title: Maternal occupational exposure to polycyclic aromatic hydrocarbons and congenital heart defects among offspring in the national birth defects prevention study.
abstract: BACKGROUND
  There is evidence in experimental model systems that exposure to polycyclic aromatic hydrocarbons (PAHs) results in congenital heart defects (CHDs); however, to our knowledge, this relationship has not been examined in humans. Therefore, we conducted a case-control study assessing the association between estimated maternal occupational exposure to PAHs and CHDs in offspring.
  
  
  METHODS
  Data on CHD cases and control infants were obtained from the National Birth Defects Prevention Study for the period of 1997 to 2002. Exposure to PAHs was assigned by industrial hygienist consensus, based on self-reported maternal occupational histories from 1 month before conception through the third month of pregnancy. Logistic regression was used to evaluate the association between maternal occupational PAH exposure and specific CHD phenotypic subtypes among offspring.
  
  
  RESULTS
  The prevalence of occupational PAH exposure was 4.0% in CHD case mothers (76/1907) and 3.6% in control mothers (104/2853). After adjusting for maternal age, race or ethnicity, education, smoking, folic acid supplementation, and study center, exposure was not associated with conotruncal defects (adjusted odds ratio [AOR], 0.98; 95% confidence interval [CI], 0.58-1.67), septal defects (AOR, 1.28; 95% CI, 0.86-1.90), or with any isolated CHD subtype.
  
  
  CONCLUSIONS
  Our findings do not support an association between potential maternal occupational exposure to PAHs and various CHDs in a large, population-based study. For CHD phenotypic subtypes in which modest nonsignificant associations were observed, future investigations could be improved by studying populations with a higher prevalence of PAH exposure and by incorporating information on maternal and fetal genotypes related to PAH metabolism. Birth Defects Research (Part A), 2012.
authors.affiliation: Division of Epidemiology, Human Genetics and Environmental Sciences, University of Texas School of Public Health, Houston, TX 77030, USA. Philip.J.Lupo@uth.tmc.edu
authors.forename: Philip J
authors.initials: PJ
authors.lastname: Lupo
authors.forename: Elaine
authors.initials: E
authors.lastname: Symanski
authors.forename: Peter H
authors.initials: PH
authors.lastname: Langlois
authors.forename: Christina C
authors.initials: CC
authors.lastname: Lawson
authors.forename: Sadia
authors.initials: S
authors.lastname: Malik
authors.forename: Suzanne M
authors.initials: SM
authors.lastname: Gilboa
authors.forename: Laura J
authors.initials: LJ
authors.lastname: Lee
authors.forename: A J
authors.initials: AJ
authors.lastname: Agopian
authors.forename: Tania A
authors.initials: TA
authors.lastname: Desrosiers
authors.forename: Martha A
authors.initials: MA
authors.lastname: Waters
authors.forename: Paul A
authors.initials: PA
authors.lastname: Romitti
authors.forename: Adolfo
authors.initials: A
authors.lastname: Correa
authors.forename: Gary M
authors.initials: GM
authors.lastname: Shaw
authors.forename: Laura E
authors.initials: LE
authors.lastname: Mitchell
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D005260:Female; D006306:Health Surveys; D006330:Heart Defects, Congenital / Q000453:epidemiology* / Q000209:etiology / Q000517:prevention & control; D006801:Humans; D007223:Infant; D016015:Logistic Models; D008297:Male; D018811:Maternal Exposure / Q000009:adverse effects*; D016273:Occupational Exposure / Q000009:adverse effects*; D016017:Odds Ratio; D011084:Polycyclic Aromatic Hydrocarbons / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000453:epidemiology* / Q000209:etiology / Q000517:prevention & control; D015995:Prevalence; D012307:Risk Factors; D014481:United States / Q000453:epidemiology
chemical_list: D011084:Polycyclic Aromatic Hydrocarbons