Ammonia in the human airways: neutralization of inspired acid sulfate aerosols.

In the human being, expired ammonia concentrations from 7 to 520 micrograms per cubic meter are controlled by the last airway segment traversed by the air, and such concentrations are higher in the mouth than nose. Inspired submicrometric sulfuric acid aerosol at a mass concentration of 600 +/- 100 micrograms per cubic meter was found to be an ammonium salt with an average ammonium to sulfate molar ratio of greater than or equal to 1, when sampled within 0.5 second after exhalation.

Sulfuric acid-ammonium sulfate aerosol: optical detection in the St. Louis region.

Nephelometric sensing of the deliquescence of ammonium sulfate produced by the reaction of sulfuric acid or ammonium bisulfate aerosol with ammonia provides a means for detecting these substances in air. Field experiments show them to be the dominant substances in the submicrometer, light-scattering aerosol in the St. Louis region.

Effects of inhalation of acidic compounds on pulmonary function in allergic adolescent subjects.

There is concern about the human health effects of inhalation of acid compounds found in urban air pollution. It was the purpose of this study to investigate three of these acid compounds, sulfur dioxide (SO2), sulfuric acid (H2SO4), and nitric acid (HNO3) in a group of allergic adolescent subjects. Subjects were exposed during rest and moderate exercise to 0.7 mumole/m3 (68 micrograms/m3) H2SO4, 4.0 mumole/m3 (0.1 ppm) SO2, or 2.0 mumole/m3 (0.05 ppm) HNO3. Pulmonary functions (FEV1, total respiratory resistance, and maximal flow) were measured before and after exposure. Preliminary analysis based on nine subjects indicates that exposure to 0.7 mumole/m3 H2SO4 alone and in combination with SO2 caused significant changes in pulmonary function, whereas exposure to air or SO2 alone did not. FEV1 decreased an average of 6% after exposure to H2SO4 alone and 4% when the aerosol was combined with SO2. The FEV1 decrease was 2% after both air and SO2 exposures. Total respiratory resistance (RT) increased 15% after the combined H2SO4 exposures, 12% after H2SO4 alone, and 7% after exposure to air. After exposures to HNO3 alone, FEV1 decreased by 4%, and RT increased by 23%. These results are preliminary; final conclusions must wait for completion of the study.

Nebulizer delivery of tobramycin to the lower respiratory tract.

We characterized a tobramycin aerosol generated by five nebulizers: Micron One, Pulmosonic, Pulmo-Aide, DeVilbiss Model 65, and UltraNeb 100 by particle size and drug concentration. The Micron One nebulizer did not produce a recoverable aerosol, while the Pulmosonic had a minimal output; therefore three machines were examined for their ability to deliver tobramycin to the lower respiratory tract of patients with cystic fibrosis (CF). The DeVilbiss 65 had the greatest output: with air as the carrier gas it produced an aerosol with > 60% of the particles having a mean mass aerodynamic diameter (MMAD) of > 5.5 microns. Using helox shifted the MMAD so that > 65% of the particles were < 5.5 microns. Increasing the power in the DeVilbiss 65 increased the output of particles > 9.2 microns, without a change in the particles < 3.3 microns. With air as the carrier gas the Pulmo-Aide and the UltraNeb 100 produced an aerosol with > 60% particles, < 3.3 microns MMAD. Using helox the UltraNeb 100 increased the amount of aerosol with a < 3.3 microns MMAD to 98%. Tobramycin delivery to the lower respiratory tract with the Pulmo-Aide and UltraNeb 100 was compared using air or helox by measuring sputum drug concentration. Pulmo-Aide failed to produce detectable tobramycin in sputum in 2 out of 9 patients with CF. With the UltraNeb 100, all patients had measurable sputum tobramycin immediately after administration (range, 16.2-3385 micrograms/g), but no statistically significant difference was found when using either compressed air, helox, or ambient air.(ABSTRACT TRUNCATED AT 250 WORDS)

Implications of air pollution effects on athletic performance.

