Diesel exhaust particulates induce nasal mucosal hyperresponsiveness to inhaled histamine aerosol.

The prevalence of allergic rhinitis is increasing in many countries. It has been reported that the prevalence rate of allergic rhinitis caused by pollens in air-polluted areas are higher than than in nonpolluted areas. Therefore, it is important to determine whether air pollutants are related to the increase in the prevalence rate of allergic rhinitis. In this respect, it is necessary to elucidate whether exposure to air pollutants affects the nasal mucosa and causes nasal mucosal hyperresponsiveness to chemical mediators released by antigen-antibody reactions. In the present study using guinea pigs, we investigated effects of diesel exhaust particulates on (1) nasal airway resistance, (2) increases in nasal airway resistance and secretion induced by histamine aerosol, and (3) vascular permeability and the increase in vascular permeability is an important factor involved in increased nasal airway resistance and secretion. Intranasal pressure and nasal secretion from the nostril were measured as markers of nasal airway resistance and exocrine activity of the nasal mucosa, respectively. A 30-min administration of a suspension of diesel exhaust particulates into the nasal cavities caused a significant increase in intranasal pressure. The administration also augmented an increase in intranasal pressure and nasal secretion induced by histamine aerosol. In dorsal skin, diesel exhaust particulates increased vascular permeability. Diesel exhaust particulates also augmented vascular permeability are potent by histamine. These properties of diesel exhaust particulates are likely derived in part from the augmentation vascular permeability by these particulates.