The pulmonary effects of ozone and nitrogen dioxide alone and combined in healthy and asthmatic adolescent subjects

Separate exposures to 0.12 ppm ozone (O3) or 0.18 ppm nitrogen dioxide (NO2) have not demonstrated consistent changes in pulmonary function in adolescent subjects. However, in polluted urban air, O3 and NO2 occur in combination. Therefore, this project was designed to investigate the pulmonary effects of combined O3 and NO2 exposures during intermittent exercise in adolescent subjects. Twelve healthy and twelve well-characterized asthmatic adolescent subjects were exposed randomly to clean air or 0.12 ppm O3 and 0.30 ppm NO2 alone or in combination during 60 minutes of intermittent moderate exercise (32.5 1/min). The inhalation exposures were carried out while the subjects breathed on a rubber mouthpiece with nose clips in place. The following pulmonary functional values were measured before and after exposure: peak flow, total respiratory resistance, maximal flow at 50 and 75 percent of expired vital capacity, forced expiratory volume in one second and forced vital capacity (FVC). Statistical significance of pulmonary function changes was tested by analysis of covariance for repeated measures. After exposure to 0.12 ppm O3 a significant decrease was seen in maximal flow at 50% of FVC in asthmatic subjects. After exposure to 0.30 ppm NO2 a significant decrease was seen in FVC also in the asthmatic subjects. One possible explanation for these changes is the multiple comparison effect. No significant changes in any parameters were seen in the asthmatic subjects after the combined O3-NO2 exposure or in the healthy subjects after any of the exposures.     

Human nasal mucosal changes after exposure to urban pollution.

Millions of people worldwide are living in areas where ozone (O3) concentrations exceed health standards (an hourly average of 235 micrograms/m3/0.12 ppm, not to be exceeded more than once per year). Ozone induces acute nasal inflammatory responses and significant epithelial lesions in experimental animals and humans. To determine the nasal effects of a 15-day exposure to an urban polluted atmosphere with O3 as the main pollutant, we studied a population of healthy, young males newly arrived to southwest metropolitan Mexico City (SWMMC). The study included 49 non-smoking residents in an unpolluted port, Veracruz City; 14 subjects stayed in the port and served as controls, while 35 subjects traveled to SWMMC and had serial nasal lavages at different times after arriving in SWMMC. Subjects had exposures to ambient O3 an average of 10.2 hr/day, with a total cumulative O3 exposure of 10.644 ppm.hr. Nasal inflammatory responses, polymorphonuclear leukocyte PMN-CD11b surface expression, rhinoscopic changes, and respiratory symptoms were evaluated. Exposed subjects had massive nasal epithelial shedding and significant responses in PMN nasal influx (p < 0.00001) and in PMN-CD11b expression (p < 0.05). Cumulative O3 exposure correlated with respiratory symptoms, PMNs (rs = 0.2374, p < 0.01), and CD11b (rs = 0.3094, p < 0.01); 94% of exposed subjects experienced respiratory symptoms, and 97% left the city with an abnormal nasal mucosa by rhinoscopy. Nasal epithelial changes persisted 2 weeks after the exposed subjects returned to their nonpolluted environment. Exposure to an urban polluted atmosphere induces significant and persistent nasal epithelial alterations in healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ozone dose-response effects of varied equivalent minute ventilation rates

While it is well known that exercise minute ventilation (V(E)) results in greater pulmonary function and subjective symptoms (SS) responses upon exposure to a given ozone (O3) dose, the magnitude of V(E) increase to produce a significant forced expiratory volume in 1 s (FEV1.0) response compared to that observed at a lower exercise V(E) for the same O3 concentration and exposure time is unclear, especially in prolonged (i.e., >2 h) exposures. Further, in prolonged exposures, the relationship of body size to FEV1.0 response to a given O3 exposure dose has not been systematically examined. In the present study, 30 young adults were exposed on four occasions for 6 h (during a 6.6-h period) to constant 03 levels of zero (filtered air, FA) or 0.12 parts per million (ppm). At the latter concentration, exercise V(E) was varied in exposures to 17, 20, and 23 l min(-1) m(-2) of BSA, respectively, for each individual to achieve an equivalent ventilation rate, EVR). In the FA exposure, EVR was 23 l min(-1) m2. Percent changes in FEV1.0 for the three 0.12 ppm O3 exposures were significantly greater than that for FA, but did not differ significantly from each other. For the 6.6-h exposures, exercise EVR at or in excess of 17 l min(-1) m(-2), SS values were significantly greater than those observed for the FA protocol. Further, SS values at 6.6 h of exposure to 0.12 ppm O3 for the exercise EVR of 23 l min(-1) m(-2) protocol were significantly greater than for the 0.12 ppm O3 exercise EVR of 17 l min(-1) m(-2) protocol. To achieve a widened EVR, two 1-h exposures to 0.30 ppm O3 with continuous exercise (CE) at a level necessitating an EVR of 17 and approximately 34 l min(-1) m(-2), respectively, were completed by each subject. All postexposure pulmonary function and SS responses were significantly greater for the higher 1-h EVR protocol. In all exposures with significant O3-induced changes in FEV1.0 and SS, it was found that the smaller subjects who exercised at the lowest absolute V(E) had significantly smaller responses than did the larger subjects. These results strongly suggest that for the O3 concentrations and exposure durations used in this study, the effect of V(E) on O3-induced FEV1.0 and SS responses is not body-size-dependent.     

Tolerance to sulfur dioxide-induced bronchoconstriction in subjects with asthma

A study to determine whether the bronchoconstriction induced by low concentration of sulfur dioxide in subjects with asthma decreases with repeated exposure was undertaken. Eight subjects with asthma performed 3 min of voluntary eucapnic hyperpnea with 0.5 ppm of SO2 in humidified filtered air three times at 30-min intervals and we measured specific airway resistance (SRaw) before and after each period of hyperpnea. Specific airway resistance increased significantly more after the first exposure to SO2 [(from 7.6 +/- 1.7 to 15.5 +/- 2.0 L x cm H2O/liter/sec (mean +/- SEM)] than after the second (from 8.1 +/- 1.3 to 10.8 +/- 1.6) or third (from 7.6 +/- 1.6 to 10.1 +/- 1.9) exposures (P less than 0.025). When seven subjects repeated hyperpnea with SO2 24 hr and 7 days later, SRaw increased as much as it had after the first exposure (from 8.2 +/- 2.5 to 15.5 +/- 4.5 at 24 hr and from 6.6 +/- 1.4 to 15.4 +/- 2.1 at 7 days). In four subjects repeated exposure to SO2 caused short-term inhibition of the bronchomotor response to SO2 but did not inhibit the bronchomotor response to histamine aerosol. It was concluded that repeated exposures to a low concentration of SO2 over a short period (on 1 day) can induce tolerance to the bronchomotor effects of SO2 in subjects with asthma. Tolerance to the bronchomotor effects of SO2 is not caused by decreased responsiveness of airway smooth muscle or a generalized decrease in the responsiveness of vagal reflex pathways since the bronchomotor response to histamine is preserved.     

Formaldehyde (CH2O) concentrations in the blood of humans and Fischer-344 rats exposed to CH2O under controlled conditions

