Documentation of the nasal nitric oxide response to humming: methods evaluation.

RATIONALE: Nitric oxide (NO) is present at higher concentrations in the nasal cavity than in the lower airway, and at even higher concentrations within the paranasal sinuses proper. When the paranasal sinus ostia are patent, acoustic activity produced by vocalization with closed lips (humming) promotes mixing of sinus with nasal gases, producing a further increase in nasal NO. We wished to evaluate procedures for the documentation of the nasal NO response to humming. MATERIALS AND METHODS: We compared two ATS-recommended sampling methods: 1) active exhalation of lower airway gas (parallel technique) and 2) passive aspiration of nasal gas with closed velopharynx (series technique). Variables controlled for included sampling rate, external resistance (parallel method), humming frequency, humming duration, and intertrial interval. Prior to upper airway sampling, exhaled lower airway NO was determined utilizing ATS-standardized technique. RESULTS: Ten volunteers (seven males and three females, aged 21-58) with no history of respiratory allergies or sino-nasal disease were studied in a single session each. The parallel technique documented an increase in nasal NO during the humming manoeuvre in all subjects (mean ratio of humming-to-quiet NO, 4.2), whereas the series technique did so in eight of 10 subjects (mean ratio 2.1). Correcting for admixture from the lower airway, the ratio of humming-to-quiet NO was greater with the parallel than series sampling technique (P < 0.05). CONCLUSIONS: Documentation of the response of nasal NO to humming in subjects without sino-nasal disease was consistently achievable by parallel sampling using commercially available equipment. Specific operational procedures are proposed.

Association between short term exposure to fine particulate matter and heart rate variability in older subjects with and without heart disease.

BACKGROUND: Short term increases in exposure to particulate matter (PM) air pollution are associated with increased cardiovascular morbidity and mortality. The mechanism behind this effect is unclear, although changes in autonomic control have been observed. It was hypothesised that increases in fine PM measured at the subjects' home in the preceding hour would be associated with decreased high frequency heart rate variability (HF-HRV) in individuals with pre-existing cardiac disease. METHODS: Two hundred and eighty five daily 20 minute measures of HRV (including a paced breathing protocol) were made in the homes of 34 elderly individuals with (n = 21) and without (n = 13) cardiovascular disease (CVD) over a 10 day period in Seattle between February 2000 and March 2002. Fine PM was continuously measured by nephelometry at the individuals' homes. RESULTS: The median age of the study population was 77 years (range 57-87) and 44% were male. Models that adjusted for health status, relative humidity, temperature, mean heart rate, and medication use did not find a significant association between a 10 microg/m3 increase in 1 hour mean outdoor PM2.5 before the HRV measurement and a change in HF-HRV power in individuals with CVD (3% increase in median HF-HRV (95% CI -19 to 32)) or without CVD (5% decrease in median HF-HRV (95% CI -34 to 36)). Similarly, no association was evident using 4 hour and 24 hour mean outdoor PM2.5 exposures before the HRV measurement. CONCLUSION: No association was found between increased residence levels of fine PM and frequency domain measures of HRV in elderly individuals.

Measurement of offline exhaled nitric oxide in a study of community exposure to air pollution.

As part of a large panel study in Seattle, Washington, we measured levels of exhaled nitric oxide (eNO) in children's homes and fixed-site particulate matter with aerodynamic diameters of 2.5 micro m or less (PM(2.5)) outside and inside the homes as well as personal PM(2.5) during winter and spring sessions of 2000-2001. Nineteen subjects 6-13 years of age participated; 9 of the 19 were on inhaled corticosteroid (ICS) therapy. Exhaled breath measurements were collected offline into a Mylar balloon for up to 10 consecutive days. Mean eNO values were 19.1 (SD +/- 11.4) ppb in winter sessions and 12.5 +/- 6.6 ppb in spring sessions. Fixed-site PM(2.5) mean concentrations were 10.1 +/- 5.7 microg/m(3) outside homes and 13.3 +/- 1.4 inside homes; the personal PM(2.5) mean was 13.4 +/- 3.2 microg/m(3). We used a linear mixed-effects model with random intercept and an interaction term for medications to test for within-subject-within-session associations between eNO and various PM(2.5) values. We found a 10 microg/m(3) increase in PM(2.5) from the outdoor, indoor, personal, and central-site measurements that was associated with increases in eNO in all subjects at lag day zero. The effect was 4.3 ppb [95% confidence interval (CI), 1.4-7.29] with the outdoor monitor, 4.2 ppb (95% CI, 1.02-7.4) for the indoor monitor, 4.5 ppb (95% CI, 1.02-7.9) with the personal monitor, and 3.8 ppb (95% CI, 1.2-6.4) for the central monitors. The interaction term for medication category (ICS users vs. nonusers) was significant in all analyses. These findings suggest that eNO can be used as an assessment tool in epidemiologic studies of health effects of air pollution.

