Most studies on the effects of ambient ozone on asthmatics have been based on ozone concentration measurements taken by air monitors in downtown areas. Using a passive ozone sampler, we investigated the effects of on-site ozone concentrations on the pulmonary function and symptoms of asthmatics. Twenty moderate to severe asthmatics who had been managed for at least 2 months without changes of their medication were enrolled from 3 June to 18 July 2005. Respiratory, nasal and ocular symptoms, peak expiratory flow (PEF), which was measured twice a day, and medication use were recorded on a daily basis during the study period. Data for 17 subjects were analyzed. The average ozone exposure level was 28.2+/-23.6 ppb (3.4-315.3 ppb). There was no significant correlation between PEF and ozone concentration (p>0.05) on the same day or 1-, 2-, or 3-day lags. Interestingly, the degree of asthma symptoms was influenced by the ozone concentration (rho=0.303, p<0.001), even at concentrations less than 80 ppb (p=0.298, p<0.001), but the correlation between ozone exposure and the frequency of reliever medication use was not statistically significant (p=0.99). Our results suggest that exposure to relatively low concentrations of ozone influences the symptoms of moderate to severe asthmatics regardless of changes in pulmonary function or medication use.
Ozone/analysis/*toxicity ; Nebulizers and Vaporizers ; Middle Aged ; Male ; Lung/*physiopathology ; Humans ; Female ; Asthma/drug therapy/*etiology/physiopathology ; Air Pollution/*adverse effects ; Aged ; Adult

Asthma ; diagnosis ; drug therapy ; physiopathology ; Child, Preschool ; Diagnosis, Differential ; Glucocorticoids ; therapeutic use ; Humans ; Infant ; Recurrence ; Respiratory Sounds ; diagnosis ; drug effects ; etiology ; Treatment Outcome

Anti-Asthmatic Agents ; therapeutic use ; Asthma, Exercise-Induced ; diagnosis ; epidemiology ; physiopathology ; therapy ; Child ; Constriction, Pathologic ; drug therapy ; etiology ; physiopathology ; Diagnosis, Differential ; Glucocorticoids ; therapeutic use ; Humans ; Risk Factors ; Treatment Outcome

Reactive oxygen species (ROS) performs a pivotal function as a signaling mediator in receptor-mediated signaling. However, the sources of ROS in this signaling have yet to be determined, but may include lipoxygenases (LOXs) and NADPH oxidase. The stimulation of lymphoid cells with TNF-alpha, IL-1beta, and LPS resulted in significant ROS production and NF-kappaB activation. Intriguingly, these responses were markedly abolished via treatment with the LOXs inhibitor nordihydroguaiaretic acid (NDGA). We further examined in vivo anti-inflammatory effects of NDGA in allergic airway inflammation. Both intraperitoneal and intravenous NDGA administration attenuated ovalbumin (OVA)-induced influx into the lungs of total leukocytes, as well as IL-4, IL-5, IL-13, and TNF-alpha levels. NDGA also significantly reduced serum levels of OVA-specific IgE and suppressed OVA-induced airway hyperresponsiveness to inhaled methacholine. The results of our histological studies and flow cytometric analyses showed that NDGA inhibits OVA-induced lung inflammation and the infiltration of CD11b+ macrophages into the lung. Collectively, our findings indicate that LOXs performs an essential function in pro-inflammatory signaling via the regulation of ROS regulation, and also that the inhibition of LOXs activity may have therapeutic potential with regard to the treatment of allergic airway inflammation.
Animals ; Antioxidants/metabolism ; Asthma/complications/metabolism/pathology/physiopathology ; Bronchial Hyperreactivity/drug therapy/pathology ; Bronchial Provocation Tests ; Bronchoalveolar Lavage Fluid/cytology ; Cells, Cultured ; Drug Evaluation, Preclinical ; Humans ; Inflammation/*etiology/metabolism ; Jurkat Cells ; Lipoxygenase/*physiology ; Lipoxygenase Inhibitors/pharmacology/therapeutic use ; Lymphocytes/drug effects/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Nordihydroguaiaretic Acid/pharmacology/therapeutic use ; Reactive Oxygen Species/*adverse effects/*metabolism