LONG-TERM EXPOSURE TO OZONE ALTERS PERIPHERAL AND CENTRAL CATECHOLAMINE ACTIVITY IN RATS

In addition to its noxious influence on lung airways, ozone inhalation can induce extrapulmonary neural dysfunctions the mechanisms of which are poorly understood. This study was intended to characterize the ef fects of long-term exposure to ozone (0.5 ppm, 5 days) on catecholamin e activity in rat sympathetic efferents and brain areas of prime impor tance to adaptation to environmental stressors. Catecholamine activity was assessed by estimating the turnover rate of catecholamines and in vivo tyrosine hydroxylase activity in peripheral and central structur es, i.e., heart, lungs, superior cervical ganglia, cerebral cortex, hy pothalamus and striatum, A2 cell group within the nucleus tractus soli tarius (NTS), and locus ceruleus (A6). Ozone inhibited norepinephrine turnover in heart (-48% of the control level) but not in lungs. Ozone failed to modify the tyrosine hydroxylase activity in superior cervica l ganglia, and the catecholamine content in the adrenal glands. In the central nervous system, ozone inhibited tyrosine hydroxylase activity in noradrenergic brainstem cell groups, including the locus ceruleus (-62%) and the caudal A2 subset (-57%). Catecholamine turnover was dec reased by ozone in the cortex (-49%) and striatum (-18%) but not in th e hypothalamus. The data show that ozone can produce marked neural dis turbances in structures involved in the integration of chemosensory in puts, arousal and motor control.