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.

Genetic polymorphisms as biomarkers of sensitivity to inhaled sulfur dioxide in subjects with asthma.

BACKGROUND: Individuals with asthma are sensitive to inhaled sulfur dioxide (SO2); decrements in pulmonary function occur after exposure to low concentrations even for a short duration of time. There is a great amount of interindividual variation in response to SO2. OBJECTIVE: It was our objective to determine whether one of the following polymorphism locations linked with asthma is associated with the bronchial hyperresponsiveness to SO2 observed in some asthmatic patients: the beta2-adrenergic receptor, interleukin-4 (IL-4) receptor alpha subunit, Clara cell secretory protein (CC16), TNF-alpha gene promoter, and first intron of the lymphotoxin alpha (LT-alpha) gene. METHODS: Subjects were volunteers with physician-diagnosed asthma requiring regular asthma medication. Spirometry was performed before and after a 10-minute exposure to 0.5 ppm SO2. Subjects were classified as SO2 responders if forced expiratory volume in 1 second (FEV1) decreased > or = 12%. DNA obtained from buccal cell samples was analyzed for genetic polymorphisms. RESULTS: Of the 62 subjects (21 male and 41 female), 13 had a 12% or greater decrement in FEV1 after SO2 exposure (range + 19% to -49%). Response to SO2 was associated with the wild-type allele of the TNF-alpha promoter polymorphism (12 of 12 SO2 responders versus 28 of 46 nonresponders; P < .05) but with no other polymorphisms. Medication category and atopic status showed no association with SO2 sensitivity. CONCLUSIONS: The wild-type allele of the TNF-alpha promoter polymorphism may be associated with mechanisms of asthmatic sensitivity to inhaled SO2.

Effects of ozone exposure on nuclear factor-kappaB activation and tumor necrosis factor-alpha expression in human nasal epithelial cells.

In this study we investigated a possible mechanism of the human airway inflammatory response to inhaled ozone (O(3)). Cultures of human nasal epithelial (HNE) cells, initiated from excised nasal turbinates and grown on collagen-coated Transwell tissue culture inserts, were exposed to 120, 240, or 500 ppb O(3) for 3 h. An electron spin resonance (ESR) signal that changed with time suggested free radical production in HNE cells exposed to O(3). Nuclear protein extracts were analyzed for the activated transcription factor NF-kappaB by electrophoretic mobility-shift assay (EMSA), and showed a small dose-response activation of NF-kappaB that coincided with O(3)-induced free radical production. Basal media were analyzed for the presence of tumor necrosis factor-alpha (TNF-alpha) using the enzyme-linked immunosorbent assay (ELISA). In cultures exposed to 120 ppb O(3), the mean TNF-alpha concentration was not significantly different from those exposed to air. However, exposure to 240 and 500 ppb O(3) significantly increased mean TNF-alpha expression, relative to controls, 16 h after exposure. These results support the hypothesis that the human airway epithelium plays a role in directing the inflammatory response to inhaled O(3) via free radical-mediated NF-kappaB activation.

Windblown dust contributes to high PM2.5 concentrations.

The revised National Ambient Air Quality Standards for PM include fine particulate standards based upon mass measurements of PM2.5. It is possible in arid and semi-arid regions to observe significant coarse mode intrusion in the PM2.5 measurement. In this work, continuous PM10, PM2.5, and PM1.0 were measured during several windblown dust events in Spokane, WA. PM2.5 constituted approximately 30% of the PM10 during the dust event days, compared with approximately 48% on the non-dusty days preceding the dust events. Both PM10 and PM2.5 were enhanced during the dust events. However, PM1.0 was not enhanced during dust storms that originated within the state of Washington. During a dust storm that originated in Asia and impacted Spokane, PM1.0 was also enhanced, although the Asian dust reached Washington during a period of stagnation and poor dispersion, so that local sources were also contributing to high particulate levels. The "intermodal" region of PM, defined as particles ranging in aerodynamic size from 1.0 to 2.5 microns, was found to represent a significant fraction of PM2.5 (approximately 51%) during windblown dust events, compared with 28% during the non-dusty days before the dust events.

