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.     

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.     

Airway effects of low concentrations of sulfur dioxide: dose-response characteristics

The acute respiratory effects of exposure to low-level, short-term sulfur dioxide (SO2) were studied in ten asthmatic and ten healthy subjects. Subjects were exposed in an environmental chamber in a double-blind, random sequence to SO2) levels of 0.00, 0.25, 0.50, 0.75, and 1.00 ppm for 40 min. During the first 10 min subjects exercised on a cycloergometer at a level of 450 kpm/min. On separate days, subjects were exposed to 0 and 1.0 ppm SO2 in the absence of exercise. In exercising asthmatic subjects, breathing 1 ppm SO2 resulted in significant changes from baseline in airway resistance (Raw), forced expiratory volume in 1 sec (FEV1.0), maximal expiratory flow at 60% of the vital capacity (VC) below total lung capacity on the partial flow volume curve [MEF40% (P)] as well as reductions in flows at 50% of VC (Vmax50%). None of these parameters showed significant changes for exposures to 0.5 ppm or less, with the exception of small decreases (i.e., less than 0.2 L/sec) in Vmax50% at 0.25 and 0.5 ppm. Ten minutes after the end of exercise, there were no statistically significant differences from baseline, even though SO2 was still present in the chamber atmosphere. For asthmatic subjects, the average changes in Raw, FEV1.0, MEF40%(P), and Vmax50% increased as SO2 levels increased, suggestive of a dose-response relationship with a consistent effect first seen at 0.75 ppm. In individual exercising asthmatics, responses may occur at levels of SO2 below 0.75 ppm. No changes were seen in healthy individuals on any day, or in asthmatic subjects at rest.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulmonary function, airway responsiveness, and respiratory symptoms in asthmatics following exercise in NO2

Two experiments were conducted to determine respiratory responses of persons with asthma performing intermittent moderate exercise while exposed to low concentrations of NO2. In the first, preliminary experiment, 13 male subjects, aged 19-35, with mild asthma were exposed on separate days in a chamber (natural breathing, 20 degrees C, 40% RH) to 0.30 ppm NO2 and to a control or "clean air" exposure (0.0 ppm NO2). Exposure included three 10-min periods of moderate treadmill exercise (VE = 44.5 liter/min), each followed by symptom measurement and pulmonary function testing. The average decrease in FEV1 following the initial 10 min exercise in 0.30 ppm was 11% which was significantly greater (p less than 0.05) than that observed in clean air (7%). Differences in FVC and SRaw were not significantly different at this time. Slight cough and dry mouth and throat were apparent only after the first exercise in NO2. After the second and third exercises, decreases in FEV1 and FVC and increases in SRaw were significantly greater in 0.30 than in 0.0 ppm NO2. Individual subject responses were variable. These results suggested that some asthmatics who perform moderate exercise while exposed to 0.30 ppm NO2 may experience bronchoconstriction and reduction in spirometric performance. Because of these preliminary findings, a more comprehensive, concentration-response experiment was conducted. Twenty-one male volunteers with mild asthma were exposed for 75 min with natural breathing to 0.0, 0.15, 0.30, and 0.60 ppm NO2. Exposure included three 10-min periods of moderate treadmill exercise (VE = 43 liter/min), each exercise followed by symptoms measurement and pulmonary function testing. In addition, airway responsiveness was measured two hr after each exposure by methacholine bronchial challenge testing. In the control exposures (0.0 ppm NO2), the exercise alone caused substantial decrements in pulmonary function. These decrements (as measured by decreases in FEV1 and FVC, and increases in SRaw) were not increased relative to the control exposure after any exercise session in any concentration of NO2. Furthermore, there was no overall group-averaged indication of a concentration-related effect of the NO2 on pulmonary function. Likewise, symptoms reported after NO2 exposure were not significantly different from those reported in clean air. Group-averaged airway responsiveness after exercise in NO2 was also not different from responsiveness after exercise in clean air. For only two subjects was there any indication of a concentration-related increase in airway responsiveness due to exposure to NO2.(ABSTRACT TRUNCATED AT 400 WORDS)     

Acute pulmonary response of asthmatics to 3.0 ppm formaldehyde

Previous studies have failed to demonstrate bronchoconstriction in unselected asthmatics after brief (less than or equal to 1/2-h), controlled exposures to formaldehyde (HCHO). This study was designed to evaluate the acute pulmonary response to 3 ppm HCHO in nine nonsmoking asthmatic volunteers over a more relevant exposure duration (3 hrs). Pulmonary function, nonspecific airway reactivity and symptoms were assessed before and at intervals during the exposure. No significant changes in pulmonary function (FVC, FEV1, FEF25-27%, SGaw, or FRC) or airway reactivity were observed. There was a significant increase in nose/throat irritation at 30 min. (P less than 0.05) and in eye irritation at 60 min (P less than 0.05) and 180 min (P less than 0.01). These results suggest that individuals with asthma will not experience significant bronchoconstriction when exposed at rest to 3 ppm HCHO; however, most will experience eye and upper respiratory tract irritation.     

