Developmental programming of obesity by maternal exposure to concentrated ambient PM 2.5 is maternally transmitted into the third generation in a mouse model

Part Fibre Toxicol. 2019 Jul 2;16(1):27. doi: 10.1186/s12989-019-0312-6.


Background: Obesity is an uncontrolled global epidemic and one of the leading global public health challenges. Maternal exposure to ambient fine particulate matter (PM2.5) may adversely program offspring's adiposity, suggesting a specialized role of PM2.5 pollution in the global obesity epidemic. However, the vulnerable window for this adverse programming and how it is cross-generationally transmitted have not been determined. Therefore, in the present study, female C57Bl/6 J mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (CAP) during different periods, and the development and adulthood adiposity of their four-generational offspring were assessed.

Results: Our data show that the pre-conceptional but not gestational exposure to CAP was sufficient to cause male but not female offspring's low birth weight, accelerated postnatal weight gain, and increased adulthood adiposity. These adverse developmental traits were transmitted into the F2 offspring born by the female but not male F1 offspring of CAP-exposed dams. In contrast, no adverse development was noted in the F3 offspring.

Conclusions: The present study identified a pre-conceptional window for the adverse programming of adiposity by maternal exposure to PM2.5, and showed that it was maternally transmitted into the third generation. These data not only call special attention to the protection of women from exposure to PM2.5, but also may facilitate the development of intervention to prevent this adverse programming.

Keywords: Cross-generational transmission; Developmental programming; Maternal exposure; Obesity; PM2.5.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiposity / drug effects*
  • Adiposity / genetics
  • Air Pollutants / toxicity*
  • Animals
  • Disease Models, Animal
  • Female
  • Gene Expression Regulation, Developmental / drug effects
  • Genetic Predisposition to Disease
  • Infant, Low Birth Weight
  • Male
  • Maternal Exposure / adverse effects*
  • Mice, Inbred C57BL
  • Obesity / chemically induced*
  • Obesity / genetics
  • Obesity / metabolism
  • Particle Size
  • Particulate Matter / toxicity*
  • Pregnancy
  • Prenatal Exposure Delayed Effects / chemically induced*
  • Prenatal Exposure Delayed Effects / genetics
  • Prenatal Exposure Delayed Effects / metabolism
  • Sex Factors
  • Weight Gain


  • Air Pollutants
  • Particulate Matter