Anyone Awarded Sc To Jet Fuel?

[deanosono]

Hey anybody,

I'm in the appeals process trying to show a connection to 4 years of servicing aircraft from 1977-81. The old A-7 Corsairs were being phased out to make room for the A-10 Warthogs. I had plenty of exposure to JP-4 daily.I filed my claim on the VA website in 2004. Seems like that was a big mistake as the VA has got all the facts screwed up and flatly denies everything. Finally decided to get a Rep. My Rep wants me to show a direct link between JP-4 and non-hodgkins lymphoma. I'm not finding any studies on the net that come right out and make that link, but there is benzene in the fuel and plenty of lawyers who chase benzene cases. The few I've contacted can't or won't deal with the VA. Even though they say I may have a good case based on symptoms and diagnoses and latency period.

In 1981 honorably discharged.

1993 lesion removed from the scalp ( lymphoma)

1995-97 several more lesions on scalp removed

1998-99 multiple lesions on the scalp, bone marrow biopsy ,radiation treatment ,migraines,cunvulsions

2001 brain tumor removed

2005 lesion in scalp requiring softball sized skin graft and artery transplant, undefined deterioration of the skull. titanium in my head

2007 lesion removed.

I'm running out of places for the docs to cut on and feel that I'm getting nowhere.

Losing control of this page ...ignorance overwhelming!

Any advice any one? Thanks for reading this!

Deanosono

[lfredrick123]

Dont know if this will help, but husband served in a tank squadron as a turret artillery repairman. Tanks were known to have heavy Carbon Dioxide from the diesel fuels in the turret and in the smoke and obliterants. We were digging for military evidence and found industrial hygiene surveys done at the base he was at that had multiple years of reporting that showed excessive levels of Carbon Monoxide in the training areas and heavy pollution levels. You might check to see if there were any surveys done at your particular base that would show it as a health hazard, and if they were doing anything at all to help. In husbands case he has COPD from it (never smoked himself) and severe lung problems now thanks to exposures and an eventual stroke.

At any rate I found a report from Dr Grace Ziem on Hydrocarvons, fuels exposures. Here it is. If you will look her info up Dr. Grace Ziem MD she is an Occupational doc who worked as a consultant to VA and there may be more info on your cancer problems in her materials. Here is what I found:

COMBUSTION PRODUCTS Being near busy traffic or vehicle exhaust causes exposure that affects lung function. 1 This is worse for those with longer exposure, such as house near traffic.1 Very small vehicle particles can easily enter an indoor environment. 1 Exposure to diesel exhaust causes lung inflammation even in healthy people. 2 Risk is greater with longer exposure as well as higher intensity. Even higher risk occurs with indoor exposure to idling vehicles.3 DANGER BELOW EXPOSURE LIMITS Harmful health effects occur from combustion product particles even at below government and commonly used exposure levels. 4 Particulate pollutants (such as combustion products) cause and exacerbate illness at levels below EPA and WHO guidelines.5 There is a direct dose-response relationship between levels of combustion particle exposure and death rate. 4 Recent scientific research shows body damage at very low levels of carbon monoxide, suggesting there is no known safe level of carbon monoxide exposure.6 HAZARDOUS GASES Combustion gases contain irritants7 8 9 and toxins.10 11 Combustion products of fuels (oil, gasoline, diesel, propane, etc.) contain the irritant oxides of nitrogen and for most fuels, oxides of sulphur. Repeated modest and even "tolerable" level irritant exposure,8 or higher level single8 or repeated9 irritant exposure can cause permanent or long term reactive airway disease rendering the individual with long-standing heightened susceptibility to exacerbating symptoms from future irritant exposures.7 9 Combustion products such as vehicle exhaust and smoke release benzene, a potent cancer agent, and these exposures increase cancer risk.10 Combustion products also contain carbon monoxide, which can cause sensitization and affect memory and learning.11 Carbon monoxide is toxic to brain/nerve cells, the heart, and other body muscle.6 Carbon monoxide exposure can cause long term neurologic damage.6 Chemical exposure can also interfere with detoxification. 11 LUNG DAMAGE FROM COMBUSTION PARTICLES Combustion particles when inhaled can cause allergic effects and other chronic respiratory damage.3 12 13 14 Combustion particles can accumulate in the lungs. 15 Gases, vapors and other air pollutants cling to particles and the particles then carry these substances into the lungs.16 They persist longer, because particles are harder to clear from the lungs. Very small particles cause lung inflammation, damage lung cells, and form lipid peroxides in lung tissue. They can also enter the body through the lungs and/or cause lung scarring. 17 Combustion Products Page 2 of 5 Fine particulates deposit in the respiratory tract.14 Smaller particles (under 2.5 microns) deposit in the deep lung sacs (alveoli).14 They cause inflammation that makes lungs more permeable (to toxins, other particles, etc).14 Fine particles can act as a physical stressor, increasing norepinephrine (adrenalin) and adrenal cortisol (body stress hormone) levels.14 EXPOSURE SOURCES All combustion releases carbon monoxide, and most combustion releases particles as well. Burning landfills and industrial releases are major sources. Vehicles are a problem especially with frequent/repeated and/or heavy traffic exposure, gas or kerosene space heaters, gas appliances and tobacco sources release indoor carbon monoxide.6 DIESEL Exposure to diesel exhaust causes eye and respiratory irritation and can lead to chronic respiratory damage.3 These very small particles entering the blood stream can impair normal function of the autonomic nervous system.17 Repeated, chronic diesel exhaust exposure can also cause brain damage with documented impairment in memory and other cognitive functions, as well as impaired balance, reaction time and other neurophysiologic functions.3 HEART DAMAGE Particles can cause changes in EKG (electrocardiogram) tests showing (reduced blood/oxygen supply and/or inflammation.18 Exposure to combustion particles and gases cause excess cardiovascular disease risk 19 20 21 and risk of death from stroke and other causes.21 HOW COMBUSTION PARTICLES CAUSE HARM When fine chemical particles are breathed in, they can pass into the blood stream and be distributed to many other body organs and cells.20 Chemical particles in those other locations also cause inflammation in those locations. They cause immune changes. They also cause toxicity20 and increased need for antioxidants due to formation of tissue-damaging substances called free radicals.20 Bigger particles breathed can penetrate and be deposited in the larynx (voice box), trachea and larger airways14 causing inflammation.14 22 Combustion particles impair lung function.23 Ultrafine particles in large numbers are present in vehicle emission, worse in diesel. These particles have a high ability to attach to lung sacs (alveoli), cause inflammation. They also enter the blood stream16 and have a large surface area to absorb gases and vapors.16 They thus carry other vapors into the body. COMBUSTION PRODUCT EXPOSURE DEPLETES ESSENTIAL ANTIOXIDANTS AND NUTRIENTS Carbon monoxide exposure11 24 25 26 can produce excess nitric oxide in the body 11 24 25 and NMDA activation.25 27 Both of these lead to inflammation.26 28 29 30 31 Particles also cause inflammation and increased nitric oxide. 22 32 These changes all deplete nutrients and require nutrients for repair.28 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 Combustion Products Page 3 of 5 This damage can be reduced by treatment with glutathione.12 Fine combustion and other particles can cause increase in the respiratory inflammation marker, exhaled nitric oxide.22 Excess nitric oxide depletes cobalamin (B12) and needs hydroxocobalamine as a scavenger. 36 37 OTHER BODY DAMAGE They can cause damage to genetic material (DNA).10 This is measured by a substance called 8-hydroxy-2-deoxyguanosine.16 This type of DNA damage could lead to increased cardiovascular and pulmonary disease, risk of mutations and cancer.16 Diesel exhaust increases lung cancer.55 They also damage essential lipids,16 causing damage to cell membranes and membranes around internal structures inside cells. Examples of these vital structures are ribosomes making proteins, mitochondria producing energy, etc.). They damage myelin in the brain and nervous system. Exposure to vehicle traffic exhaust significantly increases body exposure to these particles,16 and increased DNA damage can be measured after such exposure.16 It is worse with heavier traffic16 e.g., commuter, highway traffic, etc.). Other studies confirm a correlation between DNA damage and exposure to small particles. Inhaled ultrafine particles can penetrate through the lung and within an hour are able to penetrate cells and affect energy-generating mitochondria and other structures within body cells.16 56 Carbon monoxide can also cause inflammation of blood vessel linings.57 This can impair oxygen supply to the brain, heart and other organs. BURNING SYNTHETICS Persons exposed to combustion products from flame-retardants in plastics, electronics, fabrics and other materials can develop permanent brain and neurologic damage.58 Deca is the most widely used flame retardant and during combustion and other exposure breaks down to brominated compounds. These persist in the body for decades and are banned in the European Union and California.)58 1 D Sugiri, etal, “The influence of large-scale airborne particle decline and traffic-related exposure on children’s lung function,” Env Health Persp 114:282-288, 2006. 2 S Dubowsky Adar, etal, “Ambient and microenvironmental particles and exhaled nitric oxide before and after a group bus trip”, Env Health Persp 115: 507-512, 2007. 3 KH Kilburn “Effects of Diesel exhaust on neurobehavioral and pulmonary functions,” Archiv Env Health, 55: 11-14, 2000. 4 E Samoli, etal, “Particulate air pollution and mortality: findings from 20 US cities, N Eng J Med 343: 1742-1757. 5 SV Glinianaia etal, “Does particulate air pollution contribute to infant death? A Systematic Review,” Env Health Persp 112: 1365-1370, 2004. 6 E Samoli, etal “ Short-term effects of carbon monoxide on mortality: An analysis within the APHEA project”, Env Health Persp 115: 1578-1583, 2007. 7 HM Kipen etal., "Asthma experience in an occupational medicine clinic. Low dose reactive airway dysfunction syndrome", J Occup Med. 36: 1133-1137, 1994. 8 SM Brooks etal, "Reactive airway dysfunction syndrome", J Occup. Med. 27: 473-476, 1985. 9 M Tarbo and I Broder, “Irritant-induced occupational asthma”, Chest 96: 297-300, 1989. 10 MN Mead “A backpack’s worth of data: Elevated teen cancer risks linked to air pollution”, Env Health Persp, 114: A601, 2006. 11 NH Prahhaker and RS Fitzgerald, “Carbon monoxide: From tool to neurotransmitter”, CRC Press, 1996. 12 JE Sharmon etal., "Exposure to automotive pollution increases plasma susceptibility to oxidation", Arch Env Health 57: 536-540, 2002. 13 FD Gilliland etal., “Effect of glutathione-S-transferase M1 and P1 genotypes on xenobiotic enhancement of allergic responses: randomized, placebo controlled crossover study”, The Lancet 363: 119-124, 2004. 14 MP Sirivelu, etal “Activation of the stress axis and neurochemical alterations in specific brain areas by concentrated ambient particle exposure with concomitant allergic airway disease”, Env Health Persp 114: 870-874. Combustion Products Page 4 of 5 15 A Penn etal, “Combustion-derived ultrafine particles transport organic toxicants to target respiratory cells”, Env Health Persp 113: 953-963, 2005. 16 P Vinzents etal, “Personal exposure to ultrafine particles and oxidative DNA damage”, Env Health Persp 13: 1485-1490, 2005. 17 C Chang-Chuan etal, “Personal exposure to submicrometer particles and heart rate variability in human subjects”, Env Health Persp 112: 1063-1067, 2004. 18 DR Gold, etal, “Air pollution and ST-segment depression in elderly subjects”, Env Health Persp 113: 883-887, 2005. 19 LH Chen, etal “The association between fatal coronary heart disease and ambient particulate air pollution: are females at greater risk?” Env Health Persp 113: 1723-1729, 2005. 20 TR Nurkiewicz, etal, “Systemic microvascular dysfunction and inflammation after pulmonary particulate matter exposure”, Env Health Persp 114: 412-419, 2006. 21 A Zanobetti and J Schwartz, “Particulate air pollution, progression, and survival after myocardial infarction”, Env Health Persp, 115: 769-775, 2007. 22 F Therese, etal Exhaled nitric oxide in children with asthma and short-term PM 2,5 exposure in Seattle”, Env Health Persp 113: 1791-1794, 2005. 23 SF Suglia, etal, “Association between traffic-related black carbon exposure and lung function among urban women”, Env Health Persp 116: 1333-1337, 2008. 24 SR Thom etal “Neuronal nitric oxide synthase and n-methyl-d-aspartate neurons in experimental carbon monoxide poisoning”, Toxicol Applied Pharmacol 194: 280-295, 2004. 25 RE Lenga, Ed., Sigma-Aldrich Library of Chemical Safety Data. Sigma-Aldrich Corp, 1988. 26 R Dales, etal, “The influence of living near roadways on spirometry and exhaled nitric oxide in elementary school children” Env Health Persp 116: 1423-1428, 2008. 27 WA Pryor and G Squadrito, “The chemistry of peroxynitrite: a product of the reaction of nitric oxide and superoxide”, Am J Physiol 268:L 699-L, 722, 1995. 28 M Lafon-Cazal etal, “Nitric oxide, superoxide and peroxynitrite: putative mediation of NMDA-induced cell death in cerebellar cells”, Neuropharmacology 32: 1259-1266, 1999. 29 JS Beckman, “The double edged role of nitric oxide in brain function and superoxide-mediated injury”, J Dev Physiol 15: 53-59, 1991. 30 M Lafon-Cazal etal, “NMDA-dependent superoxide production and neurotoxicity”, Nature 364: 535-537, 1993. 31 JT Coyle, P Puttfarken, “Oxidative stress glutamate and neuro generative disorders”, Science 262: 689-695, 1993. 32 JE Haley, etal, “Evidence for spinal N-methyl-D-aspartate receptor involvement in prolonged chemical nociception in the rat”, Brain Res 518: 218-226, 1990. 33 S Moncada and J Bolanos “Nitric oxide cell bioenergetics and neurodegeneration”, J Neurochem, 97: 1676-1689, 2006. 34 JS Beckman and JP Crow, “Pathologic implications of nitric oxide, superoxide and peroxynitrite formation”, Biochem Soc Trans 21:330-333, 1993. 35 M Wolak, etal, “Kinetics and mechanism of the reversible binding of nitric oxide to reduced cobalamin B(12r) (Cob(II) alamin)” J Am Chem Soc 123: 9780-91, 2001. 36 C Zheng, etal, “Electrochemical and spectral studies of the reactions of aquacobalamin with nitric oxide and nitric ion”, Inorgan Chem, 41: 2548-2555, 2002. 37 W B Slot, etal, “Normalization of plasma vitamin B12 by intranasal hydroxycobalamine in vitamin B12 deficient patients”, Gastroenterology 113: 430-433, 1997. 38 O Stanger, M Weger, Interactions of homocysteine, nitric oxide, folate and radicals in the progressively damaged epithelium”, Clin Chem Lab Med 41: 1444-1454, 2003. 