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From: TSS ()
In Reply to: Docket No. 2004N-0081 Use of Materials Derived From Cattle in Human Food and Cosmetics posted by TSS on September 7, 2005 at 7:07 am:
I would kindly like to comment on ; Use of Materials Derived From Cattle in Human Food and Cosmetics [Docket No. 2004N-0081] RIN 0910-AF47 SUMMARY: The Food and Drug Administration (FDA) is amending the interim I would kindly like to submit the following ; I find it very very disturbing that FDA now takes the position; >>>Information was provided in comments that persuaded the agency that the TSE science is emerging and the old testing techniques for TSEs are becoming much more sensitive than when some of these old BSE tissue bio-assays were done in the distant past. I urge once again for the FDA and the USDA to put forth sound science instead of the political and corporate science they have floundered with for the last 3 decades. THERE is much new data out that dispute the position the FDA/USDA have taken on SRMs. STATEMENT ON INFECTIVITY IN BOVINE TONSIL Background 1. The views of the Committee were sought on unpublished results from an ongoing long-term study of the pathogenesis of BSE in cattle. This study is being carried out by the Veterinary Laboratory Agency and is funded by the Food Standards Agency (FSA). 2. In this study, cattle were orally dosed with 100g of BSE-infected bovine brain material. At various times after oral dosing, cattle were killed and different tissues tested for infectivity. In the first instance, the presence of infectivity was assessed by injection of various tissues into inbred mice ("mouse bioassay "). In this research infectivity was detected in: • distal ileum (the earliest infectivity was detected at 6 months after inoculation.) • brain and spinal cord and closely associated nervous tissue (infectivity was detected in the months just prior to the clinical onset of BSE in cattle) • at a single time point (around the time of clinical onset) bone marrow was also found to contain infectivity. ...snip http://www.seac.gov.uk/statements/tonsil211002.pdf UPDATE OF THE OPINION ON TSE INFECTIVITY DISTRIBUTION IN RUMINANT TISSUES INITIALLY ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 10-11 JANUARY 2002 AND AMENDED AT ITS MEETING OF 7-8 NOVEMBER 2002 following the submission of (1) a risk assessment by the German Federal Ministry of Consumer Protection, food and Agriculture and (2) new scientific evidence regarding BSE infectivity distribution in tonsils http://europa.eu.int/comm/food/fs/sc/ssc/out296_en.pdf 3. New work, work still in progress and future work The infectivity of neural and non-neural tissues by intracerebral inoculation of cattle is being assayed in projects M03006 and M03007. These studies are important since it is possible that some tissues may not yet have been found to be infective, due to the fact that infectivity in these tissues is below the detection limits of the tests applied so far. To date, this study has shown infectivity in CNS tissues, the distal ileum, tonsil tissue and the nictitating membrane (the nictitating membrane is also known as the third eyelid). Other challenged and control cattle continue to be closely monitored for clinical signs of BSE. Research is ongoing to determine the susceptibility of other food animal species to TSEs. These include a project to determine the susceptibility of pigs to scrapie through oral exposure (M03005) and a project to further study the transmission of BSE to pigs (M03010). Project M03024 aims to determine whether UK red deer are susceptible to BSE by oral exposure. These studies are important since it is highly probable that pigs and deer were historically exposed to ruminant derived meat and bone meal (MBM). ... http://www.food.gov.uk/multimedia/pdfs/annualresearchrpt04.pdf TSEs And The Environment The LANCET BSE: the final resting place snip... The first matter to consider is the distribution of infectivity in the snip...end...TSS TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY AS A ZOONOTIC DISEASE WRITTEN BY PAUL BROWN WITH CONTRIBUTIONS BY: RAYMOND BRADLEY LINDA DETWILER DOMINIQUE DORMONT NORA HUNTER GERALD A.H. WELLS JOHN WILESMITH ROBERT WILL ELIZABETH WILLIAMS PREPARED UNDER THE RESPONSIBILITY OF THE ILSI EUROPE EMERGING PATHOGEN TASK FORCE WITH THE ENDORSEMENT OF THE INTERNATIONAL FORUM FOR TSE AND FOOD SAFETY (TAFS) March 2003 snip... Despite the issuance by many governments of a package of prohibitions that could reasonably be expected to eliminate the veterinary and public health risks of BSE, loopholes often exist that could allow the spread of disease. The situation in the US is illustrative: • No rules exist that require the rendering process to be capable of sterilizing BSE infectivity. Most feed mills render carcasses under conditions that cannot be guaranteed to