I along with 7119 other enlisted men were used in chemical weapons and drug experiments at Edgewood Arsenal between 1955 - 1975. The Department of defense used us in this March 2003 Sarin Report to create a report,The problem with this report they stated it was a comprehensive health study, yet it ignored cardiovascular, gastrointestinal and pulmonary medical conditions. It only focused on nuerological and sleep disorders, they determined that 25 personnel per 100,000 would get brain tumors and unknown percentage would develop sleep problems, what? How could they ignore all these other body systems? They did it, because they wanted to, these other medical problems would cost compensation into the billions. Yesterday the NY Times did a story on a Boston University study that showed Sarin was linked to destruction of white brain matter, how did the IOM study miss this, in 2003? Article by Ian Urbina May 17, 2007
The Senators and the Congressman named in the title are all well known advocates in Congress and are known for their hard work on behalf of veterans and their families. I feel that much of the data I have sent to them, is failing to get their attention as some low level staffers sit on it, due to time constraints and the fact that I am not a doctor or a scientist, I am a disabled veteran and I have an agenda, so I am written off by the staffers.
The data I provide shows the governments own medical studies that the Department of Defense has not wanted the law makers to see on the veterans panels about "Gulf War Illness" many people claim their is no such disease, and I agree with them. The VA has a list of "undiagnosed symptoms" that have no known etiology the "list here" are the medical problems they agree are presumptive for gulf war one veterans, the problem with these medical conditions, are they are also listed in this VA Manual from October 2003 on page 24
- Causal relationships
a. The evidence found indicated a causal relationship between
exposure to mustard and Lewisite chemical warfare agents and
the following health conditions:
• Respiratory cancers
° nasopharyngeal
° laryngeal
° lung
• Skin cancer
° pigmentation abnormalities of the skin
° chronic skin ulceration and scar formation
° leukemia (typically acute non-lymphocytic type,
nitrogen mustard)
• Chronic respiratory diseases
° asthma
° chronic bronchitis
° emphysema
° chronic obstructive pulmonary disease
° chronic laryngitis
• Recurrent corneal ulcerative disease (includes corneal opacities;
acute severe injuries to eye from Lewisite will also persist)
• Delayed recurrent keratitis of the eye
• Chronic conjunctivitis
• Bone marrow depression and (resulting) immunosuppression
(an acute effect that may result in greater susceptibility to
serious infections with secondary permanent damage to vital
organ systems)
• Psychological disorders
° mood disorders
° anxiety disorders (including post-traumatic stress disorder)
° other traumatic stress disorder responses (These may result
from traumatic or stressful features of the exposure
experience, not a toxic effect of the agents themselves)
• Sexual dysfunction (scrotal and penile scarring may prevent or
inhibit normal sexual performance or activity)
- Suggested causal relationship
a. The evidence found suggested a causal relationship between
exposure and the following health conditions:
• Leukemia (acute non-lymphocytic type, sulfur mustard)
• Reproductive dysfunction (genotoxicity, mutagenicity, etc.;
mustard agents)
- Insufficient evidence of a causal relationship (NAS 1993)
a. There was insufficient evidence found to demonstrate a
causal relationship between exposure and the following
health conditions:
Health Effects from Chemical, Biological, and Radiological Weapons
Long-Term Health Effects Amongst Experimental Subjects
18
Health Effects from Chemical, Biological, and Radiological Weapons
Long-Term Health Effects Amongst Experimental Subjects
19
• Gastrointestinal diseases
• Hematologic diseases
• Neurological diseases
• Reproductive dysfunction (Lewisite)
• Cardiovascular diseases (except for those that may result from
serious infections shortly following exposure – heart disease
resulting from rheumatic fever, for example
these are KNOWN MEDICAL CONDITIONS that occur over a long period of time and are related to chemical weapon exposure. Mustard agents were present at Kamisayah, not just Sarin.
Also, the Edgewood "volunteers" also have a 40% death rate, in FY2000 when the data was gathered by the IOM 2098 men could not be found using IRS, VA or Social Security Databases, of the 4022 survivors they did find, 54% of them another 2200 men reported being disabled, yet the IOM never explained the deaths nor the disabilities in these men, despite a nearly 75% death and disability rate in veterans that were between the ages of 45-65 in FY2000, why?
