The recent case of mad cow disease in California once again has people around the world asking questions about food safety. A constructive analysis requires a broader perspective and a refined focus on the causes of all prion diseases.
Contrary to government statements, there is not an isolated case of mad cow disease or any prion disease. Prion disease contributes to deadly forms of environmental contamination that essentially recycle and redistribute the disease. Victims are infectious long before they exhibit clinical symptoms. Chronic wasting disease in various deer species is an explosive example. As prion disease is recycled in the environment and up the food chain, prions mutate and become even more lethal to people and other mammals.
Mad cow disease, also known as bovine spongiform encephalopathy (BSE), is one of many deadly prion diseases (technically referred to as Transmissible Spongiform Encephalopathy (TSE). TSEs are a spectrum disease, where CJD is the most extreme form. We know prion disease as:
The common denominator in all of these diseases is the prion (PREE-on) In addition, according to neuroscientist Laura Manuelidas, about 10-25 percent of Alzheimer’s disease cases are misdiagnosed—they are actually cases of CJD, which is further p the prion spectrum.
Prions are a form of protein that cannot be effectively stopped. They can’t be killed because they are not a virus or bacteria and they don’t contain DNA or RNA. These pathological proteins mutate, migrate, multiply, and intensify. Prion diseases kill everything in their path. In reality, there is no way to contain the disease. There is no cure—prion disease is always fatal. (Studies contend that any prion inactivation procedures must be validated by bioassay against the prion strain for which they are intended to be used.)
Prions are a lethal threat to our food and water supplies. We also risk exposure and infection at hospitals, dental offices, restaurants, and through pet food. The buildup of prions in the environment will get worse with time. Mismanagement is accelerating the process. Various forms of prion disease are already spreading around the world, building up in soil and water, and building up in the bodies of virtually every living creature on the planet. The incubation period and the onset of clinical signs of the disease usually take years, which makes these diseases easier to ignore and more difficult to study.
Dr. Stanley Prusiner, an American neuroscientist from the University of California at San Francisco, earned a Nobel Prize in 1997 for discovering and studying deadly prions. President Obama awarded Prusiner the National Medal of Science in 2010 to recognize the growing significance of his discovery. Although his research is ongoing, we know enough about prions to sound the alarm on many levels.
Prions are such a formidable threat that the U.S. government enacted the Bioterrorism Preparedness and Response Act of 2002, which included a provision to halt research on infectious prions in all but two laboratories. Now, infectious prions are classified as select agents that require special security clearance for lab research.
Thanks to Dr. Prusiner’s discovery and pioneering research, prion disease has been found in humans, livestock and a variety of wildlife species in several countries, including Austria, Canada, Czech Republic, Finland, Germany, Greece, Israel, Italy, Japan, Poland, Slovakia, Slovenia, Spain, United Kingdom, and the United States.
Not only are prion diseases a symptom of a much bigger problem, they are contributing to the buildup of prions in the environment. A person or animal with prion disease is contaminating their immediate environment and exposing nearby humans and animals to deadly prions.
The prion pathogen spreads through urine, feces, saliva, blood, milk, soil, and the tissue of infected animals and humans—including bone and muscle tissue. (Contrary to industry reports and a controversial statement from the World Health Organization, research suggests that milk is a pathway to prion exposure).
Humans with Creutzfeldt-Jakob disease (CJD) also are shedding infectious prions into toilets, public sewers and elsewhere. If a single person with prion disease discharges bodily fluids or feces into a public sewer system, that sewage system is permanently infected and the amount of contamination will multiply and intensify over time. The more infected people use the sewage system, the worse the contamination problem. Everything discharged from that sewage system—reclaimed water or biosolids—is at risk of spreading the contamination even further.
Between 2 and 25 percent of the 4.5 million cases of Alzheimer’s disease and senile dementia victims in the U.S. alone are actually infected with CJD, creating the reality that many thousands of CJD victims are shedding infectious prions throughout their home and everywhere they visit, (Manuelidis, et al, 1989; Boller, et al, 1989, 1995; Harrison, 1991; Teixeira, 1995; Warren, et al, 2005).
Similar pathways exist from an infected cow, sheep, or deer. When infected animals use fields and feedlots, their urine, feces, saliva, and blood permanently contaminates those areas. That contamination becomes bio-available to every creature that follows the path of the infected animal. Those areas are then subject to rainwater and runoff, which can carry the prions further.
