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Medical Forum / Diseases and Disorders / Asthma / December 2006

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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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http://jesuswasavegetarian.7h.com

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DEAD PEOPLE WALKING
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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

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com

Man Is A Herbivore!
http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
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
..

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com

Man Is A Herbivore!
http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
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.

No $4 to park!  No $6 admission!  http://www.INTERNET-GUN-SHOW.com
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.

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com

Man Is A Herbivore!
http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
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

--------------------------------------------------------------------------------

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.

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com

Man Is A Herbivore!
http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
 
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