[USCC] Compost Digest Vol 29, #1, et seq, relative to discussion between Al Rubin, Rufus Chaney and Edo McGowan.
The Rubins
rubinhial at cox.net
Fri Jul 7 23:13:12 CDT 2006
Edo:
Before I respond (or not respond) to your main challenge, a response to
"EPA has also recently backed out of promoting land applied sewer
sludge--------------why is this?" Response: EPA has clarified its policy on
the use/disposal of sewage sludge (biosolids). It is the responsibility of
communities that generate biosolids to choose the method of use/disposal for
the biosolids as long as the particular method of use/disposal is in
conformance to all appropriate provisions contained in the Federal EPA Part
503 Standards for that particular use/disposal method chosen . This
clarified policy is in complete conformance with the stautory language
(Sections 405(d) and (e) of the Clean Water Act of 1987).
As for your main challenge in your most recent posting below. There is no
need to answer this "challenge". In my earlier response to you, I asked you
to supply any evidence from biosolids field studies and/or operational data
from biosolids generators to support your allegations/hypotheses on
antibiotic resistance and other issues that you raised. I and others on
this list serve are still waiting for your data. Not having seen any data,
I assume that either none exists or if it does, you haven't aquired it. My
bottom line is that there have never been any observations made by either
academic institutions or Federal/State authorities to support your
allegations/theories. To honor the list serve's ground rule of not
retransmitting old text/postings, I have not retransmitted in this response
my earlier response to you.
Cheers
Alan
----- Original Message -----
From: "Edo McGowan" <edomcgowan at earthlink.net>
To: <compost at composter.com>
Sent: Friday, July 07, 2006 3:40 AM
Subject: [USCC] Compost Digest Vol 29, #1, et seq, relative to discussion
between Al Rubin, Rufus Chaney and Edo McGowan.
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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 Iâ?Tm 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 Griffithâ?Ts 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 â?oIt 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 donâ?Tt
know---itâ?Ts that simple------------we donâ?Tt 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 donâ?Tt 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
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