Cardiac and mitochondrial dysfunction following acute pulmonary exposure to mountaintop removal mining particulate matter
Supporting Files
-
12 15 2015
-
-
File Language:
English
Details
-
Alternative Title:Am J Physiol Heart Circ Physiol
-
Personal Author:
-
Description: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.
-
Subjects:
-
Keywords:
-
Source:Am J Physiol Heart Circ Physiol. 309(12):H2017-H2030
-
Pubmed ID:26497962
-
Pubmed Central ID:PMC4698426
-
Document Type:
-
Funding:K99 ES024783/ES/NIEHS NIH HHSUnited States/ ; T32 HL090610/HL/NHLBI NIH HHSUnited States/ ; S10 RR026378/RR/NCRR NIH HHSUnited States/ ; DP2 DK083095/DK/NIDDK NIH HHSUnited States/ ; U54 GM104942/GM/NIGMS NIH HHSUnited States/ ; P30 GM103488/GM/NIGMS NIH HHSUnited States/ ; DP2DK083095/DK/NIDDK NIH HHSUnited States/ ; CC999999/Intramural CDC HHSUnited States/ ; U54GM104942/GM/NIGMS NIH HHSUnited States/ ; P30RR031155/RR/NCRR NIH HHSUnited States/ ; T32HL090610/HL/NHLBI NIH HHSUnited States/ ; F32 ES023435/ES/NIEHS NIH HHSUnited States/ ; ES015022/ES/NIEHS NIH HHSUnited States/ ; P20 RR016440/RR/NCRR NIH HHSUnited States/
-
Volume:309
-
Issue:12
-
Collection(s):
-
Main Document Checksum:urn:sha256:498f911d0ef100552950098e0cdf11a5985e6749b3c72075b3ce03bca61d82a2
-
Download URL:
-
File Type:
Supporting Files
File Language:
English
ON THIS PAGE
CDC STACKS serves as an archival repository of CDC-published products including
scientific findings,
journal articles, guidelines, recommendations, or other public health information authored or
co-authored by CDC or funded partners.
As a repository, CDC STACKS retains documents in their original published format to ensure public access to scientific information.
As a repository, CDC STACKS retains documents in their original published format to ensure public access to scientific information.
You May Also Like
COLLECTION
CDC Public Access