Prenatal environmental tobacco smoke exposure promotes adult atherogenesis and mitochondrial damage in apolipoprotein E-/- mice fed a chow diet

Circulation. 2004 Dec 14;110(24):3715-20. doi: 10.1161/01.CIR.0000149747.82157.01. Epub 2004 Nov 29.


Background: Environmental tobacco smoke (ETS) exposure is recognized as a cardiovascular disease risk factor; however, the impact of prenatal ETS exposure on adult atherogenesis has not been examined. We hypothesized that in utero ETS exposure promotes adult atherosclerotic lesion formation and mitochondrial damage.

Methods and results: Atherosclerotic lesion formation, mitochondrial DNA damage, antioxidant activity, and oxidant load were determined in cardiovascular tissues from adult apolipoprotein E-/- mice exposed to either filtered air or ETS in utero and fed a standard chow diet (4.5% fat) from weaning until euthanasia. All parameters were significantly altered in male mice exposed in utero to ETS.

Conclusions: These data support the hypothesis that prenatal ETS exposure is sufficient to promote adult cardiovascular disease development.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Apolipoproteins E / genetics*
  • Arteriosclerosis / etiology*
  • Arteriosclerosis / metabolism
  • Arteriosclerosis / pathology
  • Dietary Fats / administration & dosage*
  • Female
  • Male
  • Mice
  • Mitochondria / genetics*
  • Oxidants / metabolism
  • Pregnancy
  • Prenatal Exposure Delayed Effects*
  • Risk Factors
  • Tobacco Smoke Pollution / adverse effects*


  • Antioxidants
  • Apolipoproteins E
  • Dietary Fats
  • Oxidants
  • Tobacco Smoke Pollution