This study aimed to: (a) assess whether substance P (SP) acts via neurokinin (NK)-1 and NK-2 receptors to stimulate neurogenic inflammation (indicated by formation of intracellular adhesion molecule (ICAM)-1 expression and oxidative stress) following oil smoke exposure (OSE) in rats; (b) determine if pre-treatment with antioxidants ameliorates the deleterious effects of OSE. Rats were pre-treated with NK-1 receptor antagonist CP-96345, NK-2 receptor antagonist SR-48968, vitamin C or catechins. OSE was for 30-120 mins. Rats were sacrificed 0 to 8h later. Total lung resistance (R_L), airway smooth muscle activity (ASMA), lung ICAM-1 expression, neurogenic plasma extravasation (via India ink, Evans blue dye) and bronchoalveolar lavage fluid SP concentrations and reactive oxygen species formation (via lucigenin and luminal-amplified chemiluminescence, CL) were assessed. Lung histology was performed. SP concentrations increased significantly in non pre-treated rats following OSE in a dose dependent manner. R_L and total ASMA increased over time after OSE. Vitamin C and catechin pre-treatments were associated with significantly reduced lucigenin CL 2 and 4h after OSE. Pre-treatment with catechins significantly reduced luminal CL counts 4 and 8h after OSE. Evans blue levels were significantly reduced following 60 and 120 mins of OSE in catechin and CP-96345 pre-treated rats. ICAM-1 protein expression was significantly decreased in all pre-treatment groups after OSE. Thickening of the alveolar capillary membrane, focal haemorrhaging, interstitial pneumonitis and peribronchiolar inflammation were apparent in OSE lungs. These findings suggest that SP acts via the NK-1 receptor to provoke neurogenic inflammation, oxidative stress and ICAM-1 expression after OSE in rats.