The acute effects of 0.2 ppm ozone in patients with chronic obstructive pulmonary disease.

Epidemiologic data suggest that patients with chronic obstructive pulmonary disease (COPD) might be more sensitive than normal persons to the respiratory effects of oxidant pollutant exposure. Our study was designed to determine the response of patients with COPD to ozone. Thirteen white men with nonreversible airways obstruction (mean FEV1/FVC, 58%), of whom 8 were current smokers, were randomly exposed for 2 h to air and to 0.2 ppm ozone on 2 consecutive days using a single-blind crossover design. During either exposure, subjects exercised for 7.5 min every 30 min. Measures of respiratory mechanics obtained pre-exposure and postexposure were not significantly affected by either exposure. Similarly, ventilation and gas exchange measured during exercise showed no difference either between exercise periods or exposure days. However, arterial O2 saturation (SaO2), measured by ear oximetry during the final exercise period each day was lower (94.8%) at the end of O2 exposure, than SaO2 obtained at the end of air exposure (95.3%), the difference (0.48%) being significant (p = 0.008). Because normal subjects undergoing comparable exposures show a threshold for respiratory mechanical effects at about 0.3 ppm ozone, our data suggest that mild to moderate COPD is not associated with increased sensitivity to low ozone concentrations. However, our data do not rule out the possibility that the response of such subjects might be exaggerated at higher ozone concentrations. The consistent (in 11 of 13 subjects), though small, decrease in SaO2 may indicate that indexes of ventilation/perfusion distribution might be more sensitive measures of ozone effect in this compromised patient group than are conventional respiratory mechanics measures.

Responses of subjects with chronic obstructive pulmonary disease after exposures to 0.3 ppm ozone.

We previously reported (American Review of Respiratory Disease 1982; 125:664-669) that the respiratory mechanics of intermittently exercising persons with chronic obstructive pulmonary disease (COPD) were unaffected by a 2-h exposure to 0.2 ppm ozone. Employing a single-blind, cross-over design protocol, 13 white men with nonreversible COPD (9 current smokers; mean FEV1/FVC, 56%) were randomly exposed on 2 consecutive days for 2 h to air and 0.3 ppm ozone. During exposures, subjects exercised (minute ventilation, 26.4 +/- 3.0 L/min) for 7.5 min every 30 min; ventilation and gas exchange measured during exercise showed no difference between exposure days. Pulmonary function tests (spirometry, body plethysmography) obtained before and after exposures were unchanged on the air day. On the ozone day the mean airway resistance and specific airway resistance showed the largest (25 and 22%) changes (p = 0.086 and 0.058, respectively). Arterial oxygen saturation (SaO2) obtained in 8 subjects during the last exercise interval showed a mean decrement of 0.95% on the ozone exposure day; this change did not attain significance (p = 0.074). Nevertheless, arterial oxygen desaturation may be a true consequence of low-level ozone exposure in this compromised patient group. As normal subjects undergoing exposures to ozone with slightly higher exercise intensities show a threshold for changes in their respiratory mechanics at approximately 0.3 ppm, our data indicate that persons with COPD are not unduly sensitive to the effects of low-level ozone exposure.

Medusa cells: cytostructure and cytochemistry of amoeboid eosinophils with pseudopod-like processes.

Eosinophils having one or more pseudopod-like processes of various lengths are observed in bone marrow, peripheral blood, sputum, nasal smears, and in other exfoliative cytology and tissue specimens after fixation and staining for histochemical study; they are called medusa cells. Although the conformations and lengths of the processes vary, they resemble protozoal pseudopodia. The form which first called our attention to these cells is a conical determinate projection that tapers to a fine tip, much like a protozoal axopod. A basal specialization in the form of a vesicle or thickening may be frequently observed where the process protrudes from, or appears attached to, the cell body. The processes of these eosinophil variants appear morphologically specialized to interact with other cellular elements of the blood and are occasionally seen in contact with, or engulfing, erythrocytes, platelets or other leukocytes. Two hydroperoxidases have been elucidated in eosinophils and medusa cells by virtue of different substrate specificities, subcellular localizations and inhibitor sensitivities. One of these hydroperoxidases is shown by 3,3'-diaminobenzidine, is cyanide resistant, and is never observed in granules or rods in the medusa cell processes; it is frequently polarized to the sites of contact of medusa cells with other cellular elements of the blood. The other hydroperoxidase is revealed by p-phenylenediamine-pyrocatechol, is sensitive to cyanide and is frequently observed in granules and rods in medusa cell processes as well as in a population of larger granules in the cell bodies; the granules in the processes appear to be precursors to the rods, which may be related to Charcot-Leyden crystals. The extrusion of medusa cell processes is facilitated by the divalent cations calcium and magnesium and is inhibited by anions which sequester them such as phosphate, EDTA, citrate and oxalate. Medusa cells have been observed in samples from both rodents and humans and can be very prominent when eosinophilia accompanies allergy, parasitosis and malignancy.