Short-Term Exposure to Diesel Exhaust Induces Nasal Mucosal Hyperresponsiveness to Histamine in Guinea Pigs

Abstract

The increasing prevalence of allergic rhinitis in many countries is becoming a social problem. It is important to determine whether air pollutants are related to the increase in the prevalence rate of allergic rhinitis or not. 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. A previous study revealed that diesel exhaust particulates are potent in augmenting increases in nasal congestion and nasal secretion induced by histamine (T. Kobayashi and T. Ito, 1995, Fundam. Appl. Toxicol. 27,195-202). In the present study, using a rhinitis model of guinea pigs, we investigated whether short-term (3-hr) exposure to diesel exhaust induces nasal mucosal hyperresponsiveness to histamine. Guinea pigs of each group were exposed to filtered air or to a low or high concentration of diesel exhaust (1 and 3.2 mg/m 3 particulates in diluted diesel exhaust, respectively) for 3 hr. After diesel exhaust exposure, sneezing frequency, nasal secretion from the nostril, and intranasal airway resistance induced by histamine were measured as indices of sneezing response, rhinorrhea, and nasal congestion, respectively. Short-term exposure to a low or high concentration of diesel exhaust itself did not induce sneezing, nasal secretion, or nasal congestion. However, short-term exposure to a high concentration of diesel exhaust augmented sneezing and nasal secretion, but not nasal congestion, induced by histamine. In conclusion, short-term exposure to diesel exhaust potently induces nasal mucosal hyperresponsiveness. C 1997Socfc(jrofTajdco4ogy.The recent increase in the prevalence of allergic rhinitis (Kaneko et al, 1980;Crawford and Cohen, 1985;Aberg, 1989;Barbee et al, 1991;Lundback et al, 1992) in many countries is becoming an increasingly important social prob-' To whom correspondence and reprint requests should be addressed. Fax: 81-298-50-2439. lem. A positive relationship between the prevalence rate of allergic rhinitis and concentrations of atmospheric pollutants (Kaneko et al, 1980;Ishizaki et al, 1987) has been suggested from epidemiological studies. Therefore, it is important to clarify whether diesel exhaust (DE) could be related to the increase in the prevalence rate of allergic rhinitis. From this point of view, it is necessary to elucidate whether exposure to DE enhances IgE production and whether exposure to diesel exhaust particulates (DEP) causes nasal mucosal hyperresponsiveness to chemical mediators released by antigen-antibody reactions. It has been reported that administration of DEP or exposure to DE enhances IgE antibody production in mice (Muranaka et al, 1986;Takafuji et al, 1987;Fujimaki et al, 1994) and in humans (Diaz-Sanchez etal, 1994; Takenaka etal, 1995). In nasal hyperresponsive animals, increases in nasal airway resistance, nasal secretion, and sneezing elicited by major mediators released during an allergic attack were induced by the lowering ...