Exhaled nitric oxide, susceptibility and new-onset asthma in the Children's Health Study.

A substantial body of evidence suggests an aetiological role of inflammation, and oxidative and nitrosative stress in asthma pathogenesis. Exhaled nitric oxide fraction (F(eNO)) may provide a noninvasive marker of oxidative and nitrosative stress, and aspects of airway inflammation. We examined whether children with elevated F(eNO) are at increased risk for new-onset asthma. We prospectively followed 2,206 asthma-free children (age 7-10 yrs) who participated in the Children's Health Study. We measured F(eNO) and followed these children for 3 yrs to ascertain incident asthma cases. Cox proportional hazard models were fitted to examine the association between F(eNO) and new-onset asthma. We found that F(eNO) was associated with increased risk of new-onset asthma. Children in the highest F(eNO) quartile had more than a two-fold increased risk of new-onset asthma compared to those with the lowest quartile (hazard ratio 2.1, 95% CI 1.3-3.5). This effect did not vary with the child's history of respiratory allergic symptoms. However, the effect of elevated F(eNO) on new-onset asthma was most apparent among those without a parental history of asthma. Our results indicate that children with elevated F(eNO) are at increased risk for new-onset asthma, especially if they have no parental history of asthma.

Respiratory effects of relocating to areas of differing air pollution levels.

We studied 110 children (59 boys and 51 girls, who were 10 yr of age at enrollment and 15 yr of age at follow-up) who had moved from communities participating in a 10-yr prospective study of respiratory health (The Children's Health Study [CHS]) to determine whether changes in air quality caused by relocation were associated with changes in annual lung function growth rates. The subjects were given health questionnaires and underwent spirometry in their homes across six western states, according to a protocol identical to evaluations performed annually on the CHS cohort in school. Changes in annual average exposure to particulate matter with a mean diameter of 10 microm (PM(10)) were associated with differences in annual lung function growth rates for FEV(1), maximal midexpiratory flow, and peak expiratory flow rate. As a group, subjects who had moved to areas of lower PM(10) showed increased growth in lung function and subjects who moved to communities with a higher PM(10) showed decreased growth in lung function. A stronger trend was found for subjects who had migrated at least 3 yr before the follow-up visit than for those who had moved in the previous 1 to 2 yr. We conclude that changes in air pollution exposure during adolescent growth years have a measurable and potentially important effect on lung function growth and performance.

Quality of spirometry test performance in children and adolescents : experience in a large field study.

STUDY OBJECTIVE: To determine the ability of children and adolescents to meet the American Thoracic Society (ATS) goals for spirometry quality that were based on results from adults. DESIGN: Observational. PARTICIPANTS: More than 4,000 public school students, ages 9 to 18 years. MEASUREMENTS: Spirometry was performed annually for 3 years, with the recording of maneuver quality measures of forced expiratory time, end-of-test volume, back-extrapolated volume, and time to peak expiratory flow (PEFT), and the recording of differences between best and second-best FVC, FEV(1), and peak expiratory flow (PEF) values. RESULTS: Regression analyses showed significant influences of participant age, gender, ethnicity, size, clinical status, and previous testing experience, as well as differences among individual test technicians. In general, these influences were small and explained little of the variance in performance. On average, children with a history of asthma or wheeze performed better quality spirometry than did others. Only PEFT improved significantly from year to year. Overall, only 15% of girls' tests and 32% of boys' tests met the PEFT criterion derived from adults in the Lung Health Study. CONCLUSION: Most of the children met adult-based ATS goals for spirometry test performance. Age group-specific criteria are needed to ensure adequately fast PEFT and reproducible PEF values.

Initial field evaluation of the Harvard active ozone sampler for personal ozone monitoring.

Assessing personal exposure to ozone has only been feasible recently with the introduction of passive ozone samplers. These devices are easy to use, but changes in air velocity across their collection surfaces can affect performance. The Harvard active ozone sampler (AS) was developed in response to problems with the passive methods. This active sampler has been tested extensively as a microenvironmental sampler. To test for personal sampling, 40 children attending summer day-camp in Riverside, California wore the active ozone sampler for approximately 2.6 h on July 19 and 21, 1994, when ozone concentrations were about 100 ppb and 140 ppb, respectively. The children spent 94-100% of the sampling period outside, staying within a well-defined area while participating in normal camp activities. Ambient ozone concentrations across this area were monitored by two UV photometric ozone monitors. The active sampler was worn in a small backpack that was also equipped with a passive ozone sampler. Device precision, reported as the percent difference between duplicate pairs of samplers, was +/- 3.7% and +/- 4.2% for the active and passive samplers, respectively. The active sampler measured, on average, 94.5 +/- 8.2% of the ambient ozone while the passive samplers measured, on average, 124.5 +/- 18.8%. The samplers were worn successfully for the entire sampling period by all participating children.

Acute effects of ambient ozone on asthmatic, wheezy, and healthy children.

Southern California children (10 to 12 years old) participated in a two-season study to assess the potential acute respiratory effects of ambient ozone (O3). Asthmatic (n = 49), wheezy (n = 53), and healthy (n = 93) children completed a four-day (Friday through Monday) study protocol, once in spring and again in summer, that included the use of daily activity and symptom diaries, heart rate recording devices, personal O3 samplers, and maximal effort spirometry several times per day. Data from regional monitoring stations were used to establish ambient hourly O3 concentrations. Analyses revealed that the children spent more time outdoors and were more physically active in the spring. Girls spent less time outdoors and were less physically active than boys. Personal O3 samplers correlated poorly with, and generally gave lower readings than, outdoor ambient monitors. Higher personal O3 exposures were associated generally with increased inhaler use, more outdoor time, and more physical activity. Children with asthma spent more time outdoors and were more active in the spring on high-O3 days (measured by personal sampler), and had the most trouble breathing, the most wheezing, and the most inhaler use on these days. Activity pattern data suggested that children with asthma protected themselves by being less physically active outdoors during the summer on high-O3 days. Wheezy children had the most trouble breathing during the summer on low-O3 days (measured by personal sampler). Observed relationships between O3 and pulmonary function were erratic and difficult to reconcile with existing knowledge about the acute respiratory effects of air pollution. We conclude that although asthmatic and wheezy children behave differently from their healthy peers with regard to symptoms and patterns of activity when challenged by ambient ozone, the nature of these changes remains inconsistent and ill-defined.

Temperature standardization of multiple spirometers.

In respiratory health surveys involving multiple spirometers, spirometer differences may introduce important biases. We investigated temperature measurement variability as a cause of spirometer differences. Digital thermometers recorded internal (cylinder) and external (outer casing) temperatures of six similar rolling-seal spirometers during field use and in laboratory tests at controlled room temperatures. Internal and external thermometers substantially agreed in recording spirometer temperature changes, which lagged room temperature changes. Offsets of individual thermometers from overall mean readings were roughly the same in field testing of 3908 students in > 60 schools over 5 months and in subsequent laboratory tests. Thermometers differed by as much as 1.3 degrees C, causing differences as large as 0.8% in vital capacity measurements. We conclude that (1) interior and exterior temperatures of typical rolling-seal spirometers do not differ greatly, although both may differ from surrounding air temperature; and (2) variations between individual digital thermometers may be large enough to bias spirometric data appreciably in large-scale surveys. Variations should be controlled by selection of similar-reading thermometers and/or correction to a uniform standard.

Chamber exposures of children to mixed ozone, sulfur dioxide, and sulfuric acid.

To help assess acute health effects of summer air pollution in the eastern United States, we simulated ambient "acid summer haze" as closely as was practical in a laboratory chamber. We exposed young volunteers who were thought to be sensitive to this pollutant mixture on the basis of previous epidemiologic evidence. Specifically, we exposed 41 subjects aged 9-12 y to mixed ozone (0.10 ppm), sulfur dioxide (0.10 ppm), and 0.6-microm sulfuric acid aerosol (100 +/- 40 microg/m3, mean +/- standard deviation) for 4 h, during which there was intermittent exercise. Fifteen subjects were healthy, and 26 had allergy or mild asthma. The entire group responded nonsignificantly (p > .05) to pollution exposure (relative to clean air), as determined by spirometry, symptoms, and overall discomfort level during exercise. Subjects with allergy/asthma showed a positive association (p = .01) between symptoms and acid dose; in healthy subjects, that association was negative (p = .08). In these chamber-exposure studies, we noted less of an effect than was reported in previous epidemiologic studies of children exposed to ambient "acid summer haze."

Short-term air pollution exposures and responses in Los Angeles area schoolchildren.

