CARDIOVASCULAR EFFECTS OF OZONE EXPOSURE IN HUMAN VOLUNTEERS

We hypothesized that ozone (O-3) exposure acutely affects cardiovascul ar hemodynamics in humans and, in particular, in subjects with essenti al hypertension. We studied 10 nonmedicated hypertensive and six healt hy male adults. Each subject, after catheterization of the right heart and a radial artery, was exposed in an environmentally controlled cha mber to filtered air (FA) on one day and to 0.3 ppm O-3 On the followi ng day for 3 h with intermittent exercise. Relative to FA exposure, O- 3 exposure induced no statistically significant changes in cardiac ind ex, ventricular performance, pulmonary artery pressure, pulmonary and systemic vascular resistances, EGG, serum cardiac enzymes, plasma cate cholamines and atrial natriuretic factor, and Sa(O2). The overall resu lts did not indicate major acute cardiovascular effects of O-3 in eith er the hypertensive or the control subjects. However, mean preexposure to postexposure changes were significantly (p < 0.02) larger with O-3 than with FA for rate-pressure product (1,353 beats/min/mm Hg) and fo r heart rate (8 beats/min); these responses were not significantly dif ferent between the hypertensive and the control subjects. Significant O-3 effects were also observed for mean FEV1 (-6%), and AaPO(2) (> 10 mm Hg increase), which were not significantly different between the tw o groups. These results suggest that O-3 exposure can increase myocard ial work and impair pulmonary gas exchange to a degree that might be c linically important in persons with significant preexisting cardiovasc ular impairment, with or without concomitant lung disease.