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↗

PubMedDate not supplied

Experimental studies on human health effects of air pollutants. IV. Short-term physiological and clinical effects of nitrogen dioxide exposure.

Adult male volunteers were exposed to nitrogen dioxide (NO2) at 1.0 ppm in purified air under conditions simulating ambient photochemical smog exposures (2-hr exposure with intermittent light exercise at 31 degrees C and 35% relative humidity). Sham exposures to purified air alone served as controls. Exposure effects were assessed by pulmonary physiological tests and by a standardized clinical evaluation. No statistically physiological changes attributable to NO2 exposure were found except for a marginal loss in forced vital capacity after exposure on two successive days (1.5% mean decrease, P less than .05). Reported respiratory and other symptoms were slightly increased with exposure as compared to control, but the change was not significant. Short-term toxicity of NO2 at peak ambient concentrations appears to be substantially less than that of ozone in healthy people, but adverse NO2 effects in diseased people or in long-term exposures cannot be ruled out at present.

Adult↗

PubMedDate not supplied

Nitrogen dioxide inhalation and human blood biochemistry.

Blood from ten young adult male humans, exposed to 1 ppm or 2 ppm nitrogen dioxide (NO2) for 2.5--3.0 hr, was examined for evidence of biochemical changes. The experiments lasted three days. The subjects entered an environmental chamber, performed mild exercise, and completed a series of measurements of pulmonary physiology while breathing filtered air. Blood samples were then taken and analyzed. This regimen was repeated on the second and third day, except that the chamber atmosphere now contained 1 ppm or 2 ppm NO2. Paired group analyses were performed on the data. A statistically significant decrease was observed in the activity of the erythrocyte membrane enzyme acetylcholinesterase at both NO2 levels. Levels of peroxidized red blood cell lipids showed statistically significant elevations after inhalation of 2 ppm NO2 but not 1 ppm. Glucose-6-phosphate dehydrogenase was significantly elevated only after the second 2-ppm NO2 exposure. Small but statistically significant decreases were observed in both hemoglobin and hematocrit values after exposure to both NO2 levels. The experiment was repeated with NO2, (i.e., three days of filtered air) to detect possible effects of the experimental procedure. Decreases were again seen in hemoglobin and hematocrit, and acetyecholinesterase, although of smaller magnitude than when NO2 was inhaled. Other data showed random variations that were not additive over the three-day sham exposure period. It was concluded that significant blood biochemical changes resulted from NO2 inhalation, although the three-day experimental regimen independently produced changes that account for some of the apparent response.

Acetylcholinesterase↗

PubMedDate not supplied

Ozone sensitivity in aging WI-38 cells based on acid phosphatase content.

Young [16-19 population doubling level (PDL)] and senescing (50-53 PDL) WI-38 cell populations were exposed to 1 ppm ozone for 2 hr and the resultant extracellular and intracellular acid phosphatase concentration was measured. Dose-response curves were also determined for surviving populations of young and old cells after a 1 hr ozone exposure ranging in concentration from 0 to 1.00 ppm. Senescing cells released 8 times more acid phosphatase per million cells than the young cells. Both old and young cells showed a clear dose-response to the 1 hr ozone gradient exposure. However, the older cells demonstrated a consistent 17% average lower survival rate than the young cells. The higher acid hydrolase level in older WI-38 cells is probably related to the lower survival rate observed in the older cells in vitro.

Acid Phosphatase↗

PubMedDate not supplied

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.

Aged↗

PubMedDate not supplied

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.

Adolescent↗

PubMedDate not supplied

Combined effect of sulfur dioxide and cold in exercising asthmatics.

Twenty-four asthmatic volunteers were exposed to 0, 0.3, and 0.6 ppm sulfur dioxide (SO2) in purified background air at each of three temperatures--21 degrees, 7 degrees, and -6 degrees C--in a controlled-environment chamber. Relative humidity was approximately 80%. Exposures consisted of 5 min heavy exercise periods plus brief warmup and cooldown periods. Airway resistance, thoracic gas volume, and symptoms were measured immediately before and after exposure. For the group, increasing SO2 concentration and decreasing temperature were associated with statistically significant unfavorable effects on airway resistance and respiratory symptoms, as expected from previous findings. Effects of SO2 and cold usually appeared to combine in an additive or less-than-additive fashion; there was little evidence of synergism. Individuals' response patterns were variable: a few suggested synergism, but others suggested a mitigating effect of cold on the bronchoconstrictive response to SO2.

