Acute pulmonary function response to ozone in young adults as a function of body mass index.

Recent studies have shown enhanced responsiveness to ozone in obese mice. Adiposity has not been examined as a possible modulator of ozone response in humans. We therefore examined the relationship between body mass index and the acute spirometric response to ozone (O(3)) exposure among 197 nonasthmatic young adults (aged 18-35 yr) studied in our human exposure facility from 1992 to 1998.

Distribution and reproducibility of spirometric response to ozone by gender and age.

Subjects were healthy nonsmoking men (n = 146) and women (n = 94) 18-60 yr old. Initially, each subject was exposed for 1.5 h to 0.

Time course of response to ozone exposure in healthy adult females.

Ozone exposure causes acute decrements in pulmonary function, increases airway responsiveness, and changes the breathing pattern. We examined these responses in 19 ozone-responsive (DeltaFEV(1) > 5%) young females exposed to both air and 0.35 ppm ozone.

Increased specific airway reactivity of persons with mild allergic asthma after 7.6 hours of exposure to 0.16 ppm ozone.

Background: Exposure to ozone causes decrements in lung function, increased airway reactivity to nonspecific bronchoconstrictors, and lung inflammation. Epidemiology studies show an association between ambient oxidant levels and increased asthma attacks and hospital admissions.

Objective: The purpose of our study was to evaluate the response of persons with mild asthma to inhaled allergen after ozone exposure conditions similar to those observed in urban areas of the United States.

Nociceptive mechanisms modulate ozone-induced human lung function decrements.

We have previously suggested that ozone (O3)-induced pain-related symptoms and inhibition of maximal inspiration are due to stimulation of airway C fibers (M. J. Hazucha, D.

Prediction of ozone-induced FEV1 changes. Effects of concentration, duration, and ventilation.

The purpose of this analysis of previously published data was to identify a model that accurately predicts the mean ozone-induced FEV1 response of humans as a function of concentration (C), minute ventilation (VE), duration of exposure (T), and age. Healthy young adults (n = 485) were exposed for 2 h to one of six ozone concentrations while exercising at one of three levels. Candidate models were fitted to portions of the data and evaluated on the basis of their ability to predict the mean response of independent samples.

Allergen bronchoprovocation of patients with mild allergic asthma after ozone exposure.

Background: Clinical and epidemiologic studies suggest that ambient ozone exposure may increase the response of patients with asthma to inhaled allergen.

Objectives: The study was designed to evaluate whether a resting 1-hour exposure to 0.12 ppm ozone increases the sensitivity of patients with atopic asthma to inhaled allergen.

Comparison of pulmonary responses of asthmatic and nonasthmatic subjects performing light exercise while exposed to a low level of ozone.

To determine if asthmatic subjects (ASTH, n = 17) experience greater O3-induced pulmonary decrements than nonasthmatic subjects (NONA, n = 13), both groups were exposed for 7.6 h to both clean air and 0.16 ppm O3.

Lung function response of healthy women after sequential exposures to NO2 and O3.

Since NOx emissions bear a precursor-product relation with ambient ozone (O3) levels, the sequence of peak ambient concentrations is first nitrogen dioxide (NO2) followed later in the day by ozone (O3). We ascertained whether preliminary exposure to 0.6 parts per million (ppm) NO2 would affect the lung function response to subsequent exposure to 0.

Respiratory responses to repeated prolonged exposure to 0.12 ppm ozone.

Repeated exposure to high concentrations of ozone results first in augmentation (typically on the second day) and then attenuation of pulmonary response in humans. To determine the effects of repeated prolonged low-concentration ozone exposure, we exposed 17 healthy nonsmoking male subjects to 0.12 ppm ozone for 6.

Human health effects of air pollution.

Over the past three or four decades, there have been important advances in the understanding of the actions, exposure-response characteristics, and mechanisms of action of many common air pollutants. A multidisciplinary approach using epidemiology, animal toxicology, and controlled human exposure studies has contributed to the database. This review will emphasize studies of humans but will also draw on findings from the other disciplines.

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.

Does nitrogen dioxide exposure increase airways responsiveness?

