Defense Experts Arguments: Part II

Defense Experts Arguments: Part II

In my last installment, I gave an overview of the process plaintiffs endure if they engage the legal system.  It can be difficult, stressful, costly but also can be very rewarding if victorious.  I have seen some settlements exceed $1,000,000 but I have also seen persons clearly damaged by the edifices of others walk away with nothing but legal bills.

In this the second of 3 epistles, I want to discuss a main strategy defense expert witnesses use to attempt to discredit CIRS-injured plaintiffs and the medical experts they use.  My goal is to show people what they are up against when using the legal system.  I will discuss “the negative argument” and how it is inappropriately employed to make CIRS look impossible.

A negative argument is the positive assertion that something does not exist.  The negative argument goes something like this, “CIRS  does not exist.”  Sounds simple, yes?  Think about it for a second.  How much literature is out there disputing CIRS?  How many epidemiologic studies have been published that demonstrate chronic exposure to the interiors of water-damaged buildings (WDB) is not associated with respiratory or multi-system illness?  The answers are: almost zero and almost zero.  The VAST MAJORITY of the literature supports that supposition that inhalation of the toxins, inflammagens and microbes in WDB leads to single (usually respiratory) or multi-system illness. In the literature search that Ming Dooley and I have nearly completed, the number of supporting peer-reviewed published epidemiologic articles outnumbers those which do not support mold causing health problems by over a 25:1 margin!  Those aren’t final numbers but yes, you read that right, for every epidemiologic article that does not show exposure to the interior to WDB is associated with adverse human health effects, you will find more than 25 that do show such effects. Ming presented some initial figures at the Fort Lauderdale Meeting of the Minds conference; we hope to finish this evaluation within the month, create final totals and then publish our findings.

Since there is such a dearth of non-supportive medical literature regarding the ability of mold to cause illness, those who champion that ill-fated cause invented a different ruse.  They just started saying the adverse health effects of mold do not exist.  (At least one stated outright, in writing and more than once, that there is NO supportive medical literature!)  This is the negative argument.  It is difficult to prove a negative argument.  If you cannot prove it, just say, “mold can’t cause illness,” 3 times, click your heels and the world will be a better place.  Before long, you will be back in Kansas, Dorothy.  Oh, right, that was a dream.

There are legitimate ways to prove a negative argument[1], but each method is very difficult.  You must prove not only that something does not exist, but that it CANNOT exist.  There is a saying that, “You cannot prove a negative”.  This is not true, you can prove a negative.  But even a single positive case disproves the negative proof.  Do you know even one person with CIRS?  I guess that negative proof is demolished.

Within science and philosophy, there are several methods of proving negative assertions to be correct.  One method is to shift the burden of proof.  Calledonus probandi, this shifts the burden of proving a thing does not exist to those who say it does exist.  An example would be if I said there was a raspberry in the middle of most couches made in the United States.  The negative argument is that there are not raspberries in U.S. built couches.  Shifting the burden of proof to the positive argument would then require me to show that at least some couches have raspberries in them.  In CIRS, the positive argument has vast amounts of evidence and this method will not work for the negative argument.

Another way to prove a negative is through evidence of absence.  Now, we know “absence of evidence is not evidence of absence”.  However, even more so, the presence of evidence is also not evidence of absence.  In fact, it is evidence of presence.  There is so much published data, as above, supporting the adverse human health effects of exposure to WDB, that the absence of evidence is actually found on the part of those who disagree, namely the expert defense witnesses who state that mold cannot cause multi-system illness.

A third method of proof for a negative argument is called Russell’s teapot.  It is a form of the burden of proof scheme.  The positive assertion is stated as an analogy that there is a teapot in space somewhere between the earth and the sun and that the teapot is too small to be seen by our best telescopes.  Therefore, it cannot be proven that the teapot exists, but also, it cannot be proven that it doesn’t exist.  Again, the burden of proof falls to the one claiming that the teapot exists.  Germ theory was such an argument.  Scientists postulated there were agents in the air which could transmit disease.  This could neither be proven nor disproven by our 5 unaided senses.  Germ theory was eventually proven by the invention of the microscope and experiments designed to show that some discrete but not visible to the naked eye agents were indeed in the air.  As above with the shifting of the burden of proof, this method cannot disprove CIRS.

