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Biomedical subjects

J Q Koenig

Publications and source records attributed to J Q Koenig.

At least 55 records · Page 3Linked to original sources
PubMed1988

Indoor and outdoor pollutants and the upper respiratory tract.

The health effects of both indoor and outdoor air pollutants are of increasing concern. The health effects of outdoor air pollutants traditionally have been assessed through measurements of lower respiratory tract changes. However, it has been shown that one outdoor air pollutant, sulfur dioxide, decreases nasal mucus flow and increases nasal airway resistance. Along with cigarette smoke, indoor air pollutants such as formaldehyde, cadmium, and ammonium or sulfate ions have been shown to alter upper airway mucociliary function. Emissions from wood stoves are known to irritate the upper airways. Measurement of nasal airway resistance using posterior rhinomanometry allows quantification of nasal function. This technique recently has been used to demonstrate that adolescents with allergic asthma have increased work of breathing after inhalation of 0.5 ppm sulfur dioxide. Another study using posterior rhinomanometry showed that clerical workers had increased work of breathing after exposure to carbonless copy paper as compared with bond paper. This brief review of upper respiratory tract changes after pollutant exposure should serve as a reminder that a complete clinical history must include questions designed to ascertain the patient's exposure history to both outdoor and indoor air pollutants. These exposures can have a major impact on the health of the upper respiratory system.

Air Pollutants↗
PubMed1988

Therapeutic range cromolyn dose-response inhibition and complete obliteration of SO2-induced bronchoconstriction in atopic adolescents.

Eight atopic adolescent subjects with exercise-induced bronchospasm were studied to determine whether cromolyn sodium could inhibit or block sulfur dioxide (SO2)-induced bronchoconstriction. Cromolyn or placebo were administered by turboinhaler 20 minutes before 10 minutes of SO2 exposure at 1.0 ppm during continuous moderate exercise on a treadmill. The exercise level that was chosen did not in itself produce bronchoconstriction. The cromolyn doses were 0 (placebo), 20, 40, and 60 mg. Pulmonary functions (FEV1, and total respiratory resistance) were measured before and after drug administration and after exposure. SO2 exposure after placebo produced significant bronchoconstriction. Pretreatment with 20 mg of cromolyn did not change the SO2 response, 40 mg significantly inhibited the response, and 60 mg completely abolished the pulmonary function changes. These results demonstrate for the first time a dose-response inhibition of SO2-induced bronchoconstriction in atopic subjects within a clinically acceptable dosage range and complete obliteration of SO2 sensitivity in this group with 60 mg of cromolyn pretreatment.

Adolescent↗
PubMed1988

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.

Adolescent↗
PubMed1988

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)

Adolescent↗
PubMed1987

The effects of albuterol on sulfur dioxide-induced bronchoconstriction in allergic adolescents.

Ten allergic subjects with exercise-induced bronchospasm were studied to determine whether albuterol could prevent sulfur dioxide (SO2)-induced bronchoconstriction. Albuterol or placebo (180 micrograms) were administered by metered-dose inhaler 20 minutes before a 10-minute exposure to SO2 or clean air during moderate exercise on a treadmill at an exercise level that by itself did not produce exercise-induced bronchospasm. Pulmonary functions (FEV1 and total respiratory resistance [RT]) were measured before the drug, after the drug, and after exposure to SO2 or clean air. Albuterol treatment produced significant bronchodilation and also prevented SO2-induced bronchoconstriction. Following SO2 inhalation after placebo, FEV1 decreased 15% (p less than 0.02) and RT increased 50% (p less than 0.03). Following SO2 inhalation after albuterol treatment, neither FEV1 or RT changed significantly. We conclude that albuterol, a beta 2-agonist, inhibits SO2-induced bronchoconstriction. This result suggests that the adrenergic nervous system or mast cell degranulation are involved in SO2-induced bronchoconstriction.

Adolescent↗
PubMed1987

The effects of sulfur dioxide on pulmonary function in healthy nonsmoking male subjects aged 55 years and older.

To determine whether normal nonsmoking individuals aged 55 years or greater have heightened bronchial reactivity to inhaled SO2, ten male subjects, 55 to 73 years of age, were exposed for 20 min at rest and 10 min during moderate exercise on a treadmill to the following: NaCl droplet aerosol, or 1.0 ppm of SO2 and NaCl droplet aerosol. Seven of the subjects also were exposed to 0.5 ppm SO2 and NaCl droplet aerosol. Significant decrease in forced expiratory volume in one sec (FEV1) were seen 2-3 min post-exercise following all three test modes. The reduction in FEV1 seen after NaCl aerosol + 1.0 ppm SO2 was significantly greater than that seen after NaCl aerosol alone. The results show that men aged 55 years or older are somewhat more sensitive to NaCl aerosol + 1.0 ppm SO2 than similarly exposed normal adolescents, but not nearly as sensitive as asthmatic subjects. This study also demonstrates that investigations of air pollutants and exercise can be undertaken in subjects of this age.

Aged↗
PubMed1987

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.

Adolescent↗
PubMed1986

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.

Air Pollution↗
PubMed1985

The effects of sulfur oxides on nasal and lung function in adolescents with extrinsic asthma.

