Prion information update from Helane Shields
Posted to Compost Council website
This is to respond to the issue raised by Dr.Rufus Chaney of prions in treated municipal sewage sludge “biosolids”.
Both risk assessments on prions in sewage sludge (Gale, et al, 2001, and Yamamoto, et al, 2006) agree: Prions from
SRM (specified risk materials such as brains and spinal cords) of infected animals processed at abattoirs
(slaughterhouses) may pass through drains into sewage treatment plants. The wastewater treatment process does not
inactivate infectious prions and reconcentrates those prions in the treated sewage sludge “biosolids”. Spreading the
sludge as fertilizer may expose animals including livestock to transmissible spongiform encephalopathies (TSEs).
However, as a basis for their conclusions, both Gale and Yamamoto rely on incorporation of the sewage sludge into the
soil to dilute the infectious prions.
Gale: “For pasture land, a grazing restriction of three weeks applies and the treated sludge must be deep injected or
ploughed down immediately after application.”
Yamamoto: “The level of sludge-derived fertilizer ingested by cattle was considered to be very low since the fertilizer
is mixed with ground soil, . . . “
In the United States (US), top dressing sewage sludge “biosolids” on hay fields, dairy pastures and grazing lands is
common practice. Thus, there is no incorporation to dilute the prions in the sludge.
Further, both Yamamoto and Gale consider the only prion source to be tiny amounts of Bovine Spongiform
Encephalopathy (BSE) infected SRM (specified risk material) passing through drain screens and/or filters in abattoirs to
the sewage plant. Neither Yamamoto nor Gale consider other sources of prions which are present here in the US
including Chronic Wasting Disease (CWD) and human prions from Creutzfeldt Jakob Disease (CJD).
CWD, a transmissible infectious prion disease similar to BSE, is spreading and has infected farmed and/or wild deer and
elk, (and frequently both) in Montana, Wyoming, Colorado, South Dakota, Nebraska, Kansas, Oklahoma, New Mexico,
Minnesota, Wisconsin, Illinois, and has moved east to West Virginia and New York Shedding of the CWD prions in
feces and urine is considered a plausible route for transmission and environmental contamination. (Williams, et al
2002) Infectious CWD prions are also found in muscle tissue. (Angers, et al 2006)
Disposal of infected CWD carcasses in landfills is common: “We want to reiterate that disposing of potentially
contaminated CWD carcasses and wastes in MSWLFs (Municipal Solid Waste Landfills ) that are compliant with 40 CFR
258 standards is and remains an acceptable option.” (EPA memo, Nov. 12, 2004)
“In most instances the (landfill) leachate is transferred to a wastewater treatment plant (WWTP) for treatment.” “Once
that leachate (from landfill) reaches the wastewater treatment plant the suspended solids will be separated from the
effluent. Those suspended solids will then be termed "sludge" or biosolids.” “Land application of municipal sludge that
potentially contains CWD PrP-res (prions) may result in the presence of CWD PrP-res in surface soils.” (WIDNR, 2002;
EPA Reg. 8, 2005)
Prions can survive for years in soil (Brown, et al 1991). Animals can become infected from prions in soil. (Miller, et al
2004)
Between 2 and 25% of the 4.5 million cases of Alzheimer’s Disease and senile dementia victims in the US are actually
infected with sporadic CJD. (Manuelidis, et al, 1989; Boller, et al, 1989, 1995; Harrison, 1991; Teixeira, 1995; Warren,
et al, 2005) creating the reality that many thousands of CJD victims are shedding infectious prions into public sewers to
end up in both Class B and Class A sludge compost.
Prions have been found in the blood and urine of CJD victims. (Gabizon, et al, 2001; Reichl, et al 2002) . Undertakers
and medical facilities routinely discharge CJD infected blood and body fluids into public sewers. (Yale; UC Davis, CDC)
Prions can cross the intestinal barrier by riding piggyback on ferritin, a protein normally absorbed by the intestine.
Because ferritin shares considerable homology across species, these data suggest that PrPSc-associated proteins, in
particular ferritin, may facilitate PrPSc uptake in the intestine from distant species, leading to a carrier state in humans.
(Singh, et al 2004)
“ . . . enteric infection at early as well as later stages of (CJD) disease, and regardless of the route of agent entry,
implicates potential environmental spread by fecal matter.” (Radebold, et al 2001)
Class B sewage sludge “biosolids” is expected to be pathogenic. EPA allows land applied sludge “biosolids” to contain
fecal coliform up to 2 million CFU/gram. But the EPA and waste industry promote the use of “pathogen-free” Class A
sludge “biosolids” compost on playgrounds, ball fields, public parks, and home flower and vegetable gardens
. “Pathogen free” is clearly not the case when the Class A sludge compost can contain infectious human and animal
prions. Not only are livestock and wildlife at risk from ingesting prion infected soil and sludge, but humans, and
particularly children, are especially at risk because their hand to mouth behavior results in the ingestion of dirt
(Robischon, 1971; LaGoy, 1987; Binder, et al 1986; Gerba, et al 2002 ; CDC, Callahan, 2004).
The EPA guidelines and disclosures on pathogens in Class A sludge “biosolids” compost need to be revisited.
Helane Shields, Alton, NH
J. Vet. Med. Sci.. 68(2): 137-142, 2006 http://www.jstage.jst.go.jp/article/jvms/68/2/137/_pdf
Evaluation of Bovine Spongiform Encephalopathy (BSE) Infection Risk of Cattle via Sewage Sludge from Wastewater
Treatment Facilities in Slaughterhouses in Japan
Takehisa YAMAMOTO1), Sota KOBAYASHI1), Akiko NISHIGUCHI1), Takashi NONAKA1) and Toshiyuki TSUTSUI1)
1) Applied Epidemiology Section, National Institute of Animal Health
ABSTRACT. Scattered SRM residues from BSE-infected cattle are possible to contaminate sewage during the
slaughtering process in slaughterhouses. A proportion of the sludge discharged from wastewater treatment facilities at
slaughterhouses has historically been processed into fertilizer. We therefore investigated the associated risk of BSE
infection to cattle via sludge-derived fertilizer. Each stage of the process associated with BSE exposure was qualitatively
evaluated and quantitative evaluations were subsequently performed using infectious dose as a unit of concern. Results
of these qualitative evaluations indicated that installation of filter(s) at the drains to the wastewater treatment facilities
has been undertaken by many slaughterhouses and has decreased the likelihood of SRM contamination of sewage.
The level of sludge-derived fertilizer ingested by cattle was considered to be very low since the fertilizer is mixed with the
ground soil, and the amount of soil ingested by cattle is likely to be small. Results from the quantitative analysis
indicated the total infectious dose ingested by cattle in Japan from an infected cow has been estimated to be 5.5 × 10-3
ID50. Preventing scattering of SRM during the slaughtering process, installing filters to the drains with the removal of
residues from the drain water and preventing the application of sludge-derived fertilizer to pasturelands would be
effective to reduce the risk. Although the limited extent of available information, this study should provide useful
indication for the development of an inclusive risk assessment for slaughterhouse sludge in the future.
KEY WORDS: abattoir, Bovine Spongiform Encephalopathy (BSE), fertilizer, risk assessment, sewage sludge
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Helane’s comments: In comparing this Japanese Risk Assessment on prions in sewage sludge (hereinafter referred to
as “Yamamoto”) with the similar “ prions in sludge” 2001 Risk Assessment by Gale & Stanfield (UK) (hereinafter called
“Gale”) they agree on many points. But both are at odds with the facts in the USA.
Yamamoto and Gale agree as follows:: Prions from SRM (specified risk materials such as brains and spinal cords) of
infected animals processed at abattoirs (slaughterhouses) may pass through drains into sewage treatment plants. The
wastewater treatment process does not inactivate infectious prions and reconcentrates those prions in the treated
sewage sludge “biosolids”. Spreading the sludge as fertilizer may expose grazing livestock to BSE.
One of the problems with both the Yamamoto and Gale risk assessments (RAs) is that they depend on incorporation of
the sewage sludge into the soil to dilute the infectious prions. Excerpts:
Gale: “For pasture land, a grazing restriction of three weeks applies and the treated sludge must be deep injected or
ploughed down immediately after application.”
Yamamoto: “The level of sludge-derived fertilizer ingested by cattle was considered to be very low since the fertilizer
is mixed with ground soil, and the amount of soil ingested by cattle is likely to be small.”
At least the prudent Japanese acknowledge the risks of spreading sewage sludge “biosolids” on animal pastures:
“The risk from slaughterhouse sludge was considered to arise mainly from the application of sludge-derived fertilizer to
grazing land and forage-crop growing land. Consequently, preventing the application of the sludge-derived fertilizer on
these lands would considerably reduce this risk.”
Here in the United States (US) it is common practice for the waste industry to top dress sludge on hay fields, dairy
pastures and grazing lands. This puts both livestock and wildlife at risk of ingesting dioxins, toxic metals, hazardous
organic chemicals, parasitic worms and, of course, infectious prions. (We have pictures of US cattle grazing with the
sludge clearly visible on the grass. Cattle are known to ingest up to one kilogram of soil a day with their fodder.)
Another problem with the Yamamoto and Gale RAs, is that both only consider the prion source to be tiny amounts of
BSE infected SRM (specified risk material) passing through drain screens and/or filters in abattoirs to the sewage plant.
