Pulmonary function responses of young and older adults to mixtures of O3, NO2 and PAN

The pulmonary function of 32 nonsmokers (eight men and eight women, 18-26 years of age; eight men and eight women, 51-76 years of age) was measured before and after two-hour exposures to (1) filtered air (FA), (2) 0.45 ppm ozone (O3), (3) 0.13 ppm peroxyacetyl nitrate + 0.45 ppm O3 (PAN/O3), (4) 0.60 ppm nitrogen dioxide + 0.45 ppm O3 (NO2/O3), and (5) 0.13 ppm PAN + 0.60 ppm NO2 + 0.45 ppm O3 (PAN/NO2/O3). Subjects alternated 20-minute periods of rest and exercise (ventilation = 25 L/min). Forced vital capacity (FVC) was measured pre-exposure and five-minutes after each exercise period. Forced expiratory volume in one sec (FEV1.0) and forced expiratory flow between 25 and 75 percent of FVC (FEF25-75%) were calculated from the FVC tests. Data were analyzed by 4-factor analysis of variance (sex, age, time period, exposure). The responses of men and women were similar. FA exposure induced no effects. The young subjects' decrements in FVC, FEV1.0 and FEF25-75% became significant (P less than 0.01) after the second exercise period of the O3, NO2/O3 and PAN/NO2/O3 exposures, while the PAN/O3 decrements were significant (P less than 0.01) after the first exercise period. Although PAN/O3 induced significant decrements earlier than the other conditions including O3, the mean pre- to post-exposure decrements for the four conditions including O3 were similar. In contrast, the older subjects had smaller and fewer significant decrements in pulmonary functions. They had significant mean decrements in FVC following the third exercise period of the NO2/O3 and PAN/NO2/O3 exposures, in FEV1.0 after the third exercise period of the PAN/O3 and NO2/O3 exposures, and in FEF 25-75% beginning after the second exercise period of the NO2/O3 exposure. The results suggest that older men and women are less responsive to O3 and mixtures of O3, NO2 and PAN than young men and women, and that O3 is responsible for the decrements observed in pulmonary function.     

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)     

Experimental studies on human health effects of air pollutants. III. Two-hour exposure to ozone alone and in combination with other pollutant gases.

Adult male volunteers were exposed to ozone (O3) at 0.25, 0.37, or 0.50 ppm, and to O3 in combination with nitrogen dioxide (NO2) and carbon monoxide (CO), with secondary stresses of heat, intermittent light exercise, and repeated exposure. Few important physiological changes, and only mild symptoms, were found with 0.25 ppm O3, with 0.25 ppm 03 plus 0.30 ppm NO2, or when 30 ppm CO was added to the latter mixture. With 0.37 ppm O3, more symptoms were present and some subjects developed definite decreases in pulmonary function. With 0.50 ppm O3, most subjects had symptoms and about half showed substantial pulmonary function decrement. In reactive subjects exposed on two successive days, changes were usually greater the second day, indicating that effects of successive exposures were cumulative.     

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.     

Respiratory effects of 2-hr exposure to 1.0 ppm nitric oxide in normal subjects

Eight adult healthy male volunteers were exposed to 1.0 ppm nitric oxide (NO) with intermittent light exercise for 2 hr. No one showed any symptoms during NO exposure. A small, but significant, decrease of specific airway conductance was observed in half of the subjects. As a group, a significant reduction of the percentage increase of maximal expiratory flow at 50% of forced vital capacity while breathing a HeO₂ gas mixture as compared with air was observed among various pulmonary function tests. These results suggested that some physiological responses to NO exposure might be observed in some subjects when performing exercise.     

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)     

Interaction of ozone and cigarette smoke exposure

Possible interactions of ozone and cigarette smoke exposure have been tested in 2-hr chamber exposures of 26 male and 6 female subjects, all of whom were habitual smokers. Treatment conditions were air alone, air + cigarette smoking, ozone alone, and ozone + cigarette smoking. Ozone levels were increased progressively over four trials (0.37 ppm, 0.75 ppm, 0.50 ppm + intermittent exercise, and 0.75 ppm + intermittent exercise); exercise (50 W for 15 min alternating with 15-min rest) was intended to increase ventilation by a factor of 2.5. Ozone exposure reduced the carbon monoxide intake normally seen with smoking, as judged from smaller increments of blood carboxyhemoglobin readings. Ozone exposure alone gave rise to a decrease of lung function (forced vital capacity (VC), 1-sec forced expiratory volume, and maximum flow rates at 25 and 50% of VC), but the onset was slower and the response less dramatic than previously seen in nonsmokers, suggesting that the chronic effect of smoking may be to delay bronchial irritation by ozone. Smoking increased heart rate both at rest and during exercise, but this response was not materially influenced by simultaneous ozone exposure. It is concluded that over an acute 2-hr exposure, there is no appreciable interaction between cigarette smoking and responses to ozone.     

Duration of increased pulmonary function sensitivity to an initial ozone exposure

The metabolic and pulmonary function effects were investigated in six non-smoking young adults who were exposed for 2 hours (22 degrees C WBGT) to: filtered air (FA) 0.45 ppm ozone (DAY1); and two days later to a second exposure to 0.45 ppm ozone (DAY2). The subjects alternated 20-minute periods of rest and 20-minute periods of bicycle ergometer exercise at a workload predetermined to elicit a ventilatory minute volume (VE) of 27 L/min (BTPS). Functional residual capacity (FRC) was determined pre- and post-exposure. Forced vital capacity (FVC) was determined before and after exposure, as well as 5 minutes after each exercise period. Heart rate was monitored throughout the exposure, and VE, oxygen uptake (VO2), respiratory rate (fR), and tidal volume (VT) were measured during the last 2 minutes of each exercise period. There were no changes in any variable consequent to FA exposure. Both ozone exposures induced significant (P less than 0.05) decrements in FVC; FEV1.0 (forced expiratory volume in 1 second); FEV3.0 (forced expiratory volume in 3 seconds); FEF25-75% (average flow rate between 25% and 75% of FVC); and total lung capacity (TLC). The decrements following the DAY2 ozone exposure were significantly greater than following DAY1, and averaged 7.2 percentage points greater than those following the DAY1 exposure.     

Inhaled albuterol does not protect against ozone toxicity in nonasthmatic athletes

We evaluated the acute prophylactic efficacy of albuterol aerosol in protecting nonasthmatic athletes from the untoward effects of 0.21 ppm ozone (O3) on symptoms, pulmonary function, exercise performance, and post-exposure histamine bronchoprovocation. Fifteen trained competitive cyclists participated in a randomized crossover study consisting of double-blinded inhalations of albuterol (180 micrograms) and placebo approximately 30 min prior to heavy continuous exercise (minute ventilation, [VE] greater than or equal to 80 L/min) for 60 min, followed by a maximal sprint (peak VE greater than 140 L/min) until exhaustion. Each subject was exposed randomly to either 0.21 ppm O3 or filtered air (FA) during the four single-blinded exposure sessions. Albuterol pretreatment resulted in modest but significant bronchodilation as compared to placebo. However, albuterol did not prevent O3-induced respiratory symptoms, decrements in forced vital capacity (FVC), forced expired volume in one second (FEV1.0), and maximum midexpiratory flow rate (FEF25-75%), and positive histamine challenges as compared to that with placebo/O3. There were no statistically significant differences in the metabolic data or ride times across all drugs and exposures, although the peak VE was significantly lower with O3 than FA (142.3 vs. 150.7 L/min, respectively) regardless of drug. The results indicate that acute pretreatment with inhaled albuterol is unable to prevent or ameliorate O3-induced symptoms and alterations in pulmonary function and exercise performance. The contribution of beta-adrenergic mechanisms in the acute airway responses to O3 appears to be minimal.     

Periodontal Disease in Well- and Malnourished Populations

The effects on pulmonary function of inhaling the same effective dose of ozone, as well as subjective responses during continuous exercise and intermittent exercise, were studied in 12 aerobically trained men. Each subject completed 1 h of continuous exercise at work rates that elicited a mean minute ventilation of 60 l/min, and two additional 2-h intermittent exercise exposures eliciting a mean exercise minute ventilation of 45–47 l/min (i.e., total minute ventilation for each protocol was approximately 3 600 l). Subjects were exposed in randomized sequence to 0.30 ppm ozone on three occasions and to filtered air on three occasions. Forced expiratory volume in 1 s decrements of ?17.6%, ?17.0%, and ?17.9%, respectively, for the 1-h continuous exercise exposure and the two 2-h intermittent exercise exposures to 0.30 ppm ozone were significantly different. Exposure to ozone caused significant differences between postexposure subjective symptom responses; that is, responses associated with continuous exercise were greater than those for either intermittent exercise protocol. However, the overall symptom severity responses during the last minute of exercise for the two intermittent exercise protocols (at 90 and 105 min, respectively) were not significantly different from the continuous exercise postexposure value. The findings indicate that when the ozone effective dose is equivalent at a given ozone concentration, there is no difference between pulmonary function responses to continuous exercise or intermittent exercise exposures of 2-h duration (or less), although subjective symptoms are reduced somewhat during the last rest period of intermittent exercise.     

Enhanced response to ozone exposure during the follicular phase of the menstrual cycle.

Exposure to ozone (O3), a toxic component of photochemical smog, results in significant airway inflammation, respiratory discomfort, and pulmonary function impairment. These effects can be reduced via pretreatment with anti-inflammatory agents. Progesterone, a gonadal steroid, is known to reduce general inflammation in the uterine endometrium. However, it is not known whether fluctuations in blood levels of progesterone, which are experienced during the normal female menstrual cycle, could alter O3 inflammatory-induced pulmonary responses. In this study, we tested the hypothesis that young, adult females are more responsive to O3 inhalation with respect to pulmonary function impairment during their follicular (F) menstrual phase when progesterone levels are lowest than during their mid-luteal (ML) phase when progesterone levels are highest. Nine subjects with normal ovarian function were exposed in random order for 1 hr each to filtered air and to 0.30 ppm O3 in their F and ML menstrual phases. Ozone responsiveness was measured by percent change in pulmonary function from pre- to postexposure. Significant gas concentration effects (filtered air versus O3) were observed for forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), and forced expiratory flow between 25 and 75% of FVC (FEF25-75; p < .05). More importantly, the pulmonary function flow rates, FEV1 and FEF25-75, showed a significant menstrual phase and gas concentration interaction effect, with larger decrements observed in the F menstrual phase when progesterone concentrations were significantly lower. We conclude that young, adult females appear to be more responsive to acute O3 exposure during the F phase than during the ML phase of their menstrual cycles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Respiratory response of humans exposed to low levels of ozone for 6.6 hours

Recent evidence suggests that prolonged exposures of exercising men to 0.08 ppm ozone (O3) result in significant decrements in lung function, induction of respiratory symptoms, and increases in nonspecific airway reactivity. The purpose of this study was to confirm or refute these findings by exposing 38 healthy young men to 0.08 ppm O3 for 6.6 h. During exposure, subjects performed exercise for a total of 5 h, which required a minute ventilation of 40 l/min. Significant O3-induced decrements were observed for forced vital capacity (FVC, -0.25 l), forced expiratory volume in 1 s (FEV1.0, -0.35 l), and mean expiratory flow rate between 25% and 75% of FVC (FEF25-75, -0.57 l/s), and significant increases were observed in airway reactivity (35%), specific airway resistance (0.77 cm H2O/s), and respiratory symptoms. These results essentially confirm previous findings. A large range in individual responses was noted (e.g., percentage change in FEV1.0; 4% increase to 38% decrease). Responses also appeared to be nonlinear in time under these experimental conditions.     

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.     

Effects of ozone and other pollutants on the pulmonary function of adult hikers.

