DoD Revisits Gulf War Toxic Exposures, Acknowledges Mustard Gas As Possible Cause for GWI

Written by Anthony Hardie, 91outomes.com

(91outcomes.com) - A new analysis published in a peer-reviewed medical journal takes a scientific relook at causes for Gulf War Illness (GWI) and suggests that mustard gas may have played a significant, plausible role.

The article, published in Progress in Molecular Biology and Translational Science, suggests coherent mechanisms for how the chronically debilitating condition was caused, including from a toxic mix of chemical warfare agents, pesticides, and anti nerve-agent pills.  The analysis includes a role for mustard gas based on newly emerging research showing its toxic mechanism.

Perhaps the most striking aspect of the new analysis isn't just its acceptance of mustard gas, chemical warfare agents and other chemicals as likely culprits causing GWI, but who sponsored the analysis -- the U.S. Department of Defense.

Until the advent in 2006 of a Congressionally directed Gulf War Illness (GWI) medical research program within DoD, which focused narrowly on finding treatment mechanisms and developing treatments for GWI, historically the agency had maintained a sharply adversarial role against a growing body of scientists and other advocates for the estimated 250,000 veterans (roughly one-third) of the 1991 Gulf War suffering from GWI.

"...it is now accepted that [Gulf War troops] could very well have been exposed to low levels of massive quantities of sarin, cyclosarin, and sulfur mustard."

Along with findings funded through the new GWI "CDMRP" that have identified at least one treatment, Coenzyme Q10, as potentially helpful in reducing some GWI symptoms, studies of a litany of other potential treatments and potential treatment targets are now in the program's pipeline.  

In 2010, an analysis by the insular Institute of Medicine determined following review of a large body of medical evidence that GWI is a physiological -- not psychological -- condition likely caused by the interplay of environmental factors and genetics and for which treatments can likely be found.  The 2010  report was therefore all the more groundbreaking.  

Like DoD, the purportedly independent IOM has been unduly influenced on repeated occasions by a tiny cabal -- largely operating from within DoD and VA -- that has vigorously rejected every probable cause for veterans' array of enduring symptoms that has not been psychological or psychosomatic in nature.  

Following on the heels of the GWI CDMRP, which helped turned the tide with its promising GWI treatment results, this new DoD-sponsored analysis suggests a plausible mechanism describing how Gulf War chemicals resulted in chronic disability for so many veterans of the 1991 Gulf War.  

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The abstract follows.  Special thanks to Kirt Love for finding and sharing this important new journal article.  

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Prog Mol Biol Transl Sci. http://www.ncbi. nlm.nih.gov/ pubmed/22974741# 2012;112:209- 30. doi: 10.1016/B978- 0-12-415813- 9.00007-6.

Chemicals of military deployments: revisiting gulf war syndrome in light of new information.Brimfield AA 

http://www.ncbi. nlm.nih.gov/ pubmed?term= Brimfield% 20AA%5BAuthor% 5D&cauthor= true&cauthor_ uid=22974741 .

Source

Research Division, U.S. Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Maryland, USA.

Abstract

Despite the amount of hard work that has gone into elucidating a toxicological basis for Gulf War Illness, we do not appear to have reached a mechanistic understanding. Investigation of long-term low-level exposure as a basis does not seem to have provided an answer. Nor does the deployment-related toxic soup idea, where exposure to a mixture of toxic chemicals not usually encountered in the same physical vicinity, seems to have explained the symptoms developed by Gulf War Veterans.

 The idea that an overabundance of CNS acetylcholine leftover from excessive cholinesterase inhibition is at the basis of this syndrome is intellectually appealing and offers a level of neurochemical complexity that may be just beyond the reach of our technical understanding. 

But no one has yet assembled a coherent mechanism from it either. It seems reasonable that chemical warfare agents were involved. They were not included in early work because it was felt that the toxicant plumes produced during the destruction of stockpiled Iraqi chemical weapons had not been large enough to cause an exposure of US forces and those of our allies. That misconception was disproven, and it is now accepted that people could very well have been exposed to low levels of massive quantities of sarin, cyclosarin, and sulfur mustard.

It also seems reasonable that excess acetylcholine or neurological consequences of its presence that we do not fully understand were involved. The combination of nerve agents and the insecticidal anticholinesterases plus the pyridostigmine bromide given prophylactically were probably sufficient to cause the problem. 

However, the most notable thing is the result of recent work on the toxic mechanism of sulfur mustard showing that it can inhibit the microsomal electron transport chain as a result of sulfonium ion reduction to carbon free radicals by NADPH-cytochrome P450 reductase. 

This information was not available during the work on Gulf War Illness. So this provides an opportunity to discuss the effects of the general inhibition of the cytochrome P450 system superimposed on the conditions encountered by the participants in Desert Storm and Desert Shield as an approach to the toxicology of mixtures.