ppm], and the behavior evoked by social and non-social odors was assessed whit habituation/dishabituation tests. Furthermore, the electrophysiological responses of dopaminergic olfactory bulb neurons were also observed. The results indicate that O3 differentially compromises olfactory sensitivity to odors: it reduces responses to social and non-social odors in Swiss Webster mice, while this effect was observed in C57BL/6J mice only for some non-social odors. Furthermore, it was found that exposition to O3 reduced the rate of spontaneous spike firing in periglomerular dopaminergic cells (PG-DA) of the olfactory bulb. Because this effect could reflect changes in excitability and/or synaptic inputs, the ability of O3 to alter PG-DA spontaneous activity was also tested together with cell membrane resistance, membrane potential, rheobase and chronaxia. Taken together, our data suggests the ability of ozone to affect olfactory perception.