title: Periconceptional paternal smoking and the risk of congenital heart defects: a case-control study.
abstract: BACKGROUND
  Maternal smoking during pregnancy has been consistently associated with an increased risk of congenital heart defects (CHDs). However, few studies have reported the association between paternal smoking during pregnancy and CHDs among offspring. This report presents the first case-control study to investigate the possible association between periconceptional paternal smoking and CHDs in China.
  
  
  METHODS
  From February 2010 through October 2011, 284 case fetuses with nonsyndromic CHDs and 422 control fetuses with no birth defects were recruited. The mothers of cases and controls were interviewed regarding whether the fathers of fetuses smoked and avoided the mothers while smoking during the periconceptional period. An unconditional logistic regression was used to calculate the adjusted odds ratios (AORs) and 95% confidence intervals (CIs) while controlling for potential confounders.
  
  
  RESULTS
  Light paternal smoking increased the risk of isolated conotruncal heart defects (AOR, 2.23; 95% CI, 1.05, 4.73). Medium paternal smoking seemed to be associated with septal defects (AOR, 2.04; 95% CI, 1.05, 3.98) and left ventricular outflow tract obstructions (AOR, 2.48; 95% CI, 1.04, 5.95). Heavy paternal smoking was also associated with isolated conotruncal heart defects (AOR, 8.16; 95% CI, 1.13, 58.84) and left ventricular outflow tract obstructions (AOR, 13.12; 95% CI, 2.55, 67.39). Paternal smoking with no avoidance behavior was associated with an increased risk of these CHDs subtypes.
  
  
  CONCLUSIONS
  Periconceptional paternal smoking increased the risk of isolated conotruncal heart defects, septal defects and left ventricular outflow tract obstructions. The avoidance behavior of paternal smokers may decrease the risk of selected CHDs.
authors.affiliation: National Center for Birth Defects Monitoring, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, China.
authors.forename: Kui
authors.initials: K
authors.lastname: Deng
authors.forename: Zhen
authors.initials: Z
authors.lastname: Liu
authors.forename: Yuan
authors.initials: Y
authors.lastname: Lin
authors.forename: Dezhi
authors.initials: D
authors.lastname: Mu
authors.forename: Xinlin
authors.initials: X
authors.lastname: Chen
authors.forename: Jun
authors.initials: J
authors.lastname: Li
authors.forename: Nana
authors.initials: N
authors.lastname: Li
authors.forename: Ying
authors.initials: Y
authors.lastname: Deng
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Li
authors.forename: Yanping
authors.initials: Y
authors.lastname: Wang
authors.forename: Shengli
authors.initials: S
authors.lastname: Li
authors.forename: Jun
authors.initials: J
authors.lastname: Zhu
mesh_terms: D016022:Case-Control Studies; D002681:China / Q000453:epidemiology; D004781:Environmental Exposure; D005220:Fathers; D005260:Female; D006330:Heart Defects, Congenital / Q000145:classification / Q000453:epidemiology* / Q000209:etiology*; D006343:Heart Septal Defects / Q000453:epidemiology / Q000209:etiology; D006801:Humans; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*; D014028:Tobacco Smoke Pollution / Q000009:adverse effects; D014694:Ventricular Outflow Obstruction / Q000453:epidemiology / Q000209:etiology; D055815:Young Adult
chemical_list: D014028:Tobacco Smoke Pollution