Deborah A. Shamoo

Comparative respiratory effects of ozone and ambient oxidant pollution exposure during heavy exercise.

Fifty volunteer bicyclists were exposed to purified air containing ozone (O/sub 3/) at controlled concentrations of 0, 0.08, 0.16, 0.24, and 0.32 ppm, and to oxidant polluted ambient air (mean O/sub 3/ concentration 0.15 ppm, mean total particulate concentration 295 ..mu..g/m/sup 3/) in suburban Los Angeles. Exposures (in random order, 14 days apart) involved one hour of heavy continuous exercise (mean minute volume 57 L) plus brief warm up and cool down periods. Significant forced expiratory function decrements and symptom increases occurred in ambient air exposures. In controlled O/sub 3/ exposures, responses were significant at 0.16 ppm and higher; their severity increased with increasing O/sub 3/ concentration. Effects were only partially reversed after one hours rest in purified air. Ambient exposures produced about the same response as O/sub 3/ alone at the same concentration. Thus coexisting pollutants do not appear to enhance the irritancy of O/sub 3/ in typical moderate ambient oxidant pollution episodes. However, O/sub 3/ itself can produce respiratory irritation at concentrations slightly above the health based federal ambient air quality standard of 0.12 ppm O/sub 3/, at high ventilation rates required during heavy exercise.

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)

Effects of 0.2 ppm nitrogen dioxide on pulmonary function and response to bronchoprovocation in asthmatics

To study the respiratory effects of nitrogen dioxide (NO2) at ambient concentrations, we exposed 31 asthmatic volunteers to purified air (control) and to 0.2 ppm NO2 for 2-h periods with light intermittent exercise. Bronchial reactivity (loss of forced expiratory performance in response to graded doses of methacholine chloride aerosol) was determined postexposure, using a newly developed apparatus that allowed accurate quantitation of methacholine dose. Forced expiratory performance, total respiratory resistance, and symptoms were also recorded immediately pre- and postexposure (prior to methacholine challenges). No significant direct effect of NO2 exposure on forced expiratory function or total respiratory resistance was observed. Symptoms showed a small significant (p less than 0.05) excess in purified air relative to NO2 exposures. Individual responses to methacholine varied greatly. About two-thirds of the subjects showed greater response after NO2 than after purified air, but the mean excess response was small. Mean changes attained significance in some but not all applicable statistical tests. Thus we cannot conclude unequivocally that NO2 exposure increased bronchial reactivity in this group, although there was some tendency in that direction.

Effects of Exposure to 4 PPM Nitrogen Dioxide in Healthy and Asthmatic Volunteers

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.

Respiratory effects of 0.75 ppm sulfur dioxide in exercising asthmatics: Influence of upper-respiratory defenses

To determine the influence of mouthpiece breathing on respiratory responses to sulfur dioxide (SO2), 23 young adult asthmatic volunteers were exposed in a chamber to 0.75 ppm SO2 during heavy exercise, once with breathing unencumbered and once while they wore noseclips and mouthpieces. These conditions (more severe than in typical ambient exposures) were deliberately chosen to produce significant physiological and clinical responses. Similar exposures to clean air served as controls. Exposure studies were separated by 1-week intervals and order was randomized. The protocol consisted of 10 min on a bicycle ergometer (mean load 650 kg-m/min, mean ventilation 40 liter/min), preceded and followed by response testing (body plethysmography, symptom questionnaires, and forced expiratory function tests; the last were performed only postexposure). During clean-air exposures, specific airway resistance (SRaw) and symptoms increased significantly, but no meaningful differences between mouthpiece breathing and unencumbered breathing were observed. Exposures to SO2 under these relatively severe conditions produced greater increases in SRaw than clean-air exposures regardless of the mode of breathing, but the excess increase was significantly greater with mouthpiece than with unencumbered breathing. Symptom changes and postexposure forced expiratory function showed qualitatively the same pattern of decrements with SO2 ad did SRaw, but the excess responses attributable to mouthpiece breathing did not attain statistical significance. Mouthpiece breathing can compromise upper-respiratory defenses against SO2 to the extent that responses are greater than with more natural breathing. The mode of breathing should be taken in account when applying laboratory human exposure data to air-quality risk assessment.

A Dose-Response Study of Healthy, Heavily Exercising Men Exposed To Ozone At Concentrations Near the Ambient Air Quality Standard

Twenty-four healthy, well-conditioned young adult male volun teers, free of asthma or clinical respiratory allergies, were exposed to purified air containing ozone (03) 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° 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 (∼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, dur ing, 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 03. 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 03. The comparative lack of response may relate to the favorable clinical status of the subjects, the pattern of exercise dur ing exposure, or some other factor not yet identified.