We studied 269 school children from three Southern California communities of contrasting air quality in two successive school years, to investigate short-term effects of ambient ozone (O3), nitrogen dioxide (NO2), or particulate matter (PM) on respiratory health. We measured lung function and symptoms twice daily for one week each in fall, winter and spring; and concurrently assessed time-activity patterns and personal exposures. Average daily personal exposures correlated with pollutant concentrations at central sites (r = 0.61 for O3, 0.63 for NO2, 0.48 for PM). Questionnaire-reported outdoor activity increased slightly in communities/seasons with higher pollution. Lung function differences between communities were explainable by age differences. Morning forced vital capacity (FVC) decreased significantly with increase in PM or NO2 measured over the preceding 24 hours. Morning-to-afternoon change of forced expired volume in one second (FEV1) became significantly more negative with increase in PM, NO2, or O3 on the same day. Predicted FVC or FEV1 loss on highest- vs lowest-pollution days was < 2%. Daily symptoms showed no association with current or prior 24-hour pollution, but increased with decreasing temperature. Parents' questionnaire responses suggested excess asthma and allergy in children from one polluted community while children in the other polluted community reported more symptoms, relative to the cleaner community. We conclude that Los Angeles area children may experience slight lung function changes in association with day-to-day air quality changes, reasonably similar to responses seen by others in less polluted areas. Although short-term pollution effects appear small, they should be assessed in longitudinal lung function studies when possible, to allow maximally accurate measurement of longer-term function changes.

Standardization of multiple spirometers at widely separated times and places.

We designed a system for a multiyear longitudinal study of lung function in 12 widely separated communities, intending to minimize variation in instrument-related data. We used multiple rolling-seal spirometer/personal computer systems. Calibrations were checked before, during, and after each day's field testing, using multiple calibration syringes with electronic readouts. The syringes were rotated to obtain data for each syringe-spirometer combination. Before and after each annual field testing season, a laboratory reference spirometer system was calibrated against a water-displacement device and an electronic frequency counter, and then compared against each field spirometer and syringe. Field equipment consistently met American Thoracic Society (ATS) specifications. Variance among spirometers exceeded variance among syringes. A spirometer occasionally changed its volume readout by approximately 1 to 2 %. More rarely, a syringe changed its delivered volume by approximately 1%. Syringes' electronic readouts tracked changes in delivered volume. Syringe readouts were the most stable component of the system, and were more reproducible than the laboratory water-displacement calibration. We conclude that variation in spirometers may limit the reliability of epidemiologic findings, even when these spirometers meet ATS specifications. Frequent calibration checks traceable to an independent standard, and adjustment of individual test results, can reduce measurement error.

Effects of prolonged, repeated exposure to ozone, sulfuric acid, and their combination in healthy and asthmatic volunteers.

To evaluate effects of "acid summer haze" on individuals who exercise extensively outdoors, we exposed 45 adult volunteers (15 normal or atopic, 30 asthmatic) in a chamber to a mixture of 0.12 ppm ozone (O3) and approximately 100 micrograms/m3 of respirable sulfuric acid aerosol (H2SO4). On separate occasions we exposed the same subjects to O3 alone, to H2SO4 alone, and to clean air. In exposures involving H2SO4, excess acid was generated to consume ammonia released by the subjects, and the aerosol therefore contained ammonium salts in addition to H2SO4. Subjects were exposed to each atmosphere on two successive days, for 6.5 h/d, with six 50-min exercise periods at ventilation rates averaging 29 L/min. Exposures were conducted during four successive weeks, in random order. Lung function and symptoms were measured before exposure and hourly during exposure. Bronchial reactivity to inhaled methacholine was measured just after the end of each exposure. Exposure to H2SO4 alone caused no significant changes in lung function, symptoms, or bronchial reactivity relative to clean air. Exposure to O3 alone or O3 + H2SO4 caused a progressive, statistically significant (p < 0.05) decline in forced expiratory function, smaller on the second day than the first, as previously found by others for O3 exposure. Bronchial reactivity increased significantly after exposure to O3 with or without H2SO4. Changes in mean lung function and bronchial reactivity with O3 + H2SO4 exposure were modestly larger than changes with O3 exposure, but the differences were nonsignificant or marginally significant. A minority of individual asthmatic and nonasthmatic subjects showed substantially greater declines in function with exposure to O3 + H2SO4 relative to O3 alone. Repeat exposure studies of these subjects again showed an excess response to O3 + H2SO4 on the average, but there was no significant correlation between the excess responses of individual subjects in the original and repeat studies. We conclude that for typical healthy or asthmatic adults heavily exposed to acid summer haze, O3 is more important than H2SO4 as a cause of short-term respiratory irritant effects.

