Short-term respiratory effects of photochemical oxidant exposure in exercising children.
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Biomedical subjects
Publications and source records attributed to E L Avol.
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To help assess respiratory health risks from sulfur dioxide (SO2) air pollution, we studied 24 normal, 21 atopic, 16 minimal/mild asthmatic, and 24 moderate/severe, medication-dependent asthmatic subjects classified according to history, lung function, allergy skin tests, serum IgE level, and airway reactivity to methacholine. All were exposed in a chamber (21 degrees C, 50% humidity) to 0.0, 0.2, 0.4, and 0.6 ppm SO2 in random order at 1-wk intervals; then exposures were repeated to test consistency of response. The 1-h exposures included three 10-min exercise periods (ventilation approximately 40 L/min). Physiologic response was measured early (approximately 15 min) and late (approximately 55 min) in exposure. Symptoms were evaluated during exposure and for 1 wk afterward. Normal and most atopic subjects showed little response at these SO2 levels. A few atopic subjects and many asthmatics developed bronchoconstriction and respiratory symptoms, but most were able to maintain their exercise. Effects were not markedly different between early and late measurements, nor between the first and second round of studies; however, late and second-round responses appeared slightly more favorable. No statistically significant effect of SO2 on symptoms was found 1 day or 1 wk after exposure. Minimal/mild asthmatics showed, on the average, slight responses at 0.0 ppm (attributable to exercise) and increasing responses at increasing SO2 concentrations. Moderate/severe asthmatics reacted more at 0.0 ppm, but their increments in response with increasing SO2 concentration were roughly similar to those of minimal/mild asthmatics. Thus, responses to SO2 per se were not strongly dependent on clinical severity of asthma, nor on SO2 exposure history during previous weeks.
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Twenty-four healthy, well-conditioned young adult male volunteers, free of asthma or clinical respiratory allergies, were exposed to purified air containing ozone (O3) at 0.16, 0.14, 0.12, 0.10, 0.08, and 0.00 part per million (ppm). Exposures were separated by 2-week intervals, occurred in random order, and lasted 2 hours each. Temperature was 32 +/- 1 degree C and relative humidity was 38 +/- 3%, simulating Los Angeles area smog conditions. Subjects exercised 15 minutes of each half hour, attaining ventilation rates averaging 68 L/min (approximately 35 L/min per m2 body surface area). Lung function was measured pre-exposure and after 1 hr and 2 hr of exposure. Airway responsiveness to a cold-air challenge was measured immediately following the 2-hr exposure. Symptoms were recorded before, during, and for one-week periods following exposures. For the group as a whole, no meaningful untoward effects were found except for a mild typical respiratory irritant response after 2 hr exposure to 0.16 ppm O3. Two individual subjects showed possible responses at 0.14 ppm, and one of them also at 0.12 ppm. In comparison to some previous investigations, this study showed generally less response to O3. The comparative lack of response may relate to the favorable clinical status of the subjects, the pattern of exercise during exposure, or some other factor not yet identified.
Twenty-two asthmatic young adult volunteers, predetermined to be reactive to sulfur dioxide (SO2) with exercise at normal room temperature, were studied to document short-term effects of SO2 exposure under hot conditions, both humid and dry. For comparison, similar exposures were conducted at mild temperatures. All subjects were exposed in an environmental control chamber to all possible combinations of 2 atmospheric conditions (purified air and 0.6 ppm SO2), 2 temperatures (near 21 and 38 degrees C), and 2 levels of relative humidity (near 20 and 80%). Exposures involved 5 min of heavy exercise (target ventilation rate, 50 L/min) plus brief warm-up and cool-down periods. Body plethysmographic measurements and symptom questionnaire interviews were administered before and at the end of each exposure. Response was expressed in terms of change in airway size or change in intensity of symptoms during exposure. Atmospheric condition showed the most marked and significant overall effect on physiologic responses; temperature and humidity effects were also significant. High temperature and high humidity tended to mitigate the bronchoconstriction produced by 0.6 ppm SO2 exposure: group mean specific airway resistance approximately tripled at 21 degrees C and low humidity, but increased by less than 40% at 38 degrees C and high humidity. Temperature and humidity affected symptoms less consistently than physiologic responses, but in general, symptom responses paralleled physiologic responses.