In Canada, out of 55,415 cows tested for BSE in 2006, five head of cattle were identified with BSE. If the U.S. only tests 40,000 head of cattle and detects one animal with BSE out of that small test group, we must assume that hundreds more infected animals are missed out of the millions of cattle that are milked and slaughtered each year. Based on those statistics, without comprehensive testing globally, we must assume that beef and dairy operations are producing hundreds of sick animals each year that are being milked, slaughtered and consumed by humans, pets, fish farms, and even other forms of livestock and poultry.
In addition, the land at the feedlot or dairy is contaminated with manure and urine that often is scraped out and used as compost and fertilizer on farms and gardens, which expands the pathways for deadly prions to reach unsuspecting families. “Prions can survive for years in soil,” (Brown, et al 1991). “Animals can become infected from prions in soil,” (Miller, et al 2004). Naturally occurring BSE prions can be up to 1 million times more difficult to inactivate than the most commonly used hamster prions (engineered for clinical studies).
Furthermore, prions can wash from the soil and migrate through irrigation and surface water runoff and settle in groundwater, streams, ponds, lakes, and oceans—where they proceed to multiply and mutate into even more abundant and lethal forms. Wildlife, livestock and humans (especially children) can ingest prions from soil exposure, water exposure, or food. We can’t afford to take the risk of further contaminating entire watersheds – increasing the pathway to humans, livestock, and wildlife downstream.
With these characteristics, there is not an isolated case of Mad-cow or any prion disease. The California dairy where the recent infected animal lived and produced milk is contaminated (two dairies have been quarantined since the discovery of that case of BSE). If the infected cow provided milk to a processor, that supply chain is now in question and those supply chains should be quarantined. In fact, all exposed milk should have been immediately recalled from that entire supply chain. The pathways of that milk still should be traced and condemned.
If the infected animal was rendered for pet food, that rendering plant is now permanently contaminated and will contaminate everything that is processed from now on—exposing our pets to the deadly disease and creating a new pathway in our homes—food bowls that also are permanently contaminated (in fact, an undisclosed rendering plant has been quarantined).
If cattle with BSE are actually processed at a slaughterhouse, that slaughterhouse also is permanently contaminated and will contaminate every carcass that follows the infected animal down the production line. Compounding the problem is the fact that liquid wastes from slaughterhouses are rinsed down the drainpipe and into the municipal sewage system, where they add to the risks associated with that waste stream.
Milk and Meat: As stated earlier, highly infectious risk-material (brain and spine) is not the only pathway to prion exposure. Prions have been found in muscle tissue and milk.
Lessons From The United Kingdom: Initially, UK officials insisted the Mad-cow epidemic was not a risk to humans. After 150 human vCJD deaths, they admitted that they were wrong.
“Thousands of pages of grisly detail on meat-pie making and animal-feed milling might seem like a hard read. As bureaucrats digest the final report of Britain’s BSE inquiry, handed to ministers on October 2nd, 2000 stomachs at the Ministry of Agriculture, Fisheries and Food (MAFF) and the Department of Health must be churning. Not at the finer points of carcass-rendering, but at what is expected to be a thorough dissection of bureaucratic incompetence. Ministers will be considering the findings until the report is presented to Parliament on October 23rd. Three days later, the public will at last be allowed to read the report into Britain’s biggest public-health scandal for decades.
The independent inquiry was established by the UK government to work out the history of two epidemiological crises, bovine spongiform encephalopathy (Mad-cow disease) and its human relative, new-variant Creutzfeldt-Jakob disease (vCJD). The inquiry’s three-person committee, headed by Lord Phillips, a high-court judge, was also asked to assess whether government and industry responded adequately to the situation as it evolved.
Roughly £27m ($39.4m) and 630 witnesses later, the Phillips report is widely expected to be the definitive word on what went wrong in Britain between the first documented cases of BSE in 1986 and the announcement in Parliament, ten years later, that the strange neurodegenerative condition appearing in a handful of young people, now called vCJD, was probably linked to Mad-cow disease.” – The Economist, October 5, 2000.
