Abstract

Rats of two age groups, of 119 and 163 g mean body weight, were exposed for three and thirty days, respectively, to automobile gases diluted with air. In addition, rabbits, of 1.88 kg mean body weight, were exposed for twenty-four days. The conditions of exposure were kept nearly constant as related to the concentration of CO in the chamber. The following determinations were performed: (1) Body weight measurements as evidence of growth of the animals; (2) The number of alveolar macrophages (AM) in the lung washings; (3) Damage to the integrity of the cytoplasmic membrane of AM; (4) Glucose-6-phosphate dehydrogenase activity (G6PD) in AM; (5) The acid-base balance in the capillary blood of the rabbits. The results of the 30-day exposure show that automobile exhaust gases significantly inhibit the growth of both age groups; with significant body weight losses in the older animals from the 16th day of exposure. The number of AM was elevated in both groups. The activity of G6PD increased in the AM of the younger animals and decreased in the AM of the older as compared with the controls. The number of dead AM was higher in the older than in the younger rats. After the three-day exposure, no significant difference was found in the number of AM washed from the lungs of both exposed groups, compared with the controls. However, G6PD activity and the number of viable AM in the older animals were decreased and the percent of dead phagocytes was significant. The opposite effect was seen in the younger group. Alterations of lung tissue structure in the exposed animals were apparent to the naked eye. Acid-base response showed metabolic and respiratory disturbances as evidenced by the decrease in carbon dioxide tension (PCo2), the rise of hemoglobin by the reduction of pH level and by the base excess (BE). The inhibition of the growth of the rabbits was noted. The intra- and extrapulmonary effect of automobile exhaust gases after inhalation was observed as a complex of disturbances of the fundamental metabolic processes in the organism. The gases affected the cells of lung defence-alveolar macrophages and their biosynthetic activity.

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