Qingli Zhang1, Weidong Wang1, Yue Niu1, Yongjie Xia1, Xiaoning Lei1, Juntao Huo2, Qianbiao Zhao2, Yihua Zhang2, Yusen Duan2, Jing Cai1, Zhekang Ying1, Weihua Li3, Renjie Chen4, Qingyan Fu5, Haidong Kan6. 1. School of Public Health, Key Lab of Public Health Safety of the Ministry of Education, NHC Key Lab of Health Technology Assessment, Fudan University, Shanghai 200032, China. 2. Shanghai Environmental Monitoring Center, Shanghai 200235, China. 3. Key Laboratory of Reproduction Regulation of National Population and Family Planning Commission, Shanghai Institute of Planned Parenthood Research, Institute of Reproduction and Development, Fudan University, Shanghai 200032, China. 4. School of Public Health, Key Lab of Public Health Safety of the Ministry of Education, NHC Key Lab of Health Technology Assessment, Fudan University, Shanghai 200032, China; Shanghai Key Laboratory of Meteorology and Health, Shanghai 200030, China. Electronic address: chenrenjie@fudan.edu.cn. 5. Shanghai Environmental Monitoring Center, Shanghai 200235, China. Electronic address: qingyanf@sheemc.cn. 6. School of Public Health, Key Lab of Public Health Safety of the Ministry of Education, NHC Key Lab of Health Technology Assessment, Fudan University, Shanghai 200032, China; Key Laboratory of Reproduction Regulation of National Population and Family Planning Commission, Shanghai Institute of Planned Parenthood Research, Institute of Reproduction and Development, Fudan University, Shanghai 200032, China. Electronic address: kanh@fudan.edu.cn.
Abstract
BACKGROUND: Fine particulate matter (PM2.5) has been widely associated with airway inflammation represented by increased fractional concentration of exhaled nitric oxide (FeNO). However, it remains unclear whether various PM2.5 constituents have different impacts on FeNO and its production process from the arginase (ARG)-nitric oxide synthase (NOS) pathway. OBJECTIVES: To investigate the acute effects of PM2.5 constituents on FeNO and DNA methylation of genes involved. METHODS: We conducted a longitudinal panel study among 43 young adults in Shanghai, China from May to October in 2016. We monitored the concentrations of 25 constituents of PM2.5. We applied the linear mixed-effect model to evaluate the associations of PM2.5 constituents with FeNO and DNA methylation of the ARG2 and NOS2A genes. RESULTS: Following PM2.5 exposure, NOS2A methylation decreased and ARG2 methylation increased only on the concurrent day, whereas FeNO increased most prominently on the second day. Nine constituents (OC, EC, K, Fe, Zn, Ba, Cr, Se, and Pb) showed consistent associations with elevated FeNO and decreased NOS2A methylation or increased ARG2 methylation in single-constituent models and models adjusting for PM2.5 total mass and collinearity. An interquartile range increase of these constituents was associated with respective decrements of 0.27-1.20 in NOS2A methylation (%5mC); increments of 0.48-1.56 in ARG2 methylation (%5mC); and increments of 7.12%-17.54% in FeNO. CONCLUSIONS: Our results suggested that OC, EC, and some metallic elements may be mainly responsible for the development and epigenetic regulation of airway inflammatory response induced by short-term PM2.5 exposure.
BACKGROUND: Fine particulate matter (PM2.5) has been widely associated with airway inflammation represented by increased fractional concentration of exhaled nitric oxide (FeNO). However, it remains unclear whether various PM2.5 constituents have different impacts on FeNO and its production process from the arginase (ARG)-nitric oxide synthase (NOS) pathway. OBJECTIVES: To investigate the acute effects of PM2.5 constituents on FeNO and DNA methylation of genes involved. METHODS: We conducted a longitudinal panel study among 43 young adults in Shanghai, China from May to October in 2016. We monitored the concentrations of 25 constituents of PM2.5. We applied the linear mixed-effect model to evaluate the associations of PM2.5 constituents with FeNO and DNA methylation of the ARG2 and NOS2A genes. RESULTS: Following PM2.5 exposure, NOS2A methylation decreased and ARG2 methylation increased only on the concurrent day, whereas FeNO increased most prominently on the second day. Nine constituents (OC, EC, K, Fe, Zn, Ba, Cr, Se, and Pb) showed consistent associations with elevated FeNO and decreased NOS2A methylation or increased ARG2 methylation in single-constituent models and models adjusting for PM2.5 total mass and collinearity. An interquartile range increase of these constituents was associated with respective decrements of 0.27-1.20 in NOS2A methylation (%5mC); increments of 0.48-1.56 in ARG2 methylation (%5mC); and increments of 7.12%-17.54% in FeNO. CONCLUSIONS: Our results suggested that OC, EC, and some metallic elements may be mainly responsible for the development and epigenetic regulation of airway inflammatory response induced by short-term PM2.5 exposure.
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