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The nasal irritation produced by DMEA, TMA and TEA was studied using male Swiss OF1mice. Groups of six mice each were exposed to concentrationsof 84 -216, 17 -70 and 77 -305 ppm in air respectively for 15 min to determine the concentration at which the respiratory rate was decreased by 50% (RD50) (Gagnaire et al., 1989). The head of each mouse was isolated in an inhalation chamber, and the breathing frequency was measured with a pressure transducer before and during the exposure period. The RD50for DMEA, TMA and TEA were 161, 61 and 156 ppm, respectively and maximal effects were observed within 0.5 to 1 min.

The authors also exposed groups of mice to 251 to 610 ppm of DMEA via tracheal cannulation for 120 min. The concentration that caused a 50% decrease in respiratory rate via this route (RD50TC) was 691 ppm.

Four male Ssc:CF-1 mice per group were exposed to tri-n-butylamine for 30 minutes and the concentration which reduces the respiratory rate by 50 % was deter- mined (RD50). To determine the sensory irritation of the upper respiratory tract (RD50) and irritation of the lungs (tRD50) the animals inhaled the substance via the head and nose, and a tracheal cannula, respectively. Tri-n-butylamine concentrations of more than 95 ml/m3 led to mortality both in animals cannulated and not cannulated; concentrations of 110 ppm were lethal in all animals. The lungs of the animals that died were reduced in size and a reddish grey colour compared with the lungs of the animals not exposed. The tRD50 was determined to be 96 ml/m3 (76–121 ml/m3). The RD50 for sensory irritation could not be determined because the reaction after non-lethal concentrations was not pronounced enough. The authors suggested that the 2-minute reduction in the respiratory rate observed in the beginning after head and nose exposure, the subsequent normalization and then renewed reduction in the respiratory rate were not induced by irritation of the upper respiratory tract but by irritation of the lungs (Nielsen and Yamagiwa 1989).