Both controlled human studies and observational studies suggest that air pollution adversely affects athletic performance during both training and competition. The air pollution dosage during exercise is much higher than during rest because of a higher ventilatory rate and both nasal and oral breathing in the former case. For example, sulfur dioxide, which is a highly water-soluble gas, is almost entirely absorbed in the upper respiratory tract during nasal breathing. However, with oral pharyngeal breathing, the amount of sulfur dioxide that is absorbed is significantly less, and with exercise and oral pharyngeal breathing a significant decrease in upper airway absorption occurs, resulting in a significantly larger dosage of this pollutant being delivered to the tracheobronchial tree. Recently, several controlled human studies have shown that the combination of exercise and pollutant exposure (SO2 or O3) caused a marked bronchoconstriction and reduced ventilatory flow when compared to pollution exposure at rest. In a situation like the Olympic Games where milliseconds and millimeters often determine the success of athletes, air pollution can be an important factor in affecting their performance. This paper examines possible impacts of air pollution on athletic competition.

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)

The effects of ozone and nitrogen dioxide on lung function in healthy and asthmatic adolescents.

The aim of this project was to investigate whether or not well characterized groups of healthy adolescents and adolescents with asthma differed in their sensitivity to ozone and nitrogen dioxide at near ambient concentrations of these pollutants. The project was divided into three phases. In each phase, ten healthy and ten asthmatic adolescents were exposed via a mouthpiece to three different atmospheres (filtered air, ozone, and nitrogen dioxide, at either 0.12 or 0.18 ppm) on separate days at least one week apart. During Phase I, subjects at rest inhaled the test atmospheres at 0.12 ppm for two 30-minute periods. The following pulmonary functional values were measured before, during, and after exposure: peak flow, total respiratory resistance, thoracic gas volume at functional residual capacity, maximal flow at 50 and 75 percent of expired vital capacity (performed with both room air and a helium-oxygen mixture), and forced expiratory volume in one second. Pulmonary function was not consistently altered in either the asthmatic or the healthy nonasthmatic adolescents as a result of the exposures. As a result, the study was repeated with the addition of ten minutes of exercise to the 30-minute rest exposure period (Phase II). In Phase II, small but significant increases in total respiratory resistance to all test atmospheres were seen after exposure at 0.12 ppm during exercise in both healthy and asthmatic adolescents. However, the increase in resistance between the groups of subjects was not statistically different. On the basis of these results, Phase III was conducted at higher concentrations of the pollutants (0.18 ppm). In Phase III, statistically significant changes were seen in average total respiratory resistance values in both healthy and asthmatic adolescents exposed to 0.18 ppm ozone while exercising. Again, the difference between the groups was not significant. Small decreases in average forced expiratory volume were found in healthy subjects exposed to ozone and filtered air. After exposure to nitrogen dioxide there was a 3 percent decrease in the forced expiratory volume in one second in asthmatic subjects. This change was not significant. It is concluded that there were no differences in pulmonary function responses between asymptomatic, allergic asthmatic adolescents and healthy adolescents exposed to either ozone or nitrogen dioxide under the conditions of these studies. However, an increase in total respiratory resistance was observed in both asthmatic and healthy adolescent subjects after their exercise exposure to 0.18 ppm ozone.(ABSTRACT TRUNCATED AT 400 WORDS)

Measurements of the humidification processes of hydroscopic particles.

A number of pure salt aerosols were produced in the laboratory, subjected to a controlled humidity environment. The magnitude of the electrooptic response was measured continuously over a range of relative humidity (RH), which was varied from 20 to 90%, with an integrating electrooptical nephelometer. From such observations the influence of water vapor on the salt aerosols, especially the process of phase transition that occurs at the deliquescent point, can be monitored. The use of electrooptic scattering would appear to be a more sensitive indicator of the effect of water vapor on the aerosols at low RH than conventional light scattering intensity measurements.

