A (Very Scary) Research Proposal 

May, 2008

One of the problems of epidemiological research in the sludge field is that a negative result has no meaning unless the study carefully takes into account the fact that any health problems caused by BS may not be evident for years after the fields have been sludged.  If you knock on a sludge-farmer's door and ask "How y'all feelin'?" and they say "Just great."  it may not tell you anything because those people may be infected with microorganisms or may be poisoned with toxic metals that will not produce any symptoms for years or decades.

Here I proffer a proposal for an epidemiological research project that could provide valuable data relevant to the question of the whether land applied BS causes long-term, asymptomatic, air-borne infections.

There are three levels of BS infections or poisoning.  The first level is acute infection, which means the person gets sick during or immediately after handling BS or immediately after BS is spread nearby.  The second level is chronic effects.  Here the symptoms appear over a course of weeks, or months, or years and plague the person over a long period.  The third level is asymotmatic effects.  The scariest example is cancer.  The BS causes a change in the person's cells that are not detectable at all for years or decades.  Eventually -- long, long after the BS was applied -- the symptoms appear.  

This research proposal focuses on a special type of asympotmatic infection in which symptoms can be triggered by a well-defined and and very common event -- prescribing a broad-spectrum antibiotic.

The background biology

Although the word "chemotherapy" raises fear, if not panic, in the hearts of all of us boomers, from a strictly pharmacological point of view the term is much broader than the brutal mode for treating cancer.  Technically, chemotherapy refers to any use of chemicals -- i.e., drugs -- to treat a disease.  For instance, this week I began chemotherapy with Clindamycin for an infected tooth.  

The dentist really stressed that I report back to him immediately if I had any diarrhea while taking the drug, and the pharmacist emphasized that point even more.  I didn't understand why these folks were so edgy about my scatological future.  Although I have a PhD in pharmacology,  I had no idea what they were going on about because the closest I've come to pharmacology in the last 15 years has been getting that Clindamycin prescription filled.   

So out of a mixed sense of professional embarrassment, self-preservation, and curiosity I dove for the books to refresh my memory of the side effects of Clindamycin.  If the truth be told here -- which, rest assured, it is always told on this website -- I actually had no memory of the side effects of Clindamycin to refresh.  I was barely able to recognize it as an antibiotic.  But my good friend Richard Lehne publishes the number one nursing pharmacology textbook in the world, and when every new edition comes out he sends me a copy, gratis. So I cracked the latest edition of Lehne's Pharmacology.

I found out Clindamycin can cause a condition known as pseudomembraneous colitis (abbreviated, for obvious reasons, to "PMC") or less often called "clostridial colitis."  Colitis refers to inflammation of the colon. Clostridial refers to a genus of germs -- Clostridium.  Clindamycin-induced PMC is a nasty colitis in which, if not stopped, the colon is sort of eaten away from the inside.  Occasionally we hear about Staph a or other bacteria attacking the skin of patients and eating it away -- necrotizing fasciitis, it's called.  Well, Clindamycin-induced PMC is much the same kind of phenomenon on the inside.  The culprit in PMC is not Staph a., it is Clostridium difficile.  

Many of you will recognize Clostridium.  The clostridium genus is one of those groups of bacteria that has been kicking Homo sapiens' butts for tens of thousands, if not hundreds of thousands, of years.  Gas gangrene, tetanus, and food poisoning (botulinism) are all deadly diseases caused by this group of nasties.  

There are two traits of this genus that are particularly important with respect to land-application of BS.  The first is that these organisms are all obligate anaerobes, which means that not only do they not require oxygen to survive, but oxygen is toxic to them.  When exposed to oxygen, as when they enter the sewage stream and aeration processes of sewage treatment systems, they hunker down into survival mode. 

The second BS-related trait of C. difficile, and all clostridia, is that survival mode means forming spores.  These spores are called "endospores".  A number of bacteria can form endospores, and they are, in general, pretty scary.  For instance, it was anthrax endospores that killed 5 people in the 2001 anthrax attack.  Endospores are biological cluster-bombs, waiting for the right conditions to burst open and kill lots of people.  

Within the context of Clostridium and land-applied BS, endospores are as scary as Jason, the guy in the horror movies with the hockey mask, because, like Jason, endospores keep coming back.  You almost can't kill them.  One researcher has referred to them as the most durable form of life known.  Endospores are resistant to UV radiation, boiling, extreme pH, and chemical disinfectants -- precisely the kinds of "treatments" that are applied to raw sewage sludge to convert it into . . .ha, ha, ha, . . .  "biosolids."  Yeah.  When you make biosolids, you are making clostridial endospores.  Whenever you have C. difficile flushed down a toilet -- and that is happening virtually constantly in a moderately sized city -- you are sending to the waste-treatment plant bacteria that will become the endospores in the BS that is spread on the farmers' land.  Hospitals are huge sources of C. difficile.   