No such drain screens or filters are required in slaughterhouses the US. And neither Yamamoto nor Gale consider
other sources of human and animal prions which are present here in the US including Chronic Wasting Disease and
human prions from Creutzfeldt Jakob Disease (CJD).
Chronic Wasting Disease (CWD), a transmissible encephalopathy prion disease similar to Mad Cow Disease (BSE) is
spreading and has infected either confined and/or wild deer and elk, (and frequently both) in Montana, Wyoming,
Colorado, South Dakota, Nebraska, Kansas, Oklahoma, New Mexico, Minnesota, Wisconsin, Illinois, and has moved east
to West Virginia and New York
Disposal of infected CWD carcasses in landfills is a common practice which has the approval of the US EPA:
Memo November 12, 2004 to RCRA and Superfund (Regions I-X) and Office of Solid Waste (OSW) from Matt Hale, EPA
OSW: “We want to reiterate that disposing of potentially contaminated CWD carcasses and wastes in MSWLFs* that are
compliant with 40 CFR 258 standards is and remains an acceptable option.” (* MSWLF = Municipal Solid Waste Landfill)
It is common and acceptable policy throughout the United States to discharge landfill leachate into POTWs. http://epa.
gov/waterscience/guide/landfills/final/landfact.html
Excerpt from the Wisconsin Dept. of Natural Resources Risk Assessment on CWD prions to landfills to POTWs to sludge
biosolids to farm fields:
http://www.dnr.state.wi.us/org/land/wildlife/Whealth/issues/Cwd/risk_analysis.pdf
The September 2002 Wisconsin Risk Assessment: “An Analysis of Risks Associated with the Disposal of Deer from
Wisconsin in Municipal Solid Waste Landfill” concludes “Once that leachate (from landfill) reaches the wastewater
treatment plant the suspended solids will be separated from the effluent. Those suspended solids will then be termed
"sludge" or biosolids.”
Page 4: “Land application of municipal sludge that potentially contains CWD PrP-res (prions) may result in the
presence of CWD PrP-res in surface soils.”
Peer reviewed, published research indicates between 2 and 25% of all senile dementias and the 4.5 - 5 million cases of
Alzheimer’s Disease in the US are actually sporadic CJD prion victims, creating the potential for hundreds of thousands
of CJD victims shedding infectious prions into public sewers.
http://www.chemtrailpatrol.com/cpr_alzheimer_cjd_linked.htm
"An informal survey of neuropathologists, however, registered a theoretical range of 2-12% of all dementias as actually
CJD (Harrison, 1991). And hundreds of thousands of Americans suffer from severe dementias every year (Brayne,
1994; United, 1995). Two other studies average about a 3% CJD rate among dementia patients (Mahendra, 1987;
Wade, 1987). A preliminary 1989 University of Pennsylvania study showed that 5% of patients diagnosed with dementia
were actually dying from Creutzfeldt-Jakob disease (Boller, 1989). It would seem CJD is seriously underdiagnosed at
present (Harrison, 1991). "
http://www.organicconsumers.org/madcow/times21604.cfm A 1989 study at the University of Pittsburgh examined the
case histories of 54 demented patients who, upon their death, were autopsied at the University of Pittsburgh. The study
discovered that 39 (72 percent) of the patients had Alzheimer's; 15 (27.7 percent) had central nervous system
disorders; and three (5.5 percent) had CJD.
In a study by Yale University researchers, 13% of Alzheimer's patients were found upon autopsy to actually have CJD.
"Manuelidis, Elias E. and Laura Manuelidis
Alzheimer Disease and Associated Disorders_ 3 (1989): 100-109
Suggested Links between Different Types of Dementias: Creutzfeldt-Jakob Disease, Alzheimer Disease, and Retroviral
CNS Infections
"In our own neuropathological material, in 46 cases diagnosed clinically as AD [(Alzheimer's)], 6 cases were proven to
be CJD at autopsy [13%}."
http://www.cyber-dyne.com/~tom/Alzheimer_cjd.html#clinical
http://www.jubilee-newspaper.com/mad_cow_96.htm
In Lancet Medical Journal on April 5, 1996, Dr. Robert Will reported that CJD usually has an incubation period of up to
30 years and affects people over 60 years of age. However, he found that 10 new cases of CJD were very unusual
because the age of the victims were young, between 19 and 41. The cases all had spongy holes in the brain,
characteristic of Mad Cow disease, and a waxy buildup known as plaque which is also seen in Alzheimer's, another form
of dementia.
