Abstract

Although epidemiologic evidence suggests that patients with heart and lung disease are more vulnerable to the acute toxic effects of photochemical air pollution, no laboratory studies have been reported in patients with coronary heart disease. In the present investigation, six male volunteers, ages 46 to 64 years, with clinically documented coronary heart disease and a well-defined symptomatic angina pectoris threshold, served as subjects. Each patient was exposed on three 40-minute occasions to either filtered air or ozone at concentrations of 0.20 or 0.30 parts per million (ppm), while walking on a treadmill at workloads simulating their regularly prescribed exercise training regimen. Results of standard pulmonary function tests and periodic observations of exercise ventilation, respiratory metabolism, electrocardiographic changes, hemodynamic response, and clinical signs and symptoms were recorded. Analysis of variance revealed that none of the patients' physiologic responses to ozone exposure were statistically significant. Furthermore, neither onset of angina pain or ischemic changes were related to ozone exposure in a dose-dependent fashion. Hence, the patients not only failed to exhibit any unexpected cardiovascular strain while exposed to ozone during exercise, but also evidenced no significant pulmonary function impairment or exercise ventilatory pattern alteration, as has been observed in clinically normal subjects exercising at similar ozone concentration levels. This apparent incongruity may be due to the fact that acute ozone toxicity is more closely related to the total amount of ozone inhaled, which is a function of pulmonary ventilation volume and exposure time, as well as ozone concentration. In the patients with angina, symptom-limited exercise tolerance resulted in a lower total amount of ozone inhaled than that observed to effect ozone toxicity in clinicially normal subjects who exercised at greater intensities and for longer durations. Patients with angina appear to be no more susceptible to ozone toxicity than are clinically normal subjects at the effective doses imposed. However, had the patients exercised longer, they might well have evidenced pulmonary function impairment and/or cardiovascular strain. Hence, caution is advised in generalizing these observations to other conditions and patient groups.

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