Greater ozone-induced inflammatory responses in subjects with asthma.

Abstract

In order to test the hypothesis that ozone (O3)-induced changes in lung function and respiratory tract injury/inflammation are greater in subjects with asthma than in normal subjects, we exposed 18 asthmatic subjects, on separate days, to O3 (0.2 ppm) and filtered air for 4 h during exercise. Symptom questionnaires were administered before and after exposure, and pulmonary function tests (FEV1, FVC, and specific airway resistance [SRaw]) were performed before, during, and immediately after each exposure. Fiberoptic bronchoscopy, with proximal airway lavage (PAL) of the isolated left main bronchus and bronchoalveolar lavage (BAL; bronchial fraction, the first 10 ml of fluid recovered) of the right middle lobe, was performed 18 h after each exposure. The PAL, bronchial fraction, and BAL fluids were analyzed for the following endpoints: total and differential cell counts; total protein, lactate dehydrogenase (LDH), fibronectin, interleukin-8 (IL-8), granulocyte-macrophage colony-stimulating factor (GM-CSF), myeloperoxidase (MPO), and transforming growth factor-beta (TGF beta 2) concentrations. We found a significant O3 effect on FEV1, FVC, SRaw (p < 0.04) and lower respiratory symptoms (p < 0.001) for the asthmatic subjects. Ozone exposure also significantly increased the percent neutrophils in PAL (p < 0.01); percent neutrophils, total protein, and IL-8 in the bronchial fraction (p < 0.001, p < 0.05, and p < 0.01, respectively); and the percent neutrophils, total protein, LDH, fibronectin, IL-8, GM-CSF, and MPO in BAL (p < 0.001, p < 0.01, p < 0.01, p < 0.001, p < 0.05, p < 0.01, and p < 0.001, respectively) for the asthmatic subjects. There were no significant differences in the lung function responses of the asthmatic subjects in comparison with a group of normal subjects (n = 81) previously studied using an identical protocol, although there was a trend toward a greater O3-induced increase in SRaw in the asthmatic subjects (p < 0.13). In contrast, the asthmatic subjects showed significantly greater (p < 0.05) O3-induced increases in several inflammatory endpoints (percent neutrophils and total protein concentration) in BAL as compared with normal subjects who underwent bronchoscopy (n = 20). Our results indicate that asthmatic persons may be at risk of developing more severe O3-induced respiratory tract injury/inflammation than normal persons, and may help explain the increased asthma morbidity associated with O3 pollution episodes observed in epidemiologic studies.

Short‐Term Exposure to Air Pollution and Biomarkers of Oxidative Stress: The Framingham Heart Study

“…Prior studies have yielded mixed results 14, 15, 16, 17, 18. In a recent study, positive associations of short‐term exposure to fine particulate matter (diameter ≤2.5 μm [PM 2.5 ]), black carbon (BC), and nitrogen oxides (NO x ) with myeloperoxidase were found in a group of potentially genetically susceptible participants 14…”

Climate, traffic-related air pollutants, and asthma prevalence in middle-school children in taiwan.

“…In clinical exposures of asthmatics, short exposure to air pollution produces increased airway reactivity. Thresholds in sulfur dioxide-induced bronchoconstriction were lower in asthmatics (10), and ozone-induced lung function change and respiratory tract injury and inflammation were more prominent in asthmatics (11).…”

Toxicologic methods: controlled human exposures.

“…Bronchoscopy was first used by Seltzer and colleagues (18) to detect airway inflammation in response to 03 exposure. Since then, bronchoscopy has allowed investigators to characterize the nature of the airway inflammatory response to single and repeated exposures to 03 in healthy, allergic, and asthmatic subjects (19)(20)(21)(22). It has been used to study the effects of exposure to many pollutants in addition to 03, including NO2 (23-25), SO2, (26), acid aerosols (27)(28)(29), and diesel exhaust (30).…”

“…Two recent studies suggested that mild asthmatics may experience a neutrophilic airway inflammatory response to 03 exposure that is more intense than in healthy subjects (22,93). Recent studies have also shown that, in asthmatics, 03 exposures at concentrations sufficient to induce an airway inflammatory response increase responsiveness to a subsequent allergen challenge (94).…”