Abstract

Increased incidence of respiratory infections has been mentioned in air polluted area. The incidence rates of pharygolaryngitis and common cold + bronchitis have been increased and are much higher in the air polluted area in Yokkaichi than control nonpolluted area. However, the level of SO2 in this area has decreased and averaged 0.03 ppm in 1972 compared with 0.08 ppm in 1964. The prevalence rates of rhinitis and tonsillitis of school children was significantly higher in this area in 1972.A distinct increase in DNA labeling index of the epithelial cells of the trachea was observed at the first week of exposure period to SO2 in mice. The labeling index returned to preexposure level after the second week of the exposure. In a period from the third week to 15th, the tracheal epithelium was replaced by tall ciliated columnar one which contained a large number of PAS positive cells. The mice exposed to SO2 for 4 weeks were inoculated influenza virus PR8 intranasally. The inflammatory changes in the nasal cavity in the SO2 + virus group were severer and spread much rapidly than virus control. In addition, HI titer developed much rapidly and reached higher level than virus control.The mean concentration of parotid salivary IgA of the normal school children in the polluted area was not significantly different than that of nonpolluted area. But the variance was significantly different.Individual value of serum IgG of the mice exposed to NO2 from intrauterine to the 4th week pcstpartum varied considerably compared with consistent value of control.The incresed severity of virus infection in SO2 mice appeared to result from interaction between effects of SO2 and infection. This interaction could increase the severity of infection. Although the manner of this interaction still needs to be answered, it should be considered that air pollutants may affect the immune response.

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