Iron In Black Lung Disease

[i***@rock.com]

Inflammatory stress response in A549 cells as a result of exposure to coal: Evidence for the role of pyrite in coal workers' pneumoconiosis pathogenesis.
Harrington AD, Tsirka SE, Schoonen MA.
Chemosphere. 2013 Jul 26. pii: S0045-6535(13)00939-9.
Department of Geosciences, Earth and Space Sciences Building, Stony Brook University, Stony Brook, NY 11784-2100, USA; Institute of Environmental Medicine, New York University, 57 Old Forge Road, Tuxedo, NY 10987, USA. Electronic address: ***@nyumc.org.

Abstract
On the basis of a recent epidemiological study it is hypothesized that pyrite content in coal is an important factor in coal workers' pneumoconiosis (CWP) pathogenesis. While the role of pyrite in pathogenesis remains to be resolved, the ability of the mineral to generate reactive oxygen species (ROS) through various mechanisms is likely a contributing factor. The aim of this study was to elucidate the importance of the pyrite content of coal in generating an inflammatory stress response (ISR), which is defined as the upregulation of ROS normalized by cell viability. The ISR of A549 human lung epithelial cells in the presence of natural coal samples with variable pyrite contents was measured. Normalized to surface area, five particle loadings for each coal reference standard were analyzed systematically for a total of 24h. The ISR generated by coals containing 0.00, 0.01, and 0.49wt.% pyritic sulfur is comparable to,though less than, the ISR generated by inert glass beads (299% of the control). The coals containing 0.52 and 1.15wt.% pyritic sulfur generated the greatest ISR (798% and 1426% of the control, respectively).

CONCLUSIONS: While ISR does not increase proportionally to pyrite content in coal, the two coals with the highest pyritic sulfur and available iron contents generate the greatest ISR. Therefore, the present study indicates that coals with elevated pyrite contents are likely to induce a significant health burden by stimulating inflammation within the lungs, and may contribute to the development of CWP.

doi: 10.1016/j.chemosphere.2013.06.082.

Copyright © 2013 Elsevier Ltd. All rights reserved.

KEYWORDS: Coal workers’ pneumoconiosis, Inflammatory stress response, Iron, Pyrite

PMID:23895739

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On Wednesday, July 31, 2013 10:11:13 AM UTC-7, ***@rock.com wrote: iron <<

"Iron is then transported out of the lung"

Disruption of iron homeostasis and lung disease.
Ghio AJ
Biochim Biophys Acta 2008 Dec 3.

As a result of a direct exchange with the external environment, the
lungs are exposed to both iron and agents with a capacity to disrupt
the homeostasis of this metal (e.g. particles).
An increased availability of catalytically reactive iron can result
from these exposures and, by generating an oxidative stress, this
metal can contribute to tissue injury.
By importing this Fe(3+) into cells for storage in a chemically less
reactive form, the lower respiratory tract demonstrates an ability to
mitigate both the oxidative stress presented by iron and its
potential for tissue injury.
This means that detoxification is accomplished by chemical reduction
to Fe(2+) (e.g. by duodenal cytochrome b and other ferrireductases),
iron import (e.g. by divalent metal transporter 1 and other
transporters), and storage in ferritin.
The metal can subsequently be exported from the cell (e.g. by
ferroportin 1) in a less reactive state relative to that initially
imported.
Iron is then transported out of the lung via the mucociliary pathway
or blood and lymphatic pathways to the reticuloendothelial system for
long term storage.
This coordinated handling of iron in the lung appears to be disrupted
in several acute diseases on the lung including infections, acute
respiratory distress syndrome, transfusion-related acute lung injury,
and ischemia-reperfusion.
Exposures to bleomycin, dusts and fibers, and paraquat similarly alter
iron homeostasis in the lung to affect an oxidative stress.
Finally, iron homeostasis is disrupted in numerous chronic lung
diseases including pulmonary alveolar proteinosis, transplantation,
cigarette smoking, and cystic fibrosis.


Biochimica et biophysica acta [Biochim Biophys Acta]

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