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#608 - Mad Cow Disease, Part 3, 22-Jul-1998

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;