title: The effect of tobacco exposure on the fetal hypothalamic-pituitary-adrenal axis.
abstract: OBJECTIVE
  Our objective was to determine if maternal smoking is associated with programming of the fetal hypothalamic-pituitary-adrenal (HPA) axis. Cigarette smoking, which induces a state of hypoxia in the fetus, may promote in utero'programming' of the HPA axis. In utero, adaptations to the HPA axis, which become maladaptive later in life, have been hypothesised to contribute to the development of adult cardiovascular disease and metabolic disorders.
  
  
  METHODS
  This was a prospective cohort study of term infants.
  
  
  METHODS
  The study involved 104 infants born by elective caesarean section, 21 of whom were exposed to in utero tobacco and 83 were nonexposed.
  
  
  METHODS
  Healthy women with healthy pregnancies were recruited if they were undergoing elective caesarean section. Maternal blood was drawn for cortisol and cotinine in the morning, and the umbilical blood was drawn immediately after delivery of the baby.
  
  
  METHODS
  Umbilical arterial cortisol and adrenocorticotropin hormone (ACTH) levels.
  
  
  RESULTS
  ACTH levels were significantly elevated in smoke-exposed infants [17 (4-22) pmol/l versus 4 (2-11) pmol/l, respectively, P= 0.005], while cortisol levels were similar [182 (130-240) nmol/l versus 192 (127-265) nmol/l, respectively, P= 0.541].
  
  
  CONCLUSIONS
  For the first time, it was shown that infants exposed to in utero tobacco smoke have significantly elevated ACTH levels compared with nonexposed infants. The results of this study warrant further exploration of the effect of smoking on the neonatal HPA axis as a potential set up for 'programming'.
authors.affiliation: Department of Obstetrics and Gynecology, McMaster University, Hamilton, Canada. mcdonals@mcmaster.ca
authors.forename: S D
authors.initials: SD
authors.lastname: McDonald
authors.forename: M
authors.initials: M
authors.lastname: Walker
authors.forename: S L
authors.initials: SL
authors.lastname: Perkins
authors.forename: J
authors.initials: J
authors.lastname: Beyene
authors.forename: K
authors.initials: K
authors.lastname: Murphy
authors.forename: W
authors.initials: W
authors.lastname: Gibb
authors.forename: A
authors.initials: A
authors.lastname: Ohlsson
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000378:metabolism*; D000328:Adult; D015331:Cohort Studies; D003367:Cotinine / Q000378:metabolism; D005260:Female; D005333:Fetus / Q000196:embryology* / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D007030:Hypothalamo-Hypophyseal System / Q000196:embryology*; D007231:Infant, Newborn; D008297:Male; D010913:Pituitary-Adrenal System / Q000196:embryology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011446:Prospective Studies; D012907:Smoking / Q000009:adverse effects*; D014469:Umbilical Arteries / Q000378:metabolism*
chemical_list: D000324:Adrenocorticotropic Hormone; D003367:Cotinine; D006854:Hydrocortisone