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Biomedical subjects

W S Linn

Publications and source records attributed to W S Linn.

At least 19 recordsLinked to original sources

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)

Adult

Exposures of older adults with chronic respiratory illness to nitrogen dioxide. A combined laboratory and field study.

We combined field and laboratory experimentation to evaluate the effects of nitrogen dioxide in a panel of Los Angeles area residents with chronic respiratory illness, 15 men and 11 women aged 47 to 69. All had heavy smoking history, chronic symptoms, and low FEV1; some also had low FVC. During the fall-winter high-NO2 season, they monitored themselves for 2-wk periods using spirometers in the home, passive NO2 sampling badges, and diaries to record time and activity patterns and clinical status. In the middle of each self-monitoring week they were exposed in a chamber, once to clean air and once to 0.3 ppm NO2. Chamber exposures were double blind, lasted 4 h, and included four 7-min exercise sessions with average ventilation rates near 25 L/min. Symptom reports and hourly forced expiratory function tests showed no statistically significant differences between clean air and NO2 chamber exposures, although peak flow showed a approximately 3% loss with NO2 relative to clean air during the first 2 h of exposure only (p = 0.056). No significant overall differences were found between field self-measurements and measurements of lung function in the chamber or between field measurements in clean air and NO2 exposure weeks. Field data showed that group average lung function and symptom levels were worse in the morning than later in the day (p < 0.005) but otherwise were stable over 2 wk. Even though most subjects smoked and stayed indoors 80 to 90% of the time, personal NO2 exposures correlated significantly with outdoor NO2 concentrations as reported by local monitoring stations.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged

Activity patterns in a panel of outdoor workers exposed to oxidant pollution.

We investigated summer activity patterns in a panel of volunteers drawn from a population segment with potentially high exposure to ambient oxidant pollution. The subjects were 15 men and 5 women aged 19-50, all of whom worked outdoors in the Los Angeles area at least 10 hr per week. The general approach was to (i) calibrate the relationship between ventilation rate (VR) and heart rate (HR) for each subject in controlled exercise; (ii) have subjects monitor their own normal activities with diaries and electronic HR recorders; (iii) estimate VR from HR recordings; and (iv) relate VR with diary descriptions of activities. Calibration data were fit to the equation log (VR) = (intercept) + (slope x HR), intercept and slope being determined separately for each individual to provide a specific equation to predict her/his VR from measured HR. Individuals' correlation coefficients relating log (VR) with HR ranged from 0.83 to 0.95. Subjects monitored themselves for three 24-hr periods during one week, including their most active work day and their most active non-work day. They wore Heart Watch(R) athletic training instruments which recorded HR once per minute; and recorded each change in their activity, location, or breathing rate in diaries. Breathing rates were classified as sleep, slow (like slow or normal walking), medium (like fast walking), or fast (like running). Diaries showed that sleep occupied about 33% of subject's time, slow activity 59%, medium 7%, and fast 1%. Fast activity was reported only at leisure, never at work. For the group, arithmetic means and standard deviations of predicted VR were 7 +/- 3 L/min for sleep, 12 +/- 7 for slow activity, 14 +/- 8 for medium, and 44 +/- 36 for fast. For the group and for most individuals, distributions of predicted VR within a given activity level (breathing rate) were approximately lognormal, with many values in a narrow range below the arithmetic mean and fewer values in a broader range above it. In the most active individuals, predicted VR exceeded 100 L/min for a total of 5 to 30 min during the three days. These data should prove useful in estimating outdoor workers' inhaled doses of ambient pollutants at existing or projected levels of air quality. Activity diary records are of significant value in pollutant dose estimation, but concurrent heart rate recording improves the estimates substantially.

Adult

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

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

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

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

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

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

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

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

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

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

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

Effects of ozone exposure in Canadians and Southern Californians. Evidence for adaptation?

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.

Acetylcholinesterase