A number of reports have suggested that exposure to nitrogen dioxide (NO2) may cause increased airways responsiveness (AR). Twenty studies of asthmatics and five studies of healthy subjects exposed to NO2 were used to test this hypothesis using a simple method of meta-analysis. Individual data were obtained for the above studies and the direction of change in AR was determined for each subject.

Respiratory response of humans exposed to low levels of ozone for 6.6 hours.

Recent evidence suggests that prolonged exposures of exercising men to 0.08 ppm ozone (O3) result in significant decrements in lung function, induction of respiratory symptoms, and increases in nonspecific airway reactivity. The purpose of this study was to confirm or refute these findings by exposing 38 healthy young men to 0.

An air quality data analysis system for interrelating effects, standards, and needed source reductions: Part 11. A lognormal model relating human lung function decrease to O3 exposure.

Forced expiratory volume in 1 second (FEV1) was measured in 21 men exercising while exposed to four O3 concentrations (0.0, 0.08, 0.

Ozone concentration and pulmonary response relationships for 6.6-hour exposures with five hours of moderate exercise to 0.08, 0.10, and 0.12 ppm.

The magnitudes of pulmonary responses we previously observed (1) following 6.6-h exposures to 0.12 ppm ozone (O3) suggested that responses would also occur with similar exposures at lower O3 concentrations.

Human health effects of exposure to airborne acid.

This paper summarizes and critiques a series of reports on the health effects of acid aerosol exposure, presented at the Symposium on the Health Effects of Acid Aerosols and compares these data to selected previous studies. The role of the two major defenses against acid aerosols, the conversion of acid to the ammonium salts by respiratory ammonia and buffering of acid by airway surface liquid are discussed in relation to airway acid burdens expected from typical inhalation exposures. The roles of particle size and hygroscopicity on airway deposition of aerosol are also included.

The relationship between exposure duration and sulfur dioxide-induced bronchoconstriction in asthmatic subjects.

The purpose of this study was to determine the shortest duration of exposure to 1.0 ppm sulfur dioxide (SO2) sufficient to induce bronchoconstriction significantly greater than that observed with exposure to clean air (CA) in exercising SO2-sensitive asthmatics. Asymptomatic, nonmedicated, male asthmatics (n = 12) with airway hyperresponsiveness to both methacholine and SO2 were exposed in a chamber (20 degrees C, 40% relative humidity) for 0.

Combined effect of ozone and sulfuric acid on pulmonary function in man.

A potential effect of the combination of ozone and sulfuric acid mist (H2SO4) on respiratory function has been postulated for humans simultaneously exposed to these two pollutants. Nine young men were exposed to 0.25 ppm ozone (O3), 1200-1600 micrograms/m3 sulfuric acid aerosol (H2SO4), and a combination of O3 and H2SO4.

Persistence of the acute effects of ozone exposure.

Reexposure to ozone 24 h after an initial exposure results in greater decreases in forced expiratory tests of lung function following the second exposure. The purpose of this study was to determine whether this hyperresponsiveness was present earlier than 24 h or persisted beyond 24 h. Four groups of subjects (n = 6,6,7,7) were exposed to 0.

Pulmonary response to threshold levels of sulfur dioxide (1.0 ppm) and ozone (0.3 ppm).

We exposed 22 healthy adult nonsmoking male subjects for 2 h to filtered air, 1.0 ppm sulfur dioxide (SO2), 0.3 ppm ozone (O3), or the combination of 1.

Pulmonary function changes after 1 h continuous heavy exercise in 0.21 ppm ozone.

Prediction equations developed from previous ozone (O3) exposure studies suggested that athletes exercising at near competitive intensities would be subject to alteration of pulmonary function during exposure to relatively low concentrations of O3. Accordingly we exercised seven trained athletes for 1 h at 75% of maximal O2 consumption in both room air and a 0.21 ppm O3 environment.

Effect of threshold loads on voluntary control of slow and rapid inspiratory movements.

The purpose of this study was to examine the hypothesis that voluntarily produced inspiratory movements are preplanned. Subjects performed both rapid (0.5 s) and slow (2.