In May, 1996 in Scotland, Dr. Gareth Roberts, an expert on dementia for Smith Kline Beecham Pharmaceuticals told a
conference of 2,000 European scientists that it is possible that earlier cases of CJD had been missed simply because
doctors were not looking for it. Evidence from Dr. Roberts suggests that the true number of patients currently being
treated for mental illness and dementia who die from CJD in the United Kingdom should be revised upwards every year.
http://bmj.bmjjournals.com/cgi/content/full/313/7061/833
" Teixeira, et al, found 3 out of 12 AD patients were really suffering from CJD. (25% ) Teixeira, F., et al. “Clinico-
Pathological Correlation in Dementias.” Journal of Psychiatry and Neuroscience 20 (1995): 276-282. http://www.
nealhendrickson.com/PDF/PDFMc040100NL.pdf
Peer reviewed, published research (Gabizon, et al 2001; Reichl, et al 2002) have reported the presence of prions in the
blood and urine of CJD victims. However, more recent research has indicated prions may also be present in the feces
of CJD victims which could add another significant source of prions to public sewers, to end up in the sludge:
Extensive research by CWD/prion expert from Colorado Dr. Beth Williams, (unfortunately deceased in tragic auto
accident last year), has already concluded that CWD is transmitted horizontally between animals through contact with
urine, feces and contaminated soil.
Another recent study explains how the prions cross the intestinal barrier:
“A new study from the Department of Pathology at Case Western Reserve University School of Medicine shows that the
infectious version of prion proteins, the main culprits behind the human form of mad cow disease or variant Creutzfeldt-
Jakob Disease (vCJD), are not destroyed by digestive enzymes found in the stomach. Furthermore, the study finds that
the infectious prion proteins, also known as prions, cross the normally stringent intestinal barrier by riding piggyback on
ferritin, a protein normally absorbed by the intestine and abundantly present in a typical meat dish. The study appears
in the Dec. 15 issue of the Journal of Neuroscience.”
Neurobiology of Disease
Protease-Resistant Human Prion Protein and Ferritin Are Cotransported across Caco-2 Epithelial Cells: Implications for
Species Barrier in Prion Uptake from the Intestine
Ravi Shankar Mishra, * Subhabrata Basu, * Yaping Gu, Xiu Luo, Wen-Quan Zou, Richa Mishra, Ruliang Li, Shu G.
Chen, Pierluigi Gambetti, Hisashi Fujioka, and Neena Singh
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106
“Because ferritin shares considerable homology across species, these data suggest that PrPSc-associated proteins, in
particular ferritin, may facilitate PrPSc uptake in the intestine from distant species, leading to a carrier state in humans.”
Prion expert Dr. Laura Manuelidis of Yale Medical School says there is a potential for environmental spread of CJD by
fecal matter:
Blood borne transit of CJD from brain to gut at early stages of infection
Klaus Radebold , Mark Chernyak , Daniel Martin and Laura Manuelidis
Section of Neuropathology, Yale Medical School, 310 Cedar St, New Haven, CT 06510, USA
BMC Infectious Diseases 2001, 1:20 doi:10.1186/1471-2334-1-20
“Thus the infectious inoculum must spread to the gut by a vascular route, a direction opposite to that generally
assumed. This interpretation is consistent with previous studies demonstrating white blood cell infectivity as well as
perivascular PrP accumulations in CJD. Notably, enteric infection at early as well as later stages of disease, and
regardless of the route of agent entry, implicates potential environmental spread by fecal matter.”
This memo is already way too long, but there is abundant more information available on the numerous sources of
infectious human prions from blood, urine and feces in both Class B and also Class A sewage sludge. There is a large
body of research showing prion diseases can cross species barriers. Thus, there is the question of whether if animals
(livestock and wildlife) can be infected with transmissible spongiform encephalopathies from human prions by ingesting
sewage sludge top-dressed on hay fields, dairy pastures and grazing lands.
Class B sewage sludge “biosolids” is known to be pathogenic. Common sense dictates that you don’t spread it on
grazing land to be ingested by livestock which can bioaccumulate pollutants and pass them on to humans in the meat
and milk. But it is unconscionable that the US EPA and waste industry promote spreading Class A sewage sludge
“biosolids” compost as being “pathogen-free” -- but potentially contains infectious human and animal prions in addition
to other pollutants, on playgrounds, ballfields, and for home use in flower and vegetable gardens. Family pets roll in
this stuff and bring it indoors on their fur . . . children eat dirt . . . and Pica kids eat lots of dirt.
The Swiss got it right: “Because of the presence of trace elements and the risk of BSE, effluent sludge from central
sewage systems is no longer used as fertiliser, but instead must be burned and disposed of at landfills.”
http://www.swissinfo.org/sen/swissinfo.html?siteSect=107&sid=5360272&cKey=1122372624000