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Biomedical subjects

R D Buckley

Publications and source records attributed to R D Buckley.

At least 19 recordsLinked to original sources
PubMed1979

Human biochemical response to ozone and vitamin E.

To determine whether vitamin E (dl-alpha-tocopherol) supplementation of the diet provides protection from inhaled oxidants such as ozone (O3) in community air pollution, its effects were studied in healthy adult volunteers, Experimental groups received 800 or 1600 IU of vitamin E for 9 wk or more; control groups received placebos. Double-blind conditions were maintained throughout the study. Biochemical parameters studied included red blood cell fragility; hematocrit and hemoglobin values; red cell glutathione concentration; and the enzymes acetylcholinesterase, glucose-6-phosphate dehydrogenase, and lactic acid dehydrogenase. No significant differences between the responses of the supplemented and placebo groups to a controlled O3 exposure (0.5 ppm for 2 h) were found for any of these parameters. The results indicate that vitamin E supplementation in humans, at the levels employed in this experiment, gives no added protection against blood biochemical effects of O3 in intermittently exercising subjects under exposure conditoins simulating summer ambient air pollution episodes.

Female↗
PubMed1978

Health effects of ozone exposure in asthmatics.

To investigate whether ambient air quality standards for ozone adequately protect high-risk populations, we assessed pulmonary and biochemical responses of 22 asthmatic volunteers to 2-hour controlled exposures to ozone at concentrations approximating 0.2 ppm, with secondary stresses of heat and intermittent exercise. All subjects had physician-diagnosed asthma; clinically, they covered a range from minimal wheezing to persistent marked abnormality in forced expiratory performance. Control experiments included repeated sham exposures (to purified air with no ozone added) as well as brief exposures to the odor of ozone followed by purified air. No meaningful changes in forced expiratory measures, lung volumes, or single-breath N2 indices were found after ozone exposure relative to control. Symptoms, scored semiquantitatively, increased slightly but not significantly with exposure to ozone. Small but significant (P is less than 0.05) group mean blood biochemical changes occurred with exposure to ozone; these included increased glucose-6-phosphate dehydrogenase and lactate dehydrogenase activities, increased erythrocyte fragility, and decreased concentration of reduced glutathione. Hemoglobin concentration and acetylcholinesterase activity decreased with ozone and decreased to a lesser extent in control studies. Concentrations of ozone readily attainable in smog episodes thus appear to be capable of affecting blood biochemistry in at least some asthmatic persons, in the absence of obvious adverse pulmonary responses. Whether the biochemical effects represent harm to health or a normal response to stress remains to be determined.

Acetylcholinesterase↗
PubMed1976

Studies in adaption to ambient oxidant air pollution: effects of ozone exposure in Los Angeles residents vs. new arrivals.

To test the hypothesis that adaptation protecting against acute effects of ambient ozone (O3) exposures develops in Los Angeles residents, human volunteers were exposed to 0.4 ppm O3 under conditions simulating ambient pollution exposures. Blood biochemical, pulmonary physiological, and clinical responses were assessed. Los Angeles residents (N = 6) showed only minimal clinical or physiological response to O3, while new arrivals (N = 9) showed significant losses in pulmonary function and a tendency toward increased symptoms. Most biochemical responses did not differ significantly between residents and new arrivals. These results agree with others in suggesting that exposures to elevated ambient concentrations of O3 produce adaptation in a least some residents of photochemical pollution areas. The underlying mechanisms and long-term consequences of such adaptation are unknown.

Adaptation, Physiological↗
PubMed1975

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.

Acetylcholinesterase↗
PubMed1975

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.

Air Pollutants↗
PubMed1975

Experimental studies on human health effects of air pollutants. III. Two-hour exposure to ozone alone and in combination with other pollutant gases.

Adult male volunteers were exposed to ozone (O3) at 0.25, 0.37, or 0.50 ppm, and to O3 in combination with nitrogen dioxide (NO2) and carbon monoxide (CO), with secondary stresses of heat, intermittent light exercise, and repeated exposure. Few important physiological changes, and only mild symptoms, were found with 0.25 ppm O3, with 0.25 ppm 03 plus 0.30 ppm NO2, or when 30 ppm CO was added to the latter mixture. With 0.37 ppm O3, more symptoms were present and some subjects developed definite decreases in pulmonary function. With 0.50 ppm O3, most subjects had symptoms and about half showed substantial pulmonary function decrement. In reactive subjects exposed on two successive days, changes were usually greater the second day, indicating that effects of successive exposures were cumulative.

Adult↗
PubMed1970

Ozone and vitamin E.

Vitamin E deficiency in rats is associated with a greater susceptibility to lethal levels of ozone. Exposure of rats to sublethal ozone concentrations produces an accelerated decline in serum vitamin E levels. These findings are consistent with the possibility that lipid peroxidation is a mechanism of ozone toxicity.

Aging↗