This study evaluated the acute effects of ambient ozone (O3), fine particulate matter (PM2.5), and strong aerosol acidity on the pulmonary function of exercising adults. During the summers of 1991 and 1992, volunteers (18-64 years of age) were solicited from hikers on Mt. Washington, New Hampshire. Volunteer nonsmokers with complete covariates (n = 530) had pulmonary function measured before and after their hikes. We calculated each hiker's posthike percentage change in forced expiratory volume in 1 sec (FEV1), forced vital capacity (FVC), the ratio of these two (FEV1/FVC), forced expiratory flow between 25 and 75% of FVC(FEF25-75%), and peak expiratory flow rate (PEFR). Average O3 exposures ranged from 21 to 74 ppb. After adjustment for age,sex, smoking status (former versus never), history of asthma or wheeze, hours hiked, ambient temperature, and other covariates, there was a 2.6% decline in FEV1 [95% confidence interval (CI), 0.4-4.7; p = 0.02] and a 2.2% decline in FVC (CI, 0.8-3.5; p =0.003) for each 50 ppb increment in mean O3. There were consistent associations of decrements in both FVC (0.4% decline; CI,0.2-0.6, p = 0.001) and PEFR (0.8% decline; CI, 0.01-1.6; p = 0.05) with PM2.5 and of decrements in PEFR (0.4% decline; CI, 0.1-0.7; p = 0.02) with strong aerosol acidity across the interquartile range of these exposures. Hikers with asthma or a history of wheeze (n = 40) had fourfold greater responsiveness to ozone than others. With prolonged outdoor exercise, low-level exposures to O3, PM2.5, and strong aerosol acidity were associated with significant effects on pulmonary function among adults. Hikers with a history of asthma or wheeze had significantly greater air pollution-related changes in pulmonary function.     

Dietary Antioxidants and Ozone-Induced Bronchial Hyperresponsiveness in Adults with Asthma

Ozone exposure aggravates asthma, as has been demonstrated in both controlled exposures and epidemiologic studies. In the current double-blind crossover study, the authors evaluated the effects of dietary antioxidants (i.e., 400 IU vitamin E/500 mg vitamin C) on ozone-induced bronchial hyperresponsiveness in adult subjects with asthma. Seventeen subjects were exposed to 0.12 ppm of ozone or to air for 45 min during intermittent moderate exercise. Bronchial hyperresponsiveness was assessed with 10-min sulfur dioxide (i.e., 0.10 ppm and 0.25 ppm) inhalation challenges. Subjects who were given dietary antioxidants responded less severely to sulfur dioxide challenge than subjects given a placebo (i.e., forced expiratory volume in the 1st sec: -1.2% vs. 4.4%, respectively; peak flow: +2.2% vs. -3.0%, respectively; and mid-forced expiratory flow: +2.0% vs. -4.3%, respectively). Effects were more pronounced when subjects were grouped by response to sulfur dioxide at the screening visit. The results suggest that dietary supplementation with vitamins E and C benefits asthmatic adults who are exposed to air pollutants.     

Dietary antioxidants and ozone-induced bronchial hyperresponsiveness in adults with asthma

Ozone exposure aggravates asthma, as has been demonstrated in both controlled exposures and epidemiologic studies. In the current double-blind crossover study, the authors evaluated the effects of dietary antioxidants (i.e., 400 IU vitamin E/500 mg vitamin C) on ozone-induced bronchial hyperresponsiveness in adult subjects with asthma. Seventeen subjects were exposed to 0.12 ppm of ozone or to air for 45 min during intermittent moderate exercise. Bronchial hyperresponsiveness was assessed with 10-min sulfur dioxide (i.e., 0.10 ppm and 0.25 ppm) inhalation challenges. Subjects who were given dietary antioxidants responded less severely to sulfur dioxide challenge than subjects given a placebo (i.e., forced expiratory volume in the 1st sec: -1.2% vs. 4.4%, respectively; peak flow: +2.2% vs. -3.0%, respectively; and mid-forced expiratory flow: +2.0% vs. -4.3%, respectively). Effects were more pronounced when subjects were grouped by response to sulfur dioxide at the screening visit. The results suggest that dietary supplementation with vitamins E and C benefits asthmatic adults who are exposed to air pollutants.     

Acute effect of sulphur dioxide from a power plant on pulmonary function of children, Thailand

