Next Article in Journal
A Robot-Based Tool for Physical and Cognitive Rehabilitation of Elderly People Using Biofeedback
Previous Article in Journal
English Stop-Smoking Services: One-Year Outcomes
Open AccessBrief Report

Neonatal Diesel Exhaust Particulate Exposure Does Not Predispose Mice to Adult Cardiac Hypertrophy or Heart Failure

1
Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA 98109, USA
2
Center for Cardiovascular Biology, School of Medicine, University of Washington, Box 358050, 850 Republican Street, Room 353, Seattle, WA 98109, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Paul B. Tchounwou
Int. J. Environ. Res. Public Health 2016, 13(12), 1178; https://doi.org/10.3390/ijerph13121178
Received: 14 October 2016 / Revised: 11 November 2016 / Accepted: 22 November 2016 / Published: 24 November 2016
(This article belongs to the Section Environmental Health)
Background: We have previously reported that in utero and early life exposure to diesel exhaust particulates predisposes mice to adult heart failure, and that in utero exposure alone is sufficient to confer this predisposition. This follow up study addresses whether neonatal exposure alone can also confer this predisposition. Methods: Newborn male C57BL/6 mice were exposed to diesel exhaust (DE) particulates immediately after birth until weaning at 21 days of age, whereupon they were transferred to filtered air (FA) conditions. At the age of 12 weeks, transverse aortic constriction (TAC) was performed followed by weekly echocardiography for three weeks. After the last echocardiogram, mice were euthanized for organ harvest, gravimetry and histology. Results: Neonatal exposure to DE particulates did not increase susceptibility to cardiac hypertrophy or heart failure after TAC when compared to FA exposed controls (ventricular weight/body weight ratio 7.505 vs. 7.517 mg/g, p = Not Significant (NS)). The left ventricular ejection fraction after TAC was similar between groups at one week, two weeks, and three weeks after procedure. Histological analysis showed no difference in the degree of cardiac hypertrophy or fibrosis. Conclusions: Neonatal exposure to DE particulates does not predispose mice to TAC-induced cardiac hypertrophy and heart failure in adulthood, in contrast to previously published results showing susceptibility due to in utero exposure. View Full-Text
Keywords: diesel exhaust particulates; cardiac hypertrophy; heart failure; air pollution; PM2.5 diesel exhaust particulates; cardiac hypertrophy; heart failure; air pollution; PM2.5
Show Figures

Figure 1

MDPI and ACS Style

Liu, Y.; Weldy, C.S.; Chin, M.T. Neonatal Diesel Exhaust Particulate Exposure Does Not Predispose Mice to Adult Cardiac Hypertrophy or Heart Failure. Int. J. Environ. Res. Public Health 2016, 13, 1178.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop