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      Nitrogen dioxide exposure: effects on airway and blood cells

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          Abstract

          This study examined the effects of nitrogen dioxide (NO 2) exposure on airway inflammation, blood cells, and antiviral respiratory defense. Twenty-one healthy volunteers were exposed on separate occasions to air and 0.6 and 1.5 ppm NO 2for 3 h with intermittent moderate exercise. Phlebotomy and bronchoscopy were performed 3.5 h after each exposure, and recovered cells were challenged with respiratory viruses in vitro. Blood studies revealed a 4.1% NO 2dose-related decrease in hematocrit ( P = 0.003). Circulating total lymphocytes ( P = 0.024) and T lymphocytes ( P = 0.049) decreased with NO 2exposure. Exposure to NO 2increased the blood lymphocyte CD4 +-to-CD8 +ratio from 1.74 ± 0.11 to 1.85 ± 0.12 in males but decreased it from 1.88 ± 0.19 to 1.78 ± 0.19 in females ( P < 0.001 for gender difference). Polymorphonuclear leukocytes in bronchial lavage increased with NO 2exposure ( P = 0.003). Bronchial epithelial cells obtained after exposure to 1.5 ppm NO 2released 40% more lactate dehydrogenase after challenge with respiratory syncytial virus than with air exposure ( P = 0.024). In healthy subjects, exposures to NO 2at levels found indoors cause mild airway inflammation, effects on blood cells, and increased susceptibility of airway epithelial cells to injury from respiratory viruses.

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          Most cited references28

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          Air pollution and bronchitic symptoms in Southern California children with asthma.

          The association of air pollution with the prevalence of chronic lower respiratory tract symptoms among children with a history of asthma or related symptoms was examined in a cross-sectional study. Parents of a total of 3,676 fourth, seventh, and tenth graders from classrooms in 12 communities in Southern California completed questionnaires that characterized the children's histories of respiratory illness and associated risk factors. The prevalences of bronchitis, chronic phlegm, and chronic cough were investigated among children with a history of asthma, wheeze without diagnosed asthma, and neither wheeze nor asthma. Average ambient annual exposure to ozone, particulate matter (PM(10) and PM(2.5); [less than/equal to] 10 microm and < 2.5 microm in aerodynamic diameter, respectively), acid vapor, and nitrogen dioxide (NO(2)) was estimated from monitoring stations in each community. Positive associations between air pollution and bronchitis and phlegm were observed only among children with asthma. As PM(10) increased across communities, there was a corresponding increase in the risk per interquartile range of bronchitis [odds ratio (OR) 1.4/19 microg/m(3); 95% confidence interval (CI), 1.1-1.8). Increased prevalence of phlegm was significantly associated with increasing exposure to all ambient pollutants except ozone. The strongest association was for NO(2), based on relative risk per interquartile range in the 12 communities (OR 2.7/24 ppb; CI, 1.4-5.3). The results suggest that children with a prior diagnosis of asthma are more likely to develop persistent lower respiratory tract symptoms when exposed to air pollution in Southern California. Images Figure 1 Figure 2
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            Association of air pollution with daily GP consultations for asthma and other lower respiratory conditions in London.

            Very few published studies have looked at the effects of air pollution on health in the primary care setting. As part of a large study to examine the association between air pollution and a number of health outcomes, the relationship between daily GP consultations for asthma and other lower respiratory diseases (LRD) and air pollution in London was investigated. Time-series analysis of daily numbers of GP consultations controlling for time trends, seasonal factors, day of week cycles, influenza, weather, pollen levels, and serial correlation was performed. Consultation data were available from between 268 718 and 295 740 registered patients from 45-47 London practices contributing to the General Practice Research Database during 1992-4. Positive associations, weakly significant and consistent across lags, were observed between asthma consultations and nitrogen dioxide (NO2) and carbon monoxide (CO) in children and particulate matter of less than 10 microm in diameter (PM10) in adults, and between other LRD consultations and sulphur dioxide (SO2) in children. A consistently negative association with ozone in children was observed in both disease categories. The effect estimates of most pollutants were much larger when analysed separately by season, particularly in the children: percentage change in asthma consultations during the warm season (April-September) for a 10-90th percentile increase in 24 hour NO2 lagged by one day = 13.2% (95% CI 5.6 to 21.3), with CO = 11.4% (95% CI 3.3 to 20.0), and with SO2 = 9.0% (95% CI 2.2 to 16.2). In adults the only association consistent over different lag periods was with PM10 = 9.2% (3.7 to 15.1). The associations of pollution and consultations for LRD were increased mainly in the winter months: percentage change in consultations by children in winter with NO2 = 7.2% (95% CI 2.8 to 11.6), CO = 6.2% (95% CI 2.3 to 10.2), and SO2 = 5.8% (95% CI 1.6 to 10.2). There are associations between air pollution and daily consultations for asthma and other lower respiratory disease in London. The most significant associations were observed in children and the most important pollutants were NO2, CO, and SO2. In adults the only consistent association was with PM10.
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              The inflammatory effects of 2 ppm NO2 on the airways of healthy subjects.

              Nitrogen dioxide (NO2) is a free radical and a common oxidant in polluted air. Here we present data on the time course of inflammation after NO2 exposure, as reflected in bronchial biopsy and airway lavage specimens. Healthy, nonsmoking subjects were exposed to air or 2 ppm NO2 for 4 h in random order on separate occasions. Endobronchial biopsies, bronchial washing (BW), and bronchoalveolar lavage (BAL) were done at 1.5 h (n = 15) or 6 h (n = 15) after exposure. In BW, exposure to NO2 induced a 1.5-fold increase in interleukin-8 (IL-8) (p < 0.05) at 1.5 h and a 2.5-fold increase in neutrophils (p < 0.01) at 6 h. In BAL fluid (BALF), small increases were observed in CD45RO+ lymphocytes, B-cells, and natural killer (NK) cells only. Immunohistologic examination of bronchial biopsy specimens showed no signs of upregulation of adhesion molecules, and failed to reveal any significant changes in inflammatory cells at either time point after NO2 exposure. In summary, NO2 induced a neutrophilic inflammation in the airways that was detectable in BW at 6 h after NO2 exposure. The increase in neutrophils could be related to the enhanced IL-8 secretion observed at 1.5 h after exposure. The absence of adhesion-molecule upregulation or cellular inflammation in mucosal biopsy specimens indicates that the major site of inflammation following exposure to NO2 may be in the smaller airways and not in the alveoli.
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                Author and article information

                Journal
                American Journal of Physiology-Lung Cellular and Molecular Physiology
                American Journal of Physiology-Lung Cellular and Molecular Physiology
                American Physiological Society
                1040-0605
                1522-1504
                January 01 2002
                January 01 2002
                : 282
                : 1
                : L155-L165
                Affiliations
                [1 ]Departments of Medicine,
                [2 ]Environmental Medicine, and
                [3 ]Division of Infectious Diseases, University of Texas Medical Branch, Galveston, Texas 77555-0835
                [4 ]Biostatistics, University of Rochester School of Medicine, Rochester, New York 14642-8692; and
                Article
                10.1152/ajplung.2002.282.1.L155
                548c1062-73f1-4120-a068-5d0535933fd8
                © 2002
                History

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