Did they already know from the previous published studies on personnel exposed to chemical weapons that there were a high disability rate, a high early death rate? The German government took good care, medical care and compensation of the Wermacht Soldiers after WW2 the medical report on them is here by SIPRI printed in 1975
A psychiatric delayed-effect syndrome was found as a result of systematic investigations
on former members of CW production and testing stations for the Wehrmacht. In
terms of frequency, two groups of symptoms can be distinguished–each consisting of
four separate symptoms or signs.
(1) The great majority of persons examined showed:
(a) persistently lowered vitality accompanied by marked diminution in drive;
(b) defective autonomic regulation leading to cephalalgia, gastrointestinal and
cardiovascular symptoms, and premature decline in libido and potency;
(c) intolerance symptoms (alcohol, nicotine, medicines);
(d) impression of premature aging.
(2) Further, one or more symptoms of the second group were found:
(a) depressive or subdepressive disorders of vital functions;
(b) cerebral vegetative (syncopal) attacks;
(c) slight or moderate amnestic and demential defects;
(d) slight organoneurological defects (predominantly microsymptoms and singular
signs of extrapyramidal character).
Our results are a contribution to the general question of psychopathological delayed
and permanent lesions caused by industrial poisoning. On the basis of our studies of
the etiologically different manifestations of toxication, the possibility of a relatively
uniform–though equally unspecific–cerebro-organic delayed effect syndrome is conceivable.
Hepatotoxic and hematotoxic lesions caused by organophosphorus
compounds
Parenchymatous lesions of the liver caused by organophosphorus compounds
40
were described by Maruyama as far back as 1954 (quoted in ref. [160]) and by
Maresch in 1956 [177]. The literature of succeeding years contains references
to the hepatotoxic effects of mainly organophosphorus pesticides [160, 178–
181].
In 1963, referring to his investigations on CW production workers,
Then the last know medical study on victims of chemical weapons exposure is the National Institute of Health report issued on January 1, 1994 shown here has a section on the known medical problems of exposure to Sarin also known as GB
Agent GB
GB is a very rapidly acting toxicant; there is little difference between the 15-min and the 24-hr lethal dose for animals by IV injection (Table 2) (28). GB has been thought by some to act primarily on the peripheral nervous system; however, respiratory arrest induced in cats by an IV dose equivalent to one-half the feline LD50 (48) was mediated through effects on the central nervous system. GB is very efficient at producing central respiratory arrest in guinea pigs and cats at IV doses too low to cause an effect on the respiratory muscles (32). Thus, the primary effects of GB appear to be on the CNS.
Like all other nerve agents, GB combines with and inhibits AChE, resulting in the accumulation of ACh. From studies in which small quantities of GB were injected directly into the bloodstream of human volunteers, Grob and Harvey (57) calculated that about 75% of GB combined with AChE in the muscle, about 22% with blood ChE, and about 3% with AChE in brain and liver. The inhibition of blood ChE results in no toxic effect; rather, it is the GB inhibition of brain and muscle AChE that causes the symptoms of nerve agent exposure. Within the muscles of cats, GB caused a dose-dependent inhibition of AChE activity; however, no simple relationship existed between AChE inhibition and alteration of muscle function (89).
Once GB is in the blood, it can penetrate the blood-brain barrier. Cholinesterase inhibitors vary in their ability to pass through this barrier, a property that has been related to the lipid solubility of the compound (90). Within the brains of mice injected intramuscularly with GB, Bajgar (91,92) observed regional differences in AChE inhibition. He concluded that the differences in AChE inhibition were due to regional differences in GB penetration rather than to a differential selectivity of GB for AChE in specific parts of the brain. Studies of isolated, blood-perfused in situ dog brains administered GB via intracarotid arterial injection (93) and of the brains of dogs after IV injection of GB (88) also showed regional differences in AChE activity. Studies in rats demonstrated that more than 94% of apparent GB bound to AChE in the brains 30 min after injection is actually the GB metabolite isopropyl methylphosphonic acid (94).
Mechanisms other than (or in addition to) AChE inhibition appear to be responsible for the observed toxicity of GB to the brain. In rats, Harris et al. (95) reported that 51% of the GB found in the brain was bound to sites other than AChE. In studies of spontaneous recovery from central respiratory failure in guinea pigs, respiratory recovery did not correlate with recovery of brainstem AChE levels (44). Adams and his colleagues concluded that the recovery occurred through a desensitization of the ACh receptors to the excess ACh, but it is also possible that AChE inhibition was not actually responsible for the initial respiratory failure. GB causes a number of noncholinergic effects in the brain, including effects on other neurotransmitters and enzymes. Most effects are too detailed to discuss individually in this analysis, but all emphasize the point that GB does much more than simply inhibit AChE in the brain (23,58,59,61,67,96,97).
Data on human responses to GB come from accidental exposures and from limited studies on low doses of GB given to volunteers. In one incident of accidental exposure to GB vapors (estimated at 0.09 mg/m3 for an undefined duration), two men had significantly lowered RBC-ChE for 80-90 days (one showed depression to 19% of baseline activity, the other to 84% of baseline) and extreme miosis that persisted for 30-45 days, but no other signs or symptoms of nerve agent poisoning (39). Other accidental inhalation exposures to GB with similar recovery times for RBC-ChE activity and miosis were described by Sidell (40). In one, the individual manifested severe symptoms and required respiratory assistance and extended hospitalization after cleaning a GB-contaminated area while wearing defective protective gear. In the other case, three workers who were in an area with a leaky GB storage container suffered temporary symptoms, such as transient mild respiratory distress, together with marked miosis and RBC-ChE activity depression. The RBC-ChE depression required 3 months for full recovery; the miosis (measured in the dark) recovered in 30-60 days.
Grob and Harvey (57) reported the effects in humans of administered low doses of GB. When either 0.003 or 0.005 mg/kg of GB was injected directly into an artery in the arm of one volunteer, Grob and Harvey observed some initial local effects (reduction in grip strength, tremors after exercise) followed by systemic effects, including many of the symptoms listed earlier. These doses, which correspond to 21% and 36% of the estimated human IV LD50, resulted in RBC-ChE activity reductions to 52% and 28% of original activity (i.e., depressions of 48% and 72%) and plasma ChE activity reductions to 61% and 42% (i.e., depressions of 39% and 58%), respectively.
After combining with a ChE molecule, the agent-ChE complex may either spontaneously dissociate (resulting in reactivation of the ChE) or "age," in which case the agent-ChE complex becomes resistant to reactivation by an oxime antidote. Aging is thought to result from stabilization of the nerve agent-ChE complex by loss of an alkyl or alkoxy group (Fig. 3). In agreement with Grob and Harvey's work (57), Sidell and Groff (56) observed little, if any, spontaneous reactivation of RBC-ChE after GB administration to volunteers. Furthermore, the GB-ChE complex aged at a moderate pace, with aging 50-60% complete 5 hr after GB infusion (56).
Figure 3. The nerve agent-acetylcholinesterase (AChE) complex may undergo either spontaneous reactivation by hydrolysis or stabilization ("aging") by loss of an alkyl or alkoxy group; stabilization proceeds at a faster rate than hydrolysis and therefore predominates. In humans, the GB-AChE complex is 50-60% aged by 5 hr, whereas VX ages more slowly, with only 40% aged at 48 hr after exposure (56).
When GB was given orally to 10 volunteers, approximately 3.5 times as much GB (in mg/kg) was needed to produce the same degree of plasma or RBC-ChE activity depression as previously observed with intra-arterial injection (see Table 4) (57). With the oral administration, Grob and Harvey noted a narrow margin between doses that produce mild signs and symptoms and those that produce moderately severe effects. They also noted that, after the disappearance of signs and symptoms, an increased susceptibility (in terms of type and severity of responses) remains to further GB exposure within 24 hr of the first exposure. Anorexia, nausea, and chest tightness were among the first symptoms reported; abdominal cramping, vomiting, and diarrhea were among later effects; miosis was not observed after oral administration. The possibility of oral exposure of the population to GB is remote because GB dissipates rapidly under most environmental conditions. Only when temperatures are 0° or less can GB persist for a few hours as a ground contaminant (22,98).
