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Biomedical subjects

J D Hackney

Publications and source records attributed to J D Hackney.

At least 55 records · Page 3Linked to original sources
PubMed1982

Persistence of adaptation to ozone in volunteers exposed repeatedly for six weeks.

Eleven generally healthy volunteer subjects were exposed daily to ozone at 0.47 ppm in an attempt to develop adaptation, then reexposed weekly to investigate the persistence of adaptation. Responses were assessed in terms of forced expiratory function and symptoms. Most subjects, when exposed 2 h daily for 4 days with intermittent exercise, developed adaptation as seen in previous studies. The adaptation was partly lost with a 4-day interval between successive exposures, and was more or less completely lost with a 7-day interval between exposures. One subject, who may have had a persistent low-grade respiratory infection, never adapted. Two others showed relatively little response in the initial daily exposures, but showed more severe responses at some point during the later weekly exposures. If these results are relevant to ambient oxidant pollution effects, adaptation may be of relatively little importance in a public-health sense, given that it may fail to develop or may be lost quickly in the absence of very frequent exposures.

Adaptation, Physiological↗
PubMed1982

Short-term respiratory effects of 0.12 ppm ozone exposure in volunteers with chronic obstructive pulmonary disease.

Twenty-five volunteers with chronic obstructive pulmonary disease of mild to moderately severe degree underwent 1-h exposures to 0.12 ppm ozone (O2) in purified air with intermittent mild exercise. Their responses were assessed in terms of forced expiratory performance, ear oximetry, and reported symptoms. Control studied consisted of similar exposures to purified air alone. Control studies were separated from O2 exposures by 1 month, and the order was randomized. All studies took place in a controlled-environment chamber, and were preceded by approximately 1 h of rest in a purified-air environment. No significant disturbances in forced expiratory performance or symptoms attributable to O2 exposure were found. A slight but significant tendency to decreased arterial hemoglobin oxygen saturation (SaO2) during exercise in O2 was observed. The decrement in SaO2 with O2 relative to clean air (mean 1.3%) was near the limit of resolution of the ear oximeter test and was detected by signal averaging, thus its physiologic or clinical significance is uncertain.

Adult↗
PubMed1982

Laboratory evaluation of a disposable half-face mask for protection against ozone.

The ability of disposable half-face masks containing activated carbon to protect against inhaled ozone (O2) (nominal experimental exposure concentration, 0.5 ppm) was tested using a specially designed mechanical device simulating the breathing of a moderately exercising human, and then tested further by 18 volunteers exposed to O2 in a controlled-environment chamber for 2 h with intermittent mild exercise. As a control experiment, masks containing no activated carbon were tested similarly. On the mechanical device, carbon-impregnated masks removed 96 to 98% of ambient O3, whereas masks with no carbon removed 32 to 37%. Volunteers experienced typical respiratory irritation and temporary loss of forced expiratory function during O3 exposures when they wore the masks without carbon. These untoward effects were substantially reduced when masks containing carbon were worn. Volunteers tolerated the half-masks reasonably well, although some complained of discomfort. Disposable masks may be of significant benefit in protecting sensitive people from O2 exposures that they cannot readily avoid by other means.

Adult↗
PubMed1981

Exposures of human volunteers to a controlled atmospheric mixture of ozone, sulfur dioxide and sulfuric acid.

Nineteen human volunteers with normal pulmonary function and no history of asthma were exposed on two separate days to clean air and to an atmospheric mixture containing ozone (O3), 0.37 ppm, sulfur dioxide (SO2), 0.37 ppm, and sulfuric acid aerosol (B2SO4), 100 micrograms/m3. Subjects were exposed under carefully controlled conditions for two hours. During this period, the subjects alternately exercised for 15 minutes, at a level calculated to double minute ventilation, and rested for 15 minutes. The experimental goal was to determine whether the presence of the copollutants, H2SO4 and SO2, would significantly enhance the irritant potential of ozone, or cause decrements in pulmonary function on the order of 10 - 20 percent. Statistical analysis of the group averaged data suggested that the mixture may have been slightly more irritating to the subjects than was O3 alone. A large percentage of the subjects exhibited small decrements in pulmonary function. The group averaged FEV1.0 (forced expiratory volume in one second) on the exposure day was depressed 3.7 percent from the control value. One might expect O3 alone to depress FEV1.0 by about 2.8 percent under similar exposure conditions.

Adult↗
PubMed1981

Human exposure to ferric sulfate aerosol: effects on pulmonary function and respiratory symptoms.

