Responses of older men with and without chronic obstructive pulmonary disease to prolonged ozone exposure.

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 degrees 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 (FEV1.0) declined significantly in O3 exposures, compared with controls (p approximately .01). Mean excess FEV1.0 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 FEV1.0 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.