Interference at the EPA Science

Rick Perry, Texas, BSE aka mad cow disease, CJD, and 12 years of lies there from

2011-08-28T10:19:00.000-07:00

Rick Perry, Texas, BSE aka mad cow disease, CJD, and 12 years of lies there from

Greetings,

I am sure that most of you are aware of the Texas mad cow cases that were covered up. the 1st documented cover-up was successful, the second documented case of mad cow in Texas would have been successful, but after literally, an act of Congress to override Austin, Texas officials (rick perry), only after the Honorable Fong of the OIG, and scientist all over the world, and a few others, including myself wrote to the OIG about said cover-up, and 7 months later, did they finally retest that covered-up highly suspect mad cow, and said covered up mad cow was finally _confirmed_ by Weybridge as a confirmed Texas BSE mad cow case. this 7 months after the fact on a Government BSE REDBOOK regulations of a 48 turn around on said test. over course this was all done for a reason, the BSE MRR policy was being put into place while all this was going on, and Heaven forbid if rick perry would have had a confirmed BSE mad cow case while those regulations were over riding the BSE GBR risk assessments. however, during all this political science on mad cow disease, it was nothing more than a crap shoot, and 15 years later, we now know that some of the sporadic CJD cases are indeed tied to the atypical BSE cases here in North America. How many people during the Bush/Perry era, how many did they needlessly expose to mad cow disease? how many will go clinical and die in the decades to come? Whether or not you dare care, during the Bush/Perry era, they exposed our kids to mad cow disease, by feeding them dead stock downer cows via the NSLP, for over 4 years. DEAD STOCK DOWNER COWS ARE THE MOST HIGH RISK COW FOR MAD COW DISEASE. WHO will watch the children for the next 5 decades for CJD ???

Rick Perry, Texas, BSE aka mad cow disease, CJD, and 15 years of lies there from

FRIDAY April 5, 1996

Cookout Serves Up Praise of U.S. Beef Los Angeles Times (LT) - FRIDAY April 5, 1996 State agriculture officials, undaunted by the mad cow scare sweeping Europe, held an impromptu cookout to hail the safety of U.S. beef. Munching on smoked brisket at a popular barbecue spot in Austin, Texas Agriculture Commissioner Rick Perry criticized the media for stoking fears among domestic beef consumers. The agricultural commissioner said evidence that bovine spongiform encephalopothy, known as BSE, will cause human brain disorders was "circumstantial" and that the issue has been politicized in Britain and Europe.

Separately, the U.S. beef industry is considering as an option a promotional campaign in Europe touting American beef as free of the disease, an export official said. "We'll look at all the options, and that'd certainly be one of them on the table," said Thad Lively, economist at the U.S. Meat Export Federation, an association of U.S. meat exporters based in Denver.

http://www.mad-cow.org/~tom/US_beef_sum.html#Cookout

Texas AG won't sue Howard Lyman over mad cow remarks

--------------------------------------------------------------------------------

AUSTIN, Texas (May 2, 1996 7:11 p.m. EDT)

-- Attorney General Dan Morales on Thursday rejected Agriculture Commissioner Rick Perry's request to use the state's new "veggie libel" law to go after a vegetarian who said mad cow disease could affect America's beef supply.

Though Morales labeled the comments "baloney," he said the law does not allow the state to file suit under the law approved last year by lawmakers to protect against people who make false claims about the safety of food products. Any such lawsuit would have to be filed by a private individual who feels his or her products have been unfairly disparaged, Morales said.

At issue are remarks made during an April 19 appearance on "The Oprah Winfrey Show" by Howard Lyman of Maryland, a former cattle rancher now with the Eating with Conscience Campaign, a project of the Humane Society of America. Lyman said on the show that mad cow disease "will make AIDS look like the common cold," and that the livestock industry is feeding "road kill" to cattle. A day later, cattle futures plummeted on the Chicago Mercantile Exchange.

Perry was enraged, and urged Morales to file suit against Lyman.

Can't do, said Morales, who also recommended a lower-key response to Lyman.

"Mr. Lyman's statements should be taken for what they are -- baloney," he told Perry. "The more public attention focused upon his outrageous claims, the greater the prospects for real harm being done to our beef industry. I suggest we simply ignore this foolishness."

Perry said he was disappointed in Morales' response.

"The letters and phone calls the Texas Department of Agriculture has received from folks who make their living from the land and who are suffering from these false statements tell us that they support our efforts to stop the inaccuracies and innuendo about our $6 billion industry," he said.

Mad cow disease (bovine spongiform encephalopathy) has been detected in cattle in Great Britain, but it has not been diagnosed in Texas. Perry and other agriculture officials say there is no scientific link between mad cow disease and the human disease (Creutzfeldt-Jakob Disease) that killed several Britons.

Copyright © 1996 Nando.net Copyright © 1996 Cox News Service

http://www.mad-cow.org/~tom/free_speech.html#fut

Gov. Perry Responds to Mad Cow Confirmation

AUSTIN – Gov. Rick Perry issued the following statement concerning confirmation from the USDA that a single cow in Texas has tested positive for BSE or Mad Cow:

“I want to urge calm and reassure the public that they can have the highest confidence in our beef supply, and the safeguards we have in place to protect the public from the spread of BSE. I, for one, will continue to eat red meat, and intend to do so later tonight with complete confidence it is safe to do so.”

“We have had plans in place for more than a decade to address a confirmed case of Mad Cow disease to ensure it is contained and kept out of the food supply. Working with federal officials, all precautions are being taken to protect the public.”

“We have been given no specific information from USDA on the origin of the cow that tested positive for BSE other than it came from a Texas herd.”

http://www.kcbd.com/story/3538951/gov-perry-responds-to-mad-cow-confirmation

Statement of Gov. Rick Perry on BSE Announcement

Thursday, June 30, 2005 • Press Release

AUSTIN – Gov. Rick Perry issued the following statement today on the announcement by the U.S. Department of Agriculture that a cow recently tested for Bovine Spongiform Encephalopathy – commonly known as mad cow disease – is from a Texas herd.

“I want to urge calm and reassure the public that they can have the highest confidence in our beef supply, and the safeguards we have in place to protect the public from the spread of BSE. There is not, nor has there ever been, a known instance of BSE contaminating the food supply in Texas or anywhere else in the United States.

The animal in question was not processed into food or any other product. Texans can be sure that the beef they buy at their local supermarkets or restaurants is as safe today as it was yesterday, and I encourage Texans to continue to enjoy Texas beef products.”

http://governor.state.tx.us/news/press-release/3287/

Section 2. Testing Protocols and Quality Assurance Controls

In November 2004, USDA announced that its rapid screening test, Bio-Rad Enzyme Linked Immunosorbent Assay (ELISA), produced an inconclusive BSE test result as part of its enhanced BSE surveillance program. The ELISA rapid screening test performed at a BSE contract laboratory produced three high positive reactive results.40 As required,41 the contract laboratory forwarded the inconclusive sample to the APHIS National Veterinary Services Laboratories (NVSL) for confirmatory testing. NVSL repeated the ELISA testing and again produced three high positive reactive results.42 In accordance with its established protocol, NVSL ran its confirmatory test, an immunohistochemistry (IHC) test, which was interpreted as negative for BSE. In addition, NVSL performed a histological43 examination of the tissue and did not detect lesions44 consistent with BSE.

Faced with conflicting results, NVSL scientists recommended additional testing to resolve the discrepancy but APHIS headquarters officials concluded no further testing was necessary because testing protocols were followed. In our discussions with APHIS officials, they justified their decision not to do additional testing because the IHC is internationally recognized as the "gold standard." Also, they believed that conducting additional tests would undermine confidence in USDA’s established testing protocols.

http://www.usda.gov/oig/webdocs/50601-10-KC.pdf

USDA orders silence on mad cow in Texas

Susan Combs by no means has public and consumer health at heart while she is protecting the cattle industry. She is oblivious to mad cow disease. Her soul purpose is to protect the cattle industry at all cost, including my mothers life (DOD 12/14/97), or maybe one of your family members from any strain of mad cow disease in TEXAS. SHE helped cover-up mad cow disease in TEXAS both on that inconclusive that was positive so many times it will make your head spin. PLUS, the other mad cow in TEXAS they rendered without testing at all, that came from the top out of Austin. THEY should be tried for murder. corporate homicide is what i call it. they knew for years, but kept on keeping on.

http://madcowtesting.blogspot.com/2007/10/bse-base-mad-cow-testing-texas-usa-and.html

Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE)

Date: June 21, 2007 at 2:49 pm PST

Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.

snip...

Topics that will be covered in ongoing or planned reviews under Goal 1 include:

soundness of BSE maintenance sampling (APHIS),

implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),

snip...

The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.

4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half

http://www.usda.gov/oig/webdocs/sarc070619.pdf

Texas BSE Investigation Final Epidemiology Report August 2005

Executive Summary

In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.

Background of the Investigation

On June 10, 2005, USDA announced that the November 2004 inconclusive BSE sample tested positive on SAF immunoblot. The SAF immunoblot was run at USDA’s National Animal Disease Center (NADC) upon the recommendation of USDA’s Office of the Inspector General. Samples were sent to a World Organization for Animal Health (OIE) reference laboratory for BSE in Weybridge, England, for confirmatory tests. Farm A, located in Texas, was the suspected farm of origin for the index cow and was placed under hold order on June 20, 2005 pending confirmation of the positive results and DNA analysis of the herd. Weybridge confirmed the BSE positive on June 24, 2005. The carcass of the index cow had been disposed of by incineration in November 2004.

http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/bse_final_epi_report8-05.pdf

News Release

Texas Animal Health Commission

Box l2966 * Austin, Texas 78711 * (800) 550-8242 * FAX (512) 719-0719

Bob Hillman, DVM * Executive Director

For info, contact Carla Everett, information officer, at 1-800-550-8242, ext. 710, or mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000388/!x-usc:mailto:ceverett@tahc.state.tx.us

For immediate release---

State-Federal Team Responds to Texas BSE Case

The US Department of Agriculture announced June 29 that genetic testing has verified that an aged cow that tested positive for Bovine Spongiform Encephalopathy or BSE originated from a Texas beef cattle herd. Tissues for laboratory testing were initially collected from the animal in November 2004, and the carcass was incinerated and did not enter the human food, animal feed or fertilizer supply system. While tests in November indicated the animal did not have BSE, retesting in England in June confirmed the animal had the disease. The Texas Animal Health Commission (TAHC), the state’s livestock and poultry health regulatory agency, and USDA have jointly assigned a state-federal team to conduct the epidemiological investigation and response.

“The TAHC and US Department of Agriculture’s Veterinary Services are working with a complement of experts from federal and state animal health, food safety, public health and feed regulatory agencies to ensure the continued safety and wholesomeness of our meat supply,” said Dr. Bob Hillman, Texas state veterinarian and executive director of the TAHC, the state’s livestock and poultry health regulatory agency. “Epidemiological investigations are thorough and focus on verifying the herd of origin, and when, where and how the animal and potentially, any herd mates, were exposed to the abnormal prion, or disease agent, that causes BSE. Additionally, epidemiology investigations trace the infected animal’s movement and herd mates. Animals potentially exposed to the disease will be depopulated, with proper disposal. The animals will not be introduced into the human or animal food chain.”

The USDA’s BSE testing protocol requires testing of emaciated or injured cattle, cattle that exhibit central nervous system disorder, cattle unable to rise or to walk normally, and cattle that die of unknown causes. Since June 1, 2004, brain tissue samples from more than 394,000 cattle have been tested in the U.S. and were negative for BSE. Of those, 38,320 were tested in Texas, Dr. Hillman noted. BSE surveillance has been conducted in the U.S. since l990.

The U.S. has taken preventive measures against the introduction of BSE since l989, when prohibitions were placed on cattle and other ruminants from BSE-affected countries, noted Dr. Hillman. In 1997, the importation ban was extended to all of Europe.

Dr. Hillman said the U.S. Food and Drug Administration (FDA) in 1997 banned the use of ruminant-derived protein (from animals such as cattle and sheep) in feed for cattle and other ruminants. There is no evidence that BSE spreads from live animal to animal in the herd, but cattle can be exposed by eating feed that contains rendered protein from infected animals. “These measures taken by the USDA and the FDA are safeguards that work to protect livestock, and ultimately, our meat supply,” he said.

--30--

http://www.tahc.state.tx.us/news/pr/2005/2005Jun30_BSE_Positive_Results.pdf

Second BSE case occurred in Texas, USDA says Jun 30, 2005 (CIDRAP News) – The United States' second case of bovine spongiform encephalopathy (BSE) was in a 12-year-old cow that came from a Texas herd and would have been made into pet food if it hadn't been flagged for BSE testing, federal officials announced yesterday evening.

US Department of Agriculture (USDA) officials said the cow was to be processed at a pet food plant in Waco, Tex., when it was diverted for testing because it couldn't walk. Officials didn't name the plant or say exactly where the cow came from. But an Associated Press (AP) report today identified the plant as Champion Pet Food in Waco and said the cow was already dead when brought there last November.

"The source herd is now under a hold order as we identify animals of interest within the herd," USDA Chief Veterinarian John Clifford said in a prepared statement. Investigators will look for cattle born within a year before or after the BSE-infected cow and any of the cow's offspring born within the past 2 years, he explained.

"If the age of the animal cannot be pinpointed, then we may expand our inquiry to include all animals in this herd before the feed ban went into place in 1997," Clifford said. To prevent BSE, the government banned putting cattle protein into cattle feed in August 1997.

The infected cow was incinerated, and no parts were used in human food or animal feed, according to the USDA. "The safety of our food supply is not in question," Clifford stated.

Because of the cow's age, the USDA suspects it became infected by eating contaminated feed before the government ban began in 1997. The USDA and the Food and Drug Administration (FDA) will try to trace the source herd's feed history, officials said.

The FDA will also check whether firms that may have processed meat-and-bone meal from animals from that herd have complied with the 1997 feed ban, Dr. Steve Sundlof, director of the FDA's Center for Veterinary Medicine, said at a news conference last night.

The Texas case is the first US BSE case in a native-born animal; Clifford said the cow lived on one farm all its life. The previous US case, found in December 2003, involved a Canadian-born dairy cow in Washington state.

An initial screening test on the Texas cow last November was inconclusive, and two confirmatory immunohistochemistry tests were negative. But early this month the USDA's inspector general ordered a Western blot test, which came back positive. Further confirmatory tests at an international reference lab in Britain were also positive, prompting the USDA to announce the findings last week.

The USDA waited for the results of DNA tests before announcing that the infected cow came from Texas. The step was necessary because parts of the infected cow were stored with those of four other cattle, causing some uncertainty, officials said.

"We felt that we had the correct herd; we wanted to identify that appropriately with DNA," Clifford said at the news conference. Investigators analyzed DNA from the infected animal and then looked for relatives in the presumed source herd by analyzing DNA from members of the herd, he said. The investigation turned up two cattle that are related to the infected cow, he added.

The AP report said Champion Pet Food is under contract to take samples from animals in poor health. The company's owner, Benjy Bauer, told the AP that his workers took samples from the cow and sent them to the Texas Veterinary Diagnostic Laboratory at Texas A&M University. The lab is one of several the USDA uses to screen cattle for BSE, the story said.

See also:

USDA news release http://www.aphis.usda.gov/lpa/issues/bse/BSE_statement6-29-05.pdf

USDA fact sheet on BSE epidemiologic investiation

http://www.usda.gov/documents/FactSheetbse062905.pdf

USDA press conference transcript

https://www.cidrap.umn.edu/cidrap/content/other/bse/news/june3005bse.html

THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;

CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006

In an article today for United Press International, science reporter Steve Mitchell writes:

Analysis: What that mad cow means

By STEVE MITCHELL UPI Senior Medical Correspondent

WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.

The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.

Despite this, Brown said the U.S. prevalence of mad cow, formally known as bovine spongiform encephalopathy, or BSE, did not significantly threaten human or cattle health.

"Overall, my view is BSE is highly unlikely to pose any important risk either in cattle feed or human feed," he said.

However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers should be troubled by the USDA's secrecy and its apparent plan to dramatically cut back the number of mad cow tests it conducts.

"Consumers should be very concerned about how little we know about the USDA's surveillance program and the failure of the USDA to reveal really important details," Halloran told UPI. "Consumers have to be really concerned if they're going to cut back the program," she added.

Last year the USDA tested more than 300,000 animals for the disease, but it has proposed, even in light of a third case, scaling back the program to 40,000 tests annually.

"They seem to be, in terms of actions and policies, taking a lot more seriously the concerns of the cattle industry than the concerns of consumers," Halloran said. "It's really hard to know what it takes to get this administration to take action to protect the public."

The USDA has insisted that the safeguards of a ban on incorporating cow tissue into cattle feed (which is thought to spread the disease) and removal of the most infectious parts of cows, such as the brain and spinal cord, protect consumers. But the agency glosses over the fact that both of these systems have been revealed to be inadequately implemented.

The feed ban, which is enforced by the Food and Drug Administration, has been criticized by the Government Accountability Office in two reports, the most recent coming just last year. The GAO said the FDA's enforcement of the ban continues to have weaknesses that "undermine the nation's firewall against BSE."

USDA documents released last year showed more than 1,000 violations of the regulations requiring the removal of brains and spinal cords in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. In addition, a violation of similar regulations that apply to beef exported to Japan is the reason why Japan closed its borders to U.S. beef in January six weeks after reopening them.

Other experts also question the adequacy of the USDA's surveillance system. The USDA insists the prevalence of mad cow disease is low, but the agency has provided few details of its surveillance program, making it difficult for outside experts to know if the agency's monitoring plan is sufficient.

"It's impossible to judge the adequacy of the surveillance system without having a breakdown of the tested population by age and risk status," Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments, told UPI.

"Everybody would be happier and more confident and in a sense it might be able to go away a little bit for (the USDA) if they would just publish a breakdown on the tests," Mumford added.

UPI requested detailed records about animals tested under the USDA's surveillance plan via the Freedom of Information Act in May 2004 but nearly two years later has not received any corresponding documents from the agency, despite a federal law requiring agencies to comply within 30 days. This leaves open the question of whether the USDA is withholding the information, does not have the information or is so haphazardly organized that it cannot locate it.

Mumford said the prevalence of the disease in U.S. herds is probably quite low, but there have probably been other cases that have so far gone undetected. "They're only finding a very small fraction of that low prevalence," she said.

Mumford expressed surprise at the lack of concern about the deadly disease from American consumers. "I would expect the U.S. public to be more concerned," she said.

Markus Moser, a molecular biologist and chief executive officer of Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is that if people are infected, the mad cow pathogen could become "humanized" or more easily transmitted from person to person.

"Transmission would be much easier, through all kinds of medical procedures" and even through the blood supply, Moser said.

© Copyright 2006 United Press International, Inc. All Rights Reserved

http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r

http://www.upi.com/Science_News/2003/12/30/Mad-Cow-Linked-to-thousands-of-CJD-cases/UPI-47861072816318/

CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...

http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm

PAUL BROWN COMMENT TO ME ON THIS ISSUE

Tuesday, September 12, 2006 11:10 AM

"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS

http://madcowtesting.blogspot.com/2009/07/mad-cow-cover-up-usa-masked-as-sporadic.html

OR, what the Honorable Phyllis Fong of the OIG found ;

Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program Â Phase II and Food Safety and Inspection Service

Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III

Report No. 50601-10-KC January 2006

Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain

http://www.usda.gov/oig/webdocs/50601-10-KC.pdf

FDA STATEMENT FOR IMMEDIATE RELEASE May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA

Statement on Texas Cow With Central Nervous System Symptoms

On Friday, April 30th, the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.

FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.

FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.

Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).

FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.

To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.

Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.

FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.

#

http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2004/ucm108292.htm

SEE FULL TEXT OF ALL THIS HERE ;

2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006

http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html

ALABAMA MAD COW CASE

http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/EPI_Final5-2-06.pdf

http://www.cdc.gov/ncidod/dvrd/bse/news/alabama_cow_031506.htm

Saturday, August 14, 2010

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

(see COPIOUS AMOUNTS OF mad cow feed in COMMERCE IN ALABAMA...TSS)

http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html

Texas BSE Investigation Final Epidemiology Report August 2005

http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/bse_final_epi_report8-05.pdf

State-Federal Team Responds to Texas BSE Case

JUNE 30, 2005

(please note 7+ month delay in final confirmation so the BSE MRR policy could be set in stone first. $$$...tss)

http://www.tahc.state.tx.us/news/pr/2005/2005Jun30_BSE_Positive_Results.pdf

https://www.cidrap.umn.edu/cidrap/content/other/bse/news/june3005bse.html

SEE ATTEMPTED COVER-UP BEFORE THE END AROUND BY FONG ET AL OF THE O.I.G

The U.S. Department of Agriculture confirmed June 29 that genetic testing had verified bovine spongiform encephalopathy (mad cow disease) in a 12-year-old cow that was born and raised in a Texas beef cattle herd.

Subsequent epidemiological investigations resulted in the culling and testing of 67 adult animals from the index herd. Bio-Rad tests for BSE were conducted on all 67 animals by the National Veterinary Services Laboratory (NVSL) in Ames, Iowa. All tests were negative.

On July 12, Texas officials lifted the quarantine on the source herd. At press time, USDA's Animal and Plant Health Inspection Service was tracing animals of the same age that had left the ranch.

Timeline

The BSE-positive animal was a Brahman-cross cow born and raised in a single Texas herd. The location of the ranch was not disclosed.

On Nov. 11, 2004, the 12-year-old cow was taken to a Texas auction market. Because of its condition, the cow was sent to Champion Pet Foods in Waco, Texas. The company produces several blends of dog food, primarily for the greyhound industry.

On Nov. 15, the animal arrived dead at Champion. Under procedures established by USDA's intensive surveillance program, a sample was sent to the USDA-approved Texas Veterinary Medical Diagnostic Testing Laboratory (TVMDL) at Texas A&M University.

Between June 1, 2004, and June 1, 2005, TVMDL tested nearly 34,000 samples from Texas, New Mexico, Arkansas and Louisiana. They tested the sample from Champion on Nov. 19 using a Bio-Rad ELISA rapid test for BSE. Initial results were inconclusive.

Because of the inconclusive results, a representative from USDA took the entire carcass to TVMDL where it was incinerated. USDA's Animal and Plant Health Inspection Service (APHIS) began tracing the animal and herd.

The sample was then sent to the National Veterinary Services Laboratory for further testing. Two Immunohistochemistry (IHC) tests were conducted and both were negative for BSE. At that point APHIS stopped their trace.

USDA scientists also ran an additional, experimental IHC "rapid" tissue fixation test for academic purposes. This test has not been approved internationally.

Some abnormalities were noted in the experimental test, but because the two approved tests came back negative, the results were not reported beyond the laboratory.

Monitoring by OIG

USDA's Office of Inspector General (OIG) has been monitoring implementation of the BSE expanded surveillance program and evaluating the following:

* Effectiveness of the surveillance program;

* Performance of BSE laboratories in complying with policies and procedures for conducting tests and reporting results;

* Enforcement of the ban on specified risk materials in meat products;

* Controls to prevent central nervous system tissue in advanced meat recovery products;

* Ante mortem condemnation procedures; and

* Procedures for obtaining brain tissue samples from condemned cattle.

While reviewing voluminous records, OIG auditors noticed conflicting test results on one sample-rapid inconclusive, IHC negative, experimental reactive.

Sample retested

At the recommendation of the Inspector General, the sample was retested during the week of June 5 with a second confirmatory test, the Western Blot. The results were reactive.

USDA scientists then conducted an additional IHC confirmatory test, using different antibodies from the November 2004 test. On Friday, June 10, Secretary of Agriculture Mike Johanns publicly announced the results as a "weak positive."

On June 16 an official with USDA's National Veterinary Services Laboratory hand-carried samples for further testing to the Veterinary Laboratory Agency (VLA) in Weybridge, England. Since 1991, the VLA has been a BSE reference laboratory for the World Organization for Animal Health (OIE).

Experts from the Weybridge lab confirmed the accuracy of the results of USDA's November confirmatory IHC test, concurring that the case could not have been confirmed on the basis of this sample. They also examined the November experimental IHC test and interpreted the results to be positive.

Weybridge also conducted additional tests, including IHC, OIE-prescribed Western Blot, NaTTA Western Blot and Prionics Western Blot tests.

To better understand the conflicting results, USDA also conducted Bio-Rad and IDEXX rapid screening tests, IHC and OIE-prescribed Western Blot. USDA also used DNA sequencing to determine the prion protein gene sequence of the animal.

http://findarticles.com/p/articles/mi_qa5420/is_200508/ai_n21377094

Texas even had a 'secret' test that showed that mad cow positive; experimental IHC test results, because the test was not a validated procedure, and because the two approved IHC tests came back negative, the results were not considered to be of regulatory significance and therefore were not reported beyond the laboratory. . A Western blot test conducted the week of June 5, 2005, returned positive for BSE.

http://www.usda.gov/documents/vs_bse_ihctestvar.pdf

48 hr BSE confirmation turnaround took 7+ months to confirm this case, so the BSE MRR policy could be put into place. ...TSS

-------- Original Message --------

Subject: re-USDA's surveillance plan for BSE aka mad cow disease

Date: Mon, 02 May 2005 16:59:07 -0500

From: "Terry S. Singeltary Sr."

