Experimental exposures of young asthmatic volunteers to 0.3 ppm nitrogen dioxide and to ambient air pollution.

Asthmatic volunteers aged 8 to 16 (N = 34) were exposed on separate occasions to clean air (control), to 0.30 ppm nitrogen dioxide (NO2) in otherwise clean air, and to polluted Los Angeles area ambient air on summer mornings when NO2 pollution was expected. Exposures lasted 3 hr, with alternating 10-min periods of exercise and rest. In ambient pollution exposures, 3-hr average NO2 concentrations ranged from 0.01 to 0.26 ppm, with a mean of 0.09 ppm. Ambient exposures did not significantly affect lung function, symptoms, or bronchial reactivity to cold air, relative to the control condition. Responses to 0.3 ppm NO2 exposures were equivocal. Asthma symptoms were more severe during 1-week periods before 0.3 ppm exposures, and lung function was decreased immediately before 0.3 ppm exposures, compared to other conditions. Lung function declined slightly during the first hour at 0.3 ppm, but improved over the remaining 2 hr. Compared to other conditions, symptoms were not increased during 0.3 ppm exposures, but were increased during 1-week periods afterward. These observations may reflect untoward effects of 0.3 ppm NO2, or may reflect chance increases in asthma severity prior to 0.3 ppm exposures.

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 micron, geometric standard deviation 2.5) in a chamber at 21 degrees and 50% relative humidity. Measured sulfuric acid concentrations averaged 0, 380, 1060, and 1520 micrograms/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 less than .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 degrees, median particle diameter approximately 10 micron) 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.

Dose-response study of asthmatic volunteers exposed to nitrogen dioxide during intermittent exercise.

Twenty-one mildly asthmatic volunteers were exposed to 0, 0.3, 1.0, and 3.0 ppm nitrogen dioxide (NO2) in purified background air in an environmental control chamber. Exposures were separated by 1-wk periods and occurred in random order. Each lasted 1 hr and included three 10-min bouts of moderately heavy exercise (mean ventilation rate 41 L/min). Exposure temperature was near 22 degrees C and relative humidity near 50%. Specific airway resistance and maximal forced expiratory performance were measured preexposure, after the initial exercise, and near the end of exposure. Bronchial reactivity was assessed immediately following exposure, by normocapnic hyperventilation with subfreezing air. Symptoms were recorded on questionnaires before, during, and for 1-wk after each exposure. Exercise induced significant bronchoconstriction regardless of NO2 level. No statistically significant untoward response to NO2 was observed at any exposure concentration. This negative finding agrees with our previous results, but contrasts with findings elsewhere of respiratory dysfunction after exposure to 0.3 ppm. The discrepancy is presently unexplained, but it may relate to different severity of asthma in different subject groups.

Controlled exposure to a mixture of SO2, NO2, and particulate air pollutants: effects on human pulmonary function and respiratory symptoms.

Exposure of 20 volunteers to sodium chloride (NaCl) aerosol or to a mixture containing NaCl plus irritant particles (zinc ammonium sulfate) and irritant gases (nitrogen dioxide and sulfur dioxide) produced no significant decrements in pulmonary function. There was a slight tendency for respiratory symptoms to be greater during the exposure to the mixture than during exposure to the NaCl aerosol alone; the differences were not statistically significant. The pollutant concentrations studied approximated worst-case ambient levels observed in the Los Angeles basin.

Effects of heat and humidity on the responses of exercising asthmatics to sulfur dioxide exposure.

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.

Respiratory responses of humans exposed to an aerosol-gas pollutant mixture: multivariate contrast of a complex atmosphere to clean air and sodium chloride aerosol controls.

Data from a group of 20 subjects with normal baseline pulmonary function, who were exposed for 2 h to a test atmosphere containing a complex mixture of pollutants, have been contrasted with data from two other groups exposed to presumably non-toxic control atmospheres. Group 1 was exposed to clean air, group 2 was exposed to clean air containing sodium chloride aerosol at 270 micrograms m-3, and group 3 was exposed to the complex atmosphere containing sodium chloride (332 micrograms m-3) and zinc ammonium sulfate (23 micrograms m-3) aerosols plus nitrogen dioxide (0.5 ppm) and sulfur dioxide (0.5 ppm). These atmospheres (ranked according to the presumed relative toxicities of the components; clean air = 0, sodium chloride = 1, complex mixture = 2) were contrasted using multiple regression and partial correlation analyses. The effects of exposure to the complex gas-aerosol mixture on forced expiratory performance were not significantly different from those observed in subjects exposed to clean air or to sodium chloride aerosol.

Asthmatics' responses to 6-hr sulfur dioxide exposures on two successive days.

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.

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.

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.