As mentioned previously, GB vapor is less effective as a toxic skin penetrant than as an inhalant. The estimated human LCt50 (clothed, resting) for dermal toxicity is 150 times higher than the estimated human LCt50 for inhalation (Table 2). Fielding (28) summarizes information from several sources, some still classified. Rapid evaporation from the skin is the primary factor in the relatively low dermal toxicity of GB; if evaporation is prevented (i.e., by covering the exposed skin with a cup), the toxicity of GB increases almost 100-fold (99). Another factor limiting the dermal toxicity is the reaction of GB with skin constituents, which attenuates the amount of GB that reaches target tissues (100). Fats such as lanolin and lard have been shown to enhance the skin penetration of GB, probably by dissolving the agent and by preventing evaporation (28). Mechanical abrasion of rabbit skin increased GB dermal toxicity 100-fold (101). Fielding (28) relates a tragic incident that illustrates the wide individual variability in dermal sensitivity to GB. Seventeen of 18 men exposed dermally to 200 mg of GB (12% of the estimated dermal LD50 for a 70 kg man) through two layers of clothing showed no signs or symptoms of GB poisoning; the eighteenth man died shortly after the onset of exposure, despite immediate treatment when signs of nerve agent poisoning appeared.
In a review of GB toxicity, McNamara and Leitnaker (25) state: "Absorption through the conjunctiva causes local effects but negligible systemic effects." Grob and Harvey (57) instilled 0.0003 mg GB in the eyes (conjunctival sacs) of volunteers and noted a marked miosis that began at 10 min and slowly diminished over a period of 60 hr. At a dose of 0.0009 mg, the pupillary constriction that occurred was near maximal for 72 hr and did not disappear until after 90 hr. In this study, miosis was measured in the light; other studies in which it was measured in the dark showed it persisted for weeks. No depression of blood ChE activity was noted at either dose level. In studies on GB applied to the conjunctival sac of guinea pigs, a rapid dose-dependent depression of AChE activity in the iris and cornea was noted with a lesser inhibition of AChE in the retina (retina required 10 times the iris dose to achieve the same AChE inhibition), but no examination was made of RBC-ChE depression or other systemic effects in the treated guinea pigs (102). However, ocular LD50 values are available for several animal species that are equivalent to the LD50 values for subcutaneous injection (11). This suggests that systemic effects are possible with GB absorption through the conjunctiva and possibly the cornea of the eye.
Studies of the retention and absorption of GB vapors by resting or exercising men demonstrated that the inactive men retained a higher percentage of the inhaled GB (82). Under similar exposure conditions of time and concentration, however, the active men received a larger dose of GB because of their greater air intake.
In determining the lowest concentration of GB that produces a biological effect, miosis provides a sensitive indicator for nerve agent exposure in humans. Questions, however, cloud the validity of the estimated no effects (0.5 mg-min/m3) concentration-time product (Ct) for miosis by GB (Table 2). The basis for this determination by McNamara and Leitnaker (25) is found in a report by Johns (103) of pupil diameter response in volunteers exposed to low atmospheric concentrations of GB (maximum Ct = 6 mg-min/m3 where tmax = 20 min). We consider the data insufficient to confidently predict concentrations of GB that would cause miosis in none of the population (no-effects level). The Johns study (103) was not designed to determine a no-effects level; it is not clear how McNamara and Leitnaker (25) derived their no-effects value of 0.5 mg-min/m3 from Johns's data. We consider the true no-effects level likely to lie below 0.5 mg-min/m3. The lack of raw data and absence of measures of variability in Johns's (103) report hinder precise reanalysis. Estimates of a human no-effects level for VX, as discussed below, were based in part on these for GB; the VX estimate consequently suffers from a similar question of reliability.
Given these already published medical reports on chemical weapon exposure to Sarin (GB) and Mustard agents I don't think the Department of Defense nor the Veterans Affairs needs to waste millions of dollars more on health studies and waste another 15 years of time on research, these veterans need help now.
How can the Kos Community help, send copies of this to your elected officials, Congressmen/women and Senators, demand answers for these veteran and their families, there are 500,000 veterans from Gulf War One that have been waiting for the research, Doctors and scientists gladly take the governments research funds, but as you can see the research has been done, since at least 1945 and in 1994, the March 2003 IOM report was a sham report which ignored the previous research, why because the known medical problems will cost the Veteran Affairs Billions and possibly Trillions of Dollars it's cheaper to claim ignorance, pay the disabled veterans war time pensions of 900 a month instead of the service connected payments of up to 2500 dollars a month.