sterilize. • Feed for ruminants and non-ruminants can be processed in the same feed mills, creating the potential for cross-contamination. Thus, rendered carcasses of deer and elk with chronic wasting disease could conceivably be fed to cattle. • If farmers or ranchers mistakenly or deliberately use non-ruminant feed for ruminants, the mammalian to ruminant feed ban would be bypassed. Spontaneous TSE occurring in nonmammalian species, if it occurs, would also escape the mammalian to ruminant feed ban. 1 With the advent of BSE, safe sourcing has been practiced by avoiding tissues that are known to harbour or replicate TSE agents, eliminating ruminant materials, or where there is no satisfactory alternative, sourcing them from countries, herds and animals with an acceptably low geographical BSE risk assessment. This is therefore not a table of risk, but rather a reminder of the extent to which humans are exposed to products of bovine origin. 2 Some bone material, such as skull and vertebral column (excluding the tail) from cattle over certain ages are classified as specified risk materials (SRM) in the EU. 3 SRM include skull, brain, ganglia, eyes, tonsils, intestines and spinal cord, and in the EU and some other countries these are compulsorily removed for destruction. 4 Some fat (e.g. mesenteric fat) is classified as SRM in the EU. 5 Production of mechanically recovered meat from ruminant animals in the EU is banned. Elsewhere, its inclusion in meat products usually does not exceed 5–10% by weight. 6 Tallow (bovine rendered fat) is one of the two major end products from rendering bovine carcass waste. Tallow is not used in regulated medicines, but can be used in soaps, topical creams, cosmetics, and suppositories. Tallow from SRM is not permitted for use except under license as a fuel. 7 Tallow derivatives include glycerol, fatty acids and their esters, stearates, polysorbates, and sorbitan esters. Tallow derivatives are produced from tallow by hydrolysis at temperatures and pressures that have been shown to sterilize TSE infectivity. They are used in the manufacture of some medicines and cosmetics and may also be used in plastics (food wrappers). 8 Glucagons (replaced by recombinant technology in some countries), corticosterol,chondroitin sulfate, vitamin D3, cholesterol, and cholic acid. 9 Liver, thymus, heart, mammary glands, placenta, ovary, and spleen. http://europe.ilsi.org/file/TSE.pdf From: TSS () PrPSc distribution of a natural case of bovine Yoshifumi Iwamaru, Yuka Okubo, Tamako Ikeda, Hiroko Hayashi, Mori- Priori Disease Research Center, National Institute of Animal Health, 3-1-5 Abstract Bovine spongiform encephalopathy (BSE) is a disease of cattle that causes The specified risk materials (SRM) are tissues potentially carrying BSE The 11th BSE case in Japan was detected in fallen stock surveillance. PrPSc was detected in brain, spinal cord, dorsal root ganglia, trigeminal Our results suggest that the currently accepted definitions of SRM in 179 T. Kitamoto (Ed.) ALSO from the International Symposium of Prion Diseases held in Sendai, October 31, to International Symposium of Prion Diseases held in Sendai, October 31, to Tetsuyuki Kitamoto 107 Vet Pathol 42:107–108 (2005) Letters to the Editor Editor: Absence of evidence is not always evidence of absence. In the article ‘‘Failure to detect prion protein (PrPres) by immunohistochemistry in striated muscle tissues of animals experimentally inoculated with agents of transmissible spongiform encephalopathy,’’ recently published in Veterinary Pathology (41:78–81, 2004), PrPres was not detected in striated muscle of experimentally infected elk, cattle, sheep, and raccoons by immunohistochemistry (IHC). Negative IHC, however, does not exclude the presence of PrPSc. For example, PrPres was detected in skeletal muscle in 8 of 32 humans with the prion disease, sporadic Creutzfeldt-Jakob disease (CJD), using sodium phosphotungstic acid (NaPTA) precipitation and western blot.1 The NaPTA precipitation, described by Wadsworth et al.,3 concentrates the abnormal isoform of the prion, PrPres, from a large tissue homogenate volume before western blotting. This technique has increased the sensitivity of the western blot up to three orders of magnitude and could be included in assays to detect PrPres. Extremely conspicuous deposits of PrPres in muscle were detected by IHC in a recent case report of an individual with inclusion body myositis and CJD.2 Here, PrPres was detected in the muscle by immunoblotting, IHC, and paraf- fin-embedded tissue blot. We would therefore caution that, in addition to IHC, highly sensitive biochemical assays and bioassays of muscle are needed to assess the presence or absence of prions from muscle in experimental and natural TSE cases. Christina Sigurdson, Markus Glatzel, and Adriano Aguzzi Institute of Neuropathology University Hospital of