Concealed Hard Evidence & The Gulf War Syndrome

Introduction

I first published this blog connecting the dots between pesticide exposure through smoking contaminated tobacco products and Gulf War Syndrome in 2013, and have watched the information become more relevant over the years since, as increasing numbers of Veterans and their families have shown full-blown Gulf War Syndrome.

However, if you can’t accurately diagnose a disease, condition or syndrome, you can’t treat it. And if you don’t know where to look for causes, and what to look for, you can’t diagnose.

That is currently the case with Gulf War Syndrome. Although almost all the evidence is clear, the factual evidential thread that connects all the dots is missing. That is what I would like to offer in this post.

Realizing that it is asking a lot of busy people to read a long and complex posting, here is a quick summary, followed by a discussion of the evidence.

1. Over two dozen well-done studies from 1994-2013 have all concluded that Gulf War Syndrome (GWS) diseases are caused by dual exposure to pyridostigmine bromide (an anti-nerve gas agent forcefully administered to GW troops) plus pesticides those troops were exposed to in theater.
a. It is very important to note how rarely scientific and medical studies actually state that they have identified the cause of such a complex issue as GWS.


2. RAND Corporation (2000) identified the Gulf War pesticides as:
a. One organochlorine pesticide (lindane)
b. One repellent (DEET)
c. Two pyrethroid pesticides (permethrin, rf-phenothrin)
d. Five organophosphate pesticides (azamethiphos, chlorpyrifos, diazinon dichlorvos, malathion)
e. Three carbamate pesticides (bendiocarb, methomyl, propoxur)


3. The majority of Gulf War troops were not exposed widely to most of these pesticides – in fact the numbers exposed and the subsequent numbers of Vets with GWS don’t match up at all.
a. For example, in the case of Lindane only one incident was reported, and that report is seriously questioned.
b. Something else is going on – and this post will try to reveal what that something is.


4. Studies of the persistence of symptoms after exposure show that the combination of exposure to PB and pesticides causes permanent neurological, genetic and other kinds of damage and disease in Gulf War Veterans


5. “The Defense Department estimates that approximately 250,000 personnel took at least some pyridostigmine bromide during the 1990-1991 Gulf War. During the 1990-1991 Gulf War, all U.S. troops were to have received packets containing pyridostigmine bromide pills.” http://www.gulflink.osd.mil/faq/faq_pb.jsp


6. None of the studies explain why Gulf War Veterans continue to develop NEW symptoms and diseases decades after exposure – this explicitly worries and puzzles many of the researchers, and they say so.


7. None of the studies explain why Gulf War Veterans continue to come down with these terrible diseases in far greater proportions than demographically-matched non-Veterans 20-25 years after exposure – this also puzzles and worries researchers, and they say so.


8. None of these studies explain why the children (and grandchildren) of Gulf War Veterans are coming down with developmental and neurological disorders in far greater numbers than demographically-matched cohorts – this is really troublesome to the scientists and doctors studying GWS – and again, they are very frustrated by their inability to explain this.


9. This post will present what I believe is compelling evidence that the explanation for all these missing pieces of the puzzle is the presence of residues of dozens of never-identified pesticides in cigarettes, chewing tobacco and wet snuff.

a. Remember that these research studies have PROVEN that exposure to PB and 6-10 specific pesticides are the cause of GWS.

b. So, what if the exposure isn’t to 6-10, but 60+ pesticides, many far more dangerous than the 10 or so identified in the GW studies
c. And what if the exposure wasn’t just during the Gulf War but every day since that war.


10. Many of the pesticides used on tobacco worldwide are known to be powerful carcinogens, developmental and reproductive toxins, neurotoxins, DNA mutagens, and endocrine disruptors in very small doses, especially when that dosage is chronic, sub-lethal, and in many cases bio-accumulative.


11. Here is the list of pesticides used worldwide on Tobacco, especially on tobacco grown on “contract farms” in political/economic dictatorships worldwide and therefore likely, at least in some cases, to be present as residues in US Tobacco Industry products.
a. DDT, TDE, Chlordane, Lindane, Aldrin, Endrin, Dieldrin, Heptachlor, and Toxaphene, Anilazine, AziaPhos-Methyl, Captan, Diflubenzuron, Leptophos, Malathion, Methoprene, Mirex, Cyclohexane, 1,3-dichloropropene (1,3-D), Chloropicrin, Maleic hydrazide, Acephate, Methyl Bromide, Isocarbophos, Dimethoate, Pendimethalin, Dicrotophos, Chlorpyrifos, Fenamiphos, Mancozeb, Flumetralin, Metalaxyl, Clomazone, Ethoprop, Endosulfan, Mefenoxam, Pebulate, Ethephon, Napropamide, Sulfentrazone, Imidacloprid, Aldicarb, Butralin, Dimethomorph, Methomyl, Malathion, Ethyl Parathion, Methyl Parathion, Disulfoton, Sethoxydim, Spinosad, Carbaryl, Fonofos, Benefin, Bacillus Thuringiensis, Carbofuran, Diazinon, Diphenamid, Isopropalin, Omethoate, Phismet, Phoxim, Oxamyl, Methidathion, Thiodan, Pendimethilum, and Trichlorfon. Also the solvents Toluene, Benzene, Phosgene, Hexane, and Xylene.

And here is what I found when I commissioned testing of a limited number of brands for my book “Smoke No Evil”.


12. Given the findings with regard to exposure to PB and a small number of pesticides causing Gulf War Syndrome diseases, just imagine what exposure to PB and the 60+ pesticide residues in Tobacco Industry products has been doing continually to the health of Veterans who continue to smoke, dip or chew since the early 1990s when this tragedy began.
a. Remember – we are talking about ongoing daily exposure to these pesticides for decades, not a few months exposure in the Persian Gulf several decades back.


13. Many of these pesticides, like DDT and the other Organochlorines, are banned from any use at all in most countries, but are still widely and illegally used on tobacco in the Third World.
a. US manufacturers import hundreds of thousands of tons of pesticide-contaminated tobacco stems, scrap and waste from Third World manufacturers and use proprietary processes (Like RJR’s G7 process, described in Exhibit 9 below) to convert this toxic waste into “tobacco” products.


14. With the exception of the questionable Lindane exposure, none of the pesticides identified in the GWS studies are Organochlorine pesticides– only Organophosphate and Carbamate pesticides
a. Probably because there aren’t supposed to be any Organochlorine pesticide residues anywhere, in anything.

15. There has never been a study of off-the-shelf cigarettes, wet snuff or chewing tobacco to determine in detail which pesticide residues are present in which brands.
a. Never. Not once in all the hundreds of millions of dollars spent on research into why Tobacco Industry products kill. Think about that.

16. CDC and other studies show a significantly higher proportion of all Veterans who are smokers than non-Veterans in all age groups. Details further on in the post.

17. Other studies of the proportion of Gulf War Veterans who continue to be smokers, chewers and dippers show that GW Vets continue at higher rates in every category compared to non-GW Vets and to matched demographic civilians. Details further on in the post.

18. There are no studies of the interaction of pesticide residues in Tobacco Industry products with pyridostigmine bromide.
a. None. That’s because tobacco exposure has NEVER been considered as part of the issue by any GWS researchers.
b. Could it be that every single one of the researchers missed the connection between Tobacco Industry products and GWS?
c. Is it possible that there was undue outside influence at work?

19. However, as stated in #1 above, the BIG BREAKTHROUGH is that thanks for the PB/GWS/Pesticide studies we now know unequivocally that ingesting even a few pesticides by inhalation in interaction with pyridostigmine bromide has been shown to be CAUSAL in the development of GWS diseases.

20. I believe that if proper studies are done they will show that the preponderance of Gulf War Veterans who have developed GWS disease are smokers, chewers, or dippers – or were at the time but may have stopped sometime since.
a. No such study has been done. This has gone right over everyone’s head – or else they’ve been told not to look into it.
b. OK – call me a conspiracy theorist. I won’t deny it.
c. A simple research model would prove or disprove the thesis – divide GW Vets into three groups;
i. ongoing Tobacco Industry product users since their Gulf War days,
ii. users during the Gulf War who have since quit,
iii. and never-users, and compare GWS rate for each group.

21. However, with regard to GW vets who once used but who have stopped, it’s important to note that since many of the pesticides used in Tobacco production are bio-accumulative, even years after stopping these pesticides remain in the body and their health effects remain potent.
a. This has been established conclusively in the case of exposed tobacco field workers in underdeveloped countries.

22. I believe that it is the ongoing, chronic sub-lethal exposure to pesticides in cigarettes, wet snuff, and chewing tobacco, combined with the forced administration of pyridostigmine bromide at the time of service, that is the CAUSE of most or even all of the suffering and death experienced by Gulf War Veterans and their families.
a. The PB and few pesticides identified in the studies may have started the lethal ball rolling, but it is the ongoing exposure, as well as the kinds of pesticides in Tobacco Industry products, that can explain many of the aspects of the research that puzzles and confuses researchers.

23. I believe that a study that determined which pesticide residues are present in which brands of Tobacco products, combined with a study of what proportion of Gulf War Veterans who suffer from GWS diseases are “Tobacco” product users (or who were exposed to second-hand smoke during their service), would show that it is the products of the Tobacco industry that are responsible for most of the ongoing suffering and death of our Gulf War Veterans.
a. You can’t treat if you can’t diagnose, and since doctors are almost universally ignorant of the presence of pesticides in Tobacco Industry products, how would they have a clue about where to look when a Gulf War Vet with GWS presents as a patient?
b. If they don’t have a clue about their patient’s 20-30 years of chronic, sub-lethal exposure to multiple pesticide residues, why would they consider pesticide poisoning?

24. Of course the presence of pesticide residues in so-called “tobacco” products explains a lot of the suffering and death among all smokers, dippers and chewers from all walks of life, but because Gulf War veterans were specifically forced to accept administration of pyridostigmine bromide, the culpability of this criminal industry and the US Government is magnified many times over.

25. This completes the summary of what this post contains.

The Trail Of Evidence

Please let me be clear. I am not advocating that Tobacco product pesticide contamination is the only causal factor in GWS. This is, after all, a syndrome – a collection of symptoms, diseases and consequences. For example, there is stunning evidence that a substantial portion of GWS is the result of compulsory military vaccinations against anthrax and other chem-bio weapons. The central issue I am trying to raise is that there is a significant, overlooked, and deliberately obscured connection between Tobacco industry products and GWS. If this connection can be confirmed by factual evidence, then ONE of the major factors in GWS will be revealed, and the culpability of what I am convinced is a criminal conspiracy will be evident.


The Tobacco industry is guilty of knowingly manufacturing unreasonably dangerous products and, in the case of Gulf War veterans, making an already intolerable set of circumstances even worse. Once the connection between PB and pesticides was firmly established, the Tobacco industry had to be aware of the ongoing damage their products would cause specifically for Gulf War Vets, having nothing to do with any other “dangers of smoking”. Some of these companies actually make “Organic” tobacco products, so they fully understand what their non-organic products contain. Yet they said or did nothing. Furthermore, while Gulf War Veterans with GWS can’t hold the US Government, the US Military, the PB manufacturers, the vaccine manufacturers, or the pet collar and no-pest strip manufacturers accountable for the damage they caused, holding the Tobacco industry accountable is a whole different matter, legally and morally.

Exhibit #1
Let me begin by showing you the abstract of an important study on the causes of the wide range of diseases that even today, 25 years after the fact, continue to sicken and kill Gulf War veterans.
Study Title: Acetylcholinesterase Inhibitors and Gulf War Illnesses
(by) Beatrice Alexandra Golomb
(In) Proceedings of the National Academies of Science, USA.
Mar 18, 2008; 105(11): 4295–4300.
Published online Mar 10, 2008.
doi: 10.1073/pnas.0711986105, PMCID: PMC2393741

Abstract
Increasing evidence suggests excess illness in Persian Gulf War veterans (GWV) can be explained in part by exposure of GWV to organophosphate and carbamate acetylcholinesterase inhibitors (AChEis), including pyridostigmine bromide (PB), pesticides, and nerve agents. Evidence germane to the relation of AChEis to illness in GWV was assessed. Many epidemiological studies reported a link between AChEi exposure and chronic symptoms in GWV. The link is buttressed by a dose–response relation of PB pill number to chronic symptoms in GWV and by a relation between avidity of AChEi clearance and illness, based on genotypes, concentrations, and activity levels of enzymes that detoxify AChEis. Triangulating evidence derived from studies linking occupational exposure to AChEis to chronic health symptoms that mirror those of ill GWV. Illness is again linked to lower activity of AChEi detoxifying enzymes and genotypes conferring less-avid AChEi detoxification. AChEi exposure satisfies Hill’s presumptive criteria for causality, suggesting this exposure may be causally linked to excess health problems in GWV.

Just to be clear, pyridostigmine bromide (PB) is the chemical administered, forcibly in many cases, to US troops in the Gulf War on the premise that it would protect them from Saddam’s nerve gas. And the pesticides referred to were also present in the Gulf War theater as a result – or so it was thought – of other kinds of chemical weapons, as well as the “pet collars” worn by many Gulf War troops and the “No-Pest strips” hung in living quarters and vehicles to try to ward off the man-eating fleas and other insects that live in that harsh desert environment.

For an excellent research paper on GW exposure to these pesticides please see:
http://www.gulflink.osd.mil/library/randrep/pesticides_survey/mr1018.12.chap5.html

Exhibit #2
As early as 1996 alarms were being raised, even about the DEET that the GW troops were using, much less the pesticides in the Pet Collars and No-Pest Strips..
J Toxicol Environ Health. 1996 May;48(1):35-56.
Neurotoxicity resulting from coexposure to pyridostigmine bromide, deet, and permethrin: implications of Gulf War chemical exposures.
Abou-Donia MB1, Wilmarth KR, Jensen KF, Oehme FW, Kurt TL.

Abstract
Of the three-quarters of a million service personnel involved in the Persian Gulf War, approximately 30,000 have complained of neurological symptoms of unknown etiology. One contributing factor to the emergence of such symptoms may be the simultaneous exposure to multiple agents used to protect the health of service personnel, in particular, the anti-nerve gas agent pyridostigmine bromide (PB; 3-dimethylaminocarbonyloxy-N-methylpyridinium bromide), the insect repellent DEET (N,N-diethyl-m-toluamide), and the insecticide permethrin (3-(2,2-dichloro-ethenyl)-2,2-dimethylcyclopropanecarboxylic acid (3-phenoxyphenyl) methyl ester). This study investigated neurotoxicity produced in hens by individual or simultaneous exposure to these agents (5 d/wk for 2 months to 5 mg/kg/d PB in water, po; 500 mg/kg/d DEET, neat, sc; and 500 mg/kg/d permethrin in corn oil, sc). At these dosages, exposure to single compounds resulted in minimal toxicity. Combinations of two agents produced greater neurotoxicity than that caused by individual agents. Neurotoxicity was further enhanced following concurrent administration of all three agents. We hypothesize that competition for liver and plasma esterases by these compounds leads to their decreased breakdown and increased transport of the parent compound to nervous tissues. Thus, carbamylation of peripheral esterases by PB reduces the hydrolysis of DEET and permethrin and increases their availability to the nervous system. In effect, PB “pumps” more DEET and permethrin into the central nervous system. Consistent with this hypothesis, hens exposed to the combination of the three agents exhibited neuropathological lesions with several characteristics similar to those previously reported in studies of near-lethal doses of DEET and permethrin. If this hypothesis is correct, then blood and liver esterases play an important “buffering” role in protecting against neurotoxicity in the population at large. It also suggests that individuals with low plasma esterase activity may be predisposed to neurologic deficits produced by exposure to certain chemical mixtures.”

Exhibit #3

However, even the studies of the effects of chronic exposure to PB and Permethrin in chickens (above) and lab rats – not humans – are pretty revealing. Here are a few excerpts from one of the more complete studies on this single chemical interaction. One can only imagine what a study of the effects of chronic exposure in human beings to PB and the entire list of cigarette pesticides would reveal.
TITLE: Synergistic Actions of Pyridostigmine Bromide and Insecticides on Muscle and Vascular Nociceptors
PRINCIPAL INVESTIGATOR: Brian Cooper
CONTRACTING ORGANIZATION: University of Florida
Gainesville, FL 33511
REPORT DATE: July 2012
TYPE OF REPORT: Annual
PREPARED FOR: U.S. Army Medical Research and Materiel Command
Fort Detrick, Maryland 21702-5012
www.dtic.mil/cgi-bin/GetTRDoc?AD=ADA590573

Key Research Accomplishments:
Chronic Exposure to Permethrin, Chlorpyrifos and Pyridostigmine Bromide:
• Persistent voltage and amplitude changes in Kv7 protein currents specifically in vascular
nociceptors
• Persistent amplitude changes in KDR protein currents specifically in vascular nociceptors
• Persistent increases in membrane resistance specifically in vascular nociceptors
• Muscle nociceptors unaffected (Nav1.8, Kv7, KDR)
• Skin, vascular and muscle nociceptor Nav1.8 protein inactivation and deactivation
unaffected
• Chronic effects of neurotoxicants/PB differ from acute effects of permethrin
Acute effects of permethrin on the pain system:
• Permethrin activates muscle nociceptors but not skin or vascular nociceptors via Nav1.8
• Permethrin increases muscle nociceptor excitability, but not the excitability of skin or
vascular nociceptors
• Permethrin increases skin, muscle and vascular nociceptor AP duration
• Permethrin accentuates skin, muscle and vascular nociceptor voltage dependent
activation of Nav1.8 protein (hyperpolarized V.50)
• Permethrin retards skin, muscle and vascular nociceptor voltage dependent deactivation
of Nav1.8 protein
• Permethrin slows the rate (decay) of Nav1.8 inactivation of muscle, skin or vascular
nociceptors
• Permethrin has no influence on the normalized peak amplitude of skin, muscle or
vascular nociceptor Nav1.8
• Permethrin has no influence on voltage dependence of skin, muscle or vascular
nociceptor inactivation of Nav1.8
• Permethrin has no acute influence on Kv7 amplitude or activation in muscle or vascular
nociceptors
• At physiological temperatures (~35.5C) the acute influence of permethrin on spontaneous activity and action potential duration and after hyperpolarization are greatly reduced but not eliminated.

The bottom line is that the vast preponderance of medical and scientific investigations over the last 20 years or so have concluded that it was the combination of exposure to pyridostigmine bromide and pesticides, along with smoke from burning oilfields, and in a small number of instances possible nerve gas exposure, that has resulted in the wide range of diseases and severe disability and death continuing to occur among Gulf War veterans even 25 years after exposure. Study after study has shown that the diseases related to PB and pesticide exposure are far greater among Gulf war veterans than among any comparable demographically matched group.

KEY POINT – NO OTHER SOURCES OF PESTICIDES, AND NO OTHER PESTICIDES, ARE MENTIONED IN ANY OF THE STUDIES OF THE HEALTH ISSUES SUFFERED BY GULF WAR VETERANS.

So, staying for the moment with what happened when troops in the Gulf War were exposed just to the pesticides that were documented – a total of no more than 6 pesticides – plus the PB that the US Government forced them to ingest, plus in a few cases the fumes from a single destroyed chemical weapons dump that contained mostly unknown compounds – we already have quite a high level of exposure. And we also already know what impact a sufficient level of exposure to each of these agents has on human health. So what’s new?

Exhibit #4
It turns out that it isn’t just the exposure to these individual pesticides and other chemical agents that matters. Check out the following observation:
It is not feasible to predict the toxicity of agent mixtures in general, or of pesticide mixtures (or pesticides in combination with other agents) in particular, on the basis of the toxicity of single compounds (Marinovich et al., 1996). Moreover, the number of possible combinations increases exponentially with the number of agents, as 2n; thus, 10 compounds have over 1,000 possible combinations that could have different consequences.


When agents are experienced together, the effect may be additive, synergistic, or antagonistic, and the character of the interaction may differ for different effects of the compounds.


Because of the computational intractability of studying every possible combination, the FDA does not require examination of drug combinations in determining approval for an individual drug; it does not even require examination of combinations that may commonly occur together.
Similarly, health consequences of pesticide mixtures, and co-exposures to pesticides and other factors, are in general poorly understood, and “testing even most potential mixtures with the classical toxicological protocol is unfeasible” (Marinovich et al., 1996).”


(from) “A Review of the Scientific Literature As It Pertains to Gulf War Illnesses – Volume 8, Pesticides”
So we now understand that even if the consequences of exposure to individual agents are known, we really have no idea what happens when a person is exposed to multiple agents at the same time. And – importantly – we don’t have any idea of what happens when they are co-combusted and inhaled. Don’t get me wrong – this is not the entire “Smoking Gun”. I simply have to put the pieces of the picture together for you one by one, and once the pieces are assembled I am confident that you will see the entire picture, if I’ve done my job.

Exhibit #5
So now let me offer you a few excerpts from very recent (2013) full-scale review of all of the diseases and conditions that collectively are known as “Gulf War Illness”.
Gulf War Illness and the Health of Gulf War Veterans:
Research Update and Recommendations, 2009-2013

Updated Scientific Findings and Recommendations
Research Advisory Committee on Gulf War Veterans’ Illnesses

Excerpt #1
“Overall, the Committee’s review of the many Gulf War studies published through 2008 identified only two types of exposures—pyridostigmine bromide and pesticides—that were consistently associated with a significantly increased risk for Gulf War illness. In addition, dose-response relationships between severity of exposure and probability of development of Gulf War illness were identified for both exposures.
The two exposures were also associated with significant differences in objectively measured health outcomes in Gulf War veterans, including alterations in neuro-cognitive function and hypothalamic-pituitary-adrenal measures. Taken together, the consistency of the epidemiological associations, the significant dose-response effects, and observed associations with objective biological measures led the Committee to conclude that the evidence strongly supported a causal role for both pyridostigmine bromide and pesticide exposures in the development of Gulf War illness.”


Excerpt #2
“Overall, the Committee’s review of the many Gulf War studies published through 2008 identified only two types of exposures—pyridostigmine bromide and pesticides—that were consistently associated with a significantly increased risk for Gulf War illness. In addition, dose-response relationships between severity of exposure and probability of development of Gulf War illness were identified for both exposures. The two exposures were also associated with significant differences in objectively measured health outcomes in Gulf War veterans, including alterations in neuro-cognitive function and hypothalamic-pituitary-adrenal measures.
Taken together, the consistency of the epidemiological associations, the significant dose-response effects, and observed associations with objective biological measures led the Committee to conclude that the evidence strongly supported a causal role for both pyridostigmine bromide and pesticide exposures in the development of Gulf War illness.”


Excerpt #3
“Based on its review of the epidemiological evidence published since its 2008 report, the Committee offers the following conclusions and recommendations for future directions of research efforts.

Research findings
1. Prevalence of Gulf War illness. All population-based studies conducted since the Gulf War have continued to identify a significant excess rate of chronic symptomatic illness, variously defined, in 1990-1991 Gulf War veterans. A large majority of studies indicate Gulf War illness prevalence in the 25-30% range.
2. Prognosis for veterans with Gulf War illness. Little additional information on the long-term prognosis of Gulf War illness has become available since 2008. Prior data suggest that there is little to no improvement in the health of ill Gulf War veterans over time. The effect that aging will have on this vulnerable population remains a matter of concern.
3. General health among Gulf War veterans. Studies published since 2008 continue to document poorer general health status and greater disability among Gulf War veterans. Despite the extensive number of studies conducted with Gulf War veterans in the 23 years since Desert Storm, medical surveillance of this population remains seriously inadequate.
4. Medical conditions in Gulf War veterans. Very little research has yet been conducted to determine rates at which Gulf War veterans have been affected by medical conditions of possible concern. As a result, it is not currently known if Gulf War veterans have experienced excess rates of most medical conditions.

Disorders of concern reviewed in this report include the following:
1. Neurological disorders. Although neurological conditions are a prominent concern for Gulf War veterans, and research has found an elevated incidence of amyotrophic lateral sclerosis (ALS), rates of multiple sclerosis, Parkinson’s disease and other neurological diseases (e.g., seizures, stroke, migraines) in Gulf War veterans are currently unknown. Research on the prevalence of neurological diseases has not been conducted despite repeated recommendations by this Committee and the Institute of Medicine and explicit legislation by Congress. The prevalence of these disorders is particularly important because they can be expected to increase as the Gulf War veteran population ages.
2. Cancer. Since 2008, research using state cancer registries has suggested that there may be an increased rate of lung cancer in Gulf War veterans. Brain cancer mortality has been shown in two studies conducted by VA to be significantly increased in the subgroup of Gulf War veterans with greatest exposure to oil well fire smoke and to low-level nerve agents released by the destruction of Iraqi facilities at Khamisiyah. In general, cancer risk remains unknown and understudied.
3. Other diagnosed medical conditions reported at excess rates. Research since 2008 continues to indicate that Gulf War veterans report being diagnosed with a variety of medical conditions at significantly higher rates than non-deployed era veterans. These include chronic digestive disorders, respiratory conditions, heart disease and skin disorders. Although consistently reported by Gulf War veterans, these conditions have not been further evaluated or characterized by epidemiologic or clinical studies.
4. Sleep dysfunction. A single study published since 2008 has identified sleep abnormalities in a group of Gulf War veterans compared to obesity-matched controls. Sleep disturbance is an extremely common symptom in veterans with Gulf War illness and continuous positive airway pressure (CPAP) has shown some promise for treating a range of symptoms in veterans with sleep apnea in a small treatment trial.
5. Adverse reproductive outcomes and birth defects. No definitive new information is available on birth defects in offspring of Gulf War veterans, and no research has ever been published concerning neurological or other medical conditions affecting veterans’ children. It is important that medical and reproductive outcomes be assessed in children of veteran subgroups of interest (e.g. exposure, location, illness subgroups).
6. Multi-symptom conditions: chronic fatigue syndrome, fibromyalgia, multiple chemical sensitivity. These disorders share similar symptoms with Gulf War illness, but most Gulf War illness patients do not meet criteria for them. Gulf War veterans who meet criteria for these disorders often differ significantly on tested parameters from non-veteran populations who are diagnosed with them. It may be necessary to consider people with these disorders who are and are not Gulf War Veterans separately in research studies, including treatment research.”

Let’s Zero In On That “Smoking Gun” A Bit More

I began this post by asserting that the “Tobacco Industry” is the villain behind the excessive number of Gulf War Veterans suffering from the diseases of Gulf War syndrome.

To begin the zeroing-in process, let’s look at the data on how many Veterans are smokers compared with non-Veterans who, of course, were never exposed to the combination of PB and pesticides.

Exhibit #6
The CDC tells us part of the story.
In the United States, cigarette smoking prevalence is higher among people serving in the military than among the civilian population. Cigarette smoking prevalence is even higher among military personnel who have been deployed. During 2007–2010:
• Male veterans aged 25–64 years were more likely to be current smokers than nonveterans (29% versus 24%).
• Among men aged 45–54 years, 36% of veterans reported being current smokers, compared with 24% of nonveterans
.

prevalence-bar-chart-military
http://www.cdc.gov/tobacco/campaign/tips/resources/data/cigarette-smoking-in-united-states.html
Here are two additional studies that drive home the point that FAR more Gulf War Vets were and still are smokers, chewers and dippers than Vets who served elsewhere or than other demographically-matched groups.
Exhibit # 7
J Gen Intern Med. Feb 2010; 25(2): 102–103.
Published online Jan 15, 2010. doi: 10.1007/s11606-009-1224-1
PMCID: PMC2837491
Effects of the Wars on Smoking Among Veterans
Lori A. Bastian, MD, MPH and Scott E. Sherman, MD, MPH
Although smoking rates in the US declined by 50% between 1965 and 2005, about 21% of adults are current smokers. The prevalence of smoking is estimated to be up to 40% higher in veterans than in the general population. The total burden of Veterans Affairs (VA) health-care costs associated with smoking range from 8% to 24%. While the VA has increased its efforts to fight the “war” on smoking, actual wars in Iraq and Afghanistan are producing veterans who are smoking at alarming rates. The prevalence of smoking among veterans returning from recent wars is similar to that of the US adult population during the late 1960s.”</em>
This is pretty strong evidence that Gulf War Vets who went on and exposed themselves not to a few pesticides from Pet Collars and No-Pest Strips, but to a chronic sub-lethal mix of pesticides as virtually undetectable residues in Tobacco Industry products.


Exhibit # 8
Mil Med. 1996 Mar;161(3):165-8.
Tobacco use habits of naval personnel during Desert Storm.
Forgas LB1, Meyer DM, Cohen ME.
http://www.ncbi.nlm.nih.gov/pubmed/8637647

Abstract
“This study examined availability and usage of tobacco products, and their potential impact on the oral health of naval personnel deployed to Desert Storm. Of 4,200 surveys mailed to a randomly selected sample, 45.6% were returned (N = 1,915). The respondents included 55.9% who reported a present or former smoking habit, 34.1% who identified themselves as current smokers (SM), and 23.8% who were smokeless tobacco (ST) users. Tobacco products were easily and inexpensively accessible through ship stores, exchange, or military support organizations (USO). While in the Persian Gulf, 7.0% started SM and 9.3% started ST, resulting in an overall 4.7 and 6.1% increase in SM and ST, respectively. Of those who were already tobacco users, 29.2% reported more SM use and 19.0% used ST more often. Stress (35.1%) and boredom (21.4%) were the most frequently cited reasons to start or increase use. Although 30.5% of respondents reported military personnel have encouraged them to quit, 77.2% reported that anti-smoking efforts have been unsuccessful in influencing them to quit. Since the tobacco usage rate is higher in the military than in the civilian sector, greater emphasis on preventive efforts in warranted to promote health and wellness.”
Here is a KEY FACT about the entire research literature on GWS:


A thorough search as many of the studies of Gulf War Syndrome as I coul
d find found ZERO references to (1) Smoking (2) Cigarette or (3) Tobacco. Not a single reference. And IMO never mentioned means never considered. I would hate to think that Tobacco products had been considered and that a decision was made to exclude them from the studies.


Here’s why that fact is key to understanding the role that the Tobacco Industry has played in the sickness, suffering and deaths of tens of thousands of these Veterans. Virtually every brand of cigarette, snuff and chewing tobacco manufactured in America contains a vast array of pesticide and herbicide residues, along with the residues of some of the most toxic industrial solvents and other classes of chemicals in existence.


Remembering that all the authoritative studies found that it was the combination of exposure to PB and a few relatively benign (if such a statement can be made) pesticides that is causal for Gulf War syndrome diseases, check out the following undoubtedly incomplete list of pesticides that are used on Tobacco crops in the US and worldwide. I gave you this list in the summary at the beginning of this post but I believe that it bears repeating here now that you’ve had a look at some of the supporting evidence for the “Smoking Gun” thesis.


