2035 Sherell Drive
Fort Collins, CO 80524
970-493-8068
jbw@frii.com

February 19, 2004

Mr. Jonathan Akins
Environmental Engineer
Air Pollution Control Division - Stationary Sources Program
Colorado Department of Public Health & Environment
APCD-SS-B1
4300 Cherry Creek Drive South
Denver, Colorado 80246-1530

Transmitted via Electronic Mail and U.S. Mail

Subject: Draft Permit #03ME0664 issued to Colorado State
University (CSU) for a bio-medical waste incinerator for
disposal of pathological waste, some of which could
potentially be infected with transmissible spongiform
encephalopathies (TSEs), located at 425 29 Road, Grand
Junction, Mesa County, Colorado.

Dear Mr. Akins:

The following are my comments concerning the air permit for
the proposed Grand Junction incinerator.  My comments are
primarily concerned with the question of whether this
incinerator will effectively destroy the agents thought to
cause Transmissible Spongiform Encephalopathies (TSEs).
Since I believe there is no assurance infective material
will not be released into the environment, I request that
the Air Pollution Control Division prohibit the disposal of
waste contaminated or potentially contaminated with TSEs in
this proposed incineration facility.

The proposed incinerator will be used to dispose of deer and
elk heads (and perhaps carcasses) infected or potentially
infected with Chronic Wasting Disease (CWD).  If the
facility is permitted to burn TSE-infected tissues, the
possibility exists that cattle with Bovine Spongiform
Encephalopathy (BSE) or the newly discovered Bovine
Amyloidotic Spongiform Encephalopathy (BASE)[1], and/or
sheep with scrapie may be disposed of in this incinerator as
well.

Surprisingly, the Colorado Department of Public Health &
Environment has no departmental rules, regulations,
policies, guidelines, and/or recommendations regarding the
safe and effective disposal of TSE-contaminated animal
carcasses and tissues.  Over the past several months I have
submitted Colorado Open Records Act requests asking for any
such records or documents.  None have been produced.  Given
the department's lack of regulatory guidance on this matter
and the scientific uncertainties surrounding cross-species
transmission of TSEs, it would appear to be premature and
irresponsible to allow burning of TSE-contaminated wastes in
this proposed facility.

The draft permit requires an afterburner temperature of
1800° Fahrenheit  (982° Celsius) with a retention time of
two seconds.  As you are aware, there is no scientific data
suggesting that these time and temperature parameters will
successfully eliminate detectable TSE infectivity.  The
parameters are drawn from a 1997 risk assessment prepared
for the U.K. Environment Agency by the consulting firm Det
Norske Veritas Limited (DNV).  The report looked at the
risks from disposing of BSE infected cattle in animal
carcass incinerators, specifically the Vetspeed incinerator
plant in Cambridge.  The Vetspeed incinerator has
approximately twice the capacity of the proposed Grand
Junction unit.  In addition, the Vetspeed incinerator uses a
water-spray gas scrubbing unit for removal of particulates,
which the study explains is one of the main protective
measures against incomplete combustion.[2]  The proposed
Grand Junction incinerator would have no such pollution
control equipment.

It is curious that the Colorado Department of Public Health
& Environment would utilize the parameters from this study
since the department apparently does not possess a copy of
the actual study.  The department seems to be relying on a
brief excerpt of the study contained in a later report by
the European Commission's Scientific Steering Committee
(EC-SSC)[3].  A careful reading of the actual study reveals
that the recommended conditions of operation, 850°C for at
least two seconds, are not grounded in any direct scientific
evidence.  The authors state:

"No experimental data are available on the effect of
incineration on BSE infectivity as such."[4]

The typical method of testing for residual TSE infectivity
is the bioassay.  Suspect tissue or material is injected
into the brains of test animals.  The animals are monitored
for clinical disease symptoms and are later autopsied and
tested for evidence of a TSE.  The DNV study did not use the
bioassay to test incinerator ash or emissions.  Rather, they
used a surrogate measurement: the total protein content
remaining in the ash.  The theory is that, since the
infective agent is thought to be a protein, the reduction in
infectivity will be in proportion to the reduction in
protein content.[5]

In a 2003 report, the EC-SSC looked at this methodology and
concluded that data to date suggest the assumption that TSE
degradation is proportional to the degradation of other
proteins is not necessarily justified.[6]  The heat
resistance of the TSE agent may simply be greater than other
proteins.

The department's reliance on the DNV study for minimum
time/temperature parameters for TSE waste incinerators may
be misplaced.  The study provides no direct evidence or
experimental data supporting the parameters.  And it is
unclear why the department has disregarded the DNV
recommendation calling for the use of pollution control
equipment to remove potentially infective particulates.