Air pollutants, bronchial hyperreactivity, and exercise.

The interaction of air pollutants and their effect on bronchial hyperreactivity show that sulfur dioxide and ozone both increase bronchial hyperreactivity. Sulfur dioxide concentrates as low as 0.5 ppm and ozone concentrations as low as 0.2 ppm have demonstrated this effect. Exercise with either sulfur dioxide or ozone exposure can significantly increase bronchial hyperreactivity in susceptible individuals. Other factors including ambient air temperature, time of day, wind velocity and direction, geography, climate, tobacco smoke exposure, and other indoor air pollutants may enhance the impact of air pollutants, causing bronchial hyperreactivity.

Relationship between asymmetry parameter and hemispheric backscatter ratio: implications for climate forcing by aerosols.

Calculations of direct climate forcing by anthropogenic aerosols commonly use radiative transfer parameters, including asymmetry parameter g. One method of obtaining the asymmetry parameter of a particle population is to convert measured values of the hemispheric-to-total-scatter ratio (backscatter ratio b) into their corresponding g values. We compare a conversion derived from Mie calculations with one derived from the Henyey-Greenstein (HG) phase function to show that the HG method systematically overestimates g for typical size distributions of accumulation-mode aerosols. A delta-Eddington radiative transfer calculation is used to show that a 10% overestimation of g can systematically reduce climate forcing as a result of aerosols by 12% or more. Mie computations are used to derive an empirical relationship between backscatter ratio and asymmetry parameter for log-normal accumulation-mode aerosols. This relationship can be used to convert the backscatter ratio to the asymmetry parameter, independent of geometric mean diameter D(gv) or complex refractive index m, but the conversion requires knowledge of the breadth σ(g) of the size distribution.

A method for continuous measurement of ammonia in respiratory airways.

A method has been developed that can continuously measure respiratory NH3 with a detection limit of 30 parts per billion by volume (ppbv) at an averaging time of 1 s. The method is based on the chemiluminescent detection of NO, which is produced by oxidizing NH3 at 850 degrees C. A polyethylene sampling probe, incorporating a heated capillary tip bathed in dry, NH3-free diluent air, minimizes NH3 losses due to absorption in breath condensate. In one subject, flow and tidal volume were monitored during quiet mouth breathing while NH3 and CO2 were sampled at the lips. In 10 subjects, NH3, and CO2 were sampled at the lips during quiet mouth breathing ranged from 280 to 1,280 ppbv (mean plus or minus SE, 540 PLUS OR MINUS 85 PPBV).

Respiratory effects from the inhalation of hydrogen chloride in young adult asthmatics.

Almost no human data exist from controlled studies using low levels of hydrogen chloride (HCl), and, with no existing HCl ambient standards in the United States, the need for human health effects research is evident. In this study, five female and five male 18 to 25-year-old asthmatic subjects were exposed to filtered air, 0.8 ppm and 1.8 ppm HCl while wearing half-face masks, during three separate 45-minute experimental sessions involving 15 minutes exercise (treadmill walking), 15 minutes rest, followed again by exercise. Baseline and postexposure pulmonary function measurements were taken including forced expiratory volume in 1 second (FEV1), forced expiratory volume (FVC), maximal flow at 50% of expired vital capacity (Vmax50), maximal flow at 75% of expired vital capacity (Vmax75), and total respiratory resistance as well as peak flow. Nasal work of breathing and oral ammonia levels also were measured preexposure and postexposure. No significant pulmonary effects were found at these HCl concentrations and exposure duration. Nasal power showed no significant differences between test atmospheres; however, in isolation a significant decrease (P less than .01) was found in measurements of inspiration with exposure to 0.80 ppm. Ammonia levels showed a significant rise postexposure after both concentrations of HCl (paired t test, (P less than .01)), not seen after air exposure. In summary, the asthmatic subjects in this study showed no adverse respiratory health effects of inhalation of low concentrations of HCl.

