title: Preliminary study to explore gene-PM2.5 interactive effects on respiratory system in traffic policemen.
abstract: OBJECTIVE
  Traffic-related particulate matter (PM) is one of the major sources of air pollution in metropolitan areas. This study is to observe the interactive effects of gene and fine particles (particles smaller than 2.5 μm - PM2.5) on the respiratory system and explore the mechanisms linking PM2.5 and pulmonary injury.
  
  
  METHODS
  The participants include 110 traffic policemen and 101 common populations in Shanghai, China. Continuous 24 h individual-level PM2.5 is detected and the pulmonary function, high-sensitivity C-reactive protein (hs-CRP), Clara cell protein 16 (CC16) and the polymorphism in CXCL3, NME7 and C5 genes are determined. The multiple linear regression method is used to analyze the association between PM2.5 and health effects. Meanwhile, the interactive effects of gene and PM2.5 on lung function are analyzed.
  
  
  RESULTS
  The individual PM2.5 exposure for traffic policemen was higher than that in the common population whereas the forced expiratory volume in 1 s (FEV1), the ratio of FEV1 to forced vital capacity (FEV1/FVC) and lymphocytes are lower. In contrast, the hs-CRP level is higher. In the adjusted analysis, PM2.5 exposure was associated with the decrease in lymphocytes and the increase in hs-CRP. The allele frequencies for NME7 and C5 have significant differences between FEV1/FVC ≤ 70% and FEV1/FVC > 70% participants. The results didn't find the interaction effects of gene and PM2.5 on FEV1/FVC in all the 3 genes.
  
  
  CONCLUSIONS
  The results indicated that traffic exposure to high levels of PM2.5 was associated with systemic inflammatory response and respiratory injury. Traffic policemen represent a high risk group suffering from the respiratory injury.
authors: Fudan University, Shanghai, China (Department of Environmental Health, School of Public Health, Key Laboratory of Public Health Safety). Jinzhuozhao@fudan.edu.cn.
authors: Jinzhuo
authors: J
authors: Zhao
authors: Fudan University, Shanghai, China (Department of Environmental Health, School of Public Health, Key Laboratory of Public Health Safety). Liang@163.com.
authors: Liang
authors: L
authors: Bo
authors: Fudan University, Shanghai, China (Department of Environmental Health, School of Public Health, Key Laboratory of Public Health Safety). Gong@126.com.
authors: Changyi
authors: C
authors: Gong
authors: No. 3 People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China (Department of Gastroenterology). chengp@gmail.com.
authors: Peng
authors: P
authors: Cheng
authors: Fudan University, Shanghai, China (Department of Environmental Health, School of Public Health, Key Laboratory of Public Health Safety). Haidong@gmail.com.
authors: Haidong
authors: H
authors: Kan
authors: Shanghai Jiao Tong University, Shanghai, China (Department of Cardiology, Xinhua Hospital, School of Medicine). xyqah@163.com.
authors: Yuquan
authors: Y
authors: Xie
authors: Fudan University, Shanghai, China (Department of Environmental Health, School of Public Health, Key Laboratory of Public Health Safety). wmsong1@gmail.com.
authors: Weimin
authors: W
authors: Song
mesh_terms: D000328:Adult; D000397:Air Pollution / Q000032:analysis*; D019743:Chemokines, CXC / Q000235:genetics / Q000378:metabolism; D004247:DNA / Q000235:genetics*; D004781:Environmental Exposure / Q000009:adverse effects*; D018876:Environmental Illness / Q000235:genetics* / Q000378:metabolism; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D008168:Lung / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009701:Nucleoside-Diphosphate Kinase / Q000235:genetics / Q000378:metabolism; D052638:Particulate Matter / Q000032:analysis*; D016495:Police; D011110:Polymorphism, Genetic; D001335:Vehicle Emissions / Q000032:analysis*
chemical_list: C499707:CXCL3 protein, human; D019743:Chemokines, CXC; D052638:Particulate Matter; D001335:Vehicle Emissions; D004247:DNA; C000595354:NME7 protein, human; D009701:Nucleoside-Diphosphate Kinase
keywords: SNP; fine particles; inflammation; respiratory system; single nucleotide polymorphism; traffic workers