The effect of exposure to formaldehyde (CH2O) on the CH2O concentration of the blood was determined. Eight male F-344 rats were exposed to 14.4 +/- 2.4 ppm of CH2O for 2 hours and the blood was collected immediately after exposure. Formaldehyde concentrations in the blood were determined by gas chromatography/mass spectrometry. The blood of eight rats unexposed to CH2O was collected and analyzed in the same manner. Measured CH2O concentrations (micrograms/g of blood) were: controls, 2.24 +/- 0.07; exposed, 2.25 +/- 0.07 (mean +/- S.E.). Formaldehyde concentrations in human blood were determined by analyzing samples of venous blood collected before and after exposure of six human volunteers (4 M, 2 F) to 1.9 +/- 0.1 ppm of CH2O for 40 min. Average CH2O concentrations (micrograms/g of blood) were: before exposure, 2.61 +/- 0.14; after exposure, 2.77 +/- 0.28. In neither experiment was there a statistically significant effect of exposure on the average CH2O concentration of the blood. However, human subjects differed significantly with respect to their blood CH2O concentrations, and significant differences (either an increase or a decrease) were found between the CH2O concentrations of the blood taken before and after exposure from some of the subjects, suggesting that blood CH2O concentrations may vary with time.     

Acute responses to phosgene inhalation and selected corrective measures (including surfactant)

We exposed 22 mongrel dogs to 94 ppm phosgene for 20 min from a non-rebreathing system. We expressed exposure to phosgene as ppm X VI X min X kg 1, i.e., the amount of gas containing a known phosgene concentration that was actually inhaled per min standardized to body weight, the "exposure index" (EI). In contrast, the conventional expression of exposure, i.e., ppm X min, fails to take volume inhaled (VI) and body weight into account. Five dogs received no intervention and served as controls. Fourteen dogs received basic therapy of oral cortisone (40 mg/kg) and NaHCO3 (3 mEq/kg) plus 100% O2 (FiO2 = 1.0) for 30 min after the exposure period. These animals were further divided according to the following selected additional therapies, which were started 30 min after exposure: Theophylline, 5 mg/kg iv for 20 min followed by 1 mg/kg/hr for 70 min (n = 5). Three dogs of this group were given a trial of 5 cm H2O expiratory resistance during the period of basic therapy. Because of the untoward response, expiratory resistance was discontinued and not used in other experiments. PGE2-hi, [1 microgram/kg/min] iv for 90 min (n = 3). PGE1-lo, [0.04 microgram/kg/min] iv for 90 min (n = 3). Atropine, 0.5 mg/kg iv at 30 and 50 min after exposure (n = 3). Three dogs [group 5] received oral cortisone and NaHCO3 plus inhaled supplementary surfactant, 2.7 mg/min ultrasonically nebulized (FiO2 = 0.5; phosphate buffer), for 30 min after exposure. All treated dogs, groups [1] through [4] and the surfactant group [5], received cortisone (40 mg/kg/hr iv), NaHCO3 to correct base deficit, and O2 to correct hypoxemia from 30 min to 120 min after exposure. Because of its clearly beneficial effect in group [1], theophylline was also given to all other treatment groups during this period. At the end of the study, all lungs were excised, examined and prepared for light microscopy. We found that EI, which varied among subjects because of spontaneous variations of VI during exposure, correlated significantly with the changes in base deficit induced by phosgene inhalation. We also found that the change in minute ventilation, delta VI X kg-1, correlated significantly with changes in lung compliance, peak flow and base deficit. Evaluation of the various therapeutic modalities revealed the following: Immediate therapy with O2 is vital and and FiO2 of 0.4 to 0.5 is sufficient.(ABSTRACT TRUNCATED AT 400 WORDS)     

A study of respiratory effects from exposure to 2 ppm formaldehyde in healthy subjects