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

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

Measurements of respiratory ammonia and the chemical neutralization of inhaled sulfuric acid aerosol in anesthetized dogs.

The extent of neutralization of inhaled H2SO4 aerosol by endogenous NH3 has been measured in the surgically isolated upper airways of anesthetized dogs. Neutralization was observed to be inversely proportional to particle size. The H2SO4 particles with initial dry diameters of 0.5 micrometer and 1.0 micrometer underwent 0.28 (+/- 0.08) and 0.06 (+/- 0.06)% neutralization per ppb of laryngeal NH3, respectively, during passage through the mouth and out of the larynx at a flow of 0.1 L/s. At either particle size, neutralization is related to the route of entry, being greater for entry via the mouth than the nose. Limited measurements for entry via the mouth show more neutralization of 0.7 micrometer particles at 0.1 L/s than at 0.2 L/s. These results are consistent with a reaction that is limited by the rate of NH4 diffusion to the particle's surface.

The effects of ozone and nitrogen dioxide on pulmonary function in healthy and in asthmatic adolescents.

The aim of this project was to investigate whether well-characterized asthmatic adolescent subjects were more sensitive to the inhaled effects of oxidant pollutants than were well-characterized healthy adolescent subjects. Ten healthy and 10 asthmatic subjects inhaled via a mouth-piece 0.12 or 0.18 ppm of ozone (O3) or nitrogen dioxide (NO2) or clean air for 30 min at rest followed by 10 min during moderate exercise (32.5 L/min) on a treadmill. The following pulmonary functional values were measured before and after exposure: peak flow, total respiratory resistance (RT), maximal flow at 50 and 75% of expired VC, and FEV1. After exercise exposure to 0.18 ppm O3, statistically significant increases were seen in RT in asthmatic and healthy adolescent subjects. No consistent changes were seen in either group after NO2 exposure. Also, no significant differences in response to oxidant pollutants between the 2 groups could be demonstrated. It was concluded that neither group was consistently sensitive to these pollutants.

Prior exposure to ozone potentiates subsequent response to sulfur dioxide in adolescent asthmatic subjects.

The objective of this study was to test whether prior exposure to a low concentration of ozone (120 ppb) would condition airways in asthmatic subjects to respond to a subthreshold concentration of sulfur dioxide (100 ppb). Eight male and five female subjects 12 to 18 yr of age participated. They all had allergic asthma and exercise-induced bronchospasm. Subjects were exposed to three test atmosphere sequences during intermittent moderate exercise (a 45-min exposure to one pollutant followed by a 15-min exposure to the second pollutant). The sequences were: air followed by 100 ppb SO2, 120 ppb O3 followed by 120 ppb O3, and 120 ppb O3 followed by 100 ppb SO2. The pulmonary function measurements assessed were FEV1, total respiratory resistance (RT), and maximal flow (Vmax50). Air-SO2 and O3-O3 exposures did not cause significant changes in pulmonary function. On the other hand, exposure to 100 ppb SO2 after a 45-min exposure to 120 ppb O3 caused a significant (8%) decrease in FEV1 (p = 0.046), a significant (19%) increase in RT (p = 0.048), and a significant (15%) decrease in Vmax50 (p = 0.008). It is concluded that prior O3 exposure increased bronchial hyperresponsiveness in these subjects such that they responded to an ordinarily subthreshold concentration of SO2. These data suggest that assessment of pulmonary changes to single pollutant challenges overlooks the interactive effects of common coexisting or sequentially occurring air pollutants.

The pulmonary effects of ozone and nitrogen dioxide alone and combined in healthy and asthmatic adolescent subjects.