The Full report from the UK’s BSE Inquiry is available. Furthermore, almost 4,000 Britons aged between 10 and 30 may be harboring the prion proteins that cause the human form of Mad-cow disease. The new estimate comes from direct analyses of human biopsies (tonsils), and is much higher than epidemiological projections of the likely number of deaths from variant Creutzfeldt-Jakob disease (vCJD).
For years, industry experts and government regulators insisted infectious prions could not be found in blood or muscle except for infected sheep and goats. Prions have since been found in blood and muscle of human vCJD and sCJD victims and in the leg muscle tissue of infected deer.
Even organic supplies are not immune from the prion problem. For example, if an organic farm is downstream from a traditional farm that has an animal with BSE, the water runoff from that farm will expose the organic operation downstream to deadly prions.
Let’s assume that everything that the beef and dairy industries, and the USDA, have said about the latest example of Mad-cow disease is true. The tested animal was sent to a rendering plant and was never destined for the food supply.
Growth Hormones and Blood Transfusions: Most growth hormones are made from the pituitary brain of dead cattle or cloned from the DNA of that pituitary gland (bad idea). One infected gland in the production facility and all future products are permanently contaminated. Dairy and beef producers could be injecting BSE directly into live animals with this practice. Similar practices (taking the pituitary gland from cadavers) have killed people from prion disease, including this very recent case from May 2012.
It’s time to stop using growth hormones in beef and dairy cattle. Even if the hormone itself is free of prion disease, what does a growth hormone do to a prion? Has industry or regulators even conducted studies on this dynamic? People have contracted prion disease from infected hormones, infected blood and infected organ transplants. We must assume that the same risk is present for livestock.
Recent studies of variant Creutzfeldt-Jakob disease (vCJD) indicate that this disease is transmissible by blood. One case of probable transfusion-transmitted vCJD infection has been reported, and one case of subclinical infection has been detected. On February 9, 2006, a third case was announced by the UK Health Protection Agency.
Each of the three patients had received a blood transfusion from a donor who subsequently developed clinical vCJD, which indicates that transfusion caused the infection.
Surgical and Dental Procedures: We can’t sterilize surgical equipment used on people who have prion disease. Prions are so resistant to sterilization that surgical instruments used on a person with CJD must be disposed because they are permanently contaminated. Hospitals have been sued successfully for exposing subsequent patients to deadly prions. Dental and oral surgery settings have the same challenge, but those industries have ignored those risks for the most part.
Despite the causal association between variant Creutzfeldt – Jakob disease and bovine spongiform encephalopathy (BSE), bovine origin graft materials are widely used during dental surgical procedures. The aim of this study was to assess the risk of BSE transmission through bovine bone substitutes. Methods: Electronic database of MEDLINE was searched to identify relevant studies regarding our focused questions, presence of BSE prion infectivity in raw bovine bone, BSE prion inactivation by bone substitute manufacturing process, protein contents in anorganic bovine bone substitutes, and validity of current BSE diagnostic methods. Search terms yielded 1,704 titles. After title/abstract screening and duplicates removal, 36 full-text articles were screened for inclusion. Results: A total of 16 studies were included in the final analysis. No eligible studies were identified regarding the efficacy of BSE prion inactivation by the treatments used for anorganic bovine bone manufacturing. BSE infectivity and PrP(Sc), pathological prion, were detected in bovine bone marrow and serum samples.
Prions were detected in Tutoplast® (bovine), Bio-Oss®, and tibia samples treated at the similar condition for Bio-Oss deproteinization. Inconsistent results of different BSE diagnostic tests were not unusual findings (Iwata et al. 2006; Arnold et al. 2007; Murayama et al. 2010), and a study by Balkema-Buschmann and colleagues showed an apparent discrepancy between BSE infectivity and detection of PrP(27-30), the current surrogate marker for prion disease infectivity. Conclusion: This review indicates that bovine-derived graft biomaterials may carry a risk of prion transmission to patients.
The transmission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt-Jakob Disease (vCJD) raised concerns about potential secondary transmissions due to the resistance of the agents causing transmissible spongiform encephalopathies (TSEs), sometimes known as prions, to commonly used methods of sterilization, notably steam sterilization (or autoclaving). It has been suggested that surgical instruments and other medical devices might retain sufficient infected tissue debris after cleaning and steam sterilization to infect patients on whom they are subsequently used.
