Medical Forum / Diseases and Disorders / Asthma / December 2006
Black lung / iron
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ironjustice@aol.com - 23 Dec 2006 03:19 GMT <<snip>> Coal samples that do not contain pyrite {iron] do not produce ROS nor degrade RNA. <<snip>>
Role of pyrite in formation of hydroxyl radicals in coal: possible implications for human health. Cohn CA, Laffers R, Simon SR, O'riordan T, Schoonen MA Part Fibre Toxicol. 2006 Dec 19; 3(1): 16
ABSTRACT: BACKGROUND: The harmful effects from inhalation of coal dust are well-documented. The prevalence of lung disease varies by mining region and may, in part, be related to regional differences in the bioavailable iron content of the coal. Pyrite (FeS2), a common inorganic component in coal, has been shown to spontaneously form reactive oxygen species (ROS) (i.e., hydrogen peroxide and hydroxyl radicals) and degrade nucleic acids. This raises the question regarding the potential for similar reactivity from coal that contains pyrite. Experiments were performed to specifically evaluate the role of pyrite in coal dust reactivity. Coal samples containing various amounts of FeS2 were compared for differences in their generation of ROS and degradation of RNA. RESULTS: Coals that contain iron also show the presence of FeS2, generate ROS and degrade RNA. Coal samples that do not contain pyrite do not produce ROS nor degrade RNA. The concentration of generated ROS and degradation rate of RNA both increase with greater FeS2 content in the coals. CONCLUSIONS: The prevalence of coal workers pneumoconiosis can be correlated to the amount of FeS2 in the coals. Considering the harmful effects of generation of ROS by inhaled particles, the results presented here show a possible mechanism whereby coal samples may contribute to CWP. This suggests that the toxicity of coal may be explained, in part, by the presence of FeS2.
Abstract · PubMed FullText · SFX · GS Clip Export InterDB · Terms Related · Graph Tag · Scopus · Cites 10.1186/1743-8977-3-16
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ironjustice@aol.com - 23 Dec 2006 03:46 GMT Sooo .. it seems ole .. Penn State is gonna have some .. splainin' .. to do ..
THEY are .. 'considered' .. sooo .. good at .. iron studies .. YET fail to SEE all the iron in the lungs of all their relatives ..
Or .. did .. they .. ?
Either way .. they are pretty unreliable ..
<<snip>> These results indicate that activation of AP-1 and NFAT by the Pennsylvania coal is through bioavailable **iron** present in the coal. <<snip>>
Titre du document / Document title Role of bioavailable iron in coal dust-induced activation of activator protein-1 and nuclear factor of activated T cells: Difference between Pennsylvania and Utah coal dusts Auteur(s) / Author(s) CHUANSHU HUANG ; JINGXIA LI ; QI ZHANG ; XI HUANG ; Résumé / Abstract Activator protein-1 (AP-1) and nuclear factor of activated T cells (NFAT) are two important transcription factors responsible for the regulation of cytokines, which are involved in cell proliferation and inflammation. Coal workers' pneumoconiosis (CWP) is an occupational lung disease that may be related to chronic inflammation caused by coal dust exposure. In the present study, we demonstrate that coal from the Pennsylvania (PA) coalmine region, which has a high prevalence of CWP, can activate both AP-1 and NFAT in JB6 mouse epidermal cells. In contrast, coal from the Utah (UT) coalmine region, which has a low prevalence of CWP, has no such effects. The PA coal stimulates mitogen-activated protein kinase (MAPK) family members of extracellular signal-regulated kinases (ERKs) and p38 MAPK but not c-jun-NH[2]-terminal kinases, as determined by the phosphorylation assay. The increase in AP-1 by the PA coal was completely eliminated by the pretreatment of cells with PD98059, a specific MAPK kinase inhibitor, and SB202190, a p38 kinase inhibitor, further confirming that the PA coal-induced AP-1 activation is mediated through ERKs and p38 MAPK pathways. Deferoxamine (DFO), an iron chelator, synergistically enhanced the PA coal-induced AP-1 activity, but inhibited NFAT activity. For comparison, cells were treated with ferrous sulfate and/or DFO. We have found that iron transactivated both AP-1 and NFAT, and DFO further enhanced iron-induced AP-1 activation but inhibited NFAT. These results indicate that activation of AP-1 and NFAT by the PA coal is through bioavailable iron present in the coal. These data are in agreement with our previous findings that the prevalence of CWP correlates well with levels of bioavailable iron in coals from various mining regions. Revue / Journal Title American journal of respiratory cell and molecular biology (Am. j. respir. cell mol. biol.) ISSN 1044-1549 CODEN AJRBEL Source / Source 2002, vol. 27, no5, pp. 568-574 [7 page(s) (article)] Langue / Language Anglais
Editeur / Publisher American Lung Association, New York, NY, ETATS-UNIS (1989) (Revue)
Localisation / Location INIST-CNRS, Cote INIST : 22187, 35400010544097.0070
Copyright 2006 INIST-CNRS. All rights reserved
Toute reproduction ou diffusion même partielle, par quelque procédé ou sur tout support que ce soit, ne pourra être faite sans l'accord préalable écrit de l'INIST-CNRS. No part of these records may be reproduced of distributed, in any form or by any means, without the prior written permission of INIST-CNRS.