Zurich Zurich, Switzerland References 1 Glatzel M, Abela E, et al: Extraneural pathologic prion protein in sporadic Creutzfeldt-Jakob disease. N Engl J Med 349(19):1812–1820, 2003 2 Kovacs GG, Lindeck-Pozza E, et al: Creutzfeldt-Jakob disease and inclusion body myositis: abundant diseaseassociated prion protein in muscle. Ann Neurol 55(1): 121–125, 2004 3 Wadsworth JDF, Joiner S, et al: Tissue distribution of protease resistant prion protein in variant CJD using a highly sensitive immuno-blotting assay. Lancet 358:171–180, 2001 Volume 349:1812-1820 November 6, 2003 Number 19 Methods We used a highly sensitive method of detection — involving the concentration of PrPSc by differential precipitation with sodium phosphotungstic acid, which increased the sensitivity of Western blot analysis by up to three orders of magnitude — to search for PrPSc in extraneural organs of 36 patients with sporadic Creutzfeldt–Jakob disease who died between 1996 and 2002. Results PrPSc was present in the brain tissue of all patients. In addition, we found PrPSc in 10 of 28 spleen specimens and in 8 of 32 skeletal-muscle samples. Three patients had PrPSc in both spleen and muscle specimens. Patients with extraneural PrPSc had a significantly longer duration of disease and were more likely to have uncommon molecular variants of sporadic Creutzfeldt–Jakob disease than were patients without extraneural PrPSc. Conclusions Using sensitive techniques, we identified extraneural deposition of PrPSc in spleen and muscle samples from approximately one third of patients who died with sporadic Creutzfeldt–Jakob disease. Extraneural PrPSc appears to correlate with a long duration of disease. From the Institute of Neuropathology and National Reference Center for Prion Diseases, University Hospital of Zurich, Zurich, Switzerland. Dr. Glatzel and Mr. Abela contributed equally to the article. Address reprint requests to Dr. Aguzzi at the Institute of Neuropathology, University Hospital of Zurich, Schmelzbergstr. 12, CH-8091 Zurich, Switzerland, or at adriano@pathol.unizh.ch . Gabor G. Kovacs, MD PhD 1 2, Elisabeth Lindeck-Pozza, MD 1, Leila Chimelli, MD, PhD 3, Abelardo Q. C. Araújo, MD, PhD 4, Alberto A. Gabbai, MD, PhD 5, Thomas Ströbel, PhD 1, Markus Glatzel, MD 6, Adriano Aguzzi, MD, PhD 6, Herbert Budka, MD 1 * *Correspondence to Herbert Budka, Institute of Neurology, AKH 4J, Wühringer Gürtel 18-20, POB 48, A-1097 Vienna, Austria Funded by: Abstract Pathologicalprion protein (PrPSc) is the hallmark of prion diseases affecting primarily the central nervous system. Using immunohistochemistry, paraffin-embedded tissue blot, and Western blot, we demonstrated abundant PrPSc in the muscle of a patient with sporadic Creutzfeldt-Jakob disease and inclusion body myositis. Extraneural PrPC-PrPSc conversion in Creutzfeldt-Jakob disease appears to become prominent when PrPC is abundantly available as substrate, as in inclusion body myositis muscle. -------------- Received: 16 June 2003; Revised: 11 September 2003; Accepted: 11 September 2003 http://www3.interscience.wiley.com/ http://www.emboreports.org/ http://www.bseinquiry.gov.uk/files/yb/1990/01/19009001.pdf SADLY, it's all about money, to hell with human health; The Economic Impact of BSE on the U.S. Beef Industry: Product Value Losses, Regulatory Costs, and Consumer Reactions snip... 5.4 Expanded Definition of SRM The definition of SRM in other countries with BSE does not typically recognize a 30- month age cut-off for tissues such as brain and spinal cord. When SRM controls were first introduced in the United Kingdom in 1989, the definition included the brain, spinal cord, spleen, thymus, tonsils and intestines of bovine animals aged 6 months or over. Since then, the definition has been expanded many times as more was learned about the disease. As of October 2000, SRM is defined in all European Union countries to include the following tissues (DEFRA): Skull including the brains and eyes, the tonsils, the spinal cord of animals aged over 12 months and the intestines from the duodenum to the rectum of bovine animals of all ages. The following tissues are also designated as SRMs in the United Kingdom and Portugal: The entire head, excluding the tongue, including the brains, eyes, trigeminal ganglia and tonsils; the thymus; the spleen and spinal cord of animals aged over 6 months; and the vertebral column, including dorsal root ganglia, of animals aged over 30 months. A possible extension of current U.S. regulations would be to eliminate or reduce the 30-month age limit in the current definition of SRM. As noted above, the International Review Team recommended that the SRM definition be expanded "unless aggressive surveillance showed the BSE risk to be minimal." If indigenous BSE cases are discovered, it seems likely that this change would occur. Assuming SRM is banned from all animal feed, an expanded