BACKGROUND: Epidemiological studies have shown reversible declines of lung function in response to air pollution, but research on the independent effect of short-term exposure to ambient sulphur dioxide (SO2) on pulmonary function is limited. This study evaluated the association of short-term exposure to increased ambient SO2 and daily pulmonary function changes among children with and without asthma. METHODS: The associations of daily exposure to SO2 and particulate matter 10 microm in diameter (PM10) with pulmonary function were examined in 175 asthmatic and non-asthmatic children aged 6-14 years who resided near a coal-fired power plant in Thailand. Each child performed daily pulmonary function tests during the 61-day study period. General linear mixed models were used to estimate the association of air pollution and pulmonary function controlling for time, temperature, co-pollutants, and autocorrelation. RESULTS: In the asthmatic children, a daily increase in SO2 was associated with negligible declines in pulmonary function, but a small negative association was found between PM10 and pulmonary function. A 10-microg/m(3) increment was associated with changes in the highest forced vital capacity (FVC) (-6.3 ml, 95% CI: -9.8, -2.8), forced expiratory volume at 1 second (FEV(1)) (-6.0 ml, 95% CI: -9.2, 2.7), peak expiratory flow rate (PEFR) (-18.9 ml.sec(-1), 95% CI: -28.5, -9.3) and forced expiratory flow 25 to 75% of the FVC (FEF(25-75%)) (-3.7 ml.sec(-1), 95% CI: -10.9, 3.5). No consistent associations between air pollution and pulmonary function were found for non-asthmatic children. CONCLUSION: Declines in pulmonary function among asthmatic children were associated with increases in particulate air pollution, rather than with increases in SO2.     

Obstructive pulmonary function defects among Taiwanese firebrick workers in a 2-year follow-up study.

The purpose of the study was to follow up an earlier observation of pulmonary function among workers employed in firebrick-manufacturing factories. A 2-year follow-up study of pulmonary function among 442 workers in 30 firebrick-manufacturing factories was designed. Excluding 79 workers with a history of other occupational dust exposure, changes in pulmonary function of 291 firebrick workers were compared with pulmonary function in 72 control subjects over a period of 2 years. Baseline pulmonary function values (i.e., forced expiratory volume in 1 second [FEV1]/forced vital capacity [FVC] and forced expiratory flow after 50% of vital capacity has been expelled [FEF50%] in smoking firebrick workers, and FEV1/FVC and FEF75% in nonsmoking firebrick workers) were significantly lower than those in the comparison group. The statistical method for repeated measurements was used for comparison of the difference between follow-up and baseline lung function. There was no significant difference in FVC and FEV1 changes between firebrick workers and those in the comparison group during the 2-year follow-up period. The decreases in FEV1/FVC, peak expiratory flow rate, maximal midexpiratory flow, and FEF50% in the firebrick workers were significantly greater than in the comparison group, after adjustment for smoking status. The FEV1, maximal midexpiratory flow, FEF50%, and FEF75% also showed a dose-response relationship with job titles. The decrement of pulmonary function in the 2-year follow-up period was the worst in burning work, followed by crushing and molding. The results show that workers in firebrick-manufacturing factories with exposure to silica-containing dusts may contract obstructive pulmonary function defects.     

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.     

Nitrogen dioxide exposure in vivo and human alveolar macrophage inactivation of influenza virus in vitro

Epidemiologic studies have reported an increased incidence of respiratory infections and illness in association with elevated indoor levels of nitrogen dioxide (NO2). Animal exposure studies have found that brief exposures to peak levels of NO2 produce greater morbidity than continuous lower level exposure. In order to examine the effect of NO2 inhalation on human alveolar macrophages, normal volunteers were exposed sequentially to air or NO2, by double-blind randomization, in an environmental chamber. Two exposure protocols with comparable concentration x time products were used: (a) continuous 0.60 ppm NO2 (n = 9), and (b) background 0.05 ppm NO2 with three 15-min peaks of 2.0 ppm (n = 15). Inhalation of NO2 caused no significant changes in pulmonary function or airway reactivity in either exposure protocol. Alveolar macrophages obtained by bronchoalveolar lavage 3 1/2 hr after exposure to continuous 0.60 ppm NO2 tended to inactivate influenza virus in vitro less effectively than cells collected after air exposure (1.96 vs 1.25 log10 plaque-forming units on Day 2 of incubation, P less than 0.07). Four of nine subjects accounted for the observed impairment in virus inactivation; cells from these four subjects demonstrated an increase in interleukin-1 (IL-1) production after NO2 vs air, whereas the five remaining subjects decreased IL-1 production after NO2. In contrast, intermittent peak exposure did not alter the rate of viral inactivation or IL-1 production. This methodology has the potential to identify pollutant effects on mechanisms of respiratory defense in humans.