As noted previously, TSE strains derived from BSE sources appear to be more resistant to steam sterilization and other forms of heat inactivation than other TSE sources.
Pet Food: How many infected animals are sent to a rendering plant, never tested for BSE, and are churned into food for dogs, cats, poultry, fish, and zoo animals? What is the likelihood that we are feeding deadly food to our pets? If and when contaminated, that food dish is another pathway for the prion pathogen to enter our homes and bodies, not to mention the risk to our pets. How often do you actually touch that pet food or the dish? How often do you wash that bowl in your kitchen sink?
Aquaculture: Many fish farms use specified risk material—SRM (brain and spinal cords) from slaughterhouses and rendering plants as protein meal. What is the likelihood that infected material from a slaughterhouse or a rendering plant was sent to a fish farm (either in a large lagoon or in the open ocean) and dumped into the water and consumed by farmed fish (and wild fish and mammals such as dolphins and whales). Since every microscopic prion can’t be consumed, how much water are we contaminating every year to extend this science experiment via new pathways.
This questionable practice puts the health of the fish at risk and those who eat the fish. Secondly, the water that the risk material is dumped becomes contaminated with prions, which threatens groundwater, surface water runoff, streams, rivers, and oceans with deadly prions. This factor could be contributing to the deaths of dolphins and whales and it could be contributing to prion disease in people. Many fish have contracted Whirling disease, which could be a form of prion disease (needs research that this author has not conducted, yet).
Animal Rendering & Anaerobic Digestion Of Carcasses: “It’s necessary to use additional heat at the end of the rendering process to fully inactivate pathogens. However, even with this, prions are not inactivated,” APHIS/USDA, January 2005.
“While finished compost can be spread on farmland as fertilizer, if prions are present and the compost is used as fertilizer prions can re-enter the food chain through grazing plants, hay and straw obtained from those areas. Thus, composting should not be used to dispose of infected deer, elk, sheep, goats, or cattle. Composting is especially unsuitable for specified risk materials, especially neural tissues (skull and spinal cord) encased in bones. The indiscriminate use of composting and spreading its byproducts on agricultural land is inconsistent with the FDA feed rule, would dilute its integrity and invalidate all existing BSE/TSE risk assessment models. This is similar to what may have transpired with the CWD material, given the WIDNR (Wisconsin Department of Natural Resources) disposal policy was indeed implemented,” National Renderers’ Association response to USDA and APHIS, June 2005.
Lotions & Cosmetics
How safe is collagen material? Our purified collagen material is extremely safe and is being used in the manufacture of finished medical devices currently on the market. All collagen devices manufactured by Collagen Matrix, Inc. have passed biocompatibility testing in accordance with ISO 10993 Biological Evaluation of Medical Devices. Any additional potential concerns such as viruses, BSE, bacteria, and pyrogens have been addressed thoroughly in manufacturing process control which includes a step that is proven to inactivate BSE, quality control testing, validations, and internal risk analyses.
Is Mad Cow Disease or Bovine Spongiform Encephalopathy (BSE) transmission a concern with the use of your collagen?
The risk of transmitting Mad Cow Disease, Bovine Spongiform Encephalopathy (BSE) or viruses through the use of bovine tendon or corium as a raw material source of type I collagen for medical devices is considered negligible. This conclusion is based on a thorough investigation and risk analysis process in which various aspects of the material from animal sourcing and harvesting to finished product testing were evaluated. There has been no such documented case of BSE transmission through a medical device using bovine-derived collagen material.
From cosmetics, candy and gelatins to drugs for diabetes, hay fever and arthritis, there are beef parts in dozens of products that people use every day. Worries about the safety of British beef spread beyond just steaks and chops Wednesday when the European Community ordered Britain to stop exporting all beef-derived products including ice cream, candy, cosmetics and drugs.
U.S. scientists noted, however, that very few of these products use pieces of the steer’s brain and spinal cord, the only parts of the steer’s body where mad cow disease, or bovine spongiform encepthalopathy, has been found. The most widely used beef product is collagen, the spongy substance derived from beef skin or bones. Collagen is often an ingredient in ice cream, custards, cheeses, candies, sausage casings and cosmetics.
Even if it were found to be a carrier, the vast majority of the collagen in U.S. products comes from domestic beef because it is so plentiful, said Bob Rust, professor emeritus in meat science at Iowa State University.
