The assumption that ozone is not only a strong oxidant, but also an important inflammatory mediator, is heavily supported by the ample literature on the pulmonary toxicity and biological effects of environmental ozone and by the recent discovery that antibodies, human neutrophils, and inflammatory lesions catalyze the formation of ozone in vivo. We hypothesized that the pulmonary inflammation in asthma involves a vicious circle of ozone production and recruitment of white blood cells, which produce more ozone. Accordingly, we predicted that electron-rich olefins, which are known ozone scavengers, could be used for prophylactic treatment of asthma. In particular, volatile, unsaturated monoterpenes, could saturate the pulmonary membranes and thereby equip the airways with local chemical protection against either exogenous or endogenous ozone. Here we present experimental evidence using a sensitized rat model to support this hypothesis. Examination of the pulmonary function of sensitized rats that inhaled either limonene (unsaturated, ozone scavenger) or eucalyptol (saturated, inert to ozone) showed that limonene inhalation significantly prevents bronchial obstruction while eucalyptol inhalation does not cause any effect. The anti-inflammatory effect of limonene was also evident from pathological parameters, such as diminished peribronchiolar and perivascular inflammatory infiltrates.