Active and passive ozone samplers based on a reaction with a binary reagent.

Ozone is one of the most toxic common air pollutants (judging from short-term animal and human exposure studies at realistic concentrations) and one of the most difficult and expensive pollutants to control. Because of ozone's high chemical reactivity, its concentrations may vary greatly over short distances, and fixed-site air quality monitors may not accurately estimate exposures of human populations. Epidemiologic research on ozone's long-term health effects has been inconclusive, partly because of the lack of reliable personal exposure information. The objective of this project was to develop a practical personal ozone exposure monitoring technique, and to document its precision and accuracy in actual use by representatives of freely ranging, ozone-exposed populations. The project site, Los Angeles, is the nation's metropolitan area with the highest level of ozone pollution and, thus, probably the most important locale for personal exposure assessment. Our overall strategy was (1) to select the most promising laboratory technique for ozone detection from published literature and private communications; (2) to design and test personal monitors using this technique; and (3) when feasible, to evaluate concurrently alternative methodologies developed by others. As indicated below, parts 1 and 2 of our strategy yielded a limited success with respect to short-term active sampling, i.e., measuring personal ozone exposure levels during one to two hours with a monitor incorporating a battery-powered air pump of the type used in industrial hygiene investigations. The same approach was not successful in passive sampling, i.e., measuring exposure levels during multihour or multiday periods with a light-weight, diffusion-controlled "badge" sampler having no moving parts. Passive badge samplers could be calibrated reasonably well in laboratory exposures to ozone in otherwise pure air, but they greatly overestimated ozone levels in outdoor ambient air. Part 3 of our strategy yielded more promising information on an alternative passive badge design. After testing and rejecting two other possibilities, we chose a binary organic reagents, 3-methyl-2-benzothiazolinone acetone azine with 2-phenylphenol, as the most promising chemical detector of ozone. Filter papers impregnated with the binary reagent develop a characteristic intense pink color when exposed to ozone. The inventors, J.E. Lambert and associates of Kansas State University, had intended only to develop a rough qualitative ozone monitor (Lambert et al. 1989). However, our initial laboratory testing (in exposure chambers containing ozone in otherwise very clean air, away from humans), revealed fairly accurate quantitative response.(ABSTRACT TRUNCATED AT 400 WORDS)

Exposures of older adults with chronic respiratory illness to nitrogen dioxide. A combined laboratory and field study.

We combined field and laboratory experimentation to evaluate the effects of nitrogen dioxide in a panel of Los Angeles area residents with chronic respiratory illness, 15 men and 11 women aged 47 to 69. All had heavy smoking history, chronic symptoms, and low FEV1; some also had low FVC. During the fall-winter high-NO2 season, they monitored themselves for 2-wk periods using spirometers in the home, passive NO2 sampling badges, and diaries to record time and activity patterns and clinical status. In the middle of each self-monitoring week they were exposed in a chamber, once to clean air and once to 0.3 ppm NO2. Chamber exposures were double blind, lasted 4 h, and included four 7-min exercise sessions with average ventilation rates near 25 L/min. Symptom reports and hourly forced expiratory function tests showed no statistically significant differences between clean air and NO2 chamber exposures, although peak flow showed a approximately 3% loss with NO2 relative to clean air during the first 2 h of exposure only (p = 0.056). No significant overall differences were found between field self-measurements and measurements of lung function in the chamber or between field measurements in clean air and NO2 exposure weeks. Field data showed that group average lung function and symptom levels were worse in the morning than later in the day (p < 0.005) but otherwise were stable over 2 wk. Even though most subjects smoked and stayed indoors 80 to 90% of the time, personal NO2 exposures correlated significantly with outdoor NO2 concentrations as reported by local monitoring stations.(ABSTRACT TRUNCATED AT 250 WORDS)

Controlled exposures of volunteers to respirable carbon and sulfuric acid aerosols.