Just the presence of these spores in the air are indicative of bacterial contamination in the surrounding environment.  A recent patent application from UCLA uses endospore detection as a way to assess air contamination by bacteria generally.  Surely, you say, EPA regulations protect us from these tiny endospore time-bombs.  Ha!  

EPA microorganism monitoring requirements for both Class A and Class B are nil verging on none.  You can meet the requirements, even for Class A, simply by measuring either the so-called fecal coliforms or Salmonella.  This requirement is based on the "logic" that these are "indicator organisms;" i.e., if they're there it indicates the presence of trouble, and if they're not there, then there's no trouble.  Link to the Part 503 rule.  

However, these indicator organisms are not even vaguely related to the Clostridium species or any kind of endospores.  You can count fecal coliforms in a BS sample until the cows come home (of course McElmurray's cows aren't coming home because Augusta's BS killed them) and you won't know a thing about how many C. difficile endospores are in the BS.  So, C. difficile gets a free ride as far as Part 503.  John Walker, Alan Rubin and the other EPA BS-promoters who concocted the Part 503 rules were apparently ignorant of or could have cared less about these deadly bacteria or their endospores. 

What happens after the BS is not tested for these little endospore devils?  The BS is transported to the farmers' fields in a semi-solid form, which means it still has a high water content.  The BS is slung out of a spreader machine and then it dries.  Once it dries the hydraulic adhesive forces between spores and the organic matrix disappear.  Now the spores are free to be picked up by the wind and distributed all over the county -- or at least to those parts of the county that are downwind of the sludged fields.   Do you remember the pods that were jettisoned when Darth Vader's death star was under attack?  That's exactly what's happening with the endospores being blown away from the sludged fields.  They escape certain death to live another day.   When they find themselves in a nice anaerobic environment with plenty of nutrients, and perfect pH, and a perfect temperature, like a some neighbor's intestine, they pop open and begin growing. Like I say, they are microscopic cluster-bombs waiting to go off. 

These endospores have evolved over hundreds of thousands of years to lie patiently dormant in an unfavorable environment until they are picked up by mammals, reptiles, or birds and incorporated into their gastrointestinal tracts.  Wikipedia  says humans are mammals, and I believe it, mostly, although the ones promoting BS are more like reptiles.  And being mammals, humans are targets for Clostridium difficile.  Humans inhale the wind that carries these endospores off of sludged fields.  Humans eat vegetables whose surfaces are covered with wind-borne endospores.  Small, cute humans wipe their hands across the exposed surfaces of playground gear upon which endospores have settled and transfer the endospores to their mouths.  Once inside humans' digestive tracts, the spores find the ideal conditions to revert to their bacterial state.  Bingo!  You have now effectively transported C. difficile from the toilets of Mount Sinai Hospital in Manhattan to Mrs. Brewster's first grade class in Campbell County, Virginia, and everybody else downwind from Synagro's sludged fields.  

But these infections will not be evident because the C. difficile infection is asymptomatic, which, if you remember, is where I started this essay.  Mrs. Brewster's kids who ingest the C. difficile endospores by licking their slides and swings, or their parents who eat home-grown tomatoes coated with the spores will not show a single symptom.  C. difficile just blends in with the rest of the normal bacteria that populate the gut -- the so-called normal flora.  For years and years C. difficile can just hang out there and cause no problems.  It's growth is suppressed by the normal flora. . . but it survives. 

Eventually, a fairly moderate proportion of folks with C. difficile in their gut come down with completely unrelated infections -- like my aching tooth.  Many of these infections will be treated with a broad-spectrum antibiotic, probably Clindamycin or a cephalosporin.  "Broad-spectrum" means the antibiotic kills all sorts of germs -- Gram positive, Gram negative, Strep, Staph, E. coli, you name it.  Of course, these antibiotics kill the normal gut flora, too.  But it's the normal gut flora that are holding the C. difficile in check.  So all hell breaks loose because without any competition from the normal bacteria, C. difficile grows and grows, and in the growing it releases a couple of toxins that produce the diarrhea and colitis.   