Still another method to prove a negative is called modus tollens.  This is a logical proof showing something cannot exist.  However, in the world of CIRS, we have documentable exposure and more than plausible pathophysiology explaining subjective symptoms and physical exam findings which are supported by reproducible objective lab abnormalities, NeuroQuant®changes and genomics findings.  In addition, we have reversal (or improvement) of these abnormalities using the Shoemaker Protocol therapies and resumption of abnormalities with re-exposure (similar to Koch’s postulates).  Every one of these items has been peer-reviewed and published in multiple journal articles, except for genomics.  The genomics publications are not far behind.  In the light of this evidence, there can be no logical proof showing CIRS cannot exist.

The final way to prove a negative is a mathematical proof called a proof of impossibility.  In this scheme, observed data is then calculated, or modeled and calculated, to show that a certain step necessary for the existence of the positive argument is not mathematically possible.  If the necessary step is not possible, then the positive argument cannot be possible and the negative assertion is therefore proven. 

This is the approach the infamous ACOEM 2002[2] article takes.  However, for this method to work, the mathematics have to be correct and the assumptions minimized.  As we remember from our high school math classes, if even one step of a mathematical proof is inaccurate the entire result is invalidated.  ACOEM 2002 incorporates at least 12 inaccurate assumptions and the “proof” literally falls apart.

The authors of the ACOEM 2002 paper were 3 professional mold defense expert witnesses (two toxicologists and an immunologist who had never written about mold before). They did not reveal their conflicts of interest.  They created a model to arithmetically prove that it was very unlikely to have sufficient mycotoxin in a room, such as in a home, to cause adverse human health effects beyond respiratory problems. 

Their first incorrect assumption was that adverse human health effects from fungi only occur through allergy, infection and toxicity.  GAO 2008, WHO 2009, POA 2010 and numerous other articles discuss non-IgE (not allergic) immune responses to exposure to the interior of WDB. 

The ACOEM report further hones down and wrongly assumes the effects of the damaging substances found in WDB were limited to mycotoxins.  I call this the toxicological argument.  The science of toxicology has a number of rules which require, amongst other things, a demonstrable linear dose-response curve.  The more toxin, the more response.  However, this assumption ignores the fact that CIRS, as its name implies, is primarily an immunologic illness with probably some toxic action too.  Toxins, inflammagens and microbes are inhaled and all are detected by the innate immune system as foreign.  This triggers an innate immune response in every human being on earth.  Every single toxin, inflammagen and microbe can trigger this response.  Most people handle these exposures well but those with HLA predisposition do not thus leading to innate immune system dysregulation.  Many immune responses are from cascades and hence are geometric, not linear.  The evidence that CIRS is immunological, but not allergic, is found in abnormal HLA, VIP, MSH, TGF-β1, MMP-9 and C4a assays.

The next wrong assumption was that ingestion of mycotoxin was the primary route of intoxication, even though they did not dispute that respiratory symptoms like visible lung inflammation and pulmonary hemorrhages occurred.  The authors then quoted 6 rodent studies (rats, mice and guinea pigs).  Five of these studies used acute installation of mycotoxin.  The authors stated they believed (assumed, without any reference) that “absorption of a toxic dose over a sufficiently short period of time” to effect human health effects was necessary and ignored evaluation of chronic lower dose exposures.  Only one rat study, over 3 weeks with 6 introductions of mycotoxin, simulated the equivalent of 18 months of intermittent human exposure.  The endpoints of most of these studies were usually death and sometimes lung inflammation.  Introduction of mycotoxin in each study was either intranasal or intratracheal.  The authors attempted to model expected exposure in humans using normal respiratory mechanisms from these induced rodent studies.

One example of the ridiculous math went like this.  The LC50 (concentration at which 50% of the animals die) for T-2 toxin of these rodents is known.  No rats die at 1 mg T-2 toxin/m3 when exposed for 10 minutes.  Bait and switch to Satratoxin H toxin concentrations.  No explanation of what Satratoxin H toxin dosing at 1 mg Satratoxin H toxin/m3 concentration can do to rats or human, but then the authors tell us it would take 1010 Stachybotrys spores to make this much Satratoxin H.  Their paragraph is totally meaningless gobbeldygook designed to confuse and obfuscate the truth.