Respirable carbon or fly ash particles are suspected to increase the respiratory toxicity of coexisting acidic air pollutants, by concentrating acid on their surfaces and so delivering it efficiently to the lower respiratory tract. To investigate this issue, we exposed 15 healthy and 15 asthmatic volunteers in a controlled-environment chamber (21 degrees C, 50 percent relative humidity) to four test atmospheres: (i) clean air; (ii) 0.5-microns H2SO4 aerosol at approximately 100 micrograms/m3, generated from water solution; (iii) 0.5-microns carbon aerosol at approximately 250 micrograms/m3, generated from highly pure carbon black with specific surface area comparable to ambient pollution particles; and (iv) carbon as in (iii) plus approximately 100 micrograms/m3 of ultrafine H2SO4 aerosol generated from fuming sulfuric acid. Electron microscopy showed that nearly all acid in (iv) became attached to carbon particle surfaces, and that most particles remained in the sub-micron size range. Exposures were performed double-blind, 1 week apart. They lasted 1 hr each, with alternate 10-min periods of heavy exercise (ventilation approximately 50 L/min) and rest. Subjects gargled citrus juice before exposure to suppress airway ammonia. Lung function and symptoms were measured pre-exposure, after initial exercise, and at end-exposure. Bronchial reactivity to methacholine was measured after exposure. Statistical analyses tested for effects of H2SO4 or carbon, separate or interactive, on health measures. Group data showed no more than small equivocal effects of any exposure on any health measure.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory responses of young asthmatic volunteers in controlled exposures to sulfuric acid aerosol.

Thirty-two asthmatic volunteers 8 to 16 yr of age, recruited through local schools and private physicians, were exposed in a chamber to clean air (control condition) and to sulfuric acid aerosol at a "low" concentration (46 +/- 11 micrograms/m3; mean +/- SD) and at a "high" concentration (127 +/- 21 micrograms/m3). Acid aerosols had mass median aerodynamic diameters near 0.5 microns with geometric standard deviations near 1.9. Temperature was 21 degrees C, and relative humidity was near 50%. Subjects were exposed with unencumbered oronasal breathing for 30 min at rest plus 10 min at moderate exercise (ventilation rate approximately 20 L/min/m2 of body surface). A subgroup (21 subjects) were exposed similarly to clean air and to "high" acid (134 +/- 20 micrograms/m3) with 100% oral breathing. Increased symptoms and bronchoconstriction were found after exercise under all exposure conditions. For the group, symptom and lung function responses were not statistically different during control and during acid exposures with unencumbered breathing or with oral breathing. By contrast, other investigators have reported statistically significant lung function disturbances in groups of young asthmatics exposed similarly with oral breathing. A minority of our subjects showed possibly meaningful excess bronchoconstriction with "high" acid exposure relative to control with both routes of breathing. This could be the result of chance, or it could suggest the existence of an acid-sensitive subpopulation of young asthmatics.

Effect of exposures to ambient ozone on ventilatory lung function in children.

This study was undertaken to determine if the ventilatory capacity of children is affected by hourly concentrations of ozone inhaled during their daily activity. Over a 3-wk period (June-July 1987) children who were attending a summer camp in the San Bernardino mountains of California performed spirometry up to three times per day during their stay at the camp. A total of 43 children were tested a total of 461 times. Ozone, oxides of nitrogen, sulfur dioxide, temperature, and relative humidity were measured continuously. Daily average measurements of total suspended particulate and the PM10 particulate fraction (less than or equal to 10 microns) were also made. Hourly ozone concentrations at the time of testing varied between 20 and 245 ppb. Regressions of each individual's FEV1 and FVC supported the view that high ozone levels reduced these lung function parameters. The average regression coefficient for FEV1 on ozone was -0.39 ml/ppb (SEM = 0.12) and for FVC -0.44 ml/ppb (SEM = 0.15), both of which were significantly different from zero. Statistical allowance for temperature and humidity increased the magnitude of these slopes. Nitrogen dioxide never exceeded 40 ppb during the time of testing and averaged 13 ppb. Sulfur dioxide's highest measurement was 8 ppb and often was at the limit of detection. Neither NO2 nor SO2 was considered in the statistical modeling. Data were divided based on whether each subject had been exposed to levels of ozone in excess of the National Ambient Air Quality Standard (NAAQS) during the several hours previous to being tested. Exposures exceeding the NAAQS indicated a significant negative relationship between ozone and FEV1, FVC, and PEFR. Data for nonexceedance periods did not indicate this negative relationship for any of the three lung function parameters, but it could not be determined if this was due to an absence of an ozone effect or to a combination of the increased variability and decreased size of this data subset. These data indicate that lung function changes on a daily basis relate in a negative fashion to ambient ozone levels. The magnitude of the changes are small and are reversed as ambient ozone decreases.