SRM definition would increase the cost of the regulation for under 30-month animals – i.e., from $2.16 per head to the estimate of $6.77 per head applicable for older animals.23 http://fss.k-state.edu/research/reports/CoffeyMintertFoxSchroederValentin200504.pdf BY reducing or weakening the SRM list due to the Economic Impact of BSE on the U.S. Beef Industry and while doing so, ignoring all 'sound science', again the FDA/USDA et al are willing to put every human and animal out there at risk to further exposure to this TSE agent, all for a buck. this is not 'sound science' this is what i call 'corporate science', and it is and will continue to expose people. some of these people will die from this agent either directly or indirectly via a multitude of scientific proven routes and sources. WE must remove all political and corporate science from TSE research. I find it disturbing that products that carry SRMs are still on the market for humans such as nutritional supplements ; ODD, I just picked up a catalog from STANDARD PROCESS INC. 2003 - 2004 Product Catalog NATURAL COCOA STANDARDBAR (mad cow candy bar) bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney... NATURAL PEANUT BUTTER STANDARDBAR bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney... USF (MAD COW) OINTMENT (RUB A DUB DUB, KURU ETC) ; bovine orhic glandular extract UTROPHIN PMG bovine uterus PMG VASCULIN bovine heart PMG extract, veal bone PMG extract, bovine liever, porcine duodenum, IPLEX (neighbors mom died from CJD while taking these pills for years) bovine eye PMG extract, veal bone PMG, bovine liver, porcine stomach, bovine adrenal, MYO-PLUS bovine heart PMG, bovine liver, porcine stomach, bovine orchic extract, bovine NEUROPLEX bovine orchic Cytosol extract, bovine spleen, BOVINE BRAIN PMG EXTRACT, NEUROTROPHIN PMG BOVINE BRAIN PMG NIACINAMIDE B6 VM bovine liver, porcine stomach, bovine spleen ovine spleen, OCULOTROPHIN PMG ORCHEX bovine liver, bovine orchic Cytosol extract, porcine stomch, OSTARPLEX veal bone PMG extract, veal bone PMG extract, bovine liver, PARAPLEX bovine pancreas PMG extract, porcine duodenum, bovine adrenal PMG, PITUITROPHIN PMG RUMAPLEX BOVINE BRAIN, veal bone PMG extract, bovine adrenal, bovine prostate SENAPLEX bovine liver PMG extract, bovine adrenal, BOVNE BRAIN, veal bone meal, bovine THESE are just a few of MANY of just this ONE COMPANY. Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice 253 1 DR. BOLTON: I have an additional question about 2 that. What is the assurance that additional locally sourced 3 tracheas are not added into that manufacturing process, thus 4 boosting the yield, if you will, but being returned to the 5 U.S. as being produced from U.S.-sourced raw material? 6 DR. McCURDY: Are there data to indicate how many 7 grams, or whatever, of infected brain are likely to infect 8 an organism, either animal or man, when taken orally? 9 DR. BROWN: If I am not mistaken, and I can be 10 corrected, I think a half a gram is enough in a cow, orally; 11 in other words, one good dietary-supplement pill. 12 DR. McCURDY: What I am driving at is the question 13 we are asked is really not do we wish to regulate these 14 things coming in. I think the statements about difficulties 15 in regulating things in the future or near future for new 16 regulations were probably accurate. 17 But I think that we could exhibit some quite 18 reasonable concern about blood donors who are taking dietary 19 supplements that contain a certain amount of unspecified- 20 origin brain, brain-related, brain and pituitary material. 21 If they have done this for more than a sniff or something 22 like that, then, perhaps, they should be deferred as blood 23 donors. 24 That is probably worse than spending six months in 25 the U.K. 254 1 DR. BROWN: That is exactly right. I think that 2 is why the discussion has apparently been on things that are 3 not directly related to these questions because, in order to 4 think about deferrals for blood donors who are taking 5 dietary supplements with things like bovine brain in them, 6 it is very important that we know that those products are 7 safe. 8 I think we have heard enough to suggest that they 9 may not be. 10 DR. McCURDY: There is one other item that needs 11 to be considered and that is what proportion of blood donors 12 are doing this; that is, how many blood donors would you 13 lose, and I don't know what the demographics--there is 14 fairly good information on the demography of blood donors. 15 I have no idea what the demography of people who take these 16 supplements is. Maybe they are old men like me and aren't 17 going to be blood donors anymore. 18 DR. BROWN: The wording of the question is not as 19 demanding as the wording of other deferral questions; that 20 is, the question here is consider recommending. We are 21 not even recommending at this point. We are saying to the 22 FDA, please think about this. It is worth thinking about. 23 DR. DETWILER: One point about brain from Europe, 24 and Jean Philippe is still here, those are considered 25 specified risk material and it is not correct to be 255 1 incinerated; correct? Or destroyed? Brain and spinal cord 2 and other high-risk tissues in Europe? 3 DR. NORTON: In tomorrow morning's British Medical 4 Journal, which has appeared on-line today, there is an 5 article called U.S. Takes Precautions against BSE. One 6 paragraph says, Even though the U.S. and U.K. governments 7 ban the practice of feeding cattle products to cows, in the 8 early 1990s, some U.K. renderers continued to manufacture 9 and ship contaminated meat and bonemeal around the world. 10 British export statistics show that thirty-seven tons of 11 meal made from offal was sent to the United States in 1997, 12 well after the U.S. government banned imports of such risky 13 meat. The ultimate use of these imports has not been 14 identified. 15 That will appear tomorrow morning. 16 DR. DETWILER: That actually was in The New York 17 Times. That is a direct quote out of The New York Times 18 article. We called the reporter on that. That statement, 19 the thirty-seven tons, was taken out of the U.S. 20 Geographical BSE Risk Assessment. What they didn't put in 21 there, in the statement, was the remainder of the GBR is at 22 that time, the big labeling for that category in the U.K., 23 because it was illegal for them to ship it to us from their 24 own regs. It is illegal for us to get that. 25 We did go and try and trace that so that wasn't [FULL TEXT ABOUT 600 PAGES] 3681t2.rtf http://www.fda.gov/ohrms/dockets/ac/cber01.htm http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm IN fact, we are now finding that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE ; Published online January 27, 2005 Risk of oral infection with bovine spongiform encephalopathy agent in primates Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)—which can lead to variant Creutzfeldt-Jakob disease (vCJD)—is compounded by incomplete knowledge about the ef.ciency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these .ndings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man. snip... BSE bovine brain inoculum 100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg Primate (oral route)* 1/2 (50%) Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%) RIII mice (icip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%) PrPres biochemical detection The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the .rst positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal. Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula snip...end www.thelancet.com Published online January 27, 2005 THEN you must consider cross contamination at feed mills and such. this has been well proven in both the UK and the USA to date via r-to-r feed ban violations. IT was proven in the UK that they indeed put profits before human health; [PDF] The BSE Inquiry / Statement No. 14 Issued 20 March 1998 THE ... http://www.bseinquiry.gov.uk/files/ws/s014.pdf [PDF] The BSE Inquiry / Statement No 76F (Supplementary) Mr Alan ... http://www.bseinquiry.gov.uk/files/ws/s076f.pdf STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995 snip... To minimise the risk of farmers' claims for compensation from feed To minimise the potential damage to compound feed markets through adverse publicity. To maximise freedom of action for feed compounders, notably by snip... THE FUTURE 4.......... MAFF remains under pressure in Brussels and is not skilled at 5. Tests _may_ show that ruminant feeds have been sold which 6. The threat remains real and it will be some years before feed SEE full text ; http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf ##################### Bovine Spongiform Encephalopathy ##################### From: TSS () Consumer Health WASHINGTON, DC, United States (UPI) -- The federal meat inspector who was charged with misconduct by the U.S. Department of Agriculture after he claimed mad cow disease safeguards were being violated at slaughterhouses told United Press International he plans to file charges against the agency. Stan Painter, a USDA inspector and chair of the National Joint Council of Food Inspection Locals, the inspectors union, notified the agency`s management in a letter last December he was aware of instances where the riskiest parts of older cows were not being marked or removed from processing. Painter worried these risky parts -- known as specified risk materials, or SRMs -- could enter the food supply and infect people, causing a fatal brain illness called variant Creutzfeldt Jakob disease. Two cases of mad cow have been detected in U.S. herds, and some suspect there are more. The USDA put the SRM safeguards in place in 2004 to protect the public from mad cow disease -- also known as bovine spongiform encephalopathy or BSE -- if more cases are detected. The USDA did not respond to Painter`s concerns until he made his letter known to news outlets. On Dec. 28, 2004, the agency charged Painter with personal misconduct for not revealing the names of the inspectors who told him of the SRM violations. Officials also told him he was under a formal investigation, which was dropped last month after the release of internal documents revealing more than 1,000 violations of the USDA`s SRM regulations. Painter said he thinks the USDA was attempting 'to harass and intimidate him (and) to have a chilling effect' on other inspectors. 