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.     

Pulmonary effects of sulfur dioxide and respirable carbon aerosol

Four-hour individual and combined exposures to 1.0 ppm sulfur dioxide (SO2) and 0.5 mg/m3 (1.5 micron mass median diameter) activated carbon aerosol (ACA) were studied in 20 healthy nonsmoking subjects to determine if activated carbon as a "carrier" aerosol can augment the pulmonary response to SO2. Fifteen-minute exercise stints (VE = 35 liters/min) were performed at commencement and completion of each 4-hr period. Significant increases in nose or throat irritation occurred with the SO2 and SO2 + ACA exposures and in eye irritation with the SO2 + ACA exposure. Small, statistically significant decrements in spirometric function were observed following the first exercise (t = 17 min) for both the SO2 and SO2 plus ACA exposures; no significant changes were associated with the ACA exposure. Comparing function changes between the SO2 and the SO2 + ACA exposures demonstrated no statistically significant differences, thus a lack of SO2 response enhancement by the carbon aerosol. The determination that the activated carbon sorbed only 1% of the SO2 challenge concentration could explain the observed lack of SO2 response enhancement.     

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.     

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.     

Controlled exposures of volunteers with chronic obstructive pulmonary disease to sulfur dioxide

Twenty-four volunteers with chronic obstructive pulmonary disease (COPD) were exposed to sulfur dioxide (SO2) at 0, 0.4, and 0.8 ppm in an environmental control chamber. Exposures lasted 1 hr and included two 15-min exercise periods (mean exercise ventilation rate 18 liter/min). Pulmonary mechanical function was evaluated before exposure, after initial exercise, and at the end of exposure. Blood oxygenation was measured by ear oximetry before exposure and during the second exercise period. Symptoms were recorded throughout exposure periods and for 1 week afterward. No statistically significant changes in physiology or symptoms could be attributed to SO2 exposure. Older adults with COPD seem less reactive to a given concentration of SO2 than heavily exercising young adult asthmatics. This may be due to lower ventilation rates (i.e., lower SO2 dose rates) and/or to lower airway reactivity in the COPD group.     

Relationship between the airway response to inhaled sulfur dioxide,isocapnic hyperventilation,and histamine in asthmatic subjects

Summary To determine whether bronchoconstriction induced by sulfur dioxide can be predicted by the airway response to inhaled histamine, we exposed on two days 46 patients with asthma to air or 0.5 ppm SO₂. The exposure protocol consisted of 10 min of tidal breathing followed by 10 min of isocapnic hyperventilation at a rate of 301/min. Airway response was measured before (baseline) and after hyperventilation in terms of specific airway resistance, SRaw. Exposure to air increased baseline mean (SD) SRaw from 6.27 (2.12) to mean (SD) maximum post-hyperventilation SRaw of 9.10 (4.38) cmH₂O^*s (P < 0.0001). Exposure to SO₂ increased mean (SD) baseline SRaw from 6.93 (3.29) to mean (SD) maximum posthyperventilation SRaw of 18.21 (18.69) cmH₂O^*s (P < 0.0001). Mean (SD) effect of SO₂. defined as difference between maximum post-hyperventilation SRaw after SO₂ versus air was 9.11 (16.14) cmH₂O^*s. When evaluated individually, 26 and 34 of the 46 patients showed an airway response to hyperventilation of air and SO₂, respectively. Airway response to histamine was determined as the histamine concentration necessary to increase specific airway resistance by 100%, PC₁₀₀SRaw. The airway response after SO₂ and PC₁₀₀SRaw showed a weak but significant correlation (R = –0.48), whereas the responses to hyperventilation and SO₂ did not correlate. We suggest that the mechanisms by which histamine and SO₂ exert their bronchomotor effects are different and that in asthmatic patients the risk of pollutant-induced asthmatic symptoms can be poorly predicted by histamine responsiveness.Supported by a grant from the Minister für Jugend, Familie und Gesundheit, Bonn, Federal Repubic of GermanyDedicated to Johannes Piiper on the occasion of the 65th birthday     

