UNITED STATES DISTRICT COURT 

SOUTHERN DISTRICT OF OHIO 

WESTERN DIVISION 

MELANIE BECKEMEYER, 

Plaintiff, 

v. 

GELCO CORPORATION, etc., 

Defendant. 

][ CASENO. 1:17-cv-00695 

][ 

] [ JUDGE BARRETT 

][ 

][ 

][ AFFIDAVIT OF RONALD E. GOTS, 

] [ M.D., PH.D., DABT 

][ 

][ 

][ 

][ 

I, Ronald E. Gots, M.D., Ph.D., DABT, hereby swear, affmn and state as follows: 

1. I am over 21 years of age and am competent to execute this affidavit.

2. I am a licensed physician and a Board Certified Toxicologist.

3. As a physician and toxicologist, I have specialized m occupational and

environmental medicine and toxicology for over thirty-five years. I have specialized primarily in the 

determination of cause and effect relationships of injuries and illnesses allegedly arising from 

chemical, biological (i.e., mold, bacteria and other agents) and other exposures. I have published 

extensively on the subject of general and specific causation, having written a number of articles and 

book chapters on this topic. The generally-recognized method of causation assessment in toxicology 

has been the topic of lectures I have given to physicians, nurses, medical students, attorneys and 

judges. At Georgetown University School of Medicine, I taught medical students a course on 

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environmental toxicology in which causation methodology was emphasized. That course included a 

section on mold, mold toxins and their health effects. 

4. I have been involved in hundreds of mold contamination and wet, damp building

matters since the late 1980's, including courthouses, schools, other municipal buildings, assisted 

living facilities, hotels, homes and commercial buildings. I have evaluated health effects, prepared 

remediation plans, overseen remediation and functioned to ensure that workers or residents not be 

harmed by any potential exposures. I have reviewed hundreds of scientific papers on mold, mold 

toxins, bacterial endotoxins, as well as other agents associated with wet, damp buildings, and their 

surmised, imputed and/or proven health effects and have written numerous articles on the subject. In 

May 2002, my firm sponsored, along with Georgetown University Medical School, a major 

international symposium devoted to the health effects of mold and mold toxins. My experience 

consulting on indoor air quality issues affecting schools, office buildings, residences and even 

automobiles is extensive. 

5. In the past thirty years, as CEO of the International Center for Toxicology and

Medicine and founder of Building Health Sciences, my associates and I have been involved 

extensively in indoor environmental matters. I have examined hundreds of patients, occupants of 

residential and municipal buildings, as well as schools (both students and teachers) who believed 

that mold in their facilities was making them ill. I have seen the breadth of complaints, some 

minority of which may have been mold-related, most of which were not, but were perceived to be 

so by involved individuals. 

6. I have also visited dozens of buildings-schools, homes, apartment buildings,

assisted living facilities, hotels, courthouses, and other public and commercial buildingsthroughout the United States in which there was water damage, mold growth and concern about 

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possible health effects. Some of these had exuberant mold growth covering many walls; others, 

small spots to no observable mold growth. Thus, I have personally seen all of the extremes of water 

damage and resultant growth of mold. In those investigations, it was often my responsibility to 

assess health risks, make decisions about removing individuals from the environment and, with my 

colleagues, to develop remediation plans. 

7. Consequently, I have an extensive professional background in the science of health

effects from indoor environmental contaminants, the evaluation of individuals who have been in 

such environments and the investigation of facilities which suffered varying degrees of water 

intrusions. This, plus my past and ongoing review of thousands of primary research papers, position 

papers and books dealing with the issues at hand inform my understanding of these matters and my 

ability to analyze them. 

8. I have reviewed thoroughly all of the available records and data in the matter of

Beckemeyer vs. Gelco. 

9. The basis for my opinions in this case includes my education, training in basic

science, experience in toxicology in general and as specifically related to mold spore and mycotoxin 

exposure, review and analysis of published peer reviewed and accepted literature on the effects of 

mycotoxins on a broad range of mammalian species including humans, general knowledge of the 

adverse effects of chemicals on mammalian species including humans, and records reviewed in this 

case. 

10. Mold and mold spores are ubiquitous and the construction and maintenance of a

mold-free environment, be it home or vehicle, is not possible. 

11. Ms. Beckemeyer believes that exposure to mold and associated mycotoxins in a

company car which she drove from June through September 2016 produced a generalized medical 

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disorder which has led to multiple multisystem symptoms. She is supported in this strange belief by 

a pediatrician and self-described "mold" expert named Scott McMahon. 

12. Ms. Beckemeyer has a variety of complaints, symptoms and diagnoses including

respiratory tract symptoms, lightheadedness, vertigo, "brain fog" memory loss, word finding 

difficulties and anxiety. All of these she and Dr. McMahon ascribe to exposure to mold in the 

automobile at issue. However, a careful review of the medical records shows clear alternate 

explanations for these and temporal disconnections-e.g. they preexisted the acquisition of the car or 

postdated the termination of its use. For example, a major complaint was vertigo (dizziness). 

However, the first complaint of dizziness bearing any temporal relationship to the car was in 

October, one month after she turned it in. There is absolutely no mechanism by which such a 

delayed response could occur. Moreover, she had a long preexisting history of this condition with 

major endolymph surgery (inner ear operation) for vertigo in 2004, predating the acquisition of the 

car by 12 years. Many of her symptoms are those associated with anxiety- "brain fog" and sleep 

disturbance for example. She had a prior and ongoing history of anxiety. She also had changes in 

her brain seen on MRI which would explain word finding and other cognitive disorders. Those had 

the appearance of chronic small vessel ischemia seen with ageing and hypertensive disease. She had 

a long history of poorly-controlled hypertension. Also, molds and mold toxins are not known to 

produce any brain abnormalities. Her respiratory tract problems during her car usage were 

diagnosed as ordinary respiratory infections, such as viral sinusitis. Later she was diagnosed as 

having allergic rhinitis, but she had had that for many years, long antedating the car. Moreover, she 

was not allergic to any molds associated with the car. Finally, those symptoms persisted long after 

she no longer had the car-a fact which eliminates an allergic response to the car and indicates 

responses to other sources of allergens. 

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13. When the car was tested for wetness and mold, no abnormality was found. There

was no source of mold growth and levels in the air and the carpet were low and typical of normal 

background levels of mold. Every home and every car have levels like those. 

14. Several of Ms. Beckemeyer's physicians seem to believe that mycotoxins or other

ill-defined "toxins" are responsible for her symptoms. There is no scientific support for this 

conclusion. One of the claimant's experts, Dr. McMahon, believes that various ill-defined agents in 

wet-damp indoor spaces produce some sort of toxicological effect which leads to an immunological 

disorder. He shares that belief with a small cadre of fringe practitioners whose methodology and 

self-described "disease" is not recognized or generally-accepted. They call this disorder chronic 

inflammatory response syndrome (CIRS), a "disease" known only to them, not generally-accepted 

and not recognized by the American Academy of Allergy Asthma and Immunology (AAAI), even 

though Dr. McMahon and likeminded practitioners claim this is an "immunologic disorder." It has 

no international disease (ICD-10) classification, the recognized nomenclature by which the US and 

the rest of the world identify recognized diseases. It is also not recognized by any body of 

toxicologists even though the claim is that mycotoxins are the initiator of this alleged disorder. 

Thus, Dr. McMahon's claim that toxins produce this immune system disease which they have 

personally named CIRS is not accepted by any but their personal adherents. That such a disease 

exists or that mycotoxins cause this is neither generally accepted by the relevant medical and 

scientific communities nor is general medical and scientific knowledge. It is an unreliable diagnosis 

with an inaccurately ascribed causal attribution. 

15. An immutable principle of toxicology is that toxicity depends upon the dose of the

toxic agent which enters the body. Thus, botulinum toxin is lethal in rather small quantities if eaten 

by people, but it is injected safely in millions (as Botox) to treat wrinkled skin. By diluting it a 

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million-fold, Botox is converted from highly toxic to quite safe. The same is true for mycotoxins. 

The calculated doses required for both acute and chronic exposures to result in adverse health 

effects in humans have been studied and written about in peer reviewed articles and are so high that 

it is essentially impossible for exposure in a home, let alone a car, to ever lead to a toxic adverse 

human health effect. The American College of Occupational and Environmental Medicine (2002 

and 2011), the National Academies of Sciences' Institute of Medicine (2004), the American 

Academy of Asthma, Allergy and Immunology (2006) and the World Health Organization (2009) 

all concur that the scientific and medical evidence does not support the contention that mycotoxinrelated disease (mycotoxicosis) occurs via inhalation of these agents in indoor environments. The 

current fact sheet of the us CDC concurs with that assessment: 

http://www.cdc.gov/mold/stachy.htm More specifically and pertinent to this case, none of these 

recognized organizations find any support for the proposition that either mycotoxins or other agents 

associated with damp indoor spaces, can produce either the range of symptoms alleged here or the 

"disease" "CIRS" made up by Dr. Ritchie Shoemaker of Maryland and adopted by his protege , 

Dr. McMahon. 

16. Assuming that the general causation requirements can be met, which is not the

case in the Beckemeyer matter, specific causal elements would need to be evaluated and ruled in 

or out. The causation methodology used to establish specific causation, that is, causation in an 

individual, is widely-accepted in the literature (Gots 1986, Gots 1993, Hackney 1979, Evans 

1976, Irey 1976, Schwartz 1995, Tarcher 1992, Marley 1991, Buffler 1995, Rom 1992, Black 

1990, Black 1993, Sullivan 1992, NRC 1992, Brennan 1987, Guezalian 2005, Weiner et al, 

2012). Other accepted methodologies differ in detail, but not in basic principle. The elements of 

the causation methodology used to establish specific causation include the following: 

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• How was the diagnosis made?

• Does the patient have a recognizable disease?

• Are we dealing with symptoms alone or with objective disorders?

• Have other causes been properly considered and ruled out? Has the exposure been

confirmed?

• Was the dosage sufficient considering the concentration and duration to produce

the condition(s)?

• Was the clinical pattern what one would expect from that causal agent?

• Were the temporal relationship and/or latency periods appropriate?

All of these questions and their answers are highly individual and must be addressed 

symptom (or disorder) by symptom (or disorder). Plaintiffs experts, and even some of her 

treating physicians, have not addressed it in this way. 

17. None of the specific causation requirements 1s met in this case, as the

detailed review above demonstrates. In fact, all of them are specifically refuted. 

A. How was the diagnosis made? And Does the patient have a 

recognizable disease? 

The primary diagnoses in this case made by standard practitioners were recognized 

respiratory disorders-allergies and infections. Others were major anxiety disorders. The 

subsequent diagnoses, and the subject of this claim, CIRS, is not a recognized disease, but the 

creation of non-traditional practitioners and neither scientifically-known nor generally-accepted. 

B. Are we dealing with symptoms alone or with objective disorders?

For some of Ms. Beckemeyer's symptom complaints, specific clinical findings are 

apparent in the records. These exclusively involve the respiratory tract. She allegedly has certain 

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laboratory abnormalities, according to several of her non-mainstream practitioners. Those will be 

discussed later. 

C. Have other causes been properly considered and ruled out? Has the

exposure been confirmed?

There was no exposure to high levels of mold or mycotoxins in this car. All mold levels 

were low and/or typical of everyday background levels. There was also no wetness established. 

Thus, no exposure has been confirmed. 

Other causes of her symptoms and findings have been identified including allergies, 

infections, major anxiety and depressive disorders. She is also clearly persistently anxious which 

explains many of her symptoms. 

D. Was the dosage sufficient considering the concentration and duration

to produce the condition(s)?

As a board-certified toxicologist, I can unequivocally state that there were no 

toxicological agents in this car capable of producing acute or chronic illnesses. 

E. Was the clinical pattern what one would expect from that causal

agent?

Ms. Beckemeyer's clinical pattern of symptoms, objective findings and response to 

treatment supported the allergic and infectious conditions diagnosed by her standard 

practitioners. This pattern is not consistent with the car having been the cause. 

That some mold-related or other unspecified "toxin" related to the car was causal of this 

claimant's made-up "condition," CIRS, is completely unsupportable. This condition has no 

specific clinical pattern, no objective findings or standard clinical testing; it has a variable array 

of wide-ranging, subjective symptoms which can occur in virtually any organ system in a pattern 

defined solely by the patient herself. 

F. Were the temporal relationship and/or latency periods appropriate?

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The timing of symptoms and the location of their occurrences also speaks clearly 

against the car as responsible. While Ms. Beckemeyer later claimed that she was sick from the 

moment she got the car, contemporaneous medical records do not support that. She had acute 

infectious respiratory conditions for short periods during her three months with the car. She also 

had allergic symptoms which were ascribed to non-car associated exposures. She later, after 

disposing of the car, developed most of her symptoms which persisted and, in some instances, 

intensified. Thus, there is a clear temporal disconnect between the car and her primary 

complaints. 

Very importantly, she had longstanding prior sinus and respiratory disorders as well 

as major anxiety disorders. Responsible for many of her symptoms, these long predated the 

acquisition of the car. 

The bottom line of this causation analysis is that there is clear evidence against 

specific causation. The car played no role, except a perceived one, in Ms. Beckemeyer' s illnesses 

or symptoms. 

18. The claimant's expert, Dr. McMahon, is relying upon several "evidentiary"

approaches to support his causal allegation. All are wrong and defy accepted medical and 

toxicological reasoning and are therefore no reliable. 

A. The first is the general causation belief which I have discussed above. That is, that

mycotoxins or other factors coming from indoor environmental air are capable of leading 

to the manifestations alleged and the strange self-named, unrecognized diseases CIRS. 

That is untrue, has never been shown scientifically and is not generally-accepted. The US 

CDC in its current online report agrees (http://www.cdc.gov/mold/stachy), as do all of the 

other consensus groups mentioned above. 

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B. The second is that the exposure and consequent dose of such toxins allegedly

received by Ms. Beckemeyer of mycotoxins or anything else was sufficient to cause the 

complaints. To "establish" this, the supporting practitioner is relying on several lines of 

self-developed and self-serving "evidence." The first is the unproven and likely untrue 

assertion that "toxins" were present and in sufficient quantities to exert effects. The 

second, is that those toxins came from the air of the car interior. 

C. The third is that the complained of disorders are consistent with toxicity

associated with indoor environments. 

C. Finally, the fourth is that various odd laboratory tests which he orders, supports

his diagnosis and his causal attribution. 

19. All of Dr. McMahon's "evidentiary" approaches as to causation are fallacious,

unreliable and misleading. 

20. The presence of toxin-producing molds and of mycotoxins or any other ''toxic

substance" in the car at issue has not been shown. There were no measurements performed 

during Plaintiffs period of use, and, the time period between Plaintiffs last reported use on 

September 23, 2016 and the testing performed by Plaintiffs industrial hygienist on July 9, 2018, 

the car had two subsequent owners. Furthermore, the total mold levels found in the car in July 

2018 were not unusually high or indicative of significant water intrusion and active mold growth. 

They were common everyday exposure levels. Even if the mold spores found were full of 

mycotoxins, thousands of times more than the largest amount found would have to have entered 

the body to produce toxicity. As recent studies have shown, airborne mold or mold toxins do not 

contribute to internal levels of mold toxins. Those come from dietary sources (Follman et al, 

2016, Jezak et al, 2016). Nor can it be presumed that those low levels found in 2018 were 

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sufficiently high at one point in the past and then became low due the passage of time; such logic 

is not accepted methodology for determining exposure levels. In essence, the ability of a 

substance to cause a toxic effect cannot be inferred in the absence of information on the dose or 

to how much of the environmental agent an individual is exposed. 

21. If Ms. Beckemeyer were exposed to a mycotoxin, as she and some of her experts

seem to believe, and even if they were to enter the body, they are rapidly eliminated. Any 

mycotoxins theoretically entering her body arising from the car would have been essentially 

gone by December 2016. However, everyone has levels of mycotoxins in their bodies, arising 

from dietary sources. 

22. Like all other foreign substances, such as medications and most other toxins,

mycotoxins are broken down and eliminated by the body. Mycotoxins are metabolized in the 

liver and excreted by the kidney in short order. Numerous scientific studies have examined the 

time that it takes for mycotoxins to be eliminated. In toxicology and pharmacology, this rate of 

elimination is generally called "half-life." This is the time that is required for one half of the 

absorbed dose to be eliminated. For the most part, the half-lives of studied mycotoxins occur in 

minutes to a few hours. Thus, they do not persist for weeks, months or years after exposure cease 

and, as a result, are not, capable of producing increasing or persistent symptoms or causing new 

symptoms to arise. 

23. Dr. McMahon and a couple of Ms. Beckemeyer's treating physicians are basically

followers of a Maryland physician, Ritchie Shoemaker, who popularized, among a fringe 

medical group, the diagnoses and testing which they follow. The fact is that these individuals 

belong to a small cadre of alternative practitioners who have promoted false notions about indoor 

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environments and all manners of adverse health consequences associated with them. Their 

beliefs and practices are neither generally-accepted nor scientifically-known. 

24. Dr. Shoemaker's practices came under fire by the Maryland Board of Medical

Examiners in 2013, when he was reprimanded and put on probation for failing to meet proper 

standards of care. At that point, he discontinued his clinical practice. However, he now purports 

to provide special certification to physicians who follow his diagnostic and therapeutic methods. 

Dr. McMahon, an expert in this case, and a pediatrician by training, touts his mold certification 

by Shoemaker as his primary credential in this arena. He adds to that the assertion that he has 

treated thousands of such patients, solidifying his self-proclaimed expertise and diminishing that 

of anyone who does not have such clinical experience. Medical history tells us that even large 

numbers of diagnostic and treatment experiences do not necessarily imply knowledge or 

wisdom. No doubt the colonial physician who bled George Washington would also have 

trumpeted his experience with thousands of such treatments. 

25. Since approximately 2008, Dr. Shoemaker has called his novel disorder Chronic

Inflammatory Response Syndrome (CIRS), a condition which is neither generally accepted nor 

known to exist. Ms. Beckemeyer, and Dr. McMahon use that term or a variation ofit, SIRS. Dr. 

Shoemaker and his followers further claim that this disorder results from exposure to a variety of 

"biotoxins" associated with wet/damp indoor spaces. This theory is self-generated, unproven, 

based on poor causation and scientific methodologies, and resides in questionable data. It is not 

generally-accepted. 

26. Dr. Shoemaker originally called the condition Sick Building Syndrome (SBS) and

Chronic Biotoxin-Associated Illness, before he renamed it "Chronic Inflammatory Response 

Syndrome." Initially, he attributed this entity to a mycotoxin cause. In 2002, he consistently 

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attributed symptoms to "toxin-forming species of fungi" and their mycotoxins. In his book Mold 

Warriors (2005), Dr. Shoemaker wrote similarly about the cause of illness in the cases he 

discussed. He highlighted water damage and mold growth and that certain molds make toxins, 

"our studies show repeatedly: mold makes people sick." (p. 332-333). He has subsequently 

disavowed the role of mycotoxins, believing instead that, "exposure to mycotoxins 1s a 

'relatively insignificant factor in the systemic inflammatory response these people get'." (See 

Deposition testimony in Anderson et al vs. The Ritz Carlton Hotel Co. et al., DC Superior Court 

Civil Div. CA No. 05ca (0001130). Now mycotoxins have returned as the alleged culprit as I 

will note shortly. 

27. Certain of the diagnostic tests performed on Ms. Beckemeyer, such as VCS,

MSH, TGF, and C4a, even the so-called HLA-genotype allegedly associated with environmental 

exposure leading to symptoms and a dozen others are neither scientifically-known nor accepted 

as showing what they are claimed to demonstrate. They are not described in the recognized and 

accepted medical and scientific literature for this purpose. Many of these tests have little clinical 

application at all, but are unique to certain specialized research laboratories, or to either specific 

other disease states or to other illnesses. These tests taken together are not delineated in 

textbooks or published as part of evidence-based clinical guidelines used by the general medical 

community. They are the sole province of this fringe medical group who call themselves 

"environmental physicians," or, now, "certified mold physicians." 

