title: Neonatal Diesel Exhaust Particulate Exposure Does Not Predispose Mice to Adult Cardiac Hypertrophy or Heart Failure.
abstract: 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.
authors.affiliation: Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA 98109, USA. ygliu99@u.washington.edu.
authors.forename: Yonggang
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA 98109, USA. chad.weldy@duke.edu.
authors.forename: Chad S
authors.initials: CS
authors.lastname: Weldy
authors.affiliation: Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA 98109, USA. mtchin@u.washington.edu.|Center for Cardiovascular Biology, School of Medicine, University of Washington, Box 358050, 850 Republican Street, Room 353, Seattle, WA 98109, USA. mtchin@u.washington.edu.
authors.forename: Michael T
authors.initials: MT
authors.lastname: Chin
mesh_terms: D000375:Aging; D000818:Animals; D000831:Animals, Newborn; D006332:Cardiomegaly / Q000209:etiology*; D004198:Disease Susceptibility; D004452:Echocardiography; D005500:Follow-Up Studies; D006333:Heart Failure / Q000209:etiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D052638:Particulate Matter / Q000633:toxicity*; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D052638:Particulate Matter; D001335:Vehicle Emissions
keywords: PM2.5; air pollution; cardiac hypertrophy; diesel exhaust particulates; heart failure