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Apoptosis and bax expression are increased by coal dust in the polycyclic aromatic hydrocarbon - exposed lung.

Authors
Ghanem-MM; Battelli-LA; Mercer-RR; Scabilloni-JF; Kashon-ML; Ma-JYC; Nath-J; Hubbs-AF
Source
Environ Health Perspect 2006 Sep; 114(9):1367-1373
NIOSHTIC No.
20030882
Abstract
Miners inhaling respirable coal dust (CD) frequently develop coal workers' pneumoconiosis, a dust-associated pneumoconiosis characterized by lung inflammation and variable fibrosis. Many coal miners are also exposed to polycyclic aromatic hydrocarbon (PAH) components of diesel engine exhaust and cigarette smoke, which may contribute to lung disease in these workers. Recently, apoptosis was reported to play a critical role in the development of another pneumoconiosis of miners, silicosis. In addition, CD was reported to suppress cytochrome P450 1A1 (CYP1A1) induction by PAHs. We investigated the hypothesis that apoptosis plays a critical role in lung injury and down-regulation of CYP1A1 induction in mixed exposures to CD and PAHs. We exposed rats intratracheally to 0.0, 2.5, 10.0, 20.0, or 40.0 mg/rat CD and, 11 days later, to intraperitoneal B-naphthoflavone (BNF) , a PAH. In another group of rats exposed to CD and BNF, caspase activity was inhibited by injection of the pan-caspase inhibitor Q-VD-OPH [quinoline-Val-Asp (OMe) -CH2-OPH]. In rats exposed to BNF, CD exposure increased alveolar expression of the proapoptotic mediator Bax but decreased CYP1A1 induction relative to BNF exposure alone. Pan-caspase inhibition decreased CD-associated Bax expression and apoptosis but did not restore CYP1A1 activity. Further, CD-induced lung inflammation and alveolar epithelial cell hypertrophy and hyperplasia were not suppressed by caspase inhibition. Combined BNF and CD exposure increased Bax expression and apoptosis in the lung, but Bax and apoptosis were not the major determinants of early lung injury in this model.
Keywords
Coal-dust; Dusts; Dust-particles; Polycyclic-aromatic-hydrocarbons; Pneumoconiosis; Coal-mining; Coal-miners; Miners; Mining-industry; Underground-mining; Underground-miners; Respirable-dust; Lung-fibrosis; Lung-disorders; Lung-disease; Silicosis; Laboratory-animals; Animals; Animal-studies; Exposure-levels; Exposure-assessment
Contact
A. Hubbs, Pathology and Physiology Research Branch, Health Effect Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, 1095 Willowdale Rd., Morgantown, WV 26505 USA
CODEN
EVHPAZ
Publication Date
20060901
Document Type
Journal Article
Email Address
AHubbs@cdc.gov
Fiscal Year
2006
NTIS Accession No.
NTIS Price
Issue of Publication
9
ISSN
0091-6765
NIOSH Division
HELD
Source Name
Environmental Health Perspectives
State
WV
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