The FDA, prior to approval of any drug with beef products, should require the manufacturer to certify that the beef only come from countries free of the disease. It does not. The variety of drugs derived from cattle parts is diverse and includes:
In June 2012, Nobel Laureate Stanley Prusiner, UCSF, confirmed that Alzheimer’s Disease (AD) is a prion disease like CJD and mad cow. AD victims shed infectious prions in their blood, saliva, mucous, urine and feces. The infectious prions bind to the sewage sludge, including sludge/biosolids/compost, being applied on home gardens, US cropland, grazing fields and dairy pastures, putting humans, family pets, wildlife and livestock at risk.
Other prion contaminated wastes discharged to sewers include rendering plants (which process remains of 2 million potentially BSE infected downer cows each year), slaughterhouses, embalmers and morticians, biocremation, taxidermists, butcher shops, veterinary and necropsy labs, hospitals, landfill leachates (where CWD infected and other carcasses are disposed), Drinking water is at risk for prions if it comes from a surface source (river or lake) which receives treated sewage effluent. Chlorination does not inactivate prions.
The US EPA lists prions as a contaminant of concern in sludge and water eight times.
Renown prion researcher, Dr. Joel Pedersen, University of Wisconsin, found that prions become 680 times more infective in certain soils.
Dr. Pedersen’s research also proved sewage treatment does not inactivate prions: “Our results suggest that if prions were to enter municipal wastewater treatment systems, most of the agent would partition to activated sludge solids, survive mesophilic anaerobic digestion, and be present in treated biosolids. Land application of biosolids containing prions could represent a route for their unintentional introduction into the environment. Our results argue for excluding inputs of prions to municipal wastewater treatment.”
“Prions could end up in wastewater treatment plants via slaughterhouse drains, hunted game cleaned in a sink, or humans with vCJD shedding prions in their urine or feces,” Pedersen says.
In the July 3, 2010 issue of VETERINARY RECORD, Dr. Pedersen stated: “Finally, the disposal of sewage sludge was considered to represent the greatest risk of spreading (prion) infectivity to other premises.”
It is well known that sewage sludge pathogens, pharma and chemical pollutants are taken up by plants and vegetables. The Canadian Food Inspection Agency recently warned that plants can uptake infectious prions: “. . . there is a potential risk to humans via direct ingestion of the compost or of compost particles adhered to skin or plant material (e.g. carrots). Another potential route of exposure is by ingestion of prions that have been taken up by plants.”
Thousands of tons of sewage sludge (biosolids) are spread on farmland, parks, open spaces, and even lawns and gardens every year. In addition, millions of gallons of sewage water are being reclaimed for various uses. Spreading sewage sludge and reclaimed sewage water on fields and in our watersheds is another foolish and risky practice. People with CJD (and many with Alzheimer’s disease) excrete prions in their urine, feces, saliva and blood and these recycling practices also are recycling, concentrating and expanding pathological pathways back to humans.
“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, Center for Disease Control.
Prions are not neutralized by sewage treatment. Therefore, prions become part of the sewage sludge and create pathways to the disease on fields and water runoff. It’s time to quit spreading lies and pathogens on farmland and pastures where livestock graze and where surface water runs off into streams, rivers, lakes and ponds.
Sewage treatment does not inactivate prions. In fact, it concentrates the infectious prions in the sewage sludge being applied on home gardens, cropland, grazing fields and dairy pastures, putting humans, family pets, wildlife and livestock at risk.
“Prions are extremely resistant to inactivation by ultraviolet light, irradiation, boiling, dry heat, formaline, freezing, drying and changes in pH. Methods for inactivating prions in infected tissues or wastes include incineration at very high temperatures and alkaline hydrolysis,” U.S. EPA.
Oral transmission of prion disease is enhanced by binding to soil particles. Dr. Pedersen and associates found that anaerobic digestion sewage treatment did not inactivate prions in sludge. Persistence of pathogenic prion protein during simulated wastewater treatment processes.
“Given it is unlikely that the sewage treatment or pellet production processes can effectively deactivate prions, adopting measures to prevent the entry of prions into the sewer system is advisable,” Toronto (Canada) Department of Health, Nov. 2004.
“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).
