Biomedical subjects

M J Hazucha

Publications and source records attributed to M J Hazucha.

7 recordsLinked to original sources

PubMed1992

Effects of steady-state and variable ozone concentration profiles on pulmonary function.

Measurements of ambient ozone (O2) concentration during daylight hours have shown a spectrum of concentration profiles, from a relatively stable to a variable pattern usually reaching a peak level in the early afternoon. Several recent studies have suggested that in estimating exposure dose (O3 concentration [C] x exposure time [T] x ventilation [V]), O3 concentration needs to be weighted more heavily than either ventilation or duration of exposure in the estimates. In this study we tested the hypothesis that regardless of concentration pattern and exposure rate the same exposure dose of O3 will induce the same spirometric response. We exposed 23 healthy male volunteers (20 to 35 yr of age) for 8 h to air, 0.12 ppm O3 (steady-state), and a triangular exposure pattern (concentration increased steadily from zero to 0.24 ppm over the first 4 h and decreased back to zero by 8 h). During the first 30 min of each hour, subjects exercised for 30 min at minute ventilation (VE) approximately 40 L/min. The order of the exposures was randomized, and the exposures were separated by at least 7 days. The response patterns over the 8-h periods for spirometric variables in both O3 exposures were statistically different from air exposure changes and from each other. For FEV1 the p values were 0.017 between air and steady-state profile, 0.002 between air and triangular profile, and 0.037 between steady-state and triangular profiles. Although in the triangular pattern of exposure the maximal O3 concentration was reached at 4 h, the maximum FEV1 decrement (10.2%) was observed at 6 h of exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Mechanism of action of ozone on the human lung.

Fourteen healthy normal volunteers were randomly exposed to air and 0.5 ppm of ozone (O3) in a controlled exposure chamber for a 2-h period during which 15 min of treadmill exercise sufficient to produce a ventilation of approximately 40 l/min was alternated with 15-min rest periods. Before testing an esophageal balloon was inserted, and lung volumes, flow rates, maximal inspiratory (at residual volume and functional residual capacity) and expiratory (at total lung capacity and functional residual capacity) mouth pressures, and pulmonary mechanics (static and dynamic compliance and airway resistance) were measured before and immediately after the exposure period. After the postexposure measurements had been completed, the subjects inhaled an aerosol of 20% lidocaine until response to citric acid aerosol inhalation was abolished. All of the measurements were immediately repeated. We found that the O3 exposure 1) induced a significant mean decrement of 17.8% in vital capacity (this change was the result of a marked fall in inspiratory capacity without significant increase in residual volume), 2) significantly increased mean airway resistance and specific airway resistance but did not change dynamic or static pulmonary compliance or viscous or elastic work, 3) significantly reduced maximal transpulmonary pressure (by 19%) but produced no changes in inspiratory or expiratory maximal mouth pressures, and 4) significantly increased respiratory rate (in 5 subjects by more than 6 breaths/min) and decreased tidal volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Relationship between ozone exposure and pulmonary function changes.

A detailed comparison of literature-reported averaged decrements in pulmonary function of normal subjects exposed to O3 has been undertaken. The data base was formed by including data published during the past 20 yr from studies that reported at least one of the pulmonary function variables (forced vital capacity, forced expiratory volume at 1 s, mean forced expiratory flow between 25 and 75% of forced vital capacity, and airway resistance) acquired at 2 h of exposures utilizing either original or modified Bates-Hazucha (intermittent exercise) protocol and that satisfied selection criteria. The final set of data (24 studies involving 299 subjects) was divided by ventilation rate (exercise loads) into four categories: light, moderate, high, and very high ventilation level. For each pulmonary function variable and ventilation level a quadratic function has been fitted to the data using regression procedures. The curve parameter estimates have been computed, tabulated, and statistically evaluated. The slope (quadratic coefficient) for each variable within a group and almost all variables between groups were significantly different from zero and from each other at P less than or equal to 0.0001.

Forced Expiratory Flow Rates↗

PubMed1987

Differing response of asthmatics to sulfur dioxide exposure with continuous and intermittent exercise.