A study of respiratory effects from exposure to 2.0 ppm formaldehyde in occupationally exposed workers

It has been suggested that exposure to formaldehyde (FA) induces asthmatic symptomatology. We have previously studied healthy and asthmatic individuals and found that lung function was unaltered by controlled exposures to 2.0 ppm FA with and without mild exercise. Our present study extends these observations to a group of hospital laboratory workers routinely exposed to FA. Fifteen laboratory workers were exposed in double-blind, random sequence to 0 and 2 ppm FA for 40 min in an environmental chamber with temperature and relative humidity held constant at 23 degrees C and 50%, respectively. These exposures were repeated on two more occasions with a 10-min exercise regimen (450 kpm/min) after being in the chamber 5 min. In addition, a symptom diary and measurements of peak expiratory flow rate (PEFR) were recorded for 24 hr after exposure. Lung function remained unaltered for all 4 exposure days; e.g., mean FEV1.0 for the group did not change by more than 3% at any testing time on any exposure day. Also, there were no delayed obstructive changes as measured by PEFR recordings. Symptoms were mild and transient with unusual odor and eye irritation the most frequent complaint. No lower airway symptoms were reported. We conclude that this group of healthy laboratory workers did not experience any acute or delayed lung function changes from exposure to 2.0 ppm FA at rest and with exercise and that irritative symptoms were few.     

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 submicrometer sulfuric acid aerosols on mucociliary transport and respiratory mechanics in asymptomatic asthmatics

The effects of a 1-hr inhalation of submicrometer sulfuric acid (H2SO4) aerosols via nasal mask on tracheobronchial mucociliary particle clearance and respiratory mechanics were studied in ten subjects with asthmatic histories. A brief inhalation of monodisperse 3.9-micron 99mTc-tagged Fe2O3 aerosol preceded the 1-hr H2SO4 (at 100, 300, and 1000 micrograms/m3) or a sham exposure. Thoracic retention of the gamma-tagged Fe2O3 was measured using external radiation detectors. Respiratory function was measured before, and 15 min and 3 hr after the H2SO4 or sham exposure. After exposure to 1000 micrograms/m3 of H2SO4, the six subjects not on routine medication exhibited a transient slowing of mucociliary clearance and also decrements in sGaw, FEV1/FVC, MMEF, and V25 (P less than 0.05) in both sets of measurements. The four asthmatics on daily medication exhibited stepwise mucociliary clearance that was too variable to allow detection of any H2SO4 effect on clearance. The 1000 micrograms/m3 of H2SO4 did produce decrements in V25 (P less than 0.05), but the variability of the other respiratory parameters in this small group was too great to permit detection of changes. Mucociliary clearance rates in both groups in the sham exposure tests were significantly slower than those of healthy nonsmokers studied previously using the same protocols. The extent of mucociliary clearance slowing following the 1000 micrograms/m3 exposure in the nonmedicated subjects was similar to that in the healthy nonsmokers. This similar change, from a reduced baseline rate of clearance, together with the significant change in respiratory function, indicate that asymptomatic asthmatics may respond to H2SO4 exposures with functional changes of greater potential health significance than do healthy nonsmokers.     

Duration of enhanced responsiveness upon re-exposure to ozone

It has been repeatedly observed that ozone (O3) re-exposure within 24 h elicits enhanced pulmonary function responses. However, there are only limited observations concerning re-exposure to O3 at intervals between 24 h and several days. The present study was designed to assess the effects of re-exposure to 0.35 ppm O3 at intervals of 24, 48, 72, and 120 h. Forty young adult male subjects were assigned randomly to one of four groups in ascending order of time to re-exposure (groups 1-4). Each exercised on a bicycle ergometer for 60 min at a workload that elicited a mean ventilation of 60 l/min on three occasions: protocol 1 (P1), filtered air (FA); protocol 2 (P2), 0.35 ppm O3; and protocol 3 (P3), 0.35 ppm O3. In addition to standard pulmonary function measures, specific airway resistance (SRaw); exercise ventilatory pattern, i.e., respiratory frequency (fR) and tidal volume (VT); and subjective symptoms (SS) were assessed. Statistical analysis revealed significant differences (p less than .05) for all groups between the FA (P1) responses and those for the two O3 exposures (P2, P3) for forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1.0), SRaw, fR, VT, and SS. When the two O3 exposures (P2 and P3) were compared, only group 1 (24 h) responses were statistically significant upon re-exposure: FEV1.0, -16.1 vs. -30.4% (p less than .003); SRaw, 20.5 vs. 34.5% (p less than .05); fR, 44.2 vs. 65.3% (p less than .001); and SS (p less than .015).(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of duration of exposure on sulfuric acid-induced pulmonary function changes in asthmatic adolescent subjects: a dose-response study.