Given the volumes of research that clearly point to the risks associated with sewage sludge, how many cattle are being exposed to prions by grazing on land where sewage sludge (biosolids) has been applied? This exposure alone could spawn countless cases of Mad-cow disease around the globe every year. In addition, how many humans have ingested prions directly thanks to this foolish practice? How much water has been contaminated thanks to sewage sludge applications in our watersheds and directly injected into our rivers and oceans?
Sludge proponents claim that there aren’t enough prions in sludge to constitute an infectious dose.This statement shows incompetency or a reckless disregard for human and environmental health. Prions are known to multiply, which means that one can become thousands or millions once a facility or property is contaminated with even the smallest particle.
“Critics say that one example of outdated assumptions is the Harvard study’s assumption that a cow would have to eat one gram of infected material to come down with the disease. Most scientists now believe a cow would have to eat only 10 milligrams of infected material, a piece the size of a peppercorn, to catch the disease. That’s 100 times smaller than the assumption in the Harvard study. Recent British studies suggest the infectious dose could be 400 micrograms, which is 25 times smaller than 10 milligrams,” said Dr. Michael Hansen.
*Above Sources on Sewage Risks Compliments of Helane Shields/
Additional Documents & Research of Interest
“BSE has now been transmitted orally to 16 species,” (S. Dealler, 1995). Animals which have suffered fatal prion diseases include sheep, goats, cattle, pigs, bison, elk, mule and white-tailed deer, oxen, moose, domestic house cats, several species of macaques/monkeys, several species of lemurs, farmed mink, cougars, cheetahs, puma, ocelot, tiger, lion, kudu, oryx, eland, nyala, gemsbok and ankole.Rendered sheep fed to cattle are believed to have initiated the Mad-cow epidemic. Intensive inbreeding of sheep for various genetic characteristics is thought to have spawned prion disease in sheep.
Contaminated meat and MBM feed are linked to zoo animal infections. A 1999 report documented three German zoo ostriches, which developed prion disease after eating feed made from downer cattle. An elephant at the Oakland Zoo died of prion disease.
Under ordinary circumstances, most sCJD cases go undiagnosed. Few autopsies are done on suspected sCJD victims because the families don’t want to incur the expense. What’s the point if their loved one is already dead? And the pathologist/medical examiner is reluctant to do an autopsy because he/she is concerned about their own risk of infection and the fact that expensive medical instruments may have to be discarded if the case is positive.
By binding to a common soil mineral, the misshapen proteins that cause chronic wasting disease in deer can be as much as 700 times more infectious than exposure to the proteins alone, according to researchers at UW-Madison. The finding, by UW-Madison animal health and biomedical science professor Judd Aiken, may help explain why CWD spreads orally among Wisconsin deer even though animals in the wild are exposed to relatively low levels of the infectious proteins, called prions. Herbivores, including deer and sheep, consume a fair amount of dirt each day as they graze. They also are known to consume soil as a source of minerals. Grazing cattle are known to ingest one kilogram of soil per day (2.2 pounds)
Health Risk Summary
There are many prion pathways that we need to address and this paper has just scratched the surface in an attempt to redirect the conversation about Mad-cow disease to more productive ground. We still have much to learn about prions and we can’t afford to compartmentalize our thinking based on one pathway or the species affected—prion disease is prion disease, regardless of whether it is killing an animal or a human, or whether the deadly prion is being discharged by an animal or a human. The idea of species barriers for the most part is a myth. However, some races and species appear to be more susceptible (ask the Koreans and Japanese about their research, which points to a higher susceptibility in their genetic makeup). These countries are very quick to test beef and ban beef from any countries of origin with unacceptable risks.
If prions must be tightly regulated in a laboratory environment today, the outdoor environment and other pathways should be managed accordingly. If we can’t sterilize surgical equipment used on people who have prion disease, why are we kidding ourselves that we can neutralize prions in sewage? Dilution is not a solution to prion contamination. Prions don’t have a half-life as radiation does. They multiply, which means even one will become many. They can’t be stopped and the diseases always are deadly.
It’s time to develop a comprehensive prion-management strategy that maximizes safeguards for human health, food, water, and wildlife around the globe. We have to stop the practice of using biosolids and reclaiming sewage water. We need to rethink several other health care and food-safety practices, too.
The stakes are too high for fragmented and misguided prion policies. It’s time to stop spreading pathogens, misinformation and lies.