'I plan to file charges against the agency,' he told UPI, adding he has not yet decided if he will go through the legal system, through internal USDA procedures or another avenue. Asked about Painter`s intent to bring charges, agency spokesman Steven Cohen told UPI the documents -- called noncompliance reports, or NRs -- demonstrate 'that BSE safeguard regulations are being enforced and prohibited materials did not reach the public.' Mad cow disease remains a sensitive topic for the USDA because it can have significant economic ramifications. The U.S. beef industry lost billions of dollars because more than 60 nations closed their borders in 2003 to American beef after the report of the first detected case in U.S. herds. Japan, formerly the largest importer of American beef, still has not reopened its borders. For months, USDA officials denied Painter`s allegations in media reports, saying they had investigated and found no evidence to substantiate his claims. The NRs released last month under the Freedom of Information Act, however, showed 1,036 violations of SRM regulations in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. The USDA delayed releasing the documents for eight months despite a federal law mandating a response within 30 days. Patty Lovera, of the watchdog group Public Citizen, which requested the USDA documents, said some of the violations cited in the NRs are egregious. In one, an employee at a plant in Michigan was not properly marking older cows to have their SRMs removed because he did not have a pencil. In another, an employee in a Missouri plant was loading cow heads onto his pickup truck to take home to feed to his dog. Lovera charged the USDA with attempting to silence Painter and failing to address problems with the SRM ban. 'Their behavior through this whole thing is appalling,' she told UPI. 'Stan brought them concerns about a policy and instead of investigating the policy, they investigated him.' Last December, after Painter made his letter known publicly, the USDA sent an officer to Painter`s house while he was on leave to question him about the allegations in his letter. Later, USDA officials interrogated Painter twice, asking him for the names of the inspectors who told him about the violations. Painter said he intentionally was kept ignorant of the inspectors` names because he feared the agency would retaliate against them. Painter also said USDA officials did not need the inspectors` names because they could determine where the infractions were occurring by looking at their database of NRs. Sometime around June the U.S. Embassy in Japan posted a notice on its Web site stating USDA officials had found no evidence to substantiate Painter`s claims and had requested a criminal investigation into his actions. The notice was removed in July after UPI reported its existence. Although Cohen acknowledged more than 1,000 NRs were written by USDA inspectors, he minimized their significance, saying they 'amount to less than one-half of one percent of the total written for all reasons by (USDA) inspection program personnel.' Lovera said any infraction of mad cow safeguards should be of concern, because this disease always is fatal in humans and cooking does not destroy the pathogen. 'You have very little margin of error for something you don`t want to get because you can`t cook it away and you can`t disinfect it,' she said. Painter said his concern now is what the agency will do to fix what he sees as shortcomings in the SRM policy. 'It`s a failed policy,' he said. 