To evaluate the pulmonary effects of varying doses of sulfuric acid, adolescent subjects with asthma were exposed to 35 or 70 micrograms/m3 sulfuric acid for 45 or 90 min. Exposure was carried out during intermittent moderate exercise. The pulmonary functions measured before and after exposure were FEV1, FVC, and total respiratory resistance. The 45 min exposures were associated with larger decreases in FEV1 (-6% or -3%) than the 90 min exposures (-1% or +2%). Analysis of variance of the change in FEV1 among the exposures revealed that the 45 min exposure to 35 micrograms/m3 was significant (p = 0.03). The p value for 45 min exposure to 70 micrograms/m3 was not significant (p = 0.08). Using analysis of variance, neither of the 90 min exposures was associated with a significant decrease in FEV1 compared to air exposure. Also, none of the changes in FVC or RT was significant. When baseline to post-exposure changes were compared for each of the five test atmospheres using paired t tests, both of the 45 min exposures were associated with statistical significance (p < 0.001 for 35 micrograms/m3 and p < 0.005 for 70 micrograms/m3). This baseline to post exposure change was not statistically significant for the 90 min exposures. The reason for the lesser effect on pulmonary function at increased exposure duration is not known; it may be due to changes in either varying deposition patterns or changes in buffering capacity of the cells lining the airways. With respect to individual sensitivities to H2SO4, the data showed a significant consistency across test atmospheres.     

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.     

Does nitrogen dioxide exposure increase airways responsiveness?

A number of reports have suggested that exposure to nitrogen dioxide (NO2) may cause increased airways responsiveness (AR). Twenty studies of asthmatics and five studies of healthy subjects exposed to NO2 were used to test this hypothesis using a simple method of meta-analysis. Individual data were obtained for the above studies and the direction of change in AR was determined for each subject. Only studies with available individual data were used. Subjects from these studies whose directional change in AR could not be determined were excluded. The fraction of positive responses (i.e. increased AR) was determined for all subjects within a group and tested for significance using a sign test. Data were also grouped according to NO2 concentration and by whether the exposure included exercise. There was an overall trend among asthmatics for AR to increase (60%) but this was primarily due to increased AR seen in resting exposures (70%). Among healthy subjects AR also increased with NO2 exposure but only at concentrations above 1.0 ppm. This analysis suggests that NO2 exposure causes increased airway responsiveness in healthy and asthmatic subjects but that exercise during exposure may modify this response in asthmatics.     

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.     

Does suggestibility modify acute reactions to passive cigarette smoke exposure?

The influence of suggestibility on responses to passive cigarette smoke exposure was tested in a group of 24 healthy adult nonasthmatic nonsmokers and 16 asthmatic nonsmokers. Sixty-five-min exposures to air and to moderate (17 ppm carbon monoxide) and heavy (31 ppm carbon monoxide) concentrations of machine-produced cigarette smoke were carried out according to a design that permitted all six permutations of the three treatments to be equally represented. Nonasthmatic subjects exercised intermittently at an intensity inducing a respiratory ventilation of 43.6 liters/min, while asthmatic individuals were at rest, in a 14.6-m3 chamber; all viewed a bank of burning cigarettes during each exposure. Significant dose-response relationships were observed for reported symptoms, deterioration of pulmonary function, increase in nasal airflow resistance, and increase of carboxyhemoglobin levels. These findings could reflect either a pure physiological response, or an interaction between physiological and psychological responses. For asthmatics, correlations between pulmonary function responses and baseline measures of suggestibility showed 5/45 (11%) significant correlations (P less than 0.05) for both the ratio of saline diluent/air FEV1 during methacholine inhalation challenge and an index derived from the Minnesota Multiphasic Personality Inventory (MMPI), while no significant correlations were shown with the James "locus of control" test. Nonasthmatics showed 4/45 (9%) significant correlations for both the James test and the MMPI index, and 1/45 (2%) for the ratio of saline diluent/air FEV1. It is concluded that while suggestibility may augment physiological responses to passive smoking, any effect is relatively weak.