Below is additional information describing the resistance of
TSE agents to typical inactivation methods, problems
associated with incineration, the alternative disposal
method of alkaline tissue digestion, and cross species
transmission of TSEs (particularly CWD).

TSE Inactivation

Writing in a study on prion transmission, Dr. C. Weissmann
of the Medical Research Council Prion Unit of the Institute
of Neurology in London stated:

"A striking feature of prions is their extraordinary
resistance to conventional sterilization procedures, and
their capacity to bind to surfaces of metal and plastic
without losing infectivity."[7]

The Centers for Disease Control and Prevention reports that
"Prions are characterized by extreme resistance to
conventional inactivation procedures including irradiation,
boiling, dry heat, and chemicals."[8]

The World Health Organization (WHO) writes, "TSE agents are
unusually resistant to disinfection and sterilization by
most of the physical and chemical methods in common use for
decontamination of infectious pathogens."  The WHO goes on
to note "infectivity is strongly stabilized by drying" and
that "contaminated materials should be kept wet between the
time of use and disinfection by immersion in chemical
disinfectants."[9]

In a scientific study on the heat resistance of the scrapie
agent, Dr. Paul Brown observed that TSE agents "are
notoriously resistant to most physical and chemical methods
used for inactivating pathogens, including heat".[10]  Dr.
Brown is a leading authority on prion diseases and prion
inactivation.  A 1998 article by Dr. Brown in the Lancet
includes the following discussion of prion inactivation:

"The agents that cause TSE have been known almost since
their discovery to have awesome resistance to methods that
quickly and easily inactivate most other pathogens...TSE
agents are very resistant to virtually every imaginable
method of inactivation, and those methods found to be most
effective may, in one test or another, fail to sterilise.
It seems that even when most infectious particles succumb to
an inactivating process, there may remain a small
subpopulation of particles that exhibit an extraordinary
capacity to withstand inactivation, and that, with
appropriate testing, will be found to retain the ability to
transmit disease."[11]

Dr. Brown's discussion of heat resistant subpopulations
refers to experiments by Dr. David Taylor, who is perhaps
the world's leading expert on prion inactivation.  Dr.
Taylor published a study in 1998 showing that during heat
inactivation, small subpopulations of TSE agents can become
rapidly heat-fixed, and that these thermostable
subpopulations may survive to resist further attempts at
inactivation.  The resistant subpopulations can be
differentiated by their longer incubation periods in test
animals.[12]

In a study on the effect of dry heat on the scrapie agent,
Dr. Taylor notes that prions "possess a number of properties
which differentiate them from conventional microorganisms,
including an exceptional resistance to inactivation by
chemical and physical methods".[13]

The most relevant study on heat resistance of TSE agents was
done by Dr. Paul Brown et al., published in 2000.  Brown
exposed one-gram samples of scrapie-infected hamster brains
to various time and temperature parameters.  The resulting
samples were injected intracerebrally into healthy hamsters
to test for residual infectivity.  Samples exposed to 600°C
and 1000°C for 5 minutes resulted in no detectable
infectivity.  A sample exposed to 600°C for 15 minutes,
however, infected 5 of 18 hamsters.[14]

The fact that 5 of the test animals became infected is
remarkable, since it seems likely that exposure to 600°C for
15 minutes would decompose all organic compounds.  This
enigmatic result led Brown and colleagues to propose various
explanations.  They note "combustion is a series of
pyrolysis and oxidation reactions that proceed rapidly but
incompletely," and that 600°C is a "comparatively low
combustion temperature".

They theorize that incomplete combustion may have introduced
elemental carbon into the combustion residues, and carbon
has been reported to partially protect TSE infectivity.  The
researchers observed that only at 1000°C did it appear that
most of the carbon residue had been oxidized.  The most
interesting theory proposed by Dr. Brown is that the heat
created an inorganic replica of the prion's molecular
geometry.  This inorganic "fossil template" could mimic the
infectivity of the scrapie agent.[15]

Although the study's authors write that the results suggest
that such an inorganic template would have a decomposition
point near 600°C, the fact is that this is a guess.
Measurable infectivity was found at 600°C and none was
detected at 1000°C.  No samples were exposed to intermediate
temperatures.

Incineration

Regarding incineration, the European Commission's Scientific
Steering Committee (EC-SSC) concludes that:

"With respect to TSEs, it is generally assumed that
incineration is a completely effective method for destroying
TSE-like agents.  However, there is no direct evidence for
this.  The dry heat experiments described in the literature
may not be completely relevant to incineration because
exposure to dry heat does not involve oxidative combustion,
as occurs during incineration."

