Schoolchildren's antioxidation genotypes are susceptible factors for reduced lung function and airway inflammation caused by air pollution
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- 作者：Bing-Yu Chena ; Chi-Hsien Chena ; Yu-Chen Chuanga ; Ho Kimb ; Yasushi Hondac ; Hung-Che Chiangd ; Yue Leon Guoa ; d ; leonguo@ntu.edu.tw" class="auth_mail" title="E-mail the corresponding author
- 关键词：PM2.5 ; particulate matter of aerodynamic smaller than 2.5 ; µ ; m ; GSTM1 ; glutathione S-transferase M1 ; GSTT1 ; glutathione S-transferase T1 ; GSTP1 ; glutathione S-transferase P1 ; SOD2 ; superoxide dismutases 2 ; EPA ; Environmental Protection Administration ; FVC ; forced expiratory vital capacity ; FEV1 ; forced expiratory volume in 1 ; s ; FEF25% ; forced expiratory flow at 25% of FVC ; FEF50% ; forced expiratory flow at 50% of FVC ; FEF75% ; forced expiratory flow at 75% of FVC ; FEF25&ndash ; 75% ; a
- 刊名：Environmental Research
- 出版年：2016
- 出版时间：August 2016
- 年：2016
- 卷：149
- 期：Complete
- 页码：145-150
- 全文大小：326 K
文摘
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Children with null GSTM1 genotype were susceptible to PM2.5-enhanced airway inflammation.
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Children with SOD2 Ala16 variant were susceptible to ozone-related decrement in FEF25%.
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Ozone-related decrements in FEF50%, FEF75%, and FEF25–75% were observed, regardless of genotype.
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Antioxidation genotype modifies the airway inflammation caused by PM2.5.
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Antioxidation genotype acts as an effect modifier, but not strong, in ozone-related small airway function response.