Looking at the single repeated-dose rat study, the authors make another ridiculous calculation.  They start by saying that intranasal installation of high dose Stachybotrys chartarum spores causes lung inflammation and hemorrhage, whereas low dose instillation causes lung inflammation but no hemorrhage.  Spoiler alert - both concentrations cause lung inflammation!  Then they go on to say that it would require 9400; 29,300 and 68,000 spores/m3 to achieve the low-level inflammation, from a toxic effect alone, for infants; children and adults, respectively.  Of course, it could take much less because they do not provide a group where no lung inflammation occurs.  Further, considering biopsy proven lung inflammation is never an endpoint I am looking at, this is a meaningless calculation but it is intended only to impress.  Even further, these numbers are based of an accumulation of 6 bolus doses over 3 weeks.  How does that compare to 8 hours a day, 7 days a week of inhalation?  The numbers required would be considerably smaller, even taking detoxification and lung clearance mechanisms into account.

Another assumption was based in the counting of potential particles that could be harmful.  The authors only counted spores which could be containing mycotoxins as potentially harmful.  Studies have shown between 320[3] and 514[4] fragments of molds, bacteria etc. are in a room for every spore found on spore trap testing.  Every one of those fragments has the potential to trigger the innate immune system into action so these authors’ model underestimated the amounts of harmful particles by at least 320 times.  The authors also admit that toxin can be found on fragments, but the do not include any calculation for that.

Putting all this together, the authors opined that their model demonstrated it would be very difficult to get enough mycotoxin in a room for inhalation to cause serious adverse human health effects.  I guarantee you, this study is cited in every defense expert witness’ report.

In terms of what we fondly refer to as the Scientific Method, the conclusions of the above  article would be called a hypothesis.  That hypothesis would then require testing to demonstrate its accuracy or lack thereof.  That has never occurred.  Their hypothesis, with its 12 faulty assumptions, is held as the standard of truth by defense expert witnesses and attorneys defending insurance companies, landlords and employers too.  This article has been discredited in the medical literature[5], the Wall Street Journal[6] and at least one book[7] written about the current state of science and science for sale.  The ACOEM no longer considers this paper to be its position statement.  Yet the defense still uses it as the gold standard.

I did say 12 faulty assumptions.  Let me innumerate them for you remembering that only one faulty assumption is enough to invalidate the entire result:

  1. Mold can only cause IgE-mediated allergic reactions, infections and toxic reactions
  2. Mycotoxins alone cause damage
  3. Because only mycotoxins cause damage, toxicologically, there must be a demonstrable linear dose response
  4. Since only mycotoxins can cause damage, it is not necessary to include the 320-514 times more particles containing inflammagenic substances such as β-glucans, or other microbes, such as bacteria and Actinomycetes, or their toxins
  5. The rodent studies only used one mycotoxin at a time; WDB have mycotoxins, endotoxins and other potentially toxic substances some combinations of which have been shown to be synergistic
  6. Ingestion is held to be the primary route of damage
  7. Rat, mice and guinea pig studies are comparable to human interactions
  8. Intranasal introduction of mycotoxin into rodents is comparable to introduction through normal human respiration
  9. Intratracheal introduction of mycotoxin into rodents is comparable to introduction through normal human respiration
  10. Intranasal and intratracheal introduction of mycotoxin into rodents is comparable to each other
  11. The endpoint of death or visible inflammatory lung damage in rodents is comparable to what we see in CIRS in humans
  12. One-time, high dose mycotoxin exposure is worse, or even comparable to, chronic low dose exposure in rodents or in humans – the truth is that high dose exposure may activate different pathological channels, i.e., by toxic direct effects, whereas low dose inhalation triggers primarily an immunological response

In 2011, the ACOEM withdrew the 2002 statement and published a similar paper as its position statement.  To get past the uproar of its previous position statement being produced by 3 defense expert witnesses, the ACOEM simply did not indicate who the authors of this new paper were.  That certainly is one way of fixing the transparency and conflict of interest issues!  There were no studies cited after 2004.  This paper ignored the plethora of data published after 2002 revealing immunological dysfunction (and inhalation as the source of damage) as a result of chronic mold exposure including the conclusions of the GAO 2008[8], WHO 2009[9] and POA 2010[10] studies all highlighting non-allergic immune dysfunction and the plausibility of chronic mold exposure causing adverse human health effects beyond respiratory and allergic symptoms.  By December 2014, and after continuous hounding by advocates like Sharon Kramer and Dr. Shoemaker, the ACOEM pulled the 2011 iteration of their mold position statement off their website.  The polite explanation was that it was sunsetted.  The truth is that 23 older position statements were retained when this statement was unceremoniously removed.  The rest of the story is that the article was not current, was poor science (an unproven hypothesis dangled as scientific fact) and did not reflect what the rest of the scientific community had been publishing for close to a decade.  Even so, these articles are still used by the defense.  Why?  Because they have nothing else!