Ten adolescent subjects with extrinsic asthma were exposed during intermittent exercise to filtered air, 0.5 ppm of sulfur dioxide (SO2), or 100 micrograms/m3 of sulfuric acid (H2SO4) on 5 separate days. The purpose of the study was to compare changes in nasal power (the work of nose breathing) with pulmonary functional changes depending on the route of inhalation of the sulfur oxide pollutants, oral inhalation through a rubber mouthpiece or oronasal inhalation via a face mask. Nasal power was measured with a modified skin diving mask equipped with two differential pressure transducers. Statistically significant changes in total respiratory resistance, FEV1, and maximum flow calculated at 50% and 75% vital capacity were observed after all exposures to SO2 and H2SO4. The magnitude of change in FEV1 and maximum flow calculated at 50% vital capacity was higher after oral compared to oronasal inhalation of SO2. The nasal work of breathing increased 32% after SO2 exposure by mouthpiece and 30% after SO2 exposure via face mask (p less than 0.05). The nasal power changes after the H2SO4 exposures were not different from the sham exposures. We conclude that oronasal inhalation of 0.5 ppm of SO2 produces a significant increase in the nasal work of breathing and that the route of exposure reduces but does not eliminate the lower airway reactions observed on oral exposure.

Adolescent↗
PubMed1985

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.

Adolescent↗
PubMed1984

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.

Adaptation, Physiological↗
PubMed1983

A comparison of the pulmonary effects of 0.5 ppm versus 1.0 ppm sulfur dioxide plus sodium chloride droplets in asthmatic adolescents.

The effects of inhaled sulfur dioxide (SO2) on pulmonary function in nine adolescent subjects with extrinsic asthma were studied. The exposure modes, inhaled via a mouthpiece, were (1) 1 mg/m3 sodium chloride solution droplet aerosol (NaCl); (2) 0.5 ppm SO2 + NaCl; or (3) 1.0 ppm SO2 + NaCl. All exposures were at greater than or equal to 75% relative humidity and approximately 22 degrees C. The following pulmonary functional measurements, with the subject seated in a body plethysmograph, were recorded: total respiratory resistance (RT), functional residual capacity (FRC), maximal flow at 50% and 75% expired vital capacity (Vmax50 and Vmax75), and forced expiratory volume in one second (FEV1). Following 10 min of exposure to either SO2 mode during moderate exercise on a treadmill, statistically significant changes in all pulmonary functional measurements except FRC were seen. There were no statistically significant changes following 10 min of exposure during moderate exercise to the NaCl droplet aerosol alone. Since the average pulmonary changes following exposure to 0.5 ppm SO2 mixture during moderate exercise ranged from 8 to 47%, we conclude that this dose of SO2 is above the response threshold for these subjects. To explore the effects of nasal (or oronasal) inhalation on the SO2-induced pulmonary functional changes, 7 of the 9 subjects inhaled 0.5 ppm SO2 + NaCl via a face mask with no nose clips. The average percentage changes in pulmonary functional values seen after exposure via face mask were similar to those seen after exposure via mouthpiece. However, the changes seen after exposure via face mask were not as consistent as following inhalation via mouthpiece and not statistically different from baseline. We conclude that oral, and to a lesser degree oronasal, inhalation of 0.5 ppm of SO2 elicits SO2-induced changes in pulmonary function in these subjects.

Adolescent↗
PubMed1983

The effects of inhaled sulfuric acid on pulmonary function in adolescent asthmatics.

Ten adolescent subjects with extrinsic asthma and exercise-induced bronchospasm were studied. The subjects were exposed for 30 min at rest followed by 10 min during moderate exercise on a treadmill to either 100 micrograms/m3 sodium chloride (NaCl) or 100 micrograms/m3 sulfuric acid (H2SO4) droplet aerosols. All exposures were at approximately 75% relative humidity and 22 degrees C. Pulmonary functional measurements were recorded before, during, and after exposure while the subject was seated in a body plethysmograph. Exposure to the NaCl aerosol during exercise produced a small (12%) but significant drop in maximal expiratory flow (Vmax75) (p less than 0.05). However, exposure to the H2SO4 aerosol produced larger reductions in Vmax75 (29%; p less than 0.01) and also significant changes in 3 other parameters of pulmonary function: Vmax50, FEV1, and total respiratory resistance (RT). The changes were similar to those reported for exposure to 0.5 ppm of sulfur dioxide in a similar group of adolescents with extrinsic asthma. Our results are the first report of reversible pulmonary functional changes after H2SO4 exposure in a group of adolescent asthmatic subjects.

Adolescent↗
PubMed1982

Bronchoconstrictor responses to sulfur dioxide or sulfur dioxide plus sodium chloride droplets in allergic, nonasthmatic adolescent.

Eight atopic adolescent subjects without diagnosis of clinical asthma but with signs of hyperactive airways were studied. The subjects were exposed for 30 min at rest followed by 10 min during moderate exercise on a treadmill to the following: (1) filtered air, (2) 1 mg/m3 NaCl droplet aerosol, (3) 1 ppm SO2 and NaCl droplet aerosol, or (4) 1 ppm SO2. All exposures were at 75% relative humidity and 22 degrees C. Exposures to either SO2 mode produced statistically significant changes in pulmonary function, whereas sham exposures to air on NaCl did not. These results are similar to those seen earlier in a group of extrinsic asthmatic adolescent subjects and are three to 22 times greater than changes we saw in a group of normal adolescent subjects. The changes seen after inhalation of SO2 were not statistically different from those seen after inhalation of SO2 and NaCl droplet aerosol. Our results indicate that inhalation of 1 ppm SO2 by a group of atopic adolescents can produce exercise-induced bronchospasm at a level of exercise that has no effect by itself.

Adolescent↗