title: The association between smoking quantity and hypertension mediated by inflammation in Chinese current smokers.
abstract: OBJECTIVE
  Previous studies indicated that cigarette smokers were more likely to develop hypertension, and both smoking and hypertension were associated with inflammation. Whether inflammation mediates the relationship of them is unclear. This study aims to examine whether inflammation mediates the association between smoking and hypertension.
  
  
  METHODS
  Nine hundred and eighty-four Chinese current smokers from a community-based chronic diseases survey in Guangzhou and Zhuhai were interviewed about sociodemographics, smoking, chronic conditions, and other health-related variables. Hypertension was defined according to 2007 European Society of Hypertension and European Society of Cardiology (ESH-ESC) Practice Guidelines. Inflammatory markers including C-reactive protein (CRP), interleukin (IL)-6, IL-1β, monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α), and vascular cell adhesion molecule-1 (VCAM-1) were measured by flow cytometry. Logistic regressions were performed to assess the mediation of inflammation on the relationship between smoking quantity and hypertension.
  
  
  RESULTS
  We observed a positive association between smoking quantity and hypertension (P<0.05). After controlling for potential confounders, daily cigarette consumption was significantly associated with higher level of CRP and VCAM-1 and lower level of TNF-α among six measured inflammatory markers, and the current smokers with hypertension had significantly higher level of MCP-1 and CRP than those smokers who were normotensive. Furthermore, the association between smoking quantity and hypertension was mediated by CRP, which accounted for 58.59% of the estimated causal effect of smoking on hypertension.
  
  
  CONCLUSIONS
  We have confirmed previous observations that smoking quantity was positively associated with hypertension, and the results of our study suggested that the association between smoking and hypertension was probably mediated by CRP.
authors.affiliation: aDepartment of Preventive Medicine bDepartment of Biostatistics and Epidemiology cExperimental Centre, School of Public Health, Sun Yat-Sen University, Guangzhou, China *Dan Feng and Tao Liu contributed equally to the writing of the article.
authors.forename: Dan
authors.initials: D
authors.lastname: Feng
authors.forename: Tao
authors.initials: T
authors.lastname: Liu
authors.forename: Dong-Fang
authors.initials: DF
authors.lastname: Su
authors.forename: Hui
authors.initials: H
authors.lastname: Wang
authors.forename: Peng
authors.initials: P
authors.lastname: Ding
authors.forename: Yan-Hui
authors.initials: YH
authors.lastname: He
authors.forename: Xue-Qing
authors.initials: XQ
authors.lastname: Deng
authors.forename: Meng-Jun
authors.initials: MJ
authors.lastname: Hou
authors.forename: Wen-Hua
authors.initials: WH
authors.lastname: Ling
authors.forename: Wei-Qing
authors.initials: WQ
authors.lastname: Chen
mesh_terms: D000328:Adult; D000368:Aged; D000428:Alcohol Drinking; D044466:Asian People; D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D018932:Chemokine CCL2 / Q000378:metabolism; D002681:China; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D007249:Inflammation / Q000473:pathology*; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D012907:Smoking / Q000009:adverse effects*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D015415:Biomarkers; C111835:CCL2 protein, human; D018932:Chemokine CCL2; C508600:IL6 protein, human; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D002097:C-Reactive Protein