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.

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

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

Effect of droplet size on respiratory responses to inhaled sulfuric acid in normal and asthmatic volunteers.

We exposed groups of healthy and asthmatic volunteers to sulfuric acid aerosols with volume median droplet diameters of approximately 20, 10, and 1 microns, at nominal concentrations of 2,000 micrograms/m3, and exposed them similarly to aerosols of purified water as a control. Exposures lasted 1 h each, and included three 10-min periods of exercise (ventilation rate typically 40 to 45 L/min). Exposures occurred in randomized order 7 days apart. Temperature was 10 degrees C, relative humidity was approximately 100% in 20- and 10-microns (fog) exposures, and approximately 75 to 80% in 1-micron aerosol exposures. Healthy subjects showed no statistically significant changes in lung function or in bronchial reactivity to methacholine attributable to acid exposures. They showed significant increases in lower and upper respiratory irritant symptoms when exposed to 20- or 10-microns acid fog, but not when exposed to 1-micron acid aerosol. Asthmatics showed significant excess decreases in forced expiratory performance, increases in airway resistance, and increases in irritant symptoms during acid exposures, relative to control conditions. Lung function changes in asthmatics tended to increase with time during exposure; they did not vary significantly with acid droplet size. Symptoms in asthmatics were slightly worse with 10- or 20-microns fog as compared with 1-micron aerosol. In a few instances, symptoms and lung function decrements necessitated stopping exercise or terminating the exposure early. Thus, asthma is a risk factor for unfavorable physiologic response to sulfuric acid at occupational exposure concentrations. Large droplet size (i.e., fog) tends to exacerbate short-term symptomatic response, but we have not been able to demonstrate a consistent effect of droplet size on physiologic response.

Acid fog: effects on respiratory function and symptoms in healthy and asthmatic volunteers.

Acidic air pollutants generally are dissolved in water droplets. Mean droplet diameter may range from more than 10 microns in dense fog to less than 1 micron at low relative humidity. Droplet size influences the deposition of inhaled acid within the respiratory tract and thus may influence toxicity. To help assess health risks from acid pollution, we performed controlled exposures of normal and asthmatic volunteers to sulfuric acid aerosols at nominal concentrations of 0 (control), 500, 1000, and 2000 micrograms/m3. Exposures lasted 1 hr with intermittent heavy exercise. Response was assessed by lung function tests and symptom questionnaires. Under foggy conditions (mean droplet size 10 microns, temperature 50 degrees F), no marked effects on lung function were found. However, both normal and asthmatic subjects showed statistically significant dose-related increases in respiratory symptoms. In a separate study, normal subjects exposed at 70 degrees F with mean droplet size 0.9 microns showed no marked effect on function or symptoms. Asthmatics showed dose-related decrements in forced expiratory performance and increases in symptoms, most obvious at 1000 and 2000 micrograms/m3. The different results of the two studies probably reflect an influence of droplet size, but further investigation is needed to confirm this. The aggregate results suggest that only mild, if any, short-term respiratory irritant effects are likely at acid concentrations attained in ambient pollution.

Repeated laboratory ozone exposures of volunteer Los Angeles residents: an apparent seasonal variation in response.

This study was intended to help explain individual differences in susceptibility to irritant effects of ozone (O3), by determining whether prior ambient O3 exposures and/or recent acute respiratory illness modified response to laboratory O3 exposures. Response was measured in terms of lung function changes and irritant symptoms. Initially, 59 adult volunteer Los Angeles area residents underwent screening exposures in spring, before the season of frequent high ambient O3 levels. Unusually responsive and nonresponsive individuals (N = 12 and 13 respectively) underwent followup exposures in autumn (late in the high-O3 season) and in winter (low-O3 season). All exposures were to 0.18 ppm O3 for 2 hr with intermittent heavy exercise at 31 degrees C and 35% relative humidity. Nonresponders tended to remain nonresponsive throughout. In fall, responders had lost much of their reactivity, as if they had "adapted" to summer ambient O3 exposures. They did not regain reactivity by winter. Clinical laboratory findings suggestive of acute respiratory illness did not appear to correlate with O3 response. Eight responders and 9 nonresponders underwent another followup exposure in spring, about 1 yr after screening. By that time most responders had regained their reactivity; individual function changes were significantly correlated with changes 1 yr earlier. These results suggest that response to O3 is a persistent individual characteristic, but can be modified by repeated ambient exposures.