Formaldehyde (FA) is a common indoor air pollutant with irritative properties. It has been suggested that FA may produce physiologic alterations of the respiratory system. To study such responses, 15 nonsmoking, healthy subjects were exposed in a double blind, random manner to 0 and 2 ppm FA for 40 min in an environmental chamber. In addition, the same exposures were repeated on a separate day with the subjects performing moderate exercise (450 kpm/min) for 10 min. Exposures were carried out under controlled environmental conditions (temperature = 23 degrees C, relative humidity = 50%). Pulmonary function was measured before, during, and after exposures using partial and maximal flow-volume curves and airway resistance. Symptom diaries were given to the subjects; upper and lower airway symptoms were recorded for up to 24 hr following exposures. No significant bronchoconstriction was noted in this group. In 3 subjects, sequential measurements of peak flow over a 24-hr period following FA exposure failed to reveal any delayed airway response. On a separate day, 6 healthy subjects failed to demonstrate changes from their baseline responsiveness to methacholine after exposure to 2 ppm FA. Respiratory symptoms were, in general, confined to the upper airways and were mild to moderate in severity. We conclude that short exposures to 2 ppm FA do not result in acute or subacute changes in lung function among healthy individuals either at rest or with exercise. Subjective complaints following such exposures are confined to irritative phenomena of the upper airways.     

Combined effect of ozone and sulfuric acid on pulmonary function in man

A potential effect of the combination of ozone and sulfuric acid mist (H2SO4) on respiratory function has been postulated for humans simultaneously exposed to these two pollutants. Nine young men were exposed to 0.25 ppm ozone (O3), 1200-1600 micrograms/m3 sulfuric acid aerosol (H2SO4), and a combination of O3 and H2SO4. During the 2-hr exposures, the subjects exercised (ventilation = 30 L/min) three times for 20 min each. Air temperature was 35 degrees C and relative humidity 83%. Pulmonary function changes after exposure to ozone alone were not expected and were not demonstrated. If a reaction between the combination of O3 and H2SO4 and pulmonary function occurred, pulmonary function responses may have been anticipated following the combination exposure, but no significant changes were seen. It was concluded that the combination of ozone and sulfuric acid aerosol at levels in excess of Threshold Limit Values (TLV) levels do not cause pulmonary dysfunction.     

Transient decrease of exhaled nitric oxide after acute exposure to passive smoke in healthy subjects

Nitric oxide (NO) is produced and detected in the exhalate from the respiratory tract where it plays important regulatory functions. Exhaled nitric oxide (eNO) concentrations are reduced in active cigarette smokers between cigarettes and in nonsmoking subjects during short-term exposure to environmental tobacco smoke. In this study, the authors evaluated eNO before and after an acute exposure to environmental tobacco smoke in healthy, nonsmoking subjects (n = 12). Baseline eNO levels were measured by chemiluminescence at baseline (1 hr before exposure), shortly after the end of exposure, and 10 and 30 min after the end of exposure. Mean room air NO concentration increased from 3 ppb to 4 ppm (range, 560 ppb-8.5 ppm) during the exposure period. Carboxyhemoglobin levels were assessed before and after the exposure with spectrophotometry. All subjects had decreased eNO with exposure to environmental tobacco smoke (mean +/- standard error of the mean: 16.65 +/- 1.35 ppb to 13.86 +/- 1.33 ppb; p < .001). These concentrations remained significantly decreased at 10 min and recovered within 30 min. No modifications in airway resistance or increase in carboxyhemoglobin levels were observed. Exposure to environmental tobacco smoke transiently--but consistently--decreased eNO concentration in healthy, nonsmoking subjects, suggesting that second-hand smoke can directly affect NO in the airway environment.     

Airway responses to 2.0 ppm nitrogen dioxide in normal subjects

Nitrogen dioxide (NO2) is a common indoor air pollutant. To characterize the acute respiratory responses to this gas, 18 nonsmoking normal subjects (mean age +/- standard deviation [SD] = 25 +/- 4 yr) were exposed to filtered air or 2 ppm NO2 gas for 1 hr in a 30-m3 environmental chamber on different days, typically 1 wk apart, in a double-blind randomized fashion. Lung function tests included forced vital capacity, forced expiratory volume in one second, partial expiratory flow at 40% of vital capacity (Vp40), functional residual capacity, and specific airway conductance, and were measured before and after exposure. Airway reactivity to methacholine inhalation was determined within 45 min of each exposure. The dose of methacholine in mg/ml to cause a 40% decrease in specific airway conductance (PD40) was measured. Airway reactivity to methacholine aerosol increased significantly after NO2, which is shown by a decrease in the concentration of methacholine; PD40 (AIR) = 101 +/- 44, PD40 (NO2) = 81 +/- 45 mg/ml, p = .003. No significant changes were noted in the lung function tests after NO2 exposure. These findings indicate that normal nonsmokers exposed to 2.0 ppm NO2 for 1 hr develop an increase in airway reactivity to methacholine aerosol, which is not associated with changes in lung volumes, flow rates, or respiratory symptoms.     

