title: Fetal window of vulnerability to airborne polycyclic aromatic hydrocarbons on proportional intrauterine growth restriction.
abstract: BACKGROUND
  Although the entire duration of fetal development is generally considered a highly susceptible period, it is of public health interest to determine a narrower window of heightened vulnerability to polycyclic aromatic hydrocarbons (PAHs) in humans. We posited that exposure to PAHs during the first trimester impairs fetal growth more severely than a similar level of exposure during the subsequent trimesters.
  
  
  METHODS
  In a group of healthy, non-smoking pregnant women with no known risks of adverse birth outcomes, personal exposure to eight airborne PAHs was monitored once during the second trimester for the entire cohort (n = 344), and once each trimester within a subset (n = 77). Both air monitoring and self-reported PAH exposure data were used in order to statistically estimate PAH exposure during the entire gestational period for each individual newborn.
  
  
  RESULTS
  One natural-log unit increase in prenatal exposure to the eight summed PAHs during the first trimester was associated with the largest decrement in the Fetal Growth Ratio (FGR) (-3%, 95% Confidence Interval (CI), -5 to -0%), birthweight (-105 g, 95% CI, -188 to -22 g), and birth length (-0.78 cm, 95% CI, -1.30 to -0.26 cm), compared to the unit effects of PAHs during the subsequent trimesters, after accounting for confounders. Furthermore, a unit exposure during the first trimester was associated with the largest elevation in Cephalization Index (head to weight ratio) (3 μm/g, 95% CI, 1 to 5 μm/g). PAH exposure was not associated with evidence of asymmetric growth restriction in this cohort.
  
  
  CONCLUSIONS
  PAH exposure appears to exert the greatest adverse effect on fetal growth during the first trimester. The present data support the need for the protection of pregnant women and the embryo/fetus, particularly during the earliest stage of pregnancy.
authors.affiliation: Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, United States of America. hchoi@albany.edu
authors.forename: Hyunok
authors.initials: H
authors.lastname: Choi
authors.forename: Lu
authors.initials: L
authors.lastname: Wang
authors.forename: Xihong
authors.initials: X
authors.lastname: Lin
authors.forename: John D
authors.initials: JD
authors.lastname: Spengler
authors.forename: Frederica P
authors.initials: FP
authors.lastname: Perera
mesh_terms: D000293:Adolescent; D000328:Adult; D000393:Air Pollutants / Q000009:adverse effects*; D001724:Birth Weight / Q000187:drug effects; D015331:Cohort Studies; D005260:Female; D047109:Fetal Development / Q000187:drug effects; D005317:Fetal Growth Retardation / Q000139:chemically induced*; D006801:Humans; D007231:Infant, Newborn; D011084:Polycyclic Aromatic Hydrocarbons / Q000009:adverse effects*; D011247:Pregnancy; D011261:Pregnancy Trimester, First; D011262:Pregnancy Trimester, Second; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced; D055815:Young Adult
chemical_list: D000393:Air Pollutants; D011084:Polycyclic Aromatic Hydrocarbons