Nasal and pulmonary toxicity of allyl glycidyl ether in mice.

A concentration-dependent expiratory bradypnea, indicative of irritation of the nasal mucosa, occurred during a 15-min oronasal exposure of mice to allyl glycidyl ether (AGE) in the concentration range of 1.9-8.6 ppm. The level of exposure responsible for a 50% decrease in the respiratory rate (RD50) was 5.7 ppm. Non-anaesthetized, tracheally cannulated mice exposed for 120 min to AGE at levels ranging from 105 to 185 ppm showed a concentration-dependent decrease in respiratory rate due to pulmonary toxicity. The level of exposure to AGE which produced a 50% decrease in the respiratory rate of tracheally cannulated mice (RD50TC) was 134 ppm. Mice were subjected to whole body exposure for 4, 9 or 14 days, 6 h/day to 7.1 or 2.5 ppm AGE. The 4-day exposure to 7.1 ppm AGE produced in the nasal cavities of mice lesions consisting of necrosis of the respiratory epithelium and complete erosion of the olfactory epithelium without pulmonary injury. Restorative responses were observed in the nasal cavities of mice exposed for 9 and 14 days to 7.1 ppm AGE. Exposure to 2.5 ppm AGE caused neither nasal nor pulmonary injury. The results indicate that AGE primarily affects the upper airways. They also make it questionable that the occupational standard of 5 ppm assures an adequate margin of protection against AGE-induced nasal effects.