Nº notice refdoc (ud4) : 14016726
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pc - 23 Dec 2006 05:26 GMT Um do you know of any coal fumes to be not harmful? :) Sooo .. it seems ole .. Penn State is gonna have some .. splainin' .. to do ..
THEY are .. 'considered' .. sooo .. good at .. iron studies .. YET fail to SEE all the iron in the lungs of all their relatives ..
Or .. did .. they .. ?
Either way .. they are pretty unreliable ..
<<snip>> These results indicate that activation of AP-1 and NFAT by the Pennsylvania coal is through bioavailable **iron** present in the coal. <<snip>>
Titre du document / Document title Role of bioavailable iron in coal dust-induced activation of activator protein-1 and nuclear factor of activated T cells: Difference between Pennsylvania and Utah coal dusts Auteur(s) / Author(s) CHUANSHU HUANG ; JINGXIA LI ; QI ZHANG ; XI HUANG ; Résumé / Abstract Activator protein-1 (AP-1) and nuclear factor of activated T cells (NFAT) are two important transcription factors responsible for the regulation of cytokines, which are involved in cell proliferation and inflammation. Coal workers' pneumoconiosis (CWP) is an occupational lung disease that may be related to chronic inflammation caused by coal dust exposure. In the present study, we demonstrate that coal from the Pennsylvania (PA) coalmine region, which has a high prevalence of CWP, can activate both AP-1 and NFAT in JB6 mouse epidermal cells. In contrast, coal from the Utah (UT) coalmine region, which has a low prevalence of CWP, has no such effects. The PA coal stimulates mitogen-activated protein kinase (MAPK) family members of extracellular signal-regulated kinases (ERKs) and p38 MAPK but not c-jun-NH[2]-terminal kinases, as determined by the phosphorylation assay. The increase in AP-1 by the PA coal was completely eliminated by the pretreatment of cells with PD98059, a specific MAPK kinase inhibitor, and SB202190, a p38 kinase inhibitor, further confirming that the PA coal-induced AP-1 activation is mediated through ERKs and p38 MAPK pathways. Deferoxamine (DFO), an iron chelator, synergistically enhanced the PA coal-induced AP-1 activity, but inhibited NFAT activity. For comparison, cells were treated with ferrous sulfate and/or DFO. We have found that iron transactivated both AP-1 and NFAT, and DFO further enhanced iron-induced AP-1 activation but inhibited NFAT. These results indicate that activation of AP-1 and NFAT by the PA coal is through bioavailable iron present in the coal. These data are in agreement with our previous findings that the prevalence of CWP correlates well with levels of bioavailable iron in coals from various mining regions. Revue / Journal Title American journal of respiratory cell and molecular biology (Am. j. respir. cell mol. biol.) ISSN 1044-1549 CODEN AJRBEL Source / Source 2002, vol. 27, no5, pp. 568-574 [7 page(s) (article)] Langue / Language Anglais
Editeur / Publisher American Lung Association, New York, NY, ETATS-UNIS (1989) (Revue)
Localisation / Location INIST-CNRS, Cote INIST : 22187, 35400010544097.0070
Copyright 2006 INIST-CNRS. All rights reserved
Toute reproduction ou diffusion même partielle, par quelque procédé ou sur tout support que ce soit, ne pourra être faite sans l'accord préalable écrit de l'INIST-CNRS. No part of these records may be reproduced of distributed, in any form or by any means, without the prior written permission of INIST-CNRS.
