Our previous study has shown that diesel exhaust particles (DEP), main constituents in ambient particulate matters (PM), enhance airway hyperresponsivness in a murine model of allergic asthma (Takano et al., 1998). However, it remains unknown which components in DEP are responsible for the enhancement. The present study investigated the effects of repeated pulmonary exposure to DEP components (extracted organic chemicals in DEP; DEP-OC, carbonaceous nuclei of DEP after extraction; washed DEP) on lung physiology in the presence or absence of antigen. ICR mice were divided into six experimental groups. Vehicle, DEP components, ovalbumin (OVA), or DEP components plus OVA was administered intratrachally for 6 weeks. Twenty-four hr after the last instillation, cholinergic lung reactivity was examined. DEP components alone did not induce any facilitation of lung function as compared to vehicle alone. The values of total respiratory system resistance (R), elastance (E), Newtonian resistance (R_n), tissue damping (G), and tissue elastance (H) were higher and the value of compliance (C) was lower in the OVA or the DEP component + OVA groups than in the vehicle group. In particular, the hyperreactivity was most prominent in the washed DEP + OVA group. The values in the DEP-OC + OVA group were not significantly different from those in the OVA group. These data suggest that carboneous component in DEP, rather than organic chemical one, can be attributable to the enhancement of lung hyperresponsiveness in allergic asthma.