Jack D. Hackney

Ozone and human blood.

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.

Experimental Studies on Human Health Effects of Air Pollutants: I. Design Considerations

Because of the possible threat to public health posed by photochemical air pollution, a need exists for experimental studies of short-term respiratory effects of air pollutant exposure in humans. Such studies require rigorous control and comprehensive documentation of the experimental air environment and exposure conditions to ensure that results are both reliable and relevant to public health questions. In addition to biochemical, behavioral, and clinical evaluations, comprehensive pulmonary testing is required to assure that effects at different levels of the respiratory tract are detected. An experimental design based on these principles is described. Studies using this design have shown a wide range of sensitivity to the pollutant ozone and important adverse health effects in sensitive individuals under exposure conditions similar to those experienced during ambient pollution episodes.

Comparative respiratory effects of ozone and ambient oxidant pollution exposure during heavy exercise.

Fifty volunteer bicyclists were exposed to purified air containing ozone (O/sub 3/) at controlled concentrations of 0, 0.08, 0.16, 0.24, and 0.32 ppm, and to oxidant polluted ambient air (mean O/sub 3/ concentration 0.15 ppm, mean total particulate concentration 295 ..mu..g/m/sup 3/) in suburban Los Angeles. Exposures (in random order, 14 days apart) involved one hour of heavy continuous exercise (mean minute volume 57 L) plus brief warm up and cool down periods. Significant forced expiratory function decrements and symptom increases occurred in ambient air exposures. In controlled O/sub 3/ exposures, responses were significant at 0.16 ppm and higher; their severity increased with increasing O/sub 3/ concentration. Effects were only partially reversed after one hours rest in purified air. Ambient exposures produced about the same response as O/sub 3/ alone at the same concentration. Thus coexisting pollutants do not appear to enhance the irritancy of O/sub 3/ in typical moderate ambient oxidant pollution episodes. However, O/sub 3/ itself can produce respiratory irritation at concentrations slightly above the health based federal ambient air quality standard of 0.12 ppm O/sub 3/, at high ventilation rates required during heavy exercise.

Controlled exposures of volunteers to respirable carbon and sulfuric acid aerosols

Respirable carbon or fly ash particles are suspected to increase the respiratory toxicity of coexisting acidic air pollutants, by concentrating acid on their surfaces and so delivering it efficiently to the lower respiratory tract. To investigate this issue, we exposed 15 healthy and 15 asthmatic volunteers in a controlled-environment chamber (21 degrees C, 50 percent relative humidity) to four test atmospheres: (i) clean air; (ii) 0.5-microns H2SO4 aerosol at approximately 100 micrograms/m3, generated from water solution; (iii) 0.5-microns carbon aerosol at approximately 250 micrograms/m3, generated from highly pure carbon black with specific surface area comparable to ambient pollution particles; and (iv) carbon as in (iii) plus approximately 100 micrograms/m3 of ultrafine H2SO4 aerosol generated from fuming sulfuric acid. Electron microscopy showed that nearly all acid in (iv) became attached to carbon particle surfaces, and that most particles remained in the sub-micron size range. Exposures were performed double-blind, 1 week apart. They lasted 1 hr each, with alternate 10-min periods of heavy exercise (ventilation approximately 50 L/min) and rest. Subjects gargled citrus juice before exposure to suppress airway ammonia. Lung function and symptoms were measured pre-exposure, after initial exercise, and at end-exposure. Bronchial reactivity to methacholine was measured after exposure. Statistical analyses tested for effects of H2SO4 or carbon, separate or interactive, on health measures. Group data showed no more than small equivocal effects of any exposure on any health measure.(ABSTRACT TRUNCATED AT 250 WORDS)

SYNDROME OF EXTREME OBESITY AND HYPOVENTILATION: STUDIES OF ETIOLOGY

Excerpt The syndrome of extreme obesity, hypoventilation, polycythemia and heart failure has been recognized with increasing frequency since 1955.1-18The most characteristic cardiorespiratory dysfu...

Effects of 0.2 ppm nitrogen dioxide on pulmonary function and response to bronchoprovocation in asthmatics

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.

Effects of ozone exposure in Canadians and Southern Californians

Comparison of published reports on physiological effects of exposure to ozone (O3) suggests that Canadians are more reactive than southern Californians. Responses of subjects and experimental methods were compared in a cooperative investigation of this apparent difference in reactivity. Four Canadians and four Californians were exposed to 0.37 ppm O3 in purified air at 21 degrees C and 50% relative humidity for 2 hours with intermittent light exercise. Exposures to purified air alone served as controls. Responses of subjects were similar to those observed previously: Canadians on the average showed greater clinical and physiological reactivity to exposure than did Californians, who were no more than minimally reactive. Canadians also showed larger increases in erythrocyte fragility following exposure. No methodological differences sufficient to explain different results of previous studies were found. Although other possible explanations have not been ruled out entirely, adaptation of southern Californians to chronic ambient O3 exposure is a rational hypothesis to explain these results.

Effects of Exposure to 4 PPM Nitrogen Dioxide in Healthy and Asthmatic Volunteers

Healthy and asthmatic volunteer subjects (N = 25 and N = 23, respectively) were exposed twice each to purified air (control) and to 4 ppm nitrogen dioxide (NO2) in a controlled-environment chamber. Exposures lasted 75 min, and included 15 min each of light exercise (ventilation rate near 25 L/min) and heavy exercise (near 50 L/min). Compared to control, NO2 exposure produced no statistically significant untoward effects on airway resistance, symptoms, heart rate, skin conductance, or self-reported emotional state in normal or asthmatic subjects. Exercise was associated with significantly (P less than .001) increased airway resistance in both subject groups, although the increase in normals was small. In both groups, systolic blood pressure showed small but significant (P less than .01) decreases with NO2 exposure, compared to control. This effect, if real, may relate to formation of a vasodilating nitrite or nitrate from inhaled NO2. The lack of respiratory response contrasts with previous findings elsewhere; at present, this inconsistency is unexplained.

Mutagenic effects of ozone on human cells exposed in vivo and in vitro based on sister chromatid exchange analysis

Abstract A sister chromatid exchange (SCE) analysis was performed on circulating lymphocytes collected from young human volunteers exposed to 0.5 ppm ozone for 2 hr, an exposure simulating conditions in severe air pollution episodes. SCE analysis was also performed on diploid human fetal lung cells (WI-38) exposed to 0, 0.25, 0.50, 0.75, and 1.00 ppm ozone for 1 hr in vitro . No increase in SCEs over controls was demonstrated in the lymphocyte chromosomes. However, a clear dose-related increase in SCEs was observed in the WI-38 cells exposed in vitro .

Experimental Studies on Human Health Effects of Air Pollutants. IV. Short-Term Physiological and Clinical Effects of Nitrogen Dioxide Exposure

Adult male volunteers were exposed to nitrogen dioxide (NO2) at 1.0 ppm in purified air under conditions simulating ambient photochemical smog exposures (2-hr exposure with intermittent light exercise at 31 degrees C and 35% relative humidity). Sham exposures to purified air alone served as controls. Exposure effects were assessed by pulmonary physiological tests and by a standardized clinical evaluation. No statistically physiological changes attributable to NO2 exposure were found except for a marginal loss in forced vital capacity after exposure on two successive days (1.5% mean decrease, P less than .05). Reported respiratory and other symptoms were slightly increased with exposure as compared to control, but the change was not significant. Short-term toxicity of NO2 at peak ambient concentrations appears to be substantially less than that of ozone in healthy people, but adverse NO2 effects in diseased people or in long-term exposures cannot be ruled out at present.