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Am J Physiol Heart Circ Physiol. 2015 Dec 15;309(12):H2017-30. doi: 10.1152/ajpheart.00353.2015. Epub 2015 Oct 23.

Cardiac and mitochondrial dysfunction following acute pulmonary exposure to mountaintop removal mining particulate matter.

Author information

1
West Virginia University School of Medicine, Division of Exercise Physiology, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, Morgantown, West Virginia;
2
Center for Cardiovascular and Respiratory Sciences, Morgantown, West Virginia; West Virginia University, School of Public Health, Morgantown, West Virginia;
3
Center for Cardiovascular and Respiratory Sciences, Morgantown, West Virginia;
4
Center for Cardiovascular and Respiratory Sciences, Morgantown, West Virginia; West Virginia University, Department of Physiology and Pharmacology, Morgantown, West Virginia;
5
West Virginia University, Department of Physiology and Pharmacology, Morgantown, West Virginia; National Institute for Occupational Safety and Health, Morgantown, West Virginia.
6
West Virginia University School of Medicine, Division of Exercise Physiology, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, Morgantown, West Virginia; jhollander@hsc.wvu.edu.

Abstract

Throughout the United States, air pollution correlates with adverse health outcomes, and cardiovascular disease incidence is commonly increased following environmental exposure. In areas surrounding active mountaintop removal mines (MTM), a further increase in cardiovascular morbidity is observed and may be attributed in part to particulate matter (PM) released from the mine. The mitochondrion has been shown to be central in the etiology of many cardiovascular diseases, yet its roles in PM-related cardiovascular effects are not realized. In this study, we sought to elucidate the cardiac processes that are disrupted following exposure to mountaintop removal mining particulate matter (PM MTM). To address this question, we exposed male Sprague-Dawley rats to PM MTM, collected within one mile of an active MTM site, using intratracheal instillation. Twenty-four hours following exposure, we evaluated cardiac function, apoptotic indices, and mitochondrial function. PM MTM exposure elicited a significant decrease in ejection fraction and fractional shortening compared with controls. Investigation into the cellular impacts of PM MTM exposure identified a significant increase in mitochondrial-induced apoptotic signaling, as reflected by an increase in TUNEL-positive nuclei and increased caspase-3 and -9 activities. Finally, a significant increase in mitochondrial transition pore opening leading to decreased mitochondrial function was identified following exposure. In conclusion, our data suggest that pulmonary exposure to PM MTM increases cardiac mitochondrial-associated apoptotic signaling and decreases mitochondrial function concomitant with decreased cardiac function. These results suggest that increased cardiovascular disease incidence in populations surrounding MTM mines may be associated with increased cardiac cell apoptotic signaling and decreased mitochondrial function.

KEYWORDS:

apoptosis; cardiac function; mitochondria; particulate matter

PMID:
26497962
PMCID:
PMC4698426
DOI:
10.1152/ajpheart.00353.2015
[Indexed for MEDLINE]
Free PMC Article

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