To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us

Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at OIG, ...............

snip...

There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...

Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 xxx xxx xxxx

Date: June 14, 2005 at 1:46 pm PST

In Reply to:

Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results

posted by TSS on June 13, 2005 at 7:33 pm:

Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns. Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected. just pondering... TSS

MAD COW IN TEXAS NOVEMBER 2004. ...TSS

-------- Original Message --------

Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

Date: Mon, 22 Nov 2004 17:12:15 -0600

From: "Terry S. Singeltary Sr."

To: Carla EverettReferences: [log in to unmask]; [log in to unmask] ;

Greetings Carla, still hear a rumor;

Texas single beef cow not born in Canada no beef entered the food chain?

and i see the TEXAS department of animal health is ramping up for something, but they forgot a url for update?

I HAVE NO ACTUAL CONFIRMATION YET...

can you confirm??? terry

============================================================

-------- Original Message --------

Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

Date: Fri, 19 Nov 2004 11:38:21 -0600

From: Carla Everett

To: "Terry S. Singeltary Sr."References;[log in to unmask];

The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas.

Carla

At 09:44 AM 11/19/2004, you wrote:

Greetings Carla,

i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from

TEXAS. can you comment on this either way please?

thank you,

Terry S. Singeltary Sr

======================================

-------- Original Message --------

Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

Date: Mon, 22 Nov 2004 18:33:20 -0600

From: Carla Everett

To: "Terry S. Singeltary Sr."References: <[log in to unmask]><[log in to unmask] us><[log in to unmask]> <[log in to unmask]us> <[log in to unmask]>

our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.

At 06:05 PM 11/22/2004,

you wrote:

why was the announcement on your TAHC site removed?

Bovine Spongiform Encephalopathy:

November 22: Press Release title here

star image More BSE information

terry

Carla Everett wrote:

no confirmation on the U.S.'inconclusive test...

no confirmation on location of animal. ;

FROM HERE, IT TOOK 7 MONTHS TO CONFIRM THIS MAD COW, while the BSE MRR policy was being bought and sold...(in my opinion...tss)

http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html

http://madcowtesting.blogspot.com/

Saturday, August 16, 2008

Qualitative Analysis of BSE Risk Factors in the United States February 13, 2000 at 3:37 pm PST (BSE red book)

http://bseusa.blogspot.com/2008/08/qualitative-analysis-of-bse-risk.html

TEXAS OFFICIALS DEAD WRONG ON AMOUNT OF INFECTIVITY TO CAUSE A TSE PRION DISEASE ;

"FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams – approximately a quarter ounce — of prohibited material. These animals weigh approximately 600 pounds."

5.5 GRAMS OF INFECTIOUS PROHIBITED MAD COW FEED FOR EACH OF THE 1,222 ANIMALS (5.5 GRAMS X 1,222 ANIMALS) IS ENOUGH INFECTIOUS MAD COW FEED TO KILL A SMALL HERD OF COWS...TSS

U.S. Food and Drug Administration FDA News | Today the Food and Drug Administ…U.S. Food and Drug Administration FDA News

Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle — a violation of FDA’s 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams – approximately a quarter ounce — of prohibited material. These animals weigh approximately 600 pounds.

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA’s Acting Principal Deputy Commissioner, “The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture’s (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE.”

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.

http://www.usmef.org/news-statistics/press-releases/us-food-and-drug-administration-fda-news-today-the-food-and-drug-administ-13375/

FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242 Consumer Inquiries: 888-INFO-FDA

FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT

Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.

http://www.fda.gov/bbs/topics/news/2001/new00752.html

PRION 2009 CONGRESS BOOK OF ABSTRACTS

O.4.3

Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission

Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany

Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).

Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.

Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.

Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.

Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.

http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf

P04.27

Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route

Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany

Background:

In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.

Aims:

The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.

Methods:

Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).

Results:

In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.

Conclusions:

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.

The work referenced was performed in partial fulfillment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;

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 Summary 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 efficiency 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 findings 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 (ic ip 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 first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula

Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa

Calves were challenged by mouth with homogenised brain from confirmed cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were then left to develop BSE, but were not subjected to the normal stresses that they might have encountered in a dairy herd. Animals in all four groups developed BSE. There has been a considerable spread of incubation period in some of the groups, but it appears as if those in the 1 and 10g challenge groups most closely fit the picture of incubation periods seen in the epidemic. Experiments in progress indicate that oral infection can occur in some animals with doses as low as 0.01g and 0.001g. .........

http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose

It is clear that the designing scientists must also have shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.

http://web.archive.org/web/20061003022720/http://www.bseinquiry.gov.uk/files/ws/s145d.pdf

6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.

http://web.archive.org/web/20061003022724/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf

Saturday, June 25, 2011

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque

"BSE-L in North America may have existed for decades"

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

snip...

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...

http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006

http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html

http://madcowtesting.blogspot.com/2007/10/bse-base-mad-cow-testing-texas-usa-and.html

http://madcowtesting.blogspot.com/

let's take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.

This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$

ALABAMA MAD COW g-h-BSEalabama

In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.

http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156

http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF

her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).

This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine–human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks.

Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA

NATURE|Vol 457|26 February 2009

http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html

Thursday, June 23, 2011

Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html

Saturday, July 23, 2011

CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html

Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation

http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html

Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)

PRION DISEASE UPDATE 2010 (11)

http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129

P.9.21

Molecular characterization of BSE in Canada

Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada

Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.

Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.

Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.

*** It also suggests a similar cause or source for atypical BSE in these countries.

http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf

SOME OLD MAD COW FEED BAN VIOLATIONS ;

THE SEVEN SCIENTIST REPORT ***

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf

WELL, someone did call me from Bio-Rad about this, however it was not Susan Berg. but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ;

Bio-Rad, TSS phone conversation 12/28/04

Finally spoke with ;

Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX

at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having.

X was very very cautious as to speak directly about USDA and it's policy of not using WB.

X was very concerned as a Bio-Rad official of retaliation of some sort.

X would only speak of what other countries do, and that i should take that as an answer.

I told X I understood that it was a very loaded question and X agreed several times over and even said a political one.

my question;

Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ???

ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated.

again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there.

"very difficult to answer"

"very political"

"very loaded question"

outside USA and Canada, they use many different confirmatory tech.

in house WB, SAF, along with IHC, HP, several times etc.

you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE.

again, look what the rest of the world is doing.

said something about Dr. Houston stating; any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives?

said something about ''just look at the sheep that tested IHC- but were positive''. ...

TSS

-------- Original Message --------

Subject: Your questions

Date: Mon, 27 Dec 2004 15:58:11 -0800

From: To: flounder@wt.net

Hi Terry:

............................................snip

Let me know your phone number so I can talk to you about the Bio-Rad BSE test. Thank you

Regards

Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email:

=================================

END...TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########

http://madcowtesting.blogspot.com/

HOW ABOUT THAT MAD COW FIRE WALL TOO ;

*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS

THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$

10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007

Date: March 21, 2007 at 2:27 pm PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

___________________________________

PRODUCT

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007

CODE

Cattle feed delivered between 01/12/2007 and 01/26/2007

RECALLING FIRM/MANUFACTURER

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

Firm initiated recall is ongoing.

REASON

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

42,090 lbs.

DISTRIBUTION

WI

___________________________________

PRODUCT

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007

CODE

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

RECALLING FIRM/MANUFACTURER

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

REASON

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

9,997,976 lbs.

DISTRIBUTION

ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm

Saturday, August 14, 2010

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)

BANNED MAD COW FEED IN COMMERCE IN ALABAMA

Date: September 6, 2006 at 7:58 am PST PRODUCT

a) EVSRC Custom dairy feed, Recall # V-130-6;

b) Performance Chick Starter, Recall # V-131-6;

c) Performance Quail Grower, Recall # V-132-6;

d) Performance Pheasant Finisher, Recall # V-133-6.

CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.

REASON

Dairy and poultry feeds were possibly contaminated with ruminant based protein.

VOLUME OF PRODUCT IN COMMERCE 477.72 tons

DISTRIBUTION AL

______________________________

http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html

PRODUCT Bulk custom dairy pre-mixes,

Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE 350 tons

DISTRIBUTION AL and MS

______________________________

PRODUCT

a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;

b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;

c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;

d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;

e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;

f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;

g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6

CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.

REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".

VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags

DISTRIBUTION AL, GA, MS, and TN

END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006

###

http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html

Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006

Date: August 6, 2006 at 6:16 pm PST PRODUCT

a) CO-OP 32% Sinking Catfish, Recall # V-100-6;

b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;

c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;

d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;

e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;

f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;

g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;

h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;

i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;

j) CO-OP LAYING CRUMBLES, Recall # V-109-6;

k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;

l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;

m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE

Product manufactured from 02/01/2005 until 06/06/2006

RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.

REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".

VOLUME OF PRODUCT IN COMMERCE 125 tons

DISTRIBUTION AL and FL

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html

MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II

______________________________

PRODUCT

a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;

b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;

c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;

d) Feather Meal, Recall # V-082-6 CODE

a) Bulk

b) None

c) Bulk

d) Bulk

RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.

REASON

Possible contamination of animal feeds with ruminent derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons

DISTRIBUTION Nationwide

END OF ENFORCEMENT REPORT FOR July 12, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html

please see full text ;

http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html

http://www.fda.gov/ICECI/EnforcementActions/EnforcementStory/EnforcementStoryArchive/ucm107472.htm

http://www.fda.gov/AnimalVeterinary/NewsEvents/CVMUpdates/ucm048448.htm

http://www.gao.gov/new.items/d02183.pdf

http://www.fda.gov/AnimalVeterinary/NewsEvents/CVMUpdates/ucm048431.htm

http://www.fda.gov/downloads/AnimalVeterinary/NewsEvents/FDAVeterinarianNewsletter/UCM055628.pdf

http://www.fda.gov/AnimalVeterinary/NewsEvents/FDAVeterinarianNewsletter/ucm106105.htm

http://agri.state.nv.us/GAO_FDA%20Mgmt%20Mad%20Cow%20IMprove_Feb05.pdf

http://www.gao.gov/products/GAO-05-101

http://www.gao.gov/new.items/d05101.pdf

http://www.fda.gov/AnimalVeterinary/NewsEvents/CVMUpdates/ucm115008.htm

http://www.fda.gov/AnimalVeterinary/NewsEvents/CVMUpdates/ucm048228.htm

Monday, March 1, 2010

ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010

http://madcowfeed.blogspot.com/2010/03/animal-protien-ie-mad-cow-feed-in.html

FDA BSE/Ruminant Feed Inspections Firms Inventory Report Texas Legend Ranch OAI 05/10/2008

Greetings,

AS you can see from this OAI, dated 05/10/2008, the potential for banned mad cow protein still being fed to U.S. cattle is great. I did a quick search, and this was a TEXAS firm (the last two documented mad cows in the USA were atypical BSE, one being from TEXAS, and science is showing that atypical BSE is more virulent to humans). WHAT I find odd, is how difficult it is now to look up these violators of these mad cow feed ban violations. Apparently the spread sheet is still not available (full text) ;

Display Entire FDA BSE/Ruminant Feed Inspections Firm Inventory Report as an Excel Spreadsheet

http://www.accessdata.fda.gov/BSEInspect/bse_excel.jsp

HOWEVER, if you look hard enough, yea shall find, potential mad cow protein in commerce USA MAY 2008 ;

FDA BSE/Ruminant Feed Inspections Firms Inventory Report

Data reported as of: 05/10/2008

Search by: State = TX, and FDA District = DAL-DO, and Firm Type = FR,HF,NL, and Last BSE Insp Date From 01/01/2007 To 05/31/2008 and BSE Program Risk = DP,HP,NP, and Last BSE District Decision = OAI, and Handles Feed for Rum. Animals = Y,N,R Sort by: Last BSE District Decision

FDA District

DAL-DO

Firm Id (FEI)

3006607060

Firm Name

Texas Legend Ranch

Street Address

2803 Highway 473

City

Kendalia

State

TX

Zip Code

78027-2016

Opr. Status

OPR

Firm Type(s)

FR, OF

Prgm Risk

NP

Last BSE Insp Date

03/25/2008

Last BSE Dist. Dcsn''

OAI

Handles Feed for Rum. Animals?

Y

Legend - Opr.Status:OPR=Operational,

SEA=Seasonal,

PRP=Pre-Production,

Firm Type:

AF=Animal Feed/Pet Food Salvager,

DR=Distributor/Retailer,

FL=Feed Mill (FDA Licensed),

FR=Feeder of Ruminants,

HF=Human Food Processor,

NL=Feed Mill (not FDA Licensed),

OF=On-farm Feed Mixer,

OT=Other,

PB=Protein Blender,

PF=Pet Food Manufacturer,

RE=Renderer,

RO=Feeder of Ruminants and Other Species,

TH=Transporter (Hauler),

Prgm Risk:DP=Only Distributes Prohib.Mat.(DP),

HP=Handles Prohibited Materials(HP),

NP=Does not handle Prohib.Mat.(NP),

Dist Dcsn:

OAI=Official Action Indicated (OAI),

VAI=Voluntary Action Indicated (VAI),

NAI=No Action Indicated (NAI),

RTS=Referred to State (RTS),

** District decisions listed in this report reflect the compliance status of firms when the report was generated. These district decisions may or may not represent the final Agency determination of compliance for these firms.

http://www.accessdata.fda.gov/BSEInspect/bse_results.jsp

PLEASE NOTE ;

An OAI inspection classification occurs when significant objectionable conditions or practices were found and regulatory sanctions are warranted in order to address the establishment's lack of compliance with the regulation. An example of an OAI inspection classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspections classified with OAI violations will be promptly re-inspected following the regulatory sanctions to determine whether adequate corrective actions have been implemented.

http://www.fda.gov/cvm/CVM_Updates/BSE0108.htm

PLEASE SEE ;

Unacceptable risk: When the potential harm either to animal or humans from a feed product attains a level not acceptable to decision-makers. The level may vary depending on the type of harm.

http://www.fda.gov/cvm/AFSS3rdDraftFramework.html

Friday, September 4, 2009

FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009

http://madcowfeed.blogspot.com/2009/09/foia-request-on-feed-recall-product.html

Saturday, August 29, 2009

FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009

http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html

C O N F I R M E D

----- Original Message -----

From: "Terry S. Singeltary Sr."

To:

Sent: Thursday, November 05, 2009 9:25 PM

Subject: [BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009

http://madcowfeed.blogspot.com/2009/11/re-foia-request-on-feed-recall-product.html

PLEASE UNDERSTAND, with a Transmissible Spongiform Encephalopathy, once clinical, the disease is 100% fatal. There should be NO debate of the 'unacceptable risk factor', with any TSE. ...TSS

Sunday, June 26, 2011

Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html

PLEASE be aware, for 4 years, during the BUSH/PERRY era, the USDA fed our children all across the Nation (including TEXAS) dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens. who will watch our children for CJD for the next 5+ decades ???

DID rick perry and george bush expose your child to mad cow disease via the NSLP ???

SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE

http://downercattle.blogspot.com/2009/05/who-will-watch-children.html

http://downercattle.blogspot.com/

DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???

you can check and see here ;

http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf

with an incubation period of up to 50 years or more, we will all just have to wait and see...

Subject: USDA BSE inconclusive MRR policy

Date: August 25, 2006 at 3:52 pm PST

USDA BSE inconclusive MRR policy

BESIDES THE TEXAS MAD COW THAT WAS RENDERED AND NEVER TESTED;

http://madcowtesting.blogspot.com/2007/10/bse-base-mad-cow-testing-texas-usa-and.html

Friday, March 4, 2011

Alberta dairy cow found with mad cow disease

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html

Thursday, February 10, 2011

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31

http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html

Friday, February 18, 2011

UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS ''PLEADS GUILTY"

http://bse-atypical.blogspot.com/2011/02/united-states-of-america-vs-galen-j.html

Wednesday, December 22, 2010

Manitoba veterinarian has been fined $10,000 for falsifying certification documents for U.S. bound cattle and what about mad cow disease ?

http://usdameatexport.blogspot.com/2010/12/manitoba-veterinarian-has-been-fined.html

i wonder if CFIA Canada uses the same OBEX ONLY diagnostic criteria as the USDA ?

Tuesday, November 02, 2010

BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992

http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html

Saturday, August 14, 2010

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

(see mad cow feed in COMMERCE IN ALABAMA...TSS)

http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html

Saturday, December 18, 2010

OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html

Saturday, August 20, 2011

BSE PRION Terrestrial Animal Health - Policy & Procedures / Santé des animaux terrestres - politiques et procédures 2011-08-16

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/bse-prion-terrestrial-animal-health.html

IN A NUT SHELL ; $$$

(Adopted by the International Committee of the OIE on 23 May 2006)

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries.The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to then Central Bureau............

http://www.oie.int/eng/Session2007/RF2006.pdf

Thursday, July 28, 2011

An Update on the Animal Disease Traceability Framework July 27, 2011

http://naiscoolyes.blogspot.com/2011/07/update-on-animal-disease-traceability.html

Wednesday, June 15, 2011

Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html

Thursday, June 2, 2011

USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California

http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html

Monday, June 20, 2011 2011

Annual Conference of the National Institute for Animal Agriculture ATYPICAL NOR-98 LIKE SCRAPIE UPDATE USA

http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html

Monday, June 27, 2011

Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease

http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html

Monday, November 30, 2009

USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE

http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html

I strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE. ...TSS

Friday, February 11, 2011

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html

Thursday, July 14, 2011

Histopathological Studies of “CH1641-Like” Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html

Thursday, November 18, 2010

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html

Sunday, October 3, 2010

Scrapie, Nor-98 atypical Scrapie, and BSE in sheep and goats North America, who's looking ?

http://nor-98.blogspot.com/2010/10/scrapie-nor-98-atypical-scrapie-and-bse.html

Wednesday, July 06, 2011

Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation

(see tonnage of mad cow feed in commerce USA...tss)

http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html

Monday, June 27, 2011

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html

Please see the following warning from CDC about prion TSE consumption in North America ;

Thursday, May 26, 2011

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html

Thursday, July 21, 2011

A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:

August 2011 - Volume 70 - Issue 8 - pp 698-702

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html

Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html

Sunday, August 21, 2011

The British disease, or a disease gone global, The TSE Prion Disease

snip...

CANADA CJD UPDATE 2011

CJD Deaths Reported by CJDSS1, 1994-20112 As of January 31, 2011

3. Final classification of 49 cases from 2009, 2010, 2011 is pending.

snip...

http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0111-eng.pdf

USA 2011

USA

National Prion Disease Pathology Surveillance Center

Cases Examined1

(November 1, 2010)

Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD

1996 earlier 51 33 28 5 0 0

1997 114 68 59 9 0 0

1998 87 51 43 7 1 0

1999 121 73 65 8 0 0

2000 146 103 89 14 0 0

2001 209 119 109 10 0 0

2002 248 149 125 22 2 0

2003 274 176 137 39 0 0

2004 325 186 164 21 0 13

2005 344 194 157 36 1 0

2006 383 197 166 29 0 24

2007 377 214 187 27 0 0

2008 394 231 205 25 0 0

2009 425 258 215 43 0 0

2010 333 213 158 33 0 0

TOTAL 38315 22656 1907 328 4 3

1 Listed based on the year of death or, if not available, on year of referral;

2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;

3 Disease acquired in the United Kingdom;

4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;

5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.

http://www.cjdsurveillance.com/pdf/case-table.pdf

Please notice where sporadic CJD cases in 1996 went from 28 cases, to 215 cases in 2009, the highest recorded year to date.

sporadic CJD is on a steady rise, and has been since 1996.

I also urge you to again notice these disturbing factors in lines 5 and 6 ;

5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.

========end=====tss=====2011

snip...

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html

CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER

"Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle."

http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=19:cjd-english-info&catid=9:cjd-ingles&Itemid=8

http://creutzfeldt-jakob-disease.blogspot.com/2010/03/irma-linda-andablo-cjd-victim-she-died.html

CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER

http://cjdtexas.blogspot.com/2010/03/cjd-texas-38-year-old-female-worked.html

SEE TEXAS CJD CASES HERE ;

http://creutzfeldt-jakob-disease.blogspot.com/2010/07/cjd-2-cases-mclennan-county-texas.html

http://cjdtexas.blogspot.com/

SEE CJD IN TEXAS UNDER REPORTED HERE ;

http://www.google.com/url?sa=t&source=web&cd=2&sqi=2&ved=0CCMQFjAB&url=http%3A%2F%2Fwww.dshs.state.tx.us%2Fidcu%2Fepilink%2Fvolume_64%2Fissue_8%2Fdocs%2F640804.pdf&rct=j&q=texas%20CREUTZFELDT%20JAKOB%20DISEASE&ei=Gg9YTrvwEaqusQKX3eWvDA&usg=AFQjCNGY2P9WX5PAuaSUJ0FhndFVlCjYVQ&sig2=I5s3rSEP7-ULzYQqvxp_8w

Thursday, August 4, 2011

Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011

(see video here) ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html

Sunday, August 21, 2011

The British disease, or a disease gone global, The TSE Prion Disease

(see video here)

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html

Thursday, July 08, 2010

GLOBAL CLUSTERS OF CREUTZFELDT JAKOB DISEASE - A REVIEW 2010

http://creutzfeldt-jakob-disease.blogspot.com/2010/07/global-clusters-of-creutzfeldt-jakob.html

Friday, June 17, 2011

Treatable neurological disorders misdiagnosed as Creutzfeldt-Jakob disease

http://creutzfeldt-jakob-disease.blogspot.com/2011/06/treatable-neurological-disorders.html

Friday, November 30, 2007

CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION

http://cjdquestionnaire.blogspot.com/2007/11/cjd-questionnaire.html

http://cjdquestionnaire.blogspot.com/

Wednesday, August 24, 2011

There Is No Safe Dose of Prions

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/there-is-no-safe-dose-of-prions.html

Wednesday, August 24, 2011

All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/all-clinically-relevant-blood.html

Wednesday, June 29, 2011

TSEAC Meeting August 1, 2011 donor deferral Saudi Arabia vCJD risk blood and blood products

http://tseac.blogspot.com/2011/06/tseac-meeting-august-1-2011-donor.html

Saturday, June 18, 2011

Self-propagation and transmission of misfolded mutant SOD1 Prion or Prion-like phenomenon?

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/self-propagation-and-transmission-of.html

Wednesday, March 31, 2010

Atypical BSE in Cattle

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE.

When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2

Thursday, August 12, 2010

Seven main threats for the future linked to prions

First threat

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

Second threat

snip...

http://www.neuroprion.org/en/np-neuroprion.html

http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html

http://prionpathy.blogspot.com/

Rural and Regional Affairs and Transport References Committee

The possible impacts and consequences for public health, trade and agriculture of the Government's decision to relax import restrictions on beef Final report June 2010

2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49

2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50

http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf

The conclusions state that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Active screening has allowed the identification of 3 new forms of animal TSEs (H-type atypical BSE, L-type atypical BSE, and atypical scrapie), but the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs. There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential. Transmission experiments to human PrP transgenic mice or primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential and indicate that that of the L-type atypical BSE agent appears similar or even higher than that of the classical BSE agent. A single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.

Commentary ---------- Following to a request from the European Commission, the Panel on Biological Hazards (BIOHAZ) and the European Centre for Disease Prevention and Control (ECDC) were asked to deliver a scientific opinion on any possible epidemiological or molecular association between transmissible spongiform encephalopathies (TSEs) in animals and humans. The opinion reviews and discusses the existing scientific evidence that links animal and human TSEs currently known.

The opinion first considers the definition of zoonoses and the principles for the identification of zoonotic diseases, which can be based on evidence gathered from both epidemiological and laboratory studies. The opinion describes the challenges involved in identifying TSEs as zoonoses, due to the specific characteristics of TSE infections/diseases, such as the nature of TSE agents, the occurrence of animal and human TSEs, and the type of monitoring applied, the long incubation period of TSEs etc. The example of the process that led to establishing a link between bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) is reviewed. The epidemiological and laboratory criteria that can be used to investigate such a link are described in detail, since those criteria might be useful for the identification of links between other animal and human TSEs.

The opinion discusses the strain diversity of the TSE agents described in sheep, goats, cattle, cervids, and humans, based on the current knowledge, which highlights that multiple TSE agents exist in each species. The factors influencing the capacity of TSE agents to cross the species transmission barrier are then considered in detail, including the variability in host and donor PrP gene and protein, the TSE strain type involved and its interaction with the host PrP, and the route of infection.

