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.

Potential risks to human respiratory health from "acid fog": evidence from experimental studies of volunteers.

Observations of high acidity (pH as low as 1.7) in fogwater collected in polluted areas have provoked concern for public health. Effects of exposure to acidic pollutants have not been studied under foggy conditions; thus there is no directly relevant information from which to estimate the health risk. Indirectly relevant information is available from numerous studies of volunteers exposed to "acid fog precursors" under controlled conditions at less than 100% relative humidity. The effect of fog in modifying responses to inhaled acidic pollutants is difficult to predict: depending on circumstances, fog droplets might either increase or decrease the effective dose of pollutants to the lower respiratory tract. Fog inhalation per se may have unfavorable effects in some individuals. Sulfur dioxide is known to exacerbate airway constriction in exercising asthmatics, at exposure concentrations attainable in ambient air. Nitrogen dioxide has shown little untoward respiratory effect at ambient concentrations in most studies, although it has been suggested to increase bronchial reactivity. Sulfuric acid aerosol has shown no clear effects at concentrations within the ambient range. At somewhat higher levels, increased bronchial reactivity and change in mucociliary clearance have been suggested. Almost no information is available concerning nitric acid.

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.

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.

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.

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.

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.

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)

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."

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

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

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.

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.

Effects of exposure to 4 ppm nitrogen dioxide in healthy and asthmatic volunteers.

Healthy and asthmatic volunteer subjects (N = 25 and N = 23, respectively) were exposed twice each to purified air (control) and to 4 ppm nitrogen dioxide (NO2) in a controlled-environment chamber. Exposures lasted 75 min, and included 15 min each of light exercise (ventilation rate near 25 L/min) and heavy exercise (near 50 L/min). Compared to control, NO2 exposure produced no statistically significant untoward effects on airway resistance, symptoms, heart rate, skin conductance, or self-reported emotional state in normal or asthmatic subjects. Exercise was associated with significantly (P less than .001) increased airway resistance in both subject groups, although the increase in normals was small. In both groups, systolic blood pressure showed small but significant (P less than .01) decreases with NO2 exposure, compared to control. This effect, if real, may relate to formation of a vasodilating nitrite or nitrate from inhaled NO2. The lack of respiratory response contrasts with previous findings elsewhere; at present, this inconsistency is unexplained.

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.

Dose-response study of asthmatic volunteers exposed to nitrogen dioxide during intermittent exercise.

Twenty-one mildly asthmatic volunteers were exposed to 0, 0.3, 1.0, and 3.0 ppm nitrogen dioxide (NO2) in purified background air in an environmental control chamber. Exposures were separated by 1-wk periods and occurred in random order. Each lasted 1 hr and included three 10-min bouts of moderately heavy exercise (mean ventilation rate 41 L/min). Exposure temperature was near 22 degrees C and relative humidity near 50%. Specific airway resistance and maximal forced expiratory performance were measured preexposure, after the initial exercise, and near the end of exposure. Bronchial reactivity was assessed immediately following exposure, by normocapnic hyperventilation with subfreezing air. Symptoms were recorded on questionnaires before, during, and for 1-wk after each exposure. Exercise induced significant bronchoconstriction regardless of NO2 level. No statistically significant untoward response to NO2 was observed at any exposure concentration. This negative finding agrees with our previous results, but contrasts with findings elsewhere of respiratory dysfunction after exposure to 0.3 ppm. The discrepancy is presently unexplained, but it may relate to different severity of asthma in different subject groups.

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.

Effects of heat and humidity on the responses of exercising asthmatics to sulfur dioxide exposure.

Twenty-two asthmatic young adult volunteers, predetermined to be reactive to sulfur dioxide (SO2) with exercise at normal room temperature, were studied to document short-term effects of SO2 exposure under hot conditions, both humid and dry. For comparison, similar exposures were conducted at mild temperatures. All subjects were exposed in an environmental control chamber to all possible combinations of 2 atmospheric conditions (purified air and 0.6 ppm SO2), 2 temperatures (near 21 and 38 degrees C), and 2 levels of relative humidity (near 20 and 80%). Exposures involved 5 min of heavy exercise (target ventilation rate, 50 L/min) plus brief warm-up and cool-down periods. Body plethysmographic measurements and symptom questionnaire interviews were administered before and at the end of each exposure. Response was expressed in terms of change in airway size or change in intensity of symptoms during exposure. Atmospheric condition showed the most marked and significant overall effect on physiologic responses; temperature and humidity effects were also significant. High temperature and high humidity tended to mitigate the bronchoconstriction produced by 0.6 ppm SO2 exposure: group mean specific airway resistance approximately tripled at 21 degrees C and low humidity, but increased by less than 40% at 38 degrees C and high humidity. Temperature and humidity affected symptoms less consistently than physiologic responses, but in general, symptom responses paralleled physiologic responses.

Replicated dose-response study of sulfur dioxide effects in normal, atopic, and asthmatic volunteers.

To help assess respiratory health risks from sulfur dioxide (SO2) air pollution, we studied 24 normal, 21 atopic, 16 minimal/mild asthmatic, and 24 moderate/severe, medication-dependent asthmatic subjects classified according to history, lung function, allergy skin tests, serum IgE level, and airway reactivity to methacholine. All were exposed in a chamber (21 degrees C, 50% humidity) to 0.0, 0.2, 0.4, and 0.6 ppm SO2 in random order at 1-wk intervals; then exposures were repeated to test consistency of response. The 1-h exposures included three 10-min exercise periods (ventilation approximately 40 L/min). Physiologic response was measured early (approximately 15 min) and late (approximately 55 min) in exposure. Symptoms were evaluated during exposure and for 1 wk afterward. Normal and most atopic subjects showed little response at these SO2 levels. A few atopic subjects and many asthmatics developed bronchoconstriction and respiratory symptoms, but most were able to maintain their exercise. Effects were not markedly different between early and late measurements, nor between the first and second round of studies; however, late and second-round responses appeared slightly more favorable. No statistically significant effect of SO2 on symptoms was found 1 day or 1 wk after exposure. Minimal/mild asthmatics showed, on the average, slight responses at 0.0 ppm (attributable to exercise) and increasing responses at increasing SO2 concentrations. Moderate/severe asthmatics reacted more at 0.0 ppm, but their increments in response with increasing SO2 concentration were roughly similar to those of minimal/mild asthmatics. Thus, responses to SO2 per se were not strongly dependent on clinical severity of asthma, nor on SO2 exposure history during previous weeks.

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.