Laboratory study of asthmatic volunteers exposed to nitrogen dioxide and to ambient air pollution

Adult volunteers with moderate to severe asthma (N = 59) underwent dose-response studies to assess their reactivity to nitrogen dioxide (NO2) in otherwise clean air. Exposure concentrations were 0.0 (control), 0.3 and 0.6 ppm. A subgroup (N = 36) also underwent exposures to Los Angeles area ambient air at times when NO2 pollution was expected. Concentrations of NO2 during ambient exposures were 0.086 +/- 0.024 ppm (mean +/- s.d.). All exposures took place in a movable chamber/laboratory facility. Each study lasted 2 hr, with alternating 10 min periods of exercise (mean ventilation rate 40 L/min) and rest. Lung function was measured prior to exposure and after 10 min, 1 hr and 2 hr of exposure. Symptoms were recorded prior to exposure, during exposure and for 1 week afterward. In some subjects bronchial reactivity to cold air was measured 1 hr after the end of exposure and again 24 hr later. Different exposure conditions were presented in randomized order, 1 week apart. No pollutant exposure produced statistically significant changes in lung function, symptoms, or bronchial reactivity, relative to clean air. Ambient air exposures produced the largest (still nonsignificant) mean changes in some lung function tests. Given the physiological and atmospheric variability, negative statistical results do not rule out a small unfavorable effect of ambient pollution on lung function. If any such effect occurred, it was not likely caused by NO2. Statistical results remained negative when the analysis was restricted to the 20 subjects with most severe lung dysfunction. In conclusion at least in the Los Angeles area, sensitivity to ambient concentrations of NO2 is not common, even among adult asthmatics with moderate to severe disease.     

Oral and oronasal breathing during continuous exercise produce similar responses to ozone inhalation

Breathing route has a profound effect on sulfur dioxide-induced pulmonary function response in human subjects. There is comparatively little evidence of the effects of oral, nasal, and oronasal breathing on ozone (O3)-induced responses in humans. In this study, six young adult males were exposed on five occasions to 0.40 parts per million (ppm) O3 while exercising continuously at one of two workloads (minute ventilation, VE, of approximately 30 and 75 l/min). The VE exposure time product was similar for all protocols. Four exposures were delivered randomly with a Hans-Rudolph respiratory valve attached to a silicone facemask, with breathing route effected with and without noseclip. A 2 x 2 analysis of variance revealed no statistically significant differences (p less than .05) across conditions in pulmonary function, exercise ventilatory pattern, or subjective symptoms responses. The fifth exposure, delivered via the same respiratory valve with mouthpiece, but without facemask, revealed significantly greater forced expiratory volume in 1 s (FEV1.0) impairment than that observed for the respiratory valve, facemask with noseclip exposure (-20.4% and -15.9%, respectively). The latter suggests partial O3 reactivity to the facemask and clean shaven facial surface of the subjects, although reduced oral scrubbing by mouthpiece-induced bypassing of the oral vestibule might account, in part, for this difference. Recent O3 uptake evidence from another laboratory, however, supports our conclusion that breathing route during moderate and heavy continuous exercise does not affect acute physiologic responses to 0.40 ppm O3.     