"The possibility that incineration might not be completely
effective is clearly being considered.  For example, after
incinerating materials that could be TSE-infected, the USDA
soaks the resulting ash in sodium hydroxide for two weeks
before disposal."[16]

The EC-SSC's "Opinion on the use of small incinerators for
BSE risk reduction," dated January 16-17, 2003 notes the
following:

1. Because of variability in incinerator design and
performance characteristics, each incinerator facility needs
to be the subject of a specific risk assessment.

2. There is no direct data on the TSE levels that may occur
in airborne emissions and residual ash from incinerators.

3. Because of this lack of data it is not possible to assess
the risks.

4. In the absence of reliable data on the possible residual
infectivity of the ash, it should be disposed of in
controlled landfills.

5. Unburned material is commonly noted in the ash from small
incinerators.

6. The level of expertise available for the management of
small incinerators is highly variable because few such
facilities can afford to employ specialists in incineration.

The EC-SSC's report concludes:

"In view of the uncertainty regarding the risks due to
BSE/TSE contamination of the fly and bottom ash and airborne
emissions it is recommended that further research is
conducted to identify the residual risks (along with
attendant uncertainties) from the burial of ash (without
further treatment,) in uncontained sites. It is essential
that suitable monitoring methods are developed."[17]

In a presentation to the Food and Drug Administration's
Transmissible Spongiform Encephalopathies Advisory Committee
on July 17, 2003, Captain Edward Rau explained that "ash bed
temperatures often may run 100°C lower than the actual air
temperature" (in an incinerator's burn chamber).[18]
Captain Rau is an Environmental Health Officer with the
National Institutes of Health and a co-researcher with Dr.
Brown on the scrapie heat resistance study.

A 6,000 pound capacity incinerator burns nearly 3 million
times the mass of the samples tested by Brown and Rau.  Many
factors can affect an incinerator's ability to completely
combust TSE contaminated waste material.  As Captain Rau
explains:

"Probability of survival in ash not only depends on a lot of
factors, the load density, the turbulence, the type of
equipment, other operational factors."

"Particularly, as things are just inserted into the
incinerator, you tend to get a boil off of some of the
material, a flash burn.  That can be carried over very
quickly into the second chamber."

"Reported temperatures for incinerators refer to the air.
That is what is being monitored, and not the actual
temperature in the ash.  Under abnormal conditions, a lot of
things can really go wrong, cold start up conditions,
overloading, inadequate control of the under fire air flow."
[19]

Overloading, excessive load density, inadequate air
turbulence, and insufficient control of under fire airflow
can all negatively impact incinerator performance.  Any of
these conditions can result in incomplete heat penetration
of the ash bed and insufficient residence time in the burn
chamber.

Dr. David Taylor discusses this possibility in a paper on
disposal issues related to TSE infected animals:

"Although incineration is generally regarded as the optimal
method for the destruction of all microorganisms, there have
been frequent reports of the discovery of organic material
in the resulting ash.  These findings indicate that the
incineration process does not always perform according to
the required standards."[20]

Equipment breakdowns during burn cycles are likely to occur
at some point.  These include electrical component failure,
short circuits, and failure of fuel or air delivery systems.
A common incinerator problem is refractory (firebrick)
breakage.  If the burn chamber is not inspected and repaired
on a regular basis, a damaged refractory can expose the
steel wall of the burn chamber to high temperatures
resulting in a "burn-through" and emergency shutdown.

Malfunctions can force a shutdown in mid-cycle.  The result
is an unintended release of smoke from the stack since there
is no way to effectively contain the combustion gases until
the partially combusted waste material has cooled down.
When an incinerator is in failure mode there is no way to
close or contain the system to prevent release of infectious
agents and other pollutants into the environment.

Operator training and supervision is crucial to incinerator
performance.  Operators of hazardous waste incinerators are
required by law to take classroom training courses and
annual refresher courses.[21]  The American Society of
Mechanical Engineers has developed certification programs
for hazardous and medical waste incinerator operators.[22]
The Colorado Department of Public Health & Environment,
however, does not require classroom courses, refresher
training, or operator certification.

Incinerator upsets and problems may occur often, even in new
facilities.  The Colorado Division of Wildlife (CDOW)
operated two new pathological incinerators in the town of
Craig, Colorado during the 2002-2003 hunting season.  In
daily logs obtained under the Colorado Open Records Act, the
incinerator operator documented numerous problems and
malfunctions.  Following are excerpts from the daily logs:

10-25-02  9:00 AM   8 hrs
First burn   Primary Temp. 1500°
Secondary Temp 1800°
57 Elk heads   47 Deer heads   104
Burn duration 8 hrs
9:30 A.M. - 5:30 P.M.   Cool down 2 hrs.
Cool down temp. 600° primary chamber.
was able to clean ashes out at this temp.
Produced about 40 gals of ash.
Stirred heads at 5 hrs. 6 hrs & 7 hrs during burn.
Only five heads were not completely incinerated.
Left them in with second burn.

10-25-02  2nd burn   10 hrs
8:15 P.M.   60 Elk   60 Deer   120
6:15 A.M. shut off
8:00 A.M. Temp was 700°
Load was not stirred during night.
App. 30 heads did not burn completely.
Some didn't even have the hair cinched [sic].
We have been stacking heads in front of door.
Those don't incinerate very well in this area,
was still some blood on floor in this area.

10-26-02 3rd Burn   8 hrs
9:00 A.M.   42 elk   68 Deer   112
Started pre-heating secondary chamber when loading primary.
Starting primary chamber when secondary is at 1200°-1300°
Increased primary to 1600°
Opened primary air blower to 8
Stirred heads every ½ hour after five hours of burning.

11-3-02   7th   10 hrs.
10:30 A.M   43 Elk   45 Deer   98 [sic]
#4 burner having trouble staying lit at start up

11-6-02   11th   10 hrs.
10:00 AM - 6:00 PM
66 Elk   40 Deer   106
starting to notice odor of burnt hair

11-7-02   12th   10 hr
9:45 AM - 7:45 PM
69 Elk   49 deer   118
Still odor
Secondary burning unit, paint is peeling & cracking around
large connection ring

11-12-02
Testing secondary chamber length of time to reach 1800° w/
primary chamber off.
12:45 A.M.   start  90°
1:15              1000°
1:45         1133°
1:55 1161°
2:45 1245°
3:30 1295°
4:30 1337°
5:50 1375°
shut off

11-13-02   15th   10 hrs
71 elk   46 Deer   12:15 A.M.   117
notice smoke around secondary burner when it ignited

11-14-02   16th   10 hrs
71 elk   7 Deer   78
9:15 A.M.   7:15 P.M.   Now winter fuel
50% #1 & 50% #2   won't hold temp. in secondary

11-14-02
Frank Searles. Plant manager returned my calls this A.M.
Is sending a new thermocouple for secondary chamber.
Thinks the smoke might be from fuel being to [sic] cold.
Wants me to heat tape the fuel lines.
Also the area of smoke & paint peeling is not an air tight
seal in that area

11-16-02   18th   10 hrs
Elk 75   Deer 0   75
10:00 AM - 8:00 P.M.
Secondary chamber had to be reset
Did not fire

These records document several problems:

- Unburned heads and blood in burn chamber after 10 hour
burn
- Started burning load before secondary chamber reached 1800
degrees F
- Malfunctioning burner
- Noticeable odor of burnt hair
- Secondary chamber unable to reach 1800 degrees F
- Noticeable smoke
- Possible problem with cold fuel

In a May 2, 2002 report prepared for the Northern Larimer
County Alliance, Duane Switzer interviewed Craig residents
Ed and Pat Relaford regarding their experience living about
300 feet from the two incinerators.  The Relafords told Mr.
Switzer:

- Bad smell.  Day and night when the incinerators are in
operation.  Singed hair and burning flesh.

- Wispy smoke, that is to say, not billowing clouds.  In any
case, the city attorney had told them there would be no
smoke.

- Noise. The roar of the incinerators is constant and loud,
to the point she could not sleep.

- The noise and smell are continuous day and night for 6 to
8 weeks straight.

The occupants of another house about 1,000 feet from the
incinerators told Mr. Switzer they experienced a "foul
smell" from the incinerators.[23]  In a July 15, 2003
article in the Craig Daily Press, Ed Relaford confirmed that
the stench of burning flesh permeated his neighborhood.[24]

Alkaline Tissue Digestion

Alkaline tissue digestion is the only proven technology for
prion inactivation that is capable of handling large volumes
of animal carcasses.  It is based on the process of alkaline
hydrolysis, which is the breaking of chemical bonds by the
insertion of water between atoms, catalyzed by alkali metal
hydroxides.

The technology for hydrolyzing large quantities of animal
carcasses was developed in 1992 by Dr. Gordon Kaye and Dr.
Peter Weber, professors at Albany Medical College in New
York.  The equipment consists of an insulated,
steam-jacketed, stainless steel pressure vessel with a lid.
Carcasses (or heads) are loaded into a basket that is placed
inside the vessel.  The load is automatically weighed, and
the appropriate amounts of water and alkali are
automatically added.[25]

The vessel is sealed and the contents are heated by steam.
The alkali solution is continuously recirculated and
agitated.  There are no moving parts inside the vessel.  The
tissues are dissolved and are hydrolyzed into smaller and
smaller molecules.[26]  The recommended digestion cycle time
is six hours based on experiments done by Robert Somerville
in 2002, funded by the UK Department of the Environment,
Food, and Rural Affairs (DEFRA).[27]

The Somerville experiments involved digestion of sheep heads
inoculated with mouse-passaged BSE agent.  Different
chemical and time parameters were tested.  Samples of the
resulting hydrolysate were diluted and injected into mice.
Although infectivity remained after 3-hour digestion cycles,
no infectivity was detectable after a 6-hour cycle.[28]

Due to constraints specific to the Somerville experiments,
the European Commission Scientific Steering Committee
(EC-SSC) concluded in its April 2003 opinion that further
studies are needed "before any final assurance could be
given regarding the safety of the process with respect to
TSE risks".[29]

It should be noted that the precautionary approach to
digestion by the EC-SSC has never been applied to the
process of incineration.  This is perhaps because of the
widely held, though not scientifically proven, assumption
that incineration is an effective means of inactivating
TSEs.  Regardless, with respect to TSE inactivation,
alkaline tissue digestion has been subjected to far greater
scrutiny than incineration.

Responding to an early version of the EC-SSC's opinion, Dr.
David Taylor prepared a risk assessment of alkaline
digestion assuming a digester with the capacity to process
ten BSE-infected bovine carcasses.  Dr. Taylor concluded
that "a human would have to consume at least 126,000 litres
(over 33,000 gallons) of effluent from the production
process to have a 50% chance of developing variant CJD."[30]

Further reinforcing the effectiveness of alkaline hydrolysis
are Dr. Taylor's comments in his 2000 review of prion
inactivation methods:

"The only methods that appear to be completely effective
under worst-case conditions are strong sodium hypochlorite
solutions or hot solutions of sodium hydroxide."[31]

Apparently convinced that alkaline tissue digestion is
effective, the European Commission is in the process of
adopting the final language of regulations approving
alkaline hydrolysis for disposal of TSE-infected
materials.[32,33]

Compared to incinerators, alkaline digesters are safer
particularly in the failure mode because the system is
self-contained.  In the event of loss of temperature and
pressure, or mechanical breakdown, the contents remain
inside the sealed vessel until repairs are completed and the
process is restarted.

The effluent from a digester can either be dehydrated and
the remaining solids landfilled, or an anaerobic digestion
process can be utilized.  Many facilities reduce the pH
level of the effluent and release it into municipal sewer
systems with no adverse effects.

Below is a comparison of certain aspects of digestion and
incineration:

Alkaline Digestion    Incineration
Closed system in failure mode Yes No
Tested for prion inactivation Yes No
Emission of air pollutants Not detectable Yes

Alkaline tissue digesters have already become the waste
disposal technology of choice at a variety of installations.
Health Canada's Host Genetics and Prion Diseases Federal
Laboratories in Winnipeg took delivery of a small digester
in January 2000.  In April of that year, the US Department
of Agriculture's (USDA) Animal Research Service lab in
Laramie, Wyoming installed a 1,500-pound capacity tissue
digester.  In February 2001, the USDA's Animal and Plant
Health Inspection Service in Ames, Iowa purchased a
7,000-pound digester to dispose of 350 sheep exposed to an
unidentified prion disease.[34,35]

Colorado State University's Veterinary Diagnostic Lab
(CSU-VDL) in Fort Collins installed a 2,000-pound digester
in October 2001.  The facility is a joint venture of CSU,
the Colorado Department of Agriculture, and the USDA.
During the 2002-2003 hunting season, the DOW contracted with
the CSU-VDL to dispose of 140,189 pounds of deer and elk
heads and carcasses, many infected with CWD.[36]

The College of Veterinary Medicine at the University of
Pennsylvania purchased a 7,000-pound unit last year
specifically for prion destruction.[37]  In a joint venture,
the USDA, the Wisconsin Veterinary Diagnostic Laboratory
(WVDL), and the Wisconsin Department of Agriculture, Trade
and Consumer Protection are deploying a mobile tissue
digester to be available for state use in dealing with the
CWD "emergency" as well as other animal disease outbreaks.
The USDA has provided $1 million for the purchase of the
digester as part of a homeland security grant to the state
and WVDL.[38]

The Cornell College of Veterinary Medicine (CCVM) in Ithaca,
New York is finalizing funding for an alkaline tissue
digester to replace its 18-year-old pathological
incinerator.  In the Draft Environmental Impact Statement
for the project, the CCVM concludes the following
significant positive impacts on human health are to be
expected:

"The significant reduction in air pollutants and greenhouse
gases (e.g., NOx and CO2) would result in a positive impact
on human health."