Healthy volunteers 12 to 15 yr of age (46 boys, 13 girls) were exposed to purified air and to smoggy Los Angeles ambient air on different occasions. The studies were performed in random order approximately 2 wk apart. They included 1 h of continuous bicycle exercise (mean ventilation, 32 L/min) plus brief warm-up and cool-down periods. Symptoms and forced expiratory performance were recorded preexposure in purified air, immediately postexposure, and after 1 h recovery in purified air. Mean exposure temperature was 32 degrees C, and mean relative humidity was 45%. In ambient exposure, pollutant concentrations averaged 0.144 ppm for ozone and 153 micrograms/m3 for total suspended particulates. Group mean FEV1 decreased during ambient exposure (p less than 0.01) and only partially recovered during the following 1 h. Unlike adults studied previously, this subject group reported no significant increase in respiratory symptoms accompanying changes in FEV1. Adolescents may be less aware of early respiratory irritation by oxidants and thus more at risk from ambient exposures than are adults.
Observations of high acidity (pH as low as 1.7) in fogwater collected in polluted areas have provoked concern for public health. Effects of exposure to acidic pollutants have not been studied under foggy conditions; thus there is no directly relevant information from which to estimate the health risk. Indirectly relevant information is available from numerous studies of volunteers exposed to "acid fog precursors" under controlled conditions at less than 100% relative humidity. The effect of fog in modifying responses to inhaled acidic pollutants is difficult to predict: depending on circumstances, fog droplets might either increase or decrease the effective dose of pollutants to the lower respiratory tract. Fog inhalation per se may have unfavorable effects in some individuals. Sulfur dioxide is known to exacerbate airway constriction in exercising asthmatics, at exposure concentrations attainable in ambient air. Nitrogen dioxide has shown little untoward respiratory effect at ambient concentrations in most studies, although it has been suggested to increase bronchial reactivity. Sulfuric acid aerosol has shown no clear effects at concentrations within the ambient range. At somewhat higher levels, increased bronchial reactivity and change in mucociliary clearance have been suggested. Almost no information is available concerning nitric acid.
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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.
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.
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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.
Assessing personal exposure to ozone has only been feasible recently with the introduction of passive ozone samplers. These devices are easy to use, but changes in air velocity across their collection surfaces can affect performance. The Harvard active ozone sampler (AS) was developed in response to problems with the passive methods. This active sampler has been tested extensively as a microenvironmental sampler. To test for personal sampling, 40 children attending summer day-camp in Riverside, California wore the active ozone sampler for approximately 2.6 h on July 19 and 21, 1994, when ozone concentrations were about 100 ppb and 140 ppb, respectively. The children spent 94-100% of the sampling period outside, staying within a well-defined area while participating in normal camp activities. Ambient ozone concentrations across this area were monitored by two UV photometric ozone monitors. The active sampler was worn in a small backpack that was also equipped with a passive ozone sampler. Device precision, reported as the percent difference between duplicate pairs of samplers, was +/- 3.7% and +/- 4.2% for the active and passive samplers, respectively. The active sampler measured, on average, 94.5 +/- 8.2% of the ambient ozone while the passive samplers measured, on average, 124.5 +/- 18.8%. The samplers were worn successfully for the entire sampling period by all participating children.
Asthmatic volunteers (N = 14) aged 18 to 33 yr with documented sensitivity to sulfur dioxide (SO2) were exposed in a chamber to 0.6 ppm SO2 for 6-hr periods on 2 successive days. Similar exposures to purified air, 1 wk later or earlier, served as controls. Subjects exercised heavily (target ventilation rate 50 L/min) for 5 min near the beginning of exposure (early exercise) and for an additional 5 min beginning after 5-hr of exposure (late exercise). At all other times, they rested. Body plethysmographic measurements and symptom questionnaires were administered pre-exposure, after each exercise period, and hourly during rest. Bronchoconstriction and lower respiratory symptoms were observed during or immediately following exercise--to a slight extent with clean air, and to a more marked extent with SO2. Bronchoconstriction and symptoms were modestly less severe on the second day of SO2 exposure than on the first day, but there were no meaningful differences in response between early and late exercise periods on either day.
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.