Adult↗

PubMedDate not supplied

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.

Adolescent↗

PubMedDate not supplied

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.

Adult↗

PubMedDate not supplied

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.

Aged↗

PubMedDate not supplied

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.

Adult↗

PubMedDate not supplied

Effect of metaproterenol sulfate on mild asthmatics' response to sulfur dioxide exposure and exercise.

Twenty asthmatic volunteers, most with mild disease, underwent dose-response studies with sulfur dioxide (SO2) under three pretreatment conditions: (1) drug (metaproterenol sulfate in aerosolized saline solution), (2) placebo (aerosolized saline only), and (3) no pretreatment. Sulfur dioxide exposure concentrations were 0.0, 0.3, and 0.6 ppm. Experimental conditions were presented in random order at 1-wk intervals. Exposures lasted 10 min with heavy continuous exercise. Lung function was measured at baseline, after pretreatment (immediately pre-exposure), immediately post-exposure, and during a 2-hr follow-up. Subjects could elect to take bronchodilators during follow-up. Symptoms were monitored before, during, and for 1 wk after exposure. With no pretreatment, subjects exhibited typical exercise-induced bronchospasm at 0.0 ppm, slightly increased responses at 0.3 ppm, and more marked increases at 0.6 ppm. Seven subjects took bronchodilator after 0.6-ppm exposures, compared to 2 at lower concentrations. Within 30 min post-exposure, most subjects' symptoms and lung function had returned to near pre-exposure levels. A similar sequence was observed when subjects received placebo. Drug pretreatment improved lung function relative to baseline, prevented bronchoconstrictive responses at 0.0 and 0.3 ppm, and greatly mitigated responses at 0.6 ppm. Thus, typical bronchodilator usage by asthmatics is likely to reduce their response to ambient SO2 pollution.

Adult↗

PubMedDate not supplied

Responses to sulfur dioxide and exercise by medication-dependent asthmatics: effect of varying medication levels.

Twenty-one volunteers with moderate to severe asthma were exposed to sulfur dioxide (SO2) at concentrations of 0 (control), 0.3, and 0.6 ppm in each of three medication states: (1) low (much of their usual asthma medication withheld), (2) normal (each subject on his own usual medication schedule), and (3) high (usual medication supplemented by inhaled metaproterenol before exposure). Theophylline, the medication usually taken by subjects, was often supplemented by beta-adrenergics. Exposures were for 10 min and were accompanied by continuous heavy exercise (ventilation approximately 50 l/min). Lung function and symptoms were measured before and after exposure. With normal medication, symptomatic bronchoconstriction occurred with exercise and was exacerbated by 0.6 ppm SO2, as reported for mildly unmedicated asthmatics studied previously. Both baseline and post-exposure lung function were noticeably worse in the low-medication state. High medication improved baseline lung function and prevented most bronchoconstrictive effects of SO2/exercise. High medication also increased heart rate and apparently induced tremor or nervousness in some individuals.

Adrenergic beta-Antagonists↗

PubMedDate not supplied

Vitamin E supplementation and respiratory effects of ozone in humans.

To determine whether vitamin E (di-alpha-tocopherol) supplementation could protect against short-term respiratory responses to O3 exposure its effects were investigated in young healthy adult volunteers. Experimental groups received 800 or 1600 IU vitamin E per day for 9 or more wk, while control groups received placebo. Subjects were then exposed for 2-h periods to 0.5 ppm O3, with secondary stresses of heat and intermittent light exercise. Responses to O3 exposure, evaluated in terms of symptoms, forced expiratory performance, and single-breath nitrogen washout, were not significantly different between vitamin E and placebo groups.

Adult↗