"Moreover, the Proposed Action would provide more reliable
treatment of animal remains infected with prions, the
causative agents of "Mad Cow Disease" and other
Transmissible Spongiform Encephalopathies (TSEs) compared
with current treatment (i.e., incineration) based on
research published to date, and would protect public health
to the maximum extent in the event that prion-infected
wastes were received by the CCVM."[39]

Compared to incineration, alkaline tissue digestion is a
more reliable method of TSE inactivation, has undergone
more scientific scrutiny, can be contained in failure mode,
is simpler to operate, is a less complex technology, and
costs less to operate per pound of waste.

Cross-Species Transmission of TSEs

The Raymond et al. 2000 in-vitro study found that the human
molecular barrier to CWD is approximately as effective as
the human molecular barrier to BSE.[40]  While the
transmission of BSE to humans is inefficient, it has
certainly proven to be possible.  U.K Department of Health
statistics as of February 2, 2004 indicate that 139 people
have died of definite or probable variant Creutzfeldt-Jakob
Disease (vCJD).[41]  It is believed that variant CJD is
caused by consumption of beef contaminated with BSE.

The study shows that, at the molecular level, humans are no
less susceptible to CWD than to BSE.  The study's authors
conclude "since humans have apparently been infected by BSE,
it would seem prudent to take reasonable measures to limit
exposure of humans (as well as sheep and cattle) to CWD
infectivity".[42]

Many of the 692 cases of sporadic Creutzfeldt-Jakob Disease
recorded in the U.K. since 1990 may also be linked to BSE.
Sporadic CJD has been thought to occur spontaneously and not
as a result of exposure to a pathogen.  This theory was
called into question in a 2002 study by Emmanuel Asante,
John Collinge, and others showing that BSE could produce a
disease indistinguishable from sporadic CJD.  The authors
conclude, "some patients with a phenotype consistent with
sporadic CJD may have a disease arising from BSE exposure"
..[43]

Any natural or molecular barriers humans may have against
CWD may be overcome by the agent's potential for adaptation.
In a study by scientists at the Rocky Mountain Laboratories
in Hamilton, Montana, a strain of hamster scrapie gradually
adapted to cause illness in mice that were previously not
susceptible to the disease.

The research revealed that scrapie prions could persist in
asymptomatic mice for years at levels too low for standard
lab tests to detect.  When the agent was transferred from
the original group of mice to additional groups, the disease
grew stronger making the newly infected mice sick.
Researcher Richard Race explained:

"The scrapie seemed to have learned how to deal with this
new species, and it worked much better.  It replicated
faster in additional rounds of mice and even became more
lethal to them."

Race noted the study "confirmed that prion disease can adapt
to new species", and that "the process is slow and difficult
to detect".  Applying his results to CWD, Race said:

"If BSE were derived from sheep scrapie, then adaptation
during passage in cattle may have increased its
pathogenicity for humans.  A similar situation could occur
with CWD.  CWD transmission to other cervids or livestock
could change its characteristics, including its potential
for transmission to people."[44]

In a similar study conducted in the U.K. on subclinical
prion infection, results led the researchers to caution that
"current definitions of the species barrier, which have been
based on clinical end-points, need to be fundamentally
reassessed".[45]

Noted CWD researcher Dr. Elizabeth Williams from Laramie,
Wyoming had the following to say about the risk to humans:

"I do think it is legitimate to be concerned about the
potential for humans being susceptible to CWD.  We don't
have evidence...but we can't say it could never happen and
we
have to be prudent."[46]

Regarding CWD transmission to cattle, the results are mixed.
In an ongoing study in Wyoming, cattle fed brain tissue from
CWD-infected mule deer have not gotten sick after 6 years.
A study in Ames, Iowa has yielded different results.  In
1997, 10 calves were inoculated intracerebrally with the
same inoculum used in the Wyoming experiment.  As of
mid-2003, 5 calves had developed CWD.[47]

Although the Wyoming study involves a more natural route,
ingestion may simply result in a more prolonged incubation
period.  Alternatively, based on the work done by Race, et
al. on TSE adaptation and species barriers, the test
cattle in Wyoming may be asymptomatic carriers harboring a
gradually adapting CWD agent.

Complicating matters, a recent study analyzing "glycoform"
patterns of abnormal prion protein from CWD-affected deer
and elk, scrapie-affected sheep and cattle, and BSE-affected
cattle failed to identify patterns capable of reliably
distinguishing these TSEs.  Difficulty in identifying the
source of a TSE following cross-species transmission adds to
the uncertainty surrounding CWD and possible risks to cattle
and humans.  The authors write:

"Sheep scrapie has been present in the United States since
at least 1947, and in many geographical areas, sheep, deer,
and elk share pastures and rangeland.  If scrapie-affected
sheep were present in these situations, then cross-species
transmission might have occurred.  Sheep scrapie is not
thought to cause disease in humans, although passage through
cattle appears to have changed this characteristic.  It
remains to be determined if the same will be true of CWD."
[48]

The European Commission's Scientific Steering Committee
(EC-SSC) released a lengthy, comprehensive report and
opinion on CWD in March 2003.  Cross-species
transmissibility experiments and risks are discussed in
detail.  The EC-SSC report reviews the successful
transmission of CWD by intracerebral inoculation to ferrets,
mice, a squirrel monkey, mink, a goat, and a sheep.  The
report concludes, "...it remains theoretically possible that
the CWD-agent could infect humans."[49]

Thank you for your consideration of my comments.  Please
contact me if you have any questions.

