MAD COW DISEASE, PART 3

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RACHEL'S ENVIRONMENT & HEALTH WEEKLY #608 .

 

.. ---July 23, 1998--- .

 

.. HEADLINES: .

 

.. MAD COW DISEASE, PART 3 .

 

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MAD COW DISEASE, PART 3

 

 

 

For the past several years, the U.S. Food and Drug Administration

 

(FDA) has been considering ways to prevent an epidemic of " mad

 

cow disease " in the U.S. In Britain, where the disease has

 

killed 170,000 cows and at least 24 people since 1985, the beef

 

industry has been crippled and confidence in government has

 

plummeted because no one took adequate measures to control the

 

disease. Additional human deaths are now expected in Britain

 

because millions of people ate contaminated beef for a decade

 

before authorities acknowledged that mad cow disease could

 

endanger public health. (See REHW #606, #607.) Could such a

 

thing happen in the U.S.?

 

 

 

When animals are slaughtered for human food, at least half of the

 

carcass --hide, hooves, entrails, and so forth --cannot be sold

 

for human food and must be sent to a " rendering " plant where it

 

is ground up, boiled down, dried into the consistency of brown

 

sugar and sold as feed for cows, pigs, chickens, and pets. Cows

 

--vegetarians by nature --can become infected by mad cow disease

 

when they are forced to eat parts of other infected animals.

 

 

 

June 5, 1997, FDA issued a rule making it illegal for rendered

 

animal parts from ruminants or mink to be fed to ruminants.

 

Ruminants are animals that chew their cuds --cattle, sheep,

 

goats, deer and elk, among others. Mink are included in the

 

FDA's ban because they can get a disease similar to mad cow

 

disease.

 

 

 

A small group of scientists, led by Michael K. Hansen of

 

Consumers Union, argues that the FDA ban does not go far enough

 

to protect public health, and that FDA's rule is " not

 

scientifically defensible. " [1] Hansen wants a ban on all animal

 

feed containing anything derived from rendered mammals.

 

Consumers Union publishes CONSUMER REPORTS magazine.

 

 

 

FDA says its ban is adequate because no cows in the U.S. have

 

ever been confirmed with mad cow disease, nor is there evidence

 

that any humans in the U.S. have been affected. However, last

 

week we reviewed indirect evidence indicating that some cows in

 

the U.S. may already have mad cow disease and that some people in

 

the U.S. may already have a human version of the disease. In

 

Britain, mad cow disease is thought to have infected some people

 

with a variant of an age-old, but very rare, disease called

 

Creutzfeld-Jakob disease, of CJD for short. In this country,

 

there is some evidence that CJD may not be as rare as was once

 

thought because some cases of CJD may have been misdiagnosed as

 

Alzheimer's disease. (See REHW #607.)

 

 

 

Mad cow disease is one of a family of diseases called

 

transmissible spongiform encephalopathies, or TSEs for short. In

 

sheep, the disease is called scrapie; in deer and elk it is

 

called chronic wasting syndrome. In cows, it is called BSE

 

[bovine spongiform encephalopathy] and in mink it is TME

 

[transmissible mink encephalopathy].

 

 

 

TSE diseases all have similar characteristics: they attack the

 

central nervous system, causing disintegration of the brain; they

 

have a long incubation period --months or years (even decades)

 

can pass between the initial infection and the time when symptoms

 

appear; TSEs are invariably fatal; and they are transmitted by

 

eating animals or animal parts, especially brains and spinal

 

cords.

 

 

 

TSEs are now thought to be caused by a protein called a prion

 

(pronounced PREE-on). Prions are normal proteins, present in all

 

mammals and some non-mammalian species such as salmon and

 

ostriches. According to the prion theory of disease, some prions

 

can fold abnormally and then they can kill nerve cells.

 

Furthermore, according to the theory, abnormal prions can cause

 

normal prions to fold abnormally, thus causing a chain reaction

 

leading eventually to disease and death.[2]

 

 

 

Prions are remarkably hardy. They are not destroyed by the

 

digestive system of humans or other animals. And they are very

 

heat resistant. A scientific committee of the European Union says

 

that heating prions to 271 degrees Fahrenheit (133 Celsius) under

 

three atmospheres of pressure will deactivate most, but not

 

necessarily all, of them. Prions also resist destruction by

 

ultraviolet light and by radiation, and they are not affected by

 

prolonged immersion in formalin, a potent disinfectant made from

 

formaldehyde and alcohol.[3] Prions are hard to stop.

 

 

 

Under FDA's rule, ruminants can be fed to pigs and pigs can be

 

fed to ruminants. Under the rule, even ruminants that are known

 

to be infected with a TSE can be fed to pigs. FDA allows this

 

because, the agency says, no " naturally occurring " TSE has ever

 

been confirmed in pigs. However, Dr. Hansen notes that British

 

researchers have managed to infect pigs with a TSE by exposing

 

them to high doses of contaminated brains from cattle.[4] This

 

does not answer the question whether pigs can be infected through

 

their normal diet, but it indisputably establishes that pigs,

 

like many other species, are susceptible to TSEs.

