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Biomedical subjects

J D Hackney

Publications and source records attributed to J D Hackney.

At least 73 records · Page 4Linked to original sources
PubMed1978

A factor analytic approach to an effective lung function screening protocol.

Interrelationships among simple indices of pulmonary function derived from flow-volume curves and single-breath nitrogen tests were investigated by performing a factor analysis on data obtained from a generally healthy office working population (n = 388). Smoking was regarded as the major contribution to pulmonary dysfunction. Delta nitrogen was largely independent of all other measures, while flow-volume measures, including flow rates at high and low lung volumes, were highly intercorrelated but largely independent of closing volume and closing capacity. Delta nitrogen was most affected by smoking in both sexes. Scores derived from flow-volume measurements and from closing-volume measurements were significantly different, on the average, between male smokers and male nonsmokers. The methods and results presented prove to be useful in the design of protocols for effective pulmonary testing of large populations.

Adult↗
PubMed1977

Respiratory effects of exposure to ozone plus sulfur dioxide in Southern Californians and Eastern Canadians.

Volunteer subjects were exposed in an environmentally controlled chamber in Los Angeles to SO2 and O3, separately and in combination, to study the enhanced toxicity of the O3 + SO2 mixture observed in a previous study in Montreal. Toxic responses to O3 + SO2 were less severe than observed previously, and only slightly more severe than with O3 alone. Sulfur-containing aerosols formed by chemical reactions within the chamber air may have contributed to the O3 + SO2 responses in the Montreal study. Adaptation of Los Angeles residents to ambient O3 may also contribute to response variability.

California↗
PubMed1977

Adaptation to short-term respiratory effects of ozone in men exposed repeatedly.

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.

Adaptation, Physiological↗
PubMed1976

Respiratory function and symptoms in urban office workers in relation to oxidant air pollution exposure.

Similar populations of male and female office workers in San Francisco, which has little air pollution, and in Los Angeles, which experiences frequent photochemical smog episodes, were surveyed in an attempt to document excess respiratory symptoms and dysfunction in Los Angeles relatable to air pollution. Most results of forced expiratory tests, single-breath N2 tests, and questionnaire interviews did not differ significantly between cities. Los Angeles women reported nonpersistent cough and phlegm more often than did San Francisco women. Smokers in both cities showed increased functional abnormalities. These results suggested that Los Angeles oxidant exposure is far less significant than smoking as a risk factor in development of chronic respiratory disease in sedentary indoor workers in good general health. Oxidant exposure has not been ruled out as a significant risk to more heavily exposed on more highly susceptible persons.

Adolescent↗
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. II. Four-hour exposure to ozone alone and in combination with other pollutant gases.

Eight adult male volunteers were exposed to ozone (O3) alone and then in combination with nitrogen dioxide and carbon monoxide under conditions simulating ambient air pollution exposures. Four "normal" men showed few or no effects from repeated exposures. Four male volunteers with a history of "hyperreactive" airways, but with normal base line pulmonary function spirometric studies, after O3 exposure developed definite symptoms and decrement in pulmonary function.

Adult↗
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↗
PubMed1975

Effects of 60 and 80% oxygen on cell division in lung alveoli of squirrel monkeys.

The purpose of this study was to determine the effects on cell division of 60 and 80% oxygen in the lung alveoli of squirrel monkeys. To accomplish this, squirrel monkeys were exposed to 60 and 80% oxygen for up to 8 d. Prior to sacrifice, cells preparing to divide were labeled with tritiated thymidine (3H-TdR). Labeled cells were visualized with autoradiographic techinques, counted with the light microscope, and expressed in terms of a labeling index. In the present study, it was shown that DNA synthesis was not changed by exposure to 60%; however, with exposure to 80% oxygen, cell labeling was well above control levels by 5 d. Analysis of the cell types involved showed an increase in labeling. due to an increase in dividing Type 2 cells. Other cells in the alveolar wall also showed an increase in labeling

Animals↗
PubMed1975

Effects of 100% oxygen on cell division in lung alveoli of squirrel monkeys.

The purpose of this study was to determine the effects of 100% oxygen on cell division in lung alveoli of squirrel monkeys. To accomplish this, squirrel monkeys were exposed to 100% oxygen for up to 5 d. Prior to sacrifice, cells preparing to divide were labeled with tritiated thymidine (3H-Tdr). Labeled cells were visualized with autoradiographic techniques, counted with the light microscope, and expressed in terms of a labeling index. In the present study it was shown that DNA synthesis was initially inhibited by exposure to 100% oxygen. However, within 3 d it was returning to normal and by 5 d was well above control levels. Analysis of the cell types involved showed that the large increase in labeling was due to an increase in dividing Type 2 cells, which is thought to be for replacement of damaged Type 1 cells.

Animals↗