Separate exposures to 0.12 ppm ozone (O3) or 0.18 ppm nitrogen dioxide (NO2) have not demonstrated consistent changes in pulmonary function in adolescent subjects. However, in polluted urban air, O3 and NO2 occur in combination. Therefore, this project was designed to investigate the pulmonary effects of combined O3 and NO2 exposures during intermittent exercise in adolescent subjects. Twelve healthy and twelve well-characterized asthmatic adolescent subjects were exposed randomly to clean air or 0.12 ppm O3 and 0.30 ppm NO2 alone or in combination during 60 minutes of intermittent moderate exercise (32.5 1/min). The inhalation exposures were carried out while the subjects breathed on a rubber mouthpiece with nose clips in place. The following pulmonary functional values were measured before and after exposure: peak flow, total respiratory resistance, maximal flow at 50 and 75 percent of expired vital capacity, forced expiratory volume in one second and forced vital capacity (FVC). Statistical significance of pulmonary function changes was tested by analysis of covariance for repeated measures. After exposure to 0.12 ppm O3 a significant decrease was seen in maximal flow at 50% of FVC in asthmatic subjects. After exposure to 0.30 ppm NO2 a significant decrease was seen in FVC also in the asthmatic subjects. One possible explanation for these changes is the multiple comparison effect. No significant changes in any parameters were seen in the asthmatic subjects after the combined O3-NO2 exposure or in the healthy subjects after any of the exposures.

Characterization of nonspherical atmospheric aerosol particles with electrooptical nephelometry.

An integrating nephelometer was adapted electronically to study the electrooptical properties of aerosol particles. The increase in light scattering coefficient due to orientation of nonspherical particles in the pulsed electric field and the decay of this signal were measured. Examples of the data for laboratory generated aerosols and atmospheric aerosols are presented.

Human nasal epithelium: characterization and effects of in vitro exposure to sulfur dioxide.

Human nasal turbinate tissue from surgical specimens was dissected free of connective tissue, and primary epithelial cultures were established by explant techniques. Transmission electron microscopy revealed that cultured cells retained homogeneous cytoplasmic granules, tonofilaments, and desmosomes and formed a homogeneous monolayer. The epithelial cells stained positively with cytokeratin antibodies AE1, AE3, and 35BH11 but failed to stain with two other cytokeratin antibodies, AE2 and 34BE12. Staining was also positive with anti-desmoplakin I and II but negative with antivimentin (43BE8), anti-desmin, and anti-human factor VIII antibodies. Cultured cells were exposed to filtered air or sulfur dioxide at 1-5 ppm for 30-60 min. Although there was no increase in cell lysis as measured by chromium-51 release, SO2 exposure significantly inhibited [3H]leucine incorporation compared to air exposure. This effect was dependent on both SO2 concentration and exposure duration. Control experiments revealed that these SO2 effects were not caused by the [H+] load produced by SO2 exposure. Electron microscopy of cells exposed to air or SO2 did not show any significant morphological differences.

Acute effects of 0.12 ppm ozone or 0.12 ppm nitrogen dioxide on pulmonary function in healthy and asthmatic adolescents.

Adolescent asthmatic subjects have been shown to be much more sensitive than healthy adolescents to the inhaled effects of sulfur dioxide. To test whether similar adolescent asthmatics are more sensitive to other common ambient air pollutants, 10 healthy and 10 asthmatic adolescent subjects were exposed for 60 min to filtered air, 0.12 ppm ozone (O3), and 0.12 ppm nitrogen dioxide (NO2) on separate days at rest. The following pulmonary functional values were measured before, at 30 min, and after 60 min of exposure: peak flow, total pulmonary resistance (RT), thoracic gas volume at functional residual capacity (FRC), maximal flow at 50 and 75% of expired vital capacity (Vmax50 and Vmax75), and forced expiratory volume in one second (FEV1). Following 60 min of exposure at rest to low concentrations of O3 or NO2, there were no consistent significant functional changes in either healthy or asthmatic adolescent subjects. There also were no measurable differences between the 2 groups.