'It doesn`t protect the consumer.' Cohen did not respond to whether the USDA planned to change the SRM regulations. The USDA`s Office of Inspector General has launched an investigation to determine whether the regulations are being implemented effectively, and results are due out soon. E-mail: sciencemail@upi.com Copyright 2005 by United Press International makes no difference, GW will change the SRM rules like he has the BSE GBR risk assessment to the terribly flawed BSE MRR policy, the legal trading of all strains of TSE, the 'gold card'. ...TSS IN a time when FDA/USDA et al should be strengthening the TSE regulations, it seems corporate interest has won out again over sound science and consumer protection from an agent that is 100% fatal for the ones that go clinical. With the many different atypical TSEs showing up in different parts of the world, and with GWs BSE MRR policy (the legal policy of trading all strains of TSEs), the battle that has waged for the last 25 years to eradicate this agent from this planet will be set back decades, if not lost for good. ...TSS Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission) https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt Docket Management Docket: 02N-0273 - Substances Prohibited From Use in Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed Comment Number: EC -10 Accepted - Volume 2 PART 2 PDF]Freas, William TSS SUBMISSION File Format: PDF/Adobe Acrobat - Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ... http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf Asante/Collinge et al, that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD; http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt # Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of Docket Management Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr. www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2. 03N-0009 Federal Preemption of State & Local Medical Device Requireme. ... Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater Comment Number: EC -1 Accepted - Volume 1 ... 00D-1662 Use of Xenotransplantation Products in Humans. http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm 2003D-0186 01N-0423 Substances Prohibited from use in animal food/Feed Ruminant APE 5 National Renderers Association, Inc. Vol#: 2 APE 6 Animal Protein Producers Industry Vol#: 2 APE 7 Darling International Inc. Vol#: 2 EMC 1 Terry S. Singeltary Sr. Vol#: 3 http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htm Send Post-Publication Peer Review to journal: disease in the United States I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc? LANCET INFECTIOUS DISEASE JOURNAL My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem. largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation. occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally , he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source. region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle. transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive. is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk. issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE. teeth , Singeltary argues. You get it when they want you to have it, and only what they want you to have. University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings ; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure . The USA should develop a system modelled on that established in the UK, he points out. Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans ; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further . Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison. the [Samii] cases because there is no evidence that the men ate CWD-infected meat . He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited . Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source. <<< actually, that quote was from a more recent article in the Journal of Neurology (see below), not the JAMA article... Full Text Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama BRITISH MEDICAL JOURNAL SOMETHING TO CHEW ON BMJ http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2 BMJ http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1 THE PATHOLOGICAL PROTEIN BY Philip Yam Yam Philip Yam News Editor Scientific American www.sciam.com IN light of Asante/Collinge et al findings that BSE transmission to the -------- Original Message -------- Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43 -0000 From: "Asante, Emmanuel A" To: Dear Terry, I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention. Thank you for your interest in the paper. In respect of your first question, the simple answer is, yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc. I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes. Emmanuel Asante <> ____________________________________ Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now) ____________________________________ snip... full text ; http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm Creutzfeldt-Jakob disease THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*, Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger ] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible http://www.pnas.org/cgi/content/full/041490898v1 Characterization of two distinct prion strains http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471 ALL human TSEs must be made reportable Nationally and Internationally, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
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