https://scholars.lib.ntu.edu.tw/handle/123456789/475231
標題: | Schoolchildren's antioxidation genotypes are susceptible factors for reduced lung function and airway inflammation caused by air pollution | 作者: | Chen B.-Y. CHI-HSIEN CHEN Chuang Y.-C. Kim H. Honda Y. Chiang H.-C. Yue Leon Guo |
公開日期: | 2016 | 出版社: | Academic Press Inc. | 卷: | 149 | 起(迄)頁: | 145-150 | 來源出版物: | Environmental Research | 摘要: | Background: We recently reported the relationship between exposure to ambient air pollutants and changes in lung function and nasal inflammation among schoolchildren. A study was conducted to investigate whether antioxidation genotypes influence these associations. Methods: A follow-up study of 97 schoolchildren was conducted in New Taipei City, Taiwan. A structured respiratory health questionnaire was administered in September 2007, followed by monthly spirometry and measurement of nasal inflammation from October 2007 to November 2009. During the study period, complete daily monitoring data for air pollutants were obtained from the Environmental Protection Administration monitoring station and Aerosol Supersite. The genotypes of glutathione S-transferase (GST) subunits M1, T1, P1 and superoxide dismutases subunit 2 (SOD2) were characterized. Mixed-effects models were used, adjusting for known confounders. Result: GSTM1 null children had significant PM2.5-related increment in leukocyte (8.52%; 95% confidence interval (CI): 3.13-13.92%) and neutrophil (9.68%; 95% CI: 4.51-14.85%) in nasal lavage. Ozone levels were significantly and inversely associated with forced expiratory flow at 25% of forced vital capacity (FEF25%) (-0.43 L/s; 95% CI: -0.58,-0.28 L/s) in SOD2 Ala16 variant children. Conclusion: In this longitudinal study of schoolchildren. Our data provide evidence that antioxidation genotype modifies the airway inflammation caused by PM2.5. Antioxidation genotype also acts as an effect modifier, but not strong, in ozone-related small airway function response. © 2016 Elsevier Inc.. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84968847694&doi=10.1016%2fj.envres.2016.05.007&partnerID=40&md5=473685cb0d900fb6b3916b40a0cb0330 https://scholars.lib.ntu.edu.tw/handle/123456789/475231 |
ISSN: | 0013-9351 | DOI: | 10.1016/j.envres.2016.05.007 | SDG/關鍵字: | glutathione transferase M1; glutathione transferase P1; glutathione transferase T1; manganese superoxide dismutase; ozone; air pollutant; antioxidant; glutathione transferase; manganese superoxide dismutase; superoxide dismutase; aerodynamics; ambient air; antioxidant; atmospheric pollution; child health; confidence interval; enzyme; genotype; health survey; ozone; particulate matter; pollution effect; pollution monitoring; questionnaire survey; respiratory disease; air pollutant; allergic rhinitis; Article; asthma; atopy; child; controlled study; environmental monitoring; female; follow up; forced expiratory flow; forced vital capacity; genotype; human; leukocyte; longitudinal study; lung function; major clinical study; male; nasal lavage; neutrophil; particulate matter; priority journal; respiratory tract inflammation; school child; spirometry; structured questionnaire; Taiwan; adolescent; chemically induced; city; drug effects; exposure; genetics; genotype; inflammation; lung function test; metabolism; oxidation reduction reaction; respiratory tract disease; toxicity; New Taipei; Taiwan; Adolescent; Air Pollutants; Antioxidants; Child; Cities; Environmental Monitoring; Female; Follow-Up Studies; Genotype; Glutathione Transferase; Humans; Inflammation; Inhalation Exposure; Longitudinal Studies; Male; Oxidation-Reduction; Respiratory Function Tests; Respiratory Tract Diseases; Superoxide Dismutase; Taiwan |
顯示於: | 環境職業醫學科 |
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