39 CD Klassen etal, Editors, Cassarett and Doulls Toxicology: The Basic Science of Poisons, McGraw Hill, New York, NY 2001. 40 W Watson, etal, “ A new role for glutathione: Protection of vitamin B12 from depletion by Xenobiotics”, Chem Res Toxicol 17: 1562-1567, 2004. 41 S Oja etal, Modulation of glutamate receptor functions by glutathione” Neurochemistry International 37: 299-306, 2000. 42 H Sprince etal, “Comparison of protection by L-ascorbic acid, L-cysteine, formaldehyde toxicity”, agents and actions 9: 407-414, 1979. 43 LJ Machlin and A Bendich “Free radical damage: protective role of antioxidant nutrients”, FASEB J 6: 441-445, 1987. 44 T Konrad etal, “Alpha-lipoic acid decreases serum lactate and pyruate and improves glucose effectiveness in lean and obese patients with type 2 diabetes”, Diabetes Care 22: 280-287, 1999. 45 S Hustad etal, “Riboflavin, flavin mononucleotide, flavin adenine dinucleotide in human plasma and erythrocytes at baseline and after low-dose riboflavin supplementation”, Clin Chem 48; 1571-1577, 2002. 46 A Prentice, C Bates, “A biochemical evaluation of the erythrocyte glutathione reductase (EC1.6.4.2) test for riboflavin status. Dose response relationships in chronic marginal deficiency”, Brit J Nutr 45: 53-65, 1981. 47 G Ziem, “Endocrine Changes in Patients with Chronic Illness Following Chemical Overexposure”, Invited presentation at Conference on Chemical Injury, Fairfax, VA, October 3, 2003. 48 M Jones, “Chronic neuropathic pain: pharmacological in the new millennium”, Internat J Pharmaceutical Compounding, Jan-Feb 2000. 49 S Christen etal, “Gamma-tocopherol traps mutagenic electrophiles such as NOx and complements alpha-tocopherol: Physiologic implications” Proc Natl Acad Sci 94: 3217-3222, 1997. 50 K Wagner etal, “Gamma-tocopherol-an underestimated vitamin” J Nutr 122: 2440-2446, 1992. Combustion Products Page 5 of 5 51 JO Moskaug, etal, “Dietary Polyphenols and Health: Proceedings of the 1st International Conference on Polyphenols and Health”, Am J Clin Nutr 81: 277S-283S, 2005. 52 N Kocak-Toker, etal, “Peroxynitrite induced decrease in Na+ , K+ -ATPase activity is restored by taurine.” World Journal of Gastroenterology. 11: 3554-3557, 2005. 53 T Yokozawa etal, “(-)-Epigallocatechin 3-0-gallate ameliorates the damage related to peroxynitrite production by mechanisms distinct from other free radical inhibitors”, Xenobiotica 33: 913-25, 2003. 54 AY Sun, YM Chen, “Oxidative stress and neurodegenerative disorders”, J Biomed Sci, 5: 401-14, 1998. 55 E Garshick, etal, “Lung cancer and vehicle exhaust in trucking industry workers”, Env Health Persp 116: 1327-1332, 2008. 56 B Weinhold “Particles in practice: how ultrafines disseminate in the body”, Env Health Persp 113: 758. 57 MJ Campen, “A comparison of vascular effects from complex and individual air pollutants indicates a role for monoxide gases and volatile hydrocarbons”, Env Health Persp, 118: 921-927, 2010. 58 “Labor drug sensitizes brain to pesticide injury”, Our Toxic Times, December 2004, Duke University Press Release, March 30, 2004.

Hope this helps

 

[Gastone]

Ifredrick123, this was a 06/08 topic, last post 2014.

[kensfolk]

I have applied for military disability and need more info on exposure to breathing of different petroleum fuel while in the Army from 1982-1985. I worked on a tank farm in Germany. We pumped thousands of gallons of mogas, diesel and Jp4-5. I have congestive heart failure, chronic kidney disease, and Non Hodgkin's lymphoma. I need to find research on the effects of petroleum in relation to these illness. I am going through radiation treatment for the non Hodgkin's again. I have some research on this.   

[GeekySquid]

9 hours ago, kensfolk said:

I have applied for military disability and need more info on exposure to breathing of different petroleum fuel while in the Army from 1982-1985. I worked on a tank farm in Germany. We pumped thousands of gallons of mogas, diesel and Jp4-5. I have congestive heart failure, chronic kidney disease, and Non Hodgkin's lymphoma. I need to find research on the effects of petroleum in relation to these illness. I am going through radiation treatment for the non Hodgkin's again. I have some research on this.   

start a new thread with your question. this is a kind of old thread that may not be being watched anymore