Bing-Yu Chen1, Chi-Hsien Chen1, Yu-Chen Chuang1, Ho Kim2, Yasushi Honda3, Hung-Che Chiang4, Yue Leon Guo5. 1. Department of Environmental and Occupational Medicine, National Taiwan University (NTU) College of Medicine and NTU Hospital, Taipei, Taiwan. 2. Department of Epidemiology and Biostatistics, School of Public Health & Institute of Health and Environment, Seoul National University, Seoul, Republic of Korea. 3. Environmental Epidemiology Group, School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan. 4. National Institute of Environmental Health Sciences, National Health Research Institute, Zhunan, Taiwan. 5. Department of Environmental and Occupational Medicine, National Taiwan University (NTU) College of Medicine and NTU Hospital, Taipei, Taiwan; National Institute of Environmental Health Sciences, National Health Research Institute, Zhunan, Taiwan. Electronic address: leonguo@ntu.edu.tw.
Abstract
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%) (-0.43L/s; 95% CI: -0.58,-0.28L/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.
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%) (-0.43L/s; 95% CI: -0.58,-0.28L/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.