title: Ambient air pollution and traffic exposures and congenital heart defects in the San Joaquin Valley of California.
abstract: BACKGROUND
  Congenital anomalies are a leading cause of infant morbidity and mortality. Studies suggest associations between environmental contaminants and some anomalies, although evidence is limited.
  
  
  METHODS
  We used data from the California Center of the National Birth Defects Prevention Study and the Children's Health and Air Pollution Study to estimate the odds of 27 congenital heart defects with respect to quartiles of seven ambient air pollutant and traffic exposures in California during the first 2 months of pregnancy, 1997-2006 (n = 822 cases and n = 849 controls).
  
  
  RESULTS
  Particulate matter < 10 microns (PM10 ) was associated with pulmonary valve stenosis [adjusted odds ratio (aOR)Fourth Quartile  = 2.6] [95% confidence intervals (CI) 1.2, 5.7] and perimembranous ventricular septal defects (aORThird Quartile  = 2.1) [95% CI 1.1, 3.9] after adjusting for maternal race/ethnicity, education and multivitamin use. PM2.5 was associated with transposition of the great arteries (aORThird Quartile  = 2.6) [95% CI 1.1, 6.5] and inversely associated with perimembranous ventricular septal defects (aORFourth Quartile  = 0.5) [95% CI 0.2, 0.9]. Secundum atrial septal defects were inversely associated with carbon monoxide (aORFourth Quartile  = 0.4) [95% CI 0.2, 0.8] and PM2.5 (aORFourth Quartile  = 0.5) [95% CI 0.3, 0.8]. Traffic density was associated with muscular ventricular septal defects (aORFourth Quartile  = 3.0) [95% CI 1.2, 7.8] and perimembranous ventricular septal defects (aORThird Quartile  = 2.4) [95% CI 1.3, 4.6], and inversely associated with transposition of the great arteries (aORFourth Quartile  = 0.3) [95% CI 0.1, 0.8].
  
  
  CONCLUSIONS
  PM10 and traffic density may contribute to the occurrence of pulmonary valve stenosis and ventricular septal defects, respectively. The results were mixed for other pollutants and had little consistency with previous studies.
authors.affiliation: Stanford University, Stanford 94305, USA. ampadula@stanford.edu
authors.forename: Amy M
authors.initials: AM
authors.lastname: Padula
authors.forename: Ira B
authors.initials: IB
authors.lastname: Tager
authors.forename: Suzan L
authors.initials: SL
authors.lastname: Carmichael
authors.forename: S Katharine
authors.initials: SK
authors.lastname: Hammond
authors.forename: Wei
authors.initials: W
authors.lastname: Yang
authors.forename: Frederick
authors.initials: F
authors.lastname: Lurmann
authors.forename: Gary M
authors.initials: GM
authors.lastname: Shaw
mesh_terms: D000293:Adolescent; D000328:Adult; D000393:Air Pollutants / Q000009:adverse effects*; D000397:Air Pollution / Q000009:adverse effects; D002140:California / Q000453:epidemiology; D002248:Carbon Monoxide / Q000009:adverse effects*; D004781:Environmental Exposure / Q000009:adverse effects*; D005260:Female; D006330:Heart Defects, Congenital / Q000453:epidemiology* / Q000209:etiology; D006343:Heart Septal Defects / Q000453:epidemiology / Q000209:etiology; D006801:Humans; D007231:Infant, Newborn; D016015:Logistic Models; D008297:Male; D018811:Maternal Exposure / Q000009:adverse effects*; D018986:Motor Vehicles; D052638:Particulate Matter / Q000009:adverse effects*; D011247:Pregnancy; D011256:Pregnancy Outcome; D011666:Pulmonary Valve Stenosis / Q000453:epidemiology / Q000209:etiology; D001335:Vehicle Emissions; D055815:Young Adult
chemical_list: D000393:Air Pollutants; D052638:Particulate Matter; D001335:Vehicle Emissions; D002248:Carbon Monoxide