Subject: #608: Mad Cow Disease, Part 3
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. 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.tmlmelist-archive/493/sr=1-1/002-6
[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.93/sr=1-1/002-6
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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