28. In assessing whether a physician or scientist used reliable scientific methodology

to reach his conclusions, it also is important to examine the known or potential rate of error of a 

theory. For example, if a scientist placed various qualifications on his conclusions, then the 

known rate of error is potentially very high. The rate of error cannot even be assessed for a 

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theory that has not been tested. Dr. Shoemaker's and Dr. McMahon's theories remain in the 

unreplicated, unreliable category. Their alleged scientific methodology in reaching their 

conclusions about this "CIRS" condition have, therefore, not been confirmed by others or 

accepted. 

29. Another important factor in assessing the scientific reliability of a theory is

whether the theory has gained widespread acceptance among scientists in that field. General 

acceptance indicates that other scientists agree that a theory is based upon reliable scientific 

methodology, has been replicated and has scientific validity. If, over time, a scientist's opinion 

has gained little or no support within the relevant field of science and/or medicine, it is 

appropriate to question whether the opinion is supported by reliable scientific methodology. The 

term CIRS as a disease entity has been used by Dr. Shoemaker since at least 2008. Dr. McMahon 

says that the condition was first described in 1997 (McMahon 2017). Since it is, according to 

them, a widespread immunological disorder (Dr. McMahon now claims 7% of people have 

CIRS), one would think that if it were proven, by now it would be widely-accepted. It is not. It 

is not recognized, for example, by the American Association of Allergy Asthma and 

Immunology, the major organization of immunologists in this country. It also has no ICD-10 

number, that is, no number in the International Classification of Diseases, version 10. Dr. 

McMahon dismisses this, suggesting that such numbers are only for "insurance purposes." 

Actually, the disease classification numbers are established by the World Health Organization to 

provide uniform nomenclature for study purposes, so that physicians and scientists worldwide 

are speaking about the same entity when they do studies. There is no ICD-10 number for CIRS. 

There is no national or international acceptance of this disease. 

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30. Dr. McMahon, an expert in this matter, claims proudly to be a disciple of Dr.

Ritchie Shoemaker. He diagnoses the Shoemaker disease, now named Chronic Inflammatory 

Response Syndrome (CIRS), which he believes arises from indoor exposures and attacks every 

organ in the body. He diagnoses this disease through a set of thirty or more disconnected 

symptoms and a bizarre array of laboratory tests only performed in this combination by Dr. 

Shoemaker's zealous followers. This disorder of Dr. Shoemaker's is trumpeted in papers that he 

has written, most published in obscure, non-mainstream journals or conference proceedings. At 

this point, approximately eight of his papers have been in the literature for at least ten or more 

years yet his revolutionary revelation has never found its way into mainstream, peer-reviewed, 

medical or scientific journals. 

31. It has also never made it into any of the most authoritative consensus documents,

such as the World Health Organization (WHO) and the Institute of Medicine, National Academy 

of Sciences (IOM/NAS) publications on wet damp indoor spaces. Although many of Dr. 

Shoemaker's papers were available by the time the WHO document was published, there are no 

references within it to Shoemaker or to this "CIRS disease." Dr. McMahon cites extensively 

from the WHO document and from another, the Government Accountability Office (GAO) 

document of 2008, which he claims supports him and Dr. Shoemaker. However, neither 

document mentions any of Dr. Shoemaker's "groundbreaking research," cites any of his papers, 

or contains any discussion whatsoever of this disease "CIRS." Dr. McMahon's notions, 

methodologies and diagnosis are neither generally-accepted, nor scientific knowledge, nor 

reliable. 

32. Nowhere in the GAO report which Dr. McMahon cites does it say that we now

know of an inflammatory disease described by Dr. Ritchie Shoemaker known as "CIRS" or 

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"biotoxin illness" or "mold illness" or any other, which produces widespread injury because of a 

chronically over-reactive innate immune system. In fact, that 61-page document which Dr. 

McMahon relies upon extensively contains not one mention of CIRS, of him or of Dr. 

Shoemaker 

33. Dr. McMahon claims that this disease, so-called "CIRS," is an immunological

disorder. As noted earlier, it is not recognized by mainstream immunologists or the many 

thousand members of the American Academy of Allergy Asthma and Immunology (AAAAI), 

the official AMA recognized body of immunologists. Furthermore, one wonders why, if this 

disorder is an immune system disease, Dr. McMahon doesn't refer Ms. Beckemeyer to an 

immunologist. He, after all, is a pediatrician. 

34. A key to Dr. McMahon's diagnosis of this CIRS is laboratory testing for a variety

of parameters which he claims, when taken together, establish the diagnosis. To optimize the socalled "abnormals," he creates his own normal values which, in some instances, differ from those 

of the laboratories. When Dr. Shoemaker was challenged years ago about his "normal" value for 

MSH which differed from the laboratory's norm or reference range, he asserted that the low end 

of their reference range was "skewed by all of his patients' abnormally low values.". Dr. 

McMahon has done exactly the same thing in his Beckemeyer report. The fact is that both major 

commercial laboratories, Quest and LabCorp have an MSH reference range [range of normal 

values] that start at zero and, in the case of LabCorp, range from 0-40 and, in the case of Quest, 

range from 0-100. LabCorp is the lab Dr. McMahon used. He insists that the norm should be 

greater than 3 5; thus, he asserts, Ms. Beckemeyer was abnormal at 5. In other words, he made up 

his own normal to fit his own case definition. According to both these laboratories, her MSH was 

normal. 

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He did the same thing for the ADH determination which he says was abnormal at Ms 

Beckemeyer' s level of 1. The laboratory which performed the test, LabCorp, reports its normal 

as 0-4.7. Dr. McMahon says the normal range is 1.3-8 making Ms. Beckemeyer abnormally low, 

according to him, but normal according to the testing laboratory. 

Thus, at least two of these key tests that he relies upon were, according to him, abnormal. 

His assertion is contradicted by the reference standards of the laboratory which performed those 

tests and found them normal. 

35. In order to avoid evaluation and criticism of his CIRS disorder by toxicologists,

Dr. McMahon claims, in his report, that it is not a toxicological disease, but an immunological 

one. However, in a paper which he wrote in 2017 and references in this report, he says: "In all 

patients (sic, CIRS patients) environmental exposures to biologically-produced toxins trigger 

innate immune cytokine overproduction ... " In other words, he says in this paper, as he and Dr. 

Shoemaker have said many times, that their claimed "immune system disease" is the result of a 

toxic exposure. 

36. In an attempt to enhance the respectability and acceptance of his "disease"

"CIRS," Dr. McMahon claims that there exist 100,000 references on Systemic Inflammatory 

Response Syndrome. That disorder (SIRS) is indeed coded in the ICD-9 and ICD-10, as he notes. 

However, SIRS has nothing to do with his CIRS. SIRS is a code reserved for severe multiorgansystem disease and is used predominantly in patients in ICUs or trauma centers. 

37. Dr. McMahon quotes the "Policyholders of America's Research Committee

Report on Diagnosis and Treatment of Chronic Inflammatory Response Syndrome caused by 

exposure to the interior environment of water-damaged buildings (2010)," as the most 

comprehensive paper on biotoxin-related illness to date. He claims that it shows that the world's 

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academic community recognizes this disease. It does nothing of the kind. It is a manifesto 

written by Drs. McMahon and Shoemaker, espousing the same positions promulgated in his 

report regarding Ms. Beckemeyer. The site "Policyholders of America" is devoted to "mold 

sufferers" and their supportive physicians. There is nothing academic about it. 

38. For all of the above reasons, Dr. McMahon's opinion in this case is far outside the

mainstream of medicine. It is not generally-accepted and is scientifically unreliable. 

39. Additional and more detailed opinions in this matter can be found in my complete

report dated December 1, 2018, attached hereto and incorporated herein as Exhibit 1. 

40. My curriculum vitae is attached hereto as Exhibit 2.

41. All of the foregoing opinions are held to a reasonable degree of scientific certainty.

This and my report are based on the materials reviewed and analyzed by me to date. Should 

additional information become available, I reserve the right to amend my opinions accordingly. 

FURTHER AFFIANT SA YETH N 

RONALD E. GOTS, M.D., Ph.D., DABT 

SUBSCRIBED AND SWORN TO before this, the i ( day of April, 2019.

,,, .. .,,,, LINDA FERR-ELL . 

fw� State of Florida-Notary Public 

�: •= Commission # GG 270064 

�,% �1' My commission Expires ,,,1,;;;;f,\�,,, October 22, 2022 

NOTARY PUBLIC 

18 

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INTERNATIONAL CENTER 

FOR TOXICOLOGY AND MEDICINE 

93 SW Palm Cove Drive Palm City, Florida 34990-4318 301-466-9858

CURRICULUM VITAE

Ronald E. Gots, MD, PhD, DABT 

Board Certified in Toxicology

Toxicology and Environmental Medicine 

International Center for Toxicology and Medicine 

93 SW Palm Cove Drive 

Palm City, FL 34990-4318 

E-mail: regots@ictm.com

Citizenship: USA 

EDUCATION:

1961 - 1964 A.B. (Chemistry) 

University of Pennsylvania 

Philadelphia, Pennsylvania 

1964 - 1968 M.D.

University of Pennsylvania

School of Medicine

Philadelphia, Pennsylvania

1968 - 1969 Internship (Surgery) 

Johns Hopkins University Hospital 

Baltimore, Maryland 

1969 - 1970 Fellow (General Surgery) 

Harbor UCLA Medical Center 

Torrance, California 

1970 - 1973 Ph.D. (Pharmacology) 

University of Southern California 

School of Medicine 

Los Angeles, California 

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PROFESSIONAL EXPERIENCE:

2002 - Present Chief Executive Officer 

International Center for Toxicology and Medicine 

2003 - 2009 Chief Scientist 

Building Health Sciences, Inc. 

1997 - 2002 Principal 

International Center for Toxicology and Medicine 

1975 - 2009 Medical Director and President 

National Medical Advisory Service 

1995 - 9/96 Medical Director 

Environmental Sensitivities Research Institute (ESRI) 

1984 - 1990 Chairman and Chief Executive Officer 

Medical Claims Review Services 

3/78 - 6/82 Vice President 

Emergency Medical Services, Inc. 

6/77 - 6/82 Vice President 

Quality Care Management Consultants 

10/78 - 1981 Coordinator, Pharmaceutical Class Labeling Project, Food and 

Drug Administration 

1/75 - 9/79 Medical Director and Examining Physician 

Occupational Health Units, Bureau of Economic Analysis, 

Census Bureau and Immigration and Naturalization Service, 

Washington, D.C. 

7/75 - 12/75 Emergency and House Physician 

Northern Virginia Doctor's Hospital 

5/75 - 10/75 Medical Officer, Occupational and Emergency Medicine, NASA 

1973 - 1975 Senior Investigator/Chief, Department of Gastroenterology, 

Walter Reed Army Institute of Research, Washington, D.C. 

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6/73 - 8/73 Emergency Physician 

Prince George's County Hospital 

1970 - 1973 Emergency Medicine Physician 

Westminster Community Hospital 

Orange County, California 

MEDICAL LICENSURE:

Maryland 

Michigan 

Pennsylvania 

Virginia 

CERTIFICATIONS: 

1968 National Board of Medical Examiners 

1987 Board Certified-American Board of Quality Assurance and 

Utilization Review Physicians 

Re-certification- 1993, 1996, 1999, 2001, 2003, 2005, 2007, 

 2009 

1994 - Current Fellow, American College of Forensic Examiners International 

1996 - Current Diplomate, American Board of Forensic Examiners 

2010 Diplomate, American Board of Toxicology 

2015 Diplomate, American Board of Toxicology, Recertification 

PROFESSIONAL SOCIETIES:

Alpha Omega Alpha (Medical Honor Society) 

American Association for the Advancement of Sciences 

American Board of Forensic Examiners 

American Academy of Clinical Toxicology 

American Federation for Clinical Research 

American Medical Association 

American Medical Peer Review Association 

American Public Health Association 

American Society of Law and Medicine 

American Chemical Society 

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American Council on Science and Health 

Fellow, American College of Forensic Examiners 

American College of Occupational and Environmental Medicine 

Fellow, American College of Quality Assurance and Utilization Review Physicians 

International Society of Exposure Analysis 

International Society of Regulatory Toxicology and Pharmacology 

National Association of Environmental Professionals 

New York Academy of Sciences 

Sigma Xi (Scientific Honor Society) 

Society for Health and Human Values 

Society of Toxicology 

Society for Occupational & Environmental Health 

Society for Chemical Hazard Communication 

TEACHING AND SPECIAL APPOINTMENTS

University of Hawaii - Laboratory Instructor and Tutor, Microbial Genetics. 1964. 

Pasteur Institute - Research Fellowship. Paris, France. June 1965 - August 1965. 

University of Southern California School of Medicine, Department of Pharmacology - 

Instructor, Pharmacology. 1970-1973. 

World Health Organization - Temporary Advisor, Workshop on Idiopathic

Environmental Intolerances. Berlin, Germany. 1996. 

American Petroleum Institute - Participant, Workshop on Clinical Studies and 

Particulate Matter. April 31 through May 1997. 

Georgetown University School of Medicine - Lecturer (Environmental Toxicology). 

Department of Pharmacology, Division of Toxicology and Applied Pharmacokinetics. 

1996 - Present. 

Peer Reviewer. Journal of Medical Toxicology. 2004-Present 

Georgetown University School of Graduate Studies. Adjunct Professor (Regulatory 

Toxicology). 2011-Present 

University of Virginia School of Public Health – Lecturer, Department of 

Environmental Science. 2007 

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CIVILIAN AWARDS AND HONORS:

1956 Eagle Scout 

1967 Alpha Omega Alpha (Medical Honor Society) 

1972 Sigma Xi (Scientific Honor Society) 

7/71 - 7/73 Special Postdoctoral Training Fellowship, Funded by National 

Institutes of Health 

 1973 AMA Physician Achievement Award 

MILITARY ASSIGNMENTS:

7/73 - 7/74 Investigator, Department of Gastroenterology, Division of 

Medicine 

Walter Reed Army Institute of Research 

Walter Reed Army Medical Center 

Washington, D.C. 20012 

7/74 - 7/75 Chief, Department of Gastroenterology, Division of Medicine 

Walter Reed Army Institute of Research 

Walter Reed Medical Center 

Washington, D.C. 20012 

Honorable Discharge 

SELECTED APPOINTMENTS:

National Association of Manufacturers, Medical Consultant, Occupational Disease 

Compensation 

FDA Panelist, Patient Package Insert Hearings 

Medical Society of D.C., Member, Workers' Compensation Committee 

U. S. Chamber of Commerce, Member, Workers' Compensation Committee 

International Association of Industrial Accident Board Commissioners, Member, 

Medical Committee 

Board of Scientific and Policy Advisors, American Council on Science and Health 

Chairman, Scientific Advisory Board of NEDA/TIEQ (National Environmental 

Development Association/Total Indoor Environmental Quality) 

Montgomery Medicine, Associate Editor 

American Industrial Hygiene Association, Toxigenic Molds Workshop 

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Hippocrates’ Lantern, Contributing Editor 

U.S. Congressional Working Group Mold Legislation (2002) 

Atlantic Legal Foundation - Scientific Advisory Board 

Peer Review, Journal of Clinical Toxicology 

SELECTED SPEAKING ENGAGEMENTS AND VISITING PROFESSORSHIPS:

1975 Guest Faculty Member, American College of Physicians. 

1980 Invited Speaker, Bendectin Hearings. FDA. 

1978 - 1980 Developer and Presenter, Hospital Risk Management Seminars. St. 

Paul Insurance Company. 

1980 Speaker, Annual Meeting. American College of Obstetrics and 

Gynecology. 

1982 Guest Faculty Speaker. American College of Physicians. 

1983 Speaker, Annual Meeting. National Legal Center for the Public 

Interest. 

2/85 Visiting Lecturer, Causation and Financial Compensation for Claims 

of Personal Injury from Toxic Chemical Exposure. International 

Conference, The Institute for Health Policy Analysis, Georgetown 

University and the Georgetown School of Law. 

1985 Visiting Professor, Legal Medicine. Uniformed University of the 

Health Sciences. 

7/86 Moderator, Medical Section. National Symposium on Workers' 

Compensation, 10th Annual Meeting, Orono, Maine 

8/86 Speaker, "Medical Causation Testimony: Misleading Fact Finders." 

Workers' Compensation and Employer's Liability Committee, 

American Bar Association, New York. 

1987 Speaker, Annual Meeting. IAIABC. 

1987 Speaker, Toxic Tort Seminar. American Bar Association, Chicago, 

Illinois. 

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1987 Speaker, Forum Meeting. University of Arkansas for Medical 

Sciences. 

1987 Lecture. Delaware Occupational Medicine Association. 

5/88 Speaker, Toxic and Environmental Tort Litigation Committee. 

American Bar Association, Natural Resource Section. 

6/88 Speaker, "Scientific and Legal Approaches to Proof of Causation in 

Tort Cases." American Chemical Society, Chemistry and the Law 

Division, Toronto, Canada. 

 12/88 Speaker, "Medical Cost Containment: Regulatory and Administrative 

Options for Containing Medical Costs.” Workers Compensation 

Commissioners' Symposium, National Council on Compensation 

Insurance. 

8/89 Visiting Professor, Environmental Law. Vermont Law School. 

11/89 Moderator, "Managed Medical Care." Workers Compensation 

Conference Dialogue for the Nineties. National Association of 

Manufacturers and Alliance of American Insurers, Baltimore, MD. 

12/89 Speaker, "Validity of Various Immuno-Suppression Theories & Risk 

Assessment Criteria in Toxic Tort Cases." Pennsylvania Bar Institute 

Toxic Tort Litigation Seminar, Philadelphia, PA. 

12/89 Visiting Lecturer, "State of the Art in the Use of Demonstrative 

Evidence in Proving Causation in a Toxic Tort Trial." Trying Mass 

Toxic Tort Cases: Demonstrations of Trial Techniques by Leading 

Practitioners and Jurists, American Bar Association National 

Institute, San Francisco, CA. 

3/90 Speaker, "Utilization Review." Forum II Workers' Compensation 

Healthcare Cost Containment. International Workers' Compensation 

Foundation, Inc., New Orleans, LA. 

4/90 Speaker and Panelist, Workers’ Compensation Panel "Blueprint for 

Reform." 1990 Issues Symposium and Annual Meeting. National 

Council of Compensation Insurance, New York, NY. 

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5/90 Speaker, "Assessing Chemical Hazards: Separating Scientific 

Toxicology from Regulatory Toxicology and Workers' Perceptions." 

American Industrial Hygiene Conference, Orlando, FL. 

10/90 Speaker, "Chemical Hazards and Perceptions and the Role of the 

Industrial Hygienist." Industrial Hygiene Conference. American 

Industrial Hygiene Association, Ocean City, MD. 

11/90 Visiting Lecturer, "Causation: Scientific Standards of Proof." 1990 

Toxic Torts for Trial Judges. The National Judicial College, Reno, 

Nevada. 

1/91 Speaker, "Perception of Chemical Assessment." PESA Health and 

Safety Conference. Public Employees Safety Association of 

Maryland, Baltimore, MD. 

1/91 Visiting Lecturer, "Toxins and Health: Science Versus Perception." 

The Johns Hopkins University Applied Physics Laboratory 

Colloquium. Johns Hopkins University, Laurel, MD. 

7/91 Speaker, "National Occupational Medicine Seminar." Eleventh 

Annual Conference. Cape Cod, Hyannis, MA. 

1/92 Speaker, "Dose Makes the Poison." Northern Virginia Association of 

Occupational Health Nurses Inc., Vienna, VA. 

