[USCC] Compost Digest Vol 29, #1, et seq, relative to discussion between Al Rubin, Rufus Chaney and Edo McGowan.

[Edo McGowan]

Compost Digest Vol 29, #1, et seq, relative to discussion between Al Rubin, Rufus Chaney and Edo McGowan.


Al, thanks for the reply. It tells volumes about your apparent understanding of the issues. In essence one might be tempted to say that you know as much as EPA which, although admonished by NRC to come up with data, remains silent. EPA has also recently backed out of promoting land applied sewer sludge--------------why is this?

But let me rephrase my challenge:

1. Prove that EPA has studied antibiotic resistance in sludge and have data showing that antibiotic resistance and its transfer via MGEs from pathogens to background organisms, thence back to man as a process is a fiction, hence sludge is not a source of antibiotic resistance. 
Implicit in this is the virulence islands that accrue to lysogenic viruses, e.g., Pantin-Valentine Leukocidin and whether or not these genetic bits survive to transfer. 

2.  Prove that EPA has demonstrated that transfer of MGEs conferring resistance are not transferred from pathogens to other organisms that can withstand temperatures of compost, and upon cooling, transfer that information back to re-blooming bacteria. 

3. Show that EPA has done health risk assessments related to pathogens that are found within sewer sludge, and thus there is no impact. 

4. Prove that EPA has studied antibiotic resistance in sludge and have data showing that antibiotic resistance and its transfer via MGEs from pathogens to background organisms, thence back to man as a process is a fiction, hence sludge is not a source of antibiotic resistance. 

As I’m sure you are aware and within the timeframe you mentioned in your post  (the 100-year increment) the world has considerably evolved. Thus, I am having a hard time in understanding your point. We progressed from general acceptance of the germ theory to the development of antibiotics. These medications came into general use following their release by the War Department in the 1940s; resistance was noted shortly thereafter. The general trend in chemicals development parallels that approximate time. Sewer plants are built on older design standards and can not deal with much of what they receive. In a recent issue of the trade journal, MSW, there are two good articles that are on point; I suggest that the readers of this list-serve pull them up via Google (see MSA Management, Vol 16, #4). The first of these articles discusses thermochemical conversion, the second is on how sewer plants can not deal with many incoming materials (see: Cleaning up medical waste).

Sewer plants also generate the advancement of antibiotic resistance, (see for example Nakamura S, Shirota H. Behavior of drug resistant fecal coliforms and R plasmids in a wastewater treatment plant] Nippon Koshu Eisei Zasshi 1990 Feb;37(2):83-90). These products are thus passed through and shunted into the sludge. These are all undisputed facts. I need not generate volumes of data for you; the data are there in the published literature.
Another interesting paper that is germane is one by Adrian UNC on Recovery of Escherichia coli from Soil after Addition of Sterile Organic Wastes. Applied and Environmental Microbiology, March 2006, p. 2287-2289, Vol. 72, No. 3. Thus the nutrient value of the material augments pathogen growth.

Additionally, one must remember Griffith’s work in the 1920s. He was working with two strains of Streptococcus pneumoniae; the R which form rough colonies (no carbohydrate capsule) and cannot cause disease, and S which form smooth colonies (have carbohydrate capsule) and can cause disease.

- inject live S cells into mice ... mice die

- kill S cells with high heat, then inject into mice ... mice live

- inject live R cells into mice ... mice live

- kill S cells with high heat, then inject dead S cells and live R cells together into mice ... mice die. When bacteria were isolated from the dead mice, they were S type.

- Thus, what of transfer of MGEs from sludge into this ready pool of waiting recipients? Does the treatment of sludge guarantee that genetic information is also destroyed?

Thus, even with heat-killed pathogens, assuming for a moment that sewer sludge is sterile, which we know it is not, there is the chance for regrowth.

What if this were Listeria and somehow a pregnant woman got contaminated? Listeria spp. were found in most treated waters (84.4%) and raw sludge (89.2%) of six French urban wastewater treatment plants and one composting facility, examined monthly over a 1-year period. (Delphine Paillard, et al.,  in Applied and Environmental Microbiology, November 2005, p. 7562-7566, Vol. 71, No. 11). 

The NIH notes, when speaking of Listeria, that “It was surprising to find that a single bacterium is sufficient to cause placental infection but even more surprising to find that they (the bacteria) migrated from the placenta back to the mother's liver and spleen in such large numbers. She can't clear the infection unless the placenta is expelled." (see: 05.jul.06 RxPG News National Institutes of Health PLoS Pathogens, reviewed by: Dr. Priya Saxena).

Under the old paradigm, there were dose responses for pathogens. There are general rules of thumb, it takes x number of bacteria to cause an infection. The above and other factors are now known to play havoc with these older paradigms. 

We know that once inside the gut, the transfer of resistance to the vast normal flora occurs. We know that absent further exposure to antibiotics, the washout is about 4 years. We know that the information can be passed to higher-grade pathogens. We know that community-acquired methicillin resistant Staph aureus that carries the prophage for Panton-Valentine leukocidin (PVL) can be rapidly fatal. It would be interesting to examine some of the pathology tissues from the young men that were exposed to sludge and there after rapidly expired. 

Without a pathogen risk assessment to consider these situations, we don’t know---it’s that simple------------we don’t know.

 We have examples of composted biosolids being put out as potting soils, and we have examples of Legionella found in potting soils, why not Listeria? Why not MRSA with PVL? Do we know?

Without some kind of monitoring, we don’t know. If we have that monitoring or efficacy data by industry, where are these published? In the absence of any health risk assessment, how would EPA and the industry know of this? What happens if the pathogen is multi-drug resistant? 

I feel that the forum is for the exchange of information, but not sniping at each other. I would much rather see the data that you and EPA have developed since the 2002 NRC report, as I previously mentioned. If there are no data and no pathogen risk assessments, then this is a critical finding. If you and the agency keep ducking these questions, you leave your selves open to serious question. 

I realize that from an industry perspective, the bottom line is critical. Industry must produce profit to survive. Thus there are things such as externalities that are developed during this quest for profit and in cases protection of such externalities is coveted. To off set this, society has constructed regulatory agencies to counter the negative aspects of such impacts on society. When, however those agencies and their higher management see their function as one of protecting industry in deference to the citizens, we are in trouble. This is clientele capture. I'm afraid that what I'm reading in current trends and perhaps mirrored in your response could be considered by some as reflective of this. 

To close, the questions I raised remain unanswered. 

Cheers----------Edo