title: Prenatal drinking-water exposure to tetrachloroethylene and ischemic placental disease: a retrospective cohort study.
abstract: BACKGROUND
  Prenatal drinking water exposure to tetrachloroethylene (PCE) has been previously related to intrauterine growth restriction and stillbirth. Pathophysiologic and epidemiologic evidence linking these outcomes to certain other pregnancy complications, including placental abruption, preeclampsia, and small-for-gestational-age (SGA) (i.e., ischemic placental diseases), suggests that PCE exposure may also be associated with these events. We examined whether prenatal exposure to PCE-contaminated drinking water was associated with overall or individual ischemic placental diseases.
  
  
  METHODS
  Using a retrospective cohort design, we compared 1,091 PCE-exposed and 1,019 unexposed pregnancies from 1,766 Cape Cod, Massachusetts women. Exposure between 1969 and 1990 was estimated using water distribution system modeling software. Data on birth weight and gestational age were obtained from birth certificates; mothers self-reported pregnancy complications.
  
  
  RESULTS
  Of 2,110 eligible pregnancies, 9% (N = 196) were complicated by ≥1 ischemic placental disease. PCE exposure was not associated with overall ischemic placental disease (for PCE ≥ sample median vs. no exposure, risk ratio (RR): 0.90; 95% confidence interval (CI): 0.65, 1.24), preeclampsia (RR: 0.36; 95% CI: 0.12-1.07), or SGA (RR: 0.98; 95% CI: 0.66-1.45). However, pregnancies with PCE exposure ≥ the sample median had 2.38-times the risk of stillbirth ≥27 weeks gestation (95% CI: 1.01, 5.59), and 1.35-times of the risk of placental abruption (95% CI: 0.68, 2.67) relative to unexposed pregnancies.
  
  
  CONCLUSIONS
  Prenatal PCE exposure was not associated with overall ischemic placental disease, but may increase risk of stillbirth.
authors.forename: Jenny L
authors.initials: JL
authors.lastname: Carwile
authors.forename: Shruthi
authors.initials: S
authors.lastname: Mahalingaiah
authors.forename: Michael R
authors.initials: MR
authors.lastname: Winter
authors.affiliation: Department of Epidemiology, Boston University School of Public Health, Boston, MA, USA. aaschen@bu.edu.
authors.forename: Ann
authors.initials: A
authors.lastname: Aschengrau
mesh_terms: D000328:Adult; D005260:Female; D006801:Humans; D008404:Massachusetts / Q000453:epidemiology; D018811:Maternal Exposure; D008962:Models, Theoretical; D010922:Placenta Diseases / Q000139:chemically induced / Q000453:epidemiology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000453:epidemiology*; D012189:Retrospective Studies; D050497:Stillbirth / Q000453:epidemiology*; D013750:Tetrachloroethylene / Q000633:toxicity*; D014874:Water Pollutants, Chemical / Q000633:toxicity*; D055815:Young Adult
chemical_list: D014874:Water Pollutants, Chemical; D013750:Tetrachloroethylene