Many of us have seen the Empire State Building.  It obviously exists sans existential musings.  The negative argument is that it does not exist.  How would you try to prove the Empire State Building, a famously photographed and visited structure many people have seen, touched and entered, does not exist?  First, you would state your case.  Of course, there is no evidence that you can produce that proves there is no Empire State Building (because there really is one!)  It is very difficult to prove a negative argument, i.e., that something does not exist.  So, you just say there is no Empire State Building, keep saying there is no Empire State Building and say it all the louder.  Say it to anyone who will listen.  Some people will believe you.  There are some people who do not believe the Holocaust of mass murder of Jewish persons occurred in Europe in the 1940’s despite vast evidence, pictures, eye-witness accounts etc.  Enter a small amount of disinformation and you can make even more people doubt. 

That is the state of where we are at.  The defense experts were able to publish very few opinion pieces and call them science.  A couple of reputable organizations published them as their position statements 17 and 13 years ago.  Both of these organization no longer consider these articles their position statements. However, defense expert witnesses still cling to them to state CIRS cannot exist.  Analogously, they say the Empire State building cannot exist because, mathematically, it is implausible to build a structure that tall out of cooked spaghetti and rubber bands.  But we do not employ such materials.  We use the reinforced steel and concrete of evidence-based medicine and more than 25:1 epidemiological peer-reviewed studies with plausible pathophysiology, explainable symptoms and numerous reproducible objective lab, imaging and genomics tests to forge our building.  The opposition can only speak loudly, sow disinformation and repeat their mantra, “There is no Empire State Building, there is no Empire State Building…”

Some of these professional defense expert witnesses worked heavily for the tobacco industry prior to their work with mold.  Is it coincidence that the emergence of the opinion pieces passed off as mold science started being published around the time Big Tobacco started taking hits?  The biggest was the 46-state lawsuit settled in November 1998 and the first junk-mold paper I am aware of was published in 2000.  I believe the time is coming, and has come, for these people to find a different industry to attack.

In my next article, I will look briefly at some more strategies which defense attorneys use to sway judges and juries against CIRS-injured litigants.


[2] Hardin BD, Kelman BJ, Saxon A. 2002. Adverse human health effects associated with molds in the indoor environment. Prepared for ACOEM, Council on Scientific Affairs.

[3]Górny RLReponen TWilleke KSchmechel DRobine EBoissier MGrinshpun SA. Fungal fragments as indoor air biocontaminants. Appl Environ Microbiol. 2002 Jul;68(7):3522-31.

[4]Cho S et al. (2005). Aerodynamic characteristics and respiratory deposition of fungal fragments. Atmospheric Environment, 39:5454–5465.

[5]Craner J. A critique of the ACOEM statement on mold: undisclosed conflicts of interest in the creation of an "evidence-based" statement. Int J Occup Environ Health. 2008 Oct-Dec;14(4):283-98.

[6]Found at:

[7]McGarity TO, Wagner WE. Bending Science: How Special Interests Corrupt Public Health Research.  Harvard university Press. 2008.  Pages 191-192.

[8] “GAO Report to the Chairman, Committee on Health, Education, Labor and Pensions, U.S. Senate, Indoor Mold” (September 2008). Found at: Retrieved 2010-02.

[9] HO guidelines for indoor air quality: dampness and mould. World Health Organization 2009.

[10] Shoemaker RC, Mark L, McMahon SW, Thrasher JD, Grimes C (2010). “Research Committee Report on Diagnosis and Treatment of Chronic Inflammatory Response Syndrome Caused by Exposure to the Interior Environment of Water-Damaged Buildings”. Found at: Retrieved 2010-08.

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