Associations between air pollution and mortality in Phoenix, 1995-1997.

We evaluated the association between mortality outcomes in elderly individuals and particulate matter (PM) of varying aerodynamic diameters (in micrometers) [PM(10), PM(2.5), and PM(CF )(PM(10) minus PM(2.5))], and selected particulate and gaseous phase pollutants in Phoenix, Arizona, using 3 years of daily data (1995-1997). Although source apportionment and epidemiologic methods have been previously combined to investigate the effects of air pollution on mortality, this is the first study to use detailed PM composition data in a time-series analysis of mortality. Phoenix is in the arid Southwest and has approximately 1 million residents (9. 7% of the residents are > 65 years of age). PM data were obtained from the U.S. Environmental Protection Agency (EPA) National Exposure Research Laboratory Platform in central Phoenix. We obtained gaseous pollutant data, specifically carbon monoxide, nitrogen dioxide, ozone, and sulfur dioxide data, from the EPA Aerometric Information Retrieval System Database. We used Poisson regression analysis to evaluate the associations between air pollution and nonaccidental mortality and cardiovascular mortality. Total mortality was significantly associated with CO and NO(2) (p < 0.05) and weakly associated with SO(2), PM(10), and PM(CF) (p < 0. 10). Cardiovascular mortality was significantly associated with CO, NO(2), SO(2), PM(2.5), PM(10), PM(CF) (p < 0.05), and elemental carbon. Factor analysis revealed that both combustion-related pollutants and secondary aerosols (sulfates) were associated with cardiovascular mortality.

Effects of ambient air pollution on symptoms of asthma in Seattle-area children enrolled in the CAMP study.

We observed a panel of 133 children (5-13 years of age) with asthma residing in the greater Seattle, Washington, area for an average of 58 days (range 28-112 days) during screening for enrollment in the Childhood Asthma Management Program (CAMP) study. Daily self-reports of asthma symptoms were obtained from study diaries and compared with ambient air pollution levels in marginal repeated measures logistic regression models. We defined days with asthma symptoms as any day a child reported at least one mild asthma episode. All analyses were controlled for subject-specific variables [age, race, sex, baseline height, and FEV(1) PC(20) concentration (methacholine provocative concentration required to produce a 20% decrease in forced expiratory volume in 1 sec)] and potential time-dependent confounders (day of week, season, and temperature). Because of variable observation periods for participants, we estimated both between- and within-subject air pollutant effects. Our primary interest was in the within-subject effects: the effect of air pollutant excursions from typical levels in each child's observation period on the odds of asthma symptoms. In single-pollutant models, the population average estimates indicated a 30% [95% confidence interval (CI), 11-52%] increase for a 1-ppm increment in carbon monoxide lagged 1 day, an 18% (95% CI, 5-33%) increase for a 10-microg/m(3) increment in same-day particulate matter < 1.0 microm (PM(1.0)), and an 11% (95% CI, 3-20%) increase for a 10-microg/m(3) increment in particulate matter < 10 microm (PM(10)) lagged 1 day. Conditional on the previous day's asthma symptoms, we estimated 25% (95% CI, 10-42%), 14% (95% CI, 4-26%), and 10% (95% CI, 3-16%) increases in the odds of asthma symptoms associated with increases in CO, PM(1.0), and PM(10), respectively. We did not find any association between sulfur dioxide (SO(2)) and the odds of asthma symptoms. In multipollutant models, the separate pollutant effects were smaller. The overall effect of an increase in both CO and PM(1. 0) was a 31% (95% CI, 11-55%) increase in the odds of symptoms of asthma. We conclude that there is an association between change in short-term air pollution levels, as indexed by PM and CO, and the occurrence of asthma symptoms among children in Seattle. Although PM effects on asthma have been found in other studies, it is likely that CO is a marker for vehicle exhaust and other combustion by-products that aggravate asthma.

Air pollution and asthma.

