Respiratory responses to repeated prolonged exposure to 0.12 ppm ozone.

Abstract

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 6.6 h on 5 consecutive days. Subjects were also exposed once to filtered air. Volunteers exercised at a ventilation of approximately 39 L/min for 50 min of each hour during the exposure. Spirometry, plethysmography, and symptom responses were obtained before, during, and after each exposure. Nasal lavage and aerosol bolus dispersion were obtained before and after exposure. Spirometry decreased and symptoms increased on the first day. Responses were less on the second day compared with those on the first day, and they were absent compared with control values on the subsequent 3 days of ozone exposure. Percent change in FEV1 after ozone exposure compared with that after air exposure averaged -12.79, -8.73, -2.54, -0.6, +0.18% for Days 1 to 5 of ozone exposure, respectively. FEV1 responses ranged from a zero to 34% decrease on Days 1 and 2. After each exposure, we determined the ratio of SRaw after inhaling a fixed dose of methacholine to SRaw after inhaling saline aerosol, as an index of airway responsiveness. Airway responsiveness was significantly increased after each ozone exposure. The mean ratios were 2.22, 3.67, 4.55, 3.99, 3.24, and 3.74 for filtered air and ozone Days 1 to 5, respectively. Symptoms of cough and pain on deep inspiration increased significantly on ozone Day 1 only.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary function, bronchial reactivity, and epithelial permeability are response phenotypes to ozone and develop differentially in healthy humans

“…Given the relatively complex physiologies surrounding each of these functional and epithelial responses, this suggests that more than a single host factor is likely responsible for modulating susceptibility to O 3 . Individual airway responses to ozone, for example the FEV 1 and/or AHR, have been shown by us and others to be highly repeatable if the subject is restudied under identical exposure conditions (13,14,34). Thus these response elements demonstrate high levels of reproducibility for periods of time that may extend over a period of at least 12 mo.…”

CCL7 and CXCL10 Orchestrate Oxidative Stress-Induced Neutrophilic Lung Inflammation

“…Oxidative stress from O 3 exposure has been shown to induce airway hyperesponsiveness in humans (36,37). These authors have suggested that because of these effects, O 3 exposure is likely to contribute to asthma morbidity.…”

Bronchial reactivity of healthy subjects: 18–20 h postexposure to ozone

“…The acute development of airway hyperreactivity may be vagally mediated, and the responsiveness can be reversed with atropine premedication (18,21). Investigations have utilized single-or multiple-exposure plans (9,22); however, assessments of hyperreactivity were not usually conducted at later time points (i.e., 1 day postexposure) when O 3 -induced inflammation of the airways and lung parenchyma have been well characterized (11). In one study of healthy subjects, an O 3 concentration of 200 ppb did not provoke airway responsiveness either immediately or 1 day postexposure (26), although hyperresponsive airways have been reported after exposure to high concentrations (400-600 ppb) of O 3 (18,32).…”