Respiratory dose-response study of normal and asthmatic volunteers exposed to sulfuric acid aerosol in the sub-micrometer size range.

Twenty-one healthy and 21 asthmatic volunteers were exposed to respirable sulfuric acid aerosol (mass median particle diameter approximately 0.9 pm, geometric standard deviation 2.5) in a chamber at 21° and 50% relative humidity. Measured sulfuric acid concentrations averaged 0, 380, 1060, and 1520 μg/m3 (in the occupational range, higher than concentrations observed in ambient air pollution). Exposures to different concentrations occurred in randomized order 1 week apart. They lasted 1 hr and included three 10-min periods of heavy exercise. Healthy volunteers showed no statistically significant changes in pulmonary function. airway reactivity to inhaled methacholine, or overall reporting of irritant symptoms which could be attributed to acid exposure. They did show a slight statistically significant (P <. 01) increase in cough with increasing acid concentration. At the two highest acid concentrations, asthmatics showed significant increases in irritant symptoms and decrements in pulmonary function, without significant changes in airway reactivity. Their function decrements appeared to increase with time during exposure. Previous studies in fog (10°, median particle diameter approximately 10 urn) with similar concentrations of sulfuric acid showed more symptoms but less pulmonary function change, perhaps reflecting different sites of particle deposition in airways and/or different degrees of neutralization by airway ammonia. This and earlier evidence predicts little, if any, acute irritant response in short-term (1 hr or less) exposures to sulfuric acid at concentrations found in ambient air pollution.

Short-Term Respiratory Effects of Photochemical Oxidant Exposure in Exercising Children

To assess the short-term respiratory effects of photochemical oxidant pollution in children, 66 volunteers—33 boys and 33 girls aged 8 to 11—were exposed in a movable laboratory to polluted Los Angeles area ambient air and to purified air as a control. Exposures lasted one hour, during which subjects exercised continuously at roughly 50 percent of maximal oxygen consumption. Forced expiratory function and symptoms were evaluated prior to and at the end of exposure. The mean ozone concentration in ambient exposures was 0.113 ppm, reflecting an unusually mild pollution season. As a group, the subjects showed no statistically significant untoward responses to ambient air in comparison to purified air, and no significant differences in response between sexes. Nevertheless, regression analyses of individual data indicated a significant (p < 0.05) trend toward forced expiratory dysfunction with increasing ambient ozone concentrations. When the regression analyses were expanded to include older children and adul...

Response to ozone in volunteers with chronic obstructive pulmonary disease.

Twenty-eight volunteers with chronic obstructive pulmonary disease were exposed to 0.0, 0.18, and 0.25 ppm ozone in purified air for 1-hr periods with light intermittent exercise, with exposure conditions presented in random order at 1-month intervals. No statistically significant changes attributable to ozone were found in forced expiratory performance or percent oxyhemoglobin (measured near the beginning and end of each exposure). No ozone-related changes in clinical status were found by interviews that included the time for 1 wk before to 1 wk after each exposure, except that a moderate increase in lower respiratory symptoms was reported by nonsmokers in 0.18 ppm exposures only. Thus, a slight decrement in hemoglobin saturation with ozone exposure (reported in two previous studies of chronic obstructive pulmonary disease subjects) may not be a common occurrence under typical ambient exposure conditions.

Controlled Exposure of Volunteers with Chronic Obstructive Pulmonary Disease to Nitrogen Dioxide

Twenty-two volunteers with chronic obstructive pulmonary disease were exposed to nitrogen dioxide at 0.0, 0.5, 1.0, and 2.0 ppm in a controlled environment chamber. Exposure lasted 1 hr and included two 15-min exercise periods, during which the mean ventilation rate was roughly 16 L/min. Pulmonary mechanical function was evaluated pre-exposure, after initial exercise, and at the end of exposure. Blood oxygenation was measured by ear oximetry pre-exposure and during the second exposure period. Symptoms were recorded during exposures and for 1-wk periods afterward. No statistically significant changes in symptom reporting could be attributed to nitrogen dioxide exposure at any concentration, compared to the 0.0 ppm control condition. Measures of pulmonary mechanics showed either no significant changes, or small and equivocal changes. Arterial oxygen saturation showed marginal improvement with exercise, regardless of nitrogen dioxide concentration.