The opinion critically assesses the tools and methodologies currently available to study and evaluate the possible association between animal and human TSEs. The use of epidemiology is discussed for TSEs in both animals and humans, and the possibility to compare the 2 sources of information is presented as a possible method to study the possible links.

Both in vivo and in vitro laboratory methods are considered and discussed, including neuropathology, transmission experiments involving different animal models (wild type and transgenic mice, primates and other species), biochemical methods, cell-free conversion assays, protein misfolding cyclic amplification (PMCA), and cell culture assays. Characteristics, advantages, and disadvantages of the different methods are reviewed, including the opportunity to collate data from different types of experiments for the study of potential associations between animal and human TSEs.

The opinion then reviews the scientific evidence currently available for the different animal and human TSEs, including classical BSE, atypical BSE (H-type and L-type), classical scrapie, atypical scrapie, chronic wasting disease (CWD), transmissible mink encephalopathy (TME), and human TSEs. In particular, the following aspects are systematically discussed for each TSE agent: epidemiology, pathogenesis, and in vivo and in vitro transmission experiments.

The opinion concludes that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. With regard to human TSEs, detected cases of sporadic CJD are randomly distributed in time and geographical location. These observations have been interpreted as a supportive argument that sporadic CJD is not environmentally acquired. However, the epidemiological evidence in relation to sporadic CJD cannot be regarded as definitive, and the possibility that a small proportion of cases are zoonotic cannot be excluded.

It also concludes that a series of uncertainties in relation to the epidemiological patterns of animal and human TSEs indicate that even a rough comparison of the present epidemiological patterns of human and animal TSEs other than classical BSE is unlikely to be informative. Because of these uncertainties, it is an imperative to continue to carry out systematic surveillance of human TSE diseases, and to continue and improve the surveillance of animal TSE diseases.

The opinion highlights that the active screening has allowed the identification of 3 new forms of animal TSEs (L-type atypical BSE, H-type atypical BSE, and atypical scrapie), but that the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs.

There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential.

Transmission experiments to human PrP transgenic mice suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE and classical BSE in sheep agents) might have zoonotic potential, whereas for other agents there is no evidence provided of a zoonotic potential (H-type atypical BSE and CWD), or no published studies are available (classical and atypical scrapie). In addition, transmission experiments to primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential. In particular, primates are highly permissive to L-type atypical BSE, even by the oral route.

The opinion emphasizes that laboratory transmission experiments indicate that the L-type atypical BSE agent has a significant zoonotic potential, which appears similar or even higher than that of the classical BSE agent. While transmission data for evaluating the zoonotic potential of classical scrapie in primates and human PrP transgenic mice are extremely limited or not yet available, a single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.

The opinion concludes that human PrP transgenic mice and primates are currently the most relevant models for investigating the human transmission barrier, but the extent to which such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. It is unpredictable whether a TSE agent will transmit to a new host, and if the transmission principally occurs, what the transmission rate will be.

Based on the results obtained with in vitro conversion assays, the opinion concludes that there is probably no absolute molecular barrier to transmission of TSE agents between mammalian species. Results also suggest that these assays may be developed as a tool for quantifying the transmission barriers between species for different TSE agent strains; however, there is no means at the moment to transpose in vitro results into the likelihood of in vivo interspecies transmission.

-- Communicated by: Terry S Singeltary Sr

[ProMED-mail thanks Terry S Singeltary Sr for drawing attention to this comprehensive document which provides a current evaluation of experimental work designed to explore the zoonotic potential of the various recently recognised TSEs of domestic and other animals.

It is concluded that at present the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Nor can it be entirely excluded at the present time that a small proportion of cases of sporadic CJD may be environmentally acquired. - Mod.CP]

******

http://www.promedmail.org/pls/apex/f?p=2400:1202:888892554804923::NO::F2400_P1202_CHECK_DISPLAY,F2400_P1202_PUB_MAIL_ID:X,88784

[Terry S. Singeltary Sr. has added the following comment:

"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed

http://whqlibdoc.who.int/publications/2003/9241545887.pdf

http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101

14th ICID International Scientific Exchange Brochure -

Final Abstract Number: ISE.114

Session: International Scientific Exchange

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

T. Singeltary

Bacliff, TX, USA

Background:

An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

Methods:

12 years independent research of available data

Results:

I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

Conclusion:

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf

Monday, May 23, 2011

Atypical Prion Diseases in Humans and Animals 2011

Top Curr Chem (2011)

DOI: 10.1007/128_2011_161

# Springer-Verlag Berlin Heidelberg 2011

Michael A. Tranulis, Sylvie L. Benestad, Thierry Baron, and Hans Kretzschmar

http://bse-atypical.blogspot.com/2011/05/atypical-prion-diseases-in-humans-and.html

TSS

layperson

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net

TEXAS NUCLEAR DUMP VOTE SET AMID HOLIDAY RUSH THANKS TO GOVERNOR RICK PERRY

2010-12-24T08:51:00.000-08:00

NUCLEAR DUMP VOTE SET AMID HOLIDAY RUSH

CRITICS PROTEST TIMING OF MEETING ON 38-STATE WASTE FACILITY IN TEXAS

AUSTIN — In a move decried by environmentalists, state regulators decided late Thursday to schedule a vote that could allow three dozen states to dump radioactive waste in Texas.

The Texas Compact Commission set a Jan. 4 meeting to decide whether to expand how much low-level radioactive waste could be processed at a dump in remote Andrews County, in far West Texas. The announcement came as environmentalists and critics on the commission accused regulators and a politically connected company of rushing the proposal past Texans who are too focused on the holidays to even notice.

The public comment period on the proposal ends Sunday. The timing could also be designed to get support from two commissioners from Vermont, which has an agreement to deposit waste at the facility.

"It's too much, too soon, too fast," said Bob Gregory, a commissioner who opposes the expansion plan. "This whole thing is absurd. Why are we having a comment period at midnight on the day after Christmas?"

Michael Ford, chairman of the commission, said the rule has been under review for more than a year.

"We've been working on this rule for 16 months," Ford said. "That does not meet my definition of rushed."

Waste Control Specialists, whose majority owner is Dallas billionaire and political donor Harold Simmons, wants state regulators to approve its proposal to allow low-level radioactive waste at its West Texas dump site from three dozen states. As it stands, the compact site can only get waste from Texas, Vermont and the federal government.

The incoming governor of Vermont, Democrat Peter Shumlin, has criticized the expansion proposal. But he doesn't take office until Jan. 6. By then, the two commissioners appointed by his predecessor could vote in favor of it.

Texas environmental activist Karen Hadden, director of the Texas SEED Coalition, said she was "appalled" by the timing of the meeting and warned it could make Texas a dumping ground for low-level radioactive waste.

"This is an evil Christmas present from WCS and Harold Simmons," added Tom "Smitty" Smith, director of the environmental group Public Citizen of Texas.

After a news conference Thursday, Smith and other environmentalists rolled a black barrel, with a radioactive symbol on the outside, under the state Christmas tree outside the Texas Capitol.

Chuck McDonald, a spokesman for WCS, said the process has been anything but rushed. He said the same opponents who are attacking the idea are responsible for delaying action until now.

"It is a true misnomer to say this has been rushed through in the holiday season," McDonald said.

8-member commission The decision on whether to allow the importation of waste from other states rests with the eight-member Texas commission, made up of appointees by the governors of Texas and Vermont. Those states have a compact that allows both states to bury nuclear waste at the Andrews County site.

In the early 1980s, the federal government started urging states to build low-level nuclear waste landfills, either on their own or in cooperation with other states.

Should the commission adopt the rules, low-level radioactive waste from 36 other states could also petition the group to allow their waste to be dumped at the facility.

The dump, now sized at 2.3 million cubic yards, would be one of a few in the nation that could take low-level waste, such as clothing, metal and other materials from nuclear power plants, hospitals and university labs.

Locals are split.

In 2009, voters in Andrew County narrowly approved - 642-639- a $75 million bond to pay for the construction of the dump by WCS, which would pay the county a share of its gross receipts.

For Tim Gannaway, who was born and raised in the city of Andrews but moved in 2007 to attend the University of Texas at San Antonio, the decision to bring radioactive waste to an area served only by a volunteer fire department is foolhardy.

He also doesn't like the idea of his home county becoming a national repository for dangerous waste.

"Andrews is now the new Yucca Mountain," he said, comparing the WCS site to the federal radioactive waste disposal project about 80 miles from Las Vegas that might never open.

Others disagree. The closest town to the site is Eunice, N.M., home to a uranium enrichment plant, two gas processing plants and is less than 50 miles from the U.S. Energy Department's Waste Isolation Pilot Plant designed to hold radioactive waste from the Defense Department.

"Those kind of facilities have located in this area because, generally, the people in this area are very receptive to those kind of facilities," said Curtis Schrader, Eunice's city manager.

Viewed as patriotic Across the state line, Russell Shannon, president and CEO of the National Bank of Andrews, points out that the city did a study of the WCS site, which also has undergone 10 years of review by the Energy Department and the state.

The dump, he said, is turning ranchland that gets less than 16 inches of rain a year into a money-making enterprise that would provide a national public service.

"If we can safely store the material here, why would we not want to help the rest of the country?" Shannon said. "We think of it as patriotic."

The Associated Press and San Antonio Express-News reporter Colin McDonald contributed to this report.

E-mail: rule.comment@tllrwdcc.org

Postal mail: Texas Low-Level Radioactive Waste Disposal Compact Commission, 3616 Far West Blvd., Suite 117, #294, Austin, Texas 78731

http://www.chron.com/disp/story.mpl/metropolitan/7352954.html

Greetings fellow Texicans,

THIS is typical timing of such an event. This is how our Government gets bills and reports passed by the public. They usual do it late at night, on a Friday night at that, so it will be only late weekend news. they got it down pat too.

Twas the night before Christmas, when all through the house, Not a creature was stirring, not even a mouse, but the rats they were a stirring, right in the House, Their pockets were lined, with money and greed, in hopes that St Nicholas would not have seen.

The children were nestled all snug in their beds, While visions of sugar-plums danced in there heads. And mamma in her 'kerchief, and I in my cap, Had just settled our brains for a long winter's nap, and again, our good Governor from Texas Rick Perry, stabbed us in the back.

When out on the lawn there arose such a clatter, I sprang from the bed to see what was the matter. Away to the window I flew like a flash, Tore open the shutters and threw up the sash, there was a bright glow from a far, in the west, it was a big bright flash.

The moon on the breast of the new-fallen snow, gave the lustre of mid-day to objects below. When, what to my wondering eyes should appear, but train load after train load of Nuclear Prolifer.

With a little old driver, his hair in perfect affair, all groomed and combed over, like a multi-millionaire, was atop the train of nuclear prolifer. The glow was so bright, it lit up the whole night. More rapid than eagles his coursers they came, and he whistled, and shouted, bring more, bring more, we will light up the whole game.

"Now Dasher! now, Dancer! now, Prancer and Vixen! On, Comet! On, Cupid! on, on Donner and Blitzen! To the top of the porch! to the top of the wall, thanks to Governor Rick Perry, we may all glow like a great big fire ball.

AS dry leaves that before the wild hurricane fly, When they meet with this fire ball in the sky, the money the received will be their final cry. So UP the house and the senate i say, and to you rick perry, i better not say.

end

I wrote about our good Environmental Friendly Governor Rick Perry and his willingness to bring nuclear waste from Ohio to Texas back in 2008. Seems the money is so good, he wants to now include 38 states to the list of states able to pollute the great state of Texas with Nuclear Proliferation waste. at a boy governor, you single handedly made Texas a toxic dump for nuclear waste. Course, which is worse, the air quality or the nuclear waste, which will kill you first ? This Governor has shown time and time again where his heart is, and it's NOT in Texas. ...

Wednesday, August 6, 2008

Company advances on plan for West Texas nuclear dump

(railcars loaded with MOUND COLD WAR NUCLEAR AFTER-BIRTH headed to Texas see photo)

http://sciencebushwhacked.blogspot.com/2008/08/company-advances-on-plan-for-west-texas.html

Wednesday, July 30, 2008

TEXAS WINS TO BE NEXT BIG DUMPING GROUND FOR NUCLEAR WEAPONS RADIOACTIVE WASTE

(see more photo's of railcars loaded with MOUND COLD WAR NUCLEAR AFTER-BIRTH headed to Texas)

IT seems a more correct headlines would have read ''Company bribes Governor Perry to bury nuclear waste and contaminate Texas''. Waste Control Specialists. The company is owned by Harold Simmons, a ''TOP DONOR TO GOV. RICK PERRY, WHO APPOINTS MEMBERS TO THE TCEQ.'' The good governor has sold out to the citizens of Texas for train car, after train car of nuclear waste from 'the mound' Monsanto plant in Miamisburg Ohio. It just so happens, my father-in-law, who is down visiting now with us, has pictures of those railroad cars just sitting and waiting to come down to Texas. Odd how I was watching the news today, about this small plane that had crashed, it had showed pictures of where it had crashed right up near a bunch of tractor-trailer cargo container boxes in a parking lot. What would keep this from happening with those radioactive toxic containers in Ohio, at 'the mound', and or in route to Texas? You see, it's been killing my father-in-law, he has been on oxygen for years, but his breathing is getting more and more labored now, even with the oxygen. He worked at 'the mound' for years and years, and he is now dying a slow death from asbestosis, among other ailments caused by working at 'the mound'. NOW here is what I just cannot understand. This material is so toxic, in trying to gain further medical assistance from the DOE, the evidence that was needed to show that indeed my father-in-law worked their i.e. work records, paperwork records, payment records etc., they told my father-in-law, that they could not dig those records up, that they were buried due to high nuclear contamination, it was just too toxic, and that he had to prove that he had worked there. In which he did finally prove, and did gain further assistance. Also, ''Soward said a contested hearing could either rebut or support allegations that the agency ignored it's own scientific evidence that the site is geologically unsuitable to store material that will remain radioactive for tens of thousands of years.'' This is typical of the Bush Administration, and it happens all the time. The only science that the Bush administration knows, is junk science, bought and paid for by industry scientist. This has been proven time and time again ;

Reports and Research

Interference at the EPA

Science and Politics at the U.S. Environmental Protection Agency

snip...see full text ;

http://sciencebushwhacked.blogspot.com/2008/07/texas-wins-to-be-next-big-dumping.html

I think the title should have read, "TEXAS LOOSES TO BE NEXT BIG DUMPING GROUND FOR NUCLEAR PROLIFERATION RADIOACTIVE WASTE", thanks to Governor Rick Perry.

update on my father-in-law Dana (RED) Ashcraft of Miamisburg Ohio, and my best fishing buddy, and Poisoned AT THE MONSANTO MOUND, hospice has now been called in. ...

TSS

part II December 25, 2010

WHY then, was my father-in-laws work records denied him, with the claim that his records were buried deep in a mountain due to contamination ? now i am speaking of only his work records, not the radioactive waste itself, that you claim to be 1000 % safe today. tell me that. do you know how many different folks handled all that paper work over the years. also, the swimming pool in Miamisburg Ohio, the old one right down from the Monsanto Mound. the town had to shut it down and fill the swimming pool in with cement. wonder how many kids there were exposed over the decades, including my wife ?

MONSANTO MOUND MIAMISBURG OHIO SWIMMING POOL

" We acknowledge that some people near the Mound Plant have breathed, or will likely breathe, very small amounts of plutonium-238, hydrogen-3 (tritium), and other radioactive substances that will be or have been released into the air from the Mound Plant. And some people may be exposed to radioactive materials released from the Mound Plant into the area waterways (for example, tritium in the Miamisburg Community Park swimming pool). Nevertheless, there is no evidence that current environmental levels of these substances cause adverse health effects. "

Data Evaluation: Current Exposures

ATSDR scientists reviewed the environmental data for the Mound Plant and concluded that there are no current exposure pathways to contamination from the Mound Plant that pose a public health hazard. We have considered all materials released from the Mound Plant, both radioactive and nonradioactive, individually and collectively, and their presence in all environmental media off site (such as air, water, vegetation and soil).

1.Radioactive Substances: Mound Releases Because nearly all Mound programs included work with radionuclides, the environmental and public health concerns that stakeholders most frequently discuss are those concerning radioactive substances released from the Mound Plant. The radionuclides in the environment that are a result of Mound activities and are of greatest concern today are plutonium-238 and hydrogen-3 (tritium). However, there is strong evidence from numerous environmental investigations--including our own--that plutonium-238, hydrogen-3, and all other radioactive substances from the Mound Plant contribute a very small amount to the total radiation dose that people living near the Mound Plant typically receive. Very likely, the largest radiation doses to nearby residents are those resulting from exposures to radioactive materials that are naturally occurring.

We acknowledge that some people near the Mound Plant have breathed, or will likely breathe, very small amounts of plutonium-238, hydrogen-3 (tritium), and other radioactive substances that will be or have been released into the air from the Mound Plant. And some people may be exposed to radioactive materials released from the Mound Plant into the area waterways (for example, tritium in the Miamisburg Community Park swimming pool). Nevertheless, there is no evidence that current environmental levels of these substances cause adverse health effects.

2.Nonradioactive Hazardous Substances: Mound Releases

The Mound Plant discharges small amounts of nonradioactive hazardous substances to the Great Miami River and to the air. People may occasionally be exposed to very small amounts of these materials. However, we do not think that releases of nonradioactive materials from the Mound Plant pose a public health hazard because the quantities of hazardous materials that are released are small and there is no evidence that the concentrations of these materials in the environment are high.

The pattern of nonradioactive contaminants in the environment does not suggest that those materials came from Mound. Mound's compliance record with the Ohio Environmental Protection Agency is good; their only regulatory exceedances in 1996 were NPDES (surface water) discharges from a private business on the Mound property. Copper concentrations in water exceeded the permit limit seven times. Mound officials reported the source of the problem was identified and corrected [14]. Based on current levels of contaminants off site and current levels of releases to the air and waterways, we do not expect that releases from the Mound Plant will pose a health hazard in the future, either.

3.Nonradioactive Hazardous Substances: Vicinity Air

The Regional Air Pollution Control Agency (RAPCA) collects air samples in a six-county area (including Montgomery County) for ozone, lead, carbon monoxide, sulfur dioxide, and particulate matter analyses. Based on the regional air data, the important indicators of air quality in Miamisburg are ozone and particulate matter concentrations. Ozone and particulate matter in air are pollutants that are both man-made and naturally occurring. The RAPCA reported that one air station in Dayton, Ohio, exceeded the current ozone standard once during 1997 (in June). The particulate matter air standard was not exceeded during 1997 at any of the RAPCA air stations that collect particulate matter samples [15].

The U.S. EPA is in the process of implementing changes in the air quality standards for both ozone and particulate matter to reflect newer information on their harmful effects [16, 17]. The current ambient air particulate matter standards are based on the concentration of particles in air that have a mean aerodynamic diameter equal to or less than 10 micrometers (called PM10) because particles larger than 10 micrometers are generally not inhaled deeply and usually do not cause health problems. In addition to measuring the concentration of particles in air below 10 micrometers, the new ambient air particulate matter standards will also require measuring the concentration of particles in air equal to or less than 2.5 micrometers (mean aerodynamic diameter, called PM2.5). RAPCA will be collecting PM2.5 data along with PM10 data to monitor compliance with the new particulate matter air standards when equipment becomes available during 1998 [15].

Mound scientists do not measure ozone at or near the Mound Plant, although they do collect particulate matter at their air monitors. Mound's annual environmental reports for 1995 and 1996 show the concentration of particulate matter in air samples collected off site near the Mound Plant met current state and federal standards [14, 18]. One air monitor on site exceeded the Ohio ambient air quality standard for particulate matter in 1996. The monitor is near the Miami-Erie Canal where engineers were removing trees and brush and digging up canal soils, and putting them in railroad cars to ship them off site. Mound's data indicated that air particulate matter concentrations around the site are slightly higher than is shown by the regional data. However, Mound's air monitors are designed to collect total air particulate matter, while the RAPCA's air monitors filter out particulate matter larger than 10 micrometers. Therefore, data from Mound's monitors are not directly comparable to the regional air data. Since we do not know what portion of the particulate mass collected at Mound's air monitoring stations includes particles larger than 10 micrometers, we do not know how their air data compares with the RAPCA's PM10 data.

In addition to the pollutants discussed above, the RAPCA reported that mold concentrations in air in the Miami Valley were high in the fall of 1996 [19]. Pollen and mold concentrations are measured by the Dayton Ear, Nose, and Throat Surgeons, Inc. in Centerville, Ohio, and reported to the RAPCA for publication on their Internet Home Page [19]. Pollen and mold are naturally occurring; air concentrations are affected by weather conditions.

4.Nonradioactive Hazardous Substances: Vicinity Soils

Nonradioactive contaminants, such as polyaromatic hydrocarbons (PAHs), polycyclic biphenyls (PCBs), heavy metals, and pesticides, are widespread--though not necessarily in high concentrations--in the environment. Investigations of area soils in 1994 by Mound scientists revealed that some contaminants are found near streets and highways [20]. Those data from soil samples collected from residential properties (all within 3,500 feet of the Mound Plant) indicated that pesticide levels are higher, on average, in residential soils than in other soils in the vicinity. We do not know whether anyone will ever breathe or eat the contaminants detected in vicinity soils. We also cannot say whether the available soil data is indicative of soil at any particular location, such as on someone's private property or in someone's garden. Nevertheless, the contaminants measured in residential soils are not in high enough concentrations to pose a health hazard [20, 21].

5.Nonradioactive Hazardous Substances: Vicinity Water

Mound investigations of private wells and cisterns in 1994 revealed that some wells and cisterns had unsafe levels of lead or pesticides [22]. At ATSDR's request, staff from the Combined Health District of Montgomery County followed up with those residents who may have been affected. There is no evidence or indication that the lead and pesticides found in private wells and cisterns came from the Mound Plant.

Mound scientists investigated surface waters and sediments on and around the Mound property in the fall of 1994 and spring of 1995 [23]. The concentrations of hazardous substances in surface waters and sediments near the Mound Plant do not pose a health hazard. The level of contamination is consistent with DOE's earlier measurements of nonradioactive substances in area soils and with urban environments. Low concentrations of contaminants, particularly semi-volatile organic compounds, are widespread in the environment; many of the contaminants are attributable to motor vehicle exhaust. Interestingly, Mound's 1994-1995 data show that the water in the Great Miami River contains very low levels of chemical contamination; many of the analytes that are typically found in the area soils, ponds, and streams are undetectable in the river water [23]. We recognize that there are other exposure pathways besides air, soil, and water, such as eating contaminated, locally grown produce, or eating fish from the Great Miami River. We examine some of these other exposure pathways in Appendix E. Our evaluations indicate that the contamination in the environment around the Mound Plant poses no apparent public health hazard by any exposure pathways that we have considered.

Data Evaluation: Past Exposures

We also looked carefully at the available historic data to determine whether people might have been exposed in the past to environmental contamination from the Mound site at levels that could have caused adverse health effects. We have divided our conclusions into three groups: a) conclusions about contamination that could have caused some people health problems, b) conclusions about contamination for which the data do not indicate that the releases would have caused anyone health problems, but for which we are lacking some important information, and c) conclusions about contamination for which we believe we have sufficient data to conclude that the releases did not ever pose a public health hazard. We discuss historic releases in the remainder of this section.

1.Historic Mound Releases That Could Have Caused Health Problems The first group, environmental releases that could have caused health problems, includes microbiological releases from the Mound sanitary (sewage) treatment facility. Two incidents with the Mound sewage treatment facility--one in August 1982 and one in August 1983--resulted in releases that posed a health hazard to people swimming and boating in the Great Miami River downstream from the plant.

The health hazard from releases of microbiological contamination is indicated by the results of fecal coliform testing in one of the Mound liquid effluent streams in 1982 and 1983. The standard maximum permitted level for the fecal coliform test is 2,000 MPN (most probable number of coliform colonies) per 100 milliliters (100 mL) of effluent water. In 1982 and 1983 the maximum values detected were 24,000 and 16,000 MPN per 100 mL, respectively. The fecal coliform test is an indicator test for the presence of pathogenic enteric organisms (bacteria, viruses, and protozoans); it is not a measure of them. Nevertheless, instances of high fecal coliform in effluent indicate an increased probability that pathogenic organisms are present in the effluent and that the effluent poses a public health hazard.

Undertreated sewage may contain numerous pathogenic microbiological organisms. Specific organisms responsible for disease outbreaks associated with recreational waters are often not identified [24]. In 1982 and 1983, states' health departments did not systematically report disease outbreaks associated with recreational waters to the U. S. Centers for Disease Control and Prevention (CDC). CDC estimated that the reported outbreaks during this period represented a small fraction of those that actually occurred [25]. Ohio did not report any water-related disease outbreaks of any kind to the CDC for 1982 and 1983.

The single organism most commonly identified with water-related disease outbreaks in recreational waters is Giardia lamblia, a parasite that can cause diarrhea, intestinal cramps, fatigue, and weight loss [25]. Giardia lamblia is not a fecal coliform, and it does not come from a fecal coliform. However, the fecal coliform test indicates the presence of pathogens that are not coliform bacteria as well as those that are. Gardia lamblia is difficult to identify in sewage because it is generally present in the cyst stage, which is not amenable to laboratory examination. The human incubation period (time from exposure to illness) may be 1 to 4 weeks; illness from Giardia lamblia (called Giardiasis) is treatable. Children, the elderly, and individuals with compromised immune systems are most at risk for illness from exposures.

Salmonella and Shigella bacteria, and Hepatitis A and Norwalk viruses may also be present in sanitary waste effluent [24]. Symptoms of these infections range from none to abdominal cramps, diarrhea, fever, and--very rarely--vomiting, delirium, convulsions, coma, and death.

We do not expect that anyone would suffer today from exposures to microbial pollution emanating from Mound in the early 1980s. The technical problems that Mound employees were having with the sanitary sewage treatment facility were corrected in the middle 1980s and there have been no reports of out-of-compliance fecal coliform levels in effluent since 1986.

2.Inconclusive Historic Mound Releases (Limited Data) In the second group--contaminants for which available data do not indicate that environmental releases posed a health hazard, but for which important data are missing--we have included both air and water releases of nonradioactive substances. We are not including the microbiological releases described in the first group, but we are including all nonradioactive chemical releases before 1971. In the 1950s and part of the 1960s, chemicals were released to the waste stream that flowed off site to the river without restriction. Also, in this same period, Mound Laboratory personnel disposed of solid and liquid wastes by open burning. Since we cannot identify or quantify all of the nonradioactive materials released to the air or water, we cannot estimate possible exposures to these materials.

We present a more detailed description of releases of nonradioactive substances from the Mound facility in Appendix A.

In the second group, we are also including releases of polonium-210 to the air and water. We have some air and water release data and environmental sampling results for polonium-210 collected during the 1950s. However, we do not have a continuous record of either releases to the environment or environmental sampling. The data we have do not indicate polonium-210 posed a public health hazard; however, institutional controls of releases were being developed in the 1950s and were not commensurate with today's standards. Since we have data gaps, we cannot estimate with any certainty the public's exposures to polonium-210 in the environment.

A more detailed description of releases of polonium-210 from the Mound Laboratory is in Appendix B.

3.Historic Mound Releases That Did Not Pose A Health Hazard The third group, where we have sufficient data to say that releases to the environment did not ever pose a public health hazard, includes all radioactive materials released from Mound, except polonium-210. These materials include plutonium-238 and hydrogen-3 (tritium).

A more detailed description of releases of radioactive substances to the environment, including plutonium-238 and hydrogen-3, is in Appendices C and D. Data Reviewed

ATSDR scientists reviewed many Mound documents for this public health assessment. Among the most important of these were Mound's health physics and environmental monitoring reports. The plant produced monthly reports before April 1954, quarterly reports from June 1954 through 1962, semi-annual reports from 1963-1972, and annual reports for 1972-1996. These periodic environmental reports (and others) are listed separately under Part 1 of the bibliography at the end of this document.

In addition to the periodic environmental monitoring data, ATSDR staff reviewed data collected from numerous investigations, including those of the plutonium-238 spill in the Miami-Erie Canal, the Conrail Bridge shoring, the Community Park water slide construction, the 1989 EG&G Energy Measurements overflight survey, and groundwater tritium evaluations for the Safe Drinking Water Act (Potable Water Standards Project) [26, 27]. We reviewed CERCLA-related environmental data in site-scoping reports, remedial investigation reports, and Operable Unit 9 investigations of off-site wells, regional soils, surface water and sediments, and groundwater. These Mound-related documents (and others) are listed under Part 2 in the bibliography at the end of this document.

Part 3 of the bibliography includes books and references that we reviewed for this public health assessment that are not specifically related to the Mound site.

We also obtained useful information through the environmental sampling program that we conducted with the assistance of the U.S. EPA National Air and Radiation Environmental Laboratory (NAREL) in Miamisburg in 1993 and 1994. ATSDR and NAREL personnel set up air monitors, surveyed the area with radiation equipment, and collected samples of the soil, water, air, and vegetation [28]. NAREL personnel and their contractors analyzed the environmental samples. Appendix E includes an evaluation of these data.

Prior to the Public Comment Release version of the Mound Plant public health assessment, ATSDR scientists conducted a health consultation evaluating the plutonium-238 in the Miami-Erie Canal [6]. We also wrote letters addressing off-site wells data [29], regional soils [21], Mound's proposed treatment for Operable Unit 1 (groundwater) [30], and Mound's proposed treatment plan for mixed wastes [31].

HEALTH OUTCOME DATA SUMMARY

Health outcome data are measures of disease occurrence in a population. Common sources of health outcome data are tumor registries, birth defects registries, and death certificates. Health outcome data can provide information on the general health status of a community--where, when, and what type of disease occurs and to whom it occurs. Public health officials use health outcome data to look for trends in disease occurrence by comparing disease occurrences in different populations over periods of years. This analysis is useful to help identify the need for exposure investigations or public health intervention activities such as community education. However, health outcome data are not meant to and cannot establish cause and effect between environmental exposures to hazardous materials and adverse health effects in a community.

ATSDR scientists generally look at health outcome data for one of two reasons: (1) to evaluate the possible health effects in a population that is known to have been exposed to environmental contamination, or (2) to help address community concerns. For this public health assessment, we identified one completed exposure pathway at levels of health concern: sewage wastes released to the Great Miami River in the early 1980s. We examined water-related disease outbreak surveillance reports and did not find any indication that people became ill from those exposures. However, we recognize that if illnesses did occur from those exposures, it is very possible they were never reported to health departments. We also examined other health outcome data for the population near the Mound Plant to help address community concerns.

At the request of ATSDR, staff from the Boston University School of Public Health (BU) helped us with our review of the health outcome data. We did not identify any health databases for the community that included health outcomes other than cancers (for example, birth defects). Where cancer data were available, we looked at leukemias that have been linked in the medical literature to radiation exposure; otherwise, we looked at all cancers including leukemias. The community near the Mound Plant expressed concerns to ATSDR staff about the presence of many cancers in the community.

ATSDR staff note that we do not have evidence that anyone living near the Mound facility was exposed to enough contamination from the site to cause adverse health effects. Moreover, based on the weight of evidence (described in Appendices C and D), we eliminated as probable candidates for causing health problems in the community the contaminants of greatest concern to the community, plutonium-238 and hydrogen-3.

Most of the health outcome data for populations near the Mound Plant are county data. However, the Montgomery County population is more than 30 times larger than the population of Miamisburg and more than 100 times larger than the population within a 1- mile radius of the Mound Plant (1990 U.S. Census data). Although Montgomery County may include a portion of the population that could have been exposed to environmental releases from the Mound Plant, the county also includes many people who were not exposed to the releases. Thus, counting occurrences of health outcomes in the county population would dilute the real effect from exposures because many people were not truly exposed.

Moreover; Montgomery County is approximately 462 square miles. Many industrial facilities other than the Mound Plant are located in Montgomery County as well as in nearby Warren and Butler counties. According to the Environmental Protection Agency's (EPA's) Toxic Chemical Release Inventory database, 49 facilities in Montgomery County reported releasing a total of more than 3 million pounds of hazardous substances into the environment in 1993 [32]. The contribution from the Mound Plant was less than 0.01% of this total. (Releases represent nonradioactive air emissions, surface water discharges, underground injections, and releases to land.) Since there are many other possible environmental exposures to account for, we cannot attribute the countywide health outcomes to exposures to environmental releases from the Mound Plant. For this reason, and because the county population is not a true representation of people exposed to releases from the Mound Plant, the countywide health data are not useful to us.

The only health outcome data for the general population near the Mound Plant that are not county-based are four reports from the Dayton Area Cancer Association summarizing cancer incidences (number and types of cancers reported) in nine area hospitals for the years 1985-1992 and, separately, cancer incidences for one of the reporting hospitals (Good Samaritan Hospital and Health Center) for 1984-1990. We do not know the residences of the people who checked into these hospitals, and we do not know whether they were exposed to environmental hazards from the Mound facility or from anywhere else. Without more information, we cannot calculate cancer rates from these data or compare cancer incidence between populations that may have been exposed to hazardous materials and those that were not, using these data. Therefore, these reports do not help us evaluate health outcomes that may be related to exposures to environmental releases from the Mound facility.

Finally, we identified three Mound worker studies. In general, worker studies may provide information on the health effects from documented exposures, and they may reflect on the safety record of the worker population. However, the Mound worker population is not the same as the general population near the Mound Plant. Mound worker health effects may be indicative of the types of exposures in the surrounding community; however, we expect the magnitude of exposures to workers to be more varied, and in some cases higher, than in the community. Therefore, we cannot infer that worker exposures are identical to those in the community around the Mound Plant.

We note that the Ohio Department of Health began to collect cancer incidence data at the zip code and census tract level in 1993. These data will be far more useful than the existing county-based health data in the future analysis of community health concerns. However, we note that, depending on actual environmental exposures to hazardous substances and the latency period between those exposures and the onset of adverse health effects, health outcome data collected since 1992 may not show effects from exposures occurring many years ago.

--------------------------------------------------------------------------------

1. Private conversation, September 12, 1996. 2. NIOSH is part of the Centers for Disease Control and Prevention (CDC), which is under the Department of Health and Human Services (DHHS). 3. This number is from the 1990 U.S. Census. The City of Miamisburg, Ohio, Home Page on the Internet indicates the population of Miamisburg in 1995 was 27,290. 4. Comprehensive Environmental Response, Compensation and Liability Act (CERCLA) of 1980 and the Superfund Amendments and Reauthorization Act (SARA) of 1986.

http://www.atsdr.cdc.gov/hac/pha/pha.asp?docid=634&pg=8

http://www.atsdr.cdc.gov/hac/pha/pha.asp?docid=634&pg=1

http://webcache.googleusercontent.com/search?q=cache:j5dll2sGIM4J:www.atsdr.cdc.gov/hac/pha/pha.asp%3Fdocid%3D634%26pg%3D1+monsanto+mound+miamisburg+ohio+swimming+pool&cd=3&hl=en&ct=clnk&gl=us

http://www.atsdr.cdc.gov/hac/pha/pha.asp?docid=634&pg=2

http://www.atsdr.cdc.gov/hac/pha/pha.asp?docid=634&pg=3

http://www.cdc.gov/niosh/ocas/pdfs/abrwh/waivers/gibson.pdf

Then, they send all the radioactive waste to Texas. Now, we are going to multiply this by about 38 states ?

stupid is, as stupid does, and some times you just can't fix stupid $$$

Drugs from genetically engineered animals poised to debut in US

2009-01-26T08:31:00.000-08:00

A CLOSER LOOK: BIOTECH ANIMALS

Genetically engineered animals and the FDA Are genetically engineered fish and meat coming soon? We examine the Food and Drug Administration's regulations.

By Jill U. Adams January 26, 2009

Fast-growing salmon. Pork containing heart-healthy omega-3 fatty acids. These are two examples of products you might see in your local supermarket soon -- animals developed not through conventional breeding but through genetic engineering.

On Jan. 15, the U.S. Food and Drug Administration decided how it will regulate genetically engineered animals, for the first time paving the way for such animals or their products to be sold as food and medicine. The agency has decided to categorize genetically engineered farm animals, also called transgenic animals, as an "animal drug." They will be held to the same requirements already existing for conventionally bred animals treated with hormones or antibiotics. (In the case of transgenic animals, the "drug" is a snippet of DNA.) Products derived from them or containing them as an ingredient will not necessarily require labeling.

A wide range of interested parties, including companies developing genetically engineered animals and consumer protection groups, are generally comfortable with the FDA decision. And yet, consumer acceptance of transgenic animals, particularly as food products, is still an unknown.

American consumers have been eating food from genetically engineered crops, such as corn, soybeans and canola, for a decade. However, transgenic animals have not been sold, pending the FDA deliberations on how to regulate them.

Why would someone want to genetically engineer animals?

Genetic engineering is a high-tech way to "breed" desirable traits into livestock. The benefits might be for the producer, such as a disease-resistant cow or an easy-to-raise salmon. It might be for the environment -- pigs that produce milder manure, for example -- or for the consumer, say, more nutritious meat.

The old-fashioned way of breeding farmed animals requires selecting offspring with desired traits over successive generations. Ron Stotish, chief executive of Aqua Bounty Technologies in Waltham, Mass., says the power of genetic engineering is that the same end is achieved in "one fell swoop." Transgenic animals also can be fitted with traits they probably would never develop naturally, as in the case of omega-3-producing pigs.

How is an animal genetically engineered?

An extra piece of genetic material (DNA) is inserted into the animal's genome at the earliest stages of development. Sometimes the method involves manipulating a fertilized egg that is then implanted into a surrogate mother; other times, it alters a cell from which an animal will be cloned. As the embryo grows, the DNA splice is replicated with the rest of the genetic material so that it ends up in every cell of the individual.

In fast-growing salmon developed by Aqua Bounty, the inserted gene is a salmon growth hormone, identical to the one the fish have naturally. The benefit comes from the precise placement of the added gene, which makes it active at times that the natural gene is not. "Normal salmon grow very, very slowly, and when it is cold they don't grow at all," Stotish says. "Our gene is active under a broader range of conditions and it allows the animals to grow." At 1 year old, a normal salmon might weigh 30 grams, but the transgenic fish weigh a kilogram, he says.

In pigs developed to contain omega-3 fatty acids, the added gene directs formation of an enzyme that converts naturally occurring omega-6 fatty acids to omega-3s. The gene is derived from tiny roundworms but is modified to make it more mammalian, says Randall Prather, co-director of the National Swine Resource and Research Center at the University of Missouri in Columbia, who developed these pigs.

Why did the FDA opt to regulate genetically engineered animals in this manner and what criteria are used to assess safety?

The FDA is responsible for food safety and already regulates genetically modified crops. By considering a DNA segment a drug, the agency will regulate transgenic animals in the same way it oversees dairy cows that receive growth hormone or beef cattle that get antibiotics, says FDA spokeswoman Siobhan DeLancey.

By using existing guidelines for so-called animal drugs, the FDA can put those products seeking approval into a process that is already up and running. "They have the staff and the process that allows them to look at this. They do it every day," says Stotish of Aqua Bounty, which has been seeking FDA approval for its fast-growing salmon for years.

Companies must show that their genetic manipulation is safe to the animal and that any food or animal-feed products derived from the animal are safe for the consumer and safe for the environment. Companies must also demonstrate that their claims about the gene-carried traits do occur.

Are there concerns beyond what the FDA can regulate?

Gregory Jaffe, who follows biotechnology for the consumer advocacy group Center for Science in the Public Interest, says the adopted guidelines are a good start "in the sense that the federal government has acknowledged that these animals are on the horizon and there needs to be oversight to ensure their safety."

But, he adds, genes are not the same as drugs. Drugs may have long-lasting effects on an individual, but they wouldn't get passed on to future generations. In the case of biotech animals, however, "you're altering the DNA of that animal, which gets carried on to its offspring." (Aqua Bounty says all the fish it markets will be sterile.)

Such lasting effects may have implications for preventing escape of the genes to natural populations, Jaffe says -- an issue that is beyond the FDA's expertise or authority.

Jaffe thinks the safety review should be more open and transparent. "Our regulatory processes for drugs" -- including animal drugs -- "are, on the whole, secret and done behind closed doors," he says. By law, the company controls what information is made public.

Other regulatory processes, such as those for pesticides at the Environmental Protection Agency, have been opened in past decades to invite public participation.

"Genetically engineered animals are highly controversial," Jaffe says. "I think that they [the FDA] need to have a transparent and participatory regulatory system -- where the public can review safety data and . . . expert scientists can provide comments to the agency."

Why did the FDA decide that food from genetically engineered animals doesn't have to be labeled?

The FDA labels food based on nutritional content, not manufacturing process, says the agency's DeLancey.

"So, if the food product is 'materially different' from a conventional product, then FDA can require that it be labeled. But the FDA doesn't require that a pork chop label specify whether it came from a pig produced through artificial insemination versus conventional breeding."

And similarly, now, if it came from genetically engineered animals. "We understand that consumers want transparency and labeling, but we are constrained by the regulations put in place by Congress," DeLancey says.

How will I know if the food I buy is from genetically engineered animals?

Pork from an omega-3 pig, should it gain approval, will be labeled because nutritional enhancement is a selling point -- and because the product is different from regular pork.

In other cases you may not know, although producers can voluntarily label their products. Researchers at the University of Guelph in Canada, who developed the so-called Enviropig with "greener" manure, say they intend to do so.

The U.S. Department of Agriculture has guidelines for labeling "natural meats," which would allow meat from non-transgenic animals to call attention to that fact.

mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:health@latimes.com

http://www.latimes.com/features/health/la-he-closer26-2009jan26,0,1632723.story

Tuesday, July 29, 2008

Docket No. 2005N-0373 RIN number 0910-AF54 Use of Materials Derived From Cattle in Medical Products REOPENING COMMENT PERIOD Date: March 30, 2007 at 11:37 am PST

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TSS SUBMISSION TO ;

Docket No. 2005N-0373 and RIN number 0910-AF54

Greetings FDA et al, ONCE again I would kindly like to comment on the continuous failed attempts by the FDA to regulate the use of certain cattle material in, or in the manufacture including processing) of, drugs, biologics, and medical devices intended for use in humans and human cells, tissues, and cellular and tissue-based products (HCT/Ps) (collectively, medical products for humans), and in drugs intended for use in ruminant animals (drugs for ruminants) from the proven risk factors of Transmissible Spongiform Encephalopahy i.e. TSE's in all species. I have continued to warn the FDA et al about these risk factors via the surgical and medical arena (vaccines, nutritional supplements, bovine heart valves, and other animal donor tissue), and I have continued to point out the risk factor of the UKBSENVCJD only theory, and the ramifications there from, i.e. BASE (bovine amyloidotic spongiform encephalopathy), and my greatest fears, one I have warned you about time and time again, seems to be coming true ;

64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE. Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD. A study also demonstrated that in a mouse model it was possible to alleviate the pathological changes of prion disease by suppressing expression of the prion protein gene after infection.

http://www.seac.gov.uk/minutes/95.pdf

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full text ;

http://madcowfeed.blogspot.com/2008/07/docket-no-2005n-0373-and-rin-number.html

http://madcowfeed.blogspot.com/2008/12/docket-no-fda2008d0597-draft-guidance.html

Tuesday, April 29, 2008

Interference at the EPA - Science and Politics at the U.S. Environmental Protection Agency

----- Original Message -----

From: "Terry S. Singeltary Sr." mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:flounder9@verizon.net
To: "Bovine Spongiform Encephalopathy" mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:BSE-L@aegee.org Cc: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:heggem.daniel@epa.gov; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:sibert.christopher@epa.gov; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:denne.jane@epa.gov; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:hazen.susan@epa.gov; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:mcrosby@ucsusa.org; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:erobinson@ucsusa.org; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:enegin@ucsusa.org; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:cjdvoice@yahoogroups.com; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:madcow@lists.iatp.org

Sent: Monday, April 28, 2008 9:48 PM

Subject: Interference at the EPA Science and Politics at the U.S. Environmental Protection Agency

Reports and Research

Interference at the EPA

Science and Politics at the U.S. Environmental Protection Agency

The U.S. Environmental Protection Agency (EPA) has the simple yet profound charge "to protect human health and the environment." EPA scientists apply their expertise to protect the public from air and water pollution, clean up hazardous waste, and study emerging threats such as global warming. Because each year brings new and potentially toxic chemicals into our homes and workplaces, because air pollution still threatens our public health, and because environmental challenges are becoming more complex and global, a strong and capable EPA is more important than ever.

Yet challenges from industry lobbyists and some political leaders to the agency's decisions have too often led to the suppression and distortion of the scientific findings underlying those decisions—to the detriment of both science and the health of our nation. While every regulatory agency must balance scientific findings with other considerations, policy makers need access to the highest-quality scientific information to make fully informed decisions.

Concern over this problem led the Union of Concerned Scientists (UCS) to investigate political interference in science at the EPA. The investigation combines dozens of interviews with current and former EPA staff, analysis of government documents, more than 1,600 responses to a survey sent to current EPA scientists, and written comments from EPA scientists.

The results of these investigations show an agency under siege from political pressures. On numerous issues—ranging from mercury pollution to groundwater contamination to climate change—political appointees have edited scientific documents, manipulated scientific assessments, and generally sought to undermine the science behind dozens of EPA regulations. ...

snip...please see full text ;

Interference at the EPA Science

http://sciencebushwhacked.blogspot.com/

Thu Dec 6, 2007 11:38

FDA IN CRISIS MODE, AMERICAN LIVES AT RISK

http://www.cidrap.umn.edu/cidrap/content/fs/food-disease/news/dec0407fda.html

FDA SCIENCE AND MISSION AT RISK

http://www.fda.gov/ohrms/dockets/ac/07/briefing/2007-4329b_02_01_FDA%20Report%20on%20Science%20and%20Technology.pdf

Monday, January 12, 2009

FDA scientists complain to Obama of 'corruption'

http://sciencebushwhacked.blogspot.com/2009/01/fda-scientists-complain-about.html

January 26, 2009

A kind greetings from Bacliff, Texas !

O.K., let us suppose the impossible, that indeed spontaneous Transmissible Spongiform Encephalopathy _does_ exists (to date, this has never been proven in the field, under natural conditions), at whatever rate they choose (i do not believe in the spontaneous TSE as the cause for 85%+ of all CJD i.e. the sporadic CJD's, i.e. that all these poor victims died from a 'happenstance of bad luck', or 'that a twisted funked out protein just chose this group on it's own, with no route and source of nothing involved'), BUT for now, lets say they exist.

PLEASE tell me then how a GM cow will be free from the spontaenous TSE ???

Spontaneous occurrence (14-16)

The evidence from the absence of BSE in many countries and the surveillance schemes abroad indicates that most BARBs cases cannot have arisen spontaneously, although the possibility cannot be excluded that a very few of them did so. The possibility of a very low frequency of spontaneous occurrence of BSE may be monitored from the output of surveillance in cattle populations elsewhere. R: A watching brief is kept on surveillance efforts world-wide.

http://www.defra.gov.uk/animalh/bse/pdf/hillreport.pdf

Perspectives BIOMEDICINE: A Fresh Look at BSE Bruce Chesebro*

Mad cow disease, or bovine spongiform encephalopathy (BSE), is the cattle form of a family of progressive brain diseases. These diseases include scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in humans, and chronic wasting disease (CWD) in deer and elk. They are also known as either "prion diseases" because of the association of a misfolded cellular prion protein in pathogenesis or "transmissible spongiform encephalopathies" (TSEs) because of the spongelike nature of the damaged brain tissue (1).

The recent discovery of two BSE-infected cows, one in Canada and one in the United States, has dramatically increased concern in North America among meat producers and consumers alike over the extent to which BSE poses a threat to humans as well as to domestic and wild animals. The European BSE epidemic of the late-1980s seems to have been initiated a decade earlier in the United Kingdom by changes in the production of meat and bone meal (MBM) from rendered livestock, which led to contamination of MBM with the BSE infectious agent. Furthermore, the fact that UK farmers fed this rendered MBM to younger animals and that this MBM was distributed to many countries may have contributed to the ensuing BSE epidemic in the United Kingdom and internationally (2).

Despite extensive knowledge about the spread of BSE through contaminated MBM, the source of BSE in Europe remains an unsolved mystery (2). It has been proposed that BSE could be derived from a cross-species infection, perhaps through contamination of MBM by scrapie-infected sheep tissues (see the figure). Alternatively, BSE may have been an endemic disease in cattle that went unnoticed because of its low level of horizontal transmission. Lastly, BSE might have originated by "spontaneous" misfolding of the normal cellular prion protein into the disease-associated abnormal isoform (3), which is postulated to be the infectious agent or "prion."

Five possible sources of BSE in North American cattle. Sheep, deer, and elk could spread prion diseases (TSEs) to cattle through direct animal contact or contamination of pastures. Endemic BSE has not been proven to exist anywhere in the world, but it is difficult to exclude this possibility because of the inefficient spread of BSE infectivity between individual animals (2). BSE caused by spontaneous misfolding of the prion protein has not been proven. CREDIT: KATHARINE SUTLIFF/SCIENCE

snip...

Nevertheless, the idea that BSE might originate due to the spontaneous misfolding of prion proteins has received renewed interest in the wake of reports suggesting the occurrence of atypical BSE (9-11). These results imply that new strains of cattle BSE might have originated separately from the main UK outbreak. Where and how might such strains have originated? Although such rare events cannot be studied directly, any number of sources of the original BSE strain could also explain the discovery of additional BSE strains in cattle (see the figure). However, it would be worrisome if spontaneous BSE were really a valid etiology because such a mechanism would be impossible to prevent--unlike other possible scenarios that could be controlled by large-scale eradication of TSE-positive animals.

Another way to look at this problem is to examine evidence for possible spontaneous TSE disease in other animals besides cattle. Spontaneous BSE would be extremely difficult to detect in cattle, where horizontal spread is minimal. However, in the case of the sheep TSE disease, scrapie, which spreads from ewes to lambs at birth as well as between adults, spontaneous disease should be detectable as new foci of clinical infection. In the early 1950s scrapie was eradicated in both Australia and New Zealand, and the mainland of both these countries has remained scrapie-free ever since. This scrapie-free status is not the result of selection of sheep resistant to scrapie because sheep from New Zealand are as susceptible as their UK counterparts to experimental scrapie infection (12). These experiments of man and nature appear to indicate that spontaneous clinical scrapie does not occur in sheep. Similarly, because CWD is known to spread horizontally, the lack of CWD in the deer or elk of eastern North America but its presence in western regions would also argue against a spontaneous disease mechanism. This is particularly noteworthy in New Zealand, where there are large numbers of deer and elk farms and yet no evidence of spontaneous CWD. If spontaneous scrapie does not occur in sheep or deer, this would suggest that spontaneous forms of BSE and sporadic Creutzfeldt-Jakob disease (sCJD) are unlikely to be found in cattle or humans. The main caveat to this notion is that spontaneous disease may arise in some animal species but not others. In humans, sCJD--which is considered by some researchers to begin by spontaneous misfolding of the prion protein--usually takes more than 50 years to appear. Thus, in animals with a shorter life-span, such as sheep, deer, and cattle, an analogous disease mechanism might not have time to develop.

What can we conclude so far about BSE in North America? Is the BSE detected in two North American cows sporadic or spontaneous or both? "Sporadic" pertains to the rarity of disease occurrence. "Spontaneous" pertains to a possible mechanism of origin of the disease. These are not equivalent terms. The rarity of BSE in North America qualifies it as a sporadic disease, but this low incidence does not provide information about cause. For the two reported North American BSE cases, exposure to contaminated MBM remains the most likely culprit. However, other mechanisms are still possible, including cross-infection by sheep with scrapie or cervids with CWD, horizontal transmission from cattle with endemic BSE, and spontaneous disease in individual cattle. Based on our understanding of other TSEs, the spontaneous mechanism is probably the least likely. Thus, "idiopathic" BSE--that is, BSE of unknown etiology--might be a better term to describe the origin of this malady. ...

snip...full text ;

http://www.sciencemag.org/cgi/content/full/sci;305/5692/1918

Release No. 0106.04

Contact: Office of Communications (202) 720-4623

Transcript of Remarks From Technical Briefing on BSE and Related Issues With Agriculture Secretary Ann M. Veneman and USDA Chief Veterinary Officer Dr. Ron DeHaven Washington D.C. - March 15, 2004

snip...

OPERATOR : “Yes. Our next one is coming from Elizabeth Weiss. Please state your company.”

ELIZABETH WEISS: “This is Elizabeth Weiss with USA Today.”

“I actually had two questions. First off, when you say you're looking for 1 in 10,000 cases, is USDA doing any work to find out the possibility of whether or not BSE exists in a spontaneous form in the way that it does in humans and elk populations?

“And secondly, how will any of this fit into some of the consternation that's been raised in California and with the Midwest packer that wanted to test all of its cattle?

“Thanks.”

DR. DEHAVEN: “All right. I think we've got three different questions in there, and I'll try to touch on each one of them.

“First of all, let me correct just a technical issue, and that is you mentioned 1 in 10,000. And actually our surveillance system currently is designed, the one that we have in place now is designed to detect 1 positive in 1 million cattle, and I gave some numbers between 200,000 and 268,000 that would allow us to detect 1 in 10 million as opposed to 1 in 10,000.

“So we would, if we were able to collect in the ballpark of those numbers of samples then we with increasing numbers of samples have an increasingly statistically valid sample from which to determine, one, whether or not the disease exists and, if so, at what prevalence level.

“So our real emphasis is to test as many of those animals as we can, ensure that we get an appropriate geographical distribution, but not setting a specific number as far as a target. Again, consistent with the recommendation from the International Review Team, their recommendation was to test all of them.

“So that's consistent with where we're going is to test as many as we possibly can.

“As far as spontaneous cases, that is a very difficult issue. There is no evidence to prove that spontaneous BSE occurs in cattle; but here again it's an issue of proving a negative. We do know that CJD, the human version of the disease, does occur spontaneously in humans at the rate of about 1 in 1 million. We don't have enough data to definitively say that spontaneous cases of BSE in cattle occur or do not occur.

“Again, it's a very difficult situation to prove a negative.

“So a lot of research is ongoing. Certainly if we do come up with any positive samples in the course of this surveillance we will be looking at that question in evaluating those samples but no scientifically hard evidence to confirm or refute whether or not spontaneous cases of BSE occur.

snip...

http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2004/03/0106.html

UK TESTING FINISHED NEXT WEEK

Matthews confirmed that the brain tissue samples from the US animal had arrived at Weybridge. Test results were likely to be ready by the end of next week, he said.

The suspect animal has already undergone a series of tests. A rapid screening test on Nov. 15 returned inconclusive results. Sophisticated immunohistochemistry (IHC) tests cleared the animal of any infection, but a third round of testing using a Western blot procedure showed a "weak positive".

Weybridge will do an IHC test plus three kinds of Western Blot tests on the samples. They will use "methods of slightly different analytical sensitivity that give us the greatest number of opportunities to interpret what we see," he said.

US beef industry leaders say scientists should not speculate about the unusual case.

"There's no evidence that it's atypical ... and there's absolutely no evidence that it's spontaneous," said Gary Weber, head of regulatory affairs at the National Cattlemen's Beef Association.

Matthews noted scientists are still grappling with what is typical and atypical BSE.

"Far too few people have looked at BSE in depth using all of the tests to be able to define 'this is normal and that one isn't'," he said.

Weber noted Japan used the term to describe two very young infected cattle because BSE is usually found in older animals. Italy labeled a case "atypical" because the misshaped prions were found in unexpected parts of the animal's brain. ...snip...end

http://www.agobservatory.org/headlines.cfm?refID=73207

Atypical BSE strain -- In July 2007, the UK Spongiform Encephalopathy Advisory Committee (SEAC) suggested that atypical BSE may be a distinct strain of prion disease. Unlike typical BSE, cases of atypical BSE, according to SEAC, may have risen spontaneously (although transmission through feed or the environment cannot be ruled out). Recently reported French surveillance data support this theory that unlike typical BSE, atypical BSE appears to represent sporadic disease

http://cdc.gov/ncidod/dvrd/bse/

http://www.defra.gov.uk/animalh/bse/pdf/hillreport.pdf

Spontaneous occurrence

14. Spontaneous cases of classical CJD in humans are found at a rate of about 1/million around the world (Will, 1993), without appreciable racial or geographical variation except in a few specific cases, notably Jews of Libyan origin that have a mutation in the open reading frame of the PRNP gene (Chapman and Korczyn, 1991). Thus it is theoretically possible that spontaneous cases of BSE could occur as a consequence of a germ line mutation, in which case relatives would also have a certain or increased incidence of the disease, or a somatic mutation, which would be unlikely to be detectable unless the appropriate tissue were identified, or after some transformation in the PrP protein in the animal concerned. BSE was unknown prior to its detection in Britain in the mid 1980s, and Index cases found around the world since then can all be explained in terms of export from the UK directly or indirectly of cattle or of feed components. No BSE affected animals have been reported in many developed countries with large cattle populations, including Australia, New Zealand, Norway and Sweden, which have mixed cattle populations; and the only infected animal detected in the US was of Canadian origin. The disease seems to have a highly homogeneous aetiology (e.g. Bruce, 2003).

15. Data from the USA, where the dairy population in particular is highly related to that in GB provide an upper limit to the spontaneous rate. A programme of testing is in place of a target population of adult cattle exhibiting some clinical sign that might be consistent with BSE (animals reported as having CNS or clinical signs of BSE or were non-ambulatory). In the intensive programme from June 2004 over 375000 animals were tested in the following 12 months. No positive results have yet been obtained in these or previous tests (USDA BSE Testing). This implies a putative upper limit of under 10 per million in this target group. Assuming, as analysis has shown, the relative risk in this group is about 30 times higher than in the population as a whole (European Commission, 2002c), then the incidence in the population as a whole is under 3 per 10 million. This figure could possibly be biased downwards if affected animals are diagnosed and disposed of without being tested. Taking account of testing done and the lack of clinical cases seen in many other countries also, it seems highly unlikely that the spontaneous rate can be as much as 3 per 10 million head. Nor can spontaneous occurrence explain incidences of ca. 30 cases of BARBs per year in 2002/4 in the UK adult cattle population of ca. 4 million. [NOTE ADDED 30 JUNE: The recent confirmation of a previously inconclusive case in the USA affects these calculations. If the animal did not have access to infected feed, the calculations have to be revised: they suggest a sporadic incidence in the population of 1/(375000 x 30) or almost 1 per 10 million, with the upper limit under 5 per 10 million.]

16. Calculation of a maximum rate of possible transformation from scrapie to BSE is less feasible. Nevertheless, BSE appears not to have arisen in the UK until around the early 1980s, despite the presence of scrapie in sheep here for at least 200 years. Although a change in the scrapie prion may have been the cause of the initial cases of BSE, the difference between their properties in mice and the uniformity of the BSE brain lesions suggest it is unlikely that more than one such mutation was the source of BSE. It is most unlikely that the same mutation could be occurring often enough to contribute significantly to BARBs cases. Furthermore BARBs cases do not match the geographical distribution of the sheep population. The evidence from the absence of BSE in many countries and the surveillance schemes abroad indicates that most BARBs cases cannot have arisen spontaneously, although the possibility cannot be excluded that a very ...

http://www.defra.gov.uk/animalh/bse/pdf/hillreport.pdf

242 Atypical and classical BSE are different strains based upon Western blot profiles 243 (Hill, 2004; Normile, 2004; Baron et al., 2006), and this study indicates that disease Page 11 of 23 Journal of Animal Science Downloaded from jas.fass.org by on November 12, 2008. 12 progresses via different routes for these strains. The disparate 244 routes of pathogenesis in 245 atypical BSE can occur by 1 of 2 means. One possibility is that the source of infectivity 246 in atypical BSE is exposure to contaminated feedstuffs, as is the case for classical BSE, 247 but progression occurs in a disparate manner that bypasses the influence of the indel 248 polymorphisms. The other possibility is that atypical BSE is occurring spontaneously in 249 the host. Support for atypical BSE occurring spontaneously are the parallels to sporadic 250 TSE in humans, specifically, occurrence in older hosts and a comparable low incidence 251 rate (Baron and Biacabe, 2006). Furthermore, atypical BSE occurs as isolated, sporadic 252 cases in contrast to the clustering of cases observed for feed borne classical BSE 253 (Donnelly et al., 1997). Interestingly, the only native born cases of BSE in the United 254 States identified to date have been classified as atypical BSE.

255 No experiment can conclusively confirm a spontaneous nature for atypical BSE.

snip...end

http://jas.fass.org/cgi/reprint/jas.2007-0208v1.pdf

Monday, February 11, 2008 7:00 am Registration and Morning Coffee

Emerging Concerns: De novo Formation of Prions

9:05 De novo Generation of Prion Infectivity in a Cell-Free System Joaquin Castilla, Ph.D., Assistant Professor, Department of Infectology, Scripps Research Institute-Florida Transmissible spongiform encephalopathies (TSEs) are a group of neurodegenerative disorders affecting both humans and animals. There is no available treatment or therapy for these fatal diseases. The infectious agent associated with TSEs (termed prion) appears to be composed uniquely of a protein, which is a conformationally-modified version (PrPSc) of the cellular prion protein (PrPC). The disease is propagated by the conversion of host PrPC into PrPSc induced by small quantities of PrPSc. Interestingly, prions occur in the form of different strains that show distinct biological and physicochemical properties. TSEs can have diverse origins, including genetic, sporadic (putatively spontaneous) and infectious. The occurrence of sporadic cases of prion diseases in humans and maybe in other species, i.e. atypical bovine spongiform encephalopathy (BSE) in European and USA cattle and atypical scrapie cases in sheep suggest that spontaneous prion diseases may happen infrequently but ubiquitously. However, there are no reported cases of spontaneously-occurring prion disease in experimental wild-type rodent models. We have used a novel technique, Protein Misfolding Cyclic Amplification (PMCA) to rapidly propagate prions in the test tube, using normal brain homogenate as substrate. Prions propagated in vitro are infectious in vivo and maintain their prion strain specificity. PMCA has been used to efficiently amplify a variety of prion strains from mouse, hamster, bank vole, deer, cattle, sheep and human. Therefore, to mimic spontaneous generation of infectivity in vitro becomes one of the most important challenges in the prion field. We show here, for the first time, the de novo generation of infectious prions from bank voles (Clethrionomys glareolus) starting with non-infectious brain homogenates. Several biochemically different prion strains were generated using two different wild-type vole genotypes. The de novo in vitro generated PrPSc was highly infectious after its inoculation in bank voles. We show an extensive characterization of this "spontaneous" phenomenon.

http://www.healthtech.com/Conferences_Overview.aspx?c=518&id=59662&c=518

Pathogenesis Chairperson: Suzette Priola, Ph.D.

11:10 Accumulation of Prion Protein in the Brain That is Not Associated with Transmissible Disease Pedro Piccardo, M.D., Senior Investigator, OBRR / DETTD / LBPUA, FDA (Invited)

11:35 High Levels of TSE Infectivity Can Be Associated with Little or No Detectable PrPSc in Vivo Rona Barron, Ph.D., Neuropathogenesis Unit, Roslin Institute and Royal (Dick) School of Veterinary Studies This work examines the relationship between TSE infectivity and the abnormal prion protein, PrPSc. In a mouse model of disease we have shown high titres of TSE infectivity in brain tissue which contains little or no PrP-res. We also found no evidence of other abnormal PrP isofoms such as PK-sen PrPSc. These data question the true relationship between PrPSc and TSE infectivity, and the current reliance on PrPSc as the sole diagnostic marker for TSE disease.

12:00 Conversion of the BASE Prion into the BSE Prion: The Origin of BSE? Fabrizio Tagliavini, Ph.D., Director, Division of Neurology 5 & Neuropathology, Neurological Institute "Carlo Besta" Twenty years after the identification of bovine spongiform encephalopathy (BSE), the origin of the causal agent is still unknown. This issue is of fundamental importance, since knowledge of the origin of the BSE agent is essential for prevention of future outbreak of the disease or variants thereof in cattle and other mammals. We carried out transmission studies with transgenic mice expressing bovine PrP and four lines of non-transgenic mice and found that an atypical form of spongiform encephalopathy of cattle, termed BASE or BSE-L, is caused by a prion strain distinct from that of classical BSE. Noteworthy, this newly characterized prion strain has the ability to convert into the classical BSE strain upon serial transmission to inbred mouse lines. According to these results, BASE--which is regarded as a sporadic form of prion disease in cattle--may be the origin of BSE, following conversion of the causal agent in an intermediate host.

12:45 Luncheon Technology Workshop (Sponsorship Available) or Lunch on Your Own

2:00 Sporadic CJD and Atypical BSE: Two Children of One Protein Maurizio Pocchiari, Ph.D., Director of Research, Virology, Istituto Superiore Di Sanita The identification of forms of TSE diseases in cattle caused by prion strains different from BSE has raised new concerns on the possibility that these novel agents might induce disease in humans with a phenotype resembling sporadic CJD. The analysis of the distribution of the different molecular subtypes of sporadic CJD might give some answers.

http://www.healthtech.com/Conferences_Overview.aspx?c=518&id=59662&c=518

let's see, a few examples of our extensive BSE surveillance plan ;

On December 23, 2003, the U.S. Department of Agriculture (USDA) announced a presumptive diagnosis of the first known case of BSE in the United States. It was in an adult Holstein cow from Washington State. This diagnosis was confirmed by an international reference laboratory in Weybridge, England, on December 25. Trace-back based on an ear-tag identification number and subsequent genetic testing confirmed that the BSE-infected cow was imported into the United States from Canada in August 2001. Because the animal was non-ambulatory (a “downer cow”) at slaughter, brain tissue samples were taken by USDA’s Animal and Plant Health Inspection Service as part of its targeted surveillance for BSE. However the animal’s condition was attributed to complications from calving. After the animal was examined by a USDA Food Safety and Inspection Service (FSIS) veterinary medical officer both before and after slaughter, the carcass was released for use as food for human consumption. During slaughter, the tissues considered to be at high risk for the transmission of the BSE agent were removed. On December 24, 2003, FSIS recalled beef from cattle slaughtered in the same plant on the same day as the BSE positive cow. (see Bovine Spongiform Encephalopathy in a Dairy Cow - Washington State, 2003.)

On June 24, 2005, the USDA announced receipt of final results from The Veterinary Laboratories Agency in Weybridge, England, confirming BSE in a cow that had conflicting test results in 2004. This cow was from Texas, died at approximately 12 years of age, and represented the first endemic case of BSE in the United States. (see Texas BSE Investigation, Final Epidemiology Report, August 2005 (PDF – 83 KB))

On March 15, 2006, the USDA announced the confirmation of BSE in a cow in Alabama. The newly confirmed case was identified in a non-ambulatory (downer) cow on a farm in Alabama. The animal was euthanized by a local veterinarian and buried on the farm. The age of the cow was estimated by examination of the dentition as 10-years-old. It had no ear tags or distinctive marks; the herd of origin could not be identified despite an intense investigation (see second featured item above and Alabama BSE Investigation, Final Epidemiology Report, May 2006).

snip...

Strains of BSE There is increasing evidence that there are different strains of BSE: the typical BSE strain responsible for the outbreak in the United Kingdom and two atypical strains (H and L strains).

Typical BSE strain -- The BSE strain responsible for most of the BSE cases in Canada is the same classic or typical strain linked to the outbreak in the United Kingdom. It is known to be preventable through elimination of BSE contaminated feed and has been causally linked to vCJD in humans. This typical strain has not yet been identified in any U.S.-born cattle.

Atypical BSE strain -- In July 2007, the UK Spongiform Encephalopathy Advisory Committee (SEAC) suggested that atypical BSE may be a distinct strain of prion disease. Unlike typical BSE, cases of atypical BSE, according to SEAC, may have risen spontaneously (although transmission through feed or the environment cannot be ruled out). Recently reported French surveillance data support this theory that unlike typical BSE, atypical BSE appears to represent sporadic disease

Both of the U.S.-born BSE cases and two of the 15 Canadian-born BSE cases were 10 years of age or older and three of these older North American cases for whom the strain type is presently known were linked to an atypical BSE strain known as the H-strain. Publication of the strain testing results on the 13 year-old BSE-infected Canadian cow identified in December 2007 is pending.

http://cdc.gov/ncidod/dvrd/bse/

Saturday, January 24, 2009

Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report

Research Project: Study of Atypical Bse

Location: Virus and Prion Diseases of Livestock

2008 Annual Report

snip...

Thursday, December 04, 2008 2:37 PM

"we have found that H-BSE can infect humans."

personal communication with Professor Kong. ...TSS

snip...

http://bse-atypical.blogspot.com/2009/01/bovine-spongiform-encephalopathy-h-bse.html

Sunday, December 28, 2008

MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy

Greetings,

I thought a quick review of the Bush's terribly flawed and failed mad cow disease policy, from the illegal feeding of literally millions and millions of pounds of highly suspect, and banned mad feed, to the failed BSE surveillance program, all of which exposed, needlessly, millions of people to the mad cow agent i.e. Transmissible Spongiform Encephalopathy. ...

Parentage-based DNA traceback in beef and dairy cattle 2008

http://www.ars.usda.gov/sp2UserFiles/Place/54380570/HeatonPublications/HeatonParentage-Traceback2008o.pdf

48 hour traceback for BSE mad cow disease in the USA ???

NOT in your lifetime !

8 YEARS IN REVIEW OF THE MAD COW DEBACLE IN THE USA ;

FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA

Statement on Texas Cow With Central Nervous System Symptoms

snip...full text ;

http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html

Friday, August 29, 2008

CREEKSTONE VS USDA COURT OF APPEALS, BUSH SAYS, NO WAY, NO HOW

http://madcowtesting.blogspot.com/2008/08/creekstone-vs-usda-court-of-appeals.html

Sunday, March 16, 2008

MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE

http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html

HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008

snip...

Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...

snip...

http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html

November 25, 2008

Update On Feed Enforcement Activities To Limit The Spread Of BSE

http://madcowfeed.blogspot.com/2008/11/november-2008-update-on-feed.html

"the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine." ... interesting. ... TSS

Thursday, June 05, 2008

Review on the epidemiology and dynamics of BSE epidemics

Vet. Res. (2008) 39:15 www.vetres.org DOI: 10.1051/vetres:2007053 c INRA, EDP Sciences, 2008 Review article

snip...

And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.

snip...

Cases of atypical BSE have only been found in countries having implemented large active surveillance programs. As of 1st September 2007, 36 cases (16 H, 20 L) have been described all over the world in cattle: Belgium (1 L) [23], Canada (1 H)15, Denmark (1 L)16, France (8 H, 6 L)17, Germany (1 H, 1 L) [13], Italy (3 L)18, Japan (1 L) [71], Netherlands (1 H, 2 L)19, Poland (1 H, 6 L)20, Sweden (1 H)21, United Kingdom (1 H)22, and USA (2 H)23. Another H-type case has been found in a 19 year old miniature zebu in a zoological park in Switzerland [56]. It is noteworthy that atypical cases have been found in countries that did not experience classical BSE so far, like Sweden, or in which only few cases of classical BSE have been found, like Canada or the USA.

And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.

full text 18 pages ;

http://www.vetres.org/index.php?option=article&access=standard&Itemid=129&url=/articles/vetres/pdf/2008/04/v07232.pdf

please see full text ;

http://bse-atypical.blogspot.com/2008/06/review-on-epidemiology-and-dynamics-of.html

***Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.***

Progress Report from the National Prion Disease Pathology Surveillance Center

An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD

April 3, 2008

http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45

In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.

In short, a great deal of further work will need to be done before the phenotypic features and prevalence of atypical BSE are understood. More than a single strain may have been present from the beginning of the epidemic, but this possibility has been overlooked by virtue of the absence of widespread Western blot confirmatory testing of positive screening test results; or these new phenotypes may be found, at least in part, to result from infections at an older age by a typical BSE agent, rather than neonatal infections with new "strains" of BSE. Neither alternative has yet been investigated.

http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm

Wednesday, August 20, 2008

Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?

http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html

A New Prionopathy OR more of the same old BSe and sporadic CJD

http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.html

Communicated by: Terry S. Singeltary Sr.

[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]

http://pro-med.blogspot.com/2007/11/proahedr-prion-disease-update-2007-07.html

http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963

There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.

He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf

sporadic Fatal Familial Insomnia

http://sporadicffi.blogspot.com/

JOURNAL OF NEUROLOGY

MARCH 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000071/!x-usc:mailto:flounder9@verizon.net

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?

http://www.neurology.org/cgi/eletters/60/2/176#535

THE PATHOLOGICAL PROTEIN

Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9

June 2003

BY Philip Yam

CHAPTER 14 LAYING ODDS

Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.

http://www.thepathologicalprotein.com/

Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

Terry S. Singeltary, Sr Bacliff, Tex

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT

http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

2 January 2000

British Medical Journal U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

http://www.bmj.com/cgi/eletters/320/7226/8/b#6117

15 November 1999

British Medical Journal vCJD in the USA * BSE in U.S.

http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406

Creutzfeldt Jakob Disease

http://creutzfeldt-jakob-disease.blogspot.com/

USA PRION UNIT BLOG

http://prionunitusaupdate2008.blogspot.com/

Sunday, April 20, 2008

Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008

Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.

see full text ;

http://prionunitusaupdate2008.blogspot.com/2008/04/progress-report-from-national-prion.html

CJD TEXAS (cjd clusters)

http://cjdtexas.blogspot.com/

USA WRITTEN CJD QUESTIONNAIRE ???

http://cjdquestionnaire.blogspot.com/

Attending Dr.: Date / Time Admitted : 12/14/97 1228

UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report

FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858

FINAL AUTOPSY DIAGNOSIS

I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.

http://creutzfeldt-jakob-disease.blogspot.com/2008/07/heidenhain-variant-creutzfeldt-jakob.html

2007

The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.

http://www.cjdfoundation.org/fact.html

TSS

FDA Scientists Complain About Corruption Inside The Agency

2009-01-12T07:26:00.000-08:00

FDA scientists complain to Obama of 'corruption'

By RICARDO ALONSO-ZALDIVAR

updated 5:10 p.m. CT, Thurs., Jan. 8, 2009 WASHINGTON - In an unusually blunt letter, a group of federal scientists is complaining to the Obama transition team of widespread managerial misconduct in a division of the Food and Drug Administration.

"The purpose of this letter is to inform you that the scientific review process for medical devices at the FDA has been corrupted and distorted by current FDA managers, thereby placing the American people at risk," said the letter, dated Wednesday, on the letterhead of the agency's Center for Devices and Radiological Health.

The center is responsible for medical devices ranging from stents and breast implants to MRIs and other imaging machinery. The concerns of the nine scientists who wrote to the transition team echo some of the complaints from the FDA's drug review division a few years ago during the safety debacle involving the painkiller Vioxx.

The FDA declined to publicly respond to the letter, but said it is working to address the concerns.

In their letter, the FDA dissidents alleged that agency managers use intimidation to squelch scientific debate, leading to the approval of medical devices whose effectiveness is questionable and which may not be entirely safe.

A copy of the letter, with the names of the scientists redacted, was provided to The Associated Press by a congressional official.

FDA spokeswoman Judy Leon said in response: "We have been working very closely with members of the transition team and any concerns or questions they have on any issue, we will address directly with the team. Separately, the agency is actively engaged in a process to explore the staff members' concerns and take appropriate action."

Senior Democratic and Republican lawmakers are urging Obama to appoint a commissioner who will shake up the FDA and restore the confidence of its working-level scientists and medical experts. But industry officials fear that approval of new drugs and devices could be delayed by endless scientific disputes within the agency.

Copyright 2008 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.

http://www.msnbc.msn.com/id/28565720/

FDA Scientists Complain About Corruption Inside The Agency

By Anna Boyd 13:39, January 11th 2009

A group of nine scientists at the Food and Drug Administration sent a letter to President-elect Barack Obama and his transition team, asking for immediate intervention as the agency is “fundamentally broken” and fails to fulfill its mission.

“The purpose of this letter is to inform you that the scientific review process for medical devices at the FDA has been corrupted and distorted by current FDA managers, thereby placing the American people at risk,” read the six-page letter, written on the agency’s Center for Devices and radiological letterhead.

The scientists went even further and said there is an atmosphere at FDA in which the honest employee fears the dishonest one, when it should be the other way around. Moreover, the FDA has promoted and rewarded some of the managers involved with the inappropriate practices. They also complained about devices that have not been properly labeled, about managers without appropriate experience who have been given authority to make final decisions about device regulation and have done so while ignoring serious safety and effectiveness concerns, or of FDA experts who have been excluded from product meetings because manufacturers felt that they were "biased."

Responding to the accusations, agency spokeswoman Judy Leon said the FDA has been working “very closely” with Mr. Obama’s transition team and will address any issues or concerns the team presents. She added the agency is “actively engaged in a process to explore the staff members' concerns and take appropriate action.”

Members of the transition team weren't available to discuss over the issues in the letter or whether they intend to address it publicly.

http://www.efluxmedia.com/news_FDA_Scientists_Complain_About_Corruption_Inside_The_Agency_33082.html

FDA Scientists Ask For Obama’s Help To Fight Corruption Inside The Agency

By Irene Collins 18:43, January 10th 2009

It appears that some scientists at the FDA wrote to President-Elect Barack Obama’s transition team, basically begging for help and outlining a number of problems with an agency they describe as “fundamentally broken.” Nine scientists who claim the FDA is a “fundamentally broken” agency authored the letter, sent Wednesday and written on the agency’s Center for Devices and Radiological Health letterhead.

The letter, addressed to John Podesta, says the atmosphere at the agency is one where “the honest employee fears the dishonest employee.”

Podesta is head of the Obama transition team but others receiving copies include Tom Daschle, Obama’s pick to lead the Department of Health and Human Services; Joshua Sharfstein, the physician leading the transition team’s assessment of FDA activities; and Senator Edward Kennedy, chairman of the health committee.

The scientists wrote that they have raised their concerns with FDA Commissioner Andrew von Eschenbach and Bill McConagha, an attorney and the assistant commissioner for accountability and integrity at the agency, but added that the agency has taken no action to address the issues.

In addition, they wrote that FDA has promoted and rewarded some of the managers involved with the inappropriate practices. They also complained about devices that have not been properly labeled, about managers without appropriate experience who have been given authority to make final decisions about device regulation and have done so while ignoring serious safety and effectiveness concerns, or of FDA experts who have been excluded from product meetings because manufacturers felt that they were "biased."

The Obama transition team has not issued a statement about the scientists’ complaint of corruption among FDA managers.

http://www.efluxmedia.com/news_FDA_Scientists_Ask_For_Obamas_Help_To_Fight_Corruption_Inside_The_Agency_33067.html

For whatever it's worth, myself and others have been asking for an investigation into the FDA and the USDA et al for a decade or more. ...TSS

Friday, June 13, 2008

Federal Oversight of Food Safety: FDA Has Provided Few Details GAO-08-909T June 12, 2008

http://fdafailedus.blogspot.com/2008/06/federal-oversight-of-food-safety-fda.html

Thu Dec 6, 2007 11:38

FDA IN CRISIS MODE, AMERICAN LIVES AT RISK

http://www.cidrap.umn.edu/cidrap/content/fs/food-disease/news/dec0407fda.html

FDA SCIENCE AND MISSION AT RISK

http://www.fda.gov/ohrms/dockets/ac/07/briefing/2007-4329b_02_01_FDA%20Report%20on%20Science%20and%20Technology.pdf

http://fdafailedus.blogspot.com/

UNITED STATES DEPARTMENT OF AGRICULTURE OFFICE OF INSPECTOR GENERAL WASHINGTON D.C. 20250

DEC 28, 2007

Mr. Terry S. Singeltary, Sr. P.O. Box 42 Bacliff, Texas 77518

Subject: FOIA Appeal-Log No. 08-00034 (No. 07-00060)

Dear Mr. Singeltary:

This is in response to your December 3, 2007, Freedom of Information Act (FOIA), 5 U.S.C. & 552, appeal of the November 20, 2007, decision of Ms. Deirdre MacNeil, FOIA/Privacy Act (PA) Attorney, Office of Inspector General (OIG), Department of Agriculture (USDA). As explained below, your FOIA appeal is denied.

As background, on March 1, 2007, you requested the "final results of the TSE Mouse-bioassays of those Atypical TSE in the Vermont Sheep." FOIA requires the release of agency records except where one or more of the nine enumerated exceptions apply. On November 20, 2007, Ms. MacNeil responded to your request by sending you seven pages from Hotline files PS-3340-0024, which was responsive to your request. Ms. MacNeil withheld identifying information pursuant to Exceptions 6 and 7(C) of the FOIA. See 5. U.S.C.& 552(b)(6) and (7)(C). On December 3, 2007, you appealed Ms. MacNeils decision.

12-3-07

To The Honorable Inspector General USDA,

snip...

see full history of this saga here ;

http://foiamadsheepmadrivervalley.blogspot.com/

Tuesday, April 29, 2008 Interference at the EPA - Science and Politics at the U.S. Environmental Protection Agency ----- Original Message -----

From: "Terry S. Singeltary Sr." flounder9@verizon.net To: "Bovine Spongiform Encephalopathy" BSE-L@aegee.org Cc: heggem.daniel@epa.gov; sibert.christopher@epa.gov; denne.jane@epa.gov; hazen.susan@epa.gov; mcrosby@ucsusa.org; erobinson@ucsusa.org; enegin@ucsusa.org; cjdvoice@yahoogroups.com; madcow@lists.iatp.org

Sent: Monday, April 28, 2008 9:48 PM

Subject: Interference at the EPA Science and Politics at the U.S. Environmental Protection Agency

Reports and Research

Interference at the EPA

Science and Politics at the U.S. Environmental Protection Agency

The U.S. Environmental Protection Agency (EPA) has the simple yet profound charge "to protect human health and the environment." EPA scientists apply their expertise to protect the public from air and water pollution, clean up hazardous waste, and study emerging threats such as global warming. Because each year brings new and potentially toxic chemicals into our homes and workplaces, because air pollution still threatens our public health, and because environmental challenges are becoming more complex and global, a strong and capable EPA is more important than ever.

Yet challenges from industry lobbyists and some political leaders to the agency's decisions have too often led to the suppression and distortion of the scientific findings underlying those decisions—to the detriment of both science and the health of our nation. While every regulatory agency must balance scientific findings with other considerations, policy makers need access to the highest-quality scientific information to make fully informed decisions.

Concern over this problem led the Union of Concerned Scientists (UCS) to investigate political interference in science at the EPA. The investigation combines dozens of interviews with current and former EPA staff, analysis of government documents, more than 1,600 responses to a survey sent to current EPA scientists, and written comments from EPA scientists.

The results of these investigations show an agency under siege from political pressures. On numerous issues—ranging from mercury pollution to groundwater contamination to climate change—political appointees have edited scientific documents, manipulated scientific assessments, and generally sought to undermine the science behind dozens of EPA regulations. ...

snip...please see full text ;

Interference at the EPA Science

http://sciencebushwhacked.blogspot.com/

Sunday, December 28, 2008

MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy

Greetings,

I thought a quick review of the Bush's terribly flawed and failed mad cow disease policy, from the illegal feeding of literally millions and millions of pounds of highly suspect, and banned mad feed, to the failed BSE surveillance program, all of which exposed, needlessly, millions of people to the mad cow agent i.e. Transmissible Spongiform Encephalopathy. ...

Parentage-based DNA traceback in beef and dairy cattle 2008

http://www.ars.usda.gov/sp2UserFiles/Place/54380570/HeatonPublications/HeatonParentage-Traceback2008o.pdf

48 hour traceback for BSE mad cow disease in the USA ???

NOT in your lifetime !

8 YEARS IN REVIEW OF THE MAD COW DEBACLE IN THE USA ;

FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA

Statement on Texas Cow With Central Nervous System Symptoms

snip...full text ;

http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html

USDA CERTIFIED DEADSTOCK DOWNER COW SCHOOL LUNCH PROGRAM

http://downercattle.blogspot.com/

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

EPA scientists blast FDA advice on fish

2008-12-21T14:29:00.000-08:00

EPA scientists blast FDA advice on fish

Experts insist mercury warnings for women, kids 'inadequate'

By MICHAEL HAWTHORNE Chicago Tribune Dec. 20, 2008, 5:32PM

In the waning days of the Bush presidency, the Food and Drug Administration is pushing to scuttle the government's advice about mercury-contaminated seafood, a dramatic policy change that would, in effect, encourage women and children to eat more fish despite growing concerns about the toxic metal.

The FDA's recommendations, sent recently to the White House Office of Management and Budget for approval, prompted a sharp rebuke from scientists at the Environmental Protection Agency who, in memos circulated earlier this month, described them as "scientifically flawed and inadequate."

A joint advisory issued by the two agencies in 2004 cautions women of childbearing age, nursing mothers and young children to limit seafood consumption to 12 ounces a week. But in a draft version of the FDA's new report, the agency says its own modeling shows that kids can benefit from eating fish.

The FDA argues that nutrients in fish offset the risks posed by mercury and could boost a child's IQ by three points. Its conclusion is similar to claims by the seafood industry.

EPA scientists, though, say the FDA's report reaches conclusions that aren't supported by the studies it cites, and at various points either trivializes or overstates existing research.

Moreover, the EPA scientists say, the FDA fails to consider that some species of fish tend to have much higher mercury levels than others. The EPA's comments reflect long-standing criticism that the government isn't giving Americans enough advice about which types of seafood are safest to eat.

Before Bush leaves office The FDA's proposal is among a series of controversial policy changes moving quickly as the Bush administration prepares to leave office. Seafood industry lobbyists want to scale back the government's mercury warning, which they contend is depressing sales and scaring women away from eating fish.

In contrast, President-elect Barack Obama and leaders of the Democratic-controlled Congress have pledged to enforce tougher mercury policies.

"Once again, the Bush administration seems intent on ignoring sound science on mercury poisoning," Sen. Patrick Leahy, D-Vt., said. "This backroom bouquet for special interests should be stopped in its tracks."

The Environmental Working Group, an advocacy organization that obtained the FDA report, sent a letter to EPA Administrator Stephen Johnson urging him to fight the proposal.

In an e-mail response to questions, the FDA said a final decision had not been reached. "The FDA will make no final determination until all the relevant comments and scientific analysis has been carefully considered," the agency wrote.

Choosing low-mercury fish Studies have shown that exposure to mercury in the womb, mostly from fish eaten by mothers, can irreversibly damage the brain before birth, causing subtle delays in walking and talking as well as decreased attention span and memory. Some research suggests that mercury also could increase the risk of heart disease in adults.

A recent study found that the percentage of women with high mercury levels declined from 2000 to 2004, even though those women were eating the same amount of seafood. The study's authors said their finding suggests that consumer advisories are prompting women to eat fish low in mercury.

Sniping between the FDA and EPA is nothing new. The two agencies have fought for years about how to caution women and children about mercury.

http://www.chron.com/disp/story.mpl/nation/6174650.html

TSS

Company advances on plan for West Texas nuclear dump

2008-08-06T09:01:00.000-07:00

(railcars loaded with MOUND COLD WAR NUCLEAR AFTER-BIRTH headed to Texas)

Company advances on plan for West Texas nuclear dump Construction contract awarded despite suit asking project be stopped By JANET ELLIOTT Copyright 2008 Houston Chronicle Austin Bureau Aug. 5, 2008, 11:23PM

AUSTIN — Waste Control Specialists is moving ahead with construction of a radioactive waste dump in Andrews County in West Texas, despite a pending lawsuit challenging the project.

The Dallas company said Tuesday it has awarded a three-year $80 million contract to URS, a San Francisco-based engineering and construction firm.

The contract includes the addition of a railroad loop and facilities for unloading hazardous waste from rail cars, as well as construction of two adjacent landfills for different categories of radioactive waste.

1 of 2 applications OK'd State environmental regulators in May granted Waste Control a license to dispose of byproduct material, including waste from nuclear weapons processing and uranium mining. The company has a second application pending for "low-level" waste, which would allow the disposal of a higher level of radioactive material, including waste from nuclear power plants.

Waste Control President Rodney Baltzer said construction would begin immediately on the rail facilities and byproducts landfill. No work will be done on the low-level site until the company receives a license.

Baltzer said in a news release that URS has been involved in the licensing process and is familiar with the site.

"URS used that knowledge in a competitive bidding process to provide the best value for WCS," he said.

Waste Control is owned by Harold Simmons, a major donor to Gov. Rick Perry and other state politicians.

Risk to water questioned The Sierra Club filed a lawsuit last month in Travis County to overturn the byproducts disposal license. The environmental group went to court after the Texas Commission on Environmental Quality denied its request for a contested hearing on the project.

"It's a concern that they're moving forward," said Cyrus Reed, a lobbyist for the Sierra Club. "We think the underlying geology has not been adequately studied and, therefore, confirmed as being safe for the disposal of this type of waste."

The site is controversial because of its location near underground water.

A team of geologists and engineers who reviewed the location for the Texas Commission on Environmental Quality concluded last year that the low-level waste disposal license should be denied. They said one water table may be closer than 14 feet, making it "highly likely" that water could seep into the dump as annual rainfall increases because of climate change. Both landfills would be on 1,300 acres WCS owns near the Texas-New Mexico border. Baltzer said the site has been extensively tested to ensure the material can be contained safely.

"The landfills will have similar designs, with disposal in the site's almost impenetrable red bed claystones," he said.

Among the materials to be buried are 3,776 steel containers of waste from an Ohio facility that processed uranium for Cold War-era nuclear weapons.

janet.elliott@chron.com

http://www.chron.com/disp/story.mpl/metropolitan/5927076.html

Wednesday, July 30, 2008

TEXAS WINS TO BE NEXT BIG DUMPING GROUND FOR NUCLEAR WEAPONS RADIOACTIVE WASTE

(see more photo's of railcars loaded with MOUND COLD WAR NUCLEAR AFTER-BIRTH headed to Texas)

http://sciencebushwhacked.blogspot.com/2008/07/texas-wins-to-be-next-big-dumping.html

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

TEXAS WINS TO BE NEXT BIG DUMPING GROUND FOR NUCLEAR WEAPONS RADIOACTIVE WASTE

2008-07-30T08:42:00.000-07:00

-----Original Message-----
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]
Sent: Thursday, May 22, 2008 5:01 PM To: janet.elliott@chron.com Cc: viewpoints@chron.com; tbeyerlein@DaytonDailyNews.com
Subject: re-Company wins license to bury nuclear waste

re-Company wins license to bury nuclear waste Houston Chronicle May 22, 2008

AUSTIN — State environmental regulators voted 2-1 Wednesday to grant a Dallas company a license to dispose of waste from nuclear weapons processing and uranium mining in Andrews County in West Texas.

Texas Commission on Environmental Quality Chairman Buddy Garcia and Commissioner Bryan Shaw voted to issue the "by-products" license to Waste Control Specialists. The company is owned by Harold Simmons, a top donor to Gov. Rick Perry, who appoints members to the TCEQ.

http://www.chron.com/disp/story.mpl/metropolitan/5795238.html

http://www.chron.com/disp/commnts.mpl/metropolitan/5795238.html?plckCurrentPage=2

IT seems a more correct headlines would have read ''Company bribes Governor Perry to bury nuclear waste and contaminate Texas''. Waste Control Specialists. The company is owned by Harold Simmons, a ''TOP DONOR TO GOV. RICK PERRY, WHO APPOINTS MEMBERS TO THE TCEQ.'' The good governor has sold out to the citizens of Texas for train car, after train car of nuclear waste from 'the mound' Monsanto plant in Miamisburg Ohio. It just so happens, my father-in-law, who is down visiting now with us, has pictures of those railroad cars just sitting and waiting to come down to Texas. Odd how I was watching the news today, about this small plane that had crashed, it had showed pictures of where it had crashed right up near a bunch of tractor-trailer cargo container boxes in a parking lot. What would keep this from happening with those radioactive toxic containers in Ohio, at 'the mound', and or in route to Texas? You see, it's been killing my father-in-law, he has been on oxygen for years, but his breathing is getting more and more labored now, even with the oxygen. He worked at 'the mound' for years and years, and he is now dying a slow death from asbestosis, among other ailments caused by working at 'the mound'. NOW here is what I just cannot understand. This material is so toxic, in trying to gain further medical assistance from the DOE, the evidence that was needed to show that indeed my father-in-law worked their i.e. work records, paperwork records, payment records etc., they told my father-in-law, that they could not dig those records up, that they were buried due to high nuclear contamination, it was just too toxic, and that he had to prove that he had worked there. In which he did finally prove, and did gain further assistance. Also, ''Soward said a contested hearing could either rebut or support allegations that the agency ignored it's own scientific evidence that the site is geologically unsuitable to store material that will remain radioactive for tens of thousands of years.'' This is typical of the Bush Administration, and it happens all the time. The only science that the Bush administration knows, is junk science, bought and paid for by industry scientist. This has been proven time and time again ;

Reports and Research

Interference at the EPA

Science and Politics at the U.S. Environmental Protection Agency

The results of these investigations show an agency under siege from political pressures. On numerous issues—ranging from mercury pollution to groundwater contamination to climate change—political appointees have edited scientific documents, manipulated scientific assessments, and generally sought to undermine the science behind dozens of EPA regulations.

http://www.ucsusa.org/scientific_integrity/interference/a-to-z-alphabetical.html

Executive Summary

snip...

The Bush administration’s direct abuse of science—combined with systemic changes to the regulatory system that threaten the integrity of EPA science—highlight the need for strong action by the next president and Con- gress to restore scientific integrity to the agency’s decision making. Only then can the EPA fully mobilize to serve the public good and ensure the nation’s health.

Report: Federal Science and the Public Good

http://www.ucsusa.org/scientific_integrity/interference/interference-at-the-epa.html

posted February 19, 2004 (March 8, 2004 issue) The Junk Science of George W. Bush

The Bush Administration has so violated and corrupted the institutional culture of government agencies charged with scientific research that it could take a generation for them to recover their integrity even if Bush is defeated this fall. Says Princeton University scientist Michael Oppenheimer, "If you believe in a rational universe, in enlightenment, in knowledge and in a search for the truth, this White House is an absolute disaster." .....

February 18, 2004

Preeminent Scientists Protest Bush Administration's Misuse of Science Nobel Laureates, National Medal of Science Recipients, and Other Leading Researchers Call for End to Scientific Abuses .....

snip...

* National Medal of Science † Nobel laureate

http://www.ucsusa.org/news/press_release/preeminent-scientists-protest-bush-administrations-misuse-of-science.html

full text ;

http://sciencebushwhacked.blogspot.com/

http://sciencebushwhacked.blogspot.com/2008/05/junk-science-of-george-w-bush.html

My point is this, why in the world would the Governor of Texas make a sound decision on accepting this nuclear waste$ It's simply amazing what enough money can buy, even the Governor of Texas. ''TCEQ's executive director rejected their request, saying there is not sufficient public interest because no Texas residents sought a review.'' Well, I am one Texan that does not want any more Toxic waste in Texas, nuclear or not. Why should we take other states nuclear waste? Texas is NOT a nuclear dump for the highest bidder, the good Governor may think so, but myself and many others here in Texas just cannot accept this. This is insane, or just business as usual, make your choice. Governor Perry sold us all out, and he must be held accountable. ...

PART 1

Piketon: A troubled past Cold War factory created secret dump, set own rules By Lynn Hulsey, Tom Beyerlein

Staff Writer

Sunday, November 12, 2006

PIKETON — Inside the closely guarded confines of this 3,714-acre federal complex, deer lope along roadways, chubby groundhogs munch clover and wild turkeys gather during breeding season.

But this is no nature preserve.

Thousands of metal cylinders of corrosive radioactive waste — most weighing 14 tons and many heavily etched with rust — stretch across industrial yards.

Five plumes of poisoned groundwater lie beneath the surface, one of them so close to private land that traces of contamination were found in a monitoring well on a nearby farm.

Access is restricted inside three buildings that sprawl for more than a mile and are contaminated with radiation, beryllium, polychlorinated biphenyls (PCBs) and asbestos.

What dangers lie beneath the thick concrete floors of those buildings is anybody's guess.

Welcome to the old Piketon atomic plant 100 miles southeast of Dayton, once a proud monument to Ohio's nuclear legacy.

Today that legacy is one of mounting bills for U.S. taxpayers, an environmental cleanup that has no end in sight, and thousands of former workers or their survivors who sought compensation, claiming work-related cancers and other illnesses.

Government investigators blame problems at the now-closed Portsmouth Gaseous Diffusion Plant on decades of slipshod safety practices, accidental toxic releases and routine mishandling of chemical and radioactive material.

The cleanup cost at the uranium enrichment plant, estimated at $3 billion, could eventually top the $4.5 billion spent at the U.S. Department of Energy's former Feed Materials Production Center in Fernald, according to Ohio Environmental Protection Agency officials. That would make the Piketon cleanup the most expensive environmental reclamation project in Ohio history.

For decades, operators of the government-owned plant created a secret dump, spraying PCBs and uranium-contaminated oils on dusty roads, burying hazardous waste in unlined landfills, pouring toxins into waterways, allowing radioactive incinerator ash to scatter in the wind — even tilling radioactive oils into the ground.

Former workers told the Dayton Daily News chilling tales of a workplace in which managers downplayed risks, enforced a code of silence, and failed to protect employees against some of the most dangerous substances on earth.

Gary Sexton, 56, said he didn't know hazardous levels of the metal beryllium were in the plant when he started work as a chemical operator in 1974. He now has trouble breathing because of a potentially fatal and incurable ailment known as chronic beryllium disease that afflicted about 38 Piketon workers.

"Of the ones that have chronic beryllium disease, there are more dead than living," said Sexton, a safety representative for United Steelworkers Local 5689.

Donald Cruse, 65, said he was often sent to dismantle radiation-contaminated equipment and handle PCBs and asbestos without protective gear. He recently underwent surgery for melanoma, and breathes through a tube in his neck after losing part of his larynx to cancer.

"All the hottest places on the plant site, I worked," said Cruse, who was employed there from 1975 to 1996. "They said none of that would hurt us. There wasn't enough there to bother us."

Kenny Estep coached peewee football, was an auxiliary police officer and headed the local Moose Lodge. But in his job as a truck driver at the Piketon plant, Estep hauled radioactive waste to a plant landfill. On March 7, 1978, he was handed a respirator and a pair of paper coveralls and told to dump snow on a leaking cylinder full of radioactive uranium hexafluoride, the material used to enrich uranium.

He died of a rare form of liver cancer seven years later at the age of 42.

"He had a job to do and he was told to do it, so he did it," said Estep's widow, Barbara Barker, 62, of Piketon.