DDT, TDE, Chlordane, Lindane, Aldrin, Endrin, Dieldrin, Heptachlor, and Toxaphene, Anilazine, AziaPhos-Methyl, Captan, Diflubenzuron, Leptophos, Malathion, Methoprene, Mirex, Cyclohexane, 1,3-dichloropropene (1,3-D), Chloropicrin, Maleic hydrazide, Acephate, Methyl Bromide, Isocarbophos, Dimethoate, Pendimethalin, Dicrotophos, Chlorpyrifos, Fenamiphos, Mancozeb, Flumetralin, Metalaxyl, Clomazone, Ethoprop, Endosulfan, Mefenoxam, Pebulate, Ethephon, Napropamide, Sulfentrazone, Imidacloprid, Aldicarb, Butralin, Dimethomorph, Methomyl, Malathion, Ethyl Parathion, Methyl Parathion, Disulfoton, Sethoxydim, Spinosad, Carbaryl, Fonofos, Benefin, Bacillus Thuringiensis, Carbofuran, Diazinon, Diphenamid, Isopropalin, Omethoate, Phismet, Phoxim, Oxamyl, Methidathion, Thiodan, Pendimethilum, and Trichlorfon. Also the solvents Toluene, Benzene, Phosgene, Hexane, and Xylene.


I would encourage you to pick just a few of these pesticides and do a search on health effects through inhalation or mucosal absorption (as with chewing tobacco and wet snuff).


But the presence of these terribly dangerous chemicals isn’t the whole story by a long shot. Two key points to keep in mind:
1. We have already shown that the health impact of exposure to multiple pesticides is not additive, it is exponential.
2. There have very few studies of what happens to any of these pesticides when they are heated and inhaled – a burning cigarette is in effect a “dry distillation” instrument. So, for example, when DDT is burned it produces, among other things, Dioxin. So do many of the other Organochlorine pesticides. Can I assume that I don’t have to explain why inhaling Dioxin 10, 20, 30 or more times a day is not a good idea?


Wrapping It Up


Exhibit #9

I can show through documentary evidence that I have obtained over my 30 years of working on this project that the top executives and Board members of the cigarette companies knew, or by virtue of their positions of authority should have known that their products contain these chemicals that irrefutably cause cancer, heart disease, neurological degradation, fetal malformation, and all of the other diseases that these pesticides cause without question.


Extensive documentation exists that proves that these companies know what their products contain – they have simply used their financial and political clout to prevent any research, ever, that would prove that these immensely dangerous chemicals are in their products and that they know they are there.


Since I have been making the point that most, though not all of the pesticide contamination in US Tobacco Industry products is the result of the industry’s use of highly contaminated imported foreign tobacco waste, let me offer you just one of literally hundreds of instances of documentation that I have collected over the years that, taken together, create a framework for proving guilty knowledge on the part of these companies.


This document also shows how brazen these people are – they are actually asking for an environmental tax credit for using toxic tobacco waste to manufacture their products rather than taking it to the landfill!


Waste Not; Want Not


In 1998 RJ Reynolds filed an appeal against a ruling by the North Carolina Department of Environment & Natural Resources that it could not classify the waste tobacco it uses to manufacture its cigarette products as solid waste in order to take advantage of tax breaks for disposing of solid waste in environmentally sound fashion.


RJ Reynolds argument was that since it was taking this waste and manufacturing it into cigarettes it was disposing of it in a way that qualified it for tax breaks. In other words – “We aren’t dumping this trash into the landfill, we’re pumping it into people’s lungs, so we deserve a tax break.”


The case number is no. COA01-74 in the North Carolina Court of Appeals filed: 19 February 2002. The full text of the case and the court’s ruling is available at
https://cases.justia.com/north-carolina/court-of-appeals/01-74-5.pdf?ts=1323905288

Aside from the preposterous idea that since RJ Reynolds was disposing of millions of pounds of waste by making it into products and selling those products to smokers rather than dumping the waste in a landfill and therefore deserved a tax break for being good environmental stewards, the summary of this lawsuit reveals information about how RJ Reynolds manufactures its products that ought to give any cigarette smoker pause to realize what suckers they are being made into by this cigarette giant.


