title: Effects of prenatal perfluorooctane sulfonate (PFOS) exposure on lung maturation in the perinatal rat.
abstract: BACKGROUND
  Perfluorooctane sulfonate (PFOS), found widely in wildlife and humans, is environmentally and metabolically stable. Environmental PFOS may be from its use as a surfactant, hydrolysis of perfluorooctanesulfonyl fluoride, and degradation of N-alkyl-perfluorooctanesulfonamide compounds formerly used in numerous applications. Prenatal exposure to PFOS in rodents causes neonatal mortality; treatment on gestation days (GD) 19-20 is sufficient to induce neonatal death in rats. Affected pups are born alive but present with labored breathing. Their lungs are pale and often do not expand fully on perfusion.
  
  
  METHODS
  Pregnant Sprague-Dawley rats received 0, 25, or 50 mg/kg/day PFOS/K+ orally on GD 19-20. Lungs from GD 21 fetuses and neonates were prepared for histology and morphometry. Rescue experiments included co-administration of dexamethasone or retinyl palmitate with PFOS. Pulmonary surfactant was investigated with mass spectrometry in GD 21 amniotic fluid and neonatal lungs. Microarray analysis was carried out on PND 0 lungs.
  
  
  RESULTS
  Histologically, alveolar walls were thicker in lungs of PFOS-exposed newborns compared to controls. The ratio of solid tissue:small airway was increased, suggesting immaturity. Rescue studies were ineffective. Phospholipid concentrations and molecular speciation were unaffected by PFOS. No changes in markers of alveolar differentiation were detected by microarray analysis.
  
  
  CONCLUSIONS
  Morphometric changes in lungs of PFOS exposed neonates were suggestive of immaturity, but the failure of rescue agents and normal pulmonary surfactant profile indicate that the labored respiration and mortality observed in PFOS-treated neonates was not due to lung immaturity.
authors.affiliation: Reproductive Toxicology Division, NHEERL, Office of Research and Development, U.S. EPA, Research Triangle Park, North Carolina, USA.
authors.forename: R C
authors.initials: RC
authors.lastname: Grasty
authors.forename: J A
authors.initials: JA
authors.lastname: Bjork
authors.forename: K B
authors.initials: KB
authors.lastname: Wallace
authors.forename: D C
authors.initials: DC
authors.lastname: Wolf
authors.forename: C S
authors.initials: CS
authors.lastname: Lau
authors.forename: J M
authors.initials: JM
authors.lastname: Rogers
mesh_terms: D017738:Alkanesulfonic Acids / Q000633:toxicity*; D000818:Animals; D000831:Animals, Newborn; D002454:Cell Differentiation; D003907:Dexamethasone / Q000008:administration & dosage; D004224:Diterpenes; D005260:Female; D005325:Fetal Organ Maturity / Q000187:drug effects*; D005466:Fluorocarbons / Q000633:toxicity*; D020869:Gene Expression Profiling; D008136:Longevity / Q000187:drug effects*; D018811:Maternal Exposure; D020411:Oligonucleotide Array Sequence Analysis; D010743:Phospholipids / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011650:Pulmonary Alveoli / Q000196:embryology* / Q000378:metabolism; D011663:Pulmonary Surfactants / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D000084562:Retinyl Esters; D014801:Vitamin A / Q000008:administration & dosage / Q000031:analogs & derivatives
chemical_list: D017738:Alkanesulfonic Acids; D004224:Diterpenes; D005466:Fluorocarbons; D010743:Phospholipids; D011663:Pulmonary Surfactants; D000084562:Retinyl Esters; D014801:Vitamin A; C014794:retinol palmitate; D003907:Dexamethasone; C076994:perfluorooctane sulfonic acid