In utero exposure to diesel exhaust air pollution promotes adverse intrauterine conditions, resulting in weight gain, altered blood pressure, and increased susceptibility to heart failure in adult mice

PLoS One. 2014 Feb 12;9(2):e88582. doi: 10.1371/journal.pone.0088582. eCollection 2014.


Exposure to fine particulate air pollution (PM₂.₅) is strongly associated with cardiovascular morbidity and mortality. Exposure to PM₂.₅ during pregnancy promotes reduced birthweight, and the associated adverse intrauterine conditions may also promote adult risk of cardiovascular disease. Here, we investigated the potential for in utero exposure to diesel exhaust (DE) air pollution, a major source of urban PM₂.₅, to promote adverse intrauterine conditions and influence adult susceptibility to disease. We exposed pregnant female C57Bl/6J mice to DE (≈300 µg/m³ PM₂.₅, 6 hrs/day, 5 days/week) from embryonic day (E) 0.5 to 17.5. At E17.5 embryos were collected for gravimetric analysis and assessed for evidence of resorption. Placental tissues underwent pathological examination to assess the extent of injury, inflammatory cell infiltration, and oxidative stress. In addition, some dams that were exposed to DE were allowed to give birth to pups and raise offspring in filtered air (FA) conditions. At 10-weeks of age, body weight and blood pressure were measured. At 12-weeks of age, cardiac function was assessed by echocardiography. Susceptibility to pressure overload-induced heart failure was then determined after transverse aortic constriction surgery. We found that in utero exposure to DE increases embryo resorption, and promotes placental hemorrhage, focal necrosis, compaction of labyrinth vascular spaces, inflammatory cell infiltration and oxidative stress. In addition, we observed that in utero DE exposure increased body weight, but counterintuitively reduced blood pressure without any changes in baseline cardiac function in adult male mice. Importantly, we observed these mice to have increased susceptibility to pressure-overload induced heart failure, suggesting this in utero exposure to DE 'reprograms' the heart to a heightened susceptibility to failure. These observations provide important data to suggest that developmental exposure to air pollution may strongly influence adult susceptibility to cardiovascular disease.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Air Pollutants / adverse effects*
  • Air Pollutants / analysis
  • Animals
  • Aorta / pathology
  • Blood Pressure
  • Echocardiography
  • Female
  • Heart Failure / chemically induced*
  • Inflammation
  • Inhalation Exposure / adverse effects
  • Leukocyte Common Antigens / metabolism
  • Male
  • Maternal Exposure / adverse effects*
  • Mice
  • Mice, Inbred C57BL
  • Myocardium / pathology
  • Necrosis
  • Oxidative Stress
  • Particle Size
  • Pregnancy
  • Pregnancy, Animal
  • Time Factors
  • Tyrosine / analogs & derivatives
  • Tyrosine / chemistry
  • Vehicle Emissions*
  • Weight Gain


  • Air Pollutants
  • Vehicle Emissions
  • 3-nitrotyrosine
  • Tyrosine
  • Leukocyte Common Antigens