Here are a few of the details directly from the court papers from COA01-74 North Carolina:
1. In manufacturing tobacco products, Reynolds buys tobacco leaves at auction. The tobacco is sent to a stemmery, where the stems (hard, woody part of the leaf) are separated from the lamina portion of the leaf (material in between the stems). The separation process also generates small scraps of tobacco (scraps) and very fine scraps of tobacco (dust). The usable tobacco lamina material is sent to the manufacturing operation where it is blended and processed into cigarettes.
2. The stems, scraps and dust are packed into containers and sent to a storage facility until they are either processed into reconstituted sheet tobacco, through a process known as the G-7 process, or are discarded. The reconstituted sheet tobacco is shredded and blended with the processed lamina strips and made into filler for cigarettes. The reconstituted tobacco filler is part of most brands of cigarettes made by Reynolds, and enables cigarettes to be made with lower tar and nicotine content which according to Reynolds has been “demanded” by smoking consumers.”
3. Reynolds uses approximately seventy million pounds of tobacco stems, scrap and dust each year in making reconstituted sheet tobacco. Reynolds also disposes of between five and seven million pounds of tobacco waste materials in landfills each year. This material is of a lower quality than the stems, scrap and dust used in the G-7 process; much of it is generated by the manufacturing process, rather than the stemmery, though some tobacco waste generated by the stemmery is also disposed of.
4. In order to keep up with its production requirements for reconstituted tobacco, Reynolds imports tobacco stems purchased overseas. For example, in 2006 ( the latest year for which US Government data is available), the US imported 136.8 Million pounds of Tobacco stems. In other words, there weren’t nearly enough stems being produced from US tobacco for the manufacturers to use in making their products. These manufacturers, on the other hand, would probably say “Well, Tobacco stems are Tobacco, so what’s the big deal?” The big deal of course is that many of the most dangerous pesticides used on tobacco overseas (like slug and snail control chemicals) are taken up from soil application into the roots and stems, and others translocate from the leaf where they are sprayed into the stems and stalks.
5. Reynolds sells reconstituted tobacco to other manufacturers of tobacco products, and manufactures reconstituted sheet tobacco for other tobacco manufacturers, using stems, scraps and dust supplied by them. As you can read in the case file, one of Reynolds’ witnesses testified that even if there were no tax incentives for recycling and resource recovery of or from solid waste, Reynolds would still operate the G-7 process because of its cost-effectiveness.”
6. While it’s bad enough that this cynical giant corporation wants tax breaks for selling waste to its customers, what isn’t revealed here is that the waste is toxic, carcinogenic, mutagenic and endocrine-disrupting. That single sentence “In order to keep up with its production requirements for reconstituted tobacco, Reynolds imports tobacco stems purchased overseas” holds the clue. When you look at where RJ Reynolds buys its tons of waste overseas you find that it is coming from countries that have absolutely no regulations on pesticide and other toxic chemical use on tobacco crops. This means that the waste that RJ Reynolds is putting in its cigarettes, and that Reynolds is selling to other cigarette manufacturers as reconstituted “sheet”, contains high levels of pesticides that are totally banned for use on any crop in the US.
7. These chemicals are known carcinogens, they are known to destroy nervous systems, they are known to produce deformed babies, and they are known to produce dozens of fatal diseases in humans. Furthermore, carefully-done research studies show that many of these pesticides are far more dangerous to children, young women, Hispanics and African-Americans that they are to white males.
8. I would also like to point out that RJ Reynolds could choose to manufacture its cigarette brands from pure tobacco leaf grown in the US under strict pesticide regulations. The reason it chooses to pack its products with toxic waste is because it is so damned profitable to do so, and because nobody has called them on the practice.

Exhibit # 10


Pesticide use is one of only two exposures consistently identified by Gulf War epidemiologic studies to be significantly associated with Gulf War illness. Multi-symptom illness profiles similar to Gulf War illness have been associated with low-level pesticide exposures in other human populations. In addition, Gulf War studies have identified dose-response effects, indicating that greater pesticide use is more strongly associated with Gulf War illness than more limited use. Pesticide use during the Gulf War has also been associated with neuro-cognitive deficits and neuro-endocrine alterations in Gulf War veterans in clinical studies conducted following the end of the war. The 2008 report concluded that “all available sources of evidence combine to support a consistent and compelling case that pesticide use during the Gulf War is causally associated with Gulf War illness.”
“Organophosphates are of concern to both scientists and regulators because they work by irreversibly blocking an enzyme that’s critical to nerve function in both insects and humans. Even at relatively low levels, organophosphates may be most hazardous to the brain development of fetuses and young children. The EPA banned most residential uses of organophosphates in 2001, but they are still sprayed agriculturally on fruits and vegetables. They’re also used to control pests like mosquitos in public spaces such as parks. They can be absorbed through the lungs or skin or by eating them on food

(in) Wikipedia


What Can Be Done?


The most powerful thing that can be done would cost at most a few thousand dollars, and that would be to collect a good sample of off-the-shelf so-called “Tobacco” products including cigarettes, chewing tobacco, cigars, dry snuff and even Vape, and then using good evidence-handling procedures get these samples to a qualified testing lab and have them do a comprehensive analysis for residues of chemicals that do not occur naturally in the Tobacco plant. This would include the broad list of pesticides referred to earlier in this post, plus all other non-natural chemicals such as flavoring and aroma agents as well as the “smoker satisfaction” chemicals that the industry uses to create “brand loyalty” – a cute little label for deliberate chemical addiction that has zero to do with nicotine. The analysis would also look at the actual constituents of the products themselves, especially to determine how much of each product is actually tobacco, how much is actually tobacco leaf, and how much is non-tobacco materials like municipal waste.
Believe it or not, this analysis has never been done. But with the results in hand, injured smokers of all kinds including veterans exposed to both PB and “tobacco” products but also children of smokers, spouses of smokers, chewers, and other classes of victims could mount a real class action suit – not one of those res-herring class action lawsuits that pretend to go after the “Tobacco” companies for misleading claims and consumer fraud but that actually serve the interests of the “Tobacco” industry by providing them with the excuse that they have been investigated, sued, adjudicated and either slapped on the wrist or vindicated.

2 thoughts on “Concealed Hard Evidence & The Gulf War Syndrome

    1. Hi and many thanks for your comment freemancounselor:) I would love to be able to conduct the study but would need a sponsor, which is what I hope might come from the blog posting.

      We’ll see. meanwhile, my hope is that one or more Veterans injured in this way will get a Class Action lawsuit together. There I could be helpful.

      Like

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