Patients with atherosclerotic cardiovascular disease may be adversely affected by the presence of carboxyhemoglobin, even at low concentrations. We investigated the effects of carbon monoxide exposure on myocardial ischemia during exercise in 63 men with documented coronary artery disease. On each test day, subjects performed two symptom-limited incremental exercise tests on a treadmill; the tests were separated by a recovery period and 50 to 70 minutes of exposure to either room air or air containing one of two concentrations of carbon monoxide (117 +/- 4.4 ppm or 253 +/- 6.1 ppm). The order of exposure was assigned randomly. On each occasion, neither the subjects nor the study personnel knew whether the subjects had been exposed to room air or to one of the concentrations of carbon monoxide. Exposure to room air resulted in a mean carboxyhemoglobin level of 0.6 percent, exposure to the lower level of carbon monoxide resulted in a carboxyhemoglobin level of 2.0 percent, and exposure to the higher level of carbon monoxide resulted in a level of 3.9 percent. An effect of carbon monoxide on myocardial ischemia was demonstrated objectively by electrocardiographic changes during exercise. We observed a decrease of 5.1 percent (90 percent confidence interval, 1.5 to 8.7 percent; P = 0.02) and a decrease of 12.1 percent (90 percent confidence interval, 9.0 to 15.3 percent; P less than or equal to 0.0001) in the length of time to a threshold ischemic ST-segment change (ST end point) after carbon monoxide exposures that produced carboxyhemoglobin levels of 2.0 percent and 3.9 percent, respectively. The length of time to the onset of angina decreased by 4.2 percent (90 percent confidence interval, 0.7 to 7.9 percent; P = 0.054) at the 2.0 percent carboxyhemoglobin level and by 7.1 percent (90 percent confidence interval, 3.1 to 10.9 percent; P = 0.004) at the 3.9 percent carboxyhemoglobin level. Significant dose-response relations were found in both the change in the length of time to the ST end point (P less than or equal to 0.0001) and the change in the length of time to the onset of angina (P = 0.02). We conclude that low levels of carboxyhemoglobin exacerbate myocardial ischemia during graded exercise in subjects with coronary artery disease.

Statistically significant changes (P less than .05) were observed in erythrocytes (RBC) and sera of young adult human males following a single short-term exposure to 0.50 ppm ozone (O3) for 2 3/4 hours. The RBC membrane fragility, glucose-6-phosphate dehydrogenase (G-6-PDH) and lactate dehydrogenase (LDH) enzyme activities were increased, while RBC acetylcholinesterase (AcChase) activity and reduced glutathione (GSH) levels were decreased. The RBC glutathione reductase (GSSRase) activities were not significantly altered. Serum GSSRase activity, however, was significantly decreased while serum vitamin E, and lipid peroxidation levels were significantly increased. These alterations tend to disappear gradually, but were still detectable two weeks following exposure.

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To investigate whether adaptation which modifies some acute effects of ozone (O3) exposure can develop in humans, six male volunteers with respiratory hyperreactivity were exposed in a controlled environment chamber to 0.5 ppm O3 2h/day for 4 successive days under conditions stimulating ambient pollution exposures. One subject showed little measurable response, while five showed function decrement on exposure days 1-3 which was largely reversed by day 4. Symptom responses generally paralleled the physiological responses. These results suggest that at least some humans adapt to O3 exposure at concentrations occurring in severe community air pollution episodes, to the extent that obvious acute respiratory effects are prevented. Other adverse effects of O3 may not be prevented by this adaptation.

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To help assess respiratory health risks from sulfur dioxide (SO2) air pollution, we studied 24 normal, 21 atopic, 16 minimal/mild asthmatic, and 24 moderate/severe, medication-dependent asthmatic subjects classified according to history, lung function, allergy skin tests, serum IgE level, and airway reactivity to methacholine. All were exposed in a chamber (21 degrees C, 50% humidity) to 0.0, 0.2, 0.4, and 0.6 ppm SO2 in random order at 1-wk intervals; then exposures were repeated to test consistency of response. The 1-h exposures included three 10-min exercise periods (ventilation approximately 40 L/min). Physiologic response was measured early (approximately 15 min) and late (approximately 55 min) in exposure. Symptoms were evaluated during exposure and for 1 wk afterward. Normal and most atopic subjects showed little response at these SO2 levels. A few atopic subjects and many asthmatics developed bronchoconstriction and respiratory symptoms, but most were able to maintain their exercise. Effects were not markedly different between early and late measurements, nor between the first and second round of studies; however, late and second-round responses appeared slightly more favorable. No statistically significant effect of SO2 on symptoms was found 1 day or 1 wk after exposure. Minimal/mild asthmatics showed, on the average, slight responses at 0.0 ppm (attributable to exercise) and increasing responses at increasing SO2 concentrations. Moderate/severe asthmatics reacted more at 0.0 ppm, but their increments in response with increasing SO2 concentration were roughly similar to those of minimal/mild asthmatics. Thus, responses to SO2 per se were not strongly dependent on clinical severity of asthma, nor on SO2 exposure history during previous weeks.

To study the respiratory effects of nitrogen dioxide (NO2) at ambient concentrations, we exposed 31 asthmatic volunteers to purified air (control) and to 0.2 ppm NO2 for 2-h periods with light intermittent exercise. Bronchial reactivity (loss of forced expiratory performance in response to graded doses of methacholine chloride aerosol) was determined postexposure, using a newly developed apparatus that allowed accurate quantitation of methacholine dose. Forced expiratory performance, total respiratory resistance, and symptoms were also recorded immediately pre- and postexposure (prior to methacholine challenges). No significant direct effect of NO2 exposure on forced expiratory function or total respiratory resistance was observed. Symptoms showed a small significant (p less than 0.05) excess in purified air relative to NO2 exposures. Individual responses to methacholine varied greatly. About two-thirds of the subjects showed greater response after NO2 than after purified air, but the mean excess response was small. Mean changes attained significance in some but not all applicable statistical tests. Thus we cannot conclude unequivocally that NO2 exposure increased bronchial reactivity in this group, although there was some tendency in that direction.