Asthma is a disease syndrome that has captured a great deal of attention for several years. One of the perplexing aspects to asthma is that the prevalence is increasing in most industrialized countries. The reasons for this widespread increase are largely unknown. Another aspect of industrialization is the persistence of air pollution in urban areas. Because much air pollution is due to vehicles, no solution appears in sight. The topic of this article is the association between air pollution and various signs and symptoms of asthma. Air pollution is convincingly associated with many signs of asthma aggravation. These include pulmonary function decrements, increased bronchial hyperresponsiveness, visits to emergency departments, hospital admissions, increased medication use and symptom reporting, inflammatory changes, interactions between air pollution and allergen challenges, and immune system changes. With the exception of exposure to environmental tobacco smoke, common air pollutants have not been shown to cause asthma. It seems prudent for clinicians to counsel their patients about the potential risks of asthma aggravation from common outdoor air pollutants.

Sulphur dioxide sensitivity and plasma antioxidants in adult subjects with asthma.

OBJECTIVES: To screen adult subjects with asthma for sensitivity to inhaled sulphur dioxide (SO2) and identify subject characteristics associated with that sensitivity. Medication use, symptoms, and plasma antioxidant nutrients between SO2 responders and non-responders were compared. METHODS: Adult subjects (ages 18-39 years) with asthma were exposed to 0.5 ppm SO2 for 10 minutes during moderate exercise. Pulmonary function tests and symptom ratings were assessed before and after exposure (n = 47). A subject was classified as sensitive to SO2 if forced expiratory volume in 1 second (FEV1) showed a drop > or = 8% over baseline. Blood samples were obtained from subjects (n = 38) before the SO2 challenge; plasma ascorbate, alpha-tocopherol, retinol, carotenoids, and lipids were measured. RESULTS: Of the 47 subjects screened, 53% had a drop in FEV1 > or = 8% (ranging from -8% to -44%). Among those 25 subjects, the mean drop in FEV1 was -17.2%. Baseline pulmonary function indices (FEV1% of predicted and FEV1/FVC% (forced vital capacity)) did not predict sensitivity to SO2. Although use of medication was inversely related to changes in pulmonary function after SO2 (p < 0.05), both SO2 responders and non-responders were represented in each medication category. Total symptom scores after exposure were significantly correlated with changes in FEV1 (p < 0.05), FVC (p < 0.05), and peak expiratory flow (PEF) (p < 0.01) but not forced expiratory flow between 25% and 75% vital capacity (FEF25-75). Plasma beta-carotene concentrations were inversely associated with PEF values and ascorbate concentrations were inversely associated with FEV1 and FEV1/FVC (p = 0.05 in all cases). High density lipoprotein concentrations were positively correlated with FEV1% of predicted (p < 0.05) and inversely correlated with change in FEF25-75 (p < 0.05) after SO2. CONCLUSION: These results show that the response to SO2 among adults with mild to moderate asthma is very diverse. Severity of asthma defined by medication category was not a predictor of sensitivity to SO2. Lung function values were associated with beta-carotene and ascorbate concentrations in plasma; however, plasma antioxidant nutrient concentrations were not associated with sensitivity to inhaled SO2.

An association between fine particles and asthma emergency department visits for children in Seattle.

Asthma is the most common chronic illness of childhood and its prevalence is increasing, causing much concern for identification of risk factors such as air pollution. We previously conducted a study showing a relationship between asthma visits in all persons < 65 years of age to emergency departments (EDs) and air pollution in Seattle, Washington. In that study the most frequent zip codes of the visits were in the inner city. The Seattle-King County Department of Public Health (Seattle, WA) subsequently published a report which showed that the hospitalization rate for children in the inner city was over 600/100,000, whereas it was < 100/100,000 for children living in the suburbs. Therefore, we conducted the present study to evaluate whether asthma visits to hospital emergency departments in the inner city of Seattle were associated with outdoor air pollution levels. ED visits to six hospitals for asthma and daily air pollution data were obtained for 15 months during 1995 and 1996. The association between air pollution and childhood ED visits for asthma from the inner city area with high asthma hospitalization rates were compared with those from lower hospital utilization areas. Daily ED counts were regressed against fine particulate matter (PM), carbon monoxide (CO), sulfur dioxide, and nitrogen dioxide using a semiparametric Poisson regression model. Significant associations were found between ED visits for asthma in children and fine PM and CO. A change of 11 microg/m3 in fine PM was associated with a relative rate of 1.15 [95% confidence interval (CI), 1.08-1.23]. There was no stronger association between ED visits for asthma and air pollution in the higher hospital utilization area than in the lower utilization area. These findings were seen when estimated PM2.5 concentrations were below the newly adopted annual National Ambient Air Quality Standard of 15 microg/m3.

Effects of ambient air pollution on nonelderly asthma hospital admissions in Seattle, Washington, 1987-1994.