 

 

 

Hansen offers evidence that some pigs in the U.S. may be infected

 

with a TSE.[5] In 1979, Dr. Masuo Doi, a U.S. Department of

 

Agriculture (USDA) hog inspector, began noticing pigs with

 

central nervous system (CNS) disorders arriving at a swine

 

slaughterhouse, the Tobin Packing Plant, in Albany, New York.

 

Because there was no single source of the animals, and because

 

the Tobin plant did not routinely deal in diseased animals, Dr.

 

Doi suspected that the symptoms he was observing might be present

 

in pigs nationwide.[6] During a 16-month period, Dr. Doi

 

observed CNS symptoms in 106 pigs, taking careful notes and

 

retaining tissue samples, including brains. Researchers examined

 

the brains of the 106 pigs and found telltale " spongiform damage "

 

--holes in the brain tissue --in only one of the 106. They did

 

find other brain damage that occurs in TSE diseases --so-called

 

" glial changes " in brain cells --in 40% of the animals. Dr. Doi,

 

and Dr. Langeheinreich, the pathologist who examined the brain

 

tissues, both say they believe they were dealing with a single

 

disease in all the pigs. Dr. Clarence Gibbs, the leading expert

 

on TSEs at the National Institutes of Health, has said he

 

believes all the pigs had the same disease, based on behavioral

 

abnormalities evident in motion pictures taken while the pigs

 

were alive.

 

 

 

There are 83 million pigs slaughtered in the U.S. each year.[6]

 

They are killed at an average age of only 5 months --long before

 

symptoms of a TSE would ordinarily become apparent.[1]

 

Therefore, if pigs were infected with a TSE, they still might end

 

up in food products for humans and in animal feed.

 

 

 

Even if a pig had the behavioral symptoms of a TSE disease, it

 

might not be noticed by USDA inspectors. To see the symptoms of

 

such disorders, one must observe an animal in motion. The way

 

they walk, turn corners, and hold their tails and heads can all

 

be important clues to their condition. Most pigs are so jammed

 

into pens with other pigs that they have no room to move. If the

 

animals are not in motion, symptoms of TSEs (or other CNS

 

disorders) can go unnoticed. At present, USDA observes only 5%

 

to 10% of pigs while they are in motion.[6] Thus USDA's

 

inspection program seems inadequate to detect symptoms of TSE

 

diseases in pigs. And, as we have noted, even if a pig were

 

identified with a TSE, FDA's rule would allow its infected

 

carcass to be fed to all non-ruminant animals, including pets,

 

chickens, fish, and pigs.

 

 

 

Do humans who eat pork and other pig products have high rates of

 

CJD, the human TSE associated with mad cow disease in Britain?

 

 

 

There have been two epidemiological studies on this point.[7,8]

 

Both were suggestive, though not definitive. The first study, in

 

1973, examined 38 patients with Creutzfeld-Jakob disease. The

 

control group consisted of the nearest relatives of the CJD

 

patients, often their spouses. These controls then selected a

 

friend of the patient of the same age and sex to act as a second

 

control.

 

 

 

The study revealed that this group of people had an unusual diet.

 

More than one-third of the CJD patients ate brains " and the

 

great majority of patients had a specific preference for hog

 

brains, " the authors wrote.[7] One-third of the control group

 

also ate brains, but not necessarily hog brains. Obviously the

 

control group, composed of close relatives and close friends,

 

shared dietary habits with the patients, reducing the power of

 

the study to discern differences between the two groups.[7]

 

 

 

The second study, in 1985, compared 26 patients with

 

Creutzfeld-Jakob disease with 18 of their family members and 22

 

other people selected from a hospital population.[8] Compared to

 

the control group, the CJD patients had an unusually high

 

consumption of roast pork, ham, hot dogs, pork chops, smoked

 

pork, and scrapple. Scrapple is made by adding cornmeal to the

 

liquid derived by boiling pig bones and meat (usually from the

 

head, feet and internal organs). Compared to controls, CJD

 

patients also had an excess consumption of roast lamb, rare meats

 

[meaning not thoroughly cooked], and raw oysters and clams.

 

 

 

Could TSE-infected meat enter the human food chain from other

 

sources besides pigs? The state of Colorado requires deer

 

hunters to turn in the heads of any deer they kill. In 1996, 6%

 

of the deer in northeastern Colorado were found to have a TSE.

 

In 1997, 4% of the deer there had a TSE.[9] Diseased deer in

 

Colorado are usually incinerated or buried in a landfill (where

 

the prions remain infective for an unknown period). However, if

 

any diseased roadkill deer were sent to a rendering plant, they

 

could become animal feed for pigs and chickens.

