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Proc Natl Acad Sci U S A. 2019 Jun 11;116(24):11590-11595. doi: 10.1073/pnas.1902925116. Epub 2019 May 28.

Adverse organogenesis and predisposed long-term metabolic syndrome from prenatal exposure to fine particulate matter.

Author information

1
Department of Animal Science, Texas A&M University, College Station, TX 77843; g-wu@tamu.edu mjmolina@ucsd.edu renyi-zhang@geos.tamu.edu.
2
Department of Animal Science, Texas A&M University, College Station, TX 77843.
3
Department of Atmospheric Science, Texas A&M University, College Station, TX 77843.
4
Department of Medical Physiology, Texas A&M University, College Station, TX 77843.
5
Department of Integrative Veterinary Bioscience, Texas A&M University, College Station, TX 77843.
6
Department of Chemistry, Texas A&M University, College Station, TX 77843.
7
Department of Environmental & Occupational Health, Texas A&M University, College Station, TX 77843.
8
Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093 g-wu@tamu.edu mjmolina@ucsd.edu renyi-zhang@geos.tamu.edu.
9
Department of Atmospheric Science, Texas A&M University, College Station, TX 77843; g-wu@tamu.edu mjmolina@ucsd.edu renyi-zhang@geos.tamu.edu.

Abstract

Exposure to fine particulate matter (PM) during pregnancy is associated with high risks of birth defects/fatality and adverse long-term postnatal health. However, limited mechanistic data are available to assess the detailed impacts of prenatal PM exposure. Here we evaluate fine PM exposure during pregnancy on prenatal/postnatal organogenesis in offspring and in predisposing metabolic syndrome for adult life. Between days 0 and 18 of gestation, two groups of adult female rats (n = 10 for each) were placed in a dual-exposure chamber device, one with clean ambient air (∼3 µg·m-3) and the other with ambient air in the presence of 100 to 200 µg·m-3 of ultrafine aerosols of ammonium sulfate. At birth (postnatal day 0, PND0), four males and four females were selected randomly from each litter to be nursed by dams, whereas tissues were collected from the remaining pups. At PND21, tissues were collected from two males and two females, whereas the remaining pups were fed either a high- or low-fat diet until PND105, when tissues were obtained for biochemical and physiological analyses. Maternal exposure to fine PM increased stillbirths; reduced gestation length and birth weight; increased concentrations of glucose and free fatty acids in plasma; enhanced lipid accumulation in the liver; and decreased endothelium-dependent relaxation of aorta. This lead to altered organogenesis and predisposed progeny to long-term metabolic defects in an age-, organ-, and sex-specific manner. Our results highlight the necessity to develop therapeutic strategies to remedy adverse health effects of maternal PM exposure on conceptus/postnatal growth and development.

KEYWORDS:

air pollution; metabolism; postnatal health; pregnancy outcomes

PMID:
31138695
DOI:
10.1073/pnas.1902925116

Conflict of interest statement

The authors declare no conflict of interest.

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