Barker received compensation for her husband's death, but it didn't come until after the federal government admitted for the first time in 1999 that it harmed its atomic workers.

The environmental damage at Piketon was harder to hide. The same hazards that sickened workers also poisoned the environment and continue to threaten future generations.

Along with the Mound Laboratory in Miamisburg, the plants at Fernald and Piketon once played indispensable roles in the manufacture of Cold War nuclear weapons. But the environmental footprint each of them left behind will never fully be erased, even after the billions of dollars spent cleaning contaminated groundwater, soil, waterways and buildings.

The end-date for monitoring the pollution at Piketon: never.

William E. Murphie, manager of the Energy Department office overseeing cleanup at Piketon and a sister plant in Paducah, Ky., declined to address Piketon's history of mishandling hazardous materials.

"We take a lot of lumps for the past processes and, face it, mistakes that were made," he said. "We've learned from the past. We're all smarter than we were in the past."

Murphie said the department remains committed to the cleanup and trying new solutions if those now in place don't work.

"DOE is very proud of the cleanup program here," he said. "We believe we have accomplished a lot."

Worker safety a low priority

From 1954-2001, the Piketon plant provided a ticket to the middle class for some 10,000 residents in Appalachian Ohio. A series of government contractors enriched uranium there, first for nuclear weapons and later to power nuclear reactors.

"The focus back then was to win the Cold War. Handling the waste and avoiding contamination was pretty low on the list," said Brian Blair, an Ohio EPA supervisor who participated in the state's first inspection of the site in 1986. "They were not managed even according to the best technology available at that time. That's why we have many of the contaminants out there."

The now-defunct Goodyear Atomic Corp. operated the Piketon plant for its first 32 years. A subsidiary of Martin Marietta took over management in 1986, followed by Lockheed Martin in 1995. The government privatized its enrichment operations in 1998, turning them over to USEC Inc. of Bethesda, Md.

In the early years, few environmental regulations existed across the United States and the hazards of chemical and radioactive materials weren't fully understood. By the 1970s, the government began regulating the handling and disposal of hazardous materials, and took action against companies that didn't follow the rules.

But unlike private companies, the Energy Department was allowed to set its own environmental standards, at least when it came to nuclear facilities such as Piketon. Energy officials, in effect, said, "trust us." Until the late 1980s, environmental regulators had no jurisdiction — or access — to the Piketon plant, and even now secrecy cloaks many plant practices.

All nuclear facilities must keep some practices confidential for reasons of national security. But the secrecy and self-regulation at Piketon veiled an astounding level of environmental destruction.

In 2000, the Energy Department secretary launched a massive investigation that documented the plant's grim environmental record: mishandling of hazardous and radioactive material, failure to properly monitor environmental emissions or workers' exposure to radiation, ignoring safety rules. The investigators identified 400 accidental releases of uranium gas or toxic fluorine since the 1950s, although they said the true total was unknown due to poor record keeping.

The worst of what the investigators found occurred in the plant's first 25 years, but careless and harmful practices continued even as the plant changed operators. For example:

• Two separate incidents — in 1982 and 1993 — resulted in the airborne release of 19 curies of radioactive technetium, a cancer-causing product of nuclear fission that escaped as workers cleaned equipment. "That's a significant amount, and it's certainly not desirable to have those kinds of releases in the air," Blair said.

• Uranium-contaminated solvents were burned in an incinerator designed for solids until 1986, when the Ohio EPA ordered it shut down. Maria Galanti, the agency's on-site coordinator, said soil around the incinerator site is radioactive at least 12 feet deep.

• The Energy Department didn't stop pumping waste into the plant's worst source of off-site and groundwater contamination until 1988. That unlined pond held everything from PCBs and the solvent trichloroethylene to radioactive uranium, technetium and plutonium — toxins that leached into groundwater and the Little Beaver Creek, a tributary of the Scioto River.

People who live near the plant say they had no idea all this was going on. Children swam in the creeks, and churches held baptisms in Big Run Creek. That same creek runs past two unlined landfills and near a polluted groundwater plume as it passes through the plant grounds on its way to the Scioto River.

Clyde Blanton has lived next to the plant's southern border since 1970. Not until the late 1980s, when residents near the Fernald plant began fighting for a cleanup there, did Blanton and others start asking questions about Piketon.

He said plant officials assured people it was safe.

"Now they've spent a billion bucks cleaning up," said Blanton, 64. "That tells you it's not safe. Somebody lied."

Inspectors react with shock

The cover over Piketon's secrets began to lift in 1986, when Ohio EPA inspectors were allowed inside the plant for the first time. What they saw shocked them.

In one of the plant's more egregious practices dating to the 1980s, plant operators tilled highly radioactive oils into soil, figuring the solvents would degrade over time. They didn't take into account that radiation takes millions, even billions of years to decay.

Those plots, now capped, are one of several sources of contaminants in the plant's second-largest groundwater plume.

"You had some of the best minds in the U.S. government working on enriching uranium and this is the best they could do with their waste?" Galanti said.

Plant operators dumped radioactive materials, toxic chemicals and dangerous solvents into unlined landfills and even discharged radioactive and chemical wastes into ditches leading to the Little Beaver Creek. Galanti described the ditches as "screaming hot" and said they were one of the Ohio EPA's top cleanup priorities.

The solvent trichloroethylene, a suspected carcinogen, remains the site's most pervasive groundwater contaminant.

"They'd go dump solvents out the back door," Galanti said. "And taking drums of degreasers and volatile organics and dumping them in a big pit."

Even after they were allowed to visit the plant, Ohio EPA officials were frustrated in their effort to force a cleanup. Officials at federal nuclear facilities had long argued that they were exempt from environmental rules concerning the handling and disposal of all hazardous materials, including any radioactive material.

"They thought they were above the law," said Jack Van Kley, the lead attorney in a federal court case that the state of Ohio filed in 1989 against the Energy Department.

As a result of that case, state regulators won limited authority over the department's operations at Piketon. A consent decree issued by the court required the Energy Department to follow state and federal rules for hazardous materials. But the department retained oversight of its handling of purely radioactive material.

A separate agreement was reached with the U.S. EPA, and cleanup began the same year.

Taxpayers are footing the cleanup bill because government contracts protected the contractors who ran the plant against damages, said Energy Department spokeswoman Laura Schachter. Four of those companies are defunct but their parent companies, Goodyear Corp. and Lockheed Martin Corp., are still in business. Goodyear spokesman Keith Price had no comment for this story. Lockheed Martin spokeswoman Gail E. Rymer said environmental investigations were already underway when the company's subsidiaries managed the site and those companies also assisted with cleanup.

"Since we took over the plant we have had an exemplary safety and environmental record," said USEC spokeswoman Elizabeth Stuckle.

So far, the government has spent $1 billion to dig up soil, empty ponds, cap unlined toxic landfills, treat groundwater and haul contaminants away — more than 43,000 containers of hazardous, radioactive and other waste and 8,400 tons of radioactive scrap metal.

Each year, the plant treats 28.5 million gallons of contaminated groundwater, said Sandra Childers, spokeswoman for LATA/Parallax Portsmouth, which last year replaced Bechtel Jacobs Co. as the Energy Department's cleanup contractor.

The 20,000 cylinders of depleted uranium hexafluoride — enrichment waste that piled up on the site over 50 years — will sit until they can be converted to a more stable form and shipped away. A conversion plant now under construction would eliminate the backlog by 2026, but more waste could be coming. USEC wants to replace the old gaseous diffusion plant with the American Centrifuge Plant, a high-tech uranium enrichment facility that would annually generate about 1,300 cylinders of waste.

Piketon is one of more than 100 polluted Energy Department sites across the United States. The department is the government's worst polluter, with a cleanup bill estimated at $35 billion, according to a 2004 U.S. EPA study.

But although the Piketon site is far from the Energy Department's worst offender, the sheer size of three massive enrichment buildings complicates cleanup and inflates the cost. Inside those buildings, giant machines heated uranium hexafluoride and forced it through filters to boost the concentration of the uranium isotope needed for reactor fuel and weapons.

Some of the most dangerous cleanup work is occurring in those structures. Under tight security, workers are removing uranium deposits that cling to surfaces inside equipment and 600 miles of piping. They must use extreme care because mishandling the radioactive deposits could cause a small nuclear reaction — a "criticality" — that could kill workers and spread radiation through the area.

"We've never had a criticality event, and I have no reason to believe that we ever will have a criticality event," Murphie said.

Groundwater contamination

a sore subject

The Piketon cleanup hasn't ended disputes between the Energy Department and its regulators. The Ohio EPA has fought Energy officials over everything from what to do with the thousands of contaminated cylinders at the site to the department's efforts to ease groundwater standards.

Memos obtained by the Dayton Daily News outline Ohio EPA officials' complaints about disputes over cleanup methods, wasteful spending by Energy Department contractors and botched cleanup jobs — in one instance allowing polluted groundwater to spread because of poor construction of a barrier wall.

Murphie declined to comment on the memos.

Groundwater contamination has been a flashpoint. In 1999, the Ohio EPA rejected an Energy Department attempt to cut disposal costs by loosening rules for the suspected carcinogen trichloroethylene, which permeates groundwater and has proven difficult to remove.

More recently, the department pushed for a reduced groundwater cleanup standard, arguing that the lesser standard is appropriate because no one drinks the water underneath the plant site.

"We represent the taxpayers. Our goal here is to make sure we are doing cost-effective, smart cleanup," Murphie said. "The regulators represent the taxpayers but also the regulators represent the regulations."

Ohio EPA officials are firm: There will be no reduced groundwater standard.

"We can't allow unlimited groundwater contamination just because they say it won't be used. That is a resource, and it does migrate and move," said Ken Dewey, the agency's southeast district assistant chief.

The latest point of friction between the Energy Department and its watchdogs involves the three enrichment buildings. The debate over what to do with them involves questions of money, jurisdiction and, ultimately, jobs.

Ohio EPA officials want the buildings — and the equipment inside of them — to be cleaned and demolished. It's unclear yet whether they can be safely buried at Piketon or must be shipped at great cost to disposal sites in Utah or Nevada.

Murphie has suggested still another possibility, that the contaminated buildings stay in place indefinitely under a long-term surveillance plan. But Dewey argues that leaving the structures in place will make cleanup more expensive in the long run because "we'll have to drill under and around buildings" to investigate and clean contaminated soil and groundwater.

"I hope the federal government doesn't make that choice," he said.

Even if Energy officials decide to demolish the buildings, there is one major obstacle: money.

A fund for cleaning enrichment plants in Ohio, Tennessee and Kentucky will fall as much as $5.7 billion short of what is needed to clean all three sites, according to a 2004 report by the U.S. Government Accountability Office.

The Energy Department's five-year cleanup plan shows a decline in funding for the Piketon cleanup and no money for demolition of the enrichment buildings.

Local officials, who have watched jobs disappear through the years, worry that a stalled cleanup plan will reduce current employment and derail efforts to redevelop the site.

"Now we're threatened," said Blaine Beekman, executive director of the Pike County Chamber of Commerce. "It's like every day there's a new chapter, a new battle to fight."

Concerned neighbors

take cancer survey

After denying for years that its nuclear operations harmed anyone, the federal government in 2000 launched a program to compensate atomic workers sickened by workplace exposures. So far, more than 2,900 Piketon workers or their survivors have applied for the money.

But if people inside the plant got sick, what about those outside?

In 1994, a local residents group went door-to-door and identified 247 cancer cases within a six-mile radius of the plant. The data, however, was incomplete. The volunteers did not collect information on important risk factors, such as smoking status and occupational exposures, and failed to confirm the diagnoses with medical records.

"These limitations make it difficult to generate meaningful cancer rates from these data," a federal health assessment concluded two years later. That assessment, done by the federal Agency for Toxic Substances and Disease Registry in response to residents' concerns, found that the plant posed "no off-site threat to public health."

Critics were quick to point out inaccuracies in the government report, and continue to dispute the overall finding.

"I think they're wrong with the risk," said Vina Colley, president of a local watchdog group and a former Piketon employee fighting for compensation for illnesses she believes were caused by workplace exposures.

Ohio EPA officials say the worst of the plant's contamination is confined to the federal land, in part because thick bedrock slows the spread of the poisoned groundwater. They also say the plant's environmental record improved in recent years as operators adopted modern waste-handling practices and began following rules governing discharges to air and waterways.

Still, evidence of off-site contamination remained even after enrichment operations shut down in 2001. According to its most recent environmental reports, the Energy Department in 2003 and 2004 found small amounts of radioactive contamination outside the plant.

Tests on two area deer killed by cars showed traces of uranium isotopes in the livers of both and in the muscle of one. Traces of uranium were also found in milk and egg samples from area farms, and in three vegetables taken from the gardens of plant neighbors. Air, water and sediment tests also revealed small amounts of radioactive uranium, plutonium or technetium. And three fish from area waterways had traces of uranium or plutonium. Because plutonium rarely occurs naturally, there would appear to be only one possible source: the plant.

Energy officials say none of the amounts are large enough to pose a health threat.

Activists accuse the department of minimizing the threat of off-site radioactive contamination. Noting that a fish from the Little Beaver Creek contained trace amounts of plutonium, Elisa Young of the Sierra Club's Appalachian Group asked, "Would you eat that fish?"

Although the radiation amounts detected in recent years are small, Galanti said it's impossible to know how many contaminants were carried off by the wind or waterways over the years.

"It went somewhere," she said. "We all live downstream in one aspect or another."

With polluted government nuclear facilities dotting the map from coast to coast, Galanti said the abysmal environmental record has left a legacy of phenomenal costs and immense responsibilities for future generations.

"How do we monitor this stuff in perpetuity?" she said. "That's a relic of the Cold War and our thirst for energy."

By M.J.Kraft

November 20, 2006 06:28 PM Link to this

I hired on at Mound 1980 entry level ,{labor gang].Assignments ranging from ,office moves,,assisting skilled trades in and out of contaminated areas, yards and grounds,and digging lots of holes.In 1986 I moved up to Firefighter classification. Fire prevention was top priority.For the 13 years myself, and 8 other firefighters perforfmed ispections over every inch of every building. Hot or cold. In 1990 I was diagnosed with COPD,1994Moderate Emphysema,Lung Cancer 2006.Do yourself A favor

By Mary M.

November 19, 2006 08:14 PM Link to this

Investigative reporting at it finest (and most expensive) so it isn’t often seen in daily newspapers. I am a Mound widow and also a Mound survivor as I worked on the “cool” side. At age 81 I consider myself very, very lucky.

By Paige Gibson

November 16, 2006 08:19 AM Link to this

I worked at Mound as did my father. I became aware of the occpational exposure and got involved. I now work for Mound Workers Health Protection Program. We offer Mound workers a free medical screening. Since July we have diagnosed 6 people with lung cancer or asbestosis. We are also helping people with their claims. What a mess! So Mound people if you have questions or comments call us at 937-866-6802.

By Carolyn

November 14, 2006 09:39 PM Link to this

Excellent series. Your series and others in papers near other sites where atomic workers worked and became ill should be circulated in each community so readers know the situation in the local plant was repeated over and over all over the country.

These plants, not to mention the bombs they helped create, were the American weapons of mass destruction of several generations of workers.

By WALT

November 14, 2006 09:15 PM Link to this

I WORKED AT MOUND FOR 36 YEARS IN SOME OF THE MOST HAZARDOUS CONDITIONS. I AM NOW PAYING THE PRICE WITH CHRONIC INCURABLE LUNG DISEASE. I AM TRYING TO WORK MY WAY THRU THE PAPER WORKMILL WHICH STARTED OVER 2 YEARS AGO.

By Bill Bankes

November 14, 2006 12:17 PM Link to this

I worked at Mound and my Grandfather worked at Fernald, Waverly, and GE Evendale. He died in 1963 of Cancer caused by exposure.

His claim was denied because they would not accept his time at GE and a site to be included although there were large amounts of radioactive materials there.

By Jodi Hingtgen

November 13, 2006 09:48 PM Link to this

Is anyone keeping a central repository or database of people who worked at the Mound and have since died of unnatural causes? Anyone other than the government? My mother (Doris Hill) worked there between 1956 and 1963 and died of various cancers when she was only 42 and I was 16. NIOSH has so far denied my claims. Any information on people who worked there in the late 50’ s and early 60’s would be be greatly appreciated.

Thanks, Jodi

http://www.daytondailynews.com/n/content/oh/story/news/special-reports/piketon/2006/11/11/ddn111206pkcleanup.html

LETTER ABOUT MOUND PLANT'S DEADLY LEGACY

Publication: Dayton Daily News Publish date: October 30, 2010

How was Mound Laboratory allowed to do so much harm?

I'd like to provide some first-hand information regarding the "environmental devastation" created by the Mound Laboratory during the years that my family lived on Mound Road.

In 1956, my parents bought a new home in a lovely neighborhood for their growing family. I lived there until 1966.

Beginning in 1960, the Mound released radioactive tritium into the air and contaminated the soil with plutonium-238. Our city water supply was piped up Mound hill; we played at the Adena Indian mound, spent countless hours at the Miamisburg public pool and fished in the pond.

My father worked at Presto Adhesive Paper, below Mound Lab, on Mound Avenue. He died at the age of 53 of a rare cancer multiple myeloma.

Our mother had already undergone radical mastectomy and radiation for breast cancer prior to age 50; she would later die of mesothelioma.

Our older brother died in his early sixties of bladder cancer, and my daughter had her cancerous left kidney removed while in her mid-thirties.

My family's experiences are only a small part of our neighborhood cancer history. Beginning with Mound Road, spreading back Marsha Drive and all along Meadowview Drive, one - and in most households, both - parent experienced different types of malignant disease, i.e.: multiple breast and colon cancers, parotid tumor, bladder, prostate, lung, skin, mesothelioma, brain, aplastic anemia and a child with leukemia.

I estimate that cancer occurred in 90% of the households in that neighborhood.

How did city officials allow this to happen? Where were our environmental watchdogs from the 1970s until 1989, when the Mound plant was placed on the EPA priorities list? My family and our neighbors deserve answers to those questions.

Sally Nunery Dunn

West Carrollton

A MOUND OF NUCLEAR LIES AND DEATH COMING TO TEXAS thanks to Governor Perry $$$

The Mound faclity reportedly sent 458 boxes of plant records to Los Alamos in 1993. these records were found to be contaminated with radiation and buried at Los Alamos as a health hazard. One cannot but guess what these records contained. The most significant fact being that these records were considered a health threat from uptake of radioactive particulate. This does not speak well for the historical hygiene at the facility

snip...

A bldg was administration, B was biology, C was cafeteria, D was decontamination a hot bldg. -lots of water that they tried to wash the facility with and contaminated the regional aquifer, had -to remove tons of dirt. R building was radioactive and hot. A young man got so exposed to -radiation in the T building that he died in the medical facility. The T building was far underground.

http://www.cdc.gov/niosh/ocas/pdfs/sec/mound/mound2pet.pdf

Over time, contamination leaked from these drums into the surrounding soils ...... Mound Plant OU 1 Site. Location:. Miamisburg, OH. Period of Operation: ...

http://www.frtr.gov/pdf/abstractsvol5.pdf

Air Sparging and Soil Vapor Extraction at the Mound Plant OU 1 Site, Miamisburg, Ohio 73 Costs: • The total cost for AS/SVE was $1,439,039, consisting of $116,773 for pilot testing, $221,591 for design, $398,000 for construction, $517,958 for operations, and $184,717 for sampling and analysis • As of May 2000, the overall unit cost was $420 per pound of contaminant removed Description: The Mound Plant is a government-owned and contractor-operated facility occupying a 306-acre site within the city of Miamisburg, Ohio. The OU 1 site occupies three acres on the western edge of the developed portion of the facility. The historic landfill in OU 1 was used between 1948 and 1974 for disposal of general trash and liquid wastes from Mound Plant operations. The sanitary landfill in OU 1 was constructed partially within and adjacent to the location of the historic landfill. Both disposal sites have been used for dumping, burning, moving, reworking, and burying various plant wastes. A periodic water sampling program and a Phase 1 investigation indicated that VOCS were present in the soil and groundwater at OU 1. An air sparging and soil vapor extraction (AS/SVE) system began operating at OU 1 in December 1997. The system was intended to remove chlorinated VOCs from the soil and groundwater at the site. After 2 ½ years of operation, 3,433 lbs of VOCs had been removed, and the total VOC concentrations in the unsaturated zone decreased from 618.1 to 4.54 mg/kg. If system performance is maintained, the site was projected to meet cleanup goals by December 2002. The total cost for AS/SVE at this site was $1,439,039.

http://www.frtr.gov/pdf/abstractsvol5.pdf

COMING TO TEXAS, at a nuclear dump site near somebody, thanks to the good governor perry of Texas and a lot of $$$

Thanks Gov. ...

P.S. Suggestion; I say if it must come to Texas, send all toxic nuclear waste material to Bush Ranch, Crawford, Texas USA.

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

Ex-official: Cheney wanted climate change report altered

2008-07-09T10:35:00.000-07:00

July 8, 2008, 1:56PM

Ex-official: Cheney wanted climate change report altered

By H. JOSEF HEBERT Associated Press

WASHINGTON — Vice President Dick Cheney's office pushed for major deletions in congressional testimony on the public health consequences of climate change, fearing the presentation by a leading health official might make it harder to avoid regulating greenhouse gases, a former EPA official maintains.

When six pages were cut from testimony on climate change and public health by the head of the Centers for Disease Control and Prevention last October, the White House insisted the changes were made because of reservations raised by White House advisers about the accuracy of the science.

But Jason K. Burnett, until last month the senior adviser on climate change to Environmental Protection Agency Administrator Stephen Johnson, says that Cheney's office was deeply involved in getting nearly half of the CDC's original draft testimony removed.

"The Council on Environmental Quality and the office of the vice president were seeking deletions to the CDC testimony (concerning) ... any discussions of the human health consequences of climate change," Burnett has told the Senate Environment and Public Works Committee. ...SNIP...END...TSS

http://www.chron.com/disp/story.mpl/hotstories/5876800.html

Tuesday, April 29, 2008

Interference at the EPA - Science and Politics at the U.S. Environmental Protection Agency

please see full text ;

http://sciencebushwhacked.blogspot.com/

TSS

White House invokes executive privilege in EPA inquiry

2008-06-21T09:24:00.000-07:00

White House invokes executive privilege in EPA inquiry

The Bush administration refuses to turn over subpoenaed documents related to the agency's decision to prevent California from enacting stricter emissions standards than the federal government.

By Richard Simon, Los Angeles Times Staff Writer

June 21, 2008

WASHINGTON -- Escalating a fight with Democrats on Capitol Hill, the White House on Friday invoked executive privilege in refusing to turn over documents to a congressional committee investigating the Environmental Protection Agency's decision to deny California permission to implement its own vehicle emission standards.

The Bush administration asserted executive privilege hours before the House Oversight and Government Reform Committee was to vote on whether to bring contempt-of-Congress proceedings against EPA Administrator Stephen L. Johnson and Susan Dudley, administrator of regulatory affairs in the White House Office of Management and Budget, for refusing to turn over subpoenaed documents.

Committee Chairman Henry A. Waxman (D-Beverly Hills) put off a vote on the contempt resolutions while he considers his options.

"I don't think we've had a situation like this since Richard Nixon was president," he said, appearing determined to press ahead, even if it leads to a court fight. "We don't know whether this privilege that's being asserted is valid or not."

Presidents since George Washington have claimed rights to executive branch confidentiality, according to the nonpartisan Congressional Research Service. The Bush White House invoked executive privilege to prevent officials from testifying about the dismissal of nine U.S. attorneys in 2006. President Clinton cited presidential privilege during investigations into the Monica Lewinsky scandal and on other issues.

House and Senate committees have been investigating what role the White House played in EPA decisions preventing California and other states from enacting tougher emissions rules than the federal government and in the EPA's approval of new ozone pollution standards.

The administration's claim of executive privilege is the latest twist in the escalating legal and political battle over California's efforts to implement its own law combating global warming. Critics of the EPA decision contend that it was based on politics, not science or the law.

As Waxman considered his next move in his fight with the White House, another House committee in the room next door grilled former Bush Press Secretary Scott McClellan, who wrote a revealing book about his days in the White House. The hearings were a sign of determination by Democrats not to ease up on their oversight activities, even in the final months of the Bush administration.

In asserting executive privilege in the EPA inquiry, the administration made public a copy of a letter sent to the president by Atty. Gen. Michael B. Mukasey saying that releasing internal documents "could inhibit the candor of future deliberations among the president's staff."

EPA spokesman Tim Lyons said the agency had provided the committee with more than 7,000 documents and devoted 2,200 hours of staff time to responding to requests for information, and he called it "disappointing" that the committee had decided to "politicize environmental regulations."