 

 

 

It is not known at this time whether chickens can become infected

 

by TSE diseases. However, even if it turns out that chickens

 

cannot get a TSE disease themselves, they still might carry such

 

a disease if it were in their feed. As we have noted, the FDA

 

rule allows chickens to be fed rendered animal protein even if it

 

is known to be infected with TSE diseases. Dr. Clarence Gibbs,

 

Acting Chief of the Laboratory of Central Nervous System Studies

 

at the National Institutes of Health, testified before Congress

 

January 29, 1997, saying that bone meal derived from infected

 

rendered animals has been fed to chickens. " Poultry would be

 

expected to shed massive quantities of the infectious amyloid

 

[prion protein] in their feces. Chicken manure is widely used as

 

fertilizer on vegetable crops. This means that vegetarians might

 

be at risk, " Dr. Gibbs testified.[1]

 

 

 

[To be continued, but not next week.]

 

 

 

--Peter Montague

 

(National Writers Union, UAW Local 1981/AFL-CIO)

 

 

 

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

 

[1] [Michael K. Hansen], " Consumers Union's Comments on Docket

 

No. 96N-0135, Proposed Rule: Substances Prohibited for Use in

 

Animal Food or Feed; Animal Proteins Prohibited in Ruminant

 

Feed, " February 14, 1997. Available from Michael Hansen,

 

Consumer Policy Institute, Consumers Union, 101 Truman Avenue,

 

Yonkers, NY 10703-1057; telephone (914) 378-2000. And see

 

Michael Hansen, " The Reasons Why FDA's Feed Rule Won't Protect Us

 

from BSE, " GENETIC ENGINEERING NEWS (July, 1997), pgs. 4, 40.

 

 

 

[2] Stanley B. Prusiner, " The Prion Diseases, " SCIENTIFIC

 

AMERICAN Vol. 272, No. 1 (January 1995), pgs. 48-51. Prusiner

 

was awarded the Nobel prize in 1997 for his role in elucidating

 

the prion hypothesis.

 

 

 

[3] Institute of Food Science and Technology (UK), " Bovine

 

Spongiform Encephalopathy (BSE): Part 1/6, " part 1 of a six-part

 

position paper available on the world wide web at

 

http://www.easynet.co.uk/ifst/hottop5.htm.

 

 

 

[4] M. Dawson and others, " Primary parenteral transmission of

 

bovine spongiform encephalopathy to the pig, " THE VETERINARY

 

RECORD Vol. 127, No. 13 (September 29, 1990), pg. 338.

 

 

 

[5] Letter from Michael K. Hansen, Consumer Policy Institute, to

 

Thomas Billy, Food Safety Inspection Service, U.S. Department of

 

Agriculture, Washington, D.C. dated May 5, 1997. Available from

 

Michael K. Hansen, Consumer Policy Institute, Consumers Union,

 

101 Truman Avenue, Yonkers, NY 10703-1057; telephone (914)

 

378-2000.

 

 

 

[6] Felicia Nestor, Food Safety Director, Government

 

Accountability Project, and others, letter to Dan Glickman, U.S.

 

Secretary of Agriculture, March 27, 1997. Available from Felicia

 

Nestor, Government Accountability Project, 1612 K Street, N.W.,

 

4th Floor, Washington, DC 20006; telephone 202.408.0034; fax

 

202.408.9855. Nestor reports that the Tobin plant received pigs

 

from Canada, Illinois, Indiana, New York, Ohio, and other

 

locations in the midwest.

 

 

 

[7] A. Roger Bobowick and others, " Creutzfeld-Jakob Disease: A

 

Case-Control Study, " AMERICAN JOURNAL OF EPIDEMIOLOGY Vol. 98,

 

No. 5 (November 1973), pgs. 381-394.

 

 

 

[8] Z. Davanipour and others, " A case-control study of

 

Creutzfeld-Jacob Disease. Dietary risk factors, " AMERICAN

 

JOURNAL OF EPIDEMIOLOGY Vol. 122, No. 3 (1985), pgs. 443-451.

 

 

 

[9] " Elk No Longer a Focus of Chronic Wasting Disease Research, "

 

Wildlife Report; News from the Colorado Division of Wildlife

 

[press release] February 2, 1998. Available at

 

http://www.dnr.state.co/cdnr_news/wildlife/980202172739.html.

 

 

 

Descriptor terms: mad cow disease; emerging diseases;

 

creutzfeld-jacob disease; new variant creutzfeld-jacob disease;

 

nvcjd; cjd; great britain; consumers union; bse; tse;

 

transmissible spongiform encephalopathies; scrapie; britain;

 

michael hansen; prions; prion theory of disease; fda; bans;

 

ruminants; pigs; chickens; cows; consumers union; clarence gibbs;

 

alzheimer's disease;

 

 

 

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