In utero and early life exposure to diesel exhaust air pollution increases adult susceptibility to heart failure in mice
Open accessAbstract
BACKGROUND: Fine particulate air pollution (PM2.5) is a global health concern, as exposure to PM2.5 has consistently been found to be associated with increased cardiovascular morbidity and mortality. Although adult exposure to traffic related PM2.5, which is largely derived from diesel exhaust (DE), has been associated with increased cardiac hypertrophy, there are limited investigations into the potential effect of in utero and early life exposure on adult susceptibility to heart disease. In this study, we investigate the effect of in utero and early life exposure to DE on adult susceptibility to heart failure. METHODS: Female C57BL/6 J mice were exposed to either filtered air (FA) or DE for 3 weeks (≈ 300 μg/m3 PM2.5 for 6 hours/day, 5 days/week) and then introduced to male breeders for timed matings. Female mice were exposed to either FA or DE throughout pregnancy and until offspring were 3 weeks of age. Offspring were then transferred to either FA or DE for an additional 8 weeks of exposure. At 12 weeks of age, male offspring underwent a baseline echocardiographic assessment, followed by a sham or transverse aortic constriction (TAC) surgery to induce pressure overload. Following sacrifice three weeks post surgery, ventricles were processed for histology to assess myocardial fibrosis and individual cardiomyocyte hypertrophy. mRNA from lung tissue was isolated to measure expression of inflammatory cytokines IL6 and TNFα. RESULTS: We observed that mice exposed to DE during in utero and early life development have significantly increased susceptibility to cardiac hypertrophy, systolic failure, myocardial fibrosis, and pulmonary congestion following TAC surgery compared to FA control, or adult DE exposed mice. In utero and early life DE exposure also strongly modified the inflammatory cytokine response in the adult lung. CONCLUSIONS: We conclude that exposure to diesel exhaust air pollution during in utero and early life development in mice increases adult susceptibility to heart failure. The results of this study may imply that the effects of air pollution on cardiovascular disease in human populations may be strongly mediated through a 'fetal origins' of adult disease pathway. Further investigations on this potential pathway of disease are warranted.
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In C57Bl/6 mice exposed to diesel exhaust prior to mating, during gestation, and until offspring were 8 weeks, male offspring at 12 weeks showed increased risk of cardiac hypertrophy, systolic failure, myocardial fibrosis, and pulmonary congestion following transverse aortic constriction surgery, indicative of risk for heart failure.
“Exposed mice showed increased risk of cardiac hypertrophy, systolic failure, myocardial fibrosis, and pulmonary congestion following TAC surgery, indicative of risk for heart failure.”
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 [99]
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Experimental — accuracy not yet measuredIn 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 [99]
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- Authors
- Weldy, C. S., Liu, Y., Chang, Y.-C., Medvedev, I. O., Fox, J. R., Larson, T. V., Chien, W.-M., & Chin, M. T.
- Affiliations
- University of Washington (US)
- Corresponding author
- Chin, Michael T
- Venue
- Particle and Fibre Toxicology
- Published
- 2013-11-26
- Volume
- 10
- Issue
- 1
- Pages
- 59-59
- ISSN
- 1743-8977 (ISSN-L)
- PMC
- PMC3902482
- OpenAlex
- W2095633819
- Cited by
- 63
- References
- 64
- Citations by year
- 2025: 7 · 2024: 1 · 2023: 3 · 2022: 4 · 2021: 9 · 2020: 5 · 2019: 8 · 2018: 6 · 2017: 5 · 2016: 7 · 2015: 6 · 2014: 2
- FWCI
- 3.68
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Particle and Fibre Toxicology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (T32-HL-07828, T32HL007312, T32HL007828)
- National Institute of Environmental Health Sciences (P50ES015915, ES-015915, P30ES007033, T32ES015459)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Social Sciences › Sociology and Political Science › Environmental Justice and Health Disparities
- Keywords
- diesel exhaust, PM2.5, air pollution, prenatal exposure, early life exposure, heart failure, cardiac hypertrophy, myocardial fibrosis, systolic dysfunction, pulmonary congestion, transverse aortic constriction, pressure overload, fetal origins of adult disease, interleukin-6, TNF-α, lung inflammation, cardiovascular disease
- MeSH terms
- Animals, Vehicle Emissions, Environmental Exposure, Female, Heart Failure, Pregnancy, Prenatal Exposure Delayed Effects, Cytokines, Mice
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