As part of the Clean Air Act, Congress has directed EPA to set air quality standards to protect sensitive population groups from air pollutants in the ambient environment. People with asthma represent one such group. We undertook a study of the relation between measured ambient air pollutants in Seattle and nonelderly hospital admissions with a principal diagnosis of asthma. We regressed daily hospital admissions to local hospitals for area residents from 1987 through 1994 on particulate matter less than 10 and 2.5 microm in aerodynamic diameter (PM10 and PM2.5, respectively); coarse particulate mass; sulfur dioxide (SO2); ozone (O3); and carbon monoxide (CO) in a Poisson regression model with control for time trends, seasonal variations, and temperature-related weather effects. With the exception of seasonally monitored O3, we supplemented incomplete pollutant measures in a multiple imputation model to create a complete time series of exposure measures. We found an estimated 4-5% increase in the rate of asthma hospital admissions associated with an interquartile range change in PM (19 microg/m3 PM(10),11.8 microg/m3 PM2.5, and 9.3 microg/m3 coarse particulate mass) lagged 1 day; relative rates were as follows: for PM10, 1.05 [95% confidence interval (CI) = 1.02-1.08]; for PM2.5, 1.04 (95% CI = 1.02-1.07); and for coarse particulate mass, 1.04 (95% CI = 1.01-1.07). In single-pollutant models we also found that a 6% increase in the rate of admission was associated with an interquartile range change in CO (interquartile range, 924 parts per billion; 95% CI = 1.03-1.09) at a lag of 3 days and an interquartile range change in O3 (interquartile range, 20 parts per billion; 95% CI = 1.02-1.11) at a lag of 2 days. We did not observe an association for SO2. We found PM and CO to be jointly associated with asthma admissions. We estimated the highest increase in risk in the spring and fall seasons.

Behavioral changes following participation in a home health promotional program in King County, Washington.

This study examined behavioral changes in households after participation in a home environmental assessment. Home assessment visits by a trained coach, which involved a walk-through in the home with the home residents, were conducted in 36 homes. The walk-through included a list of recommended behavioral changes that the residents could make to reduce their exposures to home pollutants in areas such as dust control, moisture problems, indoor air, hazardous household products, and hobbies. Recruited households were surveyed 3 months after the home assessment to evaluate their implementation of the recommendations. Following the home visits, 31 of 36 households reported making at least one behavioral change, and 41% of the recommendations made by the volunteer coaches were implemented. In conclusion, this study found that the majority of the households who participated in the home assessment reported implementing at least one recommendation. This home health promotional method was effective in influencing behavioral changes.

Pulmonary function and respiratory symptoms in forest firefighters.

This study evaluated effects on respiratory health of forest firefighters exposed to high concentrations of smoke during their work shift. This is the first study of cross-shift respiratory effects in forest firefighters conducted on the job. Spirometric measurements and self-administered questionnaire data were collected before and after the 1992 firefighting season. Seventy-six (76) subjects were studied for cross-shift and 53 for cross-season analysis. On average, the cross-season data were collected 77.7 days after the last occupational smoke exposure. The cross-shift analysis identified significant mean individual declines in FVC. FEV1, and FEF25 75. The preshift to midshift decreases were 0.089 L, 0.190 L, and 0.439 I/sec. respectively, with preshift to postshift declines of 0.065 L, 0.150 L, and 0.496 L/sec. Mean individual declines for FVC, FEV1 and FEF25 75 of 0.033 L, 0.104 L, and 0.275 I/sec. respectively, also were noted in the cross-season analysis. The FEV1 changed significantly (p < 0.05). The use of wood for indoor heat also was associated with the declines in FEV1. Although annual lung function changes for a small subset (n = 10) indicated reversibility of effect, this study suggests a concern for potential adverse respiratory effects in forest firefighters.

Effect of ozone on respiratory responses in subjects with asthma.

In the process of understanding the respiratory effects of individual air pollutants, it is useful to consider which populations seem to be most susceptible to the exposures. Ozone is the most ubiquitous air pollutant in the United States, and there is great interest in the extent of susceptibility to this air pollutant. This review presents evidence that individuals with asthma are more susceptible to adverse respiratory effects from ozone exposure than are nonasthmatic individuals under similar circumstances. In studies comparing patients with asthma to nonasthmatic subjects, research has shown increased pulmonary-function decrements, an increased frequency of bronchial hyperresponsiveness in ozone responders, increased signs of upper airway inflammation after ozone exposure, and an increased response to inhaled sulfur dioxide or allergen in the subjects with asthma. Subjects with asthma are indeed a population susceptible to the inhaled effects of ozone. These data need to be considered by regulators who are charged with setting air quality standards to protect even the most susceptible members of the population. They also underline the importance of strategies to reduce human exposure to ambient ozone.

