Responses of Older Men with and without Chronic Obstructive Pulmonary Disease to Prolonged Ozone Exposure

Abstract

We tested responses to ozone (O₃) under simulated “worst-case” ambient exposure conditions. Subjects included 9 men who had severe chronic obstructive pulmonary disease (COPD) with subnormal carbon monoxide diffusing capacity (i.e., an emphysemic component) and 10 age-matched healthy men. Each subject was exposed to 0.24 ppm O₃ and to clean air (control) in an environmentally controlled chamber at 24 °C and 40% relative humidity. Exposures were randomized, they occurred 1 wk apart, and they lasted 4 h. During each half-hour interval, light exercise occurred (i.e., average ventilation 20 l/min) for 15 min. During both control and O₃ exposures, group mean symptom intensity and specific airway resistance (SRaw) increased, whereas forced expiratory performance decreased. The healthy subgroup's mean arterial oxygen saturation (SaO₂) rose slightly, and the COPD subgroup's mean SaO₂ declined slightly, during exercise. Group mean forced expiratory volume in 1 s (FEV_1.0) declined significantly in O₃ exposures, compared with controls (p =.01). Mean excess FEV_1.0 loss after 4 h in O₃ (relative to control) was 8% of the preexposure value in the COPD subgroup, compared with 3% in the healthy subgroup (p > .05 [nonsignificant]). Overall FEV_1.0 loss during O₃ exposures, including exercise effects, averaged 19% in the COPD subgroup, compared with 2% in the healthy subgroup (p < .001). Symptoms, SRaw, and SaO₂ responses, as well as healthy subjects' postexposure bronchial reactivity, differed little between O₃-exposed and control subjects. We therefore concluded that in older men with or without severe COPD, O₃ causes lung dysfunction under “worst-case” ambient exposure conditions, despite older subjects' comparative unresponsiveness to O₃. The combined effect of O₃ and exercise on lung dysfunction is markedly greater with COPD. It is still unclear whether COPD causes an increased response to O₃ per se.