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

• Published in: Archives of environmental health Vol. 52; no. 1; pp. 18 - 25
• Main Authors: Gong, Henry, Shamoo, Deborah A., Anderson, Karen R., Linn, William S.
• Format: Journal Article
• Language: English
• Published: Washington, DC Taylor & Francis Group 01.01.1997; Heldref
• Subjects: Aged; Air; Air Pollutants - adverse effects; Analysis of Variance; Atmosphere Exposure Chambers; Biological and medical sciences; Environmental pollutants toxicology; Exercise; Humans; Lung - drug effects; Lung Diseases, Obstructive - physiopathology; Male; Medical sciences; Middle Aged; Oxidants, Photochemical - adverse effects; Oxygen - blood; Ozone - adverse effects; Respiratory Function Tests; Surveys and Questionnaires; Toxicology; California; United States; North America; America; Human; Lung disease; Spirometry; Urban environment; Respiratory disease; Toxicity; Ozone; Long term; Chronic; High atmospheric pollution episode; Risk factor; Bronchus disease; Air pollution; Obstructive pulmonary disease; Emphysema; Elderly
• ISSN: 0003-9896
• DOI: 10.1080/00039899709603795

We tested responses to ozone (O 3 ) 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 O 3 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 O 3 exposures, group mean symptom intensity and specific airway resistance (SRaw) increased, whereas forced expiratory performance decreased. The healthy subgroup's mean arterial oxygen saturation (SaO 2 ) rose slightly, and the COPD subgroup's mean SaO 2 declined slightly, during exercise. Group mean forced expiratory volume in 1 s (FEV 1.0 ) declined significantly in O 3 exposures, compared with controls (p =.01). Mean excess FEV 1.0 loss after 4 h in O 3 (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 O 3 exposures, including exercise effects, averaged 19% in the COPD subgroup, compared with 2% in the healthy subgroup (p < .001). Symptoms, SRaw, and SaO 2 responses, as well as healthy subjects' postexposure bronchial reactivity, differed little between O 3 -exposed and control subjects. We therefore concluded that in older men with or without severe COPD, O 3 causes lung dysfunction under "worst-case" ambient exposure conditions, despite older subjects' comparative unresponsiveness to O 3 . The combined effect of O 3 and exercise on lung dysfunction is markedly greater with COPD. It is still unclear whether COPD causes an increased response to O 3 per se.