3/92 Speaker, "Dioxin, Risk Assessment for Human Health." Talladega 

Medical Society, Talladega, AL. 

5/92 Speaker, Interdisciplinary Panel Participant, "The Physician's Role in 

Indoor Air Complaints." National Coalition on Indoor Air Quality, 

Tampa, FL. 

5/92 Speaker, "Determining Whether a Toxic Exposure Caused an 

Illness." American College of Occupational and Environmental 

Medicine. Post Graduate Seminar. Washington, D.C. 

11/92 Conference Chair. "Multiple Chemical Sensitivities. The State of 

The Science." Co-sponsors - NMAS and the International Society of 

Regulatory Toxicology and Pharmacology. 

3/93 Speaker, "Multiple Chemical Sensitivities. The State of The 

Science." RISE. Washington, D.C. 

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4/93 Presenter, Chemical Labeling. Executive Enterprises. Washington, 

D.C.

4/93 Lecturer, "Disability Assessment in Occupational Disease." 

American College of Occupational and Environmental Medicine 

Annual Meeting. Atlanta, GA. 

5/93 Speaker, "Multiple Chemical Sensitivities: The State of The Science." 

CSMA Mid-year meeting. Chicago, IL. 

5/93 Speaker, "Multiple Chemical Sensitivities: The State of The Science." 

CTFA. Washington, D.C. 

5/93 Speaker, "Risk Communication." American Industrial Hygiene 

Association. Annual Meeting. New Orleans, LA. 

2/94 Speaker, "Relating Physical Complaints to Indoor Air Pollution.” 

Occupational Safety & Health Regulation. Conference. Washington, 

D.C.

3/94 Speaker, "Health Effects and IAQ: An Overview.” Indoor 

Environment '94. Annual Meeting. Washington, D.C. 

6/94 Speaker, "The Policy of Risk Versus Individual Risk: Key to Effective 

Risk Communication." 19th Annual Conference & Exposition. 

National Association of Environmental Professionals. New Orleans, 

Louisiana. 

9/94 Lecturer, "Risk Communication.” US Army Center for Health 

Promotion and Preventive Medicine. Aberdeen Proving Ground, 

Maryland. 

9/94 Speaker, "Public Versus Personal Risk: The Challenge In 

Environmental Risk Communication." Dixy Lee Ray Memorial 

Symposium on Science-Based Environmental Management. Temple 

University, Environmental Health and Safety. Seattle, Washington. 

9/94 Moderator, "Faculty and Audience Discussion Regarding MCS,” and 

Speaker, "Conference Summary.” First Annual Aspen 

Environmental Medicine Conference. Aspen, Colorado. 

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10/94 Speaker, "Indoor Air and Health." 4th Annual Virginia Occupational 

Health Conference. Virginia Occupational Medical Association. 

Norfolk, Virginia. 

10/94 Lecturer, "Public Versus Personal Risk: The Challenge in 

Environmental Risk Communication.” Environmental Health 

Program, Department of Public Health Sciences, University of 

Alberta, University of Calgary, Canada. 

10/94 Speaker, "Low Level Chemical Exposures: What Do We Know? 

What Can We Say?" American Industrial Hygiene Association. 

Professional Development Conference. Annapolis, Maryland. 

3/95 Speaker, "Toxic Tort Litigation from Environmental Exposure." 1995 

Oregon Governor's Occupational Safety & Health Conference, 

Portland, Oregon. 

4/95 Speaker, "Cost Effective Management of Medical/Scientific Aspects 

of Toxic Tort Claims." American Corporate Counsel Association 

Greater New York Chapter. New York, New York. 

5/95 Speaker, "Perceptions: Addressing the Divergence Between Science 

and Communication." USF&G - Industrial Hygienist, Kansas City, 

Missouri. 

6/95 Speaker, "Effects of Lead Poison - What It Shows and Doesn't 

Show." Chartered Property Casualty Underwriters Society, 

Baltimore, Maryland. 

7/95 Speaker, "Multiple Chemical Sensitivities." "Sick Buildings." 

National Workers' Compensation and Occupational Medicine 

Seminar, Hyannis, Massachusetts. 

9/95 Lecturer, "Legislative and Regulatory Activity, Regarding Multiple 

Chemical Sensitivities." 2nd Aspen Environmental Medicine 

Conference, Given Institute. Aspen, Colorado. 

9/95 Visiting Lecturer, "Quantitative Risk Assessment and Tort Claims: 

What the Attorney Must Know." Indiana Continuing Legal Education 

Forum Seminar on Toxic Tort Litigation. Indianapolis, Indiana. 

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10/95 Speaker, "Environmentally Associated Symptoms (EAS): A New & 

More Appropriate Name for MCS." Chemical Specialties 

Manufacturers Association, Annapolis, Maryland. 

10/95 Conference Chair. "Multiple Chemical Sensitivities: State-of-theScience Symposium." Co-sponsors - The International Society of 

Regulatory Toxicology and Pharmacology, The Johns Hopkins 

University/NIOSH Educational Resource Center in Occupational 

Safety & Health and National Medical Advisory Service. 

11/95 Speaker, MCS: Facts and Fantasy." 52nd Annual Science 

Conference. The Cosmetic, Toiletry, and Fragrance Association. 

Lake Buena Vista, Florida. 

12/95 Lecturer, "Public Versus Personal Risk." Department of Design and 

Environmental Analysis, Cornell University, Ithaca, New York. 

12/95 Speaker, "The Scientific Aspects and Application of Daubert Motions 

in Toxic Tort Claims." The Metropolitan Corporate Counsel. New 

York, New York. 

3/96 Speaker, “Public vs. Private Risks.” A&WMA’s Waste Combustion in 

Boilers & Industrial Furnaces Conference, Kansas City, Missouri. 

6/96 Speaker, “Application of a New Assessment Tool to Environmental 

Risk Communication: Merging Health Information with Psychosocial 

Approaches.” National Association of Environmental Professionals, 

Houston, Texas. 

7/96 Speaker, “Multiple Chemical Sensitivity: an Overview of Current 

Scientific and Medical Knowledge.” ASTM 1996 Johnson 

Conference, Johnson, Vermont. 

8/96 Speaker, “Chemical Sensitivities/Environmental Intolerance: 

Evaluation, Causation and The Impact of Causation Theories on 

Treatment Strategies.” Allergy & Asthma Associates, Santa Fe, New 

Mexico. 

9/96 State of the Art Speaker, “Illusions of Pseudoscience and Silicone 

Breast Implants.” Aspen Environmental Medicine Conference, 

Aspen, Colorado. 

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9/96 Speaker, “Multiple Chemical Sensitivities/Idiopathic Environmental 

Intolerances.” AIHA Chesapeake Section, Annapolis, Maryland. 

9/96 Speaker, “Idiopathic Environmental Intolerances - Scientific 

Understanding and Regulatory/Legislative Status.” The Soap and 

Detergent Association, Chicago, IL. 

10/96 Speaker, “History, Medical Diagnoses and Causation Determination.” 

Environmental Sensitivities Research Institute Educational Seminar 

for Attorneys and Administrators, San Francisco, California. 

10/96 Speaker, “MCS-Real or Not?” Annual Association of Structural Pest 

Control Regulatory Officials, Santa Fe, New Mexico. 

11/96 Speaker, “Proliferation of Health Allegations MCS, Allergies, 

Porphyria.” The Carpet and Rug Institute Annual Conference, 

Dalton, Georgia. 

1/97 Keynote Speaker, “Pesticide Health Risks: Scientific Truths & Public 

Perception.” 1997 Delta Production Conference and AG Expo, 

Cleveland, Mississippi. 

4/97 Speaker, “Controlled Exposure of Humans to Particulate Matter.” 

1997 American Petroleum Institute Meeting, Alexandria, VA. 

5/97 Speaker, “Medical Issues” Lead Liability Litigation Seminar. Law 

Journal Seminars - Press. New York, NY. 

6/97 Panelist, “Dialogue” on “Recent Advances in Control of Air Pollution.” 

WorldNet Television, Voice of America Studio Washington, D.C. 

10/97 Speaker, “Chemical Sensitivity.” Leadership Texas, Program of the 

Foundation for Women’s Resources. Houston, TX. 

11/97 Speaker, “Multiple Chemical Sensitivity.” Montgomery County Public 

Schools. 

3/98 Speaker, “Understanding Chemical Sensitivity in the Population.” NE 

Regional Turfgrass Conference. Providence, Rhode Island. 

3/98 Panelist, “Do Mycotoxins Cause Health Effects in Indoor 

Environments?” AIHA Toxigenic Molds Workshop. Fairfax, VA. 

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6/98 Speaker, “How To Cross Examine a Scientist.” DRI. San Antonio, 

TX. 

9/98 Speaker, “New Injuries in the Workplace.” International Association 

of Industrial Accident Boards and Commissions. St. Louis, MO. 

10/98 Speaker, “Mold Evaluation and Remediation - How Complex Should 

it Be?” Association of Specialists in Cleaning and Restoration, Water 

Loss Institute’s 3rd Annual Conference & Exposition. Charlotte, NC. 

11/98 Speaker, American College of Toxicology Annual Meeting. “Multiple 

Chemical Sensitivities: Distinguishing Between Psychogenic and 

Toxicodynamic.” Orlando, FL. 

2/99 Speaker, Mealey's Daubert and Expert Admissibility Conference. 

“The Migration of Toxins to Surrounding Areas or People.” 

Jacksonville, FL. 

9/99 Speaker, 3rd Annual Mid-Atlantic Regional Conference on 

Occupational Medicine. “Multiple Chemical Sensitivity.” Philadelphia, 

PA.

9/99 Speaker, Annual Alumni Homecoming CME Seminar, Marshall 

University. “Environmental Risk Communication: The Critical Role of 

the Clinician.” Huntington, West Virginia. 

1/01 Speaker, 2nd National Sanitation Foundation (NSF) International 

Conference on Indoor Air Health. “Indoor Air and Health: Emphasize 

Health; Minimize Engineering.” Miami Beach, Florida. 

3/01 Speaker, 40th Annual Meeting of the Society for Toxicology. “Odors 

in the Workplace: Minimizing Physical Illness; Not Satisfying 

Everyone.” San Francisco, California. 

4/01 Speaker, St. Paul Insurance Group. “Indoor Air Quality: Learning 

from the Unexpected.” Baltimore, Maryland. 

4/01 Speaker, International Society of Facilities Executives (ISFE). 

“Investigating Health Complaints in the Workplace.” Kiawah Island, 

South Carolina. 

10/01 Speaker, Property Loss Research Bureau (PLRB) Mold Symposium. 

“The Science of Mold and Health.” Charlotte, NC. 

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4/02 Speaker, DRI Mold Seminar. “The Science of Mold and Health.” 

Coronado, CA. 

5/02 Speaker, Property Loss Research Bureau (PLRB) Mold Symposium. 

“The Science of Mold and Health.” San Antonio, TX. 

5/02 Speaker, American Forest and Paper Association (AFPA). “The 

Science of Mold and Health.” Washington, D.C. 

5/02 Speaker, American Agricultural Insurance Company (AAIH). “Health 

Risks Associated with Mold Claims.” Denver, CO. 

6/02 Speaker, Mealey’s Toxic Tort Conference. “Medical and Science of 

Causation Assessment.” Pasadena, CA. 

6/02 Speaker, Riverstone Resources. “Mold and Health/Managing the 

Process.” Manchester, NH. 

9/02 Speaker, Lorman Education Services Conference “Health-based 

Mold Management.” Baltimore, MD. 

11/02 Speaker, Armstrong World Meeting. “The Mold Crisis and Its Effects 

on Armstrong World Industries.” Lancaster, PA. 

12/02 Speaker, Mealey’s Texas Mold Litigation Conference. “Mold Science 

Versus Mold Hype.” Dallas, TX. 

01/03 Speaker, Mold and Indoor Environment Conference. “Mold 

Medicine/Mold Hype.” New Jersey Institute of Technology. Newark, 

NJ.

02/03 Speaker, Mealey’s California Mold Litigation Conference. “Mold 

Science Versus Mold Hype: Confusing Diagnosis with Causation in 

Mold Matters.” La Jolla, CA. 

02/03 Speaker, Minnesota Association of Realtors. “Mold Medicine/Mold 

Hype and Its Impact on Realtors.” St. Paul, MN. 

03/03 Speaker, American Conference Institute. Fifth National Forum. 

“Toxic Mold Litigation.” New York, NY. 

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05/03 Speaker, St. Louis Mold Conference. “Mold Medicine & Mold 

Science: Its Practical Applications for Patient Care, Remediation & 

Claims.” St. Louis, Missouri. 

05/03 Speaker, Peckar and Abranson and New York Construction News 

Seminar. 

“Mold, Fact Versus Fiction.” New York, N.Y. 

06/03 Speaker, “Mealey’s Mold Litigation Conference.” Amelia Island, 

Florida. 

09/03 Speaker, Advances in Environmental Mold Issues in West Virginia.” 

Charleston, West Virginia. 

09/03 Speaker, Toxic Tort Litigation Conference. “Mealey’s Practical Skill 

Series.” Philadelphia, PA. 

10/03 Speaker, Fall Meeting of ABA Seer. “Mold and Daubert Session.” 

Washington, D.C. 

10/03 Speaker, 2003 Annual DRI Meeting. “Debunking the Myths of Mold 

and the Application of Effective Defense Strategies.” Washington, 

D.C.

10/03 Speaker, Lorman Education Services. “Advances in Environmental 

Mold Issues.” Lexington, KY. 

11/03 Speaker, AIHA/ASSE. Mold PDC. “A healthcare perspective on the 

effects of mold.” Tyson’s Corner, VA. 

08/04 Speaker, ExecuSummit. Second Annual Mold and Insurance 

Industry ExecuSummit. “Medical Oversight in Water Incursion/Mold 

Management.” New York, NY. 

11/04 Speaker, Twenty Fifth Annual Meeting of the American College of 

Toxicology. “The Great Debate: Indoor Mold - Plague or Nuisance?” 

Palm Springs, CA. 

05/05 Speaker, ACOEM’s American Occupational Health Conference 

(AOHC). “Occupational Medicine: From Clinic to Courtroom.” 

Washington, D.C. 

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02/06 Speaker, Lorman Education Services. “Indoor Air Quality.” 

Telephone Conference. 

06/06 Speaker, Mealey’s Lead Litigation Conference. “The Medical Debate 

over What Levels of Lead Exposure are Safe.” Boston, MA. 

10/06 Speaker, Thirteenth Annual National Forum of Environmental and 

Toxic Tort Issues Conference. “Cost Effective, Provable Science in 

Causation Assessment for Mass Toxic Torts.” Chicago, IL. 

04/07 Speaker, AALNC National Education Conference. “Causation 

Assessment in Toxic Tort Litigation and the Critical Differences 

between Differential Diagnosis and the Assessment of Cause.” 

Austin, TX. 

08/07 Speaker, 10th Annual Force Health Protection Conference. “Public 

Health Risk versus Personal Health Risk: The Key to Health Risk 

Communications” 

Louisville, KY. 

11/07 Speaker, SETAC North America 28th Annual Meeting. “Sound 

Provable Science; The Key to Assessing Public versus Private 

Health Risk and to Developing Helpful and Ethical Health Risk 

Communication.” 

07/09 Speaker, ASTM, “Scientific and Medical Causation.” Burlington, VT 

03/10 Keynote Speaker, Environmental Information Association, 

“Environmental Issues and Health Complaints.” Austin, TX 

04/10 Speaker, 2010 DRI Product Liability Conference. “A brief history of 

tort claims arising from alleged indoor exposures: how the past 

informs the future.” Las Vegas, NV 

 10/11 Speaker, HB Conference. “Lead Toxicity.” Amelia Island, FL 

PROFESSIONAL PUBLICATIONS:

1. Gots, R.E. "Study of a super-repressed mutant of E. coli B." Undergraduate

Medical Association Journal of the University of Pennsylvania. (1966).

2. Dalal, F.R., Gots, R.E. and Gots, J.S. "Mechanism of adenine inhibition in

adenine-sensitive mutants of salmonella typhimurium." J Bacteriol. (1966):

507.

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3. Gots, R.E. "Total parenteral alimentation in newborn puppies." Undergraduate

Medical Association Journal of the University of Pennsylvania. (1968).

4. Wilmore, D.W. and Gots, R.E. "The etiology of uric acid urolithiasis following

ileostomy." Arch Surg 99. (1969): 421.

5. Gots, R.E. and Zuidema, G.D. "Dilation of the intrahepatic biliary ducts in a

patient with choledochal cysts." Am J Surg 119. (1970): 726.

6. Benfield, J.R., Gots, R.E. and Mills, D. "Anomalous single left pulmonary vein

mimicking a parenchymal nodule." Chest 59. (1971): 101.

7. Gots, R.E., Gorin, F.A. and Bessman, S.P. "Kinetic enhancement of bound

hexokinase activity of mitochondrial respiration." Biochem Biophys Res

Commun 49. (1972): 1249.

8. Gots, R.E. and Bessman, S.P. "An ultrasensitive radioassay for hexokinase."

Analyt Biochem. (1973): 272.

9. Bessman, S.P. and Gots, R.E. "The mechanism of insulin action: 

mitochondrial acceptor theory." Intrasci Chem Rep 8. (1971): 7. 

10. Gots, R.E. The Functional Interaction of Mitochondrial Hexokinase with Sites of

Oxidative Phosphorylation. Diss. University of Southern California, 1973.

11. Gots, R.E. and Bessman, S.P. "Mitochondrial hexokinase: inner membrane

location and acceptor function [abstract]." Fed Proc. (1973): 477.

12. Gots, R.E., Formal, S. and Gianella, R.A. "Indomethacin inhibition of

salmonella, shigella, and cholera toxin mediated rabbit ileal fluid [abstract]."

Clin Res 7. (1973).

13. Charney, A.N., Gots, R.E. and Gianella, R.A. "(NA+ -K+) stimulated

adenosinetriphosphatase in isolated intestinal villus tip and crypt cells."

Biochem Biophys Acta 367. (1974): 26.

14. Gots, R.E., Formal, S. and Gianella, R.A. "Indomethacin inhibition of

salmonella typhimurium, shigella flexnari and cholera mediated rabbit ileal

secretion." J Infect Dis 130. (1974): 280.

15. Charney, A.N., Gots, R.E. and Gianella, R.A. "Na-K-ATPase in isolated

intestinal villus tip and crypt cells [abstract]." Gastroenterol. (1974).

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16. Gots, R.E., Formal, S. and Gianella, R.A. "Salmonella mediated ileal secretion:

stimulation of adrenyl cyclase, inhibition by indomethacin and possible

participation of prostaglandins [abstract]." Clin Res. (1974).

17. Charney, A.N., Kinsey, M.D., Meyers, L., Gianella, R.A. and Gots, R.E. "Role of

adrenal steroids on intestinal NA+ -K+ ATPase and sodium transport [abstract]."

Clin Res. (1975).

18. Gots, R.E. "Lawyer's guide to screening medical malpractice cases." The

Retainer. June (1975).

19. Charney, A.N., Kinsey, M.D., Meyers, L., Gianella, R. A. and Gots, R.E. "Na+ -

K+ activated adenosine triphosphatase and intestinal electrolyte transport:

effect of adrenal steroids." J Clin Invest 56. (1975): 653.

20. Gianella, R.A., Gots, R.E., Charney, A.N., Greenough, W.B. and Formal, S.B.

"Pathogenesis of salmonella mediated intestinal fluid secretion: activation of

adenylate cyclase and inhibition by indomethacin." Gastroenterology 69.

(1975): 1238.

21. Bessman, S.P. and Gots, R.E. "The hexokinase acceptor theory of insulin

action -hormonal control of functional compartmenation." Life Sci 19. (1975):

1215.

22. Charney, A.N., Gots, R.E., Formal, S. and Gianella, R.A. "Activation of

adenylate cyclase by shigella dysenterial enterotoxin." Gastroenterology 70.