Jim Nussle, director of the Office of Management and Budget, took issue with Waxman's "sudden and unwarranted" move to consider contempt proceedings, noting that Dudley had appeared before Waxman's committee last month and was asked "only four questions" -- and only one by the panel chairman.

"There is no valid reason for moving from mutual cooperation to unilateral confrontation," Nussle wrote Waxman.

Waxman said: "I am very disappointed and disturbed that the administration is keeping this information from us, and I think we have a right to it."

richard.simon@latimes.com

http://www.latimes.com/news/nationworld/nation/la-na-epa21-2008jun21,0,1939720.story

snip...please see full text ;

http://sciencebushwhacked.blogspot.com/

TSS

The Junk Science of George W. Bush

2008-05-22T11:01:00.000-07:00

posted February 19, 2004 (March 8, 2004 issue)

The Junk Science of George W. Bush

The Bush Administration has so violated and corrupted the institutional culture of government agencies charged with scientific research that it could take a generation for them to recover their integrity even if Bush is defeated this fall. Says Princeton University scientist Michael Oppenheimer, "If you believe in a rational universe, in enlightenment, in knowledge and in a search for the truth, this White House is an absolute disaster."

http://www.thenation.com/doc/20040308/kennedy

http://www.nrdc.org/bushrecord/science/rfk.asp

Moreover, the UCS report is neither the first of its kind nor comprehensive. Democratic Congressman Henry Waxman released a similar report last August with many overlapping charges as well as some that go entirely unmentioned by the UCS. The most significant difference between the two reports, however, may be that the Bush administration is actually bothering to respond to the UCS document. When The New York Times reported on Waxman's document last August 8th, by contrast, White House press secretary Scott McClellan simply stated, "The only one who is playing politics about science is Congressman Waxman. His report is riddled with distortion, inaccuracies, and omissions." McClellan didn't provide any specific rebuttal at the time, however, and according to Waxman's office, the administration hasn't bothered to do so since then either. This lackluster response in and of itself suggests that the White House cares little about protecting the integrity of science.

And besides the Waxman and UCS reports, there are still other analyses documenting the Bush administration's abuses of science. For example, consider www.scienceinpolicy.org, a Web site that focuses exclusively on the environmental arena. The site details distortions and misrepresentations on issues ranging from climate change to debates on drilling in the Arctic National Wildlife Refuge. Along with policy analyses, it contains the following statement:

The Bush administration justifies environmental policies by misusing and misrepresenting science. The administration's harmful positions on climate change, pollution, forest management, and resource extraction ignore widely accepted scientific evidence. When the administration invokes science, it relies on research at odds with the scientific consensus, and contradicts, undermines, or suppresses the research of its own scientists. Furthermore, the administration cloaks environmentally damaging policies under misleading program names like "clear skies" and "healthy forests." As a result, the public and the media often wrongly believe that this administration uses sound science to help promote a healthy environment. In reality, the best available science indicates that President Bush's policies will cause and exacerbate damage to the natural systems on which we all depend.
This statement has been signed, when last I checked, by 1,225 scientists, ranging from graduate students to distinguished professors.

http://www.csicop.org/doubtandabout/sciencewars/

February 18, 2004

Preeminent Scientists Protest Bush Administration's Misuse of Science
Nobel Laureates, National Medal of Science Recipients, and Other Leading Researchers Call for End to Scientific Abuses

Call (2MB mp3)
Washington, D.C.—Today, more than 60 leading scientists—including Nobel laureates, leading medical experts, former federal agency directors and university chairs and presidents—issued a statement calling for regulatory and legislative action to restore scientific integrity to federal policymaking. According to the scientists, the Bush administration has, among other abuses, suppressed and distorted scientific analysis from federal agencies, and taken actions that have undermined the quality of scientific advisory panels.
“Across a broad range of issues, the administration has undermined the quality of the scientific advisory system and the morale of the government’s outstanding scientific personnel,” said Dr. Kurt Gottfried, emeritus professor of physics at Cornell University and Chairman of the Union of Concerned Scientists. “Whether the issue is lead paint, clean air or climate change, this behavior has serious consequences for all Americans.”

“Science, to quote President Bush's father, the former president, relies on freedom of inquiry and objectivity,” said Russell Train, head of the Environmental Protection Agency under Nixon and Ford, who joined the scientists in calling for action. “But this administration has obstructed that freedom and distorted that objectivity in ways that were unheard of in any previous administration.”

The statement notes that while scientific input to the government is rarely the only factor in public policy decisions, this input should be weighed from an objective and impartial perspective. However, the administration of George W. Bush has disregarded this principle.

“The Earth system follows laws which scientists strive to understand,” said Dr. F. Sherwood Rowland a Nobel laureate in chemistry. “The public deserves rational decisionmaking based on the best scientific advice about what is likely to happen, not what political entities might wish to happen.”

“We are not simply raising warning flags about an academic subject of interest only to scientists and doctors,” said Dr. Neal Lane, a former director of the National Science Foundation and a former Presidential Science Advisor. “In case after case, scientific input to policymaking is being censored and distorted. This will have serious consequences for public health.”

In conjunction with the statement, the Union of Concerned Scientists today released a report Scientific Integrity in Policymaking that investigates numerous allegations in the scientists’ statement involving censorship and political interference with independent scientific inquiry at the Environmental Protection Agency, the Food and Drug Administration, and the Departments of Health and Human Services, Agriculture, Interior and Defense.

One example cited in the statement and report involves the suppression of an EPA study that found the bipartisan Senate Clear Air bill would do more to reduce mercury contamination in fish and prevent more deaths than the administration's proposed Clear Skies Act. “This is akin to the White House directing the National Weather Service to alter a hurricane forecast because they want everyone to think we have clear skies ahead,” said Kevin Knobloch, president of the Union of Concerned Scientists “The hurricane is still coming, but without factual information no one will be ready for it.”

Comparing President Bush with his father, George H.W. Bush and former president Richard M. Nixon, the statement warned that had these former presidents similarly dismissed science in favor of political ends, over 200,000 deaths and millions of respiratory and cardiovascular disease cases would not have been prevented with the signing of the original Clean Air Act and the 1990 amendments to that Act.

The statement demands that the Bush administration’s “distortion of scientific knowledge for partisan political ends must cease” and calls for Congressional oversight hearings, guaranteed public access to government scientific studies and other measures to prevent such abuses in the future. The statement further calls on the scientific, engineering and medical communities to work together to reestablish scientific integrity in the policymaking process.

# # #
Among the statement signers are:

Philip W. Anderson*†
David Baltimore*†
Paul Berg*†
Lewis Branscomb
Thomas Eisner*
Jerome Friedman†
Richard Garwin*
Walter Kohn*†
Neal Lane
Leon Lederman*†
Mario Molina†
W.H.K. Panofsky*
F. Sherwood Rowland†
J. Robert Schrieffer*†
Richard Smalley†
Harold E. Varmus†
Steven Weinberg*†
E.O Wilson*

* National Medal of Science
† Nobel laureate

http://www.ucsusa.org/news/press_release/preeminent-scientists-protest-bush-administrations-misuse-of-science.html

TSS

Interference at the EPA - Science and Politics at the U.S. Environmental Protection Agency

2008-04-29T08:09:00.000-07:00

----- Original Message -----

From: "Terry S. Singeltary Sr." flounder9@verizon.net
To: "Bovine Spongiform Encephalopathy" BSE-L@aegee.org
Cc: heggem.daniel@epa.gov; sibert.christopher@epa.gov; denne.jane@epa.gov; hazen.susan@epa.gov; mcrosby@ucsusa.org; erobinson@ucsusa.org; enegin@ucsusa.org; cjdvoice@yahoogroups.com; madcow@lists.iatp.org

Sent: Monday, April 28, 2008 9:48 PM

Subject: Interference at the EPA Science and Politics at the U.S. Environmental Protection Agency

Reports and Research

Interference at the EPA

Science and Politics at the U.S. Environmental Protection Agency

The U.S. Environmental Protection Agency (EPA) has the simple yet profound charge "to protect human health and the environment." EPA scientists apply their expertise to protect the public from air and water pollution, clean up hazardous waste, and study emerging threats such as global warming. Because each year brings new and potentially toxic chemicals into our homes and workplaces, because air pollution still threatens our public health, and because environmental challenges are becoming more complex and global, a strong and capable EPA is more important than ever.

Yet challenges from industry lobbyists and some political leaders to the agency's decisions have too often led to the suppression and distortion of the scientific findings underlying those decisions—to the detriment of both science and the health of our nation. While every regulatory agency must balance scientific findings with other considerations, policy makers need access to the highest-quality scientific information to make fully informed decisions.

Concern over this problem led the Union of Concerned Scientists (UCS) to investigate political interference in science at the EPA. The investigation combines dozens of interviews with current and former EPA staff, analysis of government documents, more than 1,600 responses to a survey sent to current EPA scientists, and written comments from EPA scientists.

The results of these investigations show an agency under siege from political pressures. On numerous issues—ranging from mercury pollution to groundwater contamination to climate change—political appointees have edited scientific documents, manipulated scientific assessments, and generally sought to undermine the science behind dozens of EPA regulations.

These findings highlight the need for strong reforms to protect EPA scientists, make agency decision making more transparent, and reduce politicization of the regulatory process. Congress, the next president, and the next EPA Administrator must restore independence and scientific integrity to the EPA by:

Protecting EPA Scientists: Scientists should be free to report the distortion, manipulation, and suppression of their work without fear of retribution. Congress should pass a whistleblower law that includes protection for scientists. The EPA should adopt a communications policy that lets scientists speak freely to the press about their findings. Making the EPA More Transparent: Too many decisions are made behind closed doors with little accountability. The EPA’s scientific findings should be freely available to the public. The EPA should open up its decision-making process to congressional and public scrutiny to help reveal misuses of science Reforming the Regulatory Process: The White House should not change scientific findings in order to weaken, delay, or prevent new public protections. Ensuring Robust Scientific Input to EPA's Decision Making: The EPA should review and strengthen how it uses the scientific expertise of its staff and external advisory committees to create policies—especially when scientific input is critical or required by law. Depoliticizing Funding, Monitoring, and Enforcement: Problems with funding, monitoring and enforcement also need to be addressed by Congress and the next President to ensure that the EPA is the robust environmental agency that our country needs. Political interference is not unique to the EPA. Use the links on this page to explore surveys of scientists at other federal agencies and scores of examples of the abuse of science on issues ranging from prescription drugs to endangered species.

Program Overview Political Interference in Science Restoring Scientific Integrity Stay Informed

Sign up for our online action networks or electronic newsletters. Enter your email address for a list of options.

Contents Scientist Statement on Scientific Integrity 2008 Statement: Scientific Freedom and the Public Good Evidence of Political Interference Report: Interference at the EPA Report: Federal Science and the Public Good Examples of Political Interference in Science Surveys of Scientists at Federal Agencies Focus on Climate Science Focus on Endangered Species Science more... News & Views Scientific Integrity Update--01/2008 Scientific Integrity in the News Editorials on the Misuse of Science Poll: The Public's Belief in Independent Science Science, Evolution, and Intelligent Design Resources & Information Info for the Media Info For Congressional Staff Scientific Integrity Curriculum Guide Other Groups Addressing Scientific Integrity Science Idol: The Scientific Integrity Editorial Cartoon Contest

The Report Press Release Executive Summary (PDF) Interference at the EPA: Full Report (PDF) FAQ's about the Report (PDF) Essay Responses From Scientists Select Quotes (PDF) All Essays (PDF) Survey of EPA Scientists Survey Summary and Supporting Documents Congress Reacts Letter to EPA from Rep. Waxman (CA) Statement by Senator Whitehouse (RI) Statement by Rep. Holt (NJ) Other Resources EPA and the White House (PDF) Air Pollution and the EPA (PDF) Climate Change and the EPA (PDF) Toxics and the EPA (PDF) Focus on Region 4 (PDF) Focus on Region 9 (PDF) Related Information Take Action A-to-Z Guide to Political Interference

http://www.ucsusa.org/scientific_integrity/interference/a-to-z-alphabetical.html

Executive Summary

snip...

The Bush administration’s direct abuse of science—combined with systemic changes to the regulatory system that threaten the in- tegrity of EPA science—highlight the need for strong action by the next president and Con- gress to restore scientific integrity to the agen- cy’s decision making. Only then can the EPA fully mobilize to serve the public good and ensure the nation’s health.

Report: Federal Science and the Public Good

http://www.ucsusa.org/scientific_integrity/interference/interference-at-the-epa.html

*************************************************************

April 29, 2004 (Supercedes March 2, 2004 memorandum) Consideration of Prions as a Pest under FIFRA

http://www.epa.gov/oppad001/records_of_decision_on_prions.pdf

CHAMBER OF COMMERCE OF THE UNITED STATES OF AMERICA WILLIAM L. KOVACS 1615 H S TREET , N.W. VICE PRESIDENT WASHINGTON , D.C. 20062 ENVIRONMENT , TECHNOLOGY & (202) 463 5457 REGULATORY AFFAIRS December 22, 2005

Likewise, some agency records of decision, as well as internal memoranda, establish precedent for regulatory policy making that at times extend the regulatory reach of federal agencies far beyond the statutorily mandated powers given by Congress. A recent example of a record of decision with regulatory impact would be the EPA’s decision to regulate prions.4 Prions are protein structures which, when infectious, are suspected of causing transmissible spongiform encephalopathy diseases, such as mad cow disease in cattle.5 EPA’s decision to classify prions as “pests” under FIFRA stems from an internal agency memorandum asserting jurisdiction over prions,6 even though prions are not living things (a prerequisite for EPA jurisdiction under FIFRA).7 Moreover, acting under the authority granted to itself in this memorandum, EPA issued emergency exemptions to several states to authorize the use of pesticides not registered under FIFRA to treat prioninfected surfaces. Therefore, EPA is treating this memorandum as though it is the issuance of a rule, without providing notice to the public or the opportunity to comment on the agency’s interpretation of its authoritative scope.8 The U.S. Chamber specifically requested EPA publish its prior discussion in the Federal Register for notice and comment, but EPA did not respond to that request. 3 Letter from Robert P. Murphy, General Counsel, General Accounting Office, to The Honorable David M. McIntosh, U.S. House of Representatives, January 20, 1999. 4 S.B. Hazen, Memorandum “Consideration of Prions as a Pest under FIFRA” to the Record, April 29, 2004; accessed at: http://www.epa.gov/oppad001/records_of_decision_on_prions.pdf. 5 See definition of prion at http://en.wikipedia.org/wiki/Prion. 6 Memorandum from Susan B. Hazen, Principle Deputy Assistant Administrator, to the record, dated April 29, 2004. The memorandum is available on EPA’s Web site at: http://www.epa.gov/oppad001/records_of_decision_on_prions.pdf. 7 7 U.S.C. 136(t). 8 The Administrative Procedure Act defines a “rule” as … an agency statement of general or particular applicability and future effect designed to implement, interpret, or proscribe law or policy…5 U.S.C. 551(4).

snip...full text ;

http://www.whitehouse.gov/omb/inforeg/good_guid/c-commerce.pdf

Rulemaking to Establish Criteria for the Importation of Designated Ruminants and Ruminant Products From Canada into the United States Final Environmental Assessment, December 2004

While FSIS recommends the use of disinfectants, EPA regulates disinfectants under FIFRA. Prior to 2003, prions were not considered pests, and therefore their treatment with disinfectants was not regulated. In September of 2003, EPA classified prions as a pest (Hazen, 2004) and, therefore, the agency was required to regulate the “microorganisms” under the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA).

http://www.aphis.usda.gov/newsroom/hot_issues/bse/background/documents/03-080-3%20environmental%20assessment.pdf

BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01

[Federal Register: January 9, 2007 (Volume 72, Number 5)] [Proposed Rules] [Page 1101-1129] From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr09ja07-21]

http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8152

BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01 Date: January 9, 2007 at 9:08 am PST

http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f3412

PLEASE NOTE, THESE EPA DOCKET URLS ON MY SUBMISSION TO Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 ARE NO LONGER GOOD ???

Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION

http://docket.epa.gov/edkfed/do/EDKStaffItemDetailView?objectId=090007d480993808

http://docket.epa.gov/edkfed/do/EDKStaffAttachDownloadPDF?objectId=090007d480993808

http://docket.epa.gov/edkfed/do/EDKStaffCollectionDetailView?objectId=0b0007d48096b40d

Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA

https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed

Sent: Monday, July 24, 2006 1:09 PM

To: FSIS RegulationsComments

Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)

http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf

IN A NUT SHELL ;

(Adopted by the International Committee of the OIE on 23 May 2006)

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,

http://www.oie.int/eng/Session2007/RF2006.pdf

$$$ Science abused at the EPA $$$

Greetings,

I will be taking part in this action. Please be on the lookout for my letter to an EPA scientist. I would further like to add to the ;

A-to-Z Guide to Political Interference

http://www.ucsusa.org/scientific_integrity/interference/a-to-z-alphabetical.html

BOVINE SPONGIFORM ENCEPHALOPATHY TYPICAL AND ATYPICAL BOTH OF WHICH HAVE BEEN FOUND IN NORTH AMERICA.

The FDA/USDA et al have failed the public terribly in surveillance, testing, and mad cow feed ban. all of which were/are fraught with errors, time and time again, to a point of great suspicion $

and to add insult to injury, they have blatantly lied and covered up mad cow disease and other TSEs, to a point of finally after 5 years of request after request, they have officially denied my F.O.I.A. request for the final time. They tell me if i want that info on those mad sheep of mad river valley in Vermont, they tell me ;

"As FOIA requires an agency only to produce responsive non-exempt records to a requester, OIG is not obligated to answer questions regarding the TSE occurrence as you requested. Therefore, I am denying your appeal with respect to your questions."

Mr. Terry S. Singeltary, Sr. Page 3

"For these reasons, I am denying your FOIA appeal. This is the final agency decision. You may seek judicial review of this decision in the United States district court for the judicial district in which you reside or have your principal place of business or in the District of Columbia, pursuant to 5 U.S.C. & 552(a)(4)(B)."

please see full text ;

Thursday, April 24, 2008

RE-FOIA OF DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. OF FOREIGN ORIGIN IN THE UNITED STATES [Docket No. 00-072-1]

http://foiamadsheepmadrivervalley.blogspot.com/2008/04/re-foia-of-declaration-of-extraordinary.html

NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 2007

http://nor-98.blogspot.com/

Friday, April 25, 2008

Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46

http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.html

Wednesday, April 16, 2008

REPORT ON THE INVESTIGATION OF THE ELEVENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

http://madcowtesting.blogspot.com/2008/04/report-on-investigation-of-eleventh.html

BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA

http://madcowtesting.blogspot.com/

Sunday, March 16, 2008

MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE (please note the last two mad cows documented in the USA, in Texas and Alabama were both atypical BSE. please note, atypical BSE is more virlent than typical BSE.

http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html

PLEASE SEE THE LARGEST EVER LONG TERM LIVE CASE STUDY WITH OUR CHILDREN BEING EXPOSED TO MAD COW DISEASE IN THE NATIONS SCHOOL LUNCH PROGRAM, but does anyone in the USDA/FDA et al even care to follow them $$$

DOWNER COW SCHOOL LUNCH PROGRAM

http://downercattle.blogspot.com/

http://downercattle.blogspot.com/2008/02/transcript-technical-briefing.html

[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle

9/13/2005

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf

Creutzfeldt-Jakob Disease (Variant) and Bovine Spongiform Encephalopathy (Prion Diseases) Description Since 1996, strong evidence has accumulated for a causal relationship between ongoing outbreaks, primarily in Europe, of a disease in cattle called bovine spongiform encephalopathy (BSE, or “mad cow disease”) and a disease in humans called variant Creutzfeldt-Jakob disease (vCJD). Both disorders, which are caused by an unconventional transmissible agent, are invariably fatal brain diseases with incubation periods typically measured in years (1). Transmission of the BSE agent to humans, leading to vCJD, is believed to occur via ingestion of cattle products contaminated with the BSE agent; the specific foods associated with this transmission are unknown. However, a recently published case-control study involving 132 vCJD cases in the United Kingdom (UK) showed evidence of an increased risk for vCJD associated with the frequency of consuming beef products likely to contain mechanically recovered meat and head meat (such as burgers, meat pies, and sausages) (2). Bioassays and molecular tests have enabled identification of what World Health Organization consultants have classified as “high-infectivity” and “lower infectivity” tissues of cattle with BSE (3). The high-infectivity tissues include the brain, spinal cord, retina, optic nerve, and dorsal root and trigeminal ganglia, suggesting that these tissues can pose a relatively high risk of transmission. The lower infectivity tissues include peripheral nerves (e.g., sciatic and facial nerves), tonsils, nictitating membrane (third eye lid), distal ileum, bone marrow, and possibly thigh muscle. The latter tissue from one cow with BSE transmitted disease to highly BSE-sensitive transgenic mice at a rate indicative of trace levels of infectivity.

http://wwwn.cdc.gov/travel/yellowBookCh4-VariantPrions.aspx

Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008

Progress Report from the National Prion Disease Pathology Surveillance Center

An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD

April 3, 2008

Dear Member:

Once again we are writing to thank you for your continued support in enhancing surveillance of prion diseases in the United States and to bring you up to date on the National Prion Disease Pathology Surveillance Center (NPDPSC).

In large part because of your support, the number of cases examined by biopsy, autopsy and 14-3-3 protein determination has increased significantly over the years (see Tables 1 and 2). We are now able to establish a definitive diagnosis of prion disease in an estimated 60-70% of the cases in the United States, a percentage which exceeds that in even some major surveillance centers. In addition, we receive from you cerebrospinal fluid (CSF) for 14-3-3 determination, a surrogate protein which is helpful in the diagnosis of prion disease, probably in most if not all cases of suspected Creutzfeldt-Jakob disease (CJD). We are making constant efforts to reach our goal of at least 80% definitively diagnosed cases.

The major obstacle to our further increasing the autopsy rate remains the inadequate reporting of suspected cases of CJD to the NPDPSC or to the State Health Department, which in turn would notify us. Since you are the one likely to request the 14-3-3 test on these cases, please include in your request the information needed to contact you, which we will do if the test proves positive. If your institution uses a referral laboratory to send us the CSF, please provide your name, phone, and fax numbers to the lab, which will in turn submit it to us along with the sample. If this information is missing in the request accompanying the CSF sample (as it happens in about 30% of the cases), we will be unable to contact the caregiving physician. Having your contact information would also allow us to send results directly to you, thus reducing turnaround times. ...

snip...

Prion surveillance in cattle has been reduced by 90% (from about 470,000 to 40,000 in the U.S. in 2007 out of about 35 million cattle slaughtered). Termination of human prion surveillance would therefore remove the second line of surveillance, thereby eliminating prion surveillance in the U.S. entirely. This development would be extremely worrisome in view of recent reports that precautions to limit the spread of the prion infectious agent may not have been followed in some slaughter houses in the U.S. Cattle affected with bovine spongiform encephalopathy (BSE) continue to be discovered in Canada, which has more rigorous BSE surveillance than the U.S. At the same time, Canada imposes few limitations in the trade of potentially prion-infectious cattle with the U.S.

snip...

Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.

please see full text with additional comments and links @ ;

http://prionunitusaupdate2008.blogspot.com/

CJD USA

*Acquired in UK ** Acquired in Saudi Arabia *** Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007. **** Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1 from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006, 26 from 2007).

Notes:

-- Cases are listed based on the year of death when available. If the year of death is not available, the year of sample receipt is used.

-- Referrals: Cases with possible or probable prion disease from which brain tissue or blood in the case of familial disease were submitted.

-- Inconclusive: Cases in which the samples were not sufficient to make a diagnosis.

-- Non-vCJD type unknown are cases in which the tissue submitted was adequate to establish the presence but not the type; in all cases, vCJD could be excluded.

-- Communicated by: Terry S. Singeltary Sr.

[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]

http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963

There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.

He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf

JOURNAL OF NEUROLOGY

MARCH 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

flounder@wt.net

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?

http://www.neurology.org/cgi/eletters/60/2/176#535

THE PATHOLOGICAL PROTEIN Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9

June 2003

BY Philip Yam

CHAPTER 14 LAYING ODDS

Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.

http://www.thepathologicalprotein.com/

SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/srm-mad-cow-recall-406-thousand-pounds.html

SPECIFIED RISK MATERIALS

http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html

10 Million Baby Boomers to have Alzheimer's in the coming decades 2008 Alzheimer’s disease facts and figures

http://betaamyloidcjd.blogspot.com/2008/03/association-between-deposition-of-beta.html

re-Association between Deposition of Beta-Amyloid and Pathological Prion Protein in Sporadic Creutzfeldt-Jakob Disease

http://betaamyloidcjd.blogspot.com/2008/04/re-association-between-deposition-of.html

Alzheimer's and CJD

http://betaamyloidcjd.blogspot.com/

Terry S. Singeltary Sr. P.O. Box 42 Baycliff, Texas USA 77518