Twenty normal and 18 asthmatic human volunteers were exposed to ferric sulfate aerosol at a nominal concentration of 75 microgram/m3 (equivalent to 20 microgram iron/m3). The concentration and particle size distribution (2 micron mass median aerodynamic diameter; geometric standard deviation of 3) were selected to simulate worst case ambient conditions. Ferric sulfate was chosen for study because it is toxic, it is a respiratory system irritant, and increased use of coal and high sulfur fuel oils will lead to increased concentrations of iron and sulfate in ambient air. A double-blind protocol was followed in which each subject was exposed on two days, separated by about a three week period. The subjects were exposed to clean air (sham) on one day and to ferric sulfate aerosol on the other (exposure); the order of exposure was selected randomly. Neither the subjects nor the staff performing the clinical testing were informed as to the nature of the atmosphere on any given day. Pulmonary function tests were performed immediately before (pre) and after (post) each 2 hr sham or exposure period; this protocol included intermittent exercise. Pre- and post-exposure symptom score interviews were also administered. On the average, the two groups of subjects did not exhibit significant pre- to post-changes in total respiratory system resistance, forced expiratory flow/volume performance, and single breath nitrogen washout parameters. None of the subjects reported more than slight changes in symptoms during exposure. Five individuals showed small but significant decremental trends in pulmonary function; however, nine subjects tended to improve after exposure.

Adolescent↗
PubMed1980

Short-term respiratory effects of polluted ambient air: a laboratory study of volunteers in a high-oxidant community.

To investigate short-term health effects of community air pollution directly, we developed a mobile laboratory allowing "blind" exposures of volunteers to polluted ambient air and to purified air at similar temperature and humidity. Subjects (30 asthmatic, 34 normal) from the surrounding area were studied at Duarte, California, a Los Angeles suburb subject to frequent photochemical oxidant pollution. Each was exposed to a close approximation of outdoor ambient air for 2 h with intermittent light exercise. Lung function and symptoms were evaluated pre- and post-exposure. A control (purified air) study took place several weeks later. Mean ambient air exposure concentrations were near 0.22 ppm for ozone and 200 micrograms/m3 for total suspended particulate. Ambient air exposures were associated with small significant losses in forced expiratory performance and total lung capacity. The responses of asthmatic and normal subjects were generally not significantly different, possibly because many normal subjects had a history of allergy and appeared atypically reactive to respiratory insults. In the normal subjects, a small significant increase in reported symptoms was seen with ambient air exposures compared with the control. In the asthmatics, the increase was not significant. Over-all, only slight effects attributable to exposure were found, even though a severely polluted area and a presumed high-risk population were chosen for study.

Adolescent↗
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↗
PubMed1979

Effect of low-level exposure to ozone on arterial oxygenation in humans.

We investigated the effect on arterial blood oxygenation of exposure to 0.2 ppm of ozone in purified air for 2 hours with intermittent light exercise and heat stress. Similar exposures to purified air alone provided control data. In 12 healthy volunteers, blood gases were measured before and during exposure via an indwelling brachial cannula. Six of these subjects and 6 other subjects underwent separate similar studies in which "arterialized" earlobe capillary blood was sampled. Arterial Po2 and alveolar-arterial Po2 differences varied significantly among different experimental conditions, but the variability was similar in the presence or absence of ozone. Small significant variations in body temperature were observed; these did not appear to be sufficient to affect blood gas measurements substantially. Over-all, we found no evidence for an adverse effect of the exposure to ozone on arterial oxygenation.

Adult↗
PubMed1979

Controlled exposures of human volunteers to sulfate aerosols. Health effects and aerosol characterization.

Our laboratory has undertaken the study of possible acute adverse health effects of sulfate aerosols through controlled exposures of volunteer human subjects. Both healthy and asthmatic adult men were exposed for 2-hour periods (with intermittent exercise) to ammonium sulfate, ammonium bisulfate, and sulfuric acid of particle size distributions and concentrations intended to simulate "worst case" exposures during Los Angeles smog episodes. Lung function tests were performed by the subjects on entering and before exiting from a carefully controlled environmental chamber. Subject symptoms were evluated in a standardized manner. Aerosol concentrations and size distributions were determined by an on-line computer/aerometric monitoring system; gravimetric and chemical analyses were performed on impactor and total filter samples after test exposures. We found little or no evidence of adverse health effects from 2-hour multiple-day exposures to any of the compounds at "worst case" ambient concentrations.

Aerosols↗
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↗