Oxidant and acid aerosol exposure in healthy subjects and subjects with asthma. Part I: Effects of oxidants, combined with sulfuric or nitric acid, on the pulmonary function of adolescents with asthma.

Both peak flow decrements in children at summer camps and increased hospital admissions for asthma have been associated with summer "acid haze," which is composed of ozone and various acidic species. The objective of this study was to investigate the pulmonary effects of acid summer haze in a controlled laboratory setting. Twenty-eight adolescent subjects with allergic asthma, exercise-induced bronchospasm, and a positive response to a standardized methacholine challenge enrolled in the study; 22 completed the study. Each subject inhaled one of four test atmospheres by mouthpiece on two consecutive days. The order of exposure to the four test atmospheres was assigned via a random protocol: air, oxidants (0.12 parts per million [ppm]* ozone plus 0.30 ppm nitrogen dioxide), oxidants plus sulfuric acid at 70 micrograms/m3 of air, or oxidants plus 0.05 ppm nitric acid. Exposure to each of the different atmospheres was separated by at least one week. The exposures were carried out during alternating 15-minute periods of rest and moderate exercise for a total exposure period of 90 minutes per day. Pulmonary function was measured before and after exposure on both test days and again on the third day as a follow-up measurement. A postexposure methacholine challenge was performed on Day 3. Low methacholine concentrations were chosen for the postexposure challenge to avoid provoking a response. The protocol was designed to detect subtle changes in airway reactivity. The statistical significance of the pulmonary function values was tested using paired t tests. First, we compared the difference between baseline and postexposure measurements after air exposure on Day 1 with the differences between baseline and postexposure measurements after Day 1 exposure to each of the other three atmospheres. Second, we compared the difference between baseline and postexposure measurements after the Day 2 air exposure with the differences between baseline and postexposure measurements after the Day 2 exposure to each of the pollutant atmospheres. Third, we compared the difference between baseline measurements on Day 1 of each exposure atmosphere with measurements after exposure to the same atmosphere on Day 2 to detect delayed effects. No changes in any of the pulmonary function parameters were statistically significant when compared with changes after clean air exposure. Six subjects left the study because of uncomfortable symptoms associated with the exposures. These all occurred after exposure to pollutant atmospheres and not after exposure to clean air.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of sulfur dioxide exposure on African-American and Caucasian asthmatics.

There is concern that air pollution may be causing increases in asthma morbidity and mortality, especially among African-Americans. It is possible that there may be ethnic differences in susceptibility. To evaluate this speculation, a comparative pilot study of respiratory function in 10 African American and 12 Caucasian methacholine positive asthmatic males was conducted. Subjects were exposed to pure air or 1 ppm SO2 while breathing inside a polycarbonate head dome, for 10 min of rest and 10 min of exercise. Baseline and postexposure pulmonary function measurements were recorded, and nasal lavage fluid samples were collected and processed for epithelial and white blood counts. Although significant increases were seen in total respiratory resistance following SO2 exposure in both groups (P = 0.04), no ethic-based difference in response was seen. No significant differences were found in pulmonary or nasal measurements after exposure to SO2 between African-American and Caucasian subjects. No significant changes in epithelial or white blood cell count were found either when data were analyzed from the entire group or separately from the two subject groups. Even though there were no significant group changes, some individuals were particularly responsive to SO2. Three Caucasian and 5 African-American subjects showed greater than 20% increases in total respiratory resistance.

Health effects of outdoor air pollution.

One hundred sixty-four million Americans live in areas that fail to meet the National Ambient Air Quality Standards for six common air pollutants: particulates, sulfur dioxide, carbon monoxide, nitrogen dioxide, ozone and lead. The impact of these pollutants on health is significant. A Pollutant Standards Index (PSI) ranging from 0 to 500 is used to monitor air quality. When the PSI exceeds 100, the acceptable federal standard has been exceeded by at least one of four measured pollutants. When this occurs, all individuals should be advised to curtail physical activity between late morning and sunset and to remain indoors if possible. Athletes should be encouraged to train in the early morning, when photochemicals are usually at their lowest levels.