Fine particles and Japanese cedar pollinosis

摘要

In experiment 1, the adjuvant effects of various fine particles (Kanto loam dust, fly ash, carbon black, diesel exhaust particles, and aluminum hydroxide) on IgE antibody production in female BDF mice were examined by the intranasal administration of both Japanese cedar pollen and each particle. The results of the experiment 1 suggested the nature of the particles and/or their size may not be related to enhancement of IgE antibody production in mice. However, IgE antibody production seemed to occur earlier in mice treated with particles than in mice immunized with pollen alone. In experiment 2, 60 mice in each group were exposed to diesel exhaust (DE group: particles, 3.24 mg/m~3; NO_2, 1.0 ppm), diesel exhaust without particles (DEG group: particles, 0.01 mg/m~3; NO_2, 1.1 ppm), Kanto loam dust (KLD group: particles, 3.29 mg/m~3; NO_2, 0.01 ppm) or clean air (pollen group) for 16 h/d, 5 d/wk for 24 wk, along with exposure to around 550,000 grains of Japanese cedar pollen per cubic meter for 16 h/d, 2 d/wk for 24 wk. The results of the experiment 2 suggested air pollutants (DE, DEG, and KLD) seemed to enhance the production of IgE antibody in mice, however, the adjuvant activities of these pollutants on the production of IgE antibody in mice were almost the same. Furthermore, in the early phase of exposure in which sensitization occurred by exposure to pollen, the particles and gas components are considered to have exhibited different accelerating mechanisms as follows; (1) particles accelerated production of IgE antibodies in mice through the activations of T-lymphocytes, (2) the gas components exhibited almost no action on T-Iymphocytes, but directly induced disorders of the cytokine network and accelerated production of IgE antibody in mice.