(1976): 1085.

23. Gots, R. E. "Which of Your Patients is Likely to Sue You?" Medical Economics,

October 18:72, 1976.

24. Gots, R.E. "Don't Panic? It's not malpractice unless..." Medical Economics,

January 24:77, 1977.

25. Gots, R.E. "How Not to Alienate the Medical Expert." Trial, No. 4, April 1977.

26. Gots, R.E. "How Not to Alienate the Medical Expert." Civil Advocates Manual,

G.O. Kornblum and J. W. Rogers, Jr., eds., University of California, (1977): 175.

27. Gots, R.E. "Malpractice. Divide and conquer tactics you should know about."

Medical Economics 25. (1978): 48.

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28. Gots, R.E. "Medical Sleuthing a Must: Evaluating Injury Cases, a

Sophisticated Procedure." The Independent Adjuster, Chicago, IL, Spring

1980.

29. Gots, R.E. "Strategy. The medical causation defense." For the Defense.

January (1981).

30. Gots, R.E. "Medical/scientific decision-making in occupational disease 

compensation." Prepared for the Crum and Forster Insurance Group, 

November (1981). 

31. Gots, R.E. "Hypotheticals and the Expert Medical Witness." Legal Aspects of

Medical Practice 10. (1982).

32. Gots, R.E. and Gots, B.A. "Disarming the Treating Physician: A Cost-Saving

Approach to Medical Claims Defense." Best's Review 83. 64, May (1982).

33. Gots, R.E. "Fad Medical Claims in Personal Injury and Workers' 

Compensation." The Independent Adjuster. (1983): 29. 

34. Gots, R.E. "Science, medicine, and the compensation of toxic injury claims."

Public Policy Forum. National Association of Manufacturers, June (1983).

35. Gots, R.E. "Environmental fears and the treating physician." The Upstate

Physician. (1983): 13.

36. Gots, R.E. "Opinion Testimony of Treating Physicians: Combatting Advocacy;

Forcing Accuracy." For the Defense 26. (1984): 19-24.

37. Gots, R.E. "A response to H.R. 4813." Prepared for the Crum and Forster

Insurance Group, March (1984).

38. Gots, R.E. "Auditing the Physician." Business Insurance. September (1985):

23.

39. Gots, R.E. "Medical causation and expert testimony." Regul Toxicol Pharmacol

6. (1986): 95-102.

40. Gots, R.E. "The science of medical causation: its application in toxic tort

litigation." For the Defense. (1986): 4.

41. Gots, R.E. "Medical causation and expert testimony." Causation and Financial

Compensation: Conference Proceedings, February 20-21, 1985, Washington,

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D.C. Washington, DC: The Institute for Health Policy Analysis, Georgetown

University Medical Center, (1986): 215-23.

42. Gots, R.E. "The science of medical causation: its application in toxic tort

litigation." DRI Toxic Tort Litigation 4. (1986): 18-27.

43. Gots, R.E. "Workers' Compensation: The Last Bastion of the Open Medical

Checkbook." IAIABC Journal. (1987): 35-40.

44. Gots, R.E. "Medical Cost Containment in Workers Compensation: Controlling

Excesses in Tests and Medical Care." National Council on Compensation

Insurance. (1987).

45. Gots, R.E. and Gleeson, J.G. "Understanding and Defending Claims of

Increased Risk of Contracting Disease." DRI Damages and Jury Persuasion 6.

(1987):54-69.

46. Gots, R.E. "Scientific and legal approaches to proof of causation in tort cases."

The 3rd Chemical Congress of North America: The Book of Abstracts.

Washington, D.C.: The American Chemical Society, (1988).

47. Gots, R.E. "Medical Claims Flay Casualty Insurers." National Underwriter, pp.

86-89, September (1989).

48. Gots, R.E. "Workplace Illness: What We Know Versus What is Believed."

Convention Proceedings, IAIABC, September 17-20, 1989, Baltimore, MD.

International Association of Industrial Accident Boards and Commissions.

(1989): 226-240.

49. Gots, R.E. "Immune system dysfunction and toxic tort claims." Toxic Tort

Litigation. Harrisburg, PA: Pennsylvania Bar Institute, (1989): 88-133.

50. Gots, R.E. "Risk assessment in tort litigation." Toxic Tort Litigation. 

Harrisburg, PA: Pennsylvania Bar Institute, (1989): 85-7.

51. Gots, R.E. "Scientific truths versus legal truths in toxic tort litigation." Trying

Mass Toxic Tort Cases: Demonstrations of Trial Techniques by Leading

Practitioners and Jurists, ABA National Institute, Nov. 9-10, 1989, Washington,

DC and Dec. 14-15, 1989, San Francisco, CA. Chicago, IL: ABA Division for

Professional Education, (1989): 187-207.

52. Gots, R.E. "Medical surveillance in hazardous waste claims." Hazardous

Waste and Toxic Torts Law and Strategy 5. (1989): 3-5.

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53. Gots, R. "Managed medical care." Highlights of National Conference on

Workers Compensation, Dialogue for the Nineties, November 8-9, 1989,

Baltimore, MD. Baltimore: National Association of Manufacturers and Alliance

of American Insurers. (1989): 20-3.

54. Gots, R.E. "Applying the brakes to medical casualty costs." Best's Review

90:10, 1990.

55. Gots, R.E. "Assessing chemical hazards: separating scientific toxicology from

regulatory toxicology and workers' perceptions." Abstracts, American Industrial

Hygiene Conference: Industrial Hygiene in the World of Tomorrow. May 13-18,

1990, Orlando, Florida. American Industrial Hygiene Association and American

Conference of Governmental Industrial Hygienists, 1990. p. 20.

56. Gots, R.E. "Medical monitoring following chemical exposures." For The

Defense. November (1990): 22-26.

57. Gots, R.E. "Deciphering the sick building syndrome." Builder and Contractor

39. (1991):38-9.

58. Gots, R.E. "Proving causes of illness in environmental toxicology: `sick

buildings' as an example." Fresenius Environ Bull 1. (1992): 135.

59. Gots, R.E. "Address fears, suppress chaos." Public Risk 6. (1992): 24-7.

60. Gots, R.E. "Hypothesis and practice: autointoxication and MCS." Regulatory

Toxicology and Pharmacology 18. (1993): 2-12.

61. Gots, R.E. and Hamosh, T.D. "MCS: A symposium on the State of the

Science." Regulatory Toxicology and Pharmacology 18. (1993) 61-78.

62. Gots, R.E. "Risk communication: a few observations from a 

physician/toxicologist/ communicator." Hazardous Substances and Public 

Health. (1994): 6-7.

63. Gots, R.E. "Public versus personal risk: the challenge in environmental risk

communication." Technology: Journal of The Franklin Institute 331A. (1994):

59-65.

64. Gots, R.E. "Emphasize health to maximize problem solving." Skylines 20.

(1995): 14-17.

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65. Gots, R.E. "Multiple chemical sensitivities - public policy." Journal of 

Toxicology - Clinical Toxicology 33 (2), 111-113 (1995). 

66. Gots, R.E. “Multiple chemical sensitivities: distinguishing between psychogenic

and toxicodynamic.” Regulatory Toxicology and Pharmacology 24. (1996): S8-

S15.

67. Gots, R.E. “Multiple chemical sensitivities.” Hippocrates’ Lantern 4:3 (1997).

68. Light, E. and Gots, R.E. “Mold revisited a rebuttal” Cleaning & Restoration.

July (1998): 22-32.

69. Gots, R.E. and Lees-Haley, P. “Health complaints in office workers.” 

Hippocrates’ Lantern 5:4 (November 1998). 

70. Gots, R.E. “Evidence-based medicine and the independent medical examiner.”

Hippocrates’ Lantern 6:2 (June 1999).

71. Gots, R.E. “Forensic needs versus patient health in chemical exposure claims.”

[abstract] The Forensic Examiner 9:30(#6) (January/February 2000).

72. Gots, R.E. and Pirages, S.W. “Multiple chemical sensitivities: Psychogenic or

Toxicodynamic origins.” International Journal of Toxicology 18. (1999):393-

400.

73. Lees-Haley, P., Williams, C.W., Gots, R.E., and Pirages, S.W. “The

neuropsychology and toxicology of residential exposure.” Journal of Forensic

Neuropsychology 1:4 (1999): 21-43.

74. Robbins, C.A., Swenson, L.J., Nealley, M.L., Gots, R.E., and Kelman, B.J..

“The health effects of mycotoxins in indoor air: A critical review.” Applied

Occupational and Environmental Hygiene 15:10 (2000): 773-784.

75. Gots, R.E. and Hamilton, D.V. “Multiple chemical sensitivities: An iatrogenically

perpetuated disorder and example of the nocebo effect.” The Scientific Review

of Alternative Medicine. 5:1 (2001): 39-44.

76. Gots, R.E. and Juberg, D.R.. “Management of environmental health concerns

in institutional settings.” Journal of Healthcare Safety, Compliance & Infection

Control. 5:2 (2001): 54-56.

77. Gots, R.E. “Mold and mold toxins: the newest toxic tort.” Journal of 

Controversial Medical Claims. 8:1 (2001):1-8.

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78. Gots, R.E. “Indoor Air and Health: Emphasize Health: Minimize Engineering.”

Proceedings of the Second NSF International Conference on Indoor Air Health.

January 29, 2001: 5-15.

79. Gots, R.E. “Odors in the Workplace: Minimizing Physical Illness: Not Satisfying

Everyone.” The Toxicologist, An Official Journal of the Society of Toxicology

Supplement. 60:1 (2001): 136.

80. Gots, R.E., and S.W. Pirages. “Indoor health problems: a sound process for

resolution.” Facility Management Journal, a publication of the International

Facility Management Association. July/August 2001: 45-48.

81. Gots, R.E. and S.W. Pirages. “Mold as Toxin.” COLUMNS-Mold, March 2002.

82. Gots, R.E. and S.W. Pirages. “Toxic Mold – A Misnomer.” IAQ 

Applications/Spring 2003.

83. Gots, R.E., Layton, N.J. and S.W. Pirages. “Indoor Health: Background Levels

of Fungi.” Am Ind Hyg Assoc J., July/August 2003: 427-38.

84. Gots, R.E. “Differential Diagnosis vs. Causation Assessment: Why They Are

Separate Methodologies and How They Relate to Daubert.” BNA, Inc., Expert

Evidence Report, Analysis and Perspective. 8 November 2004. 4(21): 580-84.

85. Gots, R.E. “From Symptoms to Liability: The Distinct Roles of Differential

Diagnosis and Causation Assessment.” For the Defense. July 2005. 24-30.

86. Weiner, H.M., Gots, R.E., Hein, R.P. “Medical Causation and Expert Testimony:

Allergists at the Intersection of Medicine and Law.” Current Allergy and Asthma

Reports. December 2012.

POPULAR ARTICLES

1. Gots, R.E. "The long life diet." Family Circle 23. (1977): 14.

2. Gots, R.E. and Gots, B.A. "Drugs, coffee, alcohol, infections, and your unborn

baby." Good Housekeeping. January (1978): 68.

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3. Gots, B.A. and Gots, R.E. "Doctor's own consumer guide to surgeons." Self.

September (1979): 72.

4. Gots, R.E. "Bendectine: the new thalidomide?" Genesis. April (1979): 1-2.

BOOKS/BOOK CHAPTERS: 

1. Gots, R.E. The Truth About Medical Malpractice: Patients' Rights, Doctors'

Rights. New York: Stein and Day, 1975.

2. Gots, R.E. and Gots, B.A. Caring for Your Unborn Child. New York: Stein and

Day, 1977.

3. Gots, R.E. and Kaufman, A. The Peoples' Hospital Book. New York: Crown

Publishing Company, 1978.

4. Gots, R.E. "Diseases and the workplace: a framework for scientific clarification

and administrative separation." Perspectives on Healthcare Costs in Workers'

Compensation. A. Taricco and J. Greenwood, eds. LR Publications, 1992.

5. Gots, R.E. "Environmental fears and the treating physician." Rational

Readings on Environmental Concerns. New York: Van Nostrand Reinhold,

1992. pp. 491-3.

6. Gots, R.E. "Scientific truths versus legal truths in toxic tort litigation." Rational

Readings on Environmental Concerns. New York: Van Nostrand Reinhold,

1992. pp.493-500.

7. Gots, R.E. Toxic Risks: Science, Regulation, and Perception. New York:

Lewis Publishing Co., 1993.

8. Gots, R.E. “Applying principles of science to Daubert motions in toxic tort

claims.” 1997 Wiley Expert Witness Update New Developments In Personal

Injury Litigation. 1997 pp. 1-57.

9. Gots, R.E. “Environmental risks and the clinician: informing worried patients.”

Occupational, Industrial, and Environmental Toxicology. 1st ed. Ed. M.I.

Greenberg, R.J. Hamilton, S.D. Phillips. St. Louis: Mosby-Year Book, 1997 pp.

505-15.

10. Barrett, S.J., and Gots, R.E. Chemical Sensitivity: The Truth About 

Environmental Illness. Amherst, NY: Prometheus Books, 1998. 

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11. O’Reilly, J.T., Hagan, P., Gots, R., and Hedge, A. Keeping Buildings Healthy.

New York: John Wiley & Sons, Inc. 1998.

12. Gots, R.E. and Pirages, S.W. “Applying principles of science to Daubert

motions in toxic tort claims.” 2000 Aspen Expert Witness Update: New

Developments in Personal Injury Litigation. 2000. pp.1-88.

13. Gots, R.E. “Risk Communication.” in Occupational, Industrial, and

Environmental Toxicology. Editor, Michael I. Greenberg, MD, MPH. 2003

Philadelphia: Mosby, Inc.

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INTERNATIONAL CENTER 

FOR TOXICOLOGY AND MEDICINE 

93 SW Palm Cove Drive Palm City, Florida 34990-4318 Telephone 301-466-9858 

EXPERT REPORT OF RONALD E. GOTS, MD, PhD, DABT 

RE: Melanie Beckemeyer v Gelco Corporation d/b/a Element Fleet Management

INTRODUCTION 

My name is Ronald E. Gots, MD, Ph.D., DABT. I am a licensed physician and Board 

Certified Toxicologist. As a physician and toxicologist, I have specialized in occupational 

and environmental medicine and toxicology for over thirty-five years. I have specialized 

primarily in the determination of cause and effect relationships of injuries and illnesses 

allegedly arising from chemical, biological (i.e., mold, bacteria and other agents) and 

other exposures. I have published extensively on the subject of general and specific 

causation, having written a number of articles and book chapters on this topic. The 

generally-recognized method of causation assessment in toxicology has been the topic 

of lectures I have given to physicians, nurses, medical students, attorneys and judges. At 

Georgetown University School of Medicine, I taught medical students a course on 

environmental toxicology in which causation methodology was emphasized. That course 

included a section on mold, mold toxins and their health effects. 

I have been involved in hundreds of mold contamination and wet, damp building matters 

since the late 1980's, including courthouses, schools, other municipal buildings, assisted 

living facilities, hotels, homes and commercial buildings. I have evaluated health effects, 

prepared remediation plans, overseen remediation and functioned to insure that workers 

or residents not be harmed by any potential exposures. I have reviewed hundreds of 

scientific papers on mold, mold toxins, bacterial endotoxins, as well as other agents 

associated with wet, damp buildings, and their surmised, imputed and/or proven health 

effects and have written numerous articles on the subject. In May 2002, my firm 

sponsored, along with Georgetown University Medical School, a major international 

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symposium devoted to the health effects of mold and mold toxins. My experience 

consulting on indoor air quality issues affecting schools, office buildings and residences 

is extensive. I have overseen mold remediation activities in these structures. I have 

alsowritten about indoor health and cause/effect relationships for a diverse range of 

environmental pollutants. 

In the past thirty years, as CEO of the International Center for Toxicology and Medicine 

and founder of Building Health Sciences, my associates and I have been involved 

extensively in indoor environmental matters. I have examined over two hundred 

patients, occupants of residential and municipal buildings, as well as schools (both 

students and teachers) who believed that mold in their facilities was making them ill. I 

have seen the breadth of complaints, some minority of which may have been moldrelated, most of which were not, but were perceived to be so by involved individuals. 

I have also visited dozens of buildings—schools, homes, apartment buildings, assisted 

living facilities, hotels, courthouses, and other public and commercial buildings—

throughout the United States in which there was water damage, mold growth and 

concern about possible health effects. Some of these had exuberant mold growth 

covering many walls; others, small spots to no observable mold growth. Thus, I have 

personally seen all of the extremes of water damage and resultant growth of mold. In 

those investigations, it was often my responsibility to assess health risks, make decisions 

about removing individuals from the environment and, with my colleagues, to develop 

remediation plans. 

Consequently, I have an extensive professional background in the science of health 

effects from indoor environmental contaminants, the evaluation of individuals who have 

been in such environments and the investigation of facilities which suffered varying 

degrees of water intrusions. This, plus my past and ongoing review of thousands of 

primary research papers, position papers and books dealing with the issues at hand 

inform my understanding of these matters and my ability to analyze them. 

Attached is a true and correct copy of my Curriculum Vitae which details my experience, 

training and education with regard to toxicology, the science of causation analysis, to 

mold and other agents associated with wet, damp spaces, and their effect upon human 

health. (Appendix A) 

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In preparing this report, I have reviewed the following materials concerning Ms. 

Beckemeyer: 

MATERIALS REVIEWED 

Medical Records 

Masood Ahmad, MD (3/1/2001-12/27/2016) 

H.S. Blatman, MD (5/22/2017) 

Craig P. Cleveland, MD (9/22/2016-5/16/2017) 

Paul S. Hogya, MD (5/8/2017) 

Gary Huber, DO (5/22/2017-5/28/2018) 

Kroger Little Clinic (10/21/2013-10/28/2017) 

Suzanne Matunis, MD, Blue Ash Family Medicine (6/1/2011-9/25/2018) 

Medical University of Cincinnati (1/1/2016-8/1/2017) 

Harold Pretorius, MD (3/11-8/29/2017) 

Liberty Urgent Care (12/17/2012) 

Richard E. Sexton, PhD (5/5-5/18/2017) 

Quest Diagnostics (3/1/2017) 

Workers’ Compensation First Report of Injury (10/21/2016) 

Legal Documents 

Complaint (10/18/2017) 

Technical Data 

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Ecostratum Report (1/9/2018) 

Gelco Record Production 

Depositions 

Melanie Beckemeyer (9/27/2018) 

BACKGROUND OF THE CLAIM 

Melanie Beckemeyer believes that mold in a company car injured her. Ms. Beckemeyer, 

a pharmacist, was working for Avantir Pharmaceutical when, on June 20, 2016, she first 

drove her company-provided vehicle. She later claimed that she noted a bad smell and, 

within thirty minutes of driving the vehicle, became dizzy and lightheaded. Subsequently, 

she also complained of sinus and ear congestion, a non-productive cough, nasal 

discharge, a sore throat and intermittent shortness of breath. Nearly one month after 

exposure to the car ended, she reported developing “brain fog.” She ascribed these 

symptoms to mold in the car. However, the medical records show that the symptoms are 

temporally disconnected from the car: she had them before, less during, and more after 

giving up the car. They also have clear alternate causal explanations: infections and 

allergies primarily. Moreover, there was no mold growth identified in the car. 

The last day she drove the car was September 23, 2016. The last day she worked was 

October 20, 2016. 

Ms. Beckemeyer states in her Complaint that she is now “disabled from employment and 

suffers from severe cognitive impairment and other maladies.” She reports constant 

symptoms of dizziness, nausea, lightheadedness, confusion and brain fog. 