Nº notice refdoc (ud4) : 14016726
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ironjustice@aol.com - 23 Dec 2006 20:07 GMT > Um do you know of any coal fumes to be not harmful? :) Well since .. it is pretty .. hard .. to find anyplace that DOESN'T have iron laying somewhere .. around it or IN it .. the **percentage** OF .. iron is what is making the **difference** .. IN .. 'rate of disease' ..
It is STILL the **iron** .. though ..
AND .. therefore WOULD / could / CAN .. be .. theoretically .. REMOVED ..
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editor@netpath.net - 24 Dec 2006 19:09 GMT Being that there have been well-documented cases of mass deaths from silicosis tunneling through quartz and more recently mass debilitation among 9/11 rescuers and site relief workers - where there just wasn't any iron pyrites - I think pyrites don't have anything to do with such illnesses, but instead breathing in large amounts of fine mineral dust of ANY kind is likely to result in similar illnesses. After all, a common illness in the South is from breathing in cotton dust in textile mills - and that's not by breathing in iron pyrites.
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ironjustice@aol.com - 24 Dec 2006 21:09 GMT >>editor@netpath.net wrote: Being that there have been well-documented cases of mass deaths from silicosis tunneling through quartz <<
I don't know when the last time you picked up a piece of quartz .. but you would be **hardpressed** .. NOT .. to find any 'fools gold' {iron pyrite} in the quartz ..
They are pretty much synonymous in .. geological formation.
>>and more recently mass debilitation among 9/11 rescuers and site relief workers -<<
Actually right NOW they are **heavy metal** .. chelating ALL the workers at ground zero and have found a .. 60% decrease in symptoms. Asbestos CONTAINS iron .. in fact .. iron IS the .. problem WITH .. asbestos ..
Asbestos is a tiny piece of silica covered in iron.
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ironjustice@aol.com - 24 Dec 2006 21:52 GMT >>editor@netpath.net wrote: Being that there have been well-documented cases of mass deaths from silicosis tunneling through quartz <<
<<snip>> Rats on iron-depleted diets demonstrated a diminished fibrotic injury after dust instillation. <<snip>>
Low iron diet .. ?
<<snip>> Complexation of iron by the dust surface may be central in collagen deposition after silica exposure <<snip>>
Hmmm ..
http://ajplung.physiology.org/cgi/content/abstract/267/6/L686
Am J Physiol Lung Cell Mol Physiol 267: L686-L692, 1994; 1040-0605/94 AJP - Lung Cellular and Molecular Physiology, Vol 267, Issue 6 686-L692, Copyright ? 1994 by American Physiological Society
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ARTICLES
Lung injury after silica instillation is associated with an accumulation of iron in rats A. J. Ghio, R. H. Jaskot and G. E. Hatch Durham Veterans Affairs Medical Center, North Carolina.
It has been postulated that the incomplete complexation of host iron by the surface of mineral oxides is essential in in vivo lung injury after exposure to these dusts. We investigated the associations between in vivo iron accumulation after intratracheal instillation of silica dust in rats and 1) concentrations of antioxidants and oxidized products in the lung and 2) an index of chronic fibrotic injury. Fifty milligrams of minusil were intratracheally instilled into 60-day-old, male Sprague-Dawley rats. Ionizable Fe3+ complexed to the surface of silica increased from 12.7 +/- 1.4 mumol/g to values as high as 42.5 +/- 9.1 mumol/g dust after instillation. Corresponding to this elevation of surface-adsorbed metal, concentrations of iron in bronchoalveolar lavage fluid, lung tissue, plasma, and liver tissue all increased. Antioxidant molecules in lung tissue, including ascorbate, urate, and glutathione, all decreased, whereas superoxide dismutase increased. Oxidized products in the lung tissue, measured as thiobarbituric acid-reactive products, similarly increased, reflecting an oxidant stress. Dietary depletion of iron stores before instillation of silica dust resulted in low iron stores (hematocrit values of 21.8 +/- 1.9) and low iron concentrations in lavage fluid, lung tissue, and liver tissue. Rats on iron-depleted diets demonstrated a diminished fibrotic injury after dust instillation. Complexation of iron by the dust surface may be central in collagen deposition after silica exposure.
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