Prions, TSEs, Alzheimer’s, & Biosolids
Recently, there has been online coverage suggesting that biosolids recycling to soils may contribute to prion-related or similar diseases. This coverage is being cited by citizens concerned about biosolids recycling projects, and biosolids managers are once again learning about this bogus claim. There was a similar public discussion of this same topic a decade ago.
Prions are infectious, twisted proteins associated with bovine spongiform encephalopathy (BSE), also called “mad cow disease.” Prions are also associated with scrapie in sheep and the human Creutzfeldt-Jakob disease. The U. S. Center for Disease Control (CDC) provides information on the known prion diseases here.
In the past several years, scientists have been researching other twisted proteins associated with Alzheimer’s and other neurological diseases in humans.
Helane Shields of New Hampshire has argued for decades that use of biosolids spreads prions and associated diseases. On June 14th, Gary Chandler, a vocal opponent to biosolids recycling in the Northwest, posted similar arguments on an obscure Alzheimer’s website. He made scary statements about Alzheimer’s being an out-of-control epidemic worldwide and a leading cause of death, especially in Scandanvia, Iceland, and the U. S. – and that biosolids and sewage are implicated. He claims that transmissible spongiform encephalopathies (TSEs) are spreading rampantly: “They spread uncontrollably within victims and within the environment. They know no borders. Unlike radiation, however, prions do not deplete themselves. Unlike cancer, there is no cure. Prions migrate, mutate, multiply and kill with unparalleled efficiency. Each victim becomes an incubator and a distributor of the unstoppable pathogen.”
Shields’ and Chandler’s arguments about prions and biosolids stem from their long-standing positions against use of biosolids. They bend the science and feed on the uncertainties regarding prions and related malformed proteins to paint a scary picture about biosolids and wastewater treatment. “Finland and Sweden dump their sewage into rivers and lakes, which is contaminating waterways and communities, while exposing families to various toxins and pathogens, including Pandora‐like prions. This mismanagement is exposing millions of people, wildlife and livestock to the prion epidemic.... Every sewage system in the world has been used by someone, if not millions, of people with Alzheimer’s disease and Creutzfeldt‐Jakob disease. Sewage systems are now prion incubators and distributors. Sewage sludge, wastewater, biosolids and other byproducts are highly lethal.”
Shields and Chandler grossly simplify the scientific understanding of prion-like proteins that appear to be involved in Alzheimer’s and other neurological pathologies. They cite parts of the work of only one (Stanley Prusiner) of dozens of researchers working on understanding misformed proteins. The true complex story of the ongoing research is reported widely at easily available sources (e.g. National Institutes of Health paper, Nature article (May 2015), Washington Univ. research summary, Dana Foundation research summary).
The science is far from definitive, and, while there is some evidence of possible transmissivity or replication of various neurological diseases, including Alzheimer’s, it is currently considered to be a rare possibility. The Nature article notes that scientists studying these various twisted proteins “warn that it is too early to draw conclusions about the clinical significance of discovering different strains of Alzheimer’s plaques. Some are wary of linking neurodegenerative and prion diseases, especially when prion biology is still so poorly understood. And considering prion and non-prion diseases together ‘could give the misleading impression that you could catch Alzheimer’s from visiting your grandmother’, says Virginia Lee, who works on neurodegenerative diseases at the University of Pennsylvania in Philadelphia. ‘There is absolutely no evidence that’s possible, and it would be a dangerous thing to imply.’”
Finally, when confronted with claims of human health impacts from biosolids, it is important to consider the simple epidemiological concept of fate and exposure. People only get sick from something if exposed to a toxic or infective dose. It is implausible that biosolids-borne prions, many of which are inactivated in anaerobic digestion (see Miles et al., 2011, available from the NEBRA office), that are applied to soils where microbes break them down over time, contribute to the millions of cases of prion diseases or Alzheimer’s and other neurological diseases. The fact is, very very few people are exposed to biosolids. The most highly exposed population is in the wastewater profession. If Chandler and Shields were correct, the rate of such diseases in that population would be far greater than any other segment of the population, and there is no evidence of that.
This same issue arose 10 years ago and was addressed in a paper in the Journal of Residuals Science and Technology. There has been a lot more research since then, but it is certainly not implicating biosolids as a concern with regards to prions, TSE, Alzheimer's, and similar diseases. For example, a few years ago, researchers at the NSF-funded Water and Environmental Technology Center of Temple University, the University of Arizona, and Arizona State University "developed a new assay that only detects infectious prions. They used this assay to study of the fate of prions during wastewater treatment. Data showed that prions are actually inactivated during mesophilic or thermophilic anaerobic digestion negating the possibility of prions surviving wastewater treatment. This is significant in that if prions had survived wastewater treatment, they could have been found in biosolids and subsequently land applied with a potential for infecting cattle."
In May, 2015, Cell Reports published research on laboratory analyses showing plant binding and uptake of various prions (Pritzkow et al., 2015) with, in one experiment, subsequent infection of hamsters consuming the plants. This may help explain the transmission of prion disease (chronic wasting disease) that has been observed in deer, in the wild.
We will continue to track the research and learn from the science as it develops.