MEDICAL HISTORY 

Between June 15, 2011 and September 18, 2015, Ms. Beckemeyer was followed and 

treated at Blue Ash Family Medicine by her PCP, Dr. Suzanne Matunis, for panic 

disorder, major depression, single episode and stress-related hypertension. She 

reported being tearful all the time, unable to concentrate, trouble falling/staying asleep, 

unwilling to get up in the morning, anhedonia, racing heart, panic attacks with chest 

tightness and shortness of breath. In the past, she had had situational anxiety, but 

denied depression as severe as she was having at this time. Tearful and distraught, she 

was jumping from thought-to-thought, but denied being suicidal. Her blood pressure was 

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elevated, something she had experienced in the past with stress. She attributed her 

symptoms to work stress. She preferred taking leave and working with a therapist to 

taking medication. She later admitted that, while work stress was contributory to her 

symptoms, she had significant anxiety related to her mother’s and her dog’s illnesses. 

Medication successfully controlled her blood pressure, but she developed palpitations 

when she had to deal with work. By June 27, 2011, she felt anxious frequently, had 

decreased energy and problems with future planning, functioning and concentrating due 

to stress. She remained off work because of continued anxiety, poor focus and stress 

from contact with HR. Therapy was begun in mid-July 2011, but difficulty focusing and 

concentrating continued. She felt she could not return to work and be productive. By 

early August, she was still experiencing occasional panic attacks, had low energy, very 

poor concentration and focus. Minimal stress caused her to cry and feel anxious. She 

remained off work. She was self-administering health food supplements which she 

thought were helping. 

 By September 8, 2011 Ms. Beckemeyer’s leave of absence was up: her employer 

indicated she had to return to work or she could be terminated. She claimed she was 

having panic attacks nearly daily and was unable to return to work. Her panic attacks 

worsened when she thought about returning to her previous work environment. Celexa, 

an anti-depressant also used to treat anxiety, was begun September 8, 2011. 

In mid-September, she began another form of therapy: EMDR [eye movement 

desensitization and reprocessing]. As of September 26, 2011, she had a new job offer 

for the end of October. Despite feeling anxious with occasional heart racing, she was 

having no full-blown panic attacks. Celexa was continued through September 2015. Ms. 

Beckemeyer did not return for anxiety/depression or any other complaints after this visit 

for fifteen months. 

Ms. Beckemeyer’s medical records available to me begin with an allergist’s appointment 

in 2001. She was 43 years old and reported she had had allergies for at least ten years. 

Her symptoms, most prominent in summer and fall, included sneezing, nasal congestion 

and discharge, itchy/teary eyes, mouth-breathing/snores, sinus infections, irritability, 

hoarseness and headache. She had a past history of surgery on her turbinates, a 

septoplasty [nasal surgery], as well as surgery on the balance mechanism of her inner 

left ear. Examination revealed boggy, swollen nasal mucosa and enlarged (3+-4+) 

turbinates:all evidence of allergies. She was treated with allergy medication: pills, nasal 

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spray and allergy shots (immunotherapy). She continued throughout the available 

records to use nasal allergy spray. 

Allergy testing in 2004, by her allergist Dr. Ahmad, included only intradermal testing, not 

prick/puncture testing. She had 2+ [intradermal] reactions to cat, dog and mold mix 2 

(Phoma, Fusarium, Mucor, Pullularia, Rhizopus). On both visits, Ms. Beckemeyer 

reported having a pet dog. She had a slight reaction to mold mix 1 (Alternaria, Asp. 

niger, Helminthsporium, Pen. Notatum). Subsequently, she had allergy shots, after which 

her allergy symptoms improved. 

Sore throat, nasal congestion, dry cough, chest tightness and mild laryngitis were 

diagnosed in August 2011, as bronchitis, by Dr. Matunis. An antibiotic was prescribed. 

In April 2012, Ms. Beckemeyer, 53 years old, complained to Dr. Ahmad of sinus pressure 

and pain, as well as fatigue. Her eyes were red, the nasal mucosa was boggy, her 

turbinates were 4+ enlarged and there was nasal discharge evident. She had sinus 

tenderness and a red throat. Acute sinusitis was diagnosed and treated with antibiotics 

and steroids. 

Dr. Ahmad saw her again in December 2012. She complained of chest congestion, post 

nasal discharge and a stuffy [congested] nose. He noted her past history of allergic 

rhinitis, allergy shots, recurrent sinus infections, runny nose, nasal congestion and sinus 

pressure. She was taking Cromolyn and Nasonex for her upper respiratory allergies, as 

well as Metformin for diabetes. Her nose had yellow discharge and there was drainage in 

the back of her throat (PND). She gave a history of asthma. Dr. Ahmad prescribed an 

antibiotic and Proventil inhaler. Allergic conjunctivitis and acute pharyngitis [sore throat] 

were diagnosed. 

Five days later she was seen in Urgent Care complaining of constant, moderately-severe 

central chest congestion, with a feeling of pressure and a mildly-productive cough. Chest 

X-ray was normal. Acute bronchitis was diagnosed and treated with antibiotics,

Prednisone and a cough suppressant.

After an absence of fifteen months, Ms. Beckemeyer, on December 18, 2012, returned to 

see Dr. Matunis, complaining that she had been returning from a trip when someone on 

the plane was coughing. Four days later, she had developed a cough, chest and sinus 

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congestion, sore throat and malaise. She had seen her allergist, had taken two courses 

of antibiotic, but was still ill. Bronchitis was diagnosed and a new antibiotic prescribed. 

One year later, in December 2013, Dr. Matunis performed a yearly physical on Ms. 

Beckemeyer. The latter reported that she had had elevated blood pressure a few weeks 

earlier and started taking an old prescription given her for hypertension related to stress. 

She noted her pulse was in the “upper 80s,” when stressed. The examination was 

normal. Dr. Matunis wrote a new prescription for an anti-hypertensive, as well as for 

Celexa, an anti-depressant/anxiolytic. 

At the University of Cincinnati Medical Center, Ms. Beckemeyer, now 56 years old, was 

seen for follow up of left ear reconstructive surgery in June 2014. She had age-related, 

bilateral sensory-neural hearing loss. Gait, posture and positional function were normal. 

However, in September 2015, she complained that she was “woozy” and had vertigo 

following neck manipulation. She was treated with Valium and a steroid dose pack. 

On December 15, 2014, Dr. Matunis again saw the claimant for a yearly physical. She 

was stressed by her mother’s illness [myelodysplasia} and was looking for a new job. 

She had stopped taking blood pressure medication because her elevated pressure had 

“resolved.”Her past medical history was noted to include polycystic ovaries and 

Meniere’s disease, a condition associated with vertigo and imbalance. Examination was 

normal; Dr. Matunis again prescribed Celexa and Nasonex. 

Two weeks of ear pressure, left more than right, nausea, ear-fullness and popping, 

feeling off-balance and “swimmy,” along with nasal congestion caused Ms. Beckemeyer 

to see Dr. Matunis on September 18, 2015. She had a past history of left eustachian 

tube reconstructive surgery. Examination revealed no ear findings, but there was boggy 

mucosa in the nose with mucoid discharge. A Medrol [steroid] dose pack, Nasacort and 

Celexa were prescribed. Ms. Beckemeyer requested a letter since her employer required 

her to take a pre-arranged shuttle from the airport which made her nauseated. 

After undergoing neck manipulation for TMJ symptoms, Ms. Beckemeyer developed 

nausea and vertigo, a severe type of dizziness. She consulted her physician at the 

University of Cincinnati. She was advised to discontinue using Flonase and begin 

Nasonex. Celexa was continued. 

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Ms. Beckemeyer returned to Dr. Matunis in January 2016, for left hip pain after slipping 

on ice. Ibuprofen and a Medrol Dosepak were prescribed for lumbar tenderness and 

spasm. She continued seeing her physician for this problem through mid-September 

2016. 

Avanits Pharmaceuticals hired the claimant on April 25, 2016. She first drove a 

company-provided car on June 20, 2016. On June 28, 2016, Ms. Beckemeyer was seen 

at Kroger Little Clinic for sinus and ear congestion, headache, non-productive cough, 

chest tightness, nasal discharge and a sore throat for three days. These symptoms were 

the same ones she repeatedly reported to Dr. Ahmad as typical of her past history in 

2001 and 2012. Later, in the context of this claim, she claimed that she had noted a bad 

smell and, within thirty minutes of driving the company vehicle (June 20), she became 

dizzy and lightheaded. That is not the history she related to the medical provider on June 

28. In this contemporaneous record, there was no mention of becoming symptomatic

when she first got the car or of noticing any odor in the car.

She acknowledged, on this June 28 visit, that she had sick contacts at home (in other 

words, a source of infection). She gave a history of seasonal allergies, multiple ear 

surgeries and post nasal drip (PND). Examination revealed clear fluid behind her 

eardrums, mucoid nasal discharge, inflamed mucosa, swollen nasal turbinates and 

maxillary [sinus] tenderness. Her throat was normal; her lungs were clear. Viral sinusitis 

was diagnosed. Sudafed and Prednisone were prescribed. Thus, symptoms she later 

ascribed to the car were, eight days after she got it, diagnosed as a viral sinus infection 

which was clearly the correct diagnosis. There is not a hint of evidence or reason to 

believe from this record that exposure to mold in the car (even if there were mold in the 

car) played any contributory role. 

Dr. Matunis saw Ms. Beckemeyer September 13, 2016, for an upper respiratory infection 

that had been present for three-to-four days. Once again, this was a new-onset event, 

three months into her use of the car. There was no mention of the car or of ongoing 

symptoms. Her nasal mucosa was boggy, with a mucoid discharge. The physician 

diagnosed acute nasopharyngitis and prescribed an antibiotic to be taken if, after ten 

days, the symptoms had not improved or had worsened. Once again, Ms. Beckemeyer 

had another infection, having nothing whatsoever to do with the car. She later ascribed 

the symptoms of that infection to her perception that contamination in her car was 

responsible. 

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Nine days later, September 22, 2016, Ms. Beckemeyer appeared at the office of Dr. 

Ahmad, her allergist. She complained of symptoms similar to those she had described in 

June, at the Kroger Little Clinic and in mid-September to Dr. Matunis: nasal congestion, 

intermittent headache, some throat clearing with excessive post nasal drip (PND), severe 

sore throat. He diagnosed perennial allergic conjunctivitis and allergic rhinitis due to 

pollen. She did not tell the allergist that she was seen nine days earlier and diagnosed 

with an upper respiratory infection. Nor did she report that she was given an antibiotic 

which she did not take. She told him that all of these symptoms began after exposure to 

mold, not that she had several infections which had nothing to do with mold; or, that 

neither mold related or water damage, nor the putative leak causing it was found when 

her car was evaluated by Performance Toyota. 

All of these symptoms, she now said, had begun after being exposed to a car with mold. 

However, she acknowledged a long history of perennial allergy symptoms, of variable 

frequency during each month. She also said that she had symptoms at home, at work, 

at other people’s homes and outdoors, as well as in her car. Other symptom triggers 

included upper respiratory infection, weather changes and dusting. She denied having 

had allergy testing (she actually did in 2004) and noted she had pet dog(s). She later 

tested positive to dog on allergy testing. Her few physical findings were similar to her 

previous visits in June and September: puffy eyes, boggy, swollen, irritated nasal 

mucosa; her throat was normal. Qnasl, a steroid spray for allergies was prescribed, as 

was a saline nasal spray. Dr. Ahmad diagnosed allergic rhinitis due to pollen, perennial 

allergic conjunctivitis; he noted symptoms of nasal congestion, post nasal drip, dizziness 

and effects of change in ambient water pressure on ears. 

Ms. Beckemeyer later told Dr. Matunis that the last day she drove the car was 

September 23, 2016. She said that her allergist, Dr. Ahmad, had told her that it “was very 

difficult to get rid of [mold] and no chemical way to kill it.” He allegedly told her not to 

drive the car. 

On October 13, 2016, Ms. Beckemeyer was seen at the University of Cincinnati. She 

reported having had “excessive mold exposure” over the summer from a car leak which 

had caused her to develop respiratory issues. She had gotten rid of the car two weeks 

earlier; she was feeling better, but her symptoms were not gone. She had a history of 

Meniere’s disease, for which she had had a left endolymph shunt and a tube that had 

been in her ear for more than twenty years. That disorder produces, among other things, 

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dizziness. Since 2004, she admitted having some motion sensitivity which, she claimed, 

had been “exacerbated by this mold exposure.” She denied ear pressure, despite having 

reported ear congestion and ear pressure in June and September 2016, respectively. 

She was taking Qnasl for some PND and “persistent facial pressure,” a brand new 

complaint. Her past history included immunotherapy, after which her allergy symptoms 

had abated. Due to fly in a few days for her job, Ms. Beckemeyer was concerned about 

doing so until her symptoms improved; the physician concurred. 

Dr. Ahmad saw her the following day, October 14. She was complaining of nasal 

congestion, sneezing, some dizziness/lightheadedness, some ear pressure (denied, just 

the day before) and a frontal, mid-facial headache. She denied confusion, paresthesias, 

dysarthria or gait instability, cough, shortness of breath, wheezing, anxiety or depression. 

Physical findings on examination included red, puffy eyes, circles, as well as boggy, 

swollen, irritated nasal mucosa. Sinuses, throat, ear, voice, tonsils and chest were all 

normal. Zyrtec, an allergy pill and Singulair were prescribed. Dr. Ahmad noted nasal 

congestion, PND, moderate persistent asthma, food allergy and dizziness. This was now 

several weeks after she had stopped driving the car. This makes it quite clear that 

ongoing allergic symptomatology was related to factors having nothing to do with the car. 

If one is exposed to an allergen source, then eliminating that exposure ends the allergic 

response. The fact that the allergic symptomatology did not abate after the car was gone 

means the car was not responsible. 

When Dr. Matunis saw Ms. Beckemeyer on October 18, 2016, the history provided was 

that the car she had been provided for work had had mold which caused nasal 

congestion, ear pressure, balance problems, brain fog (a new complaint), mild headache 

and facial congestion. She believed she wasn’t getting better. The only physical findings 

were boggy nasal mucosa with a mucoid discharge. Dr. Matunis, based on the 

information given her, diagnosed allergic rhinitis due to mold. A steroid dose pack was 

prescribed. These symptoms, it is worth noting, were similar to ones reported throughout 

her medical records, beginning before she ever drove the company car in 2016, and 

associated with her general allergy symptoms, sinusitis and upper respiratory infections. 

Ms. Beckemeyer stopped working on October 20, 2016. A First Report of Injury to Ohio’s 

Bureau of Workers’ Compensation listed the diagnosis of Allergic Vestibulitis due to 

repeated mold exposure in company vehicle. The basis for this claimed diagnosis is not 

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clear. It was not listed as a diagnosis by any physician in any of the medical records 

available for this review. 

When she returned to Dr. Ahmad on October 24, Ms. Beckemeyer now complained of, 

“lots of dizziness symptoms, some sinus pressure, nasal congestion, left ear full, lots of 

post nasal drainage.” Her physical findings were similar to previous examinations: puffy 

eyes, boggy, swollen, irritated nasal mucosa. She had new symptoms of tenderness to 

palpitation of moderate degree over the right frontal and of significant degree over the 

left frontal sinuses. Singulair tablet and saline nasal spray were prescribed. Xyzol was 

discontinued. Once again, this was a month after the car was gone. Clearly, these 

allergic symptoms and manifestations were related to other sources of allergens, not to 

the car. 

The same day, she was seen by Dr. Matunis, to whom she reported persistent dizziness 

and malaise. She had not been in the car since September 23, but her symptoms had 

“continued to get worse.” The Prednisone had been of “no help,” in fact, Ms. Beckemeyer 

thought it “may have made [her] worse.” She was “unable to stay on task,” because the 

dizziness affected her ability to focus. Unable to drive or to fly, she had nasal congestion, 

no discharge, mild PND, pressure in her left ear, but no hearing loss or tinnitus, fever, 

chest congestion, cough or wheeze. Her “balance was off, but she had no full-blown 

spinning. She was taking Sudafed and Bonine, with minimal-to-no improvement. Dr. 

Matunis noted boggy nasal mucosa with mucoid discharge. She prescribed Anti-Vert and 

advised Ms. Beckemeyer to stay off work for two-to-four weeks. 

On October 27 and 28, 2016, Ms. Beckemeyer returned to the University of Cincinnati 

Medical Center for worsening of her motion sensitivity which had been present since her 

2004 ear surgery. She attributed the worsening to mold exposure. Despite changing 

vehicles, her symptoms of lightheadedness, imbalance, nausea, constant foggy thinking 

and some sensitivity to loud sounds. Her recent sinus congestion, intermittent left ear 

pain and popping had always been successfully managed with Dramamine, 

pseudoephedrine, but these were no longer working. Vertigo, headache and blurred 

vision were denied. Examination of the ears revealed poor movement of the left eardrum 

and normal central nervous system examination. VNG and VEMP testing were ordered. 

Again, she made the attribution to mold in the car, but that was clearly incorrect. She had 

not been in the car for over a month. Moreover, the car had never had a mold issue. 

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Dr. Ahmad saw Ms. Beckemeyer on October 31, 2016. She reported increased 

symptoms of dizziness, lightheadedness, a lot of throat clearing and some headaches. 

Nasal congestion, a runny, stuffy nose and sneezing were also described. She denied 

confusion, but said brain fog was still present. The only findings were puffy eyes with 

circles and boggy, swollen, irritated nasal mucosa. Qnasl was continued and 

hydroxyzine, an antihistamine, was prescribed. He again diagnosed allergic rhinitis due 

to pollen and perennial allergic conjunctivitis. The same day, Dr. Ahmad wrote a letter 

stating, “Ms. Beckemeyer is under my care and is experiencing constant dizziness, 

nausea and brain fog. Motion exacerbated these symptoms. I advise she not return to 

work until the situation is resolved.” 

Dr. Gamm, the Medical Review Officer for Ohio’s Bureau of Workers’ Compensation, on 

November 3 2016, denied Ms. Beckemeyer’s Workers’ Compensation Claim. He noted 

that “the medical documentation supported her claim of allergic rhinitis and allergic 

conjunctivitis due to mold as being directly related to the 9/22/2016 injury. However, 

nasal congestion, post nasal drip and dizziness are symptoms, not diagnoses and 

should not be considered. Finally, medical documentation did not support any additional 

conditions related to this claim nor any relevant pre-existing conditions.” 

The Workers’ Compensation form completed by Ms. Beckemeyer on November 15, 

2016, noted that she had last worked on October 20, 2016. She had left work because of 

“repeated exposure to mold in company-provided vehicle.” She listed the following 

symptoms as being related to that exposure: “dizziness, vertigo [new], nausea, motion 

sickness, brain fog, lightheadedness, confusion, spacey [new], impaired memory [new] 

and cognition.” Thus, seven weeks after use of the care ceased, she reported several 

brand new complaints. Brain fog had first been reported more than three weeks after 

she stopped using the car in which she claimed mold exposure occurred. 

For the last time, on December 13, 2016, Ms. Beckemeyer saw Dr. Ahmad. She told him 

she was “doing well, in general.” She had occasional itchy eyes and occasional 

dizziness, but no sinus symptoms, no ear pressure, headaches, chest congestion or 

coughing. At times, she had mild-to-moderately severe nasal congestion and somewhat 

increased PND. Her eyes still appeared puffy; her nasal mucosa was enlarged and 

bluish in appearance. He again diagnosed Allergic rhinitis due to pollen, perennial 

allergic conjunctivitis, nasal congestion, PND, dizziness and added food allergy. Allergy 

testing was performed on this visit. Skin prick testing was 3+ for two molds: Epicoccum 

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nigrans and Fusarium. 1+ for soy and 1-2+ for peanut. Intradermal testing, a form of 

allergy testing less likely to be associated with clinical symptoms, was 1+ for cat, dog 

and ragweed; she had no reaction to Mold mix 1. She had a 2+ reaction to Mold mix 2 

which included the two molds she was sensitive to on prick testing. It should be noted 

that neither of these molds to which she tested positive are commonly associated with 

interior wet spaces. Others are to which she did not test positive. 

On December 13, 2016, Ms. Beckemeyer saw Craig Cleveland, MD. She told Dr. 

Cleveland that her dizziness and motion sickness were improved. She had no sinus, 

vision or hearing problems, no headaches or motor difficulties. For the first time, in the 

available records she described cognitive problems: word finding difficulties, slow 

thought, being forgetful, all of which, she complained, had not significantly changed or 

improved. She had not reported these previously to any physician whose records I have. 

She claimed that she had increased her Nystatin (anti-fungal medication) to twice per 

day. I have no record of who gave her this. Dr. Cleveland noted that this appointment 

was a Workers’ Comp follow up visit, but there is no prior record from his office provided. 

He diagnosed allergic conjunctivitis, allergic rhinitis, labyrinthitis, motion sickness, 

confusion, cognitive impairment. 

From this point on, Ms. Beckemeyer saw standard medical practitioners only rarely. She 

visited her Primary Care physician, Dr. Maturnis (2/1/2017, 4/12/2017, 6/19/2017, 

12/28/2017, 3/26/2018 and 9/25/2018) for shoulder pain and urinary tract complaints. 

The available medical records end September 25, 2018, more than two years after Ms. 

Beckemeyer last drove the company car she believed contained mold. She complained 

about sinus and ear pressure, mild vertigo and feeling her balance was “off all the time.” 

She claimed that these had been problematic since her “mold allergy [exposure].” The 

only findings were in her nose: boggy tissue and mucous discharge. Although Ms. 

Beckemeyer erroneously believed she was still experiencing symptoms from her long 

past car exposure, Dr. Matunis recognized allergy-related findings and diagnosed 

“seasonal allergic rhinitis due to pollen.” An exposure, even to something to which she 

was actually clinically allergic, could not, two years after that exposure ended, cause 

continuous, protracted symptoms. 

Ms. Beckemeyer also consulted her ear surgeon at University of Cincinnati and was 

evaluated there by a neurologist, Dr. Shatz, who also tested her for her multiple cognitive 

complaints. She had become convinced, by her internet research and non-standard 

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practitioners that she had an “inflammatory process” in her brain, as well as her body, 

related to mold. 

Detailed, standard neurological evaluation at the University of Cincinnati by Dr. Shatz in 

August 2017 revealed a completely normal neurological physical examination, although 

she did comment that Ms. Beckemeyer was “very distressed about the symptoms” she 

believed were caused by mold exposure and she was “concerned about future 

employment.” Despite repeated complaints of word-finding difficulties, examination found 

that she had normal rate, rhythm and clarity of speech, as well as verbal agility. She had 

both intact grammatical expression and comprehension. Language was fluent, without 

any word-finding difficulty, blocks or circumlocutions. Testing was conducted for the 

complaints of “cognitive impairment with memory loss.” Dr. Shatz found only “mild 

cognitive impairment with memory” and concluded that the overall pattern of memory 

impairment was consistent with impaired attention and concentration, to which her 

admitted sleep disturbance contributed. 

As noted, the majority of Ms. Beckemeyer’s medical visits and care after November 2016 

was provided by non-standard medical providers who subjected her to a vast array of 

unnecessary diagnostic studies and treatments. The diagnoses and treatment regimens 

they provided were all directed at indicting mold as the cause of her complaints. Their 

practice patterns which are not generally-accepted or scientifically-supportable will be 

discussed below. 

MEDICAL ANALYSIS

Nasal and other upper respiratory tract symptoms: allergy or infection 

Although Ms. Beckemeyer has associated the onset of her symptoms to driving a 

company vehicle which she decided had mold, the contemporaneous medical records 

reveal that during this period she was diagnosed with upper respiratory infections, the 

actual cause of her symptoms. On June 28, 2016, she had sinus tenderness, inflamed 

nasal mucosa and discharge. Viral sinusitis was diagnosed and treated with steroid 

medication. 

It appears that these symptoms resolved with the prescribed treatment because when 

she saw her primary care physician, Dr. Matunis, one week later on September 7, for 

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back pain, stiffness and foot numbness, she reported no complaints like those described 

in June. Moreover, she was not taking any medications for those kinds of complaints. 

On September 19, 2016, Dr. Matunis diagnosed her with acute, that is, recent onset, 

naso-pharyngitis. Her complaints were new: she reported a three-to-four day history of 

an upper respiratory infection, nasal congestion, ear and sinus pressure, with nasal 

discharge and a morning cough. An antibiotic was given only to be taken if her 

symptoms did not improve or got worse within ten days. Thus, once again, while she had 

the car she had a non-car-related cause of symptoms. Moreover, those had not been 

continuous with the car usage, as she claimed; rather, they were intermittent and acute. 

Three days later, on September 22, she saw her allergist, Dr. Ahmad and reported a 

brand new history and set of symptoms. She claimed that “nasal congestion, some 

lightheadedness [new complaint], intermittent headaches and some throat clearing, 

severe sore throat and excess post nasal drip” had “all begun after being exposed to a 

car with mold.” A steroid spray was prescribed. She later said that Dr. Ahmad told her to 

get rid of the car. The last day she drove it was September 23, 2016. Her last day of 

work was October 20, 2016. 

Allergic symptoms arise when the allergic individual is exposed to the allergen to which 

she is sensitive. The presence of the allergen causes the immune system of an allergic 

person to react. Once the allergen is removed, stimulation of the immune system and the 

related symptoms cease. She admitted that she had a long history allergy symptoms 

throughout the year, with symptoms during each month. Ms. Beckemeyer tested positive 

to two molds in December 2016: Epicoccum nigrum and Fusarium, neither of which is 

identified as one of the water-loving molds commonly found in damp situations, as is 

alleged here. Both of these mold/fungi are found in air and are plant pathogens: the 

former grows on the surface of plant leaves, the latter is found in soil. Both can be 

transported on pet fur, shoes and clothing into the indoor environment and are commonly 

found in homes and buildings. Allergic reactions to these molds are just as, or more 

likely, to occur at home and out-of-doors than in a car. If, as alleged, the car was the 

source of her allergic symptoms, they should have improved after her exposure to the 

source ended. If Ms. Beckemeyer’s symptoms were allergic in nature, as Dr. Ahmad’s 

findings, diagnosis and treatment confirm, then the continued persistence of her eye, 

nose, throat and sinus complaints would be typical and confirm her continued exposure 

to allergens in her home, possibly her workplace and the outdoor environment. The fact 

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that the car was long gone yet symptoms continued mitigates against anything causal 

associated with the car. 

Neurological complaints: lightheaded, dizzy, balance off, motion sickness, vertigo 

Ms. Beckemeyer had longstanding problems with her middle ear and her balance 

beginning at least in 2004. She related that motion sensitivity, present since 2004 ear 

surgery, had been “exacerbated by excess mold exposure.” Lightheadedness was 

reported on October 14 and 18. On October 14, dizziness was first mentioned. 

By October 24, “lots of dizziness,” was described to Dr. Ahmad; Ms. Beckemeyer had 

not been in the car for over one month. The same day, she told Dr. Matunis that she had 

“persistent dizziness and malaise [new complaint]. Symptoms continued to worsen.” On 

October 27, she claimed that her “dizziness was getting worse.” When her subjective 

complaints of dizziness and imbalance were evaluated on October 28, at the University 

of Cincinnati, “no specific peripheral vestibular problem was found,” but abnormal 

tympanic membrane findings were present. Vestibular testing was ordered, but MS. 

Beckemeyer did not complete it. Increased dizziness was again related on October 31. 

Although Ms. Beckemeyer later claimed dizziness had begun thirty minutes after she first 

drove the car in June, the medical records confirm lightheadedness was first reported on 

September 22, months after she got the car and dizziness on October 14, 2016, after 

she gave it up. Thereafter, increasing and persistent dizziness continued to be 

described, as well as imbalance and vertigo, a unique type of dizziness. Even if 

dizziness were related to some allergic reaction to the car, it would not begin, then 

worsen and persist weeks, months and over a year after that exposure had ended, as is 

claimed here. The most likely explanation for ongoing dizziness/vertigo was related to 

her longstanding motion problems which followed her endolymphatic surgery in 2004. 

Neuropsychiatric symptoms: brain fog, confusion, disorientation, memory loss, 

trouble following conversation, trouble initiating tasks, word-finding difficulty, 

difficulty focusing, anxiety

Another of Ms. Beckemeyer’s persisting complaints is “brain fog.” Although she attributes 

this to mold in the car, it wasn’t reported until October 18, 2016, three weeks after she 

had ceased driving that car. “Brain fog” suggests unclear or confused thinking, yet she 

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specifically denied any symptoms of confusion on October 14, to Dr. Ahmad. The term 

“brain fog” is a symptom commonly associated with anxiety. 

The first time “impaired memory” appears as a claimed symptom is in the Workers’ 

Compensation form Ms. Beckemeyer completed November 15, 2016. The first time 

“word-finding” as a problem is reported is December 13, 2016, in Dr. Cleveland’s medical 

record. There is no conceivable pathophysiological mechanism that could explain the 

development of any of these new symptoms, long after the car exposure ended or their 

persistence more than a year later, as is claimed. There is also no conceivable way that 

mold could ever cause such disorders. There are no recognized, accepted brain effects 

of indoor environmental mold exposure of the type experienced by Ms. Beckemeyer. 

The absence of any organic brain injury affecting cognition (memory, speech, language, 

thought) is confirmed by the neurological evaluation and testing performed at the 

University of Cincinnati in August 2017, by Dr. Shatz. Ms. Beckemeyer admitted to mildly 

reduced overall sleep time; Dr. Shatz felt that this sleep disturbance could contribute to 

her distractibility, affecting attention/concentration and, therefore, memory. She 

specifically commented that the test result findings were non-neurodegenerative and 

attributable to the reported sleep disturbance. Ms. Beckemeyer admitted to Dr. Shatz 

that she was anxious and distressed, both of which are well-recognized as affecting 

one’s ability to attend and concentrate, thus impacting memory. The family history of 

dementia in Ms. Beckemeyer’s mother and two maternal uncles was recorded by Dr. 

Shatz, but she did not diagnose any neurodegenerative disorder or Alzheimer’s. Brain 

MRI revealed mild-to-moderate white matter changes consistent with aging and chronic 

small vessel ischemia, most often seen as a manifestation of hypertensive 

arteriosclerosis. The medical records chronicle frequent poor control of the claimant’s 

high blood pressure. There are no generally-accepted, known brain effects of mold, 

either through allergy or so-called “toxicity.” 

It has been alleged by some of Ms. Beckemeyer’s medical providers that she is 

experiencing some neurological effect induced by the claimed car mold. Short of a fungal 

mold infection of the nervous system which she clearly does not have, such an effect 

does not occur. 

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As noted earlier in this report, Ms. Beckemeyer sought the majority of her care after 

November 2016, with a series of fringe practitioners, Drs. Cleveland, Blatman, Pretorius 

and Huber, who encouraged her mistaken notions regarding mold and its health effects. 

As will become clear later in this report, their unnecessary and misleading testing, 

treatments and erroneous causal attributions only served to support her mistaken 

beliefs, hindering her ability to receive proper treatment or to recover, ultimately causing 

her to believe she is totally disabled and unemployable. Their diagnoses include Chronic 

Inflammatory Response Syndrome (CIRS), a made-up non-illness from mold and other 

biotoxins requiring detoxification; brain vasculitis; abnormal neuropsychological findings 

from “biotoxin” exposure; or, an immunological illness caused by a variety of ill-defined 

toxins. These “diagnoses” and causal attributions are not recognized by the standard 

medical community; they are neither generally-accepted nor scientific knowledge. 

Rather, they are the province of a small group of fringe practitioners who support 

vulnerable patients’ false belief systems. 

ENVIRONMENTAL DATA ANALYSIS 

Ms. Beckemeyer took her company vehicle to Performance Toyota on June 23, 2016. 

She requested the leak from the passenger side visor be fixed. According to the 

information in the Performance Toyota records, no specific leak is described; a damaged 

washer line, possible chewed by mice, was replaced. There is no description of any 

mold. At her request, the HVAC evaporator was flushed and all of the water was 

removed from the evaporator box. 

Testing of the vehicle was conducted by Ecostratum in July 2018. All levels of molds 

sampled in the car, in air and dust, were either low-to-non-existent and/or no different 

from common background levels found in non-water damaged homes. For example, the 

highest mold level found was 10,000 cfu/gm of carpet dust (Penicillium). Hicks et al 

studied never water-damaged homes in California. The average mold levels in carpets 

with low traffic were >55,000 cfu/gm of dust. Of that, approximately 12,000 was 

Penicillium. Even bedspreads had > 24,000 cfu/gm of dust. Since molds are carried into 

interior spaces like cars and homes on clothing and shoes, it is hardly surprising that car 

carpets will have mold when tested. So does all of our home carpeting. The air levels in 

the car, too, were well below those commonly found in indoor air (Gots et al 2003, Baxter 

et al 2005). 

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MEDICAL CAUSATION ANALYSIS 

Recognized effects of mold and mold toxins (general causation) 

The primary scientifically-known and generally-accepted mold effects and those of other 

factors associated with wet-damp spaces, relevant to this matter are discussed by the 

National Academies, Institute of Medicine (2004), Bush et al (2006), World Health 

Organization (2009), The German Society of Hygiene, Environmental Medicine and 

Preventive Medicine (2017) and Borchers et al (2017). They include: 

• Upper respiratory allergies (like hay fever) in some allergic people which produce:

Red, watery eyes 

Sneezing and runny nose 

 Stuffiness and congestion 

 Occasionally accompanied by loss of energy 

• Lower respiratory allergies (asthma) in some allergic people characterized by:

 Shortness of breath and Wheezing 

These symptoms commonly occur absent mold exposure. They have many other 

causes, including viruses, pollens, dust, dust mites, cat and dog dander, as well. 

General Causation and Wet-Damp Indoor Spaces 

A number of studies have linked symptoms to either wetness-dampness in indoor 

spaces or to odors of mold indoors. In those studies, the matter of causality is, however, 

far from settled. Studies of the indoor environment and health are plagued by major 

methodological problems. To begin with wetness and dampness are generally selfreported by the study group and never verified. Those self-reports of dampness may 

range from a small spot of water under a sink to a major flood. Those hardly lead to 

similar potential exposures. Complaints, too, are rarely verified, but are rather selfreported. The characterization of a moldy odor is highly variable and subjective. Finally, 

the majority of studies are populated by symptoms or disorders that are never validated 

by reviews of medical records. As a result, the current belief among some that wetCase: 1:17-cv-00695-MRB Doc #: 65-2 Filed: 05/20/19 Page: 62 of 91 PAGEID #: 2240
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damp spaces cause symptoms absent an allergic basis is the subject of extensive study, 

but remains well short of settled. 

The complexity of this issue is magnified by the many dozens of agents that have been 

associated with damp indoor spaces and to non-wet spaces as well, ranging from 

endotoxins, to mycotoxins, to glucans to bacteria. For example a study by Hicks et al 

(2005) found extensive mold in carpets of homes that had never been water damaged. 

None of the numerous identified agents found in homes has been specifically connected 

to any claimed health effects and studies of them individually often find no such 

connection. 

It has also been hypothesized that people who have symptoms are more likely to report 

wetness and dampness in their homes. In other words, the symptoms, rather than being 

caused by wetness, may actually be reason for an over-reporting of dampness. 

Lastly, there also exists a body of research which has linked early childhood exposures 

to microbiological agents in the indoor environment to protection form allergy, asthma 

and respiratory disorders. This has led to the “hygiene hypothesis,” arguing that some 

exposures are salutary rather than harmful. 

Thus, whether wet/damp indoor spaces produce symptoms or illnesses, other than by 

allergy, is argued, but far from proven. It is a complex and unsettled issue. 

For the most part, the known and accepted health effects of molds and mold toxins, as 

well as other agents associated with wet-damp indoor spaces, are well-studied and 

widely published. Mold occurs naturally both indoors and outdoors. Mold spores occur in 

far greater concentration in the out-of-doors, but are transported indoors via mechanical 

ventilation, movement through open doors and windows, transport on materials brought 

into a building, or carried on humans, plants and animals. Some indoor surfaces can 

support the growth of mold. These materials include paper backing on wallboard, some 

types of ceiling tiles, wood, carpeting, fabrics and insulation materials made of cellulose. 

Indoor plants likewise are a source of mold. An ongoing water source is also necessary. 

The clinical effects associated with mold/fungi exposure can be classified into three 

broad categories: allergic effects, infectious effects and potential toxicological effects. 

The latter, at issue here, are best known to occur following certain unusual and extreme 

exposure circumstances, not commonly related indoor air. 

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The allergic effects are primarily evident as respiratory allergies, such as hay fever or 

upper respiratory allergies, allergic rhinitis, asthma and, very rarely, hypersensitivity 

pneumonitis and allergic bronchopulmonary aspergillosis. Mold-related allergic effects 

are generally mild and occur only when actual exposure occurs. They are equally likely 

to result from exposure to molds out-of-doors, as well as from many other aeroallergens: pollen, grasses, dog and cat dander, feathers, dust mites, trees, weeds, house 

dust. Allergic responses occur to mold only in allergic people, who make up 

approximately 6-8% of the US population. Ms. Beckemeyer had some positive allergy 

tests to certain molds and to other agents as well. 

Certain infectious mold disorders occur in immunocompromised individuals: for example, 

persons taking immunosuppressant medications, or those with immune suppressant 

diseases. In these vulnerable individuals, mold exposure may lead to infection in the 

lungs, sinuses, or even generalized infections throughout the body. These infections 

have not been seen in generally healthy individuals exposed to mold in the indoor 

ambient air. The scientific and medical literature also documents infections developing 

from exposure to outdoor molds endemic to specific areas of the country. Such infections 

have almost never been associated with indoor exposures. 

The third category of adverse health effects associated with mold is that of mold toxicity. 

That seems to be what is claimed in this case. Several of Ms. Beckemeyer’s physicians 

seem to believe that mycotoxins or other ill-defined “toxins” are responsible for her 

symptoms. One of the claimant’s experts, Dr. McMahon, believes that various ill-defined 

agents in wet-damp indoor spaces produce some sort of toxicological effect which leads 

to an immunological disorder. He shares that belief with a small cadre of fringe 

practitioners whose methodology and self-described “disease” is not recognized or 

generally-accepted. They call this disorder chronic inflammatory response syndrome 

(CIRS or SIRS), a “disease” known only to them, not generally-accepted and not 

recognized by the American Academy of Allergy Asthma and Immunology (AAAI), even 

though Dr. McMahon and likeminded practitioners claim this is an “immunologic 

disorder.” 

Many molds are capable of producing mycotoxins under specific circumstances of 

moisture, temperature and nutrition. Some mycotoxins can cause adverse health effects 

in humans. Such effects include adverse impacts on a variety of organs and metabolic 

processes, for example, aflatoxin affects the liver when ingested (not inhaled) in 

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sufficient amounts. Popular perceptions notwithstanding, the literature does not provide 

valid or accepted scientific support for the proposition that toxic effects associated with 

mold exposure are caused by the kind of low-dose inhalational exposures potentially 

encountered in indoor air. The studies which I shall describe elucidate the near 

impossibility of such effects. 

No “CIRS” post Hurricane Katrina 

If wet/damp indoor spaces produced the disorders claimed in this case, it would stand to 

reason that such disorders would have been found in homes following hurricane Katrina. 

Post Katrina, despite being extremely wet and moldy, exposures in these flooded homes 

did not lead to illnesses. The Centers for Disease Control (CDC) evaluated homes in 

New Orleans after Hurricanes Katrina and Rita. The authors of that evaluation found no 

evidence of adverse health effects associated with those exposures (Barbeau et al, 

2010) 

Mycotoxins 

Specific mold species produce specific mycotoxins under specific conditions. The mere 

presence of such a mold is not evidence that it was producing any mycotoxin. Potentially 

toxigenic species of mold, including various species of the genera Aspergillus, 

Penicillium and Stachybotrys, do not always produce mycotoxins. Certain growth 

conditions are required and, in the case of Stachybotrys, different species produce 

entirely different mycotoxins ranging from nontoxic to humans to potentially-harmful at 

high doses. Some of the plaintiff’s causation experts in this case have assumed, with no 

support, that mycotoxins or other biotoxins were present in the car. None was actually 

measured. Moreover, as I will discuss later, airborne mycotoxins do not contribute to the 

body’s mycotoxin burden. On the other hand foodborne mycotoxins do. 

In order for a toxic effect to occur, the toxin must be present, a route of exposure must 

be available and a sufficient dose must be received to produce the toxic effect. 

Mycotoxins are not volatile, nor are they cumulative (Bush 2006). An immutable 

principle of toxicology is that toxicity depends upon the dose of the toxic agent which 

enters the body. Thus, botulinum toxin is lethal in rather small quantities if eaten by 

people, but it is injected safely in millions (as Botox) to treat wrinkled skin. By diluting it a 

million-fold, Botox is converted from highly toxic to quite safe. The same is true for 

mycotoxins. As is discussed below, the calculated doses required for both acute and 

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chronic exposures to result in adverse health effects in humans are so high that it is 

essentially impossible for exposure in a home, let alone a car, to ever lead to a toxic 

adverse human health effect. The American College of Occupational and Environmental 

Medicine (2002 and 2011), the National Academies of Sciences’ Institute of Medicine 

(2004), the American Academy of Asthma, Allergy and Immunology (2006) and the 

World Health Organization (2009) all concur that the scientific and medical evidence 

does not support the contention that mycotoxin-related disease (mycotoxicosis) occurs 

via inhalation of these agents in indoor environments. The current fact sheet of the US 

CDC concurs with that assessment: http://www.cdc.gov/mold/stachy.htm More 

specifically and pertinent to this case, none of these recognized organizations find any 

support for the proposition that either mycotoxins or other agents associated with damp 

indoor spaces, can produce either the range of symptoms alleged here or the “disease” 

“CIRS” made up by Dr. Shoemaker and adopted by Dr. McMahon. 

Direct toxicological calculations show quite clearly that it is almost impossible for there to 

be enough mycotoxins in indoor air to produce toxicity (Kelman et al, 2004). They 

calculated that 200,000 spores/m3 of mold spores chock full of the most toxic of 

mycotoxins would be the necessary airborne concentration to produce toxicity. All levels 

of molds sampled in the car, in air and dust, were no different from common background 

levels found in non-water damaged homes. Only a fraction of those were of the type 

which the plaintiff’s experts in this case might contend produce mycotoxins. In other 

words, even if these spores did contain those mycotoxins (a proposition which is 

speculative and unproven) the amount of those is thousands of times lower than the 

lowest level which is potentially toxic to human beings. 

Toxic doses of mycotoxins can be taken into the body, primarily through ingestion of 

heavily-contaminated foods. This has been primarily an issue in farm animals which 

have eaten contaminated hay or grains. When a toxic dose of mold/mycotoxin is taken 

into the body, as might follow ingestion of heavily contaminated spoiled food, for 

example, a specific pattern of illness, well-documented in the literature, arises which is 

specific for given mycotoxins (Kuhn et al, 2003). That foods, not air, are the source of 

mycotoxins in our bodies was illustrated in two recent studies. In one, molds were found 

in homes which, in the laboratory, produced mycotoxins. However, in the homes in which 

those molds were found, the mycotoxins were not found (Jezak et al 2016). In another 

study, workers in grain grinding mills where airborne mycotoxin levels are quite high, had 

the same urinary mycotoxin levels as a control group whose exposure was purely dietary 

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(Follman et al 2016). Mycotoxins in our bodies and found in our urine come from food, 

not from air. 

Fung and Hughson (2003) conducted a review of 416 studies in which no scientificallysound evidence of a causal relationship between inhaled indoor mold toxins and any 

adverse health impact was found. This review also included, without specific comment, 

all other substances associated with wet/damp indoor spaces since that was setting 

which gave rise to these studies. Mold toxin risk assessment was reported by the 

American College of Occupational Environmental Medicine (ACOEM) in its 2002 

consensus document which was reaffirmed in 2011. This well-respected, relevant 

medical organization determined that, even if some mycotoxins are produced and 

become airborne and accessible for human exposure, the amount and duration of 

exposure shown to cause adverse health effects was extremely high: far higher than 

ever occurs with indoor contamination. 

In 2004, the Institute of Medicine (IOM), National Academies of Sciences, thoroughly 

reviewed the available medical and scientific literature to determine whether there was 

any association between exposure to damp indoor environments where mold and other 

agents grow and a variety of symptoms, conditions and diseases. The IOM found no 

evidence of an association (not causation) between exposure to damp indoor 

environments and the majority of symptoms alleged in this claimant. 

Similarly, in its 2009 Guidelines for Indoor Air Quality: Dampness and Mould, the World 

Health Organization specifically noted that, “no study has shown that people living in 

damp buildings who complain of nervous system symptoms are exposed to effective 

levels of mycotoxins.” WHO concluded, “The evidence that [mycotoxins] play a role in 

health problems related to indoor air is extremely weak.” Further “toxicological studies” 

were called for, in order to “clarify and identify causative compounds,” but the authors of 

the Guidelines warned that, “The dosage must be considered in interpreting the findings 

and attempting extrapolation to the range of human exposures indoors.” To date, there 

exist no such studies. 

In a more recent report, the German Society of Hygiene, Environmental Medicine and 

Preventive Medicine reached similar conclusions (Hurras et al 2017). 

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For all of these reasons, the notion that any mycotoxin effects arise from mold in homes 

or from a limited period of driving in a car is erroneous. A small group of zealous 

advocates, a few of whom are involved in this case, as well as the plaintiff, may believe 

otherwise, but their views are scientifically-unsupported, out of the mainstream and not 

generally-accepted. 

Specific causation in an individual 

Assuming that the general causation requirements can be met, which is not the case in 

the Beckemeyer matter, specific causal elements would need to be evaluated and ruled 

in or out. 

The causation methodology used to establish specific causation, that is, causation in an 

individual, is widely-accepted in the literature (Gots 1986, Gots 1993, Hackney 1979, 

Evans 1976, Irey 1976, Schwartz 1995, Tarcher 1992, Marley 1991, Buffler 1995, Rom 

1992, Black 1990, Black 1993, Sullivan 1992, NRC 1992, Brennan 1987, Guezalian 

2005, Weiner et al, 2012). Other accepted methodologies differ in detail, but not in basic 

principle. The elements of the causation methodology used to establish specific 

causation include the following: 

How was the diagnosis made? 

Does the patient have a recognizable disease? 

Are we dealing with symptoms alone or with objective disorders? 

 Have other causes been properly considered and ruled out? Has the exposure been 

confirmed? 

Was the dosage sufficient considering the concentration and duration to produce the 

condition(s)? 

Was the clinical pattern what one would expect from that causal agent? 

Were the temporal relationship and/or latency periods appropriate? 

All of these questions and their answers are highly individual and must be addressed 

symptom (or disorder) by symptom (or disorder). 

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The discussion of those causal elements in this case will follow. 

Specific Causation in This Matter

None of the specific causation requirements are met in this case, as the detailed review 

above demonstrates. In fact, all of them are specifically refuted. 

How was the diagnosis made? And 

Does the patient have a recognizable disease? 

The primary diagnoses in this case made by standard practitioners were recognized 

respiratory disorders—allergies and infections. Others were major anxiety disorders. The 

subsequent diagnoses, and the subject of this claim, CIRS, are not recognized diseases, 

but the creation of non-traditional practitioners and neither scientifically-known nor 

generally-accepted. 

Are we dealing with symptoms alone or with objective disorders? 

For some of Ms. Beckemeyer’s symptom complaints, specific clinical findings are 

apparent in the records. These exclusively involve the respiratory tract. She allegedly 

has certain laboratory abnormalities, according to several of her non-mainstream 

practitioners. Those will be discussed later. 

Have other causes been properly considered and ruled out? Has the exposure been 

confirmed? 

There was no exposure to mold in this car. All levels were low and/or typical everyday 

background levels. There was also no wetness established. Thus, no exposure has been 

confirmed. 

Other causes of her symptoms and findings have been identified including allergies, 

infections, major anxiety and depressive disorders. She is also clearly persistently 

anxious which explains many of her symptoms. 

Was the dosage sufficient considering the concentration and duration to produce the 

condition(s)? 

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As a board certified toxicologist, I can unequivocally state that there were no 

toxicological agents in this car capable of producing acute or chronic illnesses. 

Was the clinical pattern what one would expect from that causal agent? 

Ms. Beckemeyer’s clinical pattern of symptoms, objective findings and response to 

treatment supported the allergic and infectious conditions diagnosed by her standard 

practitioners. This pattern is not consistent with the car having been the cause. 

That some mold-related or other unspecified “toxin” related to the car was causal of this 

claimant’s made-up “condition,” CIRS, is completely unsupportable. This condition has 

no specific clinical pattern, no objective findings or standard clinical testing; it has a 

variable array of wide-ranging, subjective symptoms which can occur in virtually any 

organ system in a pattern defined solely by the patient herself. 

Were the temporal relationship and/or latency periods appropriate? 

The timing of symptoms and the location of their occurrences also speaks clearly against 

the car as responsible. While Ms. Beckemeyer later claimed that she was sick from the 

moment she got the car, contemporaneous medical records do not support that. She had 

acute infectious respiratory conditions for short periods during her three months with the 

car. She also had allergic symptoms which were ascribed to non-car associated 

exposures. She later, after disposing of the car, developed most of her symptoms which 

persisted and, in some instances, intensified. Thus, there is a clear temporal disconnect 

between the car and her primary complaints. 

Very importantly, she had longstanding prior sinus and respiratory disorders as well as 

major anxiety disorders. Responsible for many of her symptoms, these long predated the 

car issue. 

The bottom line of this causation analysis is that there is clear evidence against specific 

causation. The car played no role, except a perceived one, in Ms. Beckemeyer’s 

illnesses or symptoms. 

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The role of perceptions of hazards in symptom development and reporting. An 

alternate specific causal factor 

An important specific causal factor in many exposure matters relates to fear or worry by 

the individual. Symptoms are frequently over reported when people believe their health 

has been threatened. A review of the scientific literature regarding self-reported 

symptoms indicates that these can be unreliable when perceived hazards exist as a 

basis for confirming health problems. Over the years, numerous authors have studied 

and reported upon the unreliability of self-reported symptoms, particularly following 

perceived toxic exposures. (Gots et al, 1992, Hopwood et al, 1988, Lees-Haley et al, 

1992, Kaye et al, 1994, Lipscomb et al, 1991, Lipscomb et al, 1992, Logue et al, 1986, 

Pennebaker et al, 1994, Roht et al, 1985). The most important reason is the well-known 

phenomenon of reporting bias. (Lipscomb et al, 1991, Logue et al, 1986, Pennebaker, et 

al, 1994, Last et al, 1992, Hennekens et al, 1987, Pennebaker et al, 1983) Reporting 

bias, a standard epidemiological term, is not a pejorative as it is in common usage. 

Rather, it reflects the normal human tendency to connect physical phenomena with 

unrelated causes, particularly when the perceived cause is viewed as a health threat. 

Extensive media coverage of hazards (such as waste sites, chemical spills, or nuclear 

accidents) affects perception of risk. (Aakko 2004) The “hazard du jour” phenomenon 

begins with media reports of a link between a health effect and a consumer product or 

environmental factor. (Kabat 2008). Mold and mold toxins is one of those current 

popularly perceived hazards.

Studies of health complaints of residents living near waste sites have explored the 

relationship between alleged low level chemical exposures and verification of the actual 

diseases. These have reported negative results in most instances. (Dunne et al, 1990, 

Naker et al, 1988, Hertzman et al, 1987, Janerich et al, 1981) When questioned, 

individuals living near a waste site almost always produced more complaints than 

individuals living in an area without such a waste site. Individuals concerned about the 

quality of indoor or workplace air tend to report a wide range of health complaints. 

These increased complaints, unassociated with verified, actual disease, emphasize the 

intensity of the belief about a toxic risk held by the reporting individuals. When 

individuals perceive a risk from something over which they have little or no control they 

experience a higher level of threat and fear. (Dunne et al, 1990, Baker et al, 1988). 

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One study illustrates quite clearly the unreliability of self-reporting. It involved a New 

Jersey community whose water supply was reported to be contaminated. When 

“unexposed” and “exposed” populations in Somerset, New Jersey, were questioned, the 

symptom responses of the group that believed it was exposed were substantially higher 

than that of the group residing in another part of New Jersey. Evidence obtained after the 

study revealed that the “exposed” group actually had not been exposed. Their water 

was not found to be contaminated, although they had believed it was. Clearly the 

symptom reporting on the part of these residents was directly related to the perception 

that exposure had occurred (NJDOH 1983). Numerous other studies in the published 

literature have reported precisely the same findings (Pennebaker 1994). When 

perceptions of hazards increase, symptom reporting increases, whether or not hazards 

actually exist. 

At times, physicians can play a role in initiating and maintaining patients’ symptoms and 

illness beliefs. Kellner (1990) made the observation that “in many somaticizing and 

hypochondriacal patients, iatrogenic (physician-induced) reinforcement played a part,” in 

encouraging and maintaining the patients’ symptoms or believed illnesses. It has been 

pointed out that with the increased awareness of chemicals in the environment and 

media attention to indoor and outdoor air issues, as well as to the hazards of chemicals, 

there is a greater tendency for psychological factors to aggravate, and even cause, a 

multiplicity of symptoms. Physicians, too, share the public’s awareness about chemicals 

and are exposed to the same media information about alleged hazards. Even when 

physical findings are few or absent, physicians, at times, will diagnose illness and 

attribute it to the exposure reported by the patient. By misattributing symptoms to a 

cause or diagnosis of questionable validity, a physician can encourage and reinforce a 

patient’s symptoms and belief in illness. 

Nontraditional practitioners and an even larger number of physicians and health care 

providers, who share some of their beliefs and practices, routinely diagnose 

environmental illnesses. Black (1996) published a paper entitled Iatrogenic [sic 

physician-caused] Multiple Chemical Sensitivities, in which he described this 

phenomenon. He noted that iatrogenic reinforcement can play a critical role in initiating 

and maintaining illness belief. In the case of mold and mold toxins, I have mentioned the 

role that Dr. Shoemaker and his followers have played. Dr. Shoemaker will be discussed 

below in more detail. 

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Finally, it is important to determine whether symptoms are the result of an emotional 

response to a perceived chemical toxicity or to an abnormal physiological interaction 

between chemical agents and organ systems. It is not possible from symptoms alone to 

tell which is the case, since either source can produce identical symptoms (Gots 1996). 

The recognition of the origin of complaints, acknowledgement of reporting bias in 

patients’ reporting of symptoms, as well as the public’s fear of environmental hazards, all 

contribute to symptom reporting, as can true pathologic health effects produced by 

environmental agents. Mood, feelings, stressors, fears and worries can all have 

profound impacts upon symptom development and even disease. The need to identify 

the primary or predominant causal factors of the symptoms, whether emotional or 

organic, is essential. Making such a distinction is neither trivial nor unnecessary. A brain 

tumor would not be treated with psychotropic drugs any more than stress-related 

headache would be treated with neurosurgery, even though both cause headaches. 

Both stage-fright and an abnormal electrical pathway in the heart can cause palpitations; 

each is treated differently. The critical distinction between an organic (i.e., toxicogenic) 

and psychogenic disorder is essential to make and can be made through proper testing 

(Gots 1996). 

The Role of Stress in Immunological parameters 

Perceived exposure to a hazard is a stressor which, as noted, can and does produce 

symptoms. It also can produce measurable immunological changes. In other words, 

laboratory values are affected by stressors. Numerous studies over the years have 

addressed this as they have studied the role of stressors in the production of a wide 

variety of illnesses—susceptibility to infection, heart disease, cancers and many others. 

One of the largest studies of this phenomenon, performed a meta-analysis of 300 

scientific articles on this subject (Segerstrom et al 2006). Chronic stressors (specifically, 

unemployment was one) had the most marked effect on measured immunologic 

parameters. Ms. Beckemeyer was unemployed and was told she was poisoned; she 

reported to Dr. Shatz her fear about her future employability. Those are clearly significant 

stressors. In addition to Segerstrom, others have discussed the mechanism by which 

stress affects immunological parameters. Among them is an article entitled 

Psychoimmunology examined (Thornton et al 2006). There is, in fact, an entire field of 

study known as “Psychoimmunology.” 

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CLAIMANT’S EXPERTS’ UNCONVENTIONAL CAUSAL THEORIES IN THIS MATTER 

A number of medical “experts” are supporting Ms. Beckemeyer’s beliefs in this matter or 

are mentioned. They are among a relatively small number of practitioners, outside the 

mainstream, whose diagnoses, attributions and treatments are neither generally 

accepted, nor scientifically supportable. In this case, they include Drs. Cleveland, 

Blatman, Pretorius, Huber, McMahon and Shoemaker. They have diagnosed SIRS or 

CIRS or toxic mold exposure or biotoxin illness. SIRS is actually a condition referring to 

terminally ill patients, most often in ICU, who have multi-system failure. CIRS is a 

diagnosis made up by Dr. Shoemaker and adopted by Dr. McMahon, but not generally 

accepted. They believe that CIRS is a “biotoxic” illness. 

To elucidate where this term “biotoxic illness,” “toxic mold exposure” and CIRS come 

from, I shall discuss two of the involved physicians—Drs. McMahon and Shoemaker—

who are central players in this non-accepted disorder. 

The claimant’s expert, Dr. McMahon, is relying upon several “evidentiary” approaches to 

support his causal allegation. All are wrong and defy accepted medical and toxicological 

reasoning. 

The first is the general causation belief which I have discussed above. That is, that 

mycotoxins or other factors coming from indoor environmental air are capable of leading 

to the manifestations alleged and the strange self-named, unrecognized diseases CIRS. 

That is untrue, has never been shown scientifically and is not generally-accepted. The 

US CDC in its current online report agrees (http://www.cdc.gov/mold/stachy), as do all of 

the other consensus groups mentioned above. 

The second is that the exposure and consequent dose of such toxins allegedly received 

by Ms. Beckemeyer of mycotoxins or anything else was sufficient to cause the 

complaints. To “establish” this, the supporting practitioner is relying on several lines of 

self-developed and self-serving “evidence.” The first is the unproven and likely untrue 

assertion that “toxins” or other inflammation-inducing agents were present and in 

sufficient quantities to exert effects. The second, is that those mold toxins, if mold toxins 

are at issue, came from the air of the car interior. The third is that the complained of 

disorders are consistent with toxicity associated with indoor environments. Finally, the 

fourth is that various odd laboratory tests which he orders, supports his diagnosis and his 

causal attribution. 

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If Ms. Beckemeyer were exposed to a mycotoxin, as she and some of her experts seem 

to believe, and even if they were to enter the body, they are rapidly eliminated. Any 

mycotoxins theoretically entering her body arising from the car would have been 

essentially gone by December 2016. However, everyone has levels of mycotoxins in 

their bodies, arising from dietary sources 

Like all other foreign substances, such as medications and most other toxins, mycotoxins 

are broken down and eliminated by the body. Mycotoxins are metabolized in the liver 

and excreted by the kidney in short order. Numerous scientific studies have examined 

the time that it takes for mycotoxins to be eliminated. In toxicology and 

pharmacologically, this rate of elimination is generally called “half-life.” This is the time 

that is required for one half of the absorbed dose to be eliminated. For the most part, the 

half-lives of studied mycotoxins occur in minutes to a few hours. Thus, they do not 

persist for weeks, months or years after exposure cease and, as a result, are not, 

capable of producing increasing or persistent symptoms or causing new symptoms to 

arise. 

The presence of toxin-producing molds and of mycotoxins or any other “toxic substance” 

in the car at issue has not been shown. There were no measurements performed. 

Furthermore, the total mold levels found in the car which is the subject of this case, were 

not unusually high or indicative of significant water intrusion and active mold growth. 

They were common everyday exposure levels. Even if the mold spores found were full of 

mycotoxins, thousands of times more than the largest amount found would have to have 

entered the body to produce toxicity. As recent studies have shown, airborne mold or 

mold toxins do not contribute to internal levels of mold toxins. Those come from dietary 

sources (Follman et al, 2016, Jezak et al, 2016). 

Dr. McMahon and a couple of Ms. Beckemeyer’s treating physicians are basically 

followers of a Maryland physician, Ritchie Shoemaker, who popularized, among a fringe 

medical group, the diagnoses and testing which they follow. The fact is that these 

individuals belong to a small cadre of alternative practitioners who have promoted false 

notions about indoor environments and all manners of adverse health consequences 

associated with them. Their beliefs and practices are neither generally-accepted nor 

scientifically-known. 

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Dr. Shoemaker’s practices came under fire by the Maryland Board of Medical Examiners 

in 2013, when he was reprimanded and put on probation for failing to meet proper 

standards of care. At that point, he discontinued his clinical practice. However, he now 

purports to provide special certification to physicians who follow his diagnostic and 

therapeutic methods. Dr. McMahon, an expert in this case, and a pediatrician by 

training, touts his mold certification by Shoemaker as his primary credential in this arena. 

He adds to that the assertion that he has treated thousands of such patients, solidifying 

his self-proclaimed expertise and diminishing that of anyone who does not have such 

clinical experience. Medical history tells us that even large numbers of diagnostic and 

treatment experiences do not necessarily imply knowledge or wisdom. No doubt the 

colonial physician who bled George Washington would also have trumpeted his 

experience with thousands of such treatments. 

Drs. Cleveland and Blatman may not have been formal students of Dr. Shoemaker, but 

they used his earlier diagnostic terminology of SIRS. They used the Shoemaker 

“protocol” to treat it in Ms. Beckemeyer. 

Since approximately 2008, Dr. Shoemaker has called his novel disorder Chronic 

Inflammatory Response Syndrome (CIRS), a condition which is neither generally 

accepted nor known to exist. Ms. Beckemeyer, Drs. Cleveland, Blatman and McMahon 

use that term or a variation of it, SIRS. Dr. Shoemaker and his followers further claim 

that this disorder results from exposure to a variety of “biotoxins” associated with 

wet/damp indoor spaces. This theory is self-generated, unproven, based on poor 

causation and scientific methodologies, and resides in questionable data. It is not 

generally-accepted. 

Dr. Shoemaker originally called the condition Sick Building Syndrome (SBS) and Chronic 

Biotoxin-Associated Illness, before he renamed it “Chronic Inflammatory Response 

Syndrome.” Initially, he attributed this entity to a mycotoxin cause. In 2002, he 

consistently attributed symptoms to “toxin-forming species of fungi” and their mycotoxins. 

In his book Mold Warriors (2005), Dr. Shoemaker wrote similarly about the cause of 

illness in the cases he discussed. He highlighted water damage and mold growth and 

that certain molds make toxins, “our studies show repeatedly: mold makes people sick.” 

(p. 332-333). He has subsequently disavowed the role of mycotoxins, believing instead 

that, “exposure to mycotoxins is a ‘relatively insignificant factor in the systemic 

inflammatory response these people get’.” (See Deposition testimony in Anderson et al 

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vs. The Ritz Carlton Hotel Co. et al., DC Superior Court Civil Div. CA No. 05ca 

(0001130).) 

 Certain of the diagnostic tests performed on Ms. Beckemeyer, such as VCS, MSH, TGF, 

and C4a, even the so-called HLA-genotype allegedly associated with environmental 

exposure leading to symptoms and a dozen others are neither scientifically-known nor 

accepted as showing what they are claimed to demonstrate. They are not described in 

the recognized and accepted medical and scientific literature for this purpose. Many of 

these tests have little clinical application at all, but are unique to certain specialized 

research laboratories, or to either specific other disease states or to other illnesses. 

These tests taken together are not delineated in textbooks or published as part of 

evidence-based clinical guidelines used by the general medical community. They are the 

sole province of this fringe medical group who call themselves “environmental 

physicians,” or, now, “certified mold physicians.” 

Like the changes in name and causes of his novel illness, Dr. Shoemaker’s diagnostic 

tests and the parameters measured by them have changed, as well. He admitted in 

testimony that, “the normal set of labs that I use also evolves over time. If you look at 

what I did in 2003, it contains many of the same elements I use in 2008. Some have 

come and gone out of that list from 2003, other new ones have come and gone and 

other new ones have come and stayed.” (Testimony in Anderson et al., 22 May 2008, p. 

28, l. 20-25). His diagnostic tests, then, are a moving target: there is no way that they 

could constitute a reliable, validated test battery which has become generally-accepted. 

With both the parameters being tested and the tests themselves changing or “evolving,” 

it is little wonder that the information upon which he and his followers base their 

conclusions is not found in journals that are generally available to and accepted by the 

medical community. They are, rather, their personal, idiosyncratic characterizations and 

creations, neither reliable nor validated for the purpose for which they are employed. 

Many of the tests are discussed in Dr. Shoemaker’s articles describing his “studies” and 

theoretical “mechanisms” for his personally-defined diseases of “sick building syndrome” 

and “chronic biotoxin-associated illness from exposure to water-damaged buildings.” 

Those were published in Neurotoxicology and Teratology (Shoemaker et al, 2005; 

Shoemaker et al, 2006). He has recently published another article dealing with 

“neuroquant testing” in that same journal (Shoemaker et al, 2014). Dr. Shoemaker has 

asserted that all articles were peer-reviewed. There is, however, no evidence that these 

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articles are peer reviewed or, if they are, that they are reviewed with serious rigor. Dr. 

McMahon, has recently published related articles in a journal called Medical Research 

Archives: a journal with an impact factor of about 1, meaning that it is rarely read or 

cited. 

The journals in which these studies were published, Neurotoxicology and Teratology, 

and Medical Research Archives are not among those journals listed by the International 

Committee of Medical Journal Editors (ICMJE) as following its “Uniform Requirements of 

Manuscripts Submitted to Biomedical Journals.” Journals which have agreed to follow its 

peer-review standards, as well as the other requirements delineated, are listed by the 

ICMJE. There are at least 1000 of those, but the two noted above are not included. 

I serve as a peer reviewer of a standard, recognized journal. Having read Dr. 

Shoemaker’s and Dr. McMahon’s papers, I can state that they would not pass generallyaccepted requirements of a peer-reviewed journal. 

In assessing whether a physician or scientist used reliable scientific methodology to 

reach his conclusions, it also is important to examine the known or potential rate of error 

of a particular theory. For example, if a scientist placed various qualifications on his 

conclusions, then the known rate of error is potentially very high. The rate of error 

cannot even be assessed for a theory that has not been tested. Dr. Shoemaker’s and 

Dr. McMahon’s theories remain in the unreplicated, unreliable category. Their alleged 

scientific methodology in reaching their conclusions about this “CIRS” condition have, 

therefore, not been shown. 

Another important factor in assessing the scientific reliability of a theory is whether the 

theory has gained widespread acceptance among scientists in that particular field. 

General acceptance indicates that other scientists agree that a theory is based upon 

reliable scientific methodology, has been replicated and has scientific validity. If, over 

time, a scientist’s opinion has gained little or no support within a particular field of 

science, it is appropriate to question whether the opinion is supported by reliable 

scientific methodology. The term CIRS as a disease entity has been used by Dr. 

Shoemaker since at least 2008. Dr. McMahon says that the condition was first described 

in 1997 (McMahon 2017). Since it is, according to them, a widespread immunological 

disorder (Dr. McMahon now claims 7% of people have CIRS), one would think that if it 

were proven, by now it would be widely-accepted. It is not. It is not recognized, for 

example, by the American Association of Allergy Asthma and Immunology, the major 

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immunology body in this country. It also has no ICD-10 number, that is, no number in the 

International Classification of Diseases, version 10. Dr. McMahon dismisses this, 

suggesting that such numbers are only for “insurance purposes.” Actually, the disease 

classification numbers are established by the World Health Organization to provide 

uniform nomenclature for study purposes, so that physicians and scientists worldwide 

are speaking about the same entity when they do studies. There is no ICD-10 number for 

CIRS. 

Thus, the notion that there exists a “biotoxic illness” or “SIRS/CIRS” due to the inhalation 

of mold toxins and other things in the indoor environment is not one which is generallyaccepted or scientific knowledge in the medical community. The current state-of-the 

science is discussed by organizations noted earlier, including the US CDC 

(http://www.cdc.gov/mold/stachy) 

Dr. McMahon, an expert in this matter, claims proudly to be a disciple of Dr. Ritchie 

Shoemaker. He diagnoses the Shoemaker disease, now named Chronic Inflammatory 

Response Syndrome (CIRS), which he believes arises from indoor exposures and 

attacks every organ in the body. He diagnoses this disease through a set of thirty or 

more disconnected symptoms and a bizarre array of laboratory tests only performed in 

this combination by Dr. Shoemaker’s zealous followers. This disorder of Dr. 

Shoemaker’s is trumpeted in papers that he has written, most published in obscure, nonmainstream journals or conference proceedings. At this point, approximately eight of his 

papers have been in the literature for at least ten or more years old, yet his revolutionary 

revelation has never found its way into mainstream medical or scientific journals. 

It has also never made it into any of the most authoritative consensus documents, such 

as the World Health Organization (WHO) and the Institute of Medicine, National 

Academy of Sciences (IOM/NAS) publications on wet damp indoor spaces. Although 

many of Dr. Shoemaker’s papers were available by the time the WHO document was 

published, there are no references within it to Shoemaker or to this “CIRS disease.” Dr. 

McMahon cites extensively from the WHO document and from another, the Government 

Accountability Office (GAO) document of 2008, which he claims supports him and Dr. 

Shoemaker. However, neither document mentions any of Dr. Shoemaker’s 

“groundbreaking research,” cites any of his papers, or contains any discussion 

whatsoever of this disease “CIRS,” which is the centerpiece of Dr. McMahon’s long 

report in the Beckemeyer matter. Dr. McMahon’s notions, methodologies and diagnosis, 

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a clone of the Shoemaker beliefs, are neither generally-accepted, nor scientific 

knowledge, nor reliable. 

Dr. McMahon’s report employs all of the well-recognized rhetorical flourishes of the selfpromoter in any area of endeavor. It touts his and Dr. Shoemaker’s thousands of patients 

experience, denounces his enemies as ”naysayers” and ill-informed troglodytes who are 

in the pocket of special interests and uses all manners of tangential “evidence” to 

support his position. Boasting of thousands of patients is the technique of the practitioner 

who is trying hard to convince the world of his miraculous breakthrough. If his notions 

were generally-accepted, however, would that be necessary? One would not expect a 

diabetologist to crow about his 3000 diabetic patients or a cardiologist to brag about the 

5000 patients he has treated with Lipitor. Considering the potential number of wet/damp 

buildings, homes and cars and the frequency of the genetic susceptibility that Dr. 

McMahon claims, hundreds of thousands of people should be suffering from this 

devastating and debilitating chronic disease and the medical community should have 

long recognized this critically important new disorder. If innumerable individuals like Ms. 

Beckemeyer were falling victim to illnesses from this CIRS, the medical community at 

large would have embraced, or at least considered, that possibility. Are all conspiring 

with homeowner’s or auto insurers or landlords? Dr. Shoemaker has been pushing his 

belief and writing about it for nearly twenty years. The simple and obvious answer is that 

Drs. Shoemaker’s and McMahon’s “disorder” and its so-called confirmatory diagnostic 

testing are scientifically bereft. 

Nowhere in the GAO report which Dr. McMahon cites does it say that we now know of an 

inflammatory disease described by Dr. Ritchie Shoemaker known as “CIRS” or “biotoxin 

illness” or “mold illness” or any other, which produces widespread injury because of a 

chronically over-reactive innate immune system. In fact, that 61 page document which 

Dr. McMahon relies upon extensively contains not one mention of CIRS, of him or of Dr. 

Shoemaker. 

The WHO report discusses many possible mechanisms which might account for 

symptoms associated with exposures to WDB’s. Within this hypothesized group are 

included possible immunological mechanisms and inflammatory mechanisms. Dr. 

McMahon and Dr. Shoemaker, have elevated these preliminary considerations by 

proclaiming them established fact and claiming that this validates their idiosyncratic 

“disease” “CIRS.” In fact, WHO considers many possible toxicological mechanisms 

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including: Immunostimulation and Immunoglobulin E-mediated allergies; Cytotoxicity 

and Immunosuppression; Autoimmunity; and Irritation (pp84-89). These postulated 

mechanisms underlie current theories and animal research, but are far from accepted, 

established answers to the human health effect questions. In the summary of that 

section, the WHO report says: “The mechanism by which non-infectious microbial 

exposures contribute to adverse health effects associated with indoor air dampness and 

mould are largely unknown.” (p 90) 

By contrast, Dr. McMahon would have us believe that the mechanism is clear and 

resolved. It is his disease “CIRS,” which explains it all, yet that term was not mentioned 

once in the WHO report. Thus, Dr. McMahon’s note that “‘immunologic aspects’ of 

illnesses and symptoms associated with WDB are considered by WHO,” is true, but it is 

not true to say that they were “emphasized” to the point of being definitive, as Dr. 

McMahon has suggested. Furthermore, “immunologic mechanisms” is a very broad 

category. Suggesting that such a category is the equivalent of the Shoemaker/McMahon 

unrecognized disease “CIRS” is highly misleading and flat out wrong. 

Dr. McMahon claims that this disease, so-called “CIRS,” is an immunological disorder. 

As noted earlier, it is not recognized by mainstream immunologists or the many thousand 

members of the American Academy of Allergy Asthma and Immunology (AAAAI), the 

official AMA recognized body of immunologists. Furthermore, one wonders why, if this 

disorder is an immune system disease, Dr. McMahon doesn’t refer Ms. Beckemeyer to 

an immunologist. He, after all, is a pediatrician. 

A key to Dr. McMahon’s diagnosis of this CIRS is laboratory testing for a variety of 

parameters which he claims, when taken together, establish the diagnosis. To optimize 

the so-called “abnormals,” he creates his own normal values which, in some instances, 

differ from those of the laboratories. When Dr. Shoemaker was challenged years ago 

about his “normal” value for MSH which differed from the laboratory’s norm or reference 

range, he asserted that the low end of their reference range was “skewed by all of his 

patients’ ” abnormally low values. Dr. McMahon has done exactly the same thing in his 

Beckemeyer report. The fact is that both major commercial laboratories, Quest and 

LabCorp have an MSH reference range [range of normal values] that start at zero and, in 

the case of LabCorp, range from 0-40 and, in the case of Quest, range from 0-100. 

LabCorp is the lab Dr. McMahon used. He insists that the norm should be greater than 

35; thus, Ms. Beckemeyer was abnormal at 5. In other words, he made up his own 

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normal to fit his own case definition. According to both these laboratories, her MSH was 

normal. 

He did the same thing for the ADH determination which he says was abnormal at Ms 

Beckemeyer’s level of 1. The laboratory which performed the test, LabCorp, reports its 

normal as 0-4.7. Dr. McMahon says the normal range is 1.3-8 making Ms. Beckemeyer 

abnormally low, according to him, but normal according to the testing laboratory. 

Thus, at least two of these key tests that he relies upon were, according to him, 

abnormal. His assertion is contradicted by the reference standards of the laboratory 

which performed those tests and found them normal. 

It is axiomatic in toxicology that the dose makes the poison. Dr. McMahon rejects this 

bedrock toxicological axiom. The reason is that he never has any idea of the nature or 

extent of his patients’ exposures. Thus, whatever the exposure, it was, according to him, 

sufficient. So by Dr. McMahon’s logic, the mycotoxins in our daily diet would have to be 

equally causal or, at least, could not be ruled out as the cause of the alleged disease in 

these individuals like Ms. Beckemeyer. Dr. McMahon’s version of toxicology would 

make commonly-used Botox an invariably lethal substance since, in its undiluted form, 

botulinum toxin is an extremely potent and lethal agent. 

In order to avoid evaluation and criticism of his CIRS disorder by toxicologists, Dr. 

McMahon claims, in his report, that it is not a toxicological disease, but an immunological 

one. However, in a paper which he wrote in 2017 and references in this report, he 

says:“In all patients (sic, CIRS patients) environmental exposures to biologicallyproduced toxins trigger innate immune cytokine overproduction... “ In other words, he 

says in this paper, as he and Dr. Shoemaker have said many times, that their claimed 

“immune system disease” is the result of a toxic exposure. 

In an attempt to enhance the respectability and acceptance of his “disease” “CIRS,” Dr. 

McMahon claims that there exist 100,000 references on Systemic Inflammatory 

Response Syndrome. That disorder (SIRS) is indeed coded in the ICD-9 and ICD-10, as 

he notes. However, SIRS has nothing to do with his CIRS. SIRS is a code reserved for 

severe multiorgan-system disease and is used predominantly in patients in ICUs or 

trauma centers. 

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Dr. McMahon quotes the “Policyholders of America‘s Research Committee Report on 

Diagnosis and Treatment of Chronic Inflammatory Response Syndrome caused by 

exposure to the interior environment of water-damaged buildings (2010),” as the most 

comprehensive paper on biotoxin-related illness to date. He claims that it shows that the 

world’s academic community recognizes this disease. It does nothing of the kind. It is a 

manifesto written by Drs. McMahon and Shoemaker, espousing the same positions 

promulgated in this report regarding Ms. Beckemeyer. The site “Policyholders of 

America” is devoted to “mold sufferers” and their supportive physicians. There is nothing 

academic about it. 

Dr. McMahon, and Dr. Shoemaker before him, treat their “CIRS” patients with 

cholestyramine (CSM) and Welchol, drugs which are marketed to reduce cholesterol 

levels, but have largely been replaced by more effective agents such as statins. They 

use these allegedly to bind mycotoxins in the GI tract, but how supposedly-inhaled 

mycotoxins get to the GI tract awaiting binding by these drugs is unclear to me and to 

other toxicologists. Furthermore, Dr. McMahon makes a major issue about why ingested 

mycotoxins pose little risk because they are digested, broken down and rendered 

inactive in the GI tract. If that is so, why would he need to remove them with CSM or 

Welchol? Additionally, he states that mycotoxins are not the primary issue, but only one 

of many. 

Despite that, he claims that his patients improve after being treated with this agent which 

allegedly eliminates mycotoxins. Lastly, as I pointed out earlier, any theoretically-present 

mycotoxins from the car at issue would have been long gone from the body by the time 

Ms. Beckemeyer received the agents in early 2017. The inconsistencies between the 

alleged efficacy of CSM and Welchol and Dr. McMahon’s various theories are enormous 

and irreconcilable. 

For all of the above reasons, Dr. McMahon’s opinion in this case is far outside the 

mainstream of medicine. It is not generally-accepted and is scientifically unreliable. 

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CONCLUSIONS 

Nothing in these records—medical or environmental testing—indicates a problem with 

this car or a disorder in Ms. Beckemeyer having anything to do with her car. Her ailments 

and symptoms have clear alternate explanations. There was no temporal connection 

between those and her use of the car. There was no in-car exposure to the alleged 

causal agents. Her primary experts have used unconventional, unaccepted 

methodologies and diagnoses to assert, incorrectly, a causal relationship. These 

opinions are expressed with scientific and toxicological certainty.

Ronald E Gots, MD, PhD, DABT December 1, 2018 

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