We have previously demonstrated that intranasal administration of ambient ultrafine particles (UFP) acts as an adjuvant for primary allergic sensitization to ovalbumin (OVA) in Balb/c mice. It is important to find out whether inhaled UFP exert the same effect on the secondary immune response as a way of explaining asthma flares in alreadysensitized individuals due to traffic exposure near a freeway. The objective of this study is to determine whether inhalation exposure to ambient UFP near an urban freeway could enhance the secondary immune response to OVA in already-sensitized mice. Prior OVAsensitized animals were exposed to concentrated ambient UFP at the time of secondary OVA challenge in our mobile animal laboratory in Los Angeles. OVA-specific antibody production, airway morphometry, allergic airway inflammation, cytokine gene expression, and oxidative stress marker were assessed. As few as five ambient UFP exposures were sufficient to promote the OVA recall immune response, including generating allergic airway inflammation in smaller and more distal airways compared with the adjuvant effect of intranasally instilled UFP on the primary immune response. The secondary immune response was characterized by the T helper 2 and IL-17 cytokine gene expression in the lung. In summary, our results demonstrated that inhalation of prooxidative ambient UFP could effectively boost the secondary immune response to an experimental allergen, indicating that vehicular traffic exposure could exacerbate allergic inflammation in already-sensitized subjects. allergic inflammation; oxidative stress; distal lung AMBIENT PARTICULATE MATTER (PM) exposure is a contributing factor to increased respiratory morbidity and mortality in an urban environment (37,48,51). Epidemiological studies have demonstrated that increased asthma prevalence, including the number of patients diagnosed with the disease as well as asthma-related hospital visits, is closely associated with PM levels in the ambient air, the regional motor vehicle traffic density, and residential proximity to freeways (21,47,52,53). Several mechanisms have been proposed to explain PM effects in asthma (44). While acute asthma flares in response to vehicle emission may be caused by an exacerbation of existing airway inflammation or airway hyperreactivity, the possibility also needs to be entertained that the increase in allergic inflammation could originate at the level of boosting of the secondary immune response to common environmental allergens in already-sensitized people (11-13, 30, 45). This would be a logical extension of the idea that ambient PM or diesel exhaust particle (DEP) exposure acts as an adjuvant that can lead to a de novo priming of the immune response to common environmental or experimental allergen (11-13, 30, 36, 45). We have recently confirmed that intranasal instillation of ambient ultrafine particles (UFP) derived from vehicular emissions close to a major Los Angeles freeway is capable of generating a new immune response to ovalbumin (OVA) in Balb/c mi...