Sincerely,

Jim Woodward
 
 

References

[1] Cristina Casalone, et al., "Identification of a Second
Bovine Amyloidotic Spongiform Encephalopathy: Molecular
Similarities with Sporadic Creutzfeldt-Jakob Disease,"
Proceedings of the National Academy of Sciences (2004 -
published online before print).
http://www.pnas.org/cgi/content/abstract/0305777101v1
[2] Det Norske Veritas Limited/DNV Technica, "Risks from
Disposing of BSE Infected Cattle in Animal Carcase
Incinerators - for the Environment Agency," Revision 4, June
19, 1997.
[3] European Commission Scientific Steering Committee,
"Scientific Report on the Risks of Non Conventional
Transmissible Agents, Conventional Infectious Agents or
Other Hazards such as Toxic Substances Entering the Human
Food or Animal Feed Chains via Raw Material from Fallen
Stock and Dead Animals or via Condemned Materials," June
24-25, 1999,
http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf
[4] Det Norske Veritas Limited/DNV Technica, "Risks from
Disposing of BSE Infected Cattle in Animal Carcase
Incinerators - for the Environment Agency," page 10.
[5] Ibid.
[6] European Commission Scientific Steering Committee,
"Final Opinion and Report on: A Treatment of Animal Waste by
Means of High Temperature (150°C, 3 Hours) and High Pressure
Alkaline Hydrolysis," April 10-11, 2003.
[7] C. Weissmann et al., "Transmission of Prions,"
Proceedings of the National Academy of Sciences 99 4 (2002):
16378-16383.
[8] Centers for Disease Control and Prevention, "Agent
Summary Statements: Section VII-D: Prions," 1999,
http://www.cdc.gov/od/ohs/biosfty/bmbl4/bmbl4s7d.htm
[9] World Health Organization, "Infection Control Guidelines
for Transmissible Spongiform Encephalopathies," March 1999.
[10] Paul Brown et al., "New Studies on the Heat Resistance
of Hamster-Adapted Scrapie Agent: Threshold Survival After
Ashing at 600°C Suggests an Inorganic Template of
Replication,"  Proceedings of the National Academy of
Sciences 97 7 (2000): 3418-3421.
[11] Paul Brown, "BSE: The Final Resting Place," Lancet 351
9110 (1998).
[12] David Taylor et al., "Observations on Thermostable
Subpopulations of the Unconventional Agents that Cause
Transmissible Degenerative Encephalopathies," Veterinary
Microbiology 64 1 (1998): 33-38.
[13] David Taylor et al., "The Effect of Dry Heat on the ME7
Strain of Mouse-Passaged Scrapie Agent," Journal of General
Virology 77 (1996): 3161-3164.
[14] Paul Brown et al., "New Studies on the Heat Resistance
of Hamster-Adapted Scrapie Agent: Threshold Survival After
Ashing at 600°C Suggests an Inorganic Template of
Replication."
[15] Ibid.
[16] European Commission Scientific Steering Committee,
"Scientific Report on the Risks of Non Conventional
Transmissible Agents, Conventional Infectious Agents or
Other Hazards such as Toxic Substances Entering the Human
Food or Animal Feed Chains via Raw Material from Fallen
Stock and Dead Animals or via Condemned Materials."
[17] European Commission Scientific Steering Committee,
"Opinion on the Use of Small Incinerators for BSE Risk
Reduction," January 16-17, 2003.
[18] United States Food and Drug Administration, transcript
of Transmissible Spongiform Encephalopathies Advisory
Committee (TSEAC) meeting in Bethesda, Maryland, July 17,
2003,
http://www.fda.gov/ohrms/dockets/ac/03/transcripts/
3969t1.htm
[19] Ibid.
[20] David Taylor, "Issues Involving the Disposal of TSE
Infected Animals." Proceedings of the 105th Annual Meeting
of the United States Animal Health Association, Hershey,
November 1-8, 2001, pp. 70-75.
[21] National Research Council, "Waste Incineration & Public
Health," (2000), National Academy Press, p. 48.
[22] Ibid. p. 69.
[23] Duane Switzer, "Report on the Craig Colorado Division
of Wildlife Animal Incinerators," May 2, 2003, prepared for
the Northern Larimer County Alliance.