The clinicians call the diarrhea "antibiotic-associated diarrhea," and it happens a lot, like in about 3 million Americans a year in hospital settings and in 20,000 in outpatient settings.  If the colitis develops into PMC, lesions can penetrate the colon.  Now you have bacteria entering the body cavity through the holes in the colon.  Septicemia it's called.  The end for this septicemic dude -- or kid -- may not be far off.  One study found that of 200 hospital patients treated with clindamycin, 20% developed diarrhea and 10% developed PMC.  These are huge numbers, nationwide.

With respect to C. difficile infections from BS, it's a perfect storm sort of situation; all of the right conditions have to come together simultaneously.  Spores from C. difficile spores are carried in BS from New York city to some farmer's field in Virginia.  They lie dormant on the ground for weeks, or months, or years.  Some of them are picked up by the wind and distributed to the farmer's own children or to neighbors where they enter the gut.  Because  C. difficile can lie dormant in the gut for years after it is acquired from sludge-dust, the effects may not be seen for years after the BS has been applied.  The infected person may long ago have moved away from the place where they contracted the C. difficile.  This is one reason why going around knocking on doors asking if the people who live near sludged fields feel OK, is probably a worthless way to conduct the epidemiological studies.  The fact that someone says "I feel fine."  doesn't mean anything.     

The hypothesis

The hypothesis is pretty obvious given the foregoing facts.  It may be stated as follows:  People exposed to sludge-dust have a greater risk for developing C. difficile infections.

Testing the hypothesis

The best science is done by setting up hypotheses like this one and then doing your best to shoot them down.  You can never be certain a hypothesis is true; the only certainty you ever achieve is when you prove your hypothesis is false.  That's why the emphasis is on the negative -- shooting down your hypothesis.  But if you try and try and you can't disprove the hypothesis, you gain confidence in its validity.

How could we try to disprove this hypothesis?  I can think of at least three ways:

  • First, conduct a retrospective survey of, say, 500 people who live in the vicinity of sludged fields -- call them the test group.  And conduct the same survey with another 500 who have never lived anywhere close to a sludged field -- call them the control group.  Then determine what percentage within those two groups have ever been treated with Clindamycin (or related broad-spectrum antibiotics).  And of those in each group who have been treated with the antibiotic, determine the percentage that have developed antibiotic-induced diarrhea, colitis, or PMC.  

The hypothesis predicts that those people from the test group who have been treated with Clindamycin will have a greater incidence of antibiotic-induced diarrhea and PMC, on a percentage basis.  

[The hypothesis makes no prediction as to whether the test group and the control group will have a similar occurrence of having been treated with Clindamycin.  But if the test group has a higher incidence of Clindamycin treatment, that in itself would be very, very interesting because these drugs are used to treat diseases that have been associated with BS -- Staph a. infections, for instance.]

  • The second way to test the hypothesis is to survey a few hundred cases of antibiotic-induced diarrhea and PMC across the country or across a state and determine statistically whether a disproportionate number of those cases are people who do, or who have, lived in the vicinity of sludged fields -- say in or next to counties that permit land-application of BS.
  • Third, one could examine veterinary records for pets and farm animals.  Humans are not the only mammals susceptible to C. difficile.  Nor are humans the only mammals treated with Clindamycin or who suffer PMC when C. difficile runs rampant after a Clindamycin treatment.  All of these happen in pets and farm animals, too.  Consequently, the hypothesis predicts that veterinarians in sludged counties will see and treat more cases of Clindamycin-induced PMC than veterinarians in counties who never get sludged.  One could review the vets' records and determine where the affected animals are with respect to sludged fields.  Some pretty strong correlations could be made without any complications due to HIPPA and (human) patient confidentiality.  

Of course, these are just skeleton suggestions for testing the hypothesis.  Skilled researchers have all sorts of ways to design such studies to take into account wind direction, proximity to sludged fields, hospitalizations unrelated to BS and other complicating variables.  


Almost always asymptomatic diseases greatly complicate the question of whether BS causes disease because an asymptomatic infection like C. difficile can be acquired from BS and not show up for years, maybe never.  But antibiotic-induced diarrhea and PMC are common examples of an asymptomatic disease that suddenly becomes visible.  Therefore one should be able to track the spreading of C. difficile by BS spreading by tracking the incidence of PMC.  

It is likely that the hypothesis can be tested by examining existing medical records, meteorological records, and records of BS-spreading.  All of the data are probably there; somebody just has to go get them. 


Copyright, 2005 - 2012, Denis O'Brien (aka The Gutter Grunt).  All rights reserved.