Ten subjects with mild asthma were initially exposed in an environmental chamber (26 degrees C 70% relative humidity) to clean air and 1.0 ppm SO2 while performing 3 sets of 10-min treadmill exercises (ventilation, 41 L/min) broken by 15-min rest periods. To evaluate the effects of the pattern and duration of exercise on the response to SO2 exposure, the subjects were then exposed to the same environmental conditions while exercising continuously for 30 min. Specific airway resistance (SRaw) was measured by body plethysmography before each exposure and after each exercise. All SO2 responses were significantly greater than the clean air responses. With intermittent exercise and SO2 exposure, mean SRaw measurements (preexposure and after 10, 20, and 30 min of exercise) were 5.4, 14.7, 12.8, and 11.1 cm H2O/s. After SO2 exposure with continuous exercise, the mean SRaw showed an increase from 5.2 to 17.3 cm H2O/s. This increase was significantly (p = 0.018) greater than the response after the third exercise in the intermittent protocol. It appears that asthmatics show an attenuated response to repetitive exercise in an atmosphere of 1.00 ppm SO2 and that the response to SO2 exposure develops rapidly and is maintained during 30 min of continuous exercise.

Adult↗

PubMed1987

An aerosol generator system for inhalation delivery of pharmacologic agents.

Most commercially available aerosol generators widely used in medical applications produce aerosols characterized by a large mass median diameter in the 4-8 micron range and the particle size in the 0.1-10.0 microns range. The desirable size of therapeutic and diagnostic aerosols, however, is about 2-4 microns mass median diameter, and less than 2.0 geometric standard deviation; this size increases the reproducibility of inhalation tests and enhances drug efficacy. We combined the commercially available DeVilbiss Model 65 nebulizer with a dilution/mixing chamber developed in our laboratory. The characteristics of this aerosol generator system were examined over a range of operating conditions and concentrations of solutions of three bronchoconstrictive agents--histamine, carbachol, and methacholine. The aerosol generator system produced a polydispersed aerosol with a mass median diameter range of 1.7-2.4 microns and geometric standard deviation of 1.5. The reliable and reproducible operation of the aerosol generator system greatly increases the power of bronchial challenge tests with bronchoconstrictive drugs.

Administration, Inhalation↗

PubMed1985

Responses of subjects with chronic obstructive pulmonary disease after exposures to 0.3 ppm ozone.

We previously reported (American Review of Respiratory Disease 1982; 125:664-669) that the respiratory mechanics of intermittently exercising persons with chronic obstructive pulmonary disease (COPD) were unaffected by a 2-h exposure to 0.2 ppm ozone. Employing a single-blind, cross-over design protocol, 13 white men with nonreversible COPD (9 current smokers; mean FEV1/FVC, 56%) were randomly exposed on 2 consecutive days for 2 h to air and 0.3 ppm ozone. During exposures, subjects exercised (minute ventilation, 26.4 +/- 3.0 L/min) for 7.5 min every 30 min; ventilation and gas exchange measured during exercise showed no difference between exposure days. Pulmonary function tests (spirometry, body plethysmography) obtained before and after exposures were unchanged on the air day. On the ozone day the mean airway resistance and specific airway resistance showed the largest (25 and 22%) changes (p = 0.086 and 0.058, respectively). Arterial oxygen saturation (SaO2) obtained in 8 subjects during the last exercise interval showed a mean decrement of 0.95% on the ozone exposure day; this change did not attain significance (p = 0.074). Nevertheless, arterial oxygen desaturation may be a true consequence of low-level ozone exposure in this compromised patient group. As normal subjects undergoing exposures to ozone with slightly higher exercise intensities show a threshold for changes in their respiratory mechanics at approximately 0.3 ppm, our data indicate that persons with COPD are not unduly sensitive to the effects of low-level ozone exposure.

Aged↗

PubMed1983

Effects of 0.1 ppm nitrogen dioxide on airways of normal and asthmatic subjects.

It has been reported (J. Clin. Invest. 57: 301-307, 1976) that inhalation of nitrogen dioxide (NO2) will enhance the bronchial reactivity of asthmatics. This study was designed to evaluate the respiratory effect of a 1-h exposure of normal subjects and of atopic asthmatics to 0.1 parts per million (ppm) NO2. Fifteen normal and 15 asthmatic subjects were exposed to air and to NO2 in a randomized double-blind crossover design. Exposure to either atmosphere was bracketed by bronchial inhalation challenge using aerosolized metacholine chloride solutions. Plethysmographic measurements of specific airway resistance (sRaw) and the forced random noise impedance spectrum (5-30 Hz) were obtained immediately after each methacholine dose. Following acute exposure to NO2, there was a slight but not significant increase in mean base-line sRaw in both normals and asthmatics. The overall base-line resistive properties of the respiratory system determined by forced random noise excitation were not significantly affected by NO2 inhalation either. Finally, there was no change in bronchial response to methacholine challenge in either group. These findings indicate that 0.1 ppm NO2 exposure for 1 h without exercise had no demonstrable airways effects in either young atopic asthmatics with mild disease or young normal subjects.

Adolescent↗