[24] Jeremy Browning, "The Air Up There," The Craig Daily
Press, July 15, 2003.
[25] WR2, Inc., "Biological Waste Management by Alkaline
Hydrolysis - Technical Data Monograph," January 29, 2002,
http://www.wr2.net/techdata.htm
[26] Ibid.
[27] European Commission Scientific Steering Committee,
"Final Opinion and Report on: A Treatment of Animal Waste by
Means of High Temperature (150°C, 3 Hours) and High Pressure
Alkaline Hydrolysis," April 10-11, 2003.
[28] Ibid.
[29] Ibid.
[30] David Taylor, letter to Dr. G. Kaye (WR2, Inc.)
including "A Risk-Assessment Relating to the Use of the Hot
Alkaline Hydrolysis Process for Disposing of the Carcasses
of Confirmed Cases of BSE," May 23, 2002,
http://www.wreurope.net/response/taylor2002.htm
[31] David Taylor, "Inactivation of Transmissible
Degenerative Encephalopathy Agents: A Review," The
Veterinary Journal 159 (2000): 10-17.
[32] Gordon Kaye, interview by J. Woodward, Fort Collins,
Colorado, August 12, 2003.
[33] Commission of the European Communities, "Draft
Commission Regulation of Implementing Regulation (EC) No
1774/2002 as Regards the Approval of Other Means of Disposal
or Uses of Animal By-Products," 2003,
http://www.defra.gov.uk/animalh/by-prods/publicat/
altdisposal.pdf
[34] WRE, Ltd., "WR2 Prion (TSE) Destruction or Research
Application Customer List,"
http://www.wreurope.net/response/custlist.htm
[35] Cheryl McMullen, "New Technology Destroys Sheep That
May Have Mad Cow Disease," Waste News, April 2, 2001,
http://www.organicconsumers.org/madcow/new4201.cfm
[36] Barb Powers, presentation to the Larimer County
Environmental Advisory Board, August 12, 2003,
http://www.co.larimer.co.us/boards/brd_info.cfm?board=5
[37] WRE, Ltd., "WR2 Prion (TSE) Destruction or Research
Application Customer List."
[38] Wisconsin Veterinary Diagnostic Laboratory, "Request
for State Building Commission Action," March 2003,
http://www.uwsa.edu/capbud/sbc/2003/Mar03/0303VetLabTissue%2
0Digster2.doc
[39] Malcolm Pirnie, Executive Summary of Draft
Environmental Impact Statement - CCVM Waste Management
Facility.
[40] G.J. Raymond et al., "Evidence of a Molecular Barrier
Limiting Susceptibility of Humans, Cattle and Sheep to
Chronic Wasting Disease," The EMBO Journal 19 17 (2000):
4425-4430.
[41] UK Department of Health, February 2004, "Monthly
Creutzfeldt-Jakob Disease Statistics," http://www.doh.gov.uk
[42] G.J. Raymond et al., "Evidence of a Molecular Barrier
Limiting Susceptibility of Humans, Cattle and Sheep to
Chronic Wasting Disease."
[43] Asante et al., "BSE Prions Propagate as Either Variant
CJD-like or Sporadic CJD-like Prion Strains in Transgenic
Mice Expressing Human Prion Protein," The EMBO Journal 21 23
(2002): 6358-6366.
[44] Richard Race et al., "Long-Term Subclinical Carrier
State Precedes Scrapie Replication and Adaptation in a
Resistant Species: Analogies to Bovine Spongiform
Encephalopathy and Variant Creutzfeldt-Jakob Disease in
Humans," Journal of Virology 75 21 (2001): 10106-10112.
[45] Andrew Hill et al., "Species-Barrier-Independent Prion
Replication in Apparently Resistant Species," Proceedings of
the National Academy of Sciences 97 18 (2000): 10248-10253.
[46] "Killer in the Herds, Chapter 1: While danger spread,"
Rocky Mountain News, June 1, 2002,
http://cfapp.rockymountainnews.com/cwd/killer/
[47] Janice Miller, reply to Terry Singletary, June 23,
2003, http://www.vegsource.com/talk/madcow/messages/650.html
[48] Richard Race et al., "Comparison of Abnormal Prion
Protein Glycoform Patterns from Transmissible Spongiform
Encephalopathy Agent-Infected Deer, Elk, Sheep, and Cattle,"
Journal of Virology 76 23 (2002): 12365-12368.
[49] European Commission Scientific Steering Committee,
"Opinion on Chronic Wasting Disease and Tissues That Might
Carry a Risk For Human and Animal Feed Chains," March 6-7,
2003,
http://europa.eu.int/comm/food/fs/sc/ssc/out323_en.pdf