Airway sensitivity of asthmatics to sulfur dioxide

The purpose of this study was to describe for asthmatic subjects the distribution of individual bronchial sensitivity to sulfur dioxide (SO2). Subjects were nonsmoking male asthmatics (n = 27) who were sensitive to inhaled methacholine. None of the subjects used corticosteroids or cromolyn sodium. Oral medications were withheld for 48 hr, inhaled medications for 12 hr prior to all testing. Each subject participated in four separate randomly ordered 10 min exposures to 0.00, 0.25, 0.50 and 1.00 ppm SO2 at 26 degrees C, 70% relative humidity. During exposures, subjects breathed naturally and performed moderate exercise (VE, normalized for body surface area = 21 1/m2 X min). Before and 3 min after exposure, specific airway resistance (SRaw) was measured by body plethysmography. Those subjects whose SRaw was not doubled by exposure to 1.00 ppm were also exposed to 2.00 ppm SO2. Dose response curves (relative change in SRaw, corrected for change in clean air vs SO2 concentration) were constructed for each subject. Bronchial sensitivity to SO2 [PC(SO2)], defined as the concentration of SO2 which provoked an increase in SRaw 100% greater than the response to clean air, was determined. Substantial variability in sensitivity was observed: for 23 subjects, PC(SO2) ranged between 0.28 and 1.90 ppm, while for the remaining 4 subjects, it was greater than 2.00 ppm SO2. The median PC(SO2) was 0.75 ppm SO2, and 6 subjects had a PC(SO2) of less than 0.50 ppm. PC(SO2) was not related (r = 0.31) to airway sensitivity to methacholine.     

Short-term effects of formaldehyde on peak expiratory flow and irritant symptoms

The authors studied the respiratory effects of formaldehyde exposure among students who dissected cadavers in a gross anatomy laboratory. Peak expiratory flow and respiratory symptoms were measured before and after each weekly laboratory session. Each of 38 students was exposed to formaldehyde for 2.5 hr/wk for 14 wk. Individual, daily formaldehyde measurements averaged 1.1 ppm (standard deviation = 0.56 ppm). Multivariate models demonstrated two different time scales of effect of formaldehyde on peak expiratory flow: (1) exposure during the previous 2.5 hr reduced peak expiratory flow by -1.0% per ppm, and (2) average exposure during all preceding weeks reduced peak expiratory flow by an additional -0.5% per ppm of formaldehyde. However, the short-term exposure effect was diminished during the first 4 wk, suggesting at least partial acclimatization. Symptom reporting was also associated with exposure during the previous 2.5 hr, and similar evidence of acclimatization was observed. These results suggest that there are two different time scales of response to formaldehyde, and they emphasize the need for longitudinal studies, characterized by quantitative exposure characterization, and frequent measurements of outcome.     

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.     

Effect of ozone on the agglutination of erythrocytes by concanavalin A. II. Study of human subjects receiving supplemental vitamin E.

Studies of the effect of ozone on the response of human erythrocytes to concanavalin A revealed a decrease in agglutinability following in vitro exposure (1 ppm ozone × 30 min) similar to that previously observed in rat erythrocytes. Incubation of human erythrocytes with malonaldehyde, an oxidation product of polyunsaturated fatty acids, also resulted in decreased agglutination by concanavalin A. Red cells obtained from 29 subjects receiving either vitamin E (800 IU) or a placebo daily were examined before and after the subjects were exposed to 0.5 ppm ozone for 2 hr. A tendency toward a decrease in agglutinability by concanavalin A following ozone exposure was present in the red cells of those subjects not receiving supplemental vitamin E. However, the results were not statistically significant.     

An evaluation of respiratory effects following exposure to 2.0 ppm formaldehyde in asthmatics: lung function, symptoms, and airway reactivity

Fifteen asthmatic volunteers were exposed in a double-blind, random manner to room air and 2.0 ppm formaldehyde for 40 min in an environmental chamber. These exposures were repeated on a separate day during moderate exercise (450 kpm/min) for 10 min. Ambient and dew point temperatures were 23.0 +/- 0.0 degrees C and 11.5 +/- 1.0 degrees C, respectively. No significant airway obstruction as measured by flow-volume parameters and airway resistance was noted in this group during or immediately after exposure. Furthermore, sequential measurements of peak flow for 24 hr following formaldehyde exposure revealed no delayed airway response. In contrast, in comparison to the baseline methacholine inhalation challenge (MIC) test on the screening day, 8 of 12 asthmatics demonstrated a lower threshold to MIC following 2.0 ppm exposure for 40 min; however, the mean and median decrements of threshold in methacholine concentration of 10.4 mg/ml and 24.3 mg/ml were not significant (p = .12). Bad odor, sore throat, and eye irritation were common during exposure but symptoms were infrequent afterward.     

Effects of exposure to 0.06 ppm ozone on FEV1 in humans: a secondary analysis of existing data

BACKGROUND: Ozone is a potent photochemical oxidant that produces transient, reversible decrements in the lung function of acutely exposed individuals. A recent study provided previously unavailable clinical data for 30 healthy young adults exposed to O(3) at 0.06 ppm. That study showed significant effects of 0.08 ppm on lung function, confirming the findings of others. However, exposure to 0.06 ppm O(3) was not reported to significantly affect lung function. OBJECTIVES: We conducted this analysis to reevaluate the existing lung function data of the volunteers previously exposed to 0.06 ppm O(3). METHODS: We obtained pre- and postexposure data on forced expiratory volume in 1 sec (FEV(1)) for all subjects who were previously exposed for 6.6 hr to filtered air or to 0.06 ppm or 0.08 ppm O(3). We used standard statistical methods appropriate for paired comparisons to reanalyze FEV(1) responses after exposure to 0.06 ppm O(3) relative to filtered air. RESULTS: Controlling for filtered air responses, 24 of the 30 subjects experienced an O(3)-induced decrement in FEV(1). On average, 0.06 ppm O(3) exposure caused a 2.85% reduction in FEV(1) (p < 0.002), which was consistent with the predicted FEV(1) response from existing models. Although the average response was small, two subjects had > 10% FEV(1) decrements. CONCLUSIONS: Exposure to 0.06 ppm O(3) causes a biologically small but highly statistically significant decrease in mean FEV(1) responses of young healthy adults.     

Effect of inhaled ozone on lung histamine in conscious guinea pigs

The effect of short-term ozone (O3) exposure on pulmonary mast cell function was examined. Guinea pigs were continuously exposed to 1.0 ppm O3 for 2, 4, and 8 hr. O3 exposure produced a significant decrease in lung histamine concentration. Two-hour exposure to O3 caused a 22.4 +/- 7.0% decrease in lung histamine concentration compared with controls. Ozone exposures of 4 and 8 hr caused lung histamine concentrations to decrease by 43.7 +/- 7.7 and 49.0 +/- 7.5% (P less than 0.05), respectively, without significant changes in lung water or protein, or evidence of cytotoxicity. These results suggest that O3 or its metabolites affect pulmonary mast cell function by stimulating the release of histamine from the lung.     

Prospective study of respiratory effects of formaldehyde among healthy and asthmatic medical students

We conducted a prospective evaluation of pulmonary function and respiratory symptoms among 103 medical students exposed to formaldehyde over a 7-month period to determine the incidence of bronchoconstriction and respiratory symptoms in response to exposure. Time-weighted average formaldehyde exposures were generally less than 1 part per million (ppm) and peak exposures were less than 5 ppm. Acute symptoms of eye and upper respiratory irritation were significantly associated with exposure. There was no pattern of bronchoconstriction in response to exposure after either 2 weeks or 7 months. Twelve subjects had a history of asthma; they were no more likely to have symptoms of respiratory irritation or changes in pulmonary function than those without such a history. These findings are consistent with previous case reports that indicate exposure to formaldehyde vapor at levels that are commonly encountered in occupational and residential settings do not commonly cause significant bronchoconstriction, even among subjects with preexisting asthma.