The adjuvant effects of various fine particles [Kanto loam dust, fly ash, carbon black, diesel exhaust particles (DEP), and aluminum hydroxide (alum)] on immunoglobulin E (IgE) antibody production in female BDF1 mice were examined. In experiment 1, animals both received 25 micrograms of each particle intranasally and were exposed to aerosolized Japanese cedar pollen allergens (JCPA) for 30 min/d at 1-wk intervals for the first 8 wk. This was followed by exposure for 30 min every 3 wk for the next 9 wk. As parameters of allergic rhinitis, measurements were made of JCPA-specific IgE and IgG antibody titers, the protein-adsorbing capacity of each type of particle, and nasal rubbing movements. The increases in anti-JCPA IgE and IgG antibody production in mice treated with aerosolized JCPA plus respective particles were significantly greater than that found with aerosolized JCPA alone. This was associated with no marked differences in the other allergic rhinitis parameters. In experiment 2, after the administration of particles as in experiment 1, about 160,000 grains of Japanese cedar pollen (JCP, native dry pollen) were dropped onto the tip of the nose of mice twice a week for 16 wk. Six weeks after the first immunization, the anti-JCPA IgE antibody titers of groups treated with the respective particles were greater than 1:20, whereas those of mice treated with JCP alone were 1:10. No significant differences in the anti-JCPA IgE and IgG antibody productions, nasal rubbing counts, or histopathological changes were observed after 18 wk. These results suggested the nature of the particles, their capacity to adsorb antigens, and/or their size may not be related to enhancement of IgG antibody production nor symptoms of allergic rhinitis. However, IgE antibody production seemed to occur earlier in mice treated with particles than in mice immunized with allergens alone.
One group of male, pathogen-free, Fischer 344 rats was exposed to about 17-fold diluted exhaust generated by an M85 methanol-fueled engine (methanol with 15% gasoline) without catalyst for 8 h, and then the rates of recovery from the resulting increased levels of plasma formaldehyde and carboxyhemoglobin in their erythrocytes were measured. The carboxyhemoglobin level in the erythrocytes was restored within 4 h, whereas the plasma formaldehyde level was still elevated after 4 h but was restored to the normal level within 8 h. No methanol or formic acid was detected in the plasma. Another group of rats was exposed to the same dilution of exhaust for 8 h/d for 7 d, and then the recovery from histopathological damage of the nasal cavity and lungs was also examined. Hyperplasia/squamous metaplasia and erosion of the respiratory epithelium lining the nasoturbinate, maxilloturbinate, or nasal septum, and infiltration of neutrophils into the submucosa at level 1 (level of the posterior edge of the upper incisor teeth) were observed immediately after the exposure period. Lesions of the respiratory epithelium at level 2 (incisive papilla) were less than those at level 1. Slight lesions at levels 1 or 2 were still noticed 1 wk after exposure, but not 4 wk after exposure. Just after exposure, decreases of Clara cells in the terminal bronchiolus and of cilia in the bronchial/bronchiolar epithelium were also observed. Moreover, focal hypertrophy of alveolar walls and increase of macrophages were observed in parts adjacent to respiratory bronchiolus. One week after the exposure period, these changes were no longer seen. These results indicate that changes in the blood and in the nasal cavity and lungs caused by methanol-fueled engine exhaust are reversible. However, complete recovery from damage of the nasal cavity caused by 7-d exposure to the exhaust takes 4 wk, and recovery from elevated plasma formaldehyde and erythrocyte carboxyhemoglobin levels caused by a single 8-h exposure takes 4-8 h.
Fischer 344 rats were exposed to three concentrations of exhaust generated by an M85 methanol-fueled engine (methanol with 15% gasoline) without catalyst for 8 h/d, 7 d/wk for 7, 14, 21, or 28 d. Concentration- and time-dependent yellowing of the fur was prominent in all treated groups. Concentration-dependent increases in the erythrocyte count, hematocrit, hemoglobin concentration, formaldehyde in plasma, and carboxyhemoglobin in the erythrocytes, and decrease in serum alkaline phosphatase activity were seen after all exposure periods. Histopathologically, lesions were found in the nasal cavity and lungs after 7 d of exposure. Squamous metaplasia of the respiratory epithelium of level 1 (level of the posterior edge of the upper incisor teeth) lining of the nasoturbinate and/or maxilloturbinate and infiltration of neutrophils into the submucosa, and decreases of Clara cells in the terminal bronchiolus and of cilia in the bronchiolar epithelium, were observed in the high-concentration group (carbon monoxide, 94 ppm; formaldehyde, 6.9 ppm; methanol, 17.9 ppm; nitrogen oxides, 52.7 ppm; nitrogen dioxide, 10.6 ppm). The histopathological extents of several lesions increased slightly with the exposure time. Slight squamous metaplasia and hyperplasia of the respiratory epithelium at level 1 were also observed in the medium-concentration group (one in three of the high-concentration group). No histopathological changes were found in the olfactory epithelium of the nasal cavity. In the low-concentration group (one in nine of the high-concentration group), no marked histopathological changes in these organs were observed. These results may suggest that the lesions observed in the nasal cavity of rats exposed to methanol-fueled engine exhaust were mainly caused by formaldehyde, although other components in the exhaust also may have affected nasal cavity and/or lungs to less extent.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.