In Utero Exposure of Hyperlipidemic Mice to Diesel Exhaust: Lack of Effects on Atherosclerosis in Adult Offspring Fed a Regular Chow Diet
Open accessAbstract
Uterine stress is associated with an increased risk of later life metabolic diseases. In this study, we investigated the effect of diesel exhaust (DE) exposure in utero on adult susceptibility to atherosclerosis in genetically hyperlipidemic mice. Pregnant apolipoprotein E-deficient mice received either DE exposure (~250–300 μg/m 3 PM 2.5 for 6 h/day, 5 days/week) or filtered air (FA) throughout gestation. Treatment effects on litter size and gender distribution were recorded. Plasma cholesterol and triglycerides were measured at 8, 12 and 16 weeks of age. Urinary 8-isoprostane and liver 8-hydroxy-deoxyguanosine levels were measured at killing at 16 weeks of age. Expression of the antioxidant genes heme oxygenase-1 and the glutamate-cysteine ligase modifier and catalytic subunits were measured in the lung, liver and aorta. The average area and frequency of atherosclerotic lesions were measured in the aortic sinus and innominate arteries. There were significantly smaller litters and higher postnatal mortality in the DE-exposed mice. There were no significant differences in plasma lipids or lipoprotein profiles, expression of antioxidant genes or markers of oxidative stress between treatment groups. There were also no significant differences in average atherosclerotic lesion area in the aortic sinus or innominate arteries of the DE and FA groups although there was a higher frequency of lesions in the DE-exposed group. Our study indicates that in utero DE exposure does not influence later life lipoprotein metabolism, redox homeostasis or the risk of developing larger atherosclerotic lesions.
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In several prenatal mouse exposure models, DE concentrations have ranged from 90 to 300 μg/m3 PM2.5.
“In several prenatal mouse exposure models, DE concentrations have ranged from 90 to 300 μg/m3 PM2.5 [97–100].”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [100]
In pregnant Apoe−/− mice exposed to diesel exhaust throughout gestation, there was higher postnatal mortality but no significant differences in plasma lipids, lipoprotein profiles, expression of antioxidant genes, or markers of oxidative stress between treatment groups at 16 weeks.
“While there was higher postnatal mortality in the DE-exposed mice, there were no significant differences in plasma lipids or lipoprotein profiles, expression of antioxidant genes or markers of oxidative stress between treatment groups at 16 weeks of age.”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [100]
DE-exposed offspring presented a higher frequency of atherosclerotic lesions, but there was no significant difference in average atherosclerotic lesion area in the aortic sinus or innominate arteries.
“DE-exposed offspring did present a higher frequency of atherosclerotic lesions, but overall, there were no significant difference in average atherosclerotic lesion area in the aortic sinus or innominate arteries.”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [100]
Atherosclerosis was not shown to be a consequence of prenatal diesel exhaust exposure in a recent Apoe−/− mouse model.
“While these studies signify the potential for developmental PM2.5 and PM0.1 exposure to influence hypertension, a major risk factor for heart disease, another risk factor, atherosclerosis, was not shown to be a consequence of prenatal exposure in a recent model.”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [100]
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Cited by
Sorted by citations
Johnson, N. M., Hoffmann, A. R., Behlen, J. C., Lau, C., Pendleton, D., Harvey, N., Shore, R., Li, Y., Chen, J., Tian, Y., et al. (2021) · Environmental Health and Preventive Medicine · doi:10.1186/s12199-021-00995-5 · Cited by 339 · see citing works
“[100] C57Bl/6 (ApoE −/−) mice Diesel exhaust particles PM2.”
Background
- Authors
- Harrigan, J., Ravi, D., Ricks, J., & Rosenfeld, M. E.
- Affiliations
- University of Washington (US)
- Corresponding author
- Rosenfeld, Michael E.
- Venue
- Cardiovascular Toxicology
- Published
- 2017-01-17
- Volume
- 17
- Issue
- 4
- Pages
- 417-425
- ISSN
- 1530-7905 (ISSN-L)
- 1559-0259
- PMC
- PMC5603628
- OpenAlex
- W2572227025
- Cited by
- 6
- References
- 2
- Citations by year
- 2024: 2 · 2021: 3 · 2019: 1
- FWCI
- 0.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Cardiovascular Toxicology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- UW Department of Environmental and Occupational Health Sciences RCR Pilot Projects Fund
- National Institute of Environmental Health Sciences (P50 ES015915)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- diesel exhaust, prenatal exposure, prenatal air pollution exposure, atherosclerosis, hyperlipidemia, ApoE-deficient mice, PM2.5, oxidative stress, antioxidant gene expression, heme oxygenase-1, glutathione synthetase, 8-isoprostane, 8-hydroxy-2'-deoxyguanosine, lipoprotein metabolism, litter size, postnatal mortality, aortic lesions
- MeSH terms
- Age Factors, Animals, Animal Feed, Vehicle Emissions, Female, Hyperlipidemias, Lipoproteins, Male, Mice, Inbred C57BL, Pregnancy, Prenatal Exposure Delayed Effects, Triglycerides, Mice, Knockout, Atherosclerosis, Mice
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