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Early life exposure to air pollution induces adult cardiac dysfunction

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Gorr, Matthew W., Velten, Markus, Nelin, Timothy D., Youtz, Dane J., Sun, Qinghua, Wold, Loren E.·2014·American Journal of Physiology-Heart and Circulatory Physiology
DOI 10.1152/ajpheart.00526.2014PMC PMC4217011
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Abstract

Exposure to ambient air pollution contributes to the progression of cardiovascular disease, particularly in susceptible populations. The objective of the present study was to determine whether early life exposure to air pollution causes persistent cardiovascular consequences measured at adulthood. Pregnant FVB mice were exposed to filtered (FA) or concentrated ambient particulate matter (PM 2.5) during gestation and nursing. Mice were exposed to PM 2.5 at an average concentration of 51.69 μg/m 3 from the Columbus, OH region for 6 h/day, 7 days/wk in utero until weaning at 3 wk of age. Birth weight was reduced in PM 2.5 pups compared with FA (1.36 ± 0.12 g FA, n = 42 mice; 1.30 ± 0.15 g PM 2.5, n = 67 P = 0.012). At adulthood, mice exposed to perinatal PM 2.5 had reduced left ventricular fractional shortening compared with FA-exposed mice (43.6 ± 2.1% FA, 33.2 ± 1.6% PM 2.5, P = 0.001) with greater left ventricular end systolic diameter. Pressure-volume loops showed reduced ejection fraction (79.1 ± 3.5% FA, 35.5 ± 9.5% PM 2.5, P = 0.005), increased end-systolic volume (10.4 ± 2.5 μl FA, 39.5 ± 3.8 μl PM 2.5, P = 0.001), and reduced dP/d t maximum (11,605 ± 200 μl/s FA, 9,569 ± 800 μl/s PM 2.5, P = 0.05) and minimum (−9,203 ± 235 μl/s FA, −7,045 ± 189 μl/s PM 2.5, P = 0.0005) in PM 2.5-exposed mice. Isolated cardiomyocytes from the hearts of PM 2.5-exposed mice had reduced peak shortening (%PS, 8.53 ± 2.82% FA, 6.82 ± 2.04% PM 2.5, P = 0.003), slower calcium reuptake (τ, 0.22 ± 0.09 s FA, 0.26 ± 0.07 s PM 2.5, P = 0.048), and reduced response to β-adrenergic stimulation compared with cardiomyocytes isolated from mice that were exposed to FA. Histological analyses revealed greater picro-sirius red-positive-stained areas in the PM 2.5 vs. FA group, indicative of increased collagen deposition. We concluded that these data demonstrate the detrimental role of early life exposure to ambient particulate air pollution in programming of adult cardiovascular diseases and the potential for PM 2.5 to induce persistent cardiac dysfunction at adulthood.

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Sorted by citations

Authors
Gorr, M. W., Velten, M., Nelin, T. D., Youtz, D. J., Sun, Q., & Wold, L. E.
Affiliations
  • The Ohio State University (US)
  • University of Bonn (DE)
Corresponding author
Wold, Loren E.
ORCID
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Publisher
American Physiological Society
Published
2014-11-01
Volume
307
Issue
9
Pages
H1353-H1360
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
DOI
10.1152/ajpheart.00526.2014
PMC
PMC4217011
OpenAlex
W2165601251
Cited by
84
References
2
Citations by year
2026: 3 · 2025: 6 · 2024: 4 · 2023: 5 · 2022: 9 · 2021: 8 · 2020: 4 · 2019: 12 · 2018: 10 · 2017: 11 · 2016: 8 · 2015: 4
FWCI
5.04
Type
journal article
Language
en
Open access
Locations
  • American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute of Nursing Research (R01NR012618)
  • National Institute of Environmental Health Sciences (R01ES019923)
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
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
Keywords
air pollution, particulate matter PM2.5, perinatal exposure, prenatal exposure, cardiac dysfunction, left ventricular function, cardiomyocyte contractility, calcium handling, oxidative stress, cardiomyocyte apoptosis, fetal growth restriction, cardiovascular disease, developmental origins of health and disease, pressure-volume loops, isolated cardiomyocytes, ejection fraction
MeSH terms
Animals, Calcium, Collagen, Female, Heart Rate, Myocardial Contraction, Pregnancy, Prenatal Exposure Delayed Effects, Stroke Volume, Ventricular Dysfunction, Left